What Does Harm Reduction Mean?

A rift in the addiction treatment community over abstinence.

What is harm reduction? How does it differ from the approaches traditionally associated with drug recovery and rehab?

Originally, I became interested in harm reduction because its advocates were highlighting the folly of prison terms over treatment for drug addicts—a sentiment with which I wholeheartedly agree. Also, the various harm reduction organizations worldwide were fastened tenaciously to the issue of clean needle exchanges as a means of reducing HIV transmission—another approach I heartily support. And at its core, harm reduction has always been about reducing the number of deaths by drug overdose. At its essence, harm reduction is sensible and necessary, given the failures of the drug war, and the inability to make a significant dent in addiction statistics by traditional socioeconomic approaches.

Harm reduction, as formally defined by Harm Reduction International, concerns itself with “policies, programs and practices that aim primarily to reduce the adverse health, social and economic consequences of the use of legal and illegal psychoactive drugs without necessarily reducing drug consumption. Harm reduction benefits people who use drugs, their families, and the community.” It’s a hopeful mission statement. But reducing harm without necessarily reducing drug consumption? What does that mean, exactly?

Lately, activists in the harm reduction movement have been leaning hard on the notion that abstinence is just so much humbug; an archaic admonition that need not be automatically imposed on addicts. Who said addicts have to become abstinent for the rest of their lives? Are we forever hostage to the religious zealotry of the Cambridge Group and it’s successor, Alcoholics Anonymous? If an alcoholic drinks one drink less today than yesterday, or a junkie shoots up a bit less junk today than yesterday, that is harm reduction in action.

But now that harm reduction has become intimately associated with the abstinence debate, egged on by activists like Stanton Peele and Jack Trimpey, the ground underneath the movement has shifted. Many harm reductionists are becoming wary, and sometimes completely hostile, to the notion of addiction as a disease syndrome with a distinct, lifelong, and incurable timeline beyond the reach of notions like “Rational” or “Smart” recovery. “Your best thinking got you here,” AA likes to say, reminding alcoholics that “being smart” or feeling full of “will power” often have less to do with recovery than one might suppose.

But in order to free themselves of the need for abstinence, extreme harm reductionists often deny that addiction is in any meaningful way a medical disorder. This has created a rift in the treatment community, and complicated the mission of recovery programs based on abstinence. Kenneth Anderson, a harm reduction advocate and the author of How to Change Your Drinking, framed it this way for me in an email exchange: “The more alcohol related problems you have, the more you need to practice harm reduction by planning safe drinking strategies, until you resolve your alcohol related problems by quitting or developing a non-problematic drinking pattern.” Like many harm reductionists, Anderson is no fan of Alcoholics Anonymous. One of the book’s sections is headed: “Everything You Always Wanted to Know About Alcohol—But you got told to go to AA and not ask.”

Anderson said that the National Institute on Alcohol Abuse and Alcoholism (NIAAA) “tells us that about half of people who overcome alcohol dependence do so by quitting, the other half overcome it by cutting back.” If even the nation’s premier scientific agency for researching alcoholism doesn’t seem so sure about whether alcoholics need to strive for abstinence, why should abstinence be a stated goal at the outset of treatment at all? Said Anderson: "When abstinence is forced on people against their will, it often backfires and leads to more drug or alcohol use."
 
A few weeks ago, on Denise Krochta’s excellent podcast, Addicted to Addicts, I suggested that part of the argument over abstinence vs. controlled drinking stemmed from a confused bundling of “problem drinkers” and “alcoholics”—a move that the National Institute on Alcohol Abuse and Alcoholism, whose very name is a testimony to the institute’s fundamental ambivalence, has been championing lately. This has helped harm reductionists center the battle precisely where the definitions are fuzziest: at the point on the spectrum where “problem drinking” becomes “alcoholism.” Nonetheless, by focusing on this imprecise edge, harm reductionists make a legitimate point: Culture and environment are major influences on the course of heavy drinking.

“I do not use the word alcoholism [in the book], because it has no scientific definition in the current day and is not found in the DSM IV” Anderson told me. “Although there is some heritability of alcohol dependence, it is a great error to overlook the importance of environmental factors. Alcohol dependence is not located on a single gene--currently there are dozens of genes implicated in alcohol dependence.” And he’s right. These are legitimate caveats that apply to many of the disease models of addiction now at play in the scientific community.

