The CDC announced the 2009 National Youth Risk Behavior Survey (YRBS) found that 1 in 5 high school students have ever taken a prescription drug such as OxyContin (oxycodone, from Purdue), Percocet (oxycodone/acetaminophen, from Endo), Vicodin (hydrocodone/acetaminophen, from Abbott), Adderall (mixed salts of a single-entity amphetamine product, from Shire), Ritalin (methylphenidate, from Novartis), or Xanax (alprazolam, from Pfizer), without a prescription. Data from the Drug Abuse Warning Network show that in 2008, people 12–20 years of age accounted for an estimated 141,417 (14.5%) of the 971,914 emergency department visits for nonmedical use of pharmaceuticals, not including suicide attempts.

Source: http://www.empr.com June 2010

Montana and other states that have legalized medical marijuana are seeing a backlash, with public anger rising and politicians passing laws to slow the proliferation of pot shops and bring order to what has become a wide-open, Wild West sort of industry.
They are looking to avoid what happened in California, which allowed the pot industry to grow so out of control that at one point Los Angeles had more medical marijuana shops than Starbucks – about 1,000 by one count.
“Yeah, it’s out of control – and it needs control, if not extinction,” Montana Sen. Jim Shockley said Friday. “There’s no control over distribution. There’s no control over who’s growing it. There’s no control in dosage.”
Fourteen states have legalized medical marijuana, beginning with California in 1996, and the District of Columbia followed suit this month. The laws allow chronically ill people to buy marijuana with permission from a doctor.
But many of these states passed their laws without working out the details. And they weren’t ready for the boom in pot shops that occurred this past year after the Obama administration announced it wouldn’t prosecute medical marijuana users.
In some places, law enforcement officials and civic leaders are complaining that there are too many marijuana dispensaries, that buyers and sellers are falling victim to robberies and break-ins, that driving-under-the-influence arrests are on the rise, and that the pot is being sold indiscriminately and winding up on the black market.
Some state and local governments are now rushing to put regulations in place.
Colorado lawmakers passed sweeping rules this month for pot growers and the estimated 1,100 shops selling marijuana, creating a new state bureaucracy led by auditors and criminal investigators who would monitor the industry to make sure, for example, that the drug is being sold only to patients who have a doctor’s recommendation.
Regulators expect only about half of the state’s dispensaries to continue operating under the stricter rules.
The Billings City Council approved a six-month moratorium on new medical marijuana businesses in May after the violence against pot businesses the previous two nights. On Thursday, the city of about 90,000 people ordered 25 of Billings’ 81 pot businesses to shut down after discovering they were not properly registered with the state.

Los Angeles officials recently took steps to shut down hundreds of dispensaries and ensure that the remaining ones meet stringent new guidelines. Owners must undergo a background check, their stores must be 1,000 feet from schools, parks and other gathering sites, and their pot must be tested at an independent laboratory.
Montana’s medical board is considering curbing mass screenings and teleconferences that make it easy for people to get a marijuana card. Montana in recent days has seen “cannabis caravans,” mobile operations that pass through town, charging people $100 to $150 for a doctor’s recommendation to smoke pot.
The push for tighter regulation has infuriated medical marijuana users.
“They are creating ordinances and moratoriums that are blatantly against the law,” said Jason Christ, founder of the Montana Caregivers Network, the group that organizes the cannabis caravans. “They do not serve to protect the welfare of our citizens, and they do no good.”
In Colorado earlier this month, veterans in wheelchairs, college students and dispensary owners packed legislative hearings to speak out against the regulations. The hearings lasted eight hours and reached a fever pitch when several people had to be removed for shouting at lawmakers.
Medical marijuana has been around for more than five years in Montana, but the boom came this past year. The number of registered users in Montana, a state with a population of just under 1 million, has gone from 2,923 last June to about 15,000 today. The number of registered suppliers has increased from 919 to about 5,000.
DUI arrests involving marijuana have skyrocketed, as have traffic fatalities where marijuana was found in the system of one of the drivers, Montana narcotics chief Mark Long told a legislative committee last month.
Also, Montana confidentiality laws prevent law enforcement from knowing where most medical marijuana businesses are, and civic leaders complain they don’t know whether the shops are up to city and fire codes or close to churches, schools or parks.
During Colorado’s legislative debate, state Sen. Chris Romer quoted the Grateful Dead as he contemplated the spectacle of lawmakers actually passing regulations for the legal sale of marijuana: “What a long, strange trip it’s been.”

Source: The Associated Press Friday, May 21, 2010

Opiate addiction-treatment admissions have risen from 16 percent to 20 percent of all admissions in the last decade, and marijuana admissions have also ticked upwards even as cocaine admissions declined, according to a new report from the Substance Abuse and Mental Health Services Administration (SAMHSA).
Marijuana admissions rose from 13 percent of total admissions in 1998 to 17 percent in 2008, while cocaine admissions fell from 15 percent to 11 percent. Admissions for addiction to stimulant drugs rose from 4 percent to 6 percent.
“Although the concurrent abuse of both alcohol and drugs has remained widespread, the proportion of treatment admissions for the co-abuse of these substances has declined gradually yet significantly during this period from 44 percent to 38 percent,” added SAMHSA. “At the same time there has been a steady rise in the proportion of treatment admissions attributed to drug abuse alone from 26 percent in 1998 to 37 percent in 2008, while the proportion of admissions attributed to alcohol alone fell from 27 percent in 1998 to 23 percent in 2008.”
Teen drug admissions dropped 10 percent between 2002 and 2008 after rising 13 percent from 1998 to 2001. Nearly 4 of 5 teen treatment admissions involved marijuana use, and about half were referrals from the criminal-justice system.
The National Admissions to Substance Abuse Treatment (TEDS) report is available online in PDF format.

Source: SAMHSA Report May 2010

Adolescent use of marijuana has become almost as acceptable as staying out a little past curfew. Most agree the latter shouldn’t happen, but it’s understandable and — as long as things don’t get worse — easy to address with a clock and threat of grounding. No big deal. Not so with marijuana. If your child is smoking pot and it starts to get worse you won’t know when or why until you have a child for whom a grounding is a mere impediment to a dangerous new lifestyle. And more importantly you will have missed critical opportunities to help your child address his problems in a healthy, positive way.

