A Nation Descends into Violence

By Mathieu von Rohr

The Mexican government has been using the army to fight the nation’s drug cartels for about four years. It isn’t working. Some critics say the army is part of the problem, even if the occasional mission removes a kingpin. But President Felipe Calderón has no one else to trust.
Ivana García didn’t flee when two headless bodies were found in front of the city hall, nor did she leave when a body without arms or legs was hanging above a downtown square. But when fighting erupted on the street in front of her house, when mercenaries working for the drug cartels began firing their Kalashnikovs from armored vehicles, and when house-to-house skirmishes went on for hours, as if Ciudad Mier were a town in Afghanistan, not bordering the United States, she had no choice but to flee. In fact, almost the entire population, about 6,000 people, left Ciudad Mier. When they realized there was no one to protect them — no government, no army — they packed their belongings and left their homes.
Ciudad Mier used to be an inconspicuous Mexican municipality on the Rio Grande River, consisting of a colonial center and a few rectangular blocks of houses. Now it is known throughout the country as a ghost town — one of those symbolic places that exist all over Mexico. Each of these towns can tell the story of a nation descending into violence.
Horrific, but Commonplace
One of them is Ciudad Juárez, where more than 3,000 murders were committed this year alone, making it the most violent city in the world. Criminals battle each other in broad daylight in the resort town of Acapulco. In the village of Praxedis, a 20-year-old woman became police chief because no one else dared to accept the job. On a ranch in northern Mexico, a 77-year-old man shot and killed four of the gunmen who had been sent to kill him, only to be murdered by the rest. He was celebrated as a hero. Horrific news reports have become commonplace in Mexico. Some 29,000 people have died in drug wars within the past four years, and this year the number of killings doubled to about 12,000. An astonishing 98 percent of the crimes committed in Mexico remain unpunished.
It has been four years since President Felipe Calderón came to office promising to defeat the cartels, multibillion-dollar organizations that supply the United States, the world’s largest drug market, with cocaine, crystal meth, heroin and marijuana. Calderón mobilized 45,000 soldiers and federal police officers for his campaign. There was no one else he could trust, including local police forces and governors. The army is his only reliable tool.
There have certainly been many spectacular arrests. Famous drug kingpins were arrested or killed, including the leader of the “La Familia” cartel, who died earlier this month. But have these successes weakened the drug cartels? There are few indications that this is the case.
At first, many citizens saw the violent excesses as the beginning of a necessary evil. Recent opinion polls, however, show that a majority now opposes the government’s strategy. The newspapers are filled with reports of kidnappings, blackmail and beheadings. There are blogs that specialize in publishing photos of severed limbs taken with mobile phones.
It is easy to picture the savagery with which this war is being waged. But it is more difficult to understand why the violence doesn’t stop, what its causes are and what can be done about it. Could the legalization of drugs be the answer, as some experts suggest? Or maybe more border controls? Would a new national police force and a reform of the government solve the problem? Or is it best to simply leave the cartels alone, which for years was the government’s policy?
These are the questions that Mexico is asking itself in 2010, the 200th anniversary of the beginning of its war of independence. The filmmaker Luis Estrada has given his native country a bitter film for its anniversary: “El Infierno” (Hell). It is the portrait of a world consisting of nothing but narcos, whores and corruption. “We have a national problem, and it’s called impunity,” says Estrada, a soft-spoken man with glasses and a gray beard. “People who break the law aren’t punished. That’s why many believe that honesty doesn’t pay. We Mexicans are in hell, that’s for sure. I just don’t know which pit of hell it is at the moment.”

A Ghost-Town Census

It is a hot day in late November, and Ivana García has screwed up the courage to return to Ciudad Mier for the first time since she left. She walks through the abandoned streets of the town that was once hers, a 34-year-old woman in jeans, wearing gold-plated earrings and carrying a plastic purse. The army has hired her to count the number of people still living in the town, but there are few left to count. They offered her 700 pesos, or €42 ($55) a week. She was afraid to take the job, but she needed the money to pay the exorbitant rent for her apartment in Ciudad Alemán, the next town, where she now lives.
García and two other young women walk from house to house, knocking on doors that no one opens. The few people they encounter couldn’t afford to leave or are very old. The questionnaires the women have brought along in clear plastic binders include questions about income and the remaining residents’ opinions about safety. They represent the government’s clumsy attempt to demonstrate that it still exists. Two dozen soldiers follow the women, on foot and in pickup trucks armed with machine guns, securing the streets. Most of the houses they pass are riddled with bullet holes. Starving dogs slink across the dirt roads.
Some 400 people still live in a refugee camp in the next town. They have been there for more than four weeks, and most do not want to return to Ciudad Mier. They say that when the army withdraws, in a few weeks or months, the whole thing will start again.

‘Some States Remind Me of Afghanistan’

Ciudad Mier is in the northwestern panhandle of the state of Tamaulipas, a narrow strip of land bordering Texas. It is one of the areas some experts compare to failed states. One expert, Edgardo Buscaglia, who specializes in drug-related organized crime, is currently working in Kandahar, Afghanistan. In a telephone interview, he said he had stopped using the expression “Colombianization” to describe what’s happening in Mexico. “There are now areas in some states that remind me of what I see here in Afghanistan,” he said. Narcos, or drug dealers, control about 12 percent of Mexican territory, according to some estimates.
There are no longer any police officers or mayors in large sections of Tamaulipas and the northern part of Nuevo León, two states in northeastern Mexico. They were either killed or have fled, and now the narcos operate checkpoints on the streets.
The two drug cartels that are at war in Tamaulipas were allies until a year ago: The Gulf cartel and its paramilitary arm, the Zetas. Here, the term drug war isn’t just a metaphor for a series of gang murders, as it is in Ciudad Juárez. Instead, it describes a level of almost military violence between cartels, which send armies of adolescent “sicarios,” or killers, into battle, often better equipped than soldiers in the Mexican army.
A Code of Silence
The mayor of Ciudad Mier, a perfumed man who wears his shirt open at the chest, is standing in the town hall. He says he cannot give an interview, or else — and he runs his finger across the neck of this reporter to demonstrate what could happen to him if he did. The citizens of his town want to talk, but they also want to remain anonymous. There has always been drug smuggling here, they say, and the Zetas have always been in power. In a town where there was hardly any work for young men, the drug lords were able to entice recruits with the promise of fast money, cocaine and the prettiest girls.
Their villas, built in the ornamental narco style, with gilded railings and decorative columns, are still standing. The owners fled when the Zetas broke with the Gulf Cartel, and today they live in the United States or in Mexico City. There was a victory parade of sorts when the Gulf Cartel captured the town on Feb. 22. A motorcade of 60 SUVs and pickup trucks carrying heavily armed fighters drove into the streets of Ciudad Mier.
They killed five police officers that had worked for the Zetas, beheaded a police chief and a female drug dealer, and laid out the remains on the village square. After that, say local residents, the new gangs were friendly. Unlike the Zetas, they said hello to people on the street. But the fighting wasn’t over yet. In mid-October, Ivana García found a dead Zeta fighter on the street. She had never seen the man. He must have been a mercenary from somewhere else, she thought, a young man wearing brown trousers and with a muscular torso. He was lying in a pool of blood.
On Nov. 2, the Zetas returned, driving 40 heavily armored SUVs with gun barrels poking out of their sides. The ensuing battle wore on for days and nights, killing many, and leading to the departure of residents and the arrival of the army.
The soldiers stalking along behind García as she walks through Ciudad Mier hold their rifles at the ready, as if someone could shoot at them at any moment. They storm suspicious-looking houses. The hooded commander says that he doesn’t know whether all of the bandits were driven out. The government of Tamaulipas claims the town is now safe and has called upon the local population to return to their homes. By the end of her first day of work, García has counted six inhabited houses.

‘Narco Saints,’ Money and Girls

Almost no other business in the world is as lucrative as the drug trade. The United Nations estimates that $72 billion (€55 billion) worth of drugs are sold each year. Cocaine is the most profitable of all drugs. Cocaine paste costs $800 a kilo (2.2 pounds) in Colombia, and in Chicago a buyer pays $100 a gram. The price goes up by 12,400 percent along the way. Mexican cartels smuggle an estimated 192 tons to the United States each year.
There are seven drug cartels in Mexico. While alliances often change, almost all the groups have their origins in Sinaloa, a state on Mexico’s west coast known as the birthplace of the narcos. The area is home to Joaquín Guzmán, also called El Chapo, the leader of the Sinaloa cartel. He’s the world’s most glamorous drug lord, as evidenced by the fact that Forbes includes him on its list of the wealthiest people in the world. (No one, however, has access to his bank statements. Culiacán, the capital of Sinaloa, is the Rotterdam of the cocaine trade, the place where prices are set. It lies between the Pacific Ocean and the green hills of the Sierra, where farmers grow marijuana and opium poppies. It is a friendly-looking city of 600,000 with whitewashed homes, though Culiacán has the second-highest murder rate in the country.
For the past two years, El Chapo has been battling his former allies, the Beltrán Leyva brothers. It is a war of kings, and when author Elmer Mendoza tells the story, it sounds like a Greek tragedy. Mendoza, 61, is a bearded, soft-spoken man born in Culiacán, where his crime novels are set. He portrays this world so realistically that some accuse him of being a narco author.
“I’ve been hearing their legends since I was a child,” he says. “These people had bigger houses and the most beautiful girls, and sometimes songs were even written in their honor.” There is a folk hero in Sinaloa, Jesús Malverde, who is known as the “narco saint,” a Robin Hood who took from the rich and gave to the poor. Many believe that El Chapo is his revenant, a hero of the people. Mendoza says that what is happening to his country is terrible. “But as an author, I admire people who do extraordinary things. Isn’t there something epic about bringing a shipment of cocaine from Medellín to Los Angeles?”

Culiacán, Ground Zero

The gang war that originated in Culiacán and eventually engulfed half the country began on Jan. 21, 2008, when the army arrested the drug lord Alfredo Beltrán Leyva, known as El Mochomo, in a simple house in the Tierra Blanca neighborhood. Did El Chapo tip off the army? Convinced that he did, the Beltrán Leyva brothers brought Zeta mercenaries into the city and began killing everyone who worked for him, including police officers, judges, politicians and journalists.
These people had believed that El Chapo would protect them, but then the Zetas shot and killed one of his sons in a shopping center parking lot. “People began to doubt their hero. They were afraid,” says Mendoza. “Isn’t that beautiful, from a purely literary point of view?” The author stands in the cemetery of Culiacán, the narcos’ final resting place. The graveyard is a city of marble and domed mausoleums known as Jardines del Humaya. It’s the size of several football fields, and it continues to grow.
They’re all buried here, side-by-side — the drug lords and their rivals, their children and the 18-year-old killers who, at the end of their brief lives, were at least able to afford some measure of splendor. The larger than life-sized portraits of young men with hard features hang in giant, 10-meter-tall mausoleums, next to pictures of their girlfriends and their weapons.
Nowhere in Culiacán is the power of the drug cartels as palpable as it is here. This is their temple city, and anyone who desecrates their graves can expect to receive death threats from the scouts and guards before long.
The Absent Government
Why isn’t El Chapo, the most powerful of all drug lords, in prison? He’s been living in a secret location for years. Is the government incompetent, or is it protecting a cartel? Many credible people believe the government has an agreement with the drug lord. Some believe that it is trying to solve the violence problem by handing over the drug trade to one cartel. In a recently published book, investigative journalists Anabel Hernández claims that former President Vicente Fox allowed El Chapo to escape from a maximum security prison in 2001 in return for a payment of $20 million. According to Hernandez, the Calderón government knows his whereabouts, but instead of arresting him it is eliminating his enemies.
There are many rumors and conspiracy theories in Mexico. What is perhaps most remarkable about them is what people believe their government to be capable of. They have little faith in federal institutions, which are weak. Mexico has been a real democracy only for the last 10 years, after being controlled for 70 years by a single party, the Institutional Revolutionary Party (PRI). The PRI protected organized crime, but also held it in check.
President Calderón declared war on the cartels, but he lacked the necessary tools. The police are corrupt at almost every level, and in some communities they’re identical with the ruling cartel, which helps to explain why so many municipal officers are murdered. The justice system is also viewed as corrupt. There are no independent prosecutors, and charges are never brought in many cases, because they are handled poorly or because defendants buy their way out.
The army is the only institution that Calderón can trust, although the story of Ciudad Mier reveals how ineffective it is. Soldiers can occupy a territory, but they cannot investigate or penetrate the structures of a cartel. According to security consultant Alberto Islas, a cartel is like a logistics company with a military arm. Instead of scrutinizing the structures, the government becomes embroiled in skirmishes with 18-year-old foot soldiers.

A ‘Decapitation Strategy’

The government has hardly any functioning investigative agencies. Mexico receives key information from US government agencies like the Drug Enforcement Administration (DEA). The Americans provide the army with information on the whereabouts of drug lords, allowing the Mexican soldiers to capture or kill them. This “decapitation strategy” produces reports of successes, but no real success. The cartels quickly replace their leaders.
The massive deployment of the military also poses a threat to society. Throughout Mexico, soldiers have been accused of hundreds of cases of human rights violations and torture, even murder. Critics say the large number of military operations is responsible for the violence in the first place, because it has destroyed equilibriums and triggered turf wars across the country.
The army cannot solve Mexico’s real problems — poverty, lack of education and weak government. Most experts agree on how Mexico ought to liberate itself. The only question is whether anyone has the political power to do it.
The country is a long way from being a stable democratic society, says Luís Astorga, a social scientist in Mexico City. The biggest challenge, according to Astorga, is to create a constitutional state strong enough to resist the power and money of the cartels. This requires nonpartisan political will; but Astorga says representatives of the three major parties all have their hands in the drug business. Astorga says he does not believe the government is cooperating with a cartel. But as long as there are no independent judges, he believes, there will always be rumors and speculation.
Many yearn for simple solutions; they believe in a return to the days when the cartels were allowed to do as they pleased. Even some high-level politicians say privately that the problem is drug consumption in the United States, and that it’s time to legalize marijuana. But the cartels are involved in up to 22 other types of crimes as well, including film piracy, human trafficking and extortion.
Vanda Felbab-Brown of the Brookings Institution in Washington says that bringing in the army was unavoidable, but that what is important now is to finally develop a functioning police force. Mexico does have plans for a national police reform, but they are making slow progress Edgardo Buscaglia, the expert on drug-related crime, and his team studied 17 countries that have successfully fought organized crime. He says that all of them took the same four important steps.
• First, says Buscaglia, comes a reform of the judicial system.
• Second, laws are needed to fight corruption in politics, because 70 percent of all election campaigns in the country are partially financed with drug money.
• Third, Mexico must investigate the flow of funds from the drug trade into the economy. According to Buscaglia, 78 percent of the Mexican economy has ties to the drug cartels.
• Finally, social programs are needed for young people, as the Colombian city of Medellín has demonstrated. Such programs are meant to turn young people’s attention away from a life working for the cartels — a life that can end quickly.

Taking Back Mexico, With PowerPoint

There are many ideas, but who is there to implement them?
Javier Treviño, the lieutenant governor of Nuevo León, has a plan that consists of a large number of PowerPoint slides. He wants to eliminate violence in Monterrey, the city where he lives, and in the surrounding state. Treviño, a short man with a moustache and glasses, speaks English with an American accent. He studied at Harvard, then worked as a diplomat and later in private industry, before he entered politics. He’s one of the few people in Mexico who have not lost faith in the ability of politics to shape the country.
Perhaps it is also a question of honor for Monterrey, Mexico’s wealthiest city. Located in the northeastern part of the country, 140 kilometers (88 miles) south of the US border and surrounded by mountains on three sides, Monterrey resembles an American city, with its glass and marble office towers. Many of the country’s most important companies are headquartered there.
It came as a shock to the city’s affluent citizens when, at the beginning of the year, members of the Zetas and the Gulf Cartel suddenly started shooting each other on their streets. The battle being waged in Ciudad Mier had moved to the middle of Monterrey, an economic center that was always immune to chaos elsewhere in Mexico. Many of the wealthy left town, or even the country — including the publisher of the country’s most important newspaper, La Reforma, who fled to Dallas.
Treviño is proud of the 29 slides in his presentation, which he shows to every visitor. His plan includes all the elements the think tanks have deemed necessary: social programs and reforms of the judiciary and the criminal code. The state of Nuevo León has also established a statewide police force that it hopes will finally be clean and effective. The officers will be required to take regular lie-detector tests. They will be paid well enough to end their dependence on bribes; they will receive scholarships for their children.
Nuevo León is to become a model for all of Mexico, says Treviño. It sounds like an effective plan. And who knows? It might even work. Once it is implemented, there might be at least one state in Mexico with a functioning police force. Treviño wants to make a start by strengthening institutions and society, and what better place to launch such an effort than Monterrey, the most advanced city in the country?
He continues clicking through his slides. The next one shows the country’s highway network. Two of the five main highways in the north are colored dark red, which means that they are safe for travel. The goal for 2011, says Treviño, is to make the three other highways safe as well.

Translated from the German by Christopher Sultan

Source: www.spiegel online 23rd Dec. 2010

Marijuana used for medical purposes has the same long term effect on the user as marijuana used for recreation. Marijuana use can cause impairment of short-term memory, attention, motor skills, reaction time, and the organization and integration of complex information. Marijuana use alters perceptions and creates time distortion and can cause drowsiness and lethargy. Heavy marijuana use can cause apathy, decreased motivation, and impair cognitive performance and can cause mental health problems. Employees who use marijuana off-duty are still effected by it. Impaired cognition that can cause lapses in judgement can remain for a long period. Memory defects can last as long as six weeks. See: Abbie Crites-Leoni, Medicinal Use of Marijuana: Is the Debate a Smoke Screen for Movement Toward Legalization? 19 J. Legal Med. 273, 280 (1998) (citing Schwartz, et al., Short- Term Memory Impairment in Cannabis-Dependent Adolescents, 143 Am. J. Dis. Child. 1214 (1989)

Employers may be liable for the actions of employee who use marijuana especially those employees in safety sensitive positions. The more chronic the use of “medical” marijuana the higher the risk.

VIOLATIONS OF FEDERAL LAW

Will employers have to accommodate marijuana use that violates federal law? Marijuana, remains illegal under federal law because of its “high potential for abuse,” its lack of any “currently accepted medical use in treatment in the United States,” and its “lack of accepted safety for use … under medical supervision.”Gonzales v. Raich, 545 U.S. 1 (2005); United States v. Oakland Cannabis Buyers’ Cooperative, 532 U.S. 483 (2001)

IF THIS BILL PASSES “MEDICAL” MARIJUANA WILL RESULT IN MORE MARIJUANA USE AMONG EMPLOYEES

As consumers we all pay for lost productivity and job-related accidents in the final costs of the produced goods and higher insurance premiums due to workplace accidents. Drug using employees are not as safe. They are 3.6 times more likely to be involved in a work-related accident than their non-using employee, and 5 times more likely to file workers’ compensation claims. As many as 50% of all workers’ compensation claims may involve substance abuse.[ EN1]

The U.S. Postal Service did a study that showed that substance abusers have 55% more accidents, experience 85% more on-the-job injuries, and have a 78% higher rate of absenteeism when compared to non-substance abusing employees.[ EN2] A report by the National Safety Council claimed that 80% of those injured in serious drug-related work accidents are not the drug using employees, but innocent employees and others.[ EN3]

Drug using employees commit workplace crimes. There is a very significant statistical correlation between drug use and criminal conduct.[ EN4]

Substance abuse also causes:

Domestic and financial difficulties for employees;

Poor judgment in employment decision making;

Potential embarrassment to the employer as a result of off-duty conduct, which may be publicized, including criminal charges, diversion of supervisory and managerial time;

Damage to company property; and

Time devoted to discipline and grievance matters.[EN5]

While the studies vary somewhat, it is clear that there is substantial substance abuse in the workplace and it has a powerful negative impact on our economy and productivity. The increased use of “medical” marijuana will magnify all these problems.

References

[EN1] Current, The Truth About Drug Testing: Answers to the Questions Everyone Is Asking, p. 3 (1st Ed., Fort Lauderdale, FL, 1998).

[EN2] “Pre-employment Drug Testing: Association with EAP, Disciplinary, and Medical Claims Information” U.S. Postal Service, Personnel Research and Development Branch, Office of Selection and Evaluation, July 1992.

[EN3] Wisotsky, The Ideology of Drug Testing [Ideology of Drug Testing], 11 Nova L Rev 763, 768 (1987).

[EN4] See Stewart, Proof Positive of Drug Link to Crime, Wall St J, May 28, 1987, at 26, col 3.

[EN5]Alcohol & Drugs in the Workplace: Costs, Control and Controversies, A BNA Special Report [Costs, Control and Controversies], 7 (Bureau of National Affairs, Washington, D.C. 1986)

Source: Attorney David Evans in email to Drug Free America Foundation June 2010

In the 15th Judicial District of Louisiana

Introduction and Review of Relevant Literature

During the second half of the twentieth century, two opposing views of drug use and abuse began to coincide. First, the disease concept of drug abuse and addiction became commonplace, as seen in the action of Congress passing the Comprehensive Alcohol Abuse and Alcoholism Prevention, Treatment and Rehabilitation Act in 1970. This led to the designation of monies for federal treatment programs, while simultaneously major health insurers began to include treatment plans for same in their coverage (Lemanski,2001). As a result, the numbers of treatment facilities increased dramatically.

Second, there was a simultaneous increase during this time period in the criminalization of drug use, with harsh penalties attached to drug related crimes (Andrews et al, 1990). The consequence was a growth in the criminal justice system’s control over drugs, resulting in a dramatic increase of drug-related incarcerations (Lock et al., 2002). Recognition of the futility of the effort to use entirely punitive measures, and overcrowding in correctional facilities and court systems has led to a search for viable alternatives. Into this abyss has entered the drug court treatment program.

The first such program began in Miami in 1989, and by the year 2000, more than 650 drug courts were in existence across the country (Dechenes et al., 2002). A decade later, there were 2,038 fully operational drug courts in the United States and 226 that were in the planning stages, as of July 2009 (Office of National Drug Control Policy, 2010). The U.S. Department of Justice, in association with the National Association of Drug Court Professionals has defined ten key components for the establishment of drug court programs, though some variation exists from program to program.

Specifically, eligibility and suitability requirements vary, as well as what types of treatment are offered. Essentially, drug courts are a compromise between punitive and treatment strategies (Dorf and Fagan, 2003). These programs combine the extensive supervision of punitive models of justice with the treatment model of drug addiction to seek a reduction in criminal recidivism and improve the life chances of participants (Belenko, 1998; Gottfredson et al., 2003). Empirical evidence has supported the view that recidivism is reduced, as well as the corresponding monetary spending on drug cases throughout the justice system (Banks et al., 2003; Gottfredson et al., 2003; Hora et al., 1999; Kalich and Evans, 2006).

The evaluation of the effectiveness of drug court programs has been necessitated by the tremendous proliferation of such programs across the United States. This paper is a follow-up report of one such program, upon the request of the program particularly due to the amount of time that has passed since program inception and also due to the
implementation of a particular type of therapy into the program (moral reconation therapy). At a time when drug court monies may be looked to for utilization in other budgetary locations, it is especially important to know whether drug court participants fare better than non-participants who qualified for drug court but refused to participate
and were instead assigned to either straight probation supervision or to a modified educational probation supervision. In only this way is it possible to really begin to address any possible savings in terms of criminal recidivism and therefore monetary and other costs. The report detailed below also examines the perceptions of drug court
graduates toward the drug court program, in order to investigate the meaning and impact of the program on the lives of its participants. The most rigorous evaluations of drug court programs compare drug offenders who enter the program to those who qualified but chose not to enter the program. Additionally, rigorous studies include those that randomly assign clients to receive drug court services. These have consistently indicated lower recidivism rates for drug court participants and graduates (Deschenes, et al., 1995; Finigan, 1998; Gottfredson et al., 1997; Peters and
Murrin 2000, Wolfe et al., 2002).

The two primary components of all drug court programs are intensive supervision and drug treatment. The implementation of these two components varies across jurisdictions. Intensive supervision typically combines elements such as small caseloads for probation officers and frequent court appearances and urinalysis testing. Treatment typically fuses several well documented types of drug abuse treatment programs. Very few studies have attempted to differentiate the impact of these two components on drug court participants and even fewer have specifically focused on long-term effectiveness. However, they do suggest the need for further evaluation of drug court outcomes, with particular attention to identification of predictors of those outcomes.

Background of the F.I.S.T. Drug Court Program and Parameters for this Study

The general criminal justice system in the 15th Judicial District is actually one which
utilizes two types of drug courts via what is known as Tract 1 and via the F.I.S.T.
(Focused Intervention Through Sanctions and Treatment) Drug Court Program.
However, of the two, only the F.I.S.T. Drug Court Program is eligible to receive federal monies from the 1994 Crime Act, and it is restricted further by that Act to accept only defendants with drug-related crimes and no history of violent offenses. Tract 1 processes all other drug defendants. Thus, Tract 1 remains the traditional adversarial drug tract, with the F.I.S.T. drug court technically under that tract as a special non-adversarial court to which eligible non-violent felony offenders may be referred (if identified as eligible by the Assistant District Attorney assigned to Drug Court).
The prosecutor is obliged to prosecute only when there is proof of guilt. Consequently, prior to declaring a defendant eligible, he is to check all available information to insure the appropriateness of prosecution. Eligibility also depends upon the lack of exclusionary factors. Exclusionary criteria for entry into the program include: violent criminal history and conviction of four or more felonies. Misdemeanor offenders are usually excluded unless they aggressively seek inclusion.

Upon referral to the Drug Court by the prosecutor, potential participants are then
clinically screened for suitability using the Substance Abuse Subtle Screening Inventory (SASSI3), the Substance Abuse Questionaire, and a personal interview. Clinically, exclusionary criteria for entry into the program include: mental illness that has not received clearance from a doctor indicating participation will not negatively affect the illness (for example, no schizophrenia diagnoses are accepted into the program because the clinical structure of the program has been deemed unacceptable for said diagnosis). Acute health problems are excluded on a case-by-case basis,

depending on the level of function present. If deemed suitable, the offender is referred for a consultation with the public defender or a privately retained defense attorney. After consultation with a defense attorney, if the offender is interested in participating in the drug court program, the defense attorney notifies the F.I.S.T Drug Court prosecutor, who files a Bill of Information. Some offenders choose to participate in drug court as a condition of probation (after admitting to the crime and receiving a suspended sentence), while others choose to remain in Tract1 and go to trial, or plead guilty and receive a suspended sentence with less intensive conditions of probation. Still others opt to participate in drug court as a condition of bond, while awaiting motion hearings in Tract 1. If found guilty in Tract 1, the probationers must attend drug education classes, monthly meetings with the judge, and comply with periodic random drug screens. One year of sobriety completes the program for these individuals.

However, if the random test is positive for drugs, drug treatment is ordered (drug
education has proven insufficient) and graduated sanctions are imposed. At the third
positive drug screen, and pending a positive determination of both eligibility and
suitability for Drug Court, probationers in Tract 1 (as of August 2002) will be given a
coerced choice: participate in drug court or go to jail for one year. This choice will not
be offered, however, if the defendant was offered drug court before entering Tract 1 and rejected that treatment option. Such rejection is final, and is justified by the F.I.S.T. Team on the grounds that although addiction to drugs is an illness, the choices individuals make also have consequences. The goal of such a stance is to encourage responsible decision-making; therefore, if an addict chooses against treatment, he/she must endure those consequences. Thus, at this stage in Tract 1, if the choice of entering the F.I.S.T. program has never before been offered, and if the probationer chooses jail rather than treatment, upon the fourth positive drug screen, probation is revoked, and a sentence is imposed.

If, however, the probationer chooses drug court at any point, the sanctions for continued positive drug screens increase according to the F.I.S.T drug court schedule of sanctions. Unless the individual has been rearrested for another felony or violent offense, no definitive point marks the termination of a drug court client=s participation. When revocation from drug court does occur, the previously suspended sentence is reinstated, minus any reductions the probationer may have earned for compliance to program requirements up to that point.

Drug court participants who are initially offered and choose drug court must plead guilty to their crime in order to receive a suspended or deferred sentence and participate in the program as a condition of probation, the outcome of their sentence pending the successful completion of the F.I.S.T. Drug Court Program. Individuals deemed eligible and suitable can also try the F.I.S.T. Drug Court Program as a condition of bond, while awaiting the outcome of their case in Tract 1. All drug court participants have 30 days to opt out of the program and to choose adjudication via Tract 1. Incentives to remain are strong, such as dismissal of the prosecution upon satisfactory completion of the drug court program (the equivalent of an acquittal) and expungement of the charge from the participants record. Defendants in the F.I.S.T. Drug Court Program, then, are voluntary participants, who agree to comply with a number of general and special conditions of their suspended sentence with active supervised probation and treatment.
A third option also exists for drug offenders in the 15th JDC, aside from the assignment to Drug Court or Tract 1. Individuals may be deemed both eligible and suitable but refuse to participate in drug court and receive supervised probation instead. In this case, the individual must report to the probation officer, comply with random urinalyses, and otherwise not violate the conditions of his/her probation. These individuals are on Tract 3 or “straight probation.” Successful completion of probation means that probation is not revoked, nor is a sentence imposed.

Statement of Purpose
The primary goal of this evaluation is to explore the effectiveness of the F.I.S.T. Drug
Court Program at reducing recidivism rates of participants when compared to nonparticipants of varying kinds. The universe of offenders who were deemed both eligible and suitable and who were offered the F.I.S.T. Drug Court Option is the population under examination. This examination will determine whether the outcome target has been met (the number and % of participants who achieve the outcome, in this case, lower recidivism rates) for all eligible and suitable individuals, regardless of the tract to which they belong. Tests of significant differences between the tracts will also be determined between the previously described tracts: Tract 1 completers (Prevention Plus), Tract 3 completers (Straight Probation), and Drug Court Completers. In the analyses that follow, the Drug Court population is further divided into two groups, those who completed the Program prior to the introduction of MRT (Moral Reconation Therapy), and those who completed the program with the MRT component in place. All analyses are controlled for time in tract and recidivism rates are calculated from time of initial arrest for which Drug Court was offered to 6 months, 6 months to 12 months, and 12 plus months. Finally, Drug Court Alumni are interviewed about their drug court experiences.

Methods
Data were obtained from several sources: F.I.S.T. Program Records, Tract 1 Program
Records, the State of Louisiana Office of Probation and Parole, and F.I.S.T. Alumni
interviews. Only variables available for all offenders were included in these analyses.

F.I.S.T. Program records have been maintained since program inception in 1998. As
such, a list of names and identification information was available for use by the Office of Probation and Parole to locate arrest records for each individual. For some individuals no records were found by the Office of Probation and Parole,and
therefore, these individuals were excluded from the analyses due to missing information. Similarly, some participant names were on some lists and not others, or on multiple lists. In each of these cases, the participants were excluded from the analyses. All coding was double coded and entered by hand into an SPSS database in electronic format. While it is possible that some bias might be present in the resulting dataset, this is not likely, as excluded cases were statistically examined for patterns in demographics or other key variables of interest. None were identified. Descriptive statistics were performed using SPSS to produce percentages, averages, and frequencies. Additionally, tests of significance were performed using the Chi Square statistic
.
In addition, qualitative interviews were obtained from 30 F.I.S.T. Alumni who were
willing to be interviewed. The interviews were conducted in Spring 2010 via

telephone. Not all participants who were contacted were willing to be interviewed (n=5), and not all of the phone numbers were still working and accurate numbers (n=22). However, it is important to note that this information was given voluntarily, and did not take place under the supervision of any Drug Court Personnel.

Findings

Most of the sample was not re-arrested in the first six months after the initial eligible drug court arrest (79%). However, the re-arrests were nearly 3 times as many for drug arrests as for violent or other crimes (n= 362 v. 143 v. 79). During the 6-12 months after the initial eligible drug court arrest, again, 79% of the total sample was rearrested. Again, the pattern emerged of nearly 3 times as many drug re-arrests than violent or other crimes (n= 376 v. 138 v. 89). Thus, the pattern emerges that for all persons in the sample, during the first year after the initial eligible drug court arrest, most re-arrests were drug related.

However, these initial data are over-general and need to be examined more closely to
identify the makeup of each tract within the drug offending population. Specifically,
when examining the total dataset by tract, it becomes clearer that those who choose to
complete drug court are slightly older than those completing Tract 1 or Tract 3 (52% are age 26 and older v. 46% and 49%, respectively). In addition, those who choose to
complete drug court are much more likely to be white (64%) than those completing Tract 1 (54%) or Tract 3 (53%). Finally, those who choose to complete drug court are much more likely to include females (31%) than what is found in Tract 1 or 3 (15% v. 20%). This pattern of older, more white and more female participants may suggest that drug court is a more appealing choice for such a population to choose to complete, or to complete successfully.

Drug Court Completers V. Prevention Plus/Tract 1 Completers
In any evaluation of outcomes, it is important to evaluate the differences between groups for statistical significance. This component of the evaluation seeks to examine the differences between drug court completers and Tract 1 completers in terms of statistical significance. Recall that participants in drug court are subject to rigorous educational and therapeutic tools, while there is a small educational component in Tract 1. First, the data were analyzed for statistically significant differences in age, and the differences that were found were found not to be significant (chi square < .12). However, this changes when the data are analyzed according to race and gender there is clearly a significant difference between completers in Tract 1 and
Drug Court completers in that Drug Court completers are significantly more likely to be white. Likewise, there is a significant difference between completers in Tract
1 and Drug Court completers in that Drug Court completers are significantly more likely to be female.

More importantly, when examining the effectiveness of these two programs with regard to recidivism, statistically significant differences are found in re-arrest records.
Specifically, when comparing Tract 1 completers to Drug Court completers
Tract 1 completers are twice as likely to be re-arrested within the first six months than are Drug Court completers This is especially the case with drug crimes,
where Tract 1 completers are nearly 5 times more likely to recidivate a drug crime than are Drug Court completers.

Finally, when looking at long term completers of either Tract 1 or Drug Court where re-arrests occur at 12 plus months, those participants who complete Drug
Court are significantly less likely (30% v. 52%) to be rearrested after 12 months,
especially for drug crimes and violent crimes than are those participants who complete Tract 1.it is clearly significant that more completers of Tract 1 are re-arrested for drug crimes than are Drug Court completers (37% v. 20%) at this point in time. It is clearly also the case that completers of Tract 1 are significantly more
likely to be re-arrested for violent crimes than are Drug Court Completers at this time
(25% v. 12%).

Drug Court Completers V. Straight Probation/Tract 3 Completers

This component of the evaluation seeks to examine the differences between drug court completers and Tract 3 completers in terms of statistical significance. Recall that participants in drug court are subject to rigorous educational and therapeutic tools, while there is no therapeutic or educational intervention in Tract 3. First, the data were analyzed for statistically significant differences in age, and the differences that were found were found not to be significant (chi square < .45). However, this changes when the data are analyzed according to race and gender .
There is clearly a significant difference between completers in Tract 3 and
Drug Court completers in that straight probationers are significantly more likely to be
non-white . Likewise, there is a significant difference between completers in
Tract 3 and Drug Court completers in that Drug Court completers are significantly more likely to be female.

Furthermore, when examining the effectiveness of these two programs with regard to
recidivism, statistically significant differences are found in re-arrest records at all levels. Specifically, when comparing Tract 3 completers to Drug Court completers in
Tract 3 completers are nearly 6 times more likely to be re-arrested within the first six
months than are Drug Court completers (28.3% v. 5.4%, Chi square <.00).
This is especially the case with drug crimes, where Tract 3 completers are nearly 8 times more likely to recidivate a drug crime than are Drug Court completers. Likewise, straight probationers are 3 times more likely to recidivate a violent
crime than are Drug Court completers within this time period . Likewise, straight probation completers are significantly more likely at the 6-12 month
time period to recidivate, and especially to recidivate drug and violent crime when
compared to completers of Drug Court .

Finally, straight probation completers on Tract 3 are also statistically more likely to reoffend after one year than are drug court completers, and they do so with both drug and violent crimes .In sum, then, Drug Court completers have a better recidivism rate at all times and for all crimes, especially drug and violent crimes in comparison to both groups of eligible and suitable persons who were offered drug court during the same time period. These other groups, tracts 1 and 3, are interesting comparisons further in that the former offers some prevention education and seems to have a better rate of recidivism than does the latter which offers no prevention education and which has the worst rate of recidivism.

Certainly these findings offer strong support for the continued use of drug courts and
prevention education to reduce recidivism rates in the communities where they are
provided.

Drug Court: Pre v. Post Moral Reconation Therapy

As part of this evaluation, analyses were conducted within the Drug Court Completer
population by further subdividing the population into those who finished the program
before Moral Reconation Therapy (MRT) was introduced (n=74) and those who finished the program after MRT was introduced in February 2005 (n=112). MRT is conducted via structured facilitated groups in order to overcome problems encountered in individual therapy for substance abusers, such as over-exploration of a client’s past and over discussion of their feelings at a particular time. MRT is a cognitive-behavioral group method which allows problems such as this to be avoided.

Furthermore, the use of MRT as a group treatment is economical and efficiently incorporates more clients with fewer hours by the group counselor. Group sessions have always been a part of Drug Court, but the MRT group is special in that it is goal oriented and present-focused. For these reasons, analyses were conducted to determine if clients receiving MRT have a lower recidivism rate than do clients receiving more traditional drug court therapies. It is important to remember, however, that regardless of the subgroup analyses, Drug Court Completers are significantly lower in recidivism than other drug crime offenders.

For the analyses between pre-MRT and post-MRT completers, the total sample of
completers (n=186) was subdivided. Each group was compared for significant
differences in age, race, and sex, and no statistically important differences in the two
groups were identified. Furthermore, time since completion of the program was
statistically controlled (as with the above analyses). Interestingly, there are no significant differences between pre and post MRT completers at time periods less than 12 months (analyses available upon request). However, over the long term, post-MRT completers appear to respond better and to recidivate less frequently than do pre-MRT completers, especially in drug and violent crimes. Thus, it seems in the short term there is no MRT advantage but over a longer period of time the advantage is statistically significant.

Qualitative Component: Drug Court Completers Perceptions of Drug Court
In this final component of the evaluation, Drug Court Completers were interviewed and asked a series of questions about their experience with drug court. Thirty interviews were obtained with detailed responses for these interviews. Each interviewee was asked the following set of open-ended questions:

1. How did you feel when you were assigned to drug court?
2. If pleased, what pleased you…
3. If disappointed, what was disappointing…
4. What was the first session like for you?
5. What do you feel worked best for you in the program?
6. Why was , best for you in the program?
7. What do you feel did not work?
8. Why do you feel did not work?
9. How did you feel when you finished?
10. If you will miss the group, why?
11. If you are just glad it’s over, why?
12. What benefits did you receive from this program?
13. Do you have any suggestions for changes to the program?

Below, a random representation of the comments given in the responses are presented in composite form for qualitative purposes.

Interview 1: I felt lucky when I was assigned to drug court; my choice was drug court or jail. I was lucky to go to drug court. What worked best for me in the program was
putting me in jail because I had never been in jail where I could not bond out and this
time I couldn’t. It’s not that drug court does not work; it’s that you don’t want it to work. If not for drug court, I would not be clean today.
Q: Do you have any suggestions for change for the program? Yes, I believe they should have more involvement with the people who graduate because I disagree with [the person] running the alumni program. She is a self admitting crack head and still drinks to this day, and if you go to NA they will tell you alcohol is a drug too. Everybody else, except for her, was very helpful to me.

Interview 2: My counselor worked best for me. He enlightened me and let me know that there was life without dope and I am grateful for that. I think it worked. I have a life. I have been clean and I am grateful I have had the same job for over two years. The day I graduated I felt good, it was the first time I had finished something in a long time. I felt accomplished. I am still active with Drug Court because I want to share with others what I learned about structure, honesty, and integrity. I have my family back in my life and God I live without drugs, life is good. I’m back in school getting my Master’s.
Q:Do you have any suggestions for change for the program? Just maybe offer the
program to more people; it will benefit them. The doors should maybe be opened to
repeat offenders so they may have this opportunity. The criteria should maybe be looked at.

Interview 3: The thing that worked best for me was the complete package. It was
probably at the very beginning they left no room for failure; it was very intensive. They had all the bases covered and there was no time to go out and relapse. I don’t think there was any part that was a waste of time. When I graduated, I was elated but scared but I had my support group in place so that when I left their nest I still had people who I could call on. I also still have a few friendships that were forged. There is a certain sense of being glad it is over due to the fact that it was time consuming, but it needed to be.
Q:What benefits did you receive from this program? The program gave me the tools I needed to continue recovery. It made me confident to become a contributing part of society. There are also legal benefits and one being having my record expunged
Q: Do you have any suggestions for change in the program? They are out-growing the building they were in; they need more space. It’s an awesome program – well worth it – it saved my life – it gave it back to me.

Interview 4: Q: What was the first session like for you? It was probably the hardest because I was miserable. I wanted to get high. I was fearful of the unknown. The first session was overwhelming. I was still loaded. I had several sanctions that were due to my use. I was still confused. But Drug Court gave me the structure to save my life. That was what worked best for me. The structure of drug court and the length of time. The different phases are really strenuous and we need the structure, we need the time because it takes all of that. What did I feel did not work? What does not work is the individual. Drug court works. It’s not drug court that failed me, but me that failed drug court. I have the experience of knowing today that at first the sanctions don’t work and then it happens that you stop and surrender to the program.
Q: If you are glad it’s over, why? One of the reasons I’m glad it’s over is because now I get to use what they taught me. I get to get back into society and make amends for the wrong I’ve done.

Interview 5: There are two types: those that need and those that want it. The ones who want it stay sober. Drug court is a long treatment that not only gives you a stable
environment but it gives you guidance. There are people like me who have flaws and
drug court has given me all of the tools I could ever need to keep me going. Now with
this change, everybody whose life I touch is better because of my experience with drug court. I am just so grateful. I was a convicted felon looking at 60 years. Drug court gave me a chance.

Interview 6: What worked best for me was the MRT book was absolutely wonderful. By the time I reached the 40th meeting it started to all click for me. I got a sponsor and saw how the MRT’s worked with the 12 steps. The discipline worked really good.
Q: How did you feel when you graduated? Relieved. I felt I had learned so much. I had high respect for the counselors there. Actually I wanted to cry. I had bonded with the people there – it was kind of sad. I love group and I still make 4 meetings a week. I really would not feel right if I didn’t go to at least 3 meetings a week, so I’m still working the 12 steps. Q: What benefits did you receive from this program? Definitely I kicked my addiction, I also quit smoking, I was given an opportunity to look at myself living life on life’s terms. I just never realized how it affected my spiritual growth. Q: Any suggestions for change to the program? I would incorporate the 12 steps into the program. The MRTs are important but I would add the 12 steps, and the meetings are very important. Something else I would add is alternate NA and AA to the meetings and what it is that the alcohol began you on your journey to drugs.

Interview 7: What worked best for me was the MRT book and the involvement of the
counselors. The book explains how and talks about social and moral responsibilities.
The involvement of the counselors gave you someone who was not your peers to
encourage you and go over things with. Q: Any suggestions for change to the
program? In some respects I think they should have more restrictions on how they
present themselves to society.

Interview 8: After graduation, I felt great, but a little nervous about stepping out into the world without being drug tested. Twenty five months sober, I feel good! Q: Are you glad it’s over? Well because of the time it took you know, to leave work early and go and UA or go to a meeting. Q: What did you learn from this program? I learned to not depend on drugs. I learned tools about what I can do when I’m stressed out about a situation instead of using.

Interview 9: Q: What do you feel worked best for you in the program? Having a
very close set of peers, because as peers it’s easier for them to relate to you on the same level. What did NOT work for me was the numerous meetings because Phase 1 is 4 of everything a week. There is no time to do anything else. Q: Any suggestions for change to the program? I think they should let people choose. I went because I wanted to andothers were forced and it makes it difficult going through phase 1 and 2 for those that want to be there. Everyone is grown enough to make their own decisions.

Interview 10: Everything worked – if you work the program it will work you. When I was finished I was happy but felt like I was losing a family. Q: What benefits did you receive from the program? I got an apartment, job, a bank account, friends, my
respect, dignity, family, peers. I benefitted a lot. Q: Any suggestions for change to the program? If they could just not have call in everyday – not weekends – and it could give people the chance to be responsible to come back on Monday. It’s too much everyday; they need to want for themselves.

Interview 11: Q: What was the first session like for you? I honestly can’t tell you
because I didn’t want to be there. I closed my mind and one week later I got sanctioned and went to the halfway house. When I came back from the halfway house I was so ready to change until I was ready to do anything and everything they told me to do. I can’t think of anything that didn’t work. Probably the assignments for each phase worked best because it got deep into the way reality really was; it helped me to be a better mother and daughter. I got my GED, I held a job for almost 2 years, I became independent, I got engaged, I mended the wounds between my parents and I, I became a friend and sponsor. They gave me my life back. I was able to keep my little girl and I really feel that if not for Drug Court I would probably be dead on the side of the road.

Interview 12: I think what worked best for me was the MRT book – it made me go deep into ME and not just blaming other people but holding myself accountable. Everything worked, but especially the MRT book. Q: How did you feel when you finished? I was proud of my accomplishment, it was the first thing I ever accomplished in my life. It will forever be a part of my life. I wear a shirt that says DRUG COURT WORKS. Q: What benefits did you receive from the program? That drug court introduced me to Narcotics Anonymous. Q: Do you have any suggestions for changes to the program? Drug court has changed a lot and now the clients are doing different drugs and they’re taking coricidin as a drug. I learned this through Narcotics Anonymous.

Interview 13: Q: What do you feel worked best for you? The meetings – they got me to interact with a bunch of people just my kind. Q: What do you feel did not work? Sanctions because I felt that drug court was being vengeful for my actions. I think they need to do away with the sanctions. What benefits did you receive from this program? Sobriety, gained new sober friends, much more clearer thinking, a new aspect on life, a greater relationship with God.

Interview 14: Q: What do you feel worked best for you? The immediate consequences if you do something wrong. Q: What do you feel did not work? They have stuff that they make you do like case management and gender group. It’s the same thing over and over. I’m sure that with their time they can come up with more and you see the same people over and over like housing – you can learn something else. Q: Any suggestions for changes to the program? Yes, just for the upper part of the program – be more equal – don’t let personal feelings get in the way they treat people.

Interview 15: Q: How did you feel when you got assigned to Drug Court? I was
glad. I had been in jail for 8 months. It was like a ticket out of jail at first. Q: What
was the first session like for you? It was kind of questionable; it was like how could
these people really help me – I like getting high. It was something I had to do to stay
free. Q: What worked best for you? It would have to be the rules that they gave me. I had to make 4 meetings, I had to UA, I had to attend meetings and go to the outside
meetings. This was what stood out to me and what helped me because my life had no
rules. I had nowhere to be. I had no structure. You see, I just lived. I would be out all
night, so when I had rules then I was there you make meetings and you hear things that relate to your life and you get exercises. They did a lot of exercises that would make you think about your life. It gave me structure. I spent a year and a half in drug court, and you know I never missed one group, I wasn’t glad it was over, but I was glad I had finished something because you know I didn’t finish much in my life. I had accomplished something. Q: Do you have any suggestions for change to the program? If it’s not broke, don’t fix it. If my car comes with a certain type of rims, and I like it, I ‘m not going to put any 20’s on it.

(Interviews 16-30 available upon request)

Conclusions and Key Findings

While different interviewees preferred different parts of the program, it seems that all
agreed that drug court worked for them and changed their lives for the better. In the U.S. we house proportionately more of our population in prison than does any other country and for longer periods of time than do many countries (Tischler, 1999). Recidivism rates of inmates suggest that prison is not successful at rehabilitation, and alternatives to incarceration such as the F.I.S.T. drug court therefore seem to offer a more viable and affordable option to the thousands of dollars spent per year on housing individual prisoners. This evaluation supports a previous evaluation completed in 2005 for the F.I.S.T. program in which findings strongly suggest the success rate of the program supersedes that of other alternatives to incarceration such as Tracts 1 and 3. Furthermore, the effect is stronger over the long term when participants have been exposed to the MRT component of the program.

Re-arrest rates are dramatically and statistically significantly lower for Drug Court completers than for Prevention Plus (Tract 1) or Straight Probation (Tract 3). This is especially true for drug crimes and violent crimes. While there may be some differences in the population of drug court versus these programs, these differences fail to explain the success of the program relative to the other two programs. This, along with the interviews of graduates of the program demonstrate overall positive perceptions
on the part of the participants. The findings of this evaluation should clearly show that a need for continued financial support of the F.I.S.T. Drug Court Program will be money well spent.

Source: www.ind.com 6th August 2010

References

Andrews, D.A., I. Zinger, R.D. Hoge, J. Bonta, P. Gendreau and F. Cullen. 1990. “Does
Correctional Treatment Work? A Clinically Relevant and Psychologically Informed
Meta-Analysis.” Criminology 28(3): 369-404.
Belenko, S. 1998. “Research on Drug Courts: A Critical Review”. National Drug Court
Institute Review 1(1): 1-43.
Deschenes, E.P., S. Turner, and P.W. Greenwood. 1995. “Drug Court or Probation? An
Experimental Evaluation of Maricopa County’s Drug Court.” The Justice System Journal
18: 55-73.
Deschenes, E., Peters, R., Goldkamp, J., and S. Belenko, 2002. Drugs courts. In J.
Sorenson, R. Rawson, J. Guydish, & J. Zweben (Eds.), Research to practice, practice to
research: Promoting scientific clinical interchange in drug abuse treatment. Washington,
D.C.: American Psychological Association.
Dorf, M.C. and J. Fagan. 2003. “Problem-Solving Courts: From Innovation to
Institutionalization.” The American Criminal Law Review 40(4): 1501-1511.
Finigan. M.W. 1998. “An Outcome Program Evaluation of the Multnomah County
S.T.O.P. Drug Diversion Program.” Portland, ORE: NPC Research Inc.
Gottfredson, D. C., K. Coblentz, and M.A. Harmon. 1997. “A short-term Outcome
Evaluation of the Baltimore City Drug Treatment Court Program.” Perspectives (Winter):
33-38.
Gottfredson, D.C., S.S. Najaka and B. Kearley. 2003. “Effectiveness of Drug Treatment
Courts: Evidence from a Randomized Trial.” Criminology and Public Policy 2(2): 401-
426.
Lemanski, M. 2001. A History of Addiction and Recovery in the United States. Tucson,
AZ: See Sharp Press.
Lock, E., J. Timberlake, and K. Rasinski. 2002. “Battle Fatigue: Is Public Support
Waning for ‘War’ –Centered Drug Control Stategies?” Crime and Delinquency 48: 380-
398.
Office of National Drug Control Policy. 2010. “National Criminal Justice Reference
Service.”http://www.ncjrs.gov/spotlight/drug_courts/facts.html Accessed 15 June 2010.
Peters, R. H. and M. R. Murrin. 2000. “Effectiveness of Treatment-Based Drug Courts in
Reducing Criminal Recidivism.” Criminal Justice and Behavior: 27(1): 72-96.
21
Wolfe, E., J. Guydish and J. Termondt. 2002 “A Drug Court Outcome Evaluation
Comparing Arrests in a Two Year Follow-Up Period.” The Journal of Drug Issues: 1155-
1172.
References
Andrews, D.A., I. Zinger, R.D. Hoge, J. Bonta, P. Gendreau and F. Cullen. 1990. “Does
Correctional Treatment Work? A Clinically Relevant and Psychologically Informed
Meta-Analysis.” Criminology 28(3): 369-404.
Belenko, S. 1998. “Research on Drug Courts: A Critical Review”. National Drug Court
Institute Review 1(1): 1-43.
Deschenes, E.P., S. Turner, and P.W. Greenwood. 1995. “Drug Court or Probation? An
Experimental Evaluation of Maricopa County’s Drug Court.” The Justice System Journal
18: 55-73.
Deschenes, E., Peters, R., Goldkamp, J., and S. Belenko, 2002. Drugs courts. In J.
Sorenson, R. Rawson, J. Guydish, & J. Zweben (Eds.), Research to practice, practice to
research: Promoting scientific clinical interchange in drug abuse treatment. Washington,
D.C.: American Psychological Association.
Dorf, M.C. and J. Fagan. 2003. “Problem-Solving Courts: From Innovation to
Institutionalization.” The American Criminal Law Review 40(4): 1501-1511.
Finigan. M.W. 1998. “An Outcome Program Evaluation of the Multnomah County
S.T.O.P. Drug Diversion Program.” Portland, ORE: NPC Research Inc.
Gottfredson, D. C., K. Coblentz, and M.A. Harmon. 1997. “A short-term Outcome
Evaluation of the Baltimore City Drug Treatment Court Program.” Perspectives (Winter):
33-38.
Gottfredson, D.C., S.S. Najaka and B. Kearley. 2003. “Effectiveness of Drug Treatment
Courts: Evidence from a Randomized Trial.” Criminology and Public Policy 2(2): 401-
426.
Lemanski, M. 2001. A History of Addiction and Recovery in the United States. Tucson,
AZ: See Sharp Press.
Lock, E., J. Timberlake, and K. Rasinski. 2002. “Battle Fatigue: Is Public Support
Waning for ‘War’ –Centered Drug Control Stategies?” Crime and Delinquency 48: 380-
398.
Office of National Drug Control Policy. 2010. “National Criminal Justice Reference
Service.”http://www.ncjrs.gov/spotlight/drug_courts/facts.html Accessed 15 June 2010.
Peters, R. H. and M. R. Murrin. 2000. “Effectiveness of Treatment-Based Drug Courts in
Reducing Criminal Recidivism.” Criminal Justice and Behavior: 27(1): 72-96.
21
Wolfe, E., J. Guydish and J. Termondt. 2002 “A Drug Court Outcome Evaluation
Comparing Arrests in a Two Year Follow-Up Period.” The Journal of Drug Issues: 1155-
1172.

The power of an attractive fallacyManuel Pinto Coelho*

Dr, Chairman of Association for a Drug Free Portugal – member of World Family Organization
Member of International Task Force on Strategic Drug Policy
Member of Drug Watch International

We grew up believing that no matter how many times affirmed, no matter how insistently repeated, a lie, as convenient as it could be, would never become the truth. Does that principle still apply today? We wonder…

Last year, Mr. Glenn Greenwald an American lawyer and writer, fluent in Portuguese, was invited and sponsored by Cato Institute – Washington think-tank committed to libertarianism that has been a long-time advocate of drug legalization – to come to our home country Portugal, with a certain task at hand. He was to develop a study concerning the results of the Portuguese drug decriminalization policy. After 3 weeks he went back to the United States and wrote a book. And on that book he characterized the Portuguese drug policy as being a huge success. An example. A lesson to the world. A model worth being replicated.

Those 33 pages do look appealing. The book was a tremendous sensation.
So many attractive indicators and positive statistics really pleased a lot of minds,
including the media, which boosted the proliferation of the “good news”. The TIME magazine published an article commending the book and its content.
It had a record number of viewing hits that day. “The Moderate Voice”, “The Kansas City Star”, the “Pittsburgh Tribune-Review”, “The Examiner”, the “Scientific American”, are just a few of the publications that mimicked the phenomena. In Portugal, the magazine “Visão” dedicated two articles in two consecutive numbers to this “happening” with the flashy title “Portugal inspires Obama”. “The Economist” was next in line and many others followed.
And so the book was flying around the world and speeding through the internet,
inflaming people all over the globe.

But…
Was the book truthful? Was the information in it reliable? Was it worth all that credit? Is that the truth?
Let’s take a look at some statements that might have helped trigger the libertarian euphoria.

It says:
–“The total number of drug-related deaths has actually decreased from the pre-decriminalization year of 1999 (when the total was close to 400) to 2006 (when the total was 290)”.

And regarding consumption, it gives the general notion of decreasing tendencies
affirming that:
-“Prevalence rates for the 15 to 19 age group have actually decreased in absolute terms since decriminalization.” -“Most significantly, the number of newly reported cases of HIV and AIDS among drug addicts has declined substantially every year since 2001.”

It looks rather good doesn’t it?

Unfortunately it does not comply with the truth. So lets abandon the artefacts and move to the real facts.

Consumption
Looking closer at the data regarding prevalence, it’s curious that the only 3 graphics presented in Mr. Greenwald’s book, mainly focus on an age span population comprised between 13 and 19 years old. Only a brief reference is made to the adjacent 20 to 24 age group, that already doesn’t show any mild decrease, but rather a boosted 50% increase. +50%

And still concerning the 13 to 15 age group in school environments, if we want to look at the same data in a different perspective, we can attest to an increase in every drug category from 1998 to 2002, with cannabis sky-rocketing the charts with its 150% raise.

Only to have a mild decrease on to 2006, with the exception of heroin, and although numbers are still not available regarding subsequent years, there is a general sense that the numbers are ascending yet again.

If we look below the age of 34 it’s nearly a 50% escalation. If one glances at the numbers related to prevalence in the total Portuguese population, there isn’t a single drug category, not one, that has decreased since 2001.

Between 2001 and 2007, the drug consumption in Portugal increased by 4.2% in absolute terms – the percentage of people who have experimented

with drugs at least once in their lifetime, climbed from 7.8% in 2001 to 12%.in 2007.

The following statistics are reported:
• Cannabis: from 12.4% to 17% (15-34 years old)
• Cocaine: from 1.3% to 2.8% (15-34 years old)
• Heroin: from 0.7% to 1.1% (15-64 years old)
• Ecstasy: from 1.4% to 2.6 (15-34 years old)
(Portuguese IDT – November 2008) +40%

Cannabis
It is difficult to assess trends in intensive cannabis use in Europe, but among the
countries that participated in both field trials between 2004 and 2007 (France, Spain, Ireland, Greece, Italy, Netherlands and Portugal), there was an average increase of approximately 20%. (EMCDDA – November 2008)

Cocaine
“There remains a notorious growing consumption of cocaine in Portugal, although not as severe as that which is verifiable in Spain. The increase in consumption of cocaine is extremely problematic.”
(EMCDDA´s Executive Director, Wolfgang Gotz, Lisbon – May 2009)

In the chapter “Trends” of cocaine use, the new data (Surveys from 2005-2007) confirms the escalating trend during the last year in France, Ireland, Spain, United Kingdom, Italy, Denmark and Portugal. (EMCDDA – November 2008)

While amphetamines and cocaine consumption rates doubled in Portugal, cocaine drug seizures have increased sevenfold between 2001 and 2006, rating us the sixth highest in the world in that matter. (WDR – June 2009)

Heroin and drug related Deaths and Homicides
In Portugal, heroin is the most responsible for internments in drug rehabilitation facilities and for overdose deaths.
Behind Luxembourg, Portugal has the highest rate of consistent drug users and IV heroin dependents. (Portuguese Drug Situation Annual Report – 2006)

Concerning drug-related deaths, in 2005 Portugal had 219 deaths, representing an increase of 40% relative to 2004 (156). (Portuguese Drug Situation Annual Report – 2006)
In 2006, the total number of deaths as a consequence of overdose did not diminish radically compared to 2000. In fact, the opposite occurred.

“With 219 deaths by drug ‘overdose’ a year, Portugal has one of the worst records, reporting more than one death every two days. Along with Greece, Austria and Finland, Portugal is one of the countries that recorded an increase in drug overdose by over 30% in 2005″. (EMCDDA – November 2007)

The number of deceased individuals that tested positive results for drugs (314) at the Portuguese Institute of Forensic Medicine in 2007, registered a 45% raise, climbing fiercely after 2006 (216). This represents the highest numbers since 2001 – roughly one death per day – therefore reinforcing the growth of the drug trend since 2005. (Portuguese IDT – November 2008)

In Portugal, since decriminalization has been implemented, the number of drug related homicides has increased by 40%. “It was the only European country with a significant increase in (drug-related) murders between 2001 and 2006″
(WDR – June 2009).

HIV and AIDS
On to the HIV and AIDS issue, by no means have the numbers declined substantially. Again, the exact opposite takes place. Portugal remains the country with the highest incidence of IDU-related AIDS and it is the only country recording a recent increase. 703 newly diagnosed infections, followed from a distance by Estonia with 191 and Latvia with 108 reported cases.
We’re top of the list, with a shameful 268% aggravation from the next worst case. (EMCDDA – November 2007)

The number of new cases of HIV / AIDS and Hepatitis C in Portugal recorded among drug users is eight times the average found in other member states of the European Union. “Portugal keeps on being the country with the most cases of injected drug related AIDS (85 new cases per one million of citizens in 2005, while the majority of other EU countries do not exceed 5 cases per million) and the only one registering a recent increase. 36 more cases per one million of citizens were estimated in 2005 comparatively to 2004, when only 30 were referred ” (EMCDDA – November 2007).

It’s rather simple and easy to grasp the reality of the facts, with one look at the real figures, the official figures. Still Mr. Glenn Greenwald managed to picture it otherwise, and most of the world press bought it, and subsequently some governments disgracefully did too.

That’s the power of an attractive fallacy.
In the same line of thought as Mr. Greenwald’s misleading book, there were recently published on the foreign press, two articles that deserved our attention.
The first one by Danny Kushlik of the Transform Drug Policy Foundation entitled
“Portuguese style decriminalization and legal regulation”. And a second one published in Oxford Journals – British Journal of Criminology with the partial funding of Beckley Foundation (usually very active in criticizing the United Nations drug Conventions) signed by Caitlin E.

Hughes and Alex Stevens: “What Can We Learn From The Portuguese Decriminalization of Illicit Drugs?”
Both , underestimating the readers understanding, suggest the contrary to what the numbers show clearly and unequivocally. In this last one, the authors are peremptory in their “Conclusion”: “ …since decriminalization in July 2001, the following changes have occurred:
…
• reduced illicit drug use among problematic drug users and adolescents, at least since 2003;
• reduced burden of drug offenders on the criminal justice system;
• reduction in opiate-related deaths and infectious diseases;
•
… and continues:
• “It is also an ethical and political choice of how the state should respond to drug use. Internationally, Portugal has gone furthest in emphasizing treatment as an alternative to prosecution. Portuguese political leaders and professionals have by and large determined that they have made the right policy choice and that this is an experiment worth continuing.”… “As this paper has shown, decriminalization of illicit drug use and possession does not appear to lead automatically to an increase in drug related harms. Nor does it eliminate all drug-related problems. But it may offer a model for other nations that wish to provide less punitive, more integrated and effective responses to drug use”.

Articles like these ones were so effective, that, as we mentioned before, already the Czech Republic, Mexico and Argentina copied the model and adopted the famous Portuguese drug decriminalization model.

Decriminalization and CDT’s

Let’s recede in time back to 2001. In early summer July 1st a law takes effect that decriminalizes every single drug, provided that it is for personal use only.
This means that yet illegally sold, purchased or consumed, you will never be criminally charged for any of it, unless you possess a quantity superior to an estimated 10 day supply, then transforming yourself into a drug dealing criminal.
Compared with this law, the Dutch famous permissiveness is a strict dictatorship!
So what did the mentors of this new law have in mind when they idealized it?
Their belief was that by eliminating the social stigma of guilt associated with
criminalized drug consumption, users would be more willing to enrol in drug dissuasion programs. This is based on the conception that most addicts avoid treatment for the fear of criminal charges.

In a article dedicated to Portugal´ s drug policy “The Economist” in it’s printed edition (August 27th 2009) says:
“Officials believe that, by lifting fears of prosecution, the policy
has encouraged addicts to seek treatment. This bears out their view that -
sanctions are not the best answer. ´Before decriminalization, addicts were afraid to seek treatment because they feared they would be denounced to the police and arrested,´ says Manuel Cardoso, deputy director of the Institute for Drugs and Drug Addiction, Portugal´ s main drugs-prevention and drugs-policy agency. ´Now they know they will be treated as patients with a problem and not stigmatised as criminals´.”

So the current Portuguese reality, that one reality the world has recently been invited to follow, is that anyone who’s drug dependent and commits a crime is not a criminal, because drug dependents are sick poor people.

In almost 20 years of experience – we directed the first private Portuguese drug
dependency rehabilitation clinic (Health Ministry Licence 1/1996) – neither ourselves nor any of our several collaborators, have ever heard or even slightly sensed this supposed fear of seeking treatment over the risk of criminal indictment.

Not even 1 of the 14.000 addicts that went through our clinics has ever showed any kind of fear concerning the authorities. Even in long sessions with psychologists, never was that a topic of conversation.This conception is a seriously distorted projection of reality. It is an unfounded lame argument.
This statement is also a serious and painful attempt against all the crowd of medical doctors, followers by obligation of the Hippocratic oath that ensures professional secrecy.

These doctors, although without proper conditions to do their job, as a consequence of a total absurd drug dependency policy, are giving their best to help drug dependents and their families.

As to the differentiation of dealers from users, official reports from the National Institute of Administration state that since 2001 is very hard to distinguish between dealer and consumer, since it is fairly easy for a dealer to organize his distributing method through smaller, below the line quantities.

As matter of fact that important document reports on Chapter XIV – The Future of the National Strategy: Main Questions – How to distinguish the consumer from the Traficant? ”Doubts rises in what concerns the main criteria explicated on the Decreto- Lei n.º 130-A/2001 of 23 de April, in which is considered a consumer everyone that does not carry drug quantity superior to10 days of use. So, it is possible to exert drug traffic with more distributed logistics avoiding the possession of quantities superior to that limit. How can we ameliorate this criterion?”

Since this neutral (INA) report was published – November 2003 – until today, nothing was done to improve the situation. Absolutely nothing was changed, and despite the disappointing results, the Portuguese strategy was renewed up until 2012. In fact, nowadays, in this country that some people insist on preaching as a role-model to the world, if you walk alone through any crowded street in Lisbon’s Bairro Alto or in certain populated spots of historical downtown, you are likely to be approached by individuals sneakily alluring with hashish, cocaine and others on their swift hands, even in broad daylight. Such daring characters were inexistent 5 years ago in places like these. There is a growing sense of fearlessness in the selling of small quantity drugs, since most police officers find it unworthy of their attention and
effort.

According to this ideology, a beneficial distinction is created when putting this law to practice: on one hand we would have dealers and traffickers sent to prison and on the other, we would have more dependents sent into treatment facilities. Furthering this notion, was the creation of the CDT´ s (Commissions for the Dissuasion of Drug Addiction) where users caught in the act, would be sent for evaluation, and if so justified, they would be persuaded to follow treatment in order to avoid Administrative fines and other light penalizations. Better explaining the CDT’s: there is no better way to illustrate how these new facilities, created as a form of diversion from imprisonment, truly work, than to present the reader the desperate appeal from the director of one of the most significant units.
The letter that follows was posted on IDT’s intranet services:

“The Portuguese CDT’s were created one for each district under the entry into force of Law 30/2000, which decriminalized the consumption of narcotic drugs and psychotropic substances. Becoming, then, the institutions or authorities with the responsibility to take knowledge of the offenses which began to be originated by the situations of consumption, leaving the realm of the courts: they began by depending on the Presidency of the Council of Ministers and subsequently by the Ministry of Health. Usually the cases that reach the CDT’s are sent by the PSP (Portuguese Public Police Force), GNR (Portuguese Military Guard) Courts and Prisons. Hence the law itself specifies in particular the existence of a multidisciplinary team in each CDT, covering the fields of psychology, sociology, social service, law and administrative and directive part. The same law provides and requires different processing in each case, since the hearing, the
technical evaluation, measures of deterrence, any work of motivation for treatment, monitoring process in its different moments (suspension, sanction if any, etc.). Similarly, the law requires that the hearing and the taking of any decision must be made only with a quorum, is to say, with at least two of the three members set out in the Board of Directors the Commission. The same law also recommends that any decision is adequately supported by a report of the technical team, observing this team the monitoring of cases in stage of suspension, creating networks and linking with support institutions or treatment.

Accordingly – and taking into account the different stages of the process (from receipt of the case, sealing of seized drugs and its transmission to the State safe deposit, the service of police officers and defendants, hearing, evaluation, decisions, reports, minutes, quotas and several information to attach to each case, the statement of measures taken and the corresponding bureaucratic processing,

correspondence sending, creation of maps and databases in constant update, ordering of the destruction of drugs after each archiving process, meetings, etc..) the law provides for eight persons employed by each Committee,
being one President, two vowels, two elements in the technical support team (psychology and social work) and three elements in the administrative support team.

What happens, however, is that despite many statements giving notice of the longstanding lack of resources to the minimum requirement: the CDT Braga as always seen increased the volume of work and decreased the number of staff to do it. In the first year, in December 2001, the

Social Service Technician left, as she lived in Vila do Conde and was admitted on Welfare Services of that city. She has never been replaced.

In January 2003, a member of the Board of Directors, the one specialized in the field of psychology, left to engage in private practice. In May of that year it was the time for one of the administrative employees, because she lived in Esposende and was able to be placed at the local Health Centre. Also in October of the same year, the psychologist of the technical support team leaves the service, being this team, since then, without any of the two members
provided by law. In February 2004, the second administrative official leaves, as she lived in Guimarães and managed to be employed in a private company in this city.
At that time, the CDT Braga was left with only one administrative employee, on top of all in nursing license which reduced in two hours her daily work schedule. Only later, in November 2007, after much insistence, another administrative employee was placed in system of mobility from the IRS of Braga. The situation deteriorated again in August 2009, when the oldest administrative employee moves to Lisbon at her request, to accompany her husband who had
been placed in a company at the capital city. In November of this year, the IRS requires the employee who is in mobility in this service but belongs to their staff.
Thus, of the three elements of the administrative team provided by law, this team – which was often short of staff and with board members assisting the many secretarial work – is now also without anyone. Like this, the CDT with one of the largest work volume in the country has

currently two members of the Board (President and Juridical Vowel), totally depleted, for more than five years, of any element in the technical support team and also completely lacking, up to the moment, administrative support. Of the eight elements that the law provides, there are only two resistant ones.

These problems have often been reported by different ways, at different times and for various departments. It is even reported that in the present context, it is almost impossible to open the doors of this service in good conditions of functionality and safety. It was further added that, given the holiday season where there will be only one person present at the service and that, even if there are two, they will have to unfold to the main administrative services and to assist to the basic office tasks: it is not possible under law to carry out hearings or to take decisions in the many cases that will be piling up, some on the verge of expiry. It should be understood that everything was always done and the effort always ensured to give the best prestige to a public service with internationally recognized merit. And
everything was always reassured even at times when the situation had become uncomfortable and suffocating. We are proud of it and feel duty done and with a clear conscience. I also believe that people who I address to could and can in many contexts be somewhat hamstrung to resolve these serious and urgent issues, denoting intention to solve… The difference is that now it became impossible to this service to give a minimally satisfactory response and with dignity – even at the level of assuring the existence of conditions to open doors… Considering this situation, we would appreciate to whom it might consider the possibility of eventually working for the CDT of Braga or had knowledge of someone available to perform duties here, either in the technical team of psychology and social work, either in the technical and
administrative staff. Thanking you in advance for the attention that you could dedicate in order to a better cooperation or easing to overcome this major constraint, we remain at your disposal.
T
he Chairman of the CDT Braga Jorge Tinoco”.

Note: the underlined parts are APLD’s responsibility.
For a better understanding of this new Portuguese reality let us give some more statistical insight on these entities – the CDT´s:

From a total number of 7.346 processes instated to caught users, 2.816 were classified has being non dependents 2.075 are pending evaluation and 783 were considered to be dependents.

Of these 783, 661 voluntarily accepted to be treated in order to temporarily suspend the legal process. From this group of 661 people, 166 had never had any prior contact with treatment facilities. 127 resumed abandoned treatment and 368 were already following treatment when they got caught practising the illegal offense.
So we can attest that the CDT units, one for every district, with a total of 99 technicians working in them, only managed to conduct towards treatment 166 addicts. Since the remaining (127 + 368) were already referenced and being followed in the CAT facilities.
This means that those supposed indicators of statistical success, come from referencing the dependents that are already referenced, once again misleading everyone into factual misinterpretation.

Plus, the 2.816 referenced as not constituting risk cases, in other words, yet not having a drug dependency, were dismissed from any kind of intervention.
This is equivalent to saying that they wait for users to get hooked on drugs, before they grant them any support. This is disastrous.

As well confirmed by the IDT 2008 Report that says that there is evident lack of
response upon this population. Five of these CDT units don’t even have any technical element on their staff, and many others lack professionals too.

Health
On the very recent 2010 World Drug Report released last June 26th, the Executive Director of the United Nations Office on Drugs and Crime (UNODC), Mr. Antonio Maria Costa (Executive Director) signed an extremely preoccupant Forward ED was peremptory:
“…Most importantly, we have returned to the roots of drug control, placing health at the core of drug policy. By recognizing that drug addiction is a treatable health condition, we have developed scientific, yet compassionate, new ways to help those affected. Slowly, people are starting to realize that drug addicts should be sent to treatment, not to jail.”… …

“While the pendulum of drug control is swinging back towards the right to health and human rights, we must not neglect development.”

…“Above all, we must move human rights into the mainstream of drug control.” …“Just because people take drugs, or are behind bars, this doesn’t abolish their right to be a person protected by law – domestic and international.”

What a strange world this we are living in, where it’s becoming increasingly difficult to distinguish right from wrong, even for good willed people sharing the same moral and ethical values. Surprisingly the United Nations still most representative official, in applying in his speech the two favorite arguments, the two “jewels of the crown” of the well known economic-social-political group that insistently and restlessly wishes to legalize drugs – “health” and “human rights” – indicates eventually that, he too was influenced by the “resounding success” of the Portuguese experience, and maybe did not find the strength to resist the pressure, dropped the towel and capitulated! Amazingly UNODC’s Forward speech is coincident with pro-legalization organizations like Drug Policy Alliance, Cato Institute, Transnational Institute, Beckley Foundation, Encod, among many others who claim that the War on Drugs cannot be won and that
drug use and dependency should be treated as a health problem and not as a criminal one.
By joining his voice to others who consider prohibition a violation of human rights, giving the idea that drugs are not the vehicle responsible for violence and crime but instead the war against drugs is, as that pledged group usually says. The ED’s Forward doesn’t invite as it should the drug dependent to live without drugs, considering instead, between the lines, a “responsible use” and not less surprisingly attracts the world tofollow the so original as promptly condemned example of Portugal and, likewise, decriminalize drugs too!

Who could have imagined this some years ago? After the ED’s speech, the model of society (in what concerns narcotic dependence), that always used to address the phenomenon in a winning optimistic and positive way, a society that would not allow drugs to be part of it, that used to carry the message that narcotic dependent behavior should always be considered unacceptable and marginal (the drug addicts used to feel uneasy on the streets), and would adopt regulation that makes life more difficult for those who decide to take drugs, surprisingly and unfortunately gave place to another model. A pessimistic, negative and ineffective one which considers utopian a society free from drugs, that doesn’t follow necessarily the goal of abstinence (in the name of compassion…), pretends above all to make the use of drugs less dangerous by making them more acceptable in society (narcotic dependents feel protected, not to say stimulated) and bases itself essentially on the concept of taking care of and supporting rather than reaching a cure – the unfortunately famous Portuguese one.

It is our understanding that contrary to what it is suggested on the last UNODC’s Forward, by the Executive Director Antonio Maria Costa (ED) we should not place health but welfare at the core of drug policy. As a matter of fact these are two completely different situations: if the key word for “health” is disease, the key word for welfare is discomfort.

Considering drug dependency a “treatable health condition” like Portuguese officials and the ED do, is another way to call it a disease – the ED labeled it countless times…”drug addicts need treatment as much as patients of chronic diseases such as cancer, diabetes and tuberculosis” (UNODC Annual Report – 2008). This opens the door to medical treatment and other harm reduction strategies, hiding that before the (un)health conditions are installed, before diseases like AIDS and other co-morbid situations are installed, there is an important panoply of other conditions much more related with psychological and social discomfort – personal and societal factors that drive the drug dependent into drug dependency.

Health problems are essentially consequences of a prior uneasiness felt by the individual. The disease model linked to “mainstream healthcare” prevents the correct scientific research of all these situations, a crucial research which could evolve into effective treatment.

Talking about “health problems” is to the public opinion the same than talking about”disease”-that-must-be-dealt-naturally-by-doctors.

But what is treatment? What can we interpret treatment to be? – This is the heart of the matter, the mother of all questions.
• Can the perpetuity of a called chemical dependency be considered a treatment?
• Can we interpret the massive 70% majority of dependents in substitute drug programs in Portugal to be an indicator of success, or are they just a deluding form of social control?
• Can dependents aspire to a life free of drugs?
• Can drug-free treatments do the job?

Deep underneath all these questions lies the fundamental one: Is the drug dependent a condemned victim of his own biology or can he work himself around that issue through the process of discovering himself and his will power?
In other words, is drug dependency an incurable disease or is essentially a cognitive behavioral entanglement? This is the fundamental question and the answer to it is determinant in the choice of treatment to be approached and the politics to be drawn. As we can see in further detail later on, the society as a whole feeling dismissed of its obligations, keeps itself away from the scene, so perpetuating the discomfort, sorry, the “illness” of the drug addict!
“Harm reduction” strategies are used in Portugal – a country where drug dependency is officially considered a disease – as the main tool to fight drug dependency, as can be confirmed by such a high percentage of drug dependents in substitution programs. This means that those strategies are prioritized, much to the detriment of prevention and treatment. In political terms, this also means that, surely well intentioned, Portuguese officials understand that to treat the drug dependent is indeed a very difficult task and that the majority of them relapse one time after
another when they try to stop using drugs.

So to the Portuguese people, drugs are awful and they are (poorly) persuaded to stayaway from them. But if someone is already using them, then… that’s OK, because they are “sick” and they don’t have any power to change that for the rest of their lives.

A letter we received some years ago from the Portuguese Prime Minister portrays
eloquently the situation and the Portuguese reality:
“…substitution treatment (methadone) that in the beginning were considered as just a means to achieve abstinence,have now been accepted as therapeutic maintenance programs, eventually definite in character, but that can in some cases work as a starting point for dependency liberation.”

UNODC’s 2008 slogan “use music, use sports, do not allow drugs to come into your life” had been in Portugal, in a symbolic way, replaced since 2001 by “use methadone, use buprenorphine, don’t allow drugs to abandon your life…!”
With a policy like the Portuguese one, Portuguese narcotic dependents feel more and more protected not to say stimulated. When they listen to their “drug czar” – Portuguese IDT and EMCDDA President’s thoughts: – “as a diabetic needs insulin, some people need an opiate”…”the demonization of drugs and the message that drugs kill is outdated”…”I am not a fundamentalist with drugs since people can live in balance with them”… “cannabis is not already seen as a gateway to other drugs” their soul disposition is not hard to guess – jumps of joy! More or less unconscientiously, policies like the these, give up helping drug dependent in their changing process on the way to abstinence and prefer to take care and support them.

Drug dependence as a chronic disease arises from this desistance process.
It is pessimistic, negative and inadequate, and all in the name of “compassionate humanism”, and as we said before, does not lead to abstinence.

But does abstinence work? Even if the regular citizen and drug therapists experience did not tell us that abstinence and spontaneous remission are familiar realities, a well known study revealed that people who completed successfully a treatment program (even if one year only after the beginning of the abstinence) reduced 60% illicit activities. The sALE of drugs fell close to 80%, imprisonment decreased more than 60%, drug dependents without a roof decreased to numbers close to 43%, dependence to Social Institutions fell 11% and finally the employment increased 20%. (National Institute on Drug Abuse, Drug Abuse Treatment Outcome Study (1997); Department of Health and Human Services, National Treatment Improvement and Evaluation Study (1996).

“Health at the core of drug policy” like has been done with an excused rigor since 2001 in Portugal is now also stated by the ED? False medical therapies have been used by successive governments not only in Portugal as a smoke curtain behind which have been hidden some of the most pressing problems that sicken our societies.
By transferring it to the authority of medical profession, they have successfully managed, so far, to transform political problems (that can not be resolved in a commission time…) into medical problems requiring specialized medical intervention, depriving us as society of the responsibility of an accurate and correct research of the true causes of entering and exiting drug dependency.

But is “drug addiction a treatable health condition”? It is very sad and worrying when the noble science of Medicine is emphasized as the solution for drug dependency. People must understand that what drug addicts really need is psychological help, not medical (while medical doctors can prescribe medicines, psychologists “prescribe” psychotherapy). To send away the indispensable psychologists with their fundamental emotional control strategies and skills to avoid the situations that lead to drug abuse, is to open perversely the door to the fantastic paraphernalia with which doctors usually feed (the Government calls it “treating”) the “disease” – syringes, needles, methadone,
buprenorphine, condoms, etc. – with the aid of large staff on the street, ingloriously and willingly doing their best to care drug abusers.

This is the case happening in Portugal. If instead the world understands the phenomenon less like a disease (of the will or whatever) and more like a psychological state, a way of dealing with life, if people understand that what those unfortunate people need is a reason to live and for this purpose doctors (as ourselves) can offer nothing, a decisive step forward will be performed.
When the ED states that “we have developed scientific, yet compassionate, new ways to help those affected” we agree that we must go on searching new ways of scientific research but as we stated previously, oriented in a different direction. In a direction that can help us better understand the discomfort or the privation of well-being induced by the unhappy situations that are mostly responsible for drug users to fall into the drug dependency.

Not the current research that tries to find out (with the disguised enthusiasm of pharmaceutical industrials) biomedical/bio-chemical reasons for one essentially cognitive-behavioral phenomenon. Betting on this “treatable health condition” betting on this conveniently shy disease conception of drug dependency, Governments like the Portuguese do not understand that on dependence people “get in”, while on the disease people “fall”. As a result, drug dependents go on pretending they are sick and the government goes on pretending they are treating them! That is the very thing.

This is turning political problems into medical ones, like sweeping dust under the carpet, pretending to recover people by patting them on the back and allowing them to maintain the same addictive pattern… This is neither humanization nor compassion.

What is indeed human and compassionate is the urgent creation of a new paradigm to the drug dependency phenomenon – the creation of a culture of observation, the creation of a new culture where one would look at the drug dependent instead the drug dependency. Attentions should be directed to individual´s health, social, familiar, economic and psychological idiosyncrasies thus leaving the “one size fits all” model and returning to tailor-made hand giving that makes him or her finally feel… like a human being. That would be the real work, the decisive one on the way to the drug dependents and their families welfare. That would be the real work, the decisive one to cure the drug dependent of his “disease”.

We can resume by saying that in philosophical terms, to confuse the concept of “treatment” with the concept of “social control” as nowadays is done in Portugal is an incorrect attitude. In psychological terms, to convince drug dependents that their metabolism is unbalanced and that they have to maintain it dependent of anopiate as methadone, buprenorphine or any another, instead of fighting for their autonomy, is distorting and deluding. Any policy that drives a significant fringe of its society to a situation of defeat or inability to fight for its growth and personal development is unethical.

Jail
“Slowly, people are starting to realize that drug addicts should be sent to treatment, not to jail” expressed the ED on the UNODC’s Forward.
Most respectfully, this is another unhappy statement by the ED, that if adopted by the international community as it was already in Portugal, can be very harmful as well.

Firstly, as we said before, this opens a precedent as it clearly invites other countries to do the same that Portugal did, to decriminalize the consumption, the possession and acquisition of drugs. And what is more extraordinary, is that it sounds like a prize to a country that did it with very bad results against the rest of the world and against UN Conventions that the EDrepresents…!

The APLD can imagine everyone who is wishing to legalize drugs clapping their hands vibrantly – Mr. Soros, Mr. Nadelmann, Mr. Trebach and relatives must feel very happy indeed, with their abstruse goal getting a little closer…

By the way, we remember when that happened in our country Portugal in July 2001, United Nations INCB was fast, as it should, to condemn our original attitude – we were the only country in the whole world to do it! Secondly, it is a nonsense and an incongruity. Who wins by weakening drug laws?
Is it not true that like the ED several times stressed out, “the rule of law” is one (the main one?) of the three pillars where any winner drug addiction policy, and not only, should sustain on?
“We are slaves of the law in order to be free” said Cicero (106 aC-43 aC). He did not mention any exceptions!

Don’t send drug addicts to jail? To legalize crime committed by drug dependents (or by “patients” – sic) doesn’t seem to be the most effective way to fight it.
As a matter of fact (and as we’ve mentioned before) in our country, since
decriminalization has been implemented in July 2001, the number of homicides related to drugs has increased 40%. It was the only European country with a significant increase in (drug-related) homicides between 2001 and 2006.
(WDR- June 2009).

Confirming national and international official data, a recent report commissioned by the IDT, the Center for Studies and Opinion Polls (CESOP) of the Portuguese Catholic University, based on direct interviews regarding the attitudes of the Portuguese towards drug addiction revealed that 83.7% of respondents indicated that the number of drug users in Portugal has increased in the last four years, 66.8% believed

that the accessibilityof drugs in their neighborhoods was easy or very easy and 77,3% stated that crime related to drugs had also increased.(IDT “Toxicodependências” No. 3, 2007).

What is happening in Portugal is very peculiar; drug dependents, with the support of the government since 2001, rely on their status as “sick people” to not be punished for their crimes. The same is to say that they do crimes but they are not criminals because they are drug dependents… But then afterwards, these addicts forget that they are “sick” and are assumed as free and responsible people who are able to decide whether they want treatment or not!

After the decriminalization in Portugal, the law punishes only when another illicit act is added to the effect of use, which works almost every time as attenuation.
The example of Portugal shows clearly that facilitating access to drugs, will not be the way to reduce the use, the decrease of drug dependencies or related crime.
In considering, through decriminalization, the drug dependent as a patient and not as a delinquent, the State cannot then choose, through a policy which prioritizes “harm reduction” measures, to feed the “disease” instead of healing it.

But people may wonder; must drug dependents be sent to prison? Of course, if they commit a crime within a certain penal frame, a crime that deserves that type of punishment, yes they must go to prison like any other citizen. Is the prison the right answer to the drug dependent problem? Although it might seem strange, yes it can be. First of all, if the drug dependent is not only a user but is also someone who carries drugs to deliver/sell to others, then yes, he deserves and he must go to the jail. What happens in Portugal – the most liberal country in the world where any citizen, as we’ve said before, is allowed to carry drugs up to a ten day supply, so being considered for personal use only, thus
not being considered a dealer, and punished only with a fine – is a perfect absurdity. No one in a civilized society should have the “human right” to harm his neighbor.

Secondly, it all depends on the prison policy system. if, as is the case in Sweden where one has a nearly perfect system that really treats the criminal drug dependent in a drug free program, with a wilful multidisciplinary team taking advantage of possessing the most important tool to help someone in his recovering process – Time, they have it in a large amount – and using it properly, then yes, it can be good. We can even go farther and say, that it can be a blessing to be arrested, to stop the dependency and to rehabilitate oneself.

In Sweden they do not feed drugs to drug dependent prisoners as it happens in Portugal, Spain – where needle machines and shooting rooms are available (in Portugal the Government has been trying every year without success – much to officials surprise and anger, for the last two years, although a nurse has been patiently available 24 hours a day, not even one prisoner has required it ever…) and a few more ingenuous countries. In Swedish prisons, drug needle machines and shooting rooms are not available and hopefully, they never will be. There’s the understanding that if you cannot make a prison a drug free place, how on earth can someone even imagine that would succeed anywhere else?!

By using drug detection dogs, searching visitors as well as staff working, the Swedish system gives the first step to clearly indicate that drugs are not welcome. Drug detection dogs are available at almost every prison in Sweden.
There are drugs in Swedish prisons as it happens in the rest of the world but at least there are very serious efforts in order to get rid of them. In Sweden, when drug dependent prison inmates leave the prison, they have less chances
to return back by drug dependency reasons. They do their best to care and rehabilitate the human being and they do not use drugs to treat drug problems.

Human rights
”Above all we must move human rights into the mainstream of drug control.”
(UNODC’s Forward) Before starting to discuss the problem of human rights, the first question we should point out is; from what point of view are we interested to discuss this so controversial subject?
The economic?
The political?
The legal?

Or are we going to discuss above all the drug dependents and their families’ so precious welfare? Considering that the reader elected this last one, if there is a correct understanding of it, then one should be absolutely familiar with commentaries like the one from “Sandra”, a former drug dependent, one among millions in drug rehabilitation centers throughout this world: “If it was not so troublesome for me being a drug dependent, I am sure that I would not have cured myself. If, everyday, when I’d wake up, I knew that it was easy for
me to get my drug of choice without any worries, I am positively convinced that I would not be able to stop using it ever. The opposite should happen. Drugs are like that”.

People should understand that this statement is the real paradigm of the drug dependent thought – everything he/she needs, is definitively not more drugs, available or not, in the name of their “human rights”. What he/she wants, what he and she are begging for is help to escape that “life” the circumstances dropped them in. If anyone has any doubts about this, please make an enquiry and ask them what they’d prefer: a costless and painless drug free program versus more drugs, and listen to the answer!

So addressing the question: In a free society, shouldn’t everyone have the freedom to do what they want with their body since that does not harm any third party? Answer: no. First of all, although the individual could be free when he begins using drugs, once he gets dependent, he looses that freedom immediately. The consumption, becoming imperative, ends-up subverting the rules of any society, no matter how authoritarian that society may be.

Secondly, we all are gregarious by nature. In modern societies nobody can be an island, we all depend upon each other. To the alcoholic or to the drug dependent, the surrounding ambience – the husband/wife, the children, the neighbour, the friends, the co-workers, the society in general – shall always be affected by his/her deviant behavior. Not to mention the suffering of the families, often greater than the dependent’s own suffering, because adding to their own sorrows and suffering they are punished as well by their relative’s drug problems.
That is why, regarding the collective, each and every individual ought to always subordinate to limitations, which mean that living in society implies to accept restrictions to individual liberty.

As it was said by the, so considered to be, father of the modern liberalism, the English philosopher John Stuart Mill (1806-1873) in his classic “On Liberty”, in 1859:
“Over himself, over his own mind and body, the individual is sovereign… …The only purpose for which power can be rightfully exercised over any member of a civilized community, against his will, is to prevent harm to others…”

It is a fact that drugs destroy the brain structure that allows us to decide freely. And free decision making is the pillar of man’s dignity and man’s right to assume responsibilities. In being enslaved to drugs, man is discarding his most fundamental right: the right to control his own actions. Man has the right to his free decision making abilities. Furthermore – in being indebted to do it in a responsible way, he cannot escape that obligation. And drugs reduce or retire him from that right of free choice.

So, we can affirm that human rights are incompatible with drug abuse. Consequently, politic officials have the moral and civil obligation to protect them.
Each and every policy that undermines human rights, each and every policy that supports, encourages and promotes the use of drugs, questions essential values like health and safety and violates established rights. Each and every policy that allows one significant part of the population to remain enslaved chemically and psychologically by drugs, is a cruel
and inhumane one, and must not be accepted.
Let’s make it clear; sometimes people do not understand, or pretend not to, that drug abuse aggravates social and emotional misery and undermines human rights. By facilitating drug consumption, addicts such as all the “Sandras” in the world are being neglected and penalized.

If society as a whole, doesn’t emerge in refusal of the concept that it is a human right to take drugs, one of these days we could be waking up in a world where the common understanding is that… the marginal ones, are those who do not use them! As someone once said, the message should be explicit: “It is in our best interest to help find solutions for drug dependency, not to let the dependents destroy themselves and all those around them!”

