By Mark Gold, MD

Knowing is not enough; we must apply. Willing is not enough; we must do. —Johann Wolfgang von Goethe

The Harvard Review of Psychiatry has recently chronicled important advances in understanding mental health disorders and, to a lesser extent Substance Use Disorder (SUD). This clinical review highlights the important contributions of Harvard experts over the past 25 years.

Addiction Research: What Have We Learned

Through my nearly 40 years of work in translational research and through the work of my colleagues, I have seen tremendous advances that changed how we understand the etiology and pathophysiology of SUD. Specifically, establishing the neurobiological basis of SUD, and the development of new and novel evidence-based pharmacologic and behavioral treatments including the discovery of the game changing and lifesaving drug, naltrexone, and thus establishing the neurobiological foundations for Medically Assisted Treatment (MAT), which resulted in important changes in the DSM.

As research established risk factors for SUD, we discovered that this disease is largely determined (40-60%) by genetic factors. Certainly, the Human Genome Project has unlocked the door to the field of epigenetics and the recognition that subtle variants in genetic transcription and coding are associated with numerous diseases, including SUD. The neuro-mechanisms and environmental stressors that conspire to “switch on” particular genes that increase the risk for SUD are not well established. Yet, our understanding of how specific neuronal circuitry mediates substance-induced reward, drug craving, compulsions and withdrawal is becoming clear. For example, when hedonically driven dopaminergic and opioidergic systems are disrupted, via the chronic use of intoxicants, neuroadaptation results in drug seeking, craving, anhedonia, depression, and chronic deficits in mood, memory and self-control. In other words, addiction.

Most recently, the discovery of ketamine’s efficacy in acute suicidality and treatment resistant depression represents a new and novel direction for research and the development of new therapeutics via the NDMA system. This discovery may supplant the 50-year-old catecholamine hypothesis for understanding addiction, mood disorders, pain and perhaps more.
But knowing is never enough in medicine—we must do.

So, in spite of all we have learned in the past few decades, the neurobiology and epigenetic risks for addiction remain underestimated and virtually unaddressed in current clinical guidelines for treating SUD. For example, we now know that early childhood trauma produces potentially heritable epigenetic changes that are highly correlated with SUD and other psychopathologies in adolescence and early adulthood. In addition, survey data reveals that approximately 70% of women in SUD treatment have suffered trauma, yet only a few of the top centers are professionally equipped to treat trauma as a comorbid disorder. Unaddressed, trauma almost always results in relapse.


The increasing prevalence and severity of SUD and the lack of available treatment is a formidable gap that is widening. By treatment, we do not mean SUD CPR or Naloxone, but rather prevention and when that fails, treatment that is safe and effective for five years. Efforts to close this gap involve many nonclinical variables (cost, access, harm reduction vs. medical model, politics, etc.), over which we have little control–but this is not to say we don’t have influence.

These are exciting times, as there is much to be learned about addictive disease and its numerous comorbidities. But, unless much more of the 23+ million currently addicted people in the US get help, research will remain simply academic.

Source: July 2017

Filed under: Addiction,Latest News :

Anybody wondering what happens to the 8 per cent of the skunk-smoking population who develop mental illness should visit any psychiatric hospital in Britain or speak to somebody who has done so What is really needed in dealing with cannabis is a “tobacco moment”, as with cigarettes 50 years ago, when a majority of people became convinced that smoking might give them cancer and kill them. Since then the number of cigarette smokers in Britain has fallen by two-thirds.

A depressing aspect of the present debate about cannabis is that so many proponents of legalisation or decriminalisation have clearly not taken on board that the causal link between cannabis and psychosis has been scientifically proven over the past ten years, just as the connection between cancer and cigarettes was proved in the late 1940s and 1950s.

The proofs have emerged in a series of scientific studies that reach the same grim conclusion: taking cannabis significantly increases the risk of schizophrenia. One study in The Lancet Psychiatry concludes that “the risk of individuals having a psychotic disorder showed a roughly three times increase in users of skunk-like cannabis, compared with those who never used cannabis”. As 94 per cent of cannabis seized by the police today is super-strength skunk, compared to 51 per cent in 2005, almost all those who take the drug today will be vulnerable to this three-fold increase in the likelihood that they will develop psychosis.

Mental health professionals have long had no doubts about the danger. Five years ago, I asked Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry in London, about them. He said that studies showed that “if the risk of schizophrenia for the general population is about one per cent, the evidence is that, if you take ordinary cannabis, it is two per cent; if you smoke regularly you might push it up to four per cent; and if you smoke ‘skunk’ every day you push it up to eight per cent”.

Anybody wondering what happens to this 8 per cent of the skunk-smoking population should visit any mental hospital in Britain or speak to somebody who has done so. Dr Humphrey Needham-Bennett, medical director and consultant psychiatrist of Cygnet Hospital, Godden Green in Sevenoaks, explained to me that among his patients “cannabis use is so common that I assume that people use or used it. It’s quite surprising when people say ‘no, I don’t use drugs’.”

The connection between schizophrenia and cannabis was long suspected by specialists but it retained its reputation as a relatively benign drug, its image softened by the afterglow of its association with cultural and sexual liberation in the 1960s and 1970s.

This ill-deserved reputation was so widespread that even 20 years ago, the possible toxic side effects of cannabis were barely considered. Zerrin Atakan, formerly head of the National Psychosis Unit at the Maudsley Psychiatric Hospital and later a researcher at the Institute of Psychiatry,

said: “I got interested in cannabis because I was working in the 1980s in an intensive care unit where my patients would be fine after we got them well. We would give them leave and they would celebrate their new found freedom with a joint and come back psychotic a few hours later.”

She did not find it easy to pursue her professional interest in the drug. She recalls: “I was astonished to discover that cannabis, which is the most widely used illicit substance, was hardly researched in the 1990s and there was no research on how it affected the brain.” She and fellow researchers made eight different applications for research grants and had them all turned down, so they were reduced to taking the almost unheard of course of pursuing their research without the support of a grant.

Studies by Dr Atakan and other psychiatrists all showed the connection between cannabis and schizophrenia, yet this is only slowly becoming conventional wisdom. Perhaps this should not be too surprising because in 1960, long after the link between cigarettes and lung cancer had been scientifically established, only a third of US doctors were persuaded that this was the case.

A difficulty is that people are frightened of mental illness and ignorant of its causes in a way that is no longer true of physical illnesses, such as cancer or even HIV. I have always found that three quarters of those I speak to at random about mental health know nothing about psychosis and its causes, and the other quarter know all too much about it because they have a relative or friend who has been affected.

Even those who do have experience of schizophrenia do not talk about it very much because they are frightened of a loved one being stigmatised. They may also be wary of mentioning the role of cannabis because they fear that somebody they love will be dismissed as a junkie who has brought their fate upon themselves.

This fear of being stigmatised affects institutions as well as individuals. Schools and universities are often happy to have a policy about everything from sex to climate change, but steer away from informing their students about the dangers of drugs. A social scientist specialising in drugs policy explained to me that the reason for this is because “they’re frightened that, if they do, everybody will think they have a drugs problem which, of course, they all do”.

The current debate about cannabis – sparked by the confiscation of the cannabis oil needed by Billy Caldwell to treat his epilepsy and by William Hague’s call for the legalisation of the drug – is missing the main point. It is all about the merits and failings of different degrees of prohibition of cannabis when it is obvious that legal restrictions alone will not stop the 2.1 million people who take cannabis from going on doing so. But the legalisation of cannabis legitimises it and sends a message that the government views it as relatively harmless. The very fact of illegality is a powerful disincentive for many potential consumers, regardless of the chances of being punished.

The legalisation of cannabis might take its production and sale out of the hands of criminal gangs, but it would put it into the hands of commercial companies who would want to make a profit, advertise their product and increase the number of their customers. Commercialisation of cannabis has as many dangers as criminalisation.

A new legal market in cannabis might be regulated and the toxicity of super-strength skunk reduced. But the argument of those who want to legalise cannabis is that the authorities are unable to enforce regulations when the drug is illegal, so why should they be more successful in regulating it when its production and sale is no longer against the law?

The problem with these rancorous but sterile arguments for and against legalisation and decriminalisation is that they divert attention from what should and can be done: a sustained campaign to persuade people of all ages that cannabis can send them insane. To a degree people are learning this already from bitter experience. As Professor Murray told me five years ago, the average 19- to 23-year-old probably knows more about the dangers of cannabis than the average doctor “because they have a friend who has gone paranoid. People know a lot more about bad trips than they used to.”

Patrick Cockburn is the co-author of Henry’s Demons: Living With Schizophrenia, A Father and Son’s Story

A depressing aspect of the present debate about cannabis is that so many proponents of legalisation or decriminalisation have clearly not taken on board that the causal link between cannabis and psychosis has been scientifically proven over the past ten years, just as the connection between cancer and cigarettes was proved in the late 1940s and 1950s.

The proofs have emerged in a series of scientific studies that reach the same grim conclusion: taking cannabis significantly increases the risk of schizophrenia. One study in The Lancet Psychiatry concludes that “the risk of individuals having a psychotic disorder showed a roughly three times increase in users of skunk-like cannabis, compared with those who never used cannabis”. As 94 per cent of cannabis seized by the police today is super-strength skunk, compared to 51 per cent in 2005, almost all those who take the drug today will be vulnerable to this three-fold increase in the likelihood that they will develop psychosis.

Home Secretary Sajid Javid: The government will carry out a review of the scheduling of cannabis for medicinal use

Mental health professionals have long had no doubts about the danger. Five years ago, I asked Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry in London, about them. He said that studies showed that “if the risk of schizophrenia for the general population is about one per cent, the evidence is that, if you take ordinary cannabis, it is two per cent; if you smoke regularly you might push it up to four per cent; and if you smoke ‘skunk’ every day you push it up to eight per cent”.

  • Cannabis is responsible for 91% of drug addiction cases involving teenagers
  • Skunk – high-potency herbal cannabis – causing more people to seek treatment 
  • Backs up research that skunk is having detrimental impact on mental health

Supporters of the drug claim it is harmless, but an official report now warns the ‘increased dominance of high-potency herbal cannabis’ – known as skunk – is causing more young people to seek treatment.

The revelation comes amid growing concerns that universities – and even some public schools – are awash with high-strength cannabis and other drugs.

The findings also back up academic research, revealed in The Mail on Sunday over the past three years, that skunk is having a serious detrimental impact on the mental health of the young. At least two studies have shown repeated use triples the risk of psychosis, with sufferers repeatedly experiencing delusional thoughts. Some victims end up taking their own lives.

The latest UK Focal Point on Drugs report, drawn up by bodies including Public Health England, the Scottish Government and the Home Office, found that:

Cannabis is responsible for 91 per cent of cases where teenagers end up being treated for drug addiction, shocking new figures reveal (file photo)
Cannabis is responsible for 91 per cent of cases where teenagers end up being treated for drug addiction, shocking new figures reveal 
  • Over the past decade, the number of under-18s treated for cannabis abuse in England has jumped 40 per cent – from 9,043 in 2006 to 12,712 in 2017;
  • Treatment for all narcotics has increased by 20 per cent – up from 11,618 to 13,961;
  • The proportion of juvenile drug treatment for cannabis use is up from four in five cases (78 per cent) to nine in ten (91 per cent);
  • There has been a ‘sharp increase’ in cocaine use among 15-year-olds, up 56 per cent from 16,700 in 2014 to 26,200 in 2016.

Last night, Lord Nicholas Monson, whose 21-year-old son Rupert Green killed himself last year after becoming hooked on high-strength cannabis, said: ‘These figures show the extent of the damage that high-potency cannabis wreaks on the young.

‘The big danger for young people – particularly teens – is that their brains can be really messed up by this stuff because they are still developing biologically. If they develop drug-induced psychosis – as Rupert did – the illness can stick for life.’

The large rise in the number of youngsters treated for cannabis abuse comes despite the fact that total usage is falling slightly.

The report concludes: ‘While fewer people are using cannabis, those who are using it are experiencing greater harm.’

Almost all cannabis on Britain’s streets is skunk, which is four times more powerful than types that dominated the market until the early 2000s. It can even trigger hallucinations.

Lord Monson said: ‘We really need Ministers to get a grip and launch a major publicity campaign about the dangers.’ 

Source:  April 2018

By William Ross Perlman, Ph.D., CMPP, NIDA Notes Contributing Writer

This research:

  • Identified a gene variant that promotes impulsive behavior and enhanced responses to heroin in rats.
  • Linked the corresponding human gene variant to increased risk for impulsivity and drug use.

People who are highly impulsive and those diagnosed with ADHD are at increased risk for substance use disorders (SUD). Recent research implicates a variant of the gene for a protein called cAMP-response element modulator (CREM) in these associations. Drs. Michael L. Miller and Yasmin L. Hurd from the Icahn School of Medicine at Mount Sinai in New York, with colleagues from several other institutions, showed that the gene variant promotes impulsive and hyperactive behavior in both animals and humans, and can contribute to a person’s risk for developing SUD.

Of Rats…

The Icahn researchers began their investigations with a strain of rats that exhibit impulsive behaviors resembling human attention-deficit/hyperactivity disorder (ADHD). Initial experiments confirmed that, compared with a strain (Western Kyoto) of rats that are not known for impulsivity, these “spontaneously hypertensive” (SH) rats:

  • Were more impatient to receive rewards, fidgeted more while waiting to receive rewards, ran around more, and were more attracted to novel experiences.
  • Self-administered more heroin and, when it was made unavailable, gave up seeking it less readily.  
  • Had enhanced elevation of dopamine levels in response to heroin.

The researchers screened the rats’ DNA for genetic differences that might contribute to these behavioral differences. The results revealed that the two strains carried different variants of the gene for CREM. As a result, the SH rats had lower concentrations of CREM in the core of the nucleus accumbens—a key brain region governing reward and movement.

…And People


Figure 1. A CREM Gene Variant Increases HyperactivityHyperactivity scores were higher in ADHD subjects than in control subjects. In addition, ADHD subjects who carried at least one copy of the less highly expressed A variant (i.e., with the G/A or A/A CREM genotype) reported significantly higher hyperactivity than did those carrying only the more highly expressed G variant (i.e., with the G/G genotype). Genotype had no effect on hyperactivity in non-ADHD control subjects

The researchers used genetic and behavioral evidence from previous studies conducted by other researchers to demonstrate that the corresponding variant in the human CREM gene similarly predisposes people to impulsivity. This variant occupies approximately the same position on the human gene that the rodent variant occupies on the rodent gene. At this site, known as rs12765063, the CREM gene exists in two versions—called A and G—and the A variant dials down CREM production. In one study, preschool children with the A variant were found to be more distractible and to engage in more dangerous activities than peers with only the G variant (Figure 1). In another, among adolescents with ADHD, those who carried the A variant reported more symptomatic hyperactivity than those who did not.

The researchers further found that by promoting impulsivity, the variant raises the risk of drug use. Thus, in two studies of adolescents, neither the A variant alone nor ADHD alone increased the risk for drug use, but the two together did. The first analysis looked at adolescents with ADHD, and found higher rates of drug use among those with the A variant than among those with only the G variant. The second analysis looked at adolescents who had the A variant of rs12765063 and histories of childhood ADHD. It found that those whose childhood ADHD still persisted reported more use of alcohol, tobacco, marijuana, and prescription stimulants than those who had outgrown their ADHD (Figure 2). Moreover, those who no longer had ADHD reported no more drug use than a comparison group who did not carry the A variant.


Figure 2. The A Variant of the CREM Gene Is Associated With Increased Drug Use in People With Persistent ADHD Among a cohort whose childhood ADHD persisted through adolescence, those with the CREM A variant reported more drug use than those with only the G variant. Genotype was not linked to risk for drug use in people without ADHD (i.e., those who never had ADHD or those with remitted ADHD).

A Key to Prevention and Treatment?

Dr. Hurd suggests that CREM may be a key link between impulsivity and vulnerability to addiction. Understanding these relationships may help identify new ways of treating or preventing SUD. The protein is known to regulate multiple gene networks and their biological functions, and to influence the growth of structures that neurons use to communicate with each other.

Dr. Hurd says, “These results highlight that CREM is a mediating factor between impulsivity and substance abuse vulnerability. It brings attention to CREM in the nucleus accumbens as a regulator of impulsive action and structural plasticity.”

The study was supported by NIH grants DA015446, DA030359, DA006470, DA038954, DA031559, and DA007135.

Source: June 2018

Another day, another troubling headline.

If you believe that the access to “safer” drugs is the problem, maybe vending machines will “fix Vancouver’s drug crisis.”

For more than a decade, we’ve been told that Vancouver is the model the US should emulate. No North American city has been more aggressive in implementing harm reduction practices—safe injection rooms, heroin maintenance, hydromorphone (dilaudid) maintenance, crack pipe vending machines and, of course, all the less sensational forms of harm reduction.

So . . . all these years later, where are they at?

“Last year, overdoses killed 1,422 people in British Columbia, the highest number ever, a 43 per cent increase over 2016.”

Pretty discouraging.

The provincial CDC’s conclusion is that they have not gone far enough.

“. . . sometime in the next several weeks, in March or April, Tyndall will launch a pilot program to distribute hydromorphone pills (a pharmaceutical narcotic derived from morphine) to registered users . . .”

What’s it like there?

“Vancouver’s Downtown Eastside, defined as a de facto colony for people who inject or smoke hard drugs, is smaller than it used to be—maybe half the 20 blocks it used to cover, with condo developments looming on all sides. On the warm January day when I visited, a lot of people are out, lining the sidewalks of East Hastings Street, a few side streets and many wide alleys off the main artery. Many are openly smoking or injecting drugs. It’s a shocking sight the first time you visit. You get used to it pretty quickly.”

How many times does recovery come up in this article? 1 time, as a glib rebuttal that equates questioning the approach to malignant neglect.

“You can’t ask people to recover if they’re dead. But the stigma goes so deep that I think a lot of people go, ‘Well, who gives a shit? They die. Better for us. We don’t have to pay their medical bills.’ ”

What’s the animating belief? (emphasis mine)

“Addiction, he says, is a chronic relapsing disease. Most addicts don’t stop.”

If you believe that addicts don’t want to and are unable to stop, then this seems like a pragmatic and compassionate approach.

If you know that addicts hate their lives and that there is hope for recovery, this is very, very sad. If you know that the hopelessness of most addicts requires that professional helpers acts as hope carriers, this will make you angry.

This does not have to be an either/or matter. There is room for a both/and approach. However, as a casual observer, I have not seen BC public health officials, politicians, researchers, or policy advocates address the need and hope for recovery.



Februrary 2018

Filed under: Addiction,Heroin/Methadone :

Interviewed by Mark Gold, MD

Frederick S. Southwick, MD
Professor of Internal Medicine and Former ​Chief of Infectious Diseases at the University of Florida

2010 Harvard University Advanced Leadership Fellow
Expert in Medicine, Infectious Disease and Medical Errors​

We see patients who smoke cigarettes, drink and/or abuse drugs. How does this affect their immune status or ability to fight common infections? Any association between a drug dependency like cigarettes and/or marijuana, smoking and/or alcohol drinking?

Smoking is a major risk factor for developing pneumonia. Those who smoke 20 or more cigarettes a day have three times the risk of developing pneumonia. Cigarette smoke damages the tracheal lining of the lungs, alters the consistency of the fluid that coats this lining, and destroys the cilia that move bacteria and other foreign substances out of the lung. When the fluid coating the tubes of the lung becomes thicker as a consequence of the inflammatory reaction to smoke, cilia can no longer transport this fluid, and the foreign particles, including bacteria, usually trapped by this fluid can no longer be transported out of the lungs. Damage to the cilia also interferes with this important protective mechanism.

Alcohol and other sedating drugs interfere with the function of the epiglottis. This large flap of tissue covers the trachea to prevent saliva, food and liquids from entering the lungs. We have all accidently choked on water when our epiglottis malfunctions and water enters the lung. We quickly cough it out. When drugs lead to sedation our epiglottis is more likely to malfunction and food, saliva and bacteria from the mouth can more easily enter the lungs. Sedation also interferes with our cough reflex, and as a consequence, severe aspiration pneumonia can follow an overdose or an episode of heavy drinking.

Drug abuse often leads to malnutrition and some drugs, particularly alcohol, can depress the body’s ability to produce white blood cells. Malnutrition and the loss of these cells can depress the normal acute immune response to infection, and as a consequence, infections are often more severe and life threatening in alcoholics and patients who suffer drug abuse.

Do substance abusers or addicts have more mono, flu, pneumonia, TB or other Infectious Diseases (ID)?

The incidence of mononucleosis is not known to be higher. Influenza is more severe in addicts with depressed immune responses. Tuberculosis may have a higher incidence in addicts because their depressed immune function allows the organism to more readily spread in the lungs and throughout the body.

What are some IDs associated with intravenous drug users?

Another major risk for infection is the use of intravenous drugs. Too often the drugs being injected into the blood stream are contaminated with bacteria, particularly Staphylococcus aureus (found on the skin) and Pseudomonas (found in tap water). These bacteria can infect the heart valves leading to endocarditis, a very serious and potentially fatal infection. Once bacteria enter the blood stream they can also lodge in small vessels of the bones, particularly the vertebral bodies or back bones resulting in bone infection or osteomyelitis. This infection is associated with chronic pain, fever and loss of energy. Osteomyelitis is very difficult to treat and requires six weeks of high dose intravenous antibiotics. Despite prolonged therapy, this infection often relapses resulting in years of pain and suffering.

In addition to bacteria contaminating intravenous drug preparations, shared needles can transmit viruses – Hepatitis B, Hepatitis C, and HIV virus.  Hepatitis B and Hepatitis C both can lead to severe liver inflammation that causes scaring of the liver called cirrhosis. Eventually the liver fails resulting in ascites (filling of the abdominal cavity with fluid), dilatation and bleeding of the esophageal veins (esophageal varices) resulting in gastrointestinal bleeding, and difficulty detoxifying substances in the blood resulting in the loss of alertness and eventually coma (called Hepatic encephalopathy).

HIV is another dreaded and all too common complication of IV drug use.

What would you evaluate all IV addicts for?

All IV addicts should be screened for Hepatitis B, Hepatitis C and HIV. They should also be screened for STDs.

What vaccinations would you suggest for patients with substance use disorders?

They should receive the influenza vaccine annually and the two pneumococcal vaccines. Also, if they are Hepatitis B antibody negative, they should receive the Hepatitis B vaccine.

Can you explain Hepatitis C. What is it? Who gets it? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

Hepatitis C is a virus that specifically infects the liver. This virus is transmitted by blood and blood products. Before the virus was recognized in the early 1990s, it contaminated our blood supply. Risk factors associated with an increased risk of Hepatitis C include:

  • persons receiving blood transfusions or transplanted organs before July of 1992
  • those who received clotting factors before 1987
  • anyone born to a mother with Hepatitis C virus
  • anyone who shared needles to inject drugs, or who had tattoos or body piercing with unsterile equipment

Addicts who use intravenous drugs and share needles are at very high risk, because the virus is transmitted by needles contaminated with virally infected blood. Individuals infected with Hep C have very high numbers of viral particles in their blood, and when they share a needle with an uninfected person, that person is at high risk of inadvertently injecting those viral particles intotheir own blood stream and infecting their liver. The best way to prevent the spread of Hep C is to avoid IV drug use.

Another alternative is to use a clean needle, and never share needles. In some areas of the country, needle exchange programs have been instituted to prevent the spread of Hep C, Hep B, and HIV. The diagnosis can be readily made with a blood test that measures antibodies directed against the virus. This is a very sensitive and specific test and anyone who falls into the above risk groups should undergo testing because we now have excellent antiviral therapy for this infection. Direct acting antiviral therapy offers high cure rates of over 95% in most cases. Treatment usually takes 8-12 weeks of a single pill once per day. In more complicated cases, treatment may be continued for 24 weeks. The cost of treatment is very high ($1,000/ pill) usually costing between $80,000-100,000 to achieve a cure.

Is there a new epidemic of STDs. Which? Who gets which? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

Drug abuse is associated with increased sexual activity and the more sexual partners one has the greater the risk of STDs. The incidence of syphilis in the U.S. has increased among women by 36% from 2015 to 2016 and 15% in men during this same period. Also, the incidence of newborn syphilis has increased by 28% as a consequence of transmission from mother to child.

The group with the highest incidence of this infection is men having sex with men (MSM), and about ½ of MSM who have syphilis also have HIV. The incidence of gonorrhea has also increased during this time period by 22%. This is a particularly worrisome development because strains of gonorrhea are increasingly becoming drug resistant meaning that we are at risk of running out of antibiotic treatments for this infection in the future. Condoms prevent the spread of these diseases; and should always be used given the high risk of STDs among drug abusers.

Public health workers try to identify contacts when a STD case is reported so that these contacts can be tested and treated to prevent the further spread of infection. All patients who have more than one sexual partner or who use illicit drugs should be screened for syphilis, gonorrhea, chlamydia, Hepatitis B and HIV, particularly sexually active women under 25, pregnant women, and men having sex with men.

Syphilis, Hepatitis B and HIV are detected primarily through blood tests. Gonorrhea and chlamydia are tested using vaginal and urethral (opening of the penis) swabs. These tests are all very sensitive and specific. Syphilis, gonorrhea and chlamydia are treated with antibiotics and can be cured. Hepatitis B, like Hepatitis C, can now be cured using antiviral agents, but at great expense. HIV requires lifelong treatment.

Can you explain HIV? AIDS? What is it? Who gets it? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

HIV stands for Human Immunodeficiency Virus and is caused by a retrovirus that is transmitted primarily through blood and through sexual contact as an STD. HIV is a lifelong infection that over time destroys immune cells and results in opportunistic infections (infections by organisms that rarely infect people with normal immune systems) including cryptococcal (fungal) meningitis, pneumocystis pneumonia, and toxoplasmosis brain infections.

When the immune system deteriorates to the point of allowing these infections to develop, HIV infection is said to have progressed to AIDS or Acquired Immune Deficiency Syndrome.  Anti-retroviral medications can lower the viral counts and reverse this immunodeficiency; however, these medications cannot completely eradicate the infection, and they must be taken for life. If anti-retroviral medications are discontinued, the infection reactivates.

Can you explain what is HPV?  Is it just a woman’s problem? Who gets it? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

Human papilloma virus (HPV) is a wart causing virus that is transmitted by close skin to skin contact and is most commonly transmitted by vaginal or anal sex. A high percentage of people become infected but our immune system often clears the virus; however, when the virus remains active it can cause genital warts that have a cauliflower like appearance. This virus can cause mouth and throat, penis, anal, vaginal and cervical cancer. The diagnosis of HPV is usually made based on examination. Cervical pap smears are recommended periodically for women to look for atypical precancerous cells. Treatment consists of removing the precancerous cells through surgical procedures. When cancer develops, chemotherapy and surgical resection are required.

There is no medical treatment for HPV. However, a very effective vaccine is now available that can prevent HPV induced cancer. The vaccine is recommended for all children at age 11-12 years and can be given up to age 21 for women and up to age 26 for men. This vaccine is strongly recommended for men who intend to have sex with men, transgenders, and adolescents who are immunocompromised, including patients with HIV.

For many years, we treated cigarette-related cancers rather than identifying smokers and helping people stop smoking. Is that still happening today with alcohol and drugs? With no drug testing or limited in Pediatrics and Medicine, how can asking the patient if they use or inject drugs identify and help treat the primary disease or users?

The newspapers and television news are now publicizing the worsening drug epidemic in our country. This epidemic has spread to people in every socioeconomic class. Given the many health risks of drug addiction, physicians and nurses have an obligation to ask questions about this potentially life-threatening behavior. Drug addiction is a disease, and to identify and treat this disease, medical caregivers are obligated to inquire about this important health issue. And those who suffer from drug addiction need not be ashamed. They should be open to help. The infectious disease risks of continuing addiction are real and potentially life threatening. Therapy for addiction is available and can be effective. Why wait until the damage has been done?

Source:  May 2018

The proliferation of retail boutiques in California did not really bother him, Evan told me, but the billboards did. Advertisements for delivery, advertisements promoting the substance for relaxation, for fun, for health. “Shop. It’s legal.” “Hello marijuana, goodbye hangover.” “It’s not a trigger,” he told me. “But it is in your face.”

When we spoke, he had been sober for a hard-fought seven weeks: seven weeks of sleepless nights, intermittent nausea, irritability, trouble focusing, and psychological turmoil. There were upsides, he said, in terms of reduced mental fog, a fatter wallet, and a growing sense of confidence that he could quit. “I don’t think it’s a ‘can’ as much as a ‘must,'” he said.

Evan, who asked that his full name not be used for fear of the professional repercussions, has a self-described cannabis-use disorder. If not necessarily because of legalization, but alongside legalization, such problems are becoming more common: The share of adults with one has doubled since the early aughts, as the share of cannabis users who consume it daily or near-daily has jumped nearly 50 percent-all “in the context of increasingly permissive cannabis legislation, attitudes, and lower risk perception,” as the National Institutes of Health put it.

Public-health experts worry about the increasingly potent options available, and the striking number of constant users. “Cannabis is potentially a real public-health problem,” said Mark A. R. Kleiman, a professor of public policy at New York University. “It wasn’t obvious to me 25 years ago, when 9 percent of self-reported cannabis users over the last month reported daily or near-daily use. I always was prepared to say, ‘No, it’s not a very abusable drug. Nine percent of anybody will do something stupid.’ But that number is now [something like] 40 percent.” They argue that state and local governments are setting up legal regimes without sufficient public-health protection, with some even warning that the country is replacing one form of reefer madness with another, careening from treating cannabis as if it were as dangerous as heroin to treating it as if it were as benign as kombucha.

But cannabis is not benign, even if it is relatively benign, compared with alcohol, opiates, and cigarettes, among other substances. Thousands of Americans are finding their own use problematic-in a climate where pot products are getting more potent, more socially acceptable to use, and yet easier to come by, not that it was particularly hard before.

For Keith Humphreys, a professor of psychiatry and behavioral sciences at Stanford University, the most compelling evidence of the deleterious effects comes from users themselves. “In large national surveys, about one in 10 people who smoke it say they have a lot of problems. They say things like, ‘I have trouble quitting. I think a lot about quitting and I can’t do it. I smoked more than I intended to. I neglect responsibilities.’ There are plenty of people who have problems with it, in terms of things like concentration, short-term memory, and motivation,” he said. “People will say, ‘Oh, that’s just you fuddy-duddy doctors.’ Actually, no. It’s millions of people who use the drug who say that it causes problems.”

Users or former users I spoke with described lost jobs, lost marriages, lost houses, lost money, lost time. Foreclosures and divorces. Weight gain and mental-health problems. And one other thing: the problem of convincing other people that what they were experiencing was real. A few mentioned jokes about Doritos, and comments implying that the real issue was that they were lazy stoners. Others mentioned the common belief that you can be “psychologically” addicted to pot, but not “physically” or “really” addicted. The condition remains misunderstood, discounted, and strangely invisible, even as legalization and white-marketization pitches ahead.

The country is in the midst of a volte-face on marijuana. The federal government still classifies cannabis as Schedule I drug, with no accepted medical use. (Meth and PCP, among other drugs, are Schedule II.) Politicians still argue it is a gateway to the use of things like heroin and cocaine. The country still spends billions of dollars fighting it in a bloody and futile drug war, and still arrests more people for offenses related to cannabis than it does for all violent crimes combined.

Yet dozens of states have pushed ahead with legalization for medical or recreational purposes, given that for decades physicians have argued that marijuana’s health risks have been overstated and its medical uses overlooked; activists have stressed prohibition’s tremendous fiscal cost and far worse human cost; and researchers have convincingly argued that cannabis is far less dangerous than alcohol. A solid majority of Americans support legalization nowadays.

Academics and public-health officials, though, have raised the concern that cannabis’s real risks have been overlooked or underplayed-perhaps as part of a counter-reaction to federal prohibition, and perhaps because millions and millions cannabis users have no problems controlling their use. “Part of how legalization was sold was with this assumption that there was no harm, in reaction to the message that everyone has smoked marijuana was going to ruin their whole life,” Humphreys told me. It was a point Kleiman agreed with. “I do think that not legalization, but the legalization movement, does have a lot on its conscience now,” he said. “The mantra about how this is a harmless, natural, and non-addictive substance-it’s now known by everybody. And it’s a lie.”

Thousands of businesses, as well as local governments earning tax money off of sales, are now literally invested in that lie. “The liquor companies are salivating,” Matt Karnes of GreenWave Advisors told me. “They can’t wait to come in full force.” He added that Big Pharma was targeting the medical market, with Wall Street, Silicon Valley, food businesses, and tobacco companies aiming at the recreational market.

Sellers are targeting broad swaths of the consumer market-soccer moms, recent retirees, folks looking to replace their nightly glass of chardonnay with a precisely dosed, low-calorie, and hangover-free mint. Many have consciously played up cannabis as a lifestyle product, a gift to give yourself, like a nice crystal or an antioxidant face cream. “This is not about marijuana,” one executive at the California retailer MedMen recently argued. “This is about the people who use cannabis for all the reasons people have used cannabis for hundreds of years. Yes for recreation, just like alcohol, but also for wellness.”

Evan started off smoking with his friends when they were playing sports or video games, lighting up to chill out after his nine-to-five as a paralegal at a law office. But that soon became couch-lock, and he lost interest in working out, going out, doing anything with his roommates. Then came a lack of motivation and the slow erosion of ambition, and law school moving further out of reach. He started smoking before work and after work. Eventually, he realized it was impossible to get through the day without it. “I was smoking anytime I had to do anything boring, and it took a long time before I realized that I wasn’t doing anything without getting stoned,” he said.

His first attempts to reduce his use went miserably, as the consequences on his health and his life piled up. He gained nearly 40 pounds, he said, when he stopped working out and cooking his own food at home. He recognized that he was just barely getting by at work, and was continually worried about getting fired. Worse, his friends were unsympathetic to the idea that he was struggling and needed help. “[You have to] try to convince someone that something that is hurting you is hurting you,” he said.

Other people who found their use problematic or had managed to quit, none of whom wanted to use their names, described similar struggles and consequences. “I was running two companies at the time, and fitting smoking in between running those companies. Then, we sold those companies and I had a whole lot of time on my hands,” one other former cannabis user told me. “I just started sitting around smoking all the time. And things just came to a halt. I was in terrible shape. I was depressed.”

Lax regulatory standards and aggressive commercialization in some states have compounded some existing public-health risks, raised new ones, and failed to tamp down on others, experts argue. In terms of compounding risks, many cite the availability of hyper-potent marijuana products. “We’re seeing these increases in the strength of cannabis, as we are also seeing an emergence of new types of products,” such as edibles, tinctures, vape pens, sublingual sprays, and concentrates, Ziva Cooper, an associate professor of clinical neurobiology in the Department of Psychiatry at Columbia University Medical Center, told me. “A lot of these concentrates can have up to 90 percent THC,” she said, whereas the kind of flower you could get 30 years ago was far, far weaker. Scientists are not sure how such high-octane products affect people’s bodies, she said, but worry that they might have more potential for raising tolerance, introducing brain damage, and inculcating dependence.

As for new risks: In many stores, budtenders are providing medical advice with no licensing or training whatsoever. “I’m most scared of the advice to smoke marijuana during pregnancy for cramps,” said Humphreys, arguing that sellers were providing recommendations with no scientific backing, good or bad, at all.

In terms of long-standing risks, the lack of federal involvement in legalization has meant that marijuana products are not being safety-tested like pharmaceuticals; measured and dosed like food products; subjected to agricultural-safety and pesticide standards like crops; and held to labelling standards like alcohol. (Different states have different rules and testing regimes, complicating things further.)

Health experts also cited an uncomfortable truth about allowing a vice product to be widely available, loosely regulated, and fully commercialized: Heavy users will make up a huge share of sales, with businesses wanting them to buy more and spend more and use more, despite any health consequences.

“The reckless way that we are legalizing marijuana so far is mind-boggling from a public-health perspective,” Kevin Sabet, an Obama administration official and a founder of the non-profit Smart Approaches to Marijuana, told me. “The issue now is that we have lobbyists, special interests, and people whose motivation is to make money that are writing all of these laws and taking control of the conversation.”

This is not to say that prohibition is a more attractive policy, or that legalization has proven a public-health disaster. “The big-picture view is that the vast majority of people who use cannabis are not going to be problematic users,” said Jolene Forman, an attorney at the Drug Policy Alliance. “They’re not going to have a cannabis-use disorder. They’re going to have a healthy relationship with it. And criminalization actually increases the harms related to cannabis, and so having like a strictly regulated market where there can be limits on advertising, where only adults can purchase cannabis, and where you’re going to get a wide variety of products makes sense.”

Still, strictly regulated might mean more strictly regulated than today, at least in some places, drug-policy experts argue. “Here, what we’ve done is we’ve copied the alcohol industry fully formed, and then on steroids with very minimal regulation,” Humphreys said. “The oversight boards of a number of states are the industry themselves. We’ve learned enough about capitalism to know that’s very dangerous.”

A number of policy reforms might tamp down on problem use and protect consumers, without quashing the legal market or pivoting back to prohibition and all its harms. One extreme option would be to require markets to be non-commercial: The District of Columbia, for instance, does not allow recreational sales, but does allow home cultivation and the gifting of marijuana products among adults. “If I got to pick a policy, that would probably be it,” Kleiman told me. “That would be a fine place to be if we were starting from prohibition, but we are starting from patchwork legalization. As the Vermont farmer says, I don’t think you can get there from here. I fear its time has passed. It’s generally true that the drug warriors have never missed an opportunity to miss an opportunity.”

There’s no shortage of other reasonable proposals, many already in place or under consideration in some states. The government could run marijuana stores, as in Canada. States could require budtenders to have some training or to refrain from making medical claims. They could ask users to set a monthly THC purchase cap and remain under it. They could cap the amount of THC in products, and bar producers from making edibles that are attractive to kids, like candies. A ban or limits on marijuana advertising are also options, as is requiring cannabis dispensaries to post public-health information.

Then, there are THC taxes, designed to hit heavy users the hardest. Some drug-policy experts argue that such levies would just push people from marijuana to alcohol, with dangerous health consequences. “It would be like saying, ‘Let’s let the beef and pork industries market and do whatever they wish, but let’s have much tougher restrictions on tofu and seitan,'” said Mason Tvert of the Marijuana Policy Project. “In light of the current system, where alcohol is so prevalent and is a more harmful substance, it is bad policy to steer people toward that.” Yet reducing the commercial appeal of all vice products-cigarettes, alcohol, marijuana-is an option, if not necessarily a popular one.

Perhaps most important might be reintroducing some reasonable skepticism about cannabis, especially until scientists have a better sense of the health effects of high-potency products, used frequently. Until then, listening to and believing the hundreds of thousands of users who argue marijuana is not always benign might be a good start.

Source:   20th August 2018

Researchers map out a cellular mechanism that offers a biological explanation for alcoholism, and could lead to treatments

Credit: Getty Images

You can lead a lab rat to sugar water, but you can’t make him drink—especially if there’s booze around.

New research published Thursday in Science may offer insights into why some humans who drink alcohol develop an addiction whereas most do not. After caffeine, alcohol is the most commonly consumed psychoactive substance in the world. For the majority of people the occasional happy hour beer or Bloody Mary brunch is where it stops. Yet we all know that others will drink compulsively, despite whatever consequence or darkness it brings.

The new research confirms earlier work showing this is true for rats; but it takes things a step further and supports a study design that could help scientists better understand addiction biology, and possibly develop more effective therapies for human addictive behaviors. Led by a team at Linköping University in Sweden, the researchers found that when given a choice between alcohol and a tastier, more biologically desirable sugar substitute, a subgroup of rats consistently preferred the alcohol. The authors further identified a specific brain region and molecular dysfunction most likely responsible for these addictive tendencies. They believe their findings and study design could be steps toward developing an effective pharmaceutical therapy for alcohol addiction, a kind of treatment that has eluded researchers for years.

A taste for sweetness is evolutionarily embedded in the mammalian brain; in the wild, sugar translates into fast calories and improved survival odds. For the new study, 32 rats were trained to sip a 20 percent alcohol solution for 10 weeks until it became habit. They were then presented with a daily choice between more alcohol or a solution of the noncaloric sweetener saccharine. (The artificial sweetener provides sugary-tasting enticement without the potential confounding variable of actual calories.) The majority of rats vastly preferred the faux sugar over the alcohol option.

But the fact that four rats—or 12.5 percent of the total—stuck with the alcohol was telling to senior author Markus Heilig, director of the Center for Social and Affective Neuroscience at Linköping, given the rate of alcohol misuse in humans is around 15 percent. So Heilig expanded the study. “There were four rats who went for alcohol despite the more natural reward of sweetness,” he says. “We built on that, and 600 animals later we found that a very stable proportion of the population chose alcohol.” What’s more, the “addicted” rats still chose alcohol even when it meant receiving an unpleasant foot shock.

To get a better sense of what was going on at a molecular level, Heilig and his colleagues analyzed which genes were expressed in the rodent subjects’ brains. The expression of one gene in particular—called GAT-3—was found to be greatly reduced in the brains of those who opted for alcohol rather than saccharine. GAT-3 codes for a protein that normally controls levels of a neurotransmitter called GABA, a common chemical in our brains and one known to be involved in alcohol dependence.

In collaboration with co-author and University of Texas at Austin research scientist Dayne Mayfield, Heilig’s team found that in brain samples from deceased humans who had suffered from alcohol addiction, GAT-3 levels were markedly lower in the amygdala—generally considered the brain’s emotional center. One might assume that any altered gene expression contributing to addictive behaviors would instead manifest in the brain’s reward circuitry—a network of centers involved in pleasurable responses to enticements like food, sex and gambling.

Yet the decrease in GAT-3 expression in both rats and humans was by far strongest in the amygdala. “Figuring out the reward circuitry has been a fantastic success story, but it’s probably of limited relevance to clinical addiction,” Heilig says. “The rewarding effect of drugs happens in everybody. It’s a completely different story in the minority of people who continue to take drugs despite adverse consequences.” He believes altered activity in the amygdala makes perfect sense, given that addiction—in both rats and humans—often brings with it negative emotions and anxiety.

Much previous addiction research has relied on models in which rodents learn to self-administer addictive substances, but without other options that could compete with drug use. It was French neuroscientist Serge Ahmed who recognized this as a major limitation to understanding addition biology given that, in reality, only a minority of humans develops addiction to a particular substance. By offering an alternative reward (that is, sweet water), his team showed only a minority of rats develop a harmful preference for drug use—a finding that has now been confirmed with several other commonly abused drugs.

Building on Ahmed’s concept, Heilig added the element of choice to his research. “You can’t determine the true reward of an addictive drug in isolation; it’s dependent on what other options are available—in our case a sugar substitute.” He says most models that have been used to study addiction, and to seek ways to treat it, were probably too limited in their design. “The availability of choice,” he adds, “is going to be fundamental to studying addiction and developing effective treatments for it.”

Paul Kenny, chair of neuroscience at Icahn School of Medicine at Mount Sinai, agrees. “In order to develop novel therapeutics for alcoholism it is critical to understand not just the actions of alcohol in the brain, but how those actions may differ between individuals who are vulnerable or resilient to the addictive properties of the drug,” he says. “This Herculean effort to impressively map out a cellular mechanism that likely contributes to alcohol dependence susceptibility will likely provide important new leads in the search for more effective therapeutics.” Kenny was not involved in the new research.

Heilig and his team believe they have already identified a promising addiction treatment based on their latest work,  and have teamed up with a pharmaceutical company in hopes of soon testing the compound in humans. The drug suppresses the release of GABA and thus could restore levels of the neurotransmitter to normal in people with a dangerous taste for alcohol. With any luck, one of civilization’s oldest  vices might soon loosen its grip.. Illumination.

Source:   June 21st 2018

The opioid crisis is unlike any drug epidemic America has ever known. It’s claiming lives at an almost unimaginable rate.

But to get an idea of why these drugs are taking such a toll, you have to look at the people who are dying.

This is not just the curse of the stereotypical addict.

Many of those admitted to the country’s fast swelling mortuaries were middle class professionals whose first fix was dealt to them by a doctor.

Back in the 90s and early 2000s, pharmaceutical firms began a major lobbying exercise, persuading doctors to prescribe their synthetic forms of heroin for pain relief.

Soon GPs across the country were handing out powerful prescriptions for relatively minor ailments.

The drugs worked, but they proved highly addictive and when patients’ prescriptions ran out, many took to the streets to feed what had fast become a habit.

That’s where the problem really starts. In pill form, this medication could be controlled, but by going to “street chemists” for their fix, people were taking a huge risk.

They’d buy the drugs, illegally imported from China, ready mixed with harmless powders. Just a few grains of opioid in each capsule, which they’d either snort, smoke or inject.

Most of the powders are phenomenally potent. One, Carfentanil, is said to be 10,000 times stronger than heroin.

Originally created as an elephant tranquiliser, a couple of grains could be enough to kill.

Others are less powerful but still deadly, and here’s the real issue – most addicts have no idea which kind of opioid they’re taking.

Yet across America people are seeking out dealers and buying this stuff for as little as two dollars per fix.

Some have reached a truly hopeless stage.

Ian Blackburn, a long-time addict, told me he’s never known anything like it. He’s felt in control of his drug habit in the past. Not any more.

“Three hits, that’s all it takes”, he told me: “You take this stuff three times and it’s forever”.

He explained how he doesn’t get a buzz from the drug any more, he simply takes it to feel normal, to take the pain of withdrawal away. Without it, his legs start to cramp, his stomach wrenches and he loses control of his functions.

“Every couple of hours you need a hit”, he says “no ifs ands or buts, you’re going to find it and you’re going to get money to get it, no matter what”.


September 2017

Submitted by Livia Edegger

Earlier this month Germany celebrated the results of the 2014 drug report which revealed a rapid decline in smoking, drinking and marijuana use among youth over the past ten years. Smoking among German teens aged 12 – 17 has halved in ten years (11.7%). Smoking rates have also dropped among 18 – 25 year olds, not as significantly though. Drinking rates have fallen from 17.9% in 2001 to 13.6% in 2012 among 12 – 17 year olds. In terms of gender differences, teenage boys are twice more likely to consume alcohol than their female counterparts. Little has changed among 18 – 25 year olds, the group that accounts for the highest alcohol consumption rate. Drinking in that age group was reported at 38.4% in 2012 which means it only dropped by a little over 1%. Cannabis ranks first among illicit drugs used with 5.6% of 12 – 17 year old teenagers using it compared to 9.2% in 2001. After years of steady consumption rates, cannabis use among 18 – 25 year olds is on the rise again and at 15.8% resembles figures of 2001.


23rd July 2014


Deaths from drug overdoses have jumped in nearly every county across the United States, driven largely by an explosion in addiction to prescription painkillers and heroin.

Some of the largest concentrations of overdose deaths were in Appalachia and the Southwest, according to new county-level estimates released by the Centers for Disease Control and Prevention.

The number of these deaths reached a new peak in 2014: 47,055 people, or the equivalent of about 125 Americans every day.

Deaths from overdoses are reaching levels similar to the H.I.V. epidemic at its peak.

The death rate from drug overdoses is climbing at a much faster pace than other causes of death, jumping to an average of 15 per 100,000 in 2014 from nine per 100,000 in 2003.

The trend is now similar to that of the human immunodeficiency virus, or H.I.V., epidemic in the late 1980s and early 1990s, said Robert Anderson, the C.D.C.’s chief of mortality statistics.

H.I.V. deaths rose in a shorter time frame, but their peak in 1995 is similar to the high point of deaths from drug overdoses reached in 2014, Mr. Anderson said. H.I.V., however, was mainly an urban problem. Drug overdoses cut across rural-urban boundaries.

In fact, death rates from overdoses in rural areas now outpace the rate in large metropolitan areas, which historically had higher rates.

Heroin abuse in states like New Hampshire make it a top campaign issue.

Drugs deaths have skyrocketed in New Hampshire. In 2014, 326 people died from an overdose of an opioid, a class of drugs that includes heroin and fentanyl, a painkiller 100 times as powerful as morphine.

Nationally, opioids were involved in more than 61 percent of deaths from overdoses in 2014. Deaths from heroin overdoses have more than tripled since 2010 and are double the rate of deaths from cocaine.

In New Hampshire, which holds this year’s first presidential primary, residents have repeatedly raised the issue of heroin addiction with visiting candidates.

“No group is immune to it — it is happening in our inner cities, rural and affluent communities,” said Timothy R. Rourke, the chairman of the New Hampshire Governor’s Commission on Alcohol and Drug Abuse.

Most of the deaths from overdose in the state are related to a version of fentanyl. “Dealers will lace heroin with it or sell pure fentanyl with the guise of being heroin,” Mr. Rourke said.  But fentanyl can be deadlier than heroin. It takes much more naloxone, a drug that reverses the effects of an opioid overdose, to revive someone who has overdosed on fentanyl.

Mr. Rourke said that high death rates in New Hampshire were symptomatic of a larger problem: The state is second to last, ahead of only Texas, in access to treatment programs. New Hampshire spends $8 per capita on treatment for substance abuse. Connecticut, for example, spends twice that amount.

Appalachia has been stricken with overdose deaths for more than a decade, in many ways because of prescription drug addiction among its workers.  West Virginia and neighboring states have many blue-collar workers, and “in that group, there’s just a lot of injuries,” said Dr. Carl R. Sullivan III, the director of addiction services at the West Virginia University School of Medicine.

“In the mid-1990s, there was a social movement that said it was unacceptable for patients to have chronic pain, and the pharmaceutical industry pushed the notion that opioids were safe,” he said.

A few years ago, as laws were passed to address the misuse of prescription painkillers, addicts began turning to heroin instead, he said. Because of a lack of workers needed to treat addicts, overdose deaths have continued to afflict states like West Virginia, which has the highest overdose death rate in the nation.

“Chances of getting treatment in West Virginia is ridiculously small,” Dr. Sullivan said. “We’ve had this uptick in overdose deaths despite enormous public interest in this whole issue.”

While New Mexico has avoided the national spotlight in the current wave of opioid addiction, it has had high death rates from heroin overdoses since the early 1990s.

Heroin addiction has been “passed down from generation to generation in small cities around New Mexico,” said Jennifer Weiss-Burke, executive director of Healing Addiction in Our Community, a non-profit group formed to curb heroin addiction. “I’ve heard stories of grandparents who have been heroin users for years, and it is passed down to younger generations; it’s almost like a way of life.”

Dr. Michael Landen, the state epidemiologist, said the state recently began grappling with prescription opioids. Addictions have shifted to younger people and to more affluent communities.

Ms. Weiss-Burke, whose son died from a heroin overdose in 2011, said it was much harder to treat young people. “Some young people are still having fun and they don’t have the desire to get sober, so they end up cycling through treatment or end up in jail,” she said.

Her center recently treated a 20-year-old man who was sober for five months before relapsing, then relapsed several more times after that.  “When you go right back to the same environment, it’s hard to stay clean,” she said. “Heroin craving continues to haunt a person for years.”

Source :


A pair of new studies has revealed that marijuana use could lead to abuse of other drugs and alcohol. Experts said that these risks need to be considered not only by doctors and patients but by policy makers as well particularly in states where marijuana is legalized for recreational or medical use.

For the first study, which was published in the journal Drug and Alcohol Dependence, the results showed that adults who smoke marijuana have five times increased odds of developing alcohol use disorder (AUD) compared with their counterparts who do not smoke.

By looking at the data of more than 27,000 adults, researchers found that the participants who did not have AUD but reported using cannabis during the first survey were 5.4 times more likely to have an AUD three years later.  The participants who already battle with an alcohol use disorder and were using marijuana were also found to aggravate their dependence on alcohol.

“Among adults with no history of AUD, cannabis use at Wave 1 was associated with increased incidence of an AUD three years later relative to no cannabis use,” study researcher Renee Goodwin, from Columbia University, and colleagues wrote. “Among adults with a history of AUD, cannabis use at Wave 1 was associated with increased likelihood of AUD persistence three years later relative to no cannabis use.”

The second study, which was published in JAMA Psychiatry and involved more than 34,000 subjects, revealed that participants who used cannabis during the first survey were about six times as likely to suffer from substance use disorder after three years.

Researchers also found an increased risk for drug use disorders and nicotine dependence among pot smokers.   Although the study authors said that their findings do not establish a cause and effect relationship between pot use and substance abuse, they noted that there may be an overlap in brain circuitry that influence drug use and dependence.

“Our study indicates that cannabis use is associated with increased prevalence and incidence of substance use disorders,” Carlos Blanco, from the National Institute on Drug Abuse, and colleagues wrote. “These adverse psychiatric outcomes should be taken under careful consideration in clinical care and policy planning.”

 Source:   22nd Feb 2016

During the late 1970s, my colleague, Dr. Herb Kleber, and I introduced a novel neuroanatomical model to explain the pathophysiology of opioid withdrawal and put forth our contention that addiction was not simply a matter of avoiding withdrawal. Using what was then a novel new drug, clonidine, we were able to effectively detox heroin and methadone addicts in half the time, and without the surge of norepinephrine release from the locus coeruleus. This minimized the agitation and somatic anxiety that can be unbearable for some patients.

This helped prove our conviction that addictive disease was the result of numerous and largely unknown factors, and not simply to avoid withdrawal. In spite of effectively and humanely withdrawing addicts from opioids, we also discovered that something was clearly different and unique about their brain and behavior. After being clean and sober for 6-8 months in a safe and secure rehab environment, most addicts returned to using heroin as soon as the door was unlocked. This looked like Pavlovian principles on steroids. Although it was not due to avoidance of withdrawal symptoms, the answer remained unclear.

In some ways, we have travelled light years in furthering our understanding of the brain and addictive disease. Yet, relapse remains the norm and not the exception for opioid addicts. The development and use of naltrexone in the 1990s followed by buprenorphine has helped many addicts achieve a better quality of life. Yet, relapse remains the norm.

In a recent placebo-controlled clinical trial by Kowalczyk, et al, participants were given (0.3 mg/d) of clonidine or placebo during 18 weeks of Medication-Assisted Treatment (MAT) with buprenorphine, and documented their mood and activities via a pre-programmed smart phone.

Study participants receiving clonidine in addition to buprenorphine had increased abstinence from opioids and were able to decouple their stress from drug craving. Additionally, participants in the buprenorphine-plus-clonidine group, not only experienced longer periods of abstinence, but were also better in managing, or coping with their “unstructured” time. In other words, clonidine helped persons deal with their boredom and inability to create or engage in healthy activities, which is a strong predictor of relapse.

Why Does This Matter?

The study replicates previous research demonstrating that 1.) unstructured time, especially during early recovery is a trigger and predictor of relapse, 2.) engaging in responsible or helpful activities is associated with better outcomes among patients receiving Medication-Assisted Treatment, and 3.) clonidine helped participants engage in unstructured-time activities with less risk of craving or use than they might otherwise have experienced.

From a personalized-medicine perspective, these data are a good reminder that addiction is a multifaceted disease requiring a multimodal approach. It is not treatable with any singular intervention. At best, psychopharmacology is adjunctive. And remember before any MAT, many addicted persons enjoyed sustained recovery via 12-step programs.

Source: November 2017

The use of buprenorphine and other Medically-Assisted Treatments (MAT) for opioid use disorder has increased rapidly in response to the opioid epidemic in the United States. From the clinician’s perspective, buprenorphine seemed like a panacea. I remember feeling the same way about methadone in the 70s and Naltrexone in the 80s.

Buprenorphine’s unique chemistry, being a partial agonist and antagonist medication, meant patients were able to detox from heroin or powerfully addictive prescription pain medications using Suboxone (a trade name for buprenorphine) and then taper off with relative ease, compared to heroin or oxycodone. In some cases, patients were not able to come off of Suboxone and remained on a small maintenance dose for months, and even years, but had attained a quality of life they never believed was possible when addicted to illicit opioids.

However, a large study by the Johns Hopkins Bloomberg School of Public Health (2017) reports that a significant proportion of patients on Suboxone therapy, or shortly after the conclusion of their therapy, were attaining and filling prescriptions for other opioid medications. Outcome measures matter. Different treatments work if your outcome measure is one month of adherence to the treatment versus five years of drug-free outcome and return to work.

The methodology in the Johns Hopkins study reviewed pharmacy claims for over 38,000 persons who had been prescribed Suboxone between 2006 and 2013. The results were shocking. Two-thirds of these patients had filled a prescription for an opioid painkiller in the first 12 months following Suboxone treatment—while 43 percent had received a prescription for an opioid during Suboxone therapy. In addition, approximately two-thirds of the patients who received Suboxone therapy stopped filling prescriptions for it after just three months.

What These Data Cannot Tell Us

At first glance these data are disappointing. Just looking at patient return to the program over a short time like six months, it is very clear that most methadone patients come back and many Suboxone patients do not. However, there is much the study results don’t tell us.

In a clinical and policy environment where the number of prescribers, the volume and nature of opioid prescriptions, overdoses, prescribing policies, laws and regulations are changing frequently and dramatically, data loses some of their value. In Florida, for example, the legislature, in response to the “Pill Mills,” enacted a monitoring program whereby all prescribed scheduled medications were on a single database, accessible by any licensed physician.

Twelve months after implementation, the outcomes were evaluated. Overall opioid prescriptions decreased by 1.4%. Opioid volume decreased by 2.5%, and a decrease of 5.6% in MME per transaction was observed. These data were limited to prescribers and patients with the highest baseline opioid prescribing and usage. The findings also accounted for potential confounding variables including sensitivity analyses, varying time windows and dynamic enrolment criteria. The opioid landscape in Florida continues to improve, and the pill mills are virtually gone. This is just one example of how a state’s policies impact the data and the outcome in longitudinal research.

In addition, prescription drug monitoring programs (PDMPs) are associated with reductions in all drug use (including opioids). Data culled from adult Medicare beneficiaries in states that utilize PDMPs compared with states that do not have PDMPs show significant reductions in prescription opioid transactions. Moreover, the top treatment centers may prescribe buprenorphine but also set up voluntary drug monitoring and continuing care programs for their patients, much as the programs do for impaired physicians, nurses and pilots who mandate random and for-cause drug testing for five years.

Most heroin addicts have multiple drug dependencies and problems. They also have multiple medical co-morbidities. It is not as simple as switching the patient’s heroin for buprenorphine. But street heroin is more than a drug, it is many drugs and dangerous adulterants. Over 80 percent of the Physician Health Program participants are treated effectively, monitored and never had a positive drug test throughout the five years of post-treatment outpatient monitoring.

Lastly, the Institute of Medicine released their exhaustive report on Pain in America, revealing that 100 million Americans currently suffer from chronic or intractable pain syndromes. The Johns Hopkins study does not indicate what percent of the study participants have a pain syndrome, requiring treatment with opioid medication, hopefully under the supervision of a specialist in pain managements and addiction medicine.

Why Does This Matter?

The findings certainly raise questions about the effectiveness and the appropriateness of Suboxone for addiction treatment. Clearly, if we were to adopt an oncology standard of five years, Suboxone is not likely to be considered an effective treatment. But it is a viable and important option and part of an arsenal of treatment modalities used to individualize treatment for our patients.

The study researchers noted, and I agree, that the continued use of pain medication during and after addiction treatment indicates that too many patients did not receive a multimodal, integrated treatment plan for their addiction or concurrent chronic pain or co-occurring mental illness, which approximately 50-65% of those with Substance Use Disorder (SUD) have.

Dr. Alexander, the lead author of the study noted: “There are high rates of chronic pain among patients receiving opioid agonist therapy, and thus concomitant use of buprenorphine and other opioids may be justified clinically. This is especially true as the absence of pain management among patients with opioid use disorders may result in problematic behaviors such as illicit drug use and misuse of other prescription medications.”

Addicts are quick to discover the probabilities of attaining a “high” from just about any drug they come across. Buprenorphine, while not commonly abused or sold on the streets, can be used to get high or to ease the pangs of withdrawal when heroin and other opioids are scarce.

The efficacy of treatment for SUD, regardless of the drug, is largely dependent upon non-medical factors. Yes, monitoring is important, but only if the potential for losing something one values is at stake. Surrendering, which cannot be described in medical or psychological language, is the single most important factor in determining recovery. Adjunctive treatments such as Suboxone, Methadone, N.A., A.A., CBT, yoga, meditation, diet and exercise can help a highly motivated individual. When treatment is

individualized and a bond of trust is established between a counselor and patient, good and even improbable things happen, and lives are restored.

MATs are not a replacement for the traditional foundations of treatment and recovery. At best, they can provide a specific need for a specific patient. They are not for everyone. When people ask me what the elements of success are in treatment, I often start with long-term. If a person has been abusing and addicted for years, it is difficult to imagine treatment in weeks. But, as a shortcut to what works, I tell them the 3 M’s: treatment that is high-dose, intense multimodal, multidisciplinary and multifaceted, staffed by dedicated professionals who are experienced and really do care about the patients.

Suboxone and the similar medications that will be developed are inherently not good or bad and certainly don’t work for every opioid addict. But I am thankful we have them. I believe they have saved thousands of lives. The real trick of successful treatment is to know your patients and collaborate with him or her in developing a plan that gives them the best shot at recovery.

Source: Author: Mark Gold, MD

Pain and pleasure rank among nature’s strongest motivators, but when mixed, the two can become irresistible. This is how opioids brew a potent and deadly addiction in the brain. Societies have coveted the euphoria and pain relief provided by opioids since Ancient Sumerians referred to opium poppies as the “joy plant” circa 3400 B.C. But the repercussions of using the drugs were ever present, too. For centuries, Chinese patients swallowed opium cocktails before major surgeries, but by 1500, they described the recreational use of opium pipes as subversive. The Chinese emperor Yung Cheng eventually restricted the use of opium for medical purposes in 1729. Less than 100 years later, a German chemist purified morphine from poppies, creating the go-to pain reliever for anxiety and respiratory conditions. But the Civil War and its many wounds spawned mass addiction to the drugs, a syndrome dubbed Soldier’s Disease. A cough syrup was concocted in the late 1800s — called heroin — to remedy these morphine addictions. Doctors thought the syrup would be “non-addictive.” Instead, it turned into a low-cost habit that spread internationally. More than 70 percent of the world’s opium — 3,410 tons — goes to heroin production, a number that has more than doubled since 1985. Approximately 17 million people around the globe used heroin, opium or morphine in 2016.

Today, prescription and synthetic opioids crowd America’s medicine cabinets and streets, driving a modern crisis that may kill half a million people over the next decade. Opioids claimed 53,000 lives in the U.S. last year, according to preliminary estimates from the Centers for Disease Control and Prevention — more than those killed in motor vehicle accidents.

How did we arrive here? Here’s a look at why our brains get hooked on opioids.

The pain divide

Let’s start with the two types of pain. They go by different names depending on which scientist you ask. Peripheral versus central pain. Nociceptive versus neuropathic pain.

The distinction is the sensation of actual damage to your body versus your mind’s perception of this injury.

Your body quiets your pain nerves through the production of natural opioids called endorphins.

Stuff that damages your skin and muscles — pin pricks and stove burns — is considered peripheral/nociceptive pain.

Pain fibers sense these injuries and pass the signal onto nerve cells — or neurons — in your spine and brain, the duo that makes up your central nervous system.

In a normal situation, your pain fibers work in concert with your central nervous system. Someone punches you, and your brain thinks “ow” and tells your body how to react.

Stress-relieving hormones get released. Your immune system counteracts the inflammation in your wounded arm.

Your body quiets your pain nerves through the production of natural opioids called endorphins. The trouble is when these pain pathways become overloaded or uncoupled.

One receptor to rule them all

Say you have chronic back pain. Your muscles are inflamed, constantly beaming pain signals to your brain. Your natural endorphins aren’t enough and your back won’t let up, so your doctor prescribes an opioid painkiller like oxycodone.

Prescription opioids and natural endorphins both land on tiny docking stations — called receptors — at the ends of your nerves. Most receptors catch chemical messengers — called neurotransmitters — to activate your nerve cells, triggering electric pulses that carry the signal forward.

But opioid receptors do the opposite. They stop electric pulses from traveling through your nerve cells in the first place. To do this, opioids bind to three major receptors, called Mu, Kappa and Delta. But the Mu receptor is the one that really sets everything in motion.

The Mu-opiate receptor is responsible for the major effects of all opiates, whether it’s heroin, prescription pills like oxycodone or synthetic opioids like fentanyl, said Chris Evans, director of Brain Research Institute at UCLA. “The depression, the analgesia [pain numbing], the constipation and the euphoria — if you take away the Mu-opioid receptor, and you give morphine, then you don’t have any of those effects,” Evans said.

Opioids receptors trigger such widespread effects because they govern more than just pain pathways. When opioid drugs infiltrate a part of the brain stem called the locus ceruleus, their receptors slow respiration, cause constipation, lower blood pressure and decrease alertness. Addiction begins in the midbrain, where opioids receptors switch off a batch of nerve cells called GABAergic neurons.

GABAergic neurons are themselves an off-switch for the brain’s euphoria and pleasure networks.

When it comes to addiction, opioids are an off-switch for an off-switch. Opioids hold back GABAergic neurons in the midbrain, which in turn keep another neurotransmitter called dopamine from flooding a brain’s pleasure circuits. Image by Adam Sarraf

Once opioids shut off GABAergic neurons, the pleasure circuits fill with another neurotransmitter called dopamine. At one stop on this pleasure highway — the nucleus accumbens — dopamine triggers a surge of happiness. When the dopamine rolls into amygdala, the brain’s fear center, it relieves anxiety and stress. Both of these events reinforce the idea that opioids are rewarding.

These areas of the brain are constantly communicating with decision-making hubs in the prefrontal cortex, which make value judgments about good and bad. When it hears “This pill feels good. Let’s do more,” the mind begins to develop habits and cravings.

Taking the drug soon becomes second nature or habitual, Evans said, much like when your mind zones out while driving home from work. The decision to seek out the drugs, rather than participate in other life activities, becomes automatic.

The opioid pendulum: When feeling good starts to feel bad

Opioid addiction becomes entrenched after a person’s neurons adapt to the drugs. The GABAergic neurons and other nerves in the brain still want to send messages, so they begin to adjust. They produce three to four times more cyclic AMP, a compound that primes the neuron to fire electric pulses, said Thomas Kosten, director of the division of alcohol and addiction psychiatry at the Baylor College of Medicine.

That means even when you take away the opioids, Kosten says, “the neurons fire extensively.”

The pendulum swings back. Now, rather than causing constipation and slowing respiration, the brain stem triggers diarrhoea and elevates blood pressure. Instead of triggering happiness, the nucleus accumbens and amygdala reinforce feelings of dysphoria and anxiety. All of this negativity feeds into the prefrontal cortex, further pushing a desire for opioids.

While other drugs like cocaine and alcohol can also feed addiction through the brain’s pleasure circuits, it is the surge of withdrawal from opioids that makes the drugs so inescapable.

Could opioid addiction be driven in part by people’s moods?

Cathy Cahill, a pain and addiction researcher at UCLA, said these big swings in emotions likely factor into the learned behaviors of opioid addiction, especially with those with chronic pain. A person with opioid use disorder becomes preoccupied with the search for the drugs. Certain contexts become triggers for their cravings, and those triggers start overlapping in their minds.

“The basic view is some people start with the pain trigger [the chronic back problem], but it gets partially substituted with the negative reinforcement of the opioid withdrawal,” Cahill said.

That’s why Cahill, Evans and other scientists think the opioid addiction epidemic might be driven, in part, by our moods.

Chronic pain patients have a very high risk of becoming addicted to opioids if they are also coping with a mood disorder. A 2017 study found most patients — 81 percent — whose addiction started with a chronic pain problem also had a mental health disorder. Another study found patients on morphine experience 40 percent less pain relief from the drug if they have mood disorder. They need more drugs to get the same benefits.

People with mood disorders alone are also more likely to abuse opioids. A 2012 survey found patients with depression were twice as likely to misuse their opioid medications.

“So, not only does a mood disorder affect a person’s addiction potential, but it also influences if the opioids will successfully treat their pain,” Cahill said.

Meanwhile, the country is living through sad times. Some research suggests social isolation is on the rise. While the opioid epidemic started long before the recession, job loss has been linked to a higher likelihood of addiction, with every 1 percent increase in unemployment linked to a 3.6 percent rise in the opioid-death rate.

Can the brain swing back?

As an opioid disorder progresses, a person needs a higher quantity of the drugs to keep withdrawal at bay. A person typically overdoses when they take so much of the drug that the brain stem slows breathing until it stops, Kosten said.

Many physicians have turned to opioid replacement therapy, a technique that swaps highly potent and addictive drugs like heroin with compounds like methadone or buprenorphine (an ingredient in Suboxone).

These substitutes outcompete heroin when they reach the opioid receptors, but do not activate the receptors to the same degree. By doing so, they reduce a person’s chances for overdosing. These replacement medications also stick to the receptors for a longer period of time, which curtails withdrawal symptoms. Buprenorphine, for instance, binds to a receptor for 80 minutes while morphine only hangs on for a few milliseconds.

For some, this solution is not perfect. The patients need to remain on the replacements for the foreseeable future, and some recovery communities are divided over whether treating opioids with more opioids can solve the crisis. Plus, opioid replacement therapy does not work for fentanyl, the synthetic opioid that now kills more Americans than heroin. Kosten’s lab is one of many working on a opioid vaccine that would direct a person’s immune system to clear drugs like fentanyl before they can enter the brain. But those are years away from use in humans.

And Evans and Cahill said many clinics in Southern California are combining psychological therapy with opioid replacement prescriptions to combat the mood aspects of the epidemic.

“I don’t think there’s going to be a magic bullet on this one,” Evans said. “It’s really an issue of looking after society and looking after of people’s psyches rather than just treatment.


Legalizing opioids may give Americans greater freedom over their decision-making, but at what cost? One painful aspect of the public debates over the opioid-addiction crisis is how much they mirror the arguments that arise from personal addiction crises.

If you’ve ever had a loved one struggle with drugs — in my case, my late brother, Josh — the national exercise in guilt-driven blame-shifting and finger-pointing, combined with flights of sanctimony and ideological righteousness, has a familiar echo. The difference between the public arguing and the personal agonizing is that, at the national level, we can afford our abstractions.

When you have skin in the game, none of the easy answers seem all that easy. For instance, “tough love” sounds great until you contemplate the possible real-world consequences. My father summarized the dilemma well. “Tough love” — i.e., cutting off all support for my brother so he could hit rock bottom and then start over — had the best chance of success. It also had the best chance for failure — i.e., death. There’s also a lot of truth to “just say no,” but once someone has already said “yes,” it’s tantamount to preaching “keep your horses in the barn” long after they’ve left.

But if there’s one seemingly simple answer that has been fully discredited by the opioid crisis, it’s that the solution lies in wholesale drug legalization. In Libertarianism: A Primer, David Boaz argues that “if drugs were produced by reputable firms, and sold in liquor stores, fewer people would die from overdoses and tainted drugs, and fewer people would be the victims of prohibition-related robberies, muggings and drive-by-shootings.”

Maybe. But you know what else would happen if we legalized heroin and opioids? More people would use heroin and opioids. And the more people who use such addictive drugs, the more addicts you get. Think of the opioid crisis as the fruit of partial legalization. In the 1990s, for good reasons and bad, the medical profession, policymakers, and the pharmaceutical industry made it much easier to obtain opioids in order to confront an alleged pain epidemic. Doctors prescribed more opioids, and government subsidies made them more affordable. Because they were prescribed by doctors and came in pill form, the stigma reserved for heroin didn’t exist. When you increase supply, lower costs, and reduce stigma, you increase use.