I see a lot of adolescents in my practice, many of whom arrive after a lengthy relationship with pot… But my first contact is usually with the anxious parents. “Something is going on,” they say. “His grades are going down; She’s spends all her time in her room; He’s moody and uncommunicative; she’s lost interest in her flute. ” “He’s different,” they say. “She’s like a stranger.”How long has this been going on I ask? Around six months says mom. Closer to a year says dad.

I ask a few questions — a sort of psychological triage looking for any recent changes or traumas that might offer a clue.Then I put it out there. “Do you think your child is involved with drugs?” Here is the answer I almost always receive. “No. I don’t think so. Maybe just a little marijuana.” So, let’s stop here. I want to say this loud and clear. The correct answer to my questions is a simple “YES.”

I realize there is a battle afoot to legalize the stuff. I understand that most parents when asked if their child smokes marijuana will usually respond in a tone rife with defeatism, “Of course. They all do.” I get it. There is comfort in numbers. But unfortunately this beleaguered answer tends to end a conversation instead of inspire a look at the heart of the matter. “Why does my child choose to do drugs?”

Certainly I know there are some teens who dabble with marijuana every so often at a party. Maybe she wants to fit in. Maybe the munchies and some frenzied laughter feel like a fun release. But this same adolescent stays on top of her grades, enjoys long term friendships and converses typically peevishly with her parents on a regular basis. I don’t meet these kids or their parents in my office. Obviously not every child who smokes marijuana is going to dance around the drain.

But from what I can see, more and more kids are doing just that . At this point you might be thinking, ” When I was young I smoked all the time. I was fine!.” Well, the truth is marijuana is more powerful now, 20 to 30 times according to some estimates, and is more often laced with other drugs. The information age has also made it far easier to get it when you want it. All of this makes a big difference.

I recently attended a lecture at a private Residential Treatment Center for adolescent drug addicts, at which the director made a point of saying there wasn’t a child there who hadn’t convinced their parents or themselves that a little marijuana was okay.

Adolescents are walking into my office in increasing numbers having grown alienated, unproductive and increasingly self-destructive. They are standing on a long road of marijuana use. These are unhappy kids and whether they are smoking a little on occasional weekends, every weekend, everyday or are already into heavier stuff, they need emotional help.

The sooner they get it the better. Which is why it is critical that every parent recognize that their pot smoking teenager, who may be doing what everyone else is doing, IS STILL DOING A DRUG and that it is a form of self-medication. This is no time to seek comfort in numbers. It’s a time NOT TO PANIC, but to pay attention.

Marijuana helps kids hide from the painful and negative feelings with which so many teens struggle. By minimizing pot, parents may be neglecting to look around for the REASON their particular teen is needing to stifle his or her feelings. They are looking away from their child’s emotional health which may in fact be far more fragile than it seems. Most kids don’t connect hating life with identifiable painful feelings. They just think life stinks and drugs offer a vacation.. So how do you help open their eyes?

If you ask your child if she is depressed or anxious she will likely say “no.” This is because she doesn’t really know what the words mean and anyway believes she’s found a way to stop feeling “bad.” Ask anyway. It’s an opportunity to teach emotional vocabulary. For example, “You’ve been so quiet lately. Not laughing much and you’re not hanging out with your friends. You seem depressed, kind of sad to me.” Your teen will most certainly say you’re wrong, but that’s okay. Her education has begun.

As for how to ask your teen about drug use it’s really quite counterintuitive. Don’t ask when he is bleary eyed, or comes home laughing hysterically, or if you walk in his room and find yourself in a haze of AXE. Wait for a quiet moment when you’re child is not going to be highly defensive, or out of it and express the question with concern as opposed to accusation.

Point out what you noticed the other night, say you’re worried about drugs including marijuana, and then center on your concern for how she is FEELING. If she closes down just smile and invite her to talk when she’s ready. If she snaps that everyone smokes a little marijuana try, “I understand the way it is out there but it doesn’t make it right or healthy.” Then let it alone. Return to the subject when there are more clues or you can sense there’s an opening. The point is not to let her waste energy being angry at you. She needs that energy to just think.

When it comes to their well-being teens rarely do that. Which is why you have to. Marijuana is a drug. For many kids it will become addictive. It could become the first step to the use of other drugs. Drugs that could ruin and even end lives.

So watch your child. If there’s a problem you’ll see it…because too many times just a little marijuana, despite what you are being told, is simply not okay. And remember, “just a little” is dangerously subjective.