The counter-argument here is that genuine alcoholics do not have, and cannot develop, a “non-problematic drinking pattern,” any more than a serious diabetic is likely to develop a non-problematic sugar doughnut strategy. What alcoholic hasn’t tried controlled drinking? Again and again? And failed? Where are the legions of former drunk-tank alcoholics who have rationally transformed themselves into social drinkers?

These are some of the terms of the current debate in the addiction recovery community. But we do a disservice by concentrating solely on points of departure. The harm reduction movement, at street level, has some very sound contributions to make regarding addiction and public policy. Anderson, in his book, drives home the overlooked but essential point that there is no one-size-fits-all treatment for destructive drinking:

• “Harm reduction never forces people to change in ways which they do not choose for themselves.”
• “Harm reduction recognizes that each of us is a unique human being different from all others.”
• “Harm reduction recognizes the need for ‘different strokes for different folks.’”
• “Harm reduction supports every positive change.”

I fervently hope that 12-Step Groups and Harm Reduction Groups can work their way toward a rapprochement. And so does Kenneth Anderson. But what stands in the way of this is, I fear, is the disease model of addiction—and medical addiction researchers aren’t likely to turn their backs on that premise any time soon. Still, we cannot say what future research will reveal. And I agree with harm reductionists that the best attitude we can bring to the subject of addiction and recovery is open-mindedness, and a willingness to treat each case as unique, in order to forestall “metabolic chauvinism.”

Graphics Credit: http://hamsnetwork.org 

Common Field Test for Marijuana is Unreliable, Critics Say

A 75-year old pot assay is due for an update.

We’ve all seen it on cop shows: The little plastic bag, the officer breaking the seal on a small pipette and inserting a bit of marijuana, then a firm shake, and voila, the liquid in the test satchel turns purple: Guilty.

Here’s an interesting twist they don’t tell you about: The so-called Duquenois-Levine test—the dominant method for field-testing marijuana since 1930—is considered by many to be wildly inaccurate, and frequently doesn’t hold up in court. One U.S. Superior Court judge referred to the test as “pseudo-scientific.”

The test itself works fine. The problem is that, in addition to identifying marijuana or hashish, the Duquenois-Levine, or D-L, frequently reads positive for tea, nutmeg, sage, and dozens of other chemicals—including resorcinols, a family of over-the-counter medicines, which, according to John Kelly at AlterNet, includes Sucrets throat lozenges. This does matter, because in New York, Washington, D.C., and elsewhere, inner-city minority kids are getting busted for pot in record numbers. Lacking a reliable test protocol, marijuana is whatever the officer says it is. In a classic case that continues to bedevil the testing industry, a middle-aged woman was busted for marijuana while bird watching. A “leafy substance” turned purple on the Duquenois-Levine (D-L) test, and the woman was arrested. The material turned out to be sage, sweetgrass, and lavender, and the woman was engaging in a Native American purifying ritual using a smudge, a concept with which the arresting officers were unfamiliar.

So, when push comes to shove, a positive D-L rarely establishes the presence of marijuana beyond a reasonable doubt, without further confirmatory testing. For at least 20 years now, a visual inspection and a NarcoPouch, as the D-L field test is called, were enough to bring on the felony charges. State courts have squabbled over the matter, but state legislatures have been reluctant to intervene, in large part because sending samples to a lab for confirmatory testing is prohibitively expensive, particularly when the busts are small. The D-L test saves money.

According to the official drug policy of the United Nations, a positive marijuana ID requires gas chromatography/mass spectrometry analysis. And even this far more sophisticated test has angered courts in Washington and Colorado, the UK Guardian reports, “because the DEA doesn’t have standard lab protocols to govern its use.” In part, the judges are furious because plea-bargaining depends upon valid drug possession evidence. So, the officers themselves, when it comes to testifying in court, become de facto expert witnesses, able to identify illegal drugs on sight. Ah, those were the days. But now, cannabis-based products come in a bewildering variety of sizes, shapes, colors, smells, and chemical compositions.