And guess what? Increased use equals more addicts. A survey by the Washington Post and the Kaiser Family Foundation found that one-third of the people who were prescribed opioids for more than two months became addicted. A Centers for Disease Control study found that a very small number of people exposed to opioids are likely to become addicted after a single use. The overdose crisis is largely driven by the fact that once addicted to legal opioids, people seek out illegal ones — heroin, for example — to fend off the agony of withdrawal once they can’t get, or afford, any more pills. Last year, 64,000 Americans died from overdoses. Some 58,000 Americans died in the Vietnam War.

Experts rightly point out that a large share of opioid addiction stems not from prescribed use but from people selling the drugs secondhand on the black market, or from teenagers stealing them from their parents. That’s important, but it doesn’t help the argument for legalization. Because the point remains: When these drugs become more widely available, more people avail themselves of them. How would stacking heroin or OxyContin next to the Jim Beam lower the availability? Liquor companies advertise — a lot. Would we let, say, Pfizer run ads for their brand of heroin? At least it might cut down on the Viagra commercials. I think it’s probably true that legalization would reduce crime, insofar as some violent illegal drug dealers would be driven out of the business.

I’m less sure that legalization would curtail crimes committed by addicts in order to feed their habits. As a rule, addiction is not conducive to sustained gainful employment, and addicts are just as capable of stealing and prostitution to pay for legal drugs as illegal ones. The fundamental assumption behind legalization is that people are rational actors and can make their own decisions. As a general proposition, I believe that. But what people forget is that drug addiction makes people irrational. If you think more addicts are worth it in the name of freedom, fine. Just be prepared to accept that the costs of such freedom are felt very close to home.



St. Petersburg, FL – Thursday, August 31, 2017 – Drug Free America Foundation today introduced a first-of-its-kind Opioid Tool Kit in an effort to help address the opioid epidemic gripping the United States.

The Opioid Tool Kit was unveiled in conjunction with International Overdose Awareness Day, a global event held on August 31st each year that aims to raise the awareness of the problem of drug overdose-related deaths.

“With more than 142 people dying each day, drug overdoses are now the leading cause of death for Americans under the age of 50,” according to Calvina Fay, Executive Director of Drug Free America Foundation. “Moreover, deaths from drug overdose are an equal opportunity killer, with no regard to race, religion or economic class,” she said.

“While alcohol and marijuana still remain the most common drugs of abuse, the nonmedical use of prescription painkillers and other opioids has resulted in a crisis-level spike in drug overdose deaths,” said Fay.

The Opioid Tool Kit has been designed to educate people about the opioid epidemic and offer strategies that can be used to address this crisis. “The Tool Kit is also intended to encourage collaboration with different community sectors and stakeholders to make successful and lasting change,” Fay continued.

The Opioid Tool Kit is a comprehensive guide that defines what an opioid is, examines the scope of the problem, and addresses why opioids are a continuing health problem.  The Tool Kit also provides strategies for the prevention of prescription drug misuse and overdose deaths and includes a community advocacy and action plan, as well as additional resources.

Fay emphasized that the best way to prevent opioid and other drug addiction is not to abuse drugs in the first place.  “The chilling reality is that the long-term use and abuse of opioids and other addictive drugs rewire the brain, making recovery a difficult and often a life-long struggle,” she concluded. The Opioid Tool Kit can be found on Drug Free America Foundation’s website at

Source:  August 2017

Just a few miles from where President Trump will address his blue-collar base here Tuesday night, exactly the kind of middle-class factory jobs he has vowed to bring back from overseas are going begging.

It’s not that local workers lack the skills for these positions, many of which do not even require a high school diploma but pay $15 to $25 an hour and offer full benefits. Rather, the problem is that too many applicants — nearly half, in some cases — fail a drug test.

The fallout is not limited to the workers or their immediate families. Each quarter, Columbiana Boiler, a local company, forgoes roughly $200,000 worth of orders for its galvanized containers and kettles because of the manpower shortage, it says, with foreign rivals picking up the slack.

“Our main competitor in Germany can get things done more quickly because they have a better labor pool,” said Michael J. Sherwin, chief executive of the 123-year-old manufacturer. “We are always looking for people and have standard ads at all times, but at least 25 percent fail the drug tests.”


Filed under: Addiction,Economic,USA :

In his last article for Pro Talk, Renaming and Rethinking Drug Treatment, psychologist Robert Schwebel, Ph.D., author and developer of The Seven Challenges program, expressed his views about problems in typical drug and alcohol treatment. In this interview, he focuses on changes that he thinks would better meet the needs of individuals with substance problems.

The Seven Challenges Program

The Seven Challenges is described as “a comprehensive counselling program for teens and young adults that incorporates work on alcohol and other drug problems.” The program addresses much more than substance issues because it also helps young people develop better life skills, as well as manage their situational and psychological problems. Although there is an established structure for each session and a framework for decision-making (see website for the youth version of “The Seven Challenges”), it is not pre-scripted as in many traditional programs. Rather it is “exceptionally flexible, in response to the immediate needs of the clients.”

Independent studies funded by The Center for Substance Abuse Treatment and published in peer-reviewed journals have provided evidence that The Seven Challenges significantly decreases substance use of adolescents and greatly improves their overall mental health status. The program has been shown to be especially effective for the many young people with drug problems who also have trauma issues.

Just recently, a new version of The Seven Challenges program was introduced for adults and is being piloted in a research project. Soon, a book geared toward the general public by Dr. Schwebel that incorporates much of the philosophy of the program, as well as many of the decision-making and behavior change strategies, will be available.

Q&A: What Should Treatment Look Like?

Q: In your last article for Pro Talk, you argued strongly against the word “treatment” and suggested that we use the word “counselling” instead. Will you reiterate why you prefer using “counselling” when talking about professional help for people with substance problems?

Dr. S.: Counselling is an active and interactive process that’s responsive to the needs of individuals. It may include education, but it’s more than that because the information is personalized and offered in the context of a discussion about what’s happening in a person’s life. Effective counsellors help clients become aware of their options, expand those options, and make their own informed choices.

Treatment, on the other hand, sounds like something imposed and passive that an authority (say a doctor) does to someone else or tells them to do. It also implies recipients receive a standardized protocol or regime with a preconceived goal, usually abstinence when we’re talking about addiction. It doesn’t suggest autonomy of choice or collaboration.


Q: You stress the importance of choice and collaboration, suggesting both are important in addiction counselling. Please tell us more.

Dr. S.: In collaborative counselling that allows choices, clients get to identify the issues they want to work on. They make the decisions. We make it clear that we’re not there to make them quit using drugs…and couldn’t even if we tried. We tell them, “We’re here to support you in working on your issues, things that are important to you; things that are not going well in your life or as well you would like them to be going.”

We also support clients in decision-making about drugs. They set their own goals about using. One person might want to quit using, while another might want to set new limits. For those who want to change their drug use behavior, we check in with them about how they’re doing regarding their decision on a session-by-session basis. If they have setbacks, we’ll provide individualized support to help them figure out why, We’re not doubting them or trying to “catch” them. Rather, we’re helping them succeed with their own decisions to change. This type of check-in would not apply to individuals who have not yet decided to make changes.


Q: Many addiction programs feel that dealing with addiction should be the first priority and that other issues are secondary. What are your thoughts about this?

Dr. S.: I’ll start by saying that they have equal importance. Drug problems have everything to do with what is going on in a person’s life. And, a person’s life is very much affected by drug problems. I do want to say, however, that not everyone who winds up in an addiction program has an addiction. That’s a ridiculous generalization. They may be having problems with binge drinking, issues with family or jobs because of substance misuse, or legal problems because they were unlucky and got caught. (For instance they got arrested for another crime and tested positive for drugs.) They often wind up in places that require abstinence and wonder, “What am I doing here?” Then they’re told they’re “in denial.”

Traditional treatment tends to focus narrowly on drug problems, usually pushing an agenda of immediate abstinence. However, drug problems – whether or not they qualify as “addiction,” are very much connected to the rest of life. Therefore, clients need comprehensive counselling that addresses what’s happening in their overall lives and helps clients make their lives better. So it’s not all about use of substances and making the individual quit. The goal is to support clients and to help them make their own decisions about life and substance use.

We use the term “issues” – not “problems.” Whatever is most important to the individual that day is what we work on. A client might say, “I have an issue with my mother.” We don’t just want to have a discussion about the issue; we want to set a session goal so that a client gets practical help with an issue each time. Ideally we try to facilitate a next step, some sort of action that can be taken between sessions. We want to support our clients in making their own lives better. We like to reassure clients that we won’t be harping on drugs all the time: At least half of what we do is about everything else besides drugs. This means that counsellors need to know how to help people with their other problems. Unfortunately, many have a narrow background in drug treatment and don’t yet know how to do that.


Q: How do you address the issue of “powerlessness” which a number of young people have told me they struggled with in12-step treatment programs they’ve attended? Don’t adolescents by nature resist anything that threatens to take away their autonomy?

Dr. S.: One of our main messages is “You are powerful; people do take control over their drug use. You have that power within you.” We also say, “You don’t need to do it alone. You are entitled to support. We’re behind you. We’re not saying it’s easy and

there won’t be setbacks along the way. If there are, we’ll help you figure out why and how to handle it differently the next time. At the same time we’ll help you with other issues in your life so you’ll have less need for drugs.”

I think there is great harm in the all-or-nothing approach to drug and alcohol problems and that more people would come for help if they were not told that they’re powerless. Also, many more would come if they felt they could make a choice about drugs and did not expect to be coerced.


A New Version of The Seven Challenges

Following is the new adult version of Dr. Schwebel’s The Seven Challenges program:

· Challenging Yourself to Make Thoughtful Decisions About Your Life, Including Your Use of Alcohol and Other Drugs

· Challenging Yourself to Look at Your Responsibility and the Responsibility of Others for Your Problems

· Challenging Yourself to Look at What You Like About Alcohol and Other Drugs, and Why You Use Them

· Challenging Yourself to Honestly Look at Your Life, Including Your Use of Alcohol and Other Drugs

· Challenging Yourself to Look at Harm That Has Happened or Could Happen From Your Use of Alcohol and Other Drugs

· Challenging Yourself to Look at Where You Are Headed, Where You Would Like to Go, and What You Would Like to Accomplish

· Challenging Yourself to Take Action and Succeed With Your Decisions About Your Life and Use of Alcohol and Other Drugs

Source:     17th July 2017

Medication-assisted treatment is often called the gold standard of addiction care. But much of the country has resisted it.

If you ask Jordan Hansen why he changed his mind on medication-assisted treatment for opioid addiction, this is the bottom line.

Several years ago, Hansen was against the form of treatment. If you asked him back then what he thought about it, he would have told you that it’s ineffective — and even harmful — for drug users. Like other critics, to Hansen, medication-assisted treatment was nothing more than substituting one drug (say, heroin) with another (methadone).

Today, not only does Hansen think this form of treatment is effective, but he readily argues — as the scientific evidence overwhelmingly shows — that it’s the best form of treatment for opioid addiction. He believes this so strongly, in fact, that he now often leads training sessions for medication-assisted treatment across the country.

“It almost hurts to say it out loud now, but it’s the truth,” Hansen told me, describing his previous beliefs. “I was kind of absorbing the collective fear and ignorance from the culture at large within the recovery community.” Hansen is far from alone. Over the past few years, America’s harrowing opioid epidemic — now the deadliest drug overdose crisis in the country’s history — has led to a lot of rethinking about how to deal with addiction. For addiction treatment providers, that’s led to new debates about the merits of the abstinence-only model — many of which essentially consider addiction a failure of willpower — so long supported in the US.

The case for prescription heroin

The Hazelden Betty Ford Foundation, which Hansen works for, exemplifies the debate. As one of the top drug treatment providers in the country, it used to subscribe almost exclusively to the abstinence-only model, based on an interpretation of the 12 steps of Alcoholics Anonymous and Narcotics Anonymous popularized in American addiction treatment in the past several decades. But in 2012, Hazelden announced a big switch: It would provide medication-assisted treatment.

“This is a huge shift for our culture and organization,” Marvin Seppala, chief medical officer of Hazelden, said at the time. “We believe it’s the responsible thing to do.”

From the outside, this might seem like a bizarre debate: Okay, so addiction treatment providers are supporting a form of treatment that has a lot of evidence behind it. So what?

But the growing embrace of medication-assisted treatment is demonstrative of how the opioid epidemic is forcing the country to take another look at its inadequate drug treatment system. With so many people dying from drug overdoses — tens of thousands a year — and hundreds of thousands more expected to die in the next decade, America is finally considering how its response to addiction can be better rooted in science instead of the moralistic stigmatization that’s existed for so long.

The problem is that the moralistic stigmatization is still fairly entrenched in how the US thinks about addiction. But the embrace of medication-assisted treatment shows that may be finally changing — and America may be finally looking at addiction as a medical condition instead of a moral failure.

The research is clear: Medication-assisted treatment works

One of the reasons opioid addiction is so powerful is that users feel like they must keep using the drugs in order to stave off withdrawal. Once a person’s body grows used to opioids but doesn’t get enough of the drugs to satisfy what it’s used to, withdrawal can pop up, causing, among other symptoms, severe nausea and full-body aches. So to avoid suffering through it, drug users often seek out drugs like heroin and opioid painkillers — not necessarily to get a euphoric high, but to feel normal and avoid withdrawal. (In the heroin world, this is often referred to as “getting straight.”)

Medications like methadone and buprenorphine (also known as Suboxone) can stop this cycle. Since they are opioids themselves, they can fulfil a person’s cravings and stop withdrawal symptoms. The key is that they do this in a safe medical setting, and when taken as prescribed do not produce the euphoric high that opioids do when they are misused. By doing this, an opioid user significantly reduces the risk of relapse, since he doesn’t have to worry about avoiding withdrawal anymore. Users can take this for the rest of their lives, or in some cases, doses may be reduced; it varies from patient to patient.

The research backs this up: Various studies, including systemic reviews of the research, have found that medication-assisted treatment can cut the all-cause mortality rate among addiction patients by half or more. Just imagine if a medication came out for any other disease — and, yes, health experts consider addiction a disease — that cuts mortality by half; it would be a momentous discovery.

“That is shown repeatedly,” Maia Szalavitz, a long time addiction journalist and author of Unbroken Brain: A Revolutionary New Way of Understanding Addiction, told me. “There’s so much data from so many different places that if you add methadone or Suboxone in, deaths go down, and if you take it away, deaths go up.” That’s why the biggest public health organizations — including the Centers for Disease Control and Prevention, the National Institute on Drug Abuse, and the World Health Organization — all acknowledge medication-assisted treatment’s medical value. And experts often describe it to me as “the gold standard” for opioid addiction care.

The data is what drove Hansen’s change in perspective. “If I wanted to view myself as an ethical practitioner and doing the best that I could for the people I served, I needed to make this change based on the overwhelming evidence,” he said. “And I needed to separate that from my personal recovery experience.”

Medication-assisted treatment is different from traditional forms of dealing with addiction in America, which tend to demand abstinence. The standards in this field are 12-step programs, which combine spiritual and moralistic ideals into a support group for people suffering from addiction. While some 12-step programs allow medication-assisted treatment, others prohibit it as part of their demand for total abstinence. The research shows this is a particularly bad idea for opioids, for which medications are considered the standard of care.

There are different kinds of medications for opioids, which will work better or worse depending on a patient’s circumstances. Methadone, for example, is only administered in a clinic, typically one to four times a day — but that means patients will have to make the trip to a clinic on a fairly regular basis. Buprenorphine is a take-home drug that’s taken once or twice a day, but the at-home access also means it might be easier to misuse and divert to the black market.

One rising medication, known as naltrexone or its brand name Vivitrol, isn’t an opioid — making it less prone to misuse — and only needs to be injected once a month. But it doesn’t work in the same way as methadone or buprenorphine. It requires full detoxification to use (usually three to 10 days of no opioid use), while buprenorphine, for example, only requires a partial detoxification process (usually 12 hours to two days). And instead of preventing withdrawal — indeed, the detox process requires going through withdrawal — it blocks the effects of opioids up to certain doses, making it much harder to get high or overdose on the drugs. It’s also relatively new, so there’s less evidence for its real-world effectiveness.

One catch is that even these medications, though the best forms of opioid treatment, do not work for as much as 40 percent of opioid users. Some patients may prefer not to take any medications because they see any drug use whatsoever as getting in the way of their recovery, in which case total abstinence may be the right answer for them. Others may not respond well physically to the medications, or the medications may for whatever reason fail to keep them from misusing drugs.

This isn’t atypical in medicine. What works for some people, even the majority, isn’t always going to work for everyone. So these are really first-line treatments, but in some cases patients may need alternative therapies if medication-assisted treatment doesn’t work. (That might even involve prescription heroin — which, while it’s perhaps counterintuitive, the research shows it works to mitigate the problems of addiction when provided in tightly controlled, supervised medical settings.)

Medication can also be paired with other kinds of treatment to better results. It can be used in tandem with cognitive behavioral therapy or similar approaches, which teach drug users how to deal with problems or settings that can lead to relapse. All of that can also be paired with 12-step programs like AA and NA or other support groups in which people work together and hold each other accountable in the fight against addiction. It all varies from patient to patient.

It is substituting one drug for another, but that’s okay

The main criticism of medication-assisted treatment is that it’s merely replacing one drug with another. Health and Human Services Secretary Tom Price recently echoed this criticism, saying, “If we’re just substituting one opioid for another, we’re not moving the dial much. Folks need to be cured so they can be productive members of society and realize their dreams.” (A spokesperson for Price later walked back the statement, saying Price supports all kinds of drug treatment.)

On its face, this argument is true. Medication-assisted treatment is replacing one drug, whether it’s opioid painkillers or heroin, with another, such as methadone or buprenorphine.

But this isn’t by itself a bad thing. Under the Diagnostic and Statistical Manual of Mental Disorders, it’s not enough for someone to be using or even physically dependent on drugs to qualify for a substance use disorder, the technical name for addiction. After all, most US adults use drugs — some every day or multiple times a day — without any problems whatsoever. Just think about that next time you sip a beer, glass of wine, coffee, tea, or any other beverage with alcohol or caffeine in it, or any time you use a drug to treat a medical condition.

The qualification for a substance use disorder is that someone is using drugs in a dangerous or risky manner, putting himself or others in danger. So someone with a substance use disorder would not just be using opioids but potentially using these drugs in a way that puts him in danger — perhaps by feeling the need to commit crimes to obtain the drugs or using the drugs so much that he puts himself at risk of overdose and inhibits his day-to-day functioning. Basically, the drug use has to hinder someone from being a healthy, functioning member of society to qualify as addiction.

The key with medication-assisted treatment is that while it does involve continued drug use, it turns that drug use into a much safer habit. So instead of stealing to get heroin or using painkillers so much that he puts his life at risk, a patient on medication-assisted treatment can simply use methadone or buprenorphine to meet his physical cravings and otherwise go about his day — going to school, work, or any other obligations.

Yet this myth of the dangers of medication-assisted treatment remains prevalent — to deadly results.

In 2013, Judge Frank Gulotta Jr. in New York ordered an opioid user arrested for drugs, Robert Lepolszki, off methadone treatment, which he began after his arrest. In January 2014, Lepolszki died of a drug overdose at 28 years old — a direct result, Lepolszki’s parents say, of failing to get the medicine he needed. In his defense,  Gulotta has continued to argue that methadone programs “are crutches — they are substitutes for drugs and drug cravings without enabling the participant to actually rid him or herself of the addiction.”

This is just one case, but it shows the real risk of denying opioid users medication: It can literally get them killed by depriving them of lifesaving medical care.

The myth is also a big reason why there are still restrictions on medication-assisted treatment. For example, the federal government still caps how many patients doctors can prescribe buprenorphine to, with strict rules about raising the cap. This limits how accessible the treatment is. A Huff Post analysis found that even if every doctor who can prescribe buprenorphine did so at the maximum rate in 2012, more than half of Americans with opioid use disorders could not get the medication. That’s on top of barriers to addiction treatment in general. According to a 2016 report by the surgeon general, just 10 percent of Americans with a drug use disorder obtain specialty treatment. The report attributed the low rate to severe shortages in the supply of care, with some areas of the country, particularly rural counties, lacking affordable options for treatment — which can lead to waiting periods of weeks or even months. Only recently has there been a broader push to fix this gap in care.

The medications used in treatment do carry some risks

None of this is to say that the medications used in these treatments are without any problems whatsoever. Methadone is tied to thousands of deadly overdoses a year, although almost entirely when it’s used for pain, not addiction, treatment — since it’s much more regulated in addiction care. Buprenorphine is safer in that, unlike common painkillers, heroin, and methadone, its effect has a ceiling — meaning it has no significant effect after a certain dose level. But it’s still possible to misuse, particularly for people with lower tolerance levels. And there are some reports of buprenorphine mills, where patients can get buprenorphine for misuse from unscrupulous doctors — similar to how pill mills popped up during the beginning of the opioid epidemic and provided patients easy access to painkillers.

Naltrexone, meanwhile, can heighten the risk of overdose and death in case of full relapse. Overdose and death are risks in any case of relapse, but they’re particularly acute for naltrexone because it requires a full detox process that eliminates prior tolerance. (Although this would typically require someone to stop taking naltrexone, since otherwise it blocks the effects of opioids up to certain doses.)

But when taken as prescribed, the medications are broadly safe and effective for addiction treatment. For regulators, it’s a matter of making sure the drugs aren’t diverted into misuse, while also providing good access to people who genuinely need them.

The fight over medication-assisted treatment is really about how we see addiction

Behind the arguments about medication-assisted treatment is a simple reality of how Americans view addiction: Many still don’t see it, as public health officials and experts do, as a disease.

With other diseases, there is no question that medication can be a legitimate answer. That medication is not viewed as a proper answer by many to addiction shows that people believe addiction is unique in some way — particularly, they view addiction as at least partly a moral failing instead of just a disease.

I get emails all the time to this effect. Here, for example, is a fairly representative reader message: “Darwin’s Theory says ‘survival of the fittest.’ Let these lost souls pay the price of their criminal choices and criminal actions. Society does not owe them multiple medical resuscitations from their own bad judgment, criminal activity, and self-inflicted wounds.”

This contradicts what addiction experts broadly agree on. As Stanford psychiatrist and Drug Dealer, MD author Anna Lembke put it, “If you see somebody who continues to use despite their lives being totally destroyed — losing their jobs, losing loved ones, ending up in jail — nobody would choose that. Nobody anywhere would ever choose that life. So clearly it is beyond this individual’s control on some level.”

Many Americans may understand this with, say, depression and anxiety. We know that people with these types of mental health problems are not in full control of their thoughts and emotions. But many don’t realize that addiction functions in a similar way — only that the thoughts and emotions drive someone to seek out drugs at just about any cost.

Some of the sentiment against medications, as Hansen can testify, is propagated by people suffering from addiction. Some of them believe that any drug use, even to treat addiction, goes against the goal of full sobriety. They may believe that if they got sober without medications, perhaps others should too. Many of them also don’t trust the health care system: If they got addicted to drugs because a doctor prescribed them opioid painkillers, they have a good reason to distrust doctors who are now trying to get them to take another medication — this time for their addiction.

The opioid epidemic, however, has gotten a lot of people in the addiction recovery world to reconsider their past beliefs. Funeral after funeral and awful statistic after awful statistic, there is a sense that there has to be a better way — and by looking at the evidence, many have come to support medication-assisted treatment.

“I remember sitting there,” Hansen said, speaking to his experience at a funeral, as a mother sang her dead son a lullaby, “thinking that we have to do better.”

Source:  German  Jul 20, 2017


Medical Illness Model:

Near the end of the Second World War researchers and leaders in the recovery community jointly formulated the problem of uncontrolled drinking into what is now known as the Disease Model of alcoholism. This model postulates that, like medical illnesses, alcoholism–more specifically alcohol dependence, or addiction—can be diagnosed, its course observed, and its physical causes understood.

Further, scientific trials can be undertaken to identify the best treatments for those who suffer from it. The diagnosis of Alcohol Dependence, in this model, rested on four symptoms: 1) a tolerance to alcohol in which a person needs to drink ever greater amounts to reach a desired effect, 2) withdrawal symptoms, such as “the shakes” and others, on stopping use, 3) the Loss of Control phenomenon in which affected persons lose the ability to control how much they drink at a sitting and thereby can no longer predict how much they will drink from one episode to the next, and 4) social or physical impairment resulting from combinations of the first three symptom categories1.

This model pictures a condition from which many alcohol dependent people emerge every year, and into which many others return. View as a disease, alcoholism takes on the characteristics of a remitting-relapsing illness with primary symptoms that direct us to brain functioning. And, because ethyl alcohol is a very small molecule with easy access to most parts of the body, moderate to heavy alcohol use often injures other organs, such as the liver and heart among others.

Uncontrolled, or dependent, alcohol use also affects the social network setting of family as well as work activities, friendships, and legal involvement. Last, however, the Disease model brings with it the possibilities of treatment and of hope. At this date, effective medicinal agents against alcoholism are very few. But hope, that necessary ingredient for recovery, waxes strong in the illness model. In the words of the alcoholic patient quoted in the Part 2, “It is much easier to think of myself as an ill person working to become well, rather than a bad person trying to become good.”

Genetic Models:

From the Disease model has come another, that of genetic influence. The observation that alcoholism often runs in families for many years meant that family cultures or mores determined who would become alcoholic and who would not. While it is clear that cultural and family life influences are very powerful, more recent studies have noted that an underlying genetic disposition may be at play in some genealogical lines2. If so, the evidence suggests a confluence of many gene effects rather than the dominant/recessive results of inheritance in Mendelian models of genetic death, as for example, in Huntington’s Disease.

Instead, the gene effects seem to have more to do with the vulnerability towards alcoholism. One form appears in those who have a genetically-based insensitivity to alcohol—an “inborn tolerance,” and develop alcohol dependence at much higher rates than alcohol sensitive comparison groups. Another form may require a combination of

gene influences and environment conditions to come together to result in alcohol-plus-multiple drug dependence, sometimes referred to as Type 2 or Type B alcoholics.

Unexpectedly, the news of gene involvement was greeted with enthusiasm among some quarters of the actively drinking alcoholic public: “Since alcoholism is genetic, we can’t escape our genes and may as well keep drinking.” As with older models however, the element of choice remains present in the sober periods between drinking episodes. As some of the other models suggest, healing from alcoholism remains an individual process.

Psychological Adaptation Models in Illness and Recovery:

Further modern research asks that we look at individuals and their abilities to adapt to the stresses of life. Careful observation has established that individual humans have the ability to adapt creatively to the painful thoughts and feelings of living and to do so in ways that connect us together rather than drive us apart3. This model of Mature human psychological adaptation, however, emphasizes that the brain function at its healthy best. Heavy, continuous use of alcohol carries often subtle, if severe, effects on the brain that are as yet poorly understood.

But we know they exist because of their effects in driving down the ability to adapt, from psychological Maturity to much more rigid Primitive mechanisms of coping, such as when an alcoholic “denies” that an obvious problem exists at all. This kind of Denial can occur in the actively drinking alcoholic who understands that resolving his or her ambivalence toward drinking is too painful to contemplate; therefore, a failure to perceive the problem seems preferable than facing it.

So it is that the Adaptation model views the First of the Twelve Steps as addressing primitive Denial in coming to recognize that the individual’s alcoholism exists. Progressing along the continuum of the Steps leads finally to the Twelfth: helping others who have the same problem. In the Psychological Adaptation model, this exemplifies the Mature mechanism of Altruism: selflessly helping others. The occurrence of brain healing as abstinence continues—along with the progression towards psychological maturity, whether viewed in the Psychological Adaptation or the Twelve Step models—suggests that brain recovery process are at work. We can only recognize their existence at this point, and need to understand their biology if we are to improve treatments in the Disease model.

Many Models, More Questions:

With this overview of the different model formulations of the problem of alcoholism and what to do about it, we are now ready to look as specific questions from a scientific point of view. As this series unfolds, we will have recourse to use all of the models mentioned—now adding the crucial ingredient of evidence, systematically gathered. In future Updates, the discussion will focus on specific problems and what we can learn about them.

Source:  14th Jan. 2014

Blue Cross Blue Shield issued a report on the opioid crisis with their data from all members in their commercial plans.  Early in the document, they report a pair of striking numbers.

First, that 21% of members filled a prescription for an opioid in 2015. I’ve heard these kinds of numbers before, but I never get numb. That’s 1 in 5 members, despite growing attention to excessive prescribing of opioids.

Second, a 493% increase in diagnosis of opioid use disorders over 7 years. My reaction is that this has to reflect changes in coding or diagnostic practices rather than the population. It’s implausible that there was an increase this large in the number of people with an opioid use disorder.

The document then devotes a great deal of attention to opioid prescribing.

Toward the end, there are a couple of graphics that caught my attention.

First, a map showing rates of opioid use disorders.


Then, this:

Though critical to treating opioid use disorder, the use of medication-assisted treatments (e.g., methadone) does not always track with rates of opioid use disorder (compare Exhibits 10 and 11). For example, New England leads the nation in use of medication-assisted treatments but it has lower levels of opioid use disorder than other parts of the country


So . . . they note that New England has average rates of opioid use disorders, yet they have high rates of utilization of medication-assisted treatment. This caught my attention because New England has higher rates of overdose, as depicted in the CDC graphics below.

Number and age-adjusted rates of drug overdose deaths by state, US 2015


Statistically significant drug overdose death rate increase from 2014 to 2015, US states

(It’s worth noting that BCBS is not among the top 3 insurers in Maine or New Hampshire, but they are the biggest in Massachusetts and Vermont.)

It begs questions about what the story is, doesn’t it?

I don’t presume to know the answers.

§ What was the sequence of events for the high OD rates and the utilization of MAT? And, what impact, if any, has the expansion of MAT had on overdose rates?

§ Is the BCBS data representative? (This brand new SAMHSA report suggest that the data about use is representative.)

§ We know that opioid maintenance meds reduce risk of OD, but we also know that people stop taking these meds at high rates. Does this imply that, in the real world, these meds end up providing less OD protection than hoped?

§ What are the policies and practices of the other insurers in the state?  (For example, we know that Anthem [the largest insurer in Maine and Vermont] recently ended prior authorization requirements for MAT. It’s not clear how restrictive they had been. They also are attempting to institute reformsto address the fact that, “only about 16 to 19 percent of the members taking the medications for opioid use disorder also were getting the recommended in-person counseling.”)

§ Are there regional differences in drug potency that explain this?

Let’s hope that more insurers follow suit and share their data.


A study by researchers from the Murdoch Children’s Research Institute (MCRI) that followed a sample of almost 2000 Victorian school children from the age of 14 until the age of 35 found that social disadvantage, anxiety, and licit and illicit substance use (in particular cannabis), were all more common in participants who had reported self-harm during adolescence.

The longitudinal study, the Victorian Adolescent Health Cohort Study, was the first in the world to document health-related outcomes in people in their 30s who had self-harmed during their adolescence. Until now, very little has been known about the longer-term health and social outcomes of adolescents who self-harm.

Published in the new Lancet Child and Adolescent Health journal, the study found the following common elements:

· People who self-harmed as teenagers were more than twice as likely to be weekly cannabis users at age 35

· Anxiety, drug use, and social disadvantage were more common at age 35 among participants who had self-harmed during their teenage years. While most of these associations can be explained by things like mental health problems during adolescence and substance use during adolescence, adolescent self-harm was strongly and independently associated with using cannabis on a weekly basis at age 35 years

· Self-harm during the adolescent years is a marker for distress and not just a ‘passing phase’

The findings suggest that adolescents who self-harm are more likely to experience a wide range of psychosocial problems later in life, said the study’s lead author, Dr Rohan Borschmann from MCRI. “Adolescent self-harm should be viewed as a conspicuous marker of emotional and behavioural problems that are associated with poor life outcomes,” Dr Borschmann said.

The study found that anxiety, drug use, and social disadvantage were more common at age 35 among participants who had self-harmed during their teenage years. “While most of this can be explained partly by things like mental healthduring adolescence and substance use during adolescence, adolescent self-harm was strongly and independently associated with using cannabis on a weekly basis at age 35 years,” Dr Borschmann said.

Interventions during adolescence which address multiple risk-taking behaviours are likely to be more successful in helping this vulnerable group adjust to adult life.

More information: Rohan Borschmann et al. 20-year outcomes in adolescents who self-harm: a population-based cohort study, The Lancet Child & Adolescent Health (2017). DOI: 10.1016/S2352-4642(17)30007-X


Residential treatment has received a lot of criticism and scepticism over the last several years, especially for opioid use disorders. (Some of it is deserved. Too many providers are hustlers and others provide little more than detox with inadequate follow-up. Of course, many of the same criticisms have been directed at medication-assisted treatment. But, that’s not what this post is about.)

At any rate, the Recovery Research Institute recently posted about a study looking at completion rates for outpatient and residential treatment.   The study looked at A LOT of treatment admissions, 318,924.  Residential completion rates appear to have surprised a lot of people:

Results: Residential programs reported a 65% completion rate compared to 52% for outpatient settings. After controlling for other confounding factors, clients in residential treatment were nearly three times as likely as clients in outpatient treatment to complete treatment.

But, what really surprised some readers was this:

Compared to clients with a primary alcohol use disorder:
Clients with marijuana use disorder were only 74% as likely to complete residential treatment.
Clients with an opioid use disorder were 1.29x MORE likely to complete residential treatment.

So opioid users were much more likely to benefit from residential treatment compared to alcohol users. . . .

We speculate that for opioid abusers, the increased structure and cloistering of residential treatment provide some protection from the environmental and social triggers for relapse or that otherwise lead to the termination of treatment that outpatient treatment settings do not afford. Indeed, environmental risk characteristics in drug abusers’ residential neighbourhoods, such as the presence of liquor stores and indicators of concentrated disadvantage at the neighbourhood level, have been found to be associated with treatment non-continuity and relapse.

Such environmental triggers may play a particularly substantial role for those addicted to opioids compared to those seeking treatment for marijuana abuse. Since opioid users have the lowest raw completion rates in general, this finding that residential treatment makes a greater positive difference for opioid users than it does for any of the other substances represents an important result that merits further investigation. Given the current epidemic of opioid-related overdoses in the U.S., our results suggest that greater use of residential treatment should be explored for opioid users in particular.

For the differences between residential and outpatient, they say the following:

In general, residential treatment completion rates are usually higher compared to outpatient settings, but what is particularly noteworthy is that even after controlling for various client characteristics and state level variations, the likelihood of treatment completion for residential programs was still nearly three times as great as for outpatient settings. Given the more highly structured nature and intensity of services of residential programs compared to outpatient treatment, it is understandable that residential treatment completion rates would be higher. It requires far less effort to end treatment prematurely in outpatient settings com-pared to residential treatment.

Given the strong association between treatment completion and positive post-treatment outcomes such as long term abstinence, the large magnitude of difference between outpatient and residential treatment represents a potentially important consideration for the choice of treatment setting for clients.


Smart Approaches to Marijuana’s 2017 publication references academic studies which suggest that marijuana primes the brain for other types of drug usage.  Here’s the summary on that subject from page 4, Marijuana and Other Drugs: A Link We Can’t Ignore :

MORE THAN FOUR in 10 people who ever use marijuana will go on to use other illicit drugs, per a large, nationally representative sample of U.S. adults.(1) The CDC also says that marijuana users are three times more likely to become addicted to heroin.(2)

Although 92% of heroin users first used marijuana before going to heroin, less than half used painkillers before going to heroin.

And according to the seminal 2017 National Academy of Sciences report, “There is moderate evidence of a statistical association between cannabis use and the development of substance dependence and/or a substance abuse disorder for substances including alcohol, tobacco, and other illicit drugs.”(3)

RECENT STUDIES WITH animals also indicate that marijuana use is connected to use and abuse of other drugs. A 2007 Journal of Neuropsychopharmacology study found that rats given THC later self -administered heroin as adults, and increased their heroin usage, while those rats that had not been treated with THC maintained a steady level of heroin intake.(4) Another 2014 study found that adolescent THC exposure in rats seemed to change the rodents’ brains, as they subsequently displayed “heroin-seeking” behaviour. Youth marijuana use could thus lead to “increased vulnerability to drug relapse in adulthood.”(5)

National Institutes of Health Report

The National Institutes of Health says that research in this area is “consistent with animal experiments showing THC’s ability to ‘prime’ the brain for enhanced responses to other drugs. For example, rats previously administered THC show heightened behavioral response not only when further exposed to THC, but also when exposed to other drugs such as morphine—a phenomenon called cross-sensitization.”(6)

Suggestions that one addictive substance replaces another ignores the problem of polysubstance abuse, the common addiction of today.

Additionally, the majority of studies find that marijuana users are often polysubstance users, despite a few studies finding limited evidence that some people substitute marijuana for opiate medication. That is, people generally do not substitute marijuana for other drugs. Indeed, the National Academy of Sciences report found that “with regard to opioids, cannabis use predicted continued opioid prescriptions 1 year after injury.  Finally, cannabis use was associated with reduced odds of achieving abstinence from alcohol, cocaine, or polysubstance use after inpatient hospitalization and treatment for substance use disorders” [emphasis added].(7)

Moreover, a three-year 2016 study of adults also found that marijuana compounds problems with alcohol. Those who reported marijuana use during the first wave of the survey were more likely than adults who did not use marijuana to develop an alcohol use disorder within three years.(8) Similarly, alcohol consumption in Colorado has increased slightly since legalization. (9)



Drug addiction is a chronic and relapsing disease that often begins during adolescence.

Epidemiological evidence documents an association between marijuana use during adolescence and subsequent abuse of drugs such as heroin and cocaine (1, 2). While many factors including societal pressures, family, culture, and drug availability can contribute to this apparent `gateway’ association, little is known about the neurobiological basis underlying such potential vulnerability.

Of the neural substrates that have been investigated, the enkephalinergic opioid system is  consistently altered by developmental marijuana exposure (3–5), perhaps reflecting neuroanatomical interactions between cannabinoid receptor type 1 and the enkephalinergic system (6, 7).

Debates exist, however, regarding the relationship between proenkephalin (Penk) dysregulation and opiate susceptibility. We previously reported that adult rats exposed to Δ9-tetrahydrocannabinol (THC; primary psychoactive component of marijuana) during adolescence exhibit increased heroin self administration (SA) as well as increased expression of Penk, the gene encoding the opioid neuropeptide enkephalin, in the nucleus accumbens shell (NAcsh), a mesolimbic structure critically involved in reward-related behaviors (3).

Although these data suggest that increased NAcsh Penk expression and heroin SA behavior are independent consequences of adolescent THC exposure, they do not address a possible causal relationship between THCinduced  Penk upregulation in NAcsh and enhanced behavioral susceptibility to opiates.

Moreover, insights regarding the neurobiological mechanisms by which adolescent THC exposure maintains upregulation of Penk into adulthood remain unknown.

Here, we take advantage of viral-mediated gene transfer strategies to show that adulthood addiction-like behaviors induced by adolescent THC exposure are dependent on discrete regulation of NAcsh Penk gene expression. A number of recent studies have demonstrated an important role for histone methylation in the regulation of drug-induced behaviors and transcriptional plasticity, particularly alteration of repressive histone H3 lysine 9 (H3K9) methylation at NAc gene promotors (8, 9).

We report here that one mechanism by which adolescent THC exposure may mediate Penk upregulation in adult NAcsh is through reduction of H3K9 di- and trimethylation, a functional consequence of which may be decreased transcriptional repression of Penk.



Marijuana use by teenagers often predates the use of harder drugs, but the neurobiological underpinnings of such vulnerability are unknown. Animal studies suggest enhanced heroin self-administration (SA) and dysregulation of the endogenous opioid system in the nucleus accumbens shell (NAcsh) of adults following adolescent Δ9-tetrahydrocannabinol (THC) exposure. However, a causal link between Penk expression and vulnerability to heroin has yet to be established.


To investigate the functional significance of NAcsh  Penk tone, selective viral mediated knockdown and overexpression of Penk was performed, followed by analysis of subsequent heroin SA behavior. To determine whether adolescent THC exposure was associated with chromatin alteration, we analyzed levels of histone H3 methylation in the NAcsh via ChIP atfive sites flanking the Penk gene transcription start site.


Here, we show that regulation of the proenkephalin (Penk) opioid neuropeptide gene in NAcsh directly regulates heroin SA behavior. Selective viral-mediated knockdown of Penk in striatopallidal neurons attenuates heroin SA in adolescent THC-exposed rats, whereas Penk overexpression potentiates heroin SA in THC-naïve rats. Furthermore, we report that adolescent THC exposure mediates Penk upregulation through reduction of histone H3 lysine 9 (H3K9) methylation in the NAcsh, thereby disrupting the normal developmental pattern of H3K9 methylation.


These data establish a direct association between THC-induced NAcsh Penk upregulation and heroin SA and indicate that epigenetic dysregulation of Penk underlies the long term effects of THC.

Source:  Biol Psychiatry. 2012 November 15; 72(10): 803–810. doi:10.1016/j.biopsych.2012.04.026.

Cannabis Use, Gender and the Brain

Cannabis is the most widely used illicit drug in the U.S. and, as a result of legalization efforts for both medical remedy and for recreational use, is now the second leading reason (behind alcohol) for admission to addiction treatment in the U.S. The health consequences, cognitive changes, academic performance and numerous neuroadaptations have been debated ad nauseam. Like other drugs and medications, effects are different if exposure occurs in the young vs. the old or in males vs. females. Exposure in utero, early childhood, adolescence-young adult, adult and elderly may have different effects on the brain and outcomes. Yet the best available independent research shows that marijuana use is associated with consistent regionally specific alterations to important brain circuitry in the striatum and pre-frontal and post orbital regions. In this study, Chye and colleagues have investigated the association between marijuana use and the size of specific brain regions that are vitally important in goal-directed behavior, focus and learning within in the orbitol frontal cortex (OFC) and caudate. This investigation suggests that marijuana dependence and recreational use have distinct and region-specific effects.

Why Does This Matter?

This is an important finding, but distinction between cannabis use, abuse and dependence is not always clear, objective, linear or well understood. However, dependence-related medial OFC volume reduction was robust and highly significant. Lateral OFC volume reduction was associated with monthly marijuana use. Greater reductions in brain volume of specific regions were stronger among females who were marijuana dependent. This finding correlates with previous evidence of gender-dependent differences towards the various physiological, behavioral and the reinforcing effect of marijuana for both recreational use and addiction.

The results highlight important neurological distinctions between occasional cannabis use and addiction. Specifically, Chye and colleagues found that smaller medial OFC volume may be driven by marijuana addiction-related mechanisms, while smaller lateral OFC volume may be due to ongoing exposure to cannabinoids. The results highlight a distinction between cannabis use and dependence and warrant future examination of gender-specific effects in studies of marijuana use and dependence.

Source:   June 2017  Author: Mark Gold, MD

Author: Mark Gold, MD

Mortality resulting from opioid use (over 33,000 in 2015) is now epidemic in the U.S., exceeding drug-related deaths from all other intoxicants. Dr. Ted Cicero of Washington University, Dr. William Jacobs, Medical Director of Bluff Plantation, and I discussed the opioid over-prescribing and switch to heroin at DEA Headquarters on November 17, 2015. Things have gone from bad to worse. In a recent JAMA article (March 2017), Dr. Bertha Madras, Professor in the Department of Psychiatry at Harvard Medical School, offers compelling analysis and recommendations to rein in this crisis.

Physicians have increasingly prescribed opioids for pain since the AMA added pain as the “fifth vital sign,” which, like blood pressure, mandated assessment during each patient encounter. As a result of this and acceptance of low-quality evidence touting opioids as a relatively benign remedy for managing both acute and chronic pain, prescriptions for opioids have risen threefold over the past two decades.

Addiction, overdose and mortality resulting directly from opioid misuse increased rapidly. In addition, the influx of cheap heroin, often combined with homemade fentanyl analogues, became increasingly popular as prescription opioids became harder to attain and cost prohibitive on the streets. Consequently, a proportion of prescription opioid misusers transitioned to cheaper, stronger and more dangerous illicit opioids.

Opioid Mortality

The breakdown in mortality was confirmed by surveys (2015) revealing a disproportionate rise in deaths specifically attributable to: fentanyl/analogs (72.2%) and heroin (20.6%) compared with only prescription opioids, at less than eight percent. The unprecedented rise in overdose deaths and association with the heroin trade catalyzed the formation of federal and state policies to reduce supply and increase the availability of treatment and of a life saving opioid antagonist overdose medication Naloxone, a short-acting, mu 1, opioid receptor antagonist. Naloxone quickly reverses the effect of opioids and acute respiratory failure provoked by overdose.

Yet, according to Dr. Madras, the current federal and state response is woefully inadequate. She writes: “Of more than 14,000 drug treatment programs in the United States, some funded by federal block grants to states, many are not staffed with licensed medical practitioners. An integrated medical and behavioral treatment system, under the supervision of a physician and substance abuse specialist, would foster comprehensive services, provide expedient access to prescription medicines, and bring care into alignment with current medical standards of care.”

Why Does This Matter?

As baby boomers age and live longer, chronic non-cancer pain is highly prevalent. Opioids for legitimate non-cancer pain are not misused or abused by most patients under proper medical supervision. Yet there is no effective, practical means in this managed care climate whereby Primary Care Physicians (PCPs) can determine who is at risk for abuse and addiction and who is not. And frankly, addicts lie to their doctors to get opioids. Without proper training, physicians, who genuinely want to help their patients, get in over their heads and don’t know how to respond.

Further complicating the issue is that many of the affordable treatment programs do not employ medical providers who are trained and Board Certified in Addiction and Pain

Medicine, not to mention addiction psychiatry, or addiction medicine physicians. Thus the outcomes are dismal, which fosters doubt and mistrust of treatment.

Lastly, the lack of well-trained providers is due, in part, to the lack of training for medical doctors in addiction and behavioral medicine. At the University of Florida, we developed a mandatory rotation for all medical students in “the Division of Addiction Medicine.” We also started Addiction as a sub-specialty within psychiatry, where residents and post-doctoral fellows were immersed in both classroom and clinical training.

Since 1990, many other similar fellowship programs have started, yet few are training all medical students in the hands-on, two-week clerkship experience in Addiction Medicine like they have in obstetrics. We took this a step further when we developed a jointly run Pain and Addiction Medicine evaluation and treatment program which focused on prevention and non-opioid treatments. Many more are needed, as well as increased CME in addictive disease for physicians in any specialty.

Source:   June 2017

One in 5 adolescents at risk of tobacco dependency, harmful alcohol consumption and illicit drug use

Researchers from the University of Bristol have found regular and occasional cannabis use as a teen is associated with a greater risk of other illicit drug taking in early adulthood.   The study by Bristol’s Population Health Science Institute, published online in the Journal of Epidemiology & Community Health, also found cannabis use was associated with harmful drinking and smoking.

Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), the researchers looked at levels of cannabis use during adolescence to determine whether these might predict other problematic substance misuse in early adulthood — by the age of 21.

The researchers looked at data about cannabis use among 5,315 teens between the ages of 13 and 18. At five time points approximately one year apart cannabis use was categorised as none; occasional (typically less than once a week); or frequent (typically once a week or more).

When the teens reached the age of 21, they were asked to say whether and how much they smoked and drank, and whether they had taken other illicit drugs during the previous three months. Some 462 reported recent illicit drug use: 176 (38%) had used cocaine; 278 (60%) had used ‘speed’ (amphetamines); 136 (30%) had used inhalants; 72 (16%) had used sedatives; 105 (23%) had used hallucinogens; and 25 (6%) had used opioids.

The study’s lead author, Dr Michelle Taylor from the School of Social and Community Medicine said:

“We tend to see clusters of different forms of substance misuse in adolescents and young people, and it has been argued that cannabis acts as a gateway to other drug use. However, historically the evidence has been inconsistent.

“I think the most important findings from this study are that one in five adolescents follow a pattern of occasional or regular cannabis use and that those individuals are more likely to be tobacco dependant, have harmful levels of alcohol consumption or use other illicit drugs in early adulthood.”

In all, complete data were available for 1571 people. Male sex, mother’s substance misuse and the child’s smoking, drinking, and behavioural problems before the age of 13 were all strongly associated with cannabis use during adolescence. Other potentially influential factors were also considered: housing tenure; mum’s education and number of children she had; her drinking and drug use; behavioural problems when the child was 11 and whether s/he had started smoking and/or drinking before the age of 13.

After taking account of other influential factors, those who used cannabis in their teens were at greater risk of problematic substance misuse by the age of 21 than those who didn’t.

Teens who regularly used cannabis were 37 times more likely to be nicotine dependent and three times more likely to have a harmful drinking pattern than non-users by the time they were 21. And they were 26 times more likely to use other illicit drugs.

Both those who used cannabis occasionally early in adolescence and those who starting using it much later during the teenage years had a heightened risk of nicotine dependence, harmful drinking, and other illicit drug use. And the more cannabis they used the greater was the likelihood of nicotine dependence by the age of 21.

This study used observational methods and therefore presents evidence for correlation but not does not determine clear cause and effect — whether the results observed are because cannabis use actually causes the use of other illicit drugs. Furthermore, it does not identify what the underlying mechanisms for this might be. Nevertheless, clear categories of use emerged.

Dr Taylor concludes:

“We have added further evidence that suggests adolescent cannabis use does predict later problematic substance use in early adulthood. From our study, we cannot say why this might be, and it is important that future research focuses on this question, as this will enable us to identify groups of individuals that might as risk and develop policy to advise people of the harms.

“Our study does not support or refute arguments for altering the legal status of cannabis use — especially since two of the outcomes are legal in the UK. This study and others do, however, lend support to public health strategies and interventions that aim to reduce cannabis exposure in young people.”

Journal Reference:

1. Michelle Taylor, Simon M Collin, Marcus R Munafò, John MacLeod, Matthew Hickman, Jon Heron. Patterns of cannabis use during adolescence and their association with harmful substance use behaviour: findings from a UK birth cohort. Journal of Epidemiology and Community Health, 2017; jech-2016-208503 DOI: 10.1136/jech-2016-208503

Source:<.htm>. 7 June 2017.

Study Finds Users Are 26 Times More Likely To Turn To Other Substances By The Age Of 21

Study is first clear evidence that cannabis is gateway to cocaine and heroin

Teen marijuana smokers are 37 times more likely to be hooked on nicotine

Findings from Bristol University provide authoritative support for those warning against the liberalisation of drugs laws

Teenagers who regularly smoke cannabis are 26 times more likely to turn to other drugs by the age of 21.

The study of the lives of more than 5,000 teenagers produced the first resounding evidence that cannabis is a gateway to cocaine, amphetamines, hallucinogens and heroin.

It also discovered that teenage cannabis smokers are 37 times more likely to be hooked on nicotine and three times more likely to be problem drinkers than non-users of the drug.

The findings from Bristol University provide authoritative support for those warning against the liberalisation of drugs laws.

Medical researchers have argued for years that cannabis is far from harmless and instead carries serious mental health risks.

Dr Michelle Taylor, who led the study, said: ‘It has been argued that cannabis acts as a gateway to other drug use. However, historically the evidence has been inconsistent.

‘The most important findings from this study are that one in five adolescents follow a pattern of occasional or regular cannabis use and that those individuals are more likely to be tobacco dependent, have harmful levels of alcohol consumption or use other illicit drugs in early adulthood.

‘Our study does not support or refute arguments for altering the legal status of cannabis use.

‘This study and others do, however, lend support to public health strategies and interventions that aim to reduce cannabis exposure in young people.’

The Bristol evidence was gathered from a long-term survey of the lives of young people around the city, the Avon Longitudinal Study of Parents and Children.

The survey, which was published in the Journal of Epidemiology & Community Health, examined 5,315 teenagers between the ages of 13 and 18. One in five used cannabis.

Dr Tom Freeman of King’s College London said: ‘This is a high quality study using a large UK cohort followed from birth. It provides further evidence that early exposure to cannabis is associated with subsequent use of other drugs.’

The study of the lives of more than 5,000 teenagers produced the first resounding evidence that cannabis is a gateway to cocaine amphetamines, hallucinogens and heroin .

Ian Hamilton, who is a mental health researcher at York University, said: ‘It adds to evidence that cannabis acts as a gateway to nicotine dependence, as the majority of people using cannabis in the UK combine tobacco with cannabis when they roll a joint.

‘This habit represents one of the greatest health risks to the greatest number of young people who use cannabis.  It suggests that adolescent cannabis use serves as a gateway to a harmful relationship with drugs as an adult.’

The report said: ‘After taking account of other influential factors, those who used cannabis in their teens were at greater risk of problematic substance misuse by the age of 21.

‘Teens who regularly used cannabis were 37 times more likely to be nicotine dependent and three times more likely to have a harmful drinking pattern than non-users by the time they were 21. And they were 26 times more likely to use other illicit drugs.

‘Both those who used cannabis occasionally early in adolescence and those who started using it much later during the teenage years had a heightened risk of nicotine dependence, harmful drinking, and other illicit drug use.

‘And the more cannabis they used the greater was the likelihood of nicotine dependence by the age of 21.’

Source:   8th June 2017


Ohio had the most overdose fatalities in the United States in 2014 and 2015.

A newspaper’s survey of county coroners has painted a grim picture of fatal overdoses in Ohio: more than 4,000 people died from drug overdoses in 2016 in the state badly hit by a heroin and opioid epidemic.

At least 4,149 died from unintentional overdoses last year, a 36 percent climb from the previous year, or a time when Ohio had the most overdose fatalities in the United States so far.

“They died in restaurants, theaters, libraries, convenience stores, parks, cars, on the streets and at home,” wrote The Columbus Dispatch in its report revealing the findings.

Survey Findings

It’s likely getting worse, too, as coroners warned that overdose deaths this year are fast outpacing these figures brought on by overdoses from heroin, synthetic opioids fentanyl and carfentanil, and other drugs.

The Dispatch obtained the number by getting in touch with coroners’ offices in all 88 Ohio counties. Coroners in six smaller counties, according to the paper, did not provide the requested figures.

Leading the counties in rapid drug overdose rises are counties such as Cuyahoga, where there were 666 deaths in 2016, as well as Franklin, Hamilton, Lucas, Montgomery, and Summit.

The devastation, added the survey, did not discriminate against big or small cities and towns, urban or rural areas, and rich and poor enclaves.

“It’s a growing, breathing animal, this epidemic,” said Medina County coroner and ER physician Dr. Lisa Deranek, who has sometimes revived the same overdose patients a few times each week.

Fentanyl Overdoses

Cuyahoga County, which covers Cleveland, had its death toll largely blamed on fentanyl use. Heroin remains a leading killer, but the autopsy reports reflected the major role of fentanyl, a synthetic opiate 50 times stronger than morphine, and animal tranquilizer carfentanil.

“We’ve done so much, but the numbers are going the other way. I don’t see the improvement,” said William Denihan, outgoing CEO of Cuyahoga County Alcohol, Drug Addiction and Mental Health Services Board.

Cuyahoga County had 400 fentanyl-linked deaths from Nov. 21 in 2015 to Dec. 31 last year, more than double related deaths of all previous years in combination. The opioid crisis, too, no longer just affected mostly white drug users, but also minority communities.

Dr. Thomas Gilson, medical examiner of Cuyahoga County, warned that cocaine is now getting mixed into the fentanyl distribution and fentanyl analogs in order to bring the drugs closer to the African-American groups.

Plans And Prospects

The state’s Department of Mental Health and Addiction Services stated that the overdose death toll back in 2015 would have been higher if not for the role of naloxone, an antidote use for opioid overdose cases. It has been administered by family members, other drug users, and friends to revive dying individuals.

State legislature moved to make naloxone accessible in pharmacies without a prescription. Ohio topped the nation’s drug overdose death numbers in 2014 and 2015. In the latter year, it was followed by New York, according to an analysis by the Kaiser Family Foundation using statistics from the U.S. Centers for Disease Control and Prevention.

Experts are pushing for expanding drug prevention as well as education initiatives from schoolkids to young and middle-aged adults, which also make up the bulk of dying people.

And while the state pioneered in crushing “pill mills” that issue prescription painkillers, health officials warned that this sent addicts to heroin and other stronger substances.

Naloxone, too, is merely an overdose treatment and not a cure for the growing addiction. Last May 22 in Pennsylvania, two drug counselors working to help others battle their drug addiction were found dead from opioid overdose at the addiction facility in West Brandywine, Chester County.

Source:  29.05.17

“I wish that all families would at least consider investigating medication-assisted treatment and reading about what’s out there,” says Alicia Murray, DO, Board Certified Addiction Psychiatrist. “I think, unfortunately, there is still stigma about medications. But what we want people to see is that we’re actually changing the functioning of the patient.” Essentially, medication-assisted treatment (MAT) can help get a patient back on track to meeting the demands of life – getting into a healthy routine, showing up for work and being the sibling, spouse or parent that they once were. “If we can change that with medication-assisted treatment and with counselling,” says Murray, “that’s so valuable.” The opioid epidemic is terrifying, especially so for a parent of someone already struggling with prescription pills or heroin use. It’s so important to consider any and all options for helping your child recover from their opioid dependence.

Part of the reason it’s so hard to overcome an opioid addiction is because it rewires your brain to focus almost exclusively on the drug over anything else, and produces extreme cravings and withdrawal symptoms as a result. By helping to reduce those feelings of cravings and withdrawal, medication-assisted treatment can help your son or daughter’s brain stop thinking constantly about the drug and focus on returning to a healthier life.

Medication-assisted treatment is often misunderstood. Many traditional treatment programs and step-based supports may tell you that MAT is simply substituting one addictive drug for another. However, taking medication for opioid addiction is like taking medication for any other chronic disease, such as diabetes or asthma. When it is used according to the doctor’s instructions and in conjunction with therapy, the medication will not create a new addiction, and can help.

As a parent, you want to explore all opportunities to get your child help for his or her opioid addiction, and get them closer and closer to functioning as a healthy adult – holding down a job, keeping a regular schedule and tapering, and eventually, stopping their misuse of opioids. Medication-assisted treatment helps them do that.

“MAT medications are most effective when they are used in conjunction with therapy and recovery work. We would never recommend medication over other forms of treatment. We would recommend it in addition to it.”

The three most-common medications used to treat opioid addiction are:

· Naltrexone (Vivitrol)

· Buprenorphine (Suboxone)

· Methadone


Naltrexone, known by its brand-name Vivitrol, is administered by a doctor monthly through an injection. Naltrexone is an opioid antagonist. Antagonists attach themselves to opioid receptors in the brain and prevent other opioids such as heroin or painkillers from exerting the effects of the drug. It has no abuse potential.


Buprenorphine, known by its brand-name Suboxone, is an oral tablet or film dissolved under the tongue or in the mouth prescribed by a doctor in an office-based setting. It is taken daily and can be dispensed at a physician’s office or taken at home. Buprenorphine is a partial agonist. Partial agonists attach to the opioid receptors in the brain and activate them, but not to the full degree as agonists. If used against the doctor’s instructions, it has the potential to be abused.


Methadone is dispensed through a certified opioid treatment program (OTP). It’s a liquid and taken orally and usually witnessed at an OTP clinic until the patient receives take-home doses. Methadone is an opioid agonist. Agonists are drugs that activate opioid receptors in the brain, producing an effect. If used against the doctor’s instructions, it has the potential to be abused. There is no “one size fits all” approach to medication-assisted treatment, or even recovery. Recovery is individual.

The most important thing to do is to consider all of your options, and speak to a medical professional to determine the best course of action for your family. The best path is the path that helps and works for your child.

Source:  19th May 2017

 A New Agenda to  Turn Back the Drug Epidemic

Robert L. DuPont, MD, President , Institute for Behavior and Health, Inc.

A. Thomas McLellan, PhD, Senior Strategy Advisor , Institute for Behavior and Health, Inc.  May 2017

Institute for Behavior and Health, Inc. , 6191 Executive Blvd , Rockville, MD 20852 , 1


The Institute for Behavior and Health, Inc. (IBH) is a 501(c)3 non-profit substance use policy and research organization that was founded in 1978. Non-partisan and non-political, IBH develops new ideas and serves as a force for change.

Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs and Health was published in November 2016. Four months later, in March 2017, IBH held a meeting of 25 leaders in addiction treatment, health care, insurance, government and research to discuss the scope and implications of this historic document. The US Surgeon General, VADM Vivek H. Murthy, MD, was an active participant in the meeting. The significance of this new Surgeon General’s Report is analogous to the historic 1964 Surgeon General’s report, Smoking and Health, a document that inspired an extraordinarily successful public health response in the United States that has reduced the rates of cigarette smoking by over 64% and continues its impact even today, more than 50 years following its release.

The following is a summary of the discussion at the March 2017 meeting and the conclusions and recommendations that were developed.

Introduction: The 2016 Surgeon General’s Report 

The two primary objectives of the US Surgeon General’s Report of 2016 are first to provide scientific evidence that shows that in addition to nicotine, other substance misuse and addiction issues (e.g., alcohol, opioids, marijuana, etc.) also are best understood and addressed as public health problems; and second to encourage the inclusion of addiction – its prevention, early recognition and intervention, treatment and active long-term recovery management – into the mainstream of American health care. At present these elements are not integrated either as a stand-alone continuum or within the general medical system. As is true for other widespread illnesses, addiction to nicotine, alcohol, marijuana, opioids, cocaine and other substances is a serious chronic illness. This perspective is contrary to the common perception that addiction reflects a moral failing, a personal weakness or poor parenting. Such opinions have stigmatized individuals who are suffering from these often deadly substance use disorders and have led to expensive and ineffective public policies that segregate prevention and treatment outside of mainstream medical care. A better public health approach encourages afflicted individuals and their family members to seek and receive help within the current health care system for these serious health problems.

An informed public health approach to reducing the prevalence and the harms associated with substance use disorders requires more than the brief treatment of serious cases. Particularly important are substance use prevention programs in schools, healthcare and in all other parts of the community to protect adolescents (ages 12 – 21), the group most at risk for the initiation of substance-related harms and substance use disorders.  Importantly, abundant tragic experience and accumulating science show that substance use disorders are not effectively treated with only short-term care. Because substance use disorders produce 2 significant long-lasting changes in the brain circuits responsible for memory, motivation, inhibition, reward sensitivity and stress tolerance, addicted individuals remain vulnerable to relapse years following specialized treatment.1, 2, 3 Thus, as is true for all other chronic illnesses, long periods of personalized treatment and monitoring are necessary to assure compliance with care, continued sobriety, and improved health and social function. In combination, science-based prevention, early intervention, continuing care and monitoring comprise a modern continuum of public health care. The overall goals of this continuum comport well with those of other chronic illnesses:

1 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 2. The Neurobiology of Substance Use, Misuse, and Addiction. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available:

2 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 5. Recovery: The Many Paths to Wellness. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available:

3 Betty Ford Institute Consensus Panel. (2007). What is recovery? A working definition from the Betty Ford Institute. Journal of Substance Abuse Treatment, 33(3), 221-228.

4 White, W. L. (2012). Recovery/remission from substance use disorders: An analysis of reported outcomes in 415 scientific reports, 1868-2011. Philadelphia, PA: Philadelphia Department of Behavioral Health and Intellectual Disability Services.

· sustained reduction of the cardinal symptom of the illness, i.e., substance use;

· improved general health and function; and,

· education and training of the patient and the family to self-manage the illness and avoid relapses.

In the addiction field achieving these goals is called “recovery.” This word is used to describe abstention from the use of alcohol, marijuana and other non-prescribed drugs as well as improved personal health and social responsibility.3,4 Over 25 million formerly addicted Americans are in stable, long-term recovery of a year or longer.4 Understanding how to consistently accomplish the life-saving goal of recovery must inform health care decisions.

The 2016 Surgeon General’s Report offers a science-informed vision and path to recovery in response to the nation’s serious addiction problem, including specifically the opioid overdose epidemic. Research shows that it is possible to prevent or delay most cases of substance misuse; and to effectively treat even the most serious substance use disorders with recovery as an expectable result of comprehensive, continuous care and sustained monitoring. To do this, substance use disorders must be recognized as serious, chronic health conditions that are both preventable and treatable. The nation must integrate the short-term siloed episodes of specialty treatment that now are isolated from mainstream healthcare into a fully integrated continuum of care comparable to that currently available to those with other chronic illnesses such as diabetes, hypertension, asthma and chronic pain.

Meeting Discussion and Conclusions 

The Surgeon General’s Report and the meeting convened by the Institute for Behavior and Health, Inc. (IBH) to promote its recommendations are significant responses to the expanding epidemic of opioid 3 and other substance use disorders, an epidemic that struck nearly 21 million Americans aged 12 and older in 2015 alone.5 That year saw more than 52,000 overdose deaths.6 This drug epidemic has devastated countless families and communities throughout the US. Unlike earlier and smaller drug epidemics, the current opioid epidemic is not limited to a few regions or communities or a narrow range of ethnicities or incomes in the United States. Instead it afflicts all communities and all socioeconomic groups; its impacts include smaller communities and rural areas as well as suburban areas and inner cities. Fuelled by the suffering of countless grieving families, the nation is in the early stages of confronting the new epidemic. A growing national determination to turn back this deadly epidemic has opened the door to innovation that is sustained by strong bipartisan political support for new and improved efforts in both prevention and treatment of substance use disorders.

5 Center for Behavioral Health Statistics and Quality. (2015). Behavioral health trends in the United States: Results from the 2014 National Survey on Drug Use and Health (HHS Publication No. SMA 15-4927, NSDUH Series H-50). Available:

6 Rudd, R. A., Seth, P., David, F., & Scholl, L. (2016, December 30). Increases in drug and opioid-involved overdose deaths – United States. Morbidity and Mortality Weekly Report, 65(50-51), 1445-1452. Available:

7 Levy, S. J., Williams, J. F., & AAP Committee on Substance Use and Prevention. (2016). Substance use screening, brief intervention, and referral to treatment. Pediatrics, 138(1), e20161211. Available:

8 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 3. Prevention Programs and Policies. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available:

Abstinence is an Achievable Goal, both for Prevention and for Treatment 

Embracing and synthesizing the 30 years of science supporting the findings of the 2016 Surgeon General’s Report, the group discussed a single goal for the prevention of addiction: no use of alcohol, nicotine, marijuana or other non-prescribed drugs by youth for reasons of health. This goal should be the core prevention message to all children from a very young age. Health care professionals, educators and parents should understand the importance of this simple, clear health message. They should continue to reinforce this message of no-use for health as children grow to adulthood. Even when prevention fails, it is possible for parents, other family members, friends, primary care clinicians, educators and others to identify and to intervene quickly to stop youth substance use from becoming addiction.7

The science behind this ambitious but attainable prevention goal is clear. Alcohol, nicotine products, marijuana and other non-prescribed drug use is uniquely harmful to the still-developing brains of adolescents. Thus any substance “use” among youth must be considered “misuse” – use that may harm self or others. The goal of no substance use is not just for the purpose of preventing addiction, though that is one clear and important by product of successful prevention. Addiction is a biological process that can take years to develop. In contrast, even a single episode of high-dose use of alcohol or other substance could immediately produce an injury, accident or even death. While it is true that most episodes of substance misuse among adults do not produce serious problems, it is also true that substance misuse is associated with 70% or more of the injuries, disabilities and deaths of young people.8 These figures are even higher for minority youth. Many adolescent deaths are preventable 4 because most are related to substance use – including substance-related motor vehicle crashes and overdose.9

9 Subramaniam, G. A., & Volkow, N. D. (2014). Substance misuse among adolescents. To screen or not to screen? JAMA Pediatrics, 168(9), 798-799. Available:

10 Data analyzed by the Center for Behavioral Health Statistics and Quality. CBHS. (2015). Behavioral health trends in the United States: Results from the 2014 National Survey on Drug Use and Health (HHS Publication No. SMA 15- 4927, NSDUH Series H-50).

11 2014 data obtained by IBH from the Monitoring the Future study. For discussion of data through 2013 see DuPont, R. L. (2015, July 1). It’s time to re-think prevention; increasing percentages of adolescents understand they should not use any addicting substances. Rockville, MD: Institute for Behavior and Health, Inc. Available:

Youth who use any one of the three most common “gateway” substances, i.e., alcohol, nicotine and marijuana, are many times more likely than those who do not use that single drug to use the other two substances as well as other illegal drugs.10 The use of any drug opens the door to an endless series of highly risky decisions about which drugs to use, how much to use, and when to use them. This perspective validates the public health goal for youth of no use of any drug.

Complete abstinence from the use of alcohol or any other drug among adolescents is not simply an idealistic goal – it is a goal that can be achieved. Data were presented at the meeting from the nationally representative Monitoring the Future study showing that 26% of American high school seniors in 2014 reported no use of alcohol, cigarettes, marijuana or other non-prescribed drugs in their lifetimes. 11 This is a remarkable increase from only 3% reported by American high school seniors in 1983. Moreover, in the same survey, 50% of high school seniors had not used any alcohol, cigarettes, marijuana or other non-prescribed substance in the past 30 days, up from 16% in 1982. These largely overlooked and important findings show that youth abstinence from any substance use is already widespread and steadily increasing.

In parallel with the goal of abstinence for prevention, the recommended goal for the treatment of those who are addicted is sustained abstinence from the use of alcohol and other drugs, with the caveat, explicitly acknowledged by the group, that individuals who are taking medications as-prescribed in the treatment of substance use disorders (e.g., buprenorphine, methadone and naltrexone) and who do not use alcohol or other non-prescribed addictive substances – are considered to be abstinent and ”in recovery.” Abstinence from all non-prescribed substance use is the scientifically-informed goal for individuals in addiction treatment. This treatment goal is widely accepted in the large national recovery community. The long-lasting effects of addiction to drugs are easily seen among cigarette smokers: smoking only a single cigarette is a serious threat to the former smoker, even decades after smoking the last cigarette. There is incontrovertible evidence from brain and genetic research showing the long-term effects of substance misuse on critical brain regions.2 It is unknown when or if these brain changes will return to being entirely normal following cessation of substance use; however, it is known that the recovering brain is particularly vulnerable to the effects of return to any substance use, often leading to overdose or rapid re-addiction. 5

Participants in the IBH meeting supported the idea that abstinence is the high-value outcome in addiction treatment; and that while any duration of abstinence is valuable, longer-term, stable abstinence of 5 years is analogous to the widely-used standard in cancer treatment of 5-year survival. The scientific basis for the value of sustained recovery is validated by the experience of the estimated 25 million Americans now in recovery. This increasingly visible recovery community is a remarkable and very positive new force in the country.

Measuring and Attaining these Goals 

The mantra from the IBH meeting was, if you don’t measure it, it won’t happen. The group of leaders recognized the paucity of current models for systematic integration of addiction treatment and general healthcare. The group encouraged the identification of promising models and the promotion of innovation to achieve the goal of sustained recovery. Even programs that include fully integrated care of other diseases, managed care and other comprehensive health programs do not reliably achieve the goal of sustained or even temporary recovery for substance use disorders. The meeting participants noted the absence of long-term outcome studies of the treatment of substance use disorders and encouraged all treatment programs not only to extend the care of discharged patients but also to systematically study the trajectories of discharged patients to improve their long-term treatment outcomes. The increasing range of recovery support services after treatment is an important and promising new trend that is now actively promoting sustained recovery.

Meeting participants noted one particularly promising model of public health goal measurement and attainment – the 90-90-90 goals for the treatment of HIV/AIDS: 90% of people with HIV will be screened to know their infection status; 90% of all people with diagnosed HIV infection will receive sustained antiretroviral therapy; and 90% of all patients receiving antiretroviral therapy will have viral suppression (i.e., zero viral load).12 These measurable goals provide an operational definition of public health success for the country, states and individual healthcare organizations.