Source: www.megfschneiderlcsw.com August 19, 2010

Legalise drugs and a worldwide epidemic of addiction will follow
Those who argue we should decriminalise the trade in narcotics are blind to the catastrophic consequences
The debate between those who dream of a world free of drugs and those who hope for a world of free drugs has been raging for years. I believe the dispute between prohibition and legalisation would be more fruitful if it focused on the appropriate degree of regulation for addictive substances (drugs, but also alcohol and tobacco) and how to attain such regulation.
Current international agreements are hard to change. All nations, with no exception, agree that illicit drugs are a threat to health and that their production, trade and use should be regulated. In fact, adherence to the UN’s drug conventions is virtually universal and no statutory changes are possible unless the majority of states agree – quite unlikely, in the foreseeable future. Yet important improvements to today’s system are needed and achievable, especially in areas where current controls have produced serious collateral damage.
Why such resistance to abolishing the controls? In part, because the conventions’ success in restraining both supply and demand of drugs is undeniable.
Look first at production. Drug controls slashed global opium supply dramatically: in 2007, it was one-third the level of 1907. What about recent trends? Over the last 10 years, world output of cocaine, amphetamines and ecstasy has stabilised, and in many instances dropped. Cannabis output has declined since 2004. Since the mid-90s, opium production moved from the Golden Triangle to Afghanistan where it grew exponentially at first, but started to decline (since 2008).
My first point is factual: in the distant past as well as recently, production controls have had measurable results. What about drug-use levels? There are 25 million addicts (daily use) in the world, 0.6% of the population. Ten times as many people (5% of the world’s population) take drugs at least once a year. As these amounts are relatively small, statements such as “there are drugs everywhere” or “everybody takes drugs” are nonsense. The drug numbers compare well with those of tobacco, a legal drug used by 30% of the world’s population. Even more people consume alcohol. Tobacco causes 5 million deaths per year and alcohol 2 million, against the 200,000 killed by illicit drugs.
My second point is logical: in the absence of controls, it is not fanciful to imagine drug addiction, and related deaths, as high as those of tobacco and alcohol. What are recent drug-use trends? In rich countries, addiction is high but declining. In North America and Australia, it has declined in the past 10 years, especially among the young. In Europe, opiates use has declined, offset by greater cocaine sales; cannabis and amphetamines are stable or lower. In developing countries, drug use is low, but growing. In South America and west Africa, this applies to cannabis and cocaine; in Asia and southern Africa to heroin.
My third point is intuitive: rich countries are addressing the drug problem, while poor countries lack resources to do so. With the building blocks of my reasoning in place (stability of the world drug supply; alcohol and tobacco hurt more than drugs; the divergent drug trends in poor and rich nations), I find it irrational to propose policies that would increase the public health damage caused by drugs by making them more freely available.
At the same time, drug controls are not working as they should. The resulting collateral damage is the platform upon which critics build the abolitionist argument.
Let’s look at health, security and human rights. Health must be at the centre of drug control, because drug addiction is a mix of genetic, personal and social factors: gene variants (predisposition), childhood (neglect), social conditions (poverty). The pharmacological effects of drugs on health are independent of their legal status. Drugs are not dangerous because they are illegal: they are illegal because they are dangerous to health. Unfortunately, ideology has displaced health from the mainstream of the drug debate and this has happened on both sides of the prohibition versus legalisation dispute.
In the past half-century, drug control rhetoric by governments has been right, but prevention and treatment programmes have lagged. Priority was wrongly given to repression and criminalisation. Similarly, those in favour of legalisation have lost sight of health as the priority. They prioritise handing out condoms and clean needles, while addicts need prevention, treatment and reintegration, not only harm reduction gadgets. In short, the debate on drug policy has turned into a political battle. But why? There are no ideological debates about curing cancer, so why so much politics in dealing with drug addiction?
But there is more. Drugs do harm to health, but they can also do good. Greater use of opiates for palliative care would overcome the socio-economic factors that deny a Nigerian suffering from Aids or a Mexican cancer patient the morphine offered to Italian or American counterparts. Yet such relief is not happening.
Next is the security question. Drugs pose a threat not only to individuals. Entire regions – think of Central America, the Caribbean and Africa – are caught in the crossfire of drug trafficking. In Mexico, a bloody drug war has erupted among crime groups fighting for the control of the US drug market. The legalisers’ argument on security is striking, though it leads to the wrong conclusion. Prohibition causes crime by creating a black market for drugs, the argument goes, so, legalise drugs to defeat organised crime. As an economist, I agree. But this is not only an economic argument. Legalisation would reduce crime profits, but it would also increase the damage to health, as drug availability leads to drug abuse.
Drug policy does not have to choose between either protecting health, through drug control, or ensuring law and order, by liberalising drugs. Society must protect both health and safety.
In a world of free drugs, the privileged rich can afford expensive treatment while poor people are condemned to a life of dependence. Now extrapolate the problem on to a global scale and imagine the impact of unregulated drug use in developing countries, with no prevention or treatment available. Legalised drugs would unleash an epidemic of addiction in the developing world.
Last but not least, there’s the question of human rights. Around the world, millions of people caught taking drugs are sent to jail. In some countries, drug treatment amounts to the equivalent of torture. People are sentenced to death for drug-related offences. Although drugs kill, governments should not kill because of them. The prohibition versus legalisation debate must stop being ideological and look for the appropriate degree of controls. Drug control is not the task of governments alone: it is a society-wide responsibility. Are we ready to engage?

Source: Antonio Maria Costa www.observer.guardian.co.uk 5th Sept 2010

Contrary to the beliefs of those who advocate the legalization of marijuana, the current balanced, restrictive, and bipartisan drug policies of the United States are working reasonably well and they have contributed to reductions in the rate of marijuana use in our nation.

The rate of current, past 30-day use of marijuana by Americans aged 12 and older in 1979 was 13.2 percent. In 2008 that figure stood at 6.1 percent. This 54-percent reduction in marijuana use over that 29-year period is a major public health triumph, not a failure.

Marijuana is the most commonly abused illegal drug in the U.S. and around the world. Those who support its legalization, for medical or for general use, fail to recognize that the greatest costs of marijuana are not related to its prohibition; they are the costs resulting from marijuana use itself.

There is a common misconception that the principle costs of marijuana use are those related to the criminal justice system. This is a false premise. Caulkins & Sevigny (2005) found that the percentage of people in prison for marijuana use is less than one half of one percent (0.1-0.2 percent). An encounter with the criminal justice system through apprehension for a drugrelated crime frequently can benefit the offender because the criminal justice system is often a path to treatment.

“A useful analogy can be made to gambling. Legalized gambling has not reduced illegal gambling in the United States; rather, it has increased it.”

More than a third, 37 percent, of treatment admissions reported in the Treatment Episode Data Set, TEDS, collected from state-funded programs were referred through the criminal justice system. Marijuana was an identified drug of abuse for 57 percent of the individuals referred to treatment from the criminal justice system.

The future of drug policy is not a choice between using the criminal justice system or treatment. The more appropriate goal is to get these two systems to work together more effectively to improve both public safety and public health. In the discussion of legalizing marijuana, a useful analogy can be made to gambling. MacCoun & Reuter (2001) conclude that making the government a beneficiary of legal gambling has encouraged the government to promote gambling, overlooking it as a problem behavior. They point out that “the moral debasement of
state government is a phenomenon that only a few academics and preachers bemoan.”
Legalized gambling has not reduced illegal gambling in the United States; rather, it has increased it. This is particularly evident in sports gambling, most of which is illegal. Legal gambling is taxed and regulated and illegal gambling is not. Legal gambling sets the stage for illegal gambling just the way legal marijuana would set the stage for illegal marijuana trafficking.
The gambling precedent suggests strongly that illegal drug suppliers would thrive by selling more potent marijuana products outside of the legal channels that would be taxed and otherwise restricted. If marijuana were legalized, the only way to eliminate its illegal trade, which is modest in comparison to that of cocaine, would be to sell marijuana untaxed and unregulated to any willing buyer.