But c’mon, if it looks like bud and it smells like bud… except that the research shows there are 120 terpenoid-type compounds involved in the odor of marijuana. No two varieties smell exactly alike. There is no characteristic marijuana smell—there are hundreds of characteristic marijuana smells. Nonetheless, in 2009 the National Academy of Sciences called the testing of controlled substances “a mature forensic science discipline,” according to AlterNet.

In a 2008 article for the Texas Tech Law Review, Frederic Whitehurst, Executive Director for the Forensic Justice Project and formerly with the FBI, concluded: “We are arresting vast numbers of citizens for possession of a substance that we cannot identify by utilizing the forensic protocol that is presently in use in most crime labs in the United States.” In another section of the article, Whitehurst asks: “Why is this protocol still being utilized to decide whether human beings should be confined to cages and at times, to death chambers?” And as Stewart J. Lawrence and John Kelly write in the Guardian, “using manifestly flawed drug identification tests to charge defendants, or pressure them to plead guilty, is hard to square with a defendant’s right to due process.”

Photo Credit: http://www.howardcountydui.com/ 

The Original Magic Bus: A Preview

Ken Kesey and His Merry Band of Pranksters Search for a Cool Place

"In 1964, Ken Kesey, the famed author of "One Flew Over the Cuckoo's Nest," set off on a legendary, LSD-fuelled cross-country road trip to the New York World's Fair. He was joined by "The Merry Band of Pranksters," a renegade group of counterculture truth-seekers, including Neal Cassady, the American icon immortalized in Kerouac's "On the Road," and the driver and painter of the psychedelic Magic Bus. Kesey and the Pranksters intended to make a documentary about their trip, shooting footage on 16MM, but the film was never finished and the footage has remained virtually unseen. With Magic Trip, Oscar-winning director Alex Gibney and Alison Ellwood were given unprecedented access to this raw footage by the Kesey family. They worked with the Film Foundation, HISTORY and the UCLA Film Archives to restore over 100 hours of film and audiotape, and have shaped an invaluable document of this extraordinary piece of American history."
--(C) Magnolia Pictures

Here's a preview of Magic Trip:

Photo Credit: http://www.key-z.com

Cigarette Sadness

The chemistry of sorrow during nicotine withdrawal.

When you smoke a cigarette, nicotine pops into acetylcholine receptors in the brain, the adrenal glands, and the skeletal muscles, and you get a nicotine rush. Just like alcohol, a cigarette alters the transmission of several important chemical messengers in the brain. “These are not trivial responses,” said Professor Ovide Pomerleau of the University of Michigan Medical School. “It’s like lighting a match in a gasoline factory.”

Experiments at NIDA’s Addiction Research Center in Baltimore have confirmed that nicotine withdrawal not only makes people irritable, but also impairs intellectual performance. Logical reasoning and rapid decision-making both suffer during nicotine withdrawal. Acetylcholine appears to enhance memory, which may help explain a common lament voiced by many smokers during early withdrawal. As summarized by one ex-smoker, “I cannot think, cannot remember, cannot concentrate.”

But there is another, less widely discussed aspect of nicotine withdrawal: profound sadness. Profound enough, in many cases, to be diagnosed as clinical unipolar depression.

 Of course, people detoxing from addictive drugs like nicotine are rarely known to be happy campers. But quitting smoking, for all its other withdrawal effects, reliably evokes a sense of acute nostalgia, like saying goodbye to a lifelong friend. The very act of abstinence produces sadness, joylessness, dysphoria, melancholia—all emotional states associated with unipolar depression.

Work undertaken by Dr. Alexander Glassman and his associates at the New York State Psychiatric Institute has nailed down an unexpectedly strong relationship between prior depression and cigarette smoking, and the findings have been confirmed in other work. This sheds important light on the question of why some smokers repeatedly fail to stop smoking, regardless of the method or the motivation.  The problem, as Glassman sees it, is “an associated vulnerability between affective [mood] disorders and nicotine.”

Now a group of Canadian researchers, working out of the Centre of Addiction and Mental Health (CAMH), and the Department of Psychiatry at the University of Toronto, believe they have isolated the specific neuronal mechanisms responsible for the profound sadness of the abstinent smoker.

