Take the Alcohol Test

CAGE questionnaire still a useful tool

Despite the time, labor, and expense that have gone into the search for a better way to diagnose alcoholism, researchers have yet to outdo what may be the simplest, most accurate test for alcoholism yet devised. A set of four simple, relatively non-controversial questions, first devised in 1970 by Dr. John A. Ewing, still serve as a useful predictive tool for alcoholism.

Neurobiology has taught us that addictive drugs cause long-lasting neural changes in the brain. The problems start when sustained, heavy drinking forces the brain to accept the altered levels of neurotransmission as the normal state of affairs. As the brain struggles to adapt to the artificial surges, it becomes more sensitized to these substances. It may grow more receptors at one site, less at another. It may cut back on the natural production of these neurotransmitters altogether, in an effort to make the best of an abnormal situation. In effect, the brain is forced to treat alcoholic drinking as normal, because that is what the drinking has become.

The likelihood that many alcoholics and other drug addicts have inherited a defect in the production and distribution of serotonin and other neurotransmitters is a far-reaching finding. While it is difficult to measure neurotransmitter levels directly in brains, there are indirect ways of doing so. One such method is to measure serotonin’s principle metabolic breakdown product, a substance called 5-HIAA, in cerebrospinal fluid. From these measurements, scientists can make extrapolations about serotonin levels in the central nervous system as a whole.

However, testing for serotonin levels is imprecise and impractical in the real world of the doctor's office and the health clinic. Despite all the promising research on neurotransmission, what can physicians and health professionals do today to identify alcoholics and attempt to help them? For starters, physicians could look beyond liver damage to the many observable “tells” that are characteristic patterns of chronic alcoholism—such manifestations as constant abdominal pain, frequent nausea and vomiting, numbness or tingling in the legs, cigarette burns between the index and middle finger, jerky eye movements, and a chronically flushed or puffy face. Such signs of acute alcoholism are not always present, of course. Many practicing alcoholics are successful in their work, physically healthy, don’t smoke, and came from happy homes.

The CAGE test takes less than a minute, requires only paper and pencil, and can be graded by test takers themselves. It goes like this:

1. Have you ever felt the need to (C)ut down on your drinking?

2. Have you ever felt (A)nnoyed by someone criticizing your drinking?

3. Have you ever felt (G)uilty about your drinking?

4. Have you ever felt the need for a drink at the beginning of the day—an “(E)ye opener?

People who answer “yes” to two or more of these questions should seriously consider whether they are drinking in an alcoholic or abusive manner.

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

Neuroaddiction and the Reward Pathway

How addictive drugs fool Mother Nature

"The addicted brain is distinctly different from the nonaddicted brain,” writes Alan Leshner, the former director of the National Institute of Drug Abuse (NIDA). “Changes in brain structure and function is what makes it, fundamentally, a brain disease. A metaphorical switch in the brain seems to be thrown as a result of prolonged drug use.”

Addiction is both a cause and a consequence of these fundamental alterations in brain function. If physical abnormalities in the brain are at the root of the problem, then any treatment program worth its weight ought to be dealing—directly or indirectly--with these differences in brain state. Writing in Lancet, researcher Charles O’Brien has suggested a similar orientation: “Addiction must be approached more like other chronic illnesses--such as diabetes and chronic hypertension--than like an acute illness, such as a bacterial infection or a broken bone."

All of this suggests that we are not likely to win a war on drugs, achieve zero tolerance, or become chemical-free any time soon. The drug problem is an artifact of the basic design of the mammalian brain. Humankind is extraordinarily susceptible to drug abuse anywhere and everywhere certain drugs are widely available—and all because of a “design quirk” in the reward pathways of the central nervous system.

Any sufficiently powerful receptor-active drug is, in its way, fooling Mother Nature. This deceit means, in a sense, that all such drugs are illicit. They are not natural, however organic they may be. Yet, the human drive to use them is all-pervasive. We have no real built-in immunity to drugs that directly target specific receptors in the limbic and cortical pleasure pathways. The act of “liking” something is controlled by the forebrain and brain stem. If you receive a pleasant reward, your reaction is to “like” it.