Marijuana is currently the leading cause of substance dependence other than alcohol in the U.S. In 2008, marijuana use accounted for 4.2 million of the 7 million people aged 12 or older classified with dependence on or abuse of an illicit drug. This means that about two thirds of Americans suffering from any substance use disorder are suffering from marijuana abuse or marijuana dependence.

If the U.S. were to legalize marijuana, the number of marijuana users would increase. Today there are 15.2 million current marijuana users in comparison to 129 million alcohol users and 70.9 million tobacco users. Though the number of marijuana users might not quickly climb to the current numbers for alcohol and tobacco, if marijuana was legalized, the increase in users would be both large and rapid with subsequent increases in addiction.

Important lessons can be learned from those two widely-used legal drugs. While both alcohol and tobacco are taxed and regulated, the tax benefits to the public are vastly overshadowed by the adverse consequences of their use. Alcohol-related costs total over $185 billion while federal and states collected an estimated $14.5 billion in tax revenue; similarly, tobacco use costs over $200 billion but only $25 billion is collected in taxes. These figures show that the costs of legal alcohol are more than 12 times the total tax revenue collected, and that the costs of legal tobacco are about 8 times the tax revenue collected. This is an economically disastrous tradeoff.

The costs of legalizing marijuana would not only be financial. New marijuana users would not be limited to adults if marijuana were legalized, just as regulations on alcohol and tobacco do not prevent use by youth. Rapidly accumulating new research shows that marijuana use is associated with increases in a range of serious mental and physical problems. Lack of public understanding on this relationship is undermining prevention efforts and adversely affecting the nation’s youth and their families.

Drug-impaired driving will also increase if marijuana is legalized. Marijuana is already a significant causal factor in highway crashes, injuries and deaths. In a recent national roadside survey of weekend nighttime drivers, 8.6 percent tested positive for marijuana or its metabolites, nearly four times the percentage of drivers with a blood alcohol concentration (BAC) of .08 g/dL (2.2 percent). In another study of seriously injured drivers admitted to a Level-1 shock trauma
center, more than a quarter of all drivers (26.9 percent) tested positive for marijuana. In a study of fatally injured drivers in Washington State, 12.7 percent tested positive for marijuana. These studies demonstrate the high prevalence of drugged driving as a result of marijuana use.
Many people who want to legalize marijuana are passionate about their perception of the alleged failures of policies aimed at reducing marijuana use but those legalization proponents seldom—if ever—describe their own plan for taxing and regulating marijuana as a legal drug. There is a reason for this imbalance; they cannot come up with a credible plan for legalization that could deliver on their exaggerated claims for this new policy.

“Reducing marijuana use is essential to improving the nation’s health, education, and productivity.”

Future drug policies must be smarter and more effective in curbing the demand for illegal drugs including marijuana. Smarter-drug prevention policies should start by reducing illegal drug use among the 5 million criminal offenders who are on parole and probation in the U.S. They are among the nation’s heaviest and most problem generating illegal drug users.

Monitoring programs that are linked to swift and certain, but not severe,
consequences for any drug use have demonstrated outstanding results including lower recidivism and lower rates of incarceration. New policies to curb drugged driving will not only make our roads and highways safer and provide an important new path to treatment, but they will also reduce illegal drug use.

Reducing marijuana use is essential to improving the nation’s health, education, and productivity. New policies can greatly improve current performance of prevention strategies which, far from failing, has protected millions of people from the many adverse effects of marijuana use.
Since legalization of marijuana for medical or general use would increase marijuana use rather than reduce it and would lead to increased rates of addiction to marijuana among youth and adults, legalizing marijuana is not a smart public health or public safety strategy for any state or for our nation.

Source: Published: Tuesday, 20 Apr 2010 Robert du Pont,Institute for Behavior and Health

For the past six months, I have attended the public forums and workshops on poverty and early childhood education in Erie and America. It is agreed that many factors cause poverty, but I will focus on issues with which I have professional experience and knowledge.

I am a registered pharmacist, and during my 35-plus years as Director of Pharmacy Services, both in government and the private industry, I have taught thousands of individuals about drug, alcohol and health issues. To increase and support early educational endeavors for our children, we must first address the abuse of drugs, both legal and illegal, and alcohol.

I was the first pharmacist on the East Coast to start the “Methadone Program” with Dr. B. Kissin in Brooklyn in the early 1970s, dispensing methadone and counseling addicts on the dangers of heroin and other drugs that could kill them or their unborn child.

I have collaborated, assisted and cooperated with local police departments, the U.S. Drug Enforcement Agency and school programs such as Drug Abuse Resistance Education (D.A.R.E.). I have also been a community instructor on medication management.

At the May 27 Economic Summit on Early Childhood Education, Dr. Judy Cameron, a University of Pittsburgh neuroscientist, gave a presentation on “The Science of Early Brain Architecture and the Future of Early Childhood Policy.” Yet there was no discussion relative to the environmental factors in a household. How many children are exposed to secondary/passive illegal and legal smoke? When a mother inhales illegal substances (marijuana and crack cocaine), the effect on the developing fetus is magnified two- to 10-fold.

Our counseling program in Brooklyn had an average success rate of 30 percent with females (some pregnant, some not) who asked me questions that I answered in plain truth: “If you keep this up, you are going to die early or you are going to lose your baby. Period.”

Those in the methadone program who did not pass the drug screen were dropped from the program after one warning. Addicts developed trust because I talked to them in confidence and was a source of good and reliable drug information. I was “the man” who knew drugs.

Many will counter this point because of their agendas. Medical marijuana has been legalized in 14 states. The dummying up of America will continue if we don’t educate individuals that marijuana has equal or more toxic effects than alcohol. It is only when deaths hit families and friends that the anti-drug message sinks in.

In the past 20 years, the family has fragmented so that there is no male hero for the child. There was an added positive response from those I helped when they came from a family unit with a mother and father, because family members have to reinforce this message.

Why has there been such an increase in Attention Deficit Hyperactivity Disorder in our children during the same time period? The fact is that drugs change the maturing of cells in the body and the brain. The mere fact that we are addressing early education for children after birth but are not addressing the effects of both legal and illegal drugs before birth, resulting in mental retardation, a decrease in the attention span and learning abilities of that young child in school, is somewhat backward.

There is debate about whether poverty causes drug abuse or drug abuse causes poverty. I believe it’s the latter.