Writing in the Archives of General Psychiatry, the investigators, who had access to what the CAMH proudly calls the only PET scanner in the world dedicated to mental health and addiction research, gave PET scans to 24 healthy smokers and 24 healthy non-smokers. Non-smokers were scanned once, while heavy and moderate cigarette smokers were scanned after smoking a cigarette, and also after a period of acute withdrawal. Earlier research of this kind had focused on nicotine’s effect on dopamine release. But Ingrid Bacher and her coworkers in Toronto were measuring MAO-A levels in the prefrontal and anterior cingulate regions, two areas known to be involved in “affect,” or emotional responses. When patients suffering from major depressive disorders get scanned, they tend to show elevated levels of MAO-A. The so-called MAO-A inhibitors Marplan, Nardil, Emsam, and Parnate are still in use as antidepressant medications. In general, the higher the levels of MAO-A, the lower the levels of various neurotransmitters crucial to pleasure and reward. A high level of MAO-A would suggest that the enzyme was significantly altering the activity of serotonin, dopamine, and norepinephrine in brain regions involved in mood.

The researchers found that smokers in withdrawal had 25-35% more MAO-A binding activity than non-smoking controls. “This finding may explain why heavy smokers are at high risk for clinical depression," says Dr. Anthony Phillips, Scientific Director of the Canadian Institutes of Health Research's (CIHR's) Institute of Neurosciences, Mental Health and Addiction, which funded this study.

Although researchers involved in these kinds of drug studies almost always claim that the work is likely to lead to new pharmacological therapies, the plain truth is that such immediate spinouts are rare. But in this case, it does seem like the study provides a clear incentive to investigate the clinical standing of MAO-A inhibitors as an adjunct therapy in stop-smoking programs. “Understanding sadness during cigarette withdrawal is important because this sad mood makes it hard for people to quit, especially in the first few days,” said Dr. Jeffrey Meyer, one of the study authors.

As one addiction researcher noted, an associated vulnerability to depression “isn’t going to cover everybody’s problem, and it doesn’t mean that if you give up smoking, you’re automatically going to plunge into a suicidal depression. However, for people who have some problems along those lines, giving up smoking definitely complicates their lives.”


Bacher, I., Houle, S., Xu, X., Zawertailo, L., Soliman, A., Wilson, A., Selby, P., George, T., Sacher, J., Miler, L., Kish, S., Rusjan, P., & Meyer, J. (2011). Monoamine Oxidase A Binding in the Prefrontal and Anterior Cingulate Cortices During Acute Withdrawal From Heavy Cigarette Smoking Archives of General Psychiatry, 68 (8), 817-826 DOI: 10.1001/archgenpsychiatry.2011.82

Photo Credit:http://jenniferonmars.wordpress.com

Is Addiction Deductible?

You're free to write off the cost of addiction treatment—if you can afford to.

The cost of addiction treatment is a legitimate medical expense, as long as you are talking about drug and alcohol addiction, which the IRS recognizes as a genuine medical disease. If you go to Betty Ford on the advice of your doctor for alcoholism, it’s deductible. If you go to Passages for cocaine addiction, it’s deductible. If you buy nicotine gum and patches and fill a prescription for Chantix, in a stop-smoking effort, it’s deductible. But if you want to write off the cost of a weight-loss clinic, or a gambling cessation program, or treatment for compulsive sexual activity, you’re a bit ahead of the curve.

According to Dave Hutchison, Planned Giving Officer at the Betty Ford Center Foundation: “Generally, medical expenses, including amounts paid for medical treatment, drugs and medicines, nursing care and certain transportation and travel required for medical care, are deductible as an itemized deduction.  Amounts paid for inpatient treatment of alcoholism or drug addiction at a therapeutic center and for meals and lodging furnished as a necessary incident to the treatment are deductible.”

Officially, IRS Topic 502 says that “payments for acupuncture treatments or inpatient treatment at a center for alcohol or drug addiction are also deductible medical expenses.” So just about any loopy treatment is covered, as long as the official diagnosis is alcoholism or drug addiction, including cigarettes.