12 UNAIDS. (2014). 90-90-90: An Ambitious Treatment Target to Help End the AIDS epidemic. Geneva, Switzerland: Joint United Nations Programme on HIV/AIDS. Available:

With this model as background, the IBH group concluded that a similar public health approach and similarly specific numeric goals should be established for preventing and treating substance use disorders. Examples of parallel national prevention goals could include 90% rates of screening for substance misuse among adolescents; 90% provision of interventions and follow-up for those screening positive; and 90% total abstinence rates among youth aged 12-21. While these are admittedly ambitious prevention goals, adoption of them could incentivize families, schools and communities to increase the percentage of youth who do not use any alcohol, nicotine, marijuana or other drugs every year.

A similar approach was adopted by the IBH group to improve the impact of addiction treatment. Again, there would be significant public health value if the US adopted the following goals: 90% of individuals aged 12 or older receive annual screening for substance misuse and substance use disorders; 90% of those who receive a diagnosis of a substance use disorder are referred and meaningfully engaged (at 6 least three sessions) in some form of addiction treatment; and 90% of those engaged in treatment achieve sustained abstinence as measured by drug testing, during and for six months following treatment.

Source:  IBH-Report-A-New-Agenda-to-Turn-Back-the-Drug-Epidemic  May 2017

In Southern Ohio, the number of drug-exposed babies in child protection custody has jumped over 200%.  The problem is so dire that workers agreed to break protocol to invite a reporter to hear their stories.  Foster care placements are at record levels, and the number of drug-exposed newborns in their custody has jumped over 200% in the past decade

Inside the Clinton County child protection office, the week has been tougher than most.

Caseworkers in this thinly populated region of southern Ohio, east of Cincinnati, have grown battle-weary from an opioid epidemic that’s leaving behind a generation of traumatized children. Drugs now account for nearly 80% of their cases. Foster-care placements are at record levels, and the number of drug-exposed newborns in their custody has jumped over 200% in the past decade. Funding, meanwhile, hasn’t budged in years.

“Many of our children have experienced such high levels of trauma that they can’t go into traditional foster homes,” said Kathi Spirk, director of Clinton County job and family services. “They need more specialized care, which is very expensive.”

The problem is so dire that workers agreed to break protocol and invite a reporter to camp out in a conference room and hear their stories. For three days, they relived their worst cases and unloaded their frustrations, in scenes that played out like marathon group therapy, for which they have no time. Many agreed that talking about it only made them feel worse, yet still they continued, one after another.

Hence the bad week.

Given the small size of their community, they asked that their names be changed out of concern for their own safety and the privacy of the children.

The caseworkers, like most, are seasoned in despair. Many worked in the 1990s when crack cocaine first arrived, followed by crystal meth in the early 2000s. In 2008, after the shipping giant DHL shuttered its domestic hub here in Wilmington and shed more than 7,000 jobs, prescription pill mills flourished while the economy staggered. Back then, a typical month saw 30 open cases, only a few of them drug-related. But the flood of cheap heroin and fentanyl, now at its highest point yet, has changed everything. A typical month now brings four times as many cases, while institutional knowledge has been flipped on its head.

“At least with meth and cocaine, there was a fight,” said Laura, a supervisor with over 20 years of experience. “Parents used to challenge you to not take their kids. And now you have them say: ‘Here’s their stuff. Here’s their formula and clothes.’ They’re just done. They’re not going to fight you any more.”

Heroin has changed how they approach every step of their jobs, they said, from the first intake calls to that painstaking decision to place a child into temporary foster care or permanent custody. Intake workers now fear what used to be routine.

“Occasionally, we’d get thrown a dirty house, something easy to close and with little trauma to the child,” said Leslie, another worker. “We’re not getting those any more.

Now they’re all serious, and most of them have a drug component. So you may get a dirty house, but it’s never just a dirty house.”

‘I had a four-year old whose mom had died in front of her and she described it like it was nothing’ Children come into the system in two ways. The first is through a court order after caseworkers deem their environment unsafe, and if no friends or family can be found.

Because of the added trauma, removing a child is always the last option, caseworkers said. But in a county with only 42,000 people spread out over 400 square miles, the magnitude of the epidemic has compromised an already delicate safety net. Relatives are overwhelmed financially. Multiple generations are now addicted, along with cousins, uncles, and neighbors. In many cases, a safe house with a grandparent or other relative will eventually attract drug activity.

Law enforcement will also bring children in, usually after parents overdose. These cases often reveal the most horrendous neglect: a three-year old who needed every tooth pulled because he’d never been made to brush them, or kids found sleeping on bug-infested mattresses, going to the toilet in buckets because the water had been shut off. Children are coming in more hardened, they said, older than their years.

“I had a four-year-old whose mom had died in front of her and she described it like it was nothing,” said Bridgette, another caseworker. “She knew how to roll up a dollar bill and snort white powder off the counter. That’s what she thought dollar bills were for.” She added that many of the children could detail how to cook heroin. One foster family had a five-year-old boy who put his medicine dropper in his shoe. “Because that’s where daddy hid his needles,” she said.

“The kids are used to surviving in that mess,” added Carole, another veteran. “Now all the sudden the system is going in and saying it’s not safe. All their survival instincts are taken away and they go ballistic. They don’t know what to do.”

During the first weeks of foster care, meltdowns, tantrums, and violence are common as children navigate new landscapes and begin to process what they’ve experienced.

One afternoon, the caseworkers brought in a foster couple who’d taken in two sisters, an infant born drug-exposed, and her four-year old sister. The baby had to be weaned off opioids and now suffered chronic respiratory problems. Part of her withdrawal had included non-stop hiccups. The older girl had lived with her parents in a drug house and displayed clear signs of post-traumatic stress. Once, a family friend sitting next to her in a car had overdosed and turned purple. She’d witnessed domestic abuse, and one day a neighbor shot and killed her dog while she watched (she’d let the dog out). After a meltdown at a classmate’s pool party, over a year after entering foster care, she revealed having seen a toddler drown in a pond while adults got high. Through therapy, she’d also revealed sexual assault. The foster mother described how the girl suffered flashbacks, triggered by stress and certain anniversaries, like the day of her removal, and other seemingly random events. When this happened, she slipped into catatonic seizures.

“Her eyes are closed and you can’t wake her,” she said. “It’s like narcolepsy, a deep, unconscious sleep. We later discovered it was a coping mechanism she’d developed in order to survive.”

Despite what they’ve endured, most children wish desperately to return to their parents. Many come to see themselves as their parents’ caretakers and feel guilty for being taken away, especially if they were the ones to report an overdose, as in the case of a four-year-old girl who climbed out of a window to alert a neighbor. “She asked me: if I took her away, who was going to take care of mommy?” Bridgette remembered.

For caseworkers, reunification is the endgame. After children enter temporary foster care, the agency spends up to two years working closely with the family while the parents try to stay sober. The only contact with their children comes in the form of twice-weekly visits held in designated rooms here at the office. Each contains a tattered sofa and some second-hand toys. Currently, the agency runs about 200 visits each week. The encounters are monitored through closed-circuit cameras. For everyone involved, it can be the most trying period.

Many parents use the time to build trust and re-establish bonds. “During those first four years, a child gets such good stuff from their parents,” said Sherry, the caseworker who monitors the visits. “The kids are just trying to get that back.” Some parents bring doughnuts and pictures, while others need more guidance. Caseworkers hold parenting classes. Some moms lost newborns at the hospital after they tested positive for drugs; workers teach them how to feed and hold the child, and encourage them to bring outfits to dress their babies.

For other children, the visits trigger a storm of emotion that churns up the trauma of removal. “We had one girl who’d scream and wail at the end of every visit,” Laura, the supervisor, remembered. “Each time she thought she’d never see her mother again. We’d have to pry her out of mom’s arms and carry her down the hallway.”

“We’d sit in our offices and just sob,” added another worker. “But that girl’s cries weren’t enough to keep Mom off heroin.”

The number of available foster families is dwindling, while the cost of supporting them has never been higher

Perhaps the greatest difference with heroin and opioids, caseworkers said, is their iron grasp. Staying sober is a herculean task, especially in this rural community short on resources, where the nearest treatment facilities are over 30 miles away in Dayton, Cincinnati, or Columbus. At some point, nearly every parent falls off the wagon. They disappear and miss visits, leaving children to wait. One of the hardest parts of the job is telling a child that mom or dad isn’t coming, or that they can’t even be found.

“You see the hurt in their eyes,” Sherry said. “It’s a look of defeat, and it just breaks your heart.” She remembered a mother who’d failed to show up for months, then made it for her twin boys’ birthday. “The next day she overdosed and died.”

A tally sheet is used to track how many times prospective clients waiting to enter the program call a detox center, in Huntington, West Virginia. Photograph: Brendan Smialowski/AFP/Getty Images

When parents fail drug screenings during the 18-month period, caseworkers use discretion. Parents might be doing better in other areas like landing a job, or finding secure housing, so workers help them to get back on the wagon. “It’s all about showing progress,” Laura said. Some parents make it 16, 17 months sober and fully engaged. “And they’re the toughest cases, because we’ve been rooting for them this whole time and helping them. We’re giving kids pep talks, saying: ‘Mom’s doing great, she’s getting it together!’ They’re so happy to be going home. And then it all falls apart.”

With heroin, defeat is something the workers have learned to reckon with. Lately they’ve started snapping photos of parents and children during their first visit together, getting medical histories and other vital information – something they used to do much later. “Because we know the parents probably aren’t going to make it,” Laura admitted. “And if we never see them again, this is the info we need.” When asked how many opioid cases had ended in reunification, only two workers raised their hands.

The repeated disappointments come as resources and morale have reached their tipping point. The number of available foster families is dwindling, they said, while the cost of supporting them – over $1.5m a year – has never been higher.

Spirk, the agency’s director, said that all the agency’s budget was paid for with federal dollars and a county tax levy, although they’ve been flat-funded for nearly 10 years. The state contributes just 10%. When it comes to investing in child protection, Ohio ranks last in the country – despite having spent nearly $1bn fighting its opioid problem in 2016 alone.

The Ohio house of representatives recently passed a new state budget with an additional $15m for child protective services, but the state senate has yet to pass its own version. The only bit of hope came in March, when the Ohio attorney general’s office announced a pilot program that will give Clinton County, along with others, additional resources to help treat children for trauma, and to assist with drug treatment. It starts in October.

The epidemic’s unrelenting barrage has also taken a toll on mental health. “Our caseworkers are experiencing secondary trauma and frustration at not being able to reunify children with their parents because of relapses,” Spirk said.

Almost every caseworker said they had experienced depression or some form of PTSD, although no one had sought professional help. The privacy of their cases also means that few can speak openly with friends or family members. Some chose to drink, while others leaned on their faiths. But most said coping mechanisms they once relied on had failed.

“I used to have a routine on my drive home,” Laura said. “I’d stop in front of a church, roll down my window, and throw out all the day’s problems. The next morning I’d pick them back up. These days, I can’t do that anymore.”

“There’s no more outlet,” added Shelly, another supervisor. “You think you’re able to separate but you can’t let it go anymore. You try to eat healthy, do yoga, whatever they tell you to do. But it’s just so horrific now, and it keeps getting worse.”

At some point, the inevitable happens. When a parent can’t stay sober, or stops showing progress, the decision is made to place the child into permanent custody and put them up for adoption. For everyone, including caseworkers, it’s the most wrenching day.

The final act of every case is the “goodbye visit”, held in one of the nicer conference rooms. It’s a chance for parents to let their children know they love them and will miss them, and that it’s time to move on. Adoptive parents can choose to stay in contact, but it isn’t mandatory.

To make the time less stressful, Sherry, the worker who monitors the visits, has them draw pictures together, which she scans and gives to them as mementoes. She also tapes the meetings for them to keep. Watching from her tiny room full of TV screens, she can’t help but cry. “What people don’t realize is that when a baby comes into our custody, they’re still in a carrier seat. By the time the case is over, we’ve helped to potty train them. Two years is a very long time with a child. So in a way, it’s like my goodbye visit, too.”

Caseworkers have started making “life books” for kids once they come into the system. It’s where they put the photos they’ve taken, plus any pictures of birth parents or relatives they can find, report cards, ribbons and medals – the souvenirs of any childhood.  “It’s their history,” Sherry said, “so that one day they can make sense of their lives.”   She noted that one kid, after turning 18, tore his to pieces, taking with him only the good memories.


COLUMBUS, Ohio — It’s being called “gray death” — a new and dangerous opioid combo that underscores the ever-changing nature of the U.S. addiction crisis.

Investigators who nicknamed the mixture have detected it or recorded overdoses blamed on it in Alabama, Georgia and Ohio. The drug looks like concrete mix and varies in consistency from a hard, chunky material to a fine powder.

The substance is a combination of several opioids blamed for thousands of fatal overdoses nationally, including heroin, fentanyl, carfentanil – sometimes used to tranquilize large animals like elephants – and a synthetic opioid called U-47700.

“Gray death is one of the scariest combinations that I have ever seen in nearly 20 years of forensic chemistry drug analysis,” Deneen Kilcrease, manager of the chemistry section at the Georgia Bureau of Investigation, said.  Gray death ingredients and their concentrations are unknown to users, making it particularly lethal, Kilcrease said. In addition, because these strong drugs can be absorbed through the skin, simply touching the powder puts users at risk, she said.

Last year, the U.S. Drug Enforcement Administration listed U-47700 in the category of the most dangerous drugs it regulates, saying it was associated with dozens of fatalities, mostly in New York and North Carolina. Some of the pills taken from Prince’s estate after the musician’s overdose death last year contained U-47700.

Gray death has a much higher potency than heroin, according to a bulletin issued by the Gulf Coast High Intensity Drug Trafficking Area. Users inject, swallow, smoke or snort it.

Georgia’s investigation bureau has received 50 overdose cases in the past three months involving gray death, most from the Atlanta area, said spokeswoman Nelly Miles.

In Ohio, the coroner’s office serving the Cincinnati area says a similar compound has been coming in for months. The Ohio attorney general ‘s office has analyzed eight samples matching the gray death mixture from around the state.

The combo is just the latest in the trend of heroin mixed with other opioids, such as fentanyl, that has been around for a few years.  Fentanyl-related deaths spiked so high in Ohio in 2015 that state health officials asked the federal Centers for Disease Control and Prevention to send scientists to help address the problem.

The mixing poses a deadly risk to users and also challenges investigators trying to figure out what they’re dealing with this time around, said Ohio Attorney General Mike DeWine, a Republican.

“Normally, we would be able to walk by one of our scientists, and say ‘What are you testing?’ and they’ll tell you heroin or ‘We’re testing fentanyl,’” DeWine said. “Now, sometimes they’re looking at it, at least initially, and say, ‘Well, we don’t know.’”

Some communities also are seeing fentanyl mixed with non-opioids, such as cocaine. In Rhode Island, the state has recommended that individuals with a history of cocaine use receive supplies of the anti-overdose drug naloxone.

These deadly combinations are becoming a hallmark of the heroin and opioid epidemic, which the government says resulted in 33,000 fatal overdoses nationally in 2015. In Ohio, a record 3,050 people died of drug overdoses last year, most the result of opioid painkillers or their relative, heroin.

Most people with addictions buy heroin in the belief that’s exactly what they’re getting, overdose survivor Richie Webber said.  But that’s often not the case, as he found out in 2014 when he overdosed on fentanyl-laced heroin. It took two doses of naloxone to revive him. He’s now sober and runs a treatment organization, Fight for Recovery, in Clyde, about 45 miles (72 kilometers) southeast of Toledo.

A typical new combination he’s seeing is heroin combined with 3-methylfentanyl, a more powerful version of fentanyl, said Webber, 25. It’s one of the reasons he tells users never to take drugs alone.

“You don’t know what you’re getting with these things,” Webber said. “Every time you shoot up you’re literally playing Russian roulette with your life.”

Source:  4th May 2017

A new study released today by JAMA Psychiatry found that rates of marijuana use and marijuana addiction increased significantly more in states that passed medical marijuana laws as compared to states that have not. Examining data from 1992 to 2013, researchers concluded that medical marijuana laws likely contributed to an increased prevalence of marijuana and marijuana-addicted users.

“Politicians and pro-pot special interests are quick to tout the benefits of medical marijuana legalization, but it’s time to see through the haze —     medical marijuana has gone completely unregulated,” said SAM President Kevin Sabet. “More people in these states are suffering from an addiction to marijuana that harms their lives and relationships, while simultaneously more have begun using marijuana. No one wants to see patients denied something that might help them, but this study underscores the fact that “medical” and “recreational” legalization are blurred lines. Smoked marijuana is not medicine, and has not been proven safe and effective as other FDA-approved medications have.”

The study’s researchers wrote that increases in marijuana use in states with medical marijuana laws “may have resulted from increasing availability, potency, perceived safety, [or] generally permissive attitudes.” They conclude that “changing state laws (medical or recreational) may also have adverse public health consequences.”  Evidence demonstrates that marijuana —     which has skyrocketed in average potency over the past decades —     is addictive and harmful to the human brain, especially when used by adolescents. Moreover, in states that have already legalized the drug, there has been an increase in drugged driving crashes and youth marijuana use. States that have legalized marijuana have also failed to shore up state budget shortfalls with marijuana taxes, continue to see a thriving black market, and are experiencing a continued rise in alcohol sales.

Source:  Alexandria, VA, April 26, 2017

About SAM

Smart Approaches to Marijuana (SAM) is a nonpartisan, non-profit alliance of physicians, policy makers, prevention workers, treatment and recovery professionals,  scientists, and other concerned citizens opposed to marijuana legalization who want health and scientific evidence to guide marijuana policies. SAM has affiliates in more than 30 states. For more information about marijuana use and its effects, visit

A disturbing majority of businesses in the U.S. are being negatively impacted by prescription painkiller abuse and addiction among employees.

A survey recently released by the National Safety Council reveals more than 70 percent of workplaces are feeling the negative effects of opioid abuse. Nearly 40 percent of employers said employees are missing work do to painkiller abuse, with roughly the same percent reporting employees abusing the drugs on the job. Despite the prevalence of addiction in offices across the country, employers are doing little to mitigate risk. Record pill abuse in workplaces is coming at a time when Americans are taking more opioids than ever before, reports The Washington Post.

A recent survey from Truven Health Analytics and NPR reveals more than half of the U.S. population reports receiving a prescription for opioids at least once from their doctor, a 7 percent increase since 2011. Data released by the Centers for Disease Control and Prevention (CDC) Friday reveals that almost half of non-cancer patients prescribed opioids for a month or more are still dependent on the pills a year later.

Experts say that current opioid and heroin abuse is driven in large part by the over-prescribing of pain pills from doctors. Despite the problems opioid abuse is causing in the workplace, many employee drug tests do not look for the substance. Fifty-seven percent of businesses test for drugs, but 41 percent of those businesses do not test for opioids.

“Employers must understand that the most dangerously misused drug today may be sitting in employees’ medicine cabinets,” Deborah Hersman, president and CEO of the National Safety Council, said in a statement. “Even when they are taken as prescribed, prescription drugs and opioids can impair workers and create hazards on the job.”

Among people not currently taking opioids, nearly half view addiction as the biggest threat from using painkillers. Among current patients on opioids, fears over unwanted side effects still dwarf fears about long-term dependence and addiction. Medical professionals say doctors need to start by prescribing the least potent and least addictive pain treatment option, and then cautiously go from there.

Experts also say the patient must take greater responsibility when they visit their doctor and always ask “why” before accepting a prescription.

Addicts may begin with a dependence on opioid pills before transitioning to heroin after building up a tolerance that makes pills too expensive. States hit particularly hard by heroin abuse are beginning to crackdown on doctors liberally doling out painkillers.

“When four out of five new heroin users are getting their start by abusing prescription drugs, you have to attack the problem at ground zero – in irresponsibly run doctors’ offices,” New Jersey Attorney General Porrino said in a statement March 1. “Physicians who grant easy access to the drugs that are turning New Jersey residents into addicts can be every bit as dangerous as street-corner dealers. Purging the medical community of over-prescribers is as important to our cause as busting heroin rings and locking up drug kingpins.”

A record 33,000 Americans died from opioid related overdoses in 2015, according to the CDC. Opioid deaths contributed to the first drop in U.S. life expectancy since 1993 and eclipsed deaths from motor vehicle accidents in 2015. Combined, heroin, fentanyl and other opiate-based painkillers account for roughly 63 percent of drug fatalities, which claimed 52,404 lives in the U.S. in 2015.


Meet Ryan Hampton, 36, recovery advocate, political activist and recovering heroin addict igniting America’s social media feeds with stories of hope, recovery and activism. From his advocacy that led Sephora to take their eyeshadow branded “druggie” off the shelves to the activism that urged an Arizona politician to apologize for a statement stigmatizing addiction, he’s certainly become a social media powerhouse for all things addiction, recovery and policy. And with an estimated 7 out of 10 people on social media platforms, it’s no coincidence he’s found success taking the addiction advocacy fight digital.

Today, more than 22 million people are struggling with addiction, and it’s estimated that as a result, more than 45 million people are affected. But what many people don’t realize is that there are more than 23 million people living in active, long-term recovery today. Yet, because of shame and stigma, many stay silent. To fight this often-lethal silence, Hampton has urged the public to speak up and share personal stories of recovery through his recently launched Voices Project. The project, a collaborative effort to encourage people across the nation to share their story, exists to put real faces and names behind the addiction epidemic.

A Personal Struggle

Before becoming a national recovery advocate and social media powerhouse, Hampton himself faced a personal struggle with addiction. A former staffer in the Clinton White House, Hampton did not appear to be a likely candidate for heroin addiction, or so stigma would say. But after an injury and subsequent prescription for pain medication, Hampton found himself addicted to opiates, eventually leading to a heroin addiction that would span more than a decade.  After a long struggle, Hampton decided to get help.

It was the phone call that started his recovery journey that changed everything – his life and his view on the power of his phone. After getting sober, he began connecting with others in recovery, amazed at the magnitude of the digital community. But still, while uncovering these online stories of recovery, Hampton lost four friends to opioid addiction.

It was a breaking point for Hampton – one that led to the beginning of a movement that would someday reach and impact millions.

A Notable Partner

Hampton began reaching out to others in recovery and started realizing the power of digital tools to connect and build an online recovery community. And as he was slowly networking and meeting others in recovery, on October 4, 2015, Hampton’s advocacy met its catalyst: Facing Addiction.   The non-profit organization hosted a concert at the National Mall in Washington, D.C., an event that drew thousands to the capitol with celebrities, musicians and other well-known names willing to publicly celebrate the reality of recovery and call for reform in the addiction industry. Hampton, a Los Angeles resident, tuned into the event from across the country through Facebook Live and was again inspired by the content delivered through his mobile phone.

After meeting co-founders of Facing Addiction, Jim Hood and Greg Williams, Hampton plugged in, partnered and even joined the Facing Addiction team as a recovery advocate.

The importance of online advocacy aligns with Facing Addictions’ national priorities, shares CEO Jim Hood, “When enough people tell enough stories and the people who are impacted by addiction look like all of us and our kids and neighbors and relatives, the stigma has to start going away. And then we can get to work.”

After partnering with Facing Addiction, Hampton understood the priorities, the strategy and the mechanism. Said by Hampton, “I stand on the shoulders of giants”.

Leveraging the power of the algorithms at his fingertips every day, Hampton has grown his online presence to be one of the most influential in the recovery movement. Digital communication helped him get to treatment, connected him with Facing Addiction, and now is the platform in which he is sharing recovery stories from across the nation.

In just one week, more than 200 stories were submitted to the Voices Project and over 500 people sent in personal messages to express their support. Among those speaking up are notable voices such as pro skateboarder and former Jackass member Brandon Novak;   Grammy Award-winning musician Sirah;  rapper Royce da 5’9’’;   American politician and mental health advocate Patrick Kennedy;  former child actress and now-addiction counselor Mackenzie Phillips, and more.

According to Royce da 5’9’’, “Addiction is a problem that we all have to deal with. It affects us all in one way or another, and having someone giving it a voice, a name and a face not only helps get rid of the stigma regarding addiction, but he’s [Ryan] on the forefront letting people know there are solutions out there and recovery is real.”

Patrick Kennedy shares the importance of building a digital recovery movement to influence and support political reform in the addiction recovery space. “With the push of a button we’ll be able to have others show up to support communities across the nation,” says Kennedy, “because their fight is our fight.”

“The face of addiction is everyone,” Sirah shares. “The Voices Project gives people a voice and a connection to hope.”

The hope offered through open dialogue about addiction and recovery has now grown into a digital movement.

The pages that Hampton started with $20 and an old computer have gained more than 200,000 followers across platforms, reaching nearly 1 million people each week. “We’re the fastest-growing social movement in history – and the funny thing is, we’re a community that nobody ever wanted to be a part of,” Novak says.

“This is the one space where we cannot be ignored. The time has come for us to speak out, and we’re a community that speaks loudly. With addiction, we’re dealing with imminent death every day,” Hampton says. “Through social media, we’ve found an innovative way to communicate with each other and connect with people we haven’t met, and now, we’re having this conversation with the rest of the world.”

Perhaps the most intriguing impact of Hampton’s work is the paradoxical ability to bring the work of addiction recovery advocacy online – only to take it back offline through real-world change in communities across the country. According to Hampton, the work he’s doing shouldn’t stay digital – it should impact community laws, help new non-profits emerge and influence real people to seek treatment and find it.

“No matter if you have social media or not – your way of doing this is talking about addiction at the dinner table, to a parent or a friend or an employer. You should not be afraid to tell your story of recovery or loss and, most importantly, your story of struggle and how you need help. It may not just change your life, it may change someone else’s life,” Hampton says.

At the crux of digital advocacy in the addiction recovery realm are real lives being saved – people finding treatment, families finding hope and those in recovery being freed of stigma that can keep them in shame and silence.  This is the mission that has fuelled Hampton’s work since the beginning. And Hampton’s reason is hard to refute: “My story is powerful, but our stories are powerful beyond measure.”


Formerly inconceivable ideas—like providing drug users a safe place to inject—are gaining traction.

America’s opioid problem has turned into a full-blown emergency now that illicit fentanyl and related synthetic drugs are turning up regularly on our streets. This fentanyl, made in China and trafficked through Mexico, is 25 to 50 times as potent as heroin. One derivation, Carfentanil, is a tranquilizer for large animals that’s a staggering 1,000 to 5,000 times as powerful.

Adding synthetic opioids to heroin is a cheap way to make it stronger—and more deadly. A user can die with the needle still in his arm, the syringe partly full. Traffickers also press these drugs into pills that they sell as OxyContin and Xanax. Most victims of synthetic opioids don’t even realize what they are taking. But they are driving the soaring rate of overdose—a total of 33,091 deaths in 2015, according to the Centers for Disease Control and Prevention.

Hence the ascendance of a philosophy known as “harm reduction,” which puts first the goal of reducing opioid-related death and disease. Cutting drug use can come second, but only if the user desires it. As an addiction psychiatrist, I believe that harm reduction and outreach to addicts have a necessary place in addressing the opioid crisis. But as such policies proliferate—including some that used to be inconceivable, such as providing facilities where drug users can safely inject—Americans shouldn’t lose sight of the virtues of coerced treatment and accountability.

What does harm reduction look like? One example is Maryland’s Overdose Survivor Outreach Program. After an overdose survivor arrives in the emergency room, he is paired with a “recovery coach,” a specially trained former addict. Coaches try to link patients to treatment centers. Generally this means counseling along with one of three options: methadone; another opioid replacement called buprenorphine, which is less dangerous if taken in excess; or an opioid blocker called naltrexone. Overdose survivors who don’t want treatment are given naloxone, a fast-acting opioid antidote. Coaches also stay in touch after patients leave the ER, helping with court obligations and social services.

Similar programs operate across the country. In Chillicothe, Ohio, police try to connect addicts to treatment by visiting the home of each person in the county who overdoses. In Gloucester, Mass., heroin users can walk into the police station, hand over their drugs, and walk into treatment within hours, without arrest or charges. It’s called the Angel Program. Macomb County, Mich., has something similar called Hope Not Handcuffs.

Another idea gaining traction is to provide “safe consumption sites,” hygienic booths where people can inject their own drugs in the presence of nurses who can administer oxygen and naloxone if needed. No one who goes to a safe consumption site is forced into treatment to quit using, since the priority is reducing risk.

In Canada, staffers at Vancouver’s consumption site urge patrons to go into treatment, but they also distribute clean needles to reduce the spread of viruses such as HIV and hepatitis C. Naloxone kits are on hand in case of overdose. One study found that opening the site has reduced overdose deaths in the area, and more than one analysis showed reduced injection in places like public bathrooms, where someone can overdose undiscovered and die.

There are no consumption sites in the U.S., but in January the board of health in King County, Wash., endorsed the creation of two in the Seattle area. A bill in the California

Assembly would allow cities to establish safe consumption sites. Politicians, physicians and public-health officials have called for them in Baltimore; Boston; Burlington, Vt.; Ithaca, N.Y.; New York City; Philadelphia and San Francisco. Drug-war-weary police officers and harm reductionists would rather see addicts opt for treatment and lasting recovery, but they’ll settle for fewer deaths.

When all else fails, handcuffs can help, too. A problem with treatment is that addicts often stay with the program only for brief periods. Dropout rates within 24 weeks of admission can run above 50%, according to the National Institute on Drug Abuse. Courts can provide unique leverage. Many drug users are involved in addiction-related crime such as shoplifting, prescription forgery and burglary. Shielding them from the criminal-justice system often is not in society’s best interests—or theirs.

Drug courts, for example, keep offender-patients in treatment through immediately delivered sanctions (e.g., a night in jail) and incentives (e.g., looser supervision). Upon successful completion of a 12- to 18-month program, many courts erase the criminal record. This seems to work. The National Association of Drug Court Professionals reports that 75% of drug court graduates nationwide “remain arrest-free at least two years after leaving the program.”

What’s more, if the carrot-and-stick method used by drug courts is scrupulously applied, treatment may not always be necessary. This approach, called “swift, certain and fair,” has been successful with methamphetamine addicts in Hawaii and alcoholics in South Dakota. Some courts in Massachusetts and New Hampshire have now adopted it with opioid addicts. I predict that the combination of anti-addiction medication plus “swift, certain, and fair” will be especially effective.

With synthetic drugs similar to fentanyl turbocharging the opioid problem, the immediate focus should be on keeping people safe and alive. But for those revived by antidotes and still in a spiral of self-destruction, the criminal-justice system may be the ultimate therapeutic safety net.

Source:  April 9, 2017

The Director of the NDPA, Peter Stoker, visited Vancouver East Side in 1999.  It was tragic to see drug dependent men and women living rough on the streets – in the alleys behind the main road – injecting in public.  A team of police officers called The Odd Squad worked the area and did everything they could to help these people – producing a great video called ‘Through the Blue Lens’ – we took this video into schools and it was the most powerful drug prevention message we had ever used.  We would urgently ask you to see this video on You Tube –

The article below is covering the same story – 19 years later.  Isn’t it about time that Canada began to promote good drug prevention instead of relaxing their drug laws? 

As overdose deaths spike, provincial health officials say more overdose prevention sites will soon open across the province.

The number of overdose deaths related to illicit drugs in British Columbia leapt to 755 by the end of November, a more than 70-per-cent jump over the number of fatalities recorded during the same time period last year.

In August, 50 people died of drug overdoses in British Columbia.  In September, 57 died. In October, the number jumped to 67 — an increase that worried health officials, who had thought that increasing the supply and training for administering the overdose reversal drug naloxone was making a difference.

In November, drug overdoses caused 128 deaths — 61 more than the previous month, and nearly double the October total. That spike has brought the total number of deaths between January and November to 755, the highest number ever recorded by the BC Coroner and a 70 per cent increase over this time last year

“We’re quite fearful that the drug supply is increasingly toxic, it’s increasingly unpredictable, and it’s very, very difficult to manage,” said Lisa Lapointe, B.C.’s chief coroner, referring to the increasing prevalence of the synthetic opioid fentanyl being added to many illicit drugs.  “Those who…attempt to use drugs safely, it’s almost impossible.”

With advance notice from the coroner that November numbers would be much higher, provincial health officials announced three weeks ago that several overdose prevention sites would open in Vancouver, Surrey and Victoria. People can go inside the sites to inject drugs, and are given first aid if they overdose.

An unofficial safe consumption site located in the alley behind the Downtown Eastside Market off East Hastings Street.

Health officials have insisted the sites are temporary and are not supervised injection sites, which are currently difficult to open because of a strict Conservative-era law that current federal health minister Jane Philpott has promised to change.

If there is any good news to be found within the grim statistics, it is that no deaths have occurred at any of those overdose prevention sites. And no one has died at a volunteer-run tent that has been operating since September, without official permission or government funding, out of an alley in the heart of the Downtown Eastside. People can smoke or snort drugs at that site, not just inject.

“We’re pretty steady, we get about 100 people a day,” said Sarah Blyth, the Downtown Eastside market coordinator and one of the organizers of the tent. “We’re coming up to welfare (day)…it’s happening this Wednesday, so I imagine up until Christmas it’s going to be pretty busy.”

A sign on the front door of VANDU’s storefront at 380 E. Hastings advertises that the location is an overdose prevention site, with volunteers trained in first aid

“A lot of people use during Christmas,” Blyth added. “Not everybody’s Christmas is as happy as others.”  At the Vancouver Area Network of Drug Users storefront further down East Hastings Street, Linda Bird confirmed the overdose prevention site located there has been busy, with around 60 people a day passing through. Volunteers, who are paid a small stipend by Vancouver Coastal Health, work two to four hour shifts. Overdoses are common, small stipend by Vancouver Coastal Health, work two to four hour shifts. Overdoses are a small stipend by Vancouver Coastal Health, work two to four hour shifts. Overdoses are common, Bird said.

“A lot of them are taking this very, very seriously,” Bird said of the volunteers. “It’s a crisis and a lot of them have seen their friends dropping.”

Vancouver Coastal Health has announced a fourth overdose prevention site in Vancouver, while Fraser Health has added more sites in Langley, Abbotsford and Maple Ridge.

Overdose deaths in November were nearly double the number seen in October

Health authorities in the Interior, Vancouver Island and the north are also planning to open sites in the future, said Perry Kendall, B.C.’s health officer.  “We’re still struggling in many communities with the idea of having these (overdose prevention) sites open,” Kendall said. “That doesn’t help.”

He urged the federal government to introduce the new legislation as soon as possible.

“You must use (drugs) in the presence of somebody who can help you,” Lapointe emphasized. “We are seeing people die with a naloxone kit open beside them, but they haven’t even had time to use it. We are seeing people die with a needle in their arm or a tablet nearby…You must go somewhere where someone is able to give you immediate medical assistance.”


Utah, more than other area of the nation, is suffering from a silent epidemic.  From 2000 to 2014, Utah has experienced a nearly 400% increase in deaths from the misuse and abuse of prescription drugs. Each month there are 24 individuals who die from prescription drug overdoses.

What can we do to help alleviate this growing epidemic? Constant education of the public is essential to prevent drug and alcohol abuse. There is great danger in legal prescription medications and illicit drugs.

What is addiction? As defined by the American Society of Addiction Medicine: “Addiction is a biological, psychological, social and spiritual illness.”   We are learning more and more that opioids now kill more young adults than alcohol. Yet, these deaths are preventable.

Addictionologist, Dr. Sean A. Ponce, M.D., at Salt Lake Behavioral Health Hospital is an advocate of prevention and clinical expert in the treatment of addiction.    Dr. Ponce relates having cancer to that of drug or alcohol addiction. “For cancer, we want to know the prognosis, how far it’s spread… we want to hear the word remission.  Do we talk about that with addiction?”

He goes onto say, “Addiction is a disease that can also spread.  It is a disease that can be mild, moderate or severe.  We want to put it into remission. When cancer reoccurs everyone rallies around that patient to help. When addiction reoccurs what happens?  We send a mixed message.  It is also a disease and we need to be able to help.”

Dr. Ponce also tells us that, “Surviving isn’t really a way to live.  Thriving is.”

Intermountain Health Care recently kicked off a prescription opioid misuse awareness campaign with new artwork in the main lobby of McKay-Dee Hospital including a chandelier built entirely of pill bottles.

This artwork highlights the hospital’s efforts to raise awareness about prescription opioid misuse and represents the 7,000 opioid prescriptions filled each day in Utah. It’s aim: to inform visitors that the risk of opioid addiction “hangs over everyone.”

The campaign’s partners include: Bonneville Communities That Care, Weber Human Services, Use Only as Directed, and Intermountain’s Community Benefit team.

There are also several elevator doors, in McKay Dee Hospital, covered with warnings against opioid use. It definitely sends a strong message to stop and think about the dangers involved.

As previously mentioned, Salt Lake Behavioral Health is a private, freestanding psychiatric hospital specializing in mental health and substance abuse treatment.

You may use this link to learn more about how to help prevent the spread of this deadly epidemic.


(Comment by NDPA:  Some shocking figures from the USA in this article)

In 1964 the Surgeon General’s report on smoking and health began a movement to shine the bright light on cigarette smoking and dramatically change individual and societal views. Today, most states ban smoking in public spaces.

Most of us avoid private smoky places and sadly watch as the die-hard huddle 15 feet from the entrance on rainy, snowy or frigid coffee breaks. Employers often charge higher health insurance premiums to employees who smoke, and taxes on cigarettes are nearly triple a gallon of gas. Yet, some heralded progressive states have passed referendums to legalize the recreational use of a different smoked drug.

Now, more than 50 years later, another very profound statement has been made in the introduction to the recent report, “Substance misuse is one of the critical public health problems of our time.”

“Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health,” was released in November 2016 and is considered to hold the same landmark status as that report from 1964. And maybe, just maybe, it will have the same impact.

Many key findings are included that are critical to garnering support in the health care and substance abuse treatment fields. But the facts are just as important for the general public to know:

— In 2015, substance use disorders affected 20.8 million Americans — almost 8 percent of the adolescent and adult population. That number is similar to the number of people who suffer from diabetes, and more than 1.5 times the annual prevalence of all cancers combined (14 million).

— 12.5 million Americans reported misusing prescription pain relievers in the past year.

— 78 people die every day in the United States from an opioid overdose, nearly quadruple the number in 1999.

— We have treatments we know are effective, yet only 1 in 5 people who currently need treatment for opioid use disorders is actually receiving it.

— It is estimated that the yearly economic impact of misuse and substance use disorders is $249 billion for alcohol misuse and alcohol use disorders and $193 billion for illicit drug use and drug use disorders ($442 billion total).

— Many more people now die from alcohol and drug overdoses each year than are killed in automobile accidents.

— The opioid crisis is fuelling this trend with nearly 30,000 people dying due to an overdose on heroin or prescription opioids in 2014. An additional roughly 20,000 people died as a result of an unintentional overdose of alcohol, cocaine or non-opioid prescription drugs.

Our community has witnessed many of these issues first hand, specifically the impact of the heroin epidemic. The recent Winnebago County Coroner’s report indicated that of 96

overdose deaths in 2016, 42 were a result of heroin, and 23 from a combination of heroin and cocaine.

We know that addiction is a complex brain disease, and that treatment is effective. It can manage symptoms of substance use disorders and prevent relapse. More than 25 million individuals are in recovery and living healthy, productive lives. I, myself, know many. Most of us do.

Locally, the disease of addiction hits very close to many of us. I’ve had the privilege of being part of Rosecrance for over four decades, and I have seen the struggle for individuals and families — the triumphs and the tragedies. Seldom does a client come to us voluntarily and without others who are suffering with them. Through research and evidence-based practices at Rosecrance, I have witnessed the miracle of recovery on a daily basis. Treatment works!

If you believe you need help, or know someone who does, seek help.  Now. Source:  4th March 2017

In this pilot study:

* Patients who received transcranial magnetic stimulation (TMS) were more likely to abstain from cocaine than patients who received medications for symptoms associated with abstinence.

* Researchers concluded that TMS appears to be safe and its efficacy as a treatment for cocaine addiction deserves to be evaluated in a larger clinical trial.

Transcranial magnetic stimulation (TMS) projects electromagnetic fields into the brain and can be used to either increase or decrease neuronal responsiveness in targeted brain areas. Researchers have hypothesized that administering TMS to strengthen activity in the prefrontal cortex (PFC) and downstream brain regions can alleviate cocaine addiction (see Narrative of Discovery: Can Magnets Treat Cocaine Addiction?). Previous findings that support the hypothesis include:

* Studies in animals and people have demonstrated that exposure to cocaine weakens neuronal activity in the PFC, and have linked that decreased activity to some of the primary manifestations of addiction, such as craving and compulsive drug-seeking.

* In a recent study, rats stopped seeking cocaine after researchers experimentally increased activity levels in their prelimbic cortex, a sub region of the rat cortex that shares functional similarities with the human dorsolateral PFC (see Prefrontal Cortex Stimulation Stops Compulsive Drug Seeking in Rats).

Figure. Patients Receiving TMS for Cocaine Addiction Achieve Higher Rates of Abstinence During a 21-day assessment period, higher proportions of TMS-receiving patients than of control patients always gave urine samples that tested negative for cocaine. At completion of the assessment period, 69 percent of those treated with TMS had been continuously abstinent from cocaine versus 19 percent of control patients.

A new pilot trial sets the stage for testing the hypothesis definitively in a large-scale placebo-controlled clinical trial. In the trial, Dr. Antonello Bonci of NIDA’s Intramural Research Program, Dr. Alberto Terraneo, Dr. Luigi Gallimberti and colleagues in Italy and the United States, administered a 29-day course of TMS to 16 patients in an outpatient clinic in Padua, Italy. Of the 16, 11 (69 percent) produced 6 cocaine-negative urine samples, and no positive samples, during a 21-day assessment period that started on treatment day 9 (to allow cocaine that the patients had taken before the study to clear their systems) (see Figure). Among a comparison group of 16 patients who received only medications to control symptoms of depression, anxiety, and insomnia, only 3 (19 percent) made it through the assessment period without using cocaine. The TMS-treated patients also reported less craving for cocaine.

In a second phase of the trial, the researchers administered TMS to 10 patients from the original comparison group, 8 of whom had used cocaine during the first phase. Of the

10, 7 (70 percent) then were followed for 63 days post-TMS and achieved abstinence—an outcome nearly identical to that of the patients who received TMS in the first phase.

The researchers have maintained contact with most of the patients in the study. Dr. Bonci says, “While this observation is not part of a rigorous clinical trial follow-up, and should be taken cautiously, the majority of patients who achieved abstinence during the stimulation pilot protocol report that they have maintained that abstinence for more than 2 years. During that time, some patients have requested additional TMS therapy once a week, twice a month, or monthly, and patients can always request additional therapy if they experience cravings. Others report that they have maintained abstinence without additional TMS after the initial set of treatments.”

Aiming and Tuning the Machine

Dr. Terraneo and colleagues’ protocol focuses the TMS electromagnetic field on the left dorsolateral region of the patients’ PFC. Dr. Bonci explains, “This region is accessible and is involved in a number of addiction processes.” In particular, it has been strongly associated with drug craving. In contrast, he adds, “Stimulating the right side can cause anxiety or discomfort in some patients.” (See “A Case for Studying Brain Asymmetry in Drug Use”).

The researchers set the TMS machine to emit magnetic pulses with a frequency of 15 Hz and an amplitude based on each patient’s baseline neuronal responsiveness. The treatment schedule was designed to induce enduring, rather than brief, increases in neuronal responsiveness. Patients underwent TMS on 5 consecutive days during the first study week, then once during each of the remaining 3 study weeks. Each session lasted 13 minutes, during which the patient’s brain was exposed to 2,400 pulses.

Dr. Bonci emphasizes the safety of TMS: “Properly administered, TMS is very safe. The magnetic pulses are much weaker than those generated in an MRI.” Some patients have experienced headaches or pain at the site of stimulation in the first couple of sessions, but, these adverse effects are generally mild and temporary. Dr. Bonci says, “Few medications have such mild side effects.”

The researchers are planning a larger trial with a more rigorous design, which will address some considerations that limit the interpretation of this pilot trial. Because patients’ responses in the pilot trial may have been influenced by knowing whether they were getting TMS or medication, all patients in the new trial will receive either active TMS or sham TMS without knowing which. The new trial will also examine the possibility that TMS helped participants in the pilot trial abstain from cocaine by reducing depression that is experienced by many cocaine users. Dr. Bonci says, “This region [the dorsolateral PFC] has been a TMS target for the treatment of depression for many years.”

“Most likely, TMS should be coupled with behavioral interventions and medication. I would expect a beneficial synergistic effect. Medication may be particularly necessary for difficult cases when TMS alone is not sufficient,” Dr. Bonci adds. Dr. Harold Gordon, of NIDA’s Epidemiology Research Branch, emphasizes the potential clinical advantages of TMS. “A non-pharmaceutical treatment for addiction would be not only cost-effective but patient-friendly in terms of both compliance and convenience.”

Source:Transcranial magnetic stimulation of dorsolateral prefrontal cortex reduces cocaine use: A pilot study. European Neuropsychopharmacology: 2016.  26(1):37-44. Epub 2015 Dec 4. PMD 26655188.

Filed under: Addiction,Cocaine :

The letter below speaks of the heroin epidemic in the USA.  The figure of heroin and opioid addiction that has destroyed countless families and killed more than 50,000 Americans in 2015 alone is salutary.

A chronicle of President Barack Obama’s tenure must include the heroin epidemic that he leaves us with. Our nation is plagued with a systemic heroin and opioid addiction that has destroyed countless families and killed more than 50,000 Americans in 2015 alone. This one-year death toll is greater than the total number of Americans killed in action during the Vietnam War.

The opioid casualty count only tells part of the story. More than half a million Americans admit to being addicted to heroin, and each of them has a very difficult, if not impossible, road to recovery. Yet, heroin flows into our nation every day and is readily available for $5 a bag 24/7 on street corners throughout the cities and suburbs of America.

How was this level of accessibility not reason enough for President Obama to make slowing our porous borders a priority?  Obama, in his final days as president is now becoming more vocal about the epidemic he leaves behind. However, this is too little, too late in the extreme. His record-setting pardoning and lessening of drug dealer sentences, which have included heroin dealers, further erodes his record on the heroin epidemic. Classifying a heroin dealer as a nonviolent criminal in the face of the American opioid death toll is nonsense.

Perhaps Obama was one of the lucky ones that didn’t have a close friend or relative addicted or taken by heroin and he just didn’t notice the plague that took root under his watch.

Robert Cochran Stafford


ASK THE DOCTOR  column –  – by Dr. Robert Ashley – Erie Times-News, December 30, 2016

Q:  Marijuana seems to be increasingly accepted in our country.  But I worry about my kids using it.  Is it addictive?

A:  Marijuana has gained greater acceptance in this country, not in small part because its medical use can stimulate appetite, control nausea and control pain.  One potential problem with this degree of acceptance is how adolescents view the drug.

In 2015, 70 percent of high school seniors viewed marijuana as not harmful, according to the National Institute on Drug Abuse’s Monitoring the Future survey;  in 1990, only 20 percent felt this way.

Perhaps the biggest risk with marijuana is how it affects the adolescent brain.  The endocannabinoid system, a vast system of receptors within the brain, spinal cord and smaller nerves, affects multiple brain and body functions.  The system continues to develop in humans until the age of 21 or so.

If used frequently in adolescence, marijuana can rewire many of these nerve pathways.  These changes aren’t seen as much in the adult brain and, if they surface, can be easily reversed by stopping use.  In adolescents, however, this rewiring of the nervous system may create addiction.  According to the NIDA, only 9 percent of people who try marijuana become addicted.  However, this number increases to 16 percent among those who start using marijuana in adolescence.  It increases further if marijuana is used daily in adolescence.

Marijuana not only causes short–term memory loss, it also affects mental abilities for days after its use.  That means a person’s ability to plan, organize, solve problems and make decisions is impaired, which has significant ramifications for adolescents trying to retain information learned in school.

Further, for those predisposed to schizophrenia, marijuana can induce psychosis and, in younger users, can decrease the age of schizophrenia’s onset.  People with a familial predisposition to schizophrenia should certainly avoid use.

Send your questions to,, or Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles CA  90095.

National statistics show 2,367 users aged 18 to 24 sought treatment in 2015-16 as drug becomes increasingly unfashionable.   A total of 149,807 opiate addicts came for treatment in England during 2015-16, down 12% on a peak of 170,032 in 2009-10.

The number of 18 to 24-year-olds in England entering treatment for addiction to heroin has plummeted 79% in 10 years, as the stigma surrounding the drug and changing tastes in intoxication have made it increasingly unfashionable.

In the year to March, 2,367 people from that age group presented with heroin and opiate addiction at the approximately 900 drug treatment services in England, compared with 11,351 10 years earlier, according to statistics from the National Drug Treatment Monitoring System (NDTMS).

They constituted a tiny fraction of the 149,807 opiate addicts who came for help to kick their habit throughout the year, a number that is itself 12% down on a peak of 170,032 who came for treatment in 2009-10. The median age of those users was 39, the statistics showed.  Michael Linnell, the coordinator of UK DrugWatch, a network of drug treatment professionals, said many of the heroin users currently accessing treatment would have become addicted during a boom in the drug’s popularity in the late 1980s. Young addicts were “as rare as hen’s teeth”, he said.

Our neglect of ageing heroin users has fuelled the rise of drug-related deaths

“For the Thatcher generation who didn’t see a future and there were no jobs or employment and the rest of it, it was an alternative lifestyle in that you were really, really busy being a heroin user: getting up, scoring, nicking stuff to get the money to score and the rest of it,” Linnell said.

“There was a whole series of factors until you got to that point where people from those communities – the poorest communities – where you were likely to get heroin users, could see the visible stigma of the scarecrow effect, as some people called it.

“They didn’t want to aspire to be a heroin user because a heroin user just had negative connotations, rather than someone who was rebelling against something.”

Overall, 288,843 adults aged 18 to 99 came into contact with structured treatment for drug addiction during 2015-16, 52% of whom were addicted to heroin or some other opiate. Among opiate addicts, 41% were also addicted to crack cocaine, with the next highest adjunctive drugs being alcohol (21%) and cannabis (19%).

About half of those presenting to treatment – 144,908 – had problems with alcohol, a fall of 4% compared with the previous year. Among those, 85,035 were treated for alcohol treatment only and 59,873 for alcohol problems alongside other substances.

The most problematic drug among the 13,231 under-25s who came into contact with drug treatment services in the past year was cannabis, which was cited as a problem by 54%, followed by alcohol (44%) and cocaine (24%).

The numbers from this age group accessing treatment had fallen 37% in 10 years, which the Public Health England report accompanying the statistics said reflected shifts in the patterns of drinking and drug use over that time, with far fewer young people experimenting with drugs than in the past.  Karen Tyrell, the spokeswoman for the drug treatment charity Addaction, said the decline in problem drug use among young people reflected what drugs workers see on a daily basis, and credited evidence-based education, prevention and early intervention programmes for the change.

The shift, though, was precarious, Tyrell said, warning that yearly spending cuts to treatment services risked reversing the gains.

She added: “Of course, what this also means is that we have an ageing population of heroin users, many of whom have been using since the 80s or 90s, and who are now dealing with poor physical health and increasing vulnerability. In an environment of ever rising drug-related deaths, it’s imperative we don’t lose sight of their needs.”


If Marijuana is Medicine, How Come it Makes People So Sick?

There’s a great irony that comes from the pot industry’s claims that marijuana is medical and it’s supposed to help with nausea.   It’s called Cannabis Hyperemesis, and it hits with a vengeance.

This past week a parent wrote to PopPot, saying: “Parents should watch for red flags of pot use in their children including frequent, long hot showers; weight loss; unexplained nausea and vomiting.”

“I took my teen to the doctor assuming the stress of a rigorous course load combined with the demands of an after school sport were taking a physical toll on my child, ” the mom wrote.  “In hindsight, these were the signs of escalating pot use as described in this Pub Med article about cannabinoid hyperemesis. Unfortunately many in the medical community are ignorant of the detrimental effects of pot use on our young people —  ranging from psychotic breaks to debilitating gastrointestinal symptoms.”

From another mother in Pueblo, Colorado who also wrote this past week:  “Last week I met a 14-year-old girl suffering from Cannabis Hyperemesis Syndrome.  When I met her, at first I thought she had an addiction to meth because she was so very thin and malnourished.  She was asking me how can she return to live with her parents who are marijuana users when marijuana is so toxic for her.”

Incidences of this severe illness appear to be on the rise since the rollout of legal weed.  The high THC content of today’s weed — 5x the amount in the 1980s — seems to be involved also.  Because of misdiagnosis or denial of drug use by patients, this syndrome is going undetected.  Furthermore, users self-medicate and exacerbate this severe illness, as a medical marijuana patient was doing for more than eight months.

From veterans hospitals to addiction specialists as well as gastroenterologists, there’s suddenly an increased interest in and diagnoses of this condition.  Further research into this mysterious illness turns up numerous medical journal articles on the link between excessive and/or long-term cannabis use and hyperemesis.

Cannabis Hyperemesis: How to Know if You or Someone You Love is Afflicted

This syndrome is still largely unknown throughout the medical profession and even among cannabis users. The most prominent cases are among long-term users that started using the drug at a very early age and have used daily for over 10 years, according to the MedScape article, Emerging Role of Chronic Cannabis Use and Hyperemesis Syndrome. The article goes on to say that it can also effect newer users and even non-daily users.

In Practical Gastroenterology, there’s a case of a 19 year old Hispanic man who contracted the problem within only two years of marijuana use.  Symptoms reported in a Current Psychiatry article include cyclic vomiting, abdominal pain, nausea, gastric pain and compulsive hot bathing or showers to ease pain.  Frequent bathing and vomiting can also lead to dehydration and excessive thirst. Mild fever, weight loss, and a drop in blood pressure upon standing are other symptoms.

Sufferers find they need to take many showers or baths a day just to get relief from the chronic nausea and vomiting. The bouts of illness are so severe and frightening they lead to frequent trips to the emergency room. And finally, this debilitating illness can be very disruptive to life and relationships. The many absences from work lead to job loss and the inability to hold down a job.

Parents may mistake this situation as bulimia, particularly if the teens hide the vomiting.  Another common way this disease is misdiagnosed as cyclic vomiting syndrome. According to the Current Psychiatry article, 50% of those diagnosed with CVS are daily cannabis users.  Another common misreading by doctors of the compulsive habit of frequent hot baths is as Obsessive Compulsive Disorder.

Further complicating matters, doctors find that even when cannabis use is consistent, the bouts of hyperemesis come and go, which further serves to keep the patient in denial about the connection to their drug use.

In Spite of Cannabis Hyperemesis, Addiction is a Stronghold

Complete cessation of marijuana use is the only known cure for Cannabis Hyperemesis Syndrome.

Sadly, even those who have greatly suffered over a long period of time, still want to be able to consume marijuana. The claim by the industry that marijuana is not addictive is easily disproved when you see the comments to a High Times article, What is Cannabinoid Hyperemesis Syndrome?  Not only do many commenters admit they suffer from this detrimental effect of this drug, they confess they still love marijuana. The commenters lament having to give up their stoner lifestyle even after years of disabling illness! A number of them state that once they are well, they plan to return to the habit, albeit to a lesser degree.

Source:   19th Nov. 2016

The surgeon general’s recent report is a much-needed call to arms around a public health crisis.

On Nov. 17, Dr. Vivek Murthy, a vice admiral of the U.S. Public Health Service Commissioned Corps and U.S. surgeon general, issued a timely and much-needed report on what has become a public health crisis and menace in this country – namely, misuse and addiction to legal and illegal psychoactive drugs.

In the report preface, Murthy remarks that before starting his current job he stopped by the hospital where he had practiced. It was the nurses who said to him, he writes, “please do something about the addiction crisis in America.” He knew they were right, and he took their wise counsel.

Why are they right? Substance use disorders, where a person is functionally impaired and often physically dependent on a drug, affect nearly 21 million Americans annually – the same number of people who have diabetes and 150 percent of those with a cancer diagnosis, of any type.

In 2015, about 67 million people reported binge drinking in the past month, and 48 million were using illegal drugs or misusing prescribed drugs. In the past year, 12.5 million Americans reported misusing prescription pain relievers. In 2014, 47,055 people died from a drug overdose, with more than half of those using an opioid (like OxyContin, Percodan, Vicodin, methadone and heroin).

The numbers chill the mind, and yet with the widespread use, abuse and potentially deadly consequences, only 1 in 10 of those with a substance use disorder obtain any treatment. The nurses to whom Murthy spoke were surely seeing the consequences of drug misuse in their emergency rooms, clinics and inpatient units. They also were likely seeing the consequences among their family, friends and co-workers. (Health professionals are prone to misuse alcohol and drugs.)

What distinguishes the surgeon general’s report is its call for a long overdue shift in alcohol and drug policy – away from a criminal justice approach to a clinical or public health approach. What also distinguishes every cover note and chapter is a spirit of hope, that substance use can be prevented, detected early, effectively treated and its manifold adverse impacts mitigated.

To start, the surgeon general urges that we begin by “improving public awareness of substance misuse and related problems.” Negative attitudes, critical judgments and moral invective towards people with addiction not only interfere with delivering good care they deter people who need services from getting them.

But the report also makes clear that there is no single solution or path, nor should we expect one with problems this broad and deep. The heart of the report then, chapter by chapter, speaks to comprehensive policy action: prevention, early intervention, ongoing treatment, so-called wellness activities, identifying and reaching out to high-risk populations and supporting research efforts.

Central to the report is that we must integrate health care services with substance use treatment: not by referral from one to the other but by embedding screening and basic forms of treatment into primary care and family practice. We screen for hypertension, lipids, diabetes and much more; why aren’t we screening for problem alcohol and drug use where these problems are most likely to appear? Screening, Brief Intervention and Referral for Treatment, or SBIRT, is perhaps the best-known and most effective means of extending substance screening and management into the general health system.

Of course, all these efforts must be financed. A powerful argument can be made that it costs more to not treat these conditions than to treat them. Substance use disorders cost the U.S. more than $400 billion every year on health care expenses, criminal justice costs, social welfare consequences and lost workplace productivity. However, our health, social welfare and criminal justice systems are simply too siloed, (separated) and we pay the human and financial price of not reaching across the ersatz boundaries of government and community agencies.

Still, some laws are making inroads to improve care. The Affordable Care Act requires treatment for substance use disorders to be an “essential benefit,” no different from any other illness. The 2008 Federal Parity Act, now finally with regulations, also requires insurers to not discriminate against people with addictions. The policy and legislative pillars are there, and we need to keep using them.

The surgeon general ends his report with a vision for the future. He is deeply sanguine that we can disrupt the addiction epidemic that has seized our country. The path is a public health one, as I have illustrated above, but the report talks also of what individuals and families can do: reach out to those we see in trouble, withhold judgment, support those in recovery, and, for parents, talk to your child about alcohol and drugs. “Making [these changes] will require a major cultural shift in the way Americans think about, talk about, look at, and act toward people with substance use disorder,” the report reads. “For example, cancer and HIV used to be surrounded by fear and judgment, but they are now regarded by most Americans as medical conditions like many others.”

We owe a great thanks to the surgeon general and the many experts and advocates who put together this call for how we can respond to what is now a public health crisis. We can do that. It will be hard, but the alternative of not taking collective action will be far harder to bear.


Teens who take opioid painkillers without a prescription also often use cannabis, according to a new study.

Researchers analyzed information from more than 11,000 children and teens ages 10 to 18, in 10 U.S. cities. Participants were asked whether they had used prescription opioids in the past 30 days, and whether they had ever used cannabis.

Overall, about 29 percent of the teens said they had used cannabis at some point in their lives. But among the 524 participants who said they had used prescription opioids in the past 30 days, nearly 80 percent had used cannabis. The findings show that among young opioid users, the prevalence of cannabis use is high, said Vicki Osborne, a doctoral student in epidemiology at the University of Florida. Osborne presented the study Oct. 31 at the meeting of the American Public Health Association in Denver.

Among teens who said they used opioids without a prescription (meaning they obtained the drugs through a friend, family member or other avenue), about 88 percent had used cannabis, compared with 61 percent of those who did have a prescription for the opioids they used.

The study also found that the teens who reported having used alcohol or tobacco in addition to opioids were much more likely to use cannabis as well. Of the participants who had used opioids, those who also reported recent alcohol use were nearly 10 times more likely to have used cannabis, compared with those who didn’t use alcohol recently. And those who currently smoked tobacco were 24 times more likely to have used cannabis than those who were not tobacco users, the study found.

Efforts to prevent young people who use opioid painkillers from also using cannabis should target those who use alcohol and tobacco, Osborne said. Efforts should also target males, who were more likely to report using cannabis than females were, she said.

Interventions should also target young people who use opioids without a prescription, Osborne said. Even though such use of opioids among youth is not as high as it is among adults, the proportion of youth using opioids without a prescription is still concerning, she said.

The researchers plan to study the data further, and look at when young people start using cannabis versus when they start using opioids, Osborne said. Previous studies have found that legalizing medical marijuana actually appears to lead to a reduction in opioid use among adults. However, Osborne said the new findings among youth may be different from those in adults, because even in states that have legalized the use of marijuana, the drug is still illegal for teens to use.

Source:  7 Nov16

There is renewed interest in the role of sex or gender in drug use. Two recent publications stand out, the first is an editorial from the journal of Addiction which argues that females have been under represented in many disciplines including addiction research (Del Boca, 2016). This not only impacts on females but may have implications for males. For example, men may be more stigmatised or viewed as vulnerable to drug related problems as a consequence of research attention and reporting. In effect, both groups have been disadvantaged by this phenomenon.

The second article from the sister publication (Addiction Biology) explores the differences and similarities between the sexes in relation to starting drug use and the risk of developing problems (Sanchis-Segura et al, 2016). As the journal title implies this is through a more biological lens with a brief nod to other factors. They conclude that it is important to report sex sameness as well as sex differences in research findings. Highlighting the lack of any attention given to reporting of sex in some studies.

The recent attention given to such a basic factor reveals the state of our collective knowledge about who is at risk of developing problems as a result of drug use. To be blunt, we know very little. So it is good to see that our ignorance is being acknowledged in the academic literature.

How has this happened?

It seems staggering that we have ignored this very basic variable in addiction research. Is it deliberate, or accidental?

In some ways it has been deliberate as it is more convenient to recruit participants from treatment settings. Unfortunately these settings tend to have more men. But that shouldn’t be interpreted as men necessarily having a greater need than women for treatment. This phenomenon needs greater scrutiny as it may be that females avoid treatment fearing that there will be consequences for their role as a mother (Lott-Lavigna 2016). Also it is possible that they perceive treatment to be dominated by males and not an environment they would feel safe in (Torrence, J 2016).

So we need to consider how females start their journey into a career of problematic drug use and how this progresses. As it stands, if we carry on recruiting research participants via treatment settings we will perpetuate a tradition that has left us ignorant of the female journey.

Cannabis and psychosis

Whether male or female, millions worldwide use cannabis. So it is important to understand and communicate the risks to mental health of using the drug. But this is an area that exemplifies the problems we have as a result of not attending to sex.

Cannabis use has been associated with psychosis for some time, but has there been equal attention given to the sexes? In short no, the seminal study by Andreasson of Swedish conscripts included no females, this study has been hugely influential in research, cited more than 1,000 times by research that followed its publication in 1987 (Andreasson et al, 1987).

Unfortunately this trend in over sampling of males has continued since this point; the only Medical Research Council funded trial in the United Kingdom on this issue included a sample of over 80% of males (Barrowclough et al, 2010).

Yet there are only twice as many men admitted to hospital with psychosis and schizophrenia as women. This potentially distorts the attention given to males and certainly limits the intelligence we gather about females (Hamilton et al 2015).

One of the few studies that does provide some information about gender differences and the risks of developing cannabis psychosis found a risk ratio of 2.6 males to every female, although this was based on data from the late 1990s. This matters as cannabis potency has changed over time, which might also increase the risk of developing psychosis for both sexes.

Sex matters

All this matters as research informs treatment, policy and commissioning of services. If we ignore females in research it is likely this has a consequence for the way mental health and addiction treatment is organised and delivered. But most importantly, it leaves men and women with inadequate information on the potential risks of using substances.

Research needs to look beyond the treatment setting, challenging as this might be, there is a pressing need for equality.

Source:   21st Sept.2016

Filed under: Addiction,Social Affairs :


* •Motives for cannabis use can predict problematic use and use-related problems.

* •A MET/CBT intervention was associated with significant reductions in motives.

* •Reductions in a subset of motives significantly predicted change in outcomes.



Heavy cannabis use has been associated with negative outcomes, particularly among individuals who begin use in adolescence. Motives for cannabis use can predict frequency of use and negative use-related problems. The purpose of the current study was to assess change in motives following a motivational enhancement therapy (MET) and cognitive behavioral therapy (CBT) intervention for adolescent users and assess whether change in motives was associated with change in use and self-reported problems negative consequences.


Participants (n = 252) were non-treatment seeking high school student cannabis users. All participants received two sessions of MET and had check-ins scheduled at 4, 7, and 10 months. Participants were randomized to either a motivational check-in condition or an assessment-only check-in. Participants in both conditions had the option of attending additional CBT sessions. Cannabis use frequency, negative consequences, and motives were assessed at baseline and at 6, 9, 12, and 15 month follow-ups.


There were significant reductions in motives for use following the intervention and reductions in a subset of motives significantly and uniquely predicted change in problematic outcomes beyond current cannabis use frequency. Change in motives was significantly higher among those who utilized the optional CBT sessions.


This study demonstrates that motives can change over the course of treatment and that this change in motives is associated with reductions in use and problematic outcomes. Targeting specific motives in future interventions may improve treatment outcomes.

Source:   1st October 2016

New research from the Icahn School of Medicine at Mount Sinai using electroencephalography, or EEG, indicates that adults addicted to cocaine may be increasingly vulnerable to relapse from day two to one month of abstinence and most vulnerable between one and six months. The findings, published online today in JAMA Psychiatry, suggest that the most intense periods of craving for illicit substances often coincide with patients’ release from addiction treatment programs and facilities.

It is not known why individuals with substance use disorders relapse even after remaining abstinent from illicit substances for long periods of time. However, it is clear that cue-induced craving—craving elicited by the exposure to cues previously associated with drug use—plays a major role in relapse. Until now, studies have used self-reported measures to assess cue-induced craving. This is the first study that uses EEG to quantify cue-induced craving in humans with cocaine use disorder, showing a similar trajectory of craving demonstrated in previous studies using animal models. In this study and in contrast to the EEG measures, self-reported craving showed a gradual decline with increasing abstinence duration, underscoring a potential disconnect between the physiological response to drug-related cues in addicted individuals and their perception of this response.

“Our results are important because they identify an objectively ascertained period of high vulnerability to relapse,” says Muhammad Parvaz, PhD, Assistant Professor of Psychiatry and Neuroscience, Icahn School of Medicine at Mount Sinai, and the study’s lead author. “Unfortunately, this period of vulnerability coincides with the window of discharge from most treatment programs, perhaps increasing a person’s propensity to relapse.”

Over five and a half years, the research team collected data from EEG recordings in 76 adults addicted to cocaine with varying durations of abstinence (two days, one week, one month, six months, and one year). EEG was recorded while participants looked at different types of pictures, including pictures that depicted cocaine and individuals preparing, using, and simulating use of cocaine. After EEG, participants also self-rated their level of craving for each cocaine-related picture.

“Results of this study are alarming in that they suggest that many people struggling with drug addiction are being released from treatment programs at the time they need the most support,” said Rita Goldstein, PhD, Professor of Psychiatry and Neuroscience at the Icahn School of Medicine and Principal Investigator of the study. “Our results could help guide the implementation of alternative, individually tailored and optimally timed intervention, prevention, and treatment strategies.”

Source:  7th Sept.2016

The foremost authority on drugs in the US just smashed a huge misconception about addiction.    If drug addiction is a disease like cancer or Alzheimer’s, how do you explain the seemingly amoral behaviour — the lying, cheating, and hiding — that has come to be linked with so many addicts?

The answer has less to do with morality and much more to do with physical changes in the brains of those who become addicted, as National Institute on Drug Abuse director Dr. Nora Volkow perfectly explains in a recent PBS episode of “The Open Mind,” on addiction.

It makes a lot of sense — especially when explained with chocolate.  Volkow is a chocolate lover, you see. She has a special weakness for dark varieties. Most of the time, she can control her cravings. But occasionally — usually when she’s frustrated or tired or bored — she gives in. Then she’ll overdo it, eating too much of the stuff.

Sound familiar?

If so, that’s because it’s a fairly common type of experience. Most of us can abstain some of the time and give in occasionally, but more often than not, most of us easily follow the rule of moderation. But in people who are vulnerable to addiction (via a mesh of factors including genetics, environment, behaviour, and exposure), this is where things start to look different, Volkow explains. And it’s at this point where the long-held notion that addiction is merely a problem of a lack of self-control begins to crumble.

“When you transition from that stage where most of the time you are able to self-regulate the desires and control and manage your behaviour even though you want to do it, you say it’s not a good idea — when you lose that capacity consistently, that’s when you start to get into the transition of addiction,” she says.

But, as she continues to explain, the problem is not simply a behavioural one. It’s also influenced by physical changes that happen in the brain — changes that produce marked differences between the brains of people who are addicted and those who are not.

One of those differences, Volkow says, is a dysfunction in areas of the frontal cortex, a part of the brain that plays a key role in helping us analyse situations and make decisions. “But if these areas of the brain are not functioning properly, which is what repeated drug use [can do] to your brain, it [can erode] the capacity of frontal cortical areas.”

When that happens, your ability to say no to that chocolate bar gets diminished, or in Volkow’s words, “your ability to make optimal decisions gets dysfunctional.”

Volkow’s ideas are bolstered by decades of research, including a 2011 review of studies that she co-authored for the journal Nature. The authors of a 2004 paper built upon similar research, concluding that addiction is a learned behaviour linked with fundamental changes to the brains of addicts.

For this reason, it’s not as simple as just choosing to use drugs — or, in Volkow’s example, overdo it on the chocolate. And the more we know about the neurological basis of addiction, the better we will be able to treat it.   See  the full “Open Mind” episode on PBS:



Photo:Gage Skidmore/Wikimedia Commons*

 “Live long and prosper.” The Vulcan salute is immediately identifiable with the actor Leonard Nimoy  and his most famous character, Mr. Spock. The  beloved cultural icon was admired for his sterling character on Star Trek and off-screen as well. In  recent years and up until his last few months, while  suffering the debilitating effects of a respiratory illness, he took steps to ensure that others would indeed “live long and prosper” by speaking clearly about the role that smoking played in the illness that caused his death.

Nimoy started smoking, like many, when he was young. He managed to quit more than 30 years before his death, but not early enough to prevent the respiratory disease that took his life late February. Nimoy took great pains to show us that cigarettes are a deadly addiction – encouraging followers on Twitter to quit or never start. While he was just one of the 480,000 people in the U.S. who will die prematurely from tobacco-related diseases in 2015, he will surely be among the most well-known and widely missed by an admiring public. That makes the steps took to tell his story so vital.

Tobacco is one of the toughest addictions to overcome and by far the most deadly product available. About 14 million major medical conditions in the U.S. can be blamed on smoking. Yet, despite that inescapable fact, more than 42 million Americans still smoke.

