How we get addicted!

I was driving up the Massachusetts Turnpike one evening last February when I knocked over a bottle of water. I grabbed for it, swerved inadvertently–and a few seconds later found myself blinking into the flashlight beam of a state trooper. „How much have you had to drink tonight, sir?“ he demanded. Before I could help myself, I blurted out an answer that was surely a new one to him. „I haven’t had a drink,“ I said indignantly, „since 1981.“

It was both perfectly true and very pertinent to the trip I was making. By the time I reached my late 20s, I’d poured down as much alcohol as normal people consume in a lifetime and plenty of drugs–mostly pot–as well. I was, by any reasonable measure, an active alcoholic. Fortunately, with a lot of help, I was able to stop. And now I was on my way to McLean Hospital in Belmont, Mass., to have my brain scanned in a functional magnetic-resonance imager (fMRI). The idea was to see what the inside of my head looked like after more than a quarter-century on the wagon.

Back when I stopped drinking, such an experiment would have been unimaginable. At the time, the medical establishment had come to accept the idea that alcoholism was a disease rather than a moral failing; the American Medical Association (AMA) had said so in 1950. But while it had all the hallmarks of other diseases, including specific symptoms and a predictable course, leading to disability or even death, alcoholism was different. Its physical basis was a complete mystery–and since nobody forced alcoholics to drink, it was still seen, no matter what the AMA said, as somehow voluntary. Treatment consisted mostly of talk therapy, maybe some vitamins and usually a strong recommendation to join Alcoholics Anonymous. Although it’s a totally nonprofessional organization, founded in 1935 by an ex-drunk and an active drinker, AA has managed to get millions of people off the bottle, using group support and a program of accumulated folk wisdom.

While AA is astonishingly effective for some people, it doesn’t work for everyone; studies suggest it succeeds about 20% of the time, and other forms of treatment, including various types of behavioral therapy, do no better. The rate is much the same with drug addiction, which experts see as the same disorder triggered by a different chemical. „The sad part is that if you look at where addiction treatment was 10 years ago, it hasn’t gotten much better,“ says Dr. Martin Paulus, a professor of psychiatry at the University of California at San Diego. „You have a better chance to do well after many types of cancer than you have of recovering from methamphetamine dependence.“

That could all be about to change. During those same 10 years, researchers have made extraordinary progress in understanding the physical basis of addiction. They know now, for example, that the 20% success rate can shoot up to 40% if treatment is ongoing (very much the AA model, which is most effective when members continue to attend meetings long after their last drink). Armed with an array of increasingly sophisticated technology, including fMRIs and PET scans, investigators have begun to figure out exactly what goes wrong in the brain of an addict–which neurotransmitting chemicals are out of balance and what regions of the brain are affected. They are developing a more detailed understanding of how deeply and completely addiction can affect the brain, by hijacking memory-making processes and by exploiting emotions. Using that knowledge, they’ve begun to design new drugs that are showing promise in cutting off the craving that drives an addict irresistibly toward relapse–the greatest risk facing even the most dedicated abstainer.

„Addictions,“ says Joseph Frascella, director of the division of clinical neuroscience at the National Institute on Drug Abuse (NIDA), „are repetitive behaviors in the face of negative consequences, the desire to continue something you know is bad for you.“

Addiction is such a harmful behavior, in fact, that evolution should have long ago weeded it out of the population: if it’s hard to drive safely under the influence, imagine trying to run from a saber-toothed tiger or catch a squirrel for lunch. And yet, says Dr. Nora Volkow, director of NIDA and a pioneer in the use of imaging to understand addiction, „the use of drugs has been recorded since the beginning of civilization. Humans in my view will always want to experiment with things to make them feel good.“

That’s because drugs of abuse co-opt the very brain functions that allowed our distant ancestors to survive in a hostile world. Our minds are programmed to pay extra attention to what neurologists call salience–that is, special relevance. Threats, for example, are highly salient, which is why we instinctively try to get away from them. But so are food and sex because they help the individual and the species survive. Drugs of abuse capitalize on this ready-made programming. When exposed to drugs, our memory systems, reward circuits, decision-making skills and conditioning kick in–salience in overdrive–to create an all consuming pattern of uncontrollable craving. „Some people have a genetic predisposition to addiction,“ says Volkow. „But because it involves these basic brain functions, everyone will become an addict if sufficiently exposed to drugs or alcohol.“

That can go for nonchemical addictions as well. Behaviors, from gambling to shopping to sex, may start out as habits but slide into addictions. Sometimes there might be a behavior-specific root of the problem. Volkow’s research group, for example, has shown that pathologically obese people who are compulsive eaters exhibit hyperactivity in the areas of the brain that process food stimuli–including the mouth, lips and tongue. For them, activating these regions is like opening the floodgates to the pleasure center. Almost anything deeply enjoyable can turn into an addiction, though.

Of course, not everyone becomes an addict. That’s because we have other, more analytical regions that can evaluate consequences and override mere pleasure seeking. Brain imaging is showing exactly how that happens.Paulus, for example, looked at methamphetamine addicts enrolled in a VA hospital’s intensive four-week rehabilitation program. Those who were more likely to relapse in the first year after completing the program were also less able to complete tasks involving cognitive skills and less able to adjust to new rules quickly. This suggested that those patients might also be less adept at using analytical areas of the brain while performing decision-making tasks. Sure enough, brain scans showed that there were reduced levels of activation in the prefrontal cortex, where rational thought can override impulsive behavior. It’s impossible to say if the drugs might have damaged these abilities in the relapsers–an effect rather than a cause of the chemical abuse–but the fact that the cognitive deficit existed in only some of the meth users suggests that there was something innate that was unique to them. To his surprise, Paulus found that 80% to 90% of the time, he could accurately predict who would relapse within a year simply by examining the scans.

Another area of focus for researchers involves the brain’s reward system, powered largely by the neurotransmitter dopamine. Investigators are looking specifically at the family of dopamine receptors that populate nerve cells and bind to the compound. The hope is that if you can dampen the effect of the brain chemical that carries the pleasurable signal, you can loosen the drug’s hold.

One particular group of dopamine receptors, for example, called D3, seems to multiply in the presence of cocaine, methamphetamine and nicotine, making it possible for more of the drug to enter and activate nerve cells. „Receptor density is thought to be an amplifier,“ says Frank Vocci, director of pharmacotherapies at NIDA. „[Chemically] blocking D3 interrupts an awful lot of the drugs‘ effects. It is probably the hottest target in modulating the reward system.“

But just as there are two ways to stop a speeding car–by easing off the gas or hitting the brake pedal–there are two different possibilities for muting addiction. If dopamine receptors are the gas, the brain’s own inhibitory systems act as the brakes. In addicts, this natural damping circuit, called GABA (gamma-aminobutyric acid), appears to be faulty. Without a proper chemical check on excitatory messages set off by drugs, the brain never appreciates that it’s been satiated.

As it turns out, vigabatrin, an antiepilepsy treatment that is marketed in 60 countries (but not yet in the U.S.), is an effective GABA booster. In epileptics, vigabatrin suppresses overactivated motor neurons that cause muscles to contract and go into spasm. Hoping that enhancing GABA in the brains of addicts could help them control their drug cravings, two biotech companies in the U.S., Ovation Pharmaceuticals and Catalyst

Pharmaceuticals, are studying the drug’s effect on methamphetamine and cocaine use. So far, in animals, vigabatrin prevents the breakdown of GABA so that more of the inhibitory compound can be stored in whole form in nerve cells. That way, more of it could be released when those cells are activated by a hit from a drug. Says Vocci, optimistically: „If it works, it will probably work on all addictions.“

Another fundamental target for addiction treatments is the stress network. Animal studies have long shown that stress can increase the desire for drugs. In rats trained to self-administer a substance, stressors such as a new environment, an unfamiliar cage mate or a change in daily routine push the animals to depend on the substance even more.

Among higher creatures like us, stress can also alter the way the brain thinks, particularly the way it contemplates the consequences of actions. Recall the last time you found yourself in a stressful situation–when you were scared, nervous or threatened. Your brain tuned out everything besides whatever it was that was frightening you–the familiar fight-or-flight mode. „The part of the prefrontal cortex that is involved in deliberative cognition is shut down by stress,“ says Vocci. „It’s supposed to be, but it’s even more inhibited in substance abusers.“ A less responsive prefrontal cortex sets up addicts to be more impulsive as well.

Hormones–of the male-female kind–may play a role in how people become addicted as well. Studies have shown, for instance, that women may be more vulnerable to cravings for nicotine during the latter part of the menstrual cycle, when the egg emerges from the follicle and the hormones progesterone and estrogen are released. „The reward systems of the brain have different sensitivities at different points in the cycle,“ notes Volkow. „There is way greater craving during the later phase.“

That led researchers to wonder about other biological differences in the way men and women become addicted and, significantly, respond to treatments. Alcohol dependence is one very promising area. For years, researchers had documented the way female alcoholics tend to progress more rapidly to alcoholism than men. This telescoping effect, they now know, has a lot to do with the way women metabolize alcohol. Females are endowed with less alcohol dehydrogenase–the first enzyme in the stomach lining that starts to break down the ethanol in liquor–and less total body water than men. Together with estrogen, these factors have a net concentrating effect on the alcohol in the blood, giving women a more intense hit with each drink. The pleasure from that extreme high may be enough for some women to feel satisfied and therefore drink less. For others, the intense intoxication is so enjoyable that they try to duplicate the experience over and over.

But it’s the brain, not the gut, that continues to get most of the attention, and one of the biggest reasons is technology. It was in 1985 that Volkow first began using PET scans to record trademark characteristics in the brains and nerve cells of chronic drug abusers, including blood flow, dopamine levels and glucose metabolism–a measure of how much energy is being used and where (and therefore a stand-in for figuring out which cells are at work). After the subjects had been abstinent a year, Volkow rescanned their brains and found that they had begun to return to their predrug state. Good news, certainly, but only as far as it goes.

„The changes induced by addiction do not just involve one system,“ says Volkow. „There are some areas in which the changes persist even after two years.“ One area of delayed rebound involves learning. Somehow in methamphetamine abusers, the ability to learn some new things remained affected after 14 months of abstinence. „Does treatment push the brain back to normal,“ asks NIDA’s Frascella, „or does it push it back in different ways?“If the kind of damage that lingers in an addict’s learning abilities also hangs on in behavioral areas, this could explain why rehabilitation programs that rely on cognitive therapy–teaching new ways to think about the need for a substance and the consequences of using it–may not always be effective, especially in the first weeks and months after getting clean. „Therapy is a learning process,“ notes Vocci. „We are trying to get [addicts] to change cognition and behavior at a time when they are least able to do so.“

One important discovery: evidence is building to support the 90-day rehabilitation model, which was stumbled upon by AA (new members are advised to attend a meeting a day for the first 90 days) and is the duration of a typical stint in a drug-treatment program. It turns out that this is just about how long it takes for the brain to reset itself and shake off the immediate influence of a drug. Researchers at Yale University have documented what they call the sleeper effect–a gradual re-engaging of proper decision making and analytical functions in the brain’s prefrontal cortex–after an addict has abstained for at least 90 days.

This work has led to research on cognitive enhancers, or compounds that may amplify connections in the prefrontal cortex to speed up the natural reversal. Such enhancement would give the higher regions of the brain a fighting chance against the amygdala, a more basal region that plays a role in priming the dopamine-reward system when certain cues suggest imminent pleasure–anything from the sight of white powder that looks like cocaine to spending time with friends you used to drink with. It’s that conditioned reflex–identical to the one that caused Ivan Pavlov’s famed dog to salivate at the ringing of a bell after it learned to associate the sound with food–that unleashes a craving. And it’s that phenomenon that was the purpose of my brain scans at McLean, one of the world’s premier centers for addiction research.

In my heyday, I would often drink even when I knew it was a terrible idea–and the urge was hardest to resist when I was with my drinking buddies, hearing the clink of glasses and bottles, seeing others imbibe and smelling the aroma of wine or beer. The researchers at McLean have invented a machine that wafts such odors directly into the nostrils of a subject undergoing an fMRI scan in order to see how the brain reacts. The reward circuitry in the brain of a newly recovering alcoholic should light up like a Christmas tree when stimulated by one of these alluring smells.

