Marijuana Withdrawal: A Survey of Symptoms (Part 1)

By Dirk Hanson

[Originally published in The Praeger International Collection on Addictions. Ed. by Angela Browne-Miller. Westport, Connecticut: Praeger, 2009. Vol. 2 Ch. 7 pp.111-124.]

(See also Marijuana Withdrawal Post)

More than 14 million Americans smoke marijuana regularly, making it the most commonly used illicit drug in America. In 2006, marijuana was the only drug used by 52.8 percent of illegal drug users (U.S. Department of Health and Human Services, 2006).

Over the past 15 years, as addiction researchers have been busily mapping out the chemical alterations in the human nervous system caused by alcohol, cocaine, nicotine, heroin, and tranquilizers, America’s most popular illegal drug has remained largely a scientific mystery. Marijuana, the drug millions of Americans have been using regularly for years, is the least studied drug of all.

Why has cannabis research lagged behind that of other drugs of abuse? For decades, the prevailing belief among users and clinical researchers alike was that marijuana did not produce dependency and therefore could not be responsible for major withdrawal symptoms. This thinking is based, quite understandably, on the widespread observation that most marijuana users do not have difficulty going without marijuana, either by choice or by necessity. However, marijuana withdrawal effects are frequently submerged in the welter of polyaddictions common to active addicts. The withdrawal rigors of, say, alcohol or heroin tend to drown out the subtler manifestations of cannabis withdrawal. As Barbara Mason, director of the Laboratory of Clinical Psychopharmacology at Scripps Research Institute, has explained: “People are deciding every day whether to use or not to use marijuana, for medical purposes or otherwise, and there is little scientific information to advise this decision” (2008).

Marijuana withdrawal, which typically affects only heavy smokers, has not been well characterized by the research community. Until recently, there was scant evidence in animal models for marijuana tolerance and withdrawal, the classic determinants of addiction. Now, however, several researchers have identified the existence of symptoms brought on by the abrupt discontinuation of regular marijuana use in both animal and human studies (de Fonseca et al., 1997, p. 2050). A growing body of evidence supports the existence of a clinically significant marijuana withdrawal syndrome in a subset of marijuana smokers. The syndrome is marked by irritability, restlessness, generalized anxiety, hostility, depression, difficulty sleeping, excessive sweating, loose stools, loss of appetite, a general “blah” feeling, and a mental state that has been described as “inner unrest.”

Recent clinical research, combined with anecdotal field reports collected by the author, demonstrate the existence of marijuana withdrawal and the consistency of the most common symptoms of withdrawal and detoxification.

Background

In 1992, molecular biologists identified the elusive brain receptor where THC, the primary active ingredient in marijuana, did its work. Shortly after that discovery, researchers at Hebrew University in Jerusalem identified the body’s own form of THC, which uses the same CB1 receptors as THC. They christened the internally manufactured substance anandamide, after the Sanskrit ananda, or “bliss” (Fackelmann, 1993).

Anandamide has a streamlined three-dimensional structure that THC mimics. Both molecules slip easily through the blood brain barrier. Some of the mystery of marijuana’s effects was resolved after researchers demonstrated that marijuana definitely increased dopamine activity in the limbic area of the brain. Tanda, Pontieri, and Di Chiara demonstrated that dopamine levels in the nucleus accumbens doubled when rats received an infusion of THC (1997, p. 2048). It appears that marijuana raises dopamine and serotonin levels through the intermediary activation of opiate and GABA receptors (Wilson & Nicoll, 2001, p. 588). THC may perform a signaling function in neurons containing GABA and glutamate.

THC and its organic cousin, anandamide, make an impressive triple play in the brain: They effect movement through receptors in the basal ganglia, they alter sensory perception through receptors in the cerebral cortex, and they impact memory by means of receptors in the hippocampus. It is clear that some of the effects of cannabis are produced in much the same way as the effects of other addictive drugs—by means of neurotransmitter alterations along the limbic system’s reward pathway.

A great deal of the early research was marred by inconsistent findings and differing definitions of addiction and withdrawal. Most recreational marijuana users find that too much pot in one day makes them lethargic and uncomfortable. Self-proclaimed marijuana addicts, on the other hand, report that pot energizes them, calms them down when they are nervous, or otherwise allows them to function normally. Heavy marijuana users claim that tolerance does build. And when they withdraw from use, many report strong cravings.