If, however, you are anticipating a reward, and are, in fact, engaging in behaviors motivated by that anticipation, it can be said that you “want” it. The wholly different act of wanting something strongly is a mesolimbic dopamine-serotonin phenomenon. We like to receive gifts, for example, but we want food, sex, and drugs. As Nesse and Berridge put it, “The ‘liking’ system is activated by receiving the reward, while the ‘wanting’ system anticipates reward and motivates instrumental behaviors. When these two systems are exposed to drugs, the “wanting” system motivates persistent pursuit of drugs that no longer give pleasure, thus offering an explanation for a core paradox in addiction."

Under the biochemical paradigm, a runaway appetite for non-stop stimulation of the reward pathway is a prescription for disaster. The harm is physical, behavioral, and psychological--as are the symptoms. Peer pressure, disciplinary difficulties, contempt for authority--none of these conditions is necessary for drug addiction to blossom. What the drug itself does to people who are biologically vulnerable is enough. No further inducements are required.

Even this brief summation of the ways in which addictive drugs alter neurotransmission should serve to demonstrate that these substances have more in common than we ordinarily assume. All these drugs are of course rewarding, so it is perhaps not too surprising, for all their differences, that they work the limbic reward pathways. All these drugs share common mechanisms of action, which is why they are addictive.

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


addiction drugs

Lethal Injections

Bloggers Unite for Human Rights

I offer the following post as a participant in "Unite For Human Rights," a campaign co-sponsored by BlogCatalog and Amnesty International USA.
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Last month, in Baze v. Rees, the U.S Supreme Court dashed the hopes of human rights activists and ruled 7-2 that lethal injection in Kentucky does not constitute cruel and unusual punishment as defined by the constitution. In a narrowly technical ruling, the Court found that this method of execution under death penalty statutes was legal so long as there was no "substantial risk" of pain that could be alleviated by participating health professionals.

In response to the court decision, Amnesty International USA released a public statement decrying the government's "preoccupation with lethal injection," calling it a "distraction from myriad problems currently plaguing the death penalty system. Incompetent counsel, prosecutorial misconduct and racial, class and geographic bias are just the tip of the iceberg in a system that is flawed at its very core. "

Lamentably, the ruling does little to address the real issues of lethal injection, and the manner in which this procedure violates the Eighth Amendment prohibiting cruel and unusual punishment. Justice Alito wrote on behalf of the majority: " ... a suggested modification of a lethal injection protocol cannot be regarded as 'feasible' or 'readily' available if the modification would require participation-- either in carrying out the execution or in training those who carry out the execution--by persons whose professional ethics rules or traditions impede their participation."

That is exactly the problem: Medical professionals want nothing to do with this procedure. In fact, the technicians in charge of inserting the IV catheters that deliver the poisonous drugs into the prisoner's veins have gone on record as opposing participation in lethal injections. In 2006, a California execution was postponed when two anesthesiologists refused to oversee the administration of a barbiturate and two other drugs at a scheduled execution. Since then, the National Association of Emergency Medical Technicians (NAEMT) has strongly opposed the participation of licensed EMTs and paramedics in execution by lethal injection.

Dennis Welch, a senior writer for Gallup, notes: "For many years, capital punishment was carried out by firing squad, the gas chamber, the electric chair, hanging, or decapitation. In light of those methods, how can lethal injection be considered 'cruel and unusual'? The argument is that human error during the lethal injection process can lead to problems, sometimes causing an extended period of time (up to 45 minutes) before the person dies."

For this reason, states have looked to the courts for help, but the recent Supreme Court decision brings more confusion than clarity to the issue. Sarah Tofte, a researcher at Human Rights Watch and co-author of a 2006 report on executions by lethal injection in the United States, states emphatically: “Lethal injection is not as humane as it might appear to be. There is mounting evidence that condemned prisoners are at risk of suffering excruciating pain."