I chose dark beer, my absolute favorite, from their impressive stock. But I haven’t gotten high for more than a quarter-century; it was an open question whether I would react that way. So after an interview with a staff psychiatrist to make sure I would be able to handle it if I experienced a craving, I was fitted with a tube that carried beer aroma from a vaporizer into my nose. I was then slid into the machine to inhale that still familiar odor while the fMRI did its work.

Even if the smells triggered a strong desire to drink, I had long since learned ways to talk myself out of it–or find someone to help me do so. Like the 90-day drying-out period that turns out to parallel the brain’s recovery cycle, such a strategy is in line with other new theories of addiction. Scientists say extinguishing urges is not a matter of getting the feelings to fade but of helping the addict learn a new form of conditioning, one that allows the brain’s cognitive power to shout down the amygdala and other lower regions. „What has to happen for that cue to extinguish is not for the amygdala to become weaker but for the frontal cortex to become stronger,“ says Vocci.

While such relearning has not been studied formally in humans, Vocci believes it will work, on the basis of studies involving, of all things, phobias. It turns out that phobias and drugs exploit the same struggle between high and low circuits in the brain. People placed in a virtual-reality glass elevator and treated with the antibiotic D-cycloserine were better able to overcome their fear of heights than those without benefit of the drug. Says Vocci: „I never thought we would have drugs that affect cognition in such a specific way.“

Such surprises have even allowed experts to speculate whether addiction can ever be cured. That notion goes firmly against current beliefs. A rehabilitated addict is always in recovery because cured suggests that resuming drinking or smoking or shooting up is a safe possibility–whose downside could be devastating. But there are hints that a cure might not in principle be impossible. A recent study showed that tobacco smokers who suffered a stroke that damaged the insula (a region of the brain involved in emotional, gut-instinct perceptions) no longer felt a desire for nicotine.

That’s exciting, but because the insula is so critical to other brain functions–perceiving danger, anticipating threats–damaging this area isn’t something you would ever want to do intentionally. With so many of the brain’s systems entangled with one another, it could prove impossible to adjust just one without throwing the others into imbalance.

Nevertheless, says Volkow, „addiction is a medical condition. We have to recognize that medications can reverse the pathology of the disease. We have to force ourselves to think about a cure because if we don’t, it will never happen.“ Still, she is quick to admit that just contemplating new ideas doesn’t make them so. The brain functions that addiction commandeers may simply be so complex that sufferers, as 12-step recovery programs have emphasized for decades, never lose their vulnerability to their drug of choice, no matter how healthy their brains might eventually look.

I’m probably a case in point. My brain barely lit up in response to the smell of beer inside the fMRI at McLean. „This is actually valuable information for you as an individual,“ said Scott Lukas, director of the hospital’s behavioral psychopharmacology research laboratory and a professor at Harvard Medical School who ran the tests. „It means that your brain’s sensitivity to beer cues has long passed.“

That’s in keeping with my real-world experience; if someone has a beer at dinner, I don’t feel a compulsion to leap across the table and grab it or even to order one for myself. Does that mean I’m cured? Maybe. But it may also mean simply that it would take a much stronger trigger for me to fall prey to addiction again–like, for example, downing a glass of beer. But the last thing I intend to do is put it to the test. I’ve seen too many others try it–with horrifying results.

This is from a old Time-Magazine: http://www.time.com/time/magazine/article/0,9171,1640436-4,00.html

Ben: Diary of a Heroin Addict

Opium-Addicted Children: Paying a Heavy Price for the Afghan War

The revelation that the number of opium-addicted Afghan children has reached new highs is a sad unintended consequence of that war. It dramatically illustrates how adult war games can doom generations of children to a miserable life, argues César Chelala. Worse, it is a growing problem in neighboring Iran and Pakistan as well.
A group of researchers hired by the U.S. Department of State found staggering levels of opium in Afghan children, some as young as 14 months old, who had been passively exposed by adult drug users in their homes.
In 25% of homes where adult addicts lived, children tested showed signs of significant drug exposure, according to the researchers.

According to one of the researchers, the children exhibit the typical behavior of opium and heroin addicts. If the drug is withdrawn, they go through a withdrawal process.

The results of the study should sound an alarm. Not only were opium products found in indoor air samples, but their concentrations were also extremely high. This suggests that, as with second-hand cigarette smoke, contaminated indoor air and surfaces pose a serious health risk to women’s and children’s health.

The extent of health problems in children as a result of such exposure is not known. What is known is that the number of Afghan drug users has increased from 920,000 in 2005 to over 1.5 million, according to Zalmai Afzali, the spokesman for the Ministry of Counter-Narcotics (MCN) in Afghanistan.

A quarter of those users are thought to be women and children. Afzali stated that Afghanistan could become the world’s top drug-using nation per capita if current trends continue.

According to the UN Office on Drugs and Crime (UNODC), no other country in the world produces as much heroin, opium and hashish as Afghanistan — a sad distinction for a country already ravaged by war.

This may explain why control efforts so far have been concentrated on poppy eradication and interdiction to stem exports, while less attention was paid to the rising domestic addiction problem, particularly in children.

Both American and Afghan counter narcotic officials have said that such widespread domestic drug addiction is a relatively new problem. Among the factors leading to increased levels of drug use is on a high unemployment rate throughout the country, the social upheaval provoked by this war and those that preceded it, as well as the return of refugees from Iran and Pakistan who became addicts while abroad.

In both those countries, the high number of opium-addicted children is also a serious problem, particularly among street children. In Tehran, although the government has opened several shelters for street children, many more centers are still needed to take care of them.

According to some estimates, there are between 35,000 and 50,000 children in Tehran who are forced by their parents or other adults to live and beg in the streets or to work in sweatshops.

These children are subject to all kinds of abuse, and many among them end up in organized prostitution rings and become part of the sex trade. They are transported to other countries where they are obliged to work as prostitutes, while others simply disappear.

The situation is equally serious in Pakistan, where in Karachi alone there are tens of thousands of children who are addicted, as drug trafficking prevails all over the city. In Karachi, the main addiction is to hashish.

According to Rana Asif Habib, president of the Initiator Human Development Foundation (IHDF), due to the increase in the number of street children, the street crime rate is also on the rise as children get involved in drug trafficking activities in the city.

Injecting drug users face the additional risk of HIV-infection through the sharing of contaminated syringes. “Drug addiction and HIV/AIDS are, together, Afghanistan’s silent tsunami,” declared Tariq Suliman, director of the Nejat’s rehabilitation center to the UN Office for Humanitarian Affairs.

There are about 40 treatment centers for addicts dispersed throughout the country, but most are small, poorly staffed and under-resourced.

For the first time ever, an international team including World Health Organization (WHO) officials and experts from Johns Hopkins University and the Medical University of Vienna have joined efforts to design a treatment regime for young children.

The United States and its allies have the resources to rapidly expand and adequately fund and resource such treatment and rehabilitation centers throughout the country. Anything less will be yet another serious indictment of an occupation gone astray.

source: http://www.theglobalist.com/printSto…x?StoryId=8472

Addiction: A Loss of Plasticity of the Brain?

Why is it that only some drug users become addicts? This is the question that has been addressed by the teams of Pier Vincenzo Piazza and Olivier Manzoni, at the Neurocentre Magendie in Bordeaux (Inserm unit 862). These researchers have just discovered that the transition to addiction could result from a persistent impairment of synaptic plasticity in a key structure of the brain. This 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.

This research is published in the journal Science on 25 June 2010.
The voluntary consumption of drugs is a behaviour found in many species of animal. However, it had long been considered that addiction, defined as compulsive and pathological drug consumption, is a 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.

Now, 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. Which of these modifications is responsible for the development of an addiction? This is the question the researchers wanted to answer in order to target possible therapeutic approaches to a disorder for which treatments are cruelly lacking.

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.“

ScienceDaily
June 24, 2010
http://www.sciencedaily.com/releases…0624140912.htm

A cautionary tale: Smart people and addiction

Rationalization and denial are key concepts in addiction treatment. To recover, addicts admit they have rationalized their habit („I use so much less than my friends.“) and denied they have a problem („I can handle it. It’s not affecting my job.“)
Here’s another barrier to recovery from addiction: „I’m too smart for this to become a problem.“

This week’s Journal of the American Medical Assn., contains a sad essay from a medical researcher who made headlines last year when his fiancee, also a medical researcher, died after the two injected themselves with what they thought was the narcotic buprenorphine for kicks.

The author of the essay, Clinton B. McCracken, a former pharmacologist at the University of Maryland, describes how he became a user of marijuana and intravenous opioids (morphine and oxycodone) over a decade while building his career as a successful neuroscientist who studied the effects of drugs on the brain.

He notes that people who work in medicine have addiction rates that are equal to, if not higher than, rates among the public. Drugs are easier to get, McCracken said. But he said an attitude of arrogance led him, as a medical professional, to believe that he could enjoy dangerous drugs and avoid serious consequences. For example, he was careful to schedule his opioid use to prove to himself that he did not need it to get through the day, made sure he was tending to his responsibilities at work and reviewed the criteria for drug dependence to assure himself that he was not an addict.

„By intellectually addressing the official criteria for abuse and dependence, I provided myself with the illusion of total control over the situation and was able to confidently tell myself that no problems existed,“ he wrote in the essay.

His world came crashing down last fall when his fiancee died while injecting Drugs with him. When the police arrived, they discovered McCracken’s Mariuhana plants. He was arrested and jailed, and he later agreed to a plea bargain to avoid more serious charges. Besides losing his girlfriend, he has since lost his career, his reputation and, as a citizen of Canada and convicted felon, he expects to be deported.

Addiction may look different in different people, but it seems that, in the end, everyone, no matter the level of intelligence, looks the same — ruined.

„The transition from my drug use having no apparent negative consequences, to both my personal and professional life being damaged possibly beyond repair, was so fast as to be instantaneous, highlighting the fact that when it comes to drug use, the perception of control is really nothing more than an illusion,“ he wrote.

— Shari Roan
May 20, 2010

Here is the „sad essay“ :

Health care professionals and physicians in particular have rates of substance abuse that are equal to and often exceed those observed in the general public.These estimates may even be low, as many studies rely on self-reported data. Health care professionals presumably use drugs for many of the same reasons as those of the general population.

Nonetheless, given the intelligence, years of education, and high levels of achievement found in this group, the relatively high incidence of substance abuse may be somewhat surprising. Ease of access to drugs is commonly cited, particularly with respect to the high rates of drug abuse among anesthesiologists; however, given the complex nature of addiction, the underlying causes are assuredly myriad.

One possible contributing factor that may receive insufficient attention is the ability of highly educated professionals to intellectualize their drug use, minimizing in their mind the potential disastrous consequences, both personal (eg, the possibility of death or serious harm due to factors such as overdose or toxicity, among others) and professional (ranging from a tarnished reputation to a ruined career). This intellectualization is particularly insidious because due to its very nature, it prevents the person from realizing the scope of the problem, or even admitting a problem exists. Thus, it is related to, yet distinct from, the phenomena of rationalization and denial. Rationalization and denial are universal components of substance abuse and unaffected by education or training.

By contrast, intellectualization actually relies on advanced education and training, particularly with respect to the effects of drugs and addiction, also incorporating confidence in one’s intelligence and abilities, and no small measure of arrogance, to provide the illusion of control or mastery. The end result of this intellectualization is the manifestation of hubris that produces blindness to the devastating consequences of drug abuse and addiction.

Here, I draw on my experience as a drug abuser who for years maintained a relatively successful career as a basic biomedical scientist studying the neuroscience of addiction and compulsion to present a cautionary tale regarding the extreme dangers of intellectualizing drug use. No matter how well versed one may be in pharmacology or the addictive process, the fact remains that severe problems due to drug abuse can arise almost instantly, and no matter how in control one may believe himself to be, these problems can lead to tragic and irreversibly life-altering consequences.

In my case, this intellectualization occurred on three main levels.

The first related to my drug use patterns. I was a daily user of cannabis for most of the past decade, and an intermittent user of opioids, primarily via the intravenous route, for approximately three years. This use occurred while I pursued a career in basic science research, with a heavy focus on addiction. Consequently, I was intimately familiar with the drug abuse literature and psychiatric diagnostic manuals such as the DSM-IV. I was able to finish my doctorate and conduct research at a high level at the same time I was a regular drug user.