And it isn’t just smoking. Smokeless tobacco products, like those used by sports legend,Tony Gwynn, and other professional baseball players, are linked to oral cancer and other illnesses. Like Nimoy, Gwynn was outspoken before his death last year in naming chewing tobacco as the cause of his cancer. His efforts to speak the truth give meaning to the efforts of a coalition working to eliminate tobacco consumption on and around American baseball fields. Knock Tobacco Out of the Park will succeed, in part, because icons like Gwynn and Nimoy shared their stories and demonstrated the painful cost of tobacco-related illness.

The glamour and appeal of smoking and the power of nicotine addiction are forces that we work to counter every day at Legacy. Even that first cigarette does damage to your body and can spur a life-long addiction and struggle. Nimoy could not imagine what would happen to him five decades after he smoked his first cigarette. By sharing his story, he may help other smokers comprehend the illness and death that lie in wait for them.

As fans remember Leonard Nimoy and Tony Gwynn for cherished memories and contributions to our shared culture, we celebrate them as ambassadors of truth and of knowledge in the fight to build a future where illness and death, caused by the use of tobacco, are things of the past.

Source: 18th March 2015

A few years ago Dr. Diana Martinez and Dr. Marco Diana decided to investigate a new technology that uses magnetic pulses to stimulate brain cells. Both had been trying to develop medications to treat cocaine addiction, and both had come to feel that the pace of progress—their own and others’—was unequal to the urgency of the need. In the new technology, transcranial brain stimulation (TMS), they saw a potential treatment that might be developed relatively rapidly for clinical use.

Dr. Martinez, a neuroimaging specialist at Columbia University Health Center in New York City, planned a preclinical study. She was using a relatively new type of TMS coil (magnetic pulse generator), and her first objective was to identify machine settings with potential clinical efficacy.

Participants in her study were cocaine users who did not want to stop. They came into the hospital research unit, and attended a self-administration session in which they repeatedly chose between smoking a dose of the drug and receiving a sum of money. They then underwent TMS for 3 weeks, after which they repeated the self-administration session. If they chose cocaine less often after treatment than they had before, the setting that was used would be a good candidate for further testing.

Dr. Diana, a research pharmacologist at the University of Sassari, Italy, designed a pilot clinical trial. Sixty people who were trying to quit cocaine would receive TMS, real or sham, every other day for a month. Dr. Diana would assess their cocaine use though interviews and hair analysis before they started TMS, at the end of the treatment month, and every 3 months thereafter for a year. He hoped that the patients who received real TMS would reduce their cocaine use.

Both researchers’ projects hit snags early on. In this installment, we follow Dr. Martinez as she resolves an initial impasse and advances her project to a new stage. Meanwhile, circumstances close in on Dr. Diana. He is forced to cut short his trial, but comes away with encouraging data and increased enthusiasm for TMS.

Frequency and Intensity

The first TMS settings Dr. Martinez tested appeared to reduce cocaine intake among participants who completed the course of treatment. However, only one third completed the course. The rest complained of pain and anxiety during their first treatment session, and refused to continue.

Dr. Martinez adjusted one of her settings to try to prevent patient dropout. Reducing the magnetic pulse frequency from 10 Hz to 1 Hz abolished the aversive responses, but also the reductions in cocaine use.

Dr. Martinez considered testing an intermediate frequency. In the end, she decided to look for a way to make 10 Hz more tolerable. She says, “If you look at the literature on TMS in psychiatric disorders, there’s a strong rationale for using 10 Hz, or even 15 or 20 Hz.”

She asked herself why so many participants hadn’t tolerated TMS at 10 Hz, when many other researchers had used it without problems. Of several possible explanations, one stood out: Cocaine users tend to have exceptionally high motor thresholds.

Dr. Martinez explains, “A person’s motor threshold is the lowest TMS intensity that will stimulate his or her motor neurons to fire and contract a muscle. The TMS technician ascertains the motor threshold to determine how much stimulus to apply in treatment. If the stimulus is strong enough to activate motor neurons, it’s presumably enough to activate neurons in other cortical areas as well.”

To ascertain the motor threshold, the technician directs the TMS pulse at an area of motor cortex that controls a muscle, for example a hand or calf muscle. The technician delivers a pulse at a low intensity setting, then dials the intensity up in small steps until the target muscle twitches. The twitch gives visible proof that motor neurons have fired.

Dr. Martinez says, “The motor thresholds of the cocaine users in our study were in the range of 80 percent to 84 percent of the power output of our TMS coil. That’s higher than the thresholds that have been recorded in other studies with coils of this type. It’s also been reported in the literature that cocaine users have high motor thresholds.”

Because of their high motor thresholds, Dr. Martinez’ study participants received exceptional amounts of stimulation during the ascertainment procedure. She says, “We had to keep turning up the intensity of the stimulus, and it would often take us a good 40 minutes to work up to the threshold.” Maybe, she thought, so much stimulation during the ascertainment, plus the additional stimulation applied during treatment, hyper-excited neurons in a way that caused pain and alarm.

Dr. Martinez tested her conjecture on herself. She recounts, “When we first started working with TMS, I was curious about the experience, so I went under the coil to ascertain my motor threshold. I found out that, like cocaine users, I tend to have a higher threshold than the average person. During the ascertainment procedure I developed a headache and some other mild symptoms, but nothing too unpleasant. Now I decided to see how I would feel if I underwent what our study participants were getting—motor threshold ascertainment followed by a 10-Hz treatment. I was miserable.”

Tweak and Succeed

Dr. Martinez considered how she might adjust her study protocol to make TMS at 10 Hz comfortable for cocaine users despite their high motor thresholds. She could obtain no guidance from colleagues or the scientific literature, because no one had ever before used the specific TMS coil she was using, called the H coil, with cocaine users.

Dr. Martinez turned for advice to Dr. Abraham Zangen, of Ben-Gurion University of the Negev, in Israel, a researcher and developer of the H coil. Brainstorming together, the two came up with two adjustments:

* Dr. Martinez had been administering TMS treatment directly after motor threshold ascertainment. Going forward, she would separate the two:  ascertain the motor threshold in the morning and deliver treatment in the afternoon. Doing so would spread the stimulation over a longer time.

* She would lower the intensity of the TMS treatment. Dr. Zangen had been using the H coil to treat patients with obsessive compulsive disease, and had found that intensities lower than the motor threshold could be effective.

Dr. Martinez says that when she returned to the TMS laboratory, “We weren’t sure that these adjustments would work. We were nervous. And the participants picked up on our unease. They were looking at us like, ‘Why are you nervous?'” The adjustments worked (see Figure). Participants no longer reported pain, and most now stayed on to complete the treatment. A further protocol adjustment—spreading motor threshold ascertainment over 4 days—further increased the completion rate.

Dr. Martinez says, “These adjustments to our protocol give people time to acclimate to the stimulation. We’ve seen that TMS definitely gets less painful over time.”

With the amended protocol, Dr. Martinez quickly reached her goal of treating 6 participants with TMS at 10 Hz. These patients reduced their choices for cocaine, from about 5.5 before the treatment to 2.2 after it. No changes in the choice for cocaine were seen in the groups that received sham or low-frequency TMS.

Dr. Martinez says, “I must thank Dr. Zangen, who spent a lot of time discussing ways to fix my protocol. I’m also grateful to Brainsway Corporation, makers of the H coil, who have a real interest in treating addiction, and provided me with the equipment to do this work.”

Judging that she had enough evidence that her TMS protocol was efficacious to warrant a pilot clinical trial, Dr. Martinez began to prepare a grant proposal. In the next installment of this Narrative of Discovery, we’ll follow Dr. Martinez into this next stage of her project.

Figure. TMS Frequency and Intensity Settings Determine Efficacy and Tolerability In Dr. Martinez’ study, participants who completed a course of TMS with a frequency of 10 hertz (Hz, pulses per second) (A) reduced their cocaine use, but many found the treatment intolerable. Participants tolerated TMS with a frequency of 1 Hz well (B), but did not reduce their cocaine use. Dr. Martinez adjusted the schedule of her TMS protocol and tried 10 Hz again, this time with success. For her final settings, she also lowered the TMS pulse intensity (amplitude) from 120 percent of motor threshold to 110 percent of motor threshold (C).

Bad News

Dr. Diana’s recruitment effort ran into a deep fund of suspicion. When Dr. Diana showed potential trial participants the TMS machine and explained its purpose, many accused him of intending to subject them to electroshock. Some declined to participate. In 2 years, he enrolled only 20 patients.

In mid-2015, Dr. Diana applied to the Italian Department of Anti-Drug Policies for an extension of his funding for the project. Weeks, then months, passed with no response. Dr. Diana’s remaining funds from the past year dwindled. In July, he stopped recruiting patients because he was out of money to pay the laboratory to test hair samples for cocaine metabolites. He continued to provide his existing patients with psychological support and ask them about their cocaine use. Without biological confirmation, however, the scientific community would accord less weight to his patients’ self-reports.

“Finally, in November, the Agency was forced to respond because I was making thousands of phone calls,” Dr. Diana says. “I reminded them that we knew from the start this was going to be a 3-year project. It would be a shame not to finish, because we had encouraging preliminary findings. They told me, ‘Look, we wish you all the luck you certainly deserve, but we don’t have money to give you.”

Striking the Tent

Unable to continue his study, Dr. Diana set out to reap what he could from his years of work.  He had administered real or sham TMS to 19 patients, far short of the 60 he needed to establish that his TMS approach was effective. “I can’t do any statistics on such a small number and hope to persuade my colleagues that our findings are predictive,” he says.

Nevertheless, Dr. Diana says, “We didn’t have any choice. We had to either analyze our data and see what was there or just throw everything out.” Although he could prove nothing with results from so few patients, at least he would find out if their outcomes were consistent with TMS being effective. If they were, his work might inspire others to try TMS.

The outcomes were indeed consistent. Patients in both the TMS- and sham-treated groups were using less cocaine 1 and 3 months after starting the treatment. The difference in the amount of reductions was not statistically significant, but a significant difference emerged at the 6-month follow-up. At that time, the patients in the TMS-treated groups were using about 70 percent less cocaine than they had before starting the trial, and the sham-treated group about 45 percent less.

In addition, Dr. Diana says, “The study participants commonly reported that their mood was much better. They were more comfortable with life. They didn’t feel overwhelmed with guilt. Their anxiety levels went down significantly after the treatment. Some also described regularization of sleep, with better circadian rhythms.”

For Dr. Diana, the persisting effect of TMS past 6 months hints that his most ambitious hope for TMS may pan out:  The treatment may not just temporarily remit cocaine addiction, but actually restore the patient’s brain to a pre-addicted state (see “Can Neurons Be Reeducated?”).

Enthused and wishing to share his findings, Dr. Diana wrote a report to submit for publication. He knew the chances were slim that a journal would accept it. As of this writing, one journal has turned down the manuscript, and Dr. Diana awaits a decision from a second journal. (Update: In July 2016, Dr. Diana’s manuscript was accepted for publication in the journal Frontiers in Psychiatry−Addictive Disorders.)

Lessons and Plans

Dr. Diana sees his loss of funding in perspective. He notes that Italy is experiencing tight economic times and the government has reduced its investment in research: “We have a new prime minister who looks very efficient, very pragmatic. Everybody seems to be reporting that the country’s situation is improving economically. But when you apply for funding for research, many times the answer you get is, ‘We are now fixing things more important than research.’ Unfortunately, they don’t understand that it’s through research and innovation that you generate more jobs and well-being for people.”

Dr. Diana’s broad perspective has not precluded disappointment. He says, “I worked on this study for five years. Before I even started to recruit patients, I worked 2 years to get it approved by the ethics committee and the hospital director, plus paperwork for this and that, endless paperwork. So it’s very frustrating. But what can I say?”  Despite his disappointment, Dr. Diana remains excited about TMS. He has already teamed up with a collaborator, Dr. Giorgio Corona, in Cagliari, Sardinia. “We are set to continue this work and to replicate my observations with a larger sample,” Dr. Diana says.

For Dr. Diana, starting over, although far from what he would have wished, presents opportunities to implement new knowledge and lessons learned. In his new trial, for example, he will measure patients’ central dopamine levels, using a technique that came to his attention too late to be used in his previous trial (see “Windows Into the Brain”).

The new trial’s recruitment protocol will incorporate another lesson, this one learned at great cost: To put to rest misperceptions and mistrust, potential recruits will receive a thorough orientation designed to put them at ease about TMS. Dr. Diana says, “Our strategy will be to persuade patients that TMS really is safe and without side effects. We’ll show them the machine. We’ll show them videos of other people who have taken the treatment. And we’ll tell them that if they perceive anything is wrong, they can leave the study whenever they decide.”

Dr. Diana is eager to get his new trial underway. He says, “The idea that TMS can be useful has been reinforced in me. Comparing the effects we observed with TMS to what others are reporting with medications, I think TMS is the way to go. The new machine is being delivered as we speak.”

Can Neurons Be Reeducated?

Dr. Diana explains, “We know from studies by Nora Volkow, Diana Martinez, and others that cocaine use over time weakens dopamine neurons. These neurons fire less often and less vigorously in the addicted brain, and this accounts for a person’s cocaine craving and compulsive responses to cocaine cues. We administer TMS to increase those neurons’ firing rate and strength back to their pre-cocaine levels. That might be therapeutic, but it won’t be so great if the neurons just revert to their weakened state after the treatment, and the patient has to keep coming back indefinitely. We want an effect that lasts for a long time.

“Therefore our aim with TMS is to induce an effect called long-term potentiation, LTP, of the dopamine neurons. LTP is something that occurs naturally when a neuron repeatedly receives intense high-frequency stimulation from other neurons. The neuron develops structural changes that make it more active and sensitive to future stimulation, and that endure for extended periods.

“In my personal opinion, the results of my trial, although they are preliminary, indicate that TMS produced LTP of our patients’ dopamine neurons. Our TMS-treated patients continued to use much less cocaine for 5 months after our 1-month treatment. The contrast in outcomes between our TMS-and sham-treated groups also supports this idea. We think that the sham TMS had a strong placebo effect that lasted 2 months after the treatment, possibly because the experience of sitting under the apparatus makes a powerful impression. After 5 months, however, the placebo effect began to wear off, while LTP kept the neurons in the TMS-treated group strong.’

Dr. Diana adds, “With TMS we were trying to tell the dopamine neurons, ‘Okay. You fire faster, and remember that you are able to fire faster.’ I think the neurons got the message.”

Windows Into the Brain

The underlying idea of using TMS to treat cocaine addiction is that stimulation with magnetic pulses can re-invigorate hypofunctional dopamine signaling in the prefrontal cortex. To make the best case for TMS’ efficacy, Dr. Martinez and Dr. Diana would like to show not only that TMS reduces cocaine use, but also that the reductions are paralleled by increases in dopamine. Retinography is a tool—albeit a tricky one—for accomplishing this. With retinography, researchers measure dopamine levels in the retina, and interpret them as indicators of levels in other parts of the central nervous system.

Source:  July 2016

COBURG, Ore.  Serenity Lane says they’re seeing a growing number of people battling “Marijuana Use Disorder.” Many people have become habitual users to start their day by using the drug In Oregon, marijuana is legal for recreational and medical use, but one local drug rehab facility is concerned about pot addiction. Serenity Lane is an alcohol and drug treatment facility in Coburg.  Staff members said they’re seeing an increase in people with what they call “Marijuana Use Disorder.”

Manager Jerry Gjesvold at Serenity Lane said they see addiction trends years in advance. “Just like the opioid epidemic”, Gjesvold , “said we are seeing the beginning stages of a growing marijuana addiction”.

“Well, we know now that in the DSM-5, which is the manual that’s used to diagnose substance use disorders, there’s a specific marijuana use disorder diagnosis,” said Gjesvold.   Gjesvold said they see more patients as young as 18 years old even though the legal age for recreational marijuana use is 21.

“[Marijuana use] has become a much more acceptable, and because of that there’s more people that are using it,” Gjesvold said.   He said youth tend to be at higher risk for addiction. It’s because they use devices like vaping and assortments of marijuana like hash oil.

Products with higher THC concentration are more dangerous, but are easier to hide from parents.  “The universal response on the part of parents is that, ‘I had no clue,'” Gjesvold said.

The interim medical director, Paul Steier, at Serenity Lane says highly concentrated levels of THC can have a negative impact on the developing brains of young people. “They have trouble sequencing, doing numbers, word recollection,” Steier said.

Steier said in some cases it creates schizophrenic types of behavior. He said side effects from marijuana use disorder persist for a minimum of five months.  “But there clearly is a withdrawal experience from cannabis, especially in the habitual users, who are the people who sort of wake and bake,” said Steier.

Steier said the withdrawal experience is the same as other addictions causing changes in heart rate, blood pressure, and body temperature.

Source:    11th July 2016

Hospital maternity units and new-born care nurseries would have to report the number of infants born addicted to drugs under a bill headed to Ohio’s governor. The state Senate unanimously passed the measure Wednesday, and Gov. John Kasich was expected to sign it.

The measure is one of several aimed at reducing the state’s prescription painkiller addiction epidemic. Supporters say tracking the number of drug-addicted babies will help the state monitor Ohio’s progress in fighting drug addiction.

The facilities would be required to report the information to the state Health Department every three months. Patients would not be identified, and the information could not be used for law enforcement purposes. Should a maternity unit, maternity home or new-born care nursery fail to comply with the requirement, the state could impose a fine or revoke or suspend its license.

Overdose drug deaths have been the leading cause of accidental death in Ohio since 2007, surpassing car crashes. Many of those deaths are from painkillers and heroin.

Opiates and narcotics taken by the mother during pregnancy can pass through the placenta through the baby, causing the infant to be born dependent on harmful drugs. The babies experience neonatal abstinence syndrome and face an array of health complications, said state Sen. Shannon Jones, a Springboro Republican.

“These new-borns are thrown into painful withdrawal symptoms, such as rapid breathing, vomiting and seizures immediately following their birth,” she said.  Jones told her colleagues on the Senate floor that she had witnessed children withdrawing. “It is the most horrifying thing that I have personally experienced,” she said.

Caring for the drug-addicted new-borns and mothers, who are often on Medicaid, can be costly to the system.  Jones said officials hope to use the information to help measure opiate and illegal drug abuse across the state and better target resources to help women and babies struggling from addiction.

Source: Wednesday, April 2, 2014

For most people, the idea of winning some money will ignite a rush of emotions – joy, anticipation, excitement.

If you were to scan their brains at that very moment, you would see a surge of activity in the part of the brain that responds to rewards.

But, for people who’ve been smoking cannabis, that rush is not as big – and gets smaller and smaller over time, new research suggests.

And that dampened, blunted response may actually increase the risk that marijuana users are more likely to become addicted to pot and other drugs.

Dr Mary Heitzeg, senior author of the new study, a neuroscientist from the University of Michigan Medical School, said: ‘What we saw was that over time, marijuana use was associated with a lower response to a monetary reward.

‘This means that something that would be rewarding to most people was no longer rewarding to them, suggesting but not proving that their reward system has been “hijacked” by the drug, and that they need the drug to feel reward – or that their emotional response has been dampened.’

The findings come from the first long-term study of young marijuana users, that tracked brain responses to rewards over time, and is published in the JAMA Psychiatry.

They reveal measurable changes in the brain’s reward system with cannabis use – even when other factors like alcohol use and cigarette smoking were taken into account.

The study involved 108 people in their early 20s – the prime age for cannabis use.

All were taking part in a larger study of substance abuse, and all had brain scans at three points over a four-year period.

Three-quarters were men, and nearly all were white.

While MRI scans were performed, participants were invited to play a game.

People who smoke cannabis regularly show less activity in the area of the brain that releases the ‘pleasure’ hormone, dopamine

They were required to click a button when they saw a target on a screen in front of them.

Before each round, they were told they could win 20 cents, or $5 – or that they might lose that amount, have no reward or loss.

The researchers were most interested in assessing what happened to the volunteers’ brains – specifically activity in the reward center – the area called the nucleus accumbens.

And the moment that was deemed most important, was the moment of anticipation – when the volunteers knew they might win some money, and were anticipating what it would take to win the simple task.

In that moment of anticipating reward, that area of the brain should spark into action, pumping out the ‘pleasure’ hormone, dopamine.

The greater a person’s response, the more pleasure or thrill a person feels – and the more likely they will be to repeat the behavior later.

The researchers found that the more marijuana use a volunteer reported, the smaller the response in this part of the brain over time.

Past research has shown the brains of people who use a high-inducing drug repeatedly respond more prominently when they are shown cues related to that drug.

That increased response means the drug has been associated in their brains with positive, rewarding feelings.

And, that can make it harder for users to stop seeking out the drug and using it.

First author, Meghan Martz, doctoral student in developmental psychology, said: ‘It may be that the brain can drive marijuana use, and that the use of marijuana can also affect the brain.

‘We’re still unable to disentangle the cause and effect in the brain’s reward system, but studies like this can help that understanding.’

Regardless of that fact, the new findings show there is a change in the reward system over time, when a person regularly uses cannabis, the researchers noted.

Dr Heitzeg and her colleagues also showed recently in a paper in Developmental Cognitive Neuroscience that marijuana use impacts emotional functioning.

The new data on response to potentially winning money may also be further evidence that long-term marijuana use dampens a person’s emotional response – something scientists call anhedonia.

‘We are all born with an innate drive to engage in behaviors that feel rewarding and give us pleasure,’ said co-author Dr Elisa Trucco, a psychologist at the Center for Children and Families at Florida International University.

‘We now have convincing evidence that regular marijuana use impacts the brain’s natural response to these rewards.

‘In the long run, this is likely to put these individuals at risk for addiction.’

Marijuana’s reputation as a ‘safe’ drug, and one that an increasing number of states are legalizing for small-scale recreational use, means that many young people are trying it – as many as a third of college-age people report using it in the past year.

But Dr Heitzeg said that her team’s findings, and work by other addiction researchers, has shown that it can cause effects including problems with emotional functioning, academic problems, and even structural brain changes.

And, the earlier in life someone tries marijuana, the faster their transition to becoming dependent on the drug, or other substances.

‘Some people may believe that marijuana is not addictive or that it’s ‘better’ than other drugs that can cause dependence,’ said Dr Heitzeg.

‘But this study provides evidence that it’s affecting the brain in a way that may make it more difficult to stop using it.

‘It changes your brain in a way that may change your behavior, and where you get your sense of reward from.’

Source:    6th July  2016

Ingenious pill formulations and the latest manufacturing technologies are helping to stem the tide of painkiller addiction.

Mary Marcuccio’s life was turned upside down by drug misuse and addiction. Her son, now 26, started with alcohol and marijuana. Then came cocaine and hallucinogens. By 14, he was stealing prescription painkillers from friends’ medicine cabinets, crushing and snorting the pills to achieve a quick and euphoric high. Within one year, he had graduated to injecting heroin.

This progression is “so stereotypical”, says Marcuccio, founder of My Bottom Line, a Florida-based consulting business for families dealing with substance misuse. According to US survey data, 77% of heroin users say that, like Marcuccio’s son (who remains addicted to heroin), they misused prescription opioids — derivatives of natural or synthetic forms of opium or morphine — before trying heroin.

“It behooves us to make a greater effort at creating unabusable formularies.”

But substance-misuse specialists think that this chain of addiction might be broken with the aid of the latest manufacturing processes to make powerful opioid pain medication more resistant to various forms of tampering. Such drug preparations could also save lives. The death toll from misusing prescription opioids has skyrocketed around the world in the past 20 years, with opioid-linked overdoses exceeding fatalities from road accidents or deaths from heroin and cocaine in countries including the United Kingdom, the United States and Australia. “It behooves us to make a greater effort at creating unabusable formularies,” Marcuccio says.

Fortunately, the science and manufacturing of misuse-deterrence are advancing rapidly — and so is the political climate. In the United States — a country that consumes more than 80% of the global opioid supply — politicians are beginning to craft bills to incentivize the development of misuse-resistant formulations. “The idea is to transition the market,” says Dan Cohen, chair of the Abuse Deterrent Coalition, a network of advocacy organizations, technology manufacturers and drug companies based in Washington DC. “There are now so many different abuse-deterrent formulations that are either in products or in development that there’s enough variety out there for any product to be able to put abuse-deterrence in it.”

The new guard

Some of the latest tablet formulations are so hard that even a hammer-blow cannot pulverize them. Many pills form a gelatinous goo when dissolved that renders them difficult to inject. Others contain reversal agents that negate the high when the tablets are messed with. The idea is to create pain-relief medicines that are less prone to misuse yet work when taken as directed.

The technologies in place today are not ironclad, though. A quick perusal of online message boards and videos reveals numerous tips on how to circumvent the defences of even the most reinforced tablets. What is more, not all prescription opioids on the market are misuse-resistant. “We’re still in abuse-deterrent formulations 1.0,” says Richard Dart, director of the Rocky Mountain Poison and Drug Center in Denver, Colorado. But, he adds with a touch of hyperbole, “there are a zillion abuse-deterrent formulations coming”.

Manufacturers have been worried about prescription-drug misuse for decades. When the first controlled-release formulation of the opioid oxycodone hit the US market 20 years ago, the drug’s manufacturer, Purdue Pharma of Stamford, Connecticut, touted the twice-a-day medicine as a less-addictive alternative to the faster-acting painkillers that provide a big opioid hit all at once. In reality, however, Purdue’s longer-lasting pill, sold under the trade name OxyContin, had the opposite effect.

Drug users easily defeated OxyContin’s time-release mechanism by crushing or chewing it. Just one OxyContin could contain more oxycodone than a dozen instant-release pills but no extra ingredients such as paracetamol that make people sick if taken at high doses. OxyContin quickly became the number one addiction problem in many parts of the world, particularly in the United States and Australia. The drug was so popular among the rural poor of Appalachia in West Virginia and Kentucky that it earned the street name ‘hillbilly heroin’.

Purdue set to work to guard against some of the worst forms of misuse. In 2010, the company introduced a misuse-averting version of OxyContin that contains a polymer made of long-chain molecules. This makes the new tablet more difficult to crush — although it is not rock hard. “It behaves more like plastic,” explains Richard Mannion, executive director of pharmaceutics and analytical development at Purdue. “So, it will deform if subjected to force, but it doesn’t break into a powder easily.” The revised formulation is thus much harder to snort. Plus, Mannion says, when combined with water, the polymer forms a gummy substance that makes it very difficult to draw into a syringe (although misuse is still possible).

The new version of OxyContin has proved to reduce the incidence of therapeutic misuse. A study1 of more than 140,000 people treated at rehabilitation centres across the United States found that misuse by injection, snorting or smoking declined by two-thirds in the two years after the reformulation. In light of these results, in 2013, Purdue won the right from the US Food and Drug Administration (FDA) to describe the misuse-deterrent benefits of OxyContin on the drug’s label and to make marketing claims accordingly. The FDA said at the time that any future generic versions of OxyContin would have to incorporate equivalent misuse-deterrent protection. (In April 2015, the FDA released a guidance document outlining the types of study needed to establish misuse-deterrence, but the report stopped short of addressing generic opioid products.)

Other painkillers that now have FDA-approved misuse-deterrent labelling include Embeda, an extended-release morphine from New York-based pharmaceutical firm Pfizer, and Targiniq, another long-acting preparation of oxycodone from Purdue. Both contain antagonist agents — offsetting ingredients that remain largely inactive when the drugs are taken as directed, but that will annul the opioid’s effects if the drugs are snorted or injected.

“These new technologies are showing some positive results,” notes Robert Jamison, a pain psychologist at the Brigham and Women’s Hospital Pain Management Center in Chestnut Hill, Massachusetts. In Australia, for example, OxyContin users accounted for more than 60% of the visits to the Medically Supervised Injecting Centre in Sydney. After the tamper-resistant version of OxyContin hit the Australian market in April 2014, a team led by Louisa Degenhardt, a drug-addiction researcher at the University of New South Wales in Sydney, found2 that the number dropped to 5%. In the United States, levels of opioid misuse have decreased from their peak in 2010, when the new formulation of OxyContin arrived on the market. Rates of opioid dispensing and overdoses have dropped appreciably, too.

These public-health benefits come with an economic bonus. According to calculations from Noam Kirson and his colleagues at Analysis Group, a consulting firm in Boston, Massachusetts, the reformulated OxyContin has reduced misuse-related medical expenses and indirect societal costs by more than US$1 billion per year in the United States3. “These are substantial savings,” Kirson says.


Old habits die hard

Despite the gains, the misuse-deterrence field still has a long way to go. Drug users who have been thwarted by one technology can switch to another prescription medicine that lacks anti-tampering defences. That is what happened in rural Appalachia following the introduction of reformulated OxyContin. Opioid misusers simply started snorting and injecting the less potent immediate-release preparations of oxycodone, most of which lack misuse-deterrence characteristics. “It’s kind of a whack-a-mole situation,” says Jennifer Havens, an epidemiologist at the University of Kentucky Center for Drug and Alcohol Research in Lexington.

Plus, even with the latest physical defences it is still possible to get high by swallowing lots of OxyContin or Embeda pills at once. Preventing oral misuse requires a different approach — which a company called Signature Therapeutics, based in Palo Alto, California, is pursuing.

Signature Therapeutics’ technology uses prodrugs, which are inactive until they undergo the appropriate chemical conversion in the body. When these pills are taken by mouth as directed, a digestive enzyme in the gut called trypsin releases part of the prodrug, initiating the process of opioid drug release. But because trypsin is not found elsewhere in the body, the prodrug remains inert when injected, snorted or smoked. Signature Therapeutics has already tested its painkilling hydromorphone prodrug in a phase I trial of healthy volunteers; the company plans to begin evaluating its oxycodone prodrug in human studies later this year.

Prodrugs alone do not prevent excessive pill-popping, but scientists at Signature Therapeutics have another trick up their sleeves. If the prodrugs look promising in the clinic, the company will add a second compound that blocks trypsin activity. This might seem counterintuitive, but it is all about threshold levels. The amount of trypsin inhibitor found in one or two pills will not interfere with the prodrug modification, but a handful of pills collectively contain enough inhibitor to shut down the conversion process. With this approach, Signature Therapeutics can create either extended-release or immediate-release opioids. Bill Schmidt, chief medical officer at the company, says that the potential of these drugs is “maximum therapeutic benefit with very low abuse liability”.

New formulations such as these could ultimately prove to be almost addiction-proof, but they are not cheap. And their benefits might not be fully realized unless authorities require drug companies to include them. “The problem with abuse-deterrence right now is the lack of incentives,” Cohen says.

Lawmakers in the US House of Representatives previously proposed legislation that would have barred the approval of any new pharmaceuticals that did not use formulas resistant to tampering. That bill died in committee, but, according to Cohen, revised legislation should be introduced again “soon”. Individual US states have also begun to pass laws that compel pharmacists exclusively to dispense, and insurers to cover, misuse-deterrent versions of opioids unless instructed otherwise by a physician.

Ultimately, the success of long-term efforts to rein in opioid addiction could depend on the regulations surrounding generic painkillers. In December 2014, Australia allowed the sale of a generic long-acting oxycodone without misuse-deterrence characteristics. Degenhardt, who is monitoring the drug-misuse data, worries that many of the gains of OxyContin’s reformulation will now be lost. By contrast, US authorities have already said that they will not approve such a product.

All of these efforts should help to bring down the number of overdose deaths and also prevent experimentation with prescription pills. In her study population in rural Appalachia, Havens has met so many young people like Marcuccio’s son — for whom easily misused opioids were the gateway to addiction — that she has reached a simple, but absolute, conclusion: “The only way that abuse-deterrent formulations are going to work is if they’re all abuse-deterring,” she says. “It can’t just be piecemeal. It’s got to be all or nothing.”

Source:   Nature  522, S60–S61 doi:10.1038/522S60a  (25 June 2015)

A stressed rat will seek a dose of cocaine that is too weak to motivate an unstressed rat. The reason, NIDA researchers report, is that the stress hormone corticosterone increases dopamine activity in the brain’s reward center. When an animal is stressed, the cocaine-induced dopamine surge that drives drug seeking rises higher because it occurs on top of the stress-related elevation.

Graduate student Evan N. Graf, Dr. Paul J. Gasser, and colleagues at Marquette University in Milwaukee, Wisconsin, traced the physiological pathway that links stress and corticosterone to increased dopamine activity and heightened responsiveness to cocaine. Their findings provide new insight into cocaine use and relapse, and point to possible new medication strategies for helping people stay drug free.

Stress Increases Sensitivity to Relapse Triggers

Former drug users who relapse often cite stress as a contributing factor. The Marquette researchers observed that when stress figures in relapse, other relapse promoters are almost always present as well. Dr. Gasser explains, “It’s never one single event that triggers relapse. It’s the convergence of many events and conditions, such as the availability of the drug, cues that remind people of their former drug use, and also stress.” On the basis of this observation, the researchers hypothesized that stress promotes relapse by making a person more sensitive to other relapse triggers.

To test their hypothesis, the researchers put stressed and unstressed rats through an experimental protocol that simulates regular drug use in people followed by abstinence and exposure to a relapse trigger. As the stressor, they used a mild electric foot shock; as the relapse trigger, they administered a low dose of cocaine (2.5 milligrams per kilogram).

The results confirmed the hypothesis. The stressed rats, but not the stress-free animals, responded to the small cocaine dose with a behavior that parallels relapse in people: They resumed pressing a lever that they had previously used to self-administer the drug (see Figure 1, top graph).



Text Description of Graphic

A Stress Hormone Underlies the Effect

Mr. Graf and colleagues turned their attention to the question of how stress sensitizes animals to cocaine’s motivational effect. One likely place to start was with the hormone corticosterone. In stressful situations, the adrenal glands release corticosterone into the blood, which carries it throughout the body and to the brain. Among corticosterone’s physiological roles is that it affects glucose metabolism and helps to restore homeostasis after stress. The Marquette researchers demonstrated that increasing cocaine’s potential to induce relapse also belongs on the list of corticosterone’s effects. Reprising their original experimental protocol with a couple of new twists, they showed that:

  • Corticosterone is necessary for stress to promote relapse to cocaine seeking: The researchers removed rats’ adrenal glands, which prevented the animals from producing corticosterone. In this condition, the animals did not exhibit relapse behavior when exposed to the stressor and low-dose cocaine.
  • Corticosterone in the brain reward center is sufficient by itself to increase cocaine’s potency as a relapse trigger:The researchers injected these same rats with corticosterone, bringing the hormone concentration up to stress levels in the brain reward center (nucleus accumbens, NAc). Now the animals exhibited relapse behavior when exposed to cocaine, even without the stressor (see Figure 1, middle graph).

Enhanced Dopamine Activity…

The researchers next took up the question: What does corticosterone do in the NAc to increase cocaine’s potency to induce relapse? A hypothesis that suggested itself immediately was that the hormone enhances dopamine activity. Dopamine is an important neuromodulator in the NAc, and all addictive drugs, including cocaine, produce their motivating effects by increasing dopamine concentrations in the NAc.

The Marquette team showed that, indeed, stress-level concentrations of corticosterone enhance the cocaine-induced rise in extracellular dopamine in the NAc. In this experiment, the researchers exposed two groups of rats to low-dose cocaine, then measured their NAc dopamine levels with in vivo microdialysis. One group, which was pretreated with corticosterone injections, had higher dopamine levels than the other, which was not pretreated.

The Marquette team firmed up their hypothesis with a further experiment. They reasoned that if corticosterone promotes relapse behavior by increasing dopamine activity, then preventing that enhancement should prevent the behavior. This indeed turned out to be the case. When the researchers injected animals with corticosterone but also gave them a compound (fluphenazine) that blocks dopamine activity, exposure to low-dose cocaine did not elicit relapse behavior.

…Due To Reduced Dopamine Clearance

So far the Marquette team had established that the stress hormone corticosterone promotes relapse behavior by increasing dopamine activity in the NAc. Now they moved on to the next question: How does corticosterone enhance dopamine activity?

To address this question, the researchers considered the cycle of dopamine release and reuptake. In the NAc, as elsewhere in the brain, dopamine activity depends on the concentration of the neurotransmitter in the extracellular space (space between neurons): the higher the concentration, the more activity there will be. In turn, the extracellular dopamine concentration depends on the balance between two reciprocal ongoing processes: specialized neurons releasing dopamine molecules into the space, and specialized proteins drawing molecules back inside the neurons.

Mr. Graf and colleagues discovered that corticosterone interferes with the removal of dopamine molecules from the extracellular space back into cells. It shares this effect with cocaine, but achieves it by a different mechanism.

In this experiment, the researchers measured real-time changes in dopamine concentration in the NAc in response to electrical stimulation of dopamine release in the area. This technique allowed the team to measure both A) the rate of increase in dopamine concentration, indicating the amount of dopamine released; and B) the rate of decrease in dopamine concentration, indicating the rate of dopamine clearance. The scientists measured stimulation-induced increases and decreases in extracellular dopamine concentrations under three conditions: at baseline, after giving the animals a compound that blocks the dopamine transporter (DAT), which is the mechanism whereby cocaine inhibits dopamine removal; and, last, after injecting the animals with corticosterone. They found that:

  • As happens with cocaine, the clearance of extracellular dopamine decreased after DAT blockade.
  • Clearance of extracellular dopamine decreased further after corticosterone.


A Candidate Mechanism

One question remained outstanding to complete the picture of how stress potentiates the response to cocaine: What is the mechanism whereby corticosterone reduces dopamine clearance?

Mr. Graf and colleagues noted that previous research provides a likely answer: Corticosterone has been shown to inhibit the functioning of the organic cation transporter 3 (OCT3), which is another of the specialized proteins that, like DAT, remove dopamine from the extracellular space. To confirm this hypothesis, the researchers resorted again to their initial experimental protocol. This time, they injected rats with a compound (normetanephrine) that blocks OCT3, followed by low-dose cocaine. The animals responded by resuming their previously abandoned lever pressing  behavior, proving that OCT3 blockade is sufficient to potentiate the response to cocaine (see Figure 1, bottom graph).

The Marquette researchers say that further studies will be required to definitively establish that OCT3 plays the role their evidence points to. Taken together, however, their experiments trace a complete pathway connecting stress to an animal’s enhanced responses to cocaine (see Figure 2):

  • Stress raises corticosterone levels.
  • Corticosterone blocks OCT3, inhibiting dopamine clearance and thereby raising dopamine activity in the NAc.
  • When a stressed animal is exposed to cocaine, the resulting dopamine surge builds on the foundation of this already higher-than-normal level of dopamine activity.
  • The added elevation of the dopamine surge increases the animal’s motivation to seek the drug.



Figure 2. Stress Amplifies Cocaine’s Effect on Dopamine Release in the Nucleus Accumbens (NAc) The schematic illustrates how stress may enhance cocaine’s motivational effect and increase the risk for relapse. A) Cocaine binds to the dopamine transporter (DAT) on dopamine-releasing neurons in the NAc, reducing dopamine (DA) clearance and, in turn, increasing extracellular dopamine. B) Stress causes release of corticosterone, which inhibits the OCT3 transporter, further reducing dopamine clearance and increasing extracellular dopamine. The resulting heightened dopamine stimulation of medium spiny neurons (MSNs) enhances drug seeking.

Text Description of Graphic

Stress–Relapse Connection Unraveled

“Our findings show that stress doesn’t just cause relapse behavior by itself, but interacts with other ongoing behaviors to influence relapse,” Dr. Gasser says. “This insight provides a better picture of how stress can affect addiction. It helps us understand why treating cocaine addiction is so difficult and will help in designing therapies whether they be based on pharmacotherapy or counseling.” The researchers believe—and are testing as a hypothesis—that stress increases the power of environmental drug-associated cues to trigger relapse, just as it does the power of low-dose cocaine.

Although researchers have long known that stress plays an important role in relapse, pinning down its role experimentally has been a challenge, says Dr. Susan Volman, program officer and health science administrator at NIDA’s Behavioral and Cognitive Science Research Branch. “This study provides a perspective of stress as a stage-setter or modulator for relapse, and it gets all the way down to the molecular mechanism. Based on this team’s findings, OCT3 offers a potential new target for developing pharmacological therapies to help with treating addiction,” Dr. Volman says.

This work was supported by NIH grants DA017328, DA15758, and DA025679.


Graf, E.N.; Wheeler, R.A.; Baker, D.A. et al. Corticosterone acts in the nucleus accumbens to enhance dopamine signalling and potentiate reinstatement of cocaine seeking. Journal of Neuroscience 33(29):11800-11810, 2013. Full text

Genetic differences may protect some who experienced childhood trauma from later marijuana dependence, study finds


Genetic variation within the endocannabinoid system may explain why some survivors of childhood adversity go on to become dependent on marijuana, while others are able to use marijuana without problems, suggests new research from Washington University in St. Louis.

“We have long known that childhood adversity, and in particular sexual abuse, is associated with the development of cannabis dependence. However, we understand very little about the individual difference factors that leave individuals vulnerable or resilient to these effects,” said Ryan Bogdan, PhD, assistant professor of psychological and brain sciences in Arts & Sciences and a senior author of the study.

Forthcoming in the Journal of Abnormal Psychology, the study is among the first to pinpoint a specific genetic variant that may influence susceptibility to cannabis dependence in the context of childhood trauma.

THC, the main psychoactive ingredient in marijuana, influences an array of mental and bodily functions because it closely mimics chemical enzymes that the endocannabinoid system naturally produces to send signals between neurons and other individual cells throughout the body. These signals trigger the production of other internal chemicals, such as adrenalin, which help the body modulate its response to external influences, such as fear, stress and hunger.

Like most bodily functions, the workings of the endocannabinoid system are closely programmed and controlled by a set of genetically coded instructions.

“In this study, we investigated whether variation in genes within the endocannabinoid system may be particularly important in setting the stage for cannabis dependence, especially in the context of childhood trauma,” said lead author Caitlin E. Carey, a PhD student working with Bogdan.

In phase one of the study, researchers examined genetic data from 1,558 Australian marijuana users who self-reported various types of sexual abuse as children. Carey and colleagues examined whether Single Nucleotide Polymorphisms (SNPs, pronounced “snips”) located in or near endocannabinoid system genes were associated with the

development of marijuana dependence symptoms in the context of childhood sexual abuse.

SNPs represent differences in a single DNA building block called a nucleotide and are the most common form of genetic variation in people, with an estimated 10 million SNPs in the human genome.

While little is known about many SNPs, some have been identified as key biological markers for genetic diseases. When SNPs occur within a gene or in a regulatory region near a gene, they may affect how that gene functions, perhaps raising disease risk or changing how an individual responds to certain environmental factors such as drugs or trauma.

The vast majority of SNPs, including those looked at in this study, have two different alleles at each locus; one of these alleles is inherited from the biological mother, with the other being inherited from the biological father. Alleles with two matching pieces of genetic information are called homozygotes (for example A/A or G/G), while those with mixed pairs are called heterozygotes (A/G).

Of the endocannabinoid variants examined, a single variant within the monoacylglycerol lipase (MGLL) gene demonstrated a significant interaction with childhood sexual abuse and later cannabis dependence.

More specifically, the study found that variation within this SNP (known as rs604300) in MGLL showed a clear association between child sexual abuse and cannabis dependence, such that increasing exposure to childhood sexual abuse was associated with a greater number of cannabis dependence symptoms only among individuals who were homozygous for the more common G allele. There was no association between child sexual abuse and cannabis dependence symptoms in heterozygotes, and a negative relationship between childhood sexual abuse and cannabis dependence symptoms in A allele homozygotes.

“As we expected, childhood sexual abuse was overall associated with individuals reporting a greater number of cannabis dependence symptoms,” Carey said. “But what was particularly intriguing is that this association was only seen among people with two copies of the more common G allele. People with at least one copy of the less common A allele did not show this pattern, so these data suggest that the A allele may provide some form of resiliency to the development of dependence.

The endocannabinoid system is known to play an important role in the body’s response to stress. Monoacylglycerol lipase, which MGLL codes for, regulates the availability of 2-

AG, an endocannabinoid neurotransmitter that binds to the same receptors as the THC in plant-based cannabis.

Findings replicated in second sample

In phase two of the study, Carey and colleagues attempted to replicate the findings using data from 859 American participants obtained from the Study of Addiction: Genetics and Environment. Here again, they found the same interaction between the rs604300 genotype and child abuse to be significantly associated with cannabis dependence symptoms.

Carey and colleagues speculate that the rs604300 minor A allele’s role in buffering against later cannabis dependence may be related to how the brain reacts to threat.

As Bogdan said: “The amygdala is a region of the brain critical for behavioral vigilance, including coordinating our behavioral responses to threat in the environment. Heightened amygdala reactivity has been consistently linked to anxiety disorders. Prior research has shown that endocannabinoids and marijuana, as well as prior childhood adversity, affect amygdala function. Endocannabinoid signaling, in particular, regulates reactivity to threat by facilitating a dampening of amygdala response (i.e., habituation) when threats are repeatedly presented with no adverse consequence.”

The amygdala (shown in red) is a region of the brain critical for behavioral vigilance, including coordinating physiologic and behavioral responses to threat. The A allele at rs604300 within MGLL, which conferred protection to cannabis dependence in the context of elevated childhood adversity, was associated with heightened threat-related amygdala habituation (i.e., a increased dampening of response over time) among those exposed to elevated childhood adversity. Such elevated amygdala habituation is associated with recovery from environmental stress.

If the rs604300 A allele is associated with relative increased amygdala habituation (such as a dampening of response over time) to threat in the context of childhood adversity, it is possible that child abuse survivors with this allele may be less prone to later use cannabis in an attempt to achieve the same mood-altering result, they speculated.

In a third phase of this study, they tested for this connection in an independent group of 312 undergraduate students from the Duke Neurogenetics Study and found increased amygdala habituation as a function of early life stress in minor A allele carriers, but not in GG individuals. The finding reinforces the possibility that MGLL rs604300 genotype may play a key role in decoupling the neurobiological link between early life stress and mental health outcomes in later life.

Collectively, while speculative, these data suggest that elevated amygdala habituation among individuals with the A allele who were exposed to childhood trauma may result in decreased reliance on marijuana to cope with future stressors and negative affect.

“It’s important to mention that these findings are unlikely to be informative at an individual level,” Carey said. “We won’t see a genetic test for cannabis dependence anytime soon, if ever, but it’s a start.”




Cannabis use is decreasing in England and Wales, while demand for cannabis treatment in addiction services continues to rise. This could be partly due to an increased availability of high-potency cannabis.


Adults residing in the UK were questioned about their drug use, including three types of cannabis (high potency: skunk; low potency: other grass, resin). Cannabis types were profiled and examined for possible associations between frequency of use and (i) cannabis dependence, (ii) cannabis-related concerns.


Frequent use of high-potency cannabis predicted a greater severity of dependence [days of skunk use per month: b = 0.254, 95% confidence interval (CI) 0.161-0.357, p < 0.001] and this effect became stronger as age decreased (b = -0.006, 95% CI -0.010 to -0.002, p = 0.004). By contrast, use of low-potency cannabis was not associated with dependence (days of other grass use per month: b = 0.020, 95% CI -0.029 to 0.070, p = 0.436; days of resin use per month: b = 0.025, 95% CI -0.019 to 0.067, p = 0.245). Frequency of cannabis use (all types) did not predict severity of cannabis-related concerns. High-potency cannabis was clearly distinct from low-potency varieties by its marked effects on memory and paranoia. It also produced the best high, was preferred, and most available.


High-potency cannabis use is associated with an increased severity of dependence, especially in young people. Its profile is strongly defined by negative effects (memory, paranoia), but also positive characteristics (best high, preferred type), which may be important when considering clinical or public health interventions focusing on cannabis potency.

Source: 26213314   July 27th 2015

These remarkable scans clearly reveal how smoking during pregnancy harms an unborn baby’s development.

New ultrasound images show how babies of mothers who smoke during pregnancy touch their mouths and faces much more than babies of non-smoking mothers.

Foetuses normally touch their mouths and faces much less the older and more developed they are. Experts said the scans show how smoking during pregnancy can mean the development of the baby’s central nervous system is delayed. Doctors have long urged pregnant women to give up cigarettes because they heighten the risk of premature birth, respiratory problems and even cot death.

Now researchers believe they can show the effects of smoking on babies in the womb – and use the images to encourage mothers who are struggling to give up.

Image shows the 4-D ultrasound scan of two foetuses at 32 weeks gestation, one whose mother was a smoker (top) and the other carried by a non-smoker (bottom). The foetus carried by the smoker touches its face and mouth much more, indicating its development is delayed

As part of the study, Dr Nadja Reissland, of Durham University, used 4-D ultrasound scan images to record thousands of tiny movements in the womb.

She monitored 20 mothers attending the James Cook University Hospital in Middlesbrough, four of whom smoked an average of 14 cigarettes a day.

After studying their scans at 24, 28, 32 and 36 weeks, she detected that foetuses whose mothers smoked continued to show significantly higher rates of mouth movement and self-touching than those carried by non-smokers. Foetuses usually move their mouths and touch themselves less as they gain more control the closer they get to birth, she explained.

The pilot study, which Dr Reissland hopes to expand with a bigger sample, found babies carried by smoking mothers may have delayed development of the central nervous system. Dr Reissland said: ‘A larger study is needed to confirm these results and to investigate specific effects, including the interaction of maternal stress and smoking.’

She believed that videos of the difference in pre-birth development could help mothers give up smoking.

But she was against demonising mothers and called for more support for them to give up. Currently, 12 per cent of pregnant women in the UK smoke but the rate is over 20 per cent in certain areas in the North East. All the babies in her study were born healthy, and were of normal size and weight.

Dr Reissland, who has an expertise in studying foetal development, thanked the mothers who took part in her study, especially those who smoked. ‘I’m really grateful, they did a good thing,’ she said. ‘These are special people and they overcame the stigma to help others.’

Co-author Professor Brian Francis, of Lancaster University, added: ‘Technology means we can now see what was previously hidden, revealing how smoking affects the development of the foetus in ways we did not realise.

‘This is yet further evidence of the negative effects of smoking in pregnancy.’ The research was published in the journal Acta Paediatrica. 

Read more:  23 March 2015

“Even at normal doses, taking psychiatric drugs can produce suicidal thinking, violent behavior,  aggressiveness, extreme anger,  hostility, irritability, loss of ability to control impulses, rage reactions, hallucinations, mania, acute psychotic episodes, akathisia, and bizarre, grandiose, highly elaborated destructive plans, including mass murder.

“Withdrawal from psychiatric drugs can cause agitation, severe depression, hallucinations, aggressiveness, hypomania, akathisia, fear, terror, panic, fear of insanity, failing self-confidence, restlessness, irritability, aggression, an urge to destroy and, in the worst cases, an urge to kill.” -  From “Drug Studies Connecting Psychotropic Drugs with Acts of Violence” – unpublished.

My previous article on Global Research discussed the frustration of large numbers of aware observers around the world that were certain that Andreas Lubitz, the suicidal mass murderer of 149 passengers and crewmembers of the of the Lufthansa airliner crash, was under the intoxicating influence of brain-disabling, brain-altering, psychotropic medicines that had been prescribed for him by his German psychiatrists and/or neurologists who were known to have been prescribing for him.

These inquiring folks wanted and needed to know precisely what drugs he had been taking or withdrawing from so that the event could become a teachable moment that would help explain what had really happened and then possibly prevent other “irrational” acts from happening in the future. For the first week after the crash, the “authorities” were closed mouthed about the specifics, but most folks were willing to wait a bit to find out the truth.

However, another week has gone by, and there has still been no revelations from the “authorities” as to the exact medications, exact doses, exact combinations of drugs, who were the prescribing clinics and physicians and what was the rationale for the drugs having been  prescribed. Inquiring minds want to know and they deserve to be informed.

There are probably plenty of reasons why the information is not being revealed. There are big toes that could be stepped on, especially the giant pharmaceutical industries. There are medico-legal implications for the physicians and clinics that did the prescribing and there are serious implications for the airline corporations because their industry is at high risk of losing consumer confidence in their products if the truth isn’t adequately covered up. And the loss of consumer confidence is a great concern for both the pharmaceutical industry and its indoctrinated medical providers.

It looks like heavily drugged German society is dealing with the situation the same way the heavily drugged United States has dealt with psychiatric drug-induced suicidality and drug-induced mass murders (such as have been known to be in a cause and effect relationship in the American epidemic of school shootings – see

The Traffickers of Illicit Drugs That Cause Dangerous and Irrational Behaviors Such as Murders and Suicides are Punished. Why not Legal Drug Traffickers as Well?

But there is a myth out there that illegal brain-altering drugs are dangerous but prescribed brain-altering drugs are safe. But anyone who knows the molecular structure and understands the molecular biology of these drugs and has seen the horrific adverse effects of usage or withdrawal of legal psychotropic drugs knows that the myth is false, and that there is a double standard being applied, thanks to the cunning advertising campaigns from Big Pharma.

But there is an epidemic of legal drug-related deaths in America, so I submit a few questions that people – as well as journalists and lawyers who are representing drug-injured plaintiffs – need to have answered, if only for educational and preventive practice purposes:

1) What cocktail of 9 different VA-prescribed psych drugs was “American Sniper” Chris Kyle’s Marine Corps killer taking after he was discharged from his psychiatric hospital the week before the infamous murder?

2) What were the psych drugs that Robin Williams got from Hazelden just before he hung himself?

3) What were the myriad of psych drugs, tranquilizers, opioids, etc that caused the overdose deaths of Philip Seymour Hoffman, Michael Jackson, Whitney Houston, Heath Ledger, Anna Nicole Smith, etc, etc, etc (not to mention Jimi Hendrix, Bruce Lee, Elvis Presley and Marilyn Monroe) – and who were the “pushers” of those drugs?

4) What was the cocktail of psychiatric and neurologic brain-altering drugs that Andreas Lubitz was taking before he intentionally crashed the passenger jet in the French Alps – and who were the prescribers?

5) What are the correctly prescribed drugs that annually kill over 100,000 hospitalized Americans per year and are estimated to kill twice that number of out-patients?


Because the giant pharmaceutical companies want these serious matters hushed up until the news cycle blows over (so that they can get on with business as usual), and because many prescribing physicians seem to be innocently unaware that any combination of two or more brain-altering psychiatric drugs have never been tested for safety (either short or long-term), even in the rat labs, future celebrities and millions of other patient-victims will continue dying – or just be sickened from a deadly but highly preventable reality.

But what about “patient confidentiality”, a common excuse for withholding specific information about patients (even if crimes such as mass murder are involved)? It turns out that what is actually being protected by that assertion are the drug providers and manufacturers. Common sense demands that such information should not be withheld in a criminal situation.

America’s corporate controlled media makes a lot of money from its relationships with its wealthy and influential corporate sponsors, contributors, advertisers, political action committees and politicians, but, tragically, the media has been clearly abandoning its historically-important investigative journalistic responsibilities (that are guaranteed and protected by the Constitution). It is obvious that the media has allied itself with the corporate “authorities” that withhold, any way they can, the important information that forensic psychiatrists (and everybody else) needs to know.

We should be calling out and condemning the authorities that are withholding the information about the reported “plethora of drugs” that is known to have been prescribed for Lubitz by his treating “neurologists and psychiatrists”, drugs that were found in his apartment on the day of the crash and identified by those same authorities who have not revealed the information to the people who need to know. Two weeks into the story and there still has been no further information given, or as far as I can ascertain, or asked for by journalists.

So, since the facts are being withheld by the authorities, I submit some useful lists of common adverse effects of commonly prescribed crazy-making psych drugs that Lubitz may have been taking. Also included are a number of withdrawal symptoms that are routinely  and conveniently mis-diagnosed as symptoms of a mental illness of unknown cause.

And at the end of the column are some excerpts from the FAA on psych drug use for American pilots. I do not know how different are the rules in Germany, but certainly both nations have to rely on voluntary information from the pilots.

1) Common Adverse Symptoms of Antidepressant Drug Use

Agitation, akathisia (severe restlessness, often resulting in suicidality), anxiety, bizarre dreams, confusion, delusions, emotional numbing, hallucinations, headache, heart attacks  hostility, hypomania (abnormal excitement), impotence, indifference (an “I don’t give a damn attitude”), insomnia, loss of appetite, mania, memory lapses, nausea, panic attacks, paranoia, psychotic episodes, restlessness, seizures, sexual dysfunction, suicidal thoughts or behaviors, violent behavior, weight loss, withdrawal symptoms (including deeper depression)

2) Common Adverse Psychological Symptoms of Antidepressant Drug Withdrawal

Depressed mood, low energy, crying uncontrollably, anxiety, insomnia, irritability, agitation, impulsivity, hallucinations or suicidal and violent urges. The physical symptoms of antidepressant withdrawal include disabling dizziness, imbalance, nausea, vomiting, flu-like aches and pains, sweating, headaches, tremors, burning sensations or electric shock-like zaps in the brain

3) Common Symptoms of Minor Tranquilizer Drug Withdrawal

Abdominal pains and cramps, agoraphobia , anxiety, blurred vision, changes in perception (faces distorting and inanimate objects moving), depression, dizziness, extreme lethargy, fears, feelings of unreality, heavy limbs, heart palpitations, hypersensitivity to light, insomnia, irritability, lack of concentration, lack of co-ordination, loss of balance, loss of memory, nightmares, panic attacks, rapid mood changes, restlessness, severe headaches, shaking, sweating, tightness in the chest, tight-headedness

4) Common (Usually Late Onset) Adverse Psychological Symptoms From Anti-Psychotic Drug Use

Blurred vision, breast enlargement/breast milk flow,  constipation, decreased sweating, dizziness, low blood pressure, imbalance and falls, drowsiness, dry mouth, headache, hyperprolactinemia (pituitary gland dysfunction), increased skin-sensitivity to sunlight, lightheadedness, menstrual irregularity (or absence of menstruation), sexual difficulty, (decline in libido, anorgasmia, genital pain).

The lethal adverse effects of antipsychotic drugs include Catatonic decline, Neuroleptic Malignant Syndrome (NMS, a condition marked by muscle stiffness or rigidity, dark urine, fast heartbeat or irregular pulse, increased sweating, high fever, and high or low blood pressure); Torsades de Pointes (a condition that affects the heart rhythm and can lead to sudden cardiac arrest”; Sudden death

5) Late and Persistent Adverse Effects of Antipsychotic Drug Use  (Some of these symptoms may even start when tapering down or discontinuing the drug!)

Aggression, akathisia (inner restlessness, often intolerable and leading to suicidality), brain atrophy (shrinkage), caffeine or other psychostimulant addiction, cataracts, creativity decline, depression, diabetes, difficulty urinating, difficulty talking, difficulty swallowing, fatigue and tiredness, hypercholesterolemia, hypothyroidism, intellectual decline (loss of IQ points), obesity, pituitary tumors, premature death, smoking – often heavy – (nicotine addiction), tardive dyskinesia (involuntary, disfiguring movement disorder), tongue edge “snaking” (early sign of movement disorder), jerky movements of head, face, mouth or neck, muscle spasms of face, neck or back, twisting the neck muscles, restlessness – physical and mental (resulting in sleep difficulty), restless legs syndrome, drooling, seizure threshold lowered, skin rashes (itching, discoloration), sore throat, staring, stiffness of arms or legs, swelling of feet, trembling of hands, uncontrollable chewing movements, uncontrollable lip movements, puckering of the mouth, uncontrollable movements of arms and legs, unusual twisting movements of body, weight gain, liver toxicity

6) Common Symptoms of Antipsychotic Drug Withdrawal

Nausea and vomiting, diarrhea, rhinorrhea (runny nose), heavy sweating, muscle pains, odd sensations such as burning, tingling, numbness,  anxiety, hypersexuality, agitation, mania, insomnia, tremor, voice-hearing

FAA Medical Certification Requirements for Psychotropic Medications

Pilots can only take one of four antidepressant drugs – Celexa (Citalopram), Lexapro (Escitalopram), Prozac (Fluoxetine) and Zoloft (Sertraline).

Most psychiatric drugs are not approved under any circumstances.

These include but are not limited to:

  • Abilify (Aripiprazole)
  • Effexor (Venlafaxine)
  • Elavil (Amitriptyline)
  • Luvox (Fluvoxamine Maleate)
  • Monoamine Oxidase Inhibitors
  • Paxil (Paroxetine)
  • Remeron (Mirtazapine)
  • Serzone (Nefazodone)
  • Sinequan (Doxepin)
  • Tofranil (Imipramine)
  • Trazodone
  • Tricyclic Antidepressants
  • Wellbutrin (Bupropion)

To assure favorable FAA consideration, the treating physician should establish that you do not need psychotropic medication. The medication should be discontinued and the condition and circumstances should be evaluated after you have been off medication for at least 60 and in most cases 90 days.

Should your physician believe you are an ideal candidate, you may be considered by the FAA on a case by case basis only. Applicants may be considered after extensive testing and evidence of successful use for one year without adverse effects. Medications used for psychiatric conditions are rarely approved by the FAA. The FAA has approved less than fifty (50) airmen under the FAA’s SSRI protocol.

After discontinuing the medication, a detailed psychiatric evaluation should be obtained. Resolved issues and stability off the medication are usually the primary factors for approval.

Dr Kohls is a retired physician who practiced holistic mental health care for the last decade of his family practice career. He writes a weekly column on various topics for the Reader Weekly, an alternative newsweekly published in Duluth, Minnesota, USA. Many of Dr Kohls’ weekly columns are archived at

Source:  April 08, 2015


Some good news, some not-so-good news about brain recovery from alcohol use disorders

According to a recent review article on recovery of behavior and brain function after abstinence from alcohol[1], individuals in recovery can rest assured that some brain functions fully recover; but others may require more work. In this article, authors looked at 22 separate studies of recovery after alcohol dependence, and drew some interesting conclusions.

First, the good news; studies show improvement or even complete recovery to the performance level of healthy participants who had never had an alcohol use disorder in many important areas, including short-term memory, long-term memory, verbal IQ, and verbal fluency. Even more promising, not only behavior, but the structure of the brain itself may recover; an increase in the volume of the hippocampus, a brain region involved in many memory functions, was associated with memory improvement.

Another study showed that after 6 months of abstinence, alcohol-dependent participants showed a reduction in a “contextual priming task” with alcohol cues; in day to day terms, this could mean that individuals in early recovery from alcohol dependence may be less likely to resume drinking when confronted with alcohol and alcohol-related cues in their natural environment because these alcohol-related triggers are eliciting less craving.- a good thing for someone seeking recovery!

Still other studies showed that sustained abstinence was associated with tissue gain in the brain; in other words, increases in the volumes of brain regions such as the insula and cingulate cortex, areas which are important in drug craving and decision-making, were seen in abstinent alcoholics. This increase is a good thing, because more tissue means more recovery from alcohol-induced damage. A greater volume of tissue in these areas may be related to a greater ability to make better decisions.

Now, the not-so-good news: these studies reported no improvement in visuospatial skills, divided attention (e.g. doing several tasks at once), semantic memory, sustained attention, impulsivity, emotional face recognition, or planning.  This means that even after abstinence from alcohol, people in recovery may still experience problems with these neurocognitive functions, which may be important for performing some jobs that require people to pay attention for long periods of time or remember long lists of requests. These functions may also be important for daily living (i.e. assessing emotions of a spouse, planning activities, etc.).

Importantly, there were many factors that influenced the degree of brain recovery; for example, the number of prior detoxifications. Those with less than two detoxifications showed greater recovery than those with more than two detoxifications.  A strong family history of alcohol use disorder was associated with less recovery. Finally, cigarette smoking may hinder recovery, as studies have shown that heavy smoking is associated with less recovery over time.

So what does all this mean? Recovery of brain function is certainly possible after abstinence, and will naturally occur in some domains, but complete recovery may be harder in other areas. Complete recovery of some kinds of behavior (e.g. sustained attention, or paying attention over long periods of time) may take more time and effort! New interventions, such as cognitive training or medication (e.g. modafinal, which improved neurocognitive function in patients with ADHD and schizophrenia, as well as in healthy groups), may be able to improve outcomes even more, but await further testing.

[1] Recovery of neurocognitive functions following sustained abstinence after substance dependence and implications for treatment

Source:  Mieke H.J. Schulte et al., Clinical Psychology Review 34 (2014) 531–550   October 2014


 Christopher Lapish, Ph.D. (left) and Alexey Kuznetsov, Ph.D. of the School of Science at Indiana University-Purdue University study how alcohol hijacks the brain’s reward system. Credit: School of Science at IUPUIWith the support of a $545,000 three-year grant from the National Institute on Alcohol Abuse and Alcoholism, researchers from the School of Science at Indiana University-Purdue University Indianapolis are conducting research on how the brain’s reward system—the circuitry that helps regulate the body’s ability to feel pleasure—is hijacked by alcohol.

Scientists have only a rudimentary understanding of how alcohol affects neurons in the brain. It is known that, as any addictive drug, alcohol directly or indirectly acts on a specific population of brain cells, called dopamine neurons. Through this action, the neurotransmitter dopamine is released, which evokes feelings of pleasure. However, the biological mechanisms of how alcohol evokes dopamine release have not been determined; exploring this question is the major goal of the grant. 

The synergistic approach of the IUPUI researchers—biomathematician Alexey Kuznetsov, Ph.D., associate professor of mathematical sciences, and neuroscientist Christopher Lapish, Ph.D., assistant professor of psychology—is novel as they marry the cutting-edge tools of mathematical modeling developed by Kuznetsov and the sophisticated experimental neuroscience experiments designed and conducted by Lapish to study the electrical properties that determine the release of the neurotransmitter dopamine in the brain. As a starting point, they are focusing on the brain’s initial exposure to alcohol. 

Kuznetsov has developed unique mathematical models as he homes in on why and how much dopamine is released when alcohol is consumed. With the same goal, Lapish is employing sophisticated tools and methods to measure and analyze electrical signals of dopamine neurons in rats. This synergy forms a two-way street with data from the recordings of the electrical impulses of the rat brains affecting how the mathematical models are constructed and the predictions generated by the mathematical models informing the study of the animal brains. 

IUPUI undergraduates and graduate students are assisting the investigators in their work.

“Our mathematical models go much further than simple logic,” Kuznetsov said. “What we are learning from experiments is critical. The direct connection of modeling and experiments enables us to test and refine our hypotheses.”

“As we begin our second year on this project we are gaining a better understanding of how the brain responds to alcohol,” Lapish said. “The cross talk between us drives this hypothesis-driven research. There are many unknowns to explore and interpret.”

The IUPUI researchers are also collaborating with French scientists. “We are working on the problem at different levels—we are modeling and studying the brains of live rodents—in vivo work—and they [the French researchers] are studying in vitro brain slices in the lab,” Kuznetsov added.

 “Alcohol addiction is among America’s largest public health concerns yet we know far less about it than most other addictions. If we are going to successfully treat alcohol addiction we need to begin with the basics and understand how alcohol directly acts on dopamine neurons in both the alcoholic and normal brain,” Lapish said. 

Provided by Indiana University-Purdue University Indianapolis School of Science

Source:     6th March  2015 


Painkiller addicted baby

 Doctors in the United States are seeing more infants born addicted to narcotic painkillers — a problem highlighted by a new Florida-based report.

These infants experience what’s called neonatal abstinence syndrome as they undergo withdrawal from the addictive drugs their mothers took during pregnancy. Most often these are narcotic painkillers, such as oxycodone, morphine or hydrocodone, according to the report from the U.S. Centers for Disease Control and Prevention.  Since 1995, the number of such newborns jumped 10-fold in Florida while tripling nationwide, the researchers said.

“These infants can experience severe symptoms that usually appear within the first two weeks of life,” said lead researcher Jennifer Lind, a CDC epidemiologist.    The symptoms can include seizures, fever, excessive crying, tremors, vomiting and diarrhea, she said. And withdrawal can take a few weeks to a month.

Dr. David Mendez is a neonatologist at Miami Children’s Hospital. He said, “Being in Florida, I can tell you there’s been an explosion in the number of babies going through neonatal abstinence syndrome. It’s clearly related to the exposure moms have to all narcotic painkillers.”

Mendez said the infants go through a difficult time, but they do recover.  Sometimes it’s enough to keep these babies in a quiet environment, but almost four out of five need treatment with morphine or the anticonvulsant phenobarbital to quell seizures and other withdrawal symptoms, Lind said.

The report — which used data from three Florida hospitals — cites a need for improved counseling and treatment of drug-abusing and drug-dependent women earlier in pregnancy.   Previous studies have found that addiction to narcotic painkillers can increase the risk for premature births, low birth weight and birth defects, Lind said. “Some of the birth defects are heart defects and defects of the brain and the spine,” she said.  “More studies are needed to look at long-term outcomes,” she added.

In 2009, the national incidence of neonatal abstinence syndrome was 3.4 per 1,000 births, less than Florida’s total of 4.4 per 1,000 births, according to background information in the report. Florida officials, alarmed by the increase, last year asked the CDC for help in assessing the problem.  According to the report, 242 infants with neonatal abstinence syndrome were identified in three Florida hospitals in the two-year period from 2010 to 2011.

The researchers found that 99.6 percent of these babies had been exposed to narcotic painkillers and had serious medical complications, according to the March 6 issue of the CDC’s Morbidity and Mortality Weekly Report.   Nearly all of the addicted infants required admission to the neonatal intensive care unit, and average length of stay was 26 days, the investigators found.  The condition is very expensive to treat, Lind said.

Mendez added that lengthy hospital stays aren’t just for treatment. “Some of it is due to the social issues that affect these babies,” he said.  The mothers are often incapable of caring for their babies, Mendez explained. “Hospitals become the babysitter while social services arrange for a new home for the baby,” he said.  Lind said that only about 10 percent of the babies’ mothers had been referred for drug counseling or rehabilitation during pregnancy, even though many tested positive for drugs in urine tests.

Neonatal abstinence syndrome is preventable simply by not taking drugs or by getting treatment for addiction, she said.  From conception on, a pregnant woman is responsible for another human being, Mendez stressed. “Anything a woman does to herself she does to her baby. So if you are engaged in high-risk behavior, if you are taking drugs, they are going to impact the baby,” he said.

Source:   6th March 2015


A study published Wednesday found that consuming large flavored alcoholic beverages can increase risk for binge drinking and related alcohol injuries for underage drinkers. PHOTO BY EMILY ZABOSKI/DAILY FREE PRESS STAFF

Super-sized flavored alcoholic beverages can increase the risk of binge drinking and alcohol-related injuries for underage drinkers, researchers from Johns Hopkins University and Boston University found in a study, a Wednesday press release stated.

The study, published in the American Journal of Public Health on Feb. 25, found that underage drinkers who reported consuming malts, premixed cocktails and alcopops drank more on average and were more likely to experience “episodic heavy drinking,” the report stated. About 1,000 people ages 13 to 20 were surveyed online.

David Jernigan, an author of the study and director of the Center on Alcohol Marketing at Johns Hopkins, said heavier drinking occurs with these flavored beverages because of the serving sizes. Most of these beverages hold the equivalent of 4 to 5 beers in one container, he said.

“We particularly found the correlations between the largest size of these drinks and negative behaviors because one of these super-sized drinks is the equivalent of four to five beers,” he said. “Even though the can may have serving size though most don’t, teens are treating them as a single serving. Some people in the field call it a binge in a can.”

Study co-author Alison Albers, a professor in BU’s School of Public Health, said the study brings up important issues and will help determine future policies.

“These findings raise important concerns about the popularity and use of flavored alcoholic beverages among young people, particularly for the supersized varieties,” she said in the release. “Public health practitioners and policymakers would be wise to consider what further steps could be taken to keep these beverages out of the hands of youth.”

Jernigan said careful packaging should be implemented in the production of super-sized beverages.

“The re-sealable top is more of a joke,” he said. “These are being treated as a single serving, and the results suggest this may be a dangerous form of packaging.”