One may ask people who use the human rights argument to reach the goal of legalization, if, to their understanding, legalization would make drugs become less available? Would then they be less attractive? Or be less addictive? Would they raise productivity? Or diminish road accidents? Diseases? Crimes? Can it ever be the solution the drug dependents and the world are expecting it to be? Can
it solve these problems? There is no need for expertise in this subject to understand that legalization, sustained by the human right to use drugs, definitely is not the best way to protect and improve the wellbeing of the individual and society. It is definitely not the most intelligent way to protect public health and to offer security and a balanced approach to the drug problem. Very often when we think about the drugs market, we forget what is primary and secondary.
The fact that Mother Nature produces plants like poppy, or that international crime cartels took property of drug distribution, is not a primary factor.
The primary factor is that millions of people are ready to break the norms and rules for the goal of using drugs, be them natural or synthetic – most of these people are children, they’re young people! We dont have to read the declaration of children’s rights to understand that, as a responsible society we have the obligation to protect them and to not allow those who carry drugs destroy them.

“Legalize drugs and send the dealer to unemployment” we very often hear.
Concerning this, there is a lot of misconceptions about the drug seller role.
Most people have the misconception that the classic “dealer” – that evil guy we see on movies usually in black clothes – is the entity responsible for a considerable amount of the miseries drugs carry to our youth. Eventually for them, were drugs to be legalized, the consequent free market of drugs
could definitely put them out of business and consequently children released from their influence could recover their normal lives and perspective a better future.
Unfortunately, anyone who studies the problem with any accuracy knows that the reality is very far from that. In real life what happens is that, the very first accountability for the very first contact with drugs is…mine, yours. It concerns most of our beloved ones, as well as our regular relatives and friends.
They’re the ones who naively and without dimensioning properly or understanding what they are really doing, want to share – since they feel good using them – through friendly complicity with their beloved ones, the source of their ever ready easy way to “happiness” – in the beginning drugs feel good, if they didn’t, they wouldn’t be the problem they are and we would not be speaking about them now.

The classic “dealer” usually appears later on when the dependence is already well
established and/or when they feel that someone wants to stay clean. Then, has it happens a lot of times, they come very nicely and give their product money free, as the “good friends” they are. With this bit of knowledge, the reader who has the responsibility to raise his children, can now easily understand why for us, the ED’s statement ”Above all we must move human rights into the mainstream of drug control”, is so, to say the least… hugely polemic!

Shall prevention strategies acting by dissuading the youth from drug use, be considered at any time obstructive or oppressive of human rights? No they can´ t. Not for the drug user, nor for all those around him or her. In the name of liberty, solidarity, equality, democracy, human dignity and…human rights, we all, be us children or adults, have the right to grow up in drug free places. To treat the drug dependent (inside or outside prison) is not a question of compassion. It is a question of love for his neighbor, a question of respect for human rights.
We are afraid that moving human rights into the mainstream of drug control, as the UNODC’s ED proposes, might be scarily similar to Goethe’s (1749-1832) pessimistic prescience anticipating the “humanist medicalization”.
He wrote: “I believe that in the end humanitarianism will triumph, but I fear that, at the same time, the world will become one big hospital, with each person acting as the other´s nurse”.
(J.W. von Goethe, “Letter to Charlotte von Stein” (June 8, 1787) in Gedenkausgabe, 11: 362. – Szasz, T. in Pharmacracy, Syracuse, 2003, pag 165.)

Manuel Pinto Coelho August 4, 2010

A Blueprint to build strong Foundations for Change.
Professor Carlo DiClemente’s Stages of Change model is feted worldwide for enhancing the understanding and skills which make a substance-abuse treatment provider effective. It helps clinicians develop thoughtful, individually tailored, scientifically grounded treatment plans – here he extends it to policy and programmes.
This article was originally published in Addiction Today journal, March 2005. As we prepare for new – and hopefully more progressive -policies to address addiction treatment, this information is increasingly relevant.
Research tells us that central qualities of the effective clinician are empathy, warmth and positive regard. It also tells us that developing and implementing a clearly articulated treatment plan and providing treatment for the problems a client presents are effective skills. But putting these qualities and skills into action is a challenge.
How does an individual clinician learn to express these central human qualities of caring and compassion with clients who are often difficult and unhappy about being in treatment, and whose central disorder is often characterised by behaviours which do not easily elicit empathy? And given the incredible heterogeneity among substance-use clients, how can a clinician develop a personalised treatment plan grounded in science?
Further, how can we apply those same principles to other workers in the field of substance-use treatment, including members of drug/alcohol action teams? Is there a common framework? Can the process of change be applied at a systemic level as well as at an individual level?
We answered these questions at ARF’s UK/European Symposium on Addictive Disorders in London (where photo on this page was taken). But let’s open up the issue… Deepening our understanding of addiction can also deepen our understanding of the implications for policy and programmes. It can let us see that we need a common framework – such as Models of Care – and a common assessment tool, which has eluded drug/alcohol action teams, to their increasingly vocal frustration. Deep understanding of what our clients are all about, and the meaning of what we are doing, can lead us to a conceptualisation of the entire process of change and the entire continuum of care.

WHAT IS THE STAGES OF CHANGE MODEL?

Developing genuine understanding of – even empathy for – a client requires professionals to look beyond that client’s behaviour when using alcohol or drugs, and to understand the nature of substance-use disorders and difficulties inherent in changing long-standing, pervasive patterns of thought and behaviour. They are helped in this by the ‘stages of change’ model, combined with a good treatment plan.

The current model posits five stages of change:
o precontemplation
o contemplation
o preparation
o action and
o maintenance.

People in the first stage show no sign of intent to change a problem behaviour, be it because of a lack of awareness, unwillingness or a lack of hope because previous attempts failed. Contemplators are more visibly distressed about their problem behaviours than precontemplators and have begun to weigh the positives and negatives of change.
The preparation stage covers people who are ready to change both attitude and behaviour, and to change soon. When people are in the action stage, behaviour change has clearly begun. So they need skills to implement specific change methods. They also need to be aware of the psychological – cognitive, behavioural and emotional – events which can work against their best efforts. And they need to learn how to prevent major reversals, such as having a relapse and returning to pre-change patterns. The action stage lasts an average of about six months.
The last major stage of change is maintenance, where people sustain and strengthen improvements they have made. They can take a few years to eel “secure”.
_____________________________________________
“The stages of change are a model of ‘how to think’
rather than ‘how to do’…
They describe attitudes, intentions and behaviours
related to tasks of change”
_____________________________________________
All of this is voluntary rather than coerced change. Indeed, the stages of change are a model of “how to think” rather than “how to do”. They describe attitudes, intentions and behaviours related to the tasks of change. Note that the “change” sought is specific: commitment to change one behaviour might say nothing about commitment to change a related behaviour. And each stage refers to a time period and to tasks which a person or organisation must complete before moving to the next stage.

COMMON CHARACTERISTICS

Let’s look at the commonalities of clients in the five stages of change – then readers can draw their own conclusions as to the similarities at a systemic level for change in our field.
The common characteristics of people in the precontemplative stage are: defensive, resistant to suggestion of problems associated with their use/ behaviour, uncommitted or passive in treatment/work, consciously or unconsciously avoiding steps to change their behaviour, lacking awareness of a problem, often pressured by others to change, feeling coerced and ‘put upon’ by significant others.
The characteristics of contemplators of change are: seeking to evaluate and understand their actions, distressed, desirous of exerting control or mastery, thinking about making change, have not begun taking action and are not yet prepared to do so, many previous attempts to change, evaluating pros and cons of their behaviour and of changing it.
Now we come to the preparation stage, where people: intend to change their behaviour, are ready to change attitude and behaviour, are on the verge of taking action, are engaged in the change process, are prepared to make firm commitments to follow through on the action option they choose, and are making or have made the decision to change.
Common characteristics of people in the action stage are that they have: decided to change, verbalised or otherwise shown a firm commitment to change, tried to modify behaviour and/or environment, demonstrated motivation, and are willing to follow suggested strategies and activities for change.
And what do we share at the maintenance stage? Characteristics are: working to sustain changes achieved to date, focusing considerable attention on avoiding slips or relapses, feeling fear or anxiety about relapse and facing high-risk situations, and less frequent but often intense temptations to return to old habits.

MOTIVATIONAL STRATEGIES to promote change include giving advice, practising empathy, removing barriers, providing feedback, providing choice, clarifying goals, decreasing desirability of unhealthy habits, and active helping.
CLINICAL STRATEGIES for people in the action stage include maintaining engagement in the change process/treatment, supporting a realistic view of change through small successive steps, acknowledging the difficulties, helping people to identify high-risk situations through a functional analysis and developing coping strategies to overcome these, helping people to find new reinforcers of positive change, and helping people to assess if they have strong support networks.
Clinical strategies for people in the maintenance stage include helping them to identify and sample drug-free sources of satisfaction, supporting lifestyle changes, affirming people’s resolve and self-efficacy, helping them to practise and apply new coping strategies to avoid a return to unhealthy habits, and maintaining supportive contact.

TREATMENT/ACTION PLANNING

Based on information gathered during assessment, this is created in collaboration with each person wishing to change and addresses mutually agreed goals. It serves a variety of purposes, including prioritising short- and long-term goals, choosing the optimal interventions for specific goals, identifying barriers to the achievement of goals, and monitoring progress towards goals over time.
For our new purposes, goals can be as much on a national or local level as they can be on a personal level. They can include decrease in or cessation of substance use, which can impact on other goals such as improving family and employment situations, extending social support networks, and returning to school or college. One obvious benefit of prioritising goals is that attention is focused on the most pressing problems.
Another is that successes in these main areas often place people in a better position to address secondary goals.
It is important to recognise the treatment/action plan as flexible and changeable. Unexpected needs or problems can arise. Some goals might depend on others. Some might take longer than anticipated.

Common features of treatment plans include:
o developed as a result of a comprehensive assessment and modified over time as warranted
o reflects participation from appropriate disciplines – medicine, psychiatry, psychology, social work or vocational rehabilitation – as warranted
o reflects the person’s presenting needs and specifies their strengths and limitations
o consists of specific goals which pertain to the attainment, maintenance and/or re-establishment of physical and emotional health
o identifies specific objectives which relate directly to the treatment/change goals
o specifies the frequency of treatment/change contacts
o includes provisions for periodic re-evaluations and revisions, as needed, of the plan, and
o identifies criteria for determining if goals have been achieved, as well as for terminating change.
Some qualities of well-formed treatment/change goals are that they are: salient and meaningful to the person or organisation wishing change, incremental and so more manageable, concrete, specific and behaviour focused, able to increase desired behaviours, realistic and achievable, seen as requiring work and effort, and are appropriate for the projected change period.

FUTURE DIRECTIONS
In addition to its popularity with many addiction counsellors and researchers, the stages of change model should prove useful in tracking and predicting change. Most people have followed problematic paths over many years and made multiple attempts to change before being successful. They get stuck at certain points in the process of change and invest more time and energy in not changing than in activities to promote change. There is an ebb and flow, and important, distinct tasks which mark the process.
People can move forward and backward through the stages, and they can do so quickly. Their tasks involve a number of dimensions – motivation, decision making, efficacy, coping activities – which have an ongoing influence on the change process, can be accomplished quickly or slowly, and can be done more or less completely. These stages of change seem to resemble the stage dimensions of personality development proposed by Erickson in 1963.
Moving through change does not appear to be a case of doing more of the same thing, but instead doing the right thing at the right time.

There is also a growing body of literature which appears to support the relationship of stages to important outcomes.
One advantages of model is that the process of change is assumed to be the same for substance-abuse problems as well as other life problems.

It has been applied to changes related to many behaviours, including anxiety, medication compliance and health protection. The stages cover considerable ground, since the process of intentional behaviour change is central in the life of an individual, with major implications for growth and development.
There are few models which can be applied to such a variety of behaviours with such consistent results… Let’s change together.

Source: Addiction Today Aug.1st 2010

July 30, 2010

We have been monitoring ALL scientific research on marijuana/cannabis since about 1994 (and before that we purchased reference material from NIDA of all previous scientific studies). My husband is a nephrologist and clinical pharmacologist and my son is a rheumatologist. Both of these medical specialties require a depth of knowledge of pharmaceutical drugs that far surpasses that of most other subspecialties. One of the most important aspects of prescribing drugs of any sort is knowing the potential side effects and knowing how the drug will interact with other drugs or foods the individual may be taking. Every person is unique and drugs that are benign to one individual may be deadly for another. Penicillin is an excellent example because though it has saved millions of lives, it is also deadly for some. To date there are more than 20,000 published studies on marijuana and none of them offer proof of its safety or efficacy. That being said, I am attaching a file of documents relating to marijuana being a leading cause of drug-related emergency room episodes.

Fifteen years ago I attended a medical conference in Auckland, NZ with my husband. The doctor sitting next to me at dinner asked what I do. I told him that I was the unpaid head of a non-profit drug prevention organization. He said he didn’t think NZ had a drug problem. The doctor sitting across from us interjected that not only did NZ have a drug problem but that it was impacting the medical system. He said that he was head of the psychiatric unit at Auckland’s main hospital and that he would venture that at least 50% of those admitted for emergency psychiatric problems were there because of marijuana. I had heard that marijuana could cause psychiatric problems because two individuals I knew had kids who would go “round the twist” as they say in Auckland, whenever they smoked pot, and would end up in psychiatric care, but I had no idea is was that severe.

Then, about ten years ago, just after my husband became director of transplant for Legacy Hospital Systems, we went to dinner with one of the administrators and his wife. The wife asked what I do and I told her. She then volunteered that she was head of a triage unit in a psychiatric ward at another hospital and that it was her opinion that at least 65% of those admitted for emergency psychiatric problems were there because of marijuana.

re ingesting cannabis. One does not always know the potency of the cannabis being used or how much is in the product. Below is an exchange between a doctor who ingested “space cakes” and the editor of High Times Magazine. You will see that Ed Rosenthal (then the editor) acknowledges that marijuana can cause problems for even experienced users.

Marijuana is such an insidious drug that it may be years before we see the full extent of its potential to do harm. But a couple of things I think are VERY important and that is that marijuana has become a major factor in infertility (see Science Magazine for starters), and it destroys brain cells.

I am also attaching a document put together in 1999 (when there were only about 10,000 studies on marijuana) by a drug prevention specialist out of Canada. This document is called The Marijuana Connection and it categorizes the studies by side effect.

Source: Marijuana Research Review July 2010

Constituents of Cannabis Sativa L. (Marijuana)

In a document entitled “Constituents of Cannabis Sativa L. (Marijuana)” published by the University of Mississippi, Research Institute of

Pharmaceutical Sciences, Department of Pharmaceutics” (Ross SA, Elsohly MA. Constituents of Cannabis Sativa L. XXVIII A review of the natural

constituents: 1980-1994. J. Pharm Science. 1995;4:1-10, it states that marijuana contains 483 substances, 66 of which are cannabinoids. No

other plant contains cannabinoids.

Up to January, 2001, over 15,000 scientific papers have been published on cannabis and its constituents and many reviews have been written on

cannabis constituents and cannabinoid chemistry. A total of 483 natural constituents have been isolated and/or identified in Cannabis sativa

L., and they have been delineated as follows:

Cannabinoids 66
Nitrogenous Compounds 27
Amino acids 18
Proteins, Glycoproteins, Enzymes 11
Sugars & related compounds 34
Hydrocarbons 50
Simple Alcohols 7
Simple Aldehydes 12
Simple Keytones 13
Simple Acids 21
Fatty Acids 22
Simple Esters & Lactones 13
Steroids 11
Terpenes 120
Non-Cannabinoids Phenols 25
Flavonoids 21
Vitamins 1
Pigments 2
Elements 9

During the last quarter of the 20th century recreational use of
cannabis increased greatly across the world.1 Cannabis consumption
came to be seen as a normal leisure activity, and was regarded
as safe even by the medical establishment.2 However, in recent
years there has been considerable controversy over the use of
cannabis, with, for example, the UK government repeatedly
reviewing its safety.3 This concern has arisen from large prospective
epidemiological studies which have reported that use of
cannabis increases the risk of schizophrenia-like psychosis.4,5
However, these studies have not collected detailed data on the
patterns of use or potency of the cannabis used, which may be
important factors moderating the associated risk.6
The principal constituents of cannabis are D9-tetrahydrocannabinol
(D9-THC) and cannabidiol. The former is the main
psychoactive ingredient and in experimental studies it produces
transient psychotic symptoms and impaired memory in a dose dependent
manner.6,7 In contrast, cannabidiol does not induce
hallucinations or delusions, and it seems to antagonise the cognitive
impairment and psychotogenic effects caused by D9-THC.6
Until the early 2000s the most freely available type of cannabis
in the UK was cannabis resin (‘hash’), which had approximately
70% of the ‘street’ market, followed by traditional imported herbal
cannabis and then sinsemilla (‘skunk’). Cannabis resin contains
2–4% D9-THC and a similar proportion of cannabidiol, whereas
herbal cannabis contains a similar percentage of D9-THC but no
cannabidiol.8,9 However, sinsemilla (skunk) has increasingly taken
over the UK market and its THC concentration, and to a lesser
extent that of imported herbal cannabis, has been consistently
rising. For example, seizures of cannabis on the streets of England
in 2008 by the police showed that sinsemilla had a market share
of more than 70%, and had reached a D9-THC concentration of
12–18% with virtually no cannabidiol.8,9

Smith has suggested that such high-potency cannabis might be
especially harmful to mental health.10 We therefore compared
patterns and types of cannabis use in people experiencing their
first episode of psychosis and in a healthy control sample.
Specifically, we sought to test the hypothesis that daily use of
high-potency cannabis is associated with a particularly high risk
of psychosis.

Method
Sample
We approached all patients aged 18–65 years who presented with a
first episode of psychosis to the Lambeth, Southwark and Croydon
adult in-patient units of the South London & Maudsley Mental
Health National Health Service (NHS) Foundation Trust between
December 2005 and October 2008. We validated clinical diagnosis
by administering the Schedules for Clinical Assessment in
Neuropsychiatry (SCAN).11 Patients who met ICD–10 criteria
for a diagnosis of psychosis (codes F20–F29 and F30–F33)12 were
invited to participate in the study; cases with a diagnosis of
organic psychosis were excluded. During the same period we
recruited a healthy control group (n = 174) from the local
population living in the area served by the Trust, by means of
internet and newspaper advertisements, and distribution of
leaflets at train stations, shops and job centres. Cannabis was
not mentioned in these advertisements. Particular attention was
directed to attempting to obtain a control sample similar to the
patient sample in age, gender, ethnicity, educational qualifications
and employment status. Those who agreed to participate were
administered the Psychosis Screening Questionnaire,13 and
excluded if they met criteria for a psychotic disorder or reported
a previous diagnosis of psychotic illness.
Ethical permission was obtained from the Trust and the
Institute of Psychiatry research ethics committee. All study
participants signed a consent form allowing publication of data
originating from the study.

Background
People who use cannabis have an increased risk of
psychosis, an effect attributed to the active ingredient D9-
tetrahydrocannabinol (D9-THC). There has recently been
concern over an increase in the concentration of D9-THC in
the cannabis available in many countries.

Aims
To investigate whether people with a first episode of
psychosis were particularly likely to use high-potency
cannabis.

Method
We collected information on cannabis use from 280 cases
presenting with a first episode of psychosis to the South
London & Maudsley National Health Service (NHS) Foundation
Trust, and from 174 healthy controls recruited from the local
population.

Results
There was no significant difference between cases and
controls in whether they had ever taken cannabis, or age at
first use. However, those in the cases group were more
likely to be current daily users (OR = 6.4) and to have smoked
cannabis for more than 5 years (OR = 2.1). Among those who
used cannabis, 78% of the cases group used high-potency
cannabis (sinsemilla, ‘skunk’) compared with 37% of the
control group (OR 6.8).

Conclusions
The finding that people with a first episode of psychosis had
smoked higher-potency cannabis, for longer and with greater
frequency, than a healthy control group is consistent with
the hypothesis that D9-THC is the active ingredient
increasing risk of psychosis. This has important public health
implications, given the increased availability and use of highpotency
cannabis.

Source: The British Journal of Psychiatry (2009)
195, 488–491. doi: 10.1192/bjp.bp.109.064220

A report of a recent heroin prescription trial in Britain published in the Lancet (29th May 2010) was widely promoted as a success. The fact is that for a very costly intervention a surprisingly small minority got off street heroin.
Of the 43 clients that received a heroin dosage of 450mg twice a day plus a nightly oral methadone supplement over a 26 week period, just 5 of them managed to get off street heroin. Hardly a measure of success.
That means that the remaining 38 although they decreased their consumption of street heroin (hardly surprising) are still involved in the illegal heroin market, and still involved in the crime, harm and misery related to it.
Regardless of the at best mixed results, the authors make the following recommendation based on their study: “UK Government proposals should be rolled out to support the positive response that can be achieved with heroin maintenance treatment for previously unresponsive chronic heroin addicts.” This is not the way policy making should be informed.
It would be a surprise if a free handout of 900 mg a day of heroin would not decrease street heroin consumption to some extent. What is a significan and surprise finding is that even when offering free heroin, the program has such a limited impact on the use of street heroin.
The cost of heroin prescription per client is estimated to be about €18.000 a year, far more than for other treatment options. The UK government has spent about €700.000 on two heroin trials last year.

Misleading media reports

Reports in the press pretend that the project kept people “off street drugs”. That is stretching the truth quite a bit. This is how Reuters (Reuters Health) quote the researchers: “Prescribing heroin to addicts who can’t kick their habit helps them stay off street drugs, British researchers said Friday”, under the headline “Prescription heroin helps addicts off street drugs”. This is clearly misleading, and it reflects badly on the researchers that are clearly unable or unwilling to present a correct picture of their results.
The clients were measured on their reduction of street heroin, not other drugs. They were in fact not even tested for other drugs. For a specialist in drug treatment and for health politicians this is not very helpful. Drug addiction must be seen as a whole and not as unrelated consumption of various substances.
Associated Press reports that “Some heroin addicts who got the drug under medical supervision had a better chance of kicking the habit than those who got methadone, a new study says”, under the title “Study: heroin better than methadone to kick habit”.
First of all, to “kick the habit” means to get off the addiction. But the aim of the trial was not to get people off addiction. It did not even measure that. Second, the study does not say that treatment with heroin is better than methadone, it suggests that for some hard to treat/reach clients (5-10% of the heroin addicts) heroine may give better results. For the vast majority of problem heroin users methadone would be more suitable.
To see such inaccurate and misleading reporting by the world’s two most serious news agencies should worry everyone who is interested in how science is translated. Much of the responsibility should however lie on the researchers since they presumably were given the text for verification before release. In any case one would expect the researchers to immediately ensure that the grossly misleading reports were corrected.

“A ripple of excitement”?

The journalists’ reports lack precision and insight; the researchers however seem to have engaged in pure spin.
Professor Strang is quoted by The Independent in an article from September last year that the “the findings have sent a ripple of excitement through the addiction treatment community, which is unused to seeing progress with hard core addicts.” The researchers claim they have uncovered “”major benefits” in cutting crime and reducing street sales of drugs”.
See Kathy Gyngells blog at Centre for Policy Studies from September last year where she reports on some of the spin behind this affair while searching for the facts behind the “excitement”.
How is it possible to be positively surprised about these results, one may ask. Anyone would understand that if you give addicts heroin they will not have to buy it. The surprise is that so many of them continue to buy street heroin nevertheless.

Moralism, determinism and a bit of science

The biased approach of the researchers gets even more evident by reading the quote by Thomas Kerr, one of the researchers. He is director of the Urban Health Research Initiative at the University of British Columbia in Vancouver. He says to Reuters “I would argue it’s completely immoral and unethical to fail to treat those individuals and to allow them to suffer and allow the community around them to suffer”.
The first question to consider is if this is at all treatment. Treatment per definition should address the addiction and the health problems. This does not. If anything, it is primarily crime prevention. If treatment was paramount then why are treatment outcome indicators not measured? Their findings of psychosocial benefits are only anecdotal.
Second, the term, “allow them to suffer” assumes that their suffering is caused by “street” heroin and relieved by prescribed heroin. This represents a very narrow and simplistic understanding of the harm and problems related to addiction and drug use.
The researcher seems wedded to the myth of the demon drug. A basic social profile of the 43 clients would show that a host of social and psychosocial problems was well established before the drug problem and the addiction became the dominant issue.
Kerr question may therefore be turned around: Is it not equally “immoral and unethical” to fail to treat those individuals’ underlying problems and “allow them to suffer and allow the community around them to suffer”?
Why is it apparently more moral and ethical to substitute street heroin with prescription heroin and thereby reducing crime levels than actually treating their addiction and underlying social problems?
Do they know what addiction is?
The researchers seem to display a profound lack of understanding of what addiction is. Strang says the results shows they have “turned around” the users drug problem. “Turned around”? What happened with the few people that started to use less street heroin and more prescribed heroin cannot be called a turnaround. Some of them would commit somewhat less crime and spend a bit less time running for the next fix. Some contact is established. But where is exactly the “turnaround” in terms of the addiction and health problems? Their drug problem is not turned around and certainly not the addiction.
What this trial illustrates is the limitations of such harm reduction measures rather than its strengths. It also illustrates how scientific results may be distorted and misleading, possibly intentionally. Heroin prescription may have some benefits for some people, but they appear to be very limited, very costly and we know too little about it to make a judgement anywhere near what the researchers did in this case.
The simple question remains: what exactly is the treatment objective? What is the health related benefit? And where is the continuum of care and treatment? The programme has managed reach this very difficult group that is hard to reach and hard to treat. A politician would ask: OK, you’ve reached some of them, so what do you do?

Source: Report by Anders Ulstein, Updated 12.06.10 , published by Drug-Watch International
The study is called “Supervised injectable heroin or injectable methadone versus optimised oral methadone as treatment for chronic heroin addicts in England after persistent failure in orthodox treatment (RIOTT): a randomised trial”, written by John Strang and colleagues.

By Douglas B. Marlowe, J.D., Ph.D.
Chief of Science & Policy

Effectiveness

More research has been published on the effects of adult drug courts than virtually all other criminal justice programs combined. By 2006, the scientific community had concluded beyond a reasonable doubt from advanced statistical procedures called meta-analyses2that drug courts reduce criminal recidivism, typically measured by fewer re-arrests for new offenses and technical violations. The Table below summarizes the results of five independent meta-analyses all reporting superior effects for drug courts over randomized or matched comparison samples of drug offenders who were on probation or undergoing traditional criminal case processing. In each analysis, the results revealed that drug courts significantly reduced crime rates by an average of approximately 8 to 26 percent, with the “average of the averages” reflecting approximately a 10 to 15 percent reduction in recidivism.
Because these figures reflect averages, they mask substantial variability in the performance of individual drug courts. Approximately three quarters of the drug courts (78%) were found to have significantly reduced crime (Shaffer, 2006), with the best drug courts reducing crime by as much as 35 to 40 percent (Lowenkamp et al., 2005; Shaffer,
2006). In well-controlled experimental studies, the reductions in recidivism were shown to last at least three years post-entry (Gottfredson et al., 2005, 2006; Turner et al., 1999), and in one study the effects lasted an astounding 14 years (Finigan et al., 2007).
In 2005, the U.S. Government Accountability Office (GAO, 2005) similarly concluded that drug courts reduce crime; however, relatively little information was available at that time about their effects on other important outcomes, such as substance abuse, employment, family functioning and mental health. In response to the GAO report, the National Institute of Justice sponsored a national study of adult drug courts, entitled the Multisite Adult Drug Court Evaluation (or MADCE). The MADCE compared outcomes for participants in 23 adult drug courts located in seven geographic clusters around the country (n = 1,156) to those of a matched comparison sample of drug offenders drawn from six non-drug court sites in four geographic clusters (n = 625). The participants in both groups were interviewed at entry and at 6 and 18-month follow-ups, and provided oral fluid specimens at the 18-month follow-up. Their official criminal records are also being examined for up to 24 months.
The 6 and 18-month findings were presented at the 2009 Annual Conference of the American Society of Criminology (Rempel & Green, 2009; Rossman et al., 2009). In addition to significantly less involvement in criminal activity, the drug court participants also reported significantly less use of illegal drugs and heavy use of alcohol3. These self-report findings were confirmed by saliva drug tests, which revealed significantly fewer positive results for the drug court participants at the 18-month assessment (29% vs. 46%, p < .01). The drug court participants also reported significantly better improvements in their family relationships, and non-significant trends favoring higher employment rates and higher annual incomes. These findings confirm that drug courts elicit substantial improvements in other outcomes apart from criminal recidivism.

Cost-Effectiveness

In line with their positive effects on crime reduction, drug courts have also proven highly cost-effective (Belenko et al., 2005). A recent cost-related meta-analysis concluded that drug courts produce an average of $2.21 in direct benefits to the criminal justice system for every $1.00 invested — a 221% return on investment (Bhati et al., 2008). When drug courts targeted their services to the more serious, higher-risk offenders, the average return on investment was determined to be even higher: $3.36 for every $1.00 invested.
These savings reflect measurable cost-offsets to the criminal justice system stemming from reduced re-arrests, law enforcement contacts, court hearings, and use of jail or prison beds. When more distal cost-offsets were also taken into account, such as savings from reduced foster care placements and healthcare service utilization, studies have reported economic benefits ranging from approximately $2.00 to $27.00 for every $1.00 invested (Carey et al., 2006; Loman, 2004; Finigan et al., 2007; Barnoski & Aos, 2003). The result has been net economic benefits to local communities ranging from approximately $3,000 to $13,000 per drug court participant (e.g., Aos et al., 2006; Carey et al., 2006; Finigan et al., 2007; Loman, 2004; Barnoski & Aos, 2003; Logan et al., 2004).

Target Population

No program should be expected to work for all people. According to the criminological paradigm of the Risk Principle, intensive programs such as drug courts are expected to have the greatest effects for high-risk offenders who have more severe antisocial backgrounds or poorer prognoses for success in standard treatments (e.g., Andrews & Bonta, 2006; Taxman & Marlowe, 2006). Such high-risk individuals ordinarily require a combined regimen of intensive supervision, behavioral accountability, and evidence-based treatment services, which drug courts are specifically structured to provide.

Consistent with the predictions of the Risk Principle, drug courts have been shown to have the greatest effects for high-risk participants who were relatively younger, had more prior felony convictions, were diagnosed with antisocial personality disorder, or had previously failed in less intensive dispositions (Lowenkamp et al., 2005; Fielding et al., 2002; Marlowe et al., 2006, 2007; Festinger et al., 2002). In one meta-analysis, the effect size for drug court was determined to be twice the magnitude for high-risk participants than for low-risk participants (Lowenkamp et al., 2005). In a county-wide evaluation of drug courts in Los Angeles, virtually all of the positive effects of the drug courts were determined to have been attributable to the higher-risk participants (Fielding et al., 2002).

Fidelity to the 10 Key Components

In fiscally challenging times, there is always the pressure to do more with less. This raises the critical question of whether certain components of the drug court model can be dropped or the dosage decreased without eroding the effects. The “key components” of drug courts are hypothesized to include a multidisciplinary team approach, an ongoing schedule of judicial status hearings, weekly drug testing, contingent sanctions and incentives, and a standardized regimen of substance abuse treatment (NADCP, 1997). Each of these hypothesized key components has been studied by researchers or evaluators to determine whether it is, in fact, necessary for effective results. The results have confirmed that fidelity to the full drug court model is necessary for optimum outcomes — assuming that the programs are treating their correct target population of high-risk, addicted drug offenders.

Multidisciplinary Team Approach

The most effective drug courts require regular attendance by the judge, defense counsel, prosecutor, treatment providers and law enforcement officers at staff meetings and status hearings (Carey et al., 2008). When any one of these professional disciplines was regularly absent from team discussions, the programs tended to have outcomes that were, on average, approximately 50 percent less favorable (Carey et al., in press). In other words, if any one professional discipline walks away from the table, there is reason to anticipate the effectiveness of a drug court could be cut by as much as one half.

Judicial Status Hearings

Research clearly demonstrates that judicial status hearings are an indispensible element of drug courts (Carey et al., 2008; Festinger et al., 2002; Marlowe et al., 2004a, 2004b, 2006, 2007). The optimal schedule appears to be no less frequently than bi-weekly hearings for at least the first phase (first few months) of the program. Subsequently, the frequency of status hearings can be ratcheted downward; however, it appears that status hearings should be held at least once per month until participants have achieved a stable period of sobriety and have completed the intensive phases of their treatment regimen
.
Drug Testing

The most effective drug courts perform urine drug testing at least twice per week during the first several months of the program (Carey et al., 2008). Because the metabolites of most common drugs of abuse remain detectable in human bodily fluids for only about one to four days, testing less frequently can leave an unacceptable time gap during which participants can use drugs and evade detection. In addition, drug testing is most effective when it is performed on a random basis. If participants know in advance when they will be drug tested, they may adjust their usage accordingly or take other countermeasures in an effort to beat the tests.

Graduated Sanctions & Rewards

The pervasive perception among both staff members and participants in drug courts is that sanctions and incentives are strong motivators of positive behavioral change (Lindquist et al., 2006; Goldkamp et al., 2002; Harrell & Roman, 2001; Farole & Cissner, 2007). Two randomized, controlled experiments have confirmed that the imposition of gradually escalating sanctions for infractions, including brief intervals of jail detention, significantly improves outcomes among drug offenders (Harrell et al., 1999; Hawken & Kleiman, 2009). Comparably less research has addressed the use of positive rewards in drug courts, but preliminary evidence suggests that tangible incentives may improve
outcomes especially for the more incorrigible, higher-risk participants (Marlowe et al., 2008).
Substance Abuse Treatment

Longer tenure in substance abuse treatment predicts better outcomes (Simpson et al., 1997) and drug courts are proven to retain offenders in treatment considerably longer than most other correctional programs (Belenko, 1998; Lindquist et al., 2009; Marlowe et al., 2003). The quality of treatment is also a critically important consideration. Significantly better outcomes have been achieved when drug courts adopted standardized, evidence-based treatments, including Moral Reconation Therapy (MRT; Heck, 2008; Kirchner & Goodman, 2007), the MATRIX Model (Marinelli-Casey et al., 2008) and Multi-Systemic Therapy (MST; Henggeler et al., 2006); as well as culturally proficient services (Vito & Tewksbury, 1998). What all of these evidence-based treatments share in common is that they are highly structured, are clearly specified in a manual or workbook, apply behavioral or cognitive-behavioral interventions, and take participants’ communities of origin into account.

Conclusion

The scientific evidence is overwhelming that adult drug courts reduce crime, reduce substance abuse, improve family relationships, and increase earning potential. In the process, they return net dollar savings back to their communities that are at least two to three times the initial investments. The optimal target population for drug courts has been identified, and fidelity to several key ingredients of the drug court model has been demonstrated to be necessary for favorable results.

The challenge now is to extend the reach of adult drug courts without diluting the intervention below effective levels. Any program can be made cheaper simply by lowering the dosage or by providing fewer services to more participants. The difficult task is to maintain effectiveness in the process. Rather than drop essential components of the drug court model, research indicates that the better course of action is to standardize the best practices of drug courts so they can be reliably implemented by a larger number of programs, each serving a larger census of clients. This is the next great challenge for the drug court field.

Source: National Association of Drug Court Professionals.

References

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Barnoski, R,. & Aos, S. (2003). Washington State’s drug courts for adult defendants: Outcome evaluation and cost-benefit analysis. Olympia, WA: Washington State Institute for Public Policy.
Belenko, S. (1998). Research on drug courts: A critical review. National Drug Court Institute Review, 1, 1-42.
Belenko, S., Patapis, N., & French, M. T. (2005). Economic benefits of drug treatment: A critical review of the evidence for policy makers. Missouri Foundation for Health, National Rural Alcohol & Drug Abuse Network.
Bhati, A. S., Roman, J. K., & Chalfin, A. (2008). To treat or not to treat: Evidence on the prospects of expanding treatment to drug-involved offenders. Washington, DC: The Urban Institute.
Carey, S. M., Finigan, M., Crumpton, D., & Waller, M. (2006). California drug courts: Outcomes, costs and promising practices: An overview of phase II in a statewide study. Journal of Psychoactive Drugs, SARC Supplement 3, 345-356.
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Carey S. M., Waller, M., & Weller, J. (in press). California drug court cost study – Phase III: Statewide costs and promising practices, final report. Portland, OR: NPC Research.
Farole, D. J., & Cissner, A. B. (2007). Seeing eye to eye: Participant and staff perspectives on drug courts. In G. Berman, M. Rempel & R. V. Wolf (Eds.), Documenting Results: Research on Problem-Solving Justice (pp. 51-73). New York: Center for Court Innovation.
Festinger, D. S., Marlowe, D. B., Lee, P. A., Kirby, K. C., Bovasso, G., & McLellan, A. T. (2002). Status hearings in drug court: When more is less and less is more. Drug & Alcohol Dependence, 68, 151-157.
Fielding, J. E., Tye, G., Ogawa, P. L., Imam, I. J., & Long, A. M. (2002). Los Angeles County drug court programs: Initial results. Journal of Substance Abuse Treatment, 23, 217-224.
Finigan, M., Carey, S. M., & Cox, A. (2007). The impact of a mature drug court over 10 years of operation: Recidivism and costs. Portland, OR: NPC Research. Available at www.npcresearch.com
Goldkamp, J. S., White, M. D., & Robinson, J. B. (2002). An honest chance: Perspectives on drug courts. Federal Sentencing Reporter, 6, 369-372.
Gottfredson, D. C., Kearley, B. W., Najaka, S. S., & Rocha, C. M. (2005). The Baltimore City Drug Treatment Court: 3-year outcome study. Evaluation Review, 29, 42-64.
Gottfredson, D. C., Najaka, S. S., Kearley, B. W., & Rocha, C. M. (2006). Long-term effects of participation in the Baltimore City drug treatment court: Results from an experimental study. Journal of Experimental Criminology, 2, 67-98.
Harrell, A., Cavanagh, S., & Roman, J. (1999). Final report: Findings From the Evaluation of the D.C. Superior Court Drug Intervention Program. Washington, DC: The Urban Institute.
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Hawken, A., & Kleiman, M. (2009). Managing drug involved probationers with swift and certain sanctions: Evaluating Hawaii’s HOPE [NCJRS no. 229023]. Washington DC: National Institute of Justice. Available at http://www.ncjrs.gov/pdffiles1/nij/grants/229023.pdf.
Heck, C. (2008). MRT: Critical component of a local drug court program. Cognitive Behavioral Treatment Review, 17(1), 1-2.
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Kirchner, R. A., & Goodman, E. (2007). Effectiveness and impact of Thurston County, Washington drug court program. Cognitive Behavioral Treatment Review, 16(2), 1-4.
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Lindquist, C. H., Krebs, C. P., & Lattimore, P. K. (2006). Sanctions and rewards in drug court programs: Implementation, perceived efficacy, and decision making. Journal of Drug Issues, 36, 119-146.
Lindquist, C. H., Krebs, C. P., Warner, T. D., & Lattimore, P. K. (2009). An exploration of treatment and supervision intensity among drug court and non-drug court participants. Journal of Offender Rehabilitation, 48, 167-193.
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Logan, T. K., Hoyt, W., McCollister, K. E., French, M. T., Leukefeld, C., & Minton, L. (2004). Economic evaluation of drug court: Methodology, results, and policy implications. Evaluation & Program Planning,27, 381-396.
Loman, L. A. (2004). A cost-benefit analysis of the St. Louis City Adult Felony Drug Court. St. Louis, MO: Institute of Applied Research.
Lowenkamp, C. T., Holsinger, A. M., & Latessa, E. J. (2005). Are drug courts effective? A meta-analytic review. Journal of Community Corrections, Fall, 5-28.
Marinelli-Casey, P., Gonzales, R., Hillhouse, M., et al. (2008). Drug court treatment for methamphetamine dependence: Treatment response and post-treatment outcomes. Journal of Substance Abuse Treatment, 34, 242-248.
Marlowe, D. B., DeMatteo, D. S., & Festinger, D. S. (2003). A sober assessment of drug courts. Federal Sentencing Reporter, 16, 153-157.
Marlowe, D. B., Festinger, D. S., Dugosh, K. L., Arabia, P. L., & Kirby, K. C. (2008). An effectiveness trial of contingency management in a felony pre-adjudication drug court. Journal of Applied Behavior Analysis, 41, 565-577.
Marlowe, D. B., Festinger, D. S., Dugosh, K. L., Lee, P. A., & Benasutti, K. M. (2007). Adapting judicial supervision to the risk level of drug offenders: Discharge and six-month outcomes from a prospective matching study. Drug & Alcohol Dependence, 88S, 4-13.
Marlowe, D. B., Festinger, D. S., & Lee, P. A. (2004a). The judge is a key component of drug court. Drug Court Review, 4 (2), 1-34.
Marlowe, D. B., Festinger, D. S., & Lee, P. A. (2004b). The role of judicial status hearings in drug court. In K. Knight & D. Farabee (Eds.), Treating addicted offenders: A continuum of effective practices (chap. 11). Kingston, NJ: Civic Research Institute.
Marlowe, D. B., Festinger, D. S., Lee, P. A., Dugosh, K. L., & Benasutti, K. M. (2006). Matching judicial supervision to clients’ risk status in drug court. Crime & Delinquency, 52, 52-76.
National Association of Drug Court Professionals. (1997). Defining drug courts: The key components. Washington, DC: Office of Justice Programs, U.S. Dept. of Justice.
Rempel, M., & Green, M. (2009, November). Do drug courts reduce crime and produce psychosocial benefits? Presentation at the 2009 Annual Conference of the American Society of Criminology, Philadelphia, PA.
Rossman, S. B., Green, M., & Rempel, M. (2009, November). Substance abuse findings from the Multi-Site Adult Drug Court Evaluation (MADCE). Presentation at the 2009 Annual Conference of the American Society of Criminology, Philadelphia, PA.
1 Updated 6/29/10
Meta-analysis is an advanced statistical procedure that yields a conservative and rigorous estimate of the average effects of an intervention. It involves systematically reviewing the research literature, selecting out only those studies that are scientifically defensible according to standardized criteria, and statistically averaging the effects of the intervention across the good-quality studies (e.g., Lipsey & Wilson, 2002).
3 “Heavy use” of alcohol was defined as = 4 drinks per day for women, and = 5 drinks per day for men.
Shaffer, D. K. (2006). Reconsidering drug court effectiveness: A meta-analytic review [Doctoral Dissertation]. Las Vegas: Dept. of Criminal Justice, University of Nevada.
Simpson, D. D., Joe, G. W., &Brown, B. S. (1997). Treatment retention and follow-up outcomes in the drug abuse treatment outcome study (DATOS). Psychology of Addictive Behaviors, 11, 294-307.
Taxman, F. S., & Marlowe, D. B. (Eds.) (2006). Risk, needs, responsivity: In action or inaction? [Special Issue]. Crime & Delinquency, 52(1).
Turner, S., Greenwood, P. Fain, T., & Deschenes, E. (1999). Perceptions of drug court: How offenders view ease of program completion, strengths and weaknesses, and the impact on their lives. National Drug Court Institute Review, 2, 61-85.
U.S. Government Accountability Office. (2005). Adult drug courts: Evidence indicates recidivism reductions and mixed results for other outcomes [No. GAO-05-219]. Washington, DC: Author.
Vito, G. F., & Tewksbury, R. A. (1998). The impact of treatment: The Jefferson County (Kentucky) drug court program. Federal Probation, 62, 46-51.
Wilson, D. B., Mitchell, O., & MacKenzie, D. L. (2006). A systematic review of drug court effects on recidivism. Journal of Experimental Criminology, 2, 459-487.

A rare finding of substantially reduced youth substance use following a media campaign demonstrates the value of well tailored content and an effective, manageable delivery mechanism.
The campaign included print materials such as posters and promotional items such as book covers, tray liners, T-shirts, water bottles, rulers and lanyards, intended to associate drug-free lives with early teen aspirations for autonomy (“Be Under Your Own Influence” was the campaign’s identifier). Over two years school staff distributed the materials to secondary school pupils while community leaders involved in drug prevention worked with project staff to devise broader campaigns intended to reinforce the school-based measures. 16 communities across the United States were randomly allocated to mount these campaigns or to act as controls. Parental permission was received for 4216 first year pupils (average age 12) to participate in the study. They were surveyed before the interventions and then three more times, the last time after they had ended.

The key question was whether growth in substance use was retarded in the media campaign communities. The answer was yes, most clearly for drinking and cannabis use and less clearly (but still substantially) for smoking.
In the two sets of communities, at the start roughly the same proportions of pupils had tried these substances. Over the next two years, half as many pupils in the campaign communities started to use each of the three.
An earlier analysis suggested that the school campaign had worked by fostering the perception that substance use was incompatible with the pupils’ aspirations.

In context

Its inexpensive strategy meant the project could afford repeated exposure in a way that would not have been possible with mass media ads. It also gave teachers and school counsellors (who often distributed the materials) a chance to amplify the effects through interaction with the pupils and for pupils to discuss the campaign among themselves. Possibly relevant too were the marketing and PR backgrounds of the leading researcher and campaign strategist, who co-opted strategies used by companies seeking to sell to young people. Effects were much larger than the norm, probably because the study incorporated principles of effective media campaigns including tailoring to the community, preparatory research with the intended audience, a theoretical foundation, targeting to relevant sub-groups (in this case, youngsters largely yet to try drugs), novel and appealing messages, and effective delivery channels.
However, a third of the pupils did not participate in the study (among whom are likely to have been those most prone to substance use) and larger conurbations were excluded. Nor we do not know whether frequent use was also retarded, though this seems likely.

Practice implications An expertly planned and adequately resourced media campaign systematically focused on preventing substance use in young people can make a difference. Localities which want to achieve this will need to maintain focus on this objective rather than the many others campaigns can explicitly or implicitly serve. Upbeat messages about the advantages of not using seem to have more effect and less potential to backfire than negative warnings. Despite the emergence of important principles ( Incontext), there is no formula which guarantees success. Especially since there are also no demonstrably successful UK examples, any campaign should be evaluated against its objectives or a close proxy. If they will cooperate, schools are an effective and inexpensive delivery mechanism, but such activities are not an alternative to drug education lessons or pastoral interventions for high-risk pupils.
Featured studies Slater M.D. et al. “Combining in-school and community-based media efforts: reducing marijuana and alcohol uptake among younger adolescents.”
Health Education Research: 2006, 21(1), p. 157–167 DS
Contacts Michael Slater, School of Communication, Ohio State University, 3022
Derby Hall, 154 North Oval Mall, Columbus, OH 43210, USA, slater.59@osu.edu.
Thanks to Neil McKeganey of the Centre for Drug Misuse Research at the University
of Glasgow for his comments.

Source: Findings.org.uk

Ryan Vandrey1 and Margaret Haney2
1 Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
2 New York State Psychiatric Institute and College of Physicians and Surgeons of Columbia University,
New York, New York, USA

Abstract

Cannabis is the most widely used illicit drug in the world. Treatment admissions for cannabis use disorders have risen considerably in recent years, and the identification of medications that can be used to improve treatment outcomes among this population is a priority for researchers and clinicians.
To date, several medications have been investigated for indications of clinically desirable effects among cannabis users (e.g. reduced withdrawal, attenuation of subjective or reinforcing effects, reduced relapse). Medications studied have included those: (i) known to be effective in the treatment of other drug use disorders; (ii) known to alleviate symptoms of cannabis withdrawal (e.g. dysphoric mood, irritability); or (iii) that directly affect endogenous cannabinoid receptor function. Results from controlled laboratory studies and small open-label clinical studies indicate that buspirone, dronabinol, fluoxetine, lithium and lofexidine may have therapeutic benefit for those seeking treatment for cannabis-related problems. However, controlled clinical trials have not been conducted and are needed to both confirm the potential clinical efficacy of these medications and to validate the laboratory models being used to study candidate medications. Although the recent increase in research towards the development of pharmacotherapy for cannabis use disorders has yielded promising leads, well controlled clinical trials are needed to support broad clinical use of these medications to treat cannabis use disorders.

Cannabis (also known as marijuana or hashish) is obtained from the plant Cannabis sativa. Cannabis contains many psychoactive compounds that affect the endogenous cannabinoid receptor system, of which D-9-tetrahydrocannabinol (THC) has been identified as the compound primarily responsible for the subjective ‘high’ experienced by users.[1] The acute effects of cannabis include subjective feelings of euphoria, relaxation, dream-like state, altered sensory perception, slowing of time, anxiety/paranoia and increased appetite. Cannabis also increases heart rate and, in rare instances, can induce hallucinations or psychosis.

THC is a partial agonist of the cannabinoid receptor type 1 (CB1), a G protein-coupled receptor that is expressed in the brain at highest concentrations in the basal ganglia (motor control), cerebellum (sensorimotor coordination), hippocampus (memory) and cortex (higher-order cognition). Like most, if not all, addictive drugs, exposure to psychoactive cannabinoids stimulates brain reward areas and can induce appetitive drug-seeking and drug-taking behaviours. Evidence of these effects includes studies in which exposure to cannabis increased dopamine release in the mesolimbic-dopamine reward pathway, enhanced electrical brain stimulation reward, established conditioned place preference and established drug self-administration.
Similarly, abrupt cessation of long-term cannabinoid exposure produces cellular changes in the brain reward pathway (increased corticotrophin releasing factor, decreased dopamine) that have been linked to the dysphoric effects associated with withdrawal from drugs such as alcohol, opioids and cocaine, and are thought to contribute to relapse. Recognizing that cannabis shares neurobiological features associated with dependence on other drugs is important when considering pharmacological treatment of cannabis use disorders.

The rationale for developing pharmacological treatments for cannabis use disorders is clear. There are an estimated 160 million current cannabis users worldwide, and the number of people who meet criteria for cannabis dependence exceeds that for dependence on any other illicit drug. Treatment admissions for cannabis use disorders in many areas have steadily increased in the past decade, including a 2-fold increase in the US and 3-fold increases in Australia and
Europe. Clinical trials have demonstrated that evidence-based psychosocial interventions (e.g.motivational enhancement, contingency management, cognitive-behavioural therapy) result in overall improved clinical outcomes compared with usual care or delayed control conditions. However, as is common with other drugs (e.g. opioids, cocaine, nicotine), adults and adolescents seeking treatment for cannabis-related disorders have great difficulty achieving and sustaining periods of abstinence: the majority relapsing to use following therapeutic interventions.Thus, there exists a clear need for the development and dissemination of interventions that improve clinical outcomes (e.g. reduced use/abstinence, fewer drug-related problems) for the increasing number of those seeking treatment for their cannabis use.

One method of improving clinical outcomes for patients seeking treatment for cannabis use disorders is to identify medications that exhibit clinical benefit and could be added to existing evidence-based psychosocial treatments. There is evidence that a combination of pharmacotherapy and psychosocial therapy can significantly improve substance abuse treatment outcomes relative to psychosocial treatments alone. Pharmacotherapies can aid in the treatment of drug dependence in several ways. One approach is to identify medications that attenuate symptoms of withdrawal. This can be achieved with agonist/substitute medications (e.g. nicotine patch for tobacco dependence, methadone for opioid dependence) or by use of medications known to alleviate specific withdrawal symptoms (e.g. clonidine for sweating, gastrointestinal disturbance and hypertension during opioid withdrawal).

Another approach for pharmacotherapy is the use of medications that attenuate the reinforcing effects of the target drug. One way this can be done is by directly blocking the receptor with an antagonist (e.g. naltrexone for opioid dependence) or partial agonist (e.g. buprenorphine for opioid dependence). A third approach is the use of medications that induce adverse effects when combined with the drug of dependence (e.g. disulfiram induces nausea when combined with alcohol). There are currently no accepted pharmacological treatment interventions for cannabis use disorders. Identification of such medications is an increasing priority among researchers and clinicians working with cannabis users and has been addressed in a number of recent papers. In this manuscript, we review the extant research investigating medications of potential therapeutic efficacy for the treatment of cannabis dependence. Because of space constraints and the clinical focus of this review, preclinical laboratory studies will not be covered but can be found in other reviews. Areas of focus will include human laboratory studies, clinical case reports and small open-label trials, and controlled clinical trials. This paper will complement and extend previous reviews on the topic.

1. Human Laboratory Studies
1.1 Attenuation of Withdrawal Symptoms Research dating back to the 1970s provides clear evidence that a valid and reliable cannabis withdrawal syndrome occurs. Common symptoms of withdrawal in humans include: anger and aggression, anxiety, depressed mood, irritability, restlessness, sleep difficulty and strange dreams, decreased appetite and weight loss. Chills, headaches, physical tension, sweating, stomach pain and general physical discomfort have also been observed during cannabis withdrawal but are less common.Most symptoms begin within the first 24 hours of cessation, peak within the first week and last approximately 1–2 weeks. Because there is evidence that cannabis withdrawal contributes to the high relapse rates among heavy cannabis users,amelioration of cannabis withdrawal symptoms may be an important target for the development of pharmacological treatment interventions for heavy cannabis users. Much of the current research in humans has been conducted by a group of researchers at Columbia University in the US. There, an inpatient human laboratory model was designed to characterize the effects of medications on the consequences of abstinence from cannabis (e.g. withdrawal symptoms). Research volunteers who smoked cannabis multiple times per day and who were not seeking treatment for their cannabis use were enrolled in a series of studies investigating several medications. Participants smoked cannabis (active or placebo) and received oral medication (active or placebo) each day under double-blind conditions. The protocol used a within-subject crossover design so that each participant received each active and placebo combination of cannabis and medication. Further, most of the laboratory studies administered
medication repeatedly each day until steady state levels were attained prior to assessing the effects of cannabis. The effect of receiving placebo versus active medication during the periods of cannabis abstinence (placebo cannabis) was then evaluated. Outcome variables included round the-clock data on mood and physical symptoms, psychomotor task performance, food intake, social behaviour and sleep. Medications investigated in this model to date have been bupropion, divalproex, nefazodone, lofexidine and dronabinol. Bupropion is used clinically as an antidepressant and for smoking cessation, and is thought to exert clinical effects by inhibiting reuptake of noradrenaline (norepinephrine) and dopamine, and possibly by acting as a nicotine receptor antagonist. Divalproex is used clinically as a mood stabilizer as well as to treat epilepsy and migraine headaches. Divalproex dissociates into valproate ions in the gastrointestinal tract and, though uncertain, clinical effects are thought to be mediated by increased GABA levels in the CNS. Nefazodone is an antidepressant and is believed to operate by blocking postsynaptic serotonin 5-HT2A receptors and, to a lesser extent, by inhibiting presynaptic serotonin and noradrenaline reuptake. Lofexidine is used to treat symptoms of opioid withdrawal and acts as an agonist at the a2-adrenergic receptor. Dronabinol is used clinically as an antiemetic and appetite stimulant, and is a partial agonist of CB1 receptors.
In laboratory studies using the methods described previously, administration of bupropion (placebo or 300 mg/day for 17 days)[42] and divalproex (placebo or 1500mg/day for 29 days) during periods of cannabis abstinence significantly worsened mood compared with placebo. Nefazodone (placebo or 450mg/day for 26 days) significantly decreased ratings of anxiety and muscle pain during abstinence but did not alter other essential features of cannabis withdrawal. Lofexidine (2.4mg/day for 8 days) significantly reduced ratings of chills, restlessness and upset stomach, and improved sleep but was associated with increased sedation during the day. Not surprisingly, the medication that has demonstrated the most clinical potential in reducing cannabis withdrawal has been dronabinol. Dronabinol is a synthetic formulation of THC, the primary psychoactive component in cannabis. In that regard, it is similar to using nicotine replacement products to suppress withdrawal during tobacco abstinence. In one study by the Columbia University researchers, dronabinol (10 mg five times daily for 6 days) significantly
decreased ratings of cannabis craving, anxiety, misery, chills and self-reported sleep disturbance,
and reversed the anorexia and weight loss associated with cannabis withdrawal. This attenuation of withdrawal symptoms occurred even though participants in this study were unable to reliably distinguish dronabinol from placebo. In a follow-up study, dronabinol administered at a higher dose and less frequently (20 mg three times daily for 8 days) again decreased ratings of restless and chills, and reversed anorexia but was associated with significant increases in drug effect, drug liking, irritability and latency to sleep compared with placebo. However, in this same study a combination of dronabinol (20 mg three times daily) and lofexidine (mg/day) decreased ratings of restlessness, chills, craving and upset stomach, and improved multiple measures of sleep but also increased sedation during the day and drug effect ratings. The effects of dronabinol (0 mg, 10 mg and 30 mg, three times daily for 15 days) on cannabis withdrawal were also recently reported in an outpatient study of daily cannabis users not seeking treatment. Dronabinol dose dependently decreased withdrawal symptoms during 5-day periods of abstinence while participants were in their home environment. Compared with placebo,
the 10 mg dose reduced participant ratings of aggression, craving, irritability, sleep difficulty and total withdrawal. Though withdrawal was attenuated at the 10 mg dose, it remained significantly elevated compared with a baseline period when participants smoked cannabis as usual. When participants received the 30 mg dose, withdrawal symptom severity was significantly reduced compared with both the placebo and 10 mg conditions and, more importantly, none of the withdrawal symptom ratings differed from the cannabis-as-usual baseline condition, indicating
a maximum therapeutic effect at this dose. Consistent with the initial study described
previously, the 10 mg dose regimen was not associated with increased ratings of intoxication and was not reliably distinguished from placebo. However, the 30 mg dose was distinguished from placebo by all participants and resulted in significantly increased drug effect ratings.

1.2 Attenuation of Subjective and Reinforcing Effects
Laboratory studies have also investigated the ability of medications to reduce the acute effects of smoked cannabis or orally administered THC. In one experiment, pretreatment with the CB1 receptor antagonist rimonabant significantly attenuated the physiological and subjective effects of smoked cannabis administered 2 hours later. Acute administration of rimonabant 90 mg reduced participant ratings of the strength and liking of the smoked cannabis by approximately 40% and reduced cannabis-induced tachycardia by 59%. In a subsequent study, acute administration of rimonabant 90 mg again reduced cannabis-induced tachycardia, but the
attenuation of subjective drug effects was not replicated. In this same study, repeated daily doses of rimonabant (40 mg) administered for 15 consecutive days to a second group of participants reduced cannabis-induced tachycardia following acute cannabis administration on days 8 and 15. The subjective effects of cannabis were also reduced by rimonabant in this group, but that reduction was only significantly different from placebo on day 8 and not on day 15. Thus, rimonabant reduced the effects of smoked cannabis in two studies, but a reduction of subjective
drug effects was not consistently observed. Additional research is needed to investigate the dose effects of this antagonism and whether it translates to clinically meaningful behaviour change (reduced use or relapse prevention). Studies have also investigated whether the m-opioid receptor antagonist naltrexone, which has been shown to decrease cannabinoid self administration in non-humans, can reduce the subjective effects of cannabinoids in humans. In cannabis users, pretreatment with high doses of naltrexone (50–200 mg) failed to attenuate,and in some cases enhanced, the subjective effects of dronabinol and smoked cannabis. By contrast, a lower, more opioid-selective dose of naltrexone (12 mg) decreased the intoxicating
effects of dronabinol 20mg but not 40 mg in a recent study. These findings indicate that the influence of naltrexone on cannabinoid effects may vary as a function of the naltrexone dose, but also that the effect of naltrexone can be overcome with higher doses of cannabis. The effect of dronabinol on the subjective and reinforcing effects of smoked cannabis has also been investigated. Participants received dronabinol 0 mg, 10 mg or 20 mg four times daily for 3 consecutive days. Each day, participants sampled the dose of cannabis cigarette available that day and were then given four choices during the course of that day to smoke the sampled dose of cannabis or receive a voucher worth $US2 that would be added to their study earnings.
Subjective drug effect ratings were obtained following the sample dose of cannabis under each dronabinol dose condition. Dronabinol attenuated the subjective effects of smoked cannabis but did not affect the choice to smoke cannabis (reinforcing effects). Of note, the competing reinforcer, a voucher worth $US2, may not have been sufficiently sensitive to detect changes in cannabis reinforcing efficacy. Also, each dronabinol dose condition only lasted for 3 days, whereas more time may be needed to see an effect of maintenance medication. Thus, more data are needed to determine whether dronabinol disrupts ongoing cannabis use.

The subjective effects of cannabis have also been evaluated in single studies for several other medications. In a small laboratory study, a 0.4mg dose of clonidine (an a2-adrenoreceptor agonist and opioid withdrawal medication) administered 3 hours prior to smoked cannabis reduced cannabisinduced tachycardia but did not reduce subjective effects. Bupropion (300 mg) decreased ratings of the ‘high’ following smoked cannabis, but, as described previously, this dose also exacerbated withdrawal effects during a period of abstinence. In two other laboratory studies described previously, the subjective effects of smoked cannabis were not altered by nefazodone (450 mg) and were increased following administration of divalproex (1500 mg).

1.3 Relapse Prevention
In one recent study, relapse was modelled in non-treatment seekers by structuring laboratory conditions (charging participants $US10 for a single initial puff of cannabis) so that a return to cannabis use was costly. The effects of dronabinol (20 mg three times daily) and lofexidine (2.4 mg/day) were evaluated both when administered alone and when administered together. In this study, neither dronabinol nor lofexidine alone reduced the number of participants who elected
to smoke any amount of cannabis compared with placebo during a 4-day maintenance period, but the combination of the two drugs doubled therate of complete abstinence (25% abstinent for each medication alone, 50% for the combination).Compared with the placebo condition, the average amount of money spent per day on cannabis was reduced in both the lofexidine alone and the combined medication conditions.

2. Case Reports and Small Open-Label Studies

Several studies have investigated the efficacy of potential treatment medications for cannabis dependence in small clinical samples. One recent open-label study investigated atomoxetine as a potential pharmacotherapy in adults presenting for treatment of cannabis dependence. Atomoxetine is a non-stimulant medication that inhibits noradrenaline reuptake and is used to treat attention-deficit hyperactivity disorder. Thirteen participants received atomoxetine (25–80 mg/day; mean 62 mg/day) for 11 weeks. A non-significant reduction in cannabis use was
observed. However, several adverse events were reported, including clinically significant gastrointestinal problems in 77% of participants. Two participants withdrew from the study because of these adverse effects. An open-label investigation was also conducted with the anxiolytic medication buspirone, a 5-HT1A receptor agonist and dopamine D2 receptor mixed agonist/antagonist.[60] Ten treatment-seeking cannabis users received buspirone (up to 60 mg/day; mean 39 mg/day) for up to 12 weeks. Self-reported cannabis use declined from
use on 73% of days prior to treatment to use on 39% of days during treatment, and 44% of urine drug screens conducted during treatment were negative for cannabis (100% positive at intake). Significant decreases in craving and irritability during treatment were also observed. However, several adverse events were reported during the trial and only two participants completed the entire 12-week study. Following a preclinical study showing that lithium, a mood stabilizer that enhances oxytocin expression, attenuated cannabis withdrawal in rats, two small open-label clinical studies were conducted. In one study, lithium was administered to nine adults presenting for treatment of cannabis dependence. All participants indicated that previous quit attempts resulted in significant withdrawal symptoms and that abstinence failed to extend beyond a few days or weeks. Lithium (600–900 mg/day) was administered for 6 days and resulted in reduced withdrawal severity in four of the nine participants. However, cannabis was admittedly smoked during this period by one of these four participants and cannabis abstinence was not verified in the others. In the second study, 20 cannabis-dependent participants received lithium (500 mg twice daily) for 7 days in an inpatient detoxification facility. Twelve participants (60%) completed the 7-day inpatient detoxification (two were removed because of adverse events). Cannabis abstinence at post-treatment follow-up sessions was 64% (day 10), 65% (day 24) and 41% (day 90). Participants also self-reported cannabis abstinence on 88% of days post-treatment, with five participants reporting continuous abstinence that was corroborated with urine toxicology tests on day 90. To date, the only published report in which dronabinol has been used clinically to treat cannabis dependence is a paper describing two case studies. In both cases, the patients used cannabis daily and had repeatedly failed in prior quit attempts. Dronabinol was started at a dosage of 30 mg/day (10 mg three times daily) and then adjusted in both cases. Both patients were able to achieve sustained periods of abstinence; however,adjunct medications were required (divalproex for case 1 and venlafaxine for case 2). In case 1, the patient was successfully tapered off dronabinol without relapse. In case 2, removal of dronabinolresulted in either relapse or heavy alcohol use. This patient continued using dronabinol (5 mg two to three times daily) as a maintenance medication. A case report has also been published in which the atypical antipsychotic medication quetiapine was administered to eight cannabis-dependent patients with a diagnosis of either schizophrenia or bipolar disorder. Following quetiapine administration at a mean dosage of 388 mg/day (range 100–1200 mg/day) for an average of approximately 6 months, cannabis use in these eight patients was reported as being reduced from an average of 35.6 g/week to 1.1 g/week. Concomitant medications administered during the
quetiapine treatment period included unspecified antidepressants (n = 4), gabapentin (n = 2) and methadone (n = 1). It is unclear from the report whether cannabis use rates were verified via objective measures (e.g. urine toxicology) or if the medication was well tolerated by all patients who received it.

3. Clinical Trials

At this time, there is only one published controlled clinical trial in which a medication was tested for efficacy in participants presenting for treatment where cannabis dependence was the primary problem. In this double-blind trial, 25 participants were randomized to receive divalproex (500–2000 mg/day; mean 1673 mg/day) or placebo for 6 weeks and were then crossed over to the opposite medication condition. Participants also received weekly relapse prevention counselling throughout the study. Cannabis use was assessed via self-reporting and quantitative urine testing. An overall reduction of cannabis use was reported, but few urine drug screens were free of cannabis, suggesting that sustained abstinence was not achieved. There was no effect of divalproex compared with placebo on any cannabis use measures. Adverse events related to divalproex were common and resulted in discontinuation for three participants, and toxicology analyses indicated that medication compliance was poor among those receiving active medication. One other controlled clinical trial has been published in which cannabis use was measured following administration of medication, but in this study participants represented a subgroup of participants within a larger trial for the treatment of alcoholism and depression primary to their cannabis dependence. Following a brief inpatient detoxification, participants were randomly assigned to receive fluoxetine 20–40 mg/day (a selective serotonin reuptake inhibitor used to treat depression) or placebo for 12 weeks (n = 11 group). Compared with placebo, those who received fluoxetine reported using less cannabis, using cannabis on fewer days, drinking less alcohol and had a greater decrease in ratings of depression. No objective measures of substance use were obtained to verify the self-reports in this study, and it is unclear whether the decrease in cannabis use was mediated by reductions in alcohol use or depression.

4. Conclusion
Efforts to identify medications that can improve treatment outcomes for cannabis use disorders have increased considerably in recent years but still lag far behind the medication development efforts for treating dependence on other drugs (e.g. alcohol, cocaine, opioids). Most of the current research is limited to laboratory models and small open-label trials, with only one published controlled clinical trial (compared with dozens to hundreds of controlled pharmacotherapy trials for treating dependence on alcohol, cocaine, nicotine and opioids). The laboratory studies described in section 1 all employed cannabis users who were not trying to reduce or quit their cannabis use. Although it is possible that this limits the generality of these studies, it is important to point out that for drugs such as cocaine and heroin, the validity of human laboratory studies of self-administration for predicting
medication efficacy in the clinic is better than most other models, including open-label clinical studies, which are often characterized by a high number of false positives. That said, controlled clinical trials for cannabis dependence are clearly needed, not only to determine the efficacy of candidate medications but also to evaluate the predictive validity of the laboratory models being used. At this point, several medications that were studied appear to warrant further investigation
(table I). Dronabinol has been the most extensively studied and appears to be the strongest candidate medication to date. Studies have indicated several clinically important effects of dronabinol (reduction of withdrawal and decreased relapse when combined with lofexidine, and possibly divalproex or venlafaxine). Moreover, agonist medications have demonstrated
efficacy in the treatment of tobacco and opioid dependence. Replication in controlled clinical trials is needed (two placebo-controlled trials are currently being conducted in patients specifically seeking treatment for their cannabis use). Dronabinol has a slow rate of onset and low rates of abuse. However, the safety and abuse liability/ diversion of dronabinol in addiction treatment settings needs to be assessed because the population seeking treatment for cannabis dependence (many adolescents, people with extensive drug use histories and a preference for cannabinoid self-administration) may present with unique safety and abuse liability concerns.
The cannabinoid receptor antagonist rimonabant reduced the effects of smoked cannabis in two studies, but a reduction of subjective drug effects was not consistently observed. Since this research began, clinical use of rimonabant for any indication has been suspended because of the risk of adverse psychiatric effects. While this will preclude the use of rimonabant for the treatment of cannabis use disorders, these data indicate that cannabinoid receptor antagonists may be clinically useful in the treatment of cannabis use disorders should alternative compounds with better safety profiles be developed. That administration of fluoxetine has been associated with reduced cannabis use among depressed alcohol-dependent individuals suggests therapeutic potential. Replication of this effect is needed in either laboratory or clinical studies in which cannabis is the primary drug of abuse among participants. A laboratory study with lofexidine showed promise, but needs to be replicated. Finally, findings with buspirone, lithium and quetiapine have also been in a positive direction, but need to be verified using placebo controlled studies. The occurrence of adverse effects may also limit the use of these medications.

In conclusion, the need for identifying medications to improve treatment outcomes for cannabis dependence is clear. Medications should be used in conjunction with evidence-based psychosocial treatments to maximize clinical benefit, and some combination of multiple medications may be needed to achieve sustained abstinence in more severe cases. At this time, although it does not appear that we are close to the broad use of pharmacotherapies for cannabis dependence, several promising candidate medications have been identified. Continued research studies, particularly controlled clinical trials, are obviously needed for the medications that have demonstrated promise to date. Moreover, there are a number of compounds (e.g. second-generation cannabinoid receptor antagonists, fatty acid amide hydrolase [FAAH] inhibitors) for which mpreclinical data indicate potential for treating cannabis use disorders once they are approved for research in humans. It will be important for scientists and clinicians to continue to investigate these and other medications that could reasonably be considered to have therapeutic potential for treating cannabis use disorders.
Acknowledgements: We thank the US National Institute on Drug Abuse (Dr Vandrey: DA12471 and DA025794; Dr Haney: DA09236 and DA19239) for its support. Dr Vandrey also thanks the Johns Hopkins University School of Medicine Department of Psychiatry and Behavioral Sciences for support. The authors have no conflicts of interest that are directly relevant to the content of this review. E-mail: rvandrey@jhmi.edu

Source: Pharmacotherapy for Cannabis Dependence 553. CNS Drugs 2009; 23 (7)

Historian looks at resistance to the “NIDA paradigm.”

The history of addiction as a brain disease “looks a lot like the history of atoms or germs, insofar as these were older and controversial ideas for which scientific confirmation later became available,” writes historian David Courtwright, author of Forces of Habit: Drugs and the Making of the Modern World.

In a recent issue of the social science journal BioSocieties, Courtwright surveys the history of the disease paradigm of drug addiction, and, in doing so, brings into focus several key dilemmas related to what former National Institute on Drug Abuse (NIDA) director Alan Leshner once characterized as the “quintessential biobehavioral disorder.”

The scientific evidence available to us at present largely supports a statement like Leshner’s. Researchers have documented long-term changes in brain structure and function due to drug abuse, and neuroimaging technologies have resulted in maps of the abnormal neuronal activity addicts exhibit. Courtwright cites the discovery of the endogenous opioid system, the mapping of receptor pathways, and the growing understanding of the mesolimbic dopamine reward pathway as evidence of clinical confirmation of theories about addictive disease that has been floating around in one form or another for many years.

Why then, Courtwright asks, does the medical profession largely stay clear of issues having to do with our law enforcement-driven drug war? Why are clinical professionals not on the front lines of revolt over this issue? “If addiction was beyond the individual’s control, then criminal punishment was as inappropriate as jailing a schizophrenic who wandered into an emergency room,” the author writes.

The most obvious reason for this conundrum, says Courtwright, is that “the brain disease model has so far failed to yield much practical therapeutic value.” The disease paradigm has not greatly increased the amount of “actionable etiology” available to medical and public health practitioners. “Clinicians have acquired some drugs, such as Wellbutrin and Chantix for smokers, Campral for alcoholics or buprenorphine for heroin addicts, but no magic bullets.” Physicians and health workers are “stuck in therapeutic limbo,” Courtwright believes. “The drug-abuse field is characterized by, at best, incomplete and contested medicalization.”

Moreover, unlike the current situation in the case of, say, diabetes or schizophrenia, “at least four important groups continue to wrestle for control of the addiction field.” (Medical personnel, police, social scientists, and political officials.) Social scientists, in particular, are frequently skeptical about the NIDA disease paradigm “as part of a broader post-World War II pattern of resistance against biological explanations of behavior, genetic research and the neo-Darwinian renaissance.”

Social scientists and neuroscientists “still live in their own gated academic communities,” Courtwright alleges. “There is a lot more at stake in the brain disease debate than our understanding of addiction.”

However, these problems do not mean that valuable findings in one area–addictive disease theory–cannot produce innovations in other research fields as well. In fact, such spinoffs happen all the time. Courtwright points to advancements in our understanding of evolution: “Michael Kuhar has argued that, because the brain co-evolved with neurotransmitters, it can usually manage its internal chemistry quite well. But it did not co-evolve with drugs, understood as recently introduced and wholly exogenous super-neurotransmitters that can override the brain’s control mechanisms.”

The author also cites spinoffs in economic studies: “The permanent alteration of neurons and the development of addiction in some, but not all, users also helped explain the commercial and tax appeal of drugs, insofar as they were nondurable goods with relatively inflexible demand curves. Even non-addicted users tended to consume more over time, because of tolerance.”

In the end, it is just possible to contemplate some sort of fusion, or meeting of the minds, over the disease model. As Courtwright speculates, “it may turn out that the tension between the personality and brain disease models is more apparent than real.” He cites as evidence such connections as the fit between impulsive, thrill-seeking behavior and an associated paucity of dopamine D2 and D3 receptors in the midbrain region. The result? Such people “have less inhibition of dopamine, and experience more reward when stimulated by risky behavior.” A nice fit. And the number of nice fits between social science and brain science continues to accumulate.

“If the brain disease model ever yields a pharmacotherapy that curbs craving, or a vaccine that blocks drug euphoria, as some researchers hope,” Courtwright says, “we should expect the rapid medicalization of the field. Under those dramatically cost-effective circumstances, politicians and police would be more willing to surrender authority to physicians.”

Graphics Credit: http://alcoholanddrugabuse.org

SOURCE:HTTP://ADDICTION-DIRKH.BLOGSPOT.COM/2010/06/ WEDNESDAY, JUNE 23, 2010

1. Executive Summary
Policymakers and other stakeholders can use cost-benefit analysis as an informative tool for decision making for substance abuse prevention. This report reveals the importance of supporting effective prevention programs as part of a comprehensive substance abuse prevention strategy. The following patterns of use, their attendant costs, and the potential cost savings are analyzed:
• Extent of substance abuse among youth;
• Costs of substance abuse to the Nation and to States;
• Cost savings that could be gained if effective prevention policies, programs, and services were implemented nationwide;
• Programs and policies that are most cost beneficial.

1.1. Costs of Substance Abuse
Studies have shown the annual cost of substance abuse to the Nation to be $510.8 billion in 1999 (Harwood, 2000). More specifically,
• Alcohol abuse cost the Nation $191.6 billion;
• Tobacco use cost the Nation $167.8 billion;
• Drug abuse cost the Nation $151.4 billion.

Substance abuse clearly is among the most costly health problems in the United States. Among national estimates of the costs of illness for 33 diseases and conditions, alcohol ranked second, tobacco ranked sixth, and drug disorders ranked seventh (National Institutes of Health [NIH], 2000). This report shows that programs designed to prevent substance abuse can reduce these costs.

1.2. Savings From Effective School-Based Substance Abuse Prevention
If effective prevention programs were implemented nationwide, substance abuse initiation would decline for 1.5 million youth and be delayed for 2 years on average. It has been well established that a delay in onset reduces subsequent problems later in life (Grant & Dawson, 1997; Lynskey et al., 2003). In 2003, an estimated:

• 5.6 percent fewer youth ages 13–15 would have engaged in drinking;
• 10.2 percent fewer youth would have used marijuana;
• 30.2 percent fewer youth would have used cocaine;
• 8.0 percent fewer youth would have smoked regularly.

The average effective school-based program in 2002 costs $220 per pupil including materials and teacher training, and these programs could save an estimated $18 per $1 invested if implemented nationwide. Nationwide, full implementation of school-based effective programming in 2002 would have had the following fiscal impact

• Saved State and local governments $1.3 billion, including $1.05 billion in educational costs within 2 years;

• Reduced social costs of substance-abuse-related medical care, other resources, and lost productivity over a lifetime by an estimated $33.7 billion;
• Preserved the quality of life over a lifetime valued at $65 billion.

Although 80 percent of American youth reported participation in school-based prevention in 2005 (SAMHSA, 2004), only 20 percent were exposed to effective prevention programs (Flewelling et al., 2005). Given this level of participation, it is possible that some expected benefits already exist for these students, and the estimates in this paper are adjusted for these probable benefits.
These cost-benefit estimates show that effective school-based programs could save $18 for every $1 spent on these programs.

In a program targeting families with low income, intensive home visitation coupled with preschool enrichment reduced infant/toddler abuse (Aos et al., 1999; Karoly et al., 1998). As these toddlers reach adolescence and adulthood, visitation programs also can reduce a range of problems including substance abuse and violence.

Among indicated programs (targeted to individuals who have detectable symptoms), cost estimates that primarily focused on substance abuse were not available. However, estimates indicating good returns on the investment were available for several violence prevention interventions that address the roots of multi-risk behavior. Moral reconation therapy for adult and youth offenders, and multi-systemic therapy and functional family therapy for youth offenders returned more than $30 per dollar invested.

1.3. Conclusion
The cost of substance abuse could be offset by a nationwide implementation of effective prevention policies and programs. SAMHSA’s Strategic Prevention Framework should include a planning step that considers cost-benefit ratios. Communities should consider a comprehensive prevention strategy based on their unique needs and characteristics and use cost-benefit ratios to help guide their decisions. Model programs should include data on costs and estimated cost-benefit ratios to help guide prevention planning.

Source:
Substance Abuse Prevention Dollars and Cents: A Cost-Benefit Analysis
Substance Abuse and Mental Health Services Administration (SAMHSA) Center for Substance Abuse Prevention (CSAP)

White House ‘drug czar’ Gil Kerlikowske lays out his most thorough arguments yet against marijuana legalization. They help clear up confusion over White House drug policy, and can serve as talking points for parents and officials.
The Obama White House has finally laid out its most thorough, reasoned rebuttal to arguments for marijuana legalization – countering a campaign that is gaining alarming momentum at the state level.
The president’s tough position was delivered in early March by his “drug czar,” Gil Kerlikowske, in a private talk before police chiefs in California – which is ground zero for this debate.
“Marijuana legalization – for any purpose – is a nonstarter in the Obama administration,” said Mr. Kerlikowske, a former police chief himself.
It’s almost certain that California voters will be asked in a November ballot initiative whether to allow local governments to regulate and tax marijuana (similar to taxes on sales of alcohol). Other states are considering similar proposals, which are really a backdoor way to legalize pot.
(For a Monitor news story on the California ballot initiative, click here)
Thirteen states have decriminalized the use or possession of small amounts of marijuana, which is not the same as legalizing it. Selling it is still illegal except in states where it is used for medical purposes. And under federal law, any sort of marijuana use or sale is a criminal offense.
The drug czar’s remarks are worth notice for two reasons. First, they provide needed talking points for those who oppose legalization but who can’t seem to make their message resonate in the face of a well-financed, well-organized pro-marijuana effort. Second, they help clear up confusion about the White House policy on legalization.
When Attorney General Eric Holder announced last year that US law enforcement officials would neither raid nor prosecute medical marijuana dispensaries or those using them, states got mixed signals. Mr. Holder explained it as a matter of the best use of scarce federal law enforcement resources, which he didn’t want to expend in the now 14 states that have approved some use of medical marijuana.
But “a lot of people believe the administration is somewhat in favor of the decriminalization of marijuana,” says Scott Kirkland, police chief for El Cerrito, in the San Francisco Bay area. In California, the public, city council members, city managers, even police chiefs have “misinterpreted” the administration’s position, says Mr. Kirkland, the spokesman for marijuana issues for the California Police Chiefs Association.
The drug czar couldn’t have been more plain. On medical marijuana, which has strong public backing in opinion polls, the former Seattle police chief said that “science should determine what a medicine is, not popular vote.” As Kerlikowske pointed out, marijuana is harmful – and he has the studies to back it up. Read the footnotes in his speech; they’re sobering, especially No. 8.
(For a previous Monitor editorial on the perils of legalizing pot, click here)
Legalization supporters argue that no one has ever died from an overdose of this “soft” drug. But here’s what “science” has found so far: Smoking marijuana can result in dependence on the drug.
More than 30 percent of people who are 18 and over and who used marijuana in the past year are either dependent on the drug or abuse it – that is, they use it repeatedly under hazardous conditions or are imparied when they’re supposed to be interacting with others, such as at work. This is according to a 2004 study in the Journal of the American Medical Association.
Pot is also associated with poor motor skills, cognitive impairment (i.e., affecting the ability to think, reason, and process information), and respiratory and mental illness.
The recent “Pentagon shooter,” John Patrick Bedell, was a heavy marijuana user. The disturbed young man’s psychiatrist told the Associated Press that marijuana made the symptoms of his mental illness more pronounced. Mr. Bedell’s brother, Jeffrey, told The Washington Post that marijuana made his brother’s thinking “more disordered” and that he had implored him to stop smoking pot, to no avail.
Kerlikowske also effectively knocked down the argument that regulating and taxing marijuana is a great way for states to make money in these deficit-dreary times. Indeed, NORML, the lead group in the legalization movement, is set to launch a digital ad campaign in Manhattan’s Times Square next week: “Money CAN grow on trees!”
It’s a claim that’s too good to be true, just as the exclamation point implies. Look at the nation’s experience with regulated alcohol. America collects nearly $15 billion a year in federal and state taxes from alcohol. But Kerlikowske says that covers less than 10 percent of the “social costs” related to healthcare, lost productivity, and law enforcement. And what about lost lives? Let’s not add marijuana to the mix of regulated substances.
“The costs of legalizing marijuana would outweigh any possible tax that could be levied,” Kerlikowske explains. In the United States, illegal drugs already cost an estimated $180 billion annually in social costs, according to the Office of National Drug Control Policy. That number would increase as marijuana became more widely and easily available.
The Dutch – so often praised by marijuana advocates – have had to greatly ratchet back the number of legal marijuana outlets because of crime, nuisance, and increased pot usage among youth. Los Angeles, too, now sees the need to scale back the number of private dispensaries of medical marijuana. Many California towns have looked at L.A. and are saying “no” to dispensaries.
The California Board of Equalization, which administers the state’s sales tax, estimates $1.4 billion of potential revenue from a marijuana tax. Found money? Its reasoning is based on either “a series of assumptions that are in some instances subject to tremendous uncertainty or in other cases not valid,” according to an independent study by the RAND Corporation.
What’s too bad about the drug czar’s speech is that it was made behind closed doors at a venue not accessible to the press, then quietly put on the administration’s website. Given the confusion over the message, the White House needs to be far more outspoken about this.
President Obama himself needs to get more involved than simply letting his drug czar reveal this critical stance below the radar. As a high-profile parent, he can help other parents who are struggling to prevent their children from going down the rabbit hole of drug use. If one message can resonate in this debate, it’s that America’s young people are most vulnerable to the threat of legalization.
They are particularly sensitive to the price of pot (and prices will come down if pot is legalized). They’re the most influenced by societal norms (and public approval is growing). And they’re the ones most heavily engaged in studying and learning – a process that pot smoking can impair.
Individuals who reach age 21 without using drugs are almost certain to never use them. But according to a study by a leading source on young people and drugs, Monitoring the Future, marijuana use among teens has increased in recent years, after a decade of decline. Teens perceive less risk in use – not surprising when states approve of it as medicine. Risk perception greatly influences drug use among young people.
The risks of marijuana – and the wisdom of knowing that joy and satisfaction are not found in a drug – are lessons that Mr. Obama could effectively teach the nation. But even so, it can’t stop there.
The momentum, for now, is with those who want to legalize marijuana. They have been generously financed by a few billionaires, including George Soros, and make strategic use of the Internet and media.
It will take clear-thinking parents, teachers, local officials, faith leaders, and law enforcement officers to convincingly articulate why the march to legalization must be stopped. They can, if they use the kinds of reasonable and fact-based arguments that the nation’s drug czar has just laid out.
(To read Gil Kerlikowske’s speech, click here.)
Kerlikowske also effectively knocked down the argument that regulating and taxing marijuana is a great way for states to make money in these deficit-dreary times. Indeed, NORML, the lead group in the legalization movement, is set to launch a digital ad campaign in Manhattan’s Times Square next week: “Money CAN grow on trees!”
It’s a claim that’s too good to be true, just as the exclamation point implies. Look at the nation’s experience with regulated alcohol. America collects nearly $15 billion a year in federal and state taxes from alcohol. But Kerlikowske says that covers less than 10 percent of the “social costs” related to healthcare, lost productivity, and law enforcement. And what about lost lives? Let’s not add marijuana to the mix of regulated substances.
“The costs of legalizing marijuana would outweigh any possible tax that could be levied,” Kerlikowske explains. In the United States, illegal drugs already cost an estimated $180 billion annually in social costs, according to the Office of National Drug Control Policy. That number would increase as marijuana became more widely and easily available.
The Dutch – so often praised by marijuana advocates – have had to greatly ratchet back the number of legal marijuana outlets because of crime, nuisance, and increased pot usage among youth. Los Angeles, too, now sees the need to scale back the number of private dispensaries of medical marijuana. Many California towns have looked at L.A. and are saying “no” to dispensaries.
The California Board of Equalization, which administers the state’s sales tax, estimates $1.4 billion of potential revenue from a marijuana tax. Found money? Its reasoning is based on either “a series of assumptions that are in some instances subject to tremendous uncertainty or in other cases not valid,” according to an independent study by the RAND Corporation.
What’s too bad about the drug czar’s speech is that it was made behind closed doors at a venue not accessible to the press, then quietly put on the administration’s website. Given the confusion over the message, the White House needs to be far more outspoken about this.
President Obama himself needs to get more involved than simply letting his drug czar reveal this critical stance below the radar. As a high-profile parent, he can help other parents who are struggling to prevent their children from going down the rabbit hole of drug use. If one message can resonate in this debate, it’s that America’s young people are most vulnerable to the threat of legalization.
They are particularly sensitive to the price of pot (and prices will come down if pot is legalized). They’re the most influenced by societal norms (and public approval is growing). And they’re the ones most heavily engaged in studying and learning – a process that pot smoking can impair.
Individuals who reach age 21 without using drugs are almost certain to never use them. But according to a study by a leading source on young people and drugs, Monitoring the Future, marijuana use among teens has increased in recent years, after a decade of decline. Teens perceive less risk in use – not surprising when states approve of it as medicine. Risk perception greatly influences drug use among young people.
The risks of marijuana – and the wisdom of knowing that joy and satisfaction are not found in a drug – are lessons that Mr. Obama could effectively teach the nation. But even so, it can’t stop there.
The momentum, for now, is with those who want to legalize marijuana. They have been generously financed by a few billionaires, including George Soros, and make strategic use of the Internet and media.
It will take clear-thinking parents, teachers, local officials, faith leaders, and law enforcement officers to convincingly articulate why the march to legalization must be stopped. They can, if they use the kinds of reasonable and fact-based arguments that the nation’s drug czar has just laid out.
Source: www.csmonitor.com  By the Monitor’s Editorial Board / March 12, 2010

UN-commissioned guidance from international experts on how to mount prevention programmes based on family skills training involving parents and children in a joint effort to improve family dynamics and child development. Engaging parents seems the major barrier.

Abstract
This review and guidance initiated by the UN Office on Drugs and Crime concerned the role of family skills training programmes in the prevention of substance use problems among children in families across the board (‘universal’), or families whose children are particularly at risk (‘selective’). Unless integrated with these types of interventions, the document did not include programmes aimed at individuals identified as at high risk or as already experiencing substance use problems (‘indicated’). A literature and website review identified 130 universal and selective programmes. Research articles and programme descriptions were solicited from the developers. Practitioners, managers, researchers and developers from these programmes throughout the world were invited to a technical consultation meeting. The guide was drafted on the basis of the discussions and the literature review. This account largely relies on its final chapter, which summarised the major points.
Families can act as powerful protective forces in healthy child development, in particular with regard to substance use. To bolster this process, universal and selective family skills training programmes generally aim at strengthening the protective factors in families, equipping parents with the skills to provide supportive parenting, supervision, monitoring and effective discipline, and giving entire families opportunities and skills to strengthen attachment between parents and children. These approaches are more intensive and differ from parent education, which typically limits itself to providing parents with information about substances and their effects and does not involve the children.
Such programmes have been extensively evaluated and found effective in preventing substance abuse and other risky behaviours – about three times more effective than life skills education programmes aimed only at children and young people, and with more long-lasting benefits. Conservative estimates indicate that for each pound spent, over the long term these programmes return a saving of nine pounds. They also form part of effective multi-component programmes which offer other interventions in other settings (such as schools, media and the community), and of tiered programmes which operate across several levels of prevention simultaneously according to the needs of the families (universal, selective and indicated).
Although the evidence is limited to few programmes in high-income countries, recommended principles for family skills training programmes can be identified. These include a solid theory of how the training will affect risk and protective factors based on research on factors related to substance abuse which can be addressed at the family level. Programmes should be matched to the target population, especially the age and developmental stage of the children and the level of risk or problems in the families. This makes accurate needs assessment vital. Programmes must be of sufficient intensity and duration to address the targeted outcomes. In general, universal programmes extend over four to eight sessions, selective programmes for higher risk families, 10 to 15. Sessions last about two to three hours and should be based on interactive techniques implemented in small groups of eight to 12 families. A typical and effective programme will provide parents with the skills and opportunities to strengthen positive family relationships, family supervision and monitoring, and improve the communication of family values and expectations.
Recruitment and retention of parents are significant barriers to the dissemination of such programmes. However, retention rates of over 80% can be achieved by addressing the practical (transportation, childcare) and psychological (fear of stigmatisation, feelings of hopelessness) barriers. Interventions are most effective if participants are ready for change, such as at major transition points like children starting school or a new school phase.
Often it most feasible and/or cost-effective to base a project on an evidence-based programme developed elsewhere for a similar target group, preferably one with the best prevention record. In this case, it is important to carefully and systematically adapt the programme to the cultural and socioeconomic needs of the target population. Such adaptations enhance recruitment and retention of families. However, during its initial use the programme should be implemented with only minimal local adaptations or changes. Feedback from participants and group facilitators on what worked or did not work so well can be used as the basis for further refinements. Experience with these and outcome evaluations should be used to assess whether a deeper adaptation is required.
As with other types of programmes, adequate training and ongoing support must be provided to carefully selected staff. Most evidence-based programmes require two to three days of training for 10 to 30 future group leaders. Training should give them the opportunity to practise their skills, but also discuss the theoretical foundations, evidence of effectiveness, and the values of the programme. Ongoing support by programme managers and supervisors (and, if possible and appropriate, from programme developers) is important, especially in the form of e-mail contacts and web-based networking of group facilitators across agencies. Site visits and debriefing sessions also enhance quality and fidelity of implementation, as well as the collection of monitoring data.
Programmes should include strong and systematic monitoring and evaluation components. This work contributes to the understanding of prevention strategies, indicating which programmes are effective, under which circumstances, and for which populations, and provides evidence of effectiveness which can be used to lobby policymakers and donors, potentially helping to sustain the programme.
There is no question that the family is a powerful influence on child development and on substance use and problems in particular, nor that interventions with families and parents can (see for example this demonstration from Sweden) help prevent substance use in various forms. What is questionable is whether the research, though sometimes promising, is sufficiently extensive and sound to warrant widespread implementation of these programmes. Searching for practical guidance, British reviewers found that research deficiencies mean that no clear choice could be made about what works best either for marginalised and vulnerable groups, or for families in general. The background notes focus on two of the best researched family skills interventions (the Strengthening Families Programme and the Family Check-Up) as a way of testing the adequacy of the evidence overall, and address the issue of engaging families of early adolescent children. For other relevant evidence run this search for pre-school and parenting interventions on the Findings site.
When in 2008 the US government analysed the costs and benefits of substance use prevention programmes, family skills training programmes were among those with the highest benefit to cost ratio, though they lagged behind some other school/community/family programmes, and also well behind some entirely different kinds of initiatives like enforcing laws on serving drunk customers in licensed premises. Estimates for the two relatively well researched family skills interventions focused on in the background notes rested on one or two studies, which in both cases provided a narrow and at best tentative basis for the calculations, casting doubt over the degree to which they can be relied on to guide prevention programme planning. Nevertheless, the same may be said of some of the other programmes included in the analysis. For the analysts, the major drawback of family training as a universal prevention modality was its higher cost relative to other types of initiatives, leading them to suggest that this approach be reserved for high risk schools, areas or families
A particular issue is whether by the time family skills training comes in to its own – from age six to 11, and in major studies not until the early years of secondary schooling – enough families can be involved to make these strategies a viable way of curbing youth substance use problems across the population as a whole. British experience so far suggests this is not the case, though high-risk families under pressure to attend and/or energetically and sensitively targeted can be engaged in and benefit from family skills training. As the featured review comments, one way cost and accessibility barriers are being addressed is through computerisation of such programmes so families can go though them at times convenient to them and in their own homes, a tactic trialled for example with some success among mothers and daughters in New Jersey.
Based on UK experience and the adequacy of the international evidence, family skills training programmes of the kind reviewed can be recommended for consideration for families who have come to attention because their children (age six upwards) are at risk of behavioural problems which may include risky substance use. Sensitive personal approaches from programme staff, perhaps preferably from the same communities, can recruit many to participate, stay in and benefit from the programmes. Universal application to all families seems at the moment to lack sufficient evidence (especially in the UK) to warrant the considerable investment required, a situation which may change if low-cost, accessible computer-based alternatives prove feasible, effective and capable of widespread implementation.