I recommend a written contract/commitment between parent(s) and assistance program managers (private or government-run) with specific guidelines to decrease the usage of illegal drugs. If the commitment is to raise a person out of poverty, then there has to be a commitment from the person to help themselves, too.

If the government orders that all recipients who receive government financial support, not including the elderly or those with disabilities and legitimate medical conditions, must submit to random drug urine tests, there will be a drastic drop in drug abuse and subsequently a reduction in poverty. If an individual fails the drug test twice in 60 days, they would forfeit financial support for 12 months and be required to attend a drug-abuse program to re-enter the program. If they fail again, they should be permanently removed from all government-assistance programs.

Many citizens have to submit to random drug screens, at any time, when we are employed but those receiving government funds have no responsibility or accountability to either the government, the program or themselves. Why do we hold these individuals to different standards?

When programs don’t contain measurements, standards and contracts for accountability, they will fail and poverty will continue.

Let me close with two quotes: “All truths are easy to understand once they are discovered the point is to discover them” (Gallileo) and “Is silence an endorsement?” (Aliota).

LOU ALIOTA of Millcreek Township, is a registered pharmacist and is a private health-care consultant.

Source: Op-Ed from Erie Times-News (Erie, Pa.) – August 20, 2010

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)

Teens may smoke to “self-medicate” against depression, but researchers in Canada say smoking may increase depressive symptoms in some adolescents.

Lead author Michael Chaiton of the Ontario Tobacco Research Unit of the University of Toronto and co-author Jennifer O’Loughlin of the University of Montreal Hospital Research Centre say the study involved 662 high-school teenagers who completed as many as 20 questionnaires from grades 7-11 about their use of cigarettes to affect mood.

Study participants were divided into groups of: teens who never smoked; smokers who did not use cigarettes to self-medicate, improve mood or physical state; and smokers who used cigarettes to self-medicate. Study participants were asked to rate on a rating scale depressive symptoms such as: felt too tired to do things; had trouble going to sleep or staying asleep; felt unhappy, sad, or depressed; felt hopeless about the future; felt nervous or tense; and worried too much about things.

Smokers who used cigarettes as mood enhancers had higher risks of elevated depressive symptoms than teens who had never smoked, researchers concluded.

Source: Journal of Addictive Behaviors.Sept 2010

Researchers at King’s College London’s Institute of Psychiatry say a personality-based intervention for substance abuse that was delivered by teachers was successful in reducing drinking rates, particularly binge drinking, among adolescents.

In the article titled “Personality-Targeted Interventions Delay Uptake of Drinking and Decrease Risk of Alcohol-Related Problems When Delivered by Teachers,” principal Investigator Dr. Patricia Conrod and colleagues evaluated 2,506 adolescents, with a mean age of 13.7, using the Substance Use Risk Profile scale; a 23-item questionnaire which assesses personality risk for substance abuse along four dimensions including sensation-seeking, impulsivity, anxiety-sensitivity, and hopelessness.

Of the 1,159 students identified by researchers as being at high risk for substance abuse, 624 received intervention as part of the Adventure Trial and a matched high risk group of 384 received no intervention. School based interventions consisted of two 90 minute group sessions conducted by a trained educational professional. In order to adequately evaluate the students, the teachers attended a 3-day rigorous workshop, followed by 4 hour supervision and feedback session. An 18 point checklist was used to determine whether the teachers demonstrated a good understanding of the aims and components of the programs.

Although the trial is designed to evaluate mental health symptoms, academic achievement, and substance use uptake over a 2 year period, the authors have focused their findings on the six month outcomes of drinking and binge-drinking rates, quantity by frequency of alcohol use, and drinking-related problems. Reporting on the efficacy of the intervention at six months, author and Trial Coordinator Maeve O’Leary-Barrett writes, “Receiving an intervention significantly decreased the likelihood of reporting drinking alcohol at follow-up, with the control group 1.7 times more likely to report alcohol use than the intervention group (odds ratio, 0.6).”

Furthermore, receiving an intervention also predicted significantly lower binge-drinking rates in students who reported alcohol use at baseline (odds ratio, 0.45), indicating a 55 percent decreased risk of binge-drinking in this group compared with controls. In addition, high-risk intervention-school students reported lower quantity by frequency of alcohol use and drinking-related problems compared with the non-treatment group at follow-up.

The Adventure Trial is the first to evaluate the success of the personality-targeted interventions as delivered by teachers. The findings at six months suggest that this approach may provide a sustainable school-base prevention program for youth at risk for substance abuse.

In the JAACAP article, Principal Investigator Dr. Patricia Conrod and colleagues comment on the success of their program by stating, “In-house personality-targeted interventions allow schools to implement early prevention strategies with youth most at risk for developing future alcohol-related problems and provide the potential for follow-up of the neediest individuals.”

Source: Journal of the American Academy of Child and Adolescent Psychiatry. Sept. 2010

Wednesday 01 September 2010

The Local Alcohol Profiles for England (LAPE 2010) have just been released by the North West Public Health Observatory – profiling 23 alcohol-related indicators for every local authority and 24 for every primary care trust in England.
The profiles provide a national ‘map’ of alcohol-related harms.
Key findings from the profiles:
• Over the five years to 2008/09 there has been around a 65% increase in the number of people being admitted to hospital due to alcohol to 606,799 individuals – an increase of over 240,000 people.
• There were 945,469 admissions to hospital for alcohol-related harm in England in 2008/09. This is 825 alcohol-related admissions a day more than five years ago.
• Two thirds (65%) of all the local authorities suffering the highest levels of overall harms are in the North West and North East regions of England (1). The ten local authority areas with the highest levels of combined alcohol-related harm (2) are, in descending order, Manchester, Salford, Liverpool, Rochdale, Tameside, Islington, Middlesbrough, Halton, Oldham and Blackpool.
• By comparison East of England and South East region contain two thirds (65%) of all the local authorities with the lowest overall harm (1). The ten local authorities with the lowest levels of alcohol-related harm (2) are, in ascending order, Broadland, East Dorset, South Northamptonshire, Babergh, Three Rivers, South Norfolk, Hart, Sevenoaks, Wokingham and North Kesteven.
• Between 2006 and 2008 there were 11,247 deaths from chronic liver disease in men. The number of male deaths from chronic liver disease continues to rise steadily and increased by 12% for the five years up to 2008.
• Across England, there were 415,059 recorded crimes attributable to alcohol in 2009/10; equivalent to 8.1 crimes per 1,000 population. The highest rates of alcohol-attributable crime occur in the London region where there were 12.2 crimes per 1,000 residents, although this has decreased by 2.1% from the previous year. The lowest rate is in the North East region at 6.2 crimes per 1,000 which also showed the largest decrease (13.5%) from the previous year.
• Trends in alcohol-related harms vary between local authority areas. For instance, 64% saw an increase of over 5% in hospital admissions for alcohol-related harm in 2008/09, whilst only 7% showed a decrease of over 5%.
(1) Local authorities are categorised into five levels of harm using a clustering methodology that assigns LAs which have similar alcohol profiles to the same category. Months of life lost due to alcohol (males), months of life lost due to alcohol (females), NI39 (alcohol-related hospital admissions), alcohol-attributable recorded crimes, claimants of Incapacity Benefits due to alcoholism, increasing risk drinking, and higher risk drinking were used to determine clusters.
(2) Ranking for highest and lowest levels of alcohol-related harm use the same data as above and are ranked according to the highest combined rank across the seven harm indicators. City of London and the Isles of Scilly are excluded (figures for these areas should always be viewed with caution due to their small resident populations).
Visit the Local Alcohol Profiles for England website.