Mindful of the DSM-IV criteria for substance abuse and dependence, I was able to rationalize my drug use in a number of different ways, all with the similar end result of deluding myself into thinking I did not have a problem. First among these was that I was able to maintain a high level of professional achievement while using drugs. In addition, I was able to form and maintain a number of fulfilling personal relationships over this time period. As such, I felt that I was not suffering dire consequences in my personal and professional lives. I was able to tell myself that those items on the DSM-IV clearly did not apply to my situation, and hence no problem existed. I used similar reasoning for other items on the DSM-IV checklists for substance abuse and dependence.

I identified my daily marijuana use as „stable“ for some time (ie, years), and I was able to cease use for weeks at a time without any serious difficulty. Thus, any worries of tolerance (ie, increased use over time) or dependence (ie, withdrawal symptoms upon cessation of use) were minimized. With respect to opioids, I was keenly aware of the potential for these drugs to produce tolerance and dependence and thus restricted my use to no more than two consecutive days spaced no closer than 2 or 3 months apart.

By intellectually addressing the official criteria for abuse and dependence, I provided myself with the illusion of total control over the situation and was able to confidently tell myself that no problems existed. This was in spite of the fact that my ongoing drug use was jeopardizing not only my health, but my career.

I was also able to intellectually justify using opioids via the intravenous route. My first experience with opioid medication came after they were prescribed for pain following an injury. I enjoyed the effects and began to seek other sources to attain these drugs. Although I was acutely aware that these drugs had strong potential to cause tolerance and dependence, I was secure in my ability to control the situation. So why inject? I initially began using these drugs via the IV route primarily to maximize bioavailability.

Many opioids, and morphine in particular, possess only a fraction of their IV bioavailability when taken orally. The euphoria due to rapid drug onset via the IV route (ie, the „rush“) was another attractive factor. While I was aware that IV use presented dangers when compared with oral administration, such as increased risk of overdose, infection, or embolism, I was confident that my technical experience (having performed injections into small-animal blood vessels) and access to sterile needles, sterile syringes, sterile saline as a diluent, and alcohol swabs would allow me to circumvent many of the typical problems associated with IV administration. In hindsight, in my overconfidence I minimized one of the key dangers of IV use—the fact that the extremely rapid onset can lead to irreversible effects if things should happen to go wrong.

The final method by which I was able to intellectualize my drug use dealt with the means by which I obtained drugs. I rationalized that small-scale marijuana cultivation was less risky than purchasing it and was associated with a relatively minimal risk of discovery and associated arrest. I obtained opioids (primarily morphine and oxycodone) from an overseas online pharmacy. In addition to less risk of arrest, I made the assumption that dosage would be more consistent and the chance of adulteration much lower than drugs purchased on the street, thus reducing the risk of possible overdose. Furthermore, in the initial stages of opioid use, I proceeded extremely cautiously to ensure the drugs I received from overseas were what they purported to be. After satisfying myself that this was indeed the case, at least at the beginning, I assumed that this form of quality control was no longer necessary.

There were no acute problems stemming from my drug use for approximately three years. My fiancée, a successful scientist in her own right, and with whom virtually all of my intravenous drug use occurred over the previous three years, lost her life after injecting a product that produced severe anaphylaxis, most likely due to some form of contamination. While waiting for the paramedics to arrive I tried unsuccessfully to resuscitate her. Despite heroic efforts, neither the paramedics nor the emergency department physicians were able to revive her.

As a consequence of her death, our house was searched by police, who then discovered the ongoing marijuana cultivation. I was immediately arrested, jailed, and charged with a number of felonies; then, in the space of a few days, my employment as a postdoctoral fellow was summarily terminated and I was evicted from my residence.

The impact of these events on my life has been enormous. First and foremost is the loss of the woman I loved, my best friend and partner, with whom I had planned to spend the rest of my life. Not only were we a team in the sense of personal life, but also professionally. We worked in the same field, attended the same meetings, and were well known as a couple in our part of the scientific community. Thus, my relationship with her came to define all aspects of both my work life and my home life.

Coming to terms with her loss has proven to be extremely challenging and will likely remain so for a long time. While paling completely compared to the loss of my fiancée, I face a number of other consequences. For one, my career as an academic research scientist has been undeniably derailed, if not destroyed. Reputation is critical in my field, and mine is likely to be damaged for the foreseeable future. I originally faced substantial time in prison; I was able to agree to a plea bargain whereby I avoided any additional incarceration. However, I have now been convicted of a felony, which will undoubtedly have a severely negative effect on any future job prospects and international travel. Finally, as a Canadian citizen, my ability to live in, work in, and even visit the United States, my home for the last ten years, is also compromised; I face imminent deportation with almost no hope of reentry in the future.

The transition from my drug use having no apparent negative consequences, to both my personal and professional life being damaged possibly beyond repair, was so fast as to be instantaneous, highlighting the fact that when it comes to drug use, the perception of control is really nothing more than illusion. Had these events not occurred as they did, it is possible, even probable, that my drug use would have escalated until it precluded a normal personal or professional life.

However, it is important to note here that problems associated with drug abuse can arise with devastating effects even in the apparent absence of many diagnostic criteria, such as overt tolerance and dependence.

Neither advanced education nor knowledge of pharmacology nor familiarity with the addictive process was able to prevent tragic consequences for me. It is my sincere hope that my experience may serve as a warning, help illuminate the dangers of intellectualizing drug use and abuse, and prevent similar tragedies in the lives of others.

Additional Contributions: I thank Lawrence R. Fishel, PhD, and Anthony A. Grace, PhD, for their comments and assistance with this article.

Enhancing Recovery with Meditation and Mindfulness

There are several promising applications of mindfulness to enhance recovery from alcohol and drug dependence and other addictions. This article explores several new trends and ways that meditation and mindfulness can be used to complement and help with recovery.

The Buddhist teachings (dharma) focus on the healing power of compassion. To recover from an adversity (i.e., addiction) gives one an opportunity to be more compassionate toward others as well as toward oneself.

Using mindfulness in counseling

Mindfulness has gained wide acceptance from counselors in the mental health and addiction recovery fields. Over the last 15 years the psychology field has seen a resurgence of mindfulness being used for the treatment of stress, anxiety, depression and personality disorders. For instance, John Kabat-Zinn used mindfulness training and meditation to help clients with stress, pain and anxiety disorders Kabat-Zinn (1992); Marsha Linehan (1993) integrated mindfulness practices in her Dialectical Behavior Therapy (DBT) for the treatment of personality disorders; Steven Hayes (1999) developed Acceptance and Commitment Therapy (ACT) for the treatment of depression and anxiety; Zindel Siegal et. al. (2002) developed Mindfulness-Based Cognitive Therapy (MBCT) as a relapse prevention approach to depression.
Thus, it makes perfect sense that Buddhist teachings (dharma), meditation and mindfulness training would be an ideal tool to help in the treatment of addictions.

Buddhism and addiction

Buddhist teachings make several references to addictions. Addictions often prevent individuals from being present and aware, conscious of what is going on with others and themselves. People often fail to realize what is really important. They often forget that they are not in control, and are prone to self-deception.

“Buddhist literature offers considerable insight into the basic nature of addiction, how addictive behavior develops, and how meditation can be used as a method of transcending a wide variety of addiction problems,” said Dr. Alan Marlatt, director of the University of Washington Addictive Behavior Research Center and an expert on alcohol/drug relapse prevention (Marlatt, 2002).

Buddhism describes addiction as being “a false refuge” — a delusional place to try to hide and escape from being present in life. Buddhism also describes addiction in the context of grasping, resisting and delusions; the mindfulness counters are listed below.

The grasping is the craving, obsession and compulsion to use alcohol/drugs, and the accompanying addiction-related behaviors. Grasping is described in the three “Cs” in our functional definition of addiction — compulsion and obsession, inability to control and continued use despite negative consequences.

The resisting is the pushing away, the isolation, the shutting down of normal human pleasure and displeasures, the withdrawal from connection with others — the invoking of the “no talk, no feel, no trust” rule, and of course, “not asking for help.” The Alcoholics Anonymous proverb “Silence is the enemy of recovery,” describes this resistance. Resistance is demonstrated by denial, delusion and rejecting advice, help and direction from others.

Addiction — “Land of the Hungry Ghosts”

Dr. Thomas Bien and Dr. Beverly Bien, authors of Mindful Recovery (2002), and Finding the Center Within (2003), describe a strange and peculiar realm in Buddhist cosmology, called the “land of hungry ghosts.” People in this land are described as having huge appetites, but unable to satisfy them.

Addiction is viewed in Buddhist teachings as the inability to see the abundance in our lives, nor the joy that is there “in the now.” Bien and Bien describe the torture of addicts as “…. not lack, but the inability to open to the surrounding abundance …”

“We do not need to fill ourselves with new things — we need to experience more fully what is already there,” the authors state in their book, Finding the Center Within (Bien & Bien, 2003).

Meditation and Alcohol/Drug Recovery

Bien and Bien, in their book Mindful Recovery, describe meditation and mindfulness as helping the person develop a “quality of calm awareness.” The authors further describe this as a perfect antidote to the “addicted state of mind.”
In a study conducted by the authors, three groups of heavy alcohol users were given different treatments: one group received deep muscle massage sessions for six weeks; another group did silent reading for six weeks; and the final group had six weeks of meditation sessions. The meditation group decreased their alcohol consumption by 50 percent (the highest of all groups). The meditation group also chose to continue their meditations for longer than the other groups continued their respective practices.

Meditation, twice a day for 20 minutes per session, allows the recovering person to let thoughts and feelings (positive and negative, pleasurable and unpleasurable) to stream through consciousness without attaching to them, holding them at arms’ length, observing and reflecting, rather than reacting.

Delusion and Denial

Recovery from alcohol and drug addiction involves breaking through “denial” and admitting you are powerless over these substances. The old joke in the alcohol/drug recovery field was that denial is a river in Egypt (de-Nile). A more contemporary description of d-e-n-i-a-l stands for: I don’t even know I am lying.

Buddhism has a similar focus on denial, and frequently talks about “delusion” and how we deceive ourselves from accepting suffering as part of our lives. In Buddhism, the goal is to be more aware and present by overcoming our deceptions in our life.

Pema Chodron says it well: “The essence of bravery is being without self-deception” (Chodron, 2001).
The 12 Steps and the Eightfold Path

Mindfulness is very compatible with Alcoholics Anonymous (AA) and Narcotics Anonymous (NA), and the 12-step principles. Kevin Griffin, author of One Breath at a Time, describes the many similarities and differences between the 12 steps and the Buddhist Eightfold path. One of the similar teachings of these two is Rigorous honesty and Right Speech.

A major problem in addiction is the addict’s deception, dishonesty and outright lying. The Big Book and AA emphasize rigorous honesty to counter the rationalized lies and deceptions that are often a part of the disease. In a similar way, the third path of the Buddhist Eightfold path talks about Right Speech, which is speech that is truthful, helpful, kind and appropriate. Lies are expanded to include exaggerations, half-truths, omissions, denials, rumors and gossiping. Right Speech goes even further in describing right speech as not harming others, being kind, melodious, aesthethic and compassionate, accepting and understanding of others.

There also are many common teachings, expressions and proverbs that are paralleled in the teachings of AA and Buddhist dharma, including:

The Eightfold Path includes the following: Right View; Right Intention; Right Speech; Right Action; Right Livelihood; Right Effort; Right Mindfulness; and Right Concentration. The term “right” is used not in the context of right or wrong, but instead as the preferred way or suggested way.  “Right” also means wholeheartedness and goodness.

Compassion for self and others

Life is difficult enough without beating yourself up. Give yourself a break, lighten up, and “stay in the now.”
“All beings want to be happy, yet so very few know how. It is out of ignorance that any of us cause suffering for ourselves or for others,” said Sharon Salzberg, in her book, Loving Kindness.  Buddhism teaches compassion for oneself and for others. Shame, self-blame, criticism, judgments, anger and isolation cause and contribute to problems with alcohol and drugs. They can be countered by developing compassion for oneself and for others. Buddhism is a different way of viewing oneself and others. It is the way of compassion, reflection and goodness. Compassion also involves forgiveness. Forgiveness can allow a person to open his or her heart and live with greater compassion and love.

In his book, The Wise Heart, Jack Kornfield said, “For most people, the work of forgiveness is a process. Practicing forgiveness, we may go through stages of grief, rage, sorrow, hurt, and confusion. As you let yourself feel the pain we still hold, forgiveness comes as a relief, a release for our heart in the end. Forgiveness acknowledges that no matter how much we may have suffered, we will not put another human being out of our heart.”