Source: K. Kumfer www.findings.org.uk 09 March 2010

TESTIMONY OF DAVID G. EVANS, ESQ.
EXECUTIVE DIRECTOR, DRUG-FREE SCHOOLS COALITION
BEFORE THE HEALTH AND HUMAN SERVICES
COMMITTEE OF THE NEW JERSEY ASSEMBLY
SEPTEMBER 20, 2004
TRENTON, NJ

IN OPPOSITION TO A-3256

SUMMARY OF THE TESTIMONY:

THE PUBLIC HEALTH BENEFITS AND SOCIAL EFFECTS OF NEEDLE EXCHANGE PROGRAMS ARE AT BEST UNCERTAIN, AND AT WORST ARE DEVASTATING TO BOTH ADDICTS AND THEIR COMMUNITIES

A.   NEEDLE EXCHANGE PROGRAMS ARE NOT SCIENTIFICALLY
       PROVEN TO REDUCE THE EPIDEMIC OF HIV OR HCV INFECTION
       AMONG INJECTION DRUG USERS

B.   NEEDLE EXCHANGE PROGRAMS DO NOT REDUCE SUBSTANCE
       ABUSE, BUT IN FACT FACILITATE AND ENCOURAGE SUBSTANCE
       ABUSE

C.   NEEDLE EXCHANGE PROGRAMS ARE DESTRUCTIVE TO THE
       COMMUNITIES IN WHICH THEY ARE USED

D.  NEEDLE EXCHANGE SENDS A BAD MESSAGE TO SCHOOL CHILDREN.
      PROVISION OF NEEDLES TO ADDICTS WILL ENCOURAGE DRUG USE.
      THE MESSAGE IS INCONSISTENT WITH THE GOALS OF OUR
      NATIONAL YOUTH-ORIENTED ANTI-DRUG CAMPAIGN.
 
A. NEEDLE EXCHANGE PROGRAMS ARE NOT SCIENTIFICALLY PROVEN TO REDUCE THE EPIDEMIC OF HIV OR HCV INFECTION AMONG INJECTION DRUG USERS 
 
(i) The New Haven Study

NEP activists frequently cite the results of a New Haven, Conn., study, published in the American Journal of Medicine, which reported a one-third reduction of HIV among NEP participants. However, the New Haven researchers tested needles from anonymous users, rather than the addicts themselves, for HIV.  They never measured “seroconversion rates,” which determine the portion of participants who become HIV positive during the study.  Also, sixty percent of the New Haven study participants dropped out; those who remained were presumably more motivated to protect themselves, while the dropouts likely continued their high risk behavior.

 Essentially, the New Haven study merely reported a one-third decrease in HIV-infected needles themselves, which, considering the fact that the NEP flooded the sampling pool with a huge number of new needles, is hardly surprising.  Even Peter Lurie, a University of Michigan researcher and avid NEP advocate, admits that “the validity of testing syringes is limited.”

Furthermore, the New Haven study was based on a mathematical model of anonymous needles using six independent variables to predict the rate of infection. The unreliability of any of the variables invalidates the result. The New Haven study also assumed that any needle returned by a participant other than the one to whom it had been given had been shared, and that any needle returned by the original recipient had not been shared. Both assumptions are suspect.   Also, the role of HIV transmission through sexual activity is downplayed. Prostitution often finances a drug habit. Non-needle using crack addicts have high incidence of HIV. Recent studies reveal that the greatest HIV threat among heterosexuals is from sexual conduct, not from dirty needles.   Less than one-third of the New Haven subjects practiced safe sex. In the New Haven study, sampling error alone could account for the 30 percent decline.
(ii) The HHS / NAS Study

In 1992, Congress directed the U.S. Department of Health and Human Services (HHS) to study NEPs. HHS in turn commissioned the National Academy of Sciences (NAS), an independent, congressionally chartered, non-government research center, to conduct the study.  According to the Congressional directive, if the NAS could show that NEPs worked and did not increase drug use, the Surgeon General could lift the ban on federal funding. The study was completed in 1995, and it concluded that well run NEPs could be effective in preventing the spread of HIV, and do not increase the use of illegal drugs. The NAS panel further recommended lifting the ban on federal funding for NEPs and legalization of injection paraphernalia. Now, seven years after the NAS study, Congress has yet to lift the NEP funding ban, clearly indicating that Congress maintains serious doubts as to the validity of the NAS/HHS conclusions regarding NEPs.  Of note is that study chairman Dr. Lincoln E. Moses cites the dubious New Haven study as a basis for the NAS findings.   The NAS panel admitted that its conclusions were not based on reviews of well-designed studies, and the authors admitted that no such studies exist.  Incredibly, the panel reported that “the limitations of individual studies do not necessarily preclude us from being able to reach scientifically valid conclusions.”

Two of the physicians on the NAS panel, Herbert D. Kleber, M.D. and Lawrence S. Brown, M.D., say the news media exaggerated the NAS’s findings. “NEPs are not the panacea their supporters hope for…We personally believe that the spread of HIV is better combated by the expansion and improvement of drug abuse treatment rather than NEPs, and any government funds should be used instead for that purpose.”   Dr. Kleber, executive vice president for medical research at Columbia University, added: “The existing data is flawed.  NEPs may, in theory, be effective, but the data doesn’t prove that they are.”  

This questionable NAS study represents the cornerstone research data used by the notoriously-politicized U.S. Department of Health and Human Services.  The pro-NEP advocacy of HHS, and its supporting data, has yet to convince Congress that NEPs are scientifically proven to reduce HIV infection while not increasing drug usage.

6 Id.
7  See Loconte, Joe, Policy Review, supra, note 2.
8  See New Jersey Family Policy Council, ANeedle Exchange Programs – Panacea or Peril, supra, note 1 
9    See Loconte, Joe, Policy Review, supra, note 2.
   (iii) The CDC Study

The Centers for Disease Control (CDC) conducted a study whose chief architect, Dr. Peter Lurie, recommended NEPs.  The CDC report calls for federal funds for NEPs and the repeal of drug paraphernalia laws
 
However, although the CDC study endorses NEPs, Dr. Lurie, the study’s author, acknowledges numerous problems:  None of the studies were randomized, and self reported behavior was often the basis for outcomes. Poor follow up and rough measurement of risk behavior also present problems, and he notes that syringe studies have limited validity. The report concludes: “Studies of needle exchange programs on HIV infection rates do not, and in part due to the need for large sample sizes and the multiple impediments to randomization, probably cannot provide clear evidence that needle exchange programs decrease HIV infection rates.”

(iv) The Montreal Study

A 1995 Montreal study, published in the American Journal of epidemiology, showed that IDUs who used the NEP were more than twice as likely to become infected with HIV as IDUs who did not use the NEP. Thirty three percent of NEP users and 13 percent of nonuser became infected.  There was an HIV seroconversion rate of 7.9 per 100 person years among NEP participants, and a rate of 3.1 per 100 person years among non-participants. 

A high percentage of both groups shared intravenous equipment in the last six months: 78 percent of NEP users and 72 percent of non-NEP users. Risk factors identified as predictors of HIV infection included previous imprisonment, needle sharing and attending an exchange in the last six months. The study authors stated: “We caution against trying to prove directly the causal relation between NEP use and reduction in HIV incidence. Evaluating the effect of NEPs per se without accounting for other interventions and changes over time in the dynamics of the epidemic may prove to be a perilous exercise.”  The study concluded:  “Observational epidemiological studies…are yet to provide unequivocal evidence of benefit for NEPs.” 
(v) The Vancouver Study
Vancouver has the largest NEP in North America, and was praised in the 1993 CDC report. It is financed by public funds, and by 1996 was distributing over 2 million needles per year.  A 1997 evaluation of the needle exchange program in Vancouver showed that since the program began in 1988, AIDS prevalence in intravenous users rose from approximately 2% to 27%.  This occurred despite the fact that 92% of the intravenous addicts in that jurisdiction participated in the needle exchange program.
 
The Vancouver study also found that 40% of the HIV-positive addicts who participated in the program had lent a used syringe in the previous six months, and that 60% of HIV-negative addicts had borrowed a used syringe in the previous six months.  Despite the enormous number of clean needles provided free of charge, active needle sharing continued at an alarming rate.  After only eight months, 18.6 percent of those initially HIV negative became HIV positive. 

The Vancouver study corroborates a previous Chicago study which also demonstrated that its NEP did not reduce needle-sharing and other risky injecting behavior among participants. The Chicago study found that 39% of program participants shared syringes, compared to 38% of non-participants; 39% of program participants, and 38% of  non-participants “handed off” dirty needles; and 68% of program participants displayed injecting risks vs. 66% of non-participants.
 
The Vancouver report noted that “it is particularly striking that 23 of the 24 seroconverters reported NEP as their most frequent source of sterile syringes, and only five reported having any difficulty accessing sterile syringes.”
The authors continue: “Our data are particularly disturbing in light of two facts:  first, Vancouver has the highest volume NEP in North America; second, HIV prevalence among this city’s IDU population was relatively low until recent years.  The fact that sharing of
injection equipment is normative, and HIV prevalence and incidence are high in a community where there is an established and remarkably active NEP is alarming.”  

What should be obvious from all of the studies above is that there is no conclusive scientific evidence that NEP’s arrest HIV infection.  Indeed, there is evidence that NEP’s breed HIV infection.

Some claim that the federal government supports NEPs. While the previous administration’s Department of Health and Human Services actively favored NEPs, those who were actually in charge of our national drug policy do not. General Barry McCaffrey, then director of the Office of National Drug Control Policy (ONDCP), when addressing the issue of NEPS stated “we have a responsibility to protect our children from ever falling victim to the false allure of drugs. We do this, first and foremost, by making sure that we send them one clear, straightforward message about drugs: They are wrong and they can kill you.” McCaffrey’s strong views influenced President Clinton not to approve federal aid money for NEPs.
A further elaboration of the ONDCP’s policy was provided by James R. McDonough, Director of Strategic Planning for ONDCP, who wrote:

       ‘  The science is uncertain. Supporters of needle exchange frequently gloss over gaping holes in the data — holes which leave significant doubt regarding whether needle exchanges exacerbate drug use and whether they uniformly lead to decreases in HIV transmission. It would be imprudent to take a key policy step on the basis of yet uncertain and insufficient evidence.

     The public health risks may outweigh potential benefits. Each day, over 8,000 young people will try an illegal drug for the first time. Heroin use rates are up among youth. While perhaps eight persons contract HIV directly or indirectly from dirty needles, 352 start using heroin each day, and more than 4,000 die each
     year from heroin/morphine-related causes (the number one drug-related cause of death).Even assuming that NEWS can further accelerate the already declining rate

  of  HIV transmission, the risk that such programs might encourage a higher rate of heroin use clearly outweighs any potential benefit.

    Treatment should be our priority. Treatment has a documented record of reducing drug use as well as HIV transmission. Our fundamental obligation is to provide treatment for those addicted to drugs. NEPS should not be funded at the expense of treatment.

Supporting NEPS will send the wrong message to our children. Government provision of needles to addicts may encourage drug use. The message sent by such government action would be inconsistent with the goals of our national youth-oriented anti-drug campaign.

NEPS do nothing to ameliorate the impact of drug use on disadvantaged neighborhoods. NEPS are normally located in impoverished neighborhoods. These programs attract addicts from surrounding areas and concentrate the negative consequences of drug use, including of criminal activity. 

 (vi) Among IV drug users, HIV is transmitted primarily through high-risk sexual      contact
 
Another reason why NEPs may not retard the spread of HIV is that HIV is transmitted primarily through high-risk sexual contact, even among IV drug users.  Contrary to prior assumptions, recent studies on the efficacy of NEPs have discovered that it is not needle exchange, but instead, high-risk sexual behavior which is the main factor in HIV infection for men and women who inject drugs, and for NEP participants. A recently released 10-year study has found that the biggest predictor of HIV infection for both male and female injecting drug users (IDUs) is high-risk sexual behavior and not sharing needles. High-risk homosexual activity was the most significant factor in HIV transmission for men and high-risk heterosexual activity the most
significant for women.  The study noted that in the past the assumption was that IDUs who were HIV positive had been infected with the virus through needle sharing.

The researchers collected data every 6 months from 1,800 IDUs in Baltimore from 1988 to 1998. Study participants were at least 18 years of age when they entered the study, had a history of injection drug use within the previous 10 years, and did not have HIV infection or AIDS. More than 90 percent of them said they had injected drugs in the 6 months prior to enrolling in the study. In their interviews, the participants reported their recent drug use and sexual behavior and submitted blood samples to determine if they had become HIV POSITIVE since their last visit. The study showed that sexual behaviors, which were thought to be less important among IDUs, are the major risk for HIV seroconversion for  both men and women. 

If the above conclusions are correct, the very presumption of NEP efficacy becomes suspect.  Indeed, the use of needle exchange programs to address a problem which is caused primarily by high-risk sexual behavior would seem to be highly misguided.

Another reason that Needle Exchange Programs do not effectively address the issue of “saving lives” is that HIV (regardless of how it is contracted) is not the primary cause of death for IVUs.  A study conducted at the University of Pennsylvania followed 415 IV drug users in Philadelphia over four years.  Twenty eight died during the study.  Only five died from causes associated with HIV.  Most died of overdose, homicide, suicide, heart or liver disease, or kidney failure.

Clean needles, even if they in fact prevent HIV, will do nothing to protect the addict from numerous more imminent fatal consequences of his addiction.  It is both misleading and unethical to give addicts the idea that they can live safely as IV drug abusers.  Only treatment
and recovery will save the addict.  The myth of “safe IV drug use” is a lie which is perpetuated by NEPs, and it is a lie which will tend to kill the addict, although his corpse may be free of HIV, for whatever consolation that will provide to the NEP proponent.  
B. NEEDLE EXCHANGE PROGRAMS DO NOT REDUCE SUBSTANCE ABUSE, BUT IN FACT FACILITATE AND ENCOURAGE SUBSTANCE ABUSE.

The rise of NEPs, with their inherent facilitation of drug use (coupled with the provision of needles in large quantities), may also explain the rapid rise in binge cocaine injection which may be injected up to 40 times a day. Some NEPs encourage cocaine and crack injection by providing “safe crack kits” with instructions on how to inject crack intravenously.  Crack cocaine can be, and generally had been, ingested through smoking.  But the easy and plentiful availability of needles facilitates crack injection, creating a new segment of IV drug users, subject to health dangers they would otherwise have been spared exposure to.  In some NEPS, needles are provided in huge batches of 1000, and although there is supposed to be a one-for-one exchange, the reality is that more needles are put out on the street than are taken in.

NEPs also facilitate drug use through lax law enforcement policies.  Police are instructed not to harass addicts in areas surrounding NEPs. Addicts are exempted from arrest because they are given an anonymous identification code number. Since police in these areas must ignore drug use, and obvious and formidable disincentive to drug use disappears.  As the presence of law enforcement declines in these areas, the supply of drugs rises, with increased purity and lower prices, attracting new and younger consumers. 

Many drug prevention experts have warned that the proliferation of NEPS would result in a rise in heroin use, and indeed, this has come to pass. (However, the increase in drug use was ignored by the federally-funded studies which recommended federally funding NEPS). The National Center on Addiction and Substance Abuse at Columbia University reported August 14, 1997 that heroin use by American teens doubled from 1991 to 1996.  In the past decade, experts
estimate that the number of US heroin addicts has risen from 550,000 to 700,000. 
In 1994, a San Francisco study regarding a local NEP falsely concluded that there was no increase in community heroin use because there was no increase in young users frequenting the NEP.  The actual rate of heroin use in the community was not measured, and the lead author, needle provider John Watters, was found dead of an IV heroin overdose in November 1995. According to the Public Statistics Institute, hospital admissions for heroin in San Francisco increased 66% from 1986 to 1995.

In Vancouver, site of the largest NEP in North America, heroin use has risen sharply.  In 1988 when the NEP started, 18 deaths were attributed to drugs.  In 1993, 200 deaths were attributed to drugs. A 1998 report notes that drug deaths were averaging 10 per week.  Now Vancouver has the highest heroin death rate in North America, and is referred to as Canada’s “drug and crime capital.”

The 1997 National Institutes of Health Consensus Panel Report on HIV Prevention praised the NEP in Glasgow, Scotland, but the report failed to note Glasgow=s massive resultant heroin epidemic. Subsequently, as revealed in an article entitled “Rethinking Harm Reduction for Glasgow Addicts,” Glasgow took the lead in the United Kingdom in deaths from heroin overdose, and its incidence of AIDS continues to rise. 

Boston’s NEP opened in July 1993, and the city became a magnet for heroin. Logan Airport has been branded the country’s “heroin port.”  Boston soon led the nation in heroin purity (average 81%), and heroin samples of 99.9% are found on Boston streets. Subsequently, Boston developed the cheapest, purest heroin in the world and a serious heroin epidemic among the youth.  The Boston NEP was supposed to be a “pilot study,” but there was no evaluation of seroconversion rates in the addicts nor of the rising level of heroin use in the Boston area.

Similarly, the Baltimore NEP is praised by those who run it, but the massive drug epidemic in the city is overlooked.  The National Institute of Health reports that heroin treatment and ER admission rates in Baltimore have increased steadily from 1991 to 1995. At one open-air drug supermarket (open 9 a.m. to 9 p.m.) customers were herded into lines  sometimes 20 or 30 people deep. Guarded by persons armed with guns and baseball bats, customers are frisked for weapons, and then allowed to purchase $10 capsules of heroin.
One thing should be clear from the foregoing: since the implementation of NEPs, heroin use in our country has boomed.  It is obvious:  a public policy of giving needles to heroin addicts facilitates and encourages heroin use. 
C. NEEDLE EXCHANGE PROGRAMS ARE DESTRUCTIVE TO THE COMMUNITIES IN WHICH THEY ARE USED.

Most citizens oppose NEPs in their communities, and are concerned about the prospect of dirty needles being discarded in public places.  These fears are not without merit.  NEPs distribute millions of needles every year, and there is little or no accountability for needles once they have been distributed.  A survey conducted in 1998 revealed that in that year 19,397,527 needles handed out, and at best 62% were exchanged, leaving 7-8 million needles unaccounted for.   Carelessly discarded needles create a well-documented public hazard:

* On February 11, 2001, a six-year old from Glade View, Florida, stabbed five children with a discarded syringe. (Kellie Patrick/Scott Davis, “Playground Attack Raises Health Worries,” Sun Sentinal, 2/9/00, p 1B).

* On February 2, 2001, a nine year old from the Bronx stabbed four children with a discarded needle. (Diane Cardwell, “Boy Accused of Needle Attack,” The New York Times, 2/2/01, p. A17.)

* On February 13, 2001, a syringe left at a bus station stuck a four year old boy. (Mike Hast, “Big Fines for Syringe Litterers,” Frankson & Hastings Independent, February 13, 2001,www.mapinc.org/drugnews/v01/n304/ a08.html.)

Besides the physical hazard created by discarded needles, there is a commonsense perception that NEPs bring an air of decay to the communities that host them.  After several years of operation, 343 Massachusetts towns and cities (out of a total of 347) continue to decline the option of approving a local NEP, although of the 10 available slots, only 4 are taken.
31  Centers for Disease Control and Prevention, Morbidity and Mortality Weekly Report, HHS,       Washington, DC 2001;50:384-388. 
32  Maginnis, Robert L., 2001 Update On The Drug Needle Debate, Insight, Number 235, July 16, 2001, Family Research Council, 801 G. St. NW, Washington, DC 2001.
In March 1997, accompanied by a New York Times reporter, a member of the Coalition for a Better Community, a New York City group opposed to NEPs, visited the Lower East Side Needle Exchange. She was not asked for identification and was promptly given 40 syringes (without having to produce any to exchange).  She was also given alcohol wipes and “cookers” for mixing the drugs, and she was given an exchange ID card that would exempt her from arrest for possession of drug paraphernalia. She was then shown how to inject herself. 

Community opposition to the Lower East Side Needle Exchange arose soon after implementation of the local NEP due to an increase in dirty syringes on neighborhood streets, in school yards and in parks. There was observed to be a dramatic increase in the public display of injecting drugs.  NEP users were seen selling their syringes to buy more drugs. Exchange workers themselves were photographed selling needles offsite.  Neighbors perceived the Lower East Side NEP as little more than a wholesale distribution center for clean needles and a social club for addicts. 

Pro-needle activist Donald Grove concurred: “Most needle exchange programs actually provide a valuable service to users beyond sterile injection equipment. They serve as sites of informal organizing and coming together. A user might be able to do the networking to find good drugs in the half an hour he spends at the street based needle exchange site networking that might otherwise have taken half a day. [Grove, D. The Harm Reduction Coalition, N.Y.C., Harm Reduction Communication, Spring 1996].

In 1998, a U.S. Government official was sent to Vancouver, site of the largest NEP in North America, to assess the high incidence of HIV among NEP participants, and the skyrocketing death rate due to drug overdose.  He reported that the highest rates of property crime in Vancouver were within two blocks of the needle exchange.  He also observed, pursuant to a tour with the Vancouver Police, that there was a 24 hour drug market and plain view injection activity in the area immediately adjacent to the needle exchange.  Most poignantly, he was told, in a private interview with an elementary school teacher, that the children at area schools are not allowed outside at recess for fear of needles. 
CONCLUSION

There is ample evidence to suggest that very fundamental premises used to justify and support NEPs are seriously flawed.  First, NEP participants routinely continue to share needles and large percentages of the NEP participants are HIV positive, meaning that NEPs do nothing more than continue the spread of HIV (and HCV).  Significantly, no one has been able to explain satisfactorily why enhanced needle availability in and of itself would discourage needle sharing: needle sharing is an intrinsic aspect of IV drug use, and a NEP-issued needle will transmit HIV as well as any other needle.

Second, NEP studies have discovered (inadvertently) that needle sharing is not even the primary cause of HIV infection for IVUs.  It is primarily through high-risk sexual behavior that IVUs contract HIV; free needles do nothing to prevent sexually transmitted disease.  Furthermore, HIV (regardless of how it is contracted) is not even the primary cause of death for IVUs.  Most die of overdose, homicide, suicide, heart or liver disease, or kidney failure.  Clean needles may protect an addict from HIV, but they do nothing to protect him from the more numerous, and more imminent fatal threats of his addiction.  Several key NEP proponents have died of heroin overdose; no doubt their needles were very clean.

Third, the science is inconclusive.  Although the proponents of NEPs uniformly aver that the scientific debate regarding the efficacy of NEPs is over, in truth, even the reports favoring NEPs are burdened with imprecise methodology, and many of the authors of those reports caution that their results should not be deemed conclusive. Today, there is still no conclusive scientific evidence: (1) that NEPs reduce the spread of HIV and HCV, or (2) that NEPs do not encourage IV drug use.  Indeed, the correlation between the rise of NEPs and the explosion of IV drug use, if it is a coincidence, is a remarkable one.  Dispassionate observers will look at the current epidemic of heroin and IV cocaine use as a tragedy which might have been averted, or mitigated, but for the misguided mercies of the NEP concept.
 
Fourth, while the benefits of NEPs may be in doubt, the costs to the surrounding communities are very real.  The overwhelming majority of communities dread the prospect of a local NEP, for self-evident and well-documented reasons.

 34  D.B. Des Roches, Information, Memorandum for the Director, Through: the Deputy Director, Subject: Vancouver Needle Exchange Trip Report, Executive Office of the President, Office of National Drug Control Policy, Washington, D.C. 20503, April 6, 1998.

 Peer-based addiction recovery support: history, theory, practice, and scientific evaluation.
White W.L.
Chicago, IL: Great Lakes Addiction Technology Transfer Center and Philadelphia Department of Behavioral Health and Mental Retardation Services, 2009.
This monograph is likely to become the handbook for the growing peer-based recovery movement in the UK. For administrators, the approaches it reviews offer a way to reconcile decreasing per-patient resources with a policy agenda now focused on reintegration and recovery.
Abstract This seventh monograph* in a series on recovery management and recovery-oriented systems of care synthesises knowledge about the history, theoretical foundations, methods, and scientific status of peer-based recovery support for individuals with the most severe and complex alcohol and other drug problems. It was written primarily for people directly involved in planning, funding, delivering, supervising, and evaluating peer-based recovery support services, but will also be of interest to policymakers, purchasers of care, treatment programme administrators, and addiction counsellors and other service professionals. Though rigorously researched, information is presented in a clear and accessible language.
The report focuses on:
• Peer-based recovery support in general, meaning any form of mutual assistance aiming for long-term recovery from alcohol and other drug problems. Such assistance can and often does occur informally. The focus here is primarily on recovery support provided through recovery mutual aid societies and abstinence-based religious and cultural revitalisation movements by people whose credentials rest on personal experience.
• Peer-based recovery support services, a narrower term for assistance directed toward the same goal but delivered through more specialised roles with more formal resources, service protocols and safeguards. The key distinction is the term ‘services’, which implies a more formal structure though which recovery support is delivered. Here the focus is on recovery community organisations other than mutual aid societies, and on peer-based services provided through addiction treatment programmes and allied health and human service agencies. These services are distinguished from other programmes by their: mobilisation of personal, family, and community recovery capital to support long-term recovery; respect for diverse pathways and styles of recovery; focus on immediate recovery-linked needs; use of self as a helping instrument; and their emphasis on continuity of recovery support over time.
After comprehensively reviewing the literature and profiling peer-based recovery support initiatives, the author reached (among others) the following conclusions:

• Peer-based recovery support services are today growing out of the failure of addiction treatment to provide a continuum of care that is accessible, affordable, and capable of helping people with the most severe and complex problems move beyond brief episodes of recovery initiation to stable long-term recovery.

• Their distinctive strategy is to improve linkage to recovery mutual aid groups and other recovery support institutions, and their value is founded in what specifically those in recovery bring to the helping process. As with any effective helpers, those in recovery relate not primarily through techniques, but through humanness. They are able to do so, not because they once experienced addiction, but because they completed their own recovery experiences and emerged as men and women committed to this demanding way of life.

• Peer-based models of care can have a transforming effect on larger systems of care and on our society, but can also be corrupted and devoured when integration in to these systems leads to pressure to emulate the ethos of current professional treatment models. Care must be taken not to over-professionalise the roles of peer helpers, but training, guidelines, supervision and recognising the limits of one’s competence and role, are as important for services based on the power of mutual identification as for professional services.

• Rather than view peer-based and professional-based styles of knowing and doing as antagonistic models rivalling for superiority, it is more helpful to view these approaches as complementary. We need a community in which both professional and peer-based services are available as needed, and are supported and integrated into a seamless system of long-term recovery support.

• One unique quality separates the addictions field from peer models in allied fields: the growth of spiritual, secular, and religious recovery mutual aid groups, and new recovery support institutions, has gifted it the oldest and largest recovery mutual aid network in the world. New peer-based models must capitalise on these strengths rather than undermining or replacing them. The long-term goal is not to create a larger treatment system or new profession, but the establishment of recovery support relationships that are non-hierarchical, non-commercialised, and enduring in recovery-friendly communities.

• The question, ‘Who is most qualified to treat the alcoholic?’ is ill-framed because it assumes a homogeneity within the label ‘alcoholic’ and within the boundaries of particular helping roles or categories of helpers. In terms of recovery status, the question is not whether professional and peer helpers with or without a history of addiction recovery are most effective, but which helper is most effective with which person or family at a particular point in time. There are so many kinds of alcoholics and so many different kinds of alcoholism that a therapist eminently qualified to treat one type may fail completely with another.

• Recovery stages might be broadly conceived in terms of:
• 1 a sudden or unfolding opportunity for change;
• 2 a commitment to recovery experimentation;
• 3 recovery initiation and stabilisation;
• 4 recovery consolidation and maintenance; and
• 5 enhanced quality and meaning of life in long-term recovery.
 Peer-based recovery support services will probably be found most critical in stages 1, 2, and 4. Traditional professionals may be most effective in stages 3 and 5.
Every effort has been made to meticulously document sources, but many critical research questions about peer recovery support have yet to be studied and many studies suffer from methodological problems, so these findings are best viewed as probationary, pending new studies of greater methodological sophistication.
Though written by an advocate of peer-based recovery, this monograph is careful to adhere to the research (more comprehensively reviewed here than in any other publication) and to point out the limitations and risks involved in this route to recovery and the continuing role of professional treatment and other formal services. In it the British reader will find unfamiliar but potentially promising manifestations of mutual aid such as recovery social clubs, recovery community centres, and recovery homes, with profiles of how these have worked in practice and relevant research. Attention is not limited to 12-step based approaches, but extends to mutual aid based on other philosophies and understandings of addiction and recovery. For the growing peer-based recovery movement in the UK, it is likely to become an essential handbook to clarify thinking, offer practical ways forward, identify pitfalls and risks, and to encourage further research.
As the author comments, most of the reviewed research lacks the methodological safeguards of a randomised trial or some other research design capable of eliminating influences on outcomes other than mutual aid or peer support. Typically studies have recorded the degree to which substance dependent individuals participated in mutual aid activities and groups, and then assessed how closely this was associated with substance use and related problems. Such designs leave open the possibility that good outcomes encourage increased mutual aid participation rather than the reverse, or that people who are in any event going to do well also tend to participate in whatever in that society is the accepted route to doing well in terms of recovery from addiction. In the USA, where most studies originate, that route entails 12-step mutual aid.
When (as in a review for the Cochrane Collaboration) the focus is limited to the few randomised or other well controlled trials, there is no convincing advantage for 12-step mutual aid or allied services over other approaches. This review was unable to take in to account an influential later study which randomly assigned patients in formal treatment to standard versus intensive referral to 12-step groups. As intended, intensive referral improved 12-step mutual aid participation and this in turn improved substance use outcomes, confirming that participation was indeed an active ingredient. However, the effects on both participation and substance use were not great. While such studies can demonstrate the value of the extra element of mutual aid participation they ‘artificially’ generate, they say nothing about the value of the bulk of mutual aid participation as it naturally occurs. For this we must turn to the less well controlled studies excluded from the Cochrane review but included in the featured report, yet these are not capable of delivering convincing answers. This bind arises from the fact that mutual aid cannot be imposed or withheld by researchers and the results observed. Rather, it is generated (or not) organically by the nature of the society and of the individuals who choose (or not) to participate. It makes little sense to ask what the recovery chances of that society or those individuals would be if they did not generate or participate in mutual aid, because then they would not be the same societies or individuals. Another limitation of the controlled research is that typically it has studied mutual aid as an add-on to current treatment models, not the thoroughgoing systemic transformation called for in the featured report.
Even if given these difficulties, peer support and mutual aid struggle to demonstrate a superiority, where they can have a distinct advantage is in accessibility and (by reducing resort to public services) cost to society. For administrators in the UK, such approaches offer a way to reconcile increasing numbers in treatment, decreasing per-patient resources, increasing pressure to move patients through and out of treatment, and a policy agenda now focused on secure reintegration and recovery. Formal services seem unlikely to be able to make major advances in the availability to dependent substance users of (among other supports to reintegration and recovery) supported housing, suitable training and education opportunities, sheltered, graduated and attractive employment, and satisfying non-drug focused social and lifestyle options. Within available resources and political and public willingness to redirect these, transformations of the kind described in the featured report may be the only feasible way to create a more recovery-friendly environment which can protect greater numbers of people leaving treatment from repeated relapse.
However, risks of the kind warned about in the report are already apparent in parts of Britain where services concerned to safeguard vulnerable adults and who have clinical responsibility for patients seem reluctant to refer those patients to untried and unqualified mutual aid organisations, leading to pressure for those organisations to implement safeguards and protocols potentially antithetical to their self-help ethos. Such pressures have also been apparent in the UK mental health service-user/survivor movement. There is also a tendency for mutual aid recovery enthusiasts to see formal treatment services and their workers as ‘part of the problem’ rather than collaborators. The result is an imperfect interface between mutual aid and formal services which impedes beneficial complementarity and movement between them. As with other collaborations between organisations with different traditions and agendas, these difficulties will need to be carefully and respectfully worked through if patients are to benefit maximally from the potentially huge reservoir of voluntary effort represented by current and former problem substance users.
In the UK employment of current or former problem substance users in drug and alcohol services may be seriously impeded by the new requirements and powers associated with the advent in 2009 of the Independent Safeguarding Authority and of a similar scheme in Scotland. Among the criteria for banning people working with vulnerable adults (which would embrace many attending drug and alcohol services) are a history of acquisitive crime or fraud, addictive behaviour, or persistent offending. Such histories are common among drug addicted populations who have recovered through treatment and who might be employed as a paid employee or volunteer to offer peer-based support to substance users in contact with services. These problems have been recognised and representations are being made to the authority.
SOURCE: Peer-based addiction recovery support: history, theory, practice, and scientific evaluation.
White W.L.
Chicago, IL: Great Lakes Addiction Technology Transfer Center and Philadelphia Department of Behavioral Health and Mental Retardation Services, 2009.

There has been a considerable scientific effort over the past three decades in to identifying and understanding the core features of alcohol and drug dependence. This work really began in 1976 when the British psychiatrist Griffith Edwards and his American colleague Milton M. Gross collaborated to produce a formulation of what had previously been understood as ‘alcoholism’ – the alcohol dependence syndrome.
The alcohol dependence syndrome was seen as a cluster of seven elements that concur. It was argued that not all elements may be present in every case, but the picture is sufficiently regular and coherent to permit clinical recognition.   The syndrome was also considered to exist in degrees of severity rather than as a categorical absolute. Thus, the proper question is not ‘whether a person is dependent on alcohol’, but ‘how far along the path of dependence has a person progressed’.   The following elements are the template for which the degree of dependence is judged:

Narrowing of the drinking repertoire

A normal drinker’s consumption and choice of drink varies from day to day and week to week, with the drinking being patterned by varying internal cues and external circumstances.   The dependent person may drink to the same extent whether it is workday, weekend or holiday, irrespective of whether he is alone or in company, and whatever his mood. With advanced dependency, the drinking may become timetabled to maintain high alcohol levels.
Increased salience of the need for alcohol over competing needs and responsibilities
As dependence advances, the person gives priority to maintaining their intake. Their partner’s distressed complaints are ignored, income is used to support their drinking rather than provide for the family, and the need for drink may become more important for the person with liver damage than consideration of survival. A person who used to have moral standards now begs, borrows and steals to pay for drinking.

An acquired tolerance of alcohol

A given amount of alcohol will have a smaller effect on the dependent person than on a naïve drinker due to changes in brain function arising from repeated consumption of alcohol. Tolerance is also shown by the dependent person being able to sustain an alcohol intake and go about their business at blood alcohol levels that would incapacitate the non-tolerant individual.   However, in later stages of dependence this tolerance declines and the drinker is incapacitated by quantities of alcohol that he would previously hold easily.

Withdrawal symptoms

These vary from a mild shaking of the hands in the morning through to convulsions and the life-threatening illness of delirium tremens (confusion, hallucinations, tremor). As dependence increases, so does the frequency and severity of the symptoms. Symptoms of withdrawal may occur during the day as blood alcohol levels drop.    The four key symptoms are tremor, nausea, sweating and mood disturbance. A person may wake in the morning with soaking sweats, or they may vomit in the morning. In the early stages, a person may feel a ‘bit edgy’, but as dependence develops, they may experience terrible agitation and depression, or may show phobic reactions. Other symptoms include muscle cramps, sleep disturbance, hallucinations and grand mal seizures.

Relief or avoidance of withdrawal symptoms by further drinking

In the earlier stages of dependence, the person may feel at lunchtime that the first drink of the day ‘will help me straighten up a bit’.   At the other extreme, a person may require a drink every morning before they can get out of bed. They may try to maintain steady alcohol levels which they may have learnt to recognise as being comfortable above the danger level for withdrawal.

Subjective awareness of compulsion to drink

The person may become aware of their ability to lose control: ‘If I have one or two, I won’t stop’. They may start to experience and express their craving for alcohol. Cues for craving include the feeling of intoxication, incipient withdrawal, mood or situational cues (e.g. seeing a drinking friend). They may constantly think about alcohol when experiencing withdrawal.

Reinstatement after abstinence

If a severely dependent drinker is abstinent for a year and then attempts to return to social drinking, it is likely that within a few days they will be back to an intensity of withdrawal experience which had previously taken many years of drinking to develop. Dependence has memory.
There is no signpost to a person becoming dependent. Whilst a severely dependent person is easy to recognise, it can be difficult to detect a problem in the early stages.    Clearly, it is essential to be able to diagnose early problems, before drinking gets out of hand and there is a precipitous decline in the quality of life that accompanies increasing dependence.
In the latter stages of dependence, there may be rapidly mounting intensity of morning distress, appalling shakes and suicidal thoughts and delirium tremens. Gross and incapacitating intoxication becomes common.
The person is intoxicated after a couple of drinks, there is a gross and repeated amnesia (they may disappear for several days but not remember where), and there are desperate attempts to avoid withdrawal by topping up.   Drinking makes the person very ill – this is partly due to mounting intensity of morning distress, but also due to various alcohol-induced physical problems (e.g. liver disease). Psychiatric disorders may become common at this stage

Source: www.wiredin.org.uk 2009

Adaptation and Testing of the Strengthening Families Programme 10-14 (SFP10-14) for use in the United Kingdom

Summary
Introduction
Numerous studies in Europe report high rates of alcohol use among young people. A European School Project on Alcohol and Drugs (Hibbell 1999) reported that the UK had among the highest rates of drunkenness and binge drinking and alcohol consumption in Europe. Participants reported that 75% had had one episode of drunkenness, while nearly one third had 20 or more episodes in their lives or 10 or more episodes in the last year. Half had been intoxicated in the last month and a quarter intoxicated at least three times in the same period. The trends of the last decade are: more young people are drinking regularly (at least once a week); weekly drinkers are drinking more; regular young drinkers are drinking more alcohol per session; there are changes in the types of alcohol consumed (alcopops/designer drinks) (Alcohol Concern 2005).

The Strengthening Families Programme 10-14 (SFP10-14) is a seven session video based family skills training programme designed to increase resilience and reduce risk factors for alcohol and substance misuse, depression, violence and aggression, delinquency and school failure in The SFP10-14 has been evaluated for primary prevention effectiveness with young people and their parents living in mainly rural areas in Iowa, U.S.A. (Spoth et al 2001a; Spoth et al 2001b).
 
Whilst initial reports of implementation of the SFP10-14 in the UK are valuable it has been recognised that the US SFP10-14 programme materials and approach might need to be adapted to meet the needs of a UK audience and that a more systematic approach to evaluation of SFP10-14 in the UK was needed (Coombes et al 2006).
This report presents the results of the adaptation process and exploratory pilot study of the adapted SFP10-14 materials and approach in the UK.
Aims of the study
1. To adapt the US SFP10-14 materials and approach for the primary prevention of alcohol and drugs misuse in the U.K.
2. To model and explore the adapted SFP10-14 (UK) materials and approach with young people in the UK.
3. To develop a protocol for a large-scale evaluation study of the SFP10-14 (UK) including a cost-effectiveness assessment.

Method
Adaptation of US SFP10-14 materials
A small number of professionals and participants who had facilitated/attended SFP10–14 programmes in the United Kingdom using the United States programme materials was recruited and an advisory group formed. Four professionals, four mothers, two fathers and five young people agreed to join the advisory group. The advisory group was established with the remit to meet on one occasion only, with any further contact being by correspondence. The advisory group reviewed the original SFP10-14 materials and made recommendations about how the original programme should be adapted for a UK audience, using a nominal group technique to collect data. The advisory group was asked to review the US SFP10–14 materials and generate an individual list of positive features, and areas for improvement. A ‘round robin’ recording of individuals’ ideas into a single list was undertaken until all ideas were exhausted, and duplicates eliminated. The advisory group was then asked to discuss each item of the final list and to reach a consensus on the areas for improvement. The final list was the pooled results of individual opinions. The process of the nominal group’s work was recorded and the completed list of suggested improvements was then sent to all participants at a later date to check for accuracy
and agreement. The US SFP10–14 materials were then revised according to the agreed lists of improvements to produce the SFP10-14 (UK) materials.

Modelling of revised SFP10-14 materials
Focus group meetings involving parents/guardians and children were held in schools in four different geographical locations in the United Kingdom: Barnsley, Chester, Oxford and Peterborough (see Table 1). The sites and participants were selected purposively guided by time and resources. The focus groups critically reviewed the revised SFP10-14 (UK) materials, identifying what they felt were their strengths and weaknesses.
At the start of each focus group, short extracts from the original US SFP10–14 materials were shown. This was done to enable participants to provide a reference point for discussion of the adapted SFP10-14 (UK) materials. Participants were then asked for their opinions about the US SFP10–14 materials. This process was repeated for the SFP10-14 (UK) materials.

All focus group interviews were audiotape recorded and transcribed. The transcripts were coded and the codes were then aggregated to form larger conceptual categories. Conceptually meaningful themes were constructed from categories of the data. Validation of the thematic analysis was achieved through the use of independent individuals to check the analysis and interpretation of data; external checks on the inquiry process and debriefing with informants.

Exploratory pilot study of SFP10-14 (UK)
The SFP10-14 (UK) materials produced from the adaptation and modelling stages were field tested in three different geographical locations. In each of the three sites sufficient families were recruited to participate in the SFP10-14 (UK) delivery sessions. Subsequently, in each of the three sites a similar number of families were non-randomly selected into a comparison group. The comparison group children received the standard alcohol and drugs education delivered as part of the school curriculum. The SFP10-14 (UK) group received the standard alcohol and drugs education delivered as part of the school curriculum plus the SFP10-14 (UK) intervention.

Study self-report questionnaires were completed by youth and their parents/carers pre- and post- intervention, and at 3 months after completion of the programme. The study questionnaires were adapted from validated tools used in previous SFP10-14 evaluations in the US (Spoth et al 2001a; Spoth et al 2001b) and those used in ESPAD (European School Survey Project on Alcohol and Drugs) research studies. To supplement and enrich the quantitative data, focus groups were held to gain feedback from participating families. Two tape-recorded, focus group interviews lasting approximately 60 minutes were undertaken with the parents/caregivers and young people in Barnsley and Chester who had completed the SFP10-14 (UK) programme. Interviews focused on the parent’s/caregiver’s and young people’s experience of the SFP10-14 materials and approach. All interviews were tape recorded and transcribed and a content analysis of transcripts undertaken. The transcripts were coded and codes aggregated to form larger conceptual categories. Conceptually meaningful themes were constructed from categories of the data. Validation of the thematic analysis was achieved through the use of independent researchers to analyse and interpret single sets of data, external checks on the inquiry process and debriefing with informants.
Findings
Adaptation & Modelling of revised SFP10-14 materials
The results from the nominal group meeting and subsequent focus group meetings provided useful information on whether and how the original US SFP10–14 materials could be adapted for use in the United Kingdom, while at the same time retaining essential ingredients of the effective US programme. Twenty-one parents/caregivers and sixteen young people participated in the focus groups. The nominal and focus group study led to the development of newly revised programme materials, now referred to as SFP10–14 (UK), that were used in the subsequent exploratory pilot study.
Exploratory pilot study of SFP10-14 (UK)

There were 23 parent/caregivers and 24 young people from 3 sites in the SFP10-14 (UK) intervention group. There were 24 parent/caregivers and 22 young people from 3 sites in the non-random comparison group.
The study questionnaires were completed by all participants without difficulty, and analysis and interpretation was straightforward. Given the small sample size and short-term follow-up in this pilot study no statistically significant effects were predicted or found, though data are summarized here for completeness: overall, there were no clear or consistent outcomes associated with the SFP10-14 programme in terms of alcohol use, substance use, parenting behaviour, general child management, parent-child affective quality, or measures of supportive and controlling family environment.
16 adults and 14 young people participated in the focus groups. Feedback from parents, carers and young people was overwhelmingly positive. The following key themes have been selected for the summary:

Expectations and reasons for attending the SFP10-14: some participants commented that they did not have any idea what to expect before attending the programme, while others identified a particular aspect of the programme that they had come to find out about. What became clear during analysis of the focus group data was that the important aspect of the programme for many parents/guardians was not necessarily to do with drug and alcohol prevention, but more to do with strengthening family functioning.

Involving youth in the programme: participants acknowledged that in some cases it had not been easy to persuade their youth to attend the first group meeting. There were examples given that showed some youths were quite determined not to go with their parents at first. However, after participating in the first group, barriers and obstacles to attendance were overcome.

What worked well for participants: participants identified that the SFP10-14 (UK) had helped strengthen the family unit and had also helped them identify different strategies to manage situations. Their responses indicated that they felt that the SFP10-14 (UK) provided parents with a range of strategies (or ‘tools’) which they can draw on to help manage different situations. Some of these strategies involved a change in the adults’ behaviour and how they responded to challenging situations.
Some participants also observed that by working with a group that were all there to learn about parenting and improving their skills helped them to be open about their problems. The sessions that focused on peer pressure were identified as being particularly helpful by participants.
When speaking about the parent sessions of the programme, the group spoke positively about the support they felt they had from one another. They felt that everyone had participated and contributed to the sessions and therefore the group had gained from that.

Use of DVDs, actors and scenario: generally, participants found the DVDs useful to illustrate particular potentially problematic aspects of family life, and felt they could identify with the families (actors) homes and the locations that were used. Some participants felt the approach taken in the DVDs was patronising when they first saw it, but generally, they developed a more positive perception as they became more engaged with the programme. Participants felt that the actors and scenarios helped get discussion going in sessions by encouraging people to reflect on their own situations and how they dealt with these.

Exercises and activities in the programme: participants were very positive about the activities and family exercises to help families have fun and learn about each other, particularly enjoying activities such as creating the family tree and the family shield. However not all comments about this aspect of the course were entirely positive. Some participants found some of the exercises or games rather frivolous, although they did understand that there was a purpose behind the group activities.

What did not work so well for participants: participants were asked if they could identify aspects of the SFP10-14 (UK) that they felt did not work so well for them or for the group as a whole. One of the issues that was identified related to the tight control of time. The delivery of the SFP10-14 (UK) relies on strict time keeping within a two hour time frame: in the first hour parents and youth work separately, in the second hour they work together. It is critical that both sessions end together, on time, or the following family session will over-run and participants will be late leaving for home. Participants felt they were sometimes rushed with not enough time being available for discussion. However they also acknowledged that there is a need for some time limits.
 
Timing of the programme: the SFP10-14 (UK) is generally facilitated in the evening as this suits most families. The timing of the programme had been negotiated with parents and carers at the information evening held prior to the programme. Participants felt that this had worked well for most members of the group.
Crèche: the programme also offered a crèche for families who had younger siblings. This was viewed very positively by both the parents and the children who attended the crèche.
 
Positive outcomes:
 throughout the focus group sessions parents and carers spoke of what they had learned and how their parenting had changed since attending the programme. The following are a selection of some of the comments made:

• “What I’ve learnt is to really, really listen to my kids feelings. Even if the answer is going to be no to whatever the request is, because some have to be no, but they need to air their feelings”
• “It changed my behaviour towards my children, I listen to what they say, I don’t lose my temper so much”
• “I used to confront him and the situation would get worse and worse and it could spoil a whole evening…but by walking away its much better, it’s a really calm approach” 
• “We have definitely got closer since doing the course, I think what they (youth) have done in combination with what we have done – I think its made her think a bit more about her behaviour at home and I’m certainly thinking about my behaviour more”
• “I’m a single parent I’m on my own, it’s very hard to be a mum and a dad, but the tools gained from the course have been extremely beneficial”
• “I feel that you have never got enough skills as a parent, I’ve learned a lot from this course, my son’s learned a lot from this course and its brought us closer together and I think it would bring any family closer together”
• “I’ve got nothing but praise for what has happened, it’s a transformation. Getting called into school and they asked ‘what has changed in ****, what have you done that is different? There is a noticeable and marked difference in the way **** has adopted a more mature attitude’ and that, that’s the proof of the pudding isn’t it? As they say”
• 
Youth Feedback: the young people who had participated in the programme were equally enthusiastic in their evaluation of their experience. They enjoyed the companionship, the role play, games and exercises. They also commented that some of the tools and strategies used in the programme had worked for them in their family setting. One example of comments from one young person is:

• “I was like a bit nervous when I first came – but then enjoyed it. I liked the first week, especially the treasure map, and the fifth week with the shield. The last week was good with the role models. I liked working with mum and dad. I enjoyed the DVDs and having the family meetings. The role play and acting was good especially ‘setting up situations’. The games were good I liked the three legged game”
• “I liked it all – no negatives”
• “I learned about drugs and keeping out of trouble. And about rules – in the driving game”
• “It has been better at home. We use the points and I earned 8 points and that meant a meal in the pizza hut. 10 points and we have an Indian meal. I get the points when I clean my room, putting my shoes away. For cleaning the car or cutting the grass”

Conclusions
Although there were no clear or consistent outcomes associated with the SFP10-14 programme on examination of the quantitative data, we need to be cautious about our interpretation of these data. The purpose of this pilot study was primarily to test the adapted materials and the evaluation tools in a “live” programme delivery setting in the UK. Further research based on a randomised controlled trial design, with adequate sample size, is required to fully evaluate the potential of the programme in the UK.
The qualitative data that were obtained allow us to draw some conclusions about the perceived benefits of the SFP10-14 (UK) from the participant’s perspective. These results suggest that parents, carers and young people enjoyed and felt that they benefited from the intervention. Parents/caregivers and young people reported that 
the SFP10-14 (UK) had played a part in improving family functioning through: strengthening the family unit, improving parent/caregiver communication, using a more consistent approach, increasing the repertoire for dealing with situations, developing better positive and negative feedback, working more together as a team, identifying family strengths, strengthening family bonds, receiving group support, working more closely with mum and dad, learning to listen more, learning to get along with each other better, helping parents/caregivers more, better understanding of what parents/caregivers/young people are saying, changing the code of behaviour and developing more interaction among the family.
A protocol for a large-scale trial of the SFP10-14 in the UK has been developed and is being submitted to various funding agencies.

Source: Research Report No. 28 ISBN: 1-902606-25-6
www.brookes.ac.uk/schools/shsc/4

In Sweden routine parent-school meetings incorporating parenting advice and encouraging commitment to take a strong stand against underage drinking had a remarkable impact on adolescent drunkenness – but would this simple, low-cost tactic work as well in the UK? 

Abstract
The Örebro Prevention Programme built on the fact that Swedish schools start each term with a parent information meeting. A survey of pupils in the final grade of compulsory schooling (roughly age 16) in the county of Örebro in central Sweden was used to select schools for the project in communities typified as inner cities, public housing areas, or small towns. Within each type of community, pairs of matched schools were selected, one of which carried on as normal, the other of which was assigned to test the prevention programme. None of the schools refused to participate in the study.
The programme was implemented across the final three years (grades seven to nine) of compulsory schooling when pupils were aged 13 to 16. Before the programme started, a survey of pupils in grade seven formed the baseline against which to assess impacts in this and the following two years. In each succeeding year the next higher grade was surveyed, meaning that largely the same pupils were followed up each year. In each year roughly 900 pupils evenly split between both sets of schools were asked to participate in the study.
Rather than through classroom lessons, the programme worked via the parents. At a seventh-grade parent information meeting, project staff gave a presentation describing the programme and advising parents to maintain a zero-tolerance stance towards youth drinking and to communicate clear rules to their children. This was reinforced by inviting attending parents to sign agreements about their positions on (among other issues) youth drinking; most did so. The agreement was mailed to all parents including those who had not been at the meeting. In each of the next two years project staff attended two further parent meetings to emphasise the key message of strict rules. Reports on the meetings were one of at least three mailings each term to parents. Mailings included letters (most co-signed by project workers and teachers) which stressed the importance of communicating family rules against alcohol and drug use and of promoting organised leisure activities.
 
The key question in the pupil surveys asked how often pupils had been drunk in the past four weeks. From virtually no times at age 13, in the control schools not participating in the programme the average rose to nearly once in four weeks at age 16  chart. From a similar starting point, it rose just half as much in programme schools, a medium to large programme impact as represented by the effect size metric. Also the proportion of pupils who had been drunk more than once during this period was twice as high (27% versus 13%) in non-programme schools.
At age 13 just under a fifth of the pupils said they had already been drunk. Among these high risk pupils the programme was just as, if not more, effective, halving the increase in the frequency of drunkenness; by age 16, without the programme these children were getting drunk on average twice a month compared to less than once a month in programme schools  chart. On all these measures for both full and high risk samples, there were statistically significant differences between programme and non-programme schools, and no indication that the programme was any less effective with boys than with girls or vice versa.
Pupils were also asked how often they had committed criminal or antisocial acts over the past year. Though the intervention had focused on drinking, here too there were statistically significant and medium to large programme benefits across the entire samples and among pupils in the top fifth of delinquency before the programme started. In respect both of drunkenness and delinquency, the there were no major differences between the three types of communities in the effectiveness of the programme.
One mechanism underlying these benefits was expected to be an extension of the parents’ strict anti-drinking norms in respect of their 13-year-old children to older ages. Based on the parents’ own accounts, the programme did significantly maintain these norms. However, there was no evidence from the children that involvement in adult-led organised group activities – another supposed means by which the programme would affect drinking – had in fact been enhanced by the intervention.
For the authors their study demonstrated that the parent programme had successfully influenced parental attitudes against underage drinking, resulting in (compared to most other prevention programmes) relatively large reductions three years later in drunkenness and delinquency across both boys and girls, among high risk pupils as well as the entire school year, and in different types of communities. It achieved these impacts despite being easily administered through existing parent–teacher meetings, costing very little to implement, and requiring just a two-day course for the people delivering the programme, who need not be specialist professionals. In the Swedish context they believed these attributes meant the programme could be implemented widely and largely within existing resources.
 In the Swedish context this was a convincing demonstration of the power of harnessing the parent involvement mechanisms and influence of the school to reinforce parental responsibility in respect of their children’s drinking. It is also a testimony to the potential power of unambiguous and simple messages congruent with the culture and to the strong influence exerted by parental attitudes and behaviours on when and then how young people drink. Whether it would work in drinking cultures like that of the UK is questionable. However, ease of implementation, low cost, the fact that no classroom time is involved, and the potential for substantial impacts, may be seen as making it worth a try, probably not as a standalone intervention, but to supplement whole school programmes, the promotion of activities which give young people a sense of achievement and belonging, and perhaps above all, cultural change which makes parents more willing and able to control drinking among underage children.
Though not clear in the featured report, it seems that parents at the initial meeting jointly develop an agreement concerning their stance on youth drinking, possibly adding group solidarity and continuing parent-to-parent reinforcement to the mix of influences leading to impacts  several times greater and more consistent than typical of alcohol prevention programmes applied universally to the entire youth population. This is the case even in respect of programmes recognised as effective and usually far more costly and difficult to implement. Confidence in the validity of these findings is weakened slightly by methodological issues; in particular, the failure to account for the grouping of children and parents within schools could have falsely magnified the apparent impacts. More in background notes.
Efforts to involve parents have generally been more elaborate but less successful than the one trialled in the featured study. A meta-analysis combining findings from randomised studies of parent-focused substance use prevention programmes found modest effects in the form of fewer adolescent children starting to drink and a lower frequency of drinking. This was particularly the case when whole schools were engaged in the intervention, offering an opportunity for pupils and parents who participated in the programme to influence those who did not. However, the findings were undermined by a general failure to account for families which were unable to be followed up.
A common practical problem is getting parents to participate in face-to-face substance use prevention programmes. Typically in Britain (see for example 1 2 3) and elsewhere in Europe, attendance is very low, especially among parents most in need of parenting support and with lenient attitudes to substance use. Generally in these studies the attempt was to encourage attendance at special add-on events. On this count the featured study’s strategy of incorporating prevention in to the school’s core parent involvement programme has a distinct advantage. The downside is that at these events schools have a limited time in which communicate with parents; educational and other social issues (such as knife-carrying, guns, bullying, illegal drugs, teenage pregnancy) are likely to be seen as higher priorities both by the school and by the parents. Other solutions tried in Australia and the USA involve mailings to parents from the school or parent-child homework assignments; more in background notes.
An obvious risk of encouraging parents to make their strictness about underage drinking known to their children, is that the children will respond by hiding their drinking, depriving parents of awareness and the opportunity to intervene. In Sweden but perhaps less so in Britain, voluntary self-disclosure is an important way parents learn about their children’s leisure-time activities. More in background notes.
As the authors acknowledged, the main question mark for readers outside Sweden will be the programme’s applicability to their cultures. Rather than having to create this, it merely had to extend the strict anti-underage drinking norms held by parents and communicated to their children when they were 13 years of age to later ages, when legal purchase was still many years away for their children. Such attitudes reflect national policy. For a European nation, Sweden has unusually restrictive alcohol laws, allowing legal purchase only at age 20 and confining the sale of anything other than low-content beverages to state-run stores, restrictions which make it clear that drinking is not mainstream and accepted.
As in Sweden, in Britain too parents seem influential in their children’s drinking, but as much in the direction of condoning as outright opposition. It would be a far bigger task to persuade the majority of British parents to harden their attitudes and keep them hardened as their child approaches the lower legal alcohol purchase age in the UK, where full-strength drinks are available in virtually every supermarket. In drinking cultures like Britain, advice originating from the school about the parent’s responsibility to communicate an unambiguous stance on drinking risks being seen as unwelcome meddling, especially by the heavy drinking parents whose children could most benefit from stronger parenting. See background notes for some relevant studies. A trial in the Netherlands of a Dutch version of the Örebro programme may be a better pointer to how it would perform in a drinking culture more like that of the UK. If so, it suggests that it would be a worthwhile addition to alcohol use prevention lessons, but not the standalone success it was in Sweden. More in background notes.
Attempts are however being made in Britain to harden parental attitudes to youth drinking. Aided perhaps by media coverage highlighting the risks of youth drinking, the relevant English national policy aims to develop a national consensus on young people and drinking. At the sharp end of the policy are court orders requiring parents whose children persistently drink in public to exercise greater control. Further down the scale are support for parents whose children are at risk of problems such as drinking, and the attempt to establish a partnership with parents based on a clear understanding of acceptable and unacceptable levels and patterns of youth drinking. So far however the message received by parents from other aspects of alcohol policy – alcohol’s mainstream position in society, and particularly the recent extension of opening hours – is that the government is not taking a stand to manage the issue of alcohol in society, undermining the credibility of calls for parents themselves to shoulder that responsibility.

Source: Koutakis N., Stattin H., Kerr M. Request reprint
Addiction: 2008, 103, p. 1629–1637.

Journalist Nick Davies has  written  about legalising Heroin before and more recently. This is a rebuttal by an Australian professor and researcher. 

Nick Davies is right about one thing; drug policy is typically surrounded by an absurd amount of disinformation and misinformation. The truth is not always easy to find.  Governments the world over are perennially advised by experts of the day and the scientific establishment. Science, like most human activities, has within it schools of different thought and is very subject to the winds of its own internal fashions.  Phrenology in the 1930’s was one glaring example and the recent man made global warming debate is another. Many of my friends in the UK and on the East coast of the US are desperate for a good dose of global warming to thaw out their cars, homes and driveways.  The dearth of quality information in this field, and in many cases its deliberate suppression implies that, to borrow another of Davies’ metaphors, the policy debate continues to impersonate a drunken man on a dark night.  The main thing I learnt from Davies’ polemic was that the political and social left dislike Margaret Thatcher – who would have guessed?

Davies dutifully recites the many alibis and mantras of the liberal drug left including principally that heroin itself is intrinsically benign, and it is the illegal status of the drug along with the high cost, the impurities with which it is mixed and injected, and the unknown purity of the drug which are responsible for its toxicity. 

Astonishingly Davies even manages to trivialize heroin overdose, and claims it is relatively rare.  Perhaps this extraordinary claim is due to the fact that his references are mainly to Wikipedia, advised by a few drug liberalization sites or other journalists.

It is well known that the rate of death amongst heroin addicts is about 16 times higher than that of non-addicts, with some estimates from Sweden placing it 55 times higher, and others 70 times higher.  Overdose is not rare amongst heroin addicts, and many studies show that it is a common feature of people who have been injecting it for several years, and more have overdosed than have not.  In some Australian studies about half overdose several times annually.  Rather than heroin being safe as suggested, the levels of opiates in the blood are often relatively low or in the therapeutic range at post-mortem.  Therefore the reason some addicts die is often not well understood, although in the overdose situation it may be mixed with other drugs.  This does not exonerate heroin as it is a depressant drug, and obviously depressant drugs can sum together, or even potentiate the effects of each other to have a super-additive effect to halt breathing.  Moreover opiate addiction, which includes methadone and heroin, likely changes the central appetite mechanism deep in the hypothalamus of the forebrain, so that the appetite for other drugs is increased.  Davies also fails to mention that many heroin programs are actually heroin and methadone programs.  Heroin works for such a short time, that the overnight doses have to be of methadone to keep patients comfortable during the night.  So heroin programs are more properly thought of as “heroin top up programs.”

Rather than heroin being benign for the brain, the scientific literature is replete with studies and claims that long term opiate use causes damage to the mood centres in the limbic system, and the extended limbic system which includes the hippocampus and hypothalamus, which it turns out are also responsible for memory formation, learning and hormone control.  There is no such thing as a drug addict with a good memory and this is not related to the legal status of the drug.  Similarly the majority of opiate addicted patients have psychological disorders with rates in various studies particularly of depression and anxiety at over 70-90%.  Similarly epilepsy is far more common in opiate dependent patients, and there are several reasons for this.  Opiates have been shown to impair the renewal of brain stem cells, particularly in the hippocampus.  As this area is in charge of memory formation and emotionality, and is frequently the site of origin of fits, disturbances in these functions are to be expected, and are in fact commonly observed.  Indeed opiates have been shown to impair the growth of all organs, likely by impairing stem cell growth and activity.  This likely accounts for the evidence of disease and dysfunction in virtually every organ system of the body in long term users.  Opiates have actually been shown to impair the ability of cells to divide by blocking the normal progression of stem cells through the cell cycle, right at the very beginning of these transitions.  This effect is exacerbated by the action of morphine and its derivates including heroin to trigger programmed cell death, which researchers refer to as “apoptosis”.  Clearly the increased cell death, and the relative inability to replace the lost cells can hardly be good either for the health of the body’s cells and organs individually, or the patient as a whole.

It has also been shown that – pure – opiates both suppress and stimulate the immune system.  Whilst some may find this dual action confusing, it is reminiscent of an old car struggling to keep up with the speed limit with a dying engine.  As the car goes up the highway it blows smoke everywhere, and gets pulled over by the police for failing to keep up to the speed limit!  It is also very noisy, as its engine rev’s hard to do its best.  It is clearly working both hard and weakly at the same time.  This seems to be the picture of the opiates saturated immune system.  It parallels other clinical disorders such as rheumatoid arthritis and lupus, where patients with an overactive immune system also display evidence of generalized immunosuppression.  This immune stimulation is particularly damaging for the body, and likely takes a big toll of all organ systems.  Such immunity has been found to be important in many diseases including dementia, atherosclerosis, diabetes, obesity, osteoporosis, chronic periodontitis, cancer development and the ageing process itself.  Opiates have been shown to directly stimulate many aspects of the innate immune system, an evolutionarily ancient and very powerful arm of the immune response which acts quickly and promptly to alert the body to danger signals, and to summon other yet more powerful components of the truly matching adaptive immune response.  Moreover components of the innate immune system have now been shown to be also involved in controlling brain formation, synapse formation between nerve cells, brain stem cell generation and differentiation, and controlling neuronal and dendrite growth in the brain.  The immunosuppressive action of opiates increases the infectivity of, and damage caused by HIV in the immune system and brain, and Hepatitis C damage in the liver.

In particular one of the most sensitive tissues are actually stem cells, as these fragile baby cells, which all carry opiate receptors, are unusually sensitive to the noxious effects both of opiate agents and immunity.  This means that opiates actually pack a triple punch on cells throughout the organism:  there is the devastating effect of opiates on cell growth, and particularly stem cell growth; there is the stimulating effects of opiates on the immune system which leads to damage to the body as a whole; and then there is the compounded interactive effect of the immune effects of opiates particularly on the stem cells, which is likely more severe than the effect of either action working alone. 

Evidence of damage to the vascular system has also been published, which has been linked with stroke and heart attack.  Evidence of widespread hormonal disruption has also been shown.  The dental disease is well known, and this in its turn has been shown to be linked with higher rates of systemic pathology including hardening of the arteries and the development of dementia, probably by further stimulating the immune system.  Opiates disrupt cellular barriers both in the gut, allowing increased access of highly toxic germs to the blood stream, and in the brain where the immune system gains increased access to the nerve cells of the critical centres of the brain through a leaky blood brain barrier.  Similarly bone healing and formation is disturbed by opiates, likely by both stem cell and immune stimulatory mechanisms.  90% of an American study of opiate dependent males, with a mean age of about 40 years, had evidence of measurable and clinically significant bone loss, called osteopaenia or osteoporosis.  This is very important as it integrates the effects of addiction over significant time.  The liberalists argue that opiates are without intrinsic harm themselves, whilst conservatives argue the obvious denigration of virtually all drug users with time.  In one sense both might be true.  If the net defect suffered is only minor – say 5% annually, then over 20 years, the total deficit suffered is 64%!  Over 40 years this is 87%!  This implies that studies which demonstrate short term efficacy, typically over 6-12 months, really have essentially nothing to say about the long term toxicity of the drugs, as none of them have the necessary sensitivity to assess damage at this high degree of precision.

In fact there are very few published studies which examine the effect on physiology over the very long term.  Those which are available all paint a very bleak picture, with one major American study recently calling for geriatricians to be appointed to those addicts who survive to the age of 50 years, as their health was essentially falling apart in many body systems with evidence of widespread physical and mental disease, disability, misery and – of course – death in those who had not survived to complete the survey.

As for giving heroin out, one must be very careful.  The recent report of the Canadian heroin trial showed that it had a primary failure rate over one year of 40%.  This makes it far from the panacea depicted in its marketing blurb.  Data from the Sydney injecting groom, a room where illegal heroin can be taken under the supervision of Government employed nurses, showed that the rate of overdose was over 30 times higher than that in the general community.  In other words, in the presence of support staff clients were more than happy to “go for the magic big hit”, with near fatal overdoses on many occasions only averted by prompt action from the attending professional staff.

Davies mentions the disrupted social networks characteristic of heroin users.  It is sad that people who are dearly loved by their families die alone.  The utter chaos surrounding the heroin addicts life is legendary.  So many patients have told me that while they are using they think they are only hurting themselves; however when they get clean they realize how destructive their drug abuse is on all their family, friends and social relationships.  Most of these patients tell me that the best thing they could do is to come upon a bag of free heroin, and when they are sick many admit praying for a free hit.  However they freely and universally admit that this is also the worst thing that could happen to their own children.  When I ask them which view is correct, their view for themselves or their view for their children, they start to see that they have been badly deceived, and wickedly seduced.  It also becomes very obvious to them that they will not be truly free from their addiction in their mind until the way they think about heroin for themselves is the same as the way they think about heroin for their children.  As much is likely also true of societies.

As to heroin use being normalized in Switzerland and Zurich, that is not what the many refugees from that city who have fled all the way to Australia have told me on many occasions, nor is it the story which is in the published medical press.  Many have fled the gross social degradation which have taken over the forced closure of the Swiss “Needlepark” [ “Platzspitz”], and the criminal explosion which accompanied it.  According to published reports the top 1 meter of soil had to be bulldozed out of the park to clean it up.  Its closure only saw it move over the road to the abandoned railway station. 

Davies’ claim that the introduction of methadone was a cunning move to push up the price of black market heroin betrays his obvious agenda.  The simple fact is that a wave of heroin abuse has taken the world since the 1960’s which the various programs were designed to allay.  I found his figures for the majority of property crime in the UK being related to heroin use interesting in that they are virtually identical to those from Australia. 

The arguments of the left are seductively simple, but they are best addressed by stating the obvious from everyday life, the social, physical and psychological nightmare of active addiction.  These are the hard lessons learnt in places such as Sweden in 1968 and in Zurich where liberal policies such as those presently advocated were tried on the basis of seductive supposedly compassionate advice such as that which Davies and his ideological colleagues presently so eloquently argue.  Whilst there is a superfluity of robust evidence available in the scientific literature to refute such claims, it is also clear that much more work in this area could be done.  Nor is it relevant only to addiction medicine.

The fact that opiate addicts notoriously suffer from exorbitant rates of atherosclerosis, dementia, psychological disorders, osteoporosis, dental disease, immune dysfunction, hormonal disturbances and disruption of their sleep-wake cycles and appetite drives, and a very high rate of some cancers, implies that if we understood more of this process we could treat these major disorders much better.  Moreover, collectively they demonstrate an acceleration of the ageing process, so we would likely begin to understand the ageing process much better, potentially developing treatments which might increase the human “healthspan”, or our number of disability free years, minimizing our risk of long term disablement and years spent in a nursing home.  And the deficit of detailed long term studies of these important issues is clearly a major gap in our understanding, which urgently needs to be addressed.  Whilst it is true that there exists enough data in the published science to effectively refute the raucous arguments for legalization of all presently proscribed drugs, it is equally true that much more could be done in the toxicological sciences to explore these issues in more detail.  That western societies allow mainstream science to continue to overlook such areas, whilst drugs pose so present and imminent a major social threat, is an international disgrace, and one which can only be overcome by the will of the people being felt by the policy makers, to properly protect the coming generations. 

For example cannabis has been shown to be linked with eight cancers, including congenital leukaemia and brain cancer, and has been shown to be mutagenic.  This may be related to its genotoxic effects mediated via AP-1 and MAP kinase pathway activation.  Opiates also stimulate these same pathways, and have also been shown to be linked with carcinogenesis.  Environment has been shown to impact gene regulation through epigenetic regulation including chromatin methylation confirming the Barker hypothesis that in utero and neonatal influences can permanently affect gene expression for decades to come.  There is no liberalization argument to address genotoxicity in this generation, and no liberalist defence of genetic mutagenicity in the next generation.  The demonstration in many studies that parental opiate use produces body and organ growth retardation, impairs brain growth, induces organ structural abnormalities, and intellectual and behavioural disabilities in affected offspring into their teenage years has no liberalist defence, and is in fact egregariously indefensible.  As developed nations we have much more to learn and much more to do

The author runs the largest heroin detox clinic in Queensland Australia, and has published many papers on heroin and drug addiction and its treatment.

Source: Stuart Reece Feb.2010

Two NIDA-funded studies identify health risks that  underscore the importance of curbing marijuana abuse.

BY PATRICK ZICKLER, NIDA Notes Contributing Writer                             

A large new epidemiological study suggests that marijuana smoke can cause the same types of respiratory damage as tobacco smoke. Significant associations between marijuana smoking and a variety of respiratory diseases also have been confirmed by an extensive review of clinical literature.

MONITORING THE EFFECTS OF TOBACCO AND MARIJUANA

Dr. Brent Moore and colleagues at Yale University, the National Cancer Institute, and the University of Vermont evaluated data from a nationally representative sample of 6,728 adults. Their analysis indicated that a history of more than 100 lifetime episodes of smoking marijuana, with at least one episode in the past month, increased an individual’s risk of chronic bronchitis, coughing on most days, wheezing, chest sounds without a cold, and increased phlegm.

“The most significant difference between tobacco smoke and marijuana smoke is their principal active ingredients—nicotine in tobacco and delta-9-tetrahydrocannabinol (THC) in marijuana. Beyond that, marijuana contains at least as much tar and half again as many carcinogens as smoke from conventional tobacco,” says Dr. Moore. “Quitting marijuana smoking may benefit respiratory health as much as quitting cigarettes, in addition to the clear and considerable health, psychological, and social benefits of no longer abusing an illicit drug.”

The information Dr. Moore and his colleagues analyzed was gathered through the third National Health and Nutrition Examination Survey (NHANES III), conducted between 1988 and 1994. Participants included 4,789 nonsmokers of either tobacco or marijuana; 1,525 smokers of tobacco but not marijuana; 320 smokers of both marijuana and tobacco; and 94 who smoked marijuana only. On average, marijuana abusers had smoked the drug on 10 of the preceding 30 days, with 16 percent reporting daily or almost daily smoking. Tobacco smokers consumed roughly the same number of cigarettes—averaging 19.2 per day—whether or not they also smoked marijuana. Survey participants answered questions about their experiences of a range of respiratory symptoms and were examined for signs of respiratory abnormalities.

The researchers concluded that tobacco smokers who also smoked marijuana had a higher prevalence of most respiratory symptoms than tobacco-only smokers. Compared with tobacco-only smokers, however, those who also smoked marijuana were less likely to have had pneumonia during the previous year or to show spirometric evidence of obstructive pulmonary disorder. Commenting on this finding, Dr. Moore says that it is important to note that the marijuana smokers in the sample were significantly younger (average age 31.2 years) than the tobacco smokers (average age 41.5 years). “The marijuana-related respiratory effects correspond to a relatively young population, and NHANES III did not ask participants older than age 59 about drug use,” he adds. “It is likely that respiratory effects will be higher in older marijuana smokers, and, because of the high prevalence of tobacco use among marijuana smokers, there appears to be an increased risk for illness due to cumulative effects of smoking both drugs.”

MARIJUANA’S LONG-TERM PULMONARY EFFECTS

Further evidence of marijuana’s respiratory toxicity emerged from a study conducted by Dr. Donald Tashkin at the University of California, Los Angeles. Dr. Tashkin conducted an extensive review of clinical and epidemiological research to determine the extent to which chronic marijuana smoking might lead to long-term pulmonary effects and diseases similar to those caused by tobacco. Unlike the NHANES III data examined by Dr. Moore, the studies evaluated by Dr. Tashkin made it possible to assess a possible association between marijuana smoking and respiratory cancers.

The results of animal and cell culture studies are mixed with respect to the carcinogenic effects of THC, some studies showing that THC promotes lung cancer growth and others showing an anti-tumoral effect on a variety of malignancies. Although the results of epidemiological studies are also mixed, a large, recently completed case-control study has failed to find a direct link between marijuana use (including heavy use) and lung, throat, or other head and neck cancers. “Nevertheless, there is evidence that suggests precarcinogenic effects in respiratory tissue,” Dr. Tashkin says. “Biopsies of bronchial tissue provide evidence that regular marijuana smoking injures airway epithelial cells, leading to dysregulation of bronchial epithelial cell growth and eventually to possible malignant changes.” Moreover, he adds, because marijuana smokers typically hold their breath four times as long as tobacco smokers after inhaling, marijuana smoking deposits significantly more tar and known carcinogens within the tar, such as polycyclic aromatic hydrocarbons, in the airways. In addition to precancerous changes, Dr. Tashkin found that marijuana smoking is associated with a range of damaging pulmonary effects, including inhibition of the tumor-killing and bactericidal activity of alveolar macrophages, the primary immune cells within the lung.

Taken together, Dr. Tashkin’s survey of clinical and epidemiological studies and Dr. Moore’s assessment of self-reported and clinically observed effects provide an extensive catalog of respiratory and pulmonary damage associated with marijuana smoking. Smokers are subject to:

·         Coughing and phlegm production on most days;

·         Wheezing and other chest sounds;

·         Acute and chronic bronchitis;

·         Injury to airway tissue, including edema (swelling), increased vascularity, and increased mucus secretion;    

·         Impaired function of immune system components (alveolar macrophages) in the lungs.

Moore, B.A., et al. Respiratory effects of marijuana and tobacco use in a U.S. sample. Journal of General Internal Medicine 20(1):33-37, 2005. [Full Text]

Tashkin, D.P. Smoked marijuana as a cause of lung injury. Monaldi Archives for Chest Disease 63(2):93-100, 2005. [Abstract]

Hashibe, M., et al. Marijuana use and aerodigestive tract cancers: a population-based case control study. Cancer Epidemiology, Biomarkers & Prevention (In Press).

Source:NIDA Notes > Vol. 21, No. 1  Oct.2006

Fred M. Jacobs, M.D., J.D., Commissioner,
New Jersey Department of Health and Senior Services
August 2007

Dear Dr. Jacobs,

Re: Establishment of Needle and Syringe Programs

I understand that the state of New Jersey is considering a needle and syringe “exchange” program. I am also advised that New Jersey is a liberal democratic society whose members for the most part believe in freedom of the individual to pursue “life, liberty and happiness”. This of course is wonderful! And also provides a useful opportunity to note that no drug addict enjoys real freedom while their will, their lives, their relationships and their resources are largely dedicated to the service and slavery of their chemical addiction. This would make your lovely part of the world an excellent place in which to pursue those liberties which should be the birthright of every human being.

To introduce myself I am a family physician in Australia, and have pursued a special interest in the treatment of addiction especially for heroin, but also other drugs of addiction for the last ten years. Health department figures indicated last year that in the years 2001-2006 I single handedly registered 11,000 of the 14,000 registrations for opiate detoxification in the state of Queensland. I have also attained one of the three largest numbers of naltrexone based rapid opiate detoxifications in the country of Australia with over 1,800 procedures performed including 600 naltrexone implants. This was done with only two overnight hospital admissions which is a world safety record. I have also submitted evidence to several Government committees and leaders on the subject of drug policy.

As the so-called “needle “exchange” programmes” make little effort to exchange syringes, and as actual exchange makes little difference to the operation or mission of the programs, it is probably more accurate to refer to them as needle and syringe distribution programs, or NSP’s. It is important that your community appreciate this because syringe disposal is a real problem with these facilities. It has been so in this country. Our lovely and world famous Bondi beach in Sydney is now said to be one of the best places in the country to get a needle stick injury, due to the many syringes hidden in the sand. Clean up patrols have operated in King’s Cross twice daily for years to clean up the extreme public nuisance of hundreds of used syringes left dangerously in the streets and side walks, to protect the public . This is a well recognized problem with NSP’s which is generally covered up while such programs are in the planning phase.

Epidemiological Evidence

Since the NSP experts readily resort to discussion of “evidence based treatments”, and since the community decision to fully implement this program has such far reaching implications both in terms of needle disposal bins in all public toilets and for the time and direction of public health policy in the management of addiction, it is very appropriate that careful consideration be given to the quality of evidence which is typically cited in support of NSP’s. In particular the evidence based literature waxes lyrical about “levels of [reliability of] evidence.”

Self-report data is widely used in the addiction literature but it has been shown many times to be highly flawed and unreliable, and to fails to correlate with more objective and hard signs of HIV rates. As was pointed out to you by Dr. Fred Payne’s letter, and as was noted in the Institute of Medicine Report on this subject, it is well recognized that most of the literature on the subject of needle exchange is based on self report. This would clearly make it the least reliable form of evidence by their own criteria. Actually one would have to wonder if the evidence based gurus would accept such data at all.

Secondly we are aware of the “ecological” studies where they repeatedly report many cities with and without NSP’s. The work of Dr. Kirsten Kall’s group from the University of Linkoping shows clearly that in such an epidemic the rate of rise of the epidemic is related to the population at risk. Epidemics it is argued have a natural life history with a rise, fall and usually stabilization levels. Depending where in the natural history of the epidemic one takes one’s samples one will get a different picture of the efficacy of the NSP’s. It is for this reason that showing either a rise or a fall in HIV incidence or prevalence after NSP introduction is irrelevant if one is not informed of the natural history of the epidemic, and unless one can adduce by other means the likely outcome in its absence. This is a severe criticism, and one which effectively invalidates the whole of this genre of studies. I am also assured by epidemiologists familiar with such matters, that such studies are given no weight in epidemiological circles for this reason. That they have been foisted upon the rest of the world and even mentioned in major UN reports shows the degree to which such sloppy unscientific methods have been adopted within such agencies.

Indeed Dr. Alex Wodak, understood to be one of the primary authors of the relevant section of the 2006 UNAIDS report which eulogized NSP’s and the harm minimization addiction management paradigm, unequivocally stated in 1995 that formal proof of the methods of harm minimization would be impossible as it would not be possible to control in real life the many confounding factors which would be acting, and thereby prove that any particular intervention alone had been salient in controlling the target disorder .

Furthermore there is a clear conflict of interest by some of the leading proponents of NSP’s . Dr. Alex Wodak was for many years the President of the International Drug Law Reform Foundation and is the current president of the Australian Drug Reform Foundation which lobbies unceasingly for drug decriminalization. Dr. Don Jaralais in the USA is also understood to be of a similar ideology, and his advocacy for NSP’s is well known. I am of the understanding that such parallels could be made repeatedly for many of the most ardent advocates of NSP’s.

Dr. Payne’s letter mentions the very high rates of HIV in Vancouver at present despite the operation of an NSP, having risen from 1% to 35%. It was also shown long ago in Montréal that the HIV rate amongst NSP attendees was 2.5 times that amongst non-attendees (3.1 Vs. 7.9%) .

In terms of its control of other virus transmission NSP’s seem to substantially lack power. They failed to control Hepatitis B in Amsterdam , or Hepatitis C in Australia where rates of HCV carriage amongst IVDU who have been involved in the lifestyle for longer than six months exceed 80%.

Special Situations

Some situations are special and require special consideration. We are well aware that the apparent success of harm minimization techniques in this country is frequently cited overseas and in international fora as proof of principal of the efficacy of harm minimization epidemic management techniques. What is repeatedly overlooked in such discussions is our record rates of other infections such as Hepatitis B and C, and the venereally transmitted agents Herpes, Warts and Chlamydia. Indeed recently released data shows 30-100% growth in the last five years in Queensland in Gonorrhea, Hepatitis C, Chlamydia and Syphilis . Indeed it has been estimated that the Australian health care system has now to plan for over 100,000 liver transplants required for Hepatitis C alone in the next 20 years. One also notes that the outcome after transplantation for Hepatitis C is inferior to that for other infections due to the universal early graft re-infection which invariably occurs in the first few post-operative days, and the clash between anti-rejection immunosuppressive therapy and the anti-viral needs of fighting an aggressive viral infection in the context of the immuno-suppression and likely immuno-senescence induced by drug addiction, which is reversed to an unknown extent by abstinence.

In Australia our HIV rate amongst IVDU who do not share other risk factors is very low by international standards of the order of 1%. New cases of HIV nationally in all groups have risen from about 100 in 1991 to around 300 in 2005 . There appears to be significant variation in the estimates for the number of syringes distributed to addicts in this country with estimates varying from 20,000,000 to 200,000,000 – a level of inexactitude which in itself should give us pause. The former number was more than our total population at the time, and the latter number is substantially greater than the number of sheep here (which says a lot for a nation which for a long time was said to ride on the sheep’s back!) One important feature then facing the advocates of any NSP program is exactly how many syringes do they want to distribute? One for every man woman and child in the state?

However in the case of Australia we would do well to heed Wodak’s warnings about the inability to control for other confounders. From a modeling point of view the epidemic began in certain well known high risk groups. Its spread would then have been related to the population at risk, the activity of the various risk taking behaviours, and the intersection of these behaviors with the wider general community. Still today over half of all HIV infections in this country occur amongst men who have sex with men. It should also be added that the rate of IVDU in this group is 10-20 times higher than it is in the general community. Clearly then the spread of the disease into the wider community is related to the behaviour of this reservoir of infected people. One of the obvious confounding factors which has never been studied or quantified is what might be termed the homosexualization of the Australian culture with many laws, many bureaucracies, and schools of public health completely subsumed by the new ideology accompanying the public health impetus of the HIV epidemic. In that this likely instilled major good will in the primary target community, and is likely to have very positively influenced the relevant risk taking behaviours, it is clearly an intimate confound which confuses and likely dilutes any effects which might be attributable strictly to NSP’s.

Another important confounding factor was that Australia made treatment for HIV free to all patients who would have benefited from it from the outset of the epidemic. Assuming that the most at risk individuals were infected near the beginning of the epidemic, then those that survived their infection might reasonably be expected to have had a lower viral load for most of this time making them les infectious. This can be expected to have significantly slowed the rate of progression of the epidemic in this country.

Sweden is an important case in point which must be mentioned in any intelligent discussion of the NSP movement. Sweden has very limited methadone treatment availability, until recently no NSP activity, and no legal “shooting galleries” and a very low rate of HIV in IVDU. Hence the methods of harm minimization cannot strictly be said to be required for HIV control. Clearly HIV control can occur in a very effective manner in the absence of the model harm minimalist strategies.

The situation in prisons, or penitentiaries, is a special one and well worth at least some specific consideration. I was privileged to give evidence to the Inquiry into the Impact of Illicit Drug Use on Families before the Federal House of Representatives of the Australian Parliament on 3rd April 2007 . During that interview I stated that “my blood ran cold at the thought of 500 inmates all sharing the same syringe barrel” as was recounted to me by one of my HIV positive patients. However typical harm minimalist solutions such as methadone, syringe distribution and bleach use have been found to be impractical in the prison environment, and in this country have triggered strikes and industrial disputes by the prison warders due to the creation of unsafe workplaces. Since making those comments to the committee I have considered what might best be done about this appalling situation. One approach follows below (see “Other Treatment Modalities”).

In essence it is my belief that where the crime for which a person is committed is referable to opiate drugs, the standard of care will become naltrexone implant insertion on admission to the jail (after appropriate detoxification procedures), naltrexone implant maintenance during incarceration, and naltrexone implant prior to discharge to prevent the overdose which so often accompanies discharge (and the ritualistic “get a whack, get a woman” routine which is invariably followed). Indeed in Perth patients discharged from the prison are taken by volunteer escort from the prison gates to the clinic for implantation before the whole destructive cycle can re-commence. This seems the most sensible, responsible and compassionate management of this problem.

Other Treatment Modalities

Naltrexone was fist synthesized in the USA 1963 at Endo laboratory by Matossian acting under Blumberg’s instruction . Naltrexone implants and depot preparations have recently received a lot of attention from the international addiction management literature, and have been commercially introduced in the USA. American developed depot injections typically last 3-4 weeks. A preparation recently developed in this country lasts typically 4-6 months. The results of the first formal clinical trial conducted in Perth will soon be announced, probably in a leading medical journal such as JAMA or New England Medical Journal. They have been extensively used in this clinic where we have inserted over 600 USA (Wedgewood) and Australian (Perth “Go Medical”) implants. I was asked by the Preventative and Community Medicine Committee of the Queensland Faculty of the Royal Australian College of General Practitioners to evaluate naltrexone medicine including the Perth naltrexone program in 1998, and since 2001 I have been involved with the development in Perth of their naltrexone implant.

Unofficially the abstinence rate in terms of not returning to dependent heroin use at five months was well in excess of 50% in a study which set new standards international medical literature for patient follow-up. Only 11% of the 70- patients were lost to follow-up compared to over 90% in a similar (larger) study conducted in leading centres in the USA reported by Hollister in 1977 for NIDA at the NIH . Naltrexone is also a widely recognized and used technique for reducing problem drinking in alcoholics. It has also been used for gambling addiction, with positive results on some occasions. Moreover other results reported from the Perth clinic indicate that naltrexone is likely to have a controlling effect on other chemical addiction such as benzodiazepines, cannabis and stimulants such as amphetamines.

It is my personal view that they are excellent and will soon revolutionize the treatment of opiate addiction. Opiate dependence of course is the most addictive and refractory of all drug addictions, and the possibility of gaining control of such patients in a drug free context, as opposed to the usual medical model involving the indefinite maintenance of addiction, must be one of the most exciting opportunities ever to be offered to physicians in addiction medicine.

Another medical agent which has shown enormous promise in the control of multiple addictions is the cannabinoid antagonist rimonabant (“Accomplia”; SR141716A) which has been used with success against opiate, tobacco, alcohol, amphetamine food and cocaine addictions. This drug has attracted attention from NIDA and is undergoing further testing. I am not sure what its regulatory status is in the USA. It was available in eight European nations when I enquired with the pharmaceutical company (Sanofi-Synthelabo) about four months ago. The drug is still under patent, so this impedes its being re-formulated into an implant or depot preparation.

The combination of naltrexone and rimonabant has yet to be tested but would appear to show obvious promise, and it would be a priority in a rational testing program to investigate this further.

Future Research Directions

Many studies show increased evidence of drug use in young people.

All senior authorities in the world agree that there is far too little resources put towards investigating the toxicological effects of addictive drugs in general, and in adolescents in particular.

If we are ever going to do more than shut the door after the horse has bolted, clearly the issue of the true toxicity of addiction must be much better investigated, and the results of such studies broadcast far and wide to our young people, to de-glamourize the dreadfully seductive marketing program to which the rock music and popular culture misleadingly subjects them. If we are ever going to contain the monster of rampant destructive drug use in our younger people, then their dangers must be better emphasized.

Given the obvious multi-system damage of long term chemical addiction which is immediately apparently to even the untrained observer, one can only conclude which a Science which espouses the relative benignity of addiction must be grossly and egregariously deficient.