And while theoretically the IRS is open to the idea of allowing deductions for the “cost of participating in a weight-loss program for a specific disease or diseases, including obesity, diagnosed by a physician,” the tax people aren’t yet persuaded that obesity, per se, is an addictive disease. They don’t allow most deductions for the cost of health food diet items or health club dues, for example, even if health food and gym workouts are doctor’s orders.

So, in theory, the cost of drug and alcohol rehab is a legitimate medical expense. Or at least those expenses over and above 7.5% of your income that haven’t been paid for by medical insurance. In practice, whether you can deduct the cost of drug rehab depends entirely on your total amount of itemized medical expenses. You can write off the cost of addiction treatment—if you can afford to.
Kelly Phillips Erb, who blogs at Forbes as Tax Girl, explains it all:

As a general rule, the costs of rehabilitation for drug and alcohol abuse and addictions are deductible as medical expenses, assuming that you itemize your deductions on Schedule A. Like other medical and dental expenses, rehab and addiction treatment expenses are only deductible to the extent that they exceed 7.5% of your adjusted gross income (AGI). So, for example, if your AGI was $40,000, you can only deduct expenses which exceed $3,000 (7.5% of $40,000). If the total of your expenses, including treatment costs $5,000, then you can deduct $2,000 ($5,000 expenses less the $3,000 threshold).

And that’s after you’ve parsed the IRS definition of qualifying medical care: “The diagnosis, cure, mitigation, treatment, or prevention of disease.” According to Tax Girl, that’s it. Other than throwing out a few examples—nursing services, x-rays, ambulance expenses—there is precious little help in defining what counts as a disease. Tax Girl says that the “IRS allows deductions for expenses related to the treatment of alcoholism and drug addiction because it agrees that those behaviors are a disease—even if many taxpayers think differently.” But the IRS won’t allow deductions for the cost of treatment with illegal drugs, thereby making the likelihood of write-offs for medical marijuana and marijuana addiction treatment unlikely, as long as marijuana remains illegal at the federal level. Furthermore, certain promising treatment options are not deductible for the same reason. Tax Girl writes that “despite evidence in Europe that “prescription” heroin taken together with methadone might lessen heroin dependence in addicts, the treatment remains illegal in the U.S. and is, therefore, not be deductible for federal income tax purposes. Methadone on its own, however, is a legal treatment for drug addiction in the U.S.” and is therefore deductible for federal income tax purposes.

Furthermore: “The IRS does not necessarily agree that all behaviors considered to be ‘addictions’ qualify as a disease.” Given the broad net cast across the medical waters in the name of addiction—everything from Internet addiction to cornstarch addiction—it’s probably just as well that the IRS is taking a jaundiced view of the so-called behavioral addictions. But they have taken some heat for being hard-nosed about obesity, while at the same time allowing write-offs for medical expenses associated with sex change operations.

Okay. But what if you’re Charlie Sheen, living on the other end of the income scale, until recently pulling down $2 million dollars per TV episode, starring in a mildly amusing sitcom? He’ll make maybe $40 million this year. How much would Charlie have to spend on rehab to make it tax-deductible? As it happens, there are tax geeks like Kay Bell at MSN Money who wonder about such things. Remember, Charlie can only deduct the amount of qualifying medical expenses that exceed 7.5% of his adjusted gross income. Bell says that Sheen “would have to spend lots of time at a pretty swanky rehab center to run up the more than $3 million required for him to claim the medical expenses deduction. He’s in Los Angeles, so it’s possible, but still, that’s a big recovery bill.”

Photo credit: http://potcouture.com/

FROM THE ARCHIVES: Sex, Drugs, and… Sex

Pharmaceuticals and sexual performance.

[Originally posted 9/5/10]

The search for aphrodisiacs is an ancient, if not always venerable, human pursuit. Named for Aphrodite, the Greek goddess of love, aphrodisiacs are compounds that have the reputation, real or imagined, of increasing sexual desire, pleasure, and potency. It’s safe to say that rhinoceros horn or tiger penis—various forms of sympathetic magic—just don’t reliably do the trick.

Writing in Hormones and Behavior, a group of Canadian behavioral neurobiologists recently concluded that “substantial clinical and epidemiological literatures suggest that [stimulants and depressants] either inhibit sexual responding or can be ‘prosexual’ in certain situations, thereby increasing the potential of risky sexual activity and the spread of sexually transmitted diseases.”