In my book, Awakening to Mindfulness, I’ve outlined 10 Steps of compassion:

1. Being sensitive to others’ suffering, as well as your own suffering
2. Being reflective (gentle) instead of reactive
3. Changing critical attitudes (greed, hatred, delusion) into caring attitudes (generosity, love and awareness)
4. Being truthful, helpful, kind and appropriate
5. Not blaming, taking responsibility
6. Not complaining or dramatizing
7. Invoking “right speech” and following the eightfold path
8. “Cherishing” others
9. Avoiding and reducing criticism, contempt, defensiveness and stonewalling in relationships
10. Having the grace to love and to be loved

Mindfulness-based behavioral relapse prevention (MBRP)

Dr. Alan Marlatt and his associates at the University of Washington have been exploring the application of mindfulness and meditation in preventing relapse to alcohol/drugs. He has found that “the heightened state of present-focused awareness that is encouraged by meditation may directly counteract the conditioned automatic response to use alcohol in response to cravings and urges” (Marlatt, 2007).

MBRP helps the recovering alcoholic/addict to recognize (not suppress) the negative emotional states, keeping them at arms’ length. Ironically, trying to suppress negative thoughts results in an increase, rather than a decrease, in negative thoughts (Bowen, 2007). The negative thoughts are identified as “normal thoughts” at various stages of recovery. These negative thoughts are accepted as thoughts that the individual does not have to choose to act on.

An example of a MBRP technique is “urge surfing,” which involves visualizing your “urge” to use (alcohol/drugs) as having a cycle much like a wave. The wave has a crest, it crashes and then rolls to shore and disappears. This technique involves using your breath as a surf board, as you ride out the wave to shore.

My own experience using MBRE

I have specialized in alcohol/drug counseling for more than 30 years, and I am very excited about the many ways meditation and mindfulness can be used as a recovery enhancement for alcohol/drug addiction. In the last two years I have been introducing meditation and mindfulness practices in my two outpatient (alcohol/drug recovery) therapy groups, and have seen firsthand the many benefits of meditation and mindfulness practices in helping my clients to be more aware, compassionate to others and themselves and enjoying life more. I have seen remarkable growth in my group members, especially in their ability to be less reactive and more reflective.

The benefits of meditation and mindfulness include helping the individual to: have a “quality of calm awareness”; be less reactive and more reflective; reduce stress; learn how to enjoy life “in the now”; see the “joy” and “abundance” in his or her own life; have a stronger spiritual well-being; be compassionate to self and others; make connections and have interdependence; feel worthwhile; and no longer need to be in the “land of hungry ghosts.”

Richard Fields, PhD is the author of the college textbook Drugs in Perspective, 7th edition, and Awakening to Mindfulness: 10 Steps for Positive Change. He is a national trainer and consultant in the field of alcohol/drug recovery and mindfulness-based recovery enhancement (MBRE), the owner/director of FACES Conferences (www.facesconferences.com) and has a private counseling practice in Bellevue, Wash.

References

Bien, Thomas & Bien, Beverly (2002). Mindfulness Recovery — A Spiritual Path to Healing from Addiction, Wiley, N.Y.
Bien, Thomas & Bien, Beverly (2003). Finding the Center Within — The Healing Way of Mindfulness meditation. Wiley, N.Y.
Bowen, Sarah, Witkiewitz, Katie, Dillworth, Tirara & Marlatt, G. Alan (2007) “The role of Thought suppression in the relationship between mindfulness, meditation, and alcohol use.” Addictive Behaviors 32, 2323-2328.
Brazier, David (1997) The Feeling Buddha: A Buddhist Psychology of Character, Adversity, and Passion. Fromm International, New York.
Chodren, Pema (2001) The Places that Scare You: A Guide to Fearlessness in Different Times. Shambhala Publications, Boston.
Chodren, Pema (2005) When Things Fall Apart: Heart Advice for Difficult Times. Shambhala Publications, Boston.
Epstein, Mark (1998) Going to Pieces Without Falling Apart: Lessons from Meditation and Psychotherapy. Broadway Books, New York.
Fields, Richard (2008) Minestrone for the Mind, Awakening to Mindfulness, 10 Steps for Positive Change. Health Communications, Deerfield Beach.
Griffin, Kevin (2004) One Breath at a Time, Buddhism and the Twelve Steps. St. Martin’s Press,
Kornfield, Jack (1993) A Path with Heart: A guide Through the Perils and Promises of Spiritual Life. Bantam, New York.
Kornfield, Jack (2008). The Wise Heart — A Guide to the Universal Teachings of Buddhist Psychology. Bantam, New York.
Marlatt, G. Alan (2002) “Buddhist Psychology and the Treatment of Addictive Behavior.” Journal of Cognitive and Behavioral Practice 9(1) (2002): 44-49.
Marlatt, G. Alan & Chawla, Neharika (2007) “Meditation and Alcohol Use.” Southern Medical Journal. Vol. 100, no. 4.
Salzberg, Sharon (1990) Lovingkindness:The Revolutionary Art of Happiness. Shambhala, Boston.

This article is published in Counselor, The Magazine for Addiction Professionals, April 2009, v.10, n.2, pp.40-44.

The incentive sensitization theory of addiction:

We present a brief overview of the incentive sensitization theory of addiction.

This posits that addiction is caused primarily by drug-induced sensitization in the brain mesocorticolimbic systems
that attribute incentive salience to reward-associated stimuli. If rendered hypersensitive, these
systems cause pathological incentive motivation (‘wanting’) for drugs. We address some current
questions including: what is the role of learning in incentive sensitization and addiction? Does
incentive sensitization occur in human addicts? Is the development of addiction-like behaviour in
animals associated with sensitization? What is the best way to model addiction symptoms using
animal models? And, finally, what are the roles of affective pleasure or withdrawal in addiction?

1. INTRODUCTION
At some time in their life, most people try a potentially
addictive drug (e.g. alcohol). However, few become
addicts. Addiction implies a pathological and compulsive
pattern of drug-seeking and drug-taking behaviours,
which occupies an inordinate amount of an individual’s
time and thoughts, and persists despite adverse
consequences (Hasin et al. 2006). Addicts also find it
difficult to reduce or terminate drug use, even when
they desire to do so. Finally, addicts are highly
vulnerable to relapse even after long abstinence and
well after symptoms of withdrawal have disappeared.
Thus, a key question in addiction research is: what is
responsible for the transition to addiction in those few
susceptible individuals?
Over the last 20 years or so there has been increasing
recognition that drugs change the brain of addicts in
complex and persistent ways, so persistent that they
far outlast other changes associated with tolerance
and withdrawal. It is important to identify the brain
changes that cause the transition to addiction from
casual or recreational drug use, and the features that
make particular individuals especially susceptible to the
transition (Robinson & Berridge 1993; Nestler 2001;
Hyman et al. 2006; Kalivas & O’Brien 2008). Persistent
drug-induced changes in the brain alter a number of
psychological processes, resulting in various symptoms
of addiction. We suggested in the incentive sensitization
theory of addiction, originally published in
1993, that the most important of these psychological
changes is a ‘sensitization’ or hypersensitivity to the
incentive motivational effects of drugs and drug-associated
stimuli (Robinson & Berridge 1993). Incentive sensitization
produces a bias of attentional processing
towards drug-associated stimuli and pathological
motivation for drugs (compulsive ‘wanting’). When
combined with impaired executive control over
behaviour, incentive sensitization culminates in the
core symptoms of addiction (Robinson & Berridge
1993, 2000, 2003). Incentive sensitization has drawn
considerable interest in the past 15 years and, therefore,
we thought it worthwhile to update our perspective.
We present here a brief and idiosyncratic overview
of this view of addiction and raise some current issues

2. WHAT IS INCENTIVE SENSITIZATION THEORY
AND WHAT IS THE ROLE OF LEARNING?
The central thesis of the incentive sensitization theory
of addiction (Robinson & Berridge 1993) is that
repeated exposure to potentially addictive drugs can,
in susceptible individuals and under particular circumstances,
persistently change brain cells and circuits
that normally regulate the attribution of incentive
salience to stimuli, a psychological process involved in
motivated behaviour. The nature of these ‘neuroadaptations’
is to render these brain circuits hypersensitive
(‘sensitized’) in a way that results in pathological levels
of incentive salience being attributed to drugs and
drug-associated cues. Persistence of incentive sensitization
makes pathological incentive motivation
(wanting) for drugs last for years, even after the
discontinuation of drug use. Sensitized incentive
salience can be manifest in behaviour via either implicit
(as unconscious wanting) or explicit (as conscious
craving) processes, depending on circumstances.
Finally, the focus on drugs in particular in addicts is

produced by an interaction between incentive salience

mechanisms with associative learning mechanisms that
normally direct motivation to specific and appropriate
targets. Learning specifies the object of desire, but it is
important to note that learning per se is not enough for
pathological motivation to take drugs. Thus, we argue
that pathological motivation arises from sensitization of
brain circuits that mediate Pavlovian conditioned
incentive motivational processes (i.e. incentive sensitization).
However, it is important to emphasize that
associative learning processes can modulate the
expression of neural sensitization in behaviour at
particular places or times (and not others), as well as
guide the direction of incentive attributions. This is why
behavioural sensitization is often expressed only in
contexts in which the drugs have previously been
experienced (Stewart & Vezina 1991; Anagnostaras &
Robinson 1996; Robinson et al. 1998), and may
reflect the operation of an ‘occasion-setting’ type of
mechanism (Anagnostaras et al. 2002). Learning might
be viewed as layered onto basic sensitization processes
in a top-down fashion, similar to how learning regulates
the expression of such non-associative motivation
processes as stress and pain. The contextual control
over the expression of sensitization provides an
additional mechanism that accounts for why addicts
‘want’ drugs most particularly when they are in drugassociated
contexts.
Finally, by spreading beyond the associative focus of
wanting on drug targets, incentive sensitization can also
sometimes spill over in animals or humans to other
targets, such as food, sex, gambling, etc. (Mitchell &
Stewart 1990; Fiorino & Phillips 1999a,b; Taylor &
Horger 1999; Nocjar & Panksepp 2002). For example,
treatment with dopaminergic medications in some
patient populations can lead to a ‘dopamine dysregulation
syndrome’ (DDS) that is manifest not only by
compulsive drug use but also sometimes by ‘pathological
gambling, hypersexuality, food bingeing . and
punding, a form of complex behavioral stereotypy’
(Evans et al. 2006, p. 852).
(a) Incentive sensitization: more than just
learning
It has become popular to refer to addiction as a ‘learning
disorder’ (Hyman 2005), but we think that this phrase
may be too narrow to fit reality. Learning is only one
part of the process and probably not the one that
contributes most to the pathological pursuit of drugs.
The most influential type of ‘learning hypothesis’
suggests that drugs promote the learning of strong
‘automatized’ stimulus–response (S–R) habits, and it is
then supposed that by their nature S–R habits confer
compulsivity to behaviour (Tiffany 1990; Berke &
Hyman 2000; Everitt et al. 2001; Hyman et al. 2006).
However, it is difficult to imagine how any influence
of drugs on learning processes alone could confer
compulsivity on behaviour, unless an additional
motivational component was also involved, and S–R
habits by definition are not modulated by motivational
factors (Robinson & Berridge 2003). Do automatic
S–R habits really become compulsive merely by virtue
of being extremely well learned? We have doubts.
Strong S–R habits do not necessarily lead to compulsive
behaviour: activities such as tying shoes, brushing
teeth, etc. are not performed compulsively by most
people, even after being performed more than 10 000
times. Additional motivational processes seem needed
to explain why an addict waking up in the morning with
no drug spends the day engaging in a complex and
sometimes new series of behaviours, such as scamming,
stealing and negotiating, all seemingly motivated
to procure drug. Addicts do what they have to do and
go where they have to go to get drugs, even if actions
and routes that have never been performed before are
required. Such focused yet flexible behaviour in
addiction shows pathological motivation for drugs
that cannot be explained by evoking S–R habits.
Indeed, a strict S–R habit theory would require the
addict, upon waking up in the morning with no drug
available, to engage ‘automatically’ in exactly the same
old sequence of habitual actions they used previously to
get drugs, whether the actions were currently effective
or not. Yet addicts in the real world are not S–R
automatons; they are, if nothing else, quite resourceful.
On the other hand, everyone must agree that S–R
habits probably contribute to the automatized
behaviours and rituals involved in consuming drugs
once obtained (Tiffany 1990), and it has been shown
that treatment with drugs facilitates the development
of S–R habits in animals (Miles et al. 2003; Nelson &
Killcross 2006), perhaps via recruitment of the dorsal
striatum (Everitt et al. 2001; Porrino et al. 2007). We
also note that habits may be especially prominent in
standard animal self-administration experiments,
where only a single response is available to be
performed (e.g. press a lever) thousands of times in a
very impoverished environment to earn injections of
drugs. Thus, we think studies on how drugs promote
the learning of S–R habits will provide important
information about the regulation of drug consumption
behaviour in addicts, but this is not the core problem
in addiction.
(b) Relation of incentive sensitization to cognitive
dysfunction
The incentive sensitization theory focuses on sensitization-
induced changes in incentive motivational processes
and related changes in the brain, but we have
acknowledged that other brain changes contribute
importantly to addiction too, including damage or
dysfunction in cortical mechanisms that underlie cognitive
choice and decision making (Robinson & Berridge
2000, 2003). Many studies have documented that
changes in ‘executive functions’, involving howalternative
outcomes are evaluated and decisions and choices made,
occur in addicts and animals given drugs (Jentsch &
Taylor 1999; Rogers & Robbins 2001; Bechara et al.
2002; Schoenbaum & Shaham 2008). We agree that the
impairment of executive control plays an important
role in making bad choices about drugs, especially when
combined with the pathological incentive motivation
for drugs induced by incentive sensitization.