Katharine Mooney, director of Wellness and Prevention Services at BU, said the university takes steps to prevent the overconsumption of alcohol.

“We discourage against any kind of risky behavior, and these oversized sugar sweetened beverages definitely all into the category of risky,” she said. “[It’s] just like a punch bowl at a party.”

Mooney said because the drinks do not taste entirely like alcohol, it is difficult to determine how much alcohol is in them, which often leads to over drinking. Over drinking can affect students’ physical, social and academic wellbeing.

The Boston University Police Department has noted that the number of alcohol violations and transports for the spring 2015 semester has increased compared to numbers from the spring 2014 semester, The Daily Free Press reported Thursday.

Mooney said BU Student Health Services tries to do whatever possible to inform students about the dangers of binge drinking and learn how to drink in a less dangerous way.

“One of the things we work really hard to educate students about our standard drink portion. A standard beer has the same alcohol content as one shot,” she said. “A student needs to be particularly aware of what they are consuming when drinking these so that they don’t drink more than they intend to.”

Several students said they recognize how super-sized flavored drinks can be risky.

Brock Guzman, a freshman in the College of Engineering, said the drinks are popular because of their cheap prices, and because some items contain caffeine, young drinkers find them even more appealing.

“It’s appealing because you can get really drunk and you stay awake,” he said. “They have caffeine in them and don’t really taste like alcohol.”

Sergio Araujo, a junior in Metropolitan College, said he has seen a friend in a dangerous scenario after consuming Four Loko, a popular super-sized alcoholic beverage. Though Four Loko’s contents used to include caffeine, the company chose to remove caffeine from their product in 2010.

“One guy I know drank them a lot, and he left a party alone, then he got lost in a snowstorm and was too drunk to find his way home,” he said. “He almost had to sleep in the snow.”

Jaqui Manning, a freshman in the College of General Studies, said she has seen firsthand the consequences when others drink the types of alcoholic beverages described in the study, as well as the products that contain caffeine.

“I’ve heard a lot of people have had really bad experiences with them,” she said. “Especially drinking them really fast is really dangerous because not only is there alcohol, but there is so much sugar and caffeine that goes into it, and your body sometimes can’t handle it.”

Source:     6th March 2015

A lot of times, a simple “no thanks” may be enough. But sometimes it’s not. It can get intense, especially if the people who want you to join in on a bad idea feel judged. If you’re all being “stupid” together, then they feel less self-conscious and don’t need to take all the responsibility. 

But knowing they are just trying to save face doesn’t end the pressure, so here are a few tips that may come in handy.

1. Offer to be the designated driver. Get your friends home safely, and everyone will be glad you didn’t drink or take drugs.

2. If you’re on a sports team, you can say you are staying healthy to maximize your athletic performance—besides, no one would argue that a hangover would help you play your best.

3. “I have to [study for a big test / go to a concert / visit my grandmother / babysit / march in a parade, etc.]. I can’t do that after a night of drinking/drugs.”

4. Keep a bottled drink like a soda or iced tea with you to drink at parties. People will be less likely to pressure you to drink alcohol if you’re already drinking something. If they still offer you something, just say “I’m covered.”

5. Find something to do so that you look busy. Get up and dance. Offer to DJ.

6. When all else fails…blame your parents. They won’t mind! Explain that your parents are really strict, or that they will check up on you when you get home.

If your friends aren’t having it—then it’s a good time to find the door. Nobody wants to leave the party or their friends, but if your friends won’t let you party without drugs, then it’s not going to be fun for you.

Sometimes these situations totally surprise us. But sometimes we know that the party we are going to has alcohol or that people plan to do drugs at a concert. These are the times when asking yourself what you could do differently is key to not having to go through this weekend after weekend.

Source:      March  9th 2015

Teens Affected by Addiction is a project aimed at raising awareness about the impact of alcoholism on families – here, they share some personal stories. 

Here, four people who grew up with an alcoholic parent share their stories.  These stories have been collected by ‘Teens Affected by Addiction’, a Young Social Innovators project from Mount Mercy College in Cork, Ireland,  with the aim of raising awareness about how addiction impacts children.

“I will never get my childhood back”

“My life as a child of an alcoholic parent was frightening and lonely. My dad was a chronic alcoholic. I had a different childhood to all my friends: no birthday parties, couldn’t invite friends over to the house, and Christmas was a nightmare.

There was no one I could talk to and no one could help me, I just had to put up with it.

When I was 17 I had no choice but to leave home. I had to live my own life. My mother was heartbroken but she knew I had to go.

When I was 18, I was able to get counselling which was a great help to me. I was able to understand that alcoholism was an illness. A few months after leaving home my dad turned his life around and stopped drinking.

I will never get my childhood back but I now have a great relationship with my father and my mother now has the life she deserves. I hope this story can give other children some hope and let them know that there is a light at the end of the tunnel.”


“Missing you”

The following is a short poem a woman sent to us about her father’s alcoholism.

I don’t miss the sense of invisibility to you, 

I don’t miss listening constantly for the front door,
I don’t miss watching your face to decipher your mood,
I don’t miss dodging your verbal assaults,
I don’t miss the sense of being so small,
I don’t miss the enormity of you and your drink,
I don’t miss the deep shame,
I don’t miss everyone covering up for you,
I don’t miss everyone knowing but me,
I don’t miss the smell of drink,
I don’t miss the fear of drink,
I don’t miss my friends knowing,
I don’t miss no-one caring about me,
I don’t miss fear,
I don’t miss loving you,
I don’t miss hating you,
I don’t miss you.


 “We had food in the house but it wasn’t for us – it was for the social worker to see.”

“My alcoholic parent was my mother. She always drank. She started when she was young. When she was a child her father abused her and her brothers. They were battered by their father constantly. They locked their doors every night to keep their father out. She was beaten badly and was always expected to act like a lady. She started drinking to forget the pain she had to go through. This doesn’t make what she did to her children any bit forgivable.

When I was a child my uncle and aunts tried to take me away from my home by taking me on day trips with my sister. Back then I thought my mother would heal. My sister and I used to beg my uncle and aunts to bring us home so we could mind our mother. We didn’t want to upset her by being away for too long. One of my uncles was like a father to me. His oldest daughter and I look like brother and sister. We are just as close too. They tried to help me and give me a better life but they couldn’t.

My mom had a lot of ‘boyfriends’. They never really stayed too long. A small few used to beat me. These men were constantly in our house so we never really questioned a strange man in our house. It was normal for us.

At 15 years old I would come home from school and meet up with my mother and grandmother in the pub. My mother would buy me beer and I would sit in the pub with my drunken mother and help her get home. My home was filthy. There used to be dogs running through the house constantly and the house was never cleaned. We had food but it wasn’t for us. The food was perfect but we were not allowed eat it as it was only for when the social workers called so it would look like she was feeding us. In reality we were starving.

I started hanging out with a very rough group where I lived. They were drinking constantly and doing drugs. Eventually, I got away from them and my mother. I ran from Ireland at 16 to the States to my father. My sister was so upset with me for leaving her with my mother back in Ireland.

Now I’m living in America with a beautiful wife and three amazing children. Sometimes what happened still affects me but I try to block it out and ignore it and carry on. I’m honestly not recommending running away. I am planning on coming back to Ireland soon to sort out a few things with my mother.


“I’ve never not known Mum to have her cans by her chair and her vodka stashed away under the bed”

Well to begin with there’s a common misconception that men are generally the alcoholics in a family but when it’s the mother, the nucleus of the family is destroyed and everything falling apart becomes an inevitable fate. I come from a small family with it just being my mum, dad and my brother and I. We’ve been battling with my mother’s alcoholism for as long as I remember, I’ve never not know her to have her cans by her chair and her vodka stashed away under the bed. It wasn’t that I always saw it as the norm but when you don’t know any different it does tend to be a bit more difficult to imagine the situation differently. I’m actually very happy to see the back of 2014 as from December 2013 my whole family spiralled out of control and I spent more times in hospital than anywhere else. My parents split in December 2013 after 21 years married (I am 20 years old) my mum’s alcoholism was at its peak. Having been in and out of hospital for the past six years due to liver failure, she was on a path to destruction. In those months, mum had fallen whilst drunk and tried to hit my father with a golf club and broke her femur. She had several serious operations and she nearly died as her blood is extremely thin due to medication and alcoholism. Mum came out of hospital and continued to drink and began running around saying that she was fine and could walk. She fell hundreds of times and it became so bad she now can’t walk properly. I live with my grandmother, having left school at 17 as I suffered from depression and I went back to do my Leaving Cert and moved out of my home. Within months a series of events led to both my father and brother leaving and moving into an apartment and my mum was left wallowing in her drunken states ringing and abusing everybody (she still does this).I contacted the HSE in January 2014 with several emails sent to all organisations that support victims of alcoholism, I got a lot of reaction. I was furious that I spent years sitting in my mothers’ doctor’s surgery with my dad begging for ways out. They would always look at us helplessly and say “move out”. I felt embarrassed and as if there were no light at the end of the tunnel. My grandmother who I live with and who’s been a mother to me all my life has had a nervous breakdown and right now I spend my days working eight hour shifts as a photographer in a studio and then I go home to this mess. 

My mum has been in hospital about eight times since February 2014 when a stomach ulcer burst and she was found in a pool of blood by my grandmother. I soon lost faith but I always tried to get help; my letter to the HSE got me six months with a councillor but I was so busy with my Leaving Cert and everything I just couldn’t find time to go.

Now I am still living with this situation but I try my very best to overcome it every day and I refuse any kind of medication such as an “anti depressant” as I believe it’s just a easy way for doctors to dose people up and make money. I wish to study politics and history and possibly then business in university in the future and I hope that one day I can actually help people.

These stories are shared by ‘Teens Affected by Addiction’, a Young Social Innovators project from Mount Mercy College in Cork. The students have recently received funding from the YSI Den to publish a book with the stories of adults who grew up with an addict in the home. 

 Please see or email: if you would like to share your story.

Follow Teens Affected by Addiction on Twitter: @affbyaddiction

Source:    March 2015

On Nov. 4, Alaskans will consider Ballot Measure 2, an initiative to legalize the sale and use of marijuana for recreational purposes. And those who support that commercial trade are investing heavily in hoping you will vote “yes.” Make no mistake about it, marijuana — like tobacco and alcohol — is big business.

Like alcohol and tobacco, the costs of marijuana to public health, public safety, our youth and lost productivity, are similarly high. It’s not surprising that Outside investors would regard Alaska as fertile territory for unconditional legalization.

In 1975, our Supreme Court found a right for Alaskans to consume small amounts of marijuana in their homes in the privacy provisions of the Alaska Constitution. And in 1998, Alaskans voted to legalize marijuana for medical purposes with 58 percent support. But Ballot Measure 2 is not about “medical marijuana,” nor is it necessary in order to protect adult Alaskans who consume marijuana in their homes from police intrusion. The measure is less about freedom than it is about profit at the expense of public health. That’s why I plan to vote “no” on Ballot Measure 2.

I came to this decision after careful consideration of the medical evidence. My guide through the scientific literature was Dr. Nora Volkow, the director of the National Institute on Drug Abuse (NIDA). Earlier this year, Dr. Volkow published a peer-reviewed paper about the health effects of marijuana in the New England Journal of Medicine, one of the nation’s most eminent medical publications. Volkow directs a component of our National Institutes of Health which is, of course, neutral on state level policy initiatives. Fortunately for all of us, NIH does not prohibit its scientists from entering the discussion by objectively sharing the science with policymakers and the public.

Here’s what Volkow has to say about the state of the evidence: “The popular notion seems to be that marijuana is a harmless pleasure, access to which should not be regulated or considered illegal.”

However popular notions are not always correct. One of the detrimental effects is addiction. “The evidence clearly indicates that long term marijuana usage can lead to addiction,” Volkow states. “About 16 (percent) of those who begin marijuana usage as teenagers will become addicted. And there seems to be a strong association between repeated use and addiction. About a quarter to a half of those who use marijuana everyday are addicted. …Marijuana use by adolescents is particularly troublesome.”

Those who begin using marijuana as teenagers, when the brain is still developing, are two to four times more likely to demonstrate dependence symptoms within two years of first use than those who first use marijuana as adults. And since marijuana use “impairs critical cognitive functions … for days after use many students could be functioning at a cognitive level that is below their natural capability for considerable period of times,” according to Volkow.

These effects could be even longer lasting. Adults who smoked marijuana during adolescence have fewer fibers in specific brain regions that are important to things like alertness, self-consciousness, learning and memory.

NIDA-funded research provides some support for long standing fears that use of marijuana may be a gateway to use of other drugs with even greater known adverse health effects. Truthfully, the same may be said of alcohol and tobacco. Whether the mechanism is chemical, cultural or some combination of the two, is less well known. No evidence is cited to suggest that marijuana use keeps young people away from other drugs.

The prevalence of impaired driving in Alaska is well known and deeply troublesome. On this, Volkow observes that “both immediate and long term exposure to marijuana impair driving ability; marijuana is the illicit drug most frequently reported in connection with impaired driving and accidents, including fatal accidents.” Moreover, the mixing of marijuana and alcohol can further exacerbate the dangers to public safety.

Perhaps the most startling revelation of Volkow’s research is that all marijuana is not alike. The potency of marijuana is determined by its Tetrahydrocannabinol, or THC, content. Analysis of seized marijuana for sale on the street demonstrates that THC concentrations have been rising from about 3 percent in 1980 to about 12 percent today. Volkow suggests that this may be the reason for increased emergency room visits associated with marijuana and a higher level of fatal crashes. Also, the initiative specifically defines marijuana to include concentrates, which can contain 80-90 percent THC. Marijuana edibles would also be legalized and commercialized under the initiative. In Colorado, child-attractive edibles like lollipops, flavored drinks and gummy bears, with multiple doses of THC, are being sold.

Marijuana is a drug and with all drugs there are risks and benefits. Research suggests that use of marijuana or some of its component chemicals can be beneficial for the alleviation of a variety of medical conditions. But patients with these conditions benefit from discussions with their healthcare providers about the risks and benefits.

The state should examine the most appropriate access for this class of users. That said, the evidence that marijuana is harmful for non-medical use is growing. That should give Alaskans pause as we enter the voting booth.

I believe strongly in working for the health, safety, educational achievement, productivity and community welfare of Alaskans. That is why I am voting “no” on Ballot Measure 2.

Lisa Murkowski is a Republican U.S. Senator representing Alaska.


Excessive alcohol consumption is a leading cause of premature death in the U.S. and responsible for one in every 10 deaths. The statistics that describe the ways in which we drink ourselves to death are staggering. A study published in the journal Preventing Chronic Disease found that nearly 70% of deaths due to excessive drinking involved working-age adults. The study also found that about 5% of the deaths involved people younger than age 21.  Moreover, excessive alcohol use shortened the lives of those who died by about 30 years. Yes, 30 years.

One strong factor that reinforces the popular culture surrounding drinking is the glamour of advertising. Researchers at the Johns Hopkins Bloomberg School of Public Health examined alcohol-advertising placements to determine whether the alcohol industry had kept its word to refrain from advertising targeting young people. This included television programs for which more than 30% of the viewing audience is likely to be younger than 21 years, the legal drinking age in every state.

The study found that alcohol related advertising increased by 71% in the last decade; this is largely attributed to exposure on cable television. That increase coincided with a reported upsurge of alcohol consumption by high school students. In conclusion, the study suggested that if the National Research Council/Institute of Medicine’s proposed threshold of 15% exposure to advertising was implemented, young viewers would see 54% fewer alcohol ads and society would see a correlating decrease in alcohol related deaths.

What about those “drink responsibly” admonitions on so many commercials? Federal regulations do not require responsibility statements in alcohol advertising. The alcohol industry’s voluntary codes for marketing and promotion emphasize responsibility, but they provide no definition for responsible drinking. So when you see the admonition to “drink responsibly” at the end of an alcohol-related television commercial, there is no idea given as to exactly what that may mean, particularly to someone under the legal drinking age.

David Jernigan, PhD, director of the Center on Alcohol Marketing and Youth at the Johns Hopkins Bloomberg School of Public Health said:

The contradiction between appearing to promote responsible drinking and the actual use of ‘drink responsibly’ messages to reinforce product promotion suggests that these messages can be deceptive and misleading.”

Youth who start drinking before age 15 years are five times more likely to develop alcohol dependence or abuse later in life than those who begin drinking at or after age 21 years according to the Centers for Disease Control and Prevention.

Alcohol advertising influences many people across a wide range of demographics. Regardless of the warning labels on alcohol containers, community prevention programs and general public knowledge of the risks of excessive alcohol consumption, people continue to drink in health-damaging ways. Drinking in public, at sporting events, in parks, during celebrations, etc., is firmly embedded in society as acceptable behavior. At the same time, the large number of alcohol related deaths among all age groups is a concern, especially when this drinking behavior is generally developed while individuals are underage.

Alcohol use is a major public health problem that can lead to social, financial, and health related setbacks and premature death. Talk to health care professional if you or someone close to you is struggling with excessive alcohol consumption.


The polarized legalization debate leads to exaggerated claims and denials about pot’s potential harms. The truth lies in between.

Pretty much everyone who has spent time smoking marijuana knows at least one diehard stoner. The guy whose eyes are always red, the girl who doesn’t use the term “wake and bake” ironically, the person who just can’t seem to ever get it together. These heavy smokers might work at a low-level job or they may be unemployed—but everyone who knows them well knows that they are capable of much more, if only they had any ambition.

Is this really addiction? I believe that it is (and I don’t think that’s an argument against legalization). In fact, the reasons why marijuana is addictive elucidate the true nature of addiction itself.  Addiction is a relationship between a person and a substance or activity; addictiveness is not a simple matter of a drug “hijacking the brain.” In fact, with all potentially addictive experiences, only a minority of those who try them get hooked—and people can even become addicted to apparently “nonaddictive” things, like carrots. Addiction depends on learning, context and psychology, not just neurotransmitters.

With two states having already legalized recreational marijuana use and several more considering doing so, understanding the nature of addiction is more important than ever. Partisans on both sides of the debate have made extreme claims here; some legalizers saying there’s no such thing as marijuana addiction, while some prohibitionists claim “cannabis as addictive as heroin.”

Our concepts of addiction, however, come primarily from cultural experience with alcohol, heroin and, later, cocaine. No one has ever argued that opioids like heroin don’t have the potential to cause addiction because the withdrawal symptoms—vomiting, shaking, pallor, sweating and diarrhea—are objectively measurable. Opioids cause physical dependence that is evident when they become unavailable. The same is true for alcohol, where withdrawal is even more severe and can sometimes even be deadly.

So early researchers focused on these measurable symptoms related to alcoholism and opioid addictions in defining addiction: Using a drug could lead to becoming tolerant to it, tolerance could lead to dose escalation, which could in turn lead to physical dependence, and then the addiction could be driven by the need to avoid the painful symptoms of withdrawal. It was simple and physical.

In this view, however, cocaine and marijuana were not “really” addictive. While people can experience withdrawal symptoms like irritability, depression, craving and sleep problems when quitting these drugs, these are much more subjective and therefore can be dismissed as “psychological” rather than physical. You might really want coke or pot, but you didn’t need it like a real junkie, the thinking went.

And since most of us like to believe that we have much more control over our minds than we do over physical symptoms, “psychological” addiction is seen as far less serious than the “physical” type. It’s the remnants of this kind of thinking that mainly underlie the idea that marijuana addiction doesn’t exist. Unfortunately, that view of addiction is stuck in the 1970s.

In the 1980s—ironically, not long after Scientific American caused a big controversy by arguing that snorted cocaine is no more addictive than eating potato chips—entrepreneurs began marketing a ready-made smokeable form of the drug. The birth of crack shattered the idea that “physical” dependence is more serious than psychological dependence because people with cocaine addictions don’t vomit or have diarrhea when they quit; while they may appear desperate, it’s not in the physically obvious way of heroin or alcohol withdrawal. And so, if you are going to argue that marijuana is not addictive because you don’t get sick when you quit, you also have to argue the same for crack.

In the 1970s view, cocaine and marijuana were not “really” addictive: You might really want coke or pot, but you didn’t need it like a real junkie, the thinking went.

Good luck with that one, I say. Clearly, crack-addicted people are every bit as compulsive as those with heroin problems—and their criminal involvement if they can’t afford the drug is at least equally likely, though not as common as has been claimed. Crack dealt a deathblow to the “psychological” vs. “physical” distinction—and if it hadn’t, neuroscience was creeping up to show that the psychological and the physical aren’t exactly distinct anyway.

In the ‘70s and ‘80s, researchers also began recognizing that simply detoxing heroin addicts—getting them through the two-week period of intense physical withdrawal symptoms—is not effective treatment. If heroin addiction was driven primarily by the need to avoid withdrawal, addicted people should be out of the woods after they complete cold turkey. But as those of us who have been through it know, that is far from the hardest part.

While kicking heroin isn’t fun, staying off it in the long run is the problem—those “mere” psychological cravings are what drive addiction. Physical dependence isn’t the main problem; it isn’t even necessary. Indeed, we now know that you can actually have physical dependence without any addiction at all: There are some blood pressure medications, for example, that can have deadly withdrawal symptoms if not tapered properly, but people on these meds don’t crave them even though they are quite dependent. Similarly, antidepressants like Paxil have physical withdrawal symptoms, but because they don’t produce a high, you don’t see people robbing drug stores to get them.

So what is addiction, then, if tolerance, withdrawal and physical dependence aren’t essential to it? All of these facts point to one definition that can sum up the problem: Addiction is compulsive use of a substance or engagement in a behavior despite negative consequences. (Put more in neuroscience, addiction is a learned distortion in the brain’s motivational systems that make us persist in pursuing things linked to evolutionary fitness like food and sex.) Anything that causes pleasure via these systems—and that’s basically anything that is possible to enjoy—can be addictive to some person at some time. And that includes marijuana (and, for that matter potato chips).

This doesn’t mean that marijuana addiction is necessarily as severe as cocaine, heroin or alcohol addiction—in fact, it typically isn’t. If given the choice, most families would vociferously prefer having a member addicted to marijuana rather than to cocaine, heroin or alcohol. The negative consequences associated with marijuana addiction tend to be subtler: lost promotions, for example, rather than lostjobsworse relationships, not no relationships. And of course, no risk of overdose death.

Marijuana addiction may quietly make your life worse without ever getting bad enough to seem worth addressing; it may not destroy your life but it may make you miss opportunities.

But this is also what can make it insidious. Marijuana addiction may quietly make your life worse without ever getting bad enough to seem worth addressing; it may not destroy your life but it may make you miss opportunities. With any pattern of regular drug use, it’s important to continually track whether the risks outweigh the benefits, keeping in mind that addiction itself may distort this calculation. This is especially true with marijuana.

However, as with all other drugs, only a minority of marijuana users ever struggle with addiction. Research suggests that about 10% get hooked—and on average, marijuana addiction lasts six years. Even more than other addictions, marijuana addiction seems to be driven by self-medication of mental health problems—90% of people with marijuana addiction also have another addiction or mental illness, typically alcoholism or antisocial personality disorder.

This suggests that exposing more of the population to marijuana won’t necessarily increase the addicted population. First, people with antisocial personality disorder, by definition, tend not to be law abiding, so most have probably already tried it. Second, the percent of people with other pre-existing mental illness will not change because marijuana becomes legal—in fact, in the UK, when they reversed their prior liberalization of marijuana law because of fears related to increased schizophrenia, psychosis rates actually went up. (The link probably wasn’t causal, but it does suggest that legal crackdowns on cannabis don’t prevent related psychosis).

If some people with alcohol, cocaine or heroin addiction switch to marijuana instead, overall harm would be reduced. As I and others have been reporting at least since 2001, using marijuana as an “exit” drug is a real phenomenon, both in cocaine and opioid addiction.

When we consider the risks of various substances, we tend to do so in isolation—but that’s not how choices are made in the real world. Most people would rather their partners have no addictions—but again, some are clearly worse than others. Marijuana craving is rarely as severe as crack craving, as is obvious.

Still, like anything that can be pleasurable, marijuana can be addictive. This doesn’t mean all addictions are the same or that it is as addictive as the currently legal drugs alcohol and tobacco—the data shows it is less so.

Pretending it can’t do any harm at all, however—or that there aren’t people who are addicted to it—does no one any good. If we want better drug policy, as with other types of recovery, we need to avoid denial.

Maia Szalavitz is one of the nation’s leading neuroscience and addiction journalists, and a columnist at She has contributed to Timethe New York TimesScientific American Mindthe Washington Post and many other publications. She has also published five books, including Help at Any Cost: How the Troubled-Teen Industry Cons Parents and Hurts Kids (Riverhead, 2006), and is currently finishing her sixth, Unbroken Brain, which examines why seeing addiction as a developmental or learning disorder can help us better understand, prevent and treat it. Her last column for was about why the oft-documented fact that most people age, or grow, out of substance misuse is not common knowledge.

Source: 15th October 2014

As social acceptance and public policy around marijuana shift, and especially if legalized recreational use becomes more widespread, we will need to consider the influence and potential regulation of its marketing.  For this, we should use what we already know from the science to guide our decisions and policies to minimize harm, because inevitably, advertising is going to reach children and adolescents, people who are addicted to marijuana, and those of all ages who are on their way to becoming addicted.

Ads for addictive substances—including tobacco and alcohol and fattening foods—have the obvious intent of generating new customers as well as enticing current users to use more, but that’s not all they do. Marketers know that by associating such products with other pleasurable stimuli and situations, ads contribute to reinforcing those positive associations in the brains of users, and thus contribute to the process of developing an addiction. 

Drug addiction is a disease of learning—learning to associate drugs with positive feelings and to associate cues that signal drug availability with similar feelings, ultimately leading to craving for the drug.  This part of the addictive progression is known as conditioning, discovered in the 1890s by Pavlov. Today we also understand the brain mechanisms that underlie the phenomenon: Once a person becomes conditioned to drug-related stimuli, those stimuli independently become associated with increases in dopamine in the brain’s reward pathway (i.e., without the drug even being present). These dopamine bursts fuel drug-seeking and craving. The same process can cause such stimuli to act as triggers contributing to relapse in those who are already addicted and are struggling to recover.

When there are salient advertisements for a product, it’s very hard to contain them, because images don’t even need to reach the level of conscious awareness to stimulate the urge to use that product. Recent neuroimaging research has confirmed the brain’s extraordinary sensitivity to “unseen” rewarding stimuli: A 2008 fMRI study by Anna Rose Childress and colleagues confirmed that limbic circuitry respond to drug (as well as sexual) reward cues that are too fleeting to be consciously registered. Also, because of the reach of the Internet, it will be hard to restrict exposure to marijuana advertising just to people in states where it is legal, or just to people old enough to purchase it.

For decades we have seen the harmful effects that alcohol and tobacco ads can have, especially those that target young people; similar associations have been found between exposure to food advertising and obesity. The relative harm of marijuana compared to other legal drugs remains hotly contested, but its potential addictiveness—especially to young people—is undisputed. Thus, it is crucial that states consider the lessons learned from tobacco and alcohol policy research and restrict (or preclude) marijuana advertising to reduce as much as possible the development of newly addicted individuals and avoid inducing relapse in people who are already addicted.

Source: October 23, 2014

Pot smokers say marijuana is a mind-expanding drug, but a new study conducted at The University of Texas at Dallas links heavy, long-term use of marijuana with smaller volume in the orbitofrontal cortex–a brain region associated with decision-making and addiction. 

The same research shows that the brains of long-term users have greater connectivity in this region than do the brains of people who don’t use pot, although this connectivity seems to disappear over time with prolonged use. The research also shows that the earlier an individual starts using marijuana, the more pronounced the brain abnormalities.

Whether these brain abnormalities cause any mental or emotional deficits isn’t yet clear.

“The orbital frontal cortex is a key part of the brain’s reward system/network and instrumental in our motivation, decision-making and adaptive learning,” study leader Dr. Francesca Filbey, director of the university’s Center for BrainHealth and an associate professor in the university’s School of Behavioral and Brain Sciences, told The Huffington Post in an email. “As such, our finding that chronic marijuana users had smaller brain volume in the orbital frontal cortex, might manifest behaviorally making it difficult for them to change learned behavior.”

For the study, Filbey and her colleagues used MRI scanners to compare the brains of 48 adults who had smoked marijuana three times a day for 10 years, on average, to the brains of 62 non-users.  While their findings are provocative, the researchers acknowledge that they do not prove that marijuana use directly causes changes in the brain–a point of view shared by Dr. Asaf Keller, a professor of anatomy and neurobiology at the University of Maryland School of Medicine, who was not involved in the study. 

“As this is a retrospective study—and not a prospective one—it is impossible to determine whether individual differences in brain anatomy are related to genetic or environmental factors other than marijuana use,” he told HuffPost Science in an email. “In sum, there is not indication that the anatomical differences in the brains of marijuana users are caused by marijuana use.”  Keller has been critical of previous research linking casual marijuana use to changes in the brain.

Still, some researchers argue that this new study is an important step forward for marijuana research.  “This is important, well-conducted research that can serve as a reminder that marijuana use may not be without risks,” Dr. Susan F. Tapert, a psychiatry professor at the University of California, San Diego, who was not involved in the study, told HuffPost Science in an email. “These findings point to the need for definitive longitudinal studies that assess future users prior to the onset of marijuana use, then again after use has started.”

Source: Journal Proceedings of the National Academy of Sciences  10th Nov  2014

Cocaine addicts can’t recognise loss – such as the consequences of a break-up or being sent to jail – because the drug changes their brain, according to a new study.

Researchers found cocaine addicts may continue their destructive drug habit despite such huge personal setbacks because their brain circuits responsible for predicting emotional loss are impaired. They say the find could be used to develop new treatments, and spot those most at risk of relapsing. 


The new study recorded the brain activity of 75 people – 50 cocaine users and 25 healthy controls – using EEG, a test that detects electrical activity in the brain, while subjects played a gambling game.  Each person had to predict whether or not they would win or lose money on each trial. 

The study, published in The Journal of Neuroscience, focuses on the difference between a likely reward, or loss, related to a given behaviour and a person’s ability to predict that outcome – a measurement known as Reward Prediction Error, or RPE.Such RPE signalling is believed to drive learning in humans, which guides future behaviour. After learning from an experience, we can, in the best case, change our behaviour without having to go through it again.

Previous research determined that predictions of actual reward or loss are managed by shifting levels of the nerve signaling chemical dopamine produced by nerve cells in the brain, where changes in dopamine levels accompany unexpected gains and losses.The new study recorded the brain activity of 75 people – 50 cocaine users and 25 healthy controls – using EEG, a test that detects electrical activity in the brain, while subjects played a gambling game. Each person had to predict whether or not they would win or lose money on each trial.

Results showed that the group of cocaine users had impaired loss prediction signaling, meaning they failed to trigger RPE signals in response to worse-than-expected outcomes compared to the 25 healthy people.

Researchers say their findings offer insights into the compromised ability of addicts to learn from unfavourable outcomes, potentially resulting in continued drug use and relapse, even after suffering major losses.

Study lead author Doctor Muhammad Parvaz, Assistant Professor of Psychiatry at the Icahn School of Medicine in the US, said: ‘We found that people who were addicted to cocaine have impaired loss prediction signalling in the brain.

‘This study shows that individuals with substance use disorder have difficulty computing the difference between expected versus unexpected outcomes, which is critical for learning and future decision making.

‘This impairment might underlie disadvantageous decision making in these individuals.’

Half had used cocaine within 72 hours of the study and the other half had abstained for at least 72 hours. 

The cocaine addicts with the more recent use had higher electrical activity associated with the brain’s reward circuit when they had an unpredicted compared to a predicted win, a pattern that was similar to the 25 healthy controls. The cocaine users who had abstained for at least 72 hours did not show the higher activity in response to an unpredicted win.

The researchers said these findings are consistent with the hypothesis that in addiction the drug is taken to normalise a certain brain function, which in this case is RPE signalling of better-than-expected outcomes. Principal investigator Doctor Rita Goldstein said: ‘This is the first time a study has targeted the prediction of both gains and losses in drug addiction, showing that deficits in prediction error signalling in cocaine addicted individuals are modulated by recent cocaine use.

‘The reductions in prediction of loss across all cocaine addicted individuals included in this study are also of great interest; they could become important markers that can be used to predict susceptibility for addiction or relapse or to develop targeted interventions to improve outcome in this devastating, chronically relapsing disorder.’ 


4th Feb.2015

Grant JD1, Scherrer JF, Neuman RJ, Todorov AA, Price RK, Bucholz KK.



Little empirical evidence exists to determine if there are alternative classification schemes for cannabis abuse and dependence beyond the definitions provided by Diagnostic and Statistical Manual (DSM) criteria. Current evidence is not conclusive regarding gender differences for cannabis use, abuse and dependence. It is not known if symptom profiles differ by gender.


Latent class analysis (LCA) was used to assess whether cannabis abuse and dependence symptom patterns suggest a severity spectrum or distinct subtypes and to test whether symptom patterns differ by gender. Data from 3312 men and 2509 women in the National Longitudinal Alcohol Epidemiologic Survey (NLAES) who had used cannabis 12 + times life-time were included in the present analyses. The comparability of the solutions for men and women was examined through likelihood ratio chi(2) tests.


Based on the Bayesian information criterion and interpretability, a four-class solution was selected, and the classes were labeled as ‘unaffected/mild hazardous use’, ‘hazardous use/abuse’, ‘abuse/moderate dependence’ and ‘severe abuse/dependence’. The solutions were generally suggestive of a severity spectrum. Compared to men, women were more likely to be in the ‘unaffected/mild hazardous use’ class and less likely to be in the ‘abuse/moderate dependence’ or ‘severe abuse/dependence’ classes. The results were generally similar for men and women. However, men had consistently and substantially higher endorsements of hazardous use than women, women in the ‘abuse/moderate dependence’ class had moderately higher rates for four dependence symptoms, and women in two of the classes were more likely to endorse withdrawal.


Our findings generally support the severity dimension for DSM-IV cannabis abuse and dependence symptomatology for both men and women. While our results indicate that public health messages may have generic and not gender-specific content, treatment providers should focus more effort on reducing hazardous use in men and alleviating withdrawal in women.

Source: Addiction. 2006 Aug;101(8):1133-42.

Day NL1, Goldschmidt L, Thomas CA.



To evaluate the effects of prenatal marijuana exposure (PME) on the age of onset and frequency of marijuana use while controlling for identified confounds of early marijuana use among 14-year-olds.


In this longitudinal cohort study, women were recruited in their fourth prenatal month. Women and children were followed throughout pregnancy and at multiple time-points into adolescence.


Recruitment was from a hospital-based prenatal clinic. The women ranged in age from 18 to 42, half were African American and half Caucasian, and most were of lower socio-economic status. The women were generally light to moderate substance users during pregnancy and subsequently. At 14 years, 580 of the 763 offspring-mother pairs (76%) were assessed. A total of 563 pairs (74%) was included in this analysis.


Socio-demographic, environmental, psychological, behavioral, biological and developmental factors were assessed. Outcomes were age of onset and frequency of marijuana use at age 14. PME predicted age of onset and frequency of marijuana use among the 14-year-old offspring. This finding was significant after controlling for other variables including the child’s current alcohol and tobacco use, pubertal stage, sexual activity, delinquency, peer drug use, family history of drug abuse and characteristics of the home environment including parental depression, current drug use and strictness/supervision.


Prenatal exposure to marijuana, in addition to other factors, is a significant predictor of marijuana use at age 14.

Source:   Addiction. 2006 Sep;101(9):1313-22.

Neurobiology of Addiction: PET Scans Show Changes in the Brain.

The world tends to look at addicts as people who have a character flaw. Are they poor decision makers? Are they narcissists? Are they anti-social? For the most part, we don’t do that with other people and their diseases.

“Oh, you’re diabetic, you must be narcissistic. You have high blood pressure, you’re a poor decision maker. No, we don’t do that. So we’ve got to really come forward with drug addiction as a disease,” said JeanAnne Johnson Talbert, DHA, APRN-BC, FNP, CARN-AP, medical director of Steps Recovery Center, Payson, UT, at the American Psychiatric Nurses Association 28th Annual Conference, held October 22-25, 2014, in Indianapolis, IN.

In the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) that was published last year, addiction is classified as a “substance abuse disorder.” According to Talbert, “the newly revised edition took out the ‘legal ramifications’ criteria and substituted ‘craving.’ And that’s where you’re starting to see some progression with treating this disease.”

What’s the big deal? Nearly 23 million Americans are addicted to alcohol or other drugs. Tobacco, alcohol, and illegal drug addiction costs this country $524 billion a year in direct and indirect costs. The economic burden is twice as much as any other disease affecting the brain.

You may know people who can drink a whole bottle of wine in one evening and then not touch it again for months. And you may know people who can drink socially or on the weekends or holidays. People can also abuse substances, but not all of those people are actually addicted. Then there is full addiction, which involves changes to structures of the brain. “A person can fluctuate in and out of occasional or social abuse, but once you get into the actual addiction, you don’t fluctuate. You’re stuck,” said Talbert.

No one starts out wanting to become an addict, she added. “You may just want to feel good or better, but the younger you are when you start using, the more likely it is that you’ll become addicted,” said Talbert.

Addiction is a chronic and progressive brain disease of the reward, motivation, and memory pathway that moves from an impulse or positive reinforcement to compulsive and negative reinforcement. Brain structure and function change.

Addiction can also affect clinicians. “What really happens in the brain to cause an addicted doctor to lose control and his license to practice medicine? Addiction hijacks your brain and makes you do things that you normally wouldn’t do,”” said Talbert. The thing that’s really important with addiction is this term ‘plasticity,’ which means that the brain actually changes in response to experiences.  This involves both excitatory and inhibitory influences,” she said.

Positron emission tomography (PET) scans and other research over the past 20 years have increased our understanding of the neurologic processes that underlie addiction. Addiction affects the brain circuits involved in reward, motivation, memory, and even inhibitory control.

Talbert said drugs release dopamine‑‑the same chemical you feel after good sex, food, and relationships‑‑in the nucleus accumbens. “You want more. But over time in an addict’s brain, the same drug of choice no longer has that appeal. Then compulsion rears its ugly head and cravings control the addict, sometimes even after years of abstinence,” she said.


 An early onset of drinking is a risk factor for subsequent heavy drinking and negative outcomes among high school students, finds a new study. 

Researchers asked 295 adolescent drinkers (163 females, 132 males) with an average age of 16 years to complete an anonymous survey about their substance use. These self-report questions assessed age at first intoxication – for example, “How old were you the first time you tried alcohol/got drunk?”  They also took stock of the previous month’s consumption of alcohol, including an assessment of the frequency of engaging in binge drinking.

“Teenagers who have their first drink at an early age drink more heavily, on average, than those who start drinking later on,” said Meghan E. Morean, an assistant professor of psychology at the Oberlin College, Ohio and adjunct assistant professor of psychiatry at Yale School of Medicine. The findings also suggest that how quickly teenagers move from having their first drink to getting drunk for the first time is an important piece of the puzzle.

“In total, having your first drink at a young age and quickly moving to drinking to the point of getting drunk are associated with underage alcohol use and binge drinking, which we defined as five or more drinks on an occasion in this study,” Morean noted. We would expect a teenager who had his first drink at age 14, and who got drunk at 15, to be a heavier drinker than a teenager who had his first drink at age 14, and waited to get drunk until age 18, researchers emphasised.

“The key finding here is that both age of first use and delay from first use to first intoxication serve as risk factors for heavy drinking in adolescence,” said William R. Corbin, associate professor and director of clinical training in the department of psychology at Arizona State University

The study is scheduled to be published in the journal Alcoholism: Clinical and Experimental Research.

Source:  20th Sept 2014

Researchers link a gene already tied to alcohol dependence with a neurotransmitter involved in anxiety and relaxation.

The neurofibromatosis type 1 (Nf1) gene, which has been previously linked to alcohol dependence, may exert its influence on alcohol intake through the regulation of gamma-aminobutyric acid (GABA), a neurotransmitter known to decrease anxiety and boost feelings of relaxation, according to a mouse study published this month (August 18) in Biological Psychiatry. The research, led by scientists at The Scripps Research Institute (TSRI), also links variations in the human Nf1 with the risk and severity of alcohol dependence.

“Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood,” co-author Vez Repunte-Canonigo said in a press release.

The team decided to look for a connection with the neurotransmitter GABA as a result of previous work that has shown GABA release in the central amygdala, a brain area involved in decision making, stress, and addiction, is “critical in the transition from recreational drinking to alcohol dependence,” said co-author Melissa Herman. Examining mouse models of alcohol dependence, the team found that mice with functional Nf1 genes started to increase their alcohol intake after a single period of withdrawal, while those with one copy of the gene knocked out did not increase their ethanol consumption. Moreover, in heterozygous Nf1 mice, intake of alcohol did not result in higher GABA release in the central amygdala, which was observed in mice with two functional copies of the Nf1 gene.

The researchers also explored variation in human Nf1 using data from some 9,000 people and found the gene correlated alcohol-dependence risk and severity. “A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy,” co-author Pietro Paolo Sanna said in the release.

Source: August 27, 2014

NHS figures show increase of 22% in number of cases over last 10 years, from 1,192 in 2004-5 to 1,536 in past 12 months

More than 7,800 babies have been born with ‘neonatal withdrawal symptons’ in the past five years, after becoming dependent on drugs their mothers took during pregnancy. Photograph: Alamy

More than 1,500 babies a year are born addicted to drugs, NHS figures show. They include cases where doctors have been forced to give opiates to babies in order to wean them off heroin.

More than 7,800 newborns have been recorded with “neonatal withdrawal symptoms” in the last five years, effectively putting them into cold turkey after becoming dependent on drugs their mothers took during pregnancy.

They include 6,599 cases in England, 738 in Scotland and 464 cases in Wales, according to data obtained by the Mirror.

The figures show a 22% increase in cases over the last 10 years, from 1,192 in 2004-5 to 1,536 in the past 12 months.

Christian Guy, director of the Centre for Social Justice thinktank, said: “The 1,500 innocent babies born into the trauma of addiction each year are being given a tragic start in life. It demonstrates that addiction is not just about individual choice – it affects children, families, communities and public services.”

Vivienne Evans, chief executive of the family support charity Adfam, said: “If pregnant women think they will be mistreated, stigmatised or have their children taken away, they will be scared to access the health services that they and their babies need. We need specialist doctors, midwives and social workers to work with them.”

A study published this year found that more than half of women drink more than the recommended amount of alcohol during the first three months of pregnancy. Women who had more than two units a week were twice as likely to give birth to unexpectedly small or premature babies as women who did not drink at all.

Source:, Saturday 2 August 2014

Filed under: Addiction,Health :

Excessive alcohol use is usually associated with damage to the liver. While that is a common side effect, researchers are now warning that heavy drinking can also take a toll on the lungs.

Alcohol can break down the immune system in the lungs, making them more vulnerable to infection, and the damage it causes. It’s why alcoholics are at increased risk of developing pneumonia and life-threatening acute respiratory distress syndrome (ARDS), for which there is no treatment.

Researchers at Thomas Jefferson University say they have discovered that one of the keys to immune system failure in the lung is a build-up of fat. It’s significant, they say, because it not only explains why alcohol is linked to lung disease but offers the possibility of a new treatment.

Alcoholic fatty lung

“We call it the alcoholic fatty lung,” said lead researcher Ross Summer, M.D. “The fat accumulation in the lungs mimics the process that causes fat to build up and destroy the liver of alcoholics.”

When you over-consume alcohol your liver cells begin to produce fat – most likely a defense against the toxic effects of alcohol. Over time that fat accumulates to the point that heavy drinkers develop so called “fatty liver disease.”

The fat build-up at first impairs liver function but can also cause scarring that eventually leads to liver failure. So, what does this have to do with the lungs?

The lungs also contain cells that produce fat. These cells expel a fatty secretion onto the inner lining of the lung to keep the airways properly lubricated during breathing. Summer and his teams speculated that these cells might act the same way liver cells do after extended alcohol exposure.

The study

Laboratory rats were enlisted for experiments and the researchers noted the lung cells increased production of triglycerides by 100% and free fatty acids by 300%. The researchers also noticed that immune cells in the lungs were less effective against infection.

From this, the researchers conclude that lipid lowering drugs might be an effective tool for doctors treating alcohol-related pneumonia. They think it might also head off development of ARDS.

Increased scrutiny

Alcohol only recently has received new scrutiny as a serious health threat. The Centers for Disease Control and Prevention (CDC) says there are approximately 88,000 deaths in the U.S. each year that can be attributed to excessive alcohol use, making it the third leading lifestyle cause of death in the nation.

“Excessive alcohol use is responsible for 2.5 million years of potential life lost (YPLL) annually, or an average of about 30 years of potential life lost for each death,” the CDC said in a report.

In 2006, there were more than 1.2 million emergency room visits and 2.7 million physician office visits due to excessive drinking, the agency said. The economic costs of excessive alcohol consumption in 2006 were estimated at $223.5 billion.

Then there is the whole category of deaths and injuries due to accidents caused by excessive alcohol consumption. And there is some evidence that the current statistics understate the problem.

In March researchers writing in the Journal of Studies on Alcohol and Drugs suggested a lot of highway deaths – and other accidents in which alcohol was a factor – might not make it into the alcohol-related statistics.

Between 1999 and 2009, more than 450,000 Americans were killed in a traffic crashes. The researchers maintain that in cases where alcohol was involved, death certificates very often failed to list alcohol as a cause of death.

Defining problem drinking

What constitutes excessive drinking? Heavy drinking is defined as 8 or more drinks per week for women and 15 or more drinks for men.

But don’t think only drinking on Saturday night – but polishing off 12 beers – will qualify you as a moderate drinker. Binge drinking, according to the CDC, is the worst kind.

Binge drinking is defined as 4 or more drinks on a single occasion for women and 5 drinks for men.

Source:  7th July 2014

Filed under: Addiction,Alcohol,Health :

People affected by binge eating, substance abuse and obsessive compulsive disorder all share a common pattern of decision making and similarities in brain structure, according to new research  from the University of Cambridge. “Compulsive disorders can have a profoundly disabling effect of individuals. Now that we know what is going wrong with their decision making, we can look at developing treatments, for example using psychotherapy focused on forward planning or interventions such as medication which target the shift towards habitual choices,” authors said.

In a study published in the journal Molecular Psychiatry and primarily funded by the Wellcome Trust, researchers show that people who are affected by disorders of compulsivity have lower grey matter volumes (in other words, fewer nerve cells) in the brain regions involved in keeping track of goals and rewards.

In our daily lives, we make decisions based either on habit or aimed at achieving a specific goal. For example, when driving home from work, we tend to follow habitual choices — our ‘autopilot’ mode — as we know the route well; however, if we move to a nearby street, we will initially follow a ‘goal-directed’ choice to find our way home — unless we slip into autopilot and revert to driving back to our old home. However, we cannot always control the decision-making process and make repeat choices even when we know they are bad for us — in many cases this will be relatively benign, such as being tempted by a cake whilst slimming, but extreme cases it can lead to disorders of compulsivity.

In order to understand what happens when our decision-making processes malfunction, a team of researchers led by the Department of Psychiatry at the University of Cambridge compared almost 150 individuals with disorders including methamphetamine dependence, obesity with binge eating and obsessive compulsive disorder, comparing them with healthy volunteers of the same age and gender.

Study participants first took part in a computerised task to test their ability to make choices aimed a receiving a reward over and above making compulsive choices. In a second study, the researchers compared brain scans taken using magnetic resonance imaging (MRI) in healthy individuals and a subset of obese individuals with or without binge eating disorder (a subtype of obesity in which the person binge eats large amounts of food rapidly).

The researchers demonstrated that all of the disorders were connected by a shift away from goal-directed behaviours towards automatic habitual choices. The MRI scans showed that obese subjects with binge eating disorder have lower grey matter volumes — a measure of the number of neurons — in the orbitofrontal cortex and striatum of the brain compared to those who do not binge eat; these brain regions are involved in keeping track of goals and rewards. Even in healthy volunteers, lower grey matter volumes were associated with a shift towards more habitual choices.

Dr Valerie Voon, principal investigator of the study, says: “Seemingly diverse choices — drug taking, eating quickly despite weight gain, and compulsive cleaning or checking — have an underlying common thread: rather that a person making a choice based on what they think will happen, their choice is automatic or habitual.

“Compulsive disorders can have a profoundly disabling effect of individuals. Now that we know what is going wrong with their decision making, we can look at developing treatments, for example using psychotherapy focused on forward planning or interventions such as medication which target the shift towards habitual choices.”

Source: University of Cambridge. “Creatures of habit: Disorders of compulsivity share common pattern, brain structure.” ScienceDaily. ScienceDaily, 29 May 2014. <>.

Dr. Robert DuPont, President, Institute for Behavior and Health   |   March 28, 2014

In a recent National Public Radio interview, Dr. Lance Dodes, co-author of a new book that attacks the efficacy of Alcoholics Anonymous (AA) and the many 12-step groups it has inspired, declared that AA — which he repeatedly misidentified as a “treatment” — probably has “the worst success rate in all of medicine,” and is “harmful” to those who do not do well within its program.

He told NPR that AA’s success rate was “between 5 and 10 percent,” and that AA harms people because “everyone believes that AA is the right treatment. AA is never wrong … If you fail in AA, it’s you that’s failed,” he said.

Moreover, Dodes criticized AA and Narcotics Anonymous’ (NA) “tally” system, which recognizes incremental periods of continued sobriety by awarding chips. “The dark side is, if you have a beer after six months of sobriety, you’re back to zero in AA,” Dodes said. “That makes no sense. It’s unscientific. It’s simply crazy. If you have only a beer in six months, you’re doing beautifully.”

I couldn’t disagree more. His message is not only inaccurate and distorted, but also dangerous. No one should be discouraged from participating in these fellowships. They save lives every day.

When people ask me the percentage of success of AA and NA, the 12-step fellowships, I say it is 100 percent — for those who follow the programs as they’re intended to be followed. This means not just going to an occasional meeting, but to many meetings every week, having a sponsor — who is similar to a sober companion — “working” each of the 12 steps in depth, specifically as they apply to the recovering addict, and making recovery the No. 1 priority.  This group of related fellowships is a modern miracle. There are many reasons to be proud of America, but none is more personally important to me — or more unique — than the founding of Alcoholics Anonymous in 1935 in Akron, Ohio.

AA is not “treatment,” and it cannot be meaningfully compared to any treatment. When can anyone find a treatment program located in virtually every part of the world? A treatment program where someone calls you daily? A treatment program where you can call someone at 3 a.m.? And a “treatment” that not only is free to the suffering addict and alcoholic, but that requires no insurance, government funding or a license, and is not subject to any regulation?

No one makes money from it. Rich folks cannot even give money to it, because it needs none, other than the few dollars for administrative costs that its members donate during the meetings themselves. No one writes books about it. The groups actually seek no publicity; in fact, publicity goes against its principles. The word “anonymous” is part of its name for a reason; members respect the anonymity of those who participate, as well as their personal stories.

Moreover, unlike what Dodes apparently believes, no one judges you if you relapse. No one makes you feel as if you’ve failed. Rather, you receive unconditional support. I know of no other programs like these. They are not treatment, nor are they religion. The only requirement is a desire to stop drinking and using drugs.

But to say, as Dodes seems to be suggesting, that AA merely is a supportive social organization completely misses what this miracle is: AA and NA are well-established, sophisticated and effective paths to “recovery,” a term adopted by these fellowships to make clear that AA does not offer to help members get back to their “premorbid” state, but rather to reach an entirely new and better state of living. Its members are not “reformed,” which has a negative connotation, but “recovering,” which is — and must be — a lifelong process.

Those in recovery serve as an inspiration, not only to drug addicts and alcoholics, but to everyone they encounter — a striking and remarkable contrast to the response they would receive if they were still using alcohol and drugs.

The bright line drawn by AA and NA — the sobriety date that marks the last time a recovering addict used alcohol or other drugs — is essential. It differs radically from the academic and professional standard for drug and alcohol addiction , which tolerates slips and relapses. The bright line of the sobriety date is a matter of importance and of huge pride for fellowship members — it is a core marker of identity in the fellowships, and a fundamental defining part of the disease of addiction. One of the true joys of this fellowship is attending a group celebration that commemorates a recovering addict’s “clean time” anniversary.

The all too common academic, professional views on addiction, well represented by Dodes, run counter to the AA and NA goal of sobriety. Many professionals and academics see continued alcohol and drug use as OK but “problem-generating use” as not quite as acceptable. They encourage controlled, responsible alcohol and drug use. They encourage cutting down, but not stopping. They view drug and alcohol use by addicts as a lifestyle alternative that, like sexual orientation, should not be “stigmatized.”

That is a reckless view. An addict who has one beer after six months of sobriety is not doing “beautifully.” Instead, he or she is courting catastrophe, and likely to easily fall back into active addiction. An addict cannot just have one beer, or one cigarette, or one pill. True lifelong recovery does not happen that way, and anyone who believes that it does is heading for a major relapse.

There are endless examples of skeptics like Dodes who seek alternatives to AA, or approaches that attack AA. I suggest to my patients who reject AA that they find one of these alternatives, and see what they think of it. They tell me that such programs are hard to find. I ask them, “Why do you think that is the case? Doesn’t that tell you something?” When they go to these alternative meetings and hear little beyond AA-bashing, I ask them, “How will this help keep you sober?”

AA and NA do not replace treatment; they enhance it. I see this daily in my own practice. Some addicts do get well without AA or NA, but far more of them fail. I encourage my patients to join the fellowships, and I rejoice with them when they do, confident that they have a better chance at lifelong recovery.

When patients tell me they have attended AA or NA meetings but they haven’t helped, it doesn’t take long to discover that their attendance was brief. I urge them to find a sponsor and speak to their sponsor daily. I tell them to work the steps with a life-or-death intensity, and to do what is known as “90/90” — attend 90 meetings in 90 days. Those who follow these suggestions almost always end up with a new outlook on life and the potential for long-term sobriety. [Most Alcoholics in ‘Serious Denial’ About Treatment ]

Clinicians like me all have come to believe that these fellowships are a blessing — not just for our patients, but for all of us.

The wisdom of the 12-step fellowships does not come simply from Bill Wilson or Bob Smith, AA’s founders. It is wisdom distilled from the experiences of millions of suffering addicts and alcoholics. That source makes it utterly different from the academic studies of addiction. With the 12 steps, what works sticks, and what doesn’t disappears. The leaders don’t abandon the latter; the entire community does.

The 12-step approach is ever-changing and growing. It also is endlessly diverse, fitting in with every culture and subculture in the world. It is adaptable and sensitive to vast diversity. It is unlicensed and uncensored. Anyone can start an AA or NA meeting anywhere he or she chooses. Those groups that meet real needs of real people will thrive and grow.

To be sure, attacking AA probably sells books. Sadly, Dodes’ view of the 12-step fellowships, while misguided and ill-informed, is held by many otherwise sensible and well-informed individuals. I never have understood their skepticism. Think about it. Why have these programs endured so long and become so widespread?

The answer: It works if you work it.

Source:  www. 28th March 2014

There’s a long-standing observation that not everyone who tries drugs becomes addicted. Some people are more vulnerable to addiction and some are more resilient. Our goal is to try to understand the individual differences that contribute to whether or not someone who takes a drug will become addicted to it.

Many factors contribute to those differences, and we break them down into three sets. One set is environmental—how a person’s experiences and exposures to drugs or other influences affect his or her risk for addiction. A simple example would be that if your friends smoke, you might be more likely to become a regular smoker and incur the risk for nicotine addiction that comes with regular smoking.  A second set of factors is developmental. The impact of an experience or an exposure often depends on when in a person’s life it occurs. Because the brain is very pliant from early life through adolescence, exposures during this period can make a profound difference in how vulnerable or resilient we are to addiction in the long run.

And finally, we are working to understand the genetics, epigenetics, and other biological processes that underlie drug use and addiction. Addictive drugs can hijack our brain circuitry and cause a rewiring that motivates a person to take more of the drug or make him crave it. So this area of research focuses on how the brain is constituted and how it works, how its neurons and other cells such as glia communicate with each other in these circuits, and then how drugs infiltrate and divert these circuits.

Do genes play a large role in addiction?

Genetic factors account for about 40 to 60 percent of a person’s vulnerability to drug addiction. Genetic studies have begun to identify gene variants that influence a person’s risk for drug use and addictive behaviors. We’ve made the most progress in relating gene variants to smoking behaviors.

We’re working toward a day when a physician might be able to review a patient’s genetic information and predict how she will respond to a particular treatment, for example an antismoking medication. Is it likely to help her, or will she experience side effects and maybe do better with an alternative treatment? There’s still a lot of work to be done in this area, but the evidence is building up and leading toward that goal.

Genetic studies are also giving us leads to the molecular and biological processes that underlie addiction. When we see which genes are involved, then we know which proteins are involved, and we can look at what those proteins do.

Using gene therapy to actually treat drug addiction is a long way off, however, and probably not a main goal. Studies have shown that addiction is a complex disease, with a large number of genes each contributing a little bit. It’s not like, for example, Huntington’s disease, where a single gene is responsible, and the problem is to find an answer to what that one gene does. And even that is a huge challenge.

What are the most promising pathways to new addiction treatments?

Nongenetic factors offer the most hope. They account for 40 to 60 percent of a person’s likelihood of becoming addicted, and they’re much more malleable than genetic factors.

Our overall strategy is to understand how addictive drugs act in the brain to produce and maintain addiction. We can then look for medications, behavioral therapies, or other interventions that will reverse or overcome those effects. This is how our current medications for smoking cessation and treating heroin dependence were developed. We’re now making a major push to identify molecules and processes involved in cocaine addiction and validate them as potential targets for pharmacological interventions.

A relatively new and very promising line of research looks at drugs’ effects on the activity levels of genes. These effects, called “epigenetic” effects, alter brain structure and function in ways that affect cognition and can give rise to addictive behavior. For example, they contribute to neuronal priming, whereby an initial drug exposure primes the brain’s reward system to react more intensely to subsequent exposures. They also underlie the long-lasting changes that distinguish addicted brains from nonaddicted brains.

Epigenetic studies, by pinpointing which genes drugs activate or silence, can shed light on the specific proteins and processes involved in addiction. And, if we can then prevent or reverse those effects, we may have powerful tools for preventing and treating addiction.

Unlike gene therapy, epigenetic treatment approaches would not involve actual manipulation of the DNA in genes. Instead, they would utilize epigenetic mechanisms that control how accessible genetic DNA is to transcription and translation into proteins. There are a number of epigenetic mechanisms at work in the body at all times. Just as drugs engage them to cause addiction, research may show us how to engage them to combat addiction.

What makes your work exciting?

One reason this is an exciting time to be studying addiction is that researchers are uncovering new knowledge at a truly unprecedented pace. That’s happening in large part because we have many new, truly cutting-edge tools and technologies at our disposal. Optogenetics is a great example. With this technology, scientists are using light to stimulate or shut down specific neurons in the brains of experimental animals. They then can observe the effects of that change on animals’ behavior, or they can track neurocircuitry by observing the fallout in other parts of the brain. We also have the ability to create very fine-tuned molecular tools—for example, molecules that we can use to modulate those epigenetic processes and observe the effects.

We’re also benefiting from the huge advances in data storage and computing power that have taken place. That’s given rise to what we call “Big Science.” The promise of Big Science is that we will be able to integrate all of our behavioral, molecular, genetic, epigenetic, and other findings into a multidimensional, reasonably complete picture of addiction—what it is, and how to prevent and cure it.

Source:   May 2014

Filed under: Addiction :


This article discusses addiction and formation of the Addiction Memory. Addiction has been described as a brain disorder involving brain structures and neural circuits. Addiction impacts long term associative memory including multiple memory systems. Addiction has pathological associations with learning, memory, attention, reasoning, and impulse control. People with addictions suffer from high levels of early maladaptive schemas. The Addiction Memory (AM) plays a crucial role in relapse occurrence and maintaining the addictive behavior. Healing the addiction memory is imperative in treating addictions. Pharmacological and psychological methods are being used to treat addictions. Among the psychological interventions Cognitive Behavior Therapy, Eye movement desensitization and reprocessing (EMDR) and Schema-Focused Therapy (SFT) can be used to heal the addiction memory.

Drug addiction has become an increased phenomenon in the modern civilization. Addiction habits have impacted individuals, families and the society. Addiction has been regarded as an individual disease as well as a social condition. Addictions cause structural changes in cultural, social, political, and economic system in society (Ajami et al., 2014). Addiction is almost universally held to be characterized by a loss of control over drug-seeking and consuming behavior (Levy, 2014).

Addiction is defined as compulsive drug use despite negative consequences (Hyman, 2005). Addiction is a multifactorial phenomenon (Shaghaghy et al., 2011). McLellan and colleagues (2000) conceptualize addiction as a brain disease. Leshner (1997) views addiction as a chronic, relapsing brain disorder that involves complex interactions between biological and environmental variables. According to Mate (2014) addictions are experience based and it has close links with pain, distress, negative emotions, loss of meaning and often connected with adverse early childhood experiences.  Drug addiction leads to profound disturbances in an individual’s behavior that affect his/her immediate environment, usually resulting in isolation, marginalization, or incarceration (Volkow et al., 2004).

 Addictions and Brain Structures

There are numerous brain structures and neural circuits involved in the addiction process. Several studies using a whole brain analysis approach have demonstrated how sensorimotor brain networks contribute to addiction (Yalachkov et al., 2010). Drug addiction causes important derangements in many areas, including pathways affecting reward and cognition (Fowler et al., 2007). Tomkins & Sellers (2001) specify that multiple neurotransmitter systems may play a key role in the development and expression of drug dependence.

Studies indicate that The ventral striatum, a region implicated in reward, motivation, and craving, and the inferior frontal gyrus and orbitofrontal cortex, regions involved in inhibitory control and goal-directed behavior become affected in addictions (Konova et al., 2013). A central concept in drug abuse research is that increased dopamine (DA) in limbic brain regions is associated with the reinforcing effects of drugs (Di Chiara andImperato, 1988; Koob &Bloom, 1988; Volkow et al., 2004). Pharmacological and behavioral studies have indicated that modulation of locus coeruleus (LC) (which is the largest noradrenergic nucleus in brain, located bilaterally on the floor of the fourth ventricle in the anterior pons) neuronal firing rates contributes to physical aspects of opiate addiction, namely, physical dependence and withdrawal, in several mammalian species, including primates (Redmond and Krystal, 1984; Rasmussen et al.,1990;Nestler, 1992).

Memory and Addiction

Inter connection between human memory process and addiction has been speculated by numerous researchers in the past few decades. Theories of addiction have mainly been developed from neurobiologic evidence and data from studies of learning behavior and memory mechanisms (Cami & Farre, 2003). Wang and colleagues (2003) hypothesized that addiction can be resulted by the abnormal engagement of long term associative memory. Volkow et al. (2003) highlight that multiple memory systems have been proposed in drug addiction, including conditioned-incentive learning (mediated in part by the NAc and the amygdala), habit learning (mediated in part by the caudate and the putamen), and declarative memory (mediated in part by the hippocampus). According to Hyman(2005)addiction represents a pathological usurpation of the neural mechanisms of learning and memory that under normal circumstances serve to shape survival behaviors related to the pursuit of rewards and the cues that predict them.

The Process of Learning and Memory in Addiction

The process of learning and memory in addiction has been proposed to involve strengthening of specific brain circuits when a drug is paired with a context or environment (Klenowski et al., 2014). Addiction has pathological associations with learning, memory, attention, reasoning, and impulse control. Addiction related behaviors arise as a result of maladaptive learning process. Following learning pathways individuals with addictions become sensitive and strongly respond to drug cues (Robinson & Berridge, 2000). Drug use in the addicted individual is controlled by automatized action schemata (Tiffany, 1990).

Robbins and colleagues (2002) point out that pathological subversion of normal brain learning and memory processes in drug addiction. They further emphasize that drug related habits evolve through a cascade of complex associative processes with Pavlovian and instrumental components that may depend on the integration and coordination of output from several somewhat independent neural systems of learning and memory, each contributing to behavioral performance.

Tiffany (1990) concluded that drug urges and drug use result from distinct cognitive processes. Some experts believe that addiction related behaviors can be explained via the Feeling-State Theory. According to the Feeling-State Theory positive feelings and behavior are fixated in the body during an intense experience such as drug ingestion creating the feeling-state (Miller, 2005).

A considerable number of researchers point out that subcortical brain region plays a key role in formation of normal as well as drug related behavioral habits. Chronic drug exposure causes stable changes in the brain at the molecular and cellular levels (Nestler, 2001). Drug abusing habits can change the structure and function of the synaptic connections allowing synaptic plasticity for long periods even for a lifetime. Synaptic plasticity may play key roles in the addiction process (Winder et al., 2002). Kelley (2004) states that the process of drug addiction shares striking commonalities with neural plasticity associated with natural reward learning and memory.

 Addictions and Maladaptive Schemas

Segal (1988) viewed schemas as the residue of past reactions and experience that often effect subsequent perception and appraisals. Bakhshi Bojed and Nikmanesh,   (2013) pointed out that drug users suffer from some early maladaptive schemas which can be the potential for drugs abuse. A study done by Shaghaghy and colleagues (2011) indicated that people with addictions suffer from high levels of early maladaptive schemas and they had a more pessimistic attributional style. Maladaptive schemas and inefficient ways the patient learns to adapt with others often lead to chronic symptoms of anxiety, depression and substance abuse (Kirsch, 2009: Shaghaghy et al., 2011).

 Memory and Craving

Craving is often depicted as the subjective experience; craving tends to be highly situationally specific, readily triggered by stimuli previously associated with drug use. Secondly, craving can persist well beyond the cessation of addicted substance (Tiffany & Conklin, 2000). Volkow and colleagues (2004) point out that drugs trigger a series of adaptations in neuronal circuits involved in saliency/reward, motivation/drive, memory/conditioning, and control/disinhibition, resulting in an enhanced (and long lasting) saliency value for the drug and its associated cues at the expense of decreased sensitivity for salient events of everyday life (including natural reinforces).

 The Addiction Memory

The Addiction Memory (AM) plays a crucial role in relapse occurrence and maintaining the addictive behavior. The drug-associated cues are highly connected with Addiction Memory and it helps to maintain drug seeking craving. Boening (2001) views the personal Addiction Memory as an individual acquired software disturbance in relation to selectively integrating “feedback loops” and “comparator systems” of neuronal information processing. The Addiction Memory becomes part of the personality represented on the molecular level via the neuronal level and the neuropsychological level, especially in the episodic memory (Boening, 2001).

 Working with the Addiction Memory

Böning (2009) discusses the difficulties in treating Addiction Memory since it is embedded above all in the episodic memory, from the molecular carrier level via the neuronal pattern level through to the psychological meaning level, and has thus meanwhile become a component of personality. Therefore healing the Addiction Memory is challenging and time consuming.

According to Leshner (1997) in addictions the most effective treatment approaches include biological, behavioral, and social-context components. Among the pharmaco-therapeutic methods Sittambalam, Vij, and Ferguson (2014) highlight Suboxone as an effective treatment method for heroin addiction and as a viable outpatient therapy option. In addition they recommend individualized treatment plans and counseling for maximum benefits.

Carroll & Onken (2005) argued that Cognitive behavior therapy, contingency management, couples and family therapy, and a variety of other types of behavioral treatment have been shown to be potent interventions for several forms of drug addiction. Kauer & Malenka (2007) suggest that reversing or preventing drug-induced synaptic modifications such as mesolimbic dopamine system is one of the key ways to treat addictions.

Gould (2010) stated that from a psychological and neurological perspective, addiction is a disorder of altered cognition. Restoration of altered cognition would be essential in working with the addiction memory. von der Goltz and colleagues (2009) conjectured   that disruption of drug-related memories may help to prevent relapses. Growing evidence from preclinical and clinical studies concur that specific treatments such as extinction training and cue-exposure therapy are effective (von der Goltz & Kiefer, 2008).

Recent researches suggest that EMDR is a potent therapeutic method to treat addictions. Addiction memory could be considered as a form of an unprocessed memory. Unprocessed memories stored in networks that govern explicit and implicit memories. EMDR helps to process unprocessed memories stored in networks. EMDR involves the transmutation of dysfunctionally stored experiences into an adaptive resolution (Solomon et al., 2008).

EMDR reprocessing sessions promote an associative process that clearly reveals the intricate connections of memories that are triggered by current life experiences (Shapiro, 2014). EMDR may be used to ameliorate the effects of earlier memories that contribute to the dysfunction, potential relapse triggers, and physical cravings. In addition, EMDR is used to incorporate new coping skills and assist in learning more adaptive behaviors (Shapiro et al. 1994).

Wide arrays of experimental studies are supportive of a working memory explanation for the effects of eye movements in EMDR therapy (de Jongh et al., 2013). EMDR therapy is guided by the adaptive information processing (AIP) model (Shapiro, 2014). Levin, Lazrov & van der Kol,k (1999) found increased activation of the anterior cingulated gyrus and of the left frontal lobe after 3 sessions of EMDR treatment. Brain scans have clearly demonstrated pre-post changes after EMDR therapy, including increases in hippocampal volume, which have implications for memory storage (Shapiro, 2012).

As reviewed by Andrade and colleagues (1997) EMDR reduces the vividness of distressing images by disrupting the function of the visuospatial sketchpad (VSSP) of working memory. Cecero& Carroll (2000) considered drug cravings as a form of disturbing thoughts and they used EMDR to reduce cocaine cravings.

Young, Zangwill,   and Behary,   (2002) proposed combination of Schema-Focused Therapy (SFT) and Eye Movement Desensitization and Reprocessing (EMDR) would give effectual results processing dysfunctional memories. According to Young , Klosko & Weishaar (2003) Schema-Focused Therapy is an integrative form of psychotherapy combining cognitive, behavioral, psychodynamic object relations, and existential/humanistic approaches. Schema-Focused Therapy helps to modify individual’s maladaptive thoughts about self and others and process the emotions connected with schemas, teach coping skills and break maladaptive behavioral patterns (Young et al., 2003).


Addiction is a chronic, relapsing brain disorder. Addiction related behaviors are complex and these behaviors are strongly connected with the memory system. Formation Addiction Memory helps to maintain the addictive behavior and drug seeking craving. It becomes a component of personality. Therefore working with addiction memory could be challenging. Reduction in maladaptive schema, restoration of drug related altered cognitions help to combat addictions. Pharmacological and Psychological interventions proved to be effective in working with addiction memory. Among the psychological interventions Cognitive Behavior Therapy (CBT) Eye movement desensitization and Focused Therapy (SFT) seem to be useful in treating addiction memory.

Source:   4th May 2014

Many people who undergo treatment for addiction will relapse and begin using drugs again soon after their therapy ends, but a new study suggests that meditation techniques may help prevent such relapses. In the study, 286 people who had been treated for substance abuse were assigned to receive one of three therapies after their initial treatment: a program that involved only group discussions, a “relapse- prevention” therapy that involved learning to avoid situations where they might be tempted to use drugs, and a mindfulness-based program that involved meditation sessions to improve self-awareness.

Six months later, participants in the both the relapse prevention and mindfulness group had a reduced risk of relapsing to using drugs or heavy drinking compared with participants in the group discussions group.

And after one year, participants in the mindfulness group reported fewer days of drug use, and were at reduced risk of heavy drinking compared with those in the relapse prevention group. This result suggests that the mindfulness-based program may have a more enduring effect, the researchers said. [Mind Games: 7 Reasons You Should Meditate]

The researchers emphasized that mindfulness-based programs are not intended to replace standard programs for preventing drug relapse.