Work by Jones, Benowitz, and Herning had helped establish certain baseline symptoms—irritability, insomnia, and lack of appetite—as early as 1981 (p. 143). Studies by Budney, Novy, and Hughes in 1999 further outlined the syndrome in heavy daily marijuana smokers (p. 1311). But the abstinence effects were often inconsistent, and frequently hard to measure. Moreover, their clinical relevance was not always evident.

For marijuana withdrawal to be considered a clinical fact, several criteria had to be met. First, the typically transient pattern of withdrawal effects must be distinguishable from rebound effects. (A rebound effect is defined as the reappearance of a preexisting symptom, and is thus not considered a true withdrawal effect.) In addition, the symptoms must occur reliably, as demonstrated by comprehensive prospective studies (Budney, Hughes, Moore, & Vandrey, 2004, p. 1970). The symptoms under consideration must also be considered clinically significant. Finally, there needs to be a clear and repeatable timeline in evidence for the withdrawal effects.

It has been suggested that the reported symptoms of abrupt marijuana cessation do not rise to the level of withdrawal typically associated with drug detox. It is now possible to lay out the neurochemical basis of marijuana withdrawal, and to demonstrate that marijuana acts on the brain in a fashion similar to other addictive drugs.

There is solid experimental evidence that chronic, heavy cannabis users develop tolerance to its subjective and cardiovascular effects. “In summary,” Budney et al. write, “cannabis withdrawal effects clearly occur in the majority of heavy, daily users” (2004, p. 1974). As a rough estimate, approximately 10 percent of marijuana users are at risk for dependence and withdrawal, the classic determinants of drug addiction (Joy, Watson, & Benson, 1999, p. 92). There is clinical and epidemiological evidence that some heavy cannabis users experience problems in controlling their cannabis use, and continue to use the drug despite experiencing adverse personal consequences of use (Hall, Solowij, & Lemon, 1999). Moreover, there is strong clinical evidence that some users experience a withdrawal syndrome upon the abrupt cessation of cannabis use. The timeline is similar to withdrawal from other addictive drugs.

In 2004, a group at the University of Vermont, funded by the National Institute of Drug Abuse (NIDA), undertook a critical review of all major relevant studies of the validity and clinical significance of marijuana withdrawal (Budney et al., p. 1967). The review of studies demonstrated with certainty that there are people with a propensity for heavy marijuana use who suffer a clearly delineated, verifiable, and frequently vivid set of withdrawal symptoms when they try to quit. One of the most striking pieces of evidence for this is the similarity of symptom sets emerging from the clinical studies to date. The most common “reliable and clinically significant” effects of abrupt withdrawal in heavy pot smokers, according to the University of Vermont research group, included “severity of craving and sleep difficulty, decreased appetite, and increased aggression, anger and irritability” (Budney, Hughes, Moore, & Novy, 2001, p. 917; Kouri, 2002, p. 30).

As another study author concluded: “Marijuana withdrawal doesn’t include dramatic physical symptoms such as the pain, nausea, heavy sweating, and cramps associated with opiate withdrawal. Nevertheless, the symptoms of marijuana withdrawal appear clinically significant” (Zickler, 2002).

A recent comprehensive outpatient study (Kouri & Pope, 2000, p. 483) with prewithdrawal baselines showed greater levels of anxiety, negative mood, physical discomfort, and decreased appetite during abstinence but not at baseline, compared with two control groups. Moreover, in a “home environment” study, researchers worked with marijuana users who provided self-ratings during marijuana withdrawal; these users smoked an average of 3.6 times daily, did not use other drugs or abuse alcohol, and were free of major psychiatric disorders. The same symptoms predominated, and onset of symptoms occurred reliably within 48 hours of cessation. Moreover, “telephone interviews with collateral observers living with the participants confirmed participants’ reports of increased irritability, aggression, and restlessness during abstinence. . . . [T]he validation of symptoms by home-based observers suggested that the effects were of a clinically significant magnitude” (Budney et al., 2004, p. 1971).

Other studies by Budney and colleagues expanded on the list of symptoms that changed significantly from baseline during withdrawal: “anger and aggression, decreased appetite, irritability, nervousness, restlessness, shakiness, sleep difficulty, stomach pain, strange dreams, sweating, and weight loss” (2003, p. 393; 2004, p. 1972). Although most effects were transient, generally lasting no more than two weeks, “strange dreams and sleep difficulties showed significant elevations throughout the study” (2003). Budney et al. conclude that, since most symptoms returned to baseline levels in the former users, “these findings were not rebound effects indicative of symptoms that existed before the use of cannabis” (2004, p. 1972).

More recent studies by Haney and others “controlled for potential confounders by using placebo conditions and excluding persons who abused other substances, had an active psychiatric disorder, or were taking psychoactive medication” ().

Overall, the research cited above confirms that the most common marijuana withdrawal symptom is low-grade anxiety and dysphoria. Anxiety of this sort has a firm biochemical substrate. A peptide known as corticotrophin-releasing factor (CRF) is primarily responsible. Neurologists at the Scripps Research Institute in La Jolla, California, found that CRF levels in the amygdalas of animals in marijuana withdrawal were as much as three times higher than the levels found in animal control groups (Wickelgren, 1997, p. 1967). Long-term marijuana use alters the function of CRF in the limbic system in a manner similar to other addictive drugs (de Fonseca et al., 1997, p. 2051). (CRF receptors in the amygdala also play a direct role in alcohol withdrawal.)

Method

Personal observations and selected case histories of frequent marijuana users were gathered from anonymous, unedited comments posted on a blog site maintained by the author. Punctuation, capitalization, and spelling have been normalized in the excerpts included here. Most of the people who have posted comments thus far (more than 100) arrived at the site by means of the search term marijuana withdrawal. This may indicate that a large number of posters are heavy smokers seeking information about abstinence symptoms. The popularity of this search phrase on the Google search engine seems to suggest an interest in, and a need for, scientific information about marijuana withdrawal.

What has surprised many observers is that the idea of treatment for marijuana dependence seems to appeal to such a large and diverse group of people. NIDA has been able to find a cohort of withdrawal-prone smokers with relative ease. According to the principal investigator of one NIDA marijuana study, “We had no difficulty recruiting dozens of people between the ages of 30 and 55 who have smoked marijuana at least 5,000 times. A simple ad in the paper generated hundreds of phone calls from such people” (NIDA, 1999). This would be roughly equivalent to 14 years of daily pot smoking.

Comments gathered from anonymous users at an open Web forum created for the discussion of marijuana withdrawal symptoms cannot be controlled for confounding variables such as other addictions or psychological disorders. The comment section of the Web site is open to anyone. What such surveys can accomplish, however, is the demonstration of parallels, or lack of them, between findings in an experimental setting and anecdotal reports from the field. Survey studies cannot offer indisputable proof. Nonetheless, when combined with the results of formal clinical studies, such surveys offer a window into real-world experience, thus complementing the growing scientific data concerning marijuana withdrawal syndrome.

The comments were generated in large part by heavy, regular smokers who either recognized or have begun to recognize in themselves an addictive propensity toward marijuana. As a group, they have great difficulty—and suffer similar symptoms—whenever, and for whatever reason, they choose to abstain.

Perhaps, most important, the present survey adds to the growing documentation of the contention that withdrawal symptoms are a frequent cause of relapse in marijuana smokers attempting to achieve abstinence.

Cont. in Part 2.

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, 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. Retrieved February 27, 2008, from http://archpsyc.ama assn.org/cgi/content/full/58/10/917?cknck

Budney, A. 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. Retrieved April 21, 2008, from http://ajp.psychiatryonline.org/cgi/content/full/161/11/1967

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., 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. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11239727

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. Retrieved April 27, 2008, from http://www.jneurosci.org/cgi/content/abstract/21/24/9867

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.

Fackelmann, K. A. (1993, February 6). Marijuana and the brain: Scientists discover the brain’s own THC-delta-9-tetrahydrocannabinol. Science News. Retrieved March 28, 2008, from http://findarticles.com/p/articles/mi_m1200/is_n6_v143/ai_13434805/pg_1

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. Retrieved February 3, 2008, from http://www.druglibrary.org/schaffer/hemp/medical/home.htm

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, C. L., Ward, A. 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.

Hanson, D. (2007, October 17). Addiction inbox: Marijuana withdrawal. Retrieved May 3, 2008, from http://addiction-dirkh.blogspot.com/2007/10/marijuana-withdrawal.html

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. Retrieved April 14, 2008, from http://www.ncbi.nlm.nih.gov/sites/entrez

Joy, J. E., Watson, S. J., & Benson, J. A. (1999). Marijuana and medicine: Assessing the science base. Institute of Medicine, Division of Neuroscience and Behavioral Health. Washington, DC: National Academy Press. Retrieved March 5, 2008, from http://www.nap.edu/html/marimed/

Kouri, E. M. (2002, February 1). Does marijuana withdrawal syndrome exist? Psychiatric Times, 19(2). Retrieved March 17, 2008, from http://www.psychiatrictimes.com/display/article/10168/54701?pageNumber3

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. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/

Lichtman, A. H., & Martin, B. R. (2002). Marijuana withdrawal syndrome in the animal model. Journal of Clinical Pharmacology, 42, 20s–27s.

Mason, B. (2008, March 15). North County Times.

National Institute on Drug Abuse. (1999, April 20). Chronic marijuana users become aggressive during withdrawal. (NIDA News Release). Rockville, MD: Author. Retrieved April 9, 2008, from http://www.nida.nih.gov/MedAdv/99/NR-420.html

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. Retrieved March 16, 2008, from http://www.nctimes.com/articles/2008/03/15/news/sandiego/16_02_343_14_08.txt

Somers, T. (2008, March 14). Study aims to clear haze surrounding pot addiction. San Diego Union-Tribune. Retrieved March 16, 2008, from http://www.signonsandiego.com/news/science/20080314–9999–1n14dope.html

Tanda, G., Pontieri, F. E., & Di Chiara, G. (1997, June 27). Cannabinoid and heroin activation of mesolimbic dopamine transmission by a common 1 opioid receptor mechanism. Science, 276, 2048–2050.

U.S. 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

Vandrey, R. G., Budney, A. J., Hughes, J. R., & Liguori, A. (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.

Photo Credit: http://hubpages.com/

Does Brain Research Worsen the Addiction Stigma?

“Once an addict, always an addict.”

When it comes to the neurobiology of addiction, the research community has made great strides in a few hectic years. However, as addiction counselor William White wrote in 2007, are we lacking a comparable neurobiology of addiction recovery?

White, a senior research consultant at Chestnut Health Systems/Lighthouse Institute, warns that in the past, campaigns seeking to reduce the stigma of mental illness by educating the public about “brain disease” have often inadvertently backfired, and invoked, instead, “harsher behavior toward the mentally ill.”

White states the matter starkly: “The vivid brain images of the addicted person may make that person’s behavior more understandable, but they do not make the person whose brain is being scanned more desirable as a friend, lover, spouse, neighbor, or employee.”

Furthermore, writes White, emphasizing the “chronic” part of a chronic brain disease can mislead the public into believing, “once an addict, always an addict.”

What can be done to balance out the downside of public perceptions related to the brain disease of addiction? White suggests that what is missing is what he refers to as the neurobiology of addiction recovery. When we convey to people that addiction is a brain disease that “alters emotional affect, compromises judgment, impairs memory, inhibits one’s capacity for new learning, and erodes behavioral impulse control,” we are not always helping to reduce the stigma of the disorder.

This state of affairs will continue, says White “unless there are two companion communications: 1) With abstinence and proper care, addiction-induced brain impairments rapidly reverse themselves, and 2) millions of individuals have achieved complete long-term recovery from addiction and have gone on to experience healthy, meaningful, and productive lives.”

White points out the lack of a specific research agenda in the field of addiction science that focuses on the “prevalence, pathways, styles and stages of LONG-TERM recovery.” Specifically, a comprehensive research agenda would need to include answers to question such as:

--“To what degree does neurobiology influence who recovers from addiction and who does not achieve such recovery?”

--“What is the time period over which such pathologies are reversed in recovery—days, months, years?

--What role can pharmacological adjuncts, social support and other services play in extending and speeding this process of brain recovery?”

--“Are there critical differences in the extent and timing of neurobiological recovery related to age of onset of use... age of onset of recovery, gender, genetic load for addiction, developmental trauma”, and other factors?

White’s paper, “In Search of the Neurobiology of Addiction Recovery: A Brief Commentary on Science and Stigma,” is available HERE.



Photo Credit: http://brain.utah.edu/

The Dutch Smoke Less Pot

One of those inconvenient truths.

Government drug policy experts don’t like the numbers, which is one of the reasons why you probably haven’t seen them. Among the nations of Europe, the Netherlands is famous, or infamous, for its lenient policy toward cannabis use—so it may come as a surprise to discover that Dutch adults smoke considerably less cannabis, on average, than citizens of almost any other European country.

A recent report by Reed Stevenson for Reuters highlights figures from the annual report by the European Monitoring Centre for Drugs and Drug Addiction, which shows the Dutch to be at the low end for marijuana usage, compared to their European counterparts. The report pegs adult marijuana usage in the Netherlands at 5.4 %. Also at the low end of the scale, along with the Netherlands, were Romania, Greece, and Bulgaria.

Leading the pack was Italy, at 14.6 %, followed closely by Spain, the Czech Republic, and France.

While cannabis use rose steady in Europe throughout the 1990s, the survey this year says that the data “point to a stabilising or even decreasing situation.” The study by the European Monitoring Centre did not include figures for countries outside Europe.

According to the Dutch government, Amsterdam is scheduled to close almost 20 per cent of its existing coffee shops—roughly 50 outlets--because of their proximity to schools. However, some local coffee shop proprietors maintain that far fewer shops, perhaps no more than 10 or 20, will actually be required to close.

What are the Dutch doing right? Are coffee shops the answer? It may be prove to be the case that cannabis coffee shops can’t be made to work everywhere—that the Dutch approach is, well, Dutch. However, the fact that it works reasonably well, if not perfectly, in the Netherlands is strong testimony on behalf of the idea of harm reduction.
Here are some excerpts from a flyer given out at some Dutch coffee shops by a group of owners known as the BCD, or Union of Cannabis Shop Owners:

--Do not smoke cannabis every day.
--There are different kinds of cannabis with different strengths, so be well informed.
--The action of alcohol and cannabis can amplify each other, so be careful when smoking and drinking at the same time.
--Do not use cannabis during pregnancy!
--Consult your doctor before using cannabis in combination with any medications you may be taking.
--Note that smoking is bad for your health anyway.
--Do not buy your drugs on the street, just look for a coffeeshop.

Customers must be over the age of 18, and in most coffee shops, as in bars and restaurants in the Netherlands and elsewhere, cigarette smoking is no longer allowed.

Photo Credit: www.us.holland.com

addiction drugs

Needle Exchange in America

AIDS/harm reduction activists press Obama.

First, the good news: After 20 years, the U.S. Congress has voted to remove the funding ban on syringe exchange programs designed to combat AIDS and to bring hard drug users within the orbit of the medical health community.

Now, the bad news: Conservative legislators have managed to insert a provision in the bill prohibiting needle exchange centers within 1,000 feet of schools, day care centers, colleges, playgrounds, youth centers, swimming pools—and just about any other institution you care to come up with. In short, the legislation would make it virtually impossible to operate a viable needle exchange program, even if sufficient levels of federal funding can be obtained. As one harm reduction activist put it in the Seattle Stranger: The only place you could put a federally-funded needle exchange program in the entire city of Chicago... is O’Hare Airport? Gee, it’s almost like Democrats aren’t really serious about allowing funding live-saving needle programs at all.”

Clearly, needle exchange activists are still waiting for an unambiguous sign from the White House that Obama plans to uphold his campaign promises in this regard. Obama’s go-slow policy on needle exchange has frustrated AIDS activists in particular.

Physicians for Human Rights, a group that supports clean syringe exchange programs, made October 14 a National Call-in Day, noting on its web site that “Senators need to hear from President Obama that his Administration supports syringe exchange. Now is the time to urge President Obama to fulfill his campaign promise to end the ban and to urge the Senate to act.”

In a post in January of this year, I wrote: “Obama’s agenda, as spelled out at Whitehouse.gov, calls for rescinding the ban in an effort to save lives by reducing the transmission of HIV/AIDS. ‘The President,’ according to the agenda, ‘supports lifting the federal ban on needle exchange, which could dramatically reduce rates of infection among drug users.’"

Syringe exchange programs, Physicians for Human Rights declares, “do more than provide clean syringes and properly dispose of used ones; they link people into the health care system and drug treatment programs that save lives.”

In short, says the group, “the presence of syringe exchange programs in communities does not increase rates of drug use, nor does it lead to a rise in crime. What it does do: decrease transmission of HIV, Hepatitis C and other diseases.”

Moreover, during his confirmation hearings drug czar Gil Kirlikowske said that “a number of studies conducted in the US have shown needle exchange programs do not increase drug use.”

It’s a confusing picture in the field: Needle exchange programs exist, in San Francisco, Toronto, New York and other major metropolitan areas, because county and other local and regional officials have authorized it, even when funding was precarious. Alongside these programs, a plethora of illegal needle exchange operations is also in place. The Drug War Chronicle quoted the Western director of the Harm Reduction Coalition: “We need to get legislation authorizing syringe exchanges on a statewide level.... Requiring local authorization means we have to deals with 54 jurisdictions instead of just one.”

Back in May, Maia Szalavitz reported in Time that the president was planning to move deliberately as part of a broader HIV/AIDS strategy, even though groups from the World Health Organization (WHO) to the American Medical Association have gone on record with the view that giving clean needles to drug addicts is a successful strategy to reduce the spread of HIV disease. Studies by Don Des Jarlais of Beth Israel Hospital in New York suggest that infection rates in New York’s drug addict population may have dropped more than 75 % over the last few years as clean needle programs became increasingly available.

In a report last month by the Drug Reform Coordination Effort (DRCNet), a spokesperson for the AIDS Action group was determined to remain positive. “I have a pretty good feeling about this,” he said. “I’m hopeful this is the year.”

addiction drugs

The Black Market for Seroquel

Speed freaks, coke heads, and antipsychotics.

Last week, writing on the Daily Beast web site, reporter Jeff Deeney profiled a startling underground market for the antipsychotic medication Seroquel (quetiapine). Deeney described street transactions in North Philadelphia for Quells or Suzie-Qs, as the drug is sometimes called. Seroquel, a drug developed for the treatment of schizophrenia and bipolar disorder, has developed an additional reputation as a “comedown” drug for stimulant abusers.

Seroquel, a so-called atypical antipsychotic, works by altering levels of dopamine. While some addicts have claimed that the drug is perfect for a cocaine or speed comedown, Seroquel has also been studied for its anti-craving properties when used for cocaine abstinence.

Why would a speed freak or a coke addict want to take a drug that might decrease their desire for their stimulant of choice? For the same reason that ecstasy users often take a morning-after dose of Prozac in a misguided attempt to compensate for possible damage to serotonin receptor arrays. Or because the drug is mildly sedating for some users. However, there may be more to it. Perhaps Seroquel is an effective anti-craving medication for cocaine and methamphetamine addicts, who misuse it as a drug to ease them through enforced periods of detox or lack of availability.

One high-traffic drug discussion site has shut down a long-standing thread on Seroquel with the warning: “Do not use Seroquel for a cocaine comedown.”

The fact that prescription Seroquel is available as a street drug, at least in some parts of the country, demonstrates the likelihood that physicians and psychiatrists are increasingly using it for off-prescription purposes—like drug detox. Deeney strongly suggests that this is the case: “Drug dealers, mandated to treatment as a condition of their probation or parole, are given off-label prescriptions for Seroquel, then sent right back to the street, where the pills can be sold for cash to users and other dealers.”

Increasing its appeal is Seroquel’s reputation for combining well with cocaine in a mixture known as a Q-Ball, or Rosemary’s Dolly—a variation on the heroin/cocaine mix known as a Speedball, to which Seroquel can also be added. An anonymous med student on a medical blog noted that “certain people say they love Seroquel when doing a speed-ball. Makes sense, think about it. It heightens the high of the heroin, it eases the crash of the cocaine.”

Seroquel’s ability to modulate the effect of illegal drugs means that the medication can possibly find a market both as a detox drug for stimulant abusers, and as an ingredient in the very stimulants they abuse.

By itself, Seroquel is not considered addictive. Some addicts told Deeney that the drug simply put them to sleep more quickly after a long meth run. Indeed, Seroquel is considered to be more sedating than similar antipsychotics such as Olanzapine and Aripiprazole. The larger issue, as the Daily Beast post makes clear, is that “Seroquel can have serious side effects including diabetes, a permanent Parkinson’s-like palsy called tardive dyskinesia, and sudden cardiac death.”

All of this confusing and sometimes contradictory input is coming well ahead of the clinical data, although a study in 2001, presented at the 4th International Conference on Bipolar disorder, found that quetiapine caused a significant reduction in cocaine use among a small group of cocaine-dependent subjects who also suffered from bipolar disorder. A report last year in the Journal of Clinical Psychopharmacology also showed positive results with cocaine users. Studies of quetiapine for the reduction of cocaine use are currently being undertaken by the Seattle Institute for Biomedical and Clinical Research.

drugs dopamine

To Flush or Not To Flush

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FDA lists meds for trash or toilet.

A recent post here on the subject of illegal bong water in Minnesota—coupled with a perceptive comment by a reader about drugs in the water supply—got me thinking again about what gets thrown in the sink or flushed down the toilet.

I was surprised to discover that, according to the Food and Drug Administration (FDA), consumers are better served by flushing some drugs down the toilet. The FDA has put up a web site dedicated to the proposition that flushing drugs is the preferred method for certain kinds of drugs—but not for every kind of drug.

While noting that “flushing is not recommended for the vast majority of medicines,” the FDA asserts at druginfo@fda.hhs.gov that “certain medicines may be especially harmful and, in some cases, fatal in a single dose...” To dangerous, in other words, to leave around the house or in the trash.

The potential for fatal overdose, particularly with prescription morphine and its derivatives, suggests that flushing will be the preferred method of disposal unless or until communities and pharmaceutical companies get serious about take-back programs and other medicine disposal services.

Specifically, drugs recommended for flushing include:

--Morphine Sulfate (Morphine, Avinza, Embeda, Kadian, MS Contin, and Oramorph).

--Fentanyl Citrate (Actiq, Duragesic, Fentora, Onsolis).

--Meperidine Hydrochloride (Demerol).

--Methylphenidate (Daytrana).

--Hydromorphone Hydrochloride (Dilaudid).

--Methadone Hydrochloride (Methadone, Methadose, Dolophine).

--Oxymorphone Hydrochloride (Opana).

--Oxycodone Hydrochloride (Oxycontin, Percocet, Percodan).

-- Sodium Oxybate (Xyrem).

The FDA says that the disposal of “these select, few medicines by flushing contributes only a small fraction of the total amount of medicine found in the water. FDA believes that any potential risk to people and the environment from flushing this small, select list of medicines is outweighed by the real possibility of life-threatening risks from accidental ingestion of these medicines.”

The preferred disposal method for all other drugs, says the FDA, is to mix them with kitty litter or coffee grounds, place the mixture in a sealed plastic bag, and throw the container in your household trash.

Photo Credit: www.pri.org

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Alcohol and In Vitro Fertilization

Do drinking women face tougher odds?

Everybody knows by now that it’s not safe to drink while pregnant. However, a new study of more than 2,500 couples enrolled in a course of in vitro fertilization (IVF) treatment at a fertility clinic found that women who drank more than a single drink per day significantly reduced their likelihood of pregnancy, according to a report by doctors at the Harvard Medical School in Boston.

Now, it may not even be a good idea for women to drink while trying to get pregnant. And that includes you men out there as well.

Dr. Brooke Rossi presented the findings last week to a meeting of the American Society of Reproductive Medicine. In the study cohort, half the women and a third of the men had less than one drink per week, while about 5% of men and women had at least one drink per day. According to Dr. Rossi, women were 18% less likely to have a successful IVF baby if they drank at the higher level. Men who had more than six drinks per week reduced the rate of successful in-vitro fertilization by 14 %.

The average age of women taking part in the study was 34, and for men, the average age was 37. Tony Rutherford, chairman of the British Fertility Society, told the UK Guardian that “this is further evidence to suggest that alcohol does have an impact.” Rutherford agreed with the study authors at Harvard that women who wish to become pregnant should stop drinking.

In 1998, the British Medical Journal published a Danish study of more than 400 couples that concluded: “A woman's alcohol intake is associated with decreased fecundability even among women with a weekly alcohol intake corresponding to five or fewer drinks.” The authors conceded, however, that other studies have found little evidence of an alcohol effect on conception rates.

“It may well be that couples who are already subfertile are more affected by alcohol than those who are perfectly fertile,” Rutherford speculated. “Eggs and sperm take at least three months to develop so women have got to stop smoking, reduce alcohol consumption, or, if you are overweight, correct that weight, that far ahead if you want to maximize your chances of conception.”

Photo Credit: www.babble.com


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