In other words, recreational drugs either sex you up, or they decrease your sex drive. And they either do or do not lead to risky sexual behavior among young people.

Not too promising a start. Nonetheless, JG Pfaus and coworkers at Concordia University’s Center for Studies in Behavioral Neurobiology examined more than 100 studies based on animal models, and teased out some commonalities:

Stimulants are, well, stimulating. Cocaine “facilitated penile erection” in male rats, while acute caffeine consumption amped up the sexual behavior of both male and female test animals. As for depressants, small amounts of alcohol decreased inhibitory tendencies in rats, while a high level “disrupted sexual performance.” Alcohol “increases rodent sexual motivation” but impairs specific parameters of sexual performance. 

Yes, well, Shakespeare said it best. Macbeth proclaims at one point that alcohol “provokes the desire but it takes away the performance.”  As with mice, so with men and women. In animal studies, low doses of alcohol increase sexual desire, moderate doses intensify those effects, and a high dose extinguishes the impulse altogether. Male rodents, too, are subject to Brewer’s Droop.

With the opiates, the story is much the same. In a National Institute on Drug Abuse (NIDA) study, the title of which--“Methadone reduces sexual performance and sexual motivation in the male Syrian golden hamster”--remains a classic, researchers found that after a dose of methadone, the critters were definitely disinclined to copulate. In general, systemic morphine inhibits sexual behavior in rats, mice, dogs, even donkeys. Animals don’t want to do it on opiates. Females stop engaging in “proceptive pacing and solicitation.”

And naturally, you’re wondering about the sex lives of castrated Japanese quail. Researchers managed to get them copulating again with the opioid antagonist naloxone. (Testosterone implants also work.)

Although it sometimes seems laughable, there is a good argument to be made for the use of animals for modeling certain aspects of human sexual behavior. Stripped of cultural and complex social overlays, animal studies afford an opportunity to focus relentlessly on the biological. But enough for now on the fascinating topic of rats having sex on drugs.

In studies of men and women, Pfaus found that alcohol “dose-dependently delayed ejaculation, reduced the intensity of orgasm, and decreased both physiological and subjective measures of sexual arousal. Nearly identical effects were observed in women, although alcohol increased, rather than decreased, their subjective levels of sexual arousal.” The nastiest example of alcohol’s effect on sex may be the blood vessel and nerve damage, sometimes permanent, known as chronic alcohol impotence. Alcohol damage can disrupt communication between the pituitary gland and the genitals—and that can’t be a good thing. Heavy smoking also reduces circulation to the blood vessels in the genitals.  Heavy smokers and drinkers often report impotence or continuing sexually disinterest even when they have been sober and smokeless for a while.

Alcohol’s effect on sexual performance is no secret, of course. But Pfaus also concludes that, in general, “drug use debilitates sexual responding in the majority of situations.”

He means the whole pantheon, the entire roster of usual suspects: Why would drugs like cocaine, marijuana, amphetamine and oxycontin all have an overall negative effect on sexuality? Do hashish and cocaine, common “love potions” found in classical literature, boost sexual ardor, or do they have the opposite effect?

The following is a mix of anecdotal data and clinical reporting related to common addictive drugs and other “drugs of abuse.”

LSD/Magic Mushrooms/Ecstasy/other Psychedelics: Some users report increased sexual awareness and sensitivity, but heavier doses tend to discourage sexual activity.

Marijuana/Hashish: Heightened sensory experiences can enhance sexual experiences, while heavier cannabis use can lower libido.

Cocaine: Equivocal. Users often report increased arousal and ease of orgasm. However, exactly the opposite effect is known to occur in heavy regular users.

Heroin/Oxycontin/other Opiates: Lowered libido and difficulty achieving orgasm are the norms. Yet even in this rather clear-cut case, there is no unanimity of opinion or experience. The familiar pattern is in evidence--a little bit might temporarily add some oomph to your sex drive. Heavier use is likely to lay a thick blanket across your libido.