“We need to consider many different approaches to addiction treatment. It’s a tough problem,” said study researcher Sarah Bowen, an assistant professor at the University of Washington’s department of psychiatry and behavioral sciences. Mindfulness therapy is “another possibility for people to explore,” she said.  More research is needed to identify which groups of people benefit most from the approach, Bowen said.

Meditation for addiction About 40 to 60 percent of people who undergo addiction treatment relapse within one year after their treatment ends, the researchers said.

Although 12-step and traditional relapse-prevention programs have value in preventing relapse, “we still have a lot of work to do,” Bowen said. Mindfulness-based relapse prevention, a program developed by Bowen and colleagues, is essentially a “training in awareness,” Bowen said.

In this program, each session is about two hours, with 30 minutes of guided meditation followed by discussions about what people experienced during meditation and how it relates to addiction or relapse, Bowen said. The meditation sessions are intended to bring heightened attention to things that patients usually ignore, such as how it feels to eat a bite of food, or other bodily sensations, as well as thoughts and feelings. The mindfulness program may work to prevent relapse in part because it makes people more aware of what happens when they have cravings.

“If you’re not aware of what’s going on, you don’t have a choice, you just react,” Bowen said.

The program also teaches people how to “be with” or accept uncomfortable feelings, such as cravings, rather than fight them, Bowen said. In this way, people learn skills that they can apply to their everyday lives, and not just situations in which they feel tempted, which is usually the focus of other prevention programs, she said.

Addiction and emotions

Dr. Scott Krakower, assistant unit chief of psychiatry at Zucker Hillside Hospital in Glen Oaks, N.Y., who was not involved in the study, said people with addiction often suffer from other conditions that involve problems regulating emotions, such as depression, anxiety or self-harm. Emotional problems, such as feelings of numbness with depression, can be a reason people turn to drugs, he said.

The mindfulness program helps teach people to “tolerate feelings of emotional distress, so when they feel like they’re going to use [drugs], they don’t,” Krakowe said. Krakower noted that mindfulness meditation programs have already been shown to be useful for depression.

Future studies are needed to examine the effectiveness of the therapy for substance abuse over longer periods, Krakower said. But at the very least, it seems that the program can be helpful for people with emotional dysregulation, which is the majority of the substance abuse population, Krakower said.

Source: JAMA Psychiatry. March 19 2014

Adolescents’ Brains Respond Differently Than Adults’ When Anticipating Rewards, Increasing Teens’ Vulnerability to Addiction and Behavioral Disorders

Pitt research team finds region in the adolescent brain associated with learning and habit formation highly responsive to reward

Teenagers are more susceptible to developing disorders like addiction and depression, according to a paper published by Pitt researchers today, Jan. 16, in the Proceedings of the National Academy of Science.

The study was led by Bita Moghaddam, coauthor of the paper and a professor of neuroscience in Pitt’s Kenneth P. Dietrich School of Arts and Sciences. She and coauthor David Sturman, a MD/PhD student in Pitt’s Medical Scientist Training Program, compared the brain activity of adolescents and adults in rats involved in a task in which they anticipated a reward. The researchers found increased brain cell activity in the adolescent rats’ brains in an unusual area: the dorsal striatum (DS)—a site commonly associated with habit formation, decision-making, and motivated learning. The adult rats’ DS areas, on the other hand, did not become activated by an anticipated reward.

“The brain region traditionally associated with reward and motivation, called the nucleus accumbens, was activated similarly in adults and adolescents,” said Moghaddam. “But the unique sensitivity of adolescent DS to reward anticipation indicates that, in this age group, reward can tap directly into a brain region that is critical for learning and habit formation.”

Typically, researchers study the correlation between different behaviors of adolescents and adults. The Pitt team, however, used a method they call “behavioral clamping” to study if the brains of adolescents process the same behavior differently. To that end, the researchers implanted electrodes into different regions of rat adolescent and adult brains, allowing the researchers to study the reactions of both individual neurons and the sum of the neurons’, or “population,” activity.

The researchers’ predictions proved accurate. Even though the behavior was the same for both adult and adolescent rats, the researchers observed age-related neural response differences that were especially dramatic in the DS during reward anticipation. This shows that not only is reward expectancy processed differently in an adolescent brain, but also it can affect brain regions directly responsible for decision-making and action selection.

“Adolescence is a time when the symptoms of most mental illnesses—such as schizophrenia and bipolar and eating disorders—are first manifested, so we believe that this is a critical period for preventing these illnesses,” Moghaddam said. “A better understanding of how adolescent brain processes reward and decision-making is critical for understanding the basis of these vulnerabilities and designing prevention strategies.”

The Pitt team will continue to compare adolescent and adult behavior, especially as it relates to stimulants—such as amphetamines—and their influence on brain activity.

The National Institute of Mental Health funded this project.

The study was led by Bita Moghaddam, coauthor of the paper and a professor of neuroscience in Pitt’s Kenneth P. Dietrich School of Arts and Sciences. She and coauthor David Sturman, a MD/PhD student in Pitt’s Medical Scientist Training Program, compared the brain activity of adolescents and adults in rats involved in a task in which they anticipated a reward. The researchers found increased brain cell activity in the adolescent rats’ brains in an unusual area: the dorsal striatum (DS)—a site commonly associated with habit formation, decision-making, and motivated learning. The adult rats’ DS areas, on the other hand, did not become activated by an anticipated reward.

“The brain region traditionally associated with reward and motivation, called the nucleus accumbens, was activated similarly in adults and adolescents,” said Moghaddam. “But the unique sensitivity of adolescent DS to reward anticipation indicates that, in this age group, reward can tap directly into a brain region that is critical for learning and habit formation.”

Typically, researchers study the correlation between different behaviors of adolescents and adults. The Pitt team, however, used a method they call “behavioral clamping” to study if the brains of adolescents process the same behavior differently. To that end, the researchers implanted electrodes into different regions of rat adolescent and adult brains, allowing the researchers to study the reactions of both individual neurons and the sum of the neurons’, or “population,” activity.

The researchers’ predictions proved accurate. Even though the behavior was the same for both adult and adolescent rats, the researchers observed age-related neural response differences that were especially dramatic in the DS during reward anticipation. This shows that not only is reward expectancy processed differently in an adolescent brain, but also it can affect brain regions directly responsible for decision-making and action selection.

“Adolescence is a time when the symptoms of most mental illnesses—such as schizophrenia and bipolar and eating disorders—are first manifested, so we believe that this is a critical period for preventing these illnesses,” Moghaddam said. “A better understanding of how adolescent brain processes reward and decision-making is critical for understanding the basis of these vulnerabilities and designing prevention strategies.”

The Pitt team will continue to compare adolescent and adult behavior, especially as it relates to stimulants—such as amphetamines—and their influence on brain activity. The National Institute of Mental Health funded this project.

Source: Proceedings of the National Academy of Science.  Jan.16th 2012


Addiction makes it difficult for people to look beyond immediate gratification to the longer term consequences of their actions. Accordingly, patients in drug abuse treatment are often coached to make and rehearse mental associations between situations that trigger drug cravings and the problems that are likely to ensue from succumbing to them. The cognitive behavioral programs that incorporate this strategy generally are effective, but researchers have shed little light on the neurological basis for their efficacy—until now.

In a study led by Dr. Kevin N. Ochsner of the Social Cognitive Neuroscience Laboratory at Columbia University, smokers reported milder cigarette cravings when they thought about smoking’s harmful effects while viewing smoking cues than when they focused on its pleasures. Brain imaging correlated the reductions in craving with altered activity levels in regions associated with emotional regulation and reward.

Mental Adjustment Alters Brain Activity

Dr. Ochsner and colleagues recruited smokers as study subjects because smoking accounts for more illness and death than any other addiction. To gain insight on the smokers’ ability to regulate cravings in general, the team also investigated their responses to cues for high-fat food.

The participants were 21 men and women who had smoked for 10 years, on average, and were not trying to quit. In preparation for the study, the participants practiced turning their thoughts to rewarding effects of cigarettes or high-fat food consumption when given the instruction “NOW” and to negative effects when given the instruction “LATER.” In the study itself, the researchers gave each participant 100 such instructions, in random order, each followed by a 6-second exposure to a screen image of either cigarettes or food. Then, after a 3-second delay with the screen blank, the participant reported how much he or she desired to smoke or eat, on a scale of 1 (not at all) to 5 (very much).

The power of thinking about negative effects proved to be considerable. The participants reported 34 percent less intense urges to smoke and 30 percent less intense food cravings after the LATER instruction compared with the NOW instruction.

Brain scans taken during the experiment showed how concentrating on long-term negative consequences alters brain activity to reduce craving. Functional magnetic resonance imaging (fMRI) of the participants’ whole brain revealed increased activity levels in areas—the dorsomedial, dorsolateral, and ventrolateral regions of the prefrontal cortex (PFC)—that support cognitive control functions, such as focusing, shifting attention, and controlling emotions. Activity decreased in regions that previous studies have linked with craving; these areas include the ventral striatum and ventral tegmental area, which are parts of the reward circuit; the amygdala; and the subgenual cingulate. Individual participants who reported larger reductions in craving exhibited these changes to a more marked degree. A specialized mediation analysis of the images found that the increase in PFC activity drove the decrease in ventral striatum activity, which, in turn, fully accounted for the reduction in craving.

“These results show that a craving-control technique from behavioral treatment influences a particular brain circuit, just as medications affect other pathways,” says Dr. Steven Grant of NIDA’s Division of Clinical Neuroscience and Behavioral Research.

The researchers noted that the study participants reduced their smoking and food cravings to the same extent, even though smoking cravings were initially more intense. This finding suggests that calling undesirable consequences to mind has potential to help people overcome a variety of unhealthy urges.

Scans Show Effects of Craving Regulation in the Brain When study participants thought of the long-term negative consequences of cigarette consumption (after receiving the instruction “LATER”), rather than short-term pleasures (“NOW”), they reduced their craving. Brain scans showed increased activity in the dorsolateral prefrontal cortex—a region critical to setting goals, planning, and controlling behavior—which, in turn, inhibited the ventral striatum, part of the reward pathway that generates craving. Text Description of Scans Show Effects of Craving Regulation in the Brain Graphic

Healing Perspectives

“Cognitive reappraisal—mentally changing the meaning of an event or object to lessen its emotional impact and therefore alter the behaviors it triggers—is a strategy that helps a variety of problems,” says Dr. Ochsner. Cognitive-behavioral therapists train patients to use this approach, among others, to cope with negative emotions, stress, and substance cravings. Dr. Ochsner says, “People may not realize that they can control cravings or emotions using cognitive strategies—for example, thinking of negative consequences and distracting and distancing oneself—but patients can learn these techniques and then must continue to apply them over time.”

Dr. Ochsner says there is broad scientific interest in the neurobiological mechanisms underlying cognitive control over thoughts and emotions that promote unhealthy behaviors. Such studies generally find that although there is some overlap in the regions of the PFC engaged when people exert cognitive control, different areas seem to support different strategies for the regulation of emotional responses.

“The mediation analysis that Dr. Ochsner and colleagues conducted is unique among imaging studies and is a particular strength of this research,” says Dr. Grant. “Because the researchers examined the interaction of brain regions, the results provide a perspective on the neural circuits involved in cognitive control of craving.”

Dr. Grant suggests two important next steps in this area of research: identifying why some people have more problems than others in controlling the desire for cigarettes and determining whether brain activity predicts the ability to quit smoking.


Kober, H., et al. Prefrontal-striatal pathway underlies cognitive regulation of craving. Proceedings of the National Academy of Sciences 107(33):14811–14816, 2010. Kober, H., et al. Regulation of craving by cognitive strategies in cigarette smokers. Drug and Alcohol Dependence 106(1):52–55, 2010.  NIDA Notes April 19, 2012

Naturally-occurring hormone could block its effects

University of Bordeaux researchers found the hormone pregnenolone cuts the brain’s sensitivity to THC – the high-inducing compound in cannabis

Discovery could lead to new approaches to treating cannabis dependence

People taking the drug medicinally could skip its psychoactive effects

A naturally occurring hormone can be used to stop the ‘high’ produced by cannabis, research has shown.  The discovery could lead to new approaches to treating cannabis intoxication and dependence.   It may also assist in the use of cannabis for medicinal purposes while blocking its psychoactive effects.

A naturally occurring hormone called pregnenolone can be used to stop the ‘high’ produced by cannabis and the discovery could lead to new approaches to treating cannabis intoxication and dependence, according to new research.

Pregnenolone is a hormone that is found in our bodies and can be made in the lab.

The chemical is used for fatigue and increasing energy, Alzheimer’s disease and enhancing memory, trauma and injuries, as well as stress and improving immunity.

It is also is used for skin disorders including psoriasis. In the body, pregnenolone is used to make all steroid hormones. Because of this, it was studied studied for stress, fatigue, and arthritis in the 1940s before lab-made hormones became available.

Researchers found that the steroid hormone pregnenolone reduces the brain’s sensitivity to THC, which is the chief high-inducing compound in cannabis. Scientists led by Dr Monique Vallee, from the University of Bordeaux in France, studied mice and rats to see how recreational drugs such as cocaine, alcohol and cannabis affected the production of steroids in the brain involved in nerve function. They found that THC triggered a dramatic spike in pregnenolone through activation of the cannabinoid receptor (CB-1) – a molecule that facilitates cannabis stimulation. This in turn had a ‘negative feedback’ effect leading to a blunting of THC activity, reducing the ‘high’ from the drug.

‘This new understanding of the role of pregnenolone has the potential to generate new therapies for the treatment of cannabis dependence,’ the scientists said.

The findings, published in the journal Science, follow the decision to legalise the recreational use of cannabis in the U.S. state of Colorado.

A recent study found teenagers who use cannabis regularly risk damaging their memory as structures in their brains appeared to shrink and collapse inward, possibly reflecting a decrease in neurons. However, while some people believe the legalisation of the drug will cut criminal activity surrounding it, others believe it will expose more people to drugs, which have been linked to health issues. A recent study found teenagers who use cannabis regularly risk damaging their memory, which can lead to poor academic performance.

They believe the brain abnormalities last for ‘at least a few years’ after users have stopped taking the drug. The researchers also said there was fresh evidence the habit may cause mental health problems in youngsters predisposed to schizophrenia.

Marijuana is the most commonly used illicit drug among adolescents in the UK, with more than four in ten admitting having taken it.

Almost 100 teenagers took part in the U.S. research examining the effects of cannabis deep in the brain. It found teenagers who smoked it daily for about three years had abnormal changes in the brain structures related to remembering and processing information and they performed poorly on memory tasks. The brain abnormalities and memory problems were found on MRI scans when study participants were in their early twenties – two years after they had stopped smoking the drug. Memory-related structures in their brains appeared to shrink and collapse inward and the researchers from Northwestern University Feinberg School of Medicine, Chicago, said such damage was linked to poor academic performance and everyday functioning.

Source:   2nd January

Women throughout the nation are dying at an unprecedented rate from prescription drug overdoses.  So many are dying that it’s been called a public health epidemic.

In fact, since 2007, more women have died annually from drug overdoses than from auto accidents, according to the Atlanta-based Centers for Disease Control and Prevention.

Although more men die from drug overdoses than women, the percentage increase in deaths since 1999 is greater among women, according to the CDC.

In 2010, the deaths of at least 15,323 women were attributed to a drug overdose, a rate of 9.8 per 100,000 population. Deaths from opioid pain relievers increased fivefold between 1999 and 2010 for women. For men, the rate increased by 3.6 times.

In 2010, some 943,365 women nationally visited an emergency room for drug misuse or abuse. The highest number of visits were for cocaine or heroin, benzodiazepines, and opioid pain relievers.

Women are more likely than men to be prescribed painkillers, use them chronically, and acquire them in higher doses. In part, that is because women are more susceptible to chronic pain and more often use the health care system, suggested Dr. James Bentler, medical director for St. Vincent Healthcare’s Emergency Department. They will seek pain relievers for migraines, chronic pelvic pain, endometriosis, cysts, and fibromyalgia, a condition of widespread pain throughout the body.  Women are also more likely to be prescribed drugs to treat depression and anxiety, which can interfere with other medications, sometimes leading to death.

“Women are the primary health care decision-makers,” said Lenette Kosovich, CEO of Rimrock Foundation. “Always have been, always will be, whether for themselves, their husband or their family. Because women are so familiar with navigating the health care system, they find it easier to manipulate and abuse the system.

Women typically have smaller body masses than men, which makes them more susceptible to overdose. They are also more likely to “doctor shop” to acquire pain pills from multiple physicians, CDC officials say.

While many of the initial complaints from women about pain are legitimate and the prescription appropriate, many pain relievers are habit-forming and can lead to addictionMany of the women who become addicted would never dream of turning to illegal drugs or alcohol, but there is no taboo associated with a prescription drug, Bentler

said. “It’s easier to hide, easier to legitimize,” said Coralee Goni, director of residential services at Rimrock Foundation. “You can put it in your Tylenol case.”

There is no single profile of women who abuse prescription drugs. They run from affluent doctors to teachers to street people.  To help curb “doctor shopping,” the 2011 Legislature passed a bill creating a State wide prescription drug registry. The registry is used to monitor certain addictive prescription drugs such as opiates and narcotics, and requires pharmacies to report weekly on the prescriptions they fill for controlled substances, according to Donna Peterson, program manager for the Montana Prescription Drug Registry.  With just a few clicks, a pharmacist can check whether a patient is filling prescriptions elsewhere in the region, Peterson said.

As of this week, the registry contains more than 4.1 million prescriptions for controlled substances, based on reporting from pharmacies that represent more than 567,000 patients, according to Peterson.

The online search feature for the registry was launched in November 2012 and has been operational for more than a year. Eventually it will maintain a full three years of a patient’s prescription history. More than 90,000 searches have been conducted since the registry launched last year, Peterson said. Between Nov. 26 and Dec. 23 of this year, health care providers conducted almost 8,000 patient history searches.

Peterson said many prescribers and pharmacists have told her that the information revealed in the registry is “invaluable. Some providers thought they knew a particular patient very well, but they were surprised at the quantity of controlled substances the (registry) showed the patient was receiving from other providers,” Peterson said.

She said she also has spoken with several prescribers who identified potential prescription forgeries by using the “Prescribing History” feature of the registry, which shows all prescriptions dispensed under the prescriber’s own Drug Enforcement Administration number.

Montana has the 21st-highest drug overdose mortality rate in the United States, with 12.9 per 100,000 people fatally overdosing, according to a recent Trust for America’s Health report.

The number of drug overdose deaths, a majority of which are from prescription drugs, has more than doubled since 1999 when the rate was 4.6 per 100,000.  West Virginia has the highest number of drug overdose deaths; the study also listed New Mexico, Kentucky, Nevada and Oklahoma in the top five in terms of drug fatalities. The study found that the Dakotas have the lowest incidence of drug overdose fatalities.

The Montana Board of Pharmacy requires pharmacies doing business in the state to report to the registry. Some 763 pharmacies, including mail-order pharmacies serving

Montana customers, participate by reporting all painkiller prescriptions to the confidential database.  As of October, authorized pharmacists, physicians and other prescribers had conducted 74,000 patient history searches.

“It’s scary business, so we need to be vigilant about giving them out,” Bentler said. “There’s plenty of blame to go around as to how we got to where we are. It’s only fair that since we’re the ones prescribing them that we accept some of that responsibility and try to become better at it. We just can’t blame it on the patients, though they have culpability, too.”

The prescription drug registry is not a cure-all. Of people ages 12 or older who in 2011-2012 used pain relievers for nonmedical reasons, 54 percent said they got them free from a friend or relative, according to the Substance Abuse and Mental Health Services Administration. About 15 percent bought or stole them from a friend. Other than physicians, the balance got pain relievers from drug dealers, strangers, the Internet and other sources.

Between Jan. 1 and Dec. 16, Billings police investigated 31 incidents of people fraudulently obtaining dangerous drugs, according to Lt. Kevin Iffland. Police say the suspects doctor shopped, forged prescriptions, falsified prescriptions and more.

The increase could be due in part of the Billings Police Department teaming with the Drug Enforcement Administration and having an officer assigned to work strictly with prescription drug cases, Iffland said. It is also due to the Prescription Drug Registry.

During the same period, Billings police received 170 cases of stolen prescription medications compared with 205 cases last year. Stopping the epidemic in both women and men is everyone’s responsibility, Bentler said. Doctors need to be careful in how they prescribe medications and patients need to be judicious in how they take them.

“You need to do the right things for people and help them, but there’s a slippery slope you can go down by using these powerful medicines,” Bentler said. “It’s fascinating trying to figure out the right approach. How do you do no harm?”

Source: Dec.2013

The number of new  born babies diagnosed with “neonatal drug withdrawal symptoms” has risen by 11 per cent in the past four years, to 1,129 last year

More than 20 babies a week are born addicted to drugs in England, NHS figures show.

In the past decade, more than 10,000 new borns effectively had to be put into cold turkey at birth because they had become dependent on substances their mothers took while pregnant.

The number diagnosed with “neonatal withdrawal symptoms” has risen by 11 per cent in the past four years, to 1,129 last year.

The figures from the NHS’s statistics agency show that the numbers stayed relatively constant between 2003 and 2009, edging up from 1,028 to 1,056. But in the past four years it has jumped by more than a tenth.

The disclosure came in an answer provided by Dr Dan Poulter, the health minister, in response to a parliamentary question tabled by Tory MP Andrew Griffiths.

It was tabled following a report by the Centre for Social Justice, the think tank founded by Iain Duncan-Smith, which said that the figures included babies born addicted to the state-supplied heroin substitute, methadone.

The group criticised drugs policy in Britain as unambitious, saying more than 40,000 heroin addicts were on substitutes such as methadone for years.

“This is a tragedy for the mothers and their children born into the horrors of addiction,” said Alex Burghart, the group’s policy director.

“We should want the best start in life for all children, but as these figures show, many have one of the worst possible starts. We have a ludicrous situation where the NHS is weaning many children off the highly addictive substances the State was supplying their mothers.

“Although methadone has a place in helping addicts move towards full recovery, too many are simply parked on it and forgotten.”

Source:  23.12.13

Young Swiss men who say that they believe in God are less likely to smoke cigarettes or pot or take ecstasy pills than Swiss men of the same age group who describe themselves as atheists. Belief is a protective factor against addictive behaviour. This is the conclusion reached by a study funded by the Swiss National Science Foundation.

Karl Marx said that religion was the opium of the people. New figures now suggest that religion plays a role in preventing substance misuse. A research team led by Gerhard Gmel from Lausanne University Hospital has shown in the journal Substance Use & Misuse that, in Switzerland, fewer religious young men consume addictive substances than men of their age group who are agnostics or atheists.

At the army recruitment centre For their study on substance use in Switzerland, Gmel and his colleagues interviewed almost twenty-year-old men at army recruitment centres in Lausanne, Windisch and Mels between August 2010 and November 2011. The researchers have now evaluated the 5387 questionnaires completed by the young men. Based on the responses, the scientists split the young men into five groups: the “religious” believe in God and attend church services, the “spiritual” believe in a higher power, but do not practice any religion, the “unsure” do not know what to believe about God, the “agnostics” assume that no-one can know whether there is a God or not, and the “atheists” do not believe in God.

The researchers found that these groups deal differently with addictive substances. Among the 543 religious young men, 30% smoked cigarettes daily, 20% smoked pot more than once a week and less than 1% had consumed ecstasy or cocaine in the past year. Among the 1650 atheists, 51% smoked cigarettes, 36% smoked pot more than once a week, 6% had consumed ecstasy and 5% cocaine in the past year. The three groups that lay between these extremes were in the mid-range both regarding their religious beliefs and the consumption of addictive substances.

A protective influence for Gmel, these figures indicate that research into addictive behaviour should not only consider risk factors, but also protective factors. The results of his study show that belief is a protective factor when it comes to the consumption of addictive substances. Whether the differences between the groups can be attributed to the ethical values of the young men or to social control in the environments in which they live, remains unanswered.

Source: Religion Is Good, Belief Is Better: Religion, Religiosity, and Substance Use Among Young Swiss Men. Substance Use & Misuse, 2013; 48 (12): 1085 DOI: 10.3109/10826084.2013.799017

Neuroscientists at Western University (London, Canada) have made a remarkable new discovery revealing the underlying molecular process by which opiate addiction develops in the brain. Opiate addiction is largely controlled by the formation of powerful reward memories that link the pleasurable effects of opiate-class drugs to environmental triggers that induce drug craving in individuals addicted to opiates. The research is published in the September 11th issue of

The Addiction Research Group led by Steven Laviolette of the Schulich School of Medicine & Dentistry was able to identify how exposure to heroin induces a specific switch in a memory molecule in a region of the brain called the basolateral amygdala, which is involved importantly in controlling memories related to opiate addiction, withdrawal, and relapse. Using a rodent model of opiate addiction, Laviolette’s team found that the process of opiate addiction and withdrawal triggered a switch between two molecular pathways in the amygdala controlling how opiate addiction memories were formed. In the non-dependent state, they found that a molecule called extracellular signal-related kinase or “ERK” was recruited for early stage addiction memories. However, once opiate addiction had developed, the scientists observed a functional switch to a separate molecular memory pathway, controlled by a molecule called calmodulin-dependent kinase II or “CaMKII.”

“These findings will shed important new light on how the brain is altered by opiate drugs and provide exciting new targets for the development of novel pharmacotherapeutic treatments for individuals suffering from chronic opiate addiction,” says Laviolette, an associate professor in the Departments of Anatomy & Cell Biology, Psychiatry, and Psychology.

Source:  September 2013: The Journal of Neuroscience.

As a nation, we are drinking much more than we used to, which is partly attributable to alcohol being cheaper and more available than ever. Many British teenagers get into the habit early, although recent trends suggest this situation is improving (alcohol consumption among teenagers is slightly lower than it was ten years ago).

Nonetheless, drinking alcohol during adolescence is not a good idea, because the younger you are when you have your first alcoholic drink, the more likely you are to develop problems later on in life. The same is true for cigarette smoking and the use of illicit drugs such as cannabis and cocaine.

Starting early carries greater risk. NatCen


Arrested development

Why are adolescents particularly vulnerable to addiction? A large part of the answer comes from our understanding of the neurobiology of brain development during adolescence. The brain does not reach maturity until fairly late in life, with new connections between brain cells being formed right up until people are in their mid-20s.

Importantly, the brain does not mature at a uniform rate. The more primitive regions of the brain, including the reward system and other areas of the subcortex such as those parts that process emotions, reach maturity relatively early (when people are in their early teens).

The prefrontal cortex is a late bloomer. National Institute of Health








The more “advanced” parts of the brain, such as the prefrontal cortex, are not fully developed until much later. In behavioural terms this means adolescents are particularly sensitive to their emotions and to things that are novel and motivationally appealing, but they are relatively unable to control their behaviour and plan for the future.

Taking risks

My research suggests this can explain why some adolescents drink more than others: teenagers who were relatively poor at exerting self-control, or who took more risks on a computer test of risk-taking, were more likely to drink heavily in the future.

This creates perfect conditions for vulnerability to addiction during adolescence, because the motivational “pull” of alcohol and other drugs is very strong, whereas the ability to control behaviour is relatively weak. Many scientists think if adolescents do drink a lot, and if they do it frequently, then this might cause long-lasting changes in the way that the brain is organised, which can make it very difficult to stop drinking.

We certainly see changes in the brains of people with alcohol problems (compared to people without problems), but it can be difficult to work out if alcohol caused those brain changes, or if those people had slightly different brains before they started drinking, and these subtle differences may have led them to start drinking in the first place.

Starting early carries greater risk. NatCen


Addiction and behaviour

In principle, adolescent brains could be vulnerable to “behavioural” addictions as well as alcohol and drug addiction, for exactly the same reason. Very few behavioural addictions are officially recognised by psychiatrists and psychologists at the moment (gambling addiction is the only exception).

The Channel 4 documentary Porn on the Brain shown this week asked whether pornography is addictive, and if adolescents could be getting hooked. As shown in the programme, it certainly seems to be the case that a minority of adolescents who use pornography exhibit some of the characteristic features of addiction, such as feeling unable to control their use of porn, and loss of interest in other activities.

Their patterns of brain activity when viewing porn seem to be similar to those seen in people with alcohol and drug addictions when they look at pictures of alcohol and other drugs. It remains to be seen whether addiction to porn will eventually be recognised as a psychological disorder, but it is clear that it can create problems for some adolescents and young adults who use it.

What can be done? Although it’s obvious, parents should do what they can to prevent their children from experimenting with alcohol, smoking and other drugs for as long as possible. The same applies to other things that might eventually be considered “addictive”. School-based prevention programmes can also be successful, including a recent program that is tailored to different personality types and has shown some promise at reducing alcohol consumption in teenagers.

Source:  2nd Oct.2013

Anti-drug advocates who have admonished for years that marijuana is a “gateway drug” may be on to something, says a study by Yale University School of Medicine researchers, reports Connecticut Post. The state director of the National Organization for the Reform of Marijuana Laws dismissed the findings as “just another propaganda study.” The Yale study, which appears online in the Journal of Adolescent Health, showed that alcohol, cigarettes, and marijuana were associated with an increased likelihood of prescription drug abuse in men 18 to 25. In women of that age, only marijuana use was linked with a higher likelihood of prescription drug abuse.

For years, researchers have looked at a connection between marijuana and hard drugs, such as cocaine and heroin, said Lynn Fiellin, the study’s lead author and an associate professor of medicine at Yale. “I don’t think the general population has a good idea of how serious the problem is with prescription opioids,” Fiellin said. “When they’re abused or misused, these are hard drugs.” Researchers focused on a sample of 55,215 18- to 25-year-olds. Of those, 6,496, about 12 percent, reported that they were abusing prescription opioids. Of the group abusing these drugs, about 57 percent had used alcohol, 56 percent had smoked cigarettes and 34 percent had used marijuana.

Source:   3rd June 2013

A new potential treatment for marijuana dependence, and the success of network therapy, which engages family and friends in a patient’s substance abuse treatment, were two of the topics discussed at the recent annual meeting of the New York Society of Addiction Medicine. This is the second of a two-part report on the meeting, “Addiction Medicine 2013: Emerging Problems, Current Treatment.”

Researchers at Columbia University in New York are studying a new treatment for marijuana dependence.

Margaret Haney, PhD, led a study of 11 people, which has not yet been published, of a synthetic version of THC—the active ingredient in marijuana—called nabilone. Marijuana-dependent patients received either a placebo or one of two doses of nabilone.

Nabilone decreased marijuana withdrawal symptoms, such as increasing sleep and appetite, and decreased marijuana self-administration, in a laboratory model of relapse. Patients did not experience a “high” from nabilone, indicating it does not have a high abuse potential. The study was funded by the National Institute on Drug Abuse.

Dr. Haney’s colleague, Ziva Cooper, PhD, of Columbia University, Department of Psychiatry, New York State Psychiatric Institute, noted that while many people do not regard marijuana dependence as a major problem, it can lead to significant impairment or distress. “Marijuana dependence is likely to become more common as marijuana becomes legal in more states,” she said at the recent New York Society of Addiction Medicine meeting.

Marijuana potency has been increasing over the last 40 to 50 years, Dr. Cooper said. There is currently no medication approved by the U.S. Food and Drug Administration for treatment of marijuana dependence. Of people who do seek treatment for marijuana dependence, many are unable to stay abstinent, Dr. Cooper observed. In one study, 71 percent returned to marijuana use within six months.

Another treatment that has shown potential for marijuana dependence is a combination of oral THC and lofexidine, a drug used in the United Kingdom for opiate withdrawal, which is not approved in the United States. In a small study, patients who took the combination treatment had decreased cravings for marijuana and cigarettes, decreased relapse rate and improved sleep compared with either THC or lofexidine alone.

Network Therapy: Involving Family and Friends in Substance Abuse Treatment

Engaging close family and friends in substance abuse counseling—a process called network therapy—can help improve abstinence rates while providing much-needed support, according to an expert at New York University School of Medicine.

Marc Galanter, MD, a psychiatrist who originated network therapy, says including family and friends provides a valuable resource for patients if they relapse, while keeping them

accountable. The therapy also provides support to those affected by patients’ substance use disorders. Dr. Galanter conducted a study, published in 2004, that found substance abuse patients who engaged in network therapy were twice as likely to be abstinent compared with those who did not engage in the treatment.

“Participants in network therapy should have a close, ongoing relationship with the patient, and should not have a substance use disorder, so they don’t undermine the course of treatment,” Dr. Galanter said at the recent annual meeting of the New York Society of Addiction Medicine.

He continues treating patients separately in addition to seeing them as part of network therapy. The friends and family members who agree to be part of network therapy must agree to be available if the patient needs help. “They secure compliance—such as making sure the patient doesn’t go to a bar,” says Dr. Galanter. They also can suggest solutions to help the patient achieve and maintain abstinence.

Patients who know their drug test results will be shared with their network will be more motivated to pass the test, because they won’t want to let their family and friends down, Dr. Galanter observed.

Network therapy can help enforce patient agreements for future behavior, he added. “For instance, a patient may agree that if he can’t become abstinent within a few weeks, he will go into residential treatment. If he backs down, it’s harder for him to dismiss what he initially agreed to if he did so in front of his network.” Source: March 5th 2013

Source: March 5th 2013

In a recent Editorial in Medical Journal Australia Wodak calls for Australia drug policy reform based on Portugal “improved outcomes and declined problematic drug use” since decriminalization.

Drug decriminalization in Portugal is a failure despite of various reports like this one published all over the world pretending the opposite (1, 2).

There is a complete and absurd campaign of manipulation of Portuguese drug policy facts and figures, which Wodak appears to have fallen for. This is not the academic standard we expect from MJA.

As the Executive Office of the President Barak Obama Drug Control Policy, states (3)

“it is safe to say that claims by drug legalization advocates regarding the impact of Portugal’s drug policy exceed the existing scientific basis”.

Let´s focus on Nuno Miranda – a drug dependent Portuguese car parker, speech: “I am lucky to live in a society that has accepted the fact that drugs and addiction are part of life” (4)

By making drug consumption less difficult, drug dependents throughout the world become neglected, have shorter and more difficult lives and reproduce this poor situation to their children.


Do you want Australia to be populated by gentlemen like Nuno?

Kofi Annan definitively does not.

“Young people need models that may help them to find a positive way – a way without drugs. The eradication of drug abuse from our Planet is a giant task, but with the human organizations joint effort from all levels and the struggle of all, we can move forward to that direction” (5).


1. The figures related to the prevalence in the Portuguese population show that the percentage of people who have tried illicit drugs at least once in their lifetime increased from 7,8% (800 000 people) in 2001 to 12% (1,3 million) in 2007 (Portuguese ex- IDT 2008 November Activities Report).

2. “The highest mortality rates caused by HIV / AIDS among drug users were reported by Portugal, followed by Estonia, Spain, Latvia and Italy. In most other countries the rates are low” (EMCDDA, 2010 Annual Report).


4. Specter M, Getting a Fix, The New Yorker, 2011 Oct; 17.

5. Annan K, International Day Against the Abusing and Illicit Traffic on Drugs. New

Filed under: Addiction,Europe :


The Los Angeles City Council voted Tuesday to ban medical marijuana dispensaries in the city, the culmination of years of controversy over the sale of pot here. Meanwhile, in Oakland, a federal crackdown closed the nation’s largest dispensary amid protests and demonstrations. But authorities rarely seem to address the real issue about marijuana in California: Is it good medicine?

Some proponents of medical marijuana argue that pot is “natural” and therefore better, or at least no worse, than legally prescribed drugs, which may be addictive and may carry dangerous side effects. But natural is not the standard for whether a drug is safe and effective.

Marijuana advocates also say that physicians who warn against marijuana merely want to push prescriptions. But just because some doctors practice bad medicine with legal drugs doesn’t make marijuana good medicine. In most cases, it isn’t.

Anyone who wants to get a medical marijuana card knows there are unscrupulous doctors who will give you a recommendation with few questions asked. Without doubt, medical marijuana hands a get-out-of-jail-free card to people who just want to get high. Those who get a card and indulge in the infrequent use of marijuana will probably experience few problems. But the situation is different with chronic marijuana use.

Marijuana acts on cannabinoid receptors in the brain. These receptors, which are the most prevalent in the nervous system, influence just about every bodily function, including memory, attention, disposition, arousal, motivation, perception, appetite and sleep.

Many chronic marijuana users insist that marijuana is not addictive the way alcohol and other drugs are. However, neuroscience, animal studies, clinical reports of withdrawal in humans and epidemiology all show that marijuana is potentially addictive.

As to its benefits, controlled clinical studies show they exist, but they are limited. Marijuana can effectively treat neuropathic pain, and it has been shown to improve appetite and reduce nausea in cancer and AIDS patients.

But other generally accepted ideas about marijuana’s effectiveness don’t hold up.

The Glaucoma Research Foundation disputes the idea that medical marijuana is good medicine for the disease. “The high dose of marijuana necessary to produce a clinically relevant effect,” the foundation’s website explains, makes it a poor choice for the treatment of glaucoma, especially given its “significant side effects” and the availability of safer effective drugs.

In addition, those who use marijuana to treat mental health symptoms might be surprised to learn that studies show it not only may not help such symptoms, it may cause them.

Increased funding for research may lead to a better understanding of the impact cannabis has on our bodies, but for now the claims that the drug is effective in the treatment of multiple disorders as distinct as lupus and anxiety seem far-fetched at best. It seems more likely that for some people, getting high just makes them feel better, the way a drink or two might. You would be shocked, however, if in response to a diagnosis of lupus, your doctor suggested you “take two drinks and call me in the morning.”

And pot’s general ineffectiveness is only part of picture. It is not a neutral substance. Chronic marijuana use is associated with a number of well-documented health problems, including a variety of cancers in adults as well as in children who were exposed to the drug in utero.

As to its mental health effects, marijuana is linked to long-term psychiatric problems such as depression, anxiety and psychosis. “Marijuana often is regarded as a ‘soft drug’ with few harmful effects,” says Dr. Joseph M. Pierre, co-chief of the Schizophrenia Treatment Unit at the Department of Veterans Affairs’ West Los Angeles Healthcare Center. “However, this benign view is now being revised, along with mounting research demonstrating a clear association between cannabis and psychosis.”

If the lack of health benefits and manifest risks aren’t enough to raise doubts about medical marijuana, consider basic questions of quality and dose. Although medical marijuana sometimes comes from “cleaner” sources than say a drug cartel, independent labs have found mold, synthetic insecticides and other toxins in pot. Molds such as Aspergillus can be highly dangerous to immune-compromised patients. And there is no way to accurately judge what a proper dose of dispensary marijuana would be.

Habitual marijuana use is helpful for very few medical conditions. It can cause insidious changes in personality and attitude that are clear to everyone but the users themselves. There are nearly 400,000 emergency room visits per year due to marijuana use. Before we advocate for medical marijuana, and before another person doses himself with it, we have to ask: Is medical marijuana making us sick?

Dr. David Sack is a psychiatrist and addiction specialist. He is chief executive of Promises Treatment Centers and Elements Behavioral Health in Southern California.

Source: Dr.David Sack. CEO Promises Treatment Centers. Southern California USA

July 26th 2012

Concerned that this might on balance cause more deaths by limiting an effective treatment for opiate addiction, an expert panel convened by the US government has changed its mind on whether the risk of a fatal heart attack potentially posed by methadone justifies routine electrocardiogram screening of patients.


The QT interval (or QTc as corrected for the heart rate) is an indicator of heart function derived from electrocardiogram measures. It refers to the delay between two phases of the electrical activity of the heart which drives it in pumping blood round the body. The health risks associated with a prolonged interval are not clear. It can lead to torsades de pointes, a potentially life threatening heart attack, but some medications prolong the interval yet rarely cause this condition, and it can occur even when the interval is normal. The risk threshold has been set variously at for example 450ms (0.45 seconds) for men and 460ms to 470ms for women or 450ms for both, though it is generally accepted that intervals greater than 500ms pose a significant risk of torsades de pointes.

Some studies have reported that methadone may contribute to the elongation of the QT interval, heightening the risk of torsades de pointes. In response the US government convened an expert panel to assess the risk to patients and make recommendations to enhance their cardiac safety. The featured article is the latest report of that panel, superseding an earlier version.

The panel framed its recommendations on the understanding that methadone must remain widely available because it has been associated with an overall reduction in deaths, there are few therapeutic alternatives, and it is cost-effective. Treatment providers are encouraged to consider the report and take action to the extent that they are clinically, administratively, and financially able to do so, but nothing in the report is intended to create a legal standard of care or accreditation requirement, or to interfere with the judgment of the clinicians treating the patients.

Main findings

Based on evidence published in the peer-reviewed literature, the panel concluded that both oral and intravenous methadone are not just associated with QT prolongation but actually cause it. Prolongation to over 500ms is thought to confer a significant risk of heart arrhythmias. In all but one study of methadone maintenance treatment, a QT of this level was seen in 2% of patients. Taken in the aggregate, the evidence also supports the view that as methadone doses increase, so too does the likelihood of significant QT prolongation.

The panel’s recommendations

Panel members agreed that their recommendations must preserve patients’ access to addiction treatment. Among patients with QT prolongation related to relatively high doses of methadone, it is unclear to what degree reducing doses would risk them relapsing [to illicit opiate use], but higher doses are associated with better treatment retention and better outcomes.

The Panel affirmed that methadone can be used with reasonable assurance that it is effective and that its benefits exceed its risks, providing that the potential for QT prolongation is recognised, that patients receive electrocardiogram screening at indicated intervals, and that appropriate clinical action is taken in the presence of significant QT prolongation.

Panel members agreed that, to the extent possible, every opioid treatment programme should have a cardiac risk management plan with the following elements:
• Clinical assessment: Intake assessments should include: a complete medication history; personal and family history of structural heart disease; any personal history of arrhythmia or syncope (fainting); and use of QT-prolonging medications or illicit drugs such as cocaine which also have this effect.
• Electrocardiogram assessment: Largely due to concerns over the resource implications and its effectiveness in achieving meaningful reductions in methadone-associated cardiac events, panel members and ex officio members could not agree whether to recommend routine electrocardiogram screening within the first 30 days of treatment. However, they did agree that a baseline electrocardiogram at the time of admission and within 30 days should be performed on patients with significant risk factors for QT prolongation. Among these patients, additional tests should be performed annually or whenever the methadone dose exceeds 120mg a day. In addition to scheduled electrocardiograms, any patient who experiences unexplained syncope or generalised seizures should be tested. If marked QT prolongation is documented, torsades de pointes should be suspected and the patient hospitalised for monitoring through telemetry.
• Risk stratification: If the QT interval is over 450ms but less than 500ms, methadone may be initiated or continued, accompanied by a risk-benefit discussion with the patient and more frequent monitoring. For methadone-maintained patients with marked QT prolongation of 500ms or more, strong consideration should be given to adopting a risk minimisation strategy, such as reducing the methadone dose, eliminating other contributing factors, transitioning the patient to an alternative treatment such as buprenorphine, or discontinuing methadone treatment.

Methadone-related cardiac risk should be mentioned in the informed consent document presented to patients at intake, and patients should receive plain-language educational materials explaining this risk. Medical staff too should be educated about the risks posed by a prolonged QT interval and trained in assessing patients for risk of torsades de pointes and other cardiac problems.

The panel acknowledged that acting on these conclusions will challenge many opioid addiction treatment programmes. Identifying clinically relevant QT prolongation remains difficult, given the variability of electrocardiogram machine measurements and the difficulty of defining the precise risk a prolonged QT portends for any given individual. Programmes will find it a challenge to integrate cardiac arrhythmia risk assessment into the care of opioid-addicted patients without reducing access to vital addiction treatment services. The panel was also aware that not all methadone maintenance treatment providers can administer an electrocardiogram to every patient in all the circumstances they recommended. Opioid addiction treatment programmes and other providers are encouraged to consider implementing these conclusions to the extent that they are practically or financially capable of doing so.

Source: Martin J.A., Campbell A., Killip T. et al.
Journal of Addictive Diseases: 2011, 30, p. 283–306.

While negative influences abound, positive messages reinforcing a drug-free lifestyle seem scarcer all the time. More responsibility than ever falls on the parents of our teens to educate them of the pitfalls of marijuana — a gateway drug. New data suggests a connection between perceived risk and frequency of use, along with an increase in escalation to more dangerous drugs after experimenting with marijuana.

According to The Partnership Attitude Tracking Study (PATS), 2011, past-month marijuana use among teens was 27 percent — up a staggering 42 percent from 2008, and marking an upward trend in teen marijuana use the past three years. These disturbing statistics hint at a more relaxed opinion of the drug among teens, which leads to heavier use.


While the PATS data reflect that about half of teens seemingly disapprove of their peers using marijuana, the data also found among teens a decrease in perceived risk involved with smoking the dangerous drug. The still small voice of anti-drug messages is waning in the face of negative pressures from pot enthusiasts, causing more and more teens to use marijuana early and often.


We can assume from the findings in the study that if more teens are using marijuana more regularly, then more teens will experiment and transition to more dangerous drugs and substances. Regular and heavy teen marijuana users are significantly more likely to use substances like cocaine (30 times more likely), Ecstasy (20 times more likely), and abuse prescription pain relievers (15 times more likely), according to PATS data. Now, teens are not only at risk of becoming addicted to marijuana, they are more likely to develop an addiction to hard-core drugs as a result.

At the root of the alarming potential trends is the decrease in perceived risk. We are losing the war for our teens’ attention, and the cost will be dear if perceptions are not changed.


Still believe the myth that marijuana’s not a gateway drug? Not only are heavy pot users more likely to experiment with heavier drugs, they are also in as much risk of developing cancer as a heavy cigarette smoker. Marijuana smoke contains some of the same carcinogens found in cigarettes and often in higher concentrations. Studies have shown that someone who smokes five joints a week may be taking in as many cancer-causing chemicals as someone who smokes a full pack of cigarettes every day.

Many people know the typical short-term effects of marijuana use — dry-mouth, anxiety or paranoia, decreased motor skills — but more disturbing are the long-term effects, which quickly can escalate into lifelong issues for abusers. The most common effect is “amotivational syndrome,” in which abusers suffer from a chronic lack of interest in their future and cease to care about things that used to be important to them. Also, as their tolerance for the narcotic agents in marijuana increase, the abuser needs larger and larger amounts of the drug to achieve the same high. This also contributes to the gateway process — once the user stops experiencing the high, he or she escalates use to other drugs to make up the difference.


Source:  3rd June 2012

When we say that someone is “addicted” to a behavior like gambling or eating or playing video games, what does that mean? Are such compulsions really akin to dependencies like drug and alcohol addiction — or is that just loose talk?

This question arose recently after the committee writing the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (D.S.M.), the standard reference work for psychiatric illnesses, announced updated definitions of substance abuse and addiction, including a new category of “behavioral addictions.” At the moment, the only disorder featured in this new category is pathological gambling, but the suggestion is that other behavioral disorders will be added in due course. Internet addiction, for instance, was initially considered for inclusion but was relegated to an appendix (as was sex addiction) pending further research.

Skeptics worry that such broad criteria for addiction will pathologize normal (if bad) behavior and lead to overdiagnosis and overtreatment. Allen J. Frances, a professor of psychiatry and behavioral sciences at Duke University who has worked on the D.S.M., has said that the new definitions amount to “the medicalization of everyday behavior” and will create “false epidemics.” Health insurance companies are fretting that the new diagnostic criteria may cost the health care system hundreds of millions of dollars annually, as addiction diagnoses multiply.

There is always potential for misuse when diagnostic criteria are expanded. But on the key scientific point, the D.S.M.’s critics are wrong. As anyone familiar with the history of the diagnosis of addiction can tell you, the D.S.M.’s changes accurately reflect our evolving understanding of what it means to be an addict.

The concept of addiction has been changing and expanding for centuries. Initially, it wasn’t even a medical notion. In ancient Rome, “addiction” referred to a legal dependency: the bond of slavery that lenders imposed upon delinquent debtors. From the second century A.D. well into the 1800s, “addiction” described a disposition toward any number of obsessive behaviors, like excessive reading and writing or slavish devotion to a hobby. The term often implied a weakness of character or a moral failing.

Addiction” entered the medical lexicon only in the late 19th century, as a result of the over-prescription of opium and morphine by physicians. Here, the concept of addiction came to include the notion of an exogenous substance taken into the body. Starting in the early 20th century, another key factor in diagnosing addiction was the occurrence of physical withdrawal symptoms upon quitting the substance in question.

This definition of addiction was not always carefully applied (it took years for alcohol and nicotine to be classified as addictive, despite their fitting the bill), nor did it turn out to be accurate. Consider marijuana: in the 1980s, when I was training to become a doctor, marijuana was considered not to be addictive because the smoker rarely developed physical symptoms upon stopping. We now know that for some users marijuana can be terribly addictive, but because clearance of the drug from the body’s fat cells takes weeks (instead of hours or days), physical withdrawal rarely occurs, though psychological withdrawal certainly can.

Accordingly, most doctors have accepted changes to the definition of addiction, but many still maintain that only those people who compulsively consume an exogenous substance can be called addicts. Over the past several decades, however, a burgeoning body of scientific evidence has indicated that an exogenous substance is less important to addiction than is the disease process that the substance triggers in the brain — a process that disrupts the brain’s anatomical structure, chemical messaging system and other mechanisms responsible for governing thoughts and actions.

For example, since the early 1990s, the neuropsychologists Kent C. Berridge and Terry E. Robinson at the University of Michigan have studied the neurotransmitter dopamine, which gives rise to feelings of craving. They have found that when you repeatedly take a substance like cocaine, your dopamine system becomes hyper-responsive, making the drug extremely difficult for the addicted brain to ignore. Though the drug itself plays a crucial role in starting this process, the changes in the brain persist long after an addict goes through withdrawal: drug-using cues and memories continue to elicit cravings even in addicts who have abstained for years.

Furthermore, a team of scientists led by Nora Volkow at the National Institute on Drug Abuse have used positron emission tomography (PET) scans to show that even when cocaine addicts merely watch videos of people using cocaine, dopamine levels increase in the part of their brains associated with habit and learning. Dr. Volkow’s group and other scientists have used PET scans and functional magnetic resonance imaging to demonstrate similar dopamine receptor derangements in the brains of drug addicts, compulsive gamblers and overeaters who are markedly obese.

The conclusion to draw here is that though substances like cocaine are very effective at triggering changes in the brain that lead to addictive behavior and urges, they are not the only possible triggers: just about any deeply pleasurable activity — sex, eating, Internet use — has the potential to become addictive and destructive.

Disease definitions change over time because of new scientific evidence. This is what has happened with addiction. We should embrace the new D.S.M. criteria and attack all the substances and behaviors that inspire addiction with effective therapies and support.

Howard Markel, a physician and a professor of the history of medicine at the University of Michigan, is the author of “An Anatomy of Addiction: Sigmund Freud, William Halsted, and the Miracle Drug Cocaine.”

Source: 5th June 2012

A 14-YEAR-old manages to get both the Prime Minister and Kevin Rudd’s wife Therese Rein on the phone, and the media flocks to his home in a bid to be the first to tell his side of the story.

This is not a child protege, nor is it a 14-year-old whose talents will deliver Olympic glory.

This Year 9 teenager is a convicted drug felon, having been caught buying 3.6g of marijuana on the streets of Kuta, and the fact that today he is at home is testament to the narrow escape he’s had from the claws of the Indonesian legal system.

His get-out-of-jail-free card is not a good luck charm he is likely to ever try again, but why after all the publicity generated by the cases of Schapelle Corby and the Bali Nine do so many continue to dice with death in Bali?

The answer is two-fold. Firstly, our acceptance of drugs inAustralia has now reached the point where we think it is relatively “normal” for a 14-year-old to have an addiction to a drug he has been smoking for two years.

A 2008 survey of 24,000 Australian high school students found that 14 per cent of students aged 12-to-17 years used cannabis, peaking at 26 per cent for 17-year-olds.

The Australian Secondary Students Alcohol and Drug survey found 80 per cent of pupils between 12 and 17 had tried alcohol. Eleven per cent of 12-year-olds had used inhalants in the previous month, and by the age of 17, seven per cent of students had used amphetamines.

So why would we raise our eyebrows when a 14-year-old Australian school student conducts a drug deal on the streets of Indonesia?

The catch here relates to where he bought the drugs and the penalties for drug-taking inAustralia, compared to our close neighbours – who make no secret of their bid to stamp it out.

Many, perhaps most, Australians are angry at Schapelle Corby’s on-going punishment, believing she has been unfairly treated. Thousands have signed petitions or offered prayers for those members of the Bali Nine who decided to wrap drugs to their bodies and smuggle it back home. Didn’t they think that other young Australians would use it – and possibly die?

Instead of ongoing outrage, we sympathise with those caught and point the finger of blame at Indonesia.

We have to change that psyche. Drugs are deadly. And in Indonesia the punishment for using them can be deadly too. It’s not a secret. And disagreeing with it doesn’t change it. In fact, in this part of the world,Australia is the odd one out, with other countries mirroring Indonesia’s stance.

So if we are serious about tackling drug use, we need to look at whether we should be ridiculing another country’s policy, or adopting tougher penalties here. Instead, we give movie-star status to a teenager who should know better. We protect him getting from the airport to his home, we don’t use his name, and his family breathes a sigh of relief that he’s relatively unscathed “considering what he went through”.

The next 14-year-old won’t receive the same easy ride, and this one is lucky authorities did not want to make an example of him – particularly at a time when we are laying down tough laws netting Indonesian teenagers lured into people-smuggling rackets in a bid to feed their families.

The problem with drugs is not Indonesia, or how it punishes users. The problem is with us, and how we have “normalised” drug use here – to the point where we’re told experimentation is typical in teenage years. To that extent, it’s not this lad’s fault either. The problem is bigger than he is, and will only grow while we accept its use and refuse to confront the consequences. The Courier-Mail spelt this out graphically in its Drug Scourge investigation, which showed greater crime, a bigger road toll and increasing mental health issues.

Several weeks ago on the Gold Coast, I walked into the female toilets used by diners of an upmarket restaurant to see a well-dressed young man sniffing cocaine off a toilet seat. He apologised – for using the female toilet not the drug-taking – and continued on his high. No shame, but is there any wonder?

Source:  Courier Mail Australia.  Dec. 2011
On Twitter: @madonnamking

As a leader of a nationally prominent anti-drug coalition in San Diego County, I was thoroughly disappointed with the California Medical Association’s recent report endorsing marijuana legalization as a way to speed research into medical marijuana. Unfortunately, the CMA conflated those two very different issues by recklessly supporting the risky proposition of legalization.

First, it is important to discuss the disastrous impact marijuana legalization would have on our state. Marijuana is illegal because it is dangerous – not dangerous because it’s illegal. Recent studies link the drug with cognitive impairment (think memory loss and other brain dysfunction), motor skills impairment (think drugged driving accidents), and mental illness (like psychosis and schizophrenia). Indeed, marijuana negatively impacts the development of the adolescent brain, which is still maturing until about age 25.

We also know, according to a recent RAND report, that the price of marijuana would fall dramatically if it were legalized. Our experience with alcohol and tobacco tells us that lower price means greater use and addiction rates. And while about 1 in 10 adults who ever start marijuana will become dependent on it, according to the National Institutes of Health, that number jumps to between 1 in 4 and 1 in 2 when the drug is initiated in adolescence. Calling for legalization for adults only and thinking it will prevent drug use among kids is naive and dangerous – just ask any kid who has easy access to alcohol and tobacco today, despite age limits.

Finally, marijuana tax revenues would pale in comparison to the social costs of the increased use of the drug. Again, our two legal drugs, alcohol and tobacco, can be used as a reference point – they bring in about one-tenth of the social costs they produce.

That one opposes legalization does not mean that one has to be all for the status quo. Indeed, we need to invest more into prevention programs to stop marijuana use before it starts, intervene on early use, and treat marijuana addiction.

Nor does opposition to legalization signal acrimony toward increased medical research into the individual components of marijuana. This is where CMA makes its mistake. The organization reasoned that legalization is the only way to achieve this kind of research. And it is wrong.

Research into the active ingredients of marijuana – and there are hundreds of them – is an important area of science that should be explored. Indeed, today we have two such drugs derived from marijuana and the FDA is currently exploring others, like Sativex. Sativex is a tongue spray that is comprised of the active ingredient in marijuana – THC – and another ingredient called CBD. The THC in marijuana is what gets someone “high,” and the CBD counteracts that so that the drug is not dangerous or dependence-inducing. Late-stage trials of the drug show promise for spasticity related to multiple sclerosis and pain related to cancer. It has been approved in other countries for these purposes, too.

The bottom line is that one of CMA’s core arguments is a myth – that the government’s prohibition of marijuana prevents proper investigation into the drug’s therapeutic properties. The National Institute on Drug Abuse grows marijuana, in several different strains and varieties, for this exact purpose. According to the Drug Enforcement Administration, which issues licenses to deal with marijuana for research purposes, over 200 researchers have access to the drug.

So it is unfortunate that the California Medical Association – representing only a small number of their doctors who pushed a legalization position from the start – is now mixing politics with science. Advocating for legalization as the only route to research not only displays an ignorance of the drug-approval process, but it also represents a platform that will have untold consequences from a profession that should, first and foremost, “do no harm.”

Source:  6th Nov 2011

The British Liver Trust however says the number now being admitted to hospitals because of alcohol is a big problem for the country and blames the problem on a combination of cheap drink and extended drinking times.

The charity figures show that more than 500 people a day are being admitted to hospital because of alcohol-induced accidents, violence and liver damage and the number of alcohol-related hospital admissions has increased by almost a third since the licensing laws were relaxed almost two years ago.

According to NHS statistics the highest number is in the North East. NHS statistics show that in 2003-04 there were 147,659 admissions to English hospitals where alcohol was given as a cause.

In 2005-06, when the drinking laws were relaxed, the total was 193,637, or 530 admissions a day. 2nd Jan.2008

As professionals in the business of preventing and treating substance abuse, we at Trinity County Behavioral Health Services spend a good deal of our time researching and reading current science based literature and studies on the addictive nature of substances in order to better treat clients. For us, it is important to dispel the myth that marijuana is not addictive.

Research on marijuana use and addiction has been ongoing for many years and it has been proven that marijuana is an addictive drug. It is classified as a Schedule 1 controlled substance. Marijuana is the most commonly abused illicit drug used in the United States and addiction to this drug is listed under the Diagnostic and Statistical Manual of Mental Disorders as Cannabis Dependence (304.30). The main active chemical of marijuana causing dependence is delta-9-tetrahydrocannabinol, otherwise known as THC.

A favorite DVD we use here at Behavioral Health Services in treating our marijuana addicted clients is “Marijuana Neurochemistry and Physiology” produced by CNS Production. In this DVD, Haight- Ashbury Free Clinic (HAFC) Fellow and Doctor of Pharmacy Darryl Inaba discusses the addictive nature of marijuana. According to Dr. Inaba, in the late 1960s and through the ‘70s, the HAFC rarely (if at all) treated clients for marijuana addiction. But this changed in the late 80s and into the 90s as THC levels in marijuana began to climb sharply (a 151 percent increase in potency between 1992 and 2002). According to Dr. Inaba, in 2005 HAFC saw about 100 people per month seeking treatment for marijuana addiction alone and aside from any other drug use.

Dr. Inaba’s observation confirms what research is telling us about both psychological and tissue dependence caused by today’s “new,” more potent hybridized marijuana strains. These new marijuana strains have had some of the biggest impacts on our youth. Substance Abuse and Mental Health Services Administration treatment episodes data show that between 1992 and 2002 treatment for marijuana cannabis dependence among adolescents increased from 23 percent to 64 percent respectively — increasing right along with average THC levels over that time period. Parents need to know that today’s marijuana is very different than when they were teens. In many ways it is no longer a “gateway drug,” but the drug of choice and with the increased potency come increased addiction rates.

Should marijuana one day be legalized, we hope that the marijuana industry will have a better social consciousness than society has experienced with the alcohol and tobacco industries, the two industries marijuana proponents most compare in justifying legalization of marijuana. Alcohol and tobacco have never been taxed at a rate high enough to compensate for the tremendous harm they have caused. It has been our experience that when such industries profit by more consumption, they rarely educate the end users about the true negative consequences of using their products, something we see happening now with the promotion of marijuana as a “benign and harmless natural herb.”


When it comes to prevention of substance use in our “tween” population, turning kids on to ‘thought control’ may just be the answer to getting them to say no, Medical News Today reports.

New research published in the Journal of Studies on Alcohol and Drugs, co-led by professors Roisin O’Connor of Concordia University and Craig Colder of State University of New York at Buffalo, has found that around the” tween-age” years, youth are decidedly ambivalent toward cigarettes and alcohol. It seems that the youngsters have both positive and negative associations with these harmful substances and have yet to decide one way or the other. Because they are especially susceptible to social influences, media portrayals of drug use and peer pressure become strong allies of substance use around these formative years.

“Initiation and escalation of alcohol and cigarette use occurring during late childhood and adolescence makes this an important developmental period to examine precursors of substance use,” O’Connor said. “We conducted this study to have a better understanding of what puts this group at risk for initiating substance use so we can be more proactive with prevention.”

The study showed that at the impulsive, automatic level, these kids thought these substances were bad but they were easily able to overcome these biases and think of them as good when asked to place them with positive words. O’Connor explains that “this suggests that this age group may be somewhat ambivalent about drinking and smoking. We need to be concerned when kids are ambivalent because this is when they may be more easily swayed by social influences.”

According to O’Connor, drinking and smoking among this age group is influenced by both impulsive (acting without thinking), and controlled (weighing the pros against the cons) decisional processes. With this study, both processes were therefore examined to best understand the risk for initiating substance use.

To do this, close to 400 children between the ages of 10 and 12 participated in a computer-based test that involved targeted tasks. The tweens were asked to place pictures of cigarettes and alcohol with negative or positive words. The correct categorization of some trials, for example, involved placing pictures of alcohol with a positive word in one category and placing pictures of alcohol with negative words in another category.

The next step in the study is to look at kids over a longer period of time. The hypothesis from the research is that as tweens begin to use these substances there will be an apparent weakening in their negative biases toward drinking and smoking. The desire will eventually outweigh the costs. It is also expected that they will continue to easily outweigh the pros relative to the cons related to substance use.

O’Connor said researchers would like to continue to track the youth, who, he said, know that drugs are inherently bad.

“The problem is the likelihood of external pressures that are pushing them past their ambivalence so that they use. In a school curriculum format I see helping kids deal with their ambivalence in the moment when faced with the choice to use or not use substances,” O’Connor concluded. 15th March 2012

Adolescents’ use of marijuana may increase the risk of heroin addiction later in life, a new study suggests. Researchers say the work adds to “overwhelming” evidence that people under 21 should not use marijuana because of the risk of damaging the developing brain.

The idea that smoking cannabis increases the user’s chance of going on to take harder drugs such as heroin is highly contentious. Some dub cannabis a “gateway” drug, arguing that peer pressure and exposure to drug dealers will tempt users to escalate their drug use. Others insist that smoking cannabis is unrelated to further drug use.

Now research in rats suggests that using marijuana reduces future sensitivity to opioids, which makes people more vulnerable to heroin addiction later in life. It does so by altering the brain chemistry of marijuana users, say the researchers.

“Adolescents in particular should never take cannabis – it’s far too risky because the brain areas essential for behaviour and cognitive functioning are still developing and are very sensitive to drug exposure,” says Jasmin Hurd, who led the study at the Karolinska Institute in Sweden.
But Hurd acknowledges that most people who use cannabis begin in their teens. A recent survey reported that as many as 20% of 16-year-olds in the US and Europe had illegally used cannabis in the previous month.

“Teenage” rats

In order to explore how the adolescent use of cannabis affects later drug use, Hurd and colleagues set up an experiment in rats aimed to mirror human use as closely as possible.

In the first part of the trial, six “teenage” rats were given a small dose of THC – the active chemical in cannabis – every three days between the ages of 28 and 49 days, which is the equivalent of human ages 12 to 18. The amount of THC given was roughly equivalent to a human smoking one joint every three days, Hurd explains. A control group of six rats did not receive THC.

One week after the first part was completed, catheters were inserted in all 12 of the adult rats and they were able to self-administer heroin by pushing a lever.
“At first, all the rats behaved the same and began to self-administer heroin frequently,” says Hurd. “But after a while, they stabilised their daily intake at a certain level. We saw that the ones that had been on THC as teenagers stabilised their intake at a much higher level than the others – they appeared to be less sensitive to the effects of heroin. And this continued throughout their lives.”

Hurd says reduced sensitivity to the heroin means the rats take larger doses, which has been shown to increase the risk of addiction.

Drug memory

The researchers then examined specific brain cells in the rats, including the opioid and cannabinoid receptors. They found that the rats that had been given THC during adolescence had a significantly altered opioid system in the area associated with reward and positive emotions. This is also the area linked to addiction.

“These are very specific changes and they are long-lasting, so the brain may ‘remember’ past cannabis experimentation and be vulnerable to harder drugs later in life,” Hurd says.
Neurologist Jim van Os, a cannabis expert at the University of Maastricht in the Netherlands told New Scientist the research was a welcome addition to our understanding of how cannabis affects the adolescent brain.

“The issue of cross-sensitisation of cannabis/opioid receptors has been a controversial one, but these findings show the drug’s damaging effects on the reward structures of the brain,” van Oshe says. “There is now overwhelming evidence that nobody in the brain’s developmental stage – under the age of 21 – should use cannabis.”

Source: On line edition of Neuropsychopharmacology. Reported in July 2006

• Young people in the UK have by far the most positive expectations of alcohol in Europe and are least likely to feel that it might cause them harm.
• Exposure to alcohol marketing increases the likelihood that young people will start to use alcohol and the amount they consume.
• The alcohol industry spends £800 million on marketing in the UK annually
• A spends £153 encouraging drinking per £1 contributed to Drinkaware – the industry led alcohol information organisation charged with promoting sensible drinking.
• Underage drinkers consume approximately the equivalent of 6.9 million pints of beer or 1.7 million bottles each week
• 630,000 11- to 17-year-olds drink twice or more each week.
• Between 2002 and 2009 – 92,220 under-18s were admitted to hospital in England for alcohol-related conditions- over 36 children or young people each day.
• Under-18s alcohol-related hospital admissions increased by 32% between 2002 and 2007.
• The latest European School Survey Project on Alcohol and Other Drugs reported that in the UK 26% of 11-15 year-olds reported suffering an accident or injury because of their drinking, the highest percentage in Europe.
• Although cases of dependence amongst underage drinkers are rare, in 2008/9 – 8,799 younger people accessed treatment for alcohol up from 4,886 in 2005/6. Nov.2011

In human populations, cigarettes and alcohol generally serve as gateway drugs, which people use first before progressing to marijuana, cocaine, or other illicit substances. To understand the biological basis of the gateway sequence of drug use, we developed an animal model in mice and used it to study the effects of nicotine on subsequent responses to cocaine. We found that pretreatment of mice with nicotine increased the response to cocaine, as assessed by addiction-related behaviors and synaptic plasticity in the striatum, a brain region critical for addiction-related reward. Locomotor sensitization was increased by 98%, conditioned place preference was increased by 78%, and cocaine-induced reduction in long-term potentiation (LTP) was enhanced by 24%. The responses to cocaine were altered only when nicotine was administered first, and nicotine and cocaine were then administered concurrently. Reversing the order of drug administration was ineffective; cocaine had no effect on nicotine-induced behaviors and synaptic plasticity. Nicotine primed the response to cocaine by enhancing its ability to induce transcriptional activation of the FosB gene through inhibition of histone deacetylase, which caused global histone acetylation in the striatum. We tested this conclusion further and found that a histone deacetylase inhibitor simulated the actions of nicotine by priming the response to cocaine and enhancing FosB gene expression and LTP depression in the nucleus accumbens. Conversely, in a genetic mouse model characterized by reduced histone acetylation, the effects of cocaine on LTP were diminished. We achieved a similar effect by infusing a low dose of theophylline, an activator of histone deacetylase, into the nucleus accumbens. These results from mice prompted an analysis of epidemiological data, which indicated that most cocaine users initiate cocaine use after the onset of smoking and while actively still smoking, and that initiating cocaine use after smoking increases the risk of becoming dependent on cocaine, consistent with our data from mice. If our findings in mice apply to humans, a decrease in smoking rates in young people would be expected to lead to a decrease in cocaine addiction.

Source:  Science Translational Medicine 2 November 2011:
Vol. 3, Issue 107, p. 107ra109




West, R., et al. (2011)

This important study assessed the effectiveness of the drug cytisine in smoking cessation programs, and a potential star was born. In a single-center, randomized, double-blind, placebo-controlled trial, the journal paper concluded that “cytisine was more effective than placebo for smoking cessation. The lower price of cytisine as compared with that of other pharmacotherapies for smoking cessation may make it an affordable treatment to advance smoking cessation globally.”


 Source: New England Journal of Medicine 365: 1193-1200. 2011




Filed under: Addiction :

   Adopted children are twice as likely to abuse drugs if their biological parents did too, suggesting that genetics do indeed play a role in the development of substance abuse problems.However, trouble or substance abuse in the adoptive family is also a risk factor, according to a study of more than 18,000 adopted children inSweden.

This suggests that both environment and biological family history can influence a child’s likelihood of future drug use.”For someone at low genetic risk, being in a bad environment conveys only a modestly increased risk of drug abuse,” says lead study author Dr. Kenneth S. Kendler, professor of psychiatry and human genetics at Virginia Commonwealth University in Richmond. “But if you are at high genetic risk, this can put your risk for drug abuse much higher.”

 The findings should be reassuring to adoptive parents, and to people who are thinking about adopting, because they show the importance of a positive environment, experts say.  “A child who is adopted, just like a child who is biological, does carry a certain genetic risk, but this shows that the environment they’re being raised in and how their genetic risk interacts with that is probably much more important for the potential development of any disease, including substance abuse and dependence,” says Dr. Lukshmi Puttanniah, director of child and adolescent psychiatry at Lenox Hill Hospital in New York, who was not involved with the study.

 The study, published this week in the Archives of General Psychiatry, included 18,115 children born inSwedenbetween 1950 and 1993 and later adopted. Overall, 4.5% of adopted individuals had drug-abuse problems as identified by Swedish medical, legal and pharmacy records, versus 2.9% of people in the general population.

But 8.6% of those who had at least one biological parent who abused drugs had their own abuse problems versus 4.2% of adoptees whose biological parents did not have a history of drug abuse.

 Adopted children had roughly double the risk of drug abuse if their biological full- or half-sibling had similar issues. But the risk was about the same if their adoptive siblings — those who had no biological connection to them — had abused drugs.

In general, trouble in the adoptive family, such as parental divorce, death, criminal activity, and alcohol problems was linked to a higher risk of drug abuse in the adopted child. There are a number of things adoptive parents — and biological parents for that matter — can do to minimize the risk of their children experimenting with drugs and alcohol, say experts.

“If parents are responsible, are monitoring their children’s behavior, paying attention to them, spending time with them, that’s going to have a positive effect and protect them from going down the path of alcohol and drug abuse,” says Maria M. Wong, Ph.D., associate professor of psychology at Idaho State University in Pocatello.

 “Knowing the medical history of children who will be adopted is always a good idea, however . . . genes are not destiny,” adds Dr. Wilson Compton, director of the division of epidemiology, services, and prevention research at the National Institute on Drug Abuse, which helped fund the study. “This study shows that in a healthy, safe, and secure environment with little exposure to drug abuse and other problems in the adoptive relatives, even children with multiple drug abusing biological relatives do much better than those whose adoptive families don’t provide such advantages.”