The New York Times reported that "while most states use a method similar to Kentucky’s, a number of them have adopted additional safeguards to ensure that an inmate is properly anesthetized by the initial drug in the sequence, a barbiturate, before administration of the second two, which paralyze the muscles and stop the heart."

Significant dissents were heard from Justices Ginsberg and Souter, according to the Times report. Their dissenting opinion "listed several of these states and described the extra steps they have taken, to show that Kentucky could and should be required to do a better job. The states she named were Alabama, California, Florida, Indiana and Missouri."

Coffee Addiction

The pharmacology of caffeine

Recent studies have documented the existence of severe caffeine addicts who suffer significant depression and lessened cognitive capacity for several weeks or months following termination of coffee drinking. Balzac, the nineteenth century French writer, reportedly died of caffeine poisoning at roughly the 50-cup-per-day level.

At low doses, caffeine sharpens cognitive processes--primarily mathematics, organization, and memory--just as nicotine does. The results of a ten-year study, reported in the Archives of Internal Medicine, showed that female nurses between the ages of 34 and 59 who drank coffee were less likely to commit suicide than women who drank no coffee at all.

Until recently, coffee and tea were rarely thought of as drugs of abuse, even though it is certainly possible to drink too much caffeine. Are the xanthines, the family of compounds that includes caffeine, addictive?

The typical caffeine dose in a cup of coffee--between 50 and 200 milligrams, with an average of about 115 milligrams--is enough to produce a measurable metabolic effect. Supermarket coffee in a can has considerably more caffeine per brewed cup than gourmet blends. Robusta beans have more caffeine than Arabica varieties. Instant coffee is the most potent coffee of all. The side effects of overdose--excessive sweating, jittery feelings, and rapid speech--tend to be transient and benign. Withdrawal is another matter: Caffeine causes a surge in limbic dopamine and norepinephrine levels--but not solely at the nucleus accumbens. The prefrontal cortex gets involved as well.

Caffeine's psychoactive power and addictive potential are easily underestimated. The primary receptor site for caffeine is adenosine, which, like GABA, is an inhibitory neurotransmitter. Adenosine normally slows down neural firing. Caffeine blocks out adenosine at its receptors, and higher dopamine and norepinephrine levels are among the results. Taken as a whole, these neurotransmitter alterations result in the bracing lift, the coffee "buzz" that coffee drinkers experience as pleasurable.

Scientists at the National Institute of Mental Health (NIMH) have demonstrated that high doses of caffeine result in the growth of additional adenosine receptors in the brains of rats. In order to feel normal, the rats must continue to have caffeine. Take away the caffeine, and the brain, now excessively sensitized to adenosine, becomes sluggish without the artificial stimulation of the newly grown adenosine receptors. Like alcoholics and cocaine addicts, people with an impressive tolerance for coffee and tea may find themselves chasing a caffeine high in a losing battle against fluctuating neuroreceptor growth patterns.

Increased tolerance and verifiable withdrawal symptoms, the primary determinants of addiction, are easily demonstrated in victims of caffeinism. Even casual coffee drinkers are susceptible to the familiar caffeine withdrawal headache, which is the result of caffeine's ability to restrict blood vessels and reduce the flow of blood to the head. When caffeine is withdrawn, the arteries in the head dilate, causing a headache. Caffeine's demonstrated talent for reducing headaches is one of the reasons pharmaceutical companies routinely include it in over-the-counter cold and flu remedies. The common habit of drinking coffee in the morning is not only a quick route to wakefulness, but also a means of avoiding the headaches associated with withdrawal from the caffeine of the day before.

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

Photo Credit: Lifehacker
[Note: For my Russian readers, a translation of this post is available here: "Зависимость от кофе translated by Health Effects of Coffee"]

U.K. Marijuana Panic Continues

British Prime Minister plans to stiffen pot penalties.

The national hysteria over "skunk" marijuana shows no signs of abating in Great Britain, as Prime Minister Gordon Brown is poised to overrule his advisors and reclassify cannabis as a more dangerous drug. Lost in the debate is any semblance of reasonable discussion about scientific research on marijuana.