Heroin is a strange case: In a 2003 study of women in methadone maintenance treatment programs, published in Addictive Behaviors, several different themes emerged: “Some women believe that drugs, particularly heroin, increase their sexual performance, libido, and pleasure, but for others, drugs, particularly crack cocaine, inhibit their sexual performance and desire. Many of the women believe that crack cocaine and heroin enhance a man’s sexual desire, performance, and pleasure. However, other women deem that these drugs are responsible for their partner’s abusive and coercive behavior.” The effect of drugs on rates of sexual violence varies. Differential effects can be found in every aspect of the effect of drugs on sexual behavior, for the same reason that individuals vary in their response to these drugs. Metabolisms are not all the same.

Amphetamine: The stimulant rush can amp up sexual encounters; heavy use leads to desensitization and difficulty achieving orgasm. Intense but sometimes rather psychologically detached sex sessions can lead to everything from genital chafing to the classic “fuck knot” of tangled hair sometimes produced by a prolonged bout of missionary-position intercourse.

If the usual roster of recreational drugs cannot be counted on to perform as aphrodisiacs, there are always efforts underway to identify “prosexual” drugs and natural sex-enhancing nutrients. Among the contenders:

Bromocriptine (Parlodel): This drug is used to treat pituitary tumors and Parkinson’s disease. It reduces prolactin, which is associated with age-related impotency in men. However, the dosage level required for the effect can cause unpleasant side effects.

Gamma-hydroxybutyrate (GHB): This one has been abused in the U.S. for its euphoric, sedative, and anabolic (body building) effects. It triggers the release of growth hormone from the pituitary. Not recommended. Combining GHB with alcohol sometimes leads to nausea and breathing problems.

DHEA: Big hopes were recently riding on this hormone. Sorry to say, Pfaus reports that in aging males, DHEA “had only transient effects in a well-controlled, double-blind study.” Women had some promising hormonal news in the early going: “Mixed estrogen/androgen replacement to postmenopausal women improved measures of sexual desire, satisfaction, and frequency of sexual activity, compared with treatment with estrogen alone.”

Yohimbe: Operating on a different receptor, this plant drug, long considered an aphrodisiac, pulls norepinephrine into the picture, at least in men. Yohimbine is an adrenoceptor agonist that fairly reliably turns on male rat mounting behavior and is reputed to be an effective sexual enhancer for some men.

Deprenyl (Seliginine): A dopamine booster, which also acts as a weird MAO inhibitor and is used for Parkinson’s and depression, l-deprenyl has a reputation as a so-called smart drug, and is popular with life extension enthusiasts. It also markedly improves the sex lives of older rats.  Another one with side effects to beware of.

There are also reports that L-dopa, used in patients with Parkinson’s disease, increases sexual interest in the elderly. (But L-dopa has a number of undesirable side effects, too.) Apomorphine, a dopamine receptor agonist, increases the “likelihood of spontaneous erections.” 

In animal models, a variety of dopamine-active drugs generally have positive effects on the sexual behavior of rodents.  As might be expected, drugs that block or reduce dopamine transmission also reduce sexual displays in animals. Our friend Drosophila melanogaster, the common fruit fly, doesn’t get in the mood when it is dopamine-depleted, a state that can be reversed with L-dopa. Give a virgin male rat a good dose of D-amphetamine and it is off to the races, its surge of sexual excitement cause by dopamine release in the nucleus accumbens. In women, “the ability of estrogen to stimulate dopamine release and to augment dopamine release and behavior in response to amphetamine has been well established,” according to James G. Pfaus and Barry J. Everitt in “The Psychopharmacology of Sexual Behavior.” But the specific mechanism by which this happens has not been identified.

 Other scientists have also managed to sexually stimulate rats with extracts of Turmera diffusa (Damina), Pfaffia paniculata (Brazilian ginseng), and Eurycoma longfolia Jak (Catuaba).

As for serotonin, Pfaus and Everitt find “minimal methodologically-sound evidence on the effects on human sexuality of manipulating the serotoninergic system.” So serotonin appears not to have much to do with sexual activity directly. In fact, it can have a negative effect, as users of SSRI antidepressants like Prozac have discovered. The common symptom in this case is difficulty achieving orgasm.  Serotonin at 5-HT receptors inhibits sexual impulses in women as well as men.