Source: www.alcoholconcern.org.uk 1.09.2010

Recent research has clarified a number of important questions concerning adverse effects of cannabis on health. A causal role of acute cannabis intoxication in motor vehicle and other accidents has now been shown by the presence of measurable levels of Delta(9)-tetrahydrocannabinol (THC) in the blood of injured drivers in the absence of alcohol or other drugs, by surveys of driving under the influence of cannabis, and by significantly higher accident culpability risk of drivers using cannabis. Chronic inflammatory and precancerous changes in the airways have been demonstrated in cannabis smokers, and the most recent case-control study shows an increased risk of airways cancer that is proportional to the amount of cannabis use. Several different studies indicate that the epidemiological link between cannabis use and schizophrenia probably represents a causal role of cannabis in precipitating the onset or relapse of schizophrenia. A weaker but significant link between cannabis and depression has been found in various cohort studies, but the nature of the link is not yet clear. A large body of evidence now demonstrates that cannabis dependence, both behavioral and physical, does occur in about 7-10% of regular users, and that early onset of use, and especially of weekly or daily use, is a strong predictor of future dependence. Cognitive impairments of various types are readily demonstrable during acute cannabis intoxication, but there is no suitable evidence yet available to permit a decision as to whether long-lasting or permanent functional losses can result from chronic heavy use in adults. However, a small but growing body of evidence indicates subtle but apparently permanent effects on memory, information processing, and executive functions, in the offspring of women who used cannabis during pregnancy. In total, the evidence indicates that regular heavy use of cannabis carries significant risks for the individual user and for the health care system.

Source: Prog Neuropsychopharmacol Biol Psychiatry. 2004 Aug;28(5):849-63.

Neurobiology of cannabis–recent data enlightening driving disturbances

Abstract

During the last decades a new landscape of cannabis has been designed on account of: the increase in its use the greater youth of its users; the increase in the content of its main active constituent tetrahydrocannabinol (THC) and a lot of new epidemiological and neurobiological data. THC displays an exceptional lipophilicity, allowing its cerebral storage, leading to long lasting effects, by far more lasting than its presence in blood, and beyond the period throughout the intoxicated people feel a disablement. This is linked to its slow release from brain areas in which large proportion of spare receptors exists (reserve receptors). THC disturbs cognition and various skills required in driving. It may be responsible for psychiatric troubles: anxiety, depression, suicide attempt, psychotic attack, triggering of schizophrenia. It potentiates the alcohol effects and incites to alcohol drinking. It displays close relationships with dependence to heroin. This new landscape of cannabis urges to make a radical alteration in the public communication about this drug of abuse as it has yet collected so many troubles, accidents or tragedies.

Source: Ann Pharm Fr. 2006 May;64(3):148-59.

Dose related risk of motor vehicle crashes after cannabis use.

Abstract

The role of Delta(9)-tetrahydrocannabinol (THC) in driver impairment and motor vehicle crashes has traditionally been established in experimental and epidemiological studies.
Experimental studies have repeatedly shown that THC impairs cognition, psychomotor function and actual driving performance in a dose related manner. The degree of performance impairment observed in experimental studies after doses up to 300 microg/kg THC were equivalent to the impairing effect of an alcohol dose producing a blood alcohol concentration (BAC) >/=0.05 g/dl, the legal limit for driving under the influence in most European countries. Higher doses of THC, i.e. >300 microg/kg THC have not been systematically studied but can be predicted to produce even larger impairment.
Detrimental effects of THC were more prominent in certain driving tasks than others. Highly automated behaviors, such as road tracking control, were more affected by THC as compared to more complex driving tasks requiring conscious control.
Epidemiological findings on the role of THC in vehicle crashes have sometimes contrasted findings from experimental research. Case-control studies generally confirmed experimental data, but culpability surveys showed little evidence that crashed drivers who only used cannabis are more likely to cause accidents than drug free drivers.
However, most culpability surveys have established cannabis use among crashed drivers by determining the presence of an inactive metabolite of THC in blood or urine that can be detected for days after smoking and can only be taken as evidence for past use of cannabis. Surveys that established recent use of cannabis by directly measuring THC in blood showed that THC positives, particularly at higher doses, are about three to seven times more likely to be responsible for their crash as compared to drivers that had not used drugs or alcohol.
Together these epidemiological data suggests that recent use of cannabis may increase crash risk, whereas past use of cannabis does not. Experimental and epidemiological research provided similar findings concerning the combined use of THC and alcohol in traffic. Combined use of THC and alcohol produced severe impairment of cognitive, psychomotor, and actual driving performance in experimental studies and sharply increased the crash risk in epidemiological analyses.