British health authorities continue to find the basics of cannabis to be an inscrutable mystery. Some months ago, they declared that "skunk" cannabis was linked to the onset of schizophrenia. Since no one knows what, exactly, causes schizophrenia, and recent findings continue to point toward genetic causes, this was a doubly astonishing claim.

Now, continuing in the same vein of misinformation, The University College of London reports that different strains of marijuana cause different types of psychological maladies. Recently, Prime Minister Brown "publically described new strains of cannabis as 'lethal,' as if they could trigger a fatal overdose," according to an editorial in the Guardian. The Guardian went on to note that "Whitehall's own panel of experts has concluded that increased marijuana use has not been matched by a corresponding rise in mental illness."

The move to shift marijuana to Class B status from its current Class C designation has been fueled by these dubious reports. As long as British politicians continue to believe that something called "skunk" is a new and lethal derivative of marijuana, and that it causes psychosis, schizophrenia and suicide, no substantive debate on cannabis regulation can possibly take place. Colin Blakemore, a prominent professor of neuroscience at the Universities of Oxford and Warwick, tackled the issue in an article for the Guardian:

And what of the alarming stories of horrifying powerful "skunk"? Some newspapers have told us that the level of THC, the active ingredient, in street cannabis today is 20 or 30 times higher than 10 years ago. That would be rather surprising, given that THC content was 7 per cent on average in 1995. In reality, two studies, due to be published later this year, concluded that the average THC content has doubled.

Professor David Clark, a British psychologist who maintains a substance abuse information service called Wired In, writes on his blog: " I have to confess that I really cannot see what reclassifying the drug will do, other than criminalise and alienate more of our young people. It won't reduce harms that the drug can cause to some people. In saying this, I am not arguing that cannabis is safe - but nor are alcohol, tobacco and a wide range of prescription drugs which are all legal. "

addiction drugs

Ten Things to Know about Addiction

From "Rethinking Substance Abuse."

In the closing chapter of their 2006 book, "Rethinking Substance Abuse,” editors William R. Miller and Kathleen M. Carroll attempt to sum up what has been learned about the science of addiction. Their useful contribution, entitled Drawing the Science Together, offers "Ten Principles" that are designed to synthesize the welter of recent scientific research on addiction and help make sense of what we know.

In vastly truncated form, they are as follows:

1. Drug Use is Chosen Behavior

At least in the beginning, people choose to take drugs, as one of the behavioral options available to them.

2. Drug Problems Emerge Gradually

"Dependence emerges over time, as the person's life becomes increasingly centered on drug use," the authors write. "The diagnostic criteria for classifying people with 'drug abuse' and 'drug dependence' represent arbitrary cut points along a gradual continuum" (p.296).

3. Once Well Established, Drug Problems Tend to Become Self-Perpetuating

Once regular drug use has caused dysregulation of limbic reward systems, addictive behaviors "take on a life of their own," and become "surprisingly resistant to ordinary forces of persuasion, religion, punishment, and self-control. It can be challenging to destabilize such a self-organizing system" (p.296).

4. Motivation is Central to Prevention and Intervention

Miller and Carroll write: "Taking action also predicts change. Better outcomes follow from attending more sessions or staying longer in treatment, going to more 12-step meetings, adhering to treatment advice, or faithfully taking one's medication. It appears that actively doing something toward change may be more important than the particular actions that are taken" (p.297).

5. Drug Use Responds to Reinforcement

"Drug use tends to be associated with a foreshortening of time perspective, so that longer term delayed rewards are discounted in value.... People who more steeply discount delayed rewards are at higher risk for drug use and problems; moreover, drug use exacerbates discounting. Some effective medications reduce the reward value of drug use, which can enhance the appeal of alternative reinforcers" (p. 298).

6. Drug Problems Do Not Occur in Isolation, but as Part of Behavior Clusters

In young people, drug abuse often co-exists with mood disorders, behavioral problems at school or the job, and anti-social behaviors. As Miller and Carroll remind us, the same is true of adults. Family violence, health problems, unemployment, and child neglect are frequently associated with cases of active addiction.