CONCLUSION
In conclusion, addiction involves drug-induced
changes in many different brain circuits, leading to
complex changes in behaviour and psychological
function.We have argued that the core changes leading
to addiction occur when incentive sensitization
combines with defects in cognitive decision making
and the resulting ‘loss of inhibitory control over
behaviour and poor judgement, combined with sensitization
of addicts’ motivational impulses to obtain
and take drugs, makes for a potentially disastrous
combination’ (Robinson & Berridge 2003, pp. 44–46).
Thus, bolstered by the evidence that has accumulated
over recent years, we remain confident in concluding
‘that at its heart, addiction is a disorder of aberrant
incentive motivation due to drug-induced sensitization
of neural systems that attribute salience to particular
stimuli. It can be triggered by drug cues as a learned
motivational response of the brain, but it is not a disorder
of aberrant learning per se. Once it exists, sensitized
wanting may compel drug pursuit whether or not an
addict has any withdrawal symptoms at all. And
because incentive salience is distinct from pleasure or
liking processes, sensitization gives impulsive drug
wanting an enduring life of its own’ (Robinson &
Berridge 2003).

For further information:Addiction_Theory2

World-Hepatitis Day (19.05.10)

World Hepatitis Day: Will CA Allow Pharmacists to Save Lives and Money through Syringes?

California is one of only three states in the U.S. that still prohibits pharmacists from selling a syringe without a prescription from a physician.

May 19th marks World Hepatitis Awareness Day – a great opportunity for California to take action to help prevent liver cancer and liver disease caused by hepatitis C and B. We ask you to join us in supporting Senate Bill 1029 to ensure all Californians have access to an essential and common-sense component of an effective hepatitis prevention strategy: the ability to purchase sterile syringes in a pharmacy.

Hepatitis C, which is commonly transmitted when syringes are shared, can lead to liver disease, cirrhosis, liver cancer, and premature death. While treatment for hepatitis C is partially effective, it is expensive and for some patients debilitating. Even with treatment, some remain chronically infected.

Long after a person has stopped using drugs, living with chronic hepatitis C can lead to other health problems, to disability, to job loss, and even homelessness. Thirty percent of people living with HIV are co-infected with hepatitis C. Hepatitis C is now one of the leading causes of death for people with HIV/AIDS in San Francisco. Hospitalizations for hepatitis C cost the California taxpayers over $1.5 billion in 2007 alone.

While all forms of hepatitis can cause severe health problems and even death, there is no vaccine for hepatitis C. The only way to prevent it is to ensure that people have the information and resources they need to avoid transmitting it.

Yet California is one of only three states in the U.S. that still prohibits pharmacists from selling a syringe without a prescription from a physician. Most states amended their laws in light of evidence that limited accesses to sterile syringes led drug users to share used ones, and that sharing syringes transmits HIV and hepatitis B and C.

The sharing of used syringes is the most common cause of new hepatitis C infections in the state and the second most common cause of HIV infection. We know from the research that pharmacy sales are a cost-effective way to combat the spread of hepatitis C and HIV without contributing to increased drug use, drug injection, crime or unsafe discard of syringes.

That is why Senate Bill 1029 is needed. It would expand the current pilot program, scheduled to end this year, to allow any pharmacy in the state to sell up to 30 syringes to individuals if the pharmacist so desires. Study after study has shown that increasing access to sterile syringes is the best way to prevent syringe sharing. By preventing HIV and hepatitis C, it is an efficient and cost-effective means of saving public dollars, and more importantly, lives. There is no cost to taxpayers through this plan, as the cost of prevention falls to the individual who purchases the syringes.

As people concerned with the health and well-being of all Californians, we ask you to stand with us in support of SB 1029. The California Department of Public Health, the Federal Centers for Disease Control & Prevention, the World Health Organization, and all leading health policy research organizations agree – safe and legal syringe access through pharmacies is a key component to the prevention of hepatitis C and HIV.
Leland Y. Yee, Ph.D. (D-San Francisco) is a California state Senator. Barry Zevin MD, is a physician specialist with the, Tom Waddell Health Center, San Francisco Department of Public Health, and assistant clinical professor at UCSF School of Medicine.

source: http://www.alternet.org/health/14690…rough_syringes

Hepatitis C can lie low for years until it wreaks havoc with your liver

WHO’S AT RISK
Hepatitis C is a disease of the liver; there are five hepatitis viruses, and this one has one of the highest rates of progression to chronic disease. “Hepatitis C is a viral infection that causes inflammation of the liver that can lead to increased scar tissue and eventually to cirrhosis,” says Kim-Schluger. “About 4 million Americans are infected with hepatitis C — 1.6% of the population.”

Hepatitis C is a blood-borne disease whose underlying virus was only isolated in 1989. “If you look the number new infections through the decades, a large percentage of patients were infected before 1992, when we developed a good test for hepatitis C,” says Kim-Schluger. “Infection rates dropped precipitously after that.” Because the blood supply wasn’t being reliably screened for hepatitis C until 1992, many americans were infected as the result of blood transfusions.

The two groups at highest risk of the disease are people who received transfusions before 1992 and IV drug users. Other groups at risk are people who have used intranasal cocaine, hemodialysis patients, and health-care workers who are pricked by needles. The virus can also be sexually transmitted. “The risk increases with high-risk behaviors like multiple partners,” says Kim-Schluger. “It’s a low risk, but it’s not zero.”

SIGNS AND SYMPTOMS:
For many patients, the diagnosis of hepatitis C comes without warning signs. “The tricky thing is that the majority of people are asymptomatic, or only have vague symptoms like feeling fatigued,” says Kim-Schluger. “So it is up to the doctor to ask about the risk factors and then screen people who are at risk.”

Up to about 15% of people infected by the hepatitis C virus are able to clear it from their bodies spontaneously. “The other 85% will continue to have virus within their blood,” says Kim-Schluger. “Of that group, about 20% of will develop cirrhosis and 1% to 5% will develop liver cancer related to cirrhosis.” With an infected population of 4 million, these percentages indicate that there will be hundreds of thousands of cases of severe liver disease caused by hepatitis C in the next 10 to 20 years.

Hepatitis C usually has a long latency period, during which the virus lies dormant. “The delay between infection and end-stage liver disease varies a lot, depending on factors like when you were infected and your gender,” says Kim. “It’s usually about 30 years from infection to cirrhosis.” Using alcohol and marijuana shortens this lag. The disease also progresses faster in people who are older than 40 when they get infected. Premenopausal women are slightly protected by estrogen, which may slow fibrosis, the growth of damaging scar tissue in the liver.

Patients do start to show symptoms when they reach end-stage liver disease. “By this time, there is often bleeding in the esophagus or the stomach,” says Kim. “That has to do with the scar tissue causing increased pressure and causing portal hypertension” — high blood pressure in the portal vein, which serves the liver. Often, fluid builds up in the abdomen, and the liver stops clearing the toxins it can ordinarily remove.

TRADITIONAL TREATMENT
Hepatitis C isn’t treated until it becomes chronic, which means the body hasn’t cleared the virus on its own. “The first line of treatment is a combination of drug therapies,” says Kim. “Pegylated interferon is an injection that you get once a week, and ribavirin is a drug that you take every day.” Depending on the genetic makeup, or genotype, of the virus you have, the therapy lasts six to 12 months. right now, the success rate for these antiviral treatments is about 50%. “If the treatment is successful, it gets rid of the virus,” says Kim. “but it’s difficult treatment, and there are many side effects.”

Patients have three types of responses to the therapy. “Responders clear the virus, and nonresponders don’t clear it at all,” says Kim. “Relapsers clear the virus during therapy, but afterward it comes back.”

For patients whose hepatitis C progresses to cirrhosis and then end-stage liver disease, a transplant is the sole remaining option. “The only way to survive end-stage liver disease is a transplant, and the overall transplant survival rate after one year is 85%,” says Kim. “Unfortunately, the virus doesn’t go away after transplant, so there are issues of recurrent disease after transplant.” Beyond liver transplant, “the next step would be a cure, and I am hopeful that there will be a cure during our lifetime,” says Kim.

RESEARCH BREAKTHROUGHS:
Doctors are continually improving the treatments available for hepatitis C so they can bring relief to a higher percentage of patients. “There are new protease and polymerase inhibitors coming out in the near future, as soon as 2011-2012,” says Kim. “You have to use this therapy in conjunction with the interferon and ribavirin, but then it increases the response rate from 50% to 70%.”

QUESTIONS FOR YOUR DOCTOR:
If you’re diagnosed and need therapy, the key question to ask is, “What can I expect in terms of side effects?” Some of the best medications can cause psychiatric side effects, so it’s essential to talk to your doctor about your psychiatric history and any other medications or herbal supplements you’re taking. Another good question is, “What genotype of hepatitis do I have, and how does

that affect the outcome of therapy?” Your options will depend on which genotype you have.

WHAT YOU CAN DO
Get screened.
If you have risk factors for hepatitis C, find out if you have the infection.

source: http://www.nydailynews.com/lifestyle…er.html?page=1

Pharmacist education in MMT.!, syringes,

Pharmacists have the unique knowledge, skills and responsibilities for assuming an important role in substance abuse prevention education and assistance…  Pharmacists, as health care providers, should be actively involved in reducing the negative effects that substance abuse has on society, health systems and the pharmacy profession.

— American Society of Health-System Pharmacists (2003)

Competency framework

Unless they have taken special training, most pharmacists are unaware of the clinical and practice issues surrounding methadone and their impact on client safety because they have had little or no exposure to them during their undergraduate pharmacy education.

The role of the pharmacist in MMT is unusual and there is no similar model in other therapeutic areas. Daily interactions with clients, along with direct clinical assessments, supervised dose administration and close monitoring do not usually occur in other types of pharmacy care. Pharmacists require a set of key competencies to ensure client safety in methadone maintenance treatment.

The panel recommends that:

15. Pharmacy managers/owners, hospital pharmacy directors and the Ontario College of Pharmacists support and encourage pharmacists providing methadone services to have education in and/or demonstrate knowledge and skills in core competency areas. These areas include:

a. Substance use disorders, including opioid dependence. [IV]

b. The varied models of substance abuse treatment, including harm reduction and its implications for pharmacy. [IV]

c. The impact of attitudes and stigma on client care. [III]

d. Methadone maintenance treatment clinical guidelines and their rationale, particularly with respect to practices to protect client safety, including:

• assessing initial and increased doses for appropriateness
• assessing methadone-dosing histories (for missed doses and irregularities in pattern of pickup) before dispensing a dose of methadone to a client
• ensuring the safe provision of “carries” (take-home doses) to clients
• dealing with intoxicated clients, including understanding the risks of polysubstance abuse. [IV]

Pharmacists need to understand substance use disorders, particularly addiction, and to understand the difference between “use” and “use disorders.” Pharmacists need to be able to identify individuals with substance use disorders and to help motivate them to seek change and treatment. As one of the most accessible health care professionals, the pharmacist can play an important role and refer patients to appropriate services and substance use treatment programs. Many MMT clients have concurrent substance use disorders with substances such as alcohol, benzodiazepines or cocaine. Pharmacists should understand the risks associated with polysubstance use and the risk of toxicity.

Although pharmacists may already be involved in harm reduction, for example, by providing sterile needles and syringes to people who use injection drugs, further involvement could include offering advice to people with substance use problems about health issues and how to minimize health risks. A random survey of 2,017 Canadian pharmacists by Myers et al. (1998) found that while more than 88 per cent of pharmacists were comfortable with the harm reduction role in providing needles and syringes, this comfort did not extend to providing methadone services. This may be due to a misunderstanding of the benefits of methadone maintenance treatment and its role as a harm reduction approach. Educational initiatives need to address such misunderstandings and other negative attitudes or misperceptions that may be held by pharmacists.

Pharmacists must have a good understanding of the critical safety issues associated with methadone. Methadone has a unique pharmacological profile that makes it useful in the treatment of opioid dependence; however, it is different from other opioids and the implications of its long half-life can lead to risks of accumulation contributing to methadone overdose and deaths.

The initiation phase of methadone treatment can be a time of high risk for toxicity and pharmacists’ understanding of dosing recommendations is critical at this stage. Pharmacists need to exercise particular vigilance in monitoring client dosing for appropriateness. For example, where clients have missed several doses (defined as three or more), or fewer (one or two) during periods of methadone dose escalation, pharmacists must understand the concept of loss of tolerance and risks to clients if the usual regular methadone dose is administered (CPSO, 2005).

Pharmacists also have to understand the safety issues associated with “carries.” Having a written carry agreement with the client is one way to help the client understand these issues as well. Pharmacists should be aware of some of the signs that indicate a formerly stable client on a high level of carries is relapsing to instability (e.g., missing observed dosing days, lost carries) (CPSO, 2005).

Pharmacists in Ontario need to be familiar with the CPSO’s most recent Methadone Maintenance Guidelines (2005), the OCP’s Policy for Dispensing Methadone (2006), and CAMH’s Methadone Maintenance: A Pharmacist’s Guide to Treatment (Isaac et al., 2004).

Understanding the risks of polysubstance use and knowing how to deal with intoxicated clients are particularly important core competency areas for pharmacists, with significant safety implications. The pharmacist should have an understanding of the impact that polysubstance use (for example, use of benzodiazepines, alcohol and cocaine) can have on the client taking MMT. Through dialogue and checking for signs of excessive dosing or substance use such as sedation, slurring of speech, smelling of alcohol and unsteady gait, the pharmacist should be able to assess if a client is intoxicated before dosing.

Recommendations from the coroner have highlighted the need for assessing clients for intoxication because deaths have occurred through combination of methadone and other drugs, including alcohol (OCP, 2008).

In an Australian survey (Peterson et al., 2007), pharmacists identified the risk of overdose associated with methadone alone and in combination with other psychoactive drugs as the greatest problematic issue for pharmacists in deciding to provide a methadone service.

In a survey of 148 pharmacists in Australia (Koutroulis et al., 2000), when asked about how they would respond to clients who presented intoxicated for their methadone dose, 44 per cent said they would withhold the dose and inform the client of this. This is the desirable course of action. However, 32 per cent of pharmacists said they would provide the usual dose, 16 per cent would dispense a reduced dose without the client knowing and nine per cent said they would blind the dose with a placebo. Only two per cent of the pharmacists indicated that they would breathalyse an intoxicated client.

Pharmacists who withheld the methadone dose were more likely to inform the prescriber (74 per cent) than pharmacists who dispensed the usual or modified dose. In a focus group, the reasons for dispensing to an intoxicated client were categorized as follows:

• insufficient communication between prescriber and pharmacist
• downplaying the risk of toxicity
• personal beliefs and values
• fear of what the client would do if dose refused
• difficulty in recognizing intoxication and lack of education and training.

Further, Koutroulis et al.’s survey suggested that pharmacists who had more than 10 methadone clients were more likely to provide the usual methadone dose than pharmacists with 10 or fewer clients.

Educational offerings

Many physicians and pharmacists don’t think they see addicts in their practice. The reality is they probably are treating them for other disorders, but the patient just hasn’t been identified as an addict. This also means that dependence treatment needs to become part of regular pharmacy practice as well.

— Open discussion, physicians and pharmacists (Raisch et al., 2005)

The panel recommends that:

16. All pharmacy students receive education on substance abuse, including opioid dependence, its treatment and practical intervention strategies, in their undergraduate curriculum. [IV]

Future pharmacists need to be adequately educated on substance use so that they are prepared upon graduation to care for patients with substance abuse disorders. In particular, opioid dependence and its treatment should be required components in the curriculum. Pharmacists who have had education in this area are likely to feel more comfortable providing pharmaceutical care to this group of clients.

Currently there are two faculties of pharmacy in Ontario, at the University of Toronto and at the University of Waterloo. The Waterloo faculty initiated their program in January 2009; therefore, their plans for curriculum on substance abuse education are still in the development phase.

At Toronto’s Faculty of Pharmacy, pharmacy students receive a rigorous scientific and clinical education over four years but receive little or no education on substance abuse and its treatment. Since the early 1990s, an elective fourth-year problem-based course has been offered (Busto et al., 1994). This course has one 2-hour segment on opioid abuse and treatment. It includes a didactic component, as well as an MMT client interview and discussion of stigma and attitudes. The course is elective and only a small proportion of the fourth-year class has taken this course offering.

Over the last five years enrolment in this elective has increased from 9.7 per cent of the class (13/134 students) in 2003–2004 to 34.2 per cent of the class (79/231 students) in 2008–2009 (personal communication, Dr. B. Sproule, April 29, 2009). Clearly, most future pharmacists have no exposure to substance use, opioid dependence and treatment with methadone.

The lack of specific undergraduate educational activities about substance abuse results in a missed opportunity to positively influence the knowledge, skills and attitudes of future pharmacists in this area.

As the most accessible of all health care professionals, pharmacists have an important role to play to help prevent and treat substance abuse disorders in their clients (Tommasello, 2004). Preparation for this role should begin in the undergraduate pharmacy training.

Experiential learning and other innovative teaching methods, for example, involving real patients (or simulated cases), audiovisual vignettes or other online modules may enhance pharmacy students’ understanding of substance dependence issues and attitudes.

One college of pharmacy in the United States, in addition to a required substance abuse course, offers an elective to illustrate addiction recovery principles. Students taking the elective are asked to give up a habit that is causing them problems for six weeks and they meet weekly to discuss the addiction recovery process. This course has been offered for 15 years and 50 per cent of the substance abuse course students are enrolled (Baldwin, 2008).

From the client consultation interviews

Clients’ need for pharmaceutical care

“I would have liked to know more about methadone before I started. It would have helped me make a better decision. You shouldn’t just tell a sick person ‘this will make you better.’ ” “There has been a lack of care and communication and confusion with my HIV meds. The methadone wasn’t holding me due to medication interactions.” “I felt sick for weeks and didn’t know it was because my dose was too high.”

The panel recommends that:

17. Professional organizations, addiction and mental health agencies and pharmacists’ employers promote the development of, and provide encouragement for all practising pharmacists to participate in, educational events on substance abuse and opioid dependence, including the growing problem of prescription opioid abuse. [III]

Most pharmacists receive little training on opioid dependence and treatment in their undergraduate experience, and it is important that all pharmacists further their knowledge in this area, even if they are not yet providing MMT services. There are indications that abuse and dependence on prescription opioids is increasing in Ontario and Canada. There was an increased number of patients addicted to prescription opioids entering the CAMH methadone maintenance program following the rapid expansion in the availability of MMT in Ontario in the 1990s (Brands et al., 2002; Brands et al., 2000). More recently, the number of individuals seeking detoxification treatment from controlled-release oxycodone at CAMH has also increased significantly (Sproule et al., 2009). In addition, in a cohort study of illicit opioid users, the proportion using prescription opioids increased from the year 2002 to 2005, with regional differences noted across Canada (Fischer et al., 2006). Pharmacists need to increase their knowledge base in prescription opioid addiction, particularly to understand the difference between addiction and physical dependence. Continuing education programs on pain treatment rarely (or inadequately) discuss the issue of opioid abuse and dependence.

A survey in British Columbia of 257 pharmacists (Cohen & McCormick, 2008) found that a slight majority reported training on how to identify signs of prescription drug misuse or abuse. This training was more common in younger pharmacists. The mean amount of training was 13.6 hours. Many pharmacists learned to identify prescription drug misuse through personal experience: they detected multi-doctoring using the provincial PharmaNet prescription drug profile or by recognizing early refills of prescriptions. Most intervened by calling the physician to confirm prescriptions or by confronting the customer directly. The primary reason they gave for not intervening was concern over how the customer might react (i.e., they were afraid that the client would be confrontational or they feared for their own safety). Pharmacists recommended additional training on prescription drug misuse.

Jones et al. (2005) surveyed 42 community pharmacists in Wales and found that at one month after a structured educational evening event there was little maintained change in attitudes. This suggests that changing attitudes is a long-term process. There is a need for reinforcing changes through continuing education.

Practising pharmacists (484) in Florida were surveyed while attending continuing education programs (Lafferty et al., 2006). Of the respondents, 67.5 per cent reported participating in two or fewer hours of addiction/ substance abuse education in pharmacy school and 29.2 per cent said they had received no addiction education. Pharmacists who had more education counselled clients more frequently and felt more confident in dealing with substance abuse clients. Of those surveyed, 53 per cent reported they had never referred a patient to substance abuse treatment in their whole career.

Brooks et al. (2001) conducted a survey in the United States of 556 pharmacists, comparing those who had taken training in addiction treatment to those who had not, and found that those who had taken training would more likely refer clients to community resources and be more involved in working with their chemically dependent clients.

The panel recommends that:

18. The Ontario College of Pharmacists revise the current requirements for pharmacies providing MMT services to mandate earlier training to promote safety. The designated manager and one pharmacist must complete the training within six months of starting to dispense methadone. [IV]

19. CAMH or another approved provider of methadone training develop a brief electronic document (e.g., one page) outlining the key safety features of providing MMT services that can be made available for immediate use by pharmacies initiating MMT services. [IV]

20. CAMH produce an electronic version of its most recent pharmacist’s guide to methadone maintenance treatment that can be purchased online and downloaded immediately so that pharmacies initiating MMT services can access it without delay. [IV]

21. CAMH make the online component of its Opioid Dependence Treatment Course available immediately upon enrolment to pharmacists new to providing MMT services, with the stipulation that these pharmacists attend the workshop component within six months of beginning the course. [IV]

22. CAMH or another approved provider of methadone training monitor and respond to waiting lists for training programs by, for example, offering the training more frequently or by exploring other delivery methods, such as webinars or video conferencing, to help meet the needs of pharmacists in remote areas. [IV]

Since undergraduate training on substance abuse and opioid dependence is lacking, most pharmacists do not have an adequate knowledge base from which to provide MMT services safely.

Having the most essential knowledge and references easily accessible and as early as possible will help facilitate pharmacies starting a methadone service and assist those who are deciding whether to provide MMT.

The online component of the CAMH Opiate Dependence Treatment Interprofessional Education Program would provide a good introduction to providing service, and a brief methadone information sheet would complement this program. The methadone information sheet could include some of the key points in providing MMT service, for example, observing dosing, diluting dose in orange drink, identifying the client, assessing the client for intoxication and informing the prescriber of missed doses.

Having a current version of the CAMH Pharmacist’s Guide available in a downloadable format would enable pharmacists to have this mandatory reference as soon as they need it. The other two references pharmacists dispensing methadone require, the CPSO Methadone Maintenance Guidelines and the OCP Policy for Dispensing Methadone, are currently available electronically.

The panel recommends that:

23. The Ontario College of Pharmacists and providers of methadone training collaborate on ongoing training requirements based on needs identified during the College’s pharmacy inspection process. [IV]

The Ontario College of Pharmacists undertakes regular inspections of community pharmacy practice in the province. Practice issues related to methadone service provision identified during these inspections could be shared with educational service providers for consideration in future training initiatives. This would be an effective mechanism for updating methadone training to reflect current practice issues in the field.

The panel recommends that:

24. CAMH or another approved provider of methadone education deliver methadone training in a manner consistent with interprofessional education principles. [IV]

Since MMT practice is best delivered in a collaborative manner (Health Canada, 2002), a multidisciplinary approach in education will prepare pharmacists to work effectively with other health professionals as a team.

The panel recommends that:

25. The Ontario College of Pharmacists and community colleges providing pharmacy technician training develop core competency requirements for regulated pharmacy technicians providing MMT services. [IV]

Pharmacy technicians are important members of the pharmacy team. They may be involved with preparing and dispensing methadone, and interact with MMT clients in the pharmacy. Core competencies should be developed and educational programs designed to optimize the role of pharmacy technicians in the safe delivery of methadone services. This issue may be particularly important in view of the new regulated status for pharmacy technicians that will be implemented soon in Ontario, where pharmacy technicians will be able to take more responsibility for dispensing.

The panel recommends that:

26. CAMH or another approved provider of methadone education undertake a needs assessment of pharmacists who have participated in the initial MMT training, and then use this information to develop an updated or advanced MMT course for pharmacists. [IV]

27. Professional pharmacy organizations, the Ontario College of Pharmacists, pharmacy managers/owners and hospital pharmacy directors encourage pharmacists to take courses on motivational interviewing, intervention strategies to use with difficult patients, and concurrent disorders, to enhance pharmacists’ skills in dealing with opioid-dependent clients. [IV]

Pharmacists who are already in MMT practice and have taken initial MMT training may wish to update and improve their skills. Since pharmacist training is recommended by the Ontario College of Pharmacists every five years, a new, higher level course would meet the needs of this experienced group of providers. Pharmacists who have taken initial MMT training should be surveyed for their input about topics to include within this higher level course. This advanced training could include, for example, methadone use in pregnancy, in patients with concurrent disorders (e.g., pain, psychiatric disorders, HIV) and in other special populations.

Any interaction with a client has therapeutic potential. Pharmacists using motivational techniques in their interactions with clients may enhance clients’ treatment. The issue of dealing with difficult, demanding clients has been identified by pharmacists as an area in which they would like more training (Cohen & McCormick, 2008). Training in de-escalation techniques to avoid potentially unsafe interactions could help pharmacists achieve greater satisfaction in their practice, as well as improve client outcomes.

The panel recommends that:

28. Drug information service providers ensure that staff is trained on and familiar with common issues in MMT treatment and have a mechanism to refer to experts when necessary. [IV]

Pharmacies must subscribe to a drug information provider service. The staff at the drug information provider should be able to respond to general questions on MMT and substance abuse. To do this they would require training in MMT to understand the patient safety issues and relevant guidelines. For more complex questions, the drug information service should have an arrangement with expert service providers to assist in consultation.

The panel recommends that:

29. Professional pharmacy organizations develop a mechanism in conjunction with the Ontario College of Pharmacists to ensure that pharmacists dispensing methadone are informed in a timely fashion of new educational resources available. [IV]

A timely direct communication via e-mail from the Ontario College of Pharmacists, the Ontario Pharmacists’ Association or another professional pharmacy organization is recommended when any new methadone-related item is posted on the website of either the OCP or the CPSO.

The panel recommends that:

30. Professional pharmacy organizations, CAMH and funding agencies develop a mentorship program to link new methadone service providers with experienced providers. [IV]

31. Professional pharmacy organizations and CAMH promote the CAMH Addiction Clinical Consultation Service to pharmacists providing MMT services. [IV]

The Addiction Clinical Consultation Service (ACCS) is a service provided by CAMH. It is designed to serve health and social service professionals, including pharmacists, who have client-specific questions related to substance abuse. The accs is not designed to deal with health emergencies or immediate or legal issues. The health care worker calls a central phone number and, depending on the question, accs may provide referral to a consultant team member (physician, therapist/counsellor or pharmacist) who will communicate with the health care worker within four hours. Awareness of the service should be promoted to support pharmacists providing methadone services.

Methadone Vs. Subutex/ Suboxone!

Very few studies have considered heroin users’ views on substitute prescribing, in
particular with regards to subutex. The aim of this study was to conduct detailed
qualitative analysis, using the Grounded theory approach, on heroin users’ views on
substitute prescribing, paying specific attention to methadone and subutex. Semistructured
interviews were conducted with nine subjects recruited from an
abstinence-based, structured day care treatment program. All of the subjects were
either currently on a subutex prescribing program, or had remained abstinent from
illicit substances following the completion of a subutex treatment program. Five major
themes emerged from the analysis. These were reasons for obtaining a methadone
prescription, experiences with methadone programs, views on methadone, views on
subutex and views on an ideal opioid treatment program. Most of the findings were
supported by previous qualitative studies such as that of Neale (1999a) and Fischer
and colleagues (2002). However, there does appear to be some discrepancies
between qualitative and quantitative research with regards to consumer satisfaction
of methadone, in comparison to subutex, as a substitute drug. This study clearly
highlights the need for further research into users’ views on substitute prescribing,
with emphasis being placed on qualitative research considering users’ experiences
with subutex.

Read the full File: methadoneversussubutex kopie

Hepatitis C Treatment of Substance Users in Pharmacotherapy for Addiction

Introduction:

Hepatitis C, Substance Use,
and Dependence
Illicit drug and alcohol abuse and dependence are problems
of major medical importance in the United States, leading
to high rates of morbidity and mortality from end-stage
liver disease. The prevalence of illicit drug use in the United
States, as estimated by the National Survey on Drug Use
and Health in 2002, stands at 19.5 million Americans above
the age of 12; half of Americans aged 12 or older (51.0%)
reported being current drinkers of alcohol, an estimated
120 million people [1•].

Salient illicit drug use and practices
are presented in Table 1. The Centers for Disease Control
has estimated that 60% of all new cases of hepatitis C are
related to injection drug use [2]. Injection drug practices
include the use of heroin, cocaine, methamphetamine, and
prescription opioids (Table 1).

It has been estimated that
there are at least 800,000 untreated injection-heroin users
[3]. However, the population of opioid-drug users may be
grossly undercounted, because some surveys have found up
to three times more illicit drug users in particular regions
than commonly estimated [4].
Drug addiction is a chronic, relapsing neurophysiologic
disease resulting from the prolonged neurologic
effects of drugs. The neurochemical abnormalities resulting
from chronic use, such as opioids, underlie many of the
observed physical and behavioral aspects of addiction
(Table 1). The brain abnormalities associated with addiction
are wide ranging, complex, and long lasting [5,6].

They can involve genetically abnormal brain signaling
pathways, social factors, psychological conditioning or
stress, and result in cravings leading to a predisposition to
relapse even months or years after drug use cessation.
Recent studies have identified risk factors for the transition
to injection drug use that include the following: emerging
drug practices, differential characteristics of opiate injectors
versus inhalers, and patient-related factors that predict
entry into substance abuse treatment [7•,8].

The importance
of limiting individuals from progressing to injection
drug use can be vividly seen from data comparing the
hepatitis C incidence between injection and noninjection
drug users [9]. This longitudinal surveillance study in
New York City showed an annual incidence rate of
hepatitis C in young noninjection drug users of 0.4 per 100
person-years compared with 35.9 per 100 person-years in
injection drug users (IDUs).

Thus, delaying or preventing
the transition to injection drug use can have a significant
health benefit by reducing the risk of comorbid conditions
associated with substance abuse and addiction.

read the full file here: 002_HP04-3-1-05

Psychose und Sucht (Doppel-Diagnose)

INHALT
Zusammenfassung
1. Einleitung
1.1. Zum Frühverlauf der Schizophrenie
1.2. Zur Komorbidität von Psychose und Sucht
1.2.1. Epidemiologie
1.2.2. Erklärungsansätze zur Komorbidität
1.2.3. Probleme in der Therapie komorbider Patienten
1.3. Fragestellungen dieser Arbeit
2. Material und Methoden
2.1. Untersuchungsrahmen
2.2. Art der Datenerhebung
2.3. Beschreibung der Gesamt-Stichprobe
2.4. Beschreibung der Stichprobe der berücksichtigten Patienten
2.5. Zusammenfassung
3. Ergebnisse
3.1. Psychopathologie im Verlauf
3.2. Bestimmung der Parallelisierungszeitpunkte
3.3. Das Konsummuster zwischen 1988 und 1997
3.4. Varianzanalyse zum Konsummuster
3.5. Das Konsummuster an den Parallelisierungszeitpunkten
3.6. Einfluß von subjektiver Symptomatik und Diagnose-Zeitpunkt
4. Diskussion
4.1. Methodische Fragen
4.2. Diskussion der Ergebnisse
4.3. Fazit und Ausblick

weiterlesen: PsychoseundSucht_Studie

Chapter 1: Organization and Function of the Nervous System

Our behaviors, including our thoughts, sensations, emotions, remembering, and even our states of consciousness, are all a result of complex interactions between neurons distributed throughout our brain. These neurons form elaborate systems that communicate their activity by releasing small amounts of transmitter substances which act both on receiving neurons as well as on the neuron sending the message. In order for us to understand just how drugs act to treat certain psychological conditions, we must first understand the intricate and sometimes subtle ways in which neurons function to regulate our behaviors. We must also appreciate the complex systems of neurons within the brain that specialize in different functions including movement, emotions, learning and memory, and our motivational states

weiter geht es hier, ein echter leckerbissen:

psychopharmacologie 1

Chapter_2

Chapter_3

Ich bringe evt. den Rest auch noch!

Science-Based Views of Drug Addiction and Its Treatment

MORE THAN TWO THIRDS OF
people with addiction see a
primary care or urgent care
physician every 6 months, and many
others are regularly seen by other medical
specialists.1,2

These physicians are
therefore in a prime position to help patients
who may have drug abuse problems
by recognizing and diagnosing the
addiction, helping to direct patients to
a program that can meet their treatment
needs, and helping to monitor
progress after specialty treatment and
during recovery.3-6

Many physicians,
however, find the domain of drug abuse
particularly daunting and often avoid
the issue with their patients. This is understandable
given the relatively short
shrift drug abuse is given in formal
medical education. There is a widespread
misperception that drug abuse
treatment is not effective, which may
account for the reluctance of physicians
to even broach the subject of drug
abuse or treatment with their patients.
On the other hand, over the past 15
to 20 years, advances in science have
revolutionized our fundamental understanding
of the nature of drug abuse
and addiction and what to do about it.
In addition, there are now extensive
data showing that addiction is eminently
treatable if the treatment is welldelivered
and tailored to the needs of
the particular patient.

There is an array
of both behavioral and pharmacological
treatments that can effectively
reduce drug use, help manage drug
cravings and prevent relapses, and restore
people to productive functioning
in society.7-9
Of course, not all drug abuse treatments
are equally effective, and there
is no single treatment appropriate for
all patients. Fortunately, recent scientific
advances have provided insights
both into the nature of drug abuse and
addiction and into the principles that
characterize the most effective treatment
approaches and programs.10 These
treatment principles should make the
primary care or nonaddiction specialty
care physician’s tasks of screening
and referral much easier.

Read more: 20.03.10

Diacetylmorphine versus Methadone for the Treatment of Opioid Addiction

Studies in Europe have suggested that injectable diacetylmorphine, the active ingredient
in heroin, can be an effective adjunctive treatment for chronic, relapsing opioid
dependence.
Methods
In an open-label, phase 3, randomized, controlled trial in Canada, we compared
injectable diacetylmorphine with oral methadone maintenance therapy in patients
with opioid dependence that was refractory to treatment. Long-term users of injectable
heroin who had not benefited from at least two previous attempts at treatment
for addiction (including at least one methadone treatment) were randomly assigned
to receive methadone (111 patients) or diacetylmorphine (115 patients). The primary
outcomes, assessed at 12 months, were retention in addiction treatment or drugfree
status and a reduction in illicit-drug use or other illegal activity according to
the European Addiction Severity Index.

Read more: heroin_vs_methadone_2009

ROLE OF NIGELLA SATIVA IN OPIOID DEPENDENCE

Opioid dependence is a chronic disorder that produces changes in brain pathways that remain long after the patient stops taking the drug. These protracted brain changes put the dependent person at greater risk of relapse. Detoxification can be successful in cleansing the person of drugs and withdrawal symptoms; it does not address the underlying disorder, and thus is not the adequate treatment. Maintenance with methadone or naltrexone is the usual practice in the long-term management of opioid dependence but both drugs have their own disadvantages because no single medication is appropriate for every individual for treating their opioid dependence, it is important that clinicians have a variety of the therapeutic agents available to them.

Calcium channel blockers, such as verapamil, diltiazem, nifedipine, nimodipine, and felodipine are useful drugs being used in cardiovascular disorders, such as hyper-tension, arrhythmias, and ischaemic heart disease. Research on calcium channel blockers has proved their therapeutic potential in a variety of disorders such as asthma, diarrhoea, premature labour, and diseases of central nervous system such as epilepsy, and opioid dependence. Modern drugs are not only expensive and beyond the reach of majority of the population of world but also have multiple side effects. Hence there is a need to explore such drugs from indigenous sources and to observe if combination of desired therapeutic efficacy exists in nature.

Nigella Sativa is in use for the treatment of variety of ailments since ancient times. Research has based its many effects on their efficacy of blocking calcium channels. As calcium channels have been tried for the treatment of opioid dependence, so Nigella Sativa was used in this study. This study was carried out on 50 patients who were divided into two groups. Patients were admitted for 12 days and then weekly followed up for 12 weeks.

Each patient received placebo orally during day-1 and day-2 of admission. Thereafter Nigella Sativa was given to the patients from day-3 of admission to eighth week. Then the dose of each drug was tapered off during 9th and 10th weeks and then no treatment was given during last two weeks.

It was observed that Nigella Sativa showed a rapid improvement in signs and symptoms of acute opioid abstinence. It was also observed that Nigella Sativa prevented the development of significant craving and relapse. It is concluded that Nigella Sativa is effective in long term management of opioid dependence and it is suggested that further long term follow up studies may be designed with greater number of patients.

First Time the Full Research Paper here:1742 niglea sativa

The WAGER Vol. 9(11) – Attribution, Addiction, and Gambling: Series Conclusion

Series Special Editor: Sarah E. Nelson

Attributions play a role in all aspects of addiction. Attributions for wins and losses can influence the development of gambling problems (see WAGER 9(6)); attributions about peers’ drinking behavior can affect a person’s own drinking behavior (see WAGER 9(7)); being labeled as a heavy smoker can alter people’s attributions about their smoking (see WAGER 9(8)); people’s attributions about their own addictive behavior differ in predictable ways from attributions they make about others’ addictive behaviors (see WAGER 9(9)); and the attributions people make about their addictions can predict their own chances for recovery or likelihood of relapse (see WAGER 9(10)). This week’s WAGER reviews an article that attempts to model the way attributions change across the course of addiction (Davies, 1996).
Davies’ theory of attribution change rests on the idea that the explanations people make for their behaviors are functional: people make different attributions for the same  event in different contexts (i.e., depending on the setting and the goals of the interaction) (Davies, 1996; Schlenker & Weigold, 1992; Tedeschi & Reiss, 1981). For example, in a group of heroin users, Davies found that subjects made different attributions for their own heroin use to an interviewer who substance using habits were unknown than they did to a fellow heroin user (Davies & Baker, 1987). When it comes to explaining our own behavior, the attributions we make often reflect an ego-defensive bias: that is, attributions about the self serve to protect self esteem, meet self-presentational goals, and preserve self-concept (Schlenker, Weigold, & Hallam, 1990). Davies’ model reflects how attributions might serve this self-protective function in relation to an addiction.

In several different studies, Davies and his colleagues conducted interviews in Scotland with drug and alcohol users both in and out of treatment. Based loosely on these interviews, Davies outlined five attributional stages through which a person might progress as an addiction develops. Each stage is marked by a different attribution style for substance-using behavior. In Davies’ model, attributions can vary in terms of purposiveness (i.e., how intentional the behavior is portrayed), hedonism (i.e., how positively the behavior is described), contradictoriness (i.e., whether attributions contradict across the course of the interview), and the inclusion of addicted self-ascription (i.e., whether attributions make use of the concept of addiction as an explanation for behavior). (1)

During the first stage, presumably before the substance using behaviors become a problem, subjects’ attributions for their drug or alcohol use are high on purposiveness and hedonism – people enjoy using the substance and consider it under their control. During stage two, as problems begin to surface, subjects’ discourse becomes contradictory, varying from context to context between the positive and negative aspects of drug use, and the controlled and uncontrolled aspects of their using behavior. These attributions reflect the ambivalence that emerges during the development of addiction (e.g., Shaffer, 1997). During stage three, people refer to themselves as addicted, explain their substance use as out of their control, and view it as negative. At stage four, people begin to reject the usefulness of the concept of addiction in explaining their behavior and their discourse again becomes mixed and contradictory. Finally, people are able to proceed to a fifth stage that is either positive or negative. In either version, their attributions are relatively stable (i.e., the attributions don’t contradict from one context to another) and do not refer to substance using behavior in terms of addiction. In the positive version, people might have given up drugs or alcohol, but return to a view of their past behavior as controllable and a description of their use that highlights both the positive and negative aspects of that behavior. In the negative version, although the concept of addiction has been dropped, people continue to use substances and see themselves as “down and out” – their behavior is uncontrollable and their substance use is negative. Although these stages tend to relate to the progression of an addiction, people can move back and forth between stages. The one exception to this, according to Davies, is an irreversible transition from stage two to stage 3, which often occurs when subjects enter treatment and may persist long after; consider the Alcoholics Anonymous practice of participants introducing themselves, “Hi, my name is X and I’m an alcoholic.” .

To test this model of attributions, interviews with drug and alcohol users were transcribed and coders rated the attributions given in each interview in terms of the dimensions outlined in the model. The investigators assigned each respondent to one of the six stages based upon those ratings. Consensus between four judges rating the same twenty subjects was good: average agreement between the judges was 71% (.’s ranged from .49 to .75). In all cases, the judges never disagreed by more than one stage.
Although Davies demonstrated the reliability of his model (i.e., ability of coders to identify the attribution patterns associated with each stage) and stated that these stages related to the stages of an addiction, he did not provide information about hwo the attributional stages correspond to the actual temporal progression of addiction in his interviewees (e.g., whether the majority of subjects classified as stage 3 were in treatment at the time of the interview). Given his claim that movement between at least two of the stages is irreversible (a claim that contradicts established research on addiction stages — see Prochaska, Norcross, & DiClemente, 1994; Shaffer, 1997), this research is needed to verify the model. Also, although he developed his model based on years of observations and interviews of substance users, in this paper he only tests it on twenty interviewees. Given the theoretical basis of the model (i.e., that attributions vary according to context), it is important to test this model and its stages in different samples of substance users and different settings.

Davies’ model of attribution change needs to be validated, but is important for the questions it raises. How do these attributional stages relate to the stages of change described in more well-studied models (e.g., precontemplation, contemplation, preparation or determination, action, maintenance, and termination; Prochaska, Norcross, & DiClemente, 1994)? If these attributional patterns do reliably correspond to different stages of an addiction, it is important to determine

whether these attributions predict change (e.g., provide explanations that refer to being addicted as precursors of treatment-seeking behavior) or reflect change (e.g., provide explanations that refer to being addicted as an attempt to understand and explain past behavior within the treatment context). Both possibilities (i.e., predictive and reflective) and the research reviewed in this WAGER series stress the importance of people’s subjective understanding and interpretation of behavior in guiding future behavior. This attribution-behavior cycle is a crucial, often neglected piece of the study of addictions.

Adolescent Exposure to Chronic Delta-9-Tetrahydrocannabinol Blocks Opiate Dependence in Maternally Deprived Rats

Maternal deprivation in rats specifically leads to a vulnerability to opiate dependence. However, the impact of cannabis exposure during
adolescence on this opiate vulnerability has not been investigated. Chronic dronabinol (natural delta-9 tetrahydrocannabinol, THC)
exposure during postnatal days 35–49 was made in maternal deprived (D) or non-deprived (animal facility rearing, AFR) rats. The effects
of dronabinol exposure were studied after 2 weeks of washout on the rewarding effects of morphine measured in the place preference
and oral self-administration tests. The preproenkephalin (PPE) mRNA levels and the relative density and functionality of CB1, and
m-opioid receptors were quantified in the striatum and the mesencephalon. Chronic dronabinol exposure in AFR rats induced an
increase in sensitivity to morphine conditioning in the place preference paradigm together with a decrease of PPE mRNA levels in the
nucleus accumbens and the caudate–putamen nucleus, without any modification for preference to oral morphine consumption. In
contrast, dronabinol treatment on D-rats normalized PPE decrease in the striatum, morphine consumption, and suppressed sensitivity to
morphine conditioning. CB1 and m-opioid receptor density and functionality were not changed in the striatum and mesencephalon of all
groups of rats. These results indicate THC potency to act as a homeostatic modifier that would worsen the reward effects of morphine
on naive animals, but ameliorate the deficits in maternally D-rats. These findings point to the self-medication use of cannabis in subgroups
of individuals subjected to adverse postnatal environment.

02.10

Europad Nr.4

HeroinAdd9-1

1. CONTENTS
   Effects of Opioid Pharmacotherapy on Psychomotor and Cognitive
   Performance: A Review of Human Laboratory Studies of
   Methadone and Buprenorphine
2. The Vincent P. Dole Research and Treatment Institute for Opiate
   Dependence: An Integrated Biopsychosocial Model for the
   Treatment of Methadone Maintained Patients
3. Opioid Substitution with Methadone and Buprenorphine: Sexual
   Dysfunction as a Side Effect of Therapy
4. Paxil (Paroxetine) in Complex Therapy in Heroin Addicts 45-54
   MAYA ROKHLINA, TATIANA KITKINA AND GEORGI GUBANOV
   Use of Sodium Gamma-Hydroxybutyrate (GHB) in Alcoholic
   Heroin Addicts and Polydrug-Abusers
   55-76

Europad-Nr.3

HeroinAdd8-4

1. CONTENTS
   Combating the Stigma: Discarding the Label “Substitution Treatment” in Favour of “Behaviour-Normalization Treatment”
2. In the Service of Patients: The Legacy of Dr. Dole
3. Injecting Buprenorphine Tablets: A Manageable Risk
4. QTc Prolongation in Methadone Maintenance: Fact and Fiction
5. Methadone: Is It Enough?

Europad-Nr.2

HeroinAdd4-3

• CONTENTS
  Harm reduction and specific treatments for heroin addiction.
  Different approaches or levels of intervention? An illnesscentred
  perspective

  Methadone Treatment in Croatia

  The renaissance of methadone treatment in America

  Methadone and commonplaces

  Methadone maintenance and HIV infection

  Breast-feeding for a methadone-maintened mother: a case
  report

  Methadone Maintenance treatments in European
  extracommunity target

Europad-Magazin!

HeroinAdd5-2

1. Introduction ………………………………………………………………………………………………….8
   The Clinical and Therapeutic Aspects of Personality Disorders
   in Addicted Patients …………………………………………………………………………………….14
   Addiction and symptoms of psychopathology ………………………………………………….14
   Addiction and psychopathological dimensions ………………………………………………..14
   Addiction and Personality Disorders ………………………………………………………………16
   Antisocial Personality Disorder (APD) …………………………………………………………………………18
   Personality and the etiopathogenesis of addiction …………………………………………..19
   The self-medication hypothesis for addictive disorders …………………………………………………..19
   The role of subjective effects: the self-selection hypothesis …………………………………………….20
   Sensation-seeking behaviour and impairment of gratification: what is too little
   or too much? ……………………………………………………………………………………………………………..21
   The psychology of addiction: evolution of theoretical models. ………………………….22
   Psychodynamic theories ………………………………………………………………………………………………22
   Beyond psychodynamics …………………………………………………………………………………………….24
   Addiction and Bipolar Spectrum ……………………………………………………………………25
   Treatment of Personality Disorders during Methadone Maintenance ……………….30
   Conclusions …………………………………………………………………………………………………31
   The Clinical and Therapeutic Aspects of Mood Disorders
   in Addicted Patients …………………………………………………………………………………….32
   Epidemiology ……………………………………………………………………………………………….32
   Assessment and evaluation of depression in addicted patients ………………………….34
   Family History of Mood Disorders …………………………………………………………………35
   Primary or secondary nature of comorbid mood disorder in relation
   to addiction ………………………………………………………………………………………………….36
   Impact of comorbid mood disorders on the natural course
   of heroin addiction ……………………………………………………………………………………….37
   Substance use among Bipolar Patients …………………………………………………………..38
   Addiction and Suicide …………………………………………………………………………………..38
   Heroin addiction and its consequences on mood …………………………………………….41