Source¨ Drug Alcohol Depend. 2004 Feb 7;73(2):109-19

Schizophr Bull. 2010 Mar 11. [Epub ahead of print]
The Impact of Substance Use on Brain Structure in People at High Risk of Developing Schizophrenia.
Welch KA, McIntosh AM, Job DE, Whalley HC, Moorhead TW, Hall J, Owens DG, Lawrie SM, Johnstone EC.
1Division of Psychiatry, School of Molecular and Clinical Medicine, University of Edinburgh, Royal Edinburgh Hospital, Edinburgh EH10 5HF, UK.
Abstract
Ventricular enlargement and reduced prefrontal volume are consistent findings in schizophrenia. Both are present in first episode subjects and may be detectable before the onset of clinical disorder. Substance misuse is more common in people with schizophrenia and is associated with similar brain abnormalities. We employ a prospective cohort study with nested case control comparison design to investigate the association between substance misuse, brain abnormality, and subsequent schizophrenia. Substance misuse history, imaging data, and clinical information were collected on 147 subjects at high risk of schizophrenia and 36 controls. Regions exhibiting a significant relationship between level of use of alcohol, cannabis or tobacco, and structure volume were identified. Multivariate regression then elucidated the relationship between level of substance use and structure volumes while accounting for correlations between these variables and correcting for potential confounders. Finally, we established whether substance misuse was associated with later risk of schizophrenia. Increased ventricular volume was associated with alcohol and cannabis use in a dose-dependent manner. Alcohol consumption was associated with reduced frontal lobe volume. Multiple regression analyses found both alcohol and cannabis were significant predictors of these abnormalities when simultaneously entered into the statistical model. Alcohol and cannabis misuse were associated with an increased subsequent risk of schizophrenia. We provide prospective evidence that use of cannabis or alcohol by people at high genetic risk of schizophrenia is associated with brain abnormalities and later risk of psychosis. A family history of schizophrenia may render the brain particularly sensitive to the risk-modifying effects of these substances.

Vlahov, D. et al. Increased Use of Cigarettes, Alcohol, and Marijuana among Manhattan, New York, Residents after the September 11th Terrorist Attacks. American Journal of Epidemiology. 155(11):988-996, June 1, 2002.
Found that New Yorkers who increased their use of marijuana, tobacco or alcohol in after September 11 had increased chances of developing Post Traumatic Symptoms. Marijuana increased both PTS symptoms and depression more than the other substances.

In a large drug use survey of men born between 1944-1954, found that marijuana users who use the drug to cope with problems are more depressed than those who do not use to cope with problems.
Musty, R. Kaback, L. Relationships between motivation and depression in chronic marijuana users. Life Sciences. Volume 56, Issues 23-24, 5 May 1995, Pages 2151-2158.
Compared heavy and moderate marijuana users on several motivation and depression scales. Found that heavy users’ lack of motivation is correlated with their level of depression.
Bovasso, G. Cannabis Abuse as a Risk Factor for Depressive Symptoms.
Am J Psychiatry 158:2033-2037, December 2001.
People with a diagnosis of cannabis abuse at baseline were four times more likely than those with no cannabis abuse diagnosis to have depressive symptoms at the follow-up assessment, after adjusting for age, gender, antisocial symptoms, and other baseline covariates. In particular, these participants were more likely to have experienced suicidal ideation and anhedonia during the follow-up period.

Source: GREEN B. RITTER C. Marijuana use and depression. Journal of health and social behavior. 2000, vol. 41, no1, pp. 40-49 (1 p.3/4)

Doctors have used the drug disulfiram to help patients stay sober for several decades. It interferes with the body’s ability to metabolize alcohol, giving a fierce hangover to someone who consumes even a small amount of alcohol.
More recently, disulfiram was shown to be effective in treating cocaine addiction as well, even though alcohol and cocaine affect the nervous system in different ways.
Now, researchers at Emory University School of Medicine have identified how disulfiram may exert its effects, and have shown that a newer drug with fewer side effects works by the same mechanism.
The results are published online this week by the journal Neuropsychopharmacology. Research assistant professor Jason Schroeder, PhD, and graduate student Debra Cooper are co-first authors of the paper, and the research also involved collaborations with P. Michael Iuvone, PhD, director of research at the Emory Eye Center, Gaylen Edwards, DVM, PhD, head of the department of physiology and pharmacology at the University of Georgia’s College of Veterinary Medicine, and Philip Holmes, PhD, professor of psychology at the University of Georgia.
“Disulfiram has several effects on the body: it interferes with alcohol metabolism, but it inhibits several other enzymes by sequestering copper, and can also damage the liver,” says senior author David Weinshenker, PhD, associate professor of human genetics at Emory University School of Medicine. “We wanted to figure out how disulfiram was working so we could come up with safer and potentially more effective treatments.”
In treating cocaine addiction, there are several challenges: not only getting people to stop taking the drug, but also preventing relapse. Cocaine boosts the levels of several neurotransmitters, including dopamine and norepinephrine, at the junctions between nerve cells by blocking the machinery the brain uses to remove them.
Under normal conditions, dopamine is important for the sensation of pleasure produced by natural rewards such as food or sex, Weinshenker says. Cocaine “hijacks” the dopamine system, which plays a large role in addiction. Similarly, norepinephrine has a role in attention and arousal, but its overactivation can trigger stress responses and relapse, he says.
Weinshenker’s team showed that disulfiram prevents rats from seeking cocaine after a break, a model for addicts tempted to relapse. At the same time, it doesn’t stop them from taking cocaine when first exposed to it, or from enjoying their food.
Disulfiram appears to work by inhibiting dopamine beta-hydroxylase, an enzyme required for the production of norepinephrine. A dose of disulfiram that lowers the levels of norepinephrine in the brain by about 40 percent is effective, while doses that do not reduce norepinephrine have no effect on relapse-like behavior in rats.
To confirm that the beneficial effects of disulfiram were because of dopamine beta-hydroxylase inhibition, the researchers turned to a drug called nepicastat, which was originally developed for the treatment of congestive heart failure in the 1990s.
“Nepicastat is a selective dopamine beta-hydroxylase inhibitor that does not sequester copper or impair a host of other enzymes like disulfiram,” Weinshenker says. “We reasoned that if disulfiram is really working through dopamine beta-hydroxylase, then nepicastat might be a better alternative.”
Researchers at the University of Texas Medical Branch at Galveston have recently completed a Phase I safety trial studying nepicastat for the treatment of cocaine addiction in human subjects.
Weinshenker is co-inventor on a patent on the use of dopamine beta-hydroxylase inhibitors for the treatment of cocaine dependence, and could benefit from their commercialization. This has been reviewed by Emory University’s Conflict of Interest Committee, and a management plan is in place.
The research was supported by the National Institute of Drug Abuse and the National Eye Center.