7. There Are Identifiable and Modifiable Risk and Protective Factors for Problem Drug Use

"It is clear that heredity contributes to risk for alcohol problems, and evidence is mounting for genetic predispositions for or against other drug use" (p.299).

8. Drug Problems Occur within a Family Context

In addition to the evidence pointing to a direct genetic mode of transmission, parental drug use is also a risk factor. Anything that delays an addiction-prone young person from first use of alcohol or other drugs decreases the risk of long-term addiction.

9. Drug Problems Are Affected by a Larger Social Context

"Social isolation is both a promoter and a consequence of the progression of drug dependence, and social bonding with nonusers can be an antidote" (p.301).

10. Relationship Matters

In formal treatment settings, effectively matching counselor to client is crucial. Confrontational counselor styles are generally "countertherapeutic."

Graphics Credit: University of Utah, Genetic Science Learning Center

Marijuana Withdrawal Syndrome: A Bibliography

Selected science references.

The idea of marijuana addiction and withdrawal remains controversial in both private and scientific circles. For an unlucky few, a well-identified set of symptoms characterizes abstinence from heavy, daily use of pot. In this respect, marijuana addiction and withdrawal does not differ greatly from alcoholism--the vast majority of recreational users and drinkers will never experience it.

For those that do, however, the withdrawal symptoms of marijuana abstinence can severely impact their quality of life. Since discussions of this topic frequently veer off into sociopolitical arguments, leaving the science behind, I offer below a sampling of the growing medical and psychiatric literature on this aspect of drug use and abuse.

For additional comments and discussions about symptoms, see Marijuana Withdrawal.

References

Aharonovich, E., Liu, X., Samet, S., Nunes, E., Waxman, R., & Hasin, D. (2005). Postdischarge Cannabis Use and Its Relationship to Cocaine, Alcohol, and Heroin Use: A Prospective Study. American Journal of Psychiatry, 162(8), 1507-1514.

Budney, Alan J., Hughes, J.R., Moore, B.A., & Vandrey, R. (2004, November). Review of the Validity and Significance of Cannabis Withdrawal Syndrome. American Journal of Psychiatry, 161, 1967-1977.

Budney, A.J., Moore, B.A., Vandrey, R., Hughes, J.R. (2003). The time course and significance of cannabis withdrawal. Journal of Abnormal Psychology, 112, 393-402.

Budney, A.J., Hughes, J.R., Moore, B.A., & Novy, P.L. (2001). Marijuana Abstinence Effects in Marijuana Smokers Maintained in Their Home Environment. Archives of General Psychiatry, 58(10), 917-924.

Budney A. J., Novy P. L., & Hughes, J. R. (1999, September 1). Marijuana withdrawal among adults seeking treatment for marijuana dependence. Addiction, 94, 1311-1322.

Copeland, J., Swift, W., & Rees, V. (2001 January). Clinical profile of participants in a brief intervention program for cannabis use disorder. Journal of Substance Abuse Treatment, 20(1), 45-52.

Cui, S.S., Gu, G.B., Hannesson, D.K., Yu, P.H., & Zhang, X. (2001, December 15). Prevention of cannabinoid withdrawal syndrome by lithium: involvement of oxytocinergic neuronal activation. Journal of Neuroscience, 21(24), 9867-9876.

de Fonseca, F.R., Rocío, M., Carrera, A., Navarro, M., Koob, G.F., & Weiss, F. (1997, June 27). Activation of Corticotropin-Releasing Factor in the Limbic System During Cannabinoid Withdrawal. Science, 276, 2050 - 2054.

Department of Health and Human Services, Substance Abuse and Mental Health Services Administration. (2006). Results from the 2006 National Survey on Drug Use and Health: National Findings. Rockville, MD: Office of Applied Studies. Retrieved March 12, 2008, from http://www.oas.samhsa.gov/NSDUH/2k6NSDUH/2k6results.cfm#Ch2

Fackelmann, K.A. (1993, February 6). Marijuana and the brain: scientists discover the brain's own THC-delta-9-tetrahydrocannabinol. Science News.

Hall, W., Solowij, N., & Lemon, J. (1999). The health and psychological consequences of cannabis use. (National Task Force on Cannabis Australia, Monograph Series No. 25). Sydney, NSW: University of New South Wales, National Drug and Alcohol Research Centre.
Haney, M., Hart, C.L., Vosburg, S.K., Nasser, J., Bennetti, A., Zubaran, C., et. al. (2004). Marijuana Withdrawal in Humans: Effects of Oral THC or Divalproex. Neuropsychopharmacology, 29, 158–170.

Haney, M., Hart, Carl L., Ward, Amie S., & Foltin, R. W. (2003, January). Nefazodone decreases anxiety during marijuana withdrawal in humans. Psychopharmacology, 165(2), 157-165.

Haney, M., Ward, A.S., Comer, S.D., Foltin, R.W., & Fischman, M.W. (1999, February). Abstinence symptoms following smoked marijuana in humans. Psychopharmacology, 141(4), 395-404.

Jones, R.T., Benowitz, N.L., & Herning, R.I. (1981, August-September). Clinical relevance of cannabis tolerance and dependence. Journal of Clinical Pharmacology, 8-9 Suppl., 143-152.

Joy, J.E., Watson, S.J.,Benson, J.A. (1999). Marijuana and Medicine: Assessing the Science Base. p.92. Institute of Medicine, Division of Neuroscience and Behavioral Health. Washington. D.C.: National Academy Press. Retrieved March 5, 2008, from

Kouri, E.M., & Pope, H.G., Jr. (2000, November). Abstinence symptoms during withdrawal from chronic marijuana use. Experimental and Clinical Psychopharmacology, 8(4), 483-492.

Kouri, E.M. (2002, February 1). Does Marijuana Withdrawal Syndrome Exist? Psychiatric Times, 19(2).

Lichtman, A.H., and Martin, B.R. (2002). Marijuana Withdrawal Syndrome in the Animal Model. Journal of Clinical Pharmacology, 42, 20s-27s.

National Institute on Drug Abuse. (1999, April 20). Chronic Marijuana Users Become Aggressive During Withdrawal. NIDA News Release. Rockville, MD: National Institutes of Health, National Institute on Drug Abuse.

Schuckit, M.A., Daeppen, J-B., Danko, G.P., Tripp, M.L., Li, T-K., Hesselbrock, V.M., et. al. (1999). Clinical implications for four drugs of the DSM-IV distinction between substance dependence with and without a physiological component. American Journal of Psychiatry, 156, 41-49.

Scripps given $4M grant to study effects of marijuana. (2008, March 15). North County Times.

Somers, T. (2008, March 14). Study aims to clear haze surrounding pot addiction. San Diego Union-Tribune.

Tanda, G., Pontieri, F.E., & Di Chiara, G. (1997, June 27). Cannabinoid and Heroin Activation of Mesolimbic Dopamine Transmission by a Common µ1 Opioid Receptor Mechanism. Science, 276, 2048 - 2050.

Vandrey, R.G., Budney, A.J., Hughes, J.R., & A. Liguori. (2008, January 1). A within-subject comparison of withdrawal symptoms during abstinence from cannabis, tobacco, and both substances. Drug and Alcohol Dependence, 92, 48-54.

Wickelgren, I. (1997, June 27). Marijuana: Harder Than Thought? Science, 76, 1967-1968.

Wilson, R.I. & Nicoll, R.A. (2001, March 29). Endogenous cannabinoids mediate retrograde signalling at hippocampal synapses. Nature, 410, 588-592.

Zickler, P. (2002, October 17). Study Demonstrates That Marijuana Smokers Experience Significant Withdrawal. NIDA Notes, 17(3). Bethesda, MD: National Institutes of Health, National Institute on Drug Abuse.