In the end, Pfaus maintains that the best way to get male rats back in action after a strenuous day of copulation is “a combination of the nonspecific dopamine receptor agonist apomorphine and the adrenergic receptor antagonist yohimbine.”

Pfaus, J., Wilkins, M., DiPietro, N., Benibgui, M., Toledano, R., Rowe, A., & Couch, M. (2010). Inhibitory and disinhibitory effects of psychomotor stimulants and depressants on the sexual behavior of male and female rats Hormones and Behavior, 58 (1), 163-176 DOI: 10.1016/j.yhbeh.2009.10.004

Photo Credit: http://www.aphrodisiacs.org.uk/

Essay: The Genuine Drug War is in Biomedicine

Knowledge, not firepower, is the key to the future.

In modern American society, heart disease, cancer, HIV\AIDS, diabetes, alcoholism, and cigarette addiction account for millions of deaths. They are all disease entities with strong psychological and behavioral components—complicated, multicellular, multi-organ disorders. But they have all been associated, at one time or another, with negative personality traits and moral flaws. The less we know about the mechanics of a human disorder, the more likely we are to view its external symptoms as signs of laziness, or neuralgia of the spirit, or as a form of damage caused by specific kinds of thoughts and emotions. Without a doubt, all kinds of flaws are sometimes expressed in the behavior of people who have these disorders. Yet none of these flaws can be considered the root cause of the diseases.

Addiction is being added to the roster of physical disorders once thought to be symptoms of insanity, but which are now seen to be disease entities with strong mental components, like most diseases. As Professor Felton J. Earls of the Harvard School of Public Health argued almost twenty years ago: “Until we have an Institute of Addictive Behaviors, we are not going to get very far on the public-policy issues because we will not have our science-policy issues properly aggregated and organized in order to move forward on the issues in any meaningful way.”  Witness the tangle over merging NIDA and the NIAAA, and you’ll have a good idea of how far we still have to go in this respect.

The genuine drug war is being fought in the arena of biomedicine. The New York State Division of Substance Abuse Services in Albany  estimated several years ago that the annual bill for successfully treating a single drug addict is $3,850, compared with $14,000 in estimated annual expenses— health, welfare and law enforcement costs—associated with one untreated addict. The real crisis is the indisputable fact that there exists today an appalling shortage of funds for biomedical research—ironically one of the fields of scientific endeavor in which the U.S. holds a clear lead.

The cause of the dilemma is a fundamental misunderstanding among politicians and the public about how diseases can be understood and conquered. Cross-fertilization among scientific disciplines yields unexpected results. Targeted research, such as the much-ballyhooed war on cancer, or the crash program to find a cure for A.I.D.S., is not necessarily the most desirable way to proceed. Insights come from unexpected places, in serendipitous ways. As the scientific understanding of cells and receptors deepens, diseases and disorders once thought to have unrelated causes are seen to have common and entirely unanticipated origins. Research into the viral mechanisms of the common cold may ultimately yield more insights into AIDS then all of the directed research now underway. In biomedicine, there is no guarantee that goals can be reached through the front door, by a systematic assault akin to an engineering project. We cannot, for example, hope to cure addiction, or even the common cold, by means of the same methods we used to put a man on the moon.

There are, however, certain things we can begin to do immediately, if, as a nation, we are serious about drug abuse. As a society, Americans have not done a very good job of laying the groundwork for an objective look at addiction and recovery. To begin with, we must attend to the staggering number of drug-related deaths, injuries, and hospitalizations caused by the abuse of prescription medications. The government itself has proven the case for this contention in numerous reports issued by the National Institute on Drug Abuse and other official bodies. According to the U.S. Department of Health and Human Services, “Older Americans account for more than half of all deaths from drug reactions,” leading one to suspect that the majority of drug fatalities stem from accidentally fatal overdoses by heavily medicated senior citizens. Our national fixation on illegal drugs has blinded us to certain verifiable facts about prescription drug abuse.

We also need to recognize the problem of underprescribing opiates and other addictive painkillers for children and adults in hospital settings. If we continue to stringently prohibit the use and sale of synthetic and designer drugs like methadone, morphine, amphetamines, and barbiturates, we will have to make one important exception: pain abatement in medical applications. One of the great scandals to come out of the drug war is the growing understