Showing posts with label drug craving. Show all posts
Showing posts with label drug craving. Show all posts

Thursday, February 28, 2013

Craving Relief


Why is it so hard for addicts to say “enough?”

One of the useful things that may yet come out of the much-derided DSM-5 manual of mental disorders is the addition of craving as a criterion for addiction. “Cravings,” writes Dr. Omar Manejwala, a psychiatrist and the former medical director of Hazelden, “are at the heart of all addictive and compulsive behaviors.” Unlike the previous two volumes in this monthful of addiction books, Manejwala’s book, Craving: Why We Can’t Seem To Get Enough,  focuses on a specific aspect common to all addiction syndromes, and looks at what people might do to lessen its grip.

Why do cravings matter? Because they are the engine of addiction, and can lead people to “throw away all the things that really matter to them in exchange for a short-term fix that is often over before it even starts.” When Dr. Manejwala asked a group of patients to explain what they were thinking when they relapsed, their answer was often the same: “I was so STUPID.” But the author had tested these people. “I knew their IQs.” And the best explanation these intelligent addicts could offer “was the one explanation that could not possibly be true.”

In my book, The Chemical Carousel, I quoted former National Institute on Alcohol Abuse and Alcoholism (NIAAA) director T.K. Li on the subject of craving: “We already have a perfect drug to make alcohol aversive—and that’s Antabuse. But people don’t take it. Why don’t they take it? Because they still crave. And so they stop taking it. You have to attack the other side, and hit the craving.” However, if you ask addicts about craving when they are high, or have ready access, they will often downplay its importance. It is drug access unexpectedly denied that sets up some of the fiercest cravings of all. Conversely, many addicts find that they crave less in a situation where they cannot possibly score drugs or alcohol—at a health retreat, or on vacation at a remote locale.

Why are cravings so hard to explain? One reason is that “people use the word to mean so many different things.” You don’t crave everything you want, as Manejwala points out. Cravings are not the same as wants, desires, urges, passions, or interests. They are “stickier.” The brain science behind craving starts with the downregulation of dopamine and other neurotransmitters. As the brain is artificially flooded with neurotransmitters triggered by drug use, the brain goes into conservation mode and cuts back on, say, the number of dopamine receptors in a given part of the brain. In the absence of the drug, the brain is suddenly “lopsided,” and time has to pass while neural plasticity copes with the new (old) state of affairs. In the interim, the unbalanced state of affairs is a prime ingredient in the experience of craving.

Cravings are “disturbingly intense” (Manejwala) and “incomprehensibly demoralizing” (AA). Alcohol researcher George Koob called craving a state of “spiraling distress.” Cravings are not necessarily about reward, but about anticipating relief. “The overwhelming biological process in addictive craving is really a complex set of desperate, survival-based drives to feel ‘normal,’” says Manejwala.

The late Alan Marlatt, a psychologist who studied cravings for years, proposed that apparently irrelevant decisions could trigger or prevent relapse, almost without the addict knowing it. Turning left at an intersection, toward the supermarket, or turning right, toward the liquor store, can feel arbitrary and dissociated from desire. We also know that environmental cues can trigger craving, such as the site of a crack house where an addict used to do his business. Manejwala points to research showing that “some relapses related to cues and context are mediated by a small subgroup of neurons in the medial prefrontal cortex,” and suggests that it may be possible in the future to target this area with drug therapy.

Manejwala is unabashedly pro-12 Step, and favors traditional group work as the standard therapy. For example, he points to a Cochrane analysis of 50 trials showing that group participation roughly doubles a smoker’s chance of quitting. One of the reasons AA works for some people is that AA attendance reduces “pro-drinking social ties.” Simply put, if you are sitting with your AA pals in a meeting, you’re not out with your drinking buddies at the tavern. The author admits, however that alternatives such as SMART recovery work for some people, and that “sadly, much energy has been wasted as members of these various organizations bicker with each other about which works best, and this leaves the newcomer perplexed…. Over 20 million American are in recovery from addiction to alcohol and drugs. I can tell you this much: they didn’t all do it the same way.”

And along the way, you can be sure that all of them became familiar with cravings. Manejwala offers several strategies for managing cravings, and I paraphrase a few of them here:

Join something. Participate. Get out of your own head and become actively involved in some group, any group, doing something you are interested in.

Hang around people who are good at recovery. Long-timers, with a solid base of sobriety. You will not only learn HOW to do it, but that it CAN be done.

Write stuff down. This makes you pay attention to what you’re doing. Keep a cigarette log. Count calories. Know what you’re spending per month on alcohol. Educate yourself about your addiction.

Tell someone. Tell somebody you trust, because if there is anything harder than dealing with cravings from drinking, smoking, or drugging, it’s doing it in secret.

Be teachable. Watch out for confirmation bias. “When you think you have the answers, it’s hard to hear alternatives.”

Empathy matters. The author notes that the Big Book insists that by gaining sobriety, “you will learn the full meaning of ‘Love thy neighbor as thyself.’” Altruism may have evolutionary, physiological, and psychological implications we haven’t worked out yet.


Thursday, August 28, 2008

Quitting When You're High


Active smokers underestimate rigors of withdrawal.

An alcoholic wraps his car around a tree in a drunken haze. He has "hit bottom" and vows never to drink again.

A meth tweaker gets so high he becomes unruly and disoriented and is arrested. In jail, cranked to the gills on speed, she pledges to go sober, starting right now.

A cigarette smoker stumbles to bed after a typical two-pack day, coughing, throat burning, reeking of tobacco, and swears that upon waking, his remaining cigarettes will go out with the trash and his life as a human ashtray is over.

Each of these addicts has started off on exactly the wrong foot, and will very likely fail quickly in their quitting attempts, according to recent research on smoking cessation from the University of Pittsburgh and Carnegie Mellon University. It is easy to say you're going to quit while you're high, sailing along on a comfortable level of nicotine in the bloodstream. Once that available nicotine is flushed out, you are going to have some serious second thoughts about the whole enterprise of abstinence. The smoker is likely to wake up the next morning, fumbling for a smokeable butt, muttering to himself: "What in the world was I thinking of last night? No way am I quitting today."

In a study to be published in the September issue of Psychological Science, researchers showed that cigarettes smokers who are not actively craving a cigarette when they vow to quit will likely not succeed, because they inevitably underestimate the rigors of the upcoming withdrawal, and the fierce intensity of their future desire to smoke.

According to lead investigator and professor of psychology Michael Sayette, "this lack of insight while not craving may lead them to make decisions--such as choosing to attend a party where there will be lots of smoking--that they may come to regret."

In the study, titled "Exploring the Cold-to-Hot Empathy Gap in Smokers," the researchers write: "In contrast to smokers in a hot (craving) state, those in a cold (noncraving) state underpredicted the value of smoking during a future session when they would be craving.... Failing to anticipate the motivational strength of cigarette craving, nonsmokers may not appreciate how easy it is to become addicted and how difficult it is to quit once addicted."

George Loewenstein, professor of economics and psychology at Carnegie Mellon and a co-author of the study, said that the research implications for non-smokers were crucial: "If smokers can't appreciate the intensity of their need to smoke when they aren't currently craving, what's the likelihood that people who have never smoked can do so?"

As further evidence of this psychological mismatch, the researchers cite earlier work performed by the University of Michigan’s Monitoring the Future longitudinal study of 1993, "which found that although only 15% of respondents who were occasional smokers (less than one cigarette per day) predicted that they might be smoking in 5 years, 43% of them were, in fact, smoking 5 years later."

All things considered, it's better to make the quitting decision when you're hurting, not when you're high.

Graphic Credit: Florida State University

Wednesday, March 12, 2008

Drug Addiction and Dissociation


Where does the “self” go during active addiction?


Where does the everyday self go during active cycles of addiction? Addiction sometimes seems to resemble a waking trance, or autohypnosis. Psychologically, it is akin to a state of dissociation. The sense of self becomes impaired through the processes of intoxication, denial, neuroadaption, withdrawal, and craving. This impaired sense of self causes behavior that is baldly contradictory to the addict's core beliefs and values. Honest men and women will lie and steal in order to get drugs.

Webster’s Unabridged Dictionary defines dissociation, rather vaguely, as “the splitting off of certain mental processes from the main body of consciousness, with varying degrees of autonomy resulting.” How autonomous were you, consciousness-wise, the last time you got drunk and parked your car somewhere you couldn’t remember?

Dissociation may be part of the way consciousness itself adapts to chronic drug use. Richard S. Sandor, a thoughtful Los Angeles physician, helped to clarify many of these issues in an excellent essay some years ago in Parabola Magazine.

Sandor compares the addictive state to a form of hypnosis accompanied by posthypnotic amnesia. This automatism, this subsequent amnesia about the drugged “I” on the part of the sober “I,” is highly reminiscent of the consequences produced by state-dependent memory:

"A hypnotized subject is instructed to imagine that helium-filled balloons are tied to his wrist; slowly the wrist lifts off the arm of the chair. The subject smiles and says, ‘It’s doing it by itself!’ The ‘I’ that lifts the arm is unrecognized (not remembered) by the ‘I’ that imagines the balloons.... One part denies knowledge of what another part does. A cocaine addict, abstinent for a year, sees a small pile of spilled baking soda on a bathroom counter and experiences an overwhelming desire to use the drug again. Who wishes to get high? Who does not?"

“Interestingly,” Sandor says, “this type of amnesia is very similar to that seen in the multiple personality disorder (see Jekyll and Hyde), in which one entire ‘personality’ seems to be unaware of the existence of another. Even more interesting is the fact that confabulation, rationalization, and outright denial are also prominent features of the addictive disorders.” Dissociation, then, can occur without the intervention of anything as dramatic as hypnosis. The common quality is automaticity, the experience of “it doing it by itself.”

Sandor points to the inability of prevailing behavioral models to produce a comprehensive framework for effective addiction treatment. “None of the current treatment methods based upon the positivist scientific paradigm—be it psychodynamics (Freud, et al.) or behavioral (Pavlov, Watson, Skinner)—has demonstrated any particular superiority in the treatment of the ‘addictive disorders,’” he writes. “Many psychoanalysts readily admit the uselessness of that method for treating addicted individuals (the patient is regarded as being ‘unanalyzable’).”

In addition, says Sandor, “It appears that the most successful means of overcoming serious physical addiction is abstinence—very often supported by participation in one of the twelve-step groups based on the Alcoholics Anonymous model.... The basis of recovery from addiction in these nonprofessional programs is unashamedly spiritual.”

All addictions, Sandor argues, more closely resemble “the whole host of automatisms that we accept as an entirely normal aspect of human behavior than to some monstrous and inexplicable aberration.” Bicycle riding is a good example of an automatism, because once learned, “…it no longer requires the subjective effort of attention; more importantly, once learned, it cannot be forgotten. It is as though the organism says to itself, ‘Riding this thing could be dangerous! It’s much too important to trust that Sandor will pay close attention to it.’”

So what does the mind do? It creates a new state called bicycle riding:

"Number one priority in this state (after breathing and a few other things, of course) will be maintaining balance. In much the same way, the organism recognizes that mind- and mood-altering chemicals disturb the equilibrium of functions and are therefore potentially dangerous. In response, it may form a new state in which the ability to function is restored, but in which a new set of priorities exerts an automatic influence. Just as one’s only hope of not riding the bicycle again (if for some reason that is important) is to never again get on one, once a particular addictive state has developed, there is no longer any such things as “one” (drink, hit, fix, roll, etc.). Addicts begin again when they forget this fact (if indeed they have ever learned it) and/or when they become unable to accept the suffering that life brings and choose to escape it without delay. Addictions can be transcended--not eliminated."


--Excerpted from The Chemical Carousel: What Science Tells Us About Beating Addiction © Dirk Hanson 2008, 2009.

Thursday, February 14, 2008

Fighting Fire with Fire


An introduction to anti-craving drugs

The early neurobehavioral research on addiction has been vindicated by the development of anti-craving drugs and new drugs for depression.

On the other hand, the psychopharmacology of addiction is not much studied in med school, and all but unknown among the general populace. Even the treatments now in existence are woefully underutilized. Moreover, there are good reasons to question whether these drugs are being prescribed with sufficient care and forethought in cases where they are being used. Legitimate, unanswered questions exist about pharmacotherapy for addictive disorders.

The most important effect--the reregulation of brain receptor arrays with time--is little understood. And we cannot say with certainty whether messing with Mother Nature’s receptors, in some cases, might disrupt other finely tuned immunological or neurological systems in the body. Finally, there is the possibility of side effects years down the road, which obviously cannot be predicted based on current studies. What we already know is that the “bodymind,” as Candace Pert refers to it, is a delicate and astonishingly complicated piece of organic machinery.

Researchers are confronted with the perpetual dilemma of designing out, or designing down, the side effects of any new class of drugs. The historical record of drugs like Thorazine, and darker cases like Oraflex and thalidomide, are reminders of the potential pitfalls of development races and corner-cutting practices in the pharmaceutical industry. The pharmacological sciences and the people who work in them are inextricably linked to the drug companies that sell the end products of any neurochemistry that yields marketable new medications. It cannot be otherwise: Market considerations drive much of the research. By 1990, the American pharmaceutical industry had surpassed the federal government’s National Institutes of Health as the world’s principal source of biomedical research and development funding. One of the stiffest challenges facing managed health care in the future will be the matter of evaluating the effectiveness of medications for addiction.

Fighting fire with fire brings scientists face to face with the problems posed by the blood-brain barrier, that superfine mesh of cells that protects the brain from unwelcome molecular intruders. Bacteriologists discovered the barrier more than two centuries ago, when they learned that dyes injected into the body stained all the organs except the brain. Normally, the capillary-rich barrier of cells is so densely packed that the only way to penetrate the tight junctions between them is by means of special transporter molecules. These specialized molecules act as chauffeurs for the amino acids, hormones, and other compounds that must pass regularly and consistently into the brain. These transporter molecules can be fussy about riders, and the only way around that is to use molecules so tiny that they are measured in units of atomic mass called “Daltons.”

Knowing this, biochemists have worked toward discovering extremely small molecules, and this is partly why so few effective psychoactive drugs come along. While scientists have had some luck with small-molecule approaches to treating epilepsy, schizophrenia, and certain mood disorders, there is no reason to assume a small molecule can always be found to fit the bill.

Current work centers on tricking existing transporter molecules into ferrying artificial cargos into the brain. Pills that easily penetrate the blood-brain barrier are rare, special, and capable of causing a host of problematic side effects. If Zyban demonstrated that there were good reasons to be hopeful about future anti-craving drugs, then the diet drugs Redux and “fen-phen” demonstrated to critics of the drug industry what seemed to be a reversion to type—unsafe drugs released to the public without sufficient attention to dangerous side effects. Eli Lilly’s earlier caution about moving forward with serotonin boosting drugs as anti-obesity medications—as anti-craving drugs for food addicts--soon came to look like a wise decision.

--Excerpted from The Chemical Carousel: What Science Tells Us About Beating Addiction © Dirk Hanson 2008, 2009.

Related posts:

Chantix and Suicide
What is Drug Craving?
Naloxone and "Receptorology"
Topamax for Alcoholism: A Closer Look

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Wednesday, December 19, 2007

What is Drug Craving?


Exploring the engine of drug relapse.


“In terms of treatment, you can’t just attack the rewarding features of the drug. In the case of alcohol, we already have a perfect drug to make alcohol aversive--and that’s Antabuse. But people don’t take it. Why don’t they take it? Because they still crave. And so they stop taking it. You have to attack the other side, and hit the craving.”
--Dr. Ting-Kai Li, 1990 interview

It causes relapses and treatment failure. It leads good people to break good promises and do harm to themselves and others. What is this thing called craving? Isn’t it just another word for lack of will power?

Scientists have gained a much deeper understanding of how and why addicts crave. For years, craving was represented by the tortured tremors and sweaty nightmares of extreme heroin and alcohol withdrawal. Significantly, however, the symptom common to all forms of withdrawal and craving is anxiety. This prominent manifestation of craving plays out along a common set of axes: depression/dysphoria, anger/irritability, and anxiety/panic. These biochemical states are the result of the “spiraling distress” (George Koob’s term) and “incomprehensible demoralization” (AA’s term) produced by the addictive cycle. The mechanism driving this distress and demoralization is the progressive dysregulation of brain reward systems, leading to biologically based craving. The chemistry of excess drives the engine of addiction, which in turn drives the body and the brain to seek more of the drug.

Whatever the neuroscientists wanted to call it, addicts knew it as “jonesing,” from the verb “to jones,” meaning to go without, to crave, to suffer the rigors of withdrawal. Most doctors don’t get it, and neither did many of the therapists, and least of all the public policy makers. Drug craving is ineffable to the outsider.

Drug craving itself is mediated by glutamate receptor activity in the hippocampus—the seat of learning and memory. A fundamental branch of what we might dub the “relapse pathway” runs through the glutamate-rich areas of the hippocampus. The puzzling matter of craving and relapse began to come into focus only when certain researchers began to rethink the matter of memory and learning as it applies to the addictive process. This led back to the role of glutamate, and it gradually became clear that the drug high and the drug craving were, in a manner of speaking, stored in separate places in the brain. Research at the National Institute for Drug Abuse (NIDA) strongly supports the hypothesis that drug memories induced by environmental triggers originate primarily in the hippocampus. And glutamate may be the substance out of which the brain fashions “trigger” memories that lead certain addicts down the road to relapse.

Glutamate is the most common neurotransmitter in the brain. (In sodium salt form, as monosodium glutamate, it is a potent food additive.) About half of the brain’s neurons are glutamate-generating neurons. Glutamate receptors are dense in the prefrontal cortex, indicating an involvement with higher thought processes like reasoning and risk assessment. The receptor for glutamate is called the N-methyl-D-aspartate (NMDA) receptor. And unfortunately, as the gifted science writer Constance Holden related in Science 292, NMDA antagonists, which might have proven to be potent anti-craving drugs, cannot be used because they induce psychosis. Dissociative drugs like PCP and ketamine are glutamate antagonists.

However, drugs that play off receptors for glutamate are already available, and more are in the pipeline. As a precursor for the synthesis of GABA, glutamate has lately become a tempting new target for drug research. Ely Lilly and others have been looking into glutamate-modulating antianxiety drugs, which might also serve as effective anti-craving medications for abstinent drug and alcohol addicts.

Photo credit: Changing Lives Foundation
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