But the current study omitted some factors, some of which might be important to current and future adoptive parents.For instance, the researchers didn’t know when the adopted child joined his or her new family.

“Children who are adopted at age 5 are in a different risk category from newborns,” says Dr. Lisa Albers, director of the Adoption Program at Children’s Hospital Boston.

 And the study probably underestimates the number of drug users given that drug abuse was identified only if a person had had a brushwith the law, had been hospitalized or had a certain prescription history. That sets a “relatively high bar,” Albers says.  In any event, rates of drug abuse in theU.S.tend to be higher than inSwedenor other Scandinavian countries, says Kendler.  Also, researchers didn’t take into account changes in adoption in the last 50 years.

 For instance, many more children placed for adoption today have birth parents with a history of substance abuse compared with 50 years ago, says Albers.

On the other hand, the medical community has moved forward “light years” in its understanding and ability to handle other risk factors for substance abuse, such as ADHD, impulse control challenges, mental health concerns like anxiety or significant trauma, which may have occurred prior to the child coming into the family — all of which are risk factors for substance abuse, says Albers.

“If we have parents with a history of drug abuse, we can probably do better . . .. if we address the early signs that put the child at risk for drug abuse,” says Albers.

“Joining an adoptive family that is supportive even if you’re genetically at high risk is a very positive thing,” she adds.

Source:  5th March 2012

Kouimtsidis C., Reynolds M., Coulton S. et al.
Drugs: Education, Prevention and Policy: 2011, early online publication.
Request reprint using your default e-mail program or write to Dr Kouimtsidis at

Compromised by an inability to interest enough patients, the only randomised UK trial of cognitive-behavioural therapy for methadone patients was unable to be definitive but did find some signs of benefit and that the therapy had pulled some of the intended psychological levers.

Summary Cognitive approaches to treating substance misuse problems are still relatively new and it is important to understand how they work. Relevant treatment models emphasise the role of: self-efficacy to cope with situations associated with drug use without using; developing skills to cope with these situations as well as skills to generate broader lifestyle changes; and changing patients’ expectations of the positives and negatives of using the substance. Successful treatment is theorised to result from a reduction in the extent to which patients expect positive outcomes from substance use, an increase in their negative expectations, and enhanced self-efficacy and coping skills.

The featured study was the first study to directly test this model in the context of substitution treatment for opiate dependence. The findings derive from the UKCBTMM United Kingdom Cognitive Behaviour Therapy Study In Methadone Maintenance Treatment. study, which investigated the effectiveness and cost-effectiveness of cognitive-behavioural therapy for patients in opiate substitute prescribing programmes, itself the first randomised controlled trial of a psychosocial intervention in this setting in the UK.

At several UK treatment centres, the study randomly allocated substitute prescribing patients to keyworking only or keyworking plus cognitive-behavioural therapy, and assessed whether the additional therapy improved outcomes six and 12 months later. Additional therapy was offered weekly for 24 weeks but typically patients attended only four sessions. Therapists and keyworkers were recruited from existing staff and the therapists were trained and supervised in the therapy.

Perhaps because so few patients were eligible for and prepared to join the trial (just 60 did so of 369 who were eligible), though there were outcome gains from the extra therapy, none were statistically significant. Nevertheless, as measured by their effect sizes, A standard way of expressing the magnitude of a difference (eg, between outcomes in control and intervention groups) applicable to most quantitative data. Enables different measures taken in different studies to be compared or (in meta-analyses) combined. Based on expressing the difference in the average outcomes between control and experimental groups as a proportion of how much the outcome varies across both groups. The most common statistic used to quantify this difference is called Cohen’s d. Conventionally this is considered to indicate a small effect when no greater than 0.2, a medium effect when around 0.5, and a large effect when at least 0.8. In the featured study effect sizes were expected to be about 0.3. the gains were as large as expected in terms of reductions in the severity of addiction and heroin use, and improved compliance with prescribed methadone use. The cost of the extra therapy was more than outweighed by savings in health, social, economic, work, and criminal justice costs. Perhaps because patients had already been in methadone treatment for on average five months, these savings were less than in some other studies, and the difference in cost savings between therapy and non-therapy groups was not statistically significant.

Main findings

However, the featured report was less concerned with whether extra cognitive-behavioural therapy improved the end result of methadone treatment, than with how it might have done so. One way was expected to be by improving how well patients coped with life’s problems, a concept measured by a standard questionnaire which assessed different aspects of this ability. Relative to keyworking only, as expected, at six months the therapy was followed by a significant improvement in the degree to which patients positively reappraised problems, and a non-significant improvement in problem solving. Other domains where additional improvements were expected (logical analysis, seeking guidance and seeking alternatives) improved to roughly the same degree regardless of the extra therapy. Six months later (and 12 months after therapy had started) a similar analysis revealed that nearly all the expected mechanisms had improved after cognitive-behavioural therapy but deteriorated without it. The exception was logical analysis, where the reverse pattern was seen. Despite these trends, none of differences between patients who had or had not been offered cognitive-behavioural therapy were statistically significant, so chance variation could not be ruled out.

As expected, the degree to which patients felt confident that they could resist the urge to use drugs (‘self-efficacy’) increased after cognitive-behavioural therapy but decreased (at six months) or increased less (at 12 months) without this therapy. Patients were also asked about the good and bad consequences they expected from cutting down their heroin use. These measures changed in the opposite to what was expected; patients offered the therapy became relatively less positive and more negative about cutting down. Again, none of these differences between the two groups of patients were statistically significant.

Further analyses not reported here assessed changes among only patients who attended at least one session of their intended psychosocial intervention and related changes to the number of therapy sessions attended.

The authors’ conclusions

Though no definite conclusions can be taken from this study, there are indications that the therapy may be effective through at least some of the intended mechanisms, but also that methadone-maintained patients at services as configured in England in the 2000s generally reject the chance for this form of extra therapy.

The fact that few patients were prepared to join the study and that those who did attended few therapy sessions suggest there could be major barriers to implementing cognitive-behavioural therapy in routine practice in the British drug treatment system, perhaps associated with a culture of limited psychological therapy and relatively low expectations of clients’ engagement and compliance with treatment.

With such a small sample there is a heightened possibility that real differences made by the therapy will fail to meet conventional criteria for statistical significance and be mistakenly dismissed as chance variation. That this might have happened is suggested by the fact that the relative increase in days free of heroin use after six months was as great as expected. With a larger sample, it might well have also proved statistically significant. Economic analyses also found non-significant but appreciable net social cost-savings. The featured analysis supplements these outcome findings with indications that cognitive-behavioural therapy may have fostered some but not all of the crucial problem-solving skills.

The main seemingly counter-productive finding related to expectations about the pros and cons of reducing heroin use as measured by a scale yet to be validated. Also, more sessions of therapy did not further enhance the presumed psychological mechanisms through which the therapy worked. Nor were these mechanisms significantly related to substance use and other outcomes – again, perhaps due to the small sample size.

While appreciating the limits set by sample size, the non-significant trends suggesting that the therapy worked though the intended mechanisms were generally small in size. Of 22 comparisons between the two sets of patients, in only one had a mechanism (positively reappraising life’s problems) changed to a statistically significant degree in the expected direction – a result to be expected purely by chance. Together with a few counterproductive trends, these minor changes in the mechanisms thought to be specific to cognitive-behavioural therapy do not suggest it has a special role (that is, over and above other forms of psychological therapy) as a supplement to routine keyworking in the circumstances of the trial. At the same time the findings suggest that extra therapeutic contact did help stabilise patients who were prepared to accept it. Whether this needed to be cognitive-behavioural or a recognised therapy of any kind is impossible to tell from the study. Broader research offers little support for a distinctive role in addiction treatment for cognitive-behavioural approaches, results from which are generally equivalent to other approaches. It also seems that, at least in the mid 2000s, a steep hill remained to be climbed before formal psychological interventions of any kind were routinely and expertly implemented inBritain’s methadone clinics. How far that has changed is unclear. Details below.

CBT in methadone treatment

Guidelines from Britain’s National Institute for Health and Clinical Excellence (NICE) recommend cognitive-behavioural therapy not as a routine means of further stabilising patients, but to help with lingering anxiety and/or depression among those already stabilised in maintenance treatment. However, the analyses which led NICE to counsel against routine use did not show that cognitive-behavioural therapy was ineffective, just that it was not convincingly more effective than other well structured therapies.

Published in 2007, these guidelines did not have available to them the latest update of an authoritative meta-analytic A study which uses recognised procedures to combine quantitative results from several studies of the same or similar interventions to arrive at composite outcome scores. Usually undertaken to allow the intervention’s effectiveness to be assessed with greater confidence than on the basis of the studies taken individually. review conducted for the Cochrane collaboration which combined results from studies comparing structured psychosocial interventions against normal counselling among methadone and other opiate substitution patients. Taking in new studies available up to 2011, it found that overall such interventions had improved neither retention nor outcomes (including opiate use) to a statistically significant degree. In particular, the same was true of the family of behavioural interventions including cognitive-behavioural therapy. Contrary to expectations, this update found contingency management conferred no significant benefits, contradicting both its earlier findings and the NICE guidelines referred to above.

In the Cochrane review, verdicts in respect of cognitive-behavioural therapy rested on three studies, one of which does not appear to have reported substance use outcomes but did find greater improvements in psychological health. Relative to drug counselling alone, so too did a study of male US ex-military personnel starting methadone treatment. A year later, in this study cognitive-behavioural patients had improved more on a much wider range of psychological, social and crime measures, but not in respect of substance use. From methadone plus routine drug counselling only, so complete were the reductions in opiate use that little space was left for additional therapy to further improve outcomes. These two US studies are supplemented by a German study which found that group cognitive-behavioural therapy led to significantly greater post-therapy reductions (at the six-month follow-up) in drug use than routine methadone maintenance alone. The effect was largely due to changes in cocaine use, but there were also minor extra improvements in abstinence from opiate-type drugs and benzodiazepines. What these three studies suggest is that offering extra psychotherapy (not necessarily cognitive-behavioural therapy in particular) improves psychological and social adjustment and perhaps too helps reduce non-opiate substance use, but that methadone maintenance itself as implemented in these studies was such a powerful anti-opiate use intervention that further gains on this front were harder to engineer.

CBT in substance use treatment generally

If in terms of core substance use outcomes, cognitive-behavioural therapy in methadone maintenance does little to improve on routine counselling, this will simply be in line with findings in respect of the therapy’s role in treating drug and alcohol problems in general. A review combining results from relevant studies suggested that it remains to be shown that cognitive-behavioural therapies are more effective than other similarly extensive and coherent approaches. Studies which directly tested this proposition often found little or no difference, even when the competing therapy amounted simply to well structured medical care.

The implication is that choice of therapy can be made on the basis of what makes most sense to patient and therapist, availability, cost, and the therapist’s training. In respect of cost and availability, cognitive-behavioural therapy may (more evidence is needed) prove to have two important advantages. The first is that effects may persist and even amplify without having to continue in therapy. The second is that it lends itself to manualisation to the point where it can be packaged as an interactive computer program and made available in services lacking trained therapists – potentially a crucial advantage for widespread implementation.

Will CBT help methadone patients leave treatment?

Beyond core substance use outcomes is what in Britain is now a priority issue – whether more intensive therapy, even if it seems to add little to the powerful opiate use reduction effect of methadone treatment, might help people gain sufficient psychological and social stability to leave this treatment, and leave it sooner. In respect of psychotherapy in general and cognitive-behavioural therapy in particular, this remains a live possibility with some support from studies of during and post-treatment changes, though none have directly tested whether these enable patients to more safely leave the shelter of substitute prescribing programmes.

However, from the starting point revealed by the featured study, there seems a long way to go before structured psychosocial interventions of any kind are routine in Britain’s methadone services. An earlier report from the study commented that services were overstretched and understaffed and suffered from high staff turnover. Very few staff had been trained in psychological interventions and sometimes even basic individual client keyworking was extremely limited. Difficulties in engaging clients in the study were attributed partly to a low level of psychological interventions in services, which in turn led to low expectations of clients engaging with these interventions. Perhaps too, the authors speculated, some clients were reluctant to become involved in more intensive treatment or to address psychological issues not previously identified in usual clinical care. Most tellingly, the researchers observed “a nihilistic view of psychological intervention and clients’ capacity for change among some staff”.

In this climate, and with the added burden of research procedures, the small proportion of patients prepared to accept therapy and attend more than a few sessions is likely to be an underestimate of the possible caseload if cognitive-behavioural therapy were well promoted as a part of usual care, especially if elements of the approach were incorporated in keyworking rather than offered as an optional add-on.

In a different set of services probably sampled in the mid-2000s, perfunctory brief encounters focused on dose, prescribing and dispensing arrangements, attendance records, and regulatory and disciplinary issues characterised the keyworking service offered by some British criminal justice teams to offenders on opiate substitute prescribing programmes. However, ‘relapse prevention’ was the most common therapeutic activity in the sessions, featuring in 44% of the last sessions recalled by the staff, a term often taken to imply cognitive-behavioural approaches. What staff included under this heading was unclear, and the time given to it averaged just seven minutes, but is does suggest that there is a platform which could be built on. Unfortunately the need to do this building to foster recovery and treatment exit has coincided with resource constraints which make widespread training in and implementation of fully fledged therapy programmes seem unlikely.

Thanks for their comments on this entry in draft to Christos Kouimtsidis of the Herts Partnership NHS Foundation Trust in England. Commentators bear no responsibility for the text including the interpretations and any remaining errors.

Last revised 16 December 2011


As marijuana use among teenagers increases and its perceived danger among this age group decreases, clinicians need to know the latest science about the harmful effects of the drug on the adolescent brain, according to a researcher at theUniversityofColorado,Denver.

Paula Riggs, PhD, Professor of Psychiatry, notes the most recent Monitoring the Future Survey shows a significant increase in marijuana use, including daily marijuana use among U. S. high school students and a decrease in perceived risk of use. “There are a number of indicators, including the increasing number of states that have passed ‘medical marijuana’ legislation, and that society as a whole tends to view marijuana as a relatively benign, recreational drug. However, scientific research does not support this.”

A growing body of research shows that adolescent marijuana use can be detrimental to the brain development and may produce long-lasting neurocognitive deficits and increased risk of mental health problems including psychosis, said Dr. Riggs, who spoke about this topic at the recent California Society of Addiction Medicine meeting.

Marijuana is the most commonly used illicit drug in the United States. Although some have questioned whether marijuana is an addictive drug, scientific research shows that one in 10 people overall, and one in six adolescents, who use marijuana develop dependence or addiction, Dr. Riggs says. Research shows that marijuana can cause structural damage, neuronal loss and impair brain function on a number of levels, from basic motor coordination to more complex tasks, such as the ability to plan, organize, solve problems, remember, make decisions and control behavior and emotions.

Dr. Riggs also cited recent studies indicating that adolescents may be more vulnerable to addiction, in part due to rapid brain development. “Emerging research suggests that individuals who start using marijuana during their teenage years may have longer-lasting cognitive impairments in executive functioning than those who start later,” she says. “Animal studies also suggest that exposure to marijuana during adolescence compared to adulthood may increase the vulnerability or risk of developing addiction to other substances of abuse such as cocaine and methamphetamine.”

She adds, “It is important for pediatricians, psychiatrists and other mental health clinicians to be aware of current research because they are on the front line to identify teens when they first start to experiment. They need to be able to effectively screen adolescents for marijuana use, and be armed with the scientific facts to educate teens and families about associated risks.”

Source  Nov. 2011

A clinical trial to test better treatment options for chronic heroin addiction is expected to begin in Vancouver at the end of this year. Led by researchers from Providence Health Care and the University of British Columbia, it’s the only clinical trial of its kind in North America.

The Study to Assess Longer-term Opioid Medication Effectiveness (SALOME) is a carefully controlled three-year clinical trial that will test whether hydromorphone (Dilaudid(R)), a licensed pain medication, is as effective as diacetylmorphine, the active ingredient of heroin, at engaging the most vulnerable long-term street heroin users, so they will enroll in treatment programs and end their use of illicit drugs.

The intent of the SALOME project is to determine whether some participants become healthier and reduce their illicit drug use or are able to switch to other forms of treatment. SALOME also intends to test if, after stabilizing patients on injectable medications, they can transition to oral formulations without losing effectiveness.

This study builds on the North American Opiate Medication Initiative (NAOMI), which was North America’s first-ever clinical trial of prescribed heroin that took place from 2005 to 2008. NAOMI, which also was led by researchers from Providence Health Care and UBC, was a randomized trial aimed at testing whether medically prescribed heroin (diacetylmorphine) was more effective than methadone therapy for individuals with chronic heroin addiction who were not benefiting from other conventional treatments.

The results, published in the New England Journal of Medicine, showed that patients treated with the prescribed heroin were more likely to stay in treatment or quit heroin altogether and more likely to reduce their use of illegal drugs and other illegal activities than patients treated with oral methadone.

In the NAOMI study, the researchers also provided a small sample of patients with injectable hydromorphone, (Dilaudid(R)). An unexpected finding was that injection patients could not accurately discriminate whether they were receiving prescribed heroin or hydromorphone. The researchers also observed similar results and benefits with both these drugs although the small number of participants receiving hydromorphone did not permit any definite and scientifically valid conclusions to be drawn as to the efficacy of hydromorphone as a viable treatment option.

Should hydromorphone be proven to be as affective as heroin, the benefits of this form of injectable treatment may be more feasible and achievable without the emotional and regulatory barriers often presented by heroin maintenance.
SALOME, led by Dr. Michael Krausz, the Providence Health Care/UBC B.C. Leadership Chair in Addiction Research and Dr. Eugenia Oviedo-Joekes, Providence Health Care researcher and an assistant professor in UBC’s School of Population and Public Health, will enroll 322 individuals with chronic heroin dependency who currently are not sufficiently benefiting from conventional therapies, such as methadone treatment, at one site based in Vancouver, BC.

In the first stage, half of the 322 participants will receive injectable prescribed heroin, and the other half will receive injectable hydromorphone. Stage I will involve six-months of treatment. All volunteers retained in injection treatment at the end of Stage I will be eligible to enter Stage II.

In Stage II, half of the participants will then continue injection treatment exactly as in Stage I on a blinded basis while the other half will switch to the oral equivalent of the same medication (prescribed heroin or hydromorphone). Stage II will also involve six-months of treatment.

Throughout the treatment period, social workers will be assigned to both groups to assist them with reaching other addiction services and community resources such as counseling, housing and job training services.

Some 60,000 to 90,000 persons are affected by opioid addiction in Canada. This study will enroll the most chronically drug-dependent members of Vancouver’s population — those who are not benefiting from other treatments, such as methadone therapy and abstinence-based programs, and continue injecting street heroin.

The SALOME study is funded by the Canadian Institutes of Health Research, the Government of Canada’s agency responsible for funding health research in Canada, Providence Health Care and the InnerChange Foundation.

Dr. Perry Kendall, BC’s Provincial Health Officer –
“SALOME addresses critical social and ethical concerns dealing with addiction. Opioid-dependent people are in need of treatment options to avoid marginalization from the health care system and this study aims to answer questions that could lead to improvements in the health of persons with chronic addictions and identify new ways of reintegrating this population into society.”

“If the SALOME study shows that hydromorphone can go head-to-head with heroin as an alternative therapy for people who have failed optimally provided methadone, then I think this should be part of the treatment continuum that’s available through licensed physicians.”

Dianne Doyle, Providence Health Care President and CEO –
“Providence Health Care is supporting this research because it is so aligned with our mission, vision and values. We have a very long tradition of providing compassionate care to the most marginalized and needy in our community, including those suffering from addictions.”

“What we need to get from this research is a better understanding of what the right approaches are to treating addicted populations. In particular our hope would be that we could find a new approach for those people who are addicted and not benefiting from current approaches to care. This treatment option would be one more component of a range of services offered by Providence Health Care and Vancouver Coastal Health, all of which are intended to reduce the harm to individuals and others from drug use, and to support recovery from addiction and mental illness.”

About Providence Health Care

Providence Health Care is one of Canada’s largest faith-based health care organizations, operating 15 facilities within Vancouver Coastal Health. Guided by the principle “How you want to be treated,” PHC’s 1,200 physicians, 6,000 staff and 1,500 volunteers deliver compassionate care to patients and residents in British Columbia. Providence’s programs and services span the complete continuum of care and serve people throughout B.C. PHC operates one of two adult academic health science centres in the province, performs cutting-edge research in more than 30 clinical specialties, and focuses its services on six “populations of emphasis”: cardiopulmonary risks and illnesses, HIV/AIDS, mental health, renal risks and illness, specialized needs in aging and urban health.

About the University of British Columbia

The University of British Columbia (UBC) is one of North America’s largest public research and teaching institutions, and one of only two Canadian institutions consistently ranked among the world’s 40 best universities. Surrounded by the beauty of the Canadian West, it is a place that inspires bold, new ways of thinking that have helped make it a national leader in areas as diverse as community service learning, sustainability and research commercialization. UBC offers more than 50,000 students a range of innovative programs and attracts $550 million per year in research funding from government, non-profit organizations and industry through 7,000 grants.

To view the first video of the SALOME project, please visit the following link:

To view the second video of the SALOME project, please visit the following link:

Source:  13th Oct. 2011

Filed under: Addiction,Heroin/Methadone :

The number of Americans who died from overdoses of prescription painkillers more than tripled in the past decade, according to the Centers for Disease Control and Prevention (CDC). More people now die from painkillers than from heroin and cocaine combined.

An estimated 14,800 people died in the United States from painkiller overdoses in 2008, a more than threefold jump from the 4,000 deaths recorded in 1999, the CDC said in a new report. Prescription and illegal drugs caused 36,450 deaths in 2008, compared with 39,973 deaths from motor vehicle crashes, according to the Associated Press.

The CDC said painkiller abuse and deaths are rising because the drugs are easier than ever to obtain. They cited the growth of “pill mills,” clinics that prescribe opioids without first conducting medical exams, and “doctor shopping,” or receiving multiple prescriptions from different doctors.   According to the CDC, enough painkillers were prescribed in 2010 to medicate every American adult around the clock for a month. “Right now, the system is awash in opioids—dangerous drugs that got people hooked and keep them hooked,” said CDC Director Thomas Frieden.

“Prescription drug abuse is a silent epidemic that is stealing thousands of lives and tearing apart communities and families across America,” Gil Kerlikowske, Director of National Drug Control Policy, said in a CDC news release. He noted health care providers and patients should be educated on the risks of prescription painkillers. “Parents and grandparents should properly dispose of any unneeded or expired medications from the home and to talk to their kids about the misuse and abuse of prescription drugs,” he noted.

Source:  2nd Nov.2011

Filed under: Addiction :

 • Marijuana is the most commonly used illicit drug in the United States.
• New research shows that the use and misuse of alcohol and marijuana are influenced by a common set of genes.
Marijuana is the most commonly used illicit drug in the United States. Roughly eight to 12 percent of marijuana users are considered “dependent” and, just like alcohol, the severity of symptoms increases with heavier use. A new study has found that use and misuse of alcohol and marijuana are influenced by a common set of genes.
Results will be published in the March 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
“Results from a large annual survey of high-school students show that in 2008, 41.8 percent of 12th graders reported having used marijuana,” explained Carolyn E. Sartor, a research instructor at Washington University School of Medicine and corresponding author for the study. “Although many may have used the drug on only a few occasions, 5.4 percent of 12th graders reported using it daily within the preceding month.”
“The active ingredient in marijuana is THC, which mimics natural cannabinoids that the brain produces,” added Christian Hopfer, associate professor at the University of Colorado School of Medicine. “The cannabinoid system is critical for learning, memory, appetite, and pain perception. Most users of marijuana will not develop an ‘addiction’ to it, but perhaps one in 12 will. What is not commonly appreciated about marijuana use is that strong evidence has emerged that it increases the risk of developing mental illnesses and possibly exacerbates pre-existing mental illnesses.”
“Like any drug, marijuana can be used in a way that negatively impacts quality of life, interfering with functioning at school or work or leading to problems with family and friends,” said Sartor. “Although at least three of six symptoms listed in the Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition (DSM-IV) are needed to meet full criteria for cannabis (marijuana) dependence … the presence of even one or two of these symptoms could create distress or interfere with day-to-day functioning. There is strong evidence for a genetic component to use and dependence on marijuana as well as alcohol, and the use (and misuse) of these substances frequently occur together.”
Researchers examined 6,257 individuals (2,761 complete twin pairs and 735 singletons) listed in the Australian Twin Registry, 24 to 36 years of age. Alcohol and marijuana use histories were gathered in telephone diagnostic interviews and used to derive levels of alcohol consumption, frequency of marijuana use, and DSM-IV alcohol and cannabis dependence symptoms.
“Our findings indicate that … many of the same genetic factors that contribute to alcohol use also contribute to marijuana use,” said Sartor. “Likewise, alcohol dependence symptoms and cannabis dependence symptoms can be traced to some of the same genetic influences. For both alcohol and marijuana, the majority of genetic factors that contribute to use also contribute to dependence symptoms.”
“In other words,” said Hopfer, “the genetic influences on drug use are not specific to individual drugs, but seem to influence a general tendency to engage in drug use. This is important to note because there is a tendency to study drugs in isolation – alcohol, tobacco, marijuana, cocaine, etc. These findings add support to the notion of common mechanisms underlying all addictions.”
“The fact that very little of the environmental influences on alcohol and marijuana use, or on alcohol and cannabis dependence symptoms, could be traced to common sources indicates that there may be important distinctions between those environmental factors that influence alcohol-related outcomes and those that influence marijuana-related outcomes,” said Sartor. “Identifying alcohol- and marijuana-specific risk factors is an important next step in this line of research.”
“Marijuana research is relatively sparse compared to alcohol or nicotine research,” added Hopfer. “However, if you look at reports of at least adolescents and young people using, it becomes clear that marijuana use, including daily marijuana use, is quite common and the effects of this are not well understood. The mental illness/marijuana connection has not received much press, although I think the evidence has grown substantially that marijuana is a causal risk factor for the development of mental illness.”



Slovenian study identifies which chemicals in the blood best identify dependent drinkers in the sense of not missing those who are dependent, confirming when they have stopped drinking, and not falsely identifying non-dependent people as dependent.


The aim of this study was to determine the value of biochemical tests for glutamate dehydrogenase (GLDH) in the blood as way of diagnosing alcohol dependence, in particular as compared to or in combination with other biochemical markers including gama-glutamyltransferase (GGT), aspartate-aminotranferase (AST), alanine-aminotransferase (ALT) and erythrocyte mean cell volume (MCV). All these levels were assessed three times in 238 alcohol dependent patients admitted to hospital (on admission, after 24 hours and after seven days) and also in healthy members of the public.
Main findings All the values were significantly higher in the patients than in healthy persons. GLDH exhibited the fastest decrease in levels after the resumption of abstinence. 24 hours of non-drinking is sufficient for a reliable evaluation of the fall in GLDH activity, even more so when alcohol dependants had not drunk for three to seven days, offering a way to confirm the cessation of drinking. The time course of changes in GLDH and AST were more applicable than for GGT after a week, but GLDH changes were most reliable. GLDH was the most specific marker with almost 90% specificity, correctly identifying nine in 10 of the healthy subjects as non-dependent. A decision tree combining MCV,  GGT and GLDH markers was selected as the best diagnostic procedure because of its simplicity, easy examination and moderate cost. It gave a model with 84.5% accuracy, excellent specificity at 90% (correctly identifying 9 in 10 healthy subjects as non-dependent) and very high sensitivity at almost 80% (correctly identifying 8 in 10 alcohol dependent patients as dependent).


The high accuracy of our classification model provides an opportunity to apply it as a helping method in finding and diagnosing alcohol dependence in everyday practice, with our exclusion criteria and differential diagnostic cautions taken into consideration. We strongly believe that watching changes in the activity of laboratory markers of alcoholism is an effective yet overlooked aid.
Thanks for their comments on this entry in draft to Matej Kravos of the Psychiatric Hospital Ormoz in Slovenia. Commentators bear no responsibility for the text including the interpretations and any remaining errors.

Source: Kravos M., Malešic I.
Alcohol and Alcoholism: 2010, 45(1), p. 39–44. Revised 22 Aug.2011


Filed under: Addiction,Alcohol,Europe :

Using an integrative meta-analysis approach, researchers from the Center for Bioinformatics at Peking University in Beijing have assembled the most comprehensive gene atlas underlying drug addiction and identified five molecular pathways common to four different addictive drugs. This novel paper appears in PLoS Computational Biology on January 4, 2008.
Drug addiction is a serious worldwide problem with strong genetic and environmental influences. So far different technologies have revealed a variety of genes and biological processes underlying addiction. However, individual technology can be biased and render only an incomplete picture. Studying individual or a small number of genes is like looking at pieces of a jigsaw puzzle – only when you gather most of the pieces from different places and arrange them together in an orderly fashion do interesting patterns emerge.
The team, led by Liping Wei, surveyed scientific literature published in the past 30 years and collected 2,343 items of evidence linking genes and chromosome regions to addiction based on single-gene strategies, microarray, proteomics, or genetic studies. They made this gene atlas freely available in the first online molecular database for addiction, named KARG (, with extensive annotations and friendly web interface.
Assembling the pieces of evidence together, the authors identified 18 molecular pathways that are statistically enriched in the addiction-related genes. They then identified five pathways that are common to addiction to four different substances. These common pathways may underlie shared rewarding and response mechanisms and may be targets for effective treatments for a wide range of addictive disorders. 7th Jan.2008

Filed under: Addiction :

A new study suggests that abuse of prescription opioids may be a first step on the path toward misuse of heroin and other injected drugs.
Science Daily reports that the researchers found four out of five injection drug users misused an opioid drug before they injected heroin. They also found that almost one out of four young injection drug users first injected a prescription opioid, and most later switched to injecting heroin.
The study, published in the International Journal of Drug Policy, found that risk factors for misusing opioid drugs include family history of drug misuse, and a past history of receiving prescriptions for opioids.
“Participants were commonly raised in households where misuse of prescription drugs, illegal drugs, or alcohol, was normalized,” lead researcher Dr. Stephen Lankenau, from Drexel University in Philadelphia, said in a news release. “Access to prescription medications – either from a participant’s own source, a family member, or a friend – was a key feature of initiation into prescription drug misuse.”
The study included 50 injection drug users between the ages of 16 to 25. They had all misused a prescription drug at least three times in the past three months. Nearly three-fourths of participants had been prescribed an opioid, often for dental procedures or sports injuries. Most had family members who misused one or more substances. The authors called on parents to carefully monitor and safeguard prescription drugs, especially opioids, in their home

Source: International Journal of Drug Policy June 2011

Lying in a hospital bed, 24-year-old Stacey Rhymes cuddles a childhood toy before putting out an arm to her mother.

‘Hold my hand, Mum,’ she whispers, then slips into a coma. A few hours later, on a spring afternoon earlier this year, the girl with a whole life ahead of her was dead.

The once radiantly pretty Stacey had drunk herself to death on cut-price bottles of wine bought from corner shops, supermarkets and local pubs. She had started drinking at 17 and seven years later her body simply gave up under the constant assault from alcohol.

Her mother, Louise, says: ‘I now want the world to know exactly what happened to Stacey and why. It was a terrible way to go.   ‘Her stomach was like a balloon, as if she was nine months pregnant. Her long hair was falling out, her urine was coloured black and she could not eat. She was scared to look in the mirror because her eyes were canary yellow. The only way to stop the pain at the end was morphine.’

The story of Stacey Rhymes is a salutary one. She is one of the youngest people in modern Britain to die of alcohol abuse. And her mother, speaking for the first time, is determined that the loss of her daughter will not be in vain.

She has set up a Facebook website in memory of Stacey to highlight the dangers of alcohol – and particularly its increased availability following New Labour’s 24-hour drinking laws – which now kills more young women than cervical cancer, and more people, generally, than hard drugs.

A film clip about Stacey on YouTube, put there by her mother, has been watched by 16,000 people in a fortnight. It is now one of the most viewed in Britain by children and teenagers.

At the family’s terrace home, in Bramcote, on the outskirts of Nottingham, where Stacey grew up with her brother, Jay, now 19, sister Katie, 21, and stepfather, Terry, her mother says: ‘Alcohol is as treacherous as a Class A drug. Yet it’s available at all hours and at rock-bottom prices.

‘This morning, I saw a pack of four cans of lager at the supermarket for 92p. You can’t get four cans of children’s pop for that! Young children should be warned about alcohol in the way they are warned about drugs.  ‘I want them to be shown a photograph of Stacey’s face when she was dying. She was killed by alcohol – a drug that is as easy and cheap to buy as a packet of sweets.’

Since the relaxation of licensing laws in November 2005 – which allowed round-the-clock sales of drink in pubs, clubs, shops and supermarkets – the cost to the nation both socially and financially has been huge. Coupled with low prices for alcohol, there is now an orgy of drunkenness that rivals the gin epidemic of early Victorian times.

The facts are stark. The numbers dying from alcohol-related health problems is rising. In 1999, there were 4,000 deaths. Today, the figure has doubled, with the age of the victims going down, too. Hospitals admit for emergency treatment more than 9,000 drunken teenagers every year.

According to Alcohol Concern, 800,000 children below the age of 15 drink regularly in Britain. Nearly two-thirds of them will have had alcohol in the past month – with one in seven consuming enough to make them sick. One in three think, it is acceptable to get drunk once a week.

Campaigners say that one in ten eight-year-old boys (double the figure ten years ago) and a quarter of 11-year-old girls (ten per cent more than in 1995) have also experimented with alcohol.    Staff at the casualty department of Alder Hey Children’s Hospital in Liverpool will not be surprised by these statistics. A survey by the hospital – which admits only under-17s – showed that more than half the children treated after binge-drinking had bought their alcohol from a pub or a shop.

Nearly three-quarters of patients are girls, and the favourite tipple is vodka. Every week, seven or eight drunken youngsters are treated at the hospital – a quarter so ill that they have to be put on a ward or go into intensive care.

According to Pat McLaren, an Alder Hey spokeswoman: ‘They come in on a Friday and Saturday night in particular. Some are found unconscious on the street or even beaten up. We get them sober and contact their parents. We try to get them to change their ways.’

Alder Hey and Liverpool are not alone. Cases of liver cirrhosis in 20 to 30-year-olds – who often started drinking as children – have doubled in less than a decade.  Eight women in Britain die each day from liver disease – often at ages younger than men with the same condition because their bodies are more sensitive to alcohol poisoning.

As Professor Ian Gilmore, President of the Royal College of Physicians, warns: ‘The damage to society from alcohol is greater than from drugs.’   Dr Gray Smith-Laing, a gastroenterologist at Medway Maritime Hospital in Gillingham, Kent, says: ‘The young of all social backgrounds think it is cool to get completely legless, yet nothing could be more uncool. This is a classless and sexless phenomenon. We have not seen the peak yet.’

Young women such as Stacey Rhymes make up half his caseload. Some have irreversible liver damage from drinking. One woman of 26 he treated recently died of liver cirrhosis.  Dr Smith-Laing says: ‘We need a dramatic rise in the price of alcohol so it is no longer affordable for the young.’

It is against this frightening background that Stacey’s mother has bravely decided to speak out.

She reaches for a pile of treasured childhood photographs. They show Stacey on her first birthday; at eight in a white hat at a family wedding. There is one of her with bright, clear eyes and long thick hair smiling at the camera  – she is just 17, and it is a few months before she began to drink.

Louise, 43, says: ‘Stacey had a wonderful childhood and we were a close family. There wasn’t a lot of money, but we did old-fashioned things. We went to the park for picnics and walks around Nottingham.  ‘She had lots of friends and when she left school at 16, she got a job in a local pub as a waitress. She met a boy, and there was even talk of an engagement.’

But things were soon to change. ‘For no apparent reason, Stacey began to drink. She had arguments with the boyfriend about it. She lost the job she loved and her boyfriend, too. She was just drinking all the time. She became foul-mouthed. She stole money from us, her family, to buy the alcohol,’ says Louise. ‘Stacey would go out drinking at night then lie in bed all day. I couldn’t get her up, even though I tried before I left for work.

‘In the end, we found her a housing association flat in Nottingham, where she moved. We thought it would be a fresh start.’ Nothing could be further from the truth.

‘Stacey then got in with a bad crowd. Her friends were all drinkers, too. She would lie in bed with a bottle. A few times, she burned the bedclothes with her cigarettes. She got involved in a serious brawl, and was sent to prison for eight weeks.

‘We were horrified, but she came out looking far better. She had not been able to drink while inside. We took her back to her flat where there were eight weeks – £800-worth – of giro cheques from the benefits’ office. Stacey spent every penny on drink. She was evicted from her flat due to debts on the rent.’   Stacey wouldn’t move back home because her mother and stepfather, a self-employed builder, refused to allow her to drink. Revolted by what alcohol had done to their daughter, they are now teetotal.   Instead, Stacey found a place at a hostel in Derby, five miles from Nottingham. ‘That lasted five days before she was thrown out for drinking,’ recalls her mother.

By now, her life was out of control. For a time, Stacey lost contact with her family. She lived rough in Derby. In desperation, Louise tried to get her daughter sectioned under the mental health laws so she would be taken into hospital. ‘But the authorities said she was quite normal, just an alcoholic.’ she recalls today.   Stacey was now drinking five litres of wine a day and some cider, too. She no longer dressed fashionably, put on weight and didn’t eat properly. ‘Her stomach was huge and she was very ill,’ her mother says.

On March 28 this year, Stacey was admitted to Derby Hospital – to Ward 308 which deals with alcohol-induced liver problems. She had been to her GP because her face had gone yellow and she was having trouble walking because her limbs were swollen. The doctor told her to go to hospital immediately  –  it took her a week to do so.

Dr Jan Freeman, a consultant in whose care she was put, says: ‘Stacey was at the end of the road. She could have been saved only by a liver transplant. Like lots of young people, she never thought it would happen to her. Well, Stacey’s death shows it can happen to some.’    There is no doubt that Stacey was well looked after in the hospital but, during the next seven weeks, until her death on May 22, she managed to discharge herself three times and return to drinking.

Once, she walked out in her pyjamas, hailed a taxi then disappeared. Derby police put out appeals for the public to look for her. Her parents searched, too.    He mother recalls: ‘We got her back to the hospital on each occasion. The last time was on May 17. She had been staying with a drinking buddy. She rang up saying she was being sick and it was streaked with blood. Her skin was itching, a symptom of alcohol poisoning.

‘I knew that we would lose her, because of her colour. I thought she wouldn’t make it over the weekend. But three days later, she had picked up and told us she was scared of dying. I told her that if she stopped drinking, she would live.’    It was, of course, a white lie. The next day, the hospital rang Louise to say Stacey had a hole in her stomach, caused by acid from a ruptured peptic ulcer. There was nothing more the doctors could do.   Within 24 hours, the family were called to the hospital for the final time. Stacey died in her mother’s arms of abdominal bleeding and alcohol-related liver disease.

As confirmation of Stacey’s tragic story, Nick Sheron, a liver specialist at Southampton General Hospital and secretary of campaign group, Alcohol Health Alliance, says drink-induced liver disease – once the preserve of middle-aged men – is affecting all ages and both sexes.

He explains: ‘If they are alive, it is never too late to stop drinking. But, often the symptoms show up so late that half the patients die before they have a chance to change their ways.

‘In the Sixties and Seventies, wine used to be nine percent proof, now it is 13 percent. Beer was 3.2 percent, now a lager is five percent. The size of a wine glass is bigger, too  –  from 125ml to 175ml, and in some cases 250ml. That is a third of a bottle.’

Dr Sheron warns that alcohol is being used as a drug, instead of a part of a social event or accompaniment to a meal. ‘The young drink to get wasted as quickly as possible. They think if they can remember the night before it is not a good night out, and 24-hour licensing is one of the problems,’ he cautions.

With prices so low, Professor Mark Bellis, director of the Department of Public Health at John Moores University in Liverpool, adds: ‘A young person with £10-a-week to spend can get drunk three times a week.’   The scale of the crisis cannot be over-stated. Alcohol abuse, leading to either injury or disease, now costs the NHS £1billion annually with 40 per cent of casualty departments’ admissions being drink-related.

Significantly, the London Ambulance Service says that alcohol-related emergency calls have increased by 12 per cent since 24-hour drinking laws were introduced.   As spokeswoman Anna Lowman says: ‘One of the aims of the new laws was to eradicate the 11pm to 2am disorder flashpoint when the pubs and off-licences used to close. But this is still our busiest period. Fourteen per cent of all calls during these hours are linked to drinking.’

Yet this is not the only catastrophic side-effect. The Cabinet Office admits the real cost of drinking is £20billion a year if you include suicides, alcohol-fuelled crime, anti-social behaviour, depressive illness, family breakdown and domestic violence.

Only this month, the Local Government Association – representing councils – warned the 24-hour drinking plan to emulate a European style cafe-culture in Britain had failed miserably. It costs £100 million a year to oversee the late licensing system, provide staff to clean town centres of vomit or urine (often both) and help for the ‘walking wounded’ at the end of a night’s hard drinking.

At Stacey Rhymes’ funeral in Bramcote, held near the park where the family used to picnic, there were 150 mourners – some were her old school friends. As her mother says: ‘Stacey chose her way – and they theirs. They have got married, have children and careers. They are enjoying life. My daughter drank herself to death.   ‘She never had any problems getting her hands on another bottle. In many ways, she was a victim of our times.’

Source  Newspaper cutting  – sent to NDPA not identified.

Filed under: Addiction,Alcohol :

Adolescents’ use of marijuana may increase the risk of heroin addiction later in life, a new study suggests. Researchers say the work adds to “overwhelming” evidence that people under 21 should not use marijuana because of the risk of damaging the developing brain.
The idea that smoking cannabis increases the user’s chance of going on to take harder drugs such as heroin is highly contentious. Some dub cannabis a “gateway” drug, arguing that peer pressure and exposure to drug dealers will tempt users to escalate their drug use. Others insist that smoking cannabis is unrelated to further drug use.
Now research in rats suggests that using marijuana reduces future sensitivity to opioids, which makes people more vulnerable to heroin addiction later in life. It does so by altering the brain chemistry of marijuana users, say the researchers.
“Adolescents in particular should never take cannabis – it’s far too risky because the brain areas essential for behaviour and cognitive functioning are still developing and are very sensitive to drug exposure,” says Jasmin Hurd, who led the study at the Karolinska Institute in Sweden.
But Hurd acknowledges that most people who use cannabis begin in their teens. A recent survey reported that as many as 20% of 16-year-olds in the US and Europe had illegally used cannabis in the previous month.

“Teenage” rats

In order to explore how the adolescent use of cannabis affects later drug use, Hurd and colleagues set up an experiment in rats aimed to mirror human use as closely as possible.
In the first part of the trial, six “teenage” rats were given a small dose of THC – the active chemical in cannabis – every three days between the ages of 28 and 49 days, which is the equivalent of human ages 12 to 18. The amount of THC given was roughly equivalent to a human smoking one joint every three days, Hurd explains. A control group of six rats did not receive THC.
One week after the first part was completed, catheters were inserted in all 12 of the adult rats and they were able to self-administer heroin by pushing a lever.
“At first, all the rats behaved the same and began to self-administer heroin frequently,” says Hurd. “But after a while, they stabilised their daily intake at a certain level. We saw that the ones that had been on THC as teenagers stabilised their intake at a much higher level than the others – they appeared to be less sensitive to the effects of heroin. And this continued throughout their lives.”
Hurd says reduced sensitivity to the heroin means the rats take larger doses, which has been shown to increase the risk of addiction.

Drug memory

The researchers then examined specific brain cells in the rats, including the opioid and cannabinoid receptors. They found that the rats that had been given THC during adolescence had a significantly altered opioid system in the area associated with reward and positive emotions. This is also the area linked to addiction.
“These are very specific changes and they are long-lasting, so the brain may ‘remember’ past cannabis experimentation and be vulnerable to harder drugs later in life,” Hurd says.
Neurologist Jim van Os, a cannabis expert at the University of Maastricht in the Netherlands told New Scientist the research was a welcome addition to our understanding of how cannabis affects the adolescent brain.
“The issue of cross-sensitisation of cannabis/opioid receptors has been a controversial one, but these findings show the drug’s damaging effects on the reward structures of the brain,” van Oshe says. “There is now overwhelming evidence that nobody in the brain’s developmental stage – under the age of 21 – should use cannabis.”

Source: On line edition of Neuropsychopharmacology. Reported in July 2006

27 October 2006

People addicted to cocaine have an impaired ability to perceive rewards and exercise control due to disruptions in the brain’s reward and control circuits, according to a series of brain-mapping studies and neuropsychological tests conducted at the U.S. Department of Energy’s Brookhaven National Laboratory.
“Our findings provide the first evidence that the brain’s threshold for responding to monetary rewards is modified in drug-addicted people, and is directly linked to changes in the responsiveness of the prefrontal cortex, a part of the brain essential for monitoring and controlling behavior,” said Rita Goldstein, a psychologist at Brookhaven Lab. “These results also attest to the benefit of using sophisticated brain-imaging tools combined with sensitive behavioral, cognitive, and emotional probes to optimize the study of drug addiction, a psychopathology that these tools have helped to identify as a disorder of the brain.”
Goldstein will present details of these studies at a press conference on neuroscience and addiction at the Society for Neuroscience (SfN) annual meeting in Atlanta, Georgia, on Sunday, October 15, 2006, 2 to 3 p.m., and at a SfN symposium on Wednesday, October 18, 8:30 a.m.
Goldstein’s experiments were designed to test a theoretical model, called the Impaired Response Inhibition and Salience Attribution (I-RISA) model, which postulates that drug-addicted individuals disproportionately attribute salience, or value, to their drug of choice at the expense of other potentially but no-longer-rewarding stimuli – with a concomitant decrease in the ability to inhibit maladaptive drug use. In the experiments, the scientists subjected cocaine-addicted and non-drug-addicted individuals to a range of tests of behavior, cognition/thought, and emotion, while simultaneously monitoring their brain activity using functional magnetic resonance imaging (fMRI) and/or recordings of event-related potentials (ERP).
In one study, subjects were given a monetary reward for their performance on an attention task. Subjects were given one of three amounts (no money, one cent, or 45 cents) for each correct response, up to a total reward of $50 for their performance. The researchers also asked the subjects how much they valued different amounts of monetary reward, ranging from $10 to $1000.
More than half of the cocaine abusers rated $10 as equally valuable as $1000, “demonstrating a reduced subjective sensitivity to relative monetary reward,” Goldstein said.
“Such a ‘flattened’ sensitivity to gradients in reward may play a role in the inability of drug-addicted individuals to use internal cues and feedback from the environment to inhibit inappropriate behavior, and may also predispose these individuals to disadvantageous decisions – for example, trading a car for a couple of cocaine hits. Without a relative context, drug use and its intense effects – craving, anticipation, and high – could become all the more overpowering,” she said.
The behavioral data collected during fMRI further suggested that, in the cocaine abusers, there was a “disconnect” between subjective measures of motivation (how much they said they were engaged in the task) and the objective measures of motivation (how fast and accurately they performed on the task).
“These behavioral data implicate a disruption in the ability to perceive inner motivational drives in cocaine addiction,” Goldstein said.
The fMRI results also revealed that non-addicted subjects responded to the different monetary amounts in a graded fashion: the higher the potential reward, the greater the response in the prefrontal cortex. In cocaine-addicted subjects, however, this region did not demonstrate a graded pattern of response to the monetary reward offered. Furthermore, within the cocaine-addicted group, the higher the sensitivity to money in the prefrontal cortex, the higher was the motivation and the self-reported ability to control behavior.
The ERP results showed a similarly graded brain response to monetary reward in healthy control subjects, but not in cocaine-addicted individuals.
“The dysfunctional interplay between reward processing and control of behavior observed in these studies could help to explain the chronically relapsing nature of drug addiction,” Goldstein said. “Our results also suggest the need for new clinical interventions aimed at helping drug abusers manage these symptoms as part of an effective treatment strategy.”

Source: Medical Research News 18th Oct.2006

EDINBURGH: The Scottish Executive’s anti-drug abuse policy was criticized sharply yesterday following a report that the government recommended heroin-substitute methadone is 97% ineffective.

Methadone, a drug used for recovery from heroin addiction, has a success rate of no more than 3.4%, according to Professor Neil McKeganey, chief researcher for Glasgow University’s Centre for Drug Misuse Research. McKeganey has just concluded a study on the effectiveness of the £12m a year Methadone programme.

The study observed a group of 695 heroin addicts who started taking treatment in 2001 at 33 different addiction centers across Scotland. A large percentage of this group was given methadone-based care while the rest were put on rehabilitation. Their progress was recorded over interviews 33 months after they started the treatment to see if they had become drug-free over a 90-day period.

The group given only-methadone had a very poor 3.4 percent recovery rate from drug addiction; whereas the group placed in residential rehabilitation (with no methadone throughout the treatment) showed a 29% success rate.

A key difference in methadone’s success rates between Scotland and England was also pointed out. While England emphasizes on getting people off drugs entirely, Scotland’s drug policy lacks any such direction; as a result, addicts simply substitute methadone with heroin.

McKeganey’s previous research had revealed a greater inclination to commit crimes among methadone patients when compared with addicts placed on abstinence programmes. People in the latter group also showed twice the level of interest in finding a job.

While the report makes no recommendation, sharp reactions have come in from various quarters demanding the Executive at least review its drug policy if not entirely scrap methadone. Tory leader Anabel Goldie said she recommended more investment in residential rehabilitation centres.

Meanwhile an official at the Greater Glasgow NHS facility said methadone may not be suitable for everyone but many addicts do benefit from it. He also said the government was looking to offer “a wider package of support” that would include rehabilitation, education and training, to addicts.

Source: 30.10.06

Mount Sinai researchers have discovered how cocaine corrupts the brain and becomes addictive. These findings — the first to connect activation of specific neurons to alterations in cocaine reward — were published in Science on October 15. The results may help researchers in developing new ways of treating those addicted to the drug.

Led by Mary Kay Lobo, PhD, Postdoctoral Fellow in the Department of Neuroscience at Mount Sinai School of Medicine and first author of the study, researchers found that the two main neurons (D1 and D2) in the nucleus accumbens region of the brain, an important part of the brain’s reward center, exert opposite effects on cocaine reward. Activation of D1 neurons increases cocaine reward whereas activation of D2 neurons decreases cocaine reward.
“The data suggest a model whereby chronic exposure to cocaine results in an imbalance in activity in the two nucleus accumbens neurons: increased activity in D1 neurons combined with decreased activity in D2 neurons,” said Dr. Lobo. “This further suggests that BDNF-TrkB signaling in D2 neurons mediates this decreased activity in D2 neurons.”
The study was conducted using optogenetics, a technology to optically control neuronal activity in freely moving rodents.

Opposite cocaine reward similar to those found when activating each neuron is achieved by disrupting brain-derived neurotrophic factor, which is a protein in the brain known for its involvement in neuronal survival, learning, and memory and drug abuse signaling through its receptor TrkB in D1 or D2 neurons.

“This new information provides fundamentally novel insight into how cocaine corrupts the brains reward center, and in particular how cocaine can differentially effect two neuronal subtypes that are heterogeneously intermixed in the nucleus accumbens,” said Eric Nestler, MD, PhD, Chair of Neuroscience, Nash Family Professor, and Director of The Friedman Brain Institute at Mount Sinai and co-author on the study. “We can use this information to potentially develop new therapies for cocaine addiction, possibly aimed at altering neuronal activity selectively in either neuronal subtype.”

Source: ScienceDaily (Oct. 18, 2010)

Scientists at the University of Liverpool have found that high levels of a stress hormone in recovering alcoholics could increase the risk of relapse.

The study showed that cortisol, a hormone produced by the adrenal gland in response to stress, is found in high levels in chronic alcoholics, as well as those recovering from the condition.

Researchers found that this could result in impaired memory, attention and decision-making functions, which could decrease the patient’s ability to engage with treatment.

Chronic alcoholism is a disabling addictive disorder, characterised by compulsive and uncontrolled consumption of alcohol despite the negative effects it has on health, relationships and social standing. Alcohol damages almost every organ of the body including the brain where it causes memory loss and impairs decision-making and attention span.

Cortisol plays an important role in the regulation of emotion, learning, attention, energy utilization, and the immune system.

The research showed that high levels of this hormone are present in alcoholic patients and continue to be elevated during withdrawal from alcohol and after long periods of abstinence.

Lead author of the review, Dr Abi Rose, from the School of Psychology, Health and Society at the University of Liverpool, said: “Both drinking and withdrawal from alcohol can affect cortisol function in humans.

“Cortisol dysfunction, including the high levels of cortisol observed during alcohol withdrawal, may contribute to the high rates of relapse reported in alcohol dependence, even after many months of abstinence.

“Drugs targeting the effects of cortisol in the brain might reduce the chances of relapse and reduce the cognitive impairments that interfere with treatment.”

The study is published in Alcoholism: Clinical & Experimental Research. The research is in collaboration with Kings College London, University of Bern, and the University of Kentucky.

Source: 26.09.2010

Cocaine is one of the oldest drugs known to humans, and its abuse has become widespread since the end of the 19th century. At the same time, we know rather little about its effects on the human brain or the mechanisms that lead to cocaine addiction. The latest article by Dr. Marco Leyton, of the Montreal Neurological Institute (MNI), McGill University and the McGill University Health Centre, which was published in the journal Biological Psychiatry on May 15, 2009, not only demonstrates a link between cocaine and the reward circuits in the brain but also associates the susceptibility to addiction with these mechanisms.

The results of this study show that sniffing cocaine triggers high levels of dopamine secretion in a central region of the brain called the striatum. Dopamine is known to play a critical role in the brain’s response to reward as well as in its response to addictive drugs.
This study was carried out in ten non-addicted users of cocaine, all of whom sniffed cocaine on one test day and placebo powder on another. Participants underwent blood tests before and after taking the drug, and dopamine release in the brain was measured using PET scans.
“The ability of cocaine to activate dopamine release varies markedly from person to person. Our study suggests that this is related to how much of the drug the person consumed in the past,” explained Dr. Leyton. The more cocaine someone has used in his or her lifetime, the more the brain will secrete dopamine during subsequent cocaine use. “It’s possible therefore that the intensity of the reward-circuit response is related to increased susceptibility to addiction,” stated Dr. Leyton.
Although the relationship between the intensity of dopamine secretion and the frequency of drug use has been demonstrated, researchers still do not fully understand its mechanism of action. Is it the repeated stimulation of the reward circuit that leads to addiction, or is it an inherent sensitivity to addiction that leads to the increased secretion of dopamine? This question is not easy to answer, especially since other factors come into play, such as other aspects of the subject’s personal history.
Whatever the answer, the relationship between dopamine and cocaine means that this hormone could be a potential target for treatment against addiction. More research is required before treatments are available, but this study opens a new door in this direction.
This study was funded with a grant from the Canadian Institutes for Health Research. Salary support was given by the Fond de recherche en santé du Québec
This study is a collaboration between several laboratories of the McGill University Health Centre and McGill University, involving : Dr Sylvia M.L. Cox, Dr Chawki Benkelfat, Dr Alain Dagher, Dr J. Scott Delaney, France Durand, Samuel A. McKenzie, Dr Theodore Kolivakis, Kevin F. Casey, Dr Marco Leyton.

Source: McGill University Health Centre (2009, May 20).

Environmental conditions play a major role in treating drug addiction and in preventing relapses, according to new research. For the first time, researchers from the Institut de physiologie et biologie cellulaire (CNRS/Université de Poitiers) have shown that positive and stimulating environmental conditions make it easier to treat cocaine addiction.

Even though numerous data exist on the mechanisms of cocaine addiction, there are as yet no effective therapies, making it very urgent that new strategies for treating the disease be developed. According to a study by Marcello Solinas and Mohamed Jaber, carried out by a group of researchers at the Institut de physiologie et biologie cellulaire in Poitiers, exposing mice to an “enriched environment (1)” during cocaine withdrawal removes abnormal behavior related to addiction. An enriched environment, for mice, is an environment which stimulates their curiosity, providing social and physical activity as well as exploration.
After addicting animals to cocaine, the researchers then exposed them to an enriched environment made up of large cages with a small house, a running wheel, tunnels and other appealing toys which were changed weekly.
Three models of animal addiction were used:
behavioral sensitization, which measures the progressive increase in the stimulating effects of cocaine after chronic administration;
the location preference, which measures the ability of a context (associated with cocaine consumption) to lead to drug-seeking behavior, and the renewal of this drug-induced location preference;
measurements of cocaine’s ability to lead to a relapse after a period of withdrawal.
The result was that after thirty days of exposure to an enriched environment, addiction behavior typical of these three models had disappeared.
To identify the brain areas involved in the beneficial effect of an enriched environment, the researchers used an approach from functional neuro-anatomy. They showed that the absence of relapse in “enriched” mice was associated with a decrease in the cocaine-induced activation of a set of brain structures involved in dopaminergic transmission and associated with relapse.
These results, which have both a medical and societal impact, suggest that the living conditions of drug addicts should be taken into account in determining their therapy. A real effort should be made to create enriched environmental conditions, providing patients with different types of social, physical and intellectual stimulation. This also suggests that under deprived environmental conditions, treating addiction can be very challenging.
1) A number of earlier studies had shown that when animals are raised in an enriched environment prior to drug exposure, their vulnerability to addiction was reduced. In such conditions, the enriched environment can be seen as preventive.

Source: Proceedings of the National Academy of Sciences, 2008; 105 (44): 17145 DOI: 10.1073/pnas.0806889105

Addictive drugs are known to induce changes in the brain’s reward circuits that may underlie drug craving and relapse after long periods of abstinence. Now, new research in the September 9 issue of the journal Neuron, uncovers a specific neural mechanism that may be linked to persistent drug-seeking behavior and could help to guide strategies for development of new therapies for cocaine addiction.

Previous research has shown that the ventral tegmental area (VTA) is a brain region that is activated when cocaine users experience a craving for cocaine after being exposed to cocaine-associated cues. The medial prefrontal cortex (mPFC), which receives input from the VTA via circuits that use the “reward” neurotransmitter dopamine, has also been implicated in drug craving after cocaine withdrawal. Further, increases in the level of brain-derived neurotrophic factor (BDNF) have been observed in the VTA and mPFC in rats after withdrawal from repeated cocaine exposure.
“BDNF plays a key role in modulating the structure and function of synapses, the sites of communication between neurons. Therefore, increased BDNF after cocaine withdrawal may drive synaptic changes that contribute to compulsive drug seeking behavior,” explains senior author, Dr. Mu-ming Poo from the University of California, Berkeley. “It has been shown that increased BDNF in the VTA after cocaine withdrawal in rats promotes the drug-dependent motivational state. However, nothing is known about the potential BDNF effect on synaptic function and plasticity in mPFC neurons after cocaine withdrawal.”
Dr. Poo and colleagues designed a study to examine how BDNF and the mPFC might contribute to relapse after cocaine addiction. The researchers found that the gradual increase in BDNF expression in the rat mPFC after terminating repeated cocaine exposure significantly enhanced the activity-induced potentiation of specific synapses. Dr. Poo’s group went on to uncover the specific cellular mechanism linking increased BDNF with enhanced synaptic plasticity and demonstrated that interference with the key molecule in the BDNF signaling process reduced behavioral sensitivity after cocaine withdrawal in rats.
“In short, our results demonstrate that elevated BDNF expression after cocaine withdrawal sensitizes the excitatory synapses in the mPFC to undergo activity-induced persistent potentiation that may contribute to cue-induced drug cravings and drug-seeking behavior,” concludes Dr. Poo. Although a clear correlation between rat and human behaviors of cocaine craving and relapse remains to be established, the cellular mechanism uncovered in this study does appear to have behavioral relevance and may represent a direct brain sensitization that is involved in triggering relapse.
The researchers include Hui Lu, Pei-lin Cheng, Byung Kook Lim, Nina Khoshnevisrad, and Mu-ming Poo, University of California, Berkeley, Berkeley, CA.

Source: . Neuron, 67(5) pp. 821 – 833 DOI: 0.1016/j.neuron.2010.08.012

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

A typical drug user’s transition to addiction could result from a persistent impairment of synaptic plasticity in a key structure of the brain, suggests a new French study.
The research, by the teams of Pier Vincenzo Piazza and Olivier Manzoni, at the Neurocentre Magendie in Bordeaux, appears in the journal Science.

This study is the first demonstration that a correlation exists between synaptic plasticity and the transition to addiction. The results from the teams at Neurocentre Magendie call into question the hitherto held idea that addiction results from pathological cerebral modifications, which develop gradually with drug usage.

Their results show that addiction may, instead, come from a form of anaplasticity, i.e. from incapacity of addicted individuals to counteract the pathological modifications caused by the drug to all users.

The voluntary consumption of drugs is a behaviour found in many species of animals. However, it had long been considered that addiction, defined as compulsive and pathological drug consumption, is behaviour specific to the human species and its social structure.

In 2004, the team of Pier Vincenzo Piazza showed that the behaviours which define addiction in humans, also appear in some rats which will self administer cocaine. Addiction exhibits astonishing similarities in men and rodents, in particular the fact that only a small number of consumers (humans or rodents) develop a drug addiction. The study of drug dependent behaviour in this mammal model thus opened the way to the study of the biology of addiction.

Today, thanks to a fruitful collaboration, the teams of Pier Vincenzo Piazza and Olivier Manzoni are reporting discovery of the first known biological mechanisms for the transition from regular but controlled drug taking to a genuine addiction to cocaine, characterised by a loss of control over drug consumption.

Chronic exposure to drugs causes many modifications to the physiology of the brain. And researchers wanted to find out which of these modifications is responsible for the development of an addiction.
The addiction model developed in Bordeaux provides a unique tool to answer this question. Thus it allows comparing animals who took identical quantities of drugs, but of which only few become addicted.

By comparing addict and non-addict animals at various time points during their history of drug taking, the teams of Pier Vincenzo Piazza and Olivier Manzoni have demonstrated that the animals which developed an addiction to cocaine exhibit a permanent loss of the capacity to produce a form of plasticity known as long-term depression (or LTD).

LTD refers to the ability of the synapses (the region of communication between neurons) to reduce their activity under the effect of certain stimulations. It plays a major role in the ability to develop new memory traces and, consequently, to demonstrate flexible behaviour.

After short-term usage of cocaine, LTD is not modified. However, after a longer use, a significant LTD deficit appears in all users. Without this form of plasticity, which allows new learning to occur, behaviour with regard to the drug becomes more and more rigid, opening the door to development of a compulsive consumption.

The brain of the majority of users is able to produce the biological adaptations which allow to counteract the effects of the drug and to recover a normal LTD.
By contrast, the anaplasticity (or lack of plasticity) exhibited by the addicts leaves them without defences and hence the LTD deficit provoked by the drug becomes chronic.

This permanent absence of synaptic plasticity would explain why drug seeking behaviour becomes resistant to environmental constraints (difficulty in procuring the substance, adverse consequences of taking the drug on health, social life, etc.) and consequently more and more compulsive. Gradually, control of the taking of the drug is lost and addiction appears.

For Pier-Vincenzo Piazza and his collaborators, these discoveries also have important implications for developing new treatment of addiction.

“We are probably not going to find new therapies by trying to understand the modifications caused by a drug in the brains of drug addicts,” explain the researchers, “since their brain is anaplastic.” For the authors, “The results of this work show that it is in the brain of the non-addicted users that we will probably find the key to a true addiction therapy.

Indeed,” the authors estimate, “understanding the biological mechanisms which enable adaptation to the drug and which help the user to maintain a controlled consumption could provide us with the tools to combat the anaplastic state that leads to addiction”. (ANI)

Source: 2010-06-29

Researchers have found that a specific and remarkably small fragment of RNA appears to protect rats against cocaine addiction – and may also protect humans.
The discovery could lead to better ways of predicting drug abuse risk and treating addictions

In the study, researchers at The Scripps Research Institute in Jupiter, Florida found that cocaine consumption increased levels of a specific microRNA sequence in the brains of rats, named microRNA-212.

As its levels increased, the rats exhibited a growing dislike for cocaine, ultimately controlling how much they consumed.
On the other hand, as levels of microRNA-212 decreased, the rats consumed more cocaine and became the rat equivalent of compulsive users.

The study’s findings suggest that microRNA-212 plays a pivotal role in regulating cocaine intake in rats and perhaps in vulnerability to addiction.
Interestingly, the same microRNA-212 identified in this study, is also expressed in the human’s dorsal striatum, a brain region that has been linked to drug abuse and habit formation.

“This study enhances our understanding of how brain mechanisms, at their most fundamental levels, may contribute to cocaine addiction vulnerability or resistance to it,” Nature quoted National Institute on Drug Abuse (NIDA) Director Dr. Nora D. Volkow, as saying.

“This research provides a wonderful example of how basic science discoveries are critical to the development of new medical treatments and targeted prevention,” he added.

Rats with a history of extended cocaine access can demonstrate behavior similar to that observed in humans who are dependent on the drug.
Current data show that about 15 percent of people who use cocaine become addicted to it.
The findings suggest that microRNAs may be important factors
contributing to this vulnerability.

“The results of this study offer promise for the development of a totally new class of anti-addiction medications. Because we are beginning to map out how this specific microRNA works, we may be able to develop new compounds to manipulate the levels of microRNA-212 therapeutically with exquisite specificity, opening the possibility of new treatments for drug addiction,” said Paul J. Kenny, senior author on the study.
The study is published in the journal Nature. (ANI) 9th July 2010-07-10

Neuropharmacologists ran clinical trials to find that a drug called topiramate is an effective therapeutic medication for decreasing heavy drinking and diminishing the physical and psychosocial harm caused by alcohol dependence.

The drug works by blocking the right amount of the feel good effects of alcohol (brought on by increased levels of dopamine), making drinking less enjoyable and thus reducing cravings and helping to stop heavy drinking.

Topiramate was also found to lower blood pressure and cholesterol levels which may lead to a decrease in heart disease in alcohol dependent patients.

Alcoholism affects over 17 million people. Without proper treatment, it’s a devastating disease that can ruin lives and relationships. A new therapy that comes in a pill is bringing new hope to alcoholics.

There was a time in Christine Flemming’s life when alcohol came before her kids.
“I can’t remember when my daughter was very little, because I was drinking so much,” said Flemming. “That affected me a lot.”

Flemming needed help, but traditional treatment methods didn’t work. Now she’s on a new kind of therapy in the form of a pill called topiramate. It has changed her life. “I can tell you that it cuts my cravings, and I don’t feel like I have to drink,” Flemming said. “I don’t feel like that’s something I need in my life and I have to do.”

Alcohol increases levels of dopamine, a chemical in the brain that makes us feel good. The drug works by blocking the right amount of the feel-good effects from alcohol to reduce cravings and help stop heavy drinking. During clinical trials, neuropharmacologists were surprised to learn it also lowers blood pressure and cholesterol levels, which may lead to a decrease in heart disease in alcohol dependent patients.

“Most of the morbidity due to alcoholism is caused by secondary effects of all these other systems, so to have a drug that begins to correct all those other physical abnormalities is extremely helpful,” said Bankhole Johnson, Ph.D., a Neuropharmacologist at the University of Virginia in Charlottesville, Va.

The drug helped improve Fleming’s health and end her dependence on alcohol. She cut her drinking from 15 beers a day to just three, so time with her kids is now a priority.
“It’s made a big difference,” Flemming said. “It’s made a really big difference, and I feel like I’m actually there for my family.”

Qualifying patients can find out how to receive the drug by contacting their primary care doctors.

WHAT IS TOPIRAMATE? Topiramate is a drug originally discovered in 1979. It is prescribed as an epilepsy medication and for migraine headaches. It is also used for a number of other purposes, including as a treatment for people with alcoholism.

Researchers believe that topiramate works in two ways. First, it reduces the release of dopamine that follows the consumption of alcohol. This reduces the positive feeling that people receive from alcohol, and thus reduce the incentive to drink. Second, topiramate interferes with the protein glutamate which normally excites dopamine neurons and again, lessening the ýfeel goodý effect of dopamine from alcohol.

WHAT IS ALCOHOL? Alcohol is created through the natural process of fermentation. This happens when yeast and sugar from vegetables and grains change the sugar into alcohol. When you drink alcohol, it is absorbed into your bloodstream, where it can affect the central nervous system, which is the control center for your entire body.

Alcohol slows down this control center with its sedative effect. In moderation it can reduce anxiety, but it also blocks some of the commands the brain sends to other parts of the body, so it alters your senses. That’s why, when drunk, people often have trouble walking, talking, and some may even “black out,” forgetting what they said or did. Drinking an excessive amount of alcohol can even be fatal.

Source www.ScienceDaily June 2010

Levels of the serotonin transporter are low in the brains of users of ecstasy, according to a US National Institute of Drug Abuse-funded study by Toronto’s Centre for Addiction and Mental Health (CAMH) and The Hospital for Sick Children (SickKids) published today in the journal Brain.

Ecstasy (MDMA) is a stimulant drug widely used recreationally that is also being tested in clinical trials for the treatment of post-traumatic stress disorder.
Led by Dr. Stephen Kish at CAMH, this study provides confirmation of a previous finding from Johns Hopkins University that levels of the serotonin transporter (SERT) are low in cerebral cortex of chronic ecstasy users. The subjects were “typical” ecstasy users who used about two tablets of the drug twice a month.

SERT is a protein responsible for regulating levels of serotonin, a neurotransmitter important for mood and impulse control. Ecstasy interacts with SERT to cause the release of serotonin, an action that probably explains some of the behavioral effects of the drug such as increased sociability.

Scientists have long suspected that ecstasy might harm brain cells that use serotonin, but 12 years of brain scan studies have produced contradictory results, even within the same laboratory.
The CAMH study used a large subject size (49 drug users, 50 control subjects), confirmed by hair analysis that ecstasy users actually used the drug, and used an imaging probe that could measure SERT throughout the brain.
“We were surprised to discover that SERT was decreased only in the cerebral cortex and not throughout the brain, perhaps because serotonin nerves to the cortex are longer and more susceptible to changes. This finding is almost identical to newer data from Johns Hopkins and is the first time that one laboratory has actually been able to replicate results of another independent laboratory in a SERT study of ecstasy users.” said Dr. Kish.

Drug hair analysis indicated that many ecstasy users, probably unknowingly, also used methamphetamine, which might itself damage serotonin cells; however, low SERT was found both in ecstasy users who used and who did not use methamphetamine. Dr. Jason Lerch at SickKids showed that those ecstasy users who also used methamphetamine had a slightly thinner cerebral cortex.

Does low SERT equal “structural brain damage”? “Not necessarily” said co-author Dr. Isabelle Boileau of CAMH. “There is no way to prove whether low SERT is explained by physical loss of the entire serotonin nerve cell, or by a loss of SERT protein within an intact nerve cell.”
Dr. Kish suggests that low SERT might explain why many ecstasy users need to keep increasing the dose to experience the same effects, since SERT is necessary for the action of ecstasy. “Most of the ecstasy users of our study complained that the first dose is always the best, but then the effects begin to decline and higher doses are needed. The need for higher doses, possibly caused by low SERT, could well increase the risk of harm caused by this stimulant drug,” said Dr. Kish.

Media Contact: Michael Torres, Media Relations, CAMH ; 416 595 6015 or email

Source: 18th May 2010

We know that there are people alive today who find it impossible to quit different kinds of behaviour once they have started it. What is it that makes one person quit cold turkey, and another smoke even while they are being treated for cancer?

Is there an addiction gene? Addiction in the genes is a hotly debated subject among scientists and researchers.

Scientists and researchers are going further back than ever before to unearth present truths. Addiction runs in the family. Again and again, they have found addictive behaviours carried down the family tree. This was their first clue that addiction may be hereditary.

There doesn’t appear to be a single ‘addict’ gene that causes specific types of people to fall into the addiction trap. There are however, several that combine to form a strong susceptibility to the behavioural patterns that addict’s exhibit. This is the addiction and genetics debate.

When a person with these genetic markers is exposed to a drug, or a habit, it can change the chemistry in their brain. This change leads to compulsive behaviour and eventual addiction. We are familiar with the concept that some illnesses – both physical and mental – can be hereditary, but it appears that this can also be applied to addiction.

Naturally, even if addiction is in the genes, there are other external factors that play their part. Why is it, for example, that a man becomes a drug addict, when his sister has never so much as smoked? External circumstances, stimuli and environmental factors also play their part in affecting people who are genetically prone to addiction.

The addiction and the genetic factor discussion will play on for years to come. The science is still quite new, and there are those out there that would prefer to blame addiction on personality disorders instead of genetics. Even if a definitive link is found, there is a still a long way to go before this information can be used to treat addiction sufferers and their families. For the time being at least, traditional addiction treatment and rehabilitation is still the most effective way to proceed.

Alcoholism, gambling, sexual and drug addiction could all be the result of inherited genes and generations of vulnerability. If you believe that addiction runs in the family, analyse yourself honestly. If it appears that you have a vulnerability to addictive behaviour, seek professional assistance. Obtaining assistance early on may help to limit any long-term damage.

Source: 5.5.2010

The brain’s nucleus accumbens (NAC) is a core region of the mesocorticolimbic dopaminergic system and is interconnected with the ventral tegmental area (VTA) and the prefrontal cortex. The mesocorticolimbic system is thought to be central to the reinforcing effects of many drugs and plays an important role in addiction. A new study has found that alcohol abuse elevated the expression of a distinct set of genes in the NAC and VTA, while nicotine blunted this effect in the VTA.

Results will be published in the July 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“In spite of their differences in pharmacology, alcohol and tobacco consumption are often intimately linked,” said Traute Flatscher-Bader, a postdoctoral research fellow at The University of Queensland and corresponding author for the study. “Nonetheless, the molecular mechanisms that underlie alcohol and nicotine abuse, and particularly their co-abuse, are still incompletely understood.”

“One thing that researchers have encountered is that it is often difficult to find ‘pure’ alcoholics, that is, alcoholics that only abuse alcohol and nothing else,” agreed Simon Worrall, director of postgraduate coursework programs in molecular biology at The University of Queensland. “Many alcoholics are poly-drug abusers, with the most common other drug being nicotine. Thus, many studies which have studied the effects of alcohol on the brain and other organs have been compromised because they have not taken account of the effects of nicotine addiction which is often superimposed on the effects of alcohol addiction.”

In the first part of the current study, Flatscher-Bader and her colleagues used DNA microarray technique to study the expression of many thousands of genes in the brains of non-smoking and smoking alcoholics and non-drinking smokers.

“We examined the impact of alcoholism and smoking on gene expression in the NAC in 20 chronic alcohol abusers and controls with and without recent smoking history,” said Flatscher-Bader. “The results revealed that in this brain region, the abuse of alcohol and nicotine had distinct effects on the expression of genes. In addition, altered expression of a number of genes was associated with both alcohol and nicotine abuse. Within the latter group was a set of genes which play a crucial role in a molecular pathway regulating cell structure.”

The researchers then went on to investigate in more detail the altered expression of six selected genes within the pathway regulating cell structure in two brain regions, using 30 cases comprised again of smoking and non-smoking controls and alcohol abusers. For this part of the study they used the method called “real time polymerase chain reaction.”

“This expanded investigation revealed that one of the genes, called RHOA, was elevated by alcohol abuse and its highest expression was evident in the smoking alcoholics in both brain regions,” said Flatscher-Bader. “The RHOA gene had previously been implicated in the initiation of tobacco smoking. In the NAC, the expression of a further four of the six selected genes was increased by alcohol abuse. Interestingly, the highest expression for each of the genes in the NAC was in the smoking alcoholics. In the other brain region called the VTA, alcohol abuse had a similar effect and elevated the expression of all six selected genes. In contrast to the NAC, however, concurrent smoking dampened the induction of five of these alcohol-sensitive genes in the VTA.”

“Many studies have analyzed the changes in gene expression in this brain system to try to untangle the molecular pathology of alcohol addiction,” said Worrall, “but this is amongst the first to take into account the effect of co-administration of nicotine with alcohol.

Flatscher-Bader stressed that there are several cell types in the brain and there are several steps between gene expression and impact on cell structure and function. “It has to be emphasized that our study is important as a first step in identifying molecular pathways underlying the effects of alcohol abuse and smoking and their co-joint abuse on the human NAC and VTA, “she said. “It now needs to be tested if our findings are, indeed, associated with changes to neuronal structure and function.”

“A better understanding of the molecular basis of withdrawal may help in the development of new treatments to ameliorate the symptoms,” added Dr Worrall. “Not many previous studies took into account the potential effects of nicotine addiction that may be superimposed on top of those from alcohol, so these results may help clinicians better use present therapy/drugs to treat patients abusing both alcohol and/or nicotine and may also lead to the development of new drugs.”

Source: 5.5.2010

 Around 44 0000 people have been recorded as entering specialised drug treatment centres in Europe in 2008 in 29 countries; data mainly cover outpatient and inpatient treatment centers
 Most clients enter treatment on their own initiative or under the pressure of family and friends (43 %); 27 % go to drug treatment through health or social services, including other drug treatment centres; around 20 % are referred to treatment by the criminal justice system, and the remaining through other referral sources
 The most frequent reason for entering treatment in 2008 (or most recent year available), is the use of heroin (48 % of all drug users and around 200 000 people), followed by cannabis (21 % and around 85 000 people) and cocaine use, (17 % and around 70 000 people), use of stimulants other than cocaine (5 % and around 22 000 clients) and other drugs use, which include hypnotics and sedatives, hallucinogens, volatile and other substances
 Among those who have entered treatment for the first time in their life the proportion of heroin users is lower and that of cocaine, cannabis users and clients consuming stimulants other than cocaine (mainly amphetamine and methamphetamine) is higher
 Differences between countries are relevant with 18 countries reporting more than 50 % of primary opioid users among drug clients, 8 countries with more than 20 % of primary cannabis clients and 3 countries with more than 20 % of cocaine clients.
 Stimulants other than cocaine, which will be the subject of one of 2010 selected issue are concentrated in some countries, namely the Scandinavian countries (amphetamine), Czech Republic and Slovakia (methamphetamine)
 Clients are mainly males (4 males for every female), with a mean age 31 years (those who have entered treatment for the first time are on average 1 year younger)
 Most clients start their drug use before the age of 20, around one third of the clients inject their primary drug, and the frequency of use varies by the main drug (the highest proportion of daily users is found among opioid clients and the lowest among users of stimulants other than cocaine)
 Social conditions of drug users entering treatment are generally poorer than in the general population (education, living and labour conditions)
 Differences are reported by primary drug and by country regarding gender, age distribution and patterns of drug use

 Recent comparable data on young people’s use of alcohol and drug come largely from surveys of 15- to 16-year-old school students. The European School Survey Project (ESPAD) conducted surveys in 1995, 1999, 2003 and more recently, 2007. The 2007 survey (Hibell et al., 2009) provides comparable data from 25 EU Member States as well as Norway and Croatia. Five countries conducted their own school surveys in 2008 (Belgium-Flemish Community, Spain, Italy, Sweden, United Kingdom-England)
 The latest ESPAD survey data from 2007 reveal that the highest lifetime prevalence of cannabis use among 15- and 16-year-old school students is in the Czech Republic (45 %) (Figure EYE-1 part (ii)). High lifetime prevalence estimates, ranging from 26 % to 32 %, are also reported in Estonia, France, the Netherlands, the Slovak Republic and the United Kingdom.
 Increases in cannabis use occurred in a number of European countries between 1995 and 2003 but have, in general, come to a halt or decreased more recently. Seven countries mainly located in Northern and Southern Europe (Greece, Cyprus, Malta, Romania, Finland, Sweden, Norway) reported overall stable and low lifetime prevalence of cannabis use during the whole period. Other western European countries, as well as Croatia and Slovenia, have shown a significant increase of lifetime cannabis use up to 2003 and since then nine of these reported a decrease of more than three percentage points, two were stable and none reported an increase. In most of central and eastern Europe the increasing trend observed between 1995 and 2003 seems not to have been reversed yet. In this region, two out of eight countries report increases of more than three percentage points since 2003, six or more a stable situation and none a significant decrease. In the five countries that conducted national school surveys in 2008, all reported stable or lower lifetime prevalence of cannabis use than reported in 2007 (Table EYE-11).
 Increases in lifetime cannabis use between 1995 and 2003 in Europe were in some countries accompanied by increases in the prevalence of cigarette smoking among school students. Since 2003, both trends have reversed, suggesting a possible link between tobacco and cannabis smoking.
 Estimates of the prevalence of other drug use among school students are much lower than those for cannabis use. For example, lifetime prevalence of cocaine use among 15- to 16-year-old school students is between 1 % and 2 % in half of the 28 reporting countries. Most of the remaining countries report prevalence levels of between 3 % and 4 %, while Spain, France, and the United Kingdom report 5 %. Among the five countries that conducted school surveys in 2008, two reported a decrease of 1%, one reported an increase of 1%, and two reported no change since the last survey (Table EYE-11). However, caution is required interpreting trends with such low prevalence.
 In the countries conducting their own national school surveys, drug prevalence questions may be considered comparable to the ESPAD questions but other aspects of the method mean the data are not strictly comparable.
Source: EMDDA July 10 2010

Some people can drink a lot of alcohol without becoming addicted, and specific genes may help explain why, researchers say.
In a new study of Australian twins, scientists found that separate genes appear to be responsible, to some degree, for dependence on alcohol — addiction — and how much people drink. Understanding how these genetic factors work together should give researchers more insight into treatment of alcoholism in its various forms, said study co-author John B. Whitfield, a researcher at Royal Prince Alfred Hospital in Australia.
Alcoholism and alcohol consumption may appear to be similar, but researchers are increasingly studying them separately. Consumption refers to the amount of alcohol that someone drinks, while addiction refers to a person’s inability to go without a drink.
“The transition from social alcohol consumption to alcohol dependence is a gradual process, and it is often hard to notice it,” said Dr. Alexei B. Kampov-Polevoi, an assistant professor of psychiatry at Mount Sinai School of Medicine. “As a result, many alcoholics and their family members continue to think that a person ‘just drinks too much’ while this person already developed alcohol dependence and requires treatment.”
Whitfield and his colleagues examined statistics about alcohol use from three studies of Australian twins completed between 1980 and 1995. The number of twins in the studies declined from 8,184 in 1980 to 3,378 in 1995.
The findings appear in the August issue of Alcoholism: Clinical & Experimental Research.
The researchers found twins who were genetically similar were more likely to consume similar amounts of alcohol. According to the study, some genes affected both addiction and alcohol intake, while some just affected addiction.
“We found (as others have also found) that alcohol dependence is partly, but not entirely, due to genetic differences between people who are affected by it and those who are not,” Whitfield said. “We also found that variation in the amount of alcohol that people habitually drink is subject to genetic influence, and that there is some — but not complete — overlap between the genes affecting these two things.”
Howard J. Edenberg, professor of biochemistry and molecular biology at Indiana University, said the findings — that genes separately affect alcoholism and drinking — are “reasonable.” But “that is a long way from identifying individual genes that actually are involved,” said Edenberg, whose own research is looking into that area.
So what should ordinary folks take from this study? “There is no direct and new message for people with alcoholism in their families; they are at higher risk than average but this has been known for some time and there is only a statistical risk, not a certainty by any means,” Whitfield said. “The more positive message for such people, and the community at large, is that we are learning more about alcohol use and alcohol-related problems and their causes.”
Source : HealthDay News 18th August 2004

Filed under: Addiction,Alcohol :

New research suggests that people who smoke and drink heavily are more at risk for oral cancer, the Researchers from King’s College in London, England, found an increase in oral cancer among men and women in their 20s and 30s who smoke and binge drink.

The researchers said that when tobacco smoke combines with alcohol, it produces dangerous levels of cancer-causing chemicals that attack the lining of the mouth.

“Our data show that smoking, drinking and poor diet are major risk factors, and that the younger people start smoking and drinking, the higher the risk,” said Newell Johnson, a professor of oral pathology at King’s College

Source: Daily Telegraph, London reported Nov. 9.2004

Young men who report an unstable pattern of alcohol consumption including binge drinking have an elevated risk for experiencing hypomania, study results show. Notably, the effect was independent of total alcohol consumption and the presence of clinical alcohol use disorders.
“This fits with the idea that instability in different biological and behavioral systems is a core feature of risk for hypomania and finally risk for bipolar disorders,” say study authors Thomas Meyer (Newcastle University, UK) and Larissa Wolkenstein (University of Tübingen, Germany) in the journal Comprehensive Psychiatry.
Recent studies have suggested that vulnerability to hypomania is related to instability in certain psychologic processes. For example, individuals at risk for hypomania do not generally sleep less than others, but report a much more unstable sleeping pattern. Similarly fluctuations in self-esteem are much more characteristic of vulnerability to hypomania than are consistently low or high levels of self-esteem.
In the current study, the researchers assessed whether alcohol use might show a similar relationship to hypomania. They recruited 120 male students who completed the Hypomanic Personality Scale and were independently interviewed with the FORM 90 to assess alcohol consumption. The latter comprised an interview about a typical weekly drinking pattern and a calendar to assess drinking behavior over the last 90 days, noting special days with unusual drinking behavior.
The researchers found that intra-individual fluctuations in alcohol consumption predicted hypomania after accounting for clinical diagnoses of abuse or dependency. In addition, vulnerability for hypomania was significantly associated with mean standard ethanol content per drinking day.
Discussing their findings, the researchers note a recent theory that bipolar disorder is related to a hypersensitivity to reward-related cues, which is due to a dysregulation of the behavioral activation system.
“To extend this work further, it would be reasonable to look more closely at the motivational and affective processes associated with drinking alcohol and bipolar disorder and how mood and drinking are related,” Meyer and Wolkenstein comment.
Source: MedWire ( 19 March 2010

Compared to drugs such as heroin and cocaine, many people consider marijuana a relatively benign substance. But two studies in this issue demonstrate disturbing similarities between marijuana’s effects on the brain and those produced by highly addictive drugs such as cocaine and heroin. One study, described on page 2050, indicates that marijuana withdrawal activates the same stress system in the brain triggered by withdrawal of opiates and alcohol, while the other, reported on page 2048, indicates that marijuana activates the same reward pathway as heroin.

Source : Science 27 June 1997: Vol. 276. no. 5321, pp. 1967 – 1968

Recurrent drinking is common among patients with alcohol dependence who have received treatment. This study assessed whether certain types of relapses are more likely to recur, are more severe, or are more amenable to a particular psychosocial therapy.
Researchers examined data from 592 of 952 outpatients with alcohol dependence who had been randomized in a larger trial to receive motivational enhancement therapy, cognitive-behavioral therapy, or twelve-step facilitation therapy. These 592 subjects had experienced a relapse (i.e., drinking after being abstinent for at least 14 days) and completed the relapse-onset section of the Relapse Questionnaire, which assesses patient-perceived influences that contribute to relapse.
• Relapses were divided into 3 types: negative affect/family influences, craving/cued, and social pressure. When relapses recurred, they were often (about half the time) the same type as the initial relapse. Social pressure relapses were most likely to repeat (58% of the time). Negative affect relapses were the most severe (i.e., associated with a greater number of drinks consumed per day).
• The 3 therapies affected the overall risk of relapse similarly. However, motivational enhancement therapy offered less protection than the other therapies against social pressure relapse.
This study provides a typology that can help clinicians efficiently assess relapse risk among patients with alcohol dependence. Clinicians who understand their patients’ prior types of relapses have the opportunity to provide individualized relapse prevention counseling or referral.
Peter Friedmann, MD, MPH

Source:Zywiak WH, Stout RL, Longabaugh R, et al. Relapse-onset factors in Project MATCH: the Relapse Questionnaire. J Subst Abuse Treat. 2006;31(4):341–345.

Filed under: Addiction,Alcohol :

A researcher at the University of Buffalo’s Research Institute on Addictions (RIA) has found a change in the brain that occurs after drug use and that may contribute to drug addiction.
The finding, reported in the January issue of Biological Psychiatry, demonstrates that repeated exposure to different types of drugs of abuse, such as cocaine, nicotine, amphetamine and alcohol, lead to a persistent or long-term reduction in the electrical activity of dopamine neurons in the brain.
Dopamine neurons are the origin of the reward pathway responsible for the “feel good” experience that is such a strong component of drug use and abuse.
“A persistent reduction in dopamine neuron electrical activity after repeated exposure to different types of drugs appears to be the result of excessive excitation of dopamine neurons,” according to Roh-Yu Shen (photo), a neuroscientist and the lead investigator on the study. “This represents a new and potentially critical neural mechanism for addiction and provides a working model that suggests how the reward pathway function is altered and how these changes can be responsible for triggering intense craving and compulsive drug-seeking.”

Source. January 2007 issue of Biological Psychiatry


DURHAM, N.C. — Within the mind of every smoker trying to quit rages a battle between the higher-order functions of the brain wanting to break the habit and the lower-order functions screaming for another cigarette, say researchers at Duke University Medical Center. More often than not, that cigarette gets lit.
Brain scans of smokers studied by the researchers revealed three specific regions deep within the brain that appear to control dependence on nicotine and craving for cigarettes. These regions play important roles in some of the key motivations for smoking: to calm down when stressed, to achieve pleasure and to help concentration.
“If you can’t calm down, can’t derive pleasure and can’t control yourself or concentrate, then it will be extremely difficult for you to break the habit,” said lead study investigator Jed E. Rose, Ph.D., director of the Duke Center for Nicotine and Smoking Cessation Research. “These brain regions may explain why most people try to quit several times before they are successful.”
Understanding how the brain responds to cigarette cravings can help doctors change nicotine cessation treatments to address all three of these components of withdrawal, Rose said. Drugs or therapies that target these regions may help smokers stave off the cravings that often spoil their attempts to quit.
The team’s findings are now online in the journal Neuropsychopharmacology. The research was funded by Phillip Morris USA.
Approximately one in five Americans smokes. Even though 70 percent of smokers report that they would like to quit, only 5 percent do so successfully.
In this study, the researchers manipulated the levels of nicotine dependence and cigarette craving among 15 smokers and then scanned their brains using positron emission tomography, or PET scans, to see which areas of the brain were most active.
Three specific regions of the brain demonstrated changes in activity when the smokers craved cigarettes versus when they did not.
One region that lights up, called the thalamus, is considered to be the key relay point for sensory information flowing into the brain. Some of the symptoms of withdrawal among people trying to quit stem from the inability to focus thoughts and the feeling of being overwhelmed, and could thus be explained by changes in this region, according to the researchers. The researchers found that changes in this region were most dramatic among those who said they smoked to calm down when under stress.
Another region that lights up is a part of the pleasure system of the brain. Changes in this region, called the striatum, were most notable in people who smoked to satisfy craving and for pleasurable relaxation, the researchers said.
A third region that lights up, called the anterior cingulate cortex, is vital to cognitive functions such as conflict, self regulation, decision making and emotion. People whose brain scans showed the most differences in this region also reported that they smoked to manage their weight.
“This knowledge gives us new clues about brain mechanisms underlying addiction to cigarettes and could allow us design better methods to help smokers quit,” Rose said.
Rose and his colleagues are now planning to perform brain scans on smokers undergoing nicotine replacement therapy, such as the nicotine patch, to determine how these treatments affect the same regions of the brain.
Other researchers participating in the study were Frederique M. Behm, Alfred N. Salley, James E. Bates, R. Edward Coleman, Thomas C. Hawk and Timothy G. Turkington.

Source: www.dukemednews March 2007

* Popular and clinical lore support the strong connection between smoking and alcohol consumption.

* Adolescent smokers appear to have a greater vulnerability to developing alcohol-use disorders.

* Results indicate that smoking “primes” the brain for subsequent addiction to alcohol and possibly other drugs.

Both academic studies and casual observation support the view that smokers tend to drink, and drinkers tend to smoke. New research using nationally representative data from the U.S. finds that smokers – particularly adolescent smokers – clearly have a greater vulnerability to alcohol-use disorders (AUDs) than do non-smokers.

Results are published in the December issue of Alcoholism: Clinical & Experimental Research.

“Smoking and alcohol – separately, or together – account for more than 20 percent of deaths in the United States,” said Richard A. Grucza, an epidemiologist at Washington University School of Medicine and corresponding author for the study. “Cigarettes and alcohol are also known to be ‘gateway’ drugs, that is, the overwhelming majority of illegal drug users begin their use with one or both of these legal drugs.”

“We have known about the link between cigarette smoking and alcohol use for a while, but we have not really asked the question, as the authors here asked, whether use of one could increase the vulnerability of becoming addicted to the other,” said Kevin W Chen, associate professor at the University of Maryland School of Medicine.

“Ours was the first,” added Grucza, “to examine quantity of drinking in relationship to smoking and AUDs. Our central questions were: Can this association be explained by the fact that smokers are heavier drinkers, or is there something else going on? In other words, do smokers appear to be more sensitive to the effects of alcohol?” The short answer appears to be yes.

Researchers examined data from an aggregate of 2002 through 2004 U.S. National Surveys on Drug Use and Health. Randomly selected, household-dwelling adolescents and young adults (n=74,836) were selected from the non-institutionalized and civilian American population and queried about their drinking and smoking practices.

Results indicate that smokers – particularly adolescent smokers -have a greater vulnerability to AUDs than do non-smokers.

“In general, smokers were at more than a 50 percent higher risk, although the differences were larger in younger adolescents and among light drinkers,” said Grucza. “For example, among 15- to 17-year-olds who drank fewer than eight drinks in the month before the survey, more than 20 percent reported an AUD, compared with about five percent among the non-smoking group with the same level of drinking. We conclude that, although smokers do drink higher rates of alcohol, this alone does not explain their higher vulnerability to AUDs.”

Grucza said that these findings go beyond the popular view that bad behaviors like smoking and drinking to excess simply tend to “go together,” especially during adolescence. “It seems that smoking makes the adolescent brain more vulnerable to other addictions,” he said. “Addictive drugs all act on a part of the brain that is described as the ‘central reward circuitry.'” Once this system is exposed to one drug, the brain may become more sensitive to the effects of other drugs, as demonstrated by a number of rodent studies.

“Studies like this will set up an alert – for those who consider adolescent smoking tolerable – to rethink the issue, or perceive the problem differently,” noted Chen. “Although we do not know the exact causal relation between the two, the damage to our health is so severe that we need to create a more objective image to reject both smoking and drinking among adolescents.”

“Ours is the first study to – establish a correlation between adolescent smoking and AUDs that cannot be explained by heavier drinking,” said Grucza. “Now we, and hopefully others, need to investigate whether or not smoking actually causes adolescents to be more susceptible to AUDs. Our results are in line with an emerging literature that shows adolescence may be a unique window of vulnerability for addictions development. If it is proven that nicotine directly impacts vulnerability to alcoholism and other addictions, then that is a new, strong message to add to the health-education arsenal. However, even if this correlation is completely non-causal, these results can help to identify kids who are at risk for AUDs.”

Source:Alcoholism: Clinical & Experimental Research. (ACER) Article Date: 30 Nov 2006 – 13:00 PDT

Filed under: Addiction,Alcohol,Nicotine :

Research Summary

Smoking among young adults has plummeted since California implemented a groundbreaking tobacco-control plan 12 years ago, according to new research from the University of California at San Diego.

The California Tobacco Control Program, established in 1989, has been credited with reducing smoking among all adult smokers, but the decline among young adults has been especially striking, researchers said. Notably, cessation rates among young Californians were higher than among young adults in New York and New Jersey, which have similarly high tobacco prices but lack comprehensive stop-smoking campaigns, as well as compared to young adults in tobacco-growing states (TGS).

“We were surprised to find that, since the advent of the California campaign, young people have increased their rate of quitting by 50 percent, far more than their older counterparts,” said study author Karen Messer, Ph.D. “It used to be that smokers over age 50 were the ones quitting because they understood the health consequences of smoking …
“These young adults have grown up in a tobacco-controlled climate, where smoking isn’t the norm and isn’t socially supported. We may be seeing the first generation who believe it’s not cool to smoke, which could pay huge dividends in their future health.”

Another UCLA study focused on tobacco consumption trends. “We found that there is a national trend of declining cigarette consumption for all age groups, but the most significant by far was observed in California smokers over age 35,” noted researcher Wael K. Al-Delaimy, M.D., Ph.D.
“The data suggest that — compared with states with no tobacco control initiatives (TGS) or states with an increased cigarette price as the principal tobacco control measure (NY/NJ) – California’s comprehensive tobacco control program is more effective in decreasing cigarette consumption for those over age 35.”

Source: journal Tobacco Control April 2007

Nicotine reaches the brain as quickly as 10 seconds after inhalation, triggering feelings of pleasure, increasing heart rate and raising blood pressure.
But alongside the nicotine, smokers breathe in a deadly cocktail of chemicals including arsenic, formaldehyde and polonium.
“Cigarette smoke contains at least 69 different cancer-causing chemicals and thousands of other poisons which can increase the risk of several different types of cancer,” said Ed Yong of Cancer Research.
“Nicotine itself doesn’t cause cancer, it just keeps the smokers hooked,” he added.
Tobacco is so addictive that doctors writing in the Lancet medical journal this year said it should be classified as an illegal drug, on a par with amphetamines and barbiturates.
The government says 70 per cent of smokers want to give up but are held back by the power nicotine has over them.
Only one in five who try quitting manage to abstain for a year, while just three per cent succeed in breaking the habit by willpower alone, according to statistics compiled by health charity Action on Smoking and Health (ASH).
One in six smokers say they light up within five minutes of waking up, with half having their first cigarette inside the first 30 minutes of the day.
The government says 106,000 people die a year in Britain from smoking-related illnesses.
From July 1 smoking is banned in enclosed public spaces across all of the United Kingdom when England introduces its own prohibition to match those already in place in Scotland, Wales and Northern Ireland.
But while this may help many adults give up, there are some groups who will need much greater assistance, says ASH.
Around a quarter of all adults smoke but among the most disadvantaged, such as single parents on benefit, the rates are as high as 70 per cent.
“It’s a response to stress,” said ASH director Deborah Arnott. “If your life is very stressful then smoking seems to help in some way.”
She said such disadvantaged groups should be prescribed nicotine patches for longer periods than the usual maximum of 12 weeks to help them quit.
“It’s the nicotine they are addicted to, but it’s the smoke that’s killing them,” she said.
Prime Minister Gordon Brown cut the value added tax on nicotine replacement products to five per cent in his last budget as chancellor of the exchequer.
The tax break will last for a year but ASH says the price reduction should be made permanent to help the most addicted and disadvantaged.

Source: June 30, 2007

Filed under: Addiction,Nicotine :

For years, scientists described the human brain as a machine with parts, each part dedicated to controlling different activities. If a part was injured, the function it controlled would be lost permanently. But as Norman Doidge shows in his new book, The Brain That Changes Itself, (Viking) new neurological evidence has emerged showing that the brain can be trained to rewire itself after an injury, such as a stroke or ear or eye damage. Through interviews with neuroscientists and neuron-rehabilitation patients, Doidge also finds that the brain is capable of improving learning disabilities and intellectual and even moral performance through techniques such as repetition of learning and implementation of regular habits. The more we know about these processes, the more doctors can help patients to find other ways perform lost functions.

Doidge is a psychiatrist, psychoanalyst, and researcher on the research faculty at Columbia University’s Center for Psychoanalytic Training and Research, in New York, and the University of Toronto’s Department of Psychiatry.

Source: Hudson Institute August 2007

For years, scientists have known that some people are biologically more susceptible to drug addiction than others, but they have only been able to speculate why.
In the August 15, 2007 issue of the Journal of Neuroscience, researchers at the University of Chicago report on a study that may help answer this question.
They discovered that rats most likely to self-administer addictive drugs had a particular receptor in the brain that is more responsive than the same receptor in rats least likely to self-administer addictive drugs.
This receptor, known as the nicotinic acetylcholine receptor (nAChR), increases excitability within in the brain’s reward centers. In the animals that were more likely to take addictive drugs, the effects of these receptors were much stronger, leading to more profound excitation of the cells and pathways associated with reward.
Stress, and the associated increases in stress hormones, will promote drug-taking behavior regardless of whether an animal is more or less susceptible, say the researchers. They showed that stress also increases the responses of nAChRs within the brain’s reward areas.
“We tested the exploratory behavior of rats in an unfamiliar cage. Rats that explore a new environment for a prolonged period of time were more interested in addictive drugs,” says Daniel McGehee, PhD, associate professor and lead researcher on this study. ” Those rats also had stronger nAChR responses, meaning their brains responded differently to the drugs. We measured receptor activity in the brain’s reward centers that are known to be activated by addictive drugs.”
“This study provides valuable insight into the mechanism of addiction,” says McGehee. “It raises the possibility that nicotinic receptors may be important targets for the treatment of multiple addictions, not just nicotine. Unfortunately, blocking these receptors may also interfere with healthy behaviors that depend upon the same brain circuitry. Precisely where these findings will lead drug treatment strategies is unclear, but this work provides insight into the role of nicotinic receptors in the vulnerability to multiple classes of addictive drugs.”

Source: University of Chicago Medical Center. Published on Eureka Alert August 2007

Drug users who can’t kick the habit can blame a dysfunctional brain for their addiction, according to new research.
A study by the University of Melbourne has found long-term drug users have more difficulty controlling impulses because their frontal cortex is impaired.

The two-year study found opiate users needed to use more of their brains to resist impulses in a test of self control than those who were clean. The findings shed new light on why drug addicts find it so hard to quit, despite the health consequences.
“Drugs can capture and hijack some parts of the brain,” said Dr Murat Yucel, a lead researcher in the study. In this study we found the frontal cortex, an area that is essential for exercising control over thoughts and behaviours, was working inefficiently. These findings may help explain why it takes addicted individuals enormous effort to exercise control over their drug taking behaviour in the face of adverse consequences and why they are vulnerable to relapse back into uncontrolled, compulsive patterns of use.”
The study – published in the journal, Molecular Psychiatry, last month – also found drug users’ brain cells in the frontal region were less healthy than normal. The research shows drug taking is not a matter of choice for long-term users, who have a reduced biological capacity to stop, Dr Yucel says.
Researchers will next examine whether reduced brain function is a consequence of addiction or a contributing factor that makes some people more vulnerable to drug abuse. Co-researcher Dan Lubman said the study would likely lead to the development of new strategies for the treatment of addiction.
“These findings tell us that we need to provide a combination of pharmaceutical and psychological treatments that will help bolster the efficiency of the frontal cortex and hence the individual’s ability to stop their urge to use drugs,” he said.

Source: Aug. 2007

A record number of young people were treated for a drugs and alcohol problem last year.
Counsellors in England alone saw 52,294 people aged 13-24, a rise of 12% in two years, according to data from the National Treatment Agency (NTA).
There’s been a sharp drop in those addicted to ‘hard’ drugs like heroin.
Instead under-25s are now more likely to have a problem with a cocktail of ‘party’ drugs like cocaine, cannabis and ecstasy, often mixed with alcohol.
Campaigners say treatment services aimed at young adults need to change quickly to deal with what some are calling the biggest shift in drug habits in a generation.
‘Taken it all’
Newsbeat went to a drug treatment scheme in Stockport to speak to 24-year-old Steve, not his real name, from Liverpool.
“It first started when I was 15,” he said.
“Cannabis led to whizz, Es, pills and coke. Alcohol and drugs were a major part of my life for five years.
“When you’re young you hate to be the one left out and most my friends at school were alcohol and drug users.
“I was taking whatever I could get my hands on and mixing them with alcohol. We would come back at one or two in the morning every night and my mum and dad would be fuming.”
Treatment rises
Officials from the NTA say the overall rise in treatment over the last three years does not necessarily mean a record number of young people are abusing drugs and alcohol.
They claim at least part of the increase can be explained by the growth in treatment services.
Young people picked up by the police are also more likely to be drug tested and referred to a treatment centre.
But the figures do show a major change in the kind of drugs young people are getting treated for.
Counsellors are seeing a dramatic shift away from heroin and crack use, the two ‘problem drugs’ typically linked to serious abuse.
18,597 people aged 13-24 were treated for an addiction to those two drugs last year, down 19% in just two years.
At the same time, more young people are having a problem with booze mixed with ‘softer’ party drugs, a phenomenon nicknamed ACCE (pronounced ‘ace’) by drug workers, short for Alcohol plus Cocaine, Cannabis and Ecstasy.
The number of under-25s getting treatment for one or more of those drugs has gone up 44% from 21,744 in 2005/6 to 31,401 in 2007/8.
“Alcohol is cheaper and more available, cannabis is far stronger, cocaine is half the price it used to be and you can get half a dozen ecstasy tablets for £10,” according to Howard Parker, Professor Emeritus at Manchester University, who coined the term ‘ACCE’ last year.
“Put those three together and you’ve got just as serious a problem for health, family life and society as heroin.”
Work carried out by Parker and researchers at Liverpool John Moores University shows the average age of a heroin user in treatment in North West England has risen to 36. The average age of someone with an ACCE problem is just 22.
But while youth services aimed at under-18s can be effective at dealing with an ACCE-type problem, when users hit their 18th birthday they are often forced to switch to an adult-only drug treatment service.
“Those [adult] services are there to deal with heroin and crack users,” said Parker. “The real issue is why there are hardly any services for ACCErs when they get to 18. It’s just pot luck; it’s a postcode lottery.”
Adult drug projects are paid twice as much for treating a heroin and crack user as someone with a powder cocaine or ecstasy problem.
As a result, those services tend to focus on medical treatment like methadone replacement, a drug used to wean heroin users off their addiction.
But there are no ‘replacement’ drugs to treat a cocaine or cannabis problem.
Instead months or even years of therapy and support are needed to get users to manage their drug problem and eventually quit.
Alcohol plus drugs
The man in charge of young people’s drug policy for the National Treatment Agency, Tom Aldridge, told Newsbeat that adult services focus on heroin and crack users for a reason.
“There are very clear links between acquisitive crime and problematic [heroin and crack] drug use,” he said.
“We want to prioritise those drugs because they have more of an impact on society in terms of criminal activity and public health.
“But we are very clear that people should be given a service depending on their need, not depending on their age.
“If you have a 20 or 21-year-old that requires treatment best given by an under-18 service then they should go to that service.”
All under-18 services in England combine alcohol and drug treatment so young people can get detox and therapy for both problems at the same time.
But almost all adult services split alcohol and drugs into two completely separate programmes in different locations with different counsellors and critics say that can often mean young people drop out.
Tom Aldridge accepts that there may be an argument for combining alcohol and drug treatment for over-18s in England, as they have recently decided to do in Northern Ireland.
“We have no responsibility for the alcohol agenda,” he said. “If that were the case, there may well be lots in advantages in that. But it’s not the case at the moment.”
The Stockport solution
But in some parts of the country a handful of treatment services are already changing the way they work to deal with the ACCE phenomenon.
Newsbeat went to see a council-run drug scheme for young people in Stockport that has increased the age range of its patients from 18 all the way up to 25.
Heidi Shaw, who runs the centre called Mosaic, said that decision was a direct result of seeing more young people with recreational drug problems come through the doors.
“We knew those young people would not get help elsewhere,” she said. “Their lives are still being devastated by drugs. They are still having problems with crime, housing, training and employment.
“The same profile of substance misuse is coming through. It’s cannabis, alcohol and then cocaine.”
Mosaic also runs a service to support parents and family members of people in treatment and carries out drug prevention work in Stockport’s 14 schools.
Steve has been getting treatment for his alcohol and drug problems there for four years.
“I feel more comfortable because they seem to understand more about you,” he said. “They contact you virtually every day to see how you are doing.
“I went through detox. They put you in a dry house for a week and give you medication to counteract the effects of alcohol and the cravings.
“Since then I’ve not touched a drop and I’ve got Mosaic to thank for that.
“My life’s changed because I’m off alcohol completely and I’m working on the drugs. Hopefully this time next year, I will be off them as well.”
Source:  BBC Newsbeat 8th June 2009

Smoking marijuana as a teenager could raise the risk of developing schizophrenia and psychotic symptoms as a young adult, according to a new study that compared the prevalence of mental illness among marijuana users and non-users.

Bloomberg News reported March 2 that researcher John McGrath of the University of Queensland, Australia, and colleagues studied 3,801 young-adult sibling pairs and concluded that those who used marijuana the longest (six or more years) were twice as likely to develop schizophrenia or delusional disorders. They also were four times more likely than non-users to score highly on a test gauging psychotic-like experiences.

Higher scores on the test also were seen among those who used marijuana for less than three years.

Source:  March 2010

Nicotine addiction relies on brain receptors that have been difficult to fully study and characterize. Scientists at the University of Colorado in Boulder have demonstrated that an immunolabeling technique can effectively analyze receptor subunits.

Background: Nicotine’s effects on the brain are triggered upon its binding to nicotinic acetylcholine receptors, each of which consists of five subunits: two alphas, one beta, one delta and one gamma. Different combinations of these subunits produce different receptor subtypes, which may vary in their pharmacology, biophysical properties, and distribution. To more fully understand how to interfere with nicotine’s effects in the brain, scientists must first understand where these different receptors are and how they work. Two of the most important subunits, a4 and b2, have been hard to study because current study methods can only locate the fully assembled receptor unit. Researchers wanted to know if an alternative strategy of immunolabeling (i.e., using antibodies to tag individual proteins), which has been fraught with technical challenges, would be able to identify, map, and quantify separate subunits.

Study Design: Scientists at the University of Colorado worked with brain sections of mice genetically engineered to express particular a4 and b2 subunit combinations. Using a sensitive immunolabeling technique, they explored the expression of the a4 and b2 subunits at both the gene and protein levels. Additional mice strains, missing the subunits under study, were used as controls.

What They Found: The two predominant nicotinic receptor subtypes (a4 and b2) were reliably detected using immunolabeling. Expression of the a4 subunit protein was almost universally dependent on b2, whereas most, but not all, b2 subunit protein expression was a4-dependent.

Comments from the Authors: Immunolabeling using specific antibodies offers a powerful approach for mapping the distribution of nicotine receptor subunits and can produce reliable quantitative results.

What’s Next: Similar studies can be designed to locate other nicotine receptor subtypes. In many cases, the antibody recognition sites are inside the cell membrane. It will likely take alternative biochemical approaches to uncover these less accessible sites. A better understanding of receptor composition and function may eventually have important implications for developing interventions at the receptor level.

Source: The study, led by Dr. Paul Whiteaker of the Institute for Behavioral Genetics at the University of Colorado, Boulder, with Dr. Jon Lindstrom of the University of Pennsylvania, was published in volume 499, number 6, pages 1016-1038 (2006) of the Journal of Comparative Neurology.

An analysis that compared the DNA of drug abusers with that of non-abusing controls has identified 89 genes that are likely to contain variants that contribute to addiction vulnerability.

Background: Vulnerability to addiction is a complex trait with strong genetic influences. Since the mid-1990s, scientists have been developing methods and tools to identify and evaluate the functional role of genes and their variants. The impact of such efforts has been greatly enhanced by the Human Genome and International HapMap Projects. By 2001, the first low-resolution genome-wide association studies from the NIDA-IRP’s Molecular Neurobiology Branch were published. Genetic research technology is now able to reliably scan the genome of individuals for genetic variants linked to specific functions.

Study Design: From 1990 to 2005, thousands of people participated in studies at NIDA-IRP’s Molecular Neurobiology Branch, providing self-reports and DSM Diagnostic Interview Schedule scores. From among this pool, researchers identified 980 African-American and European-American “drug abusers” (heavy lifetime use of illegal substances) and 740 controls (no significant history of addictive substances, no abuse, no dependence). Pooled DNA samples, prepared from blood extracted from each group were used to examine a panel of close to 640,000 genetic variations.

What They Found: Using strong statistical models that focused on the overlaps between the samples, this screen identified 89 genes that display clusters of genetic variants that are likely involved in addiction vulnerability. Most of these genes are expressed in the brain. Twenty-one of these genes influence cell adhesion, and nearly all of those are expressed in brain regions implicated in memory processes.

Comments from the Authors: The nature of the addiction-associated genes identified in this study, especially those involved in cell adhesion, suggest the critical role played by dysfunctional nerve cell connections in the addicted brain.

What’s Next: Other genes that emerged from the analysis are being tested in the context of where they are located in the brain and their likely functions: enzymes, transporters, receptors, protein processing, and transcriptional regulation. Results like these highlight characteristics that are common to human addiction and may facilitate efforts to develop targeted prevention and treatment strategies.

Source:The study, led by Drs. George Uhl and Qing-Rong Liu of the Molecular Neurobiology Branch at the National Institutes of Health Intramural Research Program at NIDA in Baltimore, was published in volume 141B, pages 1-8 (2006) of the American Journal of Medical Genetics Part B (Neuropsychiatric Genetics).

Filed under: Addiction :

In this national fellowship report, project directors from the first 10 Reclaiming Futures sites share the lessons they learned in creating and implementing a model for helping teens in trouble overcome drugs, alcohol and crime.

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.

Publication Year: 2007


Reclaiming Futures
Portland State University
527 SW Hall, Suite 400
Portland, or 97201
Phone: 503.725.8911

Filed under: Addiction,Youth :

People with a certain gene variant appear to be at higher risk of cocaine addiction, according to researchers from the Institute of Psychiatry.
Medical News Today reported March 13 that some people have a gene that stops the production of DAT, which regulates removal of extra dopamine in the brain. Cocaine works by limiting DAT, overloading the brain with dopamine.
People who have the DAT-limiting gene were found to be more likely to become addicted to cocaine; those with two copies of the gene were at even higher risk.
“This study is the first large-scale search for a genetic variant influencing the risk of developing cocaine addiction or dependence,” said lead researcher Gerome Breen. “The target we investigated, DAT, is the single most important in the development of cocaine dependence. It made sense that variation within the gene encoding DAT would influence cocaine dependence.”
Source: Proceedings of the National Academy of Sciences.March 2006

Filed under: Addiction,Cocaine :

Long-term cocaine use can alter the function of genes in the brain, leaving “pleasure circuits” stuck in the open position and increasing craving for the drug, according to a new animal study conducted by researchers at the Mount Sinai School of Medicine.
Reuters reported Jan. 9 that researcher Ian Maze and colleagues found that the gene 9A — which produces an enzyme responsible for switching other genes on and off — was repressed in the brains of mice given repeated doses of cocaine. Researchers also found that restoring the activity of gene 9A reversed cocaine preference and craving in lab mice.
“This finding is opening up our understanding about how repeated drug use modifies in long-lasting ways the function of neurons,” said Nora Volkow, director of the National Institute on Drug Abuse.
Source: Science. Jan. 8, 2010

For the first time, federal researchers have broken down the disease of alcoholism into five distinct subtypes, which experts say should help provide more targeted treatment for problem drinkers.
The National Institute on Alcohol Abuse and Alcoholism (NIAAA) reported June 28 that the five new subtypes include “Young Adult,” “Young Antisocial,” “Functional,” “Intermediate Familial,” and “Chronic Severe.”
“Our findings should help dispel the popular notion of the ‘typical alcoholic,'” said study lead author Howard B. Moss, M.D., associate director of NIAAA’s Clinical and Translational Research division. “We find that young adults comprise the largest group of alcoholics in this country, and nearly 20 percent of alcoholics are highly functional and well-educated with good incomes. More than half of the alcoholics in the United States have no multigenerational family history of the disease, suggesting that their form of alcoholism was unlikely to have genetic causes.”
“Clinicians have long recognized diverse manifestations of alcoholism, and researchers have tried to understand why some alcoholics improve with specific medications and psychotherapies while others do not,” added NIAAA Director Ting-Kai Li, M.D. “The classification system described in this study will have broad application in both clinical and research settings.”
Moss and colleagues developed their subtypes based on survey respondents’ family history of alcoholism, age of onset of regular drinking and alcohol problems, symptom patterns of alcohol dependence and abuse, and the presence of additional addictive and mental disorders.
They found that 31.5 percent of alcoholics in the U.S. fall under the Young Adult subtype, who have relatively low rates of other drug or mental-health problems, low rates of family alcoholism, and rarely seek help for their drinking. The Young Antisocial subtype accounts for 21 percent of alcoholics, the researchers said; this category includes drinkers in their mid-20s who tend to have early onset of drinking, a family history of alcoholism, mental-health problems, and co-occurring tobacco or illicit-drug use. This group was more likely to have sought help for drinking than the Young Adult subtype.
Members of the Functional subtype, accounting for 19.5 percent of alcoholics, are typically middle-aged and well-educated, with stable jobs and families. They are relatively likely to have a family history of alcoholism and a personal history of major depressive illness in their lives, and about half are smokers. A similar percentage (19 percent) of American alcoholics fall into the Intermediate subtype, who are middle-aged and more likely to have a family history of alcoholism and mental illness than the Functional subtype. Most are smokers, problems with other drug use is relatively common, and about a quarter have sought help for their drinking.
The final subtype identified by Moss and colleagues, Chronic Severe, covers 9 percent of alcoholics. Most are middle-aged, with early onset drinking, high rates of antisocial personality disorders and criminality, and a strong family history of alcoholism. This subtype is typified by the highest rates of mental-health problems, smoking, and illicit-drug use, and two-thirds of this group has sought treatment for their drinking problems
Source: Drug and Alcohol Dependence. June 2007

Filed under: Addiction,Alcohol :

Clinical studies, like those by Barbara Mason at Scripps Institute, have documented a marijuana withdrawal syndrome among a minority of users. Are we prepared to say that marijuana is addictive? Why didn’t we identify this syndrome years ago?

Nora Volkow: Absolutely, there is no doubt that some users can become addicted to marijuana. In fact, well over half of the close to 7 million Americans classified with dependence or abuse of an illicit drug are dependent on or abuse marijuana. It is important to clarify that while withdrawal is one of the criteria used to diagnose an addiction (which also includes compulsive use in spite of known adverse consequences), it is possible for an individual to suffer withdrawal symptoms without he or she being addicted to an abused substance.

Now, to answer your specific question, the reason for the relatively late realization that people who abuse marijuana can develop a cannabis withdrawal syndrome (CWS) if they try to quit is probably the result of at least two factors. First is the fact (which you hint at already) that a clinically relevant cannabis withdrawal syndrome may only be expected in a subgroup of cannabis-dependent patients. This may be partially explained by marijuana’s uptake into and slow release from fat cells, which can occur over days or weeks after last use. Thus, cessation of marijuana use may not be so abrupt, and could thereby diminish signs of withdrawal. The second factor relates to the small to negligible associations between recalled and prospectively assessed withdrawal symptoms, which may have precluded many previous, recall-based studies from detecting or properly characterizing CWS. It is also worth pointing out that other addictions (e.g., cocaine) were also not initially thought of as capable of triggering withdrawal symptoms.”

People with clinical addictions know first-hand the ravages the disease can take on almost every aspect of their lives.
So why do they continue addictive behaviors, even after a period of peaceable abstinence Some answers appear rooted in regions of the brain active during decision making.
“It’s perhaps not just that people are slaves to pleasure, but that they have trouble thinking through a decision,” said Charlotte Boettiger, an assistant professor of psychology at the University of North Carolina at Chapel Hill, and lead author of a study in the December issue of the Journal of Neuroscience that took a novel tack in addiction imaging research. Our data suggest there may be a cognitive difference in people with addictions,” Boettiger said. “Their brains may not fully process the long-term consequences of their choices. They may compute information less efficiently.”
The study also found that a variant of the COMT gene, which controls the level of the neurotransmitter dopamine in the cortex, was associated with a tendency to make impulsive decisions and with high activity in certain brain areas during decision making. Current medications for addictions are not universally effective; many either mimic the addictive substance to help people get through withdrawal periods or block the substance to prevent its effects. For stimulants, such as methamphetamines, there are no therapies yet, Boettiger said.
“What’s exciting about this study is that it suggests a new approach to therapy. We might prescribe medications, such as those used to treat Parkinson’s or early Alzheimer’s disease, or tailor cognitive therapy to improve executive function,” said Boettiger, who led the study as scientist at the University of California, San Francisco’s Gallo Clinic and Research Center. I am very excited about these results because of their clinical implications,” said Dr. Howard Fields, a professor of neurology at UCSF and an investigator in the Gallo Center.
“The genetic findings raise the hopeful possibility that treatments aimed at raising dopamine levels could be effective treatments for some individuals with addictive disorders,” said Fields, who is senior author of the study. Most addiction imaging studies have focused on the brain response to drug-related stimuli.
Boettiger used functional magnetic resonance imaging (fMRI), which shows brain activity while a subject performs a function, to see what happened inside their heads when sober alcoholics and people in a non-alcoholic control group made decisions between immediate and delayed rewards. Boettiger recruited 24 subjects; 19 provided fMRI data, nine were recovering alcoholics in abstinence and 10 had no history of substance abuse. Another five were included in the genotyping analysis.
At the fMRI research facility at the University of California, Berkeley, the subjects were asked to decide between receiving a small monetary award immediately or wait for a larger payoff. The scenarios were hypothetical, but the tasks measured rational thinking and impulsivity; sober alcoholics chose the “now” reward almost three times more often than the control group, reflecting more impulsive behavior. While decisions were being made the imaging detected activity the predicted individual choice in regions associated with decision making — the posterior parietal cortex, the dorsal prefrontal cortex, the anterior temporal lobe and the orbital frontal cortex.
People who sustain damage to the orbital frontal cortex generally suffer impaired judgment; they manage money poorly and act impulsively. Boettiger’s study revealed reduced activity in the orbital frontal cortex in the brains of subjects who preferred “now”over “later,” most of whom had a history of alcoholism. The orbital frontal cortex activity may be a neural equivalent of long-term consequences. “Think of the orbital frontal cortex as the brakes,” Boettiger said. “With the brakes on, people choose for the future; without the brakes they choose for the short-term gain.”

The dorsal prefrontal cortex and the parietal cortex often form cooperative circuits, and this study found that high activity in both is associated with a bias toward choosing immediate rewards.
The frontal and parietal cortex are also involved in working memory — being able to hold data in mind over a short delay. When asked to choose between $18 now or $20 in a month, the subjects had to calculate how much that $18 (or what it could buy now) would be worth in a month and then compare it to $20 and decide whether it would be worth the wait. The parietal cortex and the dorsal prefrontal cortex were much more active in people unwilling to wait. This could mean, Boettiger said, that the area is working less efficiently in those people.
The COMT gene has two common variants with a single amino acid difference at position 158; valine (Val) or methionine. The Val form of the gene is associated with lower dopamine levels, and Boettiger’s study showed that people with two copies of the Val allele (resulting in the lowest dopamine levels) had significantly higher frontal and parietal activity and chose now over later significantly more often.
“We have a lot to learn,” Boettiger said. But the data take a significant step toward being able to identify subtypes of alcoholics, which could help tailor treatments, and may people who are at risk for developing addictions and provide earlier intervention. The bigger picture, Boettiger said, is that her study provides more evidence that addiction is a disease, something even some of her peers do not yet believe.
“It’s not unlike chronic diseases, such as diabetes,” she said. “There are underlying genetic and other biological factors, but the disease is triggered by the choices people make.”
“It wasn’t that long ago that we believed schizophrenia was caused by bad mothers and depression wasn’t a disease. Hopefully, in 10 years, we’ll look back and it will seem silly that we didn’t think addiction was a disease, too.”
Source: 30th Dec. 2007

Filed under: Addiction :

Center for Bioinformatics, National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing, People’s Republic ofChinaThe research reveals that a subject’s brain with low beta-endorphin levels becomes accustomed to the presence of an exogenous surplus, diminishing its own supply and triggering dependence on an external source–in this case, alcohol.
According to a study by the research group “Alcoholism and drug addiction”, of the University of Granada, although there are no specific reasons to become alcoholic, many social, family, environmental, and genetic factors may contribute to its development. Thanks to this study, researchers have shown that the lack of endorphin is hereditary, and thus that there is a genetic predisposition to become addicted to alcohol. Beta-endorphin is a kind of “morphine” released by the brain in response to several situations, such as pain. In this way, beta-endorphins can be considered “endogenous analgesics” to numb or dull pains.
Researchers have focused on the low beta-endorphin levels in chronic alcohol abusers. According to José Rico Irles , professor of Medicine of the UGR, and head of the research group, this low beta-endorphin level determines whether someone may become an alcoholic. When a subjects’ brain with low beta-endorphin levels gets used to the presence of an exogenous surplus, then, when its own production stops, a dependence starts on the external source: alcohol.
Who may become and alcohol abuser?
A total of 200 families of the province of Granada participated in the research. There was at least one chronic alcoholic parent in each family. From birth, each subject presented predetermined beta-endorphin levels. However, children of this population group aged between 6 months and 10 years old, registered lower beta-endorphin levels than other children of the same age. “These levels were even lower in children whose both parents were alcohol abusers”, the researcher states. According to researcher, although alcohol consumption does not affect all people in the same way, differences in endorphin levels make some subjects more vulnerable to alcohol. Therefore, they are more likely to become alcohol dependent.
Beta-endorphins constitute a useful biological marker to identify specifically those subjects who have a higher risk of developing alcohol abuse, the research claims. Regarding the results of this study, professor Rico states the following: “alcohol-abuse prevention must consist of locating and identifying genetically predisposed subjects.” More campaigns for children and teenagers should be launched before these young people make contact with alcohol. Alcohol awareness is fundamental to prevent addiction, the researcher affirms, because alcohol is a drug with reversible effects up to a point.
In relation to the “botellculture” (Botell’s a Spanish custom in which young people congregate in a park, street or any open public place to share alcoholic drinks and converse before entering bars, nightclubs, discos, etc.), José Rico states that some of these “social drinkers” could have low beta-endorphin levels and, therefore, a higher predisposition to become “solitary drinkers” and to develop alcohol abuse. 21st Dec. 2008

Filed under: Addiction,Alcohol :

Drug addiction is a serious worldwide problem with strong genetic and environmental influences. Different
technologies have revealed a variety of genes and pathways underlying addiction; however, each individual
technology can be biased and incomplete. We integrated 2,343 items of evidence from peer-reviewed publications between 1976 and 2006 linking genes and chromosome regions to addiction by single-gene strategies, microrray, proteomics, or genetic studies. We identified 1,500 human addiction-related genes and developed KARG (http://karg., the first molecular database for addiction-related genes with extensive annotations and a friendly Web interface. We then performed a meta-analysis of 396 genes that were supported by two or more independent items of evidence to identify 18 molecular pathways that were statistically significantly enriched, covering both upstream signaling events and downstream effects. Five molecular pathways significantly enriched for all four different types of addictive drugs were identified as common pathways which may underlie shared rewarding and addictive actions, including two new ones, GnRH signaling pathway and gap junction. We connected the common pathways into a hypothetical common molecular network for addiction. We observed that fast and slow positive feedback loops were interlinked through CAMKII, which may provide clues to explain some of the irreversible features of addiction.

The addiction-related genes, (common) pathways, and networks were traditionally studied experimentally. The
explosion of genomic and proteomic data in recent years both enabled and necessitated bioinformatic studies of
addiction. Integration of data from multiple sources could remove biases of any single technology platform, and
statistical and network analysis of the integrated data could uncover high-level patterns not detectable in any individual
study. For instance, our analysis revealed not only many pathways already implicated in addiction [34–38], but also
new ones such as GnRH signaling pathway and gap junction, as well as the coupled positive feedback loops through
CAMKII. They could serve as interesting hypotheses for further experimental testing.

The collection of addiction-related genes and pathways in KARG, the first bioinformatic database for addiction, is the
most comprehensive to date. However, as new technologies continue to be developed and used, more and more genes will
be linked to addiction. In 2004, a paper asked why proteomics technology was not introduced to the field of drug addiction
[5]; since then eleven studies have identified about 100 differentially expressed proteins in drug addiction. Tillingarray
technology, another new strategy for whole-genome identification of transcription factors binding sites, has been
used to identify targets of CREB, an important transcription factor implicated in drug addiction [39]. In addition, as 100 K
and 500 K SNP arrays have been introduced recently, whole genome association studies will also identify more closely
packed and unbiased hypothesis-free vulnerable positions [40]. We will continue to integrate new data and update the
gene list and molecular pathways toward a better understanding of drug addiction.

Source: Li CY, Mao X, Wei L (2008) Genes and (common) pathways underlying drug addiction. PLoS Comput Biuo 4(1):e2. doi:10.1371/journal.p.c

The above article is of extreme interest – and in order to make the details more informative for non-specialist readers Dr. Stuart Reece from Australia has written the following explanations:

The paper means that many addiction have several links in common at the molecular level.

Many major pathways to intracellular signalling are commandeered by the various addictions which have much in common. The addictions documented are tobacco, alcohol, opiates (heroin morphine methadone) and cocaine.

The paper is a computational biology paper which means that supercomputers are used to study 2343 items which have been published in the molecular literature relating to the molecular alterations induced by drug addiction.

Its very essence and principal strongly supports my long-standing contention that molecular research could be much better undertaken in this area, and much more aggressively pursued. This paper is from China.

Of course one of the most difficult parts about addiction is the way in which behaviour which initially is volitional, becomes altered to be habitual and refractory to what would normally be the messages to desist the addictive and destructive behaviours.

What is so revolutionary about the paper -beyond providing a very concise synthesis of several vast scientific literatures – is two things:

1) The way in which the institution of irreversible (or at least refractory) changes are described at the molecular level – in other words the institution of hard core addiction and perturbed memories and behaviours
2) The critically important list of molecular pathways which are identified as key components of the cell machinery which are commandeered and effectively pirated or hijacked.

The paper suggests that when fast and slow acting feedback loops interact within the cell (particularly neuron and glial cell) circuitry changes can become irreversible. This is the molecular correlate of the behavioural change which so disturbs the world, addicts and other people.

The list of the major pathways which are perturbed by addiction is absolutely central to any modern understanding of this subject, and strongly expose the terrible fallacies of the legalization arguments. A brief list of some of these and concise notes as to their significance is as follows.

1) CAMKII – Calcium-calmodulin kinase II – this is a key co-stimulating and triggering factor of many of the key cell reactions, particularly relating to synaptic transmission, growth, movement, cell division and growth, coagulation and thousands of reactions in the cell.

2) Synaptic Transmission – this is the basic building block of neural transmission and the molecular substrate of thinking,. remembering, feeling and everything neural. Indeed the article highlights also gap junction formation. These are critical communicating points not only of physical adhesion but also for new synapse formation and cellular cross-talk as occurs between neurons and glial cells in the brain. Important communications have recently been worked out where not only are neurons involved in neural process, but glial cells also have important active and supportive and facilitatory (controlling role). Gap junctions are key features of this regulation and cross talk. synapses are formed subsequent to gap junction formation and intracellular cross talk. If these are disturbed than the key synapses, on which depend memory emotion mood and perception cannot form normally and the neural circuit looses its plasticity. This is particularly true of the new nerve cells entering the circuit and providing key contributions to plasticity which is the molecular substrate of learning.

3) Glutamate and dopamine dependent neural stimulation are also featured which are key transmitters of synaptic information in the brain and long known to be involved in addiction. Importantly they are also involved in age dependent decline in brain function, and this explains the obvious clinical and experimental parallels between brain ageing and the plethora of neuropsychiatric disorders in all the various drug addictions (ie. tobacco, alcohol, cocaine, opiates and especially cannabis).

4) MAP Kinases / ERK kinases (mitogen activated and extracellular related kinases – kinases add a high energy phosphate group to various substrates particularly enzymes which typically up-regulate their activity). These are key pathways long known to be related to cell growth. They are also involved in cancer induction. This fits again with the pro-ageing phenomena mentioned above, and also the incidence of cancer in various addictions (tobacco, alcohol and cannabis).

5) Gonadotrophins releasing hormone. Whilst much work has centred on stress as a trigger for relapse into drug use often focussing on CRH (corticotrophin releasing hormone and the cortisol system in the adrenal cortex) , relatively little has examined the role of the stress system as relates to gonadal function. This is curious to some extent as the loss of the menstrual period in the female, the lowered sperm count in males, loss of libido, osteoporosis (in part gonadally determined in that sex steroids are known in both male and female to be related to maintenance of bone density) and their impact on cardiovascular disease (with females enjoying much greater protection than males, which has long been attributed to the influence of estrogen) have all been recognized for a long period. This finding suggests that just as the general systemic stress system is activated by addiction so is the gonadal one. This might account for several of the findings of addiction, and relate to many of the differences in addiction between the sexes.

6) PKA PKC (protein kinases A and C) are also major intracellular kinases and pivotal points of intracellular cell signalling for a host of pathways. Their implication implies massive pirating of the intracellular transduction cascades.

7) The insulin signalling pathway (Table 1). I had not seen evidence of the involvement of this pathway before in the addiction literature. It is the great star of the ageing literature – more has been written on this pathway in the ageing literature than any other pathway. It is a prime candidate to mediate the pro-ageing effects of addition which my clinic is increasingly documenting, and has also been noted (in part) by studies from the NIH, Johns Hopkins and Boston University hospitals. This is a very important finding and again means the nemesis of the lying legalization juggernaut. It is important to realize that this has tremendous popular appeal. by getting the message out that addiction makes you old ugly decrepit and demented – young people – particularly young females who are normally pre-occupied with beauty – should be warned away from its horrors. This was particularly evident with the interest shown by a north American fashion magazine in the publication of our own work on premature hair graying in drug addiction.

8) VEGF (Vascular endothelial growth factor). This is a key molecule which has an established role in the formation of new blood vessels. It is also involved in cancer development, and stem cell activity. Brain stem cell growth (neurogenesis) has been shown to be blood dependent. Whilst the exact reasons for the blood to be involved in stem cell action, VEGF has been shown to be one of the key factors which facilitates neurogenesis. BDNF (brain derived growth factor ) is another principal determinant of neurogenesis, although many other factors have also been listed). since these new nerve cells are key to memory and mood and brain circuit activity, inhibition or impeding of this process by interfering with VEGF pathways, suggests irreversible damage to these key cells. It should be noted that it is not yet possible to image neurogenesis either clinical or in the living experimental animal, although this is an area of intense investigation in many labs around the world.

9) Protein folding abnormalities . This leads to prion diseases like Jacob Kreuzefeldt disease and mad cow disease. Alzheimer’s disease is also a disease in part of protein misfolding. This is what leads to the development of the senile plaques which are made up of insoluble beta amyloid particles which form macroaggregates and are associated with cell tangles and synaptic dysfunction in Alzheimer’s disease. The exact molecular pathogenesis of this disorder is however not well understood. This is a terrible blow to the legalizers. To suggest that addiction is related to protein folding disorders is a terrible thing, particularly when this is an area of such active investigation globally. There are whole research departments which are devoted to abnormalities of protein folding.

Source: Chuan-Yun Li, Xizeng Mao, Liping Wei*
Center for Bioinformatics, National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing, People’s Republic ofChina

Filed under: Addiction :

NIDA Research Reveals Subconscious Signals Can Trigger Drug Craving Circuits

Using a brain imaging technology called functional magnetic resonance imaging (fMRI), scientists have discovered that cocaine-related images trigger the emotional centers of the brains of patients addicted to drugs — even when the subjects are unaware they’ve seen anything. The study, published Jan. 30 in the journal PLoS One, was funded by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health (NIH).

A team of researchers at the University of Pennsylvania, led by Dr. Anna Rose Childress and Dr. Charles O’Brien, showed cocaine patients photos of drug-related cues like crack pipes and chunks of cocaine. The images flashed by in just 33 milliseconds — so quickly that the patients were not consciously aware of seeing them. Nonetheless, the unseen images stimulated activity in the limbic system, a brain network involved in emotion and reward, which has been implicated in drug-seeking and craving.

“This is the first evidence that cues outside one’s awareness can trigger rapid activation of the circuits driving drug-seeking behavior,” said NIDA director Dr. Nora Volkow. “Patients often can’t pinpoint when or why they start craving drugs. Understanding how the brain initiates that overwhelming desire for drugs is essential to treating addiction.”

To verify that the patterns of brain activity triggered by the subconscious cues reflected the patients’ feelings about drugs, Childress and her colleagues gave the patients a different test two days later, allowing them to look longer at the drug images. The patients who demonstrated the strongest brain response to unseen cues in the fMRI experiment also felt the strongest positive association with visible drug cues. Childress notes, “It’s striking that the way people feel about these drug-related images is accurately predicted by how strongly their brains respond within just 33 milliseconds.”

Childress and her colleagues also found that the regions of the brain activated by drug images overlapped substantially with those activated by sexual images. This finding supports the scientific consensus that addictive drugs usurp brain regions that recognize natural rewards needed for survival, like food and sex.

According to Childress, these results could improve drug treatment strategies. “We have a brain hard-wired to appreciate rewards, and cocaine and other drugs of abuse latch onto this system. We are looking at the potential for new medications that reduce the brain’s sensitivity to these conditioned drug cues and would give patients a fighting chance to manage their urges.”

Source: 29.01.08

Study could potentially help clinicians treat marijuana addiction

Research by a group of scientists studying the effects of heavy marijuana use suggests that withdrawal from the use of marijuana is similar to what is experienced by people when they quit smoking cigarettes. Abstinence from each of these drugs appears to cause several common symptoms, such as irritability, anger and trouble sleeping – based on self reporting in a recent study of 12 heavy users of both marijuana and cigarettes.

“These results indicate that some marijuana users experience withdrawal effects when they try to quit, and that these effects should be considered by clinicians treating people with problems related to heavy marijuana use,” says lead investigator in the study, Ryan Vandrey, Ph.D., of the Department of Psychiatry at the Johns Hopkins University School of Medicine.

Marijuana is the most widely used illicit drug in the United States. Admissions in substance abuse treatment facilities in which marijuana was the primary problem substance have more than doubled since the early 1990s and now rank similar to cocaine and heroin with respect to total number of yearly treatment episodes in the United States, says Vandrey.

He points out that a lack of data, until recently, has led to cannabis withdrawal symptoms not being characterized or included in medical reference literature such as the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, (DSM-IV) or the International Classification of Diseases, 10th edition (ICD-10). Since the drafting of the DSM-IV in 1994, an increasing number of studies have surfaced suggesting that cannabis has significant withdrawal symptoms. What makes Vandrey’s recent study unique is that it is the first study that compares marijuana withdrawal symptoms to withdrawal symptoms that are clinically recognized by the medical community – specifically the tobacco withdrawal syndrome.

“Since tobacco withdrawal symptoms are well documented and included in the DSM-IV and the IDC-10, we can infer from the results of this comparison that marijuana withdrawal is also clinically significant and should be included in these reference materials and considered as a target for improving treatment outcomes,” says Vandrey.

Vandrey added that this is the first “controlled” comparison of the two withdrawal syndromes in that data was obtained using rigorous scientific methods – abstinence from drugs was confirmed objectively, procedures were identical during each abstinence period, and abstinence periods occurred in a random order. That tobacco and marijuana withdrawal symptoms were reported by the same participants, thus eliminating the likelihood that results reflect physiological differences between subjects, is also a strength of the study.

Interestingly, the study also revealed that half of the participants found it easier to abstain from both substances than it was to stop marijuana or tobacco individually, whereas the remaining half had the opposite response. “Given the general consensus among clinicians that it is harder to quit more than one substance at the same time, these results suggest the need for more research on treatment planning for people who concurrently use more than one drug on a regular basis,” says Vandrey.

Vandrey’s study, which appears in the January issue of the journal Drug and Alcohol Dependence, followed six men and six women at the University of Vermont in Burlington and Wake Forest University School of Medicine in Winston-Salem, N.C., for a total of six weeks. All were over 18 (median age 28.2 years), used marijuana at least 25 days a month and smoked at least 10 cigarettes a day. None of the subjects intended to quit using either substance, did not use any other illicit drugs in the prior month, were not on any psychotropic medication, did not have a psychiatric disorder, and if female, were not pregnant.

For the first week, participants maintained their normal use of cigarettes and marijuana. For the remaining five weeks, they were randomly chosen to refrain from using either cigarettes, marijuana or both substances for five-day periods separated by nine-day periods of normal use. In order to confirm abstinence, patients were given daily quantitative urine toxicology tests of tobacco and marijuana metabolites. Withdrawal symptoms were self reported on a daily basis Monday through Friday using a withdrawal symptom checklist that listed scores for aggression, anger, appetite change, depressed mood, irritability, anxiety/nervousness, restlessness, sleep difficulty, strange dreams and other, less common withdrawal symptoms. Patients also provided an overall score for discomfort they experienced during each abstinence period.

Results showed that overall withdrawal severity associated with marijuana alone and tobacco alone was of similar frequency and intensity. Sleep disturbance seemed to be more pronounced during marijuana abstinence, while some of the general mood effects (anxiety, anger) seemed to be greater during tobacco abstinence. In addition, six of the participants reported that quitting both marijuana and tobacco at the same time was more difficult than quitting either drug alone, whereas the remaining six found that it was easier to quit marijuana or cigarettes individually than it was to abstain from the two substances simultaneously.

Vandrey recognizes that the small sample size is a limitation in this study, but the results are consistent with other studies indicating that marijuana withdrawal effects are clinically important.

Source: :
Eric Vohr Johns Hopkins Medical Institutions

Although detoxification cannot, in itself, be considered a treatment for addiction, it is one of the most pivotal phases. In order to facilitate entry into recovery and/or rehabilitation programs, a detoxification treatment has to be experienced as easy and safe by the patient. In consideration of the many inconveniences related to standard withdrawal treatments, there is an interest in developing alternative pharmacological strategies. The main rationales for using anticonvulsants in substance-abuse patients are their lack of addiction potential, evidence support a role of kindling mechanisms in withdrawal syndromes and their efficacy in comorbid psychiatric disorders. The available data currently support the utilization of carbamazepine as a treatment for detoxification from benzodiazepines, alcohol and opiates, and as a useful agent to reduce cocaine consumption. The use of valproate is well corroborated for alcohol detoxification and it seems to be a promising treatment for the reduction of cocaine use; however, it has been found to be ineffective against benzodiazepine withdrawal symptoms. Some preliminary data suggest that lamotrigine could be useful in opiate and cocaine dependence. Gabapentin shows potential as a treatment for cocaine dependence, and some case reports have stimulated interest in this agent for alcohol and benzodiazepine detoxification. Due to its particular pharmacological profile, topiramate is one of the most interesting newer anticonvulsants. It has been found to be efficacious in opiate and possibly benzodiazepine detoxification and also has theoretical potential as a preventive therapy.

Source: Drugs Today (Barc). 2004 Jul;40(7):603-19. .

Filed under: Addiction :

University of Washington researchers say that animal studies show that methamphetamine use causes lasting changes in the brain’s dopamine system, making it especially difficult for users to stop using the drug.
HealthDay News reported April 9 that researcher Nigel Bamford and colleagues found that long-term methamphetamine use depressed the synaptic dopamine-release system in the corticostriatal area of the brain — a condition that gets temporarily reversed when a dose of methamphetamine is administered.
Researchers said that methamphetamine appears to cause long-term changes in certain dopamine receptors and with the neurotransmitter acetylcholine