I have formulated a detailed plan by which such a strategy can be put in place, based around the accumulated ageing changes evident in the skin, teeth, hair, blood vessels, bones, immune system, stem cells and brains of addicts. It invites international collaboration and multi-system multilevel cooperation and the application of state of the art techniques to classical clinical problems. That however, is another story.

CONCLUSION

In summary NSP’s incur great social cost and are clearly part of the problem rather than part of the solution. Their scientific literature is remarkable for its lack of compelling evidence and methodological rigor, not to mention the prominence of adverse findings, when properly adjudicated. Rather the global penetration of NSP’s is an indicator of the strength of the marketing strategy of the ideology they enshrine. They are in any case about to be phased out like old dinosaurs by the cutting edge technologies which are moving ever closer to being a real market alternative, particularly the revolutionary long lasting Australian naltrexone implant.

I have been advised that now methadone is worth $150/week to dispensing hospitals in Federal hospital subsidies. As some of the most famous institutions in the USA have 10,000 – 20,000 patients enrolled on it, this income source forms a major stream of hospital funding. As such it is not likely to be disrupted. What the management of the Australian HIV epidemic does teach us is that it is best to get on and treat the HIV infection as soon as medically appropriate. In addiction medicine we have up until now largely done the reverse, for there we have deliberately continued indefinitely maintenance treatment designed to not to confront the addicted physiology, but rather to postpone indefinitely the definitive redress of that medical condition. The Australian success with HIV management tends to rather emphasize the reverse approach. This is the therapeutic route suggested by naltrexone implant maintenance. In all the discussion we would appear to have forgotten that in the early 1960’s New York was in urgent need of a treatment for addicted GI’s returning home from Vietnam. Methadone as the only medical solution then available was adopted and quickly came to command tremendous official support to the point where it became in time, the established industry. We have now a far more exciting opportunity to launch naltrexone implants and other new treatments in a similar and innovative manner. In would be my sincere hope that nations can move speedily to deliver proven and safe medical treatments to vulnerable populations without incurring undue, unnecessary and officious regulatory obstruction.

This would appear to be the visionary, drug free and health enhancing approach. As these concepts are more widely understood it is hoped that regulators and administrators will cooperate to mobilize international best medical practice on behalf of those with whose care they have been entrusted. I would invite the legislators of New Jersey to work with us on these issues of major cultural importance.

Yours Sincerely,

A. Stuart Reece, MBBS (Hons.), FRCS (Ed.), FRCS (Glas.), MD, FRACGP.
Family Physician, Highgate Hill Brisbane,
Senior Lecturer, Medical School, University of Queensland,
Fellow, Drug Watch International,
Fellow, Drug Free Australia,
Member, Society for Neuroscience,
Member, International Cannabinoid Research Society,
Attendee, College of the Problems of Drug Dependence Conferences 2002-2006.
Awardee, National Institute of Drug Abuse, International, 2003, 2004, 2006.

MINNESOTA COUNTY ATTORNEYS ASSOCIATION

POLICY POSITION

OPPOSING THE MEDICAL USE OF MARIJUANA IN MINNESOTA

Adopted February 16, 2007

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The Minnesota County Attorneys Association (hereafter MCAA) strongly opposes any efforts to use marijuana for medical purposes within the State of Minnesota currently under consideration in the Minnesota Legislature in Senate File No. 345 and House File No. 655 (hereafter S.F. 345). Prosecutors are not alone in our opposition to this proposal. Legalizing marijuana for medicinal uses is also opposed by the Minnesota Sheriff’s Association, the Minnesota Chiefs of Police Association, the National District Attorneys Association, and the U.S. Drug Enforcement Administration. The reasons for the strong opposition to this proposal by these law enforcement organizations are many and are set forth in outline form below.

I. Marijuana is an Addictive Drug That Poses Significant Health Consequences, Even to a Person Using it for “Medical Reasons.”

• Marijuana is an addictive drug that poses significant health consequences to its users, including those who may be using it for medical purposes.
- Marijuana has been proven to be a psychologically addictive drug. Scientists at the National Institute of Drug Abuse have demonstrated that laboratory animals will self administer THC in doses equivalent to those used by humans who smoke marijuana.
- Persons using marijuana, even for medicinal purposes, suffer withdrawal symptoms when use is stopped, such as restlessness, loss of appetite, trouble with sleeping, weight loss and shaky hands.
• The short-term effects of marijuana use include: memory loss, distorted perception, trouble with thinking and problem solving, loss of motor skills, decrease in muscle strength, increased heart rate, and anxiety.
• Long-term use of marijuana may increase the risks of chronic cough, bronchitis, and emphysema, as well as cancer of the head, neck, and lungs.
• Studies have shown smoking marijuana causes a variety of health problems, including cancer, respiratory problems, loss of motor skills, and increased heart rate. It damages the immune system by impairing the ability of T-cells to fight off infections, demonstrating that marijuana can do more harm than good in people with already compromised immune systems.
- Marijuana is a significant health hazard which contains 50-70 percent more carcinogenic hydrocarbons than does tobacco smoke. Using marijuana may promote cancer of the respiratory tract and disrupt the immune system.
- Marijuana contains more than 400 chemicals, including the harmful substances found in tobacco smoke. Smoking one marijuana cigarette deposits almost four times more tar into the lungs than a filtered tobacco cigarette.
- According to the National Institute of Health, studies show that someone who smokes five joints per week may be taking in as many cancer-causing chemicals as someone who smokes a full pack of cigarettes every day.
- Smoked marijuana has also been associated with an increased risk of the same respiratory symptoms as tobacco, including coughing, phlegm production, chronic bronchitis, shortness of breath and wheezing. Because cannabis plants are contaminated with a range of fungal spores, smoking marijuana may also increase the risk of respiratory exposure by infectious organisms (i.e., molds and fungi).
- In a 2003 study, researchers in England found that smoking marijuana for even less than six years causes a marked deterioration in lung function. The study suggests that marijuana use may rob the body of antioxidants that protect cells against damage that can lead to heart disease and cancer.
- Smoking marijuana also weakens the immune system and raises the risk of lung infections. A Columbia University study found that a control group smoking a single marijuana cigarette every other day for a year had a white-blood-cell count that was 39 percent lower than normal, thus damaging the immune system and making the user far more susceptible to infection and sickness.
• Harvard University researchers report that the risk of a heart attack is five times higher than usual in the hour after smoking marijuana.
- Marijuana can cause the heart rate, normally 70 to 80 beats per minute, to increase by 20 to 50 beats per minute or, in some cases, even to double.
• According to two studies, marijuana use narrows arteries in the brain, “similar to patients with high blood pressure and dementia,” and may explain why memory tests are difficult for marijuana users. In addition, “chronic consumers of cannabis lose molecules called CB1 receptors in the brain’s arteries,” leading to blood flow problems in the brain which can cause memory loss, attention deficits, and impaired learning ability.
• The British Medical Journal recently reported: “Cannabis use is associated with an increased risk of developing schizophrenia, consistent with a causal relation. This association is not explained by use of other psychoactive drugs or personality traits relating to social integration.”
- Dr Andrew Campbell, a member of the New South Wales (Australia) Mental Health Review Tribunal, published a study in 2005 which revealed that four out of five individuals with schizophrenia were regular cannabis users when they were teenagers. Between 75-80 percent of the patients involved in the study used cannabis habitually between the ages of 12 and 21.
- A laboratory-controlled study by Yale University scientists, published in 2004, found that THC “transiently induced a range of schizophrenia-like effects in healthy people.
• According to several recent studies, marijuana use has been linked with depression and suicidal thoughts, in addition to schizophrenia. These studies report that weekly marijuana use among teens doubles the risk of developing depression and triples the incidence of suicidal thoughts.
- Marijuana users have more suicidal thoughts and are four times more likely to report symptoms of depression than people who never used the drug.
• Carleton University researchers published a study in 2005 showing that current marijuana users who smoke at least five “joints” per week did significantly worse than non-users when tested on neurocognition tests such as processing speed, memory, and overall IQ.
• Mentions of marijuana use in emergency room visits in this country have risen 176 percent since 1994, surpassing those of heroin. In 2001, marijuana was a contributing factor in more than 110,000 emergency department visits in the United States.
• Users can become dependent on marijuana to the point they must seek treatment to stop abusing it. In 1999, more than 200,000 Americans entered substance abuse treatment primarily for marijuana abuse and dependence.

II. Marijuana Does Not Have Any Proven Medical Value and it is Not Supported for Medicinal Use by Many Prominent National Health Organizations.

Before considering the enactment of this proposed statute, the Legislature is urged to look closely at the medical facts behind this issue. These include:

• Scientific research has not demonstrated that smoked marijuana is helpful as medicine.
• Major medical and health organizations, as well as the clear majority of nationally recognized experts in the fields of medicine, science and scientific research, have concluded that smoking marijuana is not a safe and effective medicine. These organizations include: The American Medical Association, the American Cancer Society, the National Sclerosis Association, the American Glaucoma Association, the American Academy of Ophthalmology, the National Eye Institute, and the National Cancer Institute.
• The American Medical Association (AMA) has rejected pleas to endorse marijuana as a medicine, and instead has urged that marijuana remain a prohibited, Schedule I controlled substance (although it does support further studies, especially those aimed at delivering a “smoke-free inhaled delivery system for marijuana or . . . (THC) to reduce the health hazards associated with the combustion and inhalation of marijuana.”)
• The American Cancer Society “does not advocate inhaling smoke, nor the legalization of marijuana” (although the organization does support carefully controlled clinical studies for alternative delivery methods, specifically a THC skin patch) .
• The American Academy of Pediatrics (AAP) opposes the legalization of marijuana because it believes that “[a]ny change in the legal status of marijuana, even if limited to adults,” [which would include its use for medical purposes] “could affect the prevalence of use among adolescents.” (Similar to the AMA, the AAP supports scientific research on the possible medical use of cannabinoids as opposed to smoked marijuana.)

- The AAP asserted that with regard to marijuana use, “from a public health perspective, even a small increase in use, whether attributable to increased availability or decreased perception of risk, would have significant ramifications.”
• The National Multiple Sclerosis Society (NMSS) states that studies done “have not provided convincing evidence that marijuana benefits people with MS,” and thus marijuana is not a recommended treatment. Furthermore, the NMSS warns that the “long-term use of marijuana may be associated with significant serious side effects.”
• A recent study by the Mayo Clinic, showed THC to be less effective than standard treatments in helping cancer patients regain lost appetites.
• The British Medical Association (BMA) has also voiced extreme concern that down-grading the criminal status of marijuana would “mislead” the public into believing that the drug is safe. [The same holds true in reference to legalizing the use of marijuana for medical purposes.]
- The BMA maintains that marijuana “has been linked to greater risk of heart disease, lung cancer, bronchitis and emphysema.” The 2004 Deputy Chairman of the BMA’s Board of Science said that “[t]he public must be made aware of the harmful effects we know result from smoking this drug.”
• Even the 1999 landmark study of The Institute of Medicine (IOM) which reviewed the supposed medical properties of marijuana (a study often cited by “medical” marijuana advocates) clearly discounts the notion that smoked marijuana is or can become “medicine.” A close review of the IOM study reveals the following:
- While the principal investigators in the IOM study found that the active compounds in marijuana may have medicinal potential for some ailments (the IOM found “… potential therapeutic value of cannabinoid drugs, primarily THC, for pain relief, control of nausea and vomiting, and appetite stimulation.” ) They pointed out that “[t]he effects of cannabinoids on the symptoms studied are generally modest, and in most cases there are more effective medications [than smoked marijuana].”
- The IOM study concluded that, at best, there in only anecdotal information on the medical benefits of smoked marijuana for some ailments, such as muscle spasticity. For other ailments, such as epilepsy and glaucoma, the study found no evidence of medical value and did not endorse further research.
- The principal investigators of the IOM study explicitly stated that using smoked marijuana in clinical trials “should not be designed to develop it as a licensed drug, but should be a stepping stone to the development of new, safe delivery systems of cannabinoids.”
- The IOM study explained that “smoked marijuana . . . is a crude THC delivery system that also delivers harmful substances.” In addition, “plants contain a variable mixture of biologically active compounds and cannot be expected to provide a precisely defined drug effect.” Therefore, the study concluded that “there is little future in smoked marijuana as a medically approved medication.”

• The Food and Drug Administration and the U.S. Public Health Service have rejected smoking crude marijuana as a medicine. (It is important to note that the Food and Drug Administration (FDA) has never approved medications that are smoked.) This is because not only is it difficult if not impossible to administer safe and regulated dosages of medicine in a smoked form, the harmful chemicals and carcinogens that are by-products of smoking create an entirely new set of health problems.

III. There Already Exists a Legalized Form of “Medical Marijuana” in our Country – It’s Called Marinol (and other approved drugs exist as well to treat these diseases).

• Marinol is an approved pharmaceutical product that is widely available through a doctor’s prescription. It comes in the form of a pill (which can accurately regulate the dose of THC delivered, unlike smoked marijuana), and it is also being studied by researchers for suitability by other delivery methods, such as an inhaler or a patch. The active ingredient of Marinol is synthetic THC, which is the main active chemical found within marijuana. However, unlike marijuana which also contains more than 400 different chemicals (including most of the cancer-causing chemicals found in tobacco smoke), Marinol delivers therapeutic doses of THC in a manner that has been studied and approved by the medical community and the Food and Drug Administration.
• There is, therefore, no medical need to substitute a dangerous and addictive drug like marijuana for an approved prescriptive drug like Marinol that can provide a synthetic form of THC treatment with safe and controlled amounts to assist patients suffering from nausea, vomiting associated with chemo therapy and the loss of appetite associated with AIDS, two of the recognized and approved uses of Marinol.
• Numerous other approved drugs exist to treat the medical problems for which medical use of marijuana would be authorized under S.F. 345. A list of over 20 such medications is set forth in footnote 51 of this document.

IV. Marijuana’s Use As A Medicine Is Contrary to Federal Law as Upheld by Federal Court Decisions (including the U.S. Supreme Court).

• The Federal Controlled Substance Act (CSA) was enacted in 1970 as part of the Comprehensive Drug Abuse Prevention and Control Act. The CSA classifies drugs under five categories (Schedule I–V) based upon their level of danger and acceptance for medical use (among other criteria).
• Schedule I consists of the most restricted drugs under federal law – drugs which have a high potential for abuse, a lack of any accepted medical use, and an absence of any accepted safety criteria for use in medically supervised treatment.
• Marijuana is classified as a Schedule I drug, the manufacture, distribution or possession of which is a federal crime. Manufacture, distribution or possession of marijuana is also a state crime in Minnesota (except possession of small quantities of less than 1.5 oz., which is classified as a petty misdemeanor) .
• States have no authority to change the federal classifications of controlled substances under the CSA (including marijuana) under the Supremacy Clause of the United States Constitution.
• Federal Courts have consistently upheld the classification of marijuana as a Schedule I controlled substance and the fact that marijuana is a dangerous drug with no accepted medical use.
- In 1994, a U.S. Court of Appeals upheld a decision of the Administrator of the Drug Enforcement Administration, who declined to reschedule marijuana from Schedule I to Schedule II of the Controlled Substance Act, finding that marijuana was a drug with “high potential for abuse” which has “no currently accepted medical use in treatment in the United States” and that “there is a lack of accepted safety for use of the drug . . . under medical supervision.”
- The U.S. Court of Appeals found that the DEA Administrator properly relied upon “the testimony of numerous experts that marijuana’s medicinal value has never been proven in sound scientific studies,” noting that physicians supporting use of marijuana for medical purposes (in testimony before an Administrative Hearing Officer) were basing their opinions on “anecdotal evidence, on stories . . . heard from patients, and on . . . impressions about the drug.”
• The most recent and important federal court case on this topic is a 2005 decision of the United States Supreme Court in Gonzales v. Angel, et al., which upheld the authority of federal authorities to enforce federal laws prohibiting the use of marijuana in California for medical purposes as authorized under California law.
- In this decision, the U.S. Supreme Court affirmed that Congress has the authority to regulate controlled substances and “to prohibit entirely the possession or use of substances listed in Schedule I” (including marijuana), except as part of a strictly controlled research project.
• Congress has done just that through passage of the CSA under which marijuana has been designated as a Schedule I drug. In other words, marijuana has been deemed by federal regulation to be an extremely dangerous drug with no general acceptance for medical use.
• If S.F. 345 is passed, it will be in direct conflict with federal law and the U.S. Supreme Court has clearly indicated in Gonzales v. Angel, et al., that federal law takes precedence under the Supremacy Clause of the United States Constitution.
- Consequently, those granted authority to lawfully produce and use marijuana for medical purposes under state law (if S.F. 345 is enacted) will still be committing a federal crime.
• Also, as pointed out by the U.S. Supreme Court in Gonzales v. Angel, et al., legalizing marijuana use for medicinal purposes will clearly lead to increases in the marijuana supply, greater use of marijuana by non-patients and more criminal activity under state law. (See Section VII below for a more specific discussion of this issue.)
• The Minnesota Legislature should not substitute its judgment for that of Congress and the Administrators of the U.S. Drug Enforcement Administration (hereafter DEA) and the Federal Drug Administration (hereafter FDA) as to the fact that marijuana has no general acceptance for medical use and as to defining what is the appropriate way to deliver safe medications to our citizens.
• It is not sound public policy to enact state laws which encourage law abiding citizens to commit federal crimes.

V. Marijuana is a Dangerous Drug that is Associated with Crime and Violence.

• Research shows a link between frequent marijuana use and increased violent behavior.
- Young people who use marijuana weekly are nearly four times more likely than nonusers to engage in violence.
• A large percentage of those arrested for crimes test positive for marijuana. Nationwide, 40 percent of adult males tested positive for marijuana at the time of their arrest.
- Of adult males arrested in the United States for all crimes, 40 percent tested positive for marijuana at the time of their arrest, according to the Director of the U.S. Drug Enforcement Administration.

• In 2003, 3.1 million Americans aged 12 or older used marijuana daily or almost daily in the past year. Of those daily marijuana users, nearly two-thirds “used at least one other illicit drug in the past 12 months.”
- More than half (53.3 percent) of daily marijuana users were also dependent on or abused alcohol or another illicit drug compared to those who were nonusers or used marijuana less than daily.
• There is a strong correlation between drug use and crime. Drug use affects the user’s behavior. In 1997, illicit drug users were:
- approximately 16 times more likely than nonusers to report being arrested for larceny or theft;
- more than 14 times more likely to be arrested for driving under the influence, drunkenness, or liquor law violations; and
- more than 9 times more likely to be arrested on assault charges.

VI. Marijuana is Far More Powerful Today Than it Was 30 Years Ago and it Serves as a Gateway to the Use of Other Illegal Drugs.

• Marijuana is much stronger now than it was decades ago. According to data from the Potency Monitoring Project at the University of Mississippi, the tetrahydrocannabinol (THC) content of commercial-grade marijuana rose from an average of 3.71 percent in 1985 to an average of 5.57 percent in 1998. The average THC content of U.S. produced sinsemilla increased 3.2 percent in 1977 to 12.8 percent in 1997.
- The average THC levels in marijuana in the past two decades has increased form 6 percent to more than 13 percent, with some samples containing THC levels of up to 33 percent (which is far higher than the 1 percent potency levels in marijuana used in the mid-1970’s).
• Marijuana is a gateway drug to the use of other illegal drugs like methamphetamine, heroin and cocaine. Long-term studies of students who use drugs show that very few young people use other illegal drugs without first trying marijuana. The use of marijuana often lowers inhibitions about drug use and exposes users to a culture that encourages the use of other drugs.

• Studies show that of the people who have ever used marijuana, those who started early are more likely to have other problems later on. For example, adults who were early marijuana users were found to be:
- 8 times more likely to have used cocaine.
- 15 times more likely to have used heroin,
- 5 times more likely to develop a need for treatment of abuse or dependence on any drug.
• The Journal of the American Medical Association reported a study of more than 300 sets of same-sex twins. The study found that marijuana-using twins were four times more likely than their siblings to use cocaine and crack cocaine, and five times more likely to use hallucinogens such as LSD.
• The study by Columbia University’s National Center on Addiction and Substance Abuse offers further support for the fact that teens who use marijuana at least once a month are 13 times more likely than other teens to use another drug like cocaine, heroin, or methamphetamine and are almost 26 times more likely than those teens who have never used marijuana to use another illegal drug.
- Other studies show that twelve to seventeen year olds who smoke marijuana are 85 times more likely to use cocaine than those who do not. Sixty percent of adolescents who use marijuana before age 15 will later use cocaine. These correlations are many times higher than the initial relationships found between smoking and lung cancer in the 1964 Surgeon General’s report (nine to ten times higher).
• Health care workers, legal counsel, police and judges indicate that marijuana is a typical precursor to methamphetamine use. For example, Nancy Kneeland, a substance abuse counselor in Idaho, pointed out that “In almost all cases meth users began with alcohol and pot.”

VII. Legalizing Marijuana for Medical Purposes Will Lead to Increased Use of Marijuana By Other Persons, Increased Crime and the Perception that Marijuana is Harmless.
• It is foolish to think that there will be no additional use of marijuana occurring as a result of legalizing its use for medicinal purposes under S.F. 345. First of all there will be no practical way to enforce the law to ensure that marijuana obtained from medical purposes is not used by other persons, including children. Anecdotal information received from prosecutors in other states where similar legislation has been enacted indicates that this is exactly what will occur.
• Under S.F. 345, no person would be subject to arrest or prosecution “for constructive possession, conspiracy, aiding and abetting, being an accessory, or any other criminal offense for being in the presence or vicinity of the medical use.” Consequently, there will be no way to ensure that those who obtain marijuana for a medical purpose will not share it with other persons.
• If this legislation is enacted, it will authorize persons to lawfully grow and sell marijuana. Because marijuana is a widely used illegal substance, incentives will exist for some unscrupulous persons involved in the sale or distribution of “legal marijuana” to steal and distribute the substance for illegal uses.
• Institutions, which are lawfully producing marijuana if this legislation is enacted, would also become easy targets for thieves looking to break in and steal “legally produced” marijuana for illegal distribution purposes.
• It is important to note that the U.S. Supreme Court in its 2005 decision in Gonzales v. Angel, et al., specifically acknowledged that adverse impacts of increasing crime and illegal marijuana use will result from the passage of state laws similar to S.F. 345. In Gonzales, the majority of the U.S. Supreme Court made the following conclusions:
- “The exemption for cultivation by patients and caregivers can only increase the supply of marijuana in the [state] market.”
- “The likelihood that all such production will promptly terminate when patients’ medical needs during their convalescence seems remote, whereas the danger that excesses will satisfy some of the admittedly enormous demand for recreational use seems obvious.”
- “[T]he [fact that the] national and international narcotics trade has thrived in the face of vigorous criminal enforcement efforts suggests that no small number of unscrupulous people will make use of the . . . [state] exemptions to serve their commercial ends whenever it is feasible to do so.”
• Legalizing marijuana for medical purposes will lead many to conclude that the drug is in fact safe.
- In states where the issue of legalizing marijuana for medical purposes has been put on the ballot for voters to decide, well-financed and organized campaigns spearheaded by pro-marijuana legalization groups have contributed to the misperception that marijuana is harmless.
- According to the Office of National Drug Policy, these campaigns are led not by medical professionals or patients-rights groups, but by pro-drug donors and organizations in a cynical attempt to exploit the suffering of sick people.
- This misperception that marijuana is harmless is perhaps most prevalent among teens where it has led to a 140 percent increase in marijuana use among high school seniors from 1994-95.
- The mortal danger of thinking that marijuana is “medicine” was graphically illustrated by a story from California. In the spring of 2004, Irma Perez was “in the thrills of her first experience with the drug ecstasy” when, after taking one ecstasy tablet, she became ill and told friends that she felt like she was “going to die.” Two teenage acquaintances did not seek medical care and instead tried to get Perez to smoke marijuana. When it failed due to her seizures, the friends tried to force feed marijuana leaves to her, “apparently because [they] knew that drug is sometimes used to treat cancer patients.” Irma Perez lost consciousness and died a few days later when she was taken off life support. She was 14 years old.
• Legalizing marijuana for medical purposes will lead to the perception that marijuana is harmless, will result in increased use of it for illegal purposes, and will result in more crime (see Section IV above), endangering our youth and the safety of all citizens in our state.

VIII. Legalizing the Use of Marijuana for Medicinal Purposes Will Increase Dangers Associated With Impaired Driving.

Driving under the influence of marijuana can dramatically impact the safety of citizens within our state as indicated by the following:
• Smoking marijuana impairs the judgment of the smoker and increases the risk of accidents. Many car accidents are caused by drivers using marijuana. In fact, some say just as many as those caused by drivers under the influence of alcohol.
• Marijuana affects many skills required for safe driving: alertness, the ability to concentrate, coordination, and reaction time. These effects can last up to 24 hours after smoking marijuana. Marijuana use can also make it difficult to judge distances and react to signals and signs on the road.
• A roadside study of reckless drivers in Tennessee found that 33 percent of all subjects who were not under the influence of alcohol and who were tested for drugs at the scene of their arrest tested positive for marijuana.
• In a 2003 Canadian study, one in five students admitted to driving within an hour of using marijuana.
• In a 1990 report, the National Transportation Safety Board studied 182 fatal truck accidents and found that just as many of the accidents were caused by drivers using marijuana as were caused by alcohol – 12.5 percent in each case.

Some of the documented consequences of marijuana impaired driving across America include the following:
- The driver of a charter bus, whose 1999 accident resulted in the death of 22 people, had been fired from bus companies in 1989 and 1996 because he tested positive for marijuana four times. A federal investigator confirmed a report that the driver “tested positive for marijuana when he was hospitalized Sunday after the bus veered off a highway and plunged into an embankment.”
- In April 2002, four children and the driver of a van died when the van hit a concrete bridge abutment after veering off the freeway. Investigators reported that the children nicknamed the driver “Smokey” because he regularly smoked marijuana. The driver was found at the crash scene with marijuana in his pocket.
- A former nurse’s aide was convicted in 2003 of murder and sentenced to 50 years in prison for hitting a homeless man with her car and driving home with his mangled body “lodged in the windshield.” The incident happened after a night of drinking and taking drugs, including marijuana. After arriving home, the woman parked her car, with the man still ledged in the windshield, and left him there until he died.
- In April 2005, an eight year old boy was killed when he was run over by an unlicensed 16 year old driver who police believed had been smoking marijuana just before the accident.
- In 2001, George Lynard was convicted of driving with marijuana in his bloodstream, causing a head-on collision that killed a 73 year old man and a 69 year old woman. Lynard appealed this conviction because he allegedly had a “valid prescription” for marijuana. A Nevada judge agreed with Lynard and granted him a new trial. The case has been appealed to the Nevada Supreme Court.
- Duane Baehler, 47, of Tulsa, Oklahoma was “involved in a fiery crash that killed his teenage son” in 2003. Police reported that Baehler had methamphetamine, cocaine and marijuana in his system at the time of the accident.

IX. Summary

For all of the reasons outlined above, legalizing marijuana for medicinal purposes is not in the interests of protecting the public safety of Minnesota’s citizens, nor is it in the best interest of persons who suffer from the types of chronic or debilitating diseases or medical conditions specified in S.F. 345. Marijuana is a dangerous addictive drug that poses significant health risks to those who use it. Legalizing marijuana for “medicinal use” will only increase the access of both youth and adults to marijuana, which will not only increase the likelihood of violent behavior but will often lead to experimentation with other even more dangerous illegal drugs. As noted by the Office of National Drug Control Policy;

“Even if smoking marijuana makes people “feel better”, that is not enough to call it a medicine. If that were the case, tobacco cigarettes could be called medicine because they are often said to make people feel better. For that matter, heroin certainly makes people “feel better” (at least initially), but no one would suggest using heroin to treat a sick person.”

The bottom line is that at the present time, there is no proven medicinal value in using marijuana to treat illnesses or disease and, in fact, a legal form of THC, which can be controlled for its strength and which delivers none of the harmful side effects of smoking marijuana already exists for use through a doctor’s prescription.

Marijuana use, even by those using it for medicinal purposes, is significantly harmful to the body. Smoking pot delivers three to five times the amount of tars and carbon monoxide into the body as does smoking cigarettes and it also damages pulmonary immunity and impairs oxygen diffusion. We agree with the Office of National Drug Control Policy, that it is hard to understand how changes such as these could be good for someone dying of cancer or AIDS.

Perhaps most importantly of all, as a prohibited Schedule I controlled substance under the Federal Controlled Substance Act (CSA), the manufacture, distribution or possession of marijuana is a federal crime. The Minnesota Legislature should not substitute its judgment for that of Congress and the Administrators of the U.S. Drug Enforcement Administration and the Federal Drug Administration as to the fact that marijuana is a dangerous drug with no accepted medical use and as to determining what is the appropriate way to deliver safe medications to our citizens. It is not sound public policy to enact state laws which encourage law abiding citizens to commit federal crimes.

It is for all these reasons that the MCAA strongly opposes the adoption of the law in Minnesota which would legalize the use of marijuana for medicinal purposes. This opposition is shared by associations representing our law enforcement partners within Minnesota.

Abstainers Are Not Maladjusted, but Lone Users Face Difficulties

Key findings:
• Although some consider experimenting with marijuana normal behavior for adolescents, those adolescents who abstain are not maladjusted as others have reported.
• Young abstainers do better than experimenters into young adulthood.
• Even strict abstainers — youth who avoid all drugs — fare well in life.
• Solitary substance use is not uncommon among youth.
• Young solitary users are an overlooked at-risk group who face a wide range of psychosocial and behavioral difficulties as teens and young adults.

A lot of adolescents experiment with marijuana — the National Institute on Drug Abuse estimates that 46% of high school seniors have tried this drug at some time. Pushing boundaries is what young people do, and some researchers believe that trying marijuana is a normal part of growing up. Does that mean that young people who do not indulge are somehow maladjusted?

Jonathan Shedler and Jack Block[1] raised this possibility in a report in 1990. They suggested that adolescents who experimented with marijuana were better adjusted emotionally and socially than their counterparts who avoided all drugs. Specifically, abstainers were observed to be anxious, emotionally constricted, and lacking in social skills compared with experimenters. Not surprisingly, these findings caused widespread comment in the drug-prevention community.

Now, RAND Corporation researchers have revisited Shedler and Block’s classic study and have uncovered evidence that challenges those initial findings. Kids who abstained from marijuana through the last year of high school were not socially or emotionally troubled. And they had better outcomes as young adults.

A second study looked at a largely ignored group of adolescents: kids who go off by themselves to use marijuana and other harmful substances. The researchers documented a wide range of psychosocial and behavioral difficulties faced by youth who use harmful substances while alone, rather than only in social settings like parties. And the troubles followed them into young adulthood.

For policymakers, these two studies help clarify the picture of youthful marijuana use: Marijuana abstainers do well, solitary users do poorly, and kids who use marijuana only in social settings are in between.

Digging for Clues About Youthful Marijuana Use
To re-examine the provocative findings of Shedler and Block, the RAND researchers, led by Joan Tucker, a social psychologist, mined a wealth of data on youthful substance use accumulated since 1985 by the RAND Adolescent/Young Adult Panel Study. This database contains survey responses from thousands of individuals who answered questions about their use of harmful substances, about their social and emotional well-being and behavior, and about school. The survey was given in grades 7, 8, 9, 10, and 12, and again at ages 23 and 29. The database was used to evaluate the effectiveness of the Project ALERT drug use prevention program that RAND developed for middle-school students. For their study, the researchers examined responses to the surveys given in 12th grade and at age 23. They divided the responders into abstainer and experimenter categories, which replicate as closely as possible those used in the 1990 Shedler and Block study:

Abstainers — those who had never tried marijuana or any other illicit drug.

Experimenters — those who had used marijuana less than 10 times in the year before being surveyed and less than three times in the preceding month, and none or only one other illicit drug in their lifetime.

A different picture emerges of youth and marijuana
From their analyses of survey responses, the RAND researchers pieced together a picture of marijuana abstainers and experimenters as teens and as young adults that contradicts that painted by earlier studies. Their key findings, some of which are shown in the figure, include

Youth who stayed away from marijuana through their senior year of high school functioned better overall than did seniors who experimented with the drug. Compared with experimenters, abstainers

• had more parental support
• devoted more time to homework
• spent more time in extracurricular school activities
• earned better grades
• got into less trouble
• were emotionally better off.

Both groups were similar in that

• on average, they rarely felt lonely
• they reported similar levels of peer support and ease in interacting with the opposite sex.

The one exception was that,

• although abstainers were socially active, they went to parties and dances significantly less frequently than did experimenters.

By the time they turned 23, those who had avoided marijuana in high school functioned better overall as young adults than those who had experimented with it in their youth. Compared with experimenters, abstainers

• were better educated
• were happier with their friends
• were less involved in deviant behavior (stealing and drug selling).

Both groups were similar in that

• they showed no differences in their satisfaction with family life and with general mental health, or with limitations due to emotional problems.

The emotional and social well-being of strict marijuana abstainers — those who had tried neither marijuana nor cigarettes and had not used alcohol in the past year — was also compared with that of experimenters, both in high school and as young adults:

• Even this more-stringent subgroup of marijuana abstainers did not show the adjustment problems suggested by earlier studies.

Why did two different pictures emerge?
The conflicting findings may be due to methodological factors. For example, the RAND team examined longitudinal data for more than 3,000 individuals who were originally recruited from 30 California and Oregon schools. These schools were chosen to represent a wide range of community types, socioeconomic status, and racial/ethnic composition. Thus, the RAND sample was considerably larger and more diverse than the 100 or so youth from the San Francisco Bay area whom Shedler and Block followed.

Young Solitary Substance Users: An Overlooked, At-Risk Group
Surprisingly little research looks at the sizable minority of teens who use marijuana and other harmful substances when alone rather than only in social settings. In a second study, researchers again used the RAND Adolescent/Young Adult Panel Study database for clues about the extent of solitary substance use, as well as about the well-being, behavior, and future risks, of this largely ignored group. For this study, these youth are referred to as “solitary users,” even though they may also use marijuana, cigarettes, or alcohol in social settings with others. This time, the researchers analyzed responses to the surveys given in 8th grade and at age 23. They found that:

Although they constitute a small percentage, solitary users are an overlooked, at-risk group:

• In 8th grade, 4% of young people said they sometimes or often used marijuana alone rather than limiting its use to parties or other social occasions. This figure was 16% for cigarettes and 17% for alcohol.

By 8th grade, solitary substance users are worse off than classmates who use only in social settings. Compared with social-only users, solitary users

• engaged in heavier and more-frequent drug use
• got into more trouble (e.g., stealing, acting out at school)
• confided less in their parents about personal problems
• performed more poorly in school (had lower grades, spent less time on homework, participated less in extracurricular school activities).

Solitary users are not social outsiders. Contrary to what might be expected, these youth are not loners. They are socially active teens who spend more time hanging out with friends, going to parties, and dating than do youth who limit substance use to social settings. Popularity with peers may help compensate solitary users for their poorer academic track records and behavioral problems in the short term.

Solitary use foreshadows problems down the road. Compared with social-only substance users, teen solitary users faced more difficulties as young adults: They made fewer educational strides, had poorer health, and experienced more substance-use problems.

Solitary users perceive drug consequences differently than do social-only users. Solitary users more strongly believed that turning to marijuana, cigarettes, or alcohol helped them get away from their problems, relax, and have more fun — an optimistic bias that could lead them to underestimate the potential for serious negative consequences.

Implications for Drug-Prevention Programs
New insight into youthful substance use emerged from the RAND studies that can help improve drug-prevention programs for adolescents and teens.

Experimentation with drugs has sometimes been viewed as developmentally appropriate and adaptive. In contrast, the RAND results indicate that youth who experiment with marijuana are worse off in many respects than those who abstain throughout their teenage years. This insight helps the drug-prevention community put into perspective the conflicting conclusions from prior studies about marijuana use and its consequences.

The research also documented the wide range of psychosocial and behavioral difficulties that lone substance users, as opposed to strictly social users, face as teens and young adults. These findings suggest that drug-prevention programs should pay closer attention to this at-risk group of young people.

Source: http://www.rand.org/pubs/research_briefs/RB9265/index1.html 2007
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[1] Shedler J, and Block J, “Adolescent Drug Use and Psychological Health: A Longitudinal Inquiry,” American Psychologist, Vol. 45, No. 5, May 1990, pp. 612–630.
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This Highlight summarizes RAND Health research reported in the following publications:
Tucker JS, Ellickson PL, Collins RL, and Klein DJ, “Are Drug Experimenters Better Adjusted Than Abstainers and Users?: A Longitudinal Study of Adolescent Marijuana Use,” Journal of Adolescent Health, Vol. 39, No. 4, 2006, pp. 488–494.

Tucker JS, Ellickson PL, Collins RL, and Klein DJ, “Does Solitary Substance Use Increase Adolescents’ Risk for Poor Psychosocial and Behavioral Outcomes? A 9-Year Longitudinal Study Comparing Solitary and Social Users,” Psychology of Addictive Behaviors, Vol. 20, No. 4, 2006, pp. 363–372.

The human brain is also a system of subsystems and there is now overwhelming evidence that the development of the human brain continues well into adolescence up to age 20. We know that the brain is vulnerable to toxic substances that can cause cognitive dysfunctions in adults. There is substantial literature on the consequences of acute and chronic marijuana exposure in adults, including measures of cognitive and behavioral effects, as well as some measures of alterations in brain function, primarily in the domains of learning and memory. There have been relatively few studies, however, of the effects of exposure to marijuana during development,
Some have reported that a delay in adolescent brain development is common when alcohol and or other drug usage including marijuana – begins at a young age. Some frequent users feel a lack of initiative and concern about the future, find it hard to become or stay motivated, and think things will take care of them selves, (Wapner, Roger, 1995). As a result, the normal maturation process is interrupted. Development of coping skills, a code of ethics, acceptance of responsibility, and other signs of maturity frequently cease or regress. A frequent user’s emotional development may be delayed when he starts using, and may take much longer to develop once the user has become clean and sober for an extended period of time. Drug misuse usually leads to denial. Denial is one of the hallmarks of chemical dependency. Frequent users not only deny that their drug use is a problem; they may begin using denial to pretend other problems do not exist either. Forgotten birthdays, missed social engagements, and unmet commitments are all no big deal . (Wapner, Roger, 1995)
Jonathon Shedler and Jack Block (University of California, Berkeley) have done extensive studies of teenagers, which included abstainers, occasional users, and frequent users. Frequent users are described (by family and peers) as not dependable or responsible, not productive or able to get things done, guileful and deceitful, opportunistic, unpredictable and changeable in attitudes and behavior, unable to delay gratification, rebellious and nonconforming, prone to push and stretch limits, self-indulgent, not ethically consistent, not having high aspirations, and prone to express hostile feelings directly. (Shedler and Block, 1990)
Marijuana Effects
The specific effects of marijuana, however, vary greatly, depending on the quality and dosage of the drug, the personality and mood of the user, the user s past experiences with the drug, the social setting, and the user s expectations.
Considerable consensus exists however among regular users that when marijuana is smoked and inhaled, a state of slight intoxication results. This state is one of mild euphoria distinguished by increased feelings of well-being, heightened perceptual acuity, and pleasant relaxation, often accompanied by a sensation of drifting or floating away. Sensory inputs are intensified. Often a person’ s sense of time is stretched or distorted, so that an event that lasts only a few seconds may seem to cover a much longer span. Short-term memory may also be affected, as one notices that a bite has been taken out of a sandwich but does not remember having taken it. For most users, pleasurable experiences, including sexual intercourse, are reportedly enhanced. When smoked, marijuana is rapidly absorbed and its effects appear within seconds to minutes but seldom last more than 2 to 3 hours (Butcher, Mineka, & Hooley, 2004).
Marijuana may lead to unpleasant as well as pleasant experiences. For example, if a person uses the drug while in an unhappy, angry, suspicious, or frightened mood, these feelings may be magnified. With higher dosages and with certain unstable or susceptible individuals, marijuana can produce extreme euphoria, hilarity, and over talkativeness, but it can also produce intense anxiety and depression as well as delusions, hallucinations, and other psychotic-like experiences. Evidence suggests a strong relationship between daily marijuana use and the occurrence of self-reported psychotic symptoms (Tien & Anthony, 1990).

One study exploring past substance use history in incarcerated murderers reported that among men who committed murder, marijuana was the most commonly used drug. One-third indicated that they used the drug before the homicide, and two-thirds were experiencing some effects of the drug at the time of the murder (Spunt et al., 1994).
Marijuana does not lead to extreme physiological dependence, as heroin does. It can, however, lead to psychological dependence, in which the person experiences a strong need for the drug whenever he or she feels anxious or tense. In fact, recent research has reported that many marijuana use abstainers reported having withdrawal-like symptoms such as nervousness, tension, sleep problems, and appetite change (Budney, Hughes, et al., 2001; Kouri and Pope, 2000). One recent study of substance abusers reported that marijuana users were more ambivalent and less confident about stopping use than were cocaine abusers (Budney, Radonovich, et al., 1998).
Self Diagnosis
1. Does your periodic marijuana use and intoxication interfere with your performance at work or school?
2. Is your periodic marijuana use and intoxication physically hazardous in situations such as driving a car?
3. Do you or have you had legal problems as a consequence of arrests for marijuana possession?
4. Do you or have you had arguments with spouses or parents over the possession of marijuana in the home or its use in the presence of children?
If you answered Yes to any one of the above you may meet criteria for a diagnosis of Cannabis Abuse and I would recommend that you undergo an alcohol/ substance abuse evaluation by a Certified Substance Abuse Counselor (CSAC) and comply with all treatment recommendations.
If you are having psychological or physical problems associated with compulsively using marijuana, such as:

1. Craving;
2. Withdrawal symptoms;
3. Irritability;
4. Sleeplessness; and/ or
5. Anxiety
- when trying to quit, then a diagnosis of Cannabis Dependence should be considered rather than Cannabis Abuse. Likewise, I would recommend that you undergo an alcohol/ substance abuse evaluation by a Certified Substance Abuse Counselor (SAC) and comply with all treatment recommendations.
Multiple Addictions
In 2001, marijuana was a contributing factor in more than 110,000 emergency department visits in the United States. In a survey of drug-related visits to the emergency room (DAWN Report, 2001), 16 percent of drug-related visits were for marijuana abuse. Many of these emergency room visits, as one might suspect, involved the use of other substances along with marijuana. If you had trouble answering Yes to one of the above self-diagnosis questions, because you have used alcohol and/ or other drugs along with marijuana and you cannot contribute your problems to marijuana alone, then you may meet the criteria for Poly-substance Dependence and or Poly-behavioral Addiction, see below. other addictions co-exist, the initial therapeutic intervention for any addiction needs to include an assessment for other addictions. National surveys revealed that very high correlation exists between cannabis abuse and/ or other substance abuse and behavioral addictions.
Poor Prognosis
We have come to realize today more than any other time in history that the treatment of Cannabis Dependence and other lifestyle diseases and behavioral addictions related to gambling, food, sex, and/ or religion, (etc.) are often a difficult and frustrating task for all concerned. Repeated failures abound with all of the addictions, even with utilizing the most effective treatment strategies. But why do 47% of patients treated in private addiction treatment programs (for example) relapse within the first year following treatment (Gorski, T., 2001)? Have addiction specialists become conditioned to accept failure as the norm? There are many reasons for this poor prognosis. Some would proclaim that addictions are psychosomatically- induced and maintained in a semi-balanced force field of driving and restraining multidimensional forces. Others would say that failures are due simply to a lack of self-motivation or will power. Most would agree that lifestyle behavioral addictions are serious health risks that deserve our attention, but could it possibly be that patients with multiple addictions are being under diagnosed (with a single dependence) simply due to a lack of diagnostic tools and resources that are incapable of resolving the complexity of assessing and treating a patient with multiple addictions?
Diagnostic Delineation
Thus far, the DSM-IV-TR has not delineated a diagnosis for the complexity of multiple behavioral and substance addictions. It has reserved the Poly-substance Dependence diagnosis for a person who is repeatedly using at least three groups of substances during the same 12-month period, but the criteria for this diagnosis do not involve any behavioral addiction symptoms. In the Psychological Factors Affecting Medical Condition s section (DSM-IV-TR, 2000); maladaptive health behaviors (e.g., unsafe sexual practices, excessive alcohol, drug use, and over eating, etc.) may be listed on Axis I, only if they are significantly affecting the course of treatment of a medical or mental condition. Since successful treatment outcomes are dependent on thorough assessments, accurate diagnoses, and comprehensive individualized treatment planning, it is no wonder that repeated rehabilitation failures and low success rates are the norm instead of the exception in the addictions field, when the latest DSM-IV-TR does not even include a diagnosis for multiple addictive behavioral disorders. Treatment clinics need to have a treatment planning system and referral network that is equipped to thoroughly assess multiple addictive and mental health disorders and related treatment needs and comprehensively provide education/ awareness, prevention strategy groups, and/ or specific addictions treatment services for individuals diagnosed with multiple addictions. Written treatment goals and objectives should be specified for each separate addiction and dimension of an individuals life, and the desired performance outcome or completion criteria should be specifically stated, behaviorally based (a visible activity), and measurable.
New Proposed Diagnosis
To assist in resolving the limited DSM-IV-TRs diagnostic capability, a multidimensional diagnosis of Poly-behavioral Addiction, is proposed for more accurate diagnosis leading to more effective treatment planning. This diagnosis encompasses the broadest category of addictive disorders that would include an individual manifesting a combination of substance abuse addictions, and other obsessively-compulsive behavioral addictive behavioral patterns to pathological gambling, religion, and/ or sex / pornography, etc.). Behavioral addictions are just as damaging – psychologically and socially as alcohol and drug abuse. They are comparative to other life-style diseases such as diabetes, hypertension, and heart disease in their behavioral manifestations, their etiologies, and their resistance to treatments. They are progressive disorders that involve obsessive thinking and compulsive behaviors. They are also characterized by a preoccupation with a continuous or periodic loss of control, and continuous irrational behavior in spite of adverse consequences.
Poly-behavioral addiction would be described as a state of periodic or chronic physical, mental, emotional, cultural, sexual and/ or spiritual/ religious intoxication. These various types of intoxication are produced by repeated obsessive thoughts and compulsive practices involved in pathological relationships to any mood-altering substance, person, organization, belief system, and/ or activity. The individual has an overpowering desire, need or compulsion with the presence of a tendency to intensify their adherence to these practices, and evidence of phenomena of tolerance, abstinence and withdrawal, in which there is always physical and/ or psychic dependence on the effects of this pathological relationship. In addition, there is a 12 – month period in which an individual is pathologically involved with three or more behavioral and/ or substance use addictions simultaneously, but the criteria are not met for dependence for any one addiction in particular (Slobodzien, J., 2005). In essence, Poly-behavioral addiction is the synergistically integrated chronic dependence on multiple physiologically addictive substances and behaviors (e.g., using/ abusing substances – nicotine, alcohol, & drugs, and/or acting impulsively or obsessively compulsive in regards to gambling, food binging, sex, and/ or religion, etc.) simultaneously.
Multidimensional Treatment
Since chronic lifestyle diseases and disorders such as diabetes, hypertension, alcoholism, drug and behavioral addictions cannot be cured, but only managed – how should we effectively manage poly-behavioral addiction?
The Addiction Recovery Measurement System (ARMS) is proposed utilizing a multidimensional integrative assessment, treatment planning, treatment progress, and treatment outcome measurement tracking system that facilitates rapid and accurate recognition and evaluation of an individual s comprehensive life-functioning progress dimensions. The ARMS hypothesis purports that there is a multidimensional synergistically negative resistance that individual s develop to any one form of treatment to a single dimension of their lives, because the effects of an individual ‘s addiction have dynamically interacted multi-dimensionally. Having the primary focus on one dimension is insufficient. Traditionally, addiction treatment programs have failed to accommodate for the multidimensional synergistically negative effects of an individual having multiple addictions, (e.g. nicotine, alcohol, and obesity, etc.). Behavioral addictions interact negatively with each other and with strategies to improve overall functioning. They tend to encourage the use of tobacco, alcohol and other drugs, help increase violence, decrease functional capacity, and promote social isolation. Most treatment theories today involve assessing other dimensions to identify dual diagnosis or co-morbidity diagnoses, or to assess contributing factors that may play a role in the individual s primary addiction. The ARMS theory proclaims that a multidimensional treatment plan must be devised addressing the possible multiple addictions identified for each one of an individual s life dimensions in addition to developing specific goals and objectives for each dimension.
Conclusion
This article was not written with the intent to demonize or glorify the most widely used illicit and top US cash crop (U.S. growers produce nearly $35 billion worth of marijuana annually, making the illegal drug the country’s largest cash crop, bigger than corn and wheat combined, an advocate of medical marijuana use said in a study released on 18 Dec. 06, WASHINGTON), Reuters. Nor was it written to advocate the use or non-use of marijuana whether legally for medicinal purposes or illegally.
There are numerous articles readily available that already accomplish that mission. It is my hope though, that the 10 to 15 percent of individuals that have multiple complex problems involving marijuana usage will find the help that they need. Considering the wide range of addictive behaviors in our world today, one should always take into account an individual s ethnic, cultural, religious, and social background prior to making any clinical judgments, and it would be wise to not over-pathologize in this area. However, since successful treatment outcomes are dependent on thorough assessments, accurate diagnoses, and comprehensive individualized treatment planning – Poly-behavioral Addiction needs to be identified to effectively treat the complexity of multiple behavioral and substance addictions.
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United States Sentencing Commission, 2005 Sourcebook of Federal Sentencing Statistics, June 2006
National Drug Intelligence Center, National Drug Threat Assessment 2007
James Slobodzien, Psy.D. CSAC, is a Hawaii licensed psychologist and certified substance abuse counselor who earned his doctorate in Clinical Psychology. The National Registry of Health Service Providers in Psychology credentials Dr. Slobodzien. He has over 20-years of mental health experience primarily working in the fields of alcohol/ substance abuse and behavioral addictions in medical, correctional, and judicial settings. He is an adjunct professor of Psychology and also maintains a private practice as a mental health consultant.

A large multi-cohort analysis has investigated factors affecting long-term response to potent antiretroviral therapy. Four to six years after starting anti-HIV treatment, higher rates of AIDS and mortality were seen in injection drug users and in those who had had AIDS-defining events or CD4 cell counts less than 25 cells/mm3 before starting therapy. The study, conducted by the Antiretroviral Therapy Cohort Collaboration, was published in the December 15th issue of the Journal of Acquired Immune Deficiency Syndromes.

Previous studies have found that rates of AIDS-related illness and death are higher in people who begin antiretroviral therapy with lower CD4 cell counts. Poorer response has also been found in injection drug users (IDUs) compared to other patients. However, most studies to date have looked at response over relatively short time periods. In this study, the Antiretroviral Therapy Cohort Collaboration (an international alliance of investigators from sixteen cohort studies of people with HIV – see www.art-cohort-collaboration.org) analysed data from 20,379 HIV-positive adults who had been on anti-HIV drugs for up to six years.

Participating cohorts were included if they had enrolled at least 100 treatment-naïve patients, 16 years of age or older, who had begun treatment with a combination of at least three antiretroviral agents. People with baseline viral loads less than 1000 copies/ml were excluded as possibly not treatment-naïve. This yielded a total of 20,379 patients from twelve European and North American cohorts. (A prognostic model based on this same data set was recently published – see the aidsmap report here)

Baseline characteristics were as follows: median age, 36; median CD4 cell count 224 cells/mm3; median month of therapy initiation, February 1999. Before treatment initiation, 2737 patients (23%) had already had a diagnosis of AIDS; 3231 (16%) were presumed infected due to IDU.

Of the initial regimens, 66% were NRTI/PI, 24% NRTI/NNRTI, 7% NRTI only, 2% triple-class; and 2% other (NRTI-sparing, or including T-20). The majority of participants (88%) began on a three-drug regimen.

Over a total of 61,798 person-years of follow-up, 1844 participants developed at least one AIDS-defining event, and 1005 died. AIDS-defining events and deaths were analysed by: baseline CD4 cell count (<25, 25 to 49, 50 to 99, 100 to 199, 200 to 349, and >350 cells/mm3), baseline viral load (<100,000 or ≥100,000 copies/ml), presumed mode of transmission (IDU or other), and AIDS diagnosis before baseline (yes or no).

Consistent with previous studies, lower baseline CD4 cell counts were consistently the strongest predictor of poorer outcomes. The effect was strongest for the lowest baseline counts, and tended to decline with length of time on therapy for all strata of CD4 count.

Beginning therapy at a baseline CD4 cell count between 200 and 349 continued to show a benefit until the four-year mark. Compared to those beginning at >350 cells/mm3 (the comparator group), the hazard ratio for progression to AIDS at one to two years on therapy was 1.5 (95% confidence interval [CI]: 1.0 to 2.3), 1.4 at two to three years (95% CI: 1.0 to 2.1), and 1.0 at four to six years (95% CI: 0.6 to 2.0). For each time period, hazard ratios were progressively higher for each lower CD4 stratum. For baseline CD4 counts <25 cells/ mm3, the hazard ratio for developing AIDS was 3.7 at one to two years (95% CI: 2.2 to 6.1), 2.4 at two to four years (95% CI: 1.5 to 3.8), and 2.3 at four to six years (95% CI: 1.0 to 2.3). At four to six years, the hazard ratio for mortality was 2.5 (95% CI: 1.2 to 5.5) for baseline CD4 counts <25 cells/ mm3.

For people presumed infected through IDU, at four to six years on HAART, the hazard ratio for AIDS was 1.6 (95% CI: 0.8 to 3.0) and the hazard ratio for mortality was higher at 3.5 (95% CI: 2.2 to 5.5). Note that cause of death was not analysed and was not necessarily directly due to HIV; mortalities due to hepatitis-related liver disease, overdose, trauma and other causes were not excluded. Mortality rates were still lower than would be expected in the absence of anti-HIV therapy.

Diagnosis of AIDS before the initiation of anti-HIV treatment also continued to predict AIDS-defining events at four to six years, with a hazard ratio of 2.3 (95% CI: 1.2 to 4.4); the predictive value for mortality ceased to be significant. HIV viral load (greater than, or less than, 100,000 copies/ml) was not a significant predictor of progression or death at any time point.

The study was limited by declining numbers of patients in follow-up after longer periods on antiretroviral treatment. At the end of the fourth year of anti-HIV therapy, 6838 participants were still being followed (23% of the original cohort); only 791 (4%) were followed for more than six years. As most original patients were still being followed up at the time of analysis, the researchers "do not believe that informative censoring is likely to be an important source of bias." However, results may have been confounded by socioeconomic and other factors which caused people to begin treatment late in the course of HIV progression. Larger hazard ratios for mortality than for development of AIDS were seen in several groups, which may be evidence of such confounding. Also, race and ethnicity were not included in the analysis due to lack of sufficient data.

The researchers concluded that "rates of AIDS and death were persistently higher in patients infected [through injection drug use]", and that "although the prognostic value of baseline CD4 count and a prior AIDS diagnosis declined with time, patients who were severely immunodeficient when they started therapy experienced higher rates of AIDS and death up to 6 years later." They believe these results may "strengthen the case for screening for HIV, because delaying treatment… has long-term disadvantages."

Reference
Antiretroviral Therapy Cohort Collaboration. Importance of baseline prognostic factors with increasing time since initiation of highly active antiretroviral therapy: collaborative analysis of cohorts of HIV-1–infected patients. J Acquir Immune Defic Syndr 46 (5):607-615, 2007.

Source: Wednesday, January 2, 2008

http://www.aidsmap.com/en/news/8ACEB690-26EB-4583-BF14-A4353CE335EC.asp

Bertha K. Madras, Ph.D., Deputy Director, Demand Reduction, Office of National Drug Control Policy

This is the second in a series of articles on how specific drugs affect the brain and body.

The brain drain
Myths that downplay the risks associated with drug use permeate youth culture and are embraced to rationalize experimentation with addictive drugs. Scientific evidence can help educators and parents de-bunk these dangerous myths.
Adolescents and young adults are the principal age groups using addictive drugs and are at the greatest risk for experiencing adverse consequences as a result of the early introduction of drugs into their brains. Early drug use can compromise academic achievement, school attendance, homework, participation in extracurricular activities, and school behavior. Drug use at a young age is also associated with addiction, violence, accidents, delinquency, criminal activity, and even death. As with any major public health problem, the inability to predict which young people will suffer detrimental, potentially life-threatening consequences from drug use is itself a reason to engage in widespread prevention efforts.
The brain has approximately one hundred billion nerve cells, with each cell producing 10,000 or more “wires” that connect with other cells. A critical component of brain development is accurate “wiring.” Imaging technologies that compare adolescent brains with those of adults have shown that the “wiring” of the adolescent brain is still immature, compared to the adult brain. Exposure to drugs before brain maturation may affect brain development, interfering with the wiring and circuitry of the brain in much the same way as a computer technician can damage a circuit board by zapping it with electrical jolts during the assembly process.
In the short term, a single dose of a drug can result in poor performance in a school or sports activity, accidents, violence, unplanned risky behavior, and the risk of overdosing. It can trigger repeated drug use, which is associated with serious health consequences, loss of desire to fulfill obligations, truancy, disorderly conduct, and social or family problems. Repeated drug use can also lead to addiction. Studies show that the earlier an adolescent begins using drugs, the more likely he or she will be to develop a substance abuse problem or become addicted to substances. Conversely, if an individual does not start using drugs during the teen years, he or she is less likely to initiate or develop a substance abuse problem later in life.
Statistics make a compelling case for focusing on preventing youth drug use. In 2006, among persons with substance dependence or abuse, the percentage dependent on or abusing illicit drugs was much higher in the 12-17 age group (57.4 percent) than among 18- to 25-year-olds (36.9 percent) or adults age 26 or older (24.1 percent), according to the 2007 National Survey on Drug Use and Health (NSDUH). One hundred eighty-one thousand youth (12-17 year-olds) received treatment for alcohol or illicit drugs (NSDUH 2007). Although prevention is a key to interrupting the progression to addiction, deterring marijuana use and prescription-drug misuse is particularly challenging because of the myths associated with these drugs.
Myth No. 1: Marijuana is a ‘soft’ drug
Marijuana use should not be considered a rite of passage. It is neither a “soft” drug nor a safe drug. The effects of marijuana can last up to 24 hours after administration, continuing to compromise reflexes, cognitive ability, and other brain functions. Driving while under the influence of marijuana is dangerous, as the use of this drug can impair motor function, concentration, and perception, thereby increasing the likelihood of road accidents. According to the 2006 Monitoring the Future study, the percentage of high school students who reported driving under the influence of marijuana (10.6 percent) was nearly as high as the percentage of those driving under the influence of alcohol (12.4 percent).
Accumulating evidence makes a forceful case for abstention from marijuana use. One study found that high school students who abstained from marijuana functioned better than occasional or frequent users during high school and during the transition to adulthood. During high school, abstainers fared better than experimenters and frequent users of marijuana on the basis of school engagement, deviant behavior, family and peer relations, and mental health. They were more likely to do homework and get better grades. When they turned 23, abstainers were twice as likely to graduate from college and much less likely to steal or to sell illicit drugs.
A long-term analysis of marijuana potency funded by the National Institute on Drug Abuse (NIDA) reveals that the strength of marijuana has increased substantially over the past two decades. Today, marijuana is more potent than ever before, and this elevated potency may be leading to an increase in teen marijuana treatment admissions and a rise in the number of marijuana-related emergency room episodes.

These worrisome results add to the growing body of evidence that the effects of youth marijuana use may endure into adulthood. Adolescents who used marijuana are twice as likely to use illicit drugs when they become young adults. In fact, in one study, individuals of twin pairs who used marijuana by age 17 had 2.1 to 5.2 times higher risk of other drug use (cocaine, heroin), alcohol dependence, and drug abuse/dependence than their co-twin who did not use before the age of 17.
Experiments with animals seem to corroborate these findings. Animals, which were not subject to environmental stressors, were exposed to the active ingredient of marijuana during adolescence. They were given a drug-free period and then, as adults, were given access to heroin. After maturation into adulthood, the early-exposed animals consumed higher amounts of heroin and showed greater heroin-seeking behavior than the non-exposed group. The effects of early exposure to marijuana were not restricted to behavior: components of the system in the brain that modulates pain and pleasure were changed in the animals’ adult brains, after exposure during adolescence.
Collectively, these findings suggest that marijuana, introduced during adolescence, may influence the biology of the brain, promote drug-seeking behavior, and affect social function during the transition to adulthood.
How addictive is marijuana, and how realistic is the perception that it is a “soft” drug? The 2007 NSDUH reported that in 2006, among adults aged 18 or older who first tried marijuana at age 14 or younger, 12.9 percent were classified with illicit drug dependence or abuse, a considerably higher number than the percentage (2.2 percent) who had first used marijuana at age 18 or older. Marijuana also ranked first as the most reported illicit drug resulting in abuse/dependence.
Early, frequent use of marijuana may be an independent risk factor for psychosis—even if use precedes the onset of schizophrenia or another form of psychosis. Marijuana may induce acute psychotic symptoms in vulnerable people and a persistent psychosis in some individuals who have not had prior signs of psychosis. Marijuana may also exacerbate psychosis in people with symptoms of schizophrenia, and these effects can persist after the drug is cleared from the body.
As with other addictive drugs, heavy marijuana use has many health and social consequences. Heavy marijuana use into adulthood creates an expanding set of health risks, including exercise-induced heart pain and reduced lung function, as well as objective and self-reports of adverse social consequences. During pregnancy, heavy marijuana use can lead to impaired fetal growth and development.
Myth No. 2: Prescription drugs used for psychoactive effects are safer than “street drugs”
Several classes of controlled prescription drugs—medications prescribed by doctors for legitimate medical purposes—have abuse and addiction potential. These include opioids prescribed for the management of pain, drugs to treat attentional problems and anxiety, and drugs to promote sleep. These drugs are safe and effective when used according to doctors’ prescriptions and advice. Abuse or non-medical use of prescription drugs is the use of drugs not prescribed for the individual, use of drugs solely for the experience or feelings they cause, or use of drugs for which the intended person has made false or inaccurate claims to obtain them.
A disturbing trend emerged last year, when NSDUH reported that first-time non-medical users of prescription drugs now equal first time users of marijuana and that misuse of prescription drugs among 12- and 13-year-olds exceeds marijuana use. The misuse of opioid pain killers is of particular concern because of the large number of users, the high addictive potential, and the potential to induce overdose or death.
Also of concern is that approximately 598,542 visits to emergency departments during 2005 involved the non-medical use of prescription drugs or over-the-counter medication or dietary supplements, with the majority involving multiple drugs (Drug Abuse Warning Network, 2005).
There are many factors contributing to the increased misuse of prescription drugs. There is a perception among young people that prescription drugs are safer than illicit street drugs. Moreover, many teens are not aware of the consequences of prescription drug misuse. Prescription drugs are also more easily attainable from friends and family.
There are indications that long-term misuse of pain medications can lead to addiction, and that intravenous use of this class of drugs places a person at increased risk of HIV and other infectious diseases. Additionally, because many of the prescription drugs that are abused share similarities with illicit drugs in the way they act on the brain, it is probable that some of the harmful consequences will be the same.
It is important for adults to recognize this growing problem and to help young people understand the risks of using prescription drugs non-medically. When used properly, under the supervision of a doctor, prescription drugs can be safe and effective. Used improperly, however, they can have serious consequences.
Preventing initiation and identifying problem use
Using marijuana or misusing prescription drugs in any amount is not safe. Scientists, educators, counselors, community coalitions, prevention experts, and others are working to expose dangerous drug myths and to increase awareness of the adverse physical, mental, emotional, and behavioral changes that can be associated with these substances. Testing students for drug use may help prevent initiation and identify drug users at an early stage, before a dependency sets in, thereby protecting adolescents and their fragile brains from the harmful effects of drug-using behavior.
A complete list of citations for this article is available at www.randomstudentdrugtesting.org

Source: Strategies for Success, Isssue 2 Vol.1 Fall 2007

“Drug [including alcohol] addictions are medical diseases which deserve parity in national healthcare programmes…” states scientist and professor Carlton Erickson, as he reveals the neurobiological research.
Although this article was first printed in Addiction Today journal in 2002, the vast majority of alcohol and drug workers remain unaware of these vital facts. Read on…
Public and professional stigma against addictive diseases is a major social problem when dealing with conditions which have traditionally been dealt with by behavioural and spiritually-based programmes. Reducing this stigma is critical, as negative attitudes damage the level and quality of patient care – and funding for prevention, education and research.
For far too many years, the “field” of drug addiction treatment and prevention has drifted aimlessly, based on insufficient research evidence that addictions are brain diseases and about the pharmacology of addicting drugs. Much of the confusion is based on an incomplete understanding of the differences between intentional drug abuse and pathological drug dependence, the “new term for addiction”.
There is also a great deal of misinformation about the pharmacology of addicting drugs. This picture is changing rapidly, based on new neuroscience (brain) research which strongly indicates that the pleasure pathway – the medial forebrain bundle – of the brain is affected by all addictions, particularly in the pharmacological qualities of euphoria, craving and a theoretical concept of “drug need”.
This is the psychological correlate of behavioural “impaired control”. The neuroanatomical and neurochemical bases of drug need have yet to be demonstrated in the laboratory. But the research technology, such as brain scans, is now at hand to test the theories.
Everyone who cares about the victims of addiction must become more scientifically literate about the implications of new research findings, and ‘spread the news’ that biomedical research is on the threshold of proving what recovering people already know – that drug dependencies are medical diseases which deserve parity in present and future national healthcare programmes. Drug dependence must also be ‘handled’ differently from drug abuse in terms of responsibility and culpability in law enforcement.
This article covers the latest research on the neurobiology of dependence, including how the brain’s pleasure pathway works. It covers the differences between chemical abuse and chemical dependency, the latest therapies for drug dependency, and research methodologies which promise even more exciting breakthroughs in understanding “addictions” in the future. This information has important implications for prevention and education of the public about the true causes of drug problems, and how society can best deal with such problems.

SOLUTIONS
The solution. First, get rid of “Spam”: an acronym for stigma, prejudice, anger and misunderstanding. All of these lead to myths – widely-held, inaccurate beliefs – as compared to research-generated facts.
And there are some dangerous myths in this world. These include the myths that club drugs and marijuana are not addicting… that everyone who uses cocaine or heroin is addicted… that caffeine is highly addicting… that the form of a drug and how it is taken affects its “addiction potential”… and that alcoholics can stop drinking, since all they have to do is go to AA meetings.

TWO CRITICAL DEFINITIONS.

It is vital that professionals carry out assessments to distinguish between chemical abuse and dependence. As the cover story by Norman Hoffman in the last issue of Addiction Today emphasises, assessment directly affects what type of treatment is most effective for each client, and thus their care plan, choice of treatment unit and outcome results. To distinguish between the two is the most humane, most cost-effective and most professional course of action.
Chemical abuse is intentional overuse of substances in cases of celebration, anxiety, despair or ignorance. It is about people making bad choices about the use of drugs. It declines with adverse consequences, supply reduction or change in drug-use environment. Drug abusers have a major economic impact on society; for example, it is estimated that property theft to fund drug habits accounts for at least £2billion a year in the UK.
The criteria for chemical abuse, according to the DSM-IV diagnostic and statistical manual, are:
1) a maladaptive pattern of drug use leading to impairment or distress, presenting as one or more of the following over a 12-month period –
• recurrent use leading to failure to fulfill obligations
• recurrent use that is physically hazardous
• recurrent drug-related legal problems, and
• continued use despite social/interpersonal problems
2) the symptoms have never met the criteria for chemical dependence.
Dependence is “impaired control” over drug use, probably caused by a dysfunction in the brain’s pleasure pathway. This is the disease of addiction, an “I can’t stop without help” disease. It requires formal therapy and/or 12 steps and might require anti-craving drug therapy. The DSM-IV criteria for chemical dependence are:
1) a maladaptive pattern of drug use, leading to impairment or distress, presenting as three or more of the following over a 12-month period –
• tolerance to the drug’s actions
• withdrawal (generally, physical withdrawal)
• drug is used more than intended
• there is an inability to control drug use
• effort is expended to obtain the drug
• important activities are replaced by drug use, and
• drug use continues despite negative consequences
2) two types of dependence can occur –
• physiological dependence, including tolerance and withdrawal, and
• non-physiological dependence, excluding tolerance and withdrawal.
The terms “physical addiction” and “psychological addiction” are no longer valid, since the DSM-IV term includes both psychological and physical components.

DOES DRUG ABUSE LEAD TO DEPENDENCE?
A five-year follow-up of 1,300 men and women (Schuckit et al 2001) found that only 3% of abusers met criteria for dependence five years after being diagnosed as abusers. But many people believe that abuse usually leads to dependence. Instead, the two conditions appear to be separate; abuse may be a milder disorder not usually progressing to dependence.

RISK OF DEPENDENCE.
Data from the National Co-morbidity Survey of 8,100 men and women aged 15-24 years old (Wagner & Anthony 2002) showed that different drugs are associated with different rates of dependence. In the 10 year study, 15-16% of cocaine users become dependent, 12-13%of alcohol users and 8% of marijuana users. Of those who became dependent on cocaine, 5-6% became dependent in the first year of use. Fully 80% of people who became dependent on cocaine over the 10 years had become dependent in the first three years. These are only single studies which deserve more replication, but they are interesting in that they begin to break down some myths that people have about the onset of dependence in users and abusers.

EARLY vs LATE ONSET.
So, although it “looks” as if most people evolve from abuse to dependence, people can become dependent during their first year of using drugs, including alcohol. People in recovery seem to understand that some people become “instantly” dependent with the very first use of the drug; most reports concern early onset with the use of alcohol and cocaine. There is only one explanation, and it lies in the physiology of the medial forebrain bundle, or MFB, also known as the mesolimbic dopamine system.
The neurobiological model of “impaired control” characteristics.
A key point is that the “dependence” brain areas are in the part of the brain that governs unconscious thought. Dependence is not a “lack of will power” because
• the main problem with dependence lies in the MFB
• problems with the frontal cortex portion of the MFB produce a pathological impairment of decision-making.
Dependence is not mainly under conscious control.

BASIC NEUROBIOLOGY: NEUROTRANSMITTERS INVOLVED IN DEPENDENCE.

Dependence is probably due to a functional dysregulation – meaning: they aren’t working right! – of one or more neurotransmitter chemicals in the MFB. These include dopamine (which is affected by cocaine, amphetamines or alcohol), serotonin (alcohol or LSD), endorphins (alcohol or opioids such as heroin), gamma-aminobutyric acid (alcohol or benzodiazepines – antianxiety agents), glutamate (alcohol) and acetylcholine (nicotine or alcohol).
The dysregulation could be related to too much or too little neurotransmission, abnormal breakdown of neurotransmitters or abnormal receptor function. How does it come about? Is it due to genetic ‘malfunctions’, to drug-induced changes, or to other aspects of the environment? Neurobiological research points to genetics and drug-induced changes as being primary causes of dependence, whereas the environment is a major, though secondary, contributor to drug abuse and thus dependence.

THE RATIONALE BASED ON GENETICS.Abnormal genes lead to abnormal proteins. This results in abnormal transmitter-synthesising enzymes, abnormal transmitter-breakdown enzymes, or abnormal receptors. This is the cause of neurotransmitter dysregulation in the pleasure pathway. Impaired control appears to be due to this brain-chemistry disruption. It is the reason that scientists and clinicians now believe that dependence is a chronic medical brain disease.

SUMMARY.
Addicting drugs seem to ‘match’ the transmitter system that is not normal. To treat such individuals, detoxification – weaning people off the drug of choice – is the first step. Then, ideally, abstinence-based treatments are attempted, which traditionally have the greatest chance of success. But abstinence is not for everyone, so more treatment choices are becoming available through scientific research. For some, continued use of a similar drug (such as methadone for heroin- dependent people) or the initial drug (nicotine patches for people who stop smoking) is the choice, because some people report that they “need” a chemical to “feel normal” – in other words, to overcome the non-normal transmitter system.

TODAY’S TREATMENT OPTIONS.
More options create greater chances for helping people. Today’s options include some or all of the following:
• traditional – 12-step programmes/abstinence
• talk – inpatient/outpatient/aftercare
• misunderstood but useful – harm reduction, including methadone
• new – brief motivational counselling, cognitive behavioural therapy, motivational enhancement therapy, ‘significant others’ therapy, vouchers
• medical treatment – new medications to enhance abstinence, anticraving medications, methadone, buprenorphine, vaccines, drugs to alleviate withdrawal.
So, if addictions are a medical disease, why do we treat them behaviourally? What is the similarity between behavioural or talk therapies and pharmacotherapies in the way they work? Simple. Behavioural therapies probably change brain chemistry! If this is a brain disease, and people get better in behaviourally-based therapies, then brain chemistry has to change. Recent brain-scan research is confirming this rational conclusion.

DISRUPTING NERVE CELLS: EXPLANATION.

The basis of chemical dependence is dysregulation of nerve cell transmission – (see picture on the right) and there is an excellent description of this on the author’s university website here. Also, most drugs used to treat mental disorders, including chemical dependence, have their most basic action on individual nerve cells
Carlton Erickson PhD is a research scientist who has been studying the effects of alcohol on the brain for over 30 years. He is the Pfizer Centennial Professor of Pharmacology and director of the Addiction Science Research and Education Center, College of Pharmacy, University of Texas. He has published over 150 scientific and professional articles, has co-edited and co-authored books and is associate editor of the scientific journal Alcoholism: Clinical and Experimental Research. He is also a recipient of the Betty Ford Center Visionary Award 2000. He has spoken to about 70,000 professionals and people in recovery since 1978 and presents every two years at the UK/European Symposium on Addictive Disorders.
Source : www.addictiontoday.org. Sept. 17th 2008

The following extracts are taken from the NHS Statistics on Drug Misuse: England, 2009. It is quite difficult to compare many of the statistics from the body of the report – some relate to age groups 16-59, others to 16-24 year olds, others to 11-15 year olds. Some give information from l996, others mention 2001, some relate to 2007/08 and others to 2008/09. Some mention an ‘overall decrease’ but when you delve into the detail you find that this overall decrease does not apply to some groups where there is an increase. Particularly disturbing is the information that the highest levels of drug use in the last year for all age groups were in the 16-19 and 20-24 year olds.

In the age group 16-24, 22% had used drugs in the previous year, 18% used cannabis in the previous year.

The report states that between l996 and 2008 the use of Class A drugs rose as follows:

25 – 29 years of age – 3.9% – 8.4%
30 – 34 “ “ “ – 1.9% – 5.2%
35 – 44 “ “ “ – 0.5% – 1.7%

And between 2007/8 to 2008/9 the rises were:

16 – 24 years of age – 6.9% – 8.1%
25 – 29 “ “ “ – 6.4% – 8.4%
30 – 34 “ “ “ – 3.8% – 5.2%

Note the differing age groups which make total comparisons difficult.
The report then makes a statement which is impossible to understand:

‘However, Class A drug use rose from 6.9% to 8.1% between 2007/08 and 2008/09; hence Class A drug use among young people is now stable over the long term’ ??

The most notable figure, repeated in the report in several places were:
7.9% of adults used cannabis in the past year (2008/9). This figure hardly agrees with media pronouncements and ‘accepted facts’ that cannabis use is endemic throughout the population. It might be very common in the younger age groups but this report suggests that over 92% of the adult population are non-users of cannabis. Ergo restrictive drug policies work.

Main findings:

Drug misuse among adults (16 – 59 years) In England and Wales:

• In 2008/09, 10.1% of adults had used one or more illicit drug within the last year,
compared with 9.6% in 2007/08. However, over the longer term this shows an overall
decrease from 11.1% in 1996.

• In 2008/09, 3.7% of adults had used Class A drugs in the last year, compared with 3.0% in 2007/08. Over the longer term this also shows an increase from 2.7% in 1996.

• Consistent with previous findings, cannabis is the type of drug most likely to be used by adults; 7.9% of 16-59 year olds used cannabis in the last year in 2008/09.

• There have been some decreases over the longer term in the use of non-Class A drugs; between 1996 and 2008/09 use of cannabis, amphetamines and anabolic steroids within the last year among adults declined.

Drug misuse among young adults (16 – 24 years) In England and Wales:

• In 2008/09, around 22.6% of young adults had used one or more illicit drug in the last year, which shows no change from 2007/08. This shows a long term decrease from 1996 when it was 29.7%.

• In 2008/09, 8.1% of young adults had used Class A drugs in the last year, compared with 6.9% in 2007/08. Over the long term, Class A drug use among young people has stabilised since 1996.

• Cannabis remains the drug most likely to be used by young people; 18.7% of
respondents aged 16-24 had used cannabis in the last year in 2008/09.

Drug misuse among children (11 – 15 years) In England:

• There has been an overall decrease in drug use reported by 11- 15 year olds since 2001. The prevalence of lifetime drug use fell from 29% in 2001 to 22% in 2008.

• There were also decreases in the proportion of pupils who reported taking drugs in the last year; from 20% in 2001 to 15% in 2008.

• Reported drug use was more common among older pupils; for example, 4% of 11 year olds said they had used drugs in the last year, compared with 29% of 15 year olds in 2008.

• Cannabis was the most widely used drug in 2008; 9.0% of pupils reported taking it in the last year, a long term decrease from 13.4% in 2001.

• Pupils who had truanted or been excluded from school were more likely to report taking drugs at least once a month than those who had not truanted or been excluded (11% and 1% respectively) in 2008
.
• There was an overall decrease in the proportion of pupils being offered drugs from 42% in 2001 to 33% in 2008. Cannabis was the most commonly offered drug followed by volatile substances and poppers.

• Older pupils were more likely to have been offered drugs, with 11% of 11 year olds
having been offered them compared with 57% of 15 year olds in 2008.

Health outcomes

Individuals who take illicit drugs face potential health risks, as the drugs are not controlled or supervised by medical professionals. As well as health risks, drugs can become addictive and lead to long term damage to the body. Illicit drug users are also at risk of being poisoned by drugs, and overdosing which can lead to a fatality.
In England (unless otherwise stated):

• In 2008/09, there were 5,668 admissions to hospital with a primary diagnosis of a drug-related mental health and behavioural disorder. This number is 15.1% less than in 2007/08 when there were 6,675 admissions. There were more male than female
admissions (3,997 and 1,671 respectively).

• Where primary or secondary diagnosis was recorded there were 42,170 admissions in 2008/09 compared with 40,421 in 2007/08, which shows an increase of 4.3%. There were more male than female admissions in 2008/09 (28,289 and 13,875 respectively).

• Where a primary diagnosis of poisoning by drugs was recorded, 11,090 admissions were reported during 2008/09, an increase of 47.2% from 1998/99 when the number of such admissions was 7,533. This has remained stable since 2007/08. There were more male than female admissions (6,076 and 5,014 respectively).

• The Strategic Health Authorities (SHAs) with the most admissions for drug related mental health and behaviour disorders as the primary or secondary diagnosis were North West SHA (155 admissions per 100,000 population) and Yorkshire and The Humber SHA (98 admissions per 100,000 population).

• During 2008/09, there were 207,580 people in contact with structured drug treatment services (those aged 18 and over). This is a 10.4% increase from the 2007/08 figures, where the number was 187,978.

• In 2008/09, a larger number of men accessed treatment services than women (151,064 men compared to 56,516 women aged 18 or over).

• Those taking opiates only (which includes heroin) was the main type of drug for which people received treatment (48% of all treatments), with a further 31% of treatments for those who have taken both opiates and crack in 2008/09.

• There were 60,386 discharged episodes of treatment by the end of 2008/09 and there were 24,656 (41%) of clients exiting treatment who were no longer dependent on the substances that brought them into treatment; a further 9,002 (15%) were referred on for further interventions outside of community-structured treatment.

• The total number of deaths related to drug misuse in England and Wales was 1,738 in 2008; 78% of those who died were male. The most popular underlying cause of death was from accidental poisoning for both males and females (597 and 166 respectively).

The key findings from Chapter 2 of the BCS (British Crime Survey) report show that:

• Around one in three (36.8%) had ever used illicit drugs, one in ten had used drugs in the last year (10.1%) and around one in 20 (5.9%) had done so in the last
month.

• Levels of Class A drug use were, unsurprisingly, lower than overall drug use, with 15.6% having used a Class A drug at least once in their lifetime, 3.7% having done so in the last year and 1.8% in the last month.

• Consistent with previous findings, cannabis is the type of drug most likely to be used; 7.9% of 16-59 year olds used cannabis in the last year.

• Use of any illicit drug during the last year has shown an overall decrease from 11.1% in 1996 to 10.1% in 2008/09, due in part to successive declines in the use of cannabis between 2003/04 and 2007/08.

• Despite this long-term overall decline, there has been an increase in the number 16-59 year olds who have used Class A drugs within the last year between 1996 (2.7%) and 2008/09 (3.7%).

• Class A drug usage has remained generally stable over this period: year-on-year changes were not statistically significant until most recently; however there was a slight underlying upward trend, which is now significant over the long term.

• The increase in Class A drug usage since 1996 can be understood in terms of an increase in the number of people who have used cocaine powder within the last year (from 0.6% to 3.0%), partly offset by a decrease over the same period in the use of LSD (from 1.0% to 0.2%).

• In 2008/09 methamphetamine was included for the first time but this has no visible impact on the overall prevalence of Class A drug use in that survey year.

• There have been some decreases over the longer term in the use of non-Class A drugs; between 1996 and 2008/09 use of cannabis, amphetamines and anabolic
steroids within the last year among 16-59 year olds declined. Looking at more recent years, key changes between 2007/08 and 2008/09 showed:

• The overall proportion of 16-59 year olds who have used any illicit drug within the last year remained stable (9.6% in 2007/08 compared with 10.1% in 2008/09) but there was an increase in Class A drug use within the last year (from 3.0% to 3.7%).

• For individual types of drug, increases were seen in the use within the previous year of cocaine powder, ecstasy, tranquillisers,anabolic steroids and ketamine.

1.3 Young people
Chapter 3 on pages 19-33 of the BCS report focuses on the use of illicit drugs by
young people aged 16-24 years old.

Figure 3.1 on page 20 shows the percentages of 16-24 year olds who have used Class A drugs either in the last year, the last month or ever for 2008/09. Related
information showing these percentages as a time series can be found in Tables 3.1-
3.3 on pages 27-29 and similar information showing actual numbers for 2008/09 can
be found in Tables 3.4- 3.6 on pages 30-32.
Figures 3.2-3.5 on pages 21-24 show the proportion of drugs used in the last year for 16-24 year olds by various drug breakdowns or as a time series. Figure 3.6 on page 25 shows the proportion of this age group classified as frequent drug users
as a time series. Related information on frequent drug use in the last year among
16-24 year olds can be found in Tables 3.7 and 3.8 on page 33 as a time series for any drug and by drug type for 2008/09.

The key findings from Chapter 3 of the BCS report show that:

• Around two in five young people(42.9%) have ever used illicit drugs, nearly one in four had used one or more illicit drugs in the previous year (22.6%) and around one in eight in the last month (13.1%).

• Levels of Class A drug use were, unsurprisingly, lower than overall drug use, with 16.9% of young people having ever used a Class A drug, 8.1% having done so within
the last year and 4.4% in the last month.

• Cannabis remains the drug most likely to be used by young people; 18.7% of respondents aged 16-24 had used cannabis in the previous year. Long and short-term trends for young people aged 16-24 show:

• The proportion of 16-24 year olds having used drugs in the last year fell from 29.7% in 1996 to 22.6% in 2008/09, due in large part to the gradual decline in cannabis use.
Latest figures show no change between 2007/08 and 2008/09.

• The general trend for having used Class A drugs in the last year for young people shows a slight decline since 1996.

• However, Class A drug use rose from 6.9% to 8.1% between 2007/08 and 2008/09; hence Class A drug use among young people is now stable over the long term. In
2008/09 methamphetamine was included for the first time but this has no visible impact on the overall prevalence of Class A drug use in that survey year. Recent trends in types of drugs used show that between 2007/08 and 2008/09:

• There was an increase in use of cocaine powder within the last year (from 5.1% to 6.6%) and ketamine (from 0.9% to 1.9%).

• Use of methadone within the last year, and hence opiates, fell (these figures are based on small numbers).

The key findings from Chapter 4 in the BCS report show that:

• The youngest age groups (16-19 and 20-24 year olds) reported the highest levels of drug use in the last year (22.2% and 22.9% respectively) compared with all older age groups.

• A broadly similar pattern can be seen for Class A drug use, but with the peak for drug use in the last year shifting slightly later to also include the 25-29 age group, with usage then decreasing with increasing age.

• Men continued to report higher levels (around twice as high) than women of drug use in the last year of any illicit drug or any Class A drug use. Looking at trends since the survey began, the self-report drug use data collection in 1996 shows there is a decrease in drug use in the last year for the 16-19 year olds which decreased from 31.7% in 1996 to 22.2% in 2008/09 and, for those aged 20- 24, fell from 28.1% to the latest figure of 22.9%. In general, between 1996 and 2008/09, year-on-year changes in levels of Class A drug use in the last year use were not statistically significant until most recently; however, there was a slight underlying upward trend which is now significant over the long term. There were increases in Class A drug use within the following age groups between 1996 and 2008/09: 25-29 year olds (3.9%
to 8.4%), 30-34 year olds (1.9% to 5.2%) and 35-44 year olds (0.5% to 1.7%).
Looking at change over the last year:

• There were no statistically significant changes in prevalence of any drug use overall in the last year between 2007/08 and 2008/09 for any age group.

• There was a statistically significant rise between 2007/08 and 2008/09 in the proportion of 16-24 (6.9% to 8.1%), 25-29 (6.4% to 8.4%) and 30-34 year olds (3.8% to 5.2%) who took Class A drugs in the last year.

Drug-related mental health and behavioural disorders

During 2008/09 more people aged 25-34 were admitted with a primary diagnosis of drug-related mental health and behaviour disorders than any other age group. This age group accounted for nearly 40% of all such admissions in that year.

Table 3.4 shows that there were 42,170 admissions where there was a primary or
secondary diagnosis of drug-related mental health and behavioural disorders in 2008/09, which is 4.3% higher than 40,421 admissions in 2007/08

England Numbers
Total Under 16 16-24 25-34 35-44 45-54 55-64 65-74 75+

1998/99 24,236 266 7,236 10,850 4,066 1,220 258 141 162
1999/00 24,974 273 7,028 11,027 4,634 1,363 271 144 196
2000/01 25,683 292 6,904 11,357 5,112 1,426 254 116 137
2001/02 28,063 329 7,136 12,355 6,034 1,543 290 151 146
2002/03 31,490 358 7,399 13,772 7,324 1,899 412 118 146
2003/04 34,957 374 7,861 15,061 8,670 2,137 418 156 194
2004/05 35,737 396 7,547 14,872 9,388 2,414 598 204 235
2005/06 38,005 445 7,495 15,752 10,314 2,817 688 181 197
2006/07 38,170 402 6,983 15,330 10,941 3,158 793 232 183
2007/08 40,421 350 7,348 15,540 11,792 3,664 924 270 191
2008/09 42,170 318 6,721 15,817 12,815 4,385 1,181 272 212

Table 3.10 NDTMS clients in treatment, by gender and age, 2008/09

England Numbers / percentages
Total Male Female

All clients 207,580 100 151,064 100 56,516 100
18-24 29,848 14 19,656 13 10,192 18
25-29 43,778 21 31,026 21 12,752 23
30-34 44,713 22 33,031 22 11,682 21
35-39 39,215 19 29,649 20 9,566 17
40+ 50,026 24 37,702 25 12,324 22

Source:

Statistics from the National Drug Treatment Monitoring System (NDTMS) 1 April 2008 – 31
March 2009. National Treatment Agency for Substance Misuse (NTA)
1. National Drug Treatment Monitoring System (NDTMS).
2. Percentages are rounded to the nearest per cent. Totals may not add up to 100 due to rounding

3. Age is calculated at year midpoint (30th September 2008).

Table 3.13 shows the reasons why clients were discharged from treatment. A discharge is classed as successful if an individual is said to have completed their course of treatment (whether drug free or otherwise), or if the individual is referred to another agency

Table 3.13 Treatment exit reasons for individuals not retained in treatment reported to NDTMS, 2008/09

Numbers %

Total (episodes discharged) 60,386 100
Total successful completions 24,656 41

Treatment completed free of dependency 15,676 26
Treatment completed drug free 8,980 15
Referred on 9,002 15
Dropped out/ left 14,822 25
Prison 4,383 7
Treatment declined 1,769 3
Treatment withdrawn 1,328 2
Moved away 1,870 3
Died 905 1
Other 980 2
Not known 159 0
No appropriate treatment 512 1

Source:
Statistics from the National Drug Treatment Monitoring System (NDTMS) 1 April 2008 – 31
March 2009. National Treatment Agency for Substance Misuse (NTA)
Copyright © 2009, re-used with the permission of the National Treatment Agency for Substance Misuse
Copyright © 2009. Health and Social Care Information Centre, Lifestyle Statistics. All rights
Reserved

Snippets

• Drug users aged 16-34 were more likely to have used three or more illicit
drugs in the last year com

The BCS report shows an overall prevalence rate of 4% for use of more than one illicit drug (polydrug use) in the last year amongst adults aged 16-59.

There was little difference between adult drug users who were single or cohabiting in terms of taking three or more illicit drugs in the last year (both 23%) and both groups were considerably more likely to take three or more illicit drugs than those who were married (married couples accounting for 8% of those who used three or more illicit drugs in the last year).

Reported drug use was more common among older pupils; for example, 4% of 11
year olds said they had used drugs in the last year, compared with 29% of 15 year
olds.

Regular smokers and pupils who have consumed more units of alcohol in the
previous week were very much more likely to have used drugs in the last year..

Deaths related to drug misuse. In 2008, there were1,738 deaths reported as being due to drug misuse. Of those who died, 78% were male. Compared to 1993 the number of male deaths has increased by around 136% in 2008 compared to a 48% increase for females. In recent years however no overall trend is apparent. The highest numbers of deaths due to drug misuse occurred in the 30 to 39 age group for both males and females (490 and 112 respectively).

Editor’s Note: This article is the first in a two-part series on Neurofeedback in the Treatment of Substance Abuse. This article presents evidence of the neurological basis, specifically EEG dysfunction, underlying addiction that makes it such a complicated condition to treat, and explains how neurofeedback addresses cognitive, emotional and physical symptoms. The second part of this article will include a discussion of the efficacy models of neurofeedback and a review of the research applying neurofeedback to substance abuse treatment, as well as address the possible mechanisms of its effectiveness in addiction.
Over the last two decades a new research and clinical approach—neurofeedback—has shown promise in the treatment of substance abuse. This article addresses how it works, what makes it so effective, why it is a potentially important tool in addiction, the neurophysiological issues it might address, the existing promising research and, most importantly, that neurofeedback can be a significant adjunct to the therapeutic and counseling process with addicts.

The category of disorders associated with substance abuse is the most common psychiatric set of conditions affecting an estimated 22 million people in this country (SAMHSA, 2004). Furthermore, the disorder is accompanied by serious impairments of cognitive, emotional and behavioral functioning. These conditions and symptoms so significantly alter a person’s brain and its functioning, that we often refer to the drug as hijacking the brain, making it very difficult to think logically and appropriately weigh the consequences of the drug related behavior.

Detoxified addicts have been shown to have significant alterations in brain electroencephalographic (EEG) patterns and children of addicts also exhibit EEG patterns that are significantly different than normal (Sokhadze et al., 2008, for review). This indicates that, not only are we dealing with the neurological consequences of drug-related behavior, but there appears to be a genetic pattern as well, that places certain people at greater risk for addictive behaviors. The complexity of these factors makes the treatment of addiction one of the most difficult areas of mental, emotional and physical rehabilitation.

Multiple factors in addiction
Treating addiction is compounded by the many factors contributing to its onset and maintenance. Furthermore, the addiction itself masks many other clinical conditions that become more evident once the drug user becomes abstinent. In fact, it is frequently other psychiatric problems that lead to drug abuse as the addict attempts self-medication. It has also been shown that people with cognitive disabilities are more vulnerable, and more likely to have a substance abuse disorder (Moore, 1998). These impairments appear to include attentional issues as well as the hypo-functioning of the frontal cortex, sometimes referred to as the executive brain, where decision making takes place (Fowler, et al., 2007).
As a result, we are learning that no one approach has all the answers. Multiple mechanisms require multiple considerations and approaches. In addition, addicts are a diverse group, resulting in the need for many tools and approaches. It appears that programs offering the most diversified array of treatment modalities are the most effective (Vaccaro & Sideroff, 2008). That is also why, for example, most programs urge the inclusion of a 12-step program for ongoing support.

But how do you address the biological and genetic aspects while also addressing the traumatic and emotional factors, the social cognitive and attentional factors? How do you deal with the apparent “procedural memory” and conditioned factors that cause an abstinent addict, on his or her way home from work, to all of a sudden take an inappropriate turn and end up at the drug dealer? Neurofeedback appears to be a tool, a training that has the facility to address many of these factors associated with addiction.

History of promising treatmentsOver the years, there have been a number of developments that have been promising in the treatment of addiction. Each time a new approach is identified, it is immediately seen as being the long sought after “silver bullet” that will solve the addiction problem. This occurred with the development of methadone, and later Levo-Alpha Acetyl Methadol (LAAM). When I entered the field in 1976, as a post-doctoral fellow of the National Institute of Drug Abuse, Naltrexone was gaining popularity. Naltrexone is a long-acting opiate antagonist that blocks the effects of opiates, such as morphine, heroin and codeine.

It was around this time that the importance of addiction-related stimuli was becoming widely recognized (Wikler, 1984). In research examining the conditioned aspects of addiction, it was found that stimuli associated with the drug using behavior could serve as conditioned stimuli that would trigger an unconditioned psychophysiological response that had similarities to withdrawal and included anxiety, fear and physiological arousal (e.g. Sideroff & Jarvik, 1980). This conditioned patterning of response lead to the proposal that relapse liability might be determined by exposing addicts to these conditioned stimuli and monitoring their responses (Sideroff, 1980).

Following this conditioning model, one potential mechanism of Naltrexone treatment would be the behavioral extinction of some of the conditioned associations of addiction. In other words, if the addict attempted to get high while on Naltrexone, the lack of reinforcing effect might lessen the conditioned effects of drug related stimuli. This, in turn, might reduce readdiction liability. All that needed to happen was for the addict to use, without experiencing any effect; a perfectly reasonable theoretical assumption. So, not only was Naltrexone expected to be successful in keeping addicts from using, but it also could address conditioned aspects of addiction.

When I arrived at UCLA and the Veterans Administration at Brentwood in 1976, I was surprised to discover that the treatment program to which I had been awarded a fellowship, was already eliminated—almost before it began. With the help of the director of the methadone clinic, I started a new experimental Naltrexone treatment program, drawing recruits from the VA’s metha¬done maintenance population.

Unfortunately, Naltrexone did not meet its high expectations. While many methadone patients expressed interest in using Naltrexone, the long process of withdrawing from methadone—necessary in order to begin taking the opiate antagonist—eliminated more than 80 percent of volunteers. Also, as we enrolled volunteers, we found that 90 percent of the addicts who began using Naltrexone never used opiates while on the antagonist; and the 10 percent who did use, only used once. It was as if the addict immediately experienced this “no reward” condition and thus didn’t bother to waste his money. This, in itself, was an interesting finding, as it showed this population to be able to demonstrate impulse control under certain circumstances (Sideroff et al., 1978). As a result, we never had the opportunity to test our theory of extinction.
The use of Naltrexone for opiate addiction has subsequently been viewed as an unworkable model. Yet, for the small fraction of individuals who were able to detox and begin taking Naltrexone, it did change their lives.

Typically, the “Silver Bullet” has been thought of in terms of a drug; something that could either eliminate craving or eliminate the high of the drug of abuse. What have become most useful, have been drugs of substitution, such as buprenorphine, (Johnson, et al., 2000), as we continue to search for an effective treatment combination that includes psychotherapy.

EEG and addiction
The EEG is one objective representation of how the brain is functioning. The EEG is recorded from scalp electrodes, and is a representation of electrical activity produced by the collective firing of populations of neurons in the brain, in the vicinity of the electrode. Figure 1 presents a chart of brain wave frequencies and the primary functions associated with their production. It should be pointed out that this is a gross representation and that more precise differences—beyong the scope of this article – can be found when you look at specific single frequencies within each range. While all frequencies and frequency ranges are important and necessary, problems arise when there is too much or too little of a particular type of brain wave; there is difficulty shifting in response to changing needs; or the EEG is to reactive.

For example, in a healthy functioning brain, if we look at the amount of theta being produced and we compared it (using 4-8 Hz) with beta frequencies between 13 and 21 Hz (cycles per second), there is approximately a 2 to 1 ratio. When we assess the EEGs of people with Attention Deficit Disorder (ADD), we see ratios that are 3 to 1 and much higher (Lubar, 2003).

These higher ratios indicate that the brain is producing too much of the slow waves relative to the beta waves, where the beta waves represent a more focused and engaged brain. In other words, these brains are under-activated. On the other hand, if we look at the EEG patterns of people with anxiety, worry and tension, there is typically too much activity occurring in the higher frequencies, usually between 24 and 35 Hz. The EEGs of people with substance abuse problems can show both of these patterns.

It has been demonstrated that the EEGs of addicts show specific abnormalities when compared to normative data. Studies of detoxified alcoholics indicate an increase in absolute and relative power in the higher beta range, along with a decrease in alpha and delta/theta power (Saletu, et al., 2002). Low voltage fast desynchronized patterns (high beta) may be interpreted as demonstrating a hyper arousal of the central nervous system (Saletu-Z et al., 2004); and Bauer, showed a worse prognosis for the patient group with a more pronounced frontal hyper-arousal (Bauer, 2001).
The fact that these EEG patterns as well as alcohol dependence itself are highly inheritable further supports the biological nature of this disease (Gabrielli et al., 1982; Schuckit & Smith, 1996; Van Beijsterveldt & Van Baal, 2002).

These specific abnormalities show both a worse prognosis and a predisposition to development of alcoholism. Indivi¬duals with a family history of alcoholism were found to have reduced relative and absolute alpha power in occipital and frontal regions and increased relative beta in both regions compared with those with a negative family history of alcoholism. In another study, these abnormalities also were associated with risk for alcoholism (Finn & Justus, 1999).

It is a common belief that at least part of the cause of addiction is an attempt at feeling better—self-medicating. When someone with reduced or an absence of synchronous alpha rhythm takes a drink of alcohol, it results in the generation of an alpha rhythm or what is referred to as alpha synchrony, which a normal functioning brain has much greater capacity to produce (Pollock et al., 1983). Thus, it appears that the alcohol is helping the addicted person compensate for their brain’s inability to produce an alpha rhythm which is associated with a state of calmness. This mechanism helps to explain the use of alcohol by this group of addicts.

In related research on abstinent heroin-dependent subjects, it is interesting to note similar abnormalities of deficits in alpha frequencies, along with excessive high beta EEG activity (Franken et al. 2004; Polunina & Davydov, 2004). Although it appears that in some studies, these changes found in early abstinence normalize after several months of abstinence (Shufman et al., 1966; Polunina & Davydov, 2004). Cocaine-dependent subjects may show similar increases in beta activity, but in addition show increases in frontal alpha (Herning, et al., 1994). These changes, specifically the elevation of fast beta activity, appear to be correlated with relapse in cocaine abuse (Bauer, 2001). In contrast, meth¬amphetamine abusers have been shown to have significant increases in delta and theta frequency bands (Newton et al, 2003).

There are many questions that this research does not answer with regard to the relationship between abnormal EEG patterns and addiction. For example, it is not known if these dysfunctional elements are coincidental or causal. In addition, these EEG patterns are found in many mental disorders, some that are typically coincident with substance abuse. These questions do not minimize the probable conclusions that the EEG dysfunction creates specific vulnerabilities of these subjects. For example, frontal alpha, which is also found with some types of ADD, results in impairment of executive functions, such as decision making; and excessive fast beta activity can result in excess emotional and physical tension as well, as obsessive qualities.

Other substances of abuse have also been shown to correlate with abnormal EEG patterns. For example, studies have demonstrated that subjects with a chronic history of marijuana use demonstrate EEG patterns of frontal elevations of alpha frequencies. (Struve, Manno, Kemp, Patrick, & Manno 2003). This is referred to as “alpha hyper-frontality.” Another common feature of the EEG of chronic users is a reduction of alpha mean frequency, which may indicate some deficits in intellectual functioning.

Neurofeedback
Neurofeedback, as a subset of biofeedback, monitors a subject’s brain waves and feeds back selective information about these brain waves, in order to gain control over these patterns. Neurofeedback programs typically allow for the setting of thresholds within specific frequency bands or ranges so that when the EEG either rises above the threshold or drops below the threshold, some form of signal or reinforcement is presented to the subject. This feedback lets the brain know when it has been successful, thus, in an operant conditioning model, encourages this rewarded brain wave response. When the goal is to have the signal go above a threshold, we refer to this as “up training” or rewarding. When the goal is to reinforce signals that drop below a threshold, we refer to this as “down training,” or inhibiting this component of the EEG.

Joe Kamiya, a researcher at the University of Chicago, was the first researcher to discover that when a subject was informed that he was producing alpha brain wave frequencies, he would then be able to learn to detect, on his own, when he was in alpha (Kamiya, 1968). As a result of this finding, he designed a study in which he similarly gave feedback to the subjects as to their production of alpha, with the instruction to produce alpha. He found that when given this feedback, subjects were able to increase their production of synchronous alpha waves (Nowlis & Kamiya, 1970). Interestingly, his success led to the popularity of alpha training in mass culture, which coincided with its loss of credibility in the academic ¬community.

Neurofeedback research and its acceptance took on a new impetus when Sterman, working with cats, was able to train these animals using a similar operant conditioning model, to increase the amount of synchronous spindle activity in the 14 Hz frequency range (Sterman, 2000). Since these spindles occurred over the sensorimotor cortex, he labeled them sensorimotor rhythm (SMR). These studies confirmed that the production of these brain waves—associated with motoric stillness—resulted in animals that were more resistant to the triggering of seizures. Sterman, then adapted this EEG biofeedback procedure with epileptic patients and demonstrated its effectiveness in reducing the frequency and intensity of seizures.

When a subject produces SMR activity, he is mentally alert with relaxed muscles (lower muscle tone). Lubar, working in Sterman’s laboratory, recognized the potential of this discovery, and in a series of research studies, he and his colleagues were able to train children with hyperactive disorder to increase their production of SMR activity with feedback, resulting in reduced hyperactivity (Lubar, 1985).

The training procedures have evolved so that in addition to reinforcing SMR frequencies, the training of ADD also typically reinforces slightly higher frequencies of either 15 to 18, or 15 to 20 Hz activity, and at the same time, down trains the slower (theta) frequencies. The protocols address the ratio be¬tween the slower (theta) brain waves, with the faster brain waves, with a goal of training greater activation of the brain, which translates into improved attention. In one follow up study, Lubar and associates were able to demonstrate that gains made in variables of attention were maintained in subjects 10 years following training (Lubar, 1995; 2003).

At the same time that neurofeedback was being used to address attentional and cognitive deficits, primarily by training the activation of the brain, it also was being used to help people relax and establish autonomic and neuromuscular balance. With populations demonstrating aspects of anxiety, obsessive compulsive disorder and tension, the procedure has been to train increases in alpha frequencies (8-12 Hz) or a combination of alpha and theta (Moore, 2000). In these cases, the process is one of training a lowering of activation of the brain. A wide range of neurofeedback protocols have now been applied to cognitive, emotional and physical symptoms and conditions with a growing range of positive results. A bibliography covering these studies is available (Hammond 2008).

Acknowledgement: The author wishes to express his appreciation to Eleanor Criswell, Jay Gunkelman, David Kaiser and Hugh Baras for their helpful comments.

Dr. Stephen Sideroff, PhD, is a licensed clinical psychologist, consultant and Assistant Professor in the Psychiatry Department at UCLA and one of the Clinical Directors at Moonview Sanctuary. Dr. Sideroff is an internationally recognized expert in behavioral medicine, biofeedback and peak performance, and wa the founder and former clinical director of Santa Monica Hospital’s Stress Strategies, which presented programsfor individuals and corporations to better cope with stress.

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The campaign to legitimize what is called “medical” marijuana is based on two propositions: that science views marijuana as medicine, and that DEA targets sick and dying people using the drug. Neither proposition is true. Smoked marijuana has not withstood the rigors of science – it is not medicine and it is not safe. DEA targets criminals engaged in cultivation and trafficking, not the sick and dying. No state has legalized the trafficking of marijuana, including the twelve states that have decriminalized certain marijuana use.

SMOKED MARIJUANA IS NOT MEDICINE
There is no consensus of medical evidence that smoking marijuana helps patients. Congress enacted laws against marijuana in 1970 based in part on its conclusion that marijuana has no scientifically proven medical value. The Food and Drug Administration (FDA) is the federal agency responsible for approving drugs as safe and effective medicine based on valid scientific data. FDA has not approved smoked marijuana for any condition or disease. The FDA noted that “there is currently sound evidence that smoked marijuana is harmful,” and “that no sound scientific studies supported medical use of marijuana for treatment in the United States, and no animal or human data supported the safety or efficacy of marijuana for general medical use.” 2
In 2001, the Supreme Court affirmed Congress’s 1970 judgment about marijuana in United States v. Oakland Cannabis Buyers’ Cooperative et al., 532 U.S. 438 (2001), which held that, given the absence of medical usefulness, medical necessity is not a defense to marijuana prosecution. Furthermore, in Gonzales v. Raich, 125 S.Ct. 2195 (2005), the Supreme Court reaffirmed that the authority of Congress to regulate the use of potentially harmful substances through the federal Controlled Substances Act includes the authority to regulate marijuana of a purely intrastate character, regardless of a state law purporting to authorize “medical” use of marijuana.
The DEA and the federal government are not alone in viewing smoked marijuana as having no documented medical value. Voices in the medical community likewise do not accept smoked marijuana as medicine:
The American Medical Association has rejected pleas to endorse marijuana as medicine, and instead has urged that marijuana remain a prohibited, Schedule I controlled substance, at least until more research is done. 3

• The American Cancer Society “does not advocate inhaling smoke, nor the legalization of marijuana,” although the organization does support carefully controlled clinical studies for alternative delivery methods, specifically a THC skin patch. 4

• The American Academy of Pediatrics (AAP) believes that “[a]ny change in the legal status of marijuana, even if limited to adults, could affect the prevalence of use among adolescents.” While it supports scientific research on the possible medical use of cannabinoids as opposed to smoked marijuana, it opposes the legalization of marijuana. 5

• The National Multiple Sclerosis Society (NMSS) states that studies done to date “have not provided convincing evidence that marijuana benefits people with MS,” and thus marijuana is not a recommended treatment. Furthermore, the NMSS warns that the “long-term use of marijuana may be associated with significant serious side effects.” 6

• The British Medical Association (BMA) voiced extreme concern that down-grading the criminal status of marijuana would “mislead” the public into believing that the drug is safe. The BMA maintains that marijuana “has been linked to greater risk of heart disease, lung cancer, bronchitis and emphysema.” 7 The 2004 Deputy Chairman of the BMA’s Board of Science said that “[t]he public must be made aware of the harmful effects we know result from smoking this drug.”8

• The American Academy of Pediatrics asserted that with regard to marijuana use, “from a public health perspective, even a small increase in use, whether attributable to increased availability or decreased perception of risk, would have significant ramifications.” 9
In 1999, The Institute of Medicine (IOM) released a landmark study reviewing the supposed medical properties of marijuana. The study is frequently cited by “medical” marijuana advocates, but in fact severely undermines their arguments.
After release of the IOM study, the principal investigators cautioned that the active compounds in marijuana may have medicinal potential and therefore should be researched further. However, the study concluded that “there is little future in smoked marijuana as a medically approved medication.” 10

• For some ailments, the IOM found “…potential therapeutic value of cannabinoid drugs, primarily THC, for pain relief, control of nausea and vomiting, and appetite stimulation.” 11 However, it pointed out that “[t]he effects of cannabinoids on the symptoms studied are generally modest, and in most cases there are more effective medications [than smoked marijuana].”12

• The study concluded that, at best, there is only anecdotal information on the medical benefits of smoked marijuana for some ailments, such as muscle spasticity. For other ailments, such as epilepsy and glaucoma, the study found no evidence of medical value and did not endorse further research. 13

• The IOM study explained that “smoked marijuana . . . is a crude THC delivery system that also delivers harmful substances.” In addition, “plants contain a variable mixture of biologically active compounds and cannot be expected to provide a precisely defined drug effect.” Therefore, the study concluded that “there is little future in smoked marijuana as a medically approved medication.” 14

• The principal investigators explicitly stated that using smoked marijuana in clinical trials “should not be designed to develop it as a licensed drug, but should be a stepping stone to the development of new, safe delivery systems of cannabinoids.” 15
Thus, even scientists and researchers who believe that certain active ingredients in marijuana may have potential medicinal value openly discount the notion that smoked marijuana is or can become “medicine.” DEA has approved and will continue to approve research into whether THC has any medicinal use. As of May 8, 2006, DEA had registered every one of the 163 researchers who requested to use marijuana in studies and who met Department of Health and Human Services standards. 16
One of those researchers, The Center for Medicinal Cannabis Research (CMCR), conducts studies “to ascertain the general medical safety and efficacy of cannabis and cannabis products and examine alternative forms of cannabis administration.”17 The CMCR currently has 11 on-going studies involving marijuana and the efficacy of cannabis and cannabis compounds as they relate to medical conditions such as HIV, cancer pain, MS, and nausea.18
At present, however, the clear weight of the evidence is that smoked marijuana is harmful. No matter what medical condition has been studied, other drugs already approved by the FDA, such as Marinol – a pill form of synthetic THC – have been proven to be safer and more effective than smoked marijuana.
MARIJUANA IS DANGEROUS TO THE USER AND OTHERS
Legalization of marijuana, no matter how it begins, will come at the expense of our children and public safety. It will create dependency and treatment issues, and open the door to use of other drugs, impaired health, delinquent behavior, and drugged drivers. This is not the marijuana of the 1970′s; today’s marijuana is far more powerful. Average THC levels of seized marijuana rose from less than one per cent in the mid-1970′s to a national average of over eight per cent in 2004. 19
And the potency of “B.C. Bud” is roughly twice the national average – ranging from 15 per cent to as high as 25 per cent THC content.20
Dependency and Treatment:
o Adolescents are at highest risk for marijuana addiction, as they are “three times more likely than adults to develop dependency.” 21
This is borne out by the fact that treatment admission rates for adolescents reporting marijuana as the primary substance of abuse increased from 32 to 65 per cent between 1993 and 2003.22 More young people ages 12-17 entered treatment in 2003 for marijuana dependency than for alcohol and all other illegal drugs combined.23

• “Research shows that use of [marijuana] can lead to dependence. Some heavy users of marijuana develop withdrawal symptoms when they have not used the drug for a period of time. Marijuana use, in fact, is often associated with behavior that meets the criteria for substance dependence established by the American Psychiatric Association.” 24

• Of the 19.1 million Americans aged 12 or older who used illicit drugs in the past 30 days in 2004, 14.6 million used marijuana, making it the most commonly used illicit drug in 2004. 25

• Among all ages, marijuana was the most common illicit drug responsible for treatment admissions in 2003, accounting for 15 per cent of all admissions — outdistancing heroin, the next most prevalent cause. 26

• In 2003, 20 per cent (185,239) of the 919,833 adults admitted to treatment for illegal drug abuse cited marijuana as their primary drug of abuse.27
Marijuana as a Precursor to Abuse of Other Drugs:
o Marijuana is a frequent precursor to the use of more dangerous drugs, and signals a significantly enhanced likelihood of drug problems in adult life. The Journal of the American Medical Association reported, based on a study of 300 sets of twins, “that marijuana-using twins were four times more likely than their siblings to use cocaine and crack cocaine, and five times more likely to use hallucinogens such as LSD.” 28
• Long-term studies on patterns of drug usage among young people show that very few of them use other drugs without first starting with marijuana. For example, one study found that among adults (age 26 and older) who had used cocaine, 62 per cent had initiated marijuana use before age 15. By contrast, less than one per cent of adults who never tried marijuana went on to use cocaine. 29

• Columbia University’s National Center on Addiction and Substance Abuse reports that teens who used marijuana at least once in the last month are 13 times likelier than other teens to use another drug like cocaine, heroin, or methamphetamine, and almost 26 times likelier than those teens who have never used marijuana to use another drug. 30

• Marijuana use in early adolescence is particularly ominous. Adults who were early marijuana users were found to be five times more likely to become dependent on any drug, eight times more likely to use cocaine in the future, and fifteen times more likely to use heroin later in life. 31

• In 2003, 3.1 million Americans aged 12 or older used marijuana daily or almost daily in the past year. Of those daily marijuana users, nearly two-thirds “used at least one other illicit drug in the past 12 months.” More than half (53.3 per cent) of daily marijuana users were also dependent on or abused alcohol or another illicit drug compared to those who were nonusers or used marijuana less than daily. 32

• Healthcare workers, legal counsel, police and judges indicate that marijuana is a typical precursor to methamphetamine. For instance, Nancy Kneeland, a substance abuse counselor in Idaho, pointed out that “in almost all cases meth users began with alcohol and pot.” 33
Mental and Physical Health Issues Related to Marijuana:
John Walters, Director of the Office of National Drug Control Policy, Charles G. Curie, Administrator of the Substance Abuse and Mental Health Services Administration, and experts and scientists from leading mental health organizations joined together in May 005 to warn parents about the mental health dangers marijuana poses to teens. According to several recent studies, marijuana use has been linked with depression and suicidal thoughts, in addition to schizophrenia. These studies report that weekly marijuana use among teens doubles the risk of developing depression and triples the incidence of suicidal thoughts. 34

• Dr. Andrew Campbell, a member of the New South Wales (Australia) Mental Health Review Tribunal, published a study in 2005 which revealed that four out of five individuals with schizophrenia were regular cannabis users when they were teenagers. Between 75-80 per cent of the patients involved in the study used cannabis habitually between the ages of 12 and 21. 35 In addition, a laboratory-controlled study by Yale scientists, published in 2004, found that THC “transiently induced a range of schizophrenia-like effects in healthy people.”36

• Smoked marijuana has also been associated with an increased risk of the same respiratory symptoms as tobacco, including coughing, phlegm production, chronic bronchitis, shortness of breath and wheezing. Because cannabis plants are contaminated with a range of fungal spores, smoking marijuana may also increase the risk of respiratory exposure by infectious organisms (i.e., molds and fungi). 37

• Marijuana takes the risks of tobacco and raises them: marijuana smoke contains more than 400 chemicals and increases the risk of serious health consequences, including lung damage. 38

• According to two studies, marijuana use narrows arteries in the brain, “similar to patients with high blood pressure and dementia,” and may explain why memory tests are difficult for marijuana users. In addition, “chronic consumers of cannabis lose molecules called CB1 receptors in the brain’s arteries,” leading to blood flow problems in the brain which can cause memory loss, attention deficits, and impaired learning ability. 39

• Carleton University researchers published a study in 2005 showing that current marijuana users who smoke at least five “joints” per week did significantly worse than non-users when tested on neurocognition tests such as processing speed, memory, and overall IQ. 40

Delinquent Behaviors and Drugged Driving:
o In 2002, the percentage of young people engaging in delinquent behaviors “rose with [the] increasing frequency of marijuana use.” For example, according to a National Survey on Drug Use and Health (NSDUH) report, 42.2 per cent of youths who smoked marijuana 300 or more days per year and 37.1 per cent of those who did so 50-99 days took part in serious fighting at school or work. Only 18.2 per cent of those who did not use marijuana in the past year engaged in serious fighting. 41

• A large shock trauma unit conducting an ongoing study found that 17 per cent (one in six) of crash victims tested positive for marijuana. The rates were slightly higher for crash victims under the age of eighteen, 19 per cent of whom tested positive for marijuana. 42

• In a study of high school classes in 2000 and 2001, about 28,000 seniors each year admitted that they were in at least one accident after using marijuana. 43

• Approximately 15 per cent of teens reported driving under the influence of marijuana. This is almost equal to the percentage of teens who reported driving under the influence of alcohol (16 per cent). 44

• A study of motorists pulled over for reckless driving showed that, among those who were not impaired by alcohol, 45 per cent tested positive for marijuana. 45

• The National Highway Traffic Safety Administration (NHTSA) has found that marijuana significantly impairs one’s ability to safely operate a motor vehicle. According to its report, “[e]pidemiology data from road traffic arrests and fatalities indicate that after alcohol, marijuana is the most frequently detected psychoactive substance among driving populations.” Problems reported include: decreased car handling performance, inability to maintain headway, impaired time and distance estimation, increased reaction times, sleepiness, lack of motor coordination, and impaired sustained vigilance. 46
Some of the consequences of marijuana-impaired driving are startling:
The driver of a charter bus, whose 1999 accident resulted in the death of 22 people, had been fired from bus companies in 1989 and 1996 because he tested positive for marijuana four times. A federal investigator confirmed a report that the driver “tested positive for marijuana when he was hospitalized Sunday after the bus veered off a highway and plunged into an embankment.” 47

• In April 2002, four children and the driver of a van died when the van hit a concrete bridge abutment after veering off the freeway. Investigators reported that the children nicknamed the driver “Smokey” because he regularly smoked marijuana. The driver was found at the crash scene with marijuana in his pocket. 48

• A former nurse’s aide was convicted in 2003 of murder and sentenced to 50 years in prison for hitting a homeless man with her car and driving home with his mangled body “lodged in the windshield.” The incident happened after a night of drinking and taking drugs, including marijuana. After arriving home, the woman parked her car, with the man still lodged in the windshield, and left him there until he died. 49

• In April 2005, an eight year-old boy was killed when he was run over by an unlicensed 16 year-old driver who police believed had been smoking marijuana just before the accident. 50

• In 2001, George Lynard was convicted of driving with marijuana in his bloodstream, causing a head-on collision that killed a 73 year-old man and a 69 year-old woman. Lynard appealed this conviction because he allegedly had a “valid prescription” for marijuana. A Nevada judge agreed with Lynard and granted him a new trial. 51 The case has been appealed to the Nevada Supreme Court.52

• Duane Baehler, 47, of Tulsa, Okalahoma was “involved in a fiery crash that killed his teenage son” in 2003. Police reported that Baehler had methamphetamine, cocaine and marijuana in his system at the time of the accident. 53
Marijuana also creates hazards that are not always predictable. In August 2004, two Philadelphia firefighters died battling a fire that started because of tangled wires and lamps used to grow marijuana in a basement closet. 54

MARIJUANA AND INCARCERATION
Federal marijuana investigations and prosecutions usually involve hundreds of pounds of marijuana. Few defendants are incarcerated in federal prison for simple possession of marijuana.
o In 2001, there were 24,299 offenders sentenced in federal court on drug charges. Of those, only 2.3 per cent (186 people) were sentenced for simple possession. 55
In addition, it is important to recognize that many inmates were initially charged with more serious crimes but negotiated reduced charges to simple possession through plea agreements.56

• According to the latest survey data in a 2005 ONDCP study, marijuana accounted for 13 per cent of all state drug offenders in 1997, and of the inmates convicted of marijuana offenses, only 0.7 per cent were incarcerated for marijuana possession alone. 57
THE FOREIGN EXPERIENCE
The Netherlands
o Due to international pressure on permissive Dutch cannabis policy and domestic complaints over the spread of marijuana “coffee shops,” the government of the Netherlands has reconsidered its legalization measures. After marijuana became normalized, consumption nearly tripled – from 15 per cent to 44 per cent – among 18 to 20 year-old Dutch youth. 58
As a result of stricter local government policies, the number of cannabis “coffeehouses” in the Netherlands was reduced – from 1,179 in 199759 to 737 in 2004, a 37 per cent decrease in 7 years.60

• About 70 per cent of Dutch towns have a zero-tolerance policy toward cannabis cafes.61

• In August 2004, after local governments began clamping down on cannabis “coffeehouses” seven years earlier, the government of the Netherlands formally announced a shift in its cannabis policy through the United National International Narcotics Control Board (INCB). According to “an inter-ministerial policy paper on cannabis, the government acknowledged that ‘cannabis is not harmless’ – neither for the abusers, nor for the community.” Netherlands intends to reduce the number of coffee shops (especially those near border areas and schools), closely monitor drug tourism, and implement an action plan to discourage cannabis use. This public policy change brings the Netherlands “closer towards full compliance with the international drug control treaties with regard to cannabis.” 62

• Dr. Ernest Bunning, formerly with Holland’s Ministry of Health and a principal proponent of that country’s liberal drug philosophy, has acknowledged that, “there are young people who abuse soft drugs . . . particularly those that have a high THC [content]. The place that cannabis takes in their lives becomes so dominant they don’t have space for the other important things in life. They crawl out of bed in the morning, grab a joint, don’t work, smoke another joint. They don’t know what to do with their lives.” 63
Switzerland
Liberalization of marijuana laws in Switzerland has likewise produced damaging results. After liberalization, Switzerland became a magnet for drug users from many other countries. In 1987, Zurich permitted drug use and sales in a part of the city called Platzpitz, dubbed “Needle Park.” By 1992, the number of regular drug users at the park reportedly swelled from a “few hundred at the outset in 1987 to about 20,000.” The area around the park became crime-ridden, forcing closure of the park. The experiment has since been terminated. 64
Canada:
After a large decline in the 1980s, marijuana use among teens increased during the 1990s as young people became “confused about the state of federal pot law” in the wake of an aggressive decriminalization campaign, according to a special adviser to Health Canada’s Director General of drug strategy. Several Canadian drug surveys show that marijuana use among Canadian youth has steadily climbed to surpass its 26-year peak, rising to 29.6 per cent of youth in grades 7-12 in 2003. 65
United Kingdom:
In March 2005, British Home Secretary Charles Clarke took the unprecedented step of calling “for a rethink on Labour’s legal downgrading of cannabis” from a Class B to a Class C substance. Mr. Clarke requested that the Advisory Council on the Misuse of Drugs complete a new report, taking into account recent studies showing a link between cannabis and psychosis and also considering the more potent cannabis referred to as “skunk.” 66

• In 2005, during a general election speech to concerned parents, British Prime Minister Tony Blair noted that medical evidence increasingly suggests that cannabis is not as harmless as people think and warned parents that young people who smoke cannabis could move on to harder drugs. 67
THE LEGALIZATION LOBBY
The proposition that smoked marijuana is “medicine” is, in sum, false – trickery used by those promoting wholesale legalization. When a statute dramatically reducing penalties for “medical” marijuana took effect in Maryland in October 2003, a defense attorney noted that “there are a whole bunch of people who like marijuana who can now try to use this defense.” The attorney observed that lawyers would be “neglecting their clients if they did not try to find out what ‘physical, emotional or psychological’” condition could be enlisted to develop a defense to justify a defendant’s using the drug. “Sometimes people are self-medicating without even realizing it,’” he said. 68

Ed Rosenthal, senior editor of High Times, a pro-drug magazine, once revealed the legalizer strategy behind the “medical” marijuana movement. While addressing an effort to seek public sympathy for glaucoma patients, he said, “I have to tell you that I also use marijuana medically. I have a latent glaucoma which has never been diagnosed. The reason why it’s never been diagnosed is because I’ve been treating it.” He continued, “I have to be honest, there is another reason why I do use marijuana . . . and that is because I like to get high. Marijuana is fun.” 69

• A few billionaires-not broad grassroots support-started and sustain the “medical” marijuana and drug legalization movements in the United States. Without their money and influence, the drug legalization movement would shrivel. According to National Families in Action, four individuals – George Soros, Peter Lewis, George Zimmer and John Sperling – contributed $1,510,000 to the effort to pass a “medical” marijuana law in California in 1996, a sum representing nearly 60 per cent of the total contributions. 70

• In 2000, The New York Times interviewed Ethan Nadelmann, Director of the Lindesmith Center. Responding to criticism that the medical marijuana issue is a stalking horse for drug legalization, Mr. Nadelmann stated: “Will it help lead toward marijuana legalization? . . . I hope so.” 71

• In 2004, Alaska voters faced a ballot initiative that would have made it legal for adults age 21 and older to possess, grow, buy, or give away marijuana. The measure also called for state regulation and taxation of the drug. The campaign was funded almost entirely by the Washington, D.C.-based Marijuana Policy Project, which provided “almost all” the $857,000 taken in by the pro-marijuana campaign. Fortunately, Alaskan voters rejected the initiative. 72

• In October 2005, Denver voters passed Initiative 100 decriminalizing marijuana based on incomplete and misleading campaign advertisements put forth by the Safer Alternative For Enjoyable Recreation (SAFER). A Denver City Councilman complained that the group used the slogan “Make Denver SAFER” on billboards and campaign signs to mislead the voters into thinking that the initiative supported increased police staffing. Indeed, the Denver voters were never informed of the initiative’s true intent to decriminalize marijuana. 73

• The legalization movement is not simply a harmless academic exercise. The mortal danger of thinking that marijuana is “medicine” was graphically illustrated by a story from California. In the spring of 2004, Irma Perez was “in the throes of her first experience with the drug ecstasy” when, after taking one ecstasy tablet, she became ill and told friends that she felt like she was “going to die.” Two teenage acquaintances did not seek medical care and instead tried to get Perez to smoke marijuana. When that failed due to her seizures, the friends tried to force-feed marijuana leaves to her, “apparently because they knew that drug is sometimes used to treat cancer patients.” Irma Perez lost consciousness and died a few days later when she was taken off life support. She was 14 years old. 74
STILL, THERE’S GOOD NEWS
Continued Declines in Marijuana Use among Youth
In 2005, the Monitoring the Future (MTF) survey recorded an overall 19.1 per cent decrease in current use of illegal drugs between 2001 and 2005, edging the nation closer to its five-year goal of a 25 per cent reduction in illicit drug use in 2006. Specific to marijuana, the 2005 MTF survey showed:
Between 2001 and 2005, marijuana use dropped in all three categories: lifetime (13%), past year (15%) and 30-day use (19%). Current marijuana use decreased 28 per cent among 8th graders (from 9.2% to 6.6%), and 23 per cent among 10th graders (from 19.8 per cent to 15.2%). 75
Increased Eradication
As of September 20, 2005, DEA’s Domestic Cannabis Eradication/Suppression Program supported the eradication of 3,054,336 plants in the top seven marijuana producing states (California, Hawaii, Kentucky, Oregon, Tennessee, Washington and West Virginia). This is an increase of 315,628 eradicated plants over the previous year. 76

• For the 2005 eradication season, a total of 5 million marijuana plants have been eradicated across the United States. This is a one million plant increase over last year. The Departments of Agriculture and Interior combined have eradicated an estimated 1.2 million plants during this 2005 eradication season. 77
APPENDIX A
Acronyms used in “The DEA Position on Marijuana”
AAP American Academy of Pediatrics
ACS American Cancer Society
AMA American Medical Association
BBC British Broadcasting Company
B.C. Bud British Columbia Bud
BMA British Medical Association
CB1 Cannabinoid Receptor 1: one of two receptors in the brain’s endocannabinoid (EC) system associated with the intake of food and tobacco dependency.
CMCR Center for Medicinal Cannabis Research
DASIS Drug and Alcohol Services Information System
DEA Drug Enforcement Administration
FDA Food and Drug Administration
HIV Human Immunodeficiency Virus
INCB International Narcotics Control Board
IOM Institute of Medicine
IOP Intraocular Pressure
LSD Diethylamide-Lysergic Acid
MS Multiple Sclerosis
NHTSA National Highway Traffic Safety Administration
NIDA National Institute on Drug Abuse
NMSS National Multiple Sclerosis Society
NORML National Organization for the Reform of Marijuana Laws
NSDUH National Survey of Drug Use and Health
ONDCP Office of National Drug Control Policy
TEDS Treatment Episode Data Set
THC Tetrahydrocannabinol

ENDNOTES
1 As of April 2006, the eleven states that have decriminalized certain marijuana use are Arizona, Alaska, California, Colorado, Hawaii, Maine, Montana, Nevada, Oregon, Rhode Island, Vermont, and Washington. In addition, Maryland has enacted legislation that recognizes a “medical marijuana” defense
2 “Inter-Agency Advisory Regarding Claims That Smoked Marijuana Is a Medicine.” U.S. Food and Drug Administration, April 20, 2006. <

http://www.fda.gov/bbs/topics/NEWS/2006/NEW01362.html>.

3 “Policy H-95.952 ‘Medical Marijuana.’” American Medical Association. See also, American Medical Association, Featured Council on Scientific Affairs. “Medical Marijuana (A-01).” June 2001. In 2001, the AMA updated their policy regarding medical marijuana reflecting the results of this study. It should be noted that a few medical organizations have offered limited support to the concept of “medical” marijuana. For example, the American Academy of Family Physicians has said that it opposes the use of marijuana “except under medical supervision and control, for specific medical indications.” Largely at the urging of one activist – a lobbyist and former Board member of NORML – the American Nurses Association has endorsed “medical” marijuana under “appropriate prescriber supervision,” and the American Academy of HIV Medicine, a group of about 1,800 members founded in 2000, has taken the view that marijuana should not only be made available for “medical” use, but should be excluded altogether as a Schedule I drug
4 “Experts: Pot Smoking Is Not Best Choice to Treat Chemo Side-Effects.” American Cancer Society. 22 May 2001.

http://www.cancer.org/docroot/NWS/content/update/NWS_1_1xU_

Experts__Pot_Smoking_Is_Not_Best_Choice_to_Treat_Chemo_Side_Effects.asp
(9 March 2005).
5 Committee on Substance Abuse and Committee on Adolescence. “Legalization of Marijuana: Potential Impact on Youth.” Pediatrics Vol. 113, No. 6 (6 June 2004): 1825-1826. See also, Joffe, Alain, MD, MPH, and Yancy, Samuel, MD. “Legalization of Marijuana: Potential Impact on Youth.” Pediatrics Vol. 113, No. 6 (6 June 2004): e632-e638h.
6 National MS Society. “Information Sourcebook.” National MS Society. December 2004. <
www.nationalmssociety.org/pdf/sourcebook/marijuana.pdf> (1 April 2005).
7 “Doctors’ Fears at Cannabis Change.” BBC News. 21 January 2004.
8 Manchester Online. “Doctors Support Drive Against Cannabis.”
Manchester News. 21 January 2004. <

http://www.manchesteronline.co.uk/

news/s/78/78826_doctors_support_drive_against_cannabis.html> (25 March 2005).
9 Joffe, Alain, MD, MPH, Yancy, Samuel W., MD, the Committee on Substance Abuse and the Committee on Adolescence, Technical Report: “Legalization of Marijuana: Potential Impact on Youth”, American Academy of Pediatrics, 6 June 2004.
10 Institute of Medicine. “Marijuana and Medicine: Assessing the Science Base.” (1999). Summary. <
http://www.nap.edu/html/marimed> (12 April 2005).
11 Id.
12 Institute of Medicine. “Marijuana and Medicine: Assessing the Science Base.” (1999). Executive Summary. <
http://www.nap.edu/html/marimed> (11 January 2006).
13 Institute of Medicine. “Marijuana and Medicine: Assessing the Science Base.” (1999). Summary. <
http://www.nap.edu/html/marimed> (11 January 2006).
14 Institute of Medicine. “Marijuana and Medicine: Assessing the Science Base.” (1999). Summary. <
http://www.nap.edu/html/marimed> (11 January 2006).
15 Benson, John A., Jr. and Watson, Stanley J., Jr. “Strike a Balance in the Marijuana Debate.” The Standard-Times. 13 April 1999.
16 DEA, Office of Diversion Control. 8 May 2006.
17 “CMCR Mission Statement.” Center for Medicinal Cannabis Research. <
http://www.cmcr.ucsd.edu/geninfo/mission.htm> (3 February 2005).
18 DEA, Office of Diversion Control. 6 January 2006.
19 Marijuana Potency Monitoring Project. “Quarterly Report #87.” Marijuana Potency Monitoring Project. 8 November 2004.
20 “BC Bud: Growth of the Canadian Marijuana Trade.” Drug Enforcement Administration, Intelligence Division. December 2000.
21 “Teens at High Risk for Pot Addiction.” The Seattle Post-Intelligencer. 6 January 2004.
22 Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. Treatment Episode Data Set (TEDS) 1993-2003: National Admissions to Substance Abuse Treatment Services. November 2005, Table 5.1b. <
http://wwwdasis.samhsa.gov/teds03/teds_2003_rpt.pdf> (12 January 2006).
23 Id.
24 “Marijuana Myths & Facts: The Truth Behind 10 Popular Misperceptions.” Office of National Drug Control Policy. <
http://www.whitehousedrugpolicy.gov/publications/marijuana_myths_facts/index.html> (12 January 2006).
25 Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. Overview of Findings from 2004 National Survey on Drug Use and Health. September 2005.
26 Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. Treatment Episode Data Set (TEDS) 1993-2003: National Admissions to Substance Abuse Treatment Services. November 2005. Page 74; Table 2.1b. <
http://wwwdasis.samhsa.gov/teds03/teds_2003_rpt.pdf> (12 January 2006).
27 Id., Tables 2.1a and 5.1a. There were 284,361 primary marijuana admissions in 2003, with 99,122 of those being juvenile marijuana admissions, meaning that there were 185,239 adult marijuana admissions.
28 “What Americans Need to Know about Marijuana.” Office of National Drug Control Policy. October 2003.
29 Gfroerer, Joseph C., et al. “Initiation of Marijuana Use: Trends, Patterns and Implications.” Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. July 2002. Page 71.
30 “Non-Medical Marijuana II: Rite of Passage or Russian Roulette?” CASA Reports. April 2004. Chapter V, Page 15.
31 “What Americans Need to Know about Marijuana,” 9.
32 Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. “Daily Marijuana Users.” The NSDUH Report. 26 November 2004.
33 Furber, Matt. “Threat of Meth-’the Devil’s Drug’-increases.” Idaho Mountain Express and Guide. 28 December 2005.
34 “Drug Abuse; Drug Czar, Others Warn Parents that Teen Marijuana Use can Lead to Depression.” Life Science Weekly. 31 May 2005.
35 Kearney, Simon. “Cannabis is Worst Drug for Psychosis.” The Australian. 21 November 2005.
36 Curtis, John. “Study Suggests Marijuana Induces Temporary Schizophrenia-Like Effects.” Yale Medicine. Fall/Winter 2004.
37 “Marijuana Associated with Same Respiratory Symptoms as Tobacco,” YALE News Release. 13 January 2005. <
http://www.yale.edu/opa/newsr/05-01-13-01.all.htm> (14 January 2005). See also, “Marijuana Causes Same Respiratory Symptoms as Tobacco,” January 13, 2005, 14WFIE.com.
38 “What Americans Need to Know about Marijuana,” page 9.
39 “Marijuana Affects Brain Long-Term, Study Finds.” Reuters. 8 February 2005. See also: “Marijuana Affects Blood Vessels.” BBC News. 8 February 2005; “Marijuana Affects Blood Flow to Brain.” The Chicago Sun-Times. 8 February 2005; Querna, Elizabeth. “Pot Head.” US News & World Report. 8 February 2005.
40 “Neurotoxicology; Neurocognitive Effects of Chronic Marijuana Use Characterized.” Health & Medicine Week. 16 May 2005.
41 Department of Health and Human Services, Substance Abuse and Mental Health Services Administration (SAMHSA), Office of Applied Sciences. “Marijuana Use and Delinquent Behaviors Among Youths.” The NSDUH Report. 9 January 2004.
42 “Drugged Driving Poses Serious Safety Risk to Teens; Campaign to Urge Teens to ‘Steer Clear of Pot’ During National Drunk and Drugged Driving (3D) Prevention Month.” PR Newswire. 2 December 2004.
43 O’Malley, Patrick and Johnston, Lloyd. “Unsafe Driving by High School Seniors: National Trends from 1976 to 2001 in Tickets and Accidents After Use of Alcohol, Marijuana and Other Illegal Drugs.” Journal of Studies on Alcohol. May 2003.
44 Id.
45 “White House Drug Czar Launches Campaign to Stop Drugged Driving.” Office of National Drug Control Policy Press Release. 19 November 2002.
46 Couper, Fiona, J., Ph.D., page 11.
47 Orange County Register. “Nation: Drug Test Positive for Driver in Deadly Crash.” Orange County Register. 14 May 1999.
48 Edmondson, Aimee. “Drug Tests Required of Child Care Drivers – Fatal Crash Stirs Change; Many Already Test Positive.” The Commercial Appeal. 2 July 2003.
49 McDonald, Melody and Boyd, Deanna. “Jury Gives Mallard 50 Years for Murder; Victim’s Son Forgives but Says ‘Restitution is Still Required.’” Fort Worth Star Telegram. 28 June 2003.
50 “Boy, 8, Who Was Struck While Riding Bike Dies.” The Dallas Morning News. 25 April 2005.
51 “Lastest News in Brief from Northern Nevada.” The Associated Press State & Local Wire. 30 April 2005.
52 Washoe County District Attorney’s Office. 6 January 2006.
53 The Associated Press. “Police: Driver in Fatal Crash had Drugs in System.” The Associated Press. 1 June 2003.
54 The Associated Press. “Murder Charges Filed in Blaze that Killed Two Firefighters.” The Associated Press. 21 August 2004.
55 Office of National Drug Control Policy. “Who’s Really in Prison for Marijuana?” May 2005. Page 22.
56 “Marijuana Myths & Facts.” Page 22.
57 “Who’s Really in Prison for Marijuana? Page 20.
58 “What Americans Need to Know about Marijuana,” ONDCP, Page 10.
59 Dutch Health, Welfare and Sports Ministry Report. 23 April 2004.
60 INTRAVAL Bureau for Research & Consultancy. “Coffeeshops in the Netherlands 2004.” Dutch Ministry of Justice. June 2005. <

http://www.intraval.nl/en/b/b45.html>.

61 Id.
62 International Narcotics Control Board. “INCB Welcomes ‘Crucial and Significant Change in Dutch Cannabis Policy.’” United Nations Information Service. 2 March 2005. The action plan to discourage cannabis use includes elements such as drug prevention campaigns, mass-media anti-drugs campaign, increased treatment efforts to cannabis users, and encouragement of administrative and criminal law enforcement efforts. See also: “International Narcotics Control Board Annual Report Focuses on Need to Integrate Drug Demand, Supply Strategies.” SOC/NAR/924 Press Release. 3 February 2005. <
http://www.un.org/News/Press/docs/2005/socnar924.doc.htm> (18 March 2005); “Press Briefing by International Narcotics Control Board.” 3 January 2005. (18 March 2005).
63 Collins, Larry. “Holland’s Half-Baked Drug Experiment.” Foreign Affairs Vol. 73, No. 3. May-June 1999: Pages 87-88.
64 Cohen, Roger. “Amid Growing Crime, Zurich Closes a Park it Reserved for Drug Addicts.” The New York Times. 11 February 1992.
65 Adlaf, Edward M. and Paglia-Boak, Angela, Center for Addiction and Mental Health, Drug Use Among Ontario Students, 1977-2005, CAMH Research Document Series No. 16. The study does not contain data on marijuana use among 12th graders prior to 1999. See also: Canadian Addiction Survey, Highlights (November 2004) and Detailed Report (March 2005), produced by Health Canada and the Canadian Executive Council on Addictions; Youth and Marijuana Quantitative Research’ 2003 Final Report, Health Canada; Tibbetts, Janice and Rogers, Dave. “Marijuana Tops Tobacco Among Teens, Survey Says: Youth Cannabis Use Hits 25-Year Peak,” The Ottawa Citizen, 29 October 2003.
66 Koster, Olinka, Doughty, Steve, and Wright, Stephen. “Cannabis Climbdown.” Daily Mail (London). 19 March 2005. See also. Revill, Jo, and Bright, Martin. “Cannabis: the Questions that Remain Unanswered.” The Observer. 20 March 2005; Steele, John and Helm, Toby. “Clarke Reviews “Too Soft” Law on Cannabis.” The Daily Telegraph (London). 19 March 2005; Brown, Colin. “Clarke Orders Review of Blunkett Move to Downgrade Cannabis.” The Independent (London). 19 March 2005.
67 “Blair’s ‘Concern’ on Cannabis.” The Irish Times. 4 May 2005. See also, Russell, Ben. “Election 2005: Blair Rules Out National Insurance Rise.” The Independent (London). 4 May 2005.
68 Craig, Tim. “Md. Starts to Allow Marijuana Court Plea; Penalty Can be Cut for Medicinal Use.” The Washington Post. 1 October 2003, sec B.
69 From a videotape recording of Mr. Rosenthal’s speech, as shown in “Medical Marijuana: A Smoke Screen.”
70 “A Guide to Drug Related State Ballot Initiatives.” National Families in Action. 23 April 2002. <
http://www.nationalfamilies.org/guide/california215.html> (31 March 2005).
71 Wren, Christopher S. “Small But Forceful Coalition Works to Counter U.S. War on Drugs.” The New York Times, 2 January 2000.
72 Brant, Tataboline. “Marijuana Campaign Draws in $857,000.” The Anchorage Daily News. 30 October 2004.
73 Gathright, Alan. “Pot Backers Can’t Stoke Hickenlooper.” Rocky Mountain News. 27 October 2005.
74 Stannard, Matthew B. “Ecstasy Victim Told Friends She Felt Like She Was Going to Die.” The San Francisco Chronicle, 4 May 2004. The Chronicle reported that Ms. Perez was given ibuprofen and “possibly marijuana,” but DEA has confirmed that the drug given to her was indeed marijuana.
75 Monitoring the Future, 2005. Supplemented by information from the Office of National Drug Control Policy press release on the 2005 MTF Survey, December 19, 2005.)
76 DEA Domestic Cannabis Eradication/Suppression Program, 2005 eradication season.
77 Id.
Source: DrugWatch International January 2010

Motivational interviewing can yield excellent results and the basic skills and techniques are easy to learn. Dr Malcolm Thomas sets out the basics of promoting behaviour change

Helping patients or clients to change their behaviour can be frustrating. As professionals, we can get into a cycle of giving advice and making suggestions, only to feel that everything we suggest is being rejected. Specialist workers often have some training in more effective techniques – this article is aimed at frontline staff, most of whom will not have had such training.
There is now rather compelling evidence that the approach known as motivational interviewing produces better results than standard care (also called ‘business as usual’ or ‘finger wagging’). A full motivational interview takes between
45 and 60 minutes. The necessary training takes two, three or more days so it’s not surprising that this has been the preserve of specialists. However, the insights and techniques of motivational interviewing are available to ‘ordinary’ practitioners. I work for a training company and it’s our contention that everyone whose job includes counselling patients or clients regarding behaviour
change can enhance their professional effectiveness with some understanding, and judicious use, of relevant techniques.
Each of the following techniques takes no more than a few minutes to use and frontline practitioners can use them flexibly in relevant professional conversations. Regard the list as a toolkit from which the relevant tool can be unpacked as needed.

Many clients exhibit two or more behaviours that may profitably be changed, such as alcohol, drug use and diet. Usually it’s the professional who chooses which one to talk about, but allowing the client to choose the focus may enhance motivation. This can be achieved by running verbally through the options as the professional sees them and inviting the client to choose, such as:
‘It looks there are three things we could talk about today. Firstly your drug use, secondly your drinking and thirdly your diet. Does that sound right?’ Then, if the client agrees: ‘OK, so which would you like us to focus on today?’ People can be a bit vague about their habits. A typical answer to ‘how much alcohol do you drink’ is likely to be something like ‘Well, that’s a good question. It’s hard to say. Depends on this and that.’ It’s usually profitable to clarify what is going on at an early stage in your
professional relationship. A recommended technique is the ‘typical day’ question. For example, ‘I wonder if I could spend a couple of minutes learning more about your drinking? Can I ask you to talk me through a typical day, starting when you wake up
and finishing when you go to bed? Tell me where you go, what you do and where your drinking fits in.’ Variations on this include asking about a specific day (yesterday, last Saturday) or a typical week (which can be better for some behaviours). It’s normally very helpful to gauge the client’s readiness to change or consider changing. This may be apparent from things they have said and it certainly can emerge naturally from the conversation, but this is not always the case. While it’s rare for there to be no real clue, it can often be very unclear just how much readiness there is to change. It’s helpful to break readiness to change down into two components – importance and confidence. One strategy is to ask specifically about these in turn, using ‘scaling questions’. For example, ‘Can I just ask you a couple of questions? On a scale of one to ten, how important is it for you to cut down your drug use?’ Say the client responds with ‘Oh, I don’t know. Maybe around a three,’ your response could be ‘I see – thanks. Can I ask a similar question? On a scale of one to ten, if you decided to cut down, how confident would you be that you could make the change?’ Their response might be: ‘That’s a good question. Maybe six-ish. I cut down quite well for a while once. I think I could do that again.’

One advantage of this approach is that you can use it as a launch pad for further exploration, such as: ‘You told me you were at three or four for importance. So can I ask you why three and not one or two?’ ‘Well, it does sometimes get me into trouble. I’d like to think I had a bit more control over it and that it didn’t dominate my life quite so much.’ ‘Alright, so what would have to happen to move that score up to say five or six?’ ‘Well, if I got properly sick with it, I think that might do it.’ People aren’t daft. They indulge in unhealthy behaviours because there’s a payoff. Being overweight is a side effect of eating, which is usually pleasurable. Substance users get some sort of ‘high’ from their substance, or a relief from withdrawal effects if dependent. Behaviours have a social context and many people enjoy doing things with friends, whether smoking, drinking or injecting.
An axiom of motivational interviewing is that our client can see pros and cons to their behaviour. Rather than offering our professional opinion, we can help by allowing the client to bring these out into the open – and then feed it back to them: ‘Can I just try to understand a bit better? Can I ask you about the pros and cons of your marijuana use? First, what are the pros of smoking it from your point of view, the things you like about smoking marijuana? ‘Well, it relaxes me a bit, you know. And when I light up a joint with my mates, we have a good laugh. And to be honest, I prefer a smoke to a drink because you don’t
get the hangovers – you know what I mean?’ ‘Yes, I think I see that. Ok, what about the cons? The things you don’t like so much?’ ‘Well, it sometimes costs me quite a bit you know. And if I get really stoned, then I miss half the day, which isn’t right. And my girlfriend isn’t keen – I think she might not stand for it forever.’ ‘Can I recap then? You’re telling me that it relaxes you, that you do it with your mates and that you prefer it to alcohol. On the other hand, it can cost a lot, you sometimes miss half a day and your girlfriend doesn’t like it?’ ‘That’s about right, yeah.’ ‘Where does that leave you today?’ This can really help in our efficient use of interview time. The client response usually tells us if they are ready to go further and get involved in change talk – or alternatively it may be clear that it isn’t profitable to take things any further today.

At any point in the discussion, resistance may emerge. It is tempting to meet resistance with reasoned argument – pointing out all the scientific reasons on the side of a behaviour change. Unfortunately, this usually has the effect of stiffening resistance. For example, ‘You really need to lose weight you know.’ ‘I guess so.’ ‘I think you should go on a diet.’ ‘I can’t because…’ This is known as negative self-talk. It has been shown that an increase in the amount of negative self-talk in an interview is associated with a lower chance of behaviour change occurring. It seems prudent to avoid provoking such statements. For example, ‘I get the impression I may be pushing you a bit too far here. Shall we stop talking about this today?’ ‘No… It’s ok, go on. It’s just that this is difficult for me to get my head around.’ This is known as ‘rolling with resistance’. It can be a very effective tactic to
prevent the emergence of negative self-talk. It demands that professionals should be on the lookout for signs of resistance at pretty much any stage in a behaviour change discussion.

Most of us who work with clients develop a well-polished series of mini-lectures by way of explaining all the regular things that come up and need explaining. Unfortunately, these mini-lectures may not really be wanted. Or else, we may fail to address important questions on the mind of the client. A mini-seminar might be better. A useful way of looking at this is ‘elicit – provide – elicit’. Elicit any questions or information needs and provide answers or information in response. When it comes to action talk, it is better to provide a range of options to be chosen from. Finally, elicit a response – find out how your information has been received. An example: ‘Can I explain anything to you, answer any questions?’ ‘Well, have you got any information about how many units are in my various drinks. And what do you think I should do to cut down?’ ‘Ok. Let’s see. This leaflet is good for information about units. How does this look?’ ‘Very clear, actually. Can I have that?’ ‘Definitely – it’s for you to take away. Anything catch your eye?’ ‘Yes. Look at this about glasses of wine. I had no idea there were so many units.’ This approach can lead to more effective use of professional time, while again minimising the risk of negative self-talk developing. Motivational interviewing gives better results than ‘business as usual’ and many of the individual skills and techniques are easy enough to learn and can be used in routine conversations with patients or clients. I’ve outlined and demonstrated a range of the most useful
micro-skills, with examples of how they might fit into your conversations but a very readable and immensely practical textbook I’d recommend to any DDN reader is Health Behavior Change – a guide for practitioners by Stephen Rollnick, Chris Butler
and Pip Mason (Churchill Livingstone) – despite the spelling, it’s a British book.

Dr Malcolm Thomas is director of national training provider Effective Professional
Interactions Ltd. www.effectivepi.co.uk

Source: drinkanddrugsnews Jan 2010

The last few months have seen a dramatic increase in use of –
and media interest in – ‘legal highs’, especially mephedrone or ‘miaow/meow’.
David Gilliver takes a look at a legislative minefield

When the government announced its intention last year to ban a range
of ‘legal highs’ and make them class C drugs, Release accused it of
‘chasing its tail’ in an attempt to ‘stay ahead of the demand for drugs
and those who supply them’ (DDN, 7 September 2009, page 4).
The chemicals were BZP and related piperazines, GBL and a related chemical
and the synthetic cannabinoids used to make smoking products like Spice.
Release’s accusation seemed to be vindicated very quickly, however. Anecdotal
evidence soon started to filter through about a sharp increase in use of the
stimulant mephedrone (4-methylmethcathinone), known as ‘miaow’. After the drug was implicated in the death of a young woman in Brighton late last year, there was a rash of mephedrone stories in the press, followed – a couple of weeks later – by stories about how that coverage had led to a huge boost in sales, with many online suppliers selling out altogether. Luci Hammond is a young person’s alcohol worker at Brighton-based service ruok? She started to notice a very sharp increase in miaow use in the second half of last year. ‘It just hit very quickly,’ she says. ‘We started getting reports of it being used by young people and we had parents and professionals asking questions about it, but since then we’ve had a lot of young people coming to us themselves.’

There has been much talk about the drug’s growing use in clubs, with people
turning to it because of the poor quality of available ecstasy and cocaine – as little as 2 per cent purity in the latter case (DDN, 21 September 2009, page 5).
However, what Hammond has found – and what the press has been quick to pick
up on – is the worrying popularity of the drug among children. So far, her youngest client to have used miaow is 12. The majority are 14 and up, but ‘14 is common’ she says. Where are they taking it – presumably they can’t get into nightclubs? ‘The majority of them can’t, but there are under-18 nights where they use it, as well as at parties and out on the streets. They’ll sit in parks and cemeteries, so they’re putting themselves at risk just through the location.’
And what about other legal highs? ‘This is the big one. We’re hearing bits about
BZP and Spice but nothing compared to this.’ John Ramsey runs the TICTAC drug-testing database at St. George’s, University of London, and has seen a dramatic increase in the use of legal highs. ‘We analyse the contents of club amnesty bins and we test purchase stuff from websites – that’s how we come to be pretty up-to-date on new and emerging compounds,’ he says. ‘We’ve been doing this for ten or 15 years and at one time it was really unusual to find anything new. Now we find something new virtually weekly. We go to Glastonbury each year and there were huge amounts of mephedrone there last
time – there was one seizure of 120g. Two or three years ago there wasn’t any.’
Legal highs are available in ‘head’ shops but anecdotal evidence – and the
scale of use being reported – would suggest that most people are buying them
quickly and easily online. Indeed, many of the press mephedrone stories have
practically been guides to getting hold of the drug, couched in obligatory
disapproving language. ‘If you go online and put in ‘legal highs’ you get hundreds of results,’ says Renato Masetti, training coordinator at Suffolk DAAT, who puts on conference workshops to essentially it’s an online phenomenon – you’ve got comments, forums, you can write in and say which one was good and which wasn’t, just like on Amazon. There’s a whole community out there – the online forums have gone mad.’

But presumably most 13 and 14-year-olds aren’t buying the drugs online,
unless they’re using their parents’ credit cards? ‘A lot of our young people are
getting it from friends, but we’re hearing of dealers specialising in miaow and
selling it to school-age children,’ says Hammond. ‘They’re buying it in bulk online,
possibly cutting it, and selling it on. We’ve also heard reports of young people
dealing because they think it’s risk-free, a legal substance. At the start the reports were “you get no comedown, it’s all legal”. It was seen as pure – everything sounded lovely. Now it’s being used more frequently we’ve discovered it’s not so lovely.’ She’s started to see behaviour change in her clients, like paranoia, aggression and anxiety, and even signs of dependency. ‘We’ve heard about shakes and poor co-ordination with withdrawal,’ she says. How widespread is the problem in Brighton? ‘I would say in terms of speaking to young people, it’s probably about five a day,’ she says. ‘One young person will tell us that their friends are doing it, or a teacher will ring up and say that the whole class is talking about it. I’m a young person’s alcohol worker but almost all my clients have tried miaow, even the ones who’ve always said “I’d never do drugs”,
because it isn’t considered a dangerous drug. This is the message we’re trying to
get across – that it does seem to be a dangerous drug.’ How are they taking it? ‘Most are snorting, which is what we’re trying to advise against – if you are going to use it we’d rather it was bombed [swallowed]. We’ve had people smoking it as well, in a bong or cone. But it’s really painful to snort, and we’re hearing of nosebleeds that recur for days afterwards, as well as spinal and joint ache. And miaow isn’t enough now – they want to do it with ketamine or acid or nitrous oxide. There seems to be a cocktail culture out there.’

Clubbers of the ’80s and ’90s were sometimes described as the ‘guinea pig
generation’, as no one really knew what effects long-term ecstasy use might have. But with mephedrone and other legal highs – anecdotal chat room accounts aside – there really is no information, because there’s been no research. ‘How can there be – who’s going to pay for it?’ says John Ramsey. ‘For example the cannabinoids in things like Spice are completely untested and yet they clearly work – the legislation has got to control about 240 of the things. Who can research 240 new chemical compounds?’ Indeed even the names seem something of a moveable feast, with a variety of drugs passed off as miaow depending on who’s selling it and in what part of the country. ‘There are fewer dealers in the chain and there does seem to be some evidence of people selling allegedly illegal drugs which when they’re tested are found to be legal, so you have this fascinating phenomenon of the illegal market pinching from the legal market and pretending it’s illegal – because people think illegal stuff is better,’ says Masetti. ‘We’ve been told that miaow can be made up of different compounds, and it’s also being mixed with stuff now,’ says Hammond. ‘It started off a few months ago at £15 per gram and now it’s £3.50. You can get pure mephedrone but you don’t really know from mix to mix what you’re getting.’ However the miaow John Ramsey has tested has been consistent. ‘Every time we’ve analysed it it’s been 4-methylmethcathinone, and there appear to be vast amounts of it about. I get a lot of calls from police officers who are being asked what they’re going to do about it. Of course the answer is “nothing”, because it’s not illegal.’

The legal status does really appear to mean that many people think the drugs
are safe and harmless. ‘We’ve had parents saying “we’re telling our kids not to do
illegal things” and they’re saying “but it’s not illegal” says Hammond. ‘I don’t think many teenagers would think that they could buy something from a high street head shop that’s going to cause them to end up in an A&E department,’ says Ramsey. ‘They wouldn’t think people would be allowed to sell things that would do that.’ And A&E, it seems, is not an exaggeration. Luci Hammond visits regularly and whereas before her clients were there through drink or illegal drugs, now it’s often miaow. ‘We’re starting to see people coming in with miaow overdoses – anxiety, excessive aggression, disturbed sleep, being sick. One parent brought her child in because he was screaming and shaking in his sleep and they put that down to a miaow overdose. One client did it at a party and kept collapsing – his knees would just buckle underneath him.’ ‘I’ve seen a couple of forums where there was talk about it causing blue knees and blue elbows,’ adds John Ramsey. ‘That means it could be an inhibitor of muscle metabolism – that’s not beyond the realms of possibility.’ Does he think the government is really chasing its tail when it comes to legislating on legal highs? Won’t the chemists just come up with a slightly different compound? ‘To some extent, but the new legislation includes piperazines – BZP and that whole family – and it is proper generic classification, not a list of compounds, so it should cut off the piperazines as a family. While there’s always scope for somebody to innovate something that hasn’t been foreseen, it makes it much more difficult to do that. But obviously the legislation completely ignores the cathinones, like mephedrone, which haven’t even been risk-assessed yet. The alternative is to do nothing, but you’ve got teenagers buying chemicals which are completely untested for safety and using them as drugs – you’ve got to try and prevent that.’ ‘It’s an interesting challenge,’ says Renato Masetti. ‘I think we need to be creative about other responses, rather than just straight legislation. You’ve got the example of GHB and GBL – GHB was made class C a while back and yet you found the same amount of seizures of GHB as GBL. The fact that you’ve classified doesn’t seem to have made much difference. Legislation is a very heavy hammer, and it’s too clumsy with chemicals that can be altered quickly. Legislation becomes really difficult because if it’s too broad it captures useful products in industry.’ He’s also unconvinced that people are switching to these drugs on a large scale because of the declining quality of cocaine and ecstasy. ‘That upshares/downshares has been going on for ages – purity rates go up and down. I think to some extent this
is probably a separate thing – experimental people who don’t wish to break the law and are looking for legal alternatives. This happened years ago when there was a big ‘herbal highs’ thing, but they were awful, caffeine-based things. I think people have been quite surprised this time – they’ve found that actually they’re effective.’

In the myriad of online forums, the effects of mephedrone are often described
as a kind of mix of amphetamine and MDMA, but with a shorter-lasting effect than the latter. ‘The chemical structures are based on the khat plant, but the
compounds have nothing to do with the plant – they’re modifications of a molecule derived from the plant – so from a chemical point of view you’d predict that it’s going to be a stimulant,’ says Ramsey. ‘I can’t see how it’s likely to be
empathogenic like MDMA, it’s more likely to be like amphetamine or even
methylamphetamine. But it’s never been used as a drug before so there’s no data
on its half-life, its potency or anything.’ The similarity with methylamphetamine/ methamphetamine is borne out by the behaviour of Hammond’s clients. ‘We’re hearing of people aged 14 or 15 who are doing three-day binges, seven-day binges. They’re not able to go to school and we’ve had people saying “I feel like I’m dying, I can’t stop.” We’ve had people who’ve used illegal drugs saying this is the most addictive thing they’ve ever had.’

So what’s the answer – is it better education? ‘Absolutely, but it’s a fine line
between educating and promoting,’ says Ramsey. ‘We’re used to that in the drug
field, but we do need some sort of generic education.’ What about the FRANK ‘crazy chemist’ campaign launched last year? (DDN, 5 October 2009, page 4). ‘That’s not based on any sound knowledge,’ he says. ‘Just anecdotal observations.’ ‘I’m a trainer so I’m biased but I think training is really important,’ says Masetti. ‘It’s important for drug teams to know the specifics about these drugs, but not because treatment is going to be any different from what they’re doing already – it’s more around confidence-building. I’d like to see awareness-raising in services so they can engage with these clients who don’t see themselves as traditional illegal drug users. We know very little about these drugs but because they’re synthetic mimickers that work similarly to the illegal drugs they’re mimicking, the treatments will be very similar – you don’t need to learn any special techniques. But we do need to get some research going on these drugs asap, along with general harm reduction advice.’ Late last year two members of the Advisory Council on the Misuse of Drugs (ACMD) told The Times that the council had serious concerns about drugs like mephedrone and was proposing a more rapid system of appraisal, and the ACMD had in fact constituted a working group on cathinone compounds of which John Ramsey was a member. ‘But all of that’s collapsed now because everybody’s resigned,’ he says. Sacked ACMD chair Prof David Nutt has said his new organisation, the Independent Council on Drug Harms, plans to produce guidance on legal highs, but they will be operating outside of government (see page 4). ‘It’s definitely getting to the “something must be done” stage,’ says Ramsey. ‘It’s not going to go away, and it’s not likely to be controlled by the Misuse of Drugs Act in the foreseeable future as they can’t legislate under that without ACMD.

ACMD would normally conduct a risk assessment and then recommend control or
non-control but, given the disarray ACMD seems to be in, the alternative is the
same process through the EMCDDA in Lisbon. They’ve collected information about
these compounds, and it may well be that they’ll do a risk assessment and
recommend control throughout Europe, with all member states expected to follow.’ In fact the EMCDDA has called Britain the online capital of Europe for legal highs, with 37 per cent of all retailers operating from the UK compared to just 14 per cent in the Netherlands. ‘True, but we bought some from a website that had a UK address – the credit card was debited in France and the material was shipped from New Zealand,’ says Ramsey. ‘But one thing is certain – there’s very big money in it.
Source: drinkanddrugsnews 18 January 2010

By Mary Brett

In the last few years increasing concern has been expressed about the association of cannabis with mental illness. The number of cannabis users is going up. In the USA in some age groups, almost as many people are smoking cannabis as cigarettes. Children are starting to use the drug at an increasingly early age, more and more studies are emerging which link cannabis use with psychological and social problems, demand for treatment for cannabis users is rising and there is a change in the THC content of some cannabis varieties. Selectively bred strains such as skunk and nederweed have much greater percentages of THC than did the marijuana of the sixties and seventies.

Jan Ramstrom, the Swedish psychiatrist and expert on substance abuse who wrote Adverse Health Consequences of Cannabis Use (2003) said, “ At present we find ourselves in a curious situation where researchers and clinicians are becoming even more concerned, while the general public, not least in Europe, seems to grow less concerned”.

He also said, “It is worth mentioning that the opiates (heroin etc), apart only from the development of dependence, produce far fewer toxic psychiatric complications than do cannabis preparations”

Two fundamentally different psychotic manifestations are involved.

Toxic psychosis:
Cannabis-induced psychotic disorder, recognised as a diagnostic unit in the DSM 1V (Diagnostic and Statistical Manual of Mental Disorders) is caused by the toxic effects of the drug and involves a group of brain damage syndromes. The symptoms are caused by cannabis consumption and subside when drug use ceases. The use of anti-psychotic medicines to eliminate any residual symptoms means most patients make a full recovery unless he or she resumes the taking of cannabis or indeed other drugs. Symptoms of delirium often dominate, i.e. bewilderment and memory disturbance. Paranoia, hallucinations and aggression alternating with euphoria also occur. There is usually an absence of any heredity factor.

Functional psychosis:
“Functional” in this sense applies to the absence of organic damage. Cullberg 2000, said that there probably is some organic damage, possibly taking the form of some subtle vulnerability as yet unknown. This category covers schizophrenia and schizophrenia-like psychosis which usually runs a chronic course. Symptoms of delirium are absent and there is often a feeling of outside interference with thought. Often the person has a “premorbid personality” with extreme reserve, loss of interest and bizarre suspicious ideas.

To quote Jan Ramstrom again, “…what we are dealing with here are the most profound disturbances known to psychiatry; even when they are short-lived, such disturbances can leave marks on those affected and on their families which may remain for many years or even be of life-long duration.…..there is both an abuse condition and a serious mental disorder. These “dual disorders” are among the most difficult to assess in the whole of psychiatry. Moreover, conditions of this type not rarely make demands on the most costly resources available in the field of psychiatric care”.

Early Studies.
Papers as early as the 1970s saw researchers connecting cannabis consumption with psychosis.

1972. Tennant and Groesbeck studied American soldiers in Europe and found large numbers abusing drugs mostly hashish. Between 1968 and 1971, the number of acute psychotic reactions, not necessarily leading to schizophrenia increased from 16 in 1968 to 77 in 1971, an almost 5-fold increase in 4 years. They concluded that hashish smoking was the major contributor.

1974. Chopra and Smith described 200 patients admitted to a Calcutta psychiatric hospital between 1963 and 1968 with psychotic symptoms following cannabis use. Most cases were preceded by the ingestion of large quantities. One third had no previous psychiatric history and the symptoms were the same regardless of their history. The most potent cannabis preparations resulted in psychotic reactions in the shortest period of time.

1974. DA Treffert allowed 4 schizophrenic patients, all on anti-psychotic medicine to act as their own controls. Having been warned not to, all of them smoked cannabis occasionally. All of them experienced deterioration in their condition, sometimes with very serious consequences. This clearly demonstrated that there was a direct association between relapses into pot smoking and serious deterioration in the schizophrenia condition.

1974. Breakey and others pointed to some sort of association between drug use, including cannabis, and the onset of schizophrenic illness. He considered that cannabis and other drugs could precipitate latent schizophrenia, but also thought that cannabis could do this in cases where the illness would not occur otherwise. They based this conclusion on the fact that the drug induces schizophrenia on average 4 years earlier than the onset in other types of schizophrenia. The onset was also more sudden, and the premorbid personality always better than a comparative group of non-drug using schizophrenics.

1976. Thacore and Shukla made a clear attempt to demonstrate the occurrence of a specific cannabis-provoked functional psychosis.

Other papers around this time, giving support to the findings include, Talbott and Teague 1969, Weil 1970, Bernardson and Gunne 1972 and Harding and Knight 1973.

So even as long ago as the early seventies some researchers were trying to ring alarm bells about the possible psychological problems of cannabis use.

The eighties brought another crop of papers on the subject.

1981. MB Holmberg found that 10% of 16 year-old consumers of large quantities of drugs, almost exclusively cannabis, by the age of 27, would have a record of psychosis. This was much higher than the 3% in the normal population.

1985. Bier and Haastrup looked at psychological admissions over one year in a Copenhagen hospital. Thirty patients had cannabis-provoked psychosis. They then estimated that 15 in a population of 100,000 would be admitted each year with psychosis either precipitated or caused by cannabis.

1986. Negrette and others concluded that interaction between cannabis smoking and schizophrenia had the following characteristics. Cannabis smokers have more relapses, more hospital visits, the positive symptoms of schizophrenia are more dramatic and the patients are less susceptible to neuroleptic medication.

1986. Ghodse said there was clear evidence from countries where heavy cannabis use is common, that cannabis causes a short-term toxic psychosis. This was supported by laboratory experiments.

Among the large body of reports from researchers and clinicians at this time are the following: Palsson, Thulin and Tunving 1982, Rottamburg et al 1982, Tsuang et al 1982, Carney 1984, Brook 1984, Tunving 1985 and Hollister 1986.

However the most important publication at this time was the large study of Swedish conscripts by Andreasson, Allebeck et al in 1987.

Forty-five thousand conscripts had their drug-taking details taken at entry, aged 18 or 19. The levels of schizophrenia were then recorded over the next 15 years. Those on admission who claim to have taken cannabis on more than 50 occasions were found to be 6 times more likely to be diagnosed with schizophrenia in the following 15 years than those who had never consumed the drug. When confounding factors were taken into account, the risk became smaller but remained statistically significant.

Although the study attracted some criticisms, Negrette, the doyen in this field judged the connection to be reasonable taking other previous studies into account, while accepting there were some weaknesses. Andreasson in 1989 and Allebeck in 1993 strengthened their position by further research. They examined the medical records of 112 cannabis-dependent and schizophrenic patients. The findings in all significant respects confirmed the original study.

Further support came from the analysis of records of 100 schizophrenic patients between 1973 and 1977 randomly chosen by Dalman et al in 2002. A large measure of consistency was established with respect to regions, hospitals and timescale as well as the diagnostic criteria for schizophrenia, DSM-1V.

Over twenty years later in 2002, Zammit and others re-analysed the results. In the light of new research into the development of schizophrenia, they were able to discount more of the original objections.

Research continued in the nineties.

1990. Tien and Anthony conducted an epidemiological analysis of drug and alcohol use and concluded that there was an association between cannabis use and psychosis. Daily use over a year suggested a 2.4 times greater risk than non-users, any use related to a risk of 1.3 times. The daily risk figure remained significant after adjustment for other substance abuse and baseline psychiatric diagnosis.

1991. Chaudry et al studied cannabis psychosis following bhang ingestion. Bhang drinkers in Pakistan were found to have mania and paranoid features. Treated with anti-psychotic medicines, the majority recovered completely in 5 days. None had residual symptoms.

1991. Johnson, from his own long experience and a review of the current literature, estimated that 10% of all of those who had used cannabis more than once, experienced either delirium or psychosis. Later estimates confirmed this figure, notably Thomas in 1996 who sent questionnaires to young new Zealanders. Johns as recently as 2001 supported this claim.

1995. Wylie observed a group of British consumers of Dutch cannabis with a high THC content. He recorded a “wave of psychosis and confusional states”. The risk therefore becomes greater the more often cannabis is used and the greater its strength.

1998. Hall concluded that cannabis can cause psychotic like symptoms during intoxication, can lead to a “cannabis psychosis” to increase the relative risk of schizophrenia, and affect the clinical course of established schizophrenia.

Other studies which deserve mention are: Thornicroft 1990, Eikmeir et al 1991, Mathers et al 1991, Rolfe et al 1993, Kristensen 1994, McBride and Thomas 1995, Castle and Ames 1996, Hambrecht and Hafner 1996 and Fowler 1998.

A paper by J Giedd et al in 1999 on development of the adolescent brain must be mentioned here. They conclude that the brain does not finish its development till the mid twenties or beyond. So the warning is that drug abuse could alter the normal course of the maturing of the brain in the teenage years. Research by Giedd on this subject is on-going.

Since the year 2000 there has been a flood of publications. 2002. Louise Arsenault et al assessed 1100 New Zealand children at 11, 15, 18 and 26. Young adults smoking cannabis at the age of 15 were at a greater risk of developing schizophrenia or a schizophrenia-like illness by the age of 26. The risk was 10% times compared to 3% for non-users. Use at 15 was a stronger risk factor for schizophreniform disorder than use by the age of 18.

2002. The Nemesis Study by Van Os et al studied 4045 psychosis-free Dutch people and 59 who had a psychotic disorder, taken at random from 60 localities. They concluded that it must be considered proven that smoking cannabis can provoke a functional (non-toxic) schizophrenia-like psychosis. They replicated the Swedish study of Andreasson. It was of shorter duration and had fewer participants, but not the weaknesses. There was a baseline assessment and 2 follow up sessions, after 1 and 3 years, by questionnaire and clinical interviews. The study showed that individuals using cannabis at baseline were almost 3 times more likely to manifest psychotic symptoms at follow up. After confounding factors were taken into account the risk remained significant. A dose-response relationship was also found. The risk factor for the heaviest users rose to 6.8. They concluded: “cannabis use is an independent risk factor for the emergence of psychosis in psychosis-free persons and that those with an established vulnerability to psychotic disorders are particularly sensitive to its effects, resulting in poor outcome”.

2002. Nunez and Gurpegui compared 26 patients with cannabis-induced psychosis to 35 with acute schizophrenia. All used cannabis, they were repeatedly urine tested. They concluded that cannabis when continuously and heavily used can induce a psychotic disorder distinct from acute schizophrenia.

2002. Hiroshi Ujike found genetic abnormalities in the genes for the cannabinoid receptors on the brain cells of schizophrenics compared to non-schizophrenics. This implies a potential malfunction of their marijuana-linked circuitry, perhaps making them more vulnerable to schizophrenia.

Many people have argued and it seems logical that if the use of cannabis has increased then so must the incidence of schizophrenia.

2003. Boydell et al found that there was indeed a continuous and statistically significant rise in the incidence of schizophrenia between 1965 and 1997. It had doubled over the last 3 decades. The increase was greatest in people under 35.

2003. The Christchurch Health and Development Study. Fergusson et al looked at 1200 children from birth to the age of 21. The cannabis-dependent youngsters developed psychotic symptoms more often than those who were non-dependent. Individuals with cannabis-dependence disorder at 18 had a 3.7-fold increased risk of psychosis than those with no dependence disorder. At 21 the risk fell to 2.3 times.

They conclude that: “the findings are clearly consistent with the view that heavy cannabis use may make a causal contribution to the development of psychotic symptoms since they show that, independently of pre-existing psychotic symptoms and a wide range of social and contextual factors, young people who develop cannabis dependence show an elevated rate of psychotic symptoms”.

Another paper on the development of the brain appeared at this time.

2003. Chambers et al reviewed literature regarding the neurocircuitry underlying motivation, impulsivity and addiction. They focused on studies investigating adolescent neurodevelopment.

They found that adolescent neurodevelopment occurs in brain regions associated with motivation, impulsivity and addiction. These developmental processes may advantageously promote learning drives for adaptation to adult roles but may also confer greater vulnerability to the addictive actions of drugs. This has significant implications for understanding adolescent behaviour, addiction vulnerability and the prevention of addiction in adolescence and adulthood.

2004. Veen et al. One hundred and thirty-three Dutch patients with schizophrenia were interviewed. There was a strong association between the use of cannabis and an earlier age of first psychotic episode in male schizophrenics. On average they were 6.9 years younger than non-using patients.

2004. D’Souza et al. Various doses of THC were administered to 22 healthy subjects, screened for any vulnerability to schizophrenia. Some of them developed symptoms resembling schizophrenia for 30 minutes to 1 hour. There were no side effects after 1, 3 and 6 months. The study findings go along with several other lines of evidence that suggest a contribution of cannabis and/or abnormalities in the brain cannabinoid receptor system to the pathophysiology of schizophrenia.

2004. Arendt et al. Findings: 1439 heavy cannabis users seeking treatment for abuse problems in Denmark were compared to 9122 abusers of other substances.

Conclusion: Co-morbid psychiatric disorders are common among heavy cannabis users seeking treatment. Some psychiatric disorders occur more frequently in this group compared to users of other substances.

2005. Isaac and Holloway did their research in PICUs (Psychiatric Intensive Care Units). There was a high rate of cannabis abuse (71.3%) among the PICU population. Patients with cannabis abuse spent longer as their psychosis was more severe. They were also younger at first hospital admission. The conclusion was that cannabis abusers have more severe psychotic illness especially in schizophrenia. There are additional problems of weight gain.

2004. Frischer et al from Keele University monitored 3% of the population of England and Wales. The number of people using drugs and having mental illness rose by 62% between 1993 and 1998. (230 GP practices were looked at). Men accounted for 79% and women 44%.

The average age affected fell from 38 to 34. The number of cases of 25 to 34 year olds more than doubled. Drug abuse and psychosis were up by 147%, paranoia by 144% and schizophrenia by 128%.

They said, “A long-term, well funded, innovative campaign aimed at publicising the real mental health risks associated with drugs including cannabis needs to be in place as soon as possible”.

2004. Stephanis et al looked at 3500 19-year olds in Greece. Conclusions: These results add credence to the hypothesis that cannabis contributes to the population level of expression of psychosis. In particular, exposure early in adolescence may increase the risk for the sub-clinical positive and negative dimensions of psychosis, but not for depression.

2005. Favrat et al. Clinical trials of THC on psychomotor function and driving performance were conducted on 8 occasional cannabis users with no history of psychosis. Low doses were used. Two young men reacted badly. One 22 year-old showed severe anxiety and psychotic symptoms 90 minutes later, and was unable to do the tests. The other, also 22, was unable to do the tests for several hours, and experienced very unpleasant symptoms.

The doses were administered under clinical conditions and were much lower than would normally be found in a modern joint. The importance of this research is that oral administration of the THC caused significant psychotic reactions. Oral medicines are becoming increasingly available and doctors should be aware of these findings.

2005. Ferdinand. The “Zuid Holland” Study, a 14 year follow up study of 1580, initially 4 to16 year olds, drawn randomly from the Dutch population. (Because cannabis use is generally condoned in Holland, false negative reports of cannabis use may occur less frequently. This adds to the value of this study). Findings: Cannabis use in individuals who did not have psychotic symptoms before they began using cannabis, predicted future psychotic symptoms, the risk was almost 3 times greater. Also psychotic symptoms in those who had never used cannabis before the onset of psychotic symptoms also predicted future cannabis use.

Conclusion: The results either imply a common vulnerability with varying order of onset or a bi-directional causal relationship between cannabis use and psychosis.

2005. Van Os et al. Nearly 2500 young people between the ages of 14 and 24, with or without predisposition to psychosis were studied. Adjustment was done for confounding factors such as alcohol, cigarettes and other drugs. There was a dose-response relationship with increasingly frequent use of cannabis.

Conclusions: Cannabis use in young people moderately increased the risk of developing psychotic symptoms. The risk for onset of symptoms was much higher in young people with a predisposition for psychosis. Predisposition psychosis at baseline did not predict cannabis use at follow up. This rejects the self-medication hypothesis i.e. that psychotic patients take drugs to relieve the symptoms of the illness.

2005. Fergusson et al. This was a 25 year longitudinal study of 1055 New Zealand children from birth. Conclusions: “Even when all factors were taken into account, there was a clear increase in rates of psychotic symptoms after the start of regular use, with daily users of cannabis having rates that were over150% those of non-users. These findings add to a growing body of evidence from different sources, all of which suggest that heavy use of cannabis may lead to increased risks of psychotic symptoms and illness in susceptible individuals”.

Several review articles have also appeared in the last few years.

2001. Johns. Conclusion: “Heavy cannabis misuse leads to the risk of psychotic episodes and aggravates the symptoms and course of schizophrenia. For any psychiatric patient, risk management and care planning is incomplete without a thorough assessment of substance abuse”. 2003. Degenhardt and Hall. Conclusion: “Cannabis use does not appear to be causally related to the incidence of schizophrenia but its use may precipitate disorders in persons who are vulnerable to develop psychosis and worsen the course of the disorder among those who have already developed it”.

2004. Arsenault et al. A review of 5 papers was undertaken: The Swedish Conscript cohort, Andreasson 1987 and Zammit et al 2002. The Dutch Nemesis Sample, Van Os 2002. The Christchurch Study, Fergusson et al 2003. The Dunedin Study, Arsenault 2002. The overall conclusion: “A twofold increase in the relative risk for later schizophrenia. At the population level, elimination of cannabis smoking would reduce the incidence of schizophrenia by around 8% assuming a causal relationship. Cannabis is a component cause for psychosis, part of a complex constellation of factors”.

2004. Rey et al. Conclusion: The weight of evidence points in the direction of early and regular use of cannabis having substantial negative effects on psychosocial functioning and psychopathology.

2004. Drewe et al. This article appeared in response to the potential legalization of cannabis in Switzerland. Conclusion: “An increase in consumption would be expected therefore there would probably be an increase in the prevalence of psychosis, not only acute toxic but also chronic psychosis. Schizophrenic psychoses would be expected to be triggered at an earlier age so there could be deleterious consequences not only for many currently healthy individuals but for disablement pensions”.

2004. Raphael and Wooding. Conclusion: “Of primary importance is the fact that cannabis use does have a number of significant associated harms. It is not a soft or safe option and its notable co-morbidity with psychotic and non-psychotic illnesses make it a significant and growing public health issue – a fact increasingly reflected in both the national and international scientific literature”.

Other reviews deserving mention include: Leweke et al 2004, Witton and Murray 2004, John Macleod et al 2004 and Smit et al 2004.

Professor Robin Murray of the Institute of Psychiatry, London, drew attention to the fact in 2003 that recent evidence had demonstrated that THC increases the release of dopamine, thus increasing its level in the brain. Psychotic symptoms in conditions like schizophrenia are mediated by dopamine.

Two important papers are awaiting publication in scientific journals.

Caspi et al. in a paper to be published in Biological Psychiatry, have found variants in a gene (COMT) which is involved in dopamine transmission. It was found to moderate the influence of adolescent cannabis use on the development of adult psychosis. One in four people carries this gene. The research was carried out on 803 men and women born in Dunedin, New Zealand in 1972 and 1973. They were enrolled at birth. The gene comes in 2 variants, methionine and valine, and everyone has two copies of the gene. If a person inherits 2 methionine types, the rate of psychotic illness is 3%, the normal rate for non-users. However if a person has 2 valine variants, the rate rises to 15% for those who have used cannabis in their teens. Dr Caspi said, “Research has shown that the valine gene variant and cannabis affect the brain’s dopamine system in similar fashion, suggesting that they deliver a “double dose” that can be damaging”.

Markus Leweke and others from the University of Cologne in Germany addressed The International Cannabis and Mental Health Conference in Melbourne in August 2004.

The brain’s “natural cannabis” is a substance called anandamide. Much higher levels of this chemical were found in the brains of schizophrenics experiencing their first psychotic episode and before they had embarked on medication for their condition, and also the brains of people with psychotic symptoms and a strong susceptibility to schizophrenia.

Surprisingly the more severe the schizophrenia, the lower the levels of anandamide. They postulated that anandamide may actually be produced to control psychotic symptoms and dampen them down. THC binds to anandamide receptors. It makes these receptor sites less sensitive and may disrupt the system in other ways as well.

An article appeared in New Scientist in August 2004.

In 2004 Marijuana and Madness was published by Cambridge University Press. The editors were, Professor David Castle of The Mental Health Research Unit, Melbourne, and Professor Robin Murray of The Institute of Psychiatry in London.

Twenty-nine contributors to 13 chapters are listed. Many of them have been mentioned in this article. The review from the journal “Addiction” says:

“Each chapter is well written and well presented…There is little doubt that the chapters are expertly written…Marijuana and madness illustrates clearly the benefits of a multi-disciplinary perspective in providing the tools for answering a complex question”.

Mary Brett, retired biology teacher and former Head of Health Education Dr Challoner’s Grammar School Amersham Bucks. May 9th 2005.

11/17/2004

News Feature
By Erika Miles Edwards

South Boston is a close-knit community of 3 square miles and 30,000 people. It’s the kind of place where everyone knows everyone else, and gossip, good or bad, spreads like wildfire.

South Boston also is a community with a significant heroin problem. In the past three years alone, 125 young people from South Boston aged 17-24 have died from using heroin. An estimated five to ten times as many have overdosed — some several times — but lived. The community is on the front lines of an epidemic of heroin use among young adults in the greater Boston area, where the drug is $4 a bag and so potent that it can be snorted instead of injected. Heroin overdoses are one of the leading causes of death among young adults in the region.

People in communities that lose children to tragic circumstances tend to bond together, and South Boston is no exception. In response to the crisis, a group of 10 mothers with children addicted to heroin formed the South Boston Family Resource Center and started a 24-hour hotline for families who need help. The group finds treatment for those who want it, even driving people to their first appointment. For many young adults, they are a lifeline.

Strange Remedy

Sometimes crises bear solutions that, under any other circumstance, would seem strange. In the case of the mothers of the South Boston Family Resource Center, that solution came in the form of the Dorchester Drug Court, founded by Judge Robert Ziemian, presiding justice of the South Boston District Court, with help from the Robert Wood Johnson Foundation.

The drug court is a collaborative process designed to help addicted individuals facing criminal charges get through treatment, a process that can take 15 months or more. Participants start out in detox, and then go to residential treatment for a minimum of six months. When they’re ready, they move to outpatient treatment, then relapse prevention, before being left unsupervised. Then, they are on their own, their criminal charges erased.

Drug-court participants are motivated through the system with sanctions, drug testing, encouragement, and support. Most adult drug-court clients are severely addicted, with long histories in the criminal-justice and social-service systems.

“If you think someone should be in jail, that’s who we want in drug court, because we know drug court keeps people in treatment,” said Ziemian. “Most people have setbacks, but from our experience, we know when those are going to occur. We’re watching them, and we’re encouraging them to succeed.”

After Ziemian started his drug court in 1995, word spread quickly of this place where people with criminal records were getting treatment and leaving clean and sober. He soon was approached by a mother in South Boston, asking him what he could do to help stem the tide of heroin overdoses.

“We normally work with hardened addicts,” said Ziemian. “They’re older, and have had a longer history with substance abuse. It’s easier to convince them that they need treatment. But we had to do something to help these kids. We needed to stop the overdosing before another death occurred.”

Mothers of children at risk of overdoses received letters from the probation office, inviting them to discuss solutions. The result: The women decided to apply for restraining orders against their heroin-addicted kids. Since a child breaking a restraining order is subject to criminal charges, the parents reasoned, these young adults would get connected to the criminal-justice system and be supervised in the South Boston Drug Court, receiving life-saving treatment in the process.

Not surprisingly, word of the solution spread like wildfire throughout South Boston. Even with a shortage of resources, the court has produced dramatic results. “One of the things we’ve learned about drug court is that you can usually coerce someone into treatment with the threat of jail or brief incarceration,” Ziemian said. “We and the parents have a chance to get through to them.” Notably, not a single person under active supervision of the drug court has died of a drug overdose.

Building on History

For years, America has fought an expensive war against drugs, using tactics ranging from extensive eradication efforts to lengthy periods of incarceration. In 1989, a judge in Miami dared to try something different, offering people with criminal cases treatment instead of incarceration and, in doing so, created the nation’s first drug court.

Around the same time, Ziemian returned to Massachusetts from Operation Desert Storm. Assigned to the Dorchester District Court in South Boston, he processed cases involving guns and drugs, and gained a reputation for sentencing criminal defendants to lengthy periods of incarceration.

Ziemian’s first impressions of drug courts were less than positive. “I went to a workshop about it at a bar association meeting, and I thought the guy was out of his mind,” he recalled. But Ziemian was urged by the Boston Coalition Against Drugs and Violence and by Join Together to look into the concept. A turning point was when Ziemian went to Miami to see the first drug court in action.

“For those familiar with court proceedings, drug courts are very different,” said Ziemian. “You really have to go, watch what happens, talk about it afterwards. But once you’ve seen it in action, it all makes sense.”

Today, Ziemian is the driving force behind the development of more than 30 drug courts in Massachusetts, Connecticut, Maine, New Hampshire, and Rhode Island. His Dorchester drug court is a model recognized by the National Association of Drug Court Professionals.

Each drug court develops differently, but in Massachusetts and throughout New England, many follow Ziemian’s model — with his assistance. The process starts with the support of a district’s presiding judge, who brings the other justices on board. Ziemian then meets with the justices and the clerks, probation officers, lawyers, treatment providers, and public-health officials who need to work together to make the drug court succeed.

Over objections heard from every drug court he has ever established, Ziemian sets the first drug-court date for as soon after the initial meeting as possible; the only way to learn is to do, he believes. Cases stay in their courts of origin, which forces teams in those regions to work together to come up with solutions. Every probation officer, for example, has to learn how to work with serious drug offenders and treat substance use disorders holistically, coach people through treatment, even find them treatment slots.

Strong Results, But a Struggle for Funding

But do drug courts work? Research shows that addiction treatment significantly reduces drug use, crime, and additional medical problems. Drug courts specifically reduce recidivism, or re-entry into the criminal-justice system, which saves states significant amounts of money. Nationally, incarceration costs at least $20,000 annually per person, whereas drug court costs about $4,000. Additionally, one study found that the Lackawanna Drug Court in upstate New York State saved over $2.1 million annually in public assistance, foster care, substance-free births, and child support.

Despite widespread support within the criminal-justice system, however, Ziemian and his drug-court colleagues struggle for financial stability. The Massachusetts state legislature has never provided line-item funding for drug courts, so the state’s drug courts run on skeleton crews of committed lawyers, justices, and probation officers. Ziemian has received federal grant funding to hire a coordinator that he shares with other regional courts, but worries about what he will do when that support runs out.

“Drug courts have a lot of moving pieces — many more than regular courts,” said Ziemian. “People are with us for much longer than people with other types of sentences. We build relationships with them. They count on us. We don’t want to give up on it because of lack of resources.”

“We want to do everything we can to help these kids,” added Ziemian. “We need to institutionalize this system. We need data to show that it works. We need an alumni network that could mentor the kids in the system. We can’t do that without help.”

Despite such funding worries, Judge Ziemian hopes that all judicial districts in New England will soon have drug courts. “The only thing I don’t have to do is convince people that their communities have problems with drugs. Drugs are everywhere,” he says. “With drug courts, we can do something about it.”

The directors offer specific steps for planning and instigating the changes, provide real-life examples from diverse communities across the nation, and provide a road map for communities to adopt the six-step model all at once or one step at a time.

The report recommends screening each teen for drug and alcohol problems, assessing the severity of his/her drug and alcohol use, providing prompt access to a treatment plan coordinated by a service team; and connecting the teen with employers, mentors, and volunteer service projects.

The report describes how judges, probation officers, treatment specialists, families and community members can take steps right now to improve the future of these youth.

Upon completion of a brief survey, the full report is available as a PDF to download at no cost.

http://www.reclaimingfutures.org/?q=judicial_report_survey&reportname=ProjectDirectors

Publication Year: 2007

Publisher

Reclaiming Futures
Portland State University
527 SW Hall, Suite 400
Portland, or 97201
Phone: 503.725.8911
Website: http://www.reclaimingfutures.org/

The high prevalence of co-morbidity between drug use disorders and other mental illnesses does not mean that one caused the other, even if it appeared first. In fact, establishing causality or directionality is difficult for several reasons. Some symptoms of a mental disorder may not be recognized until the illness has substantially progressed, and imperfect recollections of when drug use/abuse started can also present timing issues. Still, three scenarios deserve consideration:
1. Drugs of abuse can cause abusers to experience one or more symptoms of another mental illness. The increased risk of psychosis in some marijuana abusers has been offered as evidence for this possibility.
2. Mental illnesses can lead to drug abuse. Individuals with overt, mild, or even subclinical mental disorders may abuse drugs as a form of self-medication. For example, the use of tobacco products by patients with schizophrenia is believed to lessen the symptoms of the disease and improve cognition (“Smoking and Schizophrenia: Self-Medication or Shared Brain Circuitry?”).
3. Both drug use disorders and other mental illnesses are caused by overlapping factors such as underlying brain deficits, genetic vulnerabilities, and/or early exposure to stress or trauma.
All three scenarios probably contribute, in varying degrees, to how and whether specific comorbidities manifest themselves.
Overlapping Conditions– Shared Vulnerability
High Prevalence of Drug Abuse and Dependence Among Individuals With Mood and Anxiety DisordersHigh Prevalence of Mental Disorders Among Patients With Drug Use Disorders

Higher Prevalence Smoking Among Patients With Mental Disorders

Because mood disorders increase vulnerability to drug abuse and addiction, the diagnosis and treatment of the mood disorder can reduce the risk of subsequent drug use. Because the inverse may also be true, the diagnosis and treatment of drug use disorders may reduce the risk of developing other mental illnesses and, if they do occur, lessen their severity or make them more amenable to effective treatment. Finally, because more than 40 percent of the cigarettes smoked in this country are smoked by individuals with a psychiatric disorder, such as major depressive disorder; alcoholism; post-traumatic stress disorder (PTSD); schizophrenia; or bipolar disorder, smoking by patients with mental illness contributes greatly to their increased morbidity and mortality.
Data in top two graphs reprinted from the National Epidemiologic Survey on Alcohol and Related Conditions (Conway et al., 2006).
Data in bottom graph from the 1989 U.S. National Health Interview Survey (Lasser et al., 2000).
Common Factors
Overlapping Genetic Vulnerabilities. A particularly active area of comorbidity research involves the search for genes that might predispose individuals to develop both addiction and other mental illnesses, or to have a greater risk of a second disorder occurring after the first appears. It is estimated that 40-60 percent of an individual’s vulnerability to addiction is attributable to genetics; most of this vulnerability arises from complex interactions among multiple genes and from genetic interactions with environmental influences. In some instances, a gene product may act directly, as when a protein influences how a person responds to a drug (e.g., whether the drug experience is pleasurable or not) or how long a drug remains in the body. But genes can also act indirectly by altering how an individual responds to stress or by increasing the likelihood of risk-taking and novelty-seeking behaviors, which could influence the development of both drug use disorders and other mental illnesses. Several regions of the human genome have been linked to increased risk of both, including associations with greater vulnerability to adolescent drug dependence and conduct disorders. The rate of smoking in patients with schizophrenia has ranged as high as 90 percent.
Involvement of Similar Brain Regions.
Some areas of the brain are affected by both drug use disorders and other mental illnesses. For example, the circuits in the brain that use the neurotransmitter dopamine–a chemical that carries messages from one neuron to another– are typically affected by addictive substances and may also be involved in depression, schizophrenia, and other psychiatric disorders.
Indeed, some antidepressants and essentially all antipsychotic medications target the regulation of dopamine in this system directly, whereas others may have indirect effects. Importantly, dopamine pathways have also been implicated in the way in which stress can increase vulnerability to drug addiction. Stress is also a known risk factor for a range of mental disorders and therefore provides one likely common neurobiological link between the disease processes of addiction and those of other mental disorders.
The overlap of brain areas involved in both drug use disorders and other mental illnesses suggests that brain changes stemming from one may affect the other. For example, drug abuse that precedes the first symptoms of a mental illness may produce changes in brain structure and function that kindle an underlying propensity to develop that mental illness. If the mental disorder develops first, associated changes in brain activity may increase the vulnerability to abusing substances by enhancing their positive effects, reducing awareness of their negative effects, or alleviating the unpleasant effects associated with the mental disorder or the medication used to treat it.
Smoking and Schizophrenia: Self- Medication or Shared Brain Circuitry?
Patients with schizophrenia have higher rates of alcohol, tobacco, and other drug abuse than the general population. Based on nationally representative survey data, 41 percent of respondents with past-month mental illnesses are current smokers, which is about double the rate of those with no mental illness. In clinical samples, the rate of smoking in patients with schizophrenia has ranged as high as 90 percent.
Various self-medication hypotheses have been proposed to explain the strong association between schizophrenia and smoking, although none have yet been confirmed. Most of these relate to the nicotine contained in tobacco products: Nicotine may help compensate for some of the cognitive impairments produced by the disorder and may counteract psychotic symptoms or alleviate unpleasant side effects of antipsychotic medications. Nicotine or smoking behavior may also help people with schizophrenia deal with the anxiety and social stigma of their disease.
Research on how both nicotine and schizophrenia affect the brain has generated other possible explanations for the high rate of smoking among people with schizophrenia: The presence of abnormalities in particular circuits of the brain may predispose individuals to schizophrenia; increase the rewarding effects of drugs like nicotine; or reduce an individual’s ability to quit smoking. The involvement of common mechanisms is consistent with the observation that both nicotine and the medication clozapine (which also acts at nicotine receptors) can improve attention and working memory in an animal model of schizophrenia. Clozapine is effective in treating individuals with schizophrenia. It also reduces their smoking levels. Understanding how and why patients with schizophrenia use nicotine is likely to help us develop new treatments for both schizophrenia and nicotine dependence.
The Influence of Developmental Stage
Adolescence–A Vulnerable Time. Although drug abuse and addiction can happen at any time during a person’s life, drug use typically starts in adolescence, a period when the first signs of mental illness commonly appear. It is therefore not surprising that co-morbid disorders can already be seen among youth. Significant changes in the brain occur during adolescence, which may enhance vulnerability to drug use and the development of addiction and other mental disorders. Drugs of abuse affect brain circuits involved in reward, decision making, learning and memory, and behavioral control, all of which are still maturing into early adulthood. Thus, understanding the long-term impact of early drug exposure is a critical area of co-morbidity research.
The brain continues to develop into adulthood and undergoes dramatic changes during adolescence. One of the brain areas still maturing during adolescence is the prefrontal cortex– the part of the brain that enables us to assess situations, make sound decisions, and keep our emotions and desires under control. The fact that this critical part of an adolescent’s brain is still a work in progress puts them at increased risk for poor decisions (such as trying drugs or continuing abuse). Thus, introducing drugs while the brain is still developing may have profound and long-lasting consequences.
The high rate of co-morbidity between drug abuse and addiction and other mental disorders argues for a comprehensive approach to intervention that identifies, evaluates, and treats each disorder concurrently.
Early Occurrence Increases Later Risk. Strong evidence has emerged showing early drug use to be a risk factor for later substance abuse problems; additional findings suggest that it may also be a risk factor for the later occurrence of other mental illnesses. However, this link is not necessarily a simple one and may hinge upon genetic vulnerability, psychosocial experiences, and/or general environmental influences. A recent study highlights this complexity, with the finding that frequent marijuana use during adolescence can increase the risk of psychosis in adulthood, but only in individuals who carry a particular gene variant (see sidebar, “The Influence of Adolescent Marijuana Use on Adult Psychosis Is Affected by Genetic Variables”).
The Influence of Adolescent Marijuana Use on Adult Psychosis Is Affected by Genetic Variables

Percentage of Individuals Meeting Diagnostic Criteria for Schizophreniform Disorder at Age 26

Source: Caspi A, Moffitt TE, Cannon M, et al., 2005.
The above figure shows that variations in a gene can affect the likelihood of developing psychosis in adulthood following exposure to cannabis. The Catechol-O-Methyltransferase gene regulates an enzyme that breaks down dopamine, a brain chemical involved in schizophrenia. It comes in two forms: Met and Val. Individuals with one or two copies of the Val variant have a higher risk of developing schizophrenic-type disorders if they used cannabis during adolescence (dark bars). Those with only the Met variant were unaffected by cannabis use. These findings hint at the complexity of factors that contribute to co-morbid conditions; however, more research is needed.
Source: NIDA Jan.2009

Though unable to securely document outcomes, three projects have shown that British communities can generate the kind of coordinated action which new reports from the USA and Sweden have shown curtail alcohol-related violence and injury, creating substantial cost-savings for society.
FINDINGS Rather than targeting risky drinkers, all the projects targeted high-risk neighbourhoods, aiming to modify features of the social and physical environment which generate alcohol-related violence and disorder.
UK From 2004, parallel projects Jointly known as the UK Community Alcohol Prevention Programme. in Glasgow, Cardiff and Birmingham sought to generate action locally to promote responsible service of alcohol in bars and shops, enforce licensing and allied laws, limit alcohol outlets, and to modify the environment and transport services to improve safety. Awareness-raising initiatives aimed to stimulate support from residents, politicians, licensees and local services. The projects were among only five in the UK found to meet international criteria1 for ‘multi-component’ programmes which simultaneously bring a range of influences to bear on alcohol problems.
The featured report2 documented how all three were able to generate activity of the kind they sought. In the absence of a systematic evaluation, official statistics and data gathered by the projects themselves was used to assess whether this activity had reduced alcohol-related problems – problematic, because the projects’ effects could not easily be isolated and the figures fluctuated due to factors other than the real levels of crime or injury.
Perhaps clearest was the impact in Birmingham, where in the targeted area (a transport corridor crossing three suburbs) the project started with a clean slate in terms of existing community organisation. Birmingham too seems to have had the strongest enforcement component, shown by research ( In context) to be the greatest single influence. Trading standards staff visited all the area’s alcohol outlets, alerting staff to their responsibilities and warning of future ‘sting’ operations to test whether outlets would sell to underage youngsters. Police recorded reports of licensing infringements, followed up with an advice visit, and mounted highly visible operations similar to those used in relation to illicit drugs.
Possibly as a result, offences such as vehicle crime, domestic burglary and robbery in the area fell by over a third compared to just 9% in a neighbouring area, and public place wounding fell by 30% compared to 17%, though the numbers involved were small. Unlike elsewhere, after the project was established few premises sold to underage test purchasers and most asked for proof of age.
USA The US project targeted two poor neighbourhoods relatively crowded with alcohol outlets and blighted by crime and alcohol-related problems. A robust Staggered implementation at the two sites and before and after measures benchmarked against the rest of the city offered multiple checks on whether the interventions were responsible for any improvements.evaluation3 documented reductions in violent crime and injuries, among the priorities for UK projects.
Local community organisations prioritised control of alcohol outlets to tackle underage drinking and alcohol-related violence. Training in responsible beverage service was taken up by 40–70% of outlets after personal and persistent approaches by project staff and police. Shop managers were warned that police would mount test purchases by underage youngsters. An accompanying officer immediately initiated proceedings against offending outlets. Given this backing, there was a clear reduction in sales, prompting replication city-wide. Similar operations were not undertaken in bars where, without enforcement backing, staff training on its own did not lead more premises to refuse service to drunk patrons. The bottom-line finding was that across both sites, the interventions were followed by significantly greater falls than in the rest of the city in assaults According to both police and medical records. and injuries Before the waters were muddied by city-wide implementation, there was also a greater reduction in injuries specifically related to drinking or drug use. due to traffic accidents. Some of the relative reductions were substantial – over a third for assaults and traffic accidents. Given the social costs imposed by such incidents, the project was likely to have been cost-beneficial.
SWEDEN The Swedish report4 showed that such programmes can indeed save society money. It attached monetary values to an earlier finding5 that a city-centre programme targeting licensed premises reduced violence Represented by reports to the police. by 29%. The resulting estimate was that it saved society 39 times more than it cost, primarily due to reduced criminal justice expenditures. The calculations were subject to potential error but even when savings were limited to police work, the most securely estimated element, they were seven times greater than costs. A dip in quality of life after being the victim of a crime meant that the interventions also gained one quality adjusted life year (QALY) for each 3000 Euros spent, well within the Swedish yardstick of 54,000 Euros.
After an upsurge in violence when on-licence outlets expanded, Stockholm County Council initiated the programme to curb serving of drunk patrons in the central district. Test purchases by apparently drunk actors generated support for responsible beverage service training, later made a condition of licence renewal for late-night venues. Liquor law enforcement (especially the ban on serving drunk patrons) was stepped up by police and the licensing board, largely in the form of warning letters rather than formal proceedings. Resulting reductions Inevitably the calculations incorporated arguable assumptions, but the magnitude of the gains were such that substantial benefits seem certain. in violence were estimated on the basis of before and after trends in the intervention district compared to the next most similar area. Benefits grew in line with the unfolding of the programme, reinforcing the case that this was an active ingredient. Once again, enforcement was thought to have been the main influence. Even in the comparison area, underage sales fell after activists organised test purchases and notified offenders to the police, who banned some from selling alcohol.
IN CONTEXT Reviewers6 have concluded that the ‘environmental’ approach7 (controlling the geographic, retailing and social environments in which alcohol is distributed, sold or consumed, and stepping up enforcement) tested in these studies can be more effective than trying to affect individuals through education or persuasion. However, impacts sometimes remain modest, partly because the scope for local action is limited by national or regional laws.
Police or licensing authority action backed by ultimate legal sanctions can on its own have a major impact, but requires other components to amplify and sustain its effects. Publicity makes authorities aware of the need for action and licensees aware of the potential consequences of failing to comply, while local lobbying helps gain support for the required intensity and persistence of effort.8 9 Possibly enforcement works because it stimulates defensive management actions10 such as firm and clear policies on adhering to regulations and a system for monitoring staff compliance. Commercial considerations often mitigate against such policies, but can also generate them if otherwise the business faces closure or costly restrictions.
British research includes a landmark study11 based on test purchases by underage youngsters which suggested that many vendors’ primary concern was not to avoid underage selling as such, but to avoid successful prosecution for selling to children who were clearly underage. In Cardiff,12 the main lessons of a programme to curb alcohol-related city-centre violence and disorder seemed to be that intensive implementation is needed to have a major impact. Planning and licensing decisions which increase the density of drinking outlets, and competitive and financial pressures driving the policies of large club or pub chains, can counter the benefits. However, benefits remained and were probably enough to create substantial cost-savings for society. Though not formally evaluated, similar enforcement-led programmes13 stimulated by the 2004 English national alcohol strategy have encouraged licensee compliance and appear to have reduced alcohol-related crime and disorder. Sales to underage youngsters have also been curbed by recent test purchase14 operations15 allied with trading standards and/or police follow-up.
PRACTICE IMPLICATIONS The UK report argued for environmentally-based community projects on the grounds that these probably represent the best chance for minimising harm in the face of national deregulation and promotion of alcohol consumption. Yet the leverage local projects can exert depends partly on the tools made available by national laws and policies to the projects and to the authorities they seek to influence, tools abolished or weakened or by deregulation. Given adequate powers, local lobbying and coordination can maximise their potential and tackle factors beyond the reach of the law.
So a crucial issue is how far national UK frameworks provide the required support and legislative tools. New British alcohol strategies and laws and attendant funding do provide a basis for projects similar to those featured, particularly the powerful tool of test purchases to expose underage service. But at the same time (less so in Scotland) they limit the scope for licensing authorities to respond to community concerns. Click here for summaries of the situations in England, Wales and Scotland.
Flexibility is essential because the impacts of commonly used tactics depend on the environment with which they interact; a different mix works best in different situations.1 10 The ideal16 is when national support and regulations afford localities the required tools within an accountability framework which motivates effective action, but which also gives localities discretion on what to target and how.
There are however some general principles. Regardless of the interventions built upon them, test purchasing and the construction of a database linking untoward incidents to particular premises are important in motivating and targeting action and assessing its impact. The visible and credible possibility of enforcement action against alcohol outlets must be persistently maintained if it is to have anything but a fleeting impact. Attention should be paid both to alcohol consumption and the factors17 (such as crowding, transport problems, divorcing alcohol from food, poorly kept or managed premises, glasses easily transformed in to weapons, inadequate training and monitoring of staff) which potentiate violence and disorder.
In the UK guidance on local strategies18 is available and a new database19 features examples. International lessons on community alcohol interventions have also been usefully encapsulated.20 These include: devolve decision-making to the community while supplying research-based knowledge; rapid feedback of results motivates participants and keeps projects on track; recruit influential and respected local leaders; considerable lead-in time is needed to build the social and organisational infrastructure for community action, and projects need a few years to fully deliver; project staff must expect and permit adaptation not just of methods but also aims in response to the community’s strengths and self-perceived needs; success comes easier in communities where the project’s aims are already high on the agenda; community norms and alcohol availability restrictions have their greatest impacts in self-contained, stable communities whose residents and businesses cannot easily escape their impact; a key element is the surer detection and sanctioning of transgressors brought about by the more intensive use of existing legal powers; however, these legal powers must in the first place have the potential to be effective.
Source: address http://findings.org.uk Feb.2009

In good faith, the Substance Misuse Management in General Practice issued guidance now proven to be based on unfounded figures – they were taken at face value from the National Treatment Agency for Substance Misuse. Peter O’Loughlin puts the record straight.
Many – perhaps most of us – have become accustomed, even weary, of the plethora of self-congratulatory announcements issued by the National Treatment Agency for Substance Misuse. Most of the spin aims to persuade us that protocols and implementations of the current drug treatment strategy are succcessful. Indeed, such is the glut of these proclamations of success, that there is a temptation, at least by this writer, to skip them in favour of more factual and unbiased reading.
On the other hand, when a responsible and professional network such as the Substance Misuse Management In General Practice chooses to re-issue verbatim one of the more misleading documents emanating from the NTA, and endorse it as an “important report”, this writer sits up and pays attention.
The document in question is Good Practice in Harm Reduction (NTA report, October 2008).
While acknowledging that government targets for reducing drug-related deaths have not been met, it makes the following claim: “Drug related deaths have gone down in recent years”.
It then purports to show how harm reduction “combines work aimed directly at reducing the number of drug-related deaths and blood-borne virus infections, with wider goals of preventing drug misuse and of encouraging stabilisation in treatment and support for abstinence”.
It is the intention of this article, with the aid of statistical evidence from the National Audit Office and the Health Protection Agency, to show that the claim relating to drug deaths is palpably misleading – and that the current emphasis on harm reduction is failing not only in reducing drug deaths, but that they are actually increasing. This is alongside the abysmal failure of inappropriately named “harm reduction” methods to contain the escalation of blood-borne diseases.
NATIONAL AUDIT OFFICE FIGURES.
The following facts for drug deaths arising from misuse were published by the NAO in its April 2007 and autumn 2008 reports.
• Drug deaths from heroin and morphine are increasing year on year
• In 2003-4 there was a marked increase in drug-related deaths which were largely attributed to heroin, methadone and morphine.
• Drug-related deaths are the highest in five years.
• The total number of drug-poisoning deaths arising from drug misuse in 2007 increased by 16% from 2006, to 2,640.
• In 2007, 196 deaths involving cocaine occurred, the highest number of deaths involving cocaine since records by the Office of National Statistics began in 1993.
•
Deaths attributed to methadone are at their highest since 1999. In 2007, methadone-related deaths increased by 35% over 2006 to 325.
HEALTH PROTECTION AGENCY FACTS.
The following facts were published by the Health Protection Agency.
• The level of HIV infection among injecting drug users (IDUs) in England and Wales is higher now than at the start of the decade.
• In London, where the prevalence of HIV in IDUs is higher than elsewhere in England and Wales, one in 20 IDUs is infected.
• In the remainder of England and Wales, HIV among IDUs has risen from about one in 400 in 2002 to about one in 150 in 2006.
• The prevalence of hepatitis C among IDUs has risen from 33% in 2000 to 42% in 2006.
• About one in five IDUs has hepatitis B infection, which extrapolates as an increase approaching 200% since 1997.
FACING THE FACTS.
It is self evident from the facts that the disproportionate emphasis on harm reduction is failing to achieve that which the NTA document would have us believe.
The author(s) of the document contents have – knowingly or unknowingly – resorted to a technique known as ‘perception management’. This process could be regarded as more sinister than spin, since it seeks to bury the truth under a garbage of rhetoric in order to manufacture a ‘truth’ designed to influence or change the perceptions of a targeted audience.
Via email, I expressed my disappointment to the SMMGP for publishing as a “policy update” the NTA document, together with the endorsement the SMMGP gave. I now place on record my appreciation to Dr Chris Ford for the courtesy and promptness of her response.
In an age where avoidance of responsibility is so common, I also take this opportunity of expressing my admiration and respect for the forthrightness of her “mea culpa”, together with the integrity and that rare quality of humility which she displayed in our subsequent correspondence.
PETER O’LOUGHLIN is certificated in substance misuse and dependency by the Department of Addictive Behaviours, St George’s Medical School and Addaction, is an associate member of the Medical Council on Alcohol, a registered psychotherapist and clinical hypnotherapist. His 25 years’ experience spans detox, street work, rehabilitation,1:1 and group counselling.
Source: Addiction Today Feb.22nd 2009

CASE REPORT

Cannabinoid hyperemesis syndrome: Clinical diagnosis of an underrecognised manifestation of chronic cannabis abuse

Siva P Sontineni, Sanjay Chaudhary, Vijaya Sontineni, Stephen J Lanspa
Online Submissions: wjg.wjgnet.com World J Gastroenterol 2009 March 14; 15(10): 1264-1266
wjg@wjgnet.com World Journal of Gastroenterology ISSN 1007-9327
doi:10.3748/wjg.15.1264 © 2009 The WJG Press and Baishideng. All rights reserved.
Siva P Sontineni, Sanjay Chaudhary, Vijaya Sontineni,
Stephen J Lanspa, Department of Medicine, Creighton
University, Suite 5850, 601 N 30th Street, Omaha, NE 68131,
United States
Author contributions: Sontineni SP provided the patient’s data,
organized, conceptualized and contributed to the manuscript
writing and final approval; Chaudhary S collected the patient
data, reviewed the literature and contributed to the manuscript
writing; Sontineni V reviewed the literature and compiled the
references; Lanspa SJ supervised, provided critical review
and obtained financial support from the division; All authors
approved the final manuscript.
Correspondence to: Siva P Sontineni, MD, Department
of Internal Medicine, 601 N 30th St Suite 5850, Creighton
University Medical Centre, Omaha, NE 68131,
United States. ssontineni@gmail.com
Telephone: +1-402-4158319 Fax: +1-402-2804220
Received: October 25, 2008 Revised: February 8, 2009
Accepted: February 15, 2009
Published online: March 14, 2009

Abstract

Cannabis is a common drug of abuse that is associated with various long-term and short-term adverse effects.
The nature of its association with vomiting after chronic abuse is obscure and is underrecognised by
clinicians. In some patients this vomiting can take on a pattern similar to cyclic vomiting syndrome with
a peculiar compulsive hot bathing pattern, which relieves intense feelings of nausea and accompanying
symptoms. In this case report, we describe a twentytwo year-old-male with a history of chronic cannabis
abuse presenting with recurrent vomiting, intense nausea and abdominal pain. In addition, the patient
reported that the hot baths improved his symptoms during these episodes. Abstinence from cannabis led
to resolution of the vomiting symptoms and abdominal pain. We conclude that in the setting of chronic
cannabis abuse, patients presenting with chronic severe nausea and vomiting that can sometimes be
accompanied by abdominal pain and compulsive hot bathing behaviour, in the absence of other obvious
causes, a diagnosis of cannabinoid hyperemesis syndrome should be considered.
© 2009 The WJG Press and Baishideng. All rights reserved.

INTRODUCTION
Cannabis has been used recreationally for millennia and is the third most commonly used drug after tobacco
and alcohol[1,2]. Research into the neurobiology of the compound has led to the discovery of an endogenous
cannabinoid system. The therapeutic potential of cannabinoids has been recognized and these compounds are
utilized as anti-emetics[3-5]. Recently, a distinct syndrome in chronic cannabis abusers characterized by recurrent
vomiting associated with abdominal pain and a tendency to take hot showers has been increasingly recognised.
This clinical manifestation is paradoxical to the previously identified therapeutic role of cannabinoids as antiemetics.
We describe the case of a young male seeking repeated emergency room care with recurrent nausea
and vomiting.

CASE REPORT
A 22-year male presented with recurrent episodes of nausea, refractory vomiting, and colicky epigastric pain
for one week. The symptoms were characterized by treatment-resistant nausea in the morning, continuous
vomiting, and colicky epigastric abdominal pain. Each episode lasted 2 to 3 h and increased with food intake.
He often had two or more episodes a day during the symptomatic period. He had been treated for the severe
nausea and vomiting in the emergency room on two occasions in the preceding two months. He also reported
having learned to help himself by taking a hot bath each time the symptoms appeared, which dramaticallyimproved his symptoms. This habit had become a compulsion for him for symptom relief with each episode
of hyperemesis. On physical examination his mucous membranes were dry, his pulse rate was 102/min and
blood pressure was 140/100 with positive orthostasis. The remainder of the physical examination was unremarkable.
His complete blood count and comprehensive metabolic panel were unremarkable. In addition, serum
amylase and lipase levels were within the normal range. His urine drug screen was positive for tetrahydrocannabinol
(THC). Abdominal X-ray series and ultrasonography were within normal limits.
Oesophagogastroduodenoscopy revealed Grade 2 distal oesophagitis and hiatal hernia. On further interviewing,
he admitted to consistent marijuana abuse for the past 6 years, often smoking cannabis every hour or
two on a daily basis. The patient and his mother did not recall any significant past illnesses or recurrent vomiting
when he was a child. He was treated with intravenous fluids with steady improvement in symptoms, and metoclopramide,
pantoprazole and morphine for the abdominal pain. It was explained that marijuana was the cause
of his symptoms and he was advised not to resume marijuana abuse. On subsequent follow-up, he had abstained from cannabis and remained symptom-free.

DISCUSSION
Cannabis is one of the most commonly abused drugs worldwide. Over the past decade, marijuana has
remained the most commonly used illicit substance with close to 50% of high school seniors admitting use at
some time[1]. It is estimated that each year 2.6 million individuals in the USA become new users and most are
younger than 19 years of age[6].
The long-term and short-term toxicity of cannabis abuse is associated with pathological and behavioural
effects. However, cannabis has also been suggested to have therapeutic properties with anticonvulsive,
analgesic, antianxiety and anti-emetic activities. Cannabis has also been used to treat anorexia in patients with
acquired immunodeficiency syndrome[3-5]. The actions of cannabis are mediated by specific cannabinoid
receptors. The first of the cannabinoid receptors-CB-1- was identified in 1990 and this finding revolutionized the
study of cannabinoid biology. Since then, a multitude of roles for the endogenous cannabinoid system has been
proposed. A large number of endogenous cannabinoid neurotransmitters or endocannabinoids have been
identified, and the CB-1 and CB-2 cannabinoid receptors have been characterized[7]. The CB-1 receptors exert
a neuromodulatory role in the central nervous system and enteric plexus[8]. Cannabinoid type 2 receptors
have an immunomodulatory effect and are located on tissues such as microglia[5]. The presence of other
receptors, transporters, and enzymes responsible for the synthesis or metabolism of endocannabinoids are
being recognised at an extraordinary pace. Cannabinoids have a wide variety of effects on the body systems and
physiologic states (Table 1) due to their actions on the receptors as well as direct toxic effects.
The anti-emetic effect of cannabinoids is largely mediated by CB-1 receptors in the brain and the
intestinal tract, although some of their effect may also be receptor-independent. However, in this report,
we were presented with the paradoxical effect of hyperemesis in a susceptible chronic cannabis abuser.
Such a paradoxical response has previously only been demonstrated following acute toxicity to an intravenous
injection of crude marijuana extract[9]. Proposed mechanisms of cannabinoid hyperemesis include
toxicity due to marijuana’s long half-life, fat solubility, delayed gastric emptying, and thermoregulatory and
autonomic disequilibrium via the limbic system[10].
Cannabinoids are known to impair peristalsis in a dosedependent manner[11,12], which can theoretically override
the centrally mediated anti-emetic effects, thus leading to hyperemesis. It is not known why the hyperemesis
syndrome surfaces after several years of cannabis abuse. The effects of cannabinoids on the functions of the
thermoregulatory and autonomic mechanisms of the brain can lead to behavioural changes[10]. Such effects
might be the underlying mechanism for the compulsive hot bathing behaviour. There is also a supposition that
the syndrome could represent a type of cyclic vomiting.
Cyclic vomiting syndrome (CVS) in adults is now very well recognized, and it has been proposed that marijuana
contributes to CVS[13]. However, unlike the other forms of CVS, patients with cannabinoid hyperemesis are not
likely to have a history of migraine or other psychosocial stressors and the peculiar behaviour of hot showers is
Cognitive and mental health
Impaired memory
Impaired attention, organization and integration of complex information
Association with schizophrenia
Increased risk for depression
Pulmonary
Carcinogenic effect
Obstructive lung disease
Increased propensity toward infections
Acute and chronic bronchitis
Behavioural
Weapon possession and physical fighting
Unwanted and unprotected sexual encounters
Unwanted pregnancies
School dropout
Amotivational syndrome
Impairment of driving skill and coordination
Endocrine
Decreased testosterone, sperm motility and production, disruption of
ovulatory cycle
Pregnancy
Low birth weight
Problems with attention, memory and higher cognitive function
Cardiovascular
Stroke
Dose-dependent increase in HR
Orthostasis
Decreased exercise tolerance
Precipitation of angina or myocardial infarction unique to this syndrome.

Allen et al[10] first noted this condition in a group of nineteen patients from Australia with chronic
cannabis abuse and cyclical vomiting illness. An earlier case report by de Moore et al[17] described a chronic
cannabis abuser with psychogenic vomiting, which was complicated by spontaneous pneumomediastinum.
Subsequent reports have identified similar clinical presentations[7-9,18]. Given the high prevalence of chronic
cannabis abuse worldwide and the paucity of reports in the literature, clinicians need to be more attentive to the
clinical features of this underrecognised condition.

REFERENCES
1 National Institutes of Health website: NIDA Info Facts:
Marijuana. National Institute on Drug Abuse. Available
from: URL: http//www.nida.nih.gov/Infofacts/marijuana.
html. Accessed January 23, 2008
2 Baker D, Pryce G, Giovannoni G, Thompson AJ. The
therapeutic potential of cannabis. Lancet Neurol 2003; 2: 291-298
3 Walsh D, Nelson KA, Mahmoud FA. Established and
potential therapeutic applications of cannabinoids in
oncology. Support Care Cancer 2003; 11: 137-143
4 Tramèr MR, Carroll D, Campbell FA, Reynolds DJ, Moore
RA, McQuay HJ. Cannabinoids for control of chemotherapy
induced nausea and vomiting: quantitative systematic
review. BMJ 2001; 323: 16-21
5 Davis M, Maida V, Daeninck P, Pergolizzi J. The emerging
role of cannabinoid neuromodulators in symptom
management. Support Care Cancer 2007; 15: 63-71
6 Foley JD. Adolescent use and misuse of marijuana. Adolesc
Med Clin 2006; 17: 319-334
7 Childers SR, Breivogel CS. Cannabis and endogenous
cannabinoid systems. Drug Alcohol Depend 1998; 51: 173-187
8 Simoneau II, Hamza MS, Mata HP, Siegel EM, Vanderah
TW, Porreca F, Makriyannis A, Malan TP Jr. The cannabinoid
agonist WIN55,212-2 suppresses opioid-induced emesis in
ferrets. Anesthesiology 2001; 94: 882-887
9 Vaziri ND, Thomas R, Sterling M, Seiff K, Pahl MV, Davila
J, Wilson A. Toxicity with intravenous injection of crude
marijuana extract. Clin Toxicol 1981; 18: 353-366
10 Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid
hyperemesis: cyclical hyperemesis in association with
chronic cannabis abuse. Gut 2004; 53: 1566-1570
11 Pertwee RG. Cannabinoids and the gastrointestinal tract.
Gut 2001; 48: 859-867
12 McCallum RW, Soykan I, Sridhar KR, Ricci DA, Lange
RC, Plankey MW. Delta-9-tetrahydrocannabinol delays the
gastric emptying of solid food in humans: a double-blind,
randomized study. Aliment Pharmacol Ther 1999; 13: 77-80
13 Abell TL, Adams KA, Boles RG, Bousvaros A, Chong SK,
Fleisher DR, Hasler WL, Hyman PE, Issenman RM, Li BU,
Linder SL, Mayer EA, McCallum RW, Olden K, Parkman
HP, Rudolph CD, Taché Y, Tarbell S, Vakil N. Cyclic
vomiting syndrome in adults. Neurogastroenterol Motil 2008;
20: 269-284
14 Roche E, Foster PN. Cannabinoid hyperemesis: not just a
problem in Adelaide Hills. Gut 2005; 54: 731
15 Boeckxstaens GE. [Cannabinoid hyperemesis with the
unusual symptom of compulsive bathing] Ned Tijdschr
Geneeskd 2005; 149: 1468-1471
16 Chepyala P, Olden KW. Cyclic vomiting and compulsive
bathing with chronic cannabis abuse. Clin Gastroenterol
Hepatol 2008; 6: 710-712
17 de Moore GM, Baker J, Bui T. Psychogenic vomiting
complicated by marijuana abuse and spontaneous
pneumomediastinum. Aust N Z J Psychiatry 1996; 30: 290-294
18 Chang YH, Windish DM. Cannabinoid hyperemesis relieved
by compulsive bathing. Mayo Clin Proc 2009; 84: 76-78
S- Editor Li LF L- Editor Kerr C E- Editor Yin DH
Essential for diagnosis:
History of regular cannabis use for years
Major clinical features of syndrome
Severe nausea and vomiting
Vomiting that recurs in a cyclic pattern over months
Resolution of symptoms after stopping cannabis use
Supportive features
Compulsive hot baths with symptom relief
Colicky abdominal pain
No evidence of gall bladder or pancreatic inflammation
Table 2 Clinical diagnosis of cannabinoid hyperemesis

Source: 1266 ISSN 1007-9327 CN 14-1219/R World J Gastroenterol March 14, 2009 Volume 15 Number 10
www.wjgnet.com

There were 1810 deaths from benzodiazepine overdose 1990–1996 according to Home Office Statistics and there are an estimated 1600 benzodiazepine-related traffic accidents with 110 deaths each year in the UK.
C.H. Ashton, Emeritus Professor of psychopharmacology, Newcastle UniversityThe current number of benzo addicts in the UK is estimated at one and a half million although no official figures exist. Many more people are ingesting benzos and are on their way to addiction. Many other ex-addicts have withdrawn but remain damaged. There is no treatment for benzo damage. Post-benzo sufferers are often left to struggle alone, stigmatised and excluded by the Health Service that made them ill.
Mick Behan, Parliamentary Researcher, Submission to the Health Select Committee Enquiry into the Influence ofthe Pharmaceutical Industry 2004

“It is estimated that 1.5 million people’s lives have been destroyed by involuntary tranquilliser addiction leading to long periods of mental ill health. A man whom I met recently had been on tranquillisers for 45 years. Those people want to work, but cannot do so. As far as I am aware, the only primary care trust that has introduced a withdrawal programme is Oldham. Will the Secretary of State encourage his Department and the Department of Health to
study the Oldham model with the aim of getting some of those people off prescription drugs and back to work? That would improve their quality of life, and would reduce the benefits bill as well.”
Jim Dobbin (Heywood and Middleton) (Lab/Co-op) Hansard 31 March 2008

Manslaughter by gross negligence
“Negligence is generally defined as failure to exercise a reasonable level of precaution given the circumstances and so may include both acts and omissions. The defendants in such cases are often people carrying out jobs that require special skills or care, such as doctors who fail to meet the standard which could be expected from them and cause death. In R v Bateman (1925) 19 Cr App.R. 8, the Court of Criminal Appeal held that gross negligence
manslaughter involved the following elements:

1. the defendant owed a duty to the deceased to take care
2. the defendant breached this duty
3. the breach caused the death of the deceased
4. the defendant’s negligence was gross, that is, it showed such a disregard for the life and safety of others as to amount to a crime and deserve punishment.”

Negligence
“Failure to exercise the care toward others which would reasonably be expected of a person in the circumstances,or taking action which a reasonable person would not. Failure to exercise care, resulting in injury to others.”

On 23 February 2009 the Archer report on the 4,800 or so haemophiliacs who were infected with hepatitis C (and around 1,200 who were also infected with HIV) through blood transfusions in the late 1970s and early 1980s was made public. The report plainly sets out the pattern of negligence and injustices of successive governments.
The inquiry was privately funded by donations and received no support from government, either financial or through evidence. At the time of the inquiry’s launch, in February 2007, there had been 1,757 deaths and the number is increasing. The inquiry was set up by Lord Morris of Manchester and chaired
by the former solicitor general, Lord Archer. The report runs to 113 pages and Lord Archer told the press conference that the infection of the haemophiliacs was “the worst treatment disaster in the history of the NHS” and a “horrific human tragedy”. But has there been an even greater disaster with nearly fifty years of tranquilliser over-prescribing by doctors?
As with tranquillisers, the blood scandal campaigners have been religiously rejected by the Department of Health over the years and although some have received a small degree of compensation (tranquilliser victims have received none), little has in fact been done to help them or their families. Some UK families have had nothing because their HIV-infected breadwinners died before 2003. Others live anxious and needy lives because they have been unable to work. Canada and Ireland on the other hand acted much more quickly with more generous financial help and assistance with mortgages and insurance. The report has urged the government to offer a more substantial compensation package with survivors and their families but the Department of Health has so far offered only sympathy and a promise to look at the findings. No-blame assistance could be given though it is nearly 20 years since Virginia Bottomley, as health minister, promised that the needs of haemophiliacs would be kept under constant review. That review has sunk without trace.
The Department of Health also looked at the findings of the 2004-5 Health Select Committee report on the Pharmaceutical Industry, which included criticism of the provision for prescribed Tranquilliser addicts, but then rejected almost all of them. Sympathy is cheap but action and recognition costs money and impacts on the image of the NHS and politicians. The DoH is blame averse and addicted to the avoidance of responsibility and the recognition of avoidable scandals. Charles Dickens summed it up very well:
‘Regard our place [The Circumlocution Office] from the point of view that we only ask you to leave us alone and we are as capital a Department as you will find anywhere…It’s like a limited game of cricket. A field of outsiders are always going to bowl in at the Public Service, and we block the balls…Clennam asked what became of the bowlers? The airy young Barnacle replied, that they grew tired, got dead beat, got lamed, got their backs broken,
died off, gave it up, went in for other games.’ Charles Dickens, Little Dorrit, pp 736, 737

The reality of Benzodiazepines
Benzodiazepines are much more than a question of harm done by the medical profession. There is the crucial fact that successive governments of both parties allowed them to do it. Government and medical dismissal of patient experience as relatively minor and short-term is nothing more than a repetition of false assertions, the original source of which (if it was ever known), has been lost. What cannot be rationally doubted, is the fact that benzodiazepines are frequently seriously
damaging—something which might not be immediately apparent, judging by the truly enormous quantities that doctors have prescribed over the years, both in the UK and in other countries. There were warnings from very early in the life of these drugs that this was so, but the drug companies successfully fought off the findings for nearly thirty years until benzodiazepines were old news. Benzodiazepines might well help some people in the short-term, owing to their properties as hypnotics, anticonvulsants, muscle relaxants, amnesics and anxiolytics. But benzodiazepines have potentially incredibly serious adverse effects made even worse by polypharmacy, excessive dosages and long-term use. Benzodiazepines were largely sold to doctors as being much less toxic than their predecessors the barbiturates but they are a long way from being safe drugs. High doses of benzodiazepines lead to over-sedation. Benzodiazepines impact on the ability to think, make decisions,
and to remember. They make it much harder to learn new information. There are people who have withdrawn from benzodiazepines who find they have lost whole years and decades of their lives. In the elderly, these effects can lead to a false diagnosis of Alzheimer’s disease. In spite of this fact, many occupants of old people’s homes and in the community are regularly prescribed benzodiazepines. The primary effect of benzodiazepines is one of addiction. With regular use for only a few months
or even weeks the body comes to depend on them both psychologically and physically for normal
functioning. As a consequence of this dependence, tolerance develops, so that larger doses are needed to produce the same initial effects. There is clear evidence showing that hypnotic effects are no longer effective after a few weeks and anxiolytic effects after only a few scant months. People unknowingly continue taking them mainly to prevent withdrawal effects. If dosage is insufficient once tolerance has
developed, or if the drug is completely stopped, withdrawal symptoms then develop. This is an important reason why the long-term prescribed feel so ill all the time. The Department of Health stubbornly and perversely ignores this basic scientific truth and has illogically introduced an instalment prescription plan. Quite how doling out prescriptions over days will benefit addicted patients is a question it refuses to
answer. It looks like action and to government that is probably enough of a recommendation, but doctors tempted to give it a try, may well find the ‘problem’ becoming much more noticeable in their surgeries as a result. At present there are over a million long-term prescribed benzodiazepine users in the UK. Several
studies, including those carried out by Newcastle University, have shown from computerised prescribing records, that there are 180 or so such patients in every GP practice. These long-term patients, while continuing their drug use, often suffer from adverse effects and from withdrawal effects afterwards —for
a sizeable proportion this is permanent. Long-term use is commonly accompanied by increasingly diverse illnesses.
“Withdrawal symptoms can last months or years in fifteen percent of long-term users. In some people chronic use has resulted in long-term, possibly permanent disability.” C.H. Ashton 2003

Professor C.H. Ashton, unlike those who advise government behind the scenes, ran an effective benzodiazepine withdrawal clinic from 1982–1994 at Newcastle University. She has described the morbidity in the first 50 consecutive patients who attended. They had been taking prescribed “therapeutic” doses of benzodiazepines for between five and twenty years and had decided to withdraw because they did not feel well while taking the drugs. Of these, 20% suffered from agoraphobia and/or
panic attacks, 10% had had neurological investigations (three for Multiple Sclerosis) and 18% had had gastrointestinal investigations. Backing up the argument that long-term benzodiazepines lead to other prescriptions, she said that 62% of the first group had been prescribed other psychotropic drugs since starting benzodiazepines, the most common being antidepressants. In addition, 28% had been prescribed two benzodiazepines, thereby doubling the addiction potential and the possibility of side effects. Professor Ashton has said categorically that the symptoms which led to the investigations and the polypharmacy, were not the reason for starting benzodiazepines, but developed during long-term use. She has said on several occasions, that there is a likelihood that health for everyone does not
necessarily return to normal after prescriptions cease.

“From the current evidence it appears that the symptoms that are most likely to be long-lasting are anxiety and insomnia, cognitive impairment, depression, various sensory and motor phenomena, and gastrointestinal problems. Tranquilliser drugs undoubtedly cause thought deficits and impair coping abilities. There may be an extended period after the taking of benzodiazepines has ceased when former patients find stressful situations difficult to deal
with, though of course many still taking the drugs have the same experience as well. Something as basic as queuing in a shop, or answering the phone, can often seem a frightening and stressful situation. Complete recovery may require the individual to learn new strategies to replace the years of coping through drugs. For some people whose economic and social circumstances, have been severely impacted, this learning may prove to be
inordinately difficult and sometimes impossible.”
C.H. Ashton, 2003
On any patient leaflet you will find advice saying that anxiety occurring after withdrawal is due to pre-existing symptoms recurring. Indeed it is normally cited by the profession as a reason why most doctors continue prescriptions. Patients who were not prescribed the drugs for clinical anxiety (and that is the majority) know that the self-serving ‘symptoms recurring argument’ is untrue. This can be a Catch
22 situation. Depression is common in long-term benzodiazepine users and patient experience points to the drugs being the cause. Depression also appears when patients withdraw. There may be pharmacological reasons for this but who would not be depressed by the realisation of what had been done to them by what they thought was a safe medicine? Depressive symptoms may appear for the very first time after withdrawal—often some weeks later, and may be severe and protracted for a long
time. Suicide has been reported in some studies. Government maintains a supreme indifference to this benzodiazepine research. Instead it continues a parrot-like repetition of the need to prevent addiction occurring in the first place, ignoring the plight of many thousands of people disabled through medical prescribing.
It will be difficult for most people to believe that members of a highly regarded profession could inflict such damage, but the fact is that most doctors have an affinity with potions, and with the rise of drug company influence, they developed an affinity with the manufacturers of them.

“Doctors prescribe by nature. I had a patient who told me that her doctor had warned her that if she came off her medication she might die. I just saw another patient who was on seventy tablets a day. There are doctors out there who are absolutely committed to prescribing, and if the patient doesn’t get better, they just up the dose.”
Dr Robert Lefever, Director of the Promis Recovery Centre in Kent

It was the psychopharmacalogical era beginning in the late fifties that led to the explosion of medically-induced ill health. Benzodiazepines were pushed by their manufacturers as appropriate for virtually anything. Doctors followed the logic of this advert religiously: “In the face of ill health there is anxiety and where there is anxiety either as a complicating factor or as a cause of illness itself, there is a place for LIBRIUM.”
Today, in spite of this undeniable fact, the UK Department of Health rigidly maintains an illusion that the drugs are always prescribed for clinical anxiety and therefore suffering patients fall within the psychiatric sphere of responsibility. That way, it can say that any psychological problems while taking benzodiazepines or following withdrawal, are due to pre-prescription symptoms returning. They will not engage with the fact that patients, who were given the drugs for other reasons, are as likely to experience the same psychological difficulties as those who were given them for clinical anxiety. Physical side-effects are ignored. It has been claimed that benzodiazepines are the most researched drugs in the world but much of the early research was basic and superficial to say the least, and would not meet today’s standards.

Long-term research has never taken place, either then or subsequently. Patients who took the drugs for years—many for decades—therefore have their claims of health damage ignored and rejected in the face of zero scientific evidence that it did not happen. Between the introduction of benzodiazepines and 2004, Home Office and other figures suggest 17,000 deaths associated with benzodiazepines but as with all official statistics, they may well be an underestimate. In reply to a question from the Parliamentary Health Committee in 2004, Professor Alasdair Breckenridge, the Chairman of the UK drugs regulator stated that he thought there had been
approximately 170 deaths. As Professor Heather Ashton said at the time, this represented 1% of the total and was a gross under-representation on the part of the regulator. There are people who have taken the drugs and claim to have experienced no untoward effects or problems during ingestion or in withdrawal. On one side of the argument about the benefit of benzodiazepines and possible symptoms, there is Professor David Nutt of Bristol University, who believes the downside of benzodiazepines has been over-emphasised and that medics are being unduly
constrained in their use. Nutt outlines his position on benzodiazepines in his paper “The Psychopharmacology of Anxiety”. He recommends prescribing practices that directly contradict the 1988 CSM Guidelines on prescribing and what the Department of Health says is its position. Professor Nutt takes every opportunity to air these views, most recently in a lecture to students and medical staff at Newcastle University. Professor Heather Ashton agrees that some people can withdraw from benzodiazepines with few if any symptoms and that there are probably many reasons why. Personality may play a part and this ultimately has a physical basis, shaped by genetics and environment which determines the “wiring up” of the brain—e.g. the synaptic connections which mediate the ways that individuals have learnt to cope
with anxiety and stress. There is evidence that anxious people have fewer GABA/benzodiazepine receptors in the emotional areas of the brain than more stolid people—so perhaps those without withdrawal symptoms had more GABA receptors to utilise. They may not develop so much benzodiazepine tolerance (down-regulation of GABA/benzodiazepine receptors) and so suffer less rebound of GABA under activity related to withdrawal symptoms. The distribution and sensitivity of these
receptors may vary so that some people may have more physical symptoms in withdrawal while others experience more psychological symptoms. She also says that the nature of withdrawal may depend partly on the type of benzodiazepine used. Withdrawal symptoms are usually worse in those using short acting
and/or potent benzodiazepines such as lorazepam, alprazolam, and clonazepam even if these are withdrawn slowly
A crucial ingredient, seldom if ever, ever mentioned in relation to benzodiazepine withdrawal, is the factor of polypharmacy, which Professor Ashton agrees may also play a part. She says that over 60% of the long-term dependent she saw in her National Health Service Withdrawal Clinic, had also been prescribed other drugs, usually antidepressants, along with the benzodiazepines. Antidepressants, antipsychotics, and morphine-based painkillers, all have side-effects themselves—with symptoms not dissimilar to benzodiazepine withdrawal. Any discussion by anyone on the subject of benzodiazepine withdrawal is therefore necessarily incomplete, if it does not take into account the fact that for many people, benzodiazepine prescriptions led to other drug prescriptions—many of them producing physical dependence. It is often a situation of withdrawing from multi-drug use, rather than single drug use. So, the experience of people who have taken (or who are still taking) benzodiazepines and indeed other mind-altering drugs, varies. There are a number of reasons for the individuality of response, not least, differences in human physical make-up, length of prescription and differences in personal circumstances. A person working in a job, which does not require high-level intellectual thought, or constant decision-making, for instance, may find it altogether easier to avoid the impact of benzodiazepines on cognition.
But there needs to be some sort of true representation for the stories of the very large numbers of UK citizens whose existence has been needlessly harmed and sometimes destroyed by prescribed benzodiazepine addiction. Benzodiazepines are not the only treatment to destroy health and lives as the recent Vioxx disaster and the haemophilia scandal testify. There are strong common elements between
the stories—pharmaceutical company deceit, regulatory inaction, and dogged medical belief in benefit, is common to all. But it is the scale of benzodiazepine prescribing and its longevity that makes this story unique. Benzodiazepines have been prescribed in their billions to millions of patients, based on a jigsaw
of poor and non-existent research, pharmaceutical power, amateur regulation, medical ignorance and disdain, and organised government cover-up.
How are statistics of large benefit and little harm arrived at? What rigorous investigation is it based on? Is it, for instance, based on the absence of complaint to doctors, regulators or drug companies? Is it based on collected endorsements from patients? Or is based on neither of these? Is it, in fact, not a statistic at all—merely another plank in the house built by the indoctrinators? But the desire to believe is strong. It is a sad but observable fact that we look beyond positive claims and assurances only after we have personally met the hidden downside of drugs that ‘help millions’, through our own experience.

Socio-economic cost of benzodiazepine addiction
Benzodiazepines have been a near 50 year horror story for tens of thousands of people in the UK but this medical disgrace has never been addressed. Weak, belated and spasmodic warnings have been issued over the years and they have had the unfortunate side-effect for patients, of allowing government and the benzodiazepine manufacturers to further draw a veil over the historic and ongoing impact of
inappropriate prescribing in the public mind. It is possible to make an argument that much of the medical profession does not fully realise what it has done, given the speed of consultations, the failure of regulators to pass on the horror stories they
have been told, and the distance between the patient in the doctor’s surgery and the patient’s actual life outside it. But above all, it is the chemical ability of benzodiazepines to produce apparent mental instability and engender a belief, not only in doctors but also in patients, that this drug-produced harm is genuine illness that has led to the greatest medical damage. The belief has been fostered among
doctors (and unwittingly by the patients), that the drugs and consequent ones have been necessary. It is simply not true that benzodiazepine injury has ever been addressed.
There are still far too many prescribed addicts in the UK and thousands of former addicts who took the drugs long-term, and as a result are living with ruined health which cannot be rebuilt. Many are living in poverty because of the effects of benzodiazepines. Whole lives have been lost and cannot be relived. Families have
disintegrated, never to reunite. The real severity of benzodiazepine damage has never been officially recognised. In the face of it the Department of Health believes that repeated utterance of statements such as ‘we take the problem seriously’ or ‘our priority is to prevent addiction occurring in the first place’ makes it true for actual and
former patients and is adequate support for those badly in need of it. The debate on benzodiazepines has largely centred on addiction versus efficacy, but addiction
can be seen as only part of the picture—mostly important in relation to the fact that once addicted, patients keep taking them— the far more serious side of the issue centres around what continued addiction often leads to, and its dire effects on general health, thinking abilities, and life. There are extensive costs to the patient and to society, caused by benzodiazepines but not studied by medicine, because their nature is not seen as medical. There are costs produced by benzodiazepines which are medical but which have never been researched, and which are therefore not
recognised by medicine

There are costs to the National Health Service of medical investigations for symptoms which are in reality a result of the effects of benzodiazepines. These costs must be very high indeed, if patient reporting is taken into account, but they are officially unquantified. Investigations for MS, ME, IBS, Arthritis and Thyroid deficiency and other ‘ghost illnesses’ are common—usually the results are negative.
For people taking benzodiazepines and particularly the elderly, there is a much increased risk of accidents. The cause of the accidents, whether occurring in the home, on the road, at work or in a care home is routinely not recognised, but has a cost for the individual beyond the cost to the NHS. There is a great deal of evidence that the unborn are severely affected by the addiction of the mother. The link between benzodiazepines and foetal harm was denied in Parliament in 1999 but it
undoubtedly occurs.
“The developing foetus can be congenitally malformed; it can have heart attacks in the womb. We also know that the newborn baby born to somebody taking benzodiazepines will have difficulty breathing and they would have floppy muscles—what doctors call a ‘floppy baby’ and they may be unduly cold because the temperature regulation, which is so important to a baby, is disrupted…Well I think if any doctor is prescribing benzodiazepines to a pregnant woman, he should check his indemnification status because it is in fact illegal prescribing.”
Robert Kerwin, Professor of Psychopharmacology at the Maudesley Hospital in London, ‘Face the Facts’, BBC Radio 4 1999

Prescribed benzodiazepines can lead to loss of control over actions which means in practice that drug-induced violence occurs in the home involving partners and children. Unwanted pregnancies are another side-effect of the drugs. Inhibition reduction leads to anti-social acts such as theft and vandalism. People end up in gaol because the impact on thought and emotion is not recognised. As Professor Ashton says:
“Benzodiazepines can occasionally cause paradoxical aggression and have been associated with baby-battering, wife-beating and grandma-bashing. They can also cause depression and can precipitate suicide in depressed patients. They should not be used in depression although they are still commonly prescribed long-term for depressed and anxious patients. They can also cause emotional blunting and apathy, with inability to cope with the needs of children and family, an effect bitterly regretted by many long-term users.”

Benzodiazepines cause job loss either whilst taking them or while attempting to withdraw. Not everyone loses their job of course but a significantly large number do, and it is not surprising, given the deadening effects of the addiction and the high number and severity of possible withdrawal effects. This effect on the individual and on families is totally ignored by government. In 2004 the Chief Medical
Officer, Professor Liam Donaldson, reminded doctors of their continuing over-prescribing. He referred to the cost to the NHS of the drugs themselves, but made no mention of the costs to the individual. There is a large financial impact to the state generally, which benzodiazepine addiction is responsible for. People who are unable to work pay no taxes or national insurance. Their spending power is curtailed and therefore they pay less VAT. Addicted and unemployed the benzodiazepine dependent make very little contribution to the economy. Although many iatrogenic benzodiazepine addicts are to all intents and purposes disabled, few receive disability benefits. Thousands do receive incapacity benefit at a lower figure, because of the length of their ‘illness’, and this is of course a drain on the national economy. Many iatrogenic victims have not worked for decades. Perhaps the biggest loss for a proportion of the dependent (and who knows how big this proportion is) is the loss of choice. They cannot choose to buy a house or might lose a house because of
the drug effects. They cannot take holidays or buy a new car. They cannot socialise or take up hobbies because of induced anxiety and the inability to concentrate and think clearly. Some discover after they have withdrawn from the drugs that they never left the house or indeed a room, for years because of benzo-induced agoraphobia—prisoners because of drug prescriptions. There is much exhortation from government these days about the need to build up personal pensions to maintain a secure lifestyle in retirement—we are all living longer and the state is becoming
more hard-pressed to finance pensioners. There are thousands, addicted for decades to benzodiazepines, who feel assaulted anew when they hear that message. Through state avoidance of responsibility for health protection, they had no chance to build up a personal pension, leaving them entirely dependent on the state for the future. What a supreme irony it is then, that at a time when the state is telling everyone that the state pension is completely inadequate and that they should save for a personal one, there are many condemned to poverty through state inactivity and denial.
The most insidious effect of the drugs in the estimation of many is the effect the drugs have had on their family. The family was not prescribed the drugs but it was as certainly and indelibly marked as the taker. The lack of emotional response due to benzodiazepines is something a child does not understand and may never understand, even as an adult. The life chances of children of the unemployed
and sick iatrogenic addict are necessarily reduced and their emotional needs may remain unsatisfied, leading to problems for them later in life. It can be very difficult afterwards to re-establish relationships between a formerly addicted parent and children. Where does the patient find closure in the face of orchestrated denial, lack of government recognition and help, and a spirit within the medical profession that sees each new drug as a wonder drug, taking decades each time before it exercises control? The three components of continuing good health are psychological, physical and social. Benzodiazepines have a three-pronged negative effect on health—the effects of taking of them, the realisation afterwards of the impact they had on a life and the realisation for the individual that they are powerless to achieve recognition. It is a deep and genuine kind of grief which is not in the annals of medicine. Within the present political, legal and medical structures, there is little hope of closure.

A Selection of Informed Comments on Tranquillisers
“Thousands of people could not possibly invent the bizarre symptoms caused by therapeutic use of benzodiazepines and reactions to their withdrawal. Many users have to cope, not only with a frightening range of symptoms, but also with the disbelief and hostility of their doctors and families. It is not uncommon for patients to be “struck off” if they continue to complain about withdrawal symptoms. Even when doctors are concerned and understanding about the problem, they often have little knowledge of withdrawal procedure, even less about
treatment…”
Trickett S, Withdrawal from Benzodiazepines, Journal of the Royal College of General Practitioners 1983; 33: 608

“The medical profession took nearly 20 years from the introduction of benzodiazepines to recognise officially that these minor tranquillisers and hypnotics were potentially addictive. The ‘happiness pills’, which had been propping up a fair proportion of the adult population since the early 1960s, were found to have an unexpectedly bitter aftertaste: doctors and patients alike were unprepared for the problems of dependence and withdrawal that are
now known to be common even with normal therapeutic doses.”
Editorial (Anon), The Benzodiazepine Bind, The Lancet, 22 September 1984, 706

“There’s certainly a problem, the NHS are concerned. The NHS spends about £40 million per annum on these drugs. There are a substantial number of people who do suffer from this problem long-term. I know that the withdrawal symptoms can be agonising for some people and can be very difficult indeed.”
John Patten, Health Minister, 1984

“In the UK, 11.2% of all adults take an anti-anxiety drug at some time during any one year. But over a quarter of these people (3.1% of all adults) are chronic users, taking such medication every day. Even at a conservative estimate, 20% of these will develop symptoms when they attempt to withdraw. That means a quarter of a million people in the UK. The sooner the medical profession faces up to its responsibilities towards these iatrogenic
addicts, the sooner it will regain the confidence of the anxious members of our community.”
M.H. Lader, Anna C. Higgitt, Management of benzodiazepine dependence, Update 1986, Brit J Addiction, 1986, 81, 7–10

“The benzodiazepines are probably the most addictive drugs ever created and the vast army of enthusiastic doctors who prescribed these drugs by the tonne have created the world’s largest drug addiction problem.”
Dr Vernon Coleman, ‘The Drugs Myth’, 1992

Dear Mr Haslam,
Thank you for your recent letter regarding Benzodiazepine Tranquillisers. Dawn Primarolo and myself have been taking up cases and have advised on how best the groups involved might organise a parliamentary lobby and keep attention on these issues. We have also tried to assist through both Parliamentary Questions and raising the matter on the floor of the House, in pushing the Government to accept its own responsibilities and to take action now to ensure that it does not happen again.

This is something we will be returning to both in the House and in terms of our own future policy development. I am passing your letter to Paul Boateng who, as the legal affairs spokesman, has specific responsibility for the litigation side of what is a national scandal.
David Blunkett MP, Shadow Secretary of State for Health,
24 February 1994

“…the risks [of benzodiazepines] were always obvious and…the providers of medicine between them, readily let this happen.”
Charles Medawar, Social Audit, Power and Dependence 1991

They [benzodiazepines] are very effective at relieving anxiety, but we now know that they can be addictive after only four weeks regular use. When people try to stop taking them they may experience unpleasant withdrawal symptoms which can go on for some time. These drugs should be only used for short periods, perhaps to help during a crisis. They should not be used for longer-term treatment of anxiety.
The Royal College of Psychiatrists, July 2001

“Benzos are responsible for more pain, unhappiness and damage than anything else in our society.”
Phil Woolas MP, Deputy Leader of the House of Commons and Local Government Minister, Oldham Chronicle, February 12 2004

Parallels
“My family believe my brother was murdered, and I stick by that.”
Brother of Blood Transfusion Victim, Daily Telegraph, February 23, 2009
Interviewer: I don’t want to sensationalise this Susan but, in the last couple of minutes, you’ve actually accused doctors of murder. Campaigner Sue Bibby: Well I think that they do have a case to answer – it would be very nice if one or two of them would actually stand up and speak.
Talk Radio UK Interview on Tranquillisers with Mike Dicken and Susan Bibby
December 5, 1998

Is one scandal greater than the other, a larger case of inertia and unconcern? A scandal is a scandal, both are sizeable and have involved a large number of deaths, both have involved government inaction, but the 48 year benzodiazepine scandal must be seen as the greater if only for its longevity and absence of recognition. The heyday of vast tranquilliser over-prescribing took place in the 1970s and 1980s. The 4,800 or so haemophiliac victims received their contaminated blood at that time. But the tranquilliser scandal rolled on and new addicts are still, without warnings, being created today.

“The Department of Health fails even to collect figures that might be considered unpalatable.”
Alice Miles, The Times, July 4 2007

“[Benzodiazepines] have been prescribed for sports injuries, muscle spasms, premenstrual tension, exam nerves, depression, general malaise and much else…”
Professor C.H. Ashton, Bristol and District Tranquilliser Project AGM, October 2005

The benzodiazepine story has many unique qualities and the Department of Health has developed a policy of no-admission and steadfast denial. Instead of action it has:
•Routinely insisted that its priority is “to prevent addiction occurring in the first place” in the face of much evidence of injury and the fact that those injuries have been occurring for nearly half a century. Crucially, it also maintains that doctors must be free to exercise clinical judgement, even when that judgement (as in the case of David Nutt) is likely to increase addiction and harm.

•It has made no effort to commission research into the wide variety of injuries reported by patients and sticks rigidly to the message that tranquilliser addiction is a mental health problem when in fact it is a problem of chemical addiction with physical responses to that addiction.

•It has left campaigners to provide detailed information on the scale and nature of the problem but has not accepted it; neither has it made any attempt to investigate and provide its own data.

•It has always insisted that treatment and withdrawal assistance is available when it has been shown to be non-existent and in the knowledge that prescribers who addicted patients have little interest in the addiction or the expertise to assist.

•It has consistently evaded all responsibility for the situation, preferring historically to blame it on prescribers, though lately it has moved towards the blaming of patients and stigmatising them as drug misusers. Medical and government defence of the benzodiazepine scandal has moved through several stages, not necessarily in this order and not necessarily one at a time. Sometimes previous positions are
resurrected:

•The drugs are not addictive
•And if they are, it is because of an addictive personality
•Patients ask for them
•Patients bully doctors into prescribing
•The drugs are cheap to provide for government
•Doctors have no time to assist in withdrawal/doctors find it very difficult
•There are no alternatives to pills in UK healthcare
•Aware or former iatrogenic addicts are merely seeking compensation
•It’s all down to defective genes
•It’s all in the past, it was regrettable but we have learned lessons
•Patients abuse the drugs and must be controlled
•Benzo campaigners select their evidence

In 1988 the Committee on the Safety of Medicines issued 4 week prescribing Guidelines to doctors but these were never seriously followed up and the CSM had no remit to discover whether they were being followed. There was no plan to audit the number of patients on individual prescriber lists who had already exceeded the Guidelines and offer withdrawal assistance. Hence there are tens of thousands of
people today who have been taking tranquillisers for decades without knowledge that their life is being harmed.

“GPs will be asked to trawl through their patients’ records to identify those most at risk of developing cardiovascular disease and call them in for an assessment, the National Institute for Health and Clinical Excellence proposed today.
The Guardian in June 2007

Hearing the victims of the haemophilia scandal speak is like a rerun of the tranquilliser scandal: “I would just like to see someone apologise, but they won’t do it because they think they will be subject to criminal actions.” “One of the reasons the government had been so successful in keeping the whole thing silent was because there
were so few people willing to stand in public and campaign.” “People say move on with your life, but that’s hard if you have had no resolution and you are surviving on £59 a
week.” “We need an apology, just the acknowledgement that this happened and it shouldn’t have happened. I don’t think they realise how much that means to people.”
“People need to be able to live comfortably without having to go cap in hand to the local authority or a fund whenever they need the slightest thing. All we are asking for is to be able to live with decency and dignity.”

Tranquilliser victims
“[But] for a large proportion of those on incapacity benefit—half of them claiming for five years or longer—the benefit is a (cheap) compensation for the fact that they have no future. And never will have…”
Yvonne Roberts, Where’s the Benefit? The Guardian, February 6 2008

Tranquilliser victims have received no recognition, no support, no apologies, no compensation and no closure—and this in spite of the fact that so many of them cannot work, have no pensions or security and live with ruined health because there is no agonist for the damage inflicted. Many victims do receive state benefits and the government refuses to investigate how many of those on benefits are there because of the drugs, but benefits are not large and do not represent security. In fact because the Department of Works and Pensions, reliant on Department of Health information, does not take benzodiazepine injury seriously, the victims live constantly with the fear of losing those benefits. The Archer report acknowledges how the extraordinary financial burden of long term ill-health had been placed upon people who had lost their jobs, lost their insurance and, as has so often been the case, lost the breadwinners in their families. There has been no such acknowledgement in the case of tranquillisers. In this horror story the victims have been left to their own devices.

•Government has allowed health, social and economic destruction through addiction to take place and still allows it.
•Government knows what has happened and avoids recognition of it.
•Government has left many to wither on benefits and has made no attempt at rehabilitation.
•Government now believes as part of its political struggle with other parties that such people can continue to remain unrecognised and can be viewed in exactly the same light as every other benefit claimant.

Tranquilliser Quotes

“…apart from people’s physical health going down (although luckily, some people seem to be able to stand up to that), they are described by their families as being “Jekyll and Hyde”. Agoraphobia (not being able to go out) is a very, very common symptom which very few people actually have before they’re given the drugs – sometimes they might have it, but mostly they don’t have it until they’ve been put on the drugs. This of course makes them [the
patients] incapable of doing anything much. They can’t go out to the local shops, they can’t look after their children properly; they are very distressed by this and feel it’s their own fault. Usually they go back to the GP and the GP will say: “Oh you’re an anxious personality and that’s what’s wrong with you,” and they usually give them more benzodiazepines, or other antidepressant drugs as well.
Sue Bibby Talk Radio UK Interview with Mike Dicken and Susan Bibby December 5, 1998

“In fact the drug was poisoning my central nervous system. Emotionally I felt numb…Those pills cheated me of myadult life – I lived like a robot…”

“….After 30 years of tranquillisers mixed with a variety of anti-depressants, the mother-of-six says the drugs have left her physically and mentally handicapped. Over the years Mrs Dixon’s health has deteriorated and she has suffered a host of problems including panic attacks, muscle weakness, mood swings, bowel problems, nausea and severe pelvic pain. Her condition has left her unable to leave her home for the past 10 years and watch her children
and 20 grandchildren growing up….”

“One Barnet woman, who wanted to remain anonymous, says she was left housebound after being addicted to benzodiazepines for more than 20 years. She was originally prescribed the drugs for a stomach upset, but now suffers thyroid problem, asthma, ME and leg pain so severe she can hardly walk – all of which she attributes to the drugs.”
Hendon & Finchley Times August 2003

“I was prescribed Lorazepam at 16. I am now aged 44 and have been off tranquillisers for two years, after a GP suggested that I had perhaps been on them too long! After suffering most of my life with Agoraphobia and Panic Attacks, I cannot believe that this drug is still manufactured. It is high time the drug companies were held accountable and something positive was done. How many people have to lose their quality of life and battle so hard, with little help to regain it, before someone says stop.”
The Tranquilliser Trap, May 2001

“If the government knows these drugs to be harmful why are they allowing them to be dispensed? Why have they not implemented resources to help patients come off the drugs? It takes more than a guideline…the problem will not go away…indeed it will not ‘die’ off which is one method some GPs are using to reduce their prescriptions, i.e. they are waiting for those patients who have been addicted for 20+ years to die because it is easier to give a 2
minute prescription rather than seeing a demanding patient for 20 minutes a visit every day until they get what they demand.”
The Tranquilliser Trap, May 2001

“I believe I am one of the longest addicts of Lorazepam, I started taking them in 1974 following a car accident and finished taking them in 2000 (26 years). I was 18 when I was first prescribed them and the effect upon my life has been devastating, like others I thought I was going out of my mind, a fact my doctor was only too willing to agree with…I am forty five and I can’t remember what it was like when I was 18, I can’t remember a time when my life was
not governed by fear. I may function in society, but that does not mean I can lead a normal life. However I find that the medical profession believes that now I no longer take these drugs that I am back to full fitness…I was offered no support from anywhere and yet if I was a Heroin addict, I would have had masses of help and support.” The Tranquilliser Trap, May 2001

“There are people out there…who are hooked, unknowingly, unwillingly, and they feel that society has ‘chucked them overboard’. They feel they no longer belong anywhere. They feel they’ve lost such a lot, that they can no longer regard themselves as fully human.”The Tranquilliser Trap, May 2001

Source: Published in Daily Dose 4th April 2009 Colin Downes-Grainger 25 .02.2009

BackgroundStreet drugs known as ‘ecstasy’ have been sold for
about 20 years in the UK. The active substance that
such tablets contain – or purport to contain – is
3,4-methylenedioxymethamphetamine (MDMA).
Shortly after consumption, MDMA releases
chemicals in the brain that tend to bring about
a sense of euphoria, exhilaration and increased
intimacy with others. It is thought to be the third
most commonly used illegal drug in the UK after
cannabis and cocaine, with estimates suggesting
that between 500,000 and 2 million tablets are
consumed each week. Most people who take
ecstasy also use other legal and illegal drugs,
sometimes at the same time. Ecstasy is commonly
taken in nightclubs and at parties and is very often
associated with extended sessions of dancing.
Along with the pleasurable effects sought by users
of MDMA, it has become clear that the drug can
cause a range of unintended harms. In the short
term, a range of adverse events have been reported
– some fatal – and consumption of MDMA may
also have long-term consequences, especially with
regard to users’ mental health.
Objectives
This review aims to address the question: ‘What
are the harmful health effects of taking ecstasy
(MDMA) for recreational use?’ It does not examine
the harmful indirect and/or social effects, such as
effects on driving and road traffic accidents and
the consequences of any effect MDMA may have on
sexual behaviour.

Previous research syntheses
(Level I evidence)
For each identified Level I synthesis, it was difficult
to ascertain the exact methods adopted and
evidence included. Three reviews reported worse
performance for ecstasy users compared to controls
in a variety of neurocognitive domains (attention,
verbal learning and memory, non-verbal learning
and memory, motor/psychomotor speed, executive
systems functioning, short- and long-term
memory). A fourth study reviewed self-reported
depressive symptoms and found that ecstasy users
had increased levels compared to controls. The
final synthesis was primarily concerned with the
acute intoxication effects of ecstasy rather than
health harms. In all analyses, the effect sizes seen
were considered to be small.
Controlled observational
studies (Level II evidence)
Of the 110 controlled observational studies
included, there was one prospective study, the
Netherlands XTC Toxicity (NeXT) study, which
recruited a cohort of participants likely to start
using ecstasy and followed them for a year. Those
who started using ecstasy were then compared to
a group of matched controls who had remained
ecstasy-naïve. Ecstasy-exposed participants had
poorer performance in some memory tests,
although the absolute test scores for both cohorts
were comfortably within the normal range.
Other tests suggested an association between
ecstasy exposure and certain aspects of sensation seeking,
but there was no evidence of an effect on
depression or impulsivity. The cumulative dose of
ecstasy consumed was small (median 3–6 tablets).
The remaining Level II evidence consisted of cross sectional
studies only. Data were directly pooled
for seven individual outcomes. Six were common
measures of immediate and delayed verbal recall,
in which ecstasy users performed significantly
worse than polydrug controls. Effect sizes appeared
to be small, with the mean scores for each group
falling within the normal range for the instrument
concerned. No difference was seen between ecstasy
users and polydrug and drug-naïve controls in the
remaining measure, IQ.
A total of 915 outcome measures were grouped
into broad outcome domains as suggested in
the literature and after consultation with expert
advisers. For 16 of these meta-outcomes, there
were sufficient data for meta-analysis: immediate
and delayed verbal and visual memory, working
memory, sustained and focused attention, three
measures of executive function (planning, response
inhibition and shifting), perceptual organisation,
self-rated depression, memory, and anxiety and
impulsivity measured objectively and subjectively.
Ecstasy users performed significantly worse than
polydrug controls on all outcome domains with
the exception of executive function (response
inhibition and shifting) and objective measures of
impulsivity. Fewer comparisons were possible with
drug-naïve controls, with statistically significant
effects seen for verbal and working memory and
self-rated measures of depression, memory and
impulsivity. With both control groups, former
ecstasy users frequently showed deficits that
matched or exceeded those seen among current
users.
The small effect sizes seen were not consistently
modified by any study-level demographic variables.
There was little evidence of a dose–response
effect: studies reporting heavier average use
of ecstasy did not provide more extreme effect
measures than those consisting of lighter users,
and there was no demonstrable effect of length
of abstinence from ecstasy. When assessing the
impact of inter-arm differences on results, no
consistent effect was seen for imbalances in age
or gender. However, in several cases, it appeared
that imbalances in intelligence between cohorts
may have been important. Use of other drugs also
appeared to modify effects: alcohol consumption
proved the most consistent effect modifier, with
increased exposure in ecstasy-exposed populations

apparently reducing the magnitude of deficits
across a range of neurocognitive outcomes.
For the remaining outcome domains, there
were insufficient data for quantitative synthesis
and the results were summarised narratively.
For psychopathological symptoms, there was a
significant deficit for ecstasy users compared to
polydrug controls in the obsessive–compulsive
domain only, with greater deficits seen in
comparison to drug-naïve controls. In a few studies,
ecstasy users have been shown to have higher
levels of subjectively rated aggression than drug naïve
controls. It was not possible to draw clear
conclusions about the possible effects of ecstasy
consumption on dental health, loneliness, motor
function or sleep disturbance.
Case series and case reports
(Level III evidence)
Registry data from the np-SAD and GMR are not
directly comparable due to differences in data
sources and recording of drug use. The GMR
(1993–2006) suggests that there were, on average,
17 deaths a year where ecstasy was recorded as the
sole drug involved (2.5% of all deaths ascribed to a
single drug) and another 33 per year where it was
reported as co-drug use. Ecstasy-associated deaths
appear to have increased up to 2001 but to have
stabilised thereafter. In the 10 years to 2006, the
np-SAD recorded an average of 50 drug-related
deaths in which ecstasy was present (69 in 2006; 5%
of the total for the year). Ecstasy was believed to be
the sole drug implicated in an average of 10 deaths
annually over the same time period. According to
this registry, the typical victim of an ecstasy death
is an employed white male in his twenties, who
is a known drug user co-using a number of other
substances. Nearly half of ecstasy-related deaths
occur on a Saturday or Sunday night.
Published case series and case reports document
a wide range of fatal and non-fatal acute harms,
often very selectively. Two major syndromes
are most commonly reported as the immediate
cause of death in fatal cases: hyperthermia (with
consequences including disseminated intravascular
coagulation, rhabdomyolysis and acute liver and
renal failure) and hyponatraemia (commonly
presenting with confusion and seizures due to
cerebral oedema). Ecstasy users presenting with
hyponatraemia have invariably consumed a large
amount of water. We found 41 deaths relating to
hyperthermia reported in the literature and 10
from hyponatraemia (all women).
Other acute harms associated with fatal cases
include cardiovascular dysfunction, neurological
dysfunction (seizures and haemorrhage) and
suicide. Acute renal failure and sub acute liver
failure can occur without association with
hyperthermia. All these presentations were also
seen in non-fatal cases, alongside an additional
range of symptoms including acute psychiatric
effects, urinary retention and respiratory
problems including pneumothorax and
pneumomediastinum.
There are difficulties in estimating taken dose
of MDMA from the available literature, and it is
not clear why some people seem to have acute,
even fatal, reactions to doses that are commonly
tolerated in others.
Discussion
The evidence we identified for this review
provides a fairly consistent picture of deficits in
neuro-cognitive function for ecstasy users compared
to ecstasy-naïve controls. Although the effects
are consistent and strong for some measures,
particularly verbal and working memory, the effect
sizes generally appear to be small: where single
outcome measures were pooled, the mean scores of
all participants tended to fall within normal ranges
for the instrument in question and, where multiple
measures were pooled, the estimated effect sizes
were typically in the range that would be classified
as ‘small’.
However, there are substantial shortcomings in the
methodological quality of the studies analysed.
Because none of the studies was blinded, observer
or measurement bias may account for some of
the apparent effect. There is a suggestion of
publication bias in some analyses, and we saw clear
evidence of selective reporting of outcomes.
Selection bias is an inevitable problem: due to the
observational nature of all relevant evidence, there
is no guarantee that the cohorts being compared
were not subject to differences in areas other than
exposure to ecstasy. This effect will have been
exaggerated in those studies comparing ecstasy exposed
participants to drug-naïve controls; in
these instances, it is impossible to isolate the effect
of ecstasy exposure from the impact of other
substances. Within-study imbalances in intelligence
and the use of other substances, particularly
alcohol, appeared to explain some of the effects
seen. We suggest that the apparently beneficial
Methods
The following databases were searched using
a comprehensive search syntax: MEDLINE,
EMBASE, PsycINFO (run 19 September 2007)
and Web of Knowledge (run 7 October 2007).
The search outputs were considered against pre specified
inclusion/exclusion criteria; the full text
of all papers that could not confidently be excluded
on title and abstract alone was then retrieved and
screened. Only studies published in English were
included. Meeting abstracts were included only
if sufficient methodological details were given
to allow appraisal of study quality. Studies were
categorised according to a hierarchy of research
design, with systematic research syntheses (Level
I evidence) being preferred as the most valid and
least open to bias. Where Level I evidence was
not available, controlled observational studies
(Level II evidence) were systematically reviewed. If
neither Level I nor Level II evidence was available,
uncontrolled case series and case reports (Level
III evidence) were systematically surveyed. Data
extraction was undertaken by one reviewer and a
sample checked by a second.
Synthesising Level II evidence posed substantial
challenges due to the heterogeneity of the included
studies, the number and range of outcome
measures reported, the multiplicity of comparisons
(differing ecstasy exposures, differing comparator
groups) and outcomes, repeated measures and
the observational nature of the data. Analyses
were stratified for current and former ecstasy
users, with separate analyses for control groups
using other illegal drugs but not ecstasy (polydrug
controls) or controls naïve to illegal drugs (drug naïve
controls). Random-effects meta-analyses were
used throughout. Heterogeneity was also explored
through study-level regression analysis (meta regression).
Where a sufficient number of studies
had reported identical outcomes, they were meta analysed
on their original scale. Other outcome
measures were grouped into broad domains
and effect sizes expressed as standardised mean
differences in order to combine data derived from
multiple instruments. Objective and self-reported
outcome measures within each domain were
analysed separately.
For the Level III evidence, only narrative synthesis
was possible.
Results
Of 4394 papers identified by our searches, 795
were reviewed in full and 422 met the inclusion
criteria. Five systematic syntheses, 110 controlled
observational studies and 307 uncontrolled
effect of alcohol consumption may be explained
in two ways: either alcohol may mitigate the
hyperthermic effects of ecstasy in the acute setting,
attenuating damage to the brain, or ecstasy users
who co-use alcohol may represent a population of
more casual ecstasy takers than those who tend not
to drink.
Although the NeXT study suggests that small
deficits in memory may be secondary to ecstasy
exposure, all other included studies were
cross-sectional in nature; without evidence of
the temporal relationship between exposure
and outcome, it is difficult to draw any causal
inferences.
We did not find any studies directly investigating
the quality of life of participants, and we found
no attempts to assess the clinical meaningfulness
of any inter-cohort differences. The clinical
significance of any exposure effect is thus
uncertain; it seems unlikely that these deficits
significantly impair the average ecstasy user’s
everyday functioning or quality of life. However,
our methods are unlikely to have identified
subgroups that may be particularly susceptible
to ecstasy. In addition, it is difficult to know how
representative the studies are of the ecstasy-using
population as a whole. Generalising the findings is
therefore problematic.
Ecstasy is associated with a wide range of
acute harms, but remains a rare cause of death
when reported as the sole drug associated with
death related to drug use. Hyperthermia and
hyponatraemia and their consequences are the
commonest causes of death, but a wide range of
other acute fatal and non-fatal harms are reported.
Due to the poor quality of the available evidence, it
is not possible to quantify the risk of acute harms in
any meaningful way.
Research recommendations
Large, population-based, prospective studies are
required to examine the time relationship between
ecstasy exposure and neuro-cognitive deficits and
psychopathological symptoms.
Further research synthesis of the social and other
indirect health harms of ecstasy would provide a
more complete picture. Similar synthesis of the
health harms of amphetamines generally would
provide a useful comparison.
Future cross-sectional studies will only add to the
evidence-base if they are large, as representative as
possible of the ecstasy-using population, use well validated
outcome measures, measure outcomes
as objectively as possible with researchers blind
to the ecstasy-using status of their subjects, report
on all outcomes used, and provide complete
documentation of possible effect modifiers.
Cohorts should be matched for baseline factors,
including IQ and exposure to alcohol.
The heterogeneity of outcome measures used by
different investigators is unhelpful: consensus on
the most appropriate instruments to use should be
sought. Investigators should collect data directly
reflecting the quality of life of participants and/or
attempt to assess the clinical meaningfulness of any
inter-cohort differences.
A registry of adverse events related to illegal
intoxicants presenting to medical services (akin to
the ‘yellow card’ system for prescription medicines)
would enable useful estimation of the incidence of
harmful effects of ecstasy in comparison to other
substances.
Future case reports of acute harms of ecstasy are
unlikely to contribute valuable information to the
evidence-base. Where novel findings are presented,
care should be taken to report toxicological
findings confirming the precise identity of the
substance(s) consumed by the individual(s) in
question.

Source: Rogers G, Elston J, Garside R, Roome C, Taylor
R, Younger P, et al. The harmful health effects
of recreational ecstasy: a systematic review of
observational evidence. Health Technol Assess
2009;13

Approximately 36% of East Asians (Japanese, Chinese, and Koreans) show a characteristic physiological response to drinking alcohol that includes facial flushing , nausea, and tachycardia [1] . This so-called alcohol flushing response (also known as “Asian flush” or “Asian glow”) is predominantly due to an inherited deficiency in the enzyme aldehyde dehydrogenase 2 (ALDH2) [2]. Although clinicians and the East Asian public generally know about the alcohol flushing response (e.g., http://www.echeng.com/asianblush/), few are aware of the accumulating evidence that ALDH2-deficient individuals are at much higher risk of esophageal cancer (specifically squamous cell carcinoma) from alcohol consumption than individuals with fully active ALDH2. This is particularly unfortunate as esophageal cancer is one of the deadliest cancers worldwide [3], with five-year survival rates of 15.6% in the United States, 12.3% in Europe, and 31.6% in Japan [4] Our goal in writing this article is to inform doctors firstly that their ALDH2-deficient patients have an increased risk for esophageal cancer if they drink moderate amounts of alcohol, and secondly that the alcohol flushing response is a biomarker for ALDH2 deficiency. Because of the intensity of the symptoms, most people who have the alcohol flushing response are aware of it. Therefore clinicians can determine ALDH2 deficiency simply by asking about previous episodes of alcohol-induced flushing. As a result, ALDH2-deficient patients can then be counselled to reduce alcohol consumption, and high-risk patients can be assessed for endoscopic cancer screening. Based on the sizes of the Japanese, Chinese, and Korean populations and the expected frequency of ALDH2-deficient individuals in each [1], we estimate that there are at least 540 million ALDH2-deficient individuals in the world, representing approximately 8% of the population. In a population of this size, even a small reduction in the incidence of esophageal cancer could result in a substantial reduction in esophageal cancer deaths worldwide.

Summary Points

ALDH2 eficiency resulting from the ALDH2 Lys487 allele contributes to both the alcohol flushing response and an elevated risk of squamous cell esophageal cancer from alcohol consumption.
Knowledge of the flushing response is useful clinically, as it allows doctors to identify their ALDH2-deficient patients in a simple, cost-effective, and non-invasive manner.
Doctors should counsel their ALDH2-deficient patients to limit alcohol consumption and thereby reduce the risk of developing esophageal cancer.
In view of the approximately 540 million ALDH2-deficient individuals in the world, many of whom now live in Western societies, even a small percent reduction in esophageal cancers due to a reduction in alcohol drinking would translate into a substantial number of lives saved.

A Primer on the Genetics of Alcohol Metabolism

Ethanol is first metabolized primarily by alcohol dehydrogenase (ADH) into acetaldehyde (Figure 2), a mutagen and animal carcinogen that causes DNA damage and has other cancer-promoting effects [5–7]. Acetaldehyde is subsequently metabolized to acetate, mainly by the enzyme ALDH2 [8]. In East Asian populations there are two main variants of ALDH2, resulting from the replacement of glutamate (Glu) at position 487 with lysine (Lys) [9]. The Glu allele (also designated ALDH2*1) encodes a protein with normal catalytic activity, whereas the Lys allele (ALDH2*2) encodes an inactive protein. As a result, Lys/Lys homozygotes have no detectable ALDH2 activity. Because the Lys allele acts in a semi-dominant manner, ALDH2 Lys/Glu heterozygotes have far less than half of the ALDH2 activity of Glu/Glu homozygotes; in fact, the reduction in ALDH2 activity in heterozygotes is more than 100-fold [8].

Alcohol consumed by ALDH2-deficient individuals is metabolized to acetaldehyde, which accumulates in the body due to absent ALDH2 activity and results in facial flushing, nausea, and tachycardia [2]. These unpleasant effects are the result of diverse actions of acetaldehyde in the body, including histamine release [10]. Because of the intensity of this unpleasant response, ALDH2 Lys/Lys homozygotes are unable to consume significant amounts of alcohol. As a result, they are protected against the increased risk of esophageal cancer from alcohol consumption [11]. This observation also provided evidence for a causative role for ethanol in esophageal cancer, and a key role for acetaldehyde in mediating this effect [11].
ALDH2 Lys/Glu heterozygotes experience a less severe manifestation of the flushing response due to residual but low ALDH2 enzyme activity in their cells. As a result, some are able to develop tolerance to acetaldehyde and the flushing response and become habitual heavy drinkers, due in part to the influence of societal and cultural factors (see below). Therefore, paradoxically, it is the more common low-activity ALDH2 heterozygous genotype that is associated with greatest risk of esophageal cancer from drinking alcohol.

Evidence That ALDH2 Deficiency Increases the Risk of Alcohol-Related Squamous Cell Esophageal Cancer
Following the first study [12], which was conducted in the Japanese population, case control studies in Japan and Taiwan have consistently demonstrated a strong link between the risk of esophageal squamous cell carcinoma and alcohol consumption in low-activity ALDH2 heterozygotes, with odds ratios (ORs) ranging from 3.7 to 18.1 after adjustment for alcohol consumption. Moreover, most studies show ORs of over 10 for increased risk in heterozygotes who are heavy drinkers [13,14]. An independent meta-analysis has also confirmed an increased risk, even among moderate drinking heterozygotes [11]. In the Japanese and Taiwanese studies, a strikingly high proportion (58%–69%) of the excessive risk for esophageal cancer is attributable to drinking by low-activity ALDH2 heterozygous individuals [13,14].
Consistent with the results of case control studies, prospective studies in cancer-free alcoholics have also shown that the relative hazard for future upper aerodigestive tract (UADT) cancers in low-activity ALDH2 heterozygotes is approximately 12 times higher than in individuals with active ALDH2 [15]. (The UADT includes the oral cavity, pharynx, larynx, and esophagus.) In addition, alcohol consumption in low-activity ALDH2 heterozygotes has been associated with other cancer-related outcomes, including the presence of multiple areas of esophageal dysplasia (i.e., premalignant lesions) and multiple independent UADT cancers [13].
It is important to note that ALDH2 deficiency does not influence esophageal cancer risk in non-drinkers [11]. Furthermore, the magnitude of the ALDH2-associated esophageal cancer risk depends on the relative importance of alcohol versus other risk factors in a given population. In rural areas of China, where there is a high rate of esophageal cancer but alcohol drinking plays a less important role than in Japan and Taiwan, there is a more modest positive association (ORs, 1.7 to 3.1) between low-activity ALDH2 heterozygotes and esophageal cancer risk (e.g., [16]).
Acetaldehyde Is Responsible for Facial Flushing and Esophageal Cancer Risk in ALDH2-Deficient Individuals Top
Acetaldehyde is responsible for the facial flushing and other unpleasant effects that ALDH2-deficient individuals experience when they drink alcohol [10]. Importantly, there is now direct evidence that ALDH2-deficient individuals experience higher levels of acetaldehyde-related DNA and chromosomal damage than individuals with fully active ALDH2 when they consume equivalent amounts of alcohol, providing a likely mechanism for the increased cancer risk. A study in Japanese alcoholics [17] showed that the amount of mutagenic acetaldehyde-derived DNA adducts (Figure 4) in white blood cells was significantly higher in ALDH2-deficient heterozygotes than in individuals with active ALDH2 (Table 1). In this study, while the two groups were matched for alcohol consumption, the ALDH2-deficient group consumed slightly less alcohol on average than the controls. Also, ALDH2 heterozygotes who drank alcohol had higher levels of white blood cells with chromosomal damage than drinkers with active ALDH2 [18]. Because of these as well as other data, the 2007 International Agency for Research on Cancer Working Group on alcohol and cancer specifically noted the substantial mechanistic evidence supporting a causal role for acetaldehyde in alcohol-related esophageal cancer [19].

Five Key Papers in the Field
Harada et al., 1981 [2] The first documentation of the relationship between ALDH deficiency and the flushing reaction.

Yoshida et al., 1984 [9] Identification of the amino acid variant responsible for ALDH deficiency.

Yokoyama et al., 1996 [12] The first evidence demonstrating that ALDH2-deficient individuals have a dramatically elevated risk of esophageal cancer when they drink alcohol.

Yokoyama et al., 2003 [25] Demonstrates that an updated flushing questionnaire containing two simple questions is approximately 90% sensitive and specific for identifying ALDH2-deficient individuals.

Baan et al., 2007 [19] Summary of the conclusions from the 2007 International Agency for Research on Cancer Working Group on the Consumption of Alcoholic Beverages. This is the first report to conclude that ethanol in alcoholic beverages is carcinogenic to humans. The report also adds the female breast and colorectum to the list of sites for alcohol-related carcinogenesis and notes substantial mechanistic evidence linking acetaldehyde to esophageal cancer risk based on studies from ALDH2-deficient individuals.

While the UADT is exposed to acetaldehyde from alcoholic beverages [20] and tobacco smoke, increasing evidence points to the metabolism of ethanol by microorganisms in the oral cavity as an important source of acetaldehyde in saliva and, by extension, in the esophagus. Acetaldehyde levels in saliva are 10–20 times higher than in blood, due to the local formation of acetaldehyde by oral microorganisms [21]. Importantly, ALDH2 heterozygotes had two to three times the acetaldehyde levels in their saliva compared to fully active ALDH2 individuals after a moderate dose of oral ethanol [22].

Social and Cultural Factors Modulate Alcohol Drinking by ALDH2 Heterozygotes

Alcohol consumption is a social activity, and as such can be strongly influenced by cultural and social forces. In Japan, where the risk of alcohol-related esophageal cancer in ALDH2 heterozygotes has been most well documented, going out drinking after work with colleagues is an essential element of Japanese business society, and the idea of group harmony is particularly powerful. The percentage of heavy drinking men who are low-activity ALDH2 heterozygotes has risen substantially in the last few decades, in parallel with the proliferation of business society in Japan and increases in per capita alcohol consumption. Harada et al. [23] first reported that the frequency of inactive ALDH2 was very low (only 2%) in Japanese alcoholics in 1982. In a later study using archival DNA samples, Higuchi et al. [24] determined that in 1979, 3% of Japanese alcoholics were ALDH2 heterozygotes, compared with 8% in 1986 and 13% in 1992. In a more recent study, approximately 26% of heavy drinking (consuming more than about 400 g of ethanol per week) men in Tokyo were ALDH2 Lys487 heterozygotes [35]. In other East Asian countries, estimates of the percentage of alcoholics who are low-activity ALDH2 heterozygotes range from 17% in Taiwan in 1999 [26] to 4% in Korea in 2007 [27]. Taken together, these observations indicate that the inhibitory effect of heterozygous ALDH2-deficiency on alcohol consumption can be strongly influenced by local social and cultural factors which may change over time.

There are many East Asians now living in Western societies, particularly at universities and in metropolitan areas. A sub-population of special concern is ALDH2-deficient university students who may face peer pressure for heavy drinking and binge drinking. Furthermore, anecdotal evidence indicates that some young people view the facial flushing response as a cosmetic problem and use antihistamines in an effort to blunt the flushing while continuing to drink alcohol [28]. This practice is expected to increase the likelihood of developing esophageal cancer.

Education and Early Detection Can Reduce the Global Health Burden of Esophageal Cancer

Clinicians who treat patients of East Asian descent need to be aware of the risk of esophageal cancer from alcohol consumption in their ALDH2-deficient patients. Importantly, clinicians can determine whether an individual of East Asian descent is ALDH2 deficient simply by asking whether they have experienced the alcohol flushing response. In the Japanese population, ALDH2 deficiency can be identified accurately based on the answers to a flushing questionnaire consisting of two questions (see Box 1) about previous episodes of facial flushing after drinking alcohol [25]. The two questions can be easily included as part of a standard clinical interview. In a Japanese male population, the flushing questionnaire had a 90% sensitivity and 88% specificity [25] and a positive predictive value of 87% (based on the tabulated data in [25]). The flushing questionnaire gave a similarly high sensitivity (88%) and specificity (92%) when administered to Japanese women [29].

Clinical Tests To Assess ALDH2 Deficiency Due To the ALDH2 Lys487 Allele
1. The Flushing Questionnaire

The flushing questionnaire consists of two questions: (A) Do you have a tendency to develop facial flushing immediately after drinking a glass (about 180 ml) of beer?; (B) Did you have a tendency to develop facial flushing immediately after drinking a glass of beer in the first one or two years after you started drinking? For both questions, the choice of answers are: yes, no, or unknown.
If an individual answers yes to either question A or B, they are considered to be ALDH2 deficient [25]. The addition of question B is important because some individuals can become tolerant to the facial flushing effect.
The questionnaire that was tested referred to a small (about 180 ml) glass of beer. However, it seems likely that similar results would be obtained if the question were asked about beer or other beverages containing a similar amount of alcohol (about two-thirds of a glass of wine or shot of hard liquor).

2. The Ethanol Patch Test

The ethanol patch test is performed as follows: 0.1 ml of 70% ethanol is pipetted onto a 15 × 15 mm lint pad fixed on an adhesive tape. The patch is attached to the inner surface of the upper arm for a 7-minute period and then removed. A patch area that shows erythema 10–15 minutes after removal is judged as positive. The sensitivity, specificity, and positive predictive value for inactive ALDH2 are more than 90% in Japanese youth [34].

Once ALDH2-deficient patients have been identified, they should be informed about their elevated risk of developing esophageal cancer risk from drinking alcohol. As can be seen from Figure 5, ALDH2 deficiency increases esophageal cancer risk at all three drinking levels, but the slope of the line relating alcohol consumption to esophageal cancer risk is steeper in ALDH2-deficient individuals. Clinicians might therefore use this graph to explain the increased risk when counseling their ALDH2-deficient patients to reduce alcohol consumption.

Alcohol consumption amounts: low, 1–8.9 units/week; moderate, 9–17.9 units/week; high, ≥18 units/week; where 1 unit = 22 g of ethanol. The referent (OR = 1) is never/rare drinkers (<1 unit/week) of either genotype. Odds ratios were adjusted for age, frequency of drinking strong alcohol beverages, pack-years of smoking, and intake of fruit and green-yellow vegetables, based on a multiple logistic regression model. Error bars are 95% confidence intervals. The graph is based on the data in [25].
doi:10.1371/journal.pmed.1000050.g005
The ORs in Figure 5 are adjusted for smoking. However, patients should also be informed that smoking further increases the esophageal cancer risk in a synergistic manner with alcohol [30]. As noted above, cigarette smoking dramatically increases acetaldehyde levels in saliva, and ALDH2-deficient individuals have a reduced capacity to clear salivary acetaldehyde.
For patients at high risk of esophageal cancer, doctors should also consider endoscopy for early cancer detection. A health risk assessment tool to select candidates for endoscopic cancer screening, including data on alcohol flushing as well as alcohol consumption, smoking, and dietary habits, is currently being developed and validated [31]. Using a version of the health risk assessment that includes the flushing questionnaire as a major component, it has been estimated that approximately 58% of esophageal cancers in the Japanese population could be detected by screening only the individuals with the top 10% risk scores [31].
When detected early, esophageal cancer can be treated by endoscopic mucosectomy, a standard and relatively non-invasive procedure. However, once the cancer has grown large enough to penetrate the submucosal layer, the likelihood of lymph node metastasis increases significantly [32]. Only about 20% of esophageal cancer patients survive three years after diagnosis [3], emphasizing the importance of disease prevention.
ALDH2-deficient university students may have their first experiences with heavy drinking while at university. Therefore, it is particularly important for university health professionals to be aware of the relationship between ALDH2 deficiency, facial flushing, and alcohol-related cancer risk. Informing ALDH2-deficient young people of their risk of esophageal cancer from alcohol drinking represents a valuable opportunity for cancer prevention. However, most of the data on the accuracy of the flushing questionnaire have come from individuals over 40 years old. To assess ALDH2 deficiency in young people with little experience of alcohol consumption, an ethanol patch test (see Box 1) can be used [13]. In the patch test, ethanol is applied to the skin, where it is metabolized to acetaldehyde. (Both ADH and ALDH can be detected in skin fibroblasts [33].) If the acetaldehyde is not further metabolized to acetate, it causes vasodilation, which is detected visually as localized erythema. Like the flushing questionnaire, the ethanol patch test is simple and inexpensive to perform, and the sensitivity, specificity, and positive predictive value for inactive ALDH2 have been shown to be more than 90% in Japanese youth [34].

How Many Cancers Could Be Prevented by Reducing Alcohol Consumption in ALDH2-Deficient Individuals?
Finally, it is important to consider how many esophageal cancer cases might be prevented if ALDH2-deficient individuals reduced alcohol consumption. To address this question, the tabulated data of [35] were used to recalculate the population-attributable risk by Bruzzi’s method [36]. The results of this calculation indicate that if moderate or heavy drinking ALDH2 heterozygotes were instead only light drinkers, 53% of esophageal squamous cell carcinomas might be prevented in the Japanese male population.

Source: PLoS Med 6(3): e1000050. doi:10.1371/journal.pmed.1000050
Published: March 24, 2009

Effects on Neurocognitive Functioning
Maternal cannabis use during pregnancy has subtle effects on offspring’s neurocognitive functioning.

Beginning at age three to four, children of mothers who used cannabis heavily while pregnant have demonstrated deficits in memory, verbal and perceptual skills, and verbal and visual reasoning after adjusting for potentially confounding variables (Day et al., 1994; Fried & Watkinson, 1990).

Impaired performance in verbal and quantitative reasoning and short-term memory has also been found among six-year-old children whose mothers reported smoking one or more marijuana cigarettes per day, after controlling for significant covariates (Goldschmidt, Richardson, Willford, & Day, 2008).

In children around the age of nine, prenatal cannabis exposure has been linked with impaired abstract and visual reasoning, poor performance on tasks reflecting
executive functioning (i.e., visual-motor integration, nonverbal concept formation, and problem solving), and deficits in reading, spelling, and achievement, independent of various covariates (Fried, Watkinson & Gray, 1998; Fried & Watkinson, 2000; Goldschmidt, Richardson, Cornelius, & Day, 2004; Richardson, Ryan, Willford, Day & Goldschmidt, 2002)

Vulnerability in visual-cognitive functioning has been shown to persist into early adolescence among those offspring heavily exposed to cannabis (Fried, Watkinson, & Gray, 2003). Findings from brain imaging studies of young adults aged 18–22 indicate that in utero cannabis exposure negatively impacts the neural circuitry involved in aspects of executive functioning, including response inhibition and visuospatial working memory (Smith, Fried, Hogan, & Cameron, 2004, 2006).

These findings are particularly noteworthy as they demonstrate the long-term impairing effects of prenatal exposure to cannabis on offspring’s neurocognitive functioning.Global intelligence does not appear to be impacted by prenatal cannabis exposure (Fried et al., 1998, 2003).

When children reach age six, the effects of maternal cannabis use during pregnancy become much more evident. Compared to offspring of non-users, children born to cannabis users— particularly heavy users—have been found to be more hyperactive, inattentive, and impulsive (Fried, Watkinson, & Gray, 1992; Leech, Richardson, Goldschmidt, & Day, 1999), even after controlling for extraneous variables.

At age 10, prenatally exposed children display increased hyperactivity, inattention, and impulsivity, and show increased rates of delinquency and externalizing problems as reported by their mothers and teachers, compared to those children who were not exposed prenatally to cannabis (Fried et al., 1998; Goldschmidt, Day, & Richardson, 2000).

In children aged 13–16, however, some aspects of attention (i.e., flexibility, encoding and focusing) appear to no longer be affected by cannabis exposure (Fried et al., 2003).

There is accumulating evidence that suggests prenatal cannabis exposure may contribute to the initiation and frequency of subsequent substance use during
adolescence. Porath and Fried (2005) reported that 16- to 21-year-old offspring (particularly males) of cannabis users were at increased risk, in a dose-related
manner, for the initiation of cigarette smoking and cannabis use, and daily cigarette smoking, compared to offspring of non-using mothers, independent of potential prenatal confounds. Similar results were noted by Day, Goldschmidt, and Thomas (2006); compared to offspring of non-users, youth of mothers who heavily used cannabis while pregnant not only reported using this substance more frequently at age 14, but they also initiated use at an earlier age. This result was significant even after controlling for potential confounds.

Effects on Mental Health
There is emerging evidence linking in utero cannabis exposure to depressive and anxious symptomatology. After controlling for prenatal exposure to other drugs and risk factors for childhood depression, offspring of maternal cannabis users expressed significantly more depressive and anxious symptoms at age 10 compared to children of non-users (Gray, Day, Leech, & Richardson, 2005; Leech, Larkby, Day, & Day, 2006).

Mechanisms of Action
The mechanisms responsible for the effects of prenatal cannabis exposure are not well understood. Cannabinoids are able to cross the placental barrier and may affect the expression of key genes for neural development, leading to neurotransmitter and behavioural disturbances (Gomez et al., 2003). The presence of cannabinoid receptors in the placenta and fetal brain may also mediate adverse actions of prenatal cannabis exposure (Park, Gibbons, Mitchell, & Glass, 2003), as these receptors are associated with aspects of brain functioning including cognition and memory (Kumar, Chambers, Pertwee, 2001). Animal studies have documented that cannabinoids can lead to changes in dopamine activity and impaired functioning of the hypothalamus-pituitaryadrenal axis (Kumar et al., 2001), which may affect mood and neurobehavioural outcomes in offspring. It is also possible that an underlying genetic factor may account for both the lifestyle habits of the pregnant mother (i.e., cannabis use) and her child’s neurodevelopment and behaviour.

Conclusions and Implications
Evidence does suggest that prenatal exposure to cannabis (particularly heavy exposure) has subtle adverse effects, beginning at approximately three years of age, on subsequent cognitive functioning, behaviour, substance use, and mental health in offspring. Cannabis-related deficits in the cognitive domain could impair a child’s academic functioning and may require educational remediation, enrichment or placement to help protect against future learning problems.

Prevention efforts directed towards reducing maternal cannabis use during pregnancy could have significant effects in reducing such cognitive impairment. Prevention and intervention programs aimed at reducing prenatal cannabis exposure could also help reduce the percentage of youth who experience mental health conditions and other comorbid problem behaviours, such as substance use and delinquency. It has been reported that at least half of all pregnancies in North America are unplanned (Walker, Rosenberg, & Balaban, 1999). That, combined with the fact that nearly 7% of American women of childbearing age (15–44 years) reported past-month use of marijuana and hashish in 2005 (SAMHSA, 2006) indicates the potential risk for offspring to be prenatally exposed to cannabis.

Cannabis use is a preventable prenatal risk factor; the findings reviewed from the literature suggest that it is prudent to advise pregnant women, and women thinking of becoming pregnant, of the risks associated with cannabis use during pregnancy.

Source Clearing the Smoke on Cannabis . Maternal Cannabis Use During Pregnancy http://www.ccsa.ca/ 2009

Naltrexone implants after in-patient treatment for opioid dependence: randomised controlled trial.

In the first randomised trial, implants which block opiate-type drugs for months helped heroin addicts in Norway avoid relapse after detoxification. If these or allied products gain a UK licence, they could help pave the way to abstinence for the minority of suitable addicts.
Abstract Naltrexone is a medication which blocks the effects of heroin and other opiate-type drugs. Its considerable potential in helping to prevent post-detoxification relapse has not been realised because patients generally refuse to take it or quickly discontinue. However, these limitations apply to the oral formulation which has be taken daily. Longer-lasting formulations in the form of a depot injection or an implant inserted under the skin avoid the need to take the medication daily. This is the first randomised trial of an implant whose opiate-blocking effects last for about six months.
Over 18 months from January 2006, staff at inpatient drug clinics in south-eastern Norway invited opiate-dependent patients on abstinence–oriented programmes to participate in the study. Patients who agreed were contacted by researchers at the end of their detoxification or residential treatment. The 56 who joined the study were told that for the first six months they would be randomly allocated to the implant or to usual aftercare arrangements, but that then all would be offered (re)implantation. Typically they were male injectors in their 30s who had used heroin for on average seven years; nearly all also used other drugs.

Three of the implant group left the clinic before they could be implanted and another three had the implants removed. All but three of the surviving (there were two deaths) patients were reassessed six months later. The main analysis included all the patients whether or not they had received or retained their implants. Over the six months of the follow-up, usual-care patients recalled using opiate-type drugs on average on 97 days, the implant group on just 37 days chart. This differential remained in the last month of the follow-up, when the corresponding figures were 17 and six days, a statistically significant difference. Average frequency of use was also significantly higher among the usual-care patients. At the six-month follow-up assessment, 18 out of 27 usual-care patients but just 9 of the 29 implant patients continued to meet criteria for opioid dependence. In line with this, implant patients were much less likely to experience craving. Nevertheless, during the study over half (18 of 29) tried opioids at least once.
In the last month of the follow-up, implant patients scored significantly lower on an index of multiple drug use and injected less often, but there were no significant differences in drinking or use of non-opioid drugs. Over the follow-up, usual-care patients averaged significantly more repeat detoxifications (0.71 versus 0.21); there were no significant differences in outpatient treatment attendance or use of aftercare services. By the end of the follow-up, implant patients expressed greater satisfaction with their lives but there were no significant differences in levels of depression, work, or criminal activity.
One patient in the implant group reported three non-fatal overdoses (there were four in the usual-care group) while using combinations of opioids, amphetamines and benzodiazepines. Three had implants removed due to infection, discomfort or side-effects. In another two, wound-opening required antibiotic treatment, and three had allergic reactions treated with antihistamines. The single death among patients allocated to implants was an overdose prior to implantation. There was also one overdose death among the usual-care patients.
The authors concluded that naltrexone implants safely and significantly reduced opioid use in a motivated population of patients.
As with oral naltrexone, the main limitation of the treatment is its acceptability to patients. In Norway acceptability will have been heightened by restricted access to substitute prescribing programmes, particularly for people unwilling to contract to forgo not just heroin, but persistent substance use of any kind. Nevertheless, recruitment to the study seems to have been slow. The 56 out of 667 patients who joined the study were probably unusually highly motivated to sustain abstinence from opiates, yet over half the implant patients tried resuming opiate use, and those who did used for on average 60 days. This degree of persistence seems incompatible with the implant having totally eliminated opiate-type effects. The reduction in multiple drug use seems to have been mainly due to the effect on opiate use, since drinking and use of other drugs were not significantly affected. As this study shows, implants and depot injections do not guarantee abstinence. Implants can be removed and both these and depot injections can be sidestepped by turning to non-opiate drugs (as may have happened in Australia) or overridden by very high doses of opiate-type drugs, attempts which risk overdose.
The implants were compared against relatively weak aftercare arrangements; more active and structured aftercare (for example, regular monitoring, continued well organised care from the initial service, or active referral) might have narrowed the differences between the groups. However, highly motivated patients and imperfect aftercare arrangements probably reflect the conditions in which implants would be deployed in normal practice, as does the fact that patients knew whether they had an active implant; unlike some other studies, there was no placebo comparison group.
Of the 26 patients who were implanted, eight (nearly 1 in 3) experienced complications which led three to have the implant removed. One other potential problem is that implants impede opiate-based pain relief. To cater for this, participants were given a card to carry which specified the presence of a naltrexone implant, its expected duration, possible pain relief options, and contact details for study staff. Without this (as reported in Australia) hospital staff sometimes make futile attempts to relieve pain using opiate-type medications. The same report of hospital admissions after implantation identified severe withdrawal symptoms after rapid detoxification to the point where hospitalisation was required. Long-acting naltrexone means the most effective way of relieving these symptoms (using opiate-type drugs) is denied to the patient.
Other occasionally severe reactions to implants and injections have been observed, but generally these are mild and/or short-lived and treatable. As with any abstinence-based treatment, overdose due to lost tolerance to opiate-type drugs is a serious concern. However, the few studies to date suggest these products protect against overdose while they are active, and that in caseloads prepared to undertake these procedures, opiate overdose reductions can outlast the active period of the implants. These findings are consistent with findings from Britain (1) and elsewhere (1 2 3 4 5) tentatively suggesting that long-acting naltrexone can be used to create an opiate-free period which extends beyond the initial blockade, sometimes aided by further administrations (1 2). In the UK, neither implants nor depot injections of naltrexone have been licensed for medical use; they can still be (and have been; 1 2 3 4) used, but patient and doctor have to accept the added responsibility of a product which has not yet been shown to meet the safety and efficacy requirements involved in licensing. See background notes for more on these important issues of adverse effects and overdose protection.
Among the studies is another randomised trial of a different long-acting form of naltrexone conducted in the USA. Compared to placebo, this injection lasting four weeks nearly doubled the time heroin dependent patients were retained in aftercare following inpatient detoxification. On the credible assumption that drop-outs relapsed, there was a similar impact on heroin use. At the four-week choice point when the naltrexone patients could have refused the second set of injections, few did so, most committing themselves to another period without (or with reduced) opiate effects. Though encouraging, multiple exclusions (such as psychiatric conditions or dependence on other drugs) and the recruitment procedures (partly through newspaper ads) meant the patients may not have been typical of usual caseloads.
A criticism of trials to date is that they included highly selected patients. However, in this they may have reflected normal practice. Patients will only opt for such procedures if they are prepared (irreversibly in the case of depot injections) to commit to weeks or months without the effects of heroin or other opiate-type drugs, or with severely attenuated effects requiring higher than usual doses. From the control groups in naltrexone implant/depot studies, we know that even in these caseloads, treatment drop-out and relapse are common. Long-acting naltrexone helps these highly motivated patients sustain their resolve. The clearest candidates for the treatment are patients who are motivated to return to a life without opiate-type drugs (including prescribed substitutes), have the resources, stability and support to sustain this, are unlikely to simply use other drugs instead, but who when free to experience heroin and allied drugs cannot resist using them, possibly reflected in their poor compliance with oral naltrexone regimens. The treatment may also be considered for unstable patients at very high risk of overdose, but who will not accept or do poorly in substitute prescribing programmes.
Thanks for their comments on this entry in draft to Nikolaj Kunøe of the Norwegian Centre for Addiction Research, Liv Langberg of the Drammen Council Drug Addiction Prevention Centre in Norway, and Duncan Raistrick of the Leeds Addiction Unit. Commentators bear no responsibility for the text including the interpretations and any remaining errors.
Source: Drug and Alcohol Findings July 2009 British Journal of Psychiatry: 2009, 194, p. 541–546.

Jordan Diplock, Irwin Cohen, and Darryl Plecas
School of Criminology and Criminal Justice,
University College of the Fraser Valley, Abbotsford, British Columbia, Canada
Abstract
The truth about the risks and harms associated to personal marijuana use is rarely a feature of the ongoing debate over the legal status of the drug, with advocates on both sides at fault. Some consensus over the potential harms needs to be reached before any meaningful discussion can occur on this issue. This article reviews research published between 2000 and 2007 and suggests that there are many risks associated to marijuana use with regards to impairment, academic and social development, general and mental health, and continued drug use. Although some findings highlight very serious concerns for users, the numbers that become adversely affected by marijuana use do not represent the majority of users. A debate on the legal status of marijuana based on the facts about the risks and harms of this drug will greatly aid in determining the appropriate actions to address personal marijuana use around the world.
Keywords: Academic Performance; Gateway; Harms; Health; Impairment; Marijuana; Mental Health; Risks
Introduction
The debate over the personal use of marijuana in North America and around the world is extremely contentious with supporters for decriminalization and legalization, and others who assert the importance of strict prohibition. The exceptionally adversarial nature of this debate is likely one of the main obstacles to determining the most appropriate way to address marijuana use within society. As a result of interested parties remaining resolute in their particular positions, the marijuana debate often becomes characterized by selective reporting or the misuse or misinterpretation of the available information. In addition, the popular debate rarely transcends ideological arguments on marijuana’s potential harms. With proponents of legalization championing marijuana as a benign drug and prohibitionists stressing its dangerousness, the debate often fails to consider the totality of the empirical research evidence. The purpose of this review is to discuss the harms associated with marijuana use from an objective viewpoint to provide a basis for the development of further research on how to best address the issues of marijuana use.
As research on marijuana use and its effects is constantly providing additional information, the full extent of the effects of marijuana on users will likely not be known conclusively in the near future. This should not be regarded negatively, as it is the nature of research that future studies improve upon the methodologies and results of previous research. For example, in 1997, The Independent, a popular British newspaper, was a strong supporter of the decriminalization of marijuana in the United Kingdom. In part, this support led to a pro-cannabis march that pressured the government to downgrade the classification of marijuana . Ten years later, that newspaper printed a public apology for its leadership role in the legalization campaign with a headline stating “If only we had known then what we can reveal today”. This example demonstrates the importance of considering new evidence and being willing to refine one’s position based on the best available information. By reviewing the current research on the potential harms associated with marijuana use, this review intends to synthesize the best evidence to inform the debate.
Ensuring that one considers the most current research on marijuana use is not only important because of the changing nature of academic research, but also because the drug under study has changed over the years. In other words, marijuana does not refer to cannabis with a particular level of -Tetrahydrocannabinol (THC). Over time, the level of THC in marijuana has changed; typically, it has increased. However, because there have been very few studies on the changes in potency of marijuana over the years, it cannot be confirmed conclusively that marijuana users in the 1970s were typically consuming a different drug than today’s users. The information that does exist suggests that, on average, marijuana users today are exposed to higher levels of THC than in past decades. Research on potency trends of seized marijuana between 1980 and 1997 concluded that average THC levels of marijuana seized in the United States increased from less the 1.5% in 1980 to approximately 3% in the early 1990s, to over 4% in 1997 . Moreover, in an article published by the Drug Enforcement Administration (DEA), Newell reported that average THC concentrations in marijuana from 36 samples seized in the state of Florida in 2002 were over 6%. These levels were determined to be at par with the averages reported by the Marijuana Potency Monitoring Project . In Canada , the Royal Canadian Mounted Police [RCMP] reported that on average seizures of marijuana in Canada had THC concentrations over 10%. Seizures in Europe of imported marijuana typically had THC levels between 2% and 8%, but the potency of hydroponically-grown “skunk” may be as high as double that of the imported marijuana . However, it must be kept in mind that the nature of marijuana production and distribution is such that a regular user would likely be exposed to marijuana of various different concentration levels of THC. As the majority of marijuana production remains the industry of criminals, many of whom use hydroponic operations and compete with each other to produce the most and the ‘best’ marijuana, there is no reason to believe that the quality of street marijuana has remained consistent over time.
In addition to levels of THC, the understanding of the number of different constituents of marijuana and their potential to interact with each other changes over time. ElSohly and Slade reported that the number of known natural compounds in marijuana increased from 423 to 489 between 1980 and 2005. Of those numerous chemicals, 70 were Cannabinoids, 9 of which were discovered since 1980 . The changes in knowledge about the complex chemical makeup of marijuana further complicate the study of the potential dangers of its use.
Because marijuana is used around the world by approximately 160 million people, there has been a great deal of research conducted on its effects on users . The use of marijuana results in a variety of changes within the user’s body that can have a range of effects . Given this, the focus of this review is limited to the research evidence on potential harms associated with marijuana use in the areas of: impairment; academic and social development; general physical health; mental health; and continuing drug use. Although there is also a substantial body of research on the medical use of marijuana for particular patients, a review and discussion of the research on medical marijuana is not included in this study. This exclusion is not meant to suggest that marijuana is universally accepted as a safe or effective treatment for any illness, as Voth has clearly demonstrated that the wider debate over the use of marijuana extends into the issue of the drug’s medical use. The discussion presented in this review will concentrate on the use of marijuana within the general population and the empirical evidence for how marijuana use effects the general population in the five previously listed areas.

Methodology
To ensure that this review considered the most current research, information was collected from articles published from 2000 to 2007. Articles were identified by searching a number of databases, including Medline, Pub.Med, PsychINFO, and Google Scholar. To ensure a more complete search, a variety of keywords were combined with ‘marijuana’ to search the databases. In particular, these keywords related to the five aforementioned areas. An extremely partial list of keywords included ‘impairment’, ‘academics’, ‘heart disease’, ‘respiratory’, ‘cancer’, ‘psychosis’, and ‘gateway’.
Once an article was identified, it was assessed for appropriateness based on a review of the article’s title and abstract. One potential limitation of this review was that only full-text-available articles written in English were considered for this review. However, in order to expand the number of articles considered, both original research studies and articles that reviewed topics related to the harms of marijuana use were included. In order to ensure objectivity in the selection process, the inclusion or rejection of articles occurred without consideration of authorship or the conclusions or recommendations made by the authors. Given this, the articles considered in this review represented the continuum of current research on the harms that may be associated with marijuana use. Because of the scope of this topic and the amount of literature on marijuana use, the articles included in this review do not represent all available research on the effects of marijuana use. However, because many of the articles included in this review included extensive reviews of previous literature, the areas of focus for this review were well represented.
Finally, when considering the evidence presented in this review, it is critical to keep in mind that many of the studies based their results and conclusions on self-reported effects of marijuana use by the users themselves. While self-report studies are extremely valuable, they are susceptible to a variety of methodological problems, such as social desirability effects, errors in memory, exaggeration, and deception, which must be considered when evaluating results or conclusions . In addition, it is also extremely difficult to link or establish a direct causal relationship between drug use and other specific behaviours as it is likely that behaviours or outcomes are the result of multiple factors, rather than exclusively one factor, such as drug use.
Marijuana Related Impairment
One of the important debates in the research literature is the effect of marijuana use on cognitive and motor skills. Several studies have focused on determining whether there are any negative effects on cognitive or motor skills within hours of marijuana use . A number of studies have more specifically focused on the effect of marijuana use on abilities related to operating a motor vehicle . In addition to studies of short-term impairment, research has been conducted on long-term impairments associated with prolonged marijuana use .
Short-term Impairment
Impairment immediately after the consumption of marijuana may be a concern for users and the community at large. Short-term impairment has generally been assessed anywhere from 5 – 10 minutes to several hours after use. Testing the effects of marijuana on working and episodic memory determined that focusing attention and response accuracy were impaired immediately after smoking marijuana, even marijuana with less than 4% THC. The authors concluded that the marijuana resulted in difficulty maintaining a coherent train of thought and disruptions to selective filtering processes, both of which impaired memory. Similarly, another study reported that acute marijuana intoxication was accompanied by impairment of brain function related to goal-oriented activities. Further, it was suggested that marijuana consumption inhibited impulse and anger control in some users implying a possible link between marijuana use and violent or antisocial behaviour in some individuals . However, impaired attention was not found in a study of marijuana’s effects on auditory focused attention tasks where participants responded to a tone by pressing a button as quickly as possible. Results of an examination of brain functioning hours after using marijuana found that heavy marijuana users did not present impaired abilities on simple spatial working memory tasks, as deficits were compensated for by employing regions of the brain not commonly used during such tasks.
Although the research reported that short-term cognitive impairment could occur among marijuana users, the level of impairment and its seriousness was not significant. However, this does not suggest that there are no or few short-term risks of impairment. Instead, this conclusion may be due to the small sample sizes of only 10 to 12 participants in the studies examined . In effect, the sample sizes in these studies limited the ability to draw any firm conclusions about the range or seriousness of short-term cognitive impairments associated with marijuana consumption.
Researchers also examined the relationship between marijuana induced cognitive impairment and common abilities, activities, or behaviours, such as operating a motor vehicle. Ramaekers and co-workers concluded that decision-making, planning, tracking, reaction time, and impulse control were impaired by high-potency marijuana. Although the 20 subjects were considered only light users, substantial impairment of executive and motor functioning for a period of at least six hours was found. Although the 13% THC level in the marijuana used in this study was higher than the averages reported by the DEA and RCMP , this study demonstrated that serious impairment lasting for many hours was common when consuming high potency forms of marijuana.
Operating a motor vehicle can be dangerous at any time. However, doing so while impaired by marijuana significantly increases the risks of accident. Although some studies revealed that recent marijuana use was a causal factor for only a small proportion of accidents, short-term marijuana impairment does contribute to serious motor vehicle accidents To better determine marijuana impairment among drivers, standardized field sobriety tests have been designed to detect impairment by marijuana in a manner similar to alcohol. Research on field tests concluded that, as expected, impairment increases with the level of THC . Even low levels of THC can moderately impair driving abilities, but driving is severely impaired when either higher levels of THC marijuana is consumed or marijuana with lower levels of THC is consumed with even small amounts of alcohol . Considering the research examined for this review on the relationship between marijuana consumption and impairment, there appears to be a strong consensus that marijuana use has a negative and potentially harmful effect on driving.
Long-term Impairment
There are few studies on the long-term impairment of chronic marijuana consumption compared to the acute effects of marijuana use. Still, some researchers examined the potential for impairment as a result of long-term use, even during periods of abstinence . From the results of one study of older participants (33-50 years old), it appeared that, although heavy marijuana users showed impaired cognitive abilities after a week of abstinence, there were no noticeable impairments after twenty-eight days of abstinence . When compared to a control group, long-term marijuana using teens (aged 16 – 18) had equivalent task performance on a go/no-go task after twenty-eight days of abstinence . However, marijuana users committed more errors on cognitive tests and showed increased brain processing effort during the inhibition task . When comparing early-onset users to late-onset users, even after twenty-eight days of abstinence, early-onset frequent marijuana users had a greater likelihood of suffering a range of cognitive functioning impairments, in particular verbal IQ, compared to late-onset and non-users .
One interesting finding about long-term marijuana users was that there was an increase in brain activity in more regions of the brain when performing a variety of cognitive tests when compared to non-users. The researchers concluded that this finding was the result of the brain working harder and differently to overcome the deficits resulting from the marijuana use . In addition to working harder and differently, significantly increased blood volumes in various regions of the brain have been discovered , even after a period of abstinence of six to thirty-six hours. The researchers indicated that it remained unknown how these changes affected brain functioning and whether these changes were permanent, long-lasting, or temporary. However, these findings do suggest that there is a potential for some type of long-term brain impairment. Nonetheless, with the exception of impairments caused by psychosis and other mental illnesses discussed later in this review, when considering the totality of the research literature on the relationship between marijuana use and long-term cognitive or motor impairment, there appears to be little evidence to support the assertion that serious impairment is a likely result from long-term marijuana use, especially after a period of abstinence.
The Effects of Marijuana Use on Academic and Social Development
As marijuana is the drug of choice for many young people, it is necessary to understand whether marijuana has any negative effects on academic performance and the transition from adolescence to adulthood. The evidence for both immediate impairment and the possibility of longer-term impairment supports the notion that marijuana use may have negative consequences on the development of young users. In a consideration of academic performance and graduation, a number of studies have focused on the relationship between marijuana use and absenteeism , I.Q. , and academic achievement . By examining the lifestyles of adults who reported being heavy marijuana users in their youth, other researchers have attempted to assess the effects of marijuana use on social development . The following section provides a discussion of the literature in these areas.
Marijuana and School Performance
There are many factors that contribute to academic achievement, such as general intelligence, interest/curiosity, motivation, lifestyle, and social relationships/networks. Since the adolescent human brain is still developing, it is possible that recreational marijuana use may disrupt ‘normal’ development, which may manifest in, among other things, poorer school performance. Survey research revealed that students who were absent on the day of a school-based survey were more likely to use marijuana, alcohol, and cigarettes than students who were present. Although it is unsupportable to conclude that one specific day of absence from school was caused by or related to marijuana use, this study provides some small support for the more impressive findings of Lynskey and Hall’s review of cross-sectional studies on marijuana and school-related issues. Their review of over 50 research studies concluded that marijuana appeared to have a strong relationship with absenteeism, lack of retention, and not graduating.
An examination of the relationship between academic achievement and drug use in a diverse sample of 18,726 students concluded that marijuana use, when examined alone, was statistically significantly related to lower standardized test scores in math, science, reading, and social studies. Average scores on the math comprehension test for marijuana users were further below the mean than on any other test, while reading comprehension appeared to be affected the least. However, when marijuana was combined with alcohol or cigarettes, the results were much less robust. In effect, both regular smoking and alcohol intoxication explained much more of the variance, thus reducing the influence of marijuana on test scores. The explanation provided for this finding was the relatively small number of students who reported ever being under the influence of marijuana at school compared to the number of students who regularly used alcohol and/or cigarettes at school . Similarly, a study by Diego and colleagues found that grade point averages decreased as the reported frequency of marijuana use increased. Marijuana use had a larger negative correlation with grade point average as frequency of use increased than alcohol or cigarettes. While these findings suggested a link between marijuana use and academic achievement, the research could not establish a direct causal relationship or the direction of the relationship. Nonetheless, for the most part, social scientists agree that marijuana use is detrimental to school performance .
Since marijuana has been linked to short-term impairment and a decrease in school performance, some researchers have studied the effects of marijuana on IQ (29). However, measuring the direct effects of marijuana use on IQ has been difficult as there is rarely a baseline measure of a subject’s IQ prior to their initiation into marijuana use. One longitudinal study that had baseline measures of IQ prior to the subject ever using marijuana reported a statistically significant decrease in IQ score among individuals who smoked five or more marijuana cigarettes per week. On average, a 4.1 point decrease was measured between the time the subject was 9 – 12 years old (no prior use) and 17 – 20 years old (current and/or past use). However, when considering the degree of marijuana use for the sample of 70 marijuana users, only those characterised as heavy users showed any decreases in IQ compared to slight users, former users, and non-users who demonstrated increases in IQ . These results suggested that marijuana use has an effect on general intelligence but is more severe for regular and chronic marijuana users.
Marijuana Use and Later Social Development
Success in adulthood is related to a wide range of developmental and social variables throughout childhood and adolescence. It has been hypothesised that many of these contributing dynamics could be negatively affected by the use of marijuana. For example, some people contend that one of the possible outcomes of marijuana use is chronic low motivation. In effect, the hypothesis is that marijuana use among young people contributed to the development of low motivation which has long-term effects on school and employment performance. In their research, however, Lynskey and Hall concluded that there was little evidence to support the low motivational syndrome hypothesis because the majority of supportive evidence was based on older uncontrolled studies of case histories and observational reports, while controlled field or laboratory studies did not find compelling evidence of such a syndrome. Moreover, long-term (over 20 years), regular marijuana use among males was not associated with any specific negative socio-demographic effects such as alcohol or nicotine abuse or dependence, hospitalizations, and health-related quality of life .
However, other researchers have found several adverse associations between marijuana use and social development. A study of the relationship between marijuana use in 2,842 high school students and later occupational attainment concluded that marijuana had some differential negative associations with occupational attainment for males and females . Specifically, for males, self-reported abstinence or low frequency use of marijuana had no effect on occupational attainment, although high prestige jobs typically had a greater percentage of non-users or former low frequency users. However, for male users, after a certain threshold level was passed, success in occupational attainment decreased with increased early marijuana use. The threshold for this relationship in this study was ambiguous as the linear relationship began with the category associated to between 3 and 39 occasions of marijuana use in one year. Among females, early marijuana use was found to have strong negative outcomes on occupational attainment, but the pattern was different from that of males, lacking the easily identifiable threshold and negative linear relationship .
Green and Ensminger examined the effects of marijuana use on a variety of social variables among a cohort of 530 African Americans. Frequent adolescent marijuana use was associated with poorer academic achievement, a lack of stable employment, and family dysfunction. These results suggested that using marijuana 20 or more times during adolescence was associated with being unemployed, unmarried, and becoming a parent while unmarried. Early marijuana use was also linked to dropping out of school and continued marijuana use as an adult . Although this study was specific to African Americans, when considered with other studies on occupational attainment and school performance, these results contribute to the body of literature indicating that marijuana use among young people can have a detrimental outcome on their future. However, these findings do not confirm a causal relationship between marijuana use and poor performance in school or life. Still, the evidence does suggest that, even in the absence of a direct causal link, the use of marijuana during adolescence, for many young people, is often accompanied by other factors, such as the development of delinquent peer associations or a general lack of commitment to pro-social activities and institutions, which can lead to problems with social development.
General Health Consequences of Marijuana Use
The use of marijuana introduces foreign substances into the body and produces a number of chemical changes in the user’s brain and body. Given this, there is a large amount of literature focusing on the physical effects of marijuana. To begin, there is little evidence to suggest that marijuana use poses a serious risk for an overdose death or its infrequent use is related to the development of long-term health problems . Given this research, the majority of health-related studies focused on the potential harmful health outcomes associated with long-term and heavy marijuana use. One of the most widely studied issues is the relationship between smoking marijuana and the development of respiratory ailments .
In addition, the short-term and long-term effects of marijuana use on the circulatory system have also been extensively studied . Other researchers have focused on potential reproductive harms , the effects of marijuana use on the immune system , and the risks for cancers . There is also a burgeoning research literature on the degree to which marijuana users can develop a dependency and experience withdrawal symptoms . The following section will review the research literature on these important issues.
Respiratory Ailments Related to Marijuana Use
The most common way of using marijuana is by smoking it. A direct consequence of this method of consumption is that smoke must enter the airways and lungs of the user. As a result, researchers are interested in the amount and type of harm that smoking marijuana has on the respiratory system of users. This is particularly important because marijuana smoke contains many of the same poisons found in tobacco smoke. Given this, research has focused on determining whether the respiratory outcomes of smoking marijuana are similar or worse than those associated with smoking tobacco . Taylor et al. reported that respiratory symptoms were significantly more prominent in marijuana-dependent users than in non-users. The sample consisted of 21 year old subjects from the 1970s who self-reported short histories of smoking marijuana . The associated self-reported respiratory problems included wheezing, shortness of breath after exercise, nocturnal chest tightness, and early morning phlegm and mucus. These symptoms, which are typically indicative of chronic bronchitis, were also found to be associated with smoking marijuana in other research .
In their review of the research literature, Taylor and Hall argued that marijuana should be considered as damaging to the airways as tobacco and that there was a strong possibility that smoking marijuana was a contributing factor to the development of chronic lung disease. Further research concluded that long-term marijuana smoking was also associated with an increase in airflow obstruction and obstructive lung disease. A comparison of the effects of marijuana cigarettes to tobacco cigarettes concluded that one marijuana cigarette can have the obstructing effects on the lungs equal to that of two to five tobacco cigarettes. Lower lung density and increased total lung capacity were also recorded for marijuana smokers, but macroscopic emphysema was not found to be a common symptom . These findings suggested that serious negative respiratory outcomes should be expected for regular marijuana smokers, regardless of the marijuana’s THC levels, even among youth or young adults.
Since many of the detrimental effects on the respiratory system are the direct result of smoking, there have been several studies examining whether vaporizers provide a less harmful way to consume marijuana . Based on self-reported respiratory symptoms after using vaporizers to inhale marijuana cannabinoids, Earleywine and Barnwell concluded that vaporizers did provide some measure of safety, especially as the amount of marijuana inhaled increased. Hazekamp et al. reached a similar conclusion.
While the use of vaporizers may reduce or eliminate some of the respiratory ailments for users, the THC in marijuana may pose a respiratory risk. In response to the presence of THC, human airways experience cellular changes, especially to mitochondrial energetics, which are responsible, in part, for the health of cells and their energy production . Sarafina et al. described these changes as deleterious effects, as changes to the mitochondria of lung cells affects the viability and functioning of those cells. These changes were more significant with higher concentrations of THC and longer exposure times . In effect, as a result of THC in the lungs and airways, the risk of adverse pulmonary conditions is substantially increased by the potential for damage to the airway epithelial cells .
Potential Harms of Marijuana Use on the Heart and Circulatory System
One direct outcome from using marijuana is an immediate increase in heart rate. It is estimated that marijuana use increases the heart rate 20% to 50% immediately following consumption . This has led researchers to examine the short and long-term implications of marijuana use on the heart and the circulatory system. The majority of research in this area relies on case studies . Although the conditions documented in the research literature may be serious, it must be kept in mind that there is little evidence to suggest that the outcomes discussed in the case studies are typical or the norm for marijuana users.
Based on their case study of a 34-year-old man who reported heart fluttering and near syncope after marijuana use, Rezkalla and coworkers suggested that marijuana was a likely contributor to the decrease in coronary blood flow and ventricular tachycardia experienced by their subject. Another study described two cases; one in which a man with a history of heart problems suffered arrhythmia precipitated by marijuana use, the second described a young patient who suffered an onset of myocardial infarction. The researchers concluded that marijuana was a serious concern for those who may be predisposed to heart-related illnesses. Similarly, Caldicott et al. documented the case of a young patient who suffered a heart attack after marijuana use, despite having no other identifiable risk factors for a cardiac event.
Findings may be more informative when referring to larger samples that identify cardiac risks associated with marijuana use. One study concluded that, although it was less common than other stressors, marijuana use was a trigger for myocardial infarction . In this study , the risk of onset of myocardial infarction increased approximately five-fold in the first hour after use.
The conclusion of existing research is that marijuana use may, in rare instances, trigger a heart attack. However, it is important to recognise that the evidence in support of this conclusion may be confounded by the subject’s participation in a wide range of other unhealthy habits that may also contribute to a greater or lesser degree to a heart attack. Still, there is some evidence to conclude that marijuana is harmful to the heart and researchers, such as Aryana and Williams (, have stated a belief that heart problems related to marijuana use may be more common than is currently recognized. In addition, they warned that as the population of marijuana users aged, continued use may increase the risk for a number of adverse cardiovascular issues, such as tachyarrhythmia, acute coronary syndrome, vascular complication, and congenital heart defects .
Consequences of Marijuana Use on Reproduction and Pregnancy
There is a growing body of literature on the effects of drug use on sperm and egg development and the short and long-term outcomes for the foetus. This literature focuses on the relationship between drug use and implications for fertility and healthy, successful pregnancy. For example, several studies have investigated the effects of marijuana use on male sperm fertility and female hormones . Scheul et al. found that the presence of THC in the reproductive fluids of both males and females could inhibit the ability of sperm to complete fertilization. Other research reported that THC inhibited male fertility by binding to sperm cells and impairing sperm functions. In females, marijuana was found to disrupt the endocrine system and produce an estrogenic effect, which can have detrimental effects on specific elements of the female reproductive system . It should be noted, however, that the effects were more the result of the contaminants of smoking the drug than the psychoactive chemicals . In addition, marijuana use negatively affected female reproductive hormones which could lead to delayed ovulation . In considering these studies, the conclusion is that marijuana use may have some negative effects on human reproduction and that these outcomes are increased for those already at risk for infertility or other reproductive conditions.
Research also examined the degree to which marijuana use by pregnant mothers affected the unborn foetus and whether maternal marijuana use led to negative outcomes for the child. Kuczkowski reported that THC crosses the placental barrier, but that there was no confirmation that it had a teratogenic effect. In other words, there is no evidence that marijuana use by a pregnant mother contributes or causes birth defects or malformations. However, research by Wang et al. determined that some impairment was present in foetuses exposed to marijuana. This finding led the researchers to conclude that some long-term emotional and behavioural implications existed for children exposed to marijuana while in the womb.
Fried and Smith’s review of literature concluded that the effects of prenatal exposure to marijuana were subtle, with little evidence supporting growth or behavioural effects prior to age three. Others concluded that there was a statistically significant association between prenatal exposure to marijuana and later use; however, they concluded that there were many other potential factors that could have contributed to later marijuana use among those exposed to the drug while in the womb. One common theme among the research conducted to date was that they all called for more study on this issue. Although further research is needed in this area, to date, no substantial dangers have been confirmed to be associated to smoking marijuana while pregnant. However, marijuana smoke contains hazardous chemicals and materials, many of which exist in tobacco smoke. Therefore, just as health providers caution that tobacco should not be used by pregnant mothers, the caution should extend to marijuana use.
Marijuana Use as a Potential Threat to the Immune System
THC from marijuana may act upon the immune system similarly to the way it does on cells in the reproductive system . If the immune system is compromised by the use of marijuana, there may be significant implications for health care systems around the world . The relationship between marijuana use and deficiencies of the immune system is based, in part, on the findings that THC inhibits the ability of T-cells and alveolar macrophages to protect the body from foreign pathogens . Alveolar macrophages are a main defence against infections in the lungs. A review of the research literature in this area by Copeland et al. suggested, however, that it might require high doses of THC to substantially impair immune system functioning. Still, when considering the number of respiratory problems associated with smoking marijuana, and the possibility of serious carcinogenic properties in the drug, compromising the immune system may further compound the harms of marijuana use, especially among those already suffering from weakened immune systems.
Cancer Causing Effects of Marijuana
Because marijuana smoke contains many of the same harmful carcinogens as tobacco smoke, there is a possibility that marijuana use may be associated with the onset of various types of cancers, especially lung cancer as the most common method of consuming marijuana is by smoking it . To date, however, the research does not support the association between marijuana use and cancer. In their study, Hashibe and colleagues failed to find substantial evidence for an association between marijuana use and lung or upper areodigestive tract cancers. A review of research on lung cancer and marijuana use by Mehra et al. revealed many of the methodological difficulties in attributing outcomes specifically to smoking marijuana. For example, in many instances, marijuana users also smoke tobacco, there is the challenge of determining proper thresholds for marijuana use, and the research has typically included only small sample sizes. Mehra et al. suggested that because the plausibility of an association between marijuana smoking and cancer is so apparent, improved studies are required to test this possible link. Other research has reached similar conclusions about the link between marijuana use and cancer . Although a 1999 study by Zhang and colleagues reported a potential for marijuana use to increase the risk of squamous cell carcinoma of the head and neck, the evidence for a link between marijuana use and head and neck cancers has been limited and conflicting . In a recent study, marijuana was not found to increase the risk of head and neck cancer, although the duration of use under study might have been too limited to rule out the possibility of a longer-term effect . Another large-sample study concluded that marijuana was not associated to oral squamous cell carcinoma. There was also no link between maternal or paternal marijuana use and risk of childhood acute myeloid leukaemia .
Although there is currently no evidence to confirm that marijuana use increases the risk for any type of cancer, there will likely be continued research. Already, there are many researchers who believe that the changes to a variety of cells in the body caused by marijuana use may contribute to the development of cancers including lung cancer, oral cancers, and breast cancer .
Marijuana Dependency and Withdrawal
Despite the commonly held belief that marijuana use does not lead to addiction, existing research has often referred to a dependency on the drug . Although many people use marijuana on a regular basis, Looby and Earleywine reported that fewer than half of all daily users exhibited the behaviours necessary to meet the established criteria for being classified as drug dependent. These criteria include tolerance, withdrawal, taking the drug for longer periods of time or larger doses than intended, inability to stop or reduce use, increasing the time spent obtaining the drug and recovering from its effects, ignoring other important activities, and continuing use despite undesirable consequences. The authors argued that frequent use does not necessarily result in dependence, but that it may be a contributing factor. Their research suggested that negative effects of marijuana use, such as dissatisfaction with life, low motivation, and unhappiness, were more related to dependence on the drug than regular use . When considering the results of this research with findings from Copersino et al. on withdrawal symptoms, strong support is established for the idea that a proportion of frequent marijuana users suffer negative effects resulting from a dependency.
In terms of factors that most likely contribute to the development of a marijuana dependency, Hall reported that initiation to drug use at an early age was the most significant. However, in terms of public policy, if THC levels are indeed increasing and continue to increase, there will likely be a growing number of users who find themselves dependent on marijuana. Furthermore, as the National Institute on Drug Abuse’s definition of addiction focuses on the “uncontrollable, compulsive craving, seeking and use of drugs”, the physical effects of dependency and withdrawal may be only part of the problem, as addiction can occur without physical signs of dependency. This may prove more problematic if future research establishes additional negative health consequences of long-term use as users may experience more difficulty abstaining from use even in the face of exacerbating social and health problems.
Marijuana Use and Mental Health
In addition to some potentially serious physical health problems, marijuana use has also been associated with mental health problems. The link between marijuana use and psychosis or later schizophrenia has possibly received the most attention in the research literature. This body of research focuses on the role of marijuana in triggering psychosis the risk of developing schizophrenia among those who suffered marijuana-induced psychoses, the dangers of marijuana use for those already suffering from psychosis , and a number of hypotheses on whether marijuana use contributes to the presence of psychoses or schizophrenia or whether mental health issues contribute to the onset of marijuana use To a lesser degree, researchers have also investigated the relationship between marijuana use and depression and anxiety .
Marijuana-Precipitated Psychosis and Schizophrenia
An association between marijuana use and the onset of psychosis recently emerged as a serious concern. Given this, it is necessary to understand the potential for marijuana to contribute to psychosis and what proportion of marijuana users are at risk for developing psychosis. Research suggests that 8% to 10% of all cases of psychosis may be triggered by the use of marijuana Others concluded that marijuana use was linked to psychosis independent of any previous mental pathology. Given this, there is a growing consensus that, although it is relatively rare, marijuana induced psychosis is a potential threat to users, specifically to those who are already vulnerable for this type of mental affliction In order to explain this relationship, Caspi et al. reported that there may be an interaction between the chemicals typically present in marijuana and a number of ‘susceptible’ genes in the user that contributes to the onset of marijuana-induced psychosis and schizophrenia.
Research findings suggested that if marijuana use triggered psychosis, it might be a risk factor for schizophrenia in determining whether those who suffered from an episode of marijuana-induced psychosis were at risk of developing later schizophrenia, a group of such individuals was compared to a group of people referred for schizophrenia-spectrum disorders for the first time who had no history of marijuana psychosis . Although suffering from some recognized methodological problems, this study found that marijuana-induced psychosis was an important risk factor for developing schizophrenia and that it often had an earlier age of onset compared to those who self-reported no marijuana use. In partial support, Solowij and Michie found similarities between the cognitive effects of marijuana use and the cognitive endophenotypes of schizophrenia. This suggested that there was little reason to believe that marijuana is a direct cause of schizophrenia, but that marijuana likely aggravates pre-existing susceptibilities to schizophrenia . This hypothesis may explain why those prone to suffering from marijuana-related psychosis are also more susceptible to later schizophrenia.
One of the complications for fully understanding marijuana’s association with psychosis and later schizophrenia is that people with mental illness may continue to use the drug. The effects of marijuana use in patients who had recently suffered from psychosis were studied to determine whether symptoms were prolonged and worsened by the drug . Findings suggested that those who continued to use marijuana were at a greater risk of having more symptoms and a continuous course of mental illness . It could not be confirmed from the study, however, if marijuana caused the symptoms to worsen or the degree to which marijuana directly contributed to the symptoms.
There were a number of relational hypotheses tested in the research literature . The most common hypotheses were that: marijuana use caused psychosis and schizophrenia without any existing predisposition; marijuana use triggered the onset of these symptoms in people who were previously vulnerable; marijuana use exacerbated the symptoms in those already suffering; and those already suffering from these symptoms were more likely to self-medicate with marijuana. Although the current state of the research does not support the hypothesis that the relationship between marijuana and psychotic symptoms is one of self-medication , other hypotheses found more support.
The strongest support was for the second and third hypotheses. However, the causal hypothesis remains debatable. Degenhardt and Hall found that cases of schizophrenia in the general population did not rise with an increase in reported marijuana use, thus weakening the case for the causal hypothesis. Although further research is needed to more fully understand the causal association between marijuana use and psychosis, based on the research to date, psychosis and later schizophrenia as a result of marijuana use is a risk for a small portion of the marijuana using population.
Depression and Anxiety Among Marijuana Users
Although psychosis and schizophrenia were researched more than other mental health issues associated with marijuana use, there is a body of research on other issues such as depression, anxiety, and violence. Research found that increased marijuana use among high school students was associated with increased self-reports of depression. However, others found that past-year marijuana use was not a significant predictor of future development of depression. Similarly, research by Bonn-Miller et al. found that marijuana use was a predictor of anxiety symptoms, but not of depression. Again, it remains a challenge to determine whether marijuana use is a cause of these symptoms or if the symptoms play a contributing role in marijuana use.
Marijuana’s Role in Continuing Drug Use
The discussion of potential harms of marijuana use presented thus far indicated that marijuana poses a number of potential risks to the general population of users and some specific negative outcomes for a relatively small subgroup. The risk or actual harms associated with marijuana use can be seriously compounded by the use of other drugs and can become overshadowed by the dangers associated with becoming addicted to ‘harder drugs’. Moreover, there has long been the suggestion that marijuana can act as a ‘gateway’ for much harder drug use. It would appear that the probability that marijuana acts as a gateway to other illicit drugs is much higher than the other way around . According to Fergusson and Horwood , when adjusting for other common covariate factors such as childhood, family, and life-style factors, regular marijuana use (fifty or more times in a year) was strongly related to the onset of further illicit drug use. However, others found that the opportunities presented by the lifestyle accompanying marijuana use were just as likely as the actual use of marijuana to predict the use of other illicit drugs. Currently, there is no evidence to prove or disprove that any biological effects of marijuana use increases the likelihood of using other illicit drugs, although researchers continue to test this hypothesis . Based on twin studies, it is well established that marijuana use is a strong predictor of future illicit drug use regardless of the familial and environmental similarities between twins .
Still, since the majority of marijuana users do not continue on to other illicit drugs , it is important to understand what factors distinguish between those who do and those who do not go on to use harder drugs. The appropriate policy and control responses may be very different depending on whether the relationship was based on the biological effects of marijuana use or on the lifestyles that accompanied marijuana and other illicit drug use. Currently, it can be concluded that, for those who use marijuana, there is a risk of using other illicit drugs. However, without a better understanding of what causes or correlates with an increased risk, it is impossible to determine what effects changes to marijuana’s current legal status would have on patterns and rates of drug use.
Conclusions
The debate over the most appropriate policy to have with respect to the personal use of marijuana has generally been polarized because of differing positions on the drug’s harms. In addition to the unknown extent of the potential for harm caused by existence and interaction of over 800 natural chemical components of marijuana, including 70 cannabinoids, it can be concluded that marijuana does pose some considerable confirmed risks to users. Some concern over marijuana is merited by findings regarding its ability to create short-term impairment, specifically on driving ability. Academic performance and social development appear to be negatively affected by marijuana use, but the causal role that the drug plays in the lack of future success of young people remains unconfirmed. As expected, smoking the drug contributes to considerable harm to the lungs and airways. Even though the use of vaporizers removes the contaminants of combustion and reduces some major respiratory problems, THC exposure to the lungs appears to be unhealthy. The immune system is also compromised by the use of marijuana, specifically the ability of the lungs to defend against foreign pathogens. Although cancers, heart problems, and threats to human reproduction are not common among marijuana users, most experts contend that further investigation is required, and the potential for risk should not be dismissed. The development of psychosis and later schizophrenia should also remain a concern for a small proportion of those who use marijuana. Dependency and regular, long-term use of the drug are also factors that likely exacerbate the potential for the majority of the harms previously identified in this review. Of course, these harms are often compounded by the fact the marijuana users have an increased likelihood of continuing on to other illicit drugs.
It is important to remain cognizant of the fact that the harms associated with marijuana use, though very serious in some cases, are not experienced by the majority of users, although prolonged regular use will generally put a person at a greater risk than occasional use. The debate over marijuana use requires advocates of both decriminalization and prohibition to concede that marijuana is neither harmless, nor is it particularly dangerous to the majority of users. It should be acknowledged by all that the lives of a small proportion of the population will be seriously disrupted by marijuana use.
With an understanding of the potential harms associated to marijuana use forming the basis of the debate, politicians, policymakers, and citizens can begin to answer the important questions that will form the basis for discussing policy options. For example, what can be learned from other jurisdictions about ways to respond to the social and personal harms associated with marijuana use? What lessons can be learned from the experiences with alcohol that might apply to marijuana? Are there other or better approaches than prohibition to manage the problems that marijuana use creates? Further research will also be required to better understand whether decriminalization promotes increased use. In other words, would the decriminalization of marijuana create better opportunities to regulate the drug, or would it result in greater social harm?
To date, the research evidence shows that marijuana has a number of associated harms. In some cases, these harms are worse than those associated with regulated substances such as alcohol or tobacco. Based on the course of research, it is likely that future studies will further refine our understanding of the harms of marijuana use. However, because marijuana continues to be a popular recreational drug, it is necessary that researchers disseminate their latest findings in a wide range of ways in order for the public to have the best information at their disposal about the harms and risks associated with using marijuana.

Source: Journal of Global Drug Policy and Practice Vol. 3. Issue 2 Summer 2009

William L. White

The difference between the right word and the almost right word is the difference between lightning and the lightning bug.—Mark Twain

At every word a reputation dies.—Alexander Pope

By our silence, we let others define us.—Susan Rook (Missouri Recovery Network campaign slogan)

Addiction treatment organizations and a variety of policy-making, planning, and funding authorities are changing their historical focus on acute biopsychosocial stabilization to a broader vision of sustained long-term recovery for individuals and families. This shift can be seen in widespread discussions and practices that embrace “recovery management” and “recovery-oriented systems of care.” This change in organizing concepts and service practices will not be possible without the meaningful involvement of individuals and families in or seeking recovery in the planning and decision-making processes.
The word “consumer” is cropping up more frequently, with references to “our consumers,” “consumer representation,” ”consumer councils,” and “consumer-based” or “consumer-directed” services. This latest term joins a long list of terms—patients, clients, service users/recipients/participants, alumni—that have described people needing, receiving, or completing addiction treatment and recovery support services.
Historically, language applied to and chosen by historically disenfranchised groups evolves over time. People who were recovering from severe mental illness began their own recovery revolution in the 1970s and 1980s and chose to self-designate themselves as “consumers” and “survivors” as a less stigmatizing alternative to “mental patient.” The surge in “consumer” language was a positive development within the history of the mental health recovery advocacy movement—one that at the time was experienced as personally empowering. It is likely that this language will continue to evolve as the mental health recovery advocacy movement continues to evolve.
With the growing integration of addiction treatment and mental health treatment services, the introduction of new medications for the treatment of addiction, and expanded efforts to include coverage for addiction treatment and recovery support services as part of comprehensive health care reform, the use of the word “consumer” is gaining prominence within the addiction treatment and recovery support communities. This brief essay describes why this “consumer” terminology is counterproductive and suggests other ways to describe the critical role that people seeking or in long-term recovery, their families, and friends play in the design, delivery, and evaluation of addiction treatment and recovery support services.

Rejecting the “Consumer” Designation
There are nine reasons to reject the spread of “consumer” language when talking about addiction treatment and recovery support services.

1. The term “consumer” is ill-defined and as such, may create further misunderstanding by the general public and policymakers about people experiencing addiction or who are in long-term addiction recovery. There is no generally understood meaning of what exactly is being consumed, and members of the public may well think the term refers to people who continue to consume excessive amounts of alcohol and/or drugs.
“The ‘consumer’ language suggests that the person in treatment is a social ‘taker,’ that they suck up community resources and give nothing in return—a parasitic relationship to others.”
People in active addiction are often involved in a parasitic process of using (in the manipulative sense) family, friends, and community resources to sustain their alcohol and drug use. “Consumer” is a more apt description of someone in active addiction than of a person in long-term recovery. Furthermore, the most cursory search of “consumer” on the internet reveals meanings that include a person who drinks alcohol to excess (See http://www.thefreedictionary.com/consumer). A person in recovery is more aptly described as a person who ceases being a consumer.

2. The term “consumer” fails to provide an alternative identity for persons attempting to disengage from alcohol/drug-saturated lifestyles and subcultures. Addiction treatment can be a transitional bridge from a culture of addiction to a culture of recovery or a revolving door within a person’s active addiction career. The “consumer” identity tends to reinforce the latter; focusing on the repeated “consumption” of services as well as the “consumption” of alcohol and other drugs. “Person in recovery,” in contrast, builds a new identity for an individual moving forward to a new life. “Consumer” defines a person in terms of a part of the self while ignoring the whole. Participating in addiction treatment is an activity, not who a person is.
The term “consumer” had value at a particular point in time for persons recovering from mental illness. New language that had value within a particular historical context can become old language and stand as an obstacle to progress as contexts change. We need a different term to describe people seeking and in long-term recovery from addiction and people who participate in addiction treatment as part of that long-term journey. Does that mean that any alternative language we embrace today may need to be given up in the future? We need to be open to that possibility.

3. The term “consumer” ties an individual’s identity to a service delivery system, be it a treatment provider or a physician prescribing medications, and can be paternalistic and disempowering. There are words other than “consumer” that can be used to describe a relationship between a person receiving professional care and the caregiver. For example, in the HIV/AIDS community, people who receive medications from a physician often describe themselves as patients when talking about their relationship with their doctor. Similarly, many people using medications in their recovery describe themselves as a “person in long-term recovery using medication,” as a “patient” when describing their relationship with their physician, or as a “client” when describing their relationship with a clinic.
The problem is that when “consumer” is juxtaposed against “professional” or “provider,” as it often is, “consumer” conveys a person of less value and authority and implies that the individual has value only to the extent to which they consume professional services or products. This juxtaposition further creates the delusion that the “provider” is whole/well and the consumer is “broken/sick.” Both are dehumanized by this process, with one denied of weakness and the other denied of strength. The “consumer” designation reflects a hierarchical relational model that rests on twin propositions: 1) “the professional knows best” and 2) the role of the “patient/consumer is to listen and comply.”
“Consumer” also defines a person in terms of his or her problems. It relegates the person to being one, albeit critical, component of a system of care, rather than as the driver of that care and the person around whom all care is to be organized so that the person is able to get well. There is nothing in the term that conveys autonomy (or even healthy interdependence), competence, responsibility, or describes the assets that the person brings to others and the community. “Consumer” does not convey the status of, or hope for, recovery and seems alien when linked to words like liberation, journey, transformation, Higher Power, redemption, spirituality, and service, to name just a few of the words and concepts that are associated with recovery. If we need a name, then let’s use words that convey wholeness and wellness, words like “citizen,” “person in long-term recovery,” or “person seeking recovery.”

4. Using the term “consumer” to convey the involvement of people in recovery and their families in advisement or decision-making roles narrowly restricts the pool of people considered for such participation. For example, the term “consumer” would not include individuals/families in need of recovery who have never sought professional help, individuals who did not complete and may have had a “bad” experience in treatment, and individuals and families who achieve long-term recovery without the aid of professional treatment. Referring to such people as “consumers” (of addiction treatment services) is simply inaccurate. Individuals in treatment constitute only a small, unrepresentative sample of those who have experienced and/or have resolved alcohol and other drug problems. Too often, “consumer” represents an even smaller sample: individuals who have successfully “graduated” from treatment and, out of deep gratitude for their personal recovery, can offer testimony to a particular program’s effectiveness.
“Consumer” councils that guide federal, state, or local recovery-focused initiatives must include a wide range of voices as part of the advisory process. The term “consumer” does not adequately describe the scope of needed representative. Voices must be heard who represent diverse levels of problem severity/complexity, recovery capital, and pathways and styles of long-term recovery. The homogenous designation “consumer” ignores the distinct cultural histories and the enormous diversity of needs and circumstances people bring to the experiences of recovery initiation and recovery maintenance.

5. The “consumer” designation inadvertently serves as a mechanism of “outing.” To routinely introduce someone as a “consumer representative” or a member of “our consumer council” discloses the person’s status as a former treatment recipient or person in recovery and places the institution rather than the individual in control of when, where, to whom, and under what circumstances his or her recovery status is disclosed. For professional treatment institutions, such communications often constitute an inadvertent breach of ethics (confidentiality) and etiquette (respect, privacy, discretion). For the people serving in this role, the “consumer representative” designation diminishes and restricts how they are perceived by others and how they perceive themselves.

6. Terms such as “consumer,” “client,” “patient,” and “previously incarcerated person (PIP)” are inappropriate in the context of peer-based recovery support services. These terms imply a hierarchical service relationship model that is incongruent with peer-based recovery support. For example, when a recovery coach commented to a treatment professional that they did not refer to the people they served as “clients” or “consumers,” the professional asked, “Well then, what do you call them?” The simple response was, “Collectively, we call them people; individually, we call them by their names.” This response indicates a different relationship—not only one of mutual respect, but one that embraces the reciprocity that is at the core of peer recovery support relationships. The term “consumer” reflects the role dichotomy of helper (a producer of services) and helpee (a user of services); in the world of peer recovery support services, each person both gives and receives.

As more people return to communities from prison in search of sustained recovery, new acronyms are popping up. Unfortunately, these names and acronyms continue to objectify and turn individuals into an aggregate object, e.g., previously incarcerated persons (PIPs) and formerly incarcerated persons (FIPs). Such names and acronyms have no place in the world of addiction treatment and recovery support services.
( Referrals from the criminal justice system increased from 38% of total referrals in 1990 to 59% of referrals in 2004. During this same time period, referrals from welfare and child protection systems increased from 8% to 16%. McLellan, A.T. (2006). Addiction is changing: How changes in systems and customers may affect the Betty Ford Institute. Presentation to Betty Ford Institute Executive Council, February, Rancho Mirage, CA)
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7. Embracing this term in the addiction treatment and addiction recovery support arenas may amplify stigma by pairing the stigma already attached to addiction with the stigma attached to mental illness.
Given the dominance of the term “consumer” within the mental health field over the past two decades and the existing Consumer Advisory Councils for people with mental illness in each state, “consumer” has become a code word for mental illness. Joint use of “consumer” by the two fields may compound social stigma by inadvertently signaling that all “consumers” have histories of both mental illness and alcohol/drug addiction.
The use of “consumer,” because of its association with the mental health field, may also reinforce the view that addiction is a symptom of mental illness and not a primary disorder. It is critical that people with co-occurring addiction and mental illness receive the specialized and integrated services that they need to achieve long-term recovery. However, it is imperative that addiction is recognized and treated as a primary disorder.

8. The term “consumer” used in the context of addiction treatment mistakenly conveys the image of a seller-buyer relationship, with an informed customer having substantial autonomy, power, and choice and rights of redress if the product or service is faulty. This is not an accurate depiction of most persons entering addiction treatment in the United States today. The growing percentages of people entering treatment via external coercion, the substantial power differential between addiction professionals and their “patients,” the limited choices available to those forced into treatment, the lack of knowledge about those choices, the absence of lobbyists and advocacy organizations representing individuals and families in addiction treatment, and the lack of any significant mechanisms of redress for ineffective or harmful treatment are all obscured by referring to those entering addiction treatment as “consumers.” The term “consumer” is used in few other contexts in which choice and redress are so limited.

9. The term “consumer” has a commercial/marketing/sales connotation that overemphasizes the business aspects of addiction treatment and is particularly ill-suited for people involved in volunteer, peer-based recovery support services provided by recovery community organizations.
The term “consumer,” perhaps not unexpectedly, came into prominence in the roaring “greed is good” days of the 1980s when addiction treatment organizations were told they needed to shift their identity from that of a service program to one of a business.
( Acker, C.J. (1993). Stigma or legitimation? A historical examination of the social potentials of addiction disease models. Journal of Psychoactive Drugs, 25(3), 193-205, quotation from page 203.
“Americans are urged through ubiquitous advertising to construct their identities through consumerism; they are expected to be positive economic actors through consumption.”)

The commodification of addiction treatment and its accompanying language has been a corrupting force within the treatment field and set the stage for calls to de-commercialize and re-humanize the service relationship. The “consumer” designation is incongruent with the sustained person-professional and peer-peer partnerships being advocated as the ideal models of long-term recovery support. The commercial/commodity aspects of the term “consumer” are also part of a value system that attributes personal value to the possession/consumption of goods and services. It conflicts with a recovery value system that defines personal identity in terms of humility, restitution (paying rather than incurring debt), service (an emphasis on giving rather than owning), and simplicity.

Final Reflection
The addictions field could learn much from the larger disabilities movement of recent decades. Some of the central ideas of this movement include the following:

• Language matters. It is far more than superficial concerns about political correctness.

• Language is imbedded with values and judgments of a culture; cultural change involves a transformation in language.

• The labels applied to individuals affect how they are perceived by others and how they perceive themselves.

• Language is a vehicle of social control and social isolation. Stigma and discrimination are couched in a language that reinforces stereotypes and elicits fear.

• Recovery and community integration require claiming one’s own language.

• Language that focuses on the person is more respectful and less stigmatizing than language that defines a person in terms of an illness.

It will be interesting to see how the language of addiction treatment and recovery evolves in tandem with the dramatic changes that are unfolding within these worlds. I hope we will not be talking much longer about “consumers” or “consumer councils” but will instead be talking about people in recovery and recovery (or citizen) advisory councils. I also hope that the paternalistic “our patients,” “our clients,” and “those we treat” will evolve in the near future to “people we serve.”

Words can elicit fear, contempt, anger, or pity, but they can also elicit understanding, compassion, and respect. Individuals and families in recovery are awakening culturally and politically. As they do, they will forge their own language to collectively convey their “experience, strength, and hope.” They will challenge the traditional language that has been used culturally and professionally to depict alcohol and other drug problems and their resolution. Most importantly, they will claim entitlement to select the words used to refer to those who have experienced addiction and recovery.

Source: Daily Dose 21st July 2009

The following paper consists of detailed extracts from a paper which analyses carefully the costs and benefits of effective drug prevention initiatives. I makes sobering reading when the costs to society of substance abuse are revealed. Good drug prevention clearly benefits the whole of society – and especially tax-payers – not just the individual.
Whilst this document relates to the United States there is no doubt that similar results would be attainable in the United Kingdom.

1. Executive Summary
Policymakers and other stakeholders can use cost-benefit analysis as an informative tool for decision making for substance abuse prevention. This report reveals the importance of supporting effective prevention programs as part of a comprehensive substance abuse prevention strategy. The following patterns of use, their attendant costs, and the potential cost savings are analyzed:
Extent of substance abuse among youth
• Costs of substance abuse to the Nation and to States
• Cost savings that could be gained if effective prevention policies, programs, and services were implemented nationwide
• Programs and policies that are most cost beneficial

1.1. Costs of Substance Abuse
Studies have shown the annual cost of substance abuse to the Nation to be $510.8 billion in 1999 (Harwood, 2000). More specifically,

• Alcohol abuse cost the Nation $191.6 billion.

• Tobacco use cost the Nation $167.8 billion.

• Drug abuse cost the Nation $151.4 billion.

Substance abuse clearly is among the most costly health problems in the United States. Among national estimates of the costs of illness for 33 diseases and conditions, alcohol ranked second, tobacco ranked sixth, and drug disorders ranked seventh (National Institutes of Health [NIH], 2000). This report shows that programs designed to prevent substance abuse can reduce these costs.

1.2. Savings From Effective School-Based Substance Abuse Prevention
If effective prevention programs were implemented nationwide, substance abuse initiation would decline for 1.5 million youth and be delayed for 2 years on average. It has been well established that a delay in onset reduces subsequent problems later in life (Grant & Dawson, 1997; Lynskey et al., 2003). In 2003, an estimated:
• 8 percent fewer youth ages 13 to 15 would not have engaged in binge drinking
• 11.5 percent fewer youth would not have used marijuana
• 45.8 percent fewer youth would not have used cocaine
• 10.7 percent fewer youth would not have smoked regularly

The average effective school-based program in 2002 costs $220 per pupil including materials and teacher training, and these programs could save an estimated $18 per $1 invested if implemented nationwide. Nationwide, full implementation of school-based effective programming in 2002 would have had the following fiscal impact:
• Saved State and local governments $1.3 billion, including $1.05 billion in educational costs within 2 years
• Reduced social costs of substance-abuse–related medical care, other resources, and lost productivity over a lifetime by an estimated $33.5 billion
• Preserved the quality of life over a lifetime valued at $65 billion

Although 80 percent of American youth reported participation in school-based prevention in 2005 (SAMHSA, 2004), only 20 percent were exposed to effective prevention programs (Flewelling et al., 2005). Given this level of participation, it is possible that some expected benefits already exist for these students, and the estimates in this paper are adjusted for these probable benefits. These cost-benefit estimates show that effective school-based programs could save $18 for every $1 spent on these programs.

Table A1 in the appendix lists 35 effective prevention programs and strategies and the estimated cost-benefit ratios for each program. The array of demonstrated effectiveness among prevention programs and strategies is impressive. Of the 35 substance abuse prevention programs, practices, or related interventions, 15 reduced medical, criminal justice, and other spending by more than the cost to implement the program.

1.3. Conclusion
The cost of substance abuse could be offset by a nationwide implementation of effective prevention policies and programs. SAMHSA’s Strategic Prevention Framework should include a planning step that considers cost-benefit ratios. Communities should consider a comprehensive prevention strategy based on their unique needs and characteristics and use cost-benefit ratios to help guide their decisions. Model programs should include data on costs and estimated cost-benefit ratios to help guide prevention planning.

Increasingly, the American public supports investment in prevention programs as a strategy for dealing with America’s substance abuse problems (Blendon & Young, 1998; Maguire & Pastore, 1996). Research demonstrates that substance abuse prevention programs work: they can reduce rates of substance use and can delay the age of first use. Studies also have shown that prevention programs not only prevent substance abuse; they can contribute to cost savings (Aos et al., 2004; Caulkins et al., 2002; Miller & Hendrie, 2005; Swisher et al., 2003).

As well as reporting the ratio of benefits to costs, a cost-benefit analysis typically provides a net benefits estimate, which is computed by subtracting the cost of intervention from the benefits of the intervention (Mishan, 1988). For example, the All Stars program has a cost-benefit ratio of 34:1 which means it returns $34 dollars in savings for every dollar invested, yielding net benefits of $4,670 per pupil ($4,810 in social cost savings minus $140 in program costs). By comparison, the Life Skills Training program has a cost-benefit ratio of 21:1 and yields net benefits of $4,380 per pupil.

Although the All Stars and Project Northland programs save more than it costs to develop and deliver them, the return on investment in All Stars is 34:1, and the return on Project Northland is just 17:1. However, other factors should be considered, e.g., the level of outcome and long-term effects. For example, Project Northland also involves developing a community coalition that remains after the program and can address related issues without additional costs. In allocating resources, analysts often trade off the most efficient investments—those with the highest cost-benefit ratios against those with a broader reach that can produce a larger total benefit.

Direct Economic Impact of Substance Abuse
NIH ranks alcohol second, tobacco sixth, and drug disorders seventh among estimated costs of illness for 33 diseases and conditions (NIH, 2000). The year 1999 is the most recent year, with estimates available for all three categories of substance abuse. Despite a smaller number of deaths from alcohol use, alcohol-related costs are greater than tobacco costs because alcohol-related mortality tends to occur at younger ages than smoking-related mortality.
The categories used to develop the alcohol and drug abuse estimates include specialty alcohol and drug services; medical consequences; lost earnings due to premature death; lost earnings due to substance-abuse–related illness; goods or services related to crashes, fires, criminal justice, other; and lost earnings resulting from crime. The categories used to develop the smoking estimates were medical consequences and lost earnings due to morbidity and premature death. Tobacco prevention costs are excluded; the largest share of these prevention costs, State spending, averages $600 million annually (Campaign for Tobacco-Free Kids, 2004).

The social cost of alcohol, tobacco, and drug abuse in the United States by substance are as follows:. Alcohol abuse was responsible for $191.6 billion (37.5 percent) of the $510.8 billion, tobacco use was responsible for $167.8 billion (32.9 percent), and drug abuse was responsible for $151.4 billion (29.6 percent).

Loss of potential productivity and earnings: Smoking accounted for almost 440,000 deaths in 1999 (Fellows et al., 2002), alcohol abuse accounted for 42,000 (Harwood, 2000) to 76,000 deaths (Midanik et al., 2004), and drug abuse accounted for an additional 23,000 deaths (Harwood & Bouchery, 2001). Additional productivity losses occurred when individuals who abused substance

Lost productivity makes up two-thirds of the costs of substance abuse. Lifetime wage and household work lost to premature death is the largest component of these costs, followed closely by work lost to acute and chronic illness and injury. Incarceration results in $32 billion in earnings losses. Almost $25 billion more is lost when people who abuse substances pursue criminal careers rather than enter the labor force.

These estimates are conservative; they omit some costs that result from substance abuse. Specifically, they exclude (1) the impact on the quality of life of those who abuse substances and the people they harm and (2) the health care costs and work losses of victims who were involved in alcohol-attributable crashes even though they had not been drinking. These estimates also exclude the impact on the quality of life.

Costs and Benefits of Preventing Substance Abuse
This section uses the percentage of youth who might have started using substances in the United States and published estimates of prevention effectiveness to analyze the probable impact of a nationwide implementation of effective school-based substance abuse prevention programming. The following were estimated:
• Potential reduction in substance use and abuse as a result of providing effective school-based prevention interventions to all U.S. youth ages 12–14 in middle school
• Potential social cost savings as a result of providing effective school-based prevention interventions to all U.S. youth ages 12–14
• Social return on investment in preventive intervention measured in terms of costs and benefits
• Potential State government savings in juvenile justice and education costs as a result of providing effective school-based prevention interventions to all U.S. youth ages 12–14

The analyses primarily draw on data from the following sources:
• A report by Caulkins and colleagues (1999) for RAND titled An Ounce of Prevention, a Pound of Uncertainty: The Cost-Effectiveness of School-Based Drug Prevention Programs
• The NCASA report titled Shoveling Up: The Impact of Substance Abuse on State Budgets (NCASA, 2001)
• National Survey on Drug Use and Health (NSDUH) (SAMHSA, 2004))
• Youth Risk Behavior Survey (YRBS) (Centers for Disease Control and Prevention, 2003)
Two meta-analyses on the effectiveness of school-based youth substance abuse prevention programs (Aos et al., 2004; Hansen et al., 2004)

4.1. Youth Delaying or Never Using Substances
Nearly every youth ages 12–14 is at risk for trying alcohol, tobacco, and drugs and may be aware of social norms and feel peer pressure to start using these substances. The initial analysis involved estimating the number of youth who would not have tried or would not regularly use these substances if effective school-based prevention programs were in place nationwide. To determine these estimates, the number of youth ages 12–14 was multiplied by three factors: the low, medium, and high estimates of the percentage of youth who would delay initiating use of each substance if they received effective school-based prevention programming. The effectiveness estimates were drawn from two meta-analyses on the effectiveness of school-based youth substance abuse prevention programs (Aos et al., 2004; Hansen et al., 2004

The midrange estimates of youth receiving effective school-based prevention services across intervention programs are as follows:
• 4.7 percent will delay using alcohol
• 4.1 percent will delay using marijuana
• 2.7 percent will delay using cocaine
• 4.7 percent will delay smoking

These estimates represent the mean values from an array of school-based prevention programs that evaluations found significantly (>.05) delayed or prevented initiation of youth substance use. The individual estimates of effectiveness were derived from meta-analyses that generally excluded evaluations that did not use some sort of comparison or control group. Prevention programs for cocaine use had the smallest range of effectiveness from 2.3 percent to 5.3 percent of youth delaying or never initiating use. Prevention programs that delayed or prevented initiation of alcohol use had the greatest range of 1 percent to 10.3 percent.

Table 4 shows a range of estimates of the number of youth who would delay substance use if they received effective school-based prevention programming. For all youth ages 12–14, universal prevention programming in 2002 would have delayed 1.5 million initiations of substance use, with a range from 0.7 to 3 million. The largest absolute impact would be on drinking, with 446,000 youth delaying their first drink, followed closely by smoking with 436,000 youth delaying their first smoke. (A youth who delays both smoking and drinking is counted in both categories.
For drug abuse, the corresponding estimates are 247,000 youth delaying their first cocaine use and 389,000 delaying their first use of marijuana.

The rationale for this analysis is that when youth delay onset of substance use, on average, two years less of lifetime use occurs. When prevention programs delay the onset of substance use, the number of future dependent users also decreases (Grant & Dawson, 1997), but the analysis does not estimate that further saving.

Effective nationwide school-based prevention programming for youth ages 12–14 in 2002 would have prevented 267,000 youth from drinking during 2003, 183,000 from using marijuana, 138,000 from using cocaine, and 205,000 from using tobacco . Prevention programming also would have prevented 169,000 youth from binge drinking in 2003, and 72,000 youth from smoking regularly.

Effective prevention programs would reduce binge drinking by 8 percent, marijuana use by 11.5 percent, cocaine use by 45.8 percent, and regular smoking by 10.7 percent

The impact of substance abuse prevention may extend over a lifetime and is most obvious when prevention fails to deter an individual from substance abuse, and the abuse results in premature death. Substance abuse may last many years and often entails periods of recovery and relapse. Furthermore, the effects of substance abuse may continue well beyond the period of time when an individual is actively abusing substances.

The following cost factors were considered:
• Medical costs
• Other resource costs, ranging from property damage to police, criminal justice, litigation, and insurance administration expenses
• Lost wage and household work
• Value of pain, suffering, and loss in quality of life

Cost-Benefit Ratios
To achieve these savings school-based prevention programming would cost an estimated $220 per pupil nationwide. This cost represents the average across the 11 school-based prevention programs analyzed in this section. Knowledge of program costs makes it possible to estimate the cost-benefit measures defined in Section 2. The return on investment in school-based prevention services would range between $7.40 and $36 per dollar invested, with a medium estimate of $18 The best estimate equates to a net saving of $3,740 per youth served, including a $74 net savings in medical and other resource costs ($294–$220). Since expected medical and other resource cost savings exceed program costs, the program would yield net cost savings to society. School-based substance abuse prevention programming that effectively addresses substance abuse appears to be an excellent investment and is likely to pay for itself in resource cost savings alone.

For every dollar spent per pupil, society would save $18.

SAMHSA’s continuum of care suggests some overlap in prevention programs (i.e., universal, selected, and indicated). For example, when the Strengthening Families Program prevents a youth from adopting multi-risk behavior, it clearly is prevention. Similarly, when Project Northland prevents a youth from ever trying cocaine or delays initiation of cocaine use, it unambiguously prevents illicit substance use. Indicated prevention programs can also work to prevent an increase or expansion of early experimental substance use behaviors. When the topic is preventing the costs of substance abuse, the distinction blurs between programs that prevent binge drinking per se and those that prevent costly adverse consequences attributable to substance abuse (e.g., programs to prevent drinking and driving).

Universal preventive interventions are targeted to the general public or a segment of the entire population with an average probability of developing a disorder, risk, or condition. Selected preventive interventions are targeted to specific populations whose risk of a disorder is significantly higher than average, either imminently or over a lifetime. Indicated preventive interventions are targeted to designated individuals who have minimal but detectable signs or symptoms suggesting a disorder or who carry biological markers for a disorder often referred to as high risk. Youth ages 12–17 who abuse substances constitute approximately 11 percent of people who engage in binge drinking and 15 percent of people involved in illicit drug use in the United States

Family-centered interventions with a school component generally are more costly than school-based life skills training, but they offer larger benefits per youth assisted. The most effective programs strengthen youth bonds to family, school, and community, increasing protective factors while reducing risk factors. These include Adolescent Transitions, Strengthening Families, Guiding Good Choices, Project Northland, and SOAR. Although family-centered programs achieve more in terms of bonding and protective factors, some narrower life skills programs offer larger returns per dollar invested. With a limited budget, life skills programs allow a school system to reach the most children. However, the same money probably would yield greater benefits per youth assisted if spent targeting the broader family-centered programs and related mentoring to the schools at highest risk.

As these findings indicate, the costs of substance abuse to society are significant, and cost savings may offset the cost of providing effective prevention

Substance abuse has a wide range of adverse consequences. In order to optimally reduce consumption and its adverse consequences, a comprehensive package of prevention programs and strategies is required. No single intervention will reduce the problem so dramatically that no further public action is desirable. Given the number and diversity of proven interventions, optimal resource allocation requires selecting the most complementary, politically feasible, and culturally and demographically appropriate set to maximize a return on investment within the available funding. Of critical concern is to identify a sensible package of interventions that complements existing interventions. Policymakers selecting substance abuse interventions can apply a series of filters. The estimates in this report provide the first filter: eliminating interventions that offer a questionable return on investment.

However, new and improved versions of the original DARE program, Here’s Looking At You (Farley & Associates 2002) and the Adolescent Substance Abuse Prevention Study (Sloboda & Hawthorne, 2003) have produced better results and consequently better cost-benefit ratios and should not be dismissed arbitrarily. This financial information should be used as only one of an array of measures in selecting effective programs. Additional filters that policymakers can use in selecting interventions are political feasibility, local priorities, appropriateness for the target population, cultural sensitivity, affordability, and the immediacy of the impact (weeks versus years). Political feasibility is especially important. A slightly less cost-beneficial program can be superior if the alternative with the higher return has a lower chance of widespread implementation or involves a long delay in implementation. As the subsections that follow describe, all things are not equal when selecting a package that yields the maximum gains at the lowest possible price. Other factors, such as aggregate benefits obtained, overlapping effects, spillover costs and benefits, and government cost can and should weigh into the decision process.

Conclusion
If effective prevention programs were implemented nationwide, substance abuse initiation would decline for 1.5 million youth and be delayed for 2 years on average. In 2003, an estimated:
• 8 percent fewer youth ages 13–15 would not have engaged in binge drinking
• 11.5 percent fewer youth would not have used marijuana
• 45.8 percent fewer youth would not have used cocaine
• 10.7 percent fewer youth would not have smoked regularly

The average effective school-based program costs $220 per pupil. It would save an estimated $18 per $1 invested if implemented nationwide. Nationwide school-based effective programming in 2002 would have had the following fiscal impact:
• Saved State and local governments $1.3 billion, including $1.05 billion in educational costs during 2003 and 2004
• Reduced social costs of substance-abuse–related medical care, other resources, and lost productivity over a lifetime by an estimated $33.5 billion
• Preserved the quality of life over a lifetime valued at $65 billion

These cost-benefit estimates show that effective school-based programs pay for themselves and more. For every dollar spent on these programs, an average of $18 dollars per student would be saved over their lifetime. Among 10 effective school-based life skills programs, the average return on investment exceeded $15 to 1. That is, every dollar spent on these programs returned an average of $15 dollars per student. The probable costs and cost savings involved in implementing a composite of these programs for middle school youth ages 12–14 nationwide were estimated. The average program would delay more than a million initiations of alcohol, cocaine, marijuana, or tobacco use by youth for an average of 2 years. Its cost would be $220 per pupil.29
The out-of-pocket expenses would be repaid by savings to the education system alone in less than 2 years. The program would offer additional savings to State and local governments by reducing spending on Medicaid, police, and other criminal justice services. School-based programs that offer a particularly large return on investment include All Stars, Family Matters, Keepin’ It Real, Life Skills Training, and Project Northland. Although Project TND and STARS for Families yielded lesser returns than competing NREPP programs, they still yielded $4 in savings per $1 invested. Programs designed to strengthen families generally cost more than the school-based life skills programs. Several of them also were highly cost-beneficial and offered much larger returns in the aggregate per youth served than the school-based life skills programs.
In a program targeting families with low income, intensive home visitation, coupled with preschool enrichment, reduced infant/toddler abuse (Aos et al., 1999; Karoly et al., 1998). As these toddlers reach adolescence and adulthood, visitation programs also can reduce a range of problems including substance abuse and violence. However, the net returns are often realized in the long term (for actual longitudinal cost-benefit results see Karoly, et al., 1998; Schweinhart, et al., 1993). The proven interventions often cover different aspects of the problem (such as youth drug use initiation, impaired driving, and violence), which make a complementary set of interventions more beneficial. Several interventions are best directed toward different aspects of the problem. If they are massed against the same aspect, the size of that aspect will shrink, and the return on added interventions will decline below the levels shown in this study. Taken as a whole, the benefits of substance abuse prevention well outweigh the costs of providing that service. Cost-benefit ratios can guide the selection of an optimal intervention package within the available resources. Political feasibility, cultural and demographic differences, and local priorities also must be considered.

Source: Miller, T. and Hendrie, D. Substance Abuse Prevention Dollars and Cents: A Cost-Benefit Analysis, DHHS Pub. No. (SMA) 07-4298. 2008

The PATS surveys also included questions related to a variety of factors associated with drug usage. We used responses to these questions as input to our model. Perceived susceptibility was measured by asking respondents to rate three items (on 4-point scales) indicating the degree to which people risk harming themselves by using drugs. Perceived severity was measured by having respondents rate four items (on 4-point scales) indicating the degree to which they would fear the consequences of being caught with drugs. Attitudes toward drugs were measured by having respondents indicate their level of agreement with 14 items (on 5-point scales) describing benefits of drug use. Attitudes toward drug users were measured by having respondents indicate whether each of 27 personality characteristics would describe a marijuana, cocaine, or crack user. Other factors measured included peer pressure, and how difficult it was to obtain drugs. Finally, respondents were asked to read a short description of six advertisements that were aired nationally, and to indicate how often they had seen each advertisement.
The probabilities of a respondent’s reporting use of marijuana and cocaine/crack over the previous 12 months were expressed in a standard “probit” formulation as a function of both the attributes of the individual (e.g., demographic characteristics) and his or her attitudes towards drugs and drug users, and perceptions of drug use itself (e.g., perceived severity). We considered three versions of this formulation, each of which involved a slightly different assumption about the relationship between the cocaine/crack and marijuana use decisions.

An Independent Choice?
First, we estimated the marijuana and cocaine/crack equations independently, assuming that the decision to try the two drugs is independent. (Empirical research suggests that the process may be sequential; that is, one first tries marijuana and then cocaine/crack.) Second, the common syndrome theory suggests that individuals have a “predisposition” to use drugs that manifests itself first in marijuana use. Third, certain factors associated with the experience of using marijuana could lead people to use harder drugs, such as cocaine/crack. This has been referred to as a “gateway” or “stepping stone” theory. These three alternatives resulted in different statistical specifications, which allowed us to test the hypotheses with the available data. In addition to the “use” choice, we investigated the decision regarding how much to use (the “volume” decision), given that an individual has reported using marijuana or cocaine/crack. For this analysis, individuals were categorized as “light” or “heavy” users.
The result is a classic sequential-choice decision: an individual uses the drug and then, on the basis of his or her experience and additional information (e.g., anti-drug advertising), decides whether or not to use the drug again. Accordingly, for each drug, we initially estimated stage one probability equations and then estimated the probability of a given individual’s being a light or heavy user conditional on previous use. Thus, including only those who had previously used drugs, we estimated each second-stage equation using a dichotomous dependent variable indicating heavy or light usage.
The first “wave” of PATS (conducted before the initiation of anti-drug advertising) provided us with the data necessary to assess the determinants of drug use in the absence of PDFA advertising. This was the “control” in our natural experiment. We were then able to assess the significance of recall of PDFA advertising in terms of use and volume decisions via a series of “treatment” groups consisting of each of the subsequent waves exposed to advertising.
We began by estimating the three sets of probability-of-use equations (“independent,” “gateway,” and “predisposition”) using the wave one data for marijuana and cocaine/crack. Then, on the basis of the best fitting of these equations, we estimated the second stage regressions for the probability of being a light vs. heavy user, also using the wave one data. This provided us with a detailed analysis of the factors influencing the decision to use and the volume of use for each drug before the commencement of PDFA advertising.
So what did we find? Using nested tests, we concluded that the “predisposition” formulation – i.e. that individuals have a “predisposition to use drugs” that manifests itself first in marijuana use – fit significantly better than the notion that the decision to try the two drugs is independent. Consequently, we used this formulation throughout. In addition, the data led us to reject the hypothesis that marijuana use increases the probability of cocaine/crack use. To be sure, individuals who have used marijuana in the past are indeed more likely to use cocaine/crack. But the reason is that – statistically speaking – individuals who are predisposed to try marijuana are also predisposed to try cocaine/crack.

Does Anti-Drug Advertising Work?
This analysis, conducted with the wave one “control” group, provided the basis for analyzing the significance of recall of PDFA advertising in waves two, three, and four. The findings demonstrate that recall of anti-drug advertising was associated with a decreased probability of marijuana use. The advertising coefficients in the marijuana use equation were all statistically significant and of the “correct” sign. In the case of cocaine/crack use, the advertising variables were also significant in waves two through four. The estimated advertising coefficients in the volume portion of our results were all statistically nonsignificant with the exception of the wave four marijuana volume-of-use equation. This suggests that recall of PDFA’s anti-drug advertising had little or no impact on the volume of use among existing users.

In England, the proportion of young people aged between 11-15 who reported having drunk alcohol decreased from 62% to 54%, between 1988 and 2007. However, the amount consumed by the young people who drink increased from 6.4 units per week in 1994 to 12.7 units per week in 2007 [1]. The largest increase was seen in 14 year olds who increased their alcohol consumption from 6.1 to 9.9 units per week over this period. Furthermore, this increase was not gender specific. For both boys and girls there was a substantial increase in
the amount of alcohol consumed [1]. Moreover, one in four young people aged 14 reported consuming over 10 units of alcohol on their last drinking occasion; this level of consumption increased to one in three by the age of 15 [2]. In 2001 it was reported that young people’s drinking tends to be confined to fewer days than adults, and in particular at weekends .

Thus young people (aged 11-15), who drink, tend to do less frequently but at a higher intensity than adults.

In young people (aged 16-24), the latest NHS Information Statistics on Alcohol (2008) reported that 26% of males and 24% of females drink over the recommended weekly limits for low risk drinking in adults, which are 21 units for men and 14 units for women. Moreover it is shown that 9% of young males and 6% of young females drank over 50 units per week which is indicative of high risk drinking in adults . It is not clear whether current adult guidance on low risk drinking is pertinent to young people or if specific recommendations are required for individuals who are in the midst of ongoing physiological and emotional
development.

During the last 30 years the number of deaths due to chronic liver disease and cirrhosis has risen steadily in England and this trend is particularly marked in the 25-34 year group with the number rising from 16 in 1970 to 68 in 2000 for men and from 7 in 1970 to 60 in 2000 for women . The majority of liver disease in this country is due to heavy drinking . However, the most significant physical health risks associated with alcohol consumption in young people at the present moment are those relating to accidents and injuries. The ESPAD study reported that 13% of all 15-16 year olds had been involved in an accident or had an injury as a result of drinking .

In Scotland, it has been reported that on a daily basis, 15 children under the age of 17 attend Emergency Departments, intoxicated and in need of medical assistance or treatment .Indeed an audit of 21 emergency departments over a 6 week period showed that 648 children and young people under the age of 17 required medical treatment; 15 of these cases were below the age of 12 and one was as young as 8 years old. On average these young people had consumed 13 units of alcohol within the 24 hours leading up to their attendance . If this number were to be extrapolated for England it would give an estimate of around 1245 young people per week requiring medical assistance or treatment in England (64,750 per year).

In England some 35,472 young people aged 16-24 were admitted to hospital in 2005 with alcohol-related conditions . The largest proportion (19,533) were male and the figures increased with increasing age. Whilst it is clear from these figures that excessive drinking by young people is a significant concern in the UK, it is not clear what impact this alcohol misuse has on their health and well-being beyond the immediate hospital episode.

Heavy drinking by young people is more pronounced in areas with high social deprivation. The highest levels of alcohol consumption are reported by young people in the North-East of England and Yorkshire and Humberside where they are 1.5 times more likely to have drunk alcohol during the last week than young people living in the rest of England . In 2008, a survey of 1,250 young people living in deprived communities in Britain found that over a third did not know what a unit of alcohol was and did not understand the term binge drinking. Of
these young people, 39% drank up to 20 units per week and 15% drank over 20 units per week . Thus the adverse effects of social deprivation on young people may be compounded by possible health and social problems related to heavy drinking.

In a survey of school children aged 15 and 16 from the North West of England, participants reported that being aged 16, receiving a greater amount of income per week and not having a hobby or being a member of a club or sports team was associated with higher levels of alcohol . In addition, a higher percentage of girls reported drinking in public places whilst a higher percentage of binge drinkers were male . The 2005/2006 Health Behaviour in School-aged Children (HBSC) Survey (on patterns of health among young people in 41 countries and regions across Europe and North America) provides an international comparison . Notably, findings suggest that young people in the UK have some of the
highest rates of drunkenness internationally. England had the highest proportion of girls (24%) that reported that they had first been drunk at the age of 13 or younger. Rates for English boys were also high 23% reported they had been drunk at age 13 or younger .

Thus there are clear grounds for concern about alcohol consumption in young people in England and it seems that many aspects of young people’s drinking may be situational or culturally determined. Moreover, whilst there is some evidence that parents’ attitudes about alcohol may shape their children’s views (particularly in younger children) about drinking, it seems that other direct mechanisms such as access to pocket money and involvement in diversionary activities (or not) may also determine if, when and how much their children
drink. However, it is currently not clear to parents what risks arise for their children from early exposure to, or different levels of, alcohol consumption. Many parents may feel that early introduction to alcohol by them is preferable to its use in unsupervised experimentation.

However, there is currently insufficient information to base such decisions on.
In adults there are some health and social benefits associated with alcohol consumption. However, the health benefits are linked to cardio-protective effects of low to moderate consumption of alcohol which have generally been identified in older adults, that is men aged over 40 and post-menopausal women . The positive social effects of drinking are well known to the majority of the adult population that chooses to drink alcohol, although these effects are rarely studied in research terms. In young people, it is not clear whether there is any health benefits associated with drinking in early life. It is likely that young people will
perceive positive social effects of drinking . However, it is possible that these may be tempered by adverse consequences that may arise from drinking at an age before alcohol is legal.

On the basis of current epidemiological evidence on adverse consequences of drinking, particularly in young people who become intoxicated, the alcohol harm reduction strategy for England has highlighted that underage drinking is a major public health priority and outlined three objectives for tackling it:

• 1.Delaying the onset of regular drinking, primarily by changing the attitudes of 11-15 year olds and their parents about alcohol.
• 2. Reducing harm to young people who have already started to drink.
• 3. Creating a culture in which young people feel they can have fun without needing to drink.

Recent NICE guidelines on alcohol interventions in schools and the Government’s recent Youth Alcohol Action Plan also set out clear priorities concerning alcohol and young people under the age of 18. One of the actions in the Action Plan is to issue advice to parents about young people and alcohol, which will include guidelines for low risk drinking

This ‘guidance will also offer wider information on the health and social impacts of
drinking at young ages, sources of help and support for parents including evidence-based approaches for them to use with their children. Furthermore, the 2007 Chief Medical Officers Report recognised that young people’s health is the key to the nation’s future. He identified six priority risk-taking areas of which one was alcohol and drugs . In order to inform the proposed guidelines on alcohol and young people, this review was commissioned to identify published evidence on both the harms and benefits of drinking in early life. Given that there was a limited time-frame available for the work, the commissioning brief asked for a focus on existing reviews in this field. The purpose of this work was to provide an assessment of this evidence to an expert group of clinicians/researchers
convened by the Department for Children, Families and Schools to enable them to make recommendations to parents about their children’s drinking.

The aim of the study were to:

• produce a thorough review of the most up-to-date, robust and reliable evidence on the harms and benefits of alcohol consumption for children and young people;
• undertake a systematic search of existing reviews and weigh-up the quality of the evidence base;
• communicate and discuss the findings with the expert panel on alcohol and young people;
• support the Department in accurately and appropriately interpreting and using the evidence;
• ensure the guidance for parents is based on a firm evidence base; and
• identify evidence gaps that longer term research needs to address.

The following electronic databases were searched for relevant reviews:

• ETOH Alcohol and Alcohol Problems Science database (1972-2003)
• TRIP (May 2008)
• MEDLINE (1950-May 2008)
• EMBASE (1980-May 2008)
• CINAHL (1982-May 2008)
• PsycINFO (1806-May 2008)
• Social Science Citation Index (1970-May 2008)
• Science Citation Index (1970-May 2008)
• Scopus (1996-May 2008)

We also used key words (see below) to search the following websites

• Institute http://www.intute.ac.uk/
• Department for Children, Schools and Families http://www.dcsf.gov.uk/
• Department of Health http://www.dh.gov.uk/en/Publicationsandstatistics/index.htm
• Home office http://www.homeoffice.gov.uk/rds/alcohol1.html
• UK Statistics Authority http://www.statistics.gov.uk
• EU Statistics UK http://www.eustatistics.gov.uk/
• NHS Information Centre http://www.ic.nhs.uk/
• UK Data Archive http://www.data-archive.ac.uk/
• NICE http://www.nice.org.uk/
• WHO http://www.who.int/topics/alcohol_drinking/en/
• Alcohol Concern http://www.alcoholconcern.org.uk/
• Alcohol Education and Research Council http://www.aerc.org.uk/
• National Center on Addiction and Substance Abuse http://www.casacolumbia.org/
• Alcohol and Drug Abuse Institute http://depts.washington.edu/adai/
• Australian Drug Information Network http://www.adin.com.au/
• SoRAD http://www.sorad.su.se/
• Diversity Health Institute Clearinghouse

http://www.dhi.gov.au/clearinghouse/default.htm

• European Alcohol Policy Alliance http://www.eurocare.org/
• ADCA library http://tinyurl.com/4t8ds2
• DrinkandDrugs.net http://www.drinkanddrugs.net/
• Daily Dose http://www.dailydose.net/
• Google and Google Scholar http://www.google.co.uk
• NIAAA: http://www.niaaa.nih.gov/

Just as in the 1970s, the drug legalization movement has received a great deal of media attention. Also just as in the 1970s, this movement, unfortunately, has contributed to the rise in drug use by painting the picture that drug laws – not drugs – are the villains. Legalization advocates attempt to support their position with faulty analogies, misrepresentations, and unsupported theories. This fact sheet will address the myths propagated by the pro-drug movement.

MYTH: Drug laws infringe on individual freedom and privacy as well as make criminals out of otherwise law-abiding citizens.

FACT: All laws, by their nature, restrict a certain degree of freedom – the freedom to do as one pleases, whenever one pleases, regardless of the harm or potential harm to oneself or others. Civilized society has the right and the responsibility to regulate behavior in order to protect individuals from their own poor decisions as well as others from the risks of certain behavior. Drunk driving, traffic regulations, possession of explosives and weapons, incest, and child labor are but a few examples.

Those who want to legalize drugs would have you believe that individuals who choose to engage in illegal behavior bear no responsibility; but, instead, the law is to blame, even though most of our citizens elect not to violate the law. The legalization advocates focus on the rights of drug users while ignoring the rights of the public. Based on their philosophy, it is acceptable to allow a very small segment of our society to get high with impunity while placing the majority in great jeopardy from their intoxicated state. Based on their theory, drunk driving should not be against the law. A drunk should only be punished after he or she has a traffic accident and kills or maims someone.

Additionally, the majority of our citizens do not fear law enforcement. It is those few who choose to violate the law who feel threatened by the police. They seek protection of their own freedom while they choose to violate the freedom of others.

MYTH: Drug use is a victimless crime.

FACT: There are actually four classes of drug use victims: the users themselves, the family and friends of users, the individuals who are victimized by the acts of those under the influence, and the taxpayers/consumers who are paying the price. Tell these people, who have had firsthand experience with drug abusers, that they are not victims. Tell the mother and father whose child was killed by a drugged driver, or the husband whose wife was raped by somebody loaded on cocaine, or the sister whose brother was brutally beaten by a “speed freak” that they are not victims of drug use. The nexus between violence and being under the influence is indisputable. Tragic stories of promising young adults dropping out or children beaten by their drug-using parents are all too common. How anyone, assuming that they truly understand the drug culture, can suggest a policy that would facilitate drug use is beyond comprehension.

MYTH: Alcohol and illicit drugs are no different; thus, it is hypocritical for society to allow alcohol use while outlawing other drugs.

FACT: Alcohol and illicit drugs have a major difference. Most people use alcohol as a beverage and don’t drink to become intoxicated; whereas, with drugs, intoxication is the sole purpose. That is why marijuana smokers seek the higher THC content in marijuana and why crack is so popular among cocaine users. A more factual analogy would be to compare drug use with drunkenness. In addition, illicit drugs are far more addicting than alcohol. Also, approximately one-half of our citizens use alcohol, whereas only approximately 6 percent use all of the illicit drugs combined – the simple reason being that alcohol is legal, relatively inexpensive, readily available, and socially acceptable, whereas illicit drugs are not.

MYTH: The legalization of illicit drugs should be based on the alcohol model.

FACT: Alcohol is hardly the model to use to justify legalizing illicit drugs. Legal alcohol has been consumed by a majority of our young people, whereas only a small percentage use illegal drugs. There are more people addicted to alcohol than use all the illicit drugs combined. Alcohol kills five times more people, the medical costs are triple, and economic costs are double those of all illicit drugs combined. There are also three times as many arrests for alcohol offenses as there are for drug offenses. The paradox is, while society is strengthening and demanding stricter enforcement of alcohol laws, there are those who want to decriminalize and even abolish drug laws.

MYTH: We tried alcohol prohibition, which was a failure, proving that prohibition against drugs does not work.

FACT: Alcohol prohibition, under quite different circumstances in the 1920s, was an attempt to pass laws that the majority of the people did not support. Even with that, there was an approximate 50 percent reduction in alcohol consumption, deaths from alcohol-related diseases, admissions to mental institutions, and alcohol-related psychosis. Unlike the legalizers would lead you to believe, crime did not skyrocket. Prior to enforcing drug laws and alcohol prohibition, from 1900 to 1920, the murder rate jumped 300% (1.5 to 8 per 100,000) from 1905 to 1919. During prohibition, the rate climbed only 30% (8 to 9.5 per 100,000). Rescinding prohibition after only 13 years was insufficient time to change society’s attitude following 2,000 years of acceptance. Regardless of whether you drink alcohol or not, you would probably agree that our society would be much better off if we didn’t have alcoholic beverages.

MYTH Elimination of drugs would reduce crime and free prison space for the more serious violent offenders.

FACT: Removal of laws would reduce incidents for those specific violations, but the behavior would not change. Lowering the age consent to 12 would reduce the number of child molestation crimes, but it would not change the fact that predators were molesting young children ages 12 to 18. The advocates fail to recognize what drug experts are well aware of: that a high percentage of drug dealers and addicts were criminals first and foremost. They would continue their criminal behavior in order to acquire sources of income. The Mafia did not disband after Prohibition nor would the Crips and Bloods become choirboys if drugs were legalized. The drug black market would continue unless all drugs for all ages were legalized, a proposal few support.

The nexus between being under the influence of alcohol and/or drugs and violence is well documented. Because drugs alter the mental state, drug users commit a disproportionate number of violent crimes. These acts of violence are often against family members and friends. Fifty percent of all child abuse cases are attributed to drug-using parents. Drug users are five to ten times more likely to be involved in fatal traffic accidents than drunk drivers. The perpetrator was under the influence in well over half of the violent crimes such as murder, rape, and serious assault. Only 5 percent of all murders are committed because of drug laws, whereas approximately 25 percent are committed because the murderer was under the influence of drugs.

There are three times as many arrests for alcohol violations as there are for drug violations. Legalizing substances such as alcohol was supposed to reduce crime, or is it that intoxication leads to more crime?

Ninety-three percent of all state prison inmates are violent and/or serious repeat offenders. Only 1.4 percent are first time, “non-violent” drug offenders. Keep in mind that “non-violent” only describes the act for which individuals are incarcerated and not their past history or previous behavior. If an organized crime “hit man” were convicted for income tax evasion, then he would be considered a non-violent inmate. In addition, only approximately 10 percent of those arrested for drug offenses actually end up in prison. The simple truth is that if we legalize or decriminalize drugs, the acts of violence against our citizens would skyrocket.

MYTH: Other countries have had successful experience with a more lenient and/or pseudo-legalized drug policy.

FACT: In the 1970s legalization advocates cited Great Britain’s decriminalization of heroin as a model drug policy. When Britain’s failed policy resulted in increased addiction, while the addict population remained stable in the United States, the advocates discontinued citing Britain. They then pointed to Platzspitz Park in Zurich, Switzerland, which essentially offered free drugs. This program was to prove all the so-called positive benefits of legalized drugs. The advocates expected less crime, more addicts accepting treatment, decreased AIDS, and the isolation of addicts. After five years, this experiment was abandoned because crime increased, drug-related deaths doubled, AIDS rose, and the health care system was overwhelmed. The very persistent advocates then began focusing on the Netherlands and its “enlightened” drug policy of not enforcing laws against selling and using marijuana in certain areas. After a number of years, the Netherlands began experiencing the consequences of lenient drug laws with increased drug use, unemployment, and crime. From 1984 to 1992, teenage drug use in the Netherlands increased 250 percent, while in the United States, at the same time, teenage drug use was reduced by 50 percent. Crimes of violence in the Netherlands – for instance, serious assault – increased 65 percent.

The advocates actually don’t have to look beyond this country to examine the results of legalization. The experience in Alaska with decriminalized marijuana resulted in twice as many Alaskan teenagers using the drug as those in the rest of the nation. Also, in the early 1900s, prior to legal sanctions, when drugs were inexpensive, available, and legal, the drug crisis per capita was triple today’s drug problem.

The advocates failed to examine the assertive drug policies of Japan and Singapore that resulted in the virtual elimination of the drug problem. Along with some Muslim countries, Japan and Singapore have proven that tough drug laws, coupled with aggressive enforcement, work.

MYTH: The cost of enforcing drug laws is too expensive, and the money could better be spent on social programs dealing with the root causes of drug abuse.

FACT: What the legalization advocates fail to address is the cost to this country if drug laws were not enforced. Making illicit drugs legal, inexpensive, and readily available would lead to a significant increase in the number of users and increased consumption among current users. Increased use and consumption would result in corresponding greater costs for homelessness, unemployment, welfare, lost productivity, disability payments, school dropouts, lawsuits, medical care, chronic mental illness, accidents, crime, and child neglect, to name a few.

Fifty to sixty percent of mental health care patients are substance abusers. Drug-using teens are three times more likely to commit suicide than their non-using peers. Seventy-five percent of teenage runaways are substance abusers. Hundreds of thousands of newborns are drug-exposed and impaired, costing taxpayers over $100,000 per child.

The current economic cost of illicit drug abuse is still half that of one legal drug – alcohol. The money raised in taxing alcohol covers less than 10 percent of all social and health expenditures due to that drug. Federal, state, and local government expenditures for drug law enforcement, which includes police, prosecutors, public defenders, courts, and prisons, is approximately $10 billion, which is less than 1 percent of total government expenditures. Relatively speaking, this is not a significant investment considering drug law enforcement, when compared to alcohol, helps save hundreds of thousands of lives and hundreds of billions of dollars.

Putting drug law enforcement expenditures into perspective, our federal government spent ten times that amount paying the interest on the public debt, ten times that amount on the war on poverty, and more money on the Food Stamp Program alone than all federal, state, and local expenditures for drug law enforcement.

There is also an assumption that with legalization there would be no governmental costs to regulate and control the distribution, sale, and use of drugs similar to those we currently have with alcohol. In addition, drug law enforcement would still be required for those drugs that remain illegal or to police the sale to and use by those under age.

Most importantly, the cost-saving argument, referred to as “blind-side economics,” only addresses economic issues and not the more tragic costs in terms of loss of life, pain and suffering, broken families, child neglect, and the general poisoning of Americans.

MYTH: The answer to the drug problem is increased drug prevention and treatment and not law enforcement.

FACT: It is interesting to note that most drug treatment and prevention professionals are against legalizing drugs. They consider law enforcement an essential precursor to both successful prevention and treatment. Good drug policy requires all three disciplines. Drug treatment experts agree that law enforcement offers strong incentives not only to receive treatment, but once treatment has been completed, to stay off of drugs. Making drugs legal, inexpensive, and readily available would eliminate that important incentive. Drug prevention experts agree that legal sanctions and public attitude against drug use are essential for successful education and prevention programs.

MYTH: This country’s 80-year war on drugs has been a failure, proving that strict laws and enforcement do not work.

FACT: It should be noted that there is not actually a “war” on drugs, but a limited engagement. Even with that, drug sanctions and enforcement have been successful during this 80-year period. Experts estimate that in the early 1900s, prior to drug laws or enforcement, there were as many addicts in this country as there are today, even though the population was one-third smaller. Recognizing the tremendous costs and problems associated with drug use, citizens, through their government, elected to pass and strictly enforce drug laws. The drug problem was significantly reduced so that by the 1940s and ‘50s, it was relatively minor. Anyone attending high school during that period could testify that drugs were virtually non-existent for most people.

In the 1960s and 1970s, there was a major shift in attitude regarding drug use. Terms such as “recreational drug use” were coined; the legalization movement gained momentum; drug use was glorified; and drug law enforcement was de-emphasized. This resulted in a tremendous increase in drug use and related problems in America. In the 1980s, through a combination of increased law enforcement, highly publicized prevention messages, and more effective treatment, drug use was reduced by 50 percent in just twelve years. In 1979 there were 24 million drug users and by 1992 there were only 11.4 million. It was during that period that drug arrests and incarcerations doubled. High school seniors graduating in the class of 1992 were 50 percent less likely to use drugs than their counterparts in the class of 1979.

Studies and surveys show that while 70 percent of eighth graders had used alcohol, only 10 percent had tried marijuana, and only 2 percent cocaine. Additional studies demonstrate that a majority of students cite the fear of getting into trouble with the law as a major deterrent to drug use. Yet another study shows that 79 percent of those responding stated they had no chance to use cocaine. Of the 21 percent who did have a chance to use cocaine, over half did. The U.S. military’s tough drug policy dropped drug use from 28 percent in 1980 to 3 percent in 1992. Private industry has repeatedly proven that tough anti-drug sanctions are successful.

There have been few modern social problems in this country, such as welfare, teenage pregnancy, homelessness, high school dropouts, and test scores for American students that have shown the same degree of success as our country’s drug policy. If, for instance, teen pregnancies were reduced by 50 percent, homelessness reduced by 50 percent, or SAT scores raised by 50 percent, the successes would be applauded. Instead, a 50 percent reduction in the number of drug users is considered a failure.

Conclusion

You don’t have to be a drug-abuse expert, an intellectual, or hold a variety of degrees to understand that to make illicit drugs legal, readily available, relatively inexpensive, and reduce the risk would lead to increased numbers of drug users as well as increased consumption among current users. Likewise, common sense would dictate that with increased drug use and consumption, the problems affecting this country would be overwhelming. Drug abuse exacerbates most social problems facing this country and touches all segments of our population. There would be no greater threat to destroy our country from within than making drugs inexpensive, available, and legal. I don’t think this is a legacy that we want to leave our children or our grandchildren. Instead of repeating the mistake of the 1970s, we should build on the successes of the 1980s. It is a mystery as to what drug culture the legalization advocates are referencing. Drug abuse experts are positive it isn’t the one they deal with on a daily basis. Intellectual theory, although interesting, often has no basis in reality

Source: Executive Director Thomas J. Gorman The Rocky Mountain HIDTA (CO)

It’s not unusual any more to see people in Libertarian circles attacking the war on drugs as a waste of tax dollars and an infringement on personal liberties. In my opinion, that is misguided thinking that comes from trying to apply unworkable theoretical concepts in the real world.
For example, you often hear advocates of drug legalization say that we’re never going to win the war on drugs and that it would free up space in our prisons if we simply legalized drugs. While it’s true that we may not ever win the war against drugs, we’re not ever going to win the war against murder, robbery and rape either. Moreover, it’s true that it would free up lots of space in our prisons if we legalized drugs, but you could say the same thing about most crimes. In fact, we could reduce the crime rate to zero and save enormous amounts of money on police, lawyers, and courts if we simply made everything legal. But, that doesn’t mean it would be a net plus for society.
Another point that’s often brought up is that if we legalized drugs, we’d be able to tax them and bring in more revenue for the state. But, how is that working out with alcohol and cigarettes? In 2004 and 2005, 39% of all traffic-related deaths was related to alcohol consumption and 36% of convicted offenders “had been drinking alcohol when they committed their conviction offense.” When it comes to cigarettes, adult smokers “die 14 years earlier than nonsmokers.” But, will we ever get rid of tobacco or alcohol? No, both products are too societally accepted for that and perhaps more importantly, the government makes enormous amounts of revenue from their sale. Do we really want to get into that same position with Crack, Acid, or Meth? Do we really want to be sitting around 10 or 15 years from now saying, “Gee, we’d like to get rid of heroin, but how could we replace the revenue we make from taxing it at an exorbitant rate?”
Moreover, the drug legalization crowd claims that we can manufacture drugs here in the U.S., tax them heavily, thereby making money for the government, and yet still be able to sell the drugs cheaper than the dealers can. That would seem to be a dubious proposition. Drug dealers who pay no taxes, have no unions, and don’t have to pay their labor the minimum wage, may very well be able to produce drugs more cheaply than corporations in the U.S. that will be under strict FDA guidelines (It typically costs a billion dollars to bring a new drug to market), that will be faced with a never ending stream of lawsuits, that will have to pay taxes, and then, additionally, will have to sell a product that will be taxed to the high heavens. That means it’s entirely possible that the cost of illegal drugs could go up, not down, with the government running the show and that would be a problem in and of itself because currently, “16% of convicted jail inmates said that they committed their offense to get money for drugs.”
Of course, the number of people using what are currently illegal drugs would skyrocket if they were legalized, so we’d see a new wave of drug addled burglars if we “legalized it.” Now, maybe you think that’s not the case. Some people certainly argue that if illicit drugs were legalized, their usage would drop. However, the fact that drugs are illegal is certainly holding down their usage. Just look at what happened during prohibition if you want proof of that. Per Ann Coulter in her book, “How to Talk to a Liberal if you Must:”
“Prohibition resulted in startling reductions in alcohol consumption (over 50 percent), cirrhosis of the liver (63 percent), admissions to mental health clinics for alcohol psychosis (60 percent), and arrests for drunk and disorderly conduct (50 percent).” — P.311
That’s what happened when alcohol was made illegal. However, on the other hand, if we make drugs legal, safer, easier to obtain, more societally accepted, and some people say even cheaper as well, there would almost have to be an enormous spike in usage.
Certainly that’s what happened in the Netherlands where “consumption of marijuana…nearly tripled from 15 to 44% among 18-20 year olds” after the drug was legalized.
But, some people may say, “so what if drug usage does explode? They’re not hurting anyone but themselves.” That might be true in a purely capitalistic society, but in the sort of welfare state that we have in this country, the rest of us would end up paying a significant share of the bills of people who don’t hold jobs or end up strung out in the hospital without jobs — and that’s even if you forget about the thugs who’d end up robbing our houses to get things to pawn to buy more drugs. Even setting that aside, we make laws that prevent people from harming themselves all the time in our society. In many states there are helmet laws, laws that require us to wear seatbelts, laws against prostitution, and it’s even illegal to commit suicide. So banning harmful drugs is just par for the course.
And make no mistake about it, drugs do wreck a lot of lives. Of course drugs aren’t the only things that wreck lives and not every person who does drugs ends up as a crackhead burglar or a dirty bum living in an alley. Heck, Barack Obama, a man some people would like to see as our next President has used cocaine — and doesn’t it seem like every few weeks we read about another celebrity who comes out of rehab and goes on to have a successful career?
Sure, that’s true. But, every person who plays Russian Roulette doesn’t end up with a bullet in his head either. Look at the flip side of the equation. How many homeless people are drug addicts? How many women have had crack babies? How many people are in jail today because they got high and committed a crime? How many lives have been wrecked in some form or fashion by drug use? There’s probably not a person reading this column who doesn’t know someone who has faced terrible consequences in his life because of drug use.
That’s why once, way back when William Bennett was the drug czar, he responded like so to a caller on the Larry King show who told him that he should “behead the damn drug dealers.”
“I mean what the caller suggests is morally plausible. Legally, it’s difficult. But somebody selling drugs to a kid? Morally, I don’t have any problem with that at all.” — Bill Bennett
Bennett was right then, he’s right now, and my guess is that most parents, upon finding out that someone was peddling drugs to their kid, would agree with him. Since that’s the case, do we really want the federal government to take over the role of a pusher and get our kids hooked on drugs to make a profit? No, we don’t.
Source: www.rightwingnews.com Jan 2007

More Author Affiliations: ORYGEN
Research Centre (Drs Yu¨ cel,
Whittle, and Lubman) and
Melbourne Neuropsychiatry
Centre, Department of
Psychiatry, The University of
Melbourne and Melbourne
Health (Drs Yu¨ cel, Whittle,
Fornito, and Pantelis),
Melbourne, Australia; School of
Psychology and Illawarra
Institute for Mental Health,
University of Wollongong,
Wollongong, Australia
(Dr Solowij and
Ms Respondek); and
Schizophrenia Research
Institute, Sydney, Australia
(Dr Solowij).
(REPRINTED) ARCH GEN PSYCHIATRY/VOL 65 (NO. 6), JUNE 2008 WWW.ARCHGENPSYCHIATRY.COM
694
©2008 American Medical Association. All rights reserved.
Downloaded from www.archgenpsychiatry.com , on June 3, 2008

recent structural magnetic resonance imaging (MRI) studies
have also reported contradictory findings, ranging from
no global or regional changes in brain tissue volume or
composition14-16 to gray and white matter density changes,
either globally17 or in focal regions, most notably in the
hippocampal and parahippocampal areas.18,19 However,
these previous studies used imaging techniques with relatively
coarse spatial and anatomical resolution and typically
focused on samples with multiple substance use or
comorbid psychiatric disorders and on only moderate levels
of cannabis use (ie, _2 joints per day). Indeed, despite
strong evidence of neurotoxicity in the animal literature,
6-9 to our knowledge, no neuroimaging study has
examined the neurobiologic sequelae of long-term heavy
cannabis use while controlling for the important confounds
of polydrug abuse and co-occurring psychiatric
disorders.
In this study, we used high-resolution 3-T MRI to assess
volumetric changes in 2 cannabinoid-rich regions
of the brain (the hippocampus and the amygdala) known
to be susceptible to the neurotoxic effects of cannabis exposure
in a sample of long-term heavy users carefully
screened for polysubstance abuse and mental disorders.
Given the growing literature regarding an association between
cannabis use and the development of psychosis20
and cognitive impairment,16,21 we also assessed for subthreshold
psychotic symptoms and verbal learning ability
in this otherwise psychologically healthy sample.
METHODS
PARTICIPANTS
Male cannabis users with long histories of regular and heavy
cannabis use (n=15) and nonusing healthy male volunteers
(n=16) matched on age, estimated premorbid intelligence (National
Adult Reading Test),22 years of education, and state and
trait anxiety (Spielberger State-Trait Anxiety Inventory)23 were
recruited from the general community via a variety of advertisements
(Table). Cannabis users had lower Global Assessment
of Functioning scale scores and greater depressive symptoms
(as measured using the Hamilton Depression Rating Scale)24
than the comparison group; however, there were no current
or lifetime histories of diagnosable medical, neurologic, or psychiatric
conditions as assessed using the Structured Clinical Interview
for DSM-IV Axis I Disorders, Patient Edition.25 All the
control subjects also underwent a Structured Clinical Interview
for DSM-IV Axis I Disorders, Non-Patient Edition.25 Subthreshold
psychotic symptoms were probed using the Scale for the
Assessment of Positive Symptoms26 and the Scale for the Assessment
of Negative Symptoms.27 Regarding alcohol use, the
groups did not differ in levels of current consumption, lifetime
use, or history of abuse or dependence; and no participant
drank more than 24 standard alcoholic drinks per week.
Significantly more cannabis users were also tobacco smokers
(_2=22.9, P_.001) (Table). For all users, cannabis was the primary
drug of abuse, with only limited experimental use of other
illicit drugs (generally _10 lifetime episodes).
PROCEDURE
Participants were assessed on 2 occasions, usually 1 week apart.
In the first test session, participants completed demographic,
clinical, and substance use history assessments. In the second
test session, they completed the Rey Auditory Verbal Learning
Test (RAVLT) and underwent structural MRI.
Participants were asked to abstain from using substances for
at least 12 hours before each test session, and cannabis users
reported abstaining from cannabis for a mean of 21.3 hours before
the first test session (median, 14 hours; range, 10-72 hours)
and a mean of 19.8 hours before the second test session (median,
17 hours; range, 12-48 hours). Urine samples were obtained
from users on 4 occasions and from controls on 2 occasions
to corroborate self-reported abstinence. Specifically, for
cannabis users, samples were obtained on the evening before
each test session and on the day of testing. For controls, samples
were collected only on the day of testing. Examination of these
samples demonstrated that all but 1 cannabis user had cannabinoid
metabolites (11-nor-_9-tetrahydrocannabinol-9-
carboxylic acid creatinine normalized) detected in urine samples
from the first test session, and levels were generally high
(evening: median, 467 ng/mg [range, 0-2320 ng/mg]; day of
testing: median, 447 ng/mg [range, 0-11 293 ng/mg]). From the
second test session, 2 users returned a 0 reading; otherwise,
cannabinoid metabolite levels were again high (evening: median,
456 ng/mg [range, 0-3511 ng/mg]; day of testing: median,
389 ng/mg [range, 0-4470 ng/mg]). The levels of urinary
cannabinoid metabolites generally corroborate the selfreported
patterns of heavy cannabis use in the sample. All but
2 control subjects returned a 0 reading for cannabinoid metabolites
across both test sessions. The 2 controls with positive
urine samples reported only minimal and very occasional
exposure to cannabis. The median level of cannabinoid metabolites
in controls at the first test session was 0 ng/mg (range,
0-184 ng/mg) and at the second test session was 0 ng/mg (range,
0-180 ng/mg).
STRUCTURAL MRI
The MRI data were obtained using a 3-T scanner (Intera; Phillips
Medical Systems NA, Bothell, Washington) at the Symbion
Clinical Research Imaging Centre, Prince of Wales Medical
Research Institute, Sydney. A 3-dimensional volumetric
spoiled gradient–recalled echo sequence generated 180 contiguous
coronal slices. The imaging parameters were as follows:
echo time, 2.9 milliseconds; repetition time, 6.4 milliseconds;
flip angle, 8°; matrix size, 256_256; and 1-mm3 voxels.
Hippocampal, amygdala, whole brain, and intracranial volumes
were measured using established reliable protocols28-31
and were delineated by a trained rater (S.W.) masked to group
information. Specifically, the hippocampal boundaries were as
follows: posterior, the slice with the greatest length of continuous
fornix; medial, the open end of the hippocampal fissure
posteriorly, the uncal fissure in the hippocampal body, and the
medial aspect of the ambient gyrus anteriorly; lateral, the temporal
horn of the lateral ventricle; inferior, the white matter inferior
to the hippocampus; superior, the superior border of the
hippocampus; and anterior, the alveus was used to differentiate
the hippocampal head from the amygdala. The anterior border
was the most difficult to identify consistently and was aided
by moving between slices before and after the index slice. The
amygdala boundaries were as follows: posterior, the appearance
of amygdala gray matter above the temporal horn; superolateral,
the thin strip of white matter that separates the amygdala
from the claustrum and the tail of the caudate; medial, the
angular bundle, which separates the amygdala from the entorhinal
cortex; superomedial, the semilunar gyrus; inferior, the
hippocampus; inferolateral, the temporal lobe white matter and
the extension of the temporal horn; and anterior, the slice anterior
to the appearance of the optic chiasm. Whole brain volumes
were estimated using the Brain Extraction Tool method32
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to separate brain from nonbrain tissue. After brain/nonbrain
segmentation, each voxel was classified into gray matter, white
matter, or cerebrospinal fluid using FAST Model statistical software.
33 Only gray and white matter were used in the estimate
of whole brain volumes. The intracranial cavity was delineated
from a sagittal reformat of the original 3-dimensional data
set. The major anatomical boundary was the dura mater below
the inner table, which was generally visible as a white line.
Where the dura mater was not visible, the cerebral contour was
outlined. Other landmarks included the undersurfaces of the
frontal lobes, the dorsum sellae, the clivus, and the posterior
arch of the craniovertebral junction.
Interrater and intrarater reliabilities were assessed by means
of the intraclass correlation coefficient (ICC) (absolute agreement)
using 15 brain images from a separate MRI database established
specifically for this purpose and that has previously
been delineated by another expert rater. For the hippocampus,
interrater ICC reliabilities were 0.92 (right) and 0.91 (left)
and intrarater ICC reliabilities were 0.98 (right) and 0.95 (left).
For the amygdala, interrater ICC reliabilities were 0.85 (right)
and 0.88 (left) and intrarater ICC reliabilities were 0.93 (right)
and 0.97 (left). Once reliability was established, the rater (S.W.)
delineated the regions of interest for the images acquired from
the present study.
STATISTICAL ANALYSES
Whole brain volume, age, educational level, and estimated IQ
were not significantly different between the 2 groups and were,
therefore, not used as covariates (Table). Regional gray matter
volumes for the hippocampus and amygdala were corrected for
the effect of the intracranial cavity using a previously described
formula34 and were analyzed using analyses of variance,
with hemisphere (left or right) and region (hippocampus
and amygdala) as within-subject factors and group as the
between-subject factor. Main effects and interactions were evalu-
Table. Demographic, Clinical, Drug Use, and MRI Volumetric Measures
Measure
Long-term Cannabis Users
(n=15)
Nonusing Control Subjects
(n=16) P Valuea
Age, mean (SD), y 39.8 (8.9) 36.4 (9.8) .31
IQ, mean (SD) 109.2 (6.3) 113.9 (8.1) .09
RAVLT score, mean (SD)
Sum of 5 learning trials 43.8 (8.8) 57.4 (10.1) _.001
20-min delay 8.9 (4.1) 12.3 (3.7) .009b
Educational level, mean (SD), y 13.4 (3.2) 14.8 (3.7) .28
GAF scale score, mean (SD) 72.0 (11.2) 80.8 (9.4) .02
HAM-D score, mean (SD) 5.87 (3.2) 2.56 (1.9) _.001b
STAI, mean (SD)
State anxiety 34.3 (9.8) 32.9 (9.4) .67
Trait anxiety 39.3 (9.7) 39.0 (8.2) .92
SAPS score, mean (SD) 8.1 (7.9) 0.6 (1.2) _.001b
SANS score, mean (SD) 11.7 (8.5) 1.4 (1.4) _.001b
Cannabis use
Duration of regular use, mean (SD) [range], yc 19.7 (7.3) [10-32] NA NA
Age started regular use, mean (SD) [range], yc 20.1 (6.9) [12-34] NA NA
Current use, mean (SD), d/mod 28 (4.6) NA NA
Current use, mean (SD), cones/mod,e 636 (565) NA NA
Cumulative exposure, past 10 y, mean (SD)f 77 816 (66 542) NA NA
Cumulative exposure, lifetime, mean (SD)f 186 184 (210 022) 12.7 (12.2) _.001
Estimated episodes of use, median (range) 62 000 (4600-288 000) 11 (0-30) _.001
Alcohol use, mean (SD), standard drinks/wk 9.6 (6.1) 6.8 (5.0) .19
Tobacco use, mean (SD), cigarettes/d 16.5 (8.9) 7.5 (9.2) .20
Brain volumes, mean (SD), mm3
Intracranial cavity 1 546 237 (94 018) 1 607 590 (136 386) .14
Whole brain 1 310 780 (90 778) 1 374 123 (105 673) .09
Hippocampus .002g
Left hemisphere 2849 (270) 3240 (423)
Right hemisphere 2949 (244) 3348 (400)
Amygdala .01g
Left hemisphere 1766 (98) 1878 (190)
Right hemisphere 1601 (143) 1744 (158)
Abbreviations: GAF, Global Assessment of Functioning; HAM-D, Hamilton Depression Rating Scale; MRI, magnetic resonance imaging; NA, not applicable;
RAVLT, Rey Auditory Verbal Learning Test; SAPS, Scale for the Assessment of Positive Symptoms; SANS, Scale for the Assessment of Negative Symptoms;
STAI, State-Trait Anxiety Inventory.
aTwo-tailed t test unless otherwise indicated.
bMann-Whitney test.
cRegular use was defined as at least twice a month.
dCannabis users had used at this level for most of their drug-using history.
eA cone is the small funnel into which cannabis is packed to consume through a water pipe in a single inhalation. Without the loss of sidestream smoke, the
quantity of tetrahydrocannabinol delivered by this method is estimated as equating 3 cones to 1 cigarette-sized joint. Thus, the cannabis users in this study
smoked the equivalent of 212 joints per month, or approximately 7 joints per day.
fExpressed as cones for users and as episodes for controls. Estimates of lifetime exposure beyond 10 years in these very long-term users became skewed and
unreliable; hence, the 10-year estimate was used in correlational analyses.
gRegion_group analysis of variance.
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ated using Greenhouse-Geisser–corrected degrees of freedom,
with _=.05. Effect sizes, expressed as Cohen d, are also reported
for pairwise contrasts. Only effects involving group (cannabis
users vs nonusers) and associations with cannabis use
parameters are reported because this was the primary focus of
the present study. Group comparisons of performance on the
RAVLT and measures of subthreshold psychotic symptoms
(using the Scale for the Assessment of Positive Symptoms and
the Scale for the Assessment of Negative Symptoms) were conducted
using independent-samples t tests or Mann-Whitney tests
for nonnormally distributed data. Pearson product moment correlational
analyses were conducted to examine the behavioral
(ie, symptom and cognitive) relevance of any identified group
differences in regional brain volumes and the association
between these brain changes and parameters of cannabis use.
These analyses were necessarily exploratory given the limited
sample size.
RESULTS
GROUP CONTRASTS
In the analysis of regional gray matter volumes, there
was a significant main effect of group (F1,29=12.98,
P=.001) and a region_group interaction (F1,29=6.25,
P=.02). This result and the post hoc pairwise analyses
demonstrated reduced hippocampal volumes in cannabis
users (F1,29=11.14, P=.002 corrected; a reduction of
12.1% in the left and 11.9% in the right hippocampus
relative to controls), with a very large effect size (Cohen
d: left hippocampus, 1.17; and right hippocampus,
1.27) (Figure 1). Cannabis users also had smaller
amygdala volumes (F1,29=7.31, P=.01 corrected; a
reduction of 6.0% in the left amygdala and 8.2% in the
right amygdala relative to controls), with large effect
sizes (Cohen d: left amygdala, 0.80; and right amygdala,
0.99). The region _ group interaction reflects that the
overall reduction in hippocampal volume was relatively
(and significantly) greater than the reduction in amygdala
volume (12.0% in the hippocampus vs 7.1% in the
amygdala). In the analysis of subthreshold psychotic
symptoms, cannabis users reported significantly higher
positive symptoms (Scale for the Assessment of Positive
Symptoms; z=−3.57, P_.001) and negative symptoms
(Scale for the Assessment of Negative Symptoms;
z=−3.66, P_.001) than nonusing controls. Regarding
verbal learning, cannabis users displayed significantly
poorer performance than controls on the RAVLT measures
(sum of words recalled across the 5 learning trials:
z=−3.97, P_.001; and free recall after a 20-minute
delay: z=−2.61, P=.009).
CORRELATIONAL ANALYSES
There was a significant inverse association between left
hippocampal volume and cumulative cannabis exposure
during the previous 10 years (r=−0.62, P=.01; accounting
for 38% of the variance in left hippocampal volume)
(Figure 2A). When 1 participant with relatively
higher cumulative cannabis exposure and small hippocampal
volume was excluded, 22% of the variance was
still accounted for despite falling short of significance in
the reduced sample (r=−0.47, P=.09). There was also an
association between left hippocampal volume and positive
symptoms (r=−0.77, P_.001) (Figure 2B) and between
positive symptoms and cumulative cannabis exposure
(r=0.52, P=.048) (Figure 2C). The associations
between left hippocampal volume and cumulative cannabis
exposure and between left hippocampal volume and
positive symptoms remained after controlling for the effects
of global functioning (Global Assessment of Functioning
scale) and depressive symptoms (Hamilton Depression
Rating Scale). No other associations were found
between other brain volumetric measures, cannabis use,
and psychotic symptoms, and they did not vary as a function
of alcohol or tobacco use. Measures of RAVLT performance
did not correlate with hippocampal or amygdala
volumes in either controls or cannabis users.
COMMENT
To our knowledge, this is the first human study of longterm
heavy cannabis users to demonstrate marked
exposure-related hippocampal volume reductions.
These findings corroborate previous animal research,6-9
suggesting that long-term heavy cannabis use is associated
with significant and localized hippocampal volume
reductions that relate to increasing cumulative cannabis
exposure. In addition, the present findings are consis-
tent with the view that cannabis use increases the risk
of psychotic symptoms and informs the debate concerning
the potential long-term hazardous effects of cannabis
in this regard. The bilateral reduction in amygdala
volume is a novel but not unexpected finding given the
dense concentration of cannabinoid receptors in this
region.35
Although these findings are consistent with those of
a previous study,18 it is difficult to directly compare these
results with those of other human studies given that past
work used MRI with lower magnetic field strength and
spatial resolution and did not conduct region-of-interest–
based analyses (eg, performed whole-brain voxel-based
analyses18). Tzilos et al14 conducted the only other study,
to our knowledge, that investigated cannabis users with
a relatively long history of use (specifically, an average
duration of use of 22.6 years, or 18.9 years of daily use)
and their study is, therefore, most comparable with the
present study. Although they found no effects of longterm
cannabis use on hippocampal volume, the authors
acquired their images at a lower field strength and with
a coarser spatial resolution (1.5 T with 3-mm-thick slices
vs 3 T with 1-mm-thick slices in the present study), an
important consideration given the size of the brain structures
investigated. Moreover, their region of interest was
less specific to the hippocampus relative to the present
measure because they also included the parahippocampal
gyrus. Furthermore, there was a relatively large age
discrepancy between their users and controls (38.1 vs 29.5
years), and the minimum duration of exposure to cannabis
was considerably lower in their sample (as little as
1 year of cannabis exposure), but, overall, their sample
reported an average of 20 100 lifetime episodes of use.
In contrast, the minimum duration of exposure to cannabis
in the present sample was 10 years, with an average
of 62 000 episodes of use. Thus, despite a similar mean
duration of use, the present sample used more than 3 times
as much cannabis, which may explain the finding of a
dose-response relationship between hippocampal volume
and cumulative cannabis use. Further highresolution
MRI work is necessary to characterize precisely
the dosage of cannabis required for significant brain
changes to occur.
The pattern of use in the present sample is consistent
with heavy cannabis use patterns that have previously
been reported in other Australian studies. For example,
Copeland and colleagues36 reported median daily intake
of 8 cones (the small funnel into which cannabis is packed
to consume through a water pipe in a single inhalation)
in an Australian sample of cannabis users seeking treatment
for cannabis dependence, ranging up to 125 cones
per day in the heaviest user, with 11% reporting cannabis
smoking throughout the day. The heaviest user herein
reported smoking 80 cones per day (approximately 25
joints smoked throughout the day). This pattern of cannabis
use is not dissimilar to the heaviest cannabis users
from other studies of non–treatment-seeking samples of
Australian cannabis users.37,38
Despite the large magnitude of effects observed, it remains
unclear whether these volumetric reductions
reflect neuronal or glial loss, a change in cell size, or a
reduction in synaptic density (eg, dendritic arborization),
all of which have been reported in rodent studies.
6-9 For example, Scallet and colleagues9 found striking
tetrahydrocannabinol-induced residual decreases in
the mean volume of hippocampal neurons and their nuclei
and a 44% reduction in the number of synapses up
to 7 months after the last exposure to tetrahydrocannabinol.
Moreover, Landfield and colleagues7 administered
tetrahydrocannabinol 5 times a week for 8 months
(approximately 30% of the rat lifespan, and comparable
in frequency and duration to the present sample) and
found significant tetrahydrocannabinol-induced decreases
in neuronal density in the hippocampus. Such
findings may help explain the mechanisms underlying
gross hippocampal and amygdala volume loss seen in this
sample of long-term heavy cannabis users.
Left Hippocampal Volume, mm3
In the present study, hippocampal volume in the cannabis-
using group was inversely correlated with cumulative
exposure to the drug in the left, but not right, hemisphere.
Previous functional imaging studies16,39 have found
reduced left hippocampal activation during cognitive performance
in cannabis users, and there is evidence to suggest
that hippocampal abnormalities in psychiatric disorders
such as schizophrenia are more prominent in the
left hemisphere.40 These findings converge to suggest that
the left hippocampus may be particularly vulnerable to
the effects of cannabis exposure and may be more closely
related to the emergence of psychotic symptoms. In this
context, it is interesting that we found a significant inverse
correlation between left hippocampal volume and
positive symptoms. Cannabis use was also positively correlated
with positive symptoms, suggesting that there are
complex associations among exposure to cannabis, hippocampal
volume reductions, and psychotic symptoms.
Given these relationships, it is possible that the exposurerelated
hippocampal reduction may reflect heavy cannabis
use in response to preexisting or developing psychotic
symptoms. However, there is limited empirical
support for long-term self-medication of subthreshold psychotic
symptoms with cannabis and stronger support for
the induction of psychotic symptoms subsequent to cannabis
exposure.20 As such, it seems more likely that prolonged
heavy use of cannabis induced subthreshold psychotic
symptoms and that both of these factors are
associated with hippocampal volume loss. These symptoms
were subthreshold because these cannabis-using participants
were carefully screened for current and past history
of mental disorders. Furthermore, the fact that the
mean age of the present cannabis-using sample was nearly
40 years suggests that these symptoms are unlikely to reflect
a prodrome. One speculation is that the present participants
were less genetically vulnerable to developing
a psychotic disorder subsequent to cannabis use,41,42 allowing
them to smoke heavily for many years. Future longitudinal
work assessing the emergence of hippocampal
reductions and psychotic symptoms with continued exposure
to cannabis, and how these are related to polymorphic
variations in susceptibility genes for psychotic
disorders, will prove useful in better characterizing these
relationships.
Given that cannabis users had significantly greater depressive
symptom scores than controls and that there is
an association between depression and hippocampal volume
reduction,43 it could also be argued that depressive
symptoms may be another mediating factor in the relationship
between cannabis use and hippocampal volume
reduction. However, there are a variety of important
considerations that make this unlikely. First, there
was no significant association between hippocampal volumes
and depressive symptom scores. Second, the relationship
between left hippocampal volume and quantity
of cannabis used was maintained after statistically
controlling for depressive symptoms. Finally, the overwhelming
evidence suggests that hippocampal reductions
in major depressive disorder tend to occur in the
more persistent forms of the disorder (eg, multiple episodes,
repeated relapses, or long illness duration).43,44 This
was not the case in the present sample of cannabis users,
who scored less than 6.0 on the Hamilton Depression
Rating Scale, had never been diagnosed as having
major depression, and did not seek treatment for any depressive
disorder.
Cannabis users showed poorer performance on measures
of verbal learning, consistent with previous findings.
Although some functional imaging studies have
found reduced left hippocampal blood flow and activation
during verbal (and visual) learning tasks in cannabis
users, we found no correlation between RAVLT
performance measures and hippocampal volume in either
controls or cannabis users. It is likely that anatomical volume
is a less sensitive measure than brain activation for
identifying correlations with behavioral performance. This
is a particularly pertinent consideration given that the
performance measures on the RAVLT are likely to reflect
the operation of numerous cognitive processes not
necessarily related to hippocampal function. Future work
using experimental tasks designed to more specifically
probe memory functions mediated by the hippocampus
may be useful in this regard.
The bilateral reduction in amygdala volume is a novel
but not unexpected finding given the dense concentration
of cannabinoid receptors in this region.35 There were
no cognitive, psychotic, or depressive symptom associations
with reduced volume in the amygdala. However,
this region has been significantly implicated in cannabinoid-
associated emotional and reward-related learning
and memory processes.47,48 Given that these aspects of
learning have not been examined in human cannabis users,
they would seem to serve as a potentially informative
avenue forward to help elucidate the functional relevance
of such volumetric reduction in the amygdala.
The relationship between long-term cannabis use and
brain abnormalities is complex. Although a limitation of
this study may be the residual effects of cannabis in light
of the fact that the cannabis users in this study were required
to be cannabis free for only 12 to 24 hours before
MRI, such issues are likely to be more pertinent for studies
examining more dynamic aspects of brain functioning
(eg, activations and cognition).49 The present structural
findings are unlikely to relate to the recent effects
of cannabis use because we are unaware of any evidence
that suggests that the hippocampus and amygdala can
change in volume by 6% to 12% in short periods. However,
although we maintain that the present results reflect
brain changes associated with long-term heavy cannabis
use rather than the consequences of recent exposure,
further longitudinal work is required to assess whether
such changes are reversible across more protracted periods
of abstinence.
Another limitation of this study is the relatively small
sample size, although the sample was exceptionally unique
in that participants were very long-term and heavy cannabis
users (mean of 5-7 joints per day for _10 years)
without polydrug use or co-occurring neurologic or diagnosable
mental disorders. As such, we conducted the
first, to our knowledge, “pure” examination of the effects
of heavy and protracted exposure to cannabis in humans.
The large effect sizes of the main findings suggest
that these results are robust and reproducible. These findings
are further strengthened by the observed dose-
response relationships between hippocampal volume reductions
and cumulative cannabis use.
There is ongoing controversy concerning the longterm
effects of cannabis on the brain.  These findings
challenge the widespread perception of cannabis as having
limited or no neuroanatomical sequelae. Although
modest use may not lead to significant neurotoxic effects,
these results suggest that heavy daily use might indeed
be toxic to human brain tissue. Further prospective,
longitudinal research is required to determine the
degree and mechanisms of long-term cannabis-related
harm and the time course of neuronal recovery after abstinence.
Correspondence: MuratYu¨ cel, PhD,MAPS,ORYGENResearch
Centre, 35 Poplar Rd (Locked Bag 10), Melbourne,

 In Brief

• In 2002 and 2003, 21% of persons aged 16 to 20 reported that they had driven in the past year while under the influence of alcohol or illicit drugs

• Among persons aged 16 to 20, whites and American Indians/Alaska Natives were more likely to report DUI than other racial/ethnic groups

• In 2002 and 2003, approximately 4% of persons who reported DUI in the past year had been arrested and booked for DUI in the past year

 Motor vehicle crashes were the leading cause of death among young persons aged 16 to 20 in 2002.(Ref.1).   In that year, 6,327 persons aged 16 to 20 were involved in fatal crashes, representing a 10% increase since 1999. In addition, 29% of drivers aged 15 to 20 who were killed in motor vehicle crashes in 2002 had been drinking alcohol.(Ref.2) The National Survey on Drug Use and Health (NSDUH) asks persons aged 12 or older if they had driven a vehicle while under the influence of alcohol or illicit drugs in the past year (Ref.3) and if they had been arrested for driving under the influence (DUI).(Ref.4) The survey also asks about the use of alcohol and any illicit drugs in the past year and past month. Alcohol measures used in this report include any past month use, binge use, and heavy use. Binge alcohol use is defined as drinking five or more drinks on the same occasion (i.e., at the same time or within a couple of hours of each other) on at least 1 day in the past 30 days. Heavy alcohol use is defined as drinking five or more drinks on the same occasion on each of 5 or more days in the past 30 days; all heavy alcohol users also are binge alcohol users. NSDUH defines “illicit drugs” to include marijuana/hashish, cocaine (including crack), inhalants, hallucinogens, heroin, or prescription-type drugs used non-medically.

In 2002 and 2003, more than 4 million persons (21%) aged 16 to 20 reported DUI involving either alcohol or illicit drugs in the past year (Figure 1). In this age group, 17% reported past year DUI involving alcohol, 14 % reported DUI involving illicit drugs, and 8% reported DUI involving a combination of alcohol and illicit drugs used together.

Figure 1. percentages of Persons Aged 16 to 20 Who Reported Driving a Vehicle Under the Influence of Alcohol or Illicit Drugs in the Past Year: 2002 and 2003	Figure 2. percentages of Persons Aged 16 to 20 Who Reported Driving a Vehicle Under the Influence of Alcohol or Illicit Drugs in the Past Year, by Age: 2002 and 2003

 Among persons aged 16 to 20, older persons had a higher reported prevalence of DUI involving alcohol or illicit drugs than those who were younger (Figure 2). For example, persons aged 20 were nearly 3 times more likely to have driven under the influence than persons aged 16 (28 vs. 10%). Among all persons aged 16 to 20, males (24%) were more likely to report DUI involving alcohol or illicit drugs than females (18%). Among racial/ethnic groups, whites (26%) and American Indians/Alaska Natives (28%) were more likely to report DUI involving alcohol or illicit drugs than members of other racial/ethnic groups (Figure 3).

 (25%), followed by persons who lived in small MSAs (23%) and persons who lived in large MSAs
(19%).(Ref.7).

2. National Highway Traffic Safety Administration. (2003, August). Traffic safety facts 2002: Young drivers.  from http://www-nrd.nhtsa.dot.gov/pdf/nrd-30/NCSA/TSF2002/2002ydrfacts.pdf   Dec.2 2004

3. Respondents were asked, in three different questions, if during the past 12 months they had driven a vehicle while under the influence of (a) alcohol only, (b) illicit drugs only, or (c) a combination of alcohol and illicit drugs used together. Responses to these questions then were recoded to determine the prevalence of DUI involving (a) alcohol, (b) illicit drugs, (c) either alcohol or illicit drugs, or (d) both alcohol and illicit drugs.

4. Respondents were asked if during the past 12 months they had been arrested and booked for DUI involving alcohol or illicit drugs.

5. Persons aged 15 or younger were not included in these analyses because a substantial portion of persons aged 15 or younger are prohibited from driving by State laws.

6. The Midwest has 12 States: IL, IN, IA, KS, MI, MN, MO, NE, ND, OH, SD, and WI. The South has 17 States: AL, AR, DC, DE, FL, GA, KY, LA, MD, MS, NC, OK, SC, TN, TX, VA, and WV. The Northeast has 9 States: CT, MA, ME, NH, NJ, NY, PA, RI, and VT. And the West has 13 States: AK, AZ, CA, CO, HI, ID, MT, NM, NV, OR, UT, WA, and WY.

7. Large metropolitan areas have a population of 1 million or more. Small metropolitan areas have a population of fewer than 1 million. Non-metropolitan areas are outside metropolitan statistical areas (MSAs), as defined by the Office of Management and Budget. See the U.S. Bureau of the Census. (2003, June 12). About metropolitan and micropolitan statistical areas. Retrieved December 1, 2004, from http://www.census.gov/population/www/estimates/aboutmetro.html

8. This excludes an estimated 38,000 persons who reported they had been arrested and booked for DUI in the past year but indicated elsewhere that they had not driven under the influence of alcohol or drugs in the past year.

Figure Note

Office of Applied Studies. (2004). Results from the 2003 National Survey on Drug Use and Health: National findings (DHHS Publication No. SMA 04–3964, NSDUH Series H–25). Rockville, MD: Substance Abuse and Mental Health Services Administration.

Each day, more than 9,000 new driver’s licenses are issued to 16- and 17-year-olds nationwide, the very same age group that is at greatest risk for marijuana use, and a 2005 survey reveals that these teens say that cars are the second most popular place for smoking marijuana. The Office of National Drug Control Policy (ONDCP) is partnering with driving schools and other leading health, safety and youth-serving organizations to warn parents of the prevalence and dangers of drugged driving and to provide information to help teens “Steer Clear of Pot.”

More than 2.9 million driving-age teens reported lifetime use of marijuana, and last year more than 750,000 16- and 17-year-olds reported driving under the influence of illicit drugs. According to the 2004-2005 PRIDE Surveys, when asked where they use, approximately one in seven (14%) high school seniors cited “in a car,” making cars the second most popular location after at “a friend’s house” (20.4%).

“Parents need to realize that drugged driving is nearly as common today among teens as alcohol-impaired driving,” said John P. Walters, Director, National Drug Control Policy. “Marijuana impairs many of the skills required for safe driving, such as concentration, coordination, perception and reaction time, and these effects can last up to 24 hours after smoking the drug — It is critical that parents know the dangers associated with drugged driving and are vigilant in monitoring their teen drivers, especially young, less experienced drivers.”

Monitoring the Future data shows that approximately one in six (15%) teens reported driving under the influence of marijuana, a number nearly equivalent to those who reported driving under the influence of alcohol (16%). A recent study from a large shock trauma unit found that 19 percent of automobile crash victims under age 18 tested positive for marijuana.

“Getting a driver’s license is a milestone in a teen’s life that goes beyond the road to symbolize independence and freedom,” said Thomas “Buddy” Gleaton, Ed.D., President, PRIDE Surveys. “In the more than 20 years that PRIDE Surveys has been tracking teen drug use, teens consistently report engaging in risky behaviors in cars. Parents need to keep a watchful eye to be effective in reversing these trends.”

ONDCP’s National Youth Anti-Drug Media Campaign is providing parents and teens with information about the risks of drugged driving through a renewed “Steer Clear of Pot” initiative. The Media Campaign will underscore the harmful effects of teen marijuana use and drugged driving through the promotion of free materials, including a “New Drivers Kit” for teens and parents, available with other new content on the Media Campaign’s Web site for parents, http://www.TheAntiDrug.com .

In addition, “Steer Clear of Pot” partners will distribute drugged driving and marijuana prevention materials to driver’s education teachers, teens, and parents nationwide:

– The American College of Emergency Physicians will inform its nationwide membership base of 15,000 in 49 chapters of “Steer Clear of Pot” resources through its newsletter and Web site;

– The Driving School Association of the Americas will include information about the initiative in its magazine, The Dual News, which is distributed to 8,000 professional driving schools and 50,000 driving school educators, and will promote available resources on the organization’s Web site;

– The Emergency Nurses Association will inform its 28,000 members about available resources through its monthly newsletter; and

– GEICO, the fifth-largest private passenger auto insurer in the United States, has incorporated the Media Campaign’s messages into its existing “Can I Borrow the Car?” teen driving and safety materials and is providing co-branded versions of those materials through the Campaign’s “New Drivers Kit.” The company continues to distribute co-branded “Steer Clear of Pot” materials and promote the Media Campaign’s resources to its 5.5 million policyholders and 22,000 GEICO associates.

“Driver’s education and behind-the-wheel training are at the foundation for developing safe driving skills,” said Bradley Huspek, President, Driving School Association of the Americas. “Parents and driving instructors play a critical role in educating teens about being responsible drivers and steering clear from drugs.”

Experts say parental supervision and setting clear rules are associated with less risky teen behavior. A recent SADD/Liberty Mutual Group report found that nearly 60 percent of teens who drive say their parents have the most influence on their driving, followed by 27 percent who say their friends are most influential. Parents can take action and help their teen “steer clear of pot” with simple steps such as:

– checking the car for signs of drug paraphernalia;

– setting limits on driving in risky conditions;

– knowing where their teen is going and what route they intend to drive; and

– reinforcing safe driving practices by driving together.

Since its inception in 1998, the National Youth Anti-Drug Media Campaign has conducted outreach to millions of parents, teens and communities to reduce and prevent teen drug use. Counting on an unprecedented blend of public and private partnerships, non-profit community service organizations, volunteerism, and youth-to-youth communications, the Campaign is designed to reach Americans of diverse backgrounds with effective anti-drug messages.

For more information on the ONDCP National Youth Anti-Drug Media Campaign, visit

The Road Safety Monitor, a national telephone survey conducted each year involving Canadian drivers indicates that drug impaired driving is seen as second only to alcohol impaired driving as a serious issue and that illicit drugs are seen as a more serious problem than prescription or over the counter drugs. Overall, 17.7%, or 3.7 million Canadian drivers report driving within two hours of using illicit, prescription or over the counter drugs.

Collisions remain a major cause of death and injury in Canada, and concerns about the role of cannabis in road safety in this country date back many years. Much less is known about the impact of cannabis on road safety than the impact of alcohol, in part because of the much greater difficulty involved in measuring the presence and amount of cannabinoids compared to alcohol. However, there is renewed interest in this issue stimulated in part by proposed legislative changes on the part of the Government of Canada to reduce substantially the penalties for possession of small amounts of cannabis.

Objectives

The purpose of this paper is to provide an overview of available research and evidence on the potential impact of cannabis on road safety in Canada focusing on two areas: 1) research on the prevalence of cannabis use in Canada; and 2) research on the prevalence of driving after cannabis use in Canada.

Prevalence of Cannabis Use in Canada

Little information is available on the prevalence of cannabis use in Canada prior to the 1960s. However, in that decade, cannabis use increased substantially. While a variety of possible sources of information on cannabis in the Canadian population have been used over the years, including such measures as amounts of the drug seized by police and the number of individuals prosecuted by the courts for cannabis offences, the most direct and the most accurate measures of the prevalence of cannabis use are those derived from surveys. Although cannabis is an illegal drug and there are concerns that survey responses may be influenced by its legal status, research demonstrates that respondents to anonymous surveys, where there are no adverse consequences involved, generally provide valid responses.

Smart and Fejer presented one of the very first estimates of the prevalence of cannabis use in a Canadian population, based on a survey of a representative sample of residents of Toronto conducted in 1971. They found that 12.2% of males and 5.5% of females had used cannabis at least once in the preceding year. The prevalence of use differed substantially by age group and gender. Among males, 41.5% of those aged 18-25, 20.8% of those aged 26-30, and 1.8% of those aged 31 and over had used cannabis in the preceding year. Among females, 20.0% of those aged 18-25, 6.3% of those aged 26-30, and 1.8% of those aged 31 and over had used cannabis in the previous year. These data clearly demonstrate that, by the end of the 1960’s, cannabis use had become very common among young people.

Ogborne and Smart reported on cannabis use in the general population of Canada aged 15 and over based on the National Alcohol and Other Drugs Survey conducted in 1994. This survey was the largest representative survey with information on cannabis use ever made in Canada, with a sample size of 12,155. Use of cannabis at that time was relatively uncommon, but not rare. Only 7.3% of respondents reported using cannabis in the preceding year, and 2.0% reported using it as often as once per week. However, nearly a third (29%) reported that they had used cannabis at least once in their lives. Substantial regional differences were observed, with the proportion reporting use at least once in the past year ranging from a low of 4.9% in Ontario to a high of 11.4% in British Columbia.

While these data provide a valuable perspective on the use of cannabis across Canada, unfortunately there is little information on other important issues, such as change in rates of use over time. However, in Ontario a series of surveys has been conducted over the past 20 years that allow a picture of current use and changes in use over time in that part of the country.

The Use of Cannabis in Ontario

Repeated cross-sectional surveys conducted in Ontario by the Centre for Addiction and Mental Health provide the most comprehensive picture of the use of cannabis and other drugs use in Canada. These surveys have been conducted among the student population and adult population since the late 1970s.

A summary of recent data on the use of cannabis and other drugs (any use in the past year) among students in grades 7 and 126, and among adults aged 18-29 (young adults), 40-49 (the middle-aged) and 65 and over (seniors) showed cannabis is the most widely used illicit substance. Nearly half of grade 12 students reporting cannabis use at least once in the past year. It is worth noting that by grade 12 most students will have reached the age when they will be eligible to drive. Use of cannabis drops with increasing age, however, and is used by less than 2% of seniors. Use of other illicit drugs is much less common than the use of cannabis, with highest levels occurring for Hallucinogens and Ecstasy among grade 12 students. Not surprisingly, alcohol is the most commonly used substance.

Trends in Cannabis Use Over Time

information is presented on the proportion of students in Grades 7, 9, 11 and 13 who report using cannabis and alcohol between 1977 and 20016. While cannabis is used by a smaller proportion of students than alcohol; it is still used by a substantial minority of students. There have been important changes in the use of cannabis over time. The general trend appears to have been one of reduced use of cannabis and alcohol from the late 1970′s to the early 1990′s. The proportion reporting use of cannabis declined from a peak of 31.7% in 1979 to 11.7% in 1991. However, since the mid-1990’s self-reported use of both substances has increased, with 28.6% reporting cannabis use in 2001. Data is presented since 1977 on the proportion of the adult population (age 18 and above) who report using cannabis, drinking alcohol, or using cocaine at least once in the preceding 12 months. Cannabis use has continued among a much smaller proportion of the adult population than among students. Alcohol is used by the large majority of the adult population, while the use of cocaine is reported by only a very small percentage. The trends among adults are not as clear as those among the student population. For example, the proportion reporting use of alcohol has been relatively consistent, with perhaps a slight increase to the early 1990s followed by a slight decrease. Among users of cannabis and cocaine, enduring trends over time cannot be ascertained.

Prevalence of Cannabis Use and Driving in Canada: Estimates from Survey Data

Survey data on the prevalence of driving under the influence of cannabis are available. In the first reported data from the general population in Canada, Jonah reported on the prevalence of driving after use of cannabis at least once in the preceding 12 months. The survey included 9943 persons aged 16-69, obtained through random digit dialing. Jonah found that the prevalence of DUIC varied with age. While the prevalence of DUIC was relatively low, it was higher in younger age groups. Jonah also observed that DUIC was significantly associated with a variety of other risk behaviours, such as driving after drinking, use of illicit drugs other than cannabis, and collision involvement.

Conclusions

The data presented here indicate that cannabis use is relatively common in Canada, particularly among young people. The prevalence of use appears to have increased substantially in the 1960s and ‘70s, while since then some fluctuations have occurred. Driving after cannabis use is less common, but among cannabis users it does appear to occur with some frequency. In particular, young cannabis users appear more likely to report DUIC. Among high school students, DUIC appears to occur as frequently, or more frequently, than driving after drinking. These data provide grounds for concern about this behaviour, particularly among younger drivers. Further research on the prevalence of DUIC in Canada, including differences between provinces, is needed.

Frequently Asked Questions About Pot & Driving

On November 21, 2005, the Canadian Public Health Association, with funding from Canada’s Drug Strategy, Health Canada, launched a Pot and Driving campaign (http://potanddriving.cpha.ca) to raise awareness among young Canadian drivers and passengers of the risks of cannabis-impaired driving. Campaign materials include:

• A poster of airplane pilots smoking up with the campaign message, “If it doesn’t make sense here, why does it make sense when you drive?”

• 10 Questions (to provoke thought and dialogue)

• The thinking behind the questions (to encourage discussion)

• This FAQ (to inform the discussion).  This FAQ provides information on a range of issues related to cannabis use in the context of driving. It draws on up-to-date, relevant studies and surveys, insights given by key informants from Canada and several other countries, and the opinions of young Canadians who took part in focus groups held in several locations across the country.

Recent research on pot is showing that it can play an important role in road vehicle crashes, especially when combined with driver inexperience and difficult road conditions. Road accidents are often the result of a combination of factors and pot can be one of them.

The data presented by Parker et al. (1995) and Graham and Bowling (1995) indicate that, for young people, having used a drug is a far from unusual experience. By the time that the majority of Parker et al (1995) respondents were 15, 42% of them indicated that they had, at some point in their lives, used at least one illicit drug. This increased to 51% by the time they were 16. Turning to the national position, over a third (36%) of the ISRD respondents (all of whom were aged 14—21) reported ever having used a drug (Graham and Bowling 1995).

Given that proponents of the normalisation thesis have tended to concentrate on measures of lifetime use (whether a respondent has used an illicit drug at some time in their life) it is worth noting that the extent to which such measures illuminate young people’s drug using habits is limited. Arguments based on such measurements should be interpreted extremely cautiously. The inflexibility of lifetime measures means that they cannot capture the processual character of people’s drug-use (Becker 1963). As a consequence, not only are they unable to distinguish one-off use from regular polydrug use but they also fail to distinguish between current and ex-users. Given these problems it is reasonable to suggest that measures based on shorter time-frames — such as the previous year or month — are likely to provide somewhat more reliable estimates of the extent of current or regular use. Parker et al. (1995) included questions about drug use during the year and the month prior to each of their surveys, and the ISRD asked respondents about their drug use during the previous year (1992).

Inevitably, data concerning drug-related behaviour during the last year/month give a more conservative picture than those based on lifetime measures. As Figure 1 shows, in Parker et al’s second and third surveys, when the majority of the respondents were aged 15 and 16 respectively, drug use during the previous year was limited to approximately two fifths of the sample. During the month preceding the respective surveys, it was limited to about a quarter of them. Following their third survey, Parker et al. (1995:19) estimated that 20 per cent of respondents (approximately three quarters of past month users) were ‘regular users’.
We have already mentioned the fact that Parker and colleagues recognise that their research is unlikely to be typical of the national picture. The situation relating to the nation as a whole is outlined in Figure 2. According to the ISRD slightly less than a third of males and less than a quarter of females aged 14—21 used drugs in 1992 and could, therefore, be thought of as ‘current’ users (Graham and Bowling 1995). While respondents aged 18—21 were, by some way, the most likely to have used a drug in 1992, less than half of the males and less than a quarter of the females in this age category had done so.

As indicated earlier, it is the work of Howard Parker and colleagues (Parker et al. 1995; Measham et al. 1994) that has been most influential in this area. Beginning in 1991 their major study to date involved three surveys conducted annually which recorded the drug-related experiences of a group of 776 young people who were first contacted during the penultimate year of their compulsory education when most were 14 years old. These surveys were administered in the metropolitan North-West of England, an area which includes Manchester, the ‘rave capital of Great Britain’ (Coffield and Gofton 1994:5), and the researchers have acknowledged the dangers of extrapolating from their data to the national situation. Referring to the area’s higher than average levels of smoking, drinking and heroin use, they note that ‘we must therefore anticipate that young people from this region are likely to report higher levels of illicit drug use during the l990s than their peers elsewhere’ (Parker et al. 1995:21). Although the location of their research is therefore in this sense ‘unusual’, this is not the basis of our criticism of the conclusions they draw.

In order to reflect upon the national situation we have drawn, in some detail, upon the domestic element of the International Self—Report Delinquency Study (ISRD) which, focusing on the 14-21
age range, is the most recent survey of a representative sample of the nation’s youth to consider drug use (Howling et al. 1994;Graham and Bowling 1995). We will also consider, albeit more briefly, the evidence from the 1994 British Crime Survey, although it should be noted that this focuses on people aged 16 and above and is not a specialist youth survey (Ramsey and Percy 1996). Although Parker et al. (1995) survey, the ISRD and British Crime Survey vary in the details of their administration, they are similar in that the drugs components of these surveys are all based on a self-completion approach in which respondents are provided with a list of drugs or illicit substances and asked about their knowledge and use of them.

Although more illuminating than measures of lifetime use, those which focus on behaviour during the last year or month are of limited use if they fail to distinguish between different types of drug. Measures which aggregate a variety of different drugs simplify the decisions that young people make and fail to acknowledge the discerning approach many young people take towards drug use. That young people distinguish between different drugs is clearly reflected in their patterns of use. Both Parker et al. (1995) and the ISRD found that levels of use varied greatly by type of drug. Thus, reflecting its position as ‘undoubtedly the most widely used drug in the UK’ (ISDD 1994:28), cannabis had been used by 45 per cent of respondents to Parker et al’s (1995) third survey, when the majority of them were aged 16, and 33 per cent of ISRD respondents. At the other end of the popularity spectrum are heroin and cocaine. Lifetime use of cocaine was limited to 4 and 3 per cent of Parker et al’s (1995) respondents when they were aged 15 and 16 respectively, and 2 per cent of ISRD respondents. Heroin use was even more unusual: 3 and 1 per cent respectively of Parker et al’s respondents disclosed lifetime heroin use as did 1 per cent of ISRD respondents.The rise of the dance/rave scene (Redhead 1993) and its associated drug use has a special position within the normalisation thesis (Coffield and Gofton 1994; Measham et al. 1993). The late 1980s and early 1990s did witness an apparently significant increase in the use of ‘dance drugs’, which became a relatively important part of the youth drug scene (Measham 1993; Clements 1993). In the case of ecstasy and LSD, however, this increase started from a very low baseline (Clements 1993) and the popularity of these drugs can easily be overstated.
Even though LSD was the most popular dance drug among Parker et al’s (1995) respondents when they were aged 15 and 16 (and the second most widely used drug by them) it had only ever been used by approximately a quarter of them. In view of ecstasy’s high media profile it is worth noting that only one in twenty respondents to Parker a al’s (1995) third survey, when the majority of them were aged 16, had used this drug. Nationally, use of dance-drugs appears to be limited to a small sub-section of the youthful population.

Source: Michael Shiner and Tim Newburn
pub. ‘Sociology’ Vol.31 No. 3. Aug 97

Figure 2 – Drug use by young people in England and Wales during 1992 (percentage use) Source: Graham & Howling (1995:26)

By Maxie Richards, Glasgow, Scotland
Director, Maxie Richards Foundation
www.maxirichards.org

Two-and-a-half-year-old, weakened by starvation, cold, deprivation, and physical abuse, paid the scapegoat price for
this careless society and gave up the fight to live. Scott was a victim of malignant neglect, not just by his drug-crazed parents, but
by the society into which he was born, where neglect, in various forms, has become commonplace. A parent’s’ right to choose, at any
cost, a pleasure-seeking lifestyle, rules, while laws change to allow drug-taking on an unprecedented scale. The silent sufferers are the children.

The long-term effect becomes all too clear, as children, unable to cope with the chaos in their lives, become aggressive and disruptive, serving an
apprenticeship for addiction. This Government’s answer is so-called “harm reduction.” This evil drug policy has been in place for 30 years or so. Its cornerstone is free choice for individuals to take drugs, and it promotes “safe use” – whatever that means. It focuses on the individual, never the family, the dependants, or the community. This policy promotes the lie that drugs are here to stay, and there is nothing we can do about it except “reduce harm.” Addicts are enabled to take drugs and are given, at the taxpayers’ expense, all necessary means.

“Harm reduction” adherents are fanatical about protecting this system,even though it has been responsible for the drug crisis in society. We have
built a gigantic business on the backs of drug addicts (called ‘clients’), and people grow fat on the proceeds. The tax-paying public remains in denial. Perhaps people believe this couldn’t be happening. It is. Parents of addicted children, exploited by the system, live the nightmare daily. The society we are creating through malignant neglect is not one we will want to live in. Scott Saunders is not the first to endure a living hell and prolonged death. Unless we act, the rot won’t stop.

Forty years ago, the Scandinavian countries looked at “harm reduction.” Their findings led them to scrap any notion of adopting such a policy.
Every government agency had to adopt a drug-free stance and promote drug prevention. It was made abundantly clear that drug addiction was not an acceptable way of living. Sweden set up European Cities Against Drugs, developing strategies for a safe, drug-free society, and proving that it can be done.

In Rutherglen, an outwardly respectable neighbourhood of Glasgow, Scott Saunders was subjected to appalling abuse and neglect. One hundred fifty wounds were found on his body; he had been systematically deprived of food, and his eventual death from starvation came after he had been left alone in the house for three days.

We must be brave enough to face up to our failures and to the treason yes, treason – which is undermining our way of life, canceling our workforce,and damaging, often terminally, our young people, while imperceptibly luring us into accepting the unacceptable. Don’t believe the lies, the platitudes,the excuses, the cover-up of so-called “harm reduction” drug policies. We are all responsible for the death of Scott through negligence.

Back to Papers

In Brief

• In 2004, an estimated 14% of youths aged 12 to 17, approximately 3.5 million youths, had experienced at least one major depressive episode (MDE) in their lifetime

• Over 7%, an estimated 1.8 million youths, had lifetime MDE and thought about killing themselves at the time of their worst or most recent episode

• An estimated 712,000 youths had tried to kill themselves during their worst or most recent MDE; this represents 2.9% of those aged 12 to 17

In 2003, suicide was the 11th leading cause of death among persons of all ages in the United States. However, among young people aged 15 to 24, suicide, or intentional self-harm, was the third leading cause of death, with 3,921 deaths, following accidents/unintentional injuries (14,966 deaths) and assaults/homicides (5,148 deaths).

The 2004 National Survey on Drug Use and Health (NSDUH) asked youths aged 12 to 17 about symptoms of depression, including thoughts about death or suicide. Major Depressive Episode (MDE) is defined as a period of at least 2 weeks when a person experienced a depressed mood or loss of interest or pleasure in daily activities and had at least five of the nine symptoms of depression as described in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).

The suicide-related questions asked youths if (during their worst or most recent episode of depression) they thought it would be better if they were dead, thought about killing themselves, and, if they had thought about killing themselves, whether they made a plan to kill themselves and whether they tried to kill themselves. This report presents estimates of the prevalence of lifetime MDE among youths. The report also presents the numbers and percentages of youths who had both lifetime MDE and suicidal thoughts.

Prevalence of MDE

An estimated 14% of youths aged 12 to 17, approximately 3.5 million youths, had experienced at least one MDE in their lifetime (Table 1). Almost 20% of females aged 12 to 17 and 8.5% of males had at least one of these depressive episodes. Rates of lifetime MDE were similar among racial/ethnic groups and increased with age.

MDE and Suicidal Thoughts

Among youths aged 12 to 17, about 9%, an estimated 2.3 million youths, had experienced MDE in their lifetime and thought, during their worst or most recent MDE, that it would be better if they were dead. Over 7%, an estimated 1.8 million youths, thought about killing themselves at the time of their worst or most recent MDE.

Females aged 12 to 17 were significantly more likely than their male peers to have had MDE and to report thinking about suicide and believing it would be better if they were dead (Figure 1).

Both 14 or 15 year olds and 16 or 17 year olds were significantly more likely than those aged 12 or 13 to have had MDE accompanied by thoughts that it would be better if they were dead and thoughts about committing suicide (Figure 2).

MDE with suicidal thoughts did not vary by urbanicity.4 Youths in large metropolitan areas, small metropolitan areas, and non-metropolitan areas were equally likely to have MDE with suicidal thoughts.

MDE and Suicide Attempts

An estimated 900,000 youths, or 3.6% of 12 to 17 year olds, made a plan to kill themselves at the time they were having their worst or most recent MDE. An estimated 712,000 youths had tried to kill themselves during such an episode; this represents 2.9% of those aged 12 to 17.

Female youths were more likely than male youths to have had MDE and made a plan to kill themselves (5.6% of females and 1.7% of males) or to have attempted suicide (4.7% of females and 1.1% of males).