Source: . ScienceDaily. Retrieved August 30, 2010

The number of people admitted into hospital because of GHB poisoning has quadrupled in the period 2004-2009. In total, 1200 persons were admitted in the ER’s of hospitals who had swallowed the party drug (23 persons per week). This was reported by the Consumer and Safety Foundation last Sunday.
Almost sixty percent of the treatments took place in the weekend. It mainly concerns males (69 percent). Something more than half of the victims was in the age of 20 to 29 years, one in five in the age of 30 to 39 (22 percent) and fourteen percent between 15 and 19.

Many of the patients not only used GHB, but also alcohol (34%) or other drugs like XTC (10%), cocaine (7%) or speed (1%). Almost all victims at the ER’s suffer from GHB poisoning, 40 percent need to be admitted into hospital, half of which even at the IC department.

Going ‘out’ because of GHB is regarded as something normal. The Consumer and Safety Foundation wants there to be more education and information on GHB. According to the foundation the party drug now has a too positive image: “It’s cheap, simply to get, people break loose and become jolly and do not suffer a hangover. That image has to change for reality. GHB is addictive and can even be life threatening. And the long term damage to health is not yet known.”

(Source: http://www.veiligheid.nl/csi/veilighe id.nsf/wwwVwContent/M_7CC86ED715F24DE9C125778500330C70) Aug 2010

Smoking cannabis is more harmful than cigarettes and more likely to
trigger cancer, according to a report.

Just three cannabis ‘joints’ a day can cause the same amount of damage to the lungs as an entire packet of 20 cigarettes.

The British Lung Foundation says that when cannabis and tobacco are
smoked together, the harmful effects are significantly worse.

Its research suggests young cannabis smokers may also be at greater risk of throat and gullet cancers.

The foundation found that tar from cannabis joints contains 50 per cent more cancer-causing toxins than cigarettes made from tobacco alone.

Eight million Britons are thought to smoke cannabis, which some experts believe is a ‘gateway’ to harder drugs such as heroin and cocaine.

Earlier this year, researchers found that 79 per cent of children
thought cannabis was safe while only 2 per cent recognised there are
health risks from smoking the drug.

Dame Helena Shovelton, chief executive of the British Lung Foundation, said the harmful effects of cannabis had been swept under the carpet.

‘People are under the illusion it is safe to smoke cannabis. Our report
shows it is very dangerous to lung health, at least as dangerous as tobacco.

‘It seems society is in the same position as when research first showed the harm caused by tobacco. It took 15 years for the Government to take notice but we don’t want to repeat the mistakes of the past.’

Dame Helena said cannabis available today is 15 times stronger than the drug smoked in the 1960s. ‘This means studies carried out at that time will probably have underestimated the effects of cannabis smoking,’ she explained.

‘Puff and inhalation volume with cannabis is up to four times higher
than with tobacco – in other words you inhale deeper and hold your
breath with the smoke for longer before exhaling.

‘This results in more poisonous carbon monoxide and tar entering into
the lungs,’ Dame Helena said.

The foundation’s report – A Smoking Gun? – analyses research from around the world.

It found cannabis smokers have a higher level of chronic and acute
respiratory-conditions such as coughingwheezing and bronchitis. ‘When cannabis is smoked together with tobacco then the effects are additive’, it says.

Some studies suggest cannabis smoking may trigger chronic obstructive pulmonary disease which kills 32,000 people in Britain every year, the foundation’s report adds.

‘Research linking cannabis smoking to the development of respiratory
cancer exists although there have also been conflicting findings.

‘Not only does the tar in a cannabis cigarette contain many of the same carcinogens as tobacco smoke, but the concentrations of these are up to 50 per cent higher in the smoke of a cannabis cigarette,’ it says.

Benzyprene, found in the tar of cannabis joints, can change the make-up of one of the genes which suppresses tumours and could therefore make cancer more likely for people who smoke joints.

There are also more than 75 case studies of young cannabis smokers with cancers of the throat and gullet – diseases usually rare in people under 60.

Source: Daily Mail
Monday 11 Nov 2002

Friday, 20 August 2010 06:42

The British Home Office has restated its position on drugs, after the outgoing president of the Royal College of Physicians Ian Gilmore called for a review of the law.
Speaking to the BBC, Sir Ian Gilmore said that the present policy of prohibition is not a success.
Responding to Sir Ian’s comments, a Home Office spokesperson said: Drugs such as heroin, cocaine and cannabis are extremely harmful and can cause misery to communities across the country. The government does not believe that decriminalisation is the right approach. Our priorities are clear; we want to reduce drug use, crack down on drug related crime and disorder and help addicts come off drugs for good.

The journalist who chose the headline would have known that ‘Cold Turkey’ implies a harsh treatment. Using residential rehabs to help those addicted to recover may be tough but it is not inhumane – and far better than allowing drug dependents to languish for years in addiction to methadone….. The great sadness is the number of residential rehabs which were forced to close when the NTA preferred methadone maintenance to treatment towards abstinence. NDPA

David Cameron is to push ahead with radical “abstinence” plans for the most serious drug addicts.

There are estimated to be 200,000 seriously-addicted users of heroin, crack and cocaine Photo: ALAMY

The Coalition is working on proposals to stop the widespread prescription of methadone for heroin users and instead increase the use of “cold turkey” residential treatment programmes.

Drug services are expected to be paid by results if they manage to get addicts off heroin and cocaine. It also emerged last week that ministers are considering withholding benefits from those refusing treatment.

Theresa May, the Home Secretary, has been charged with drawing up the new strategy despite pressure from the Department of Work and Pensions to take the lead in tackling addiction.

There are estimated to be 200,000 seriously-addicted users of heroin, crack and cocaine and many existing programmes have focused on keeping them away from crime rather than treating their addiction.

James Brokenshire, the Drugs Minister, said: “We are looking to have greater emphasis on recovery rather than simply on treatment itself. The aim is to get people clear of addiction.”

Mr Brokenshire said that there should only be a limited role for methadone in treatment. “[Methadone] should be seen as part of a pathway taking people to a position where they are clear of addiction,” he said.

Source: Telegraph 23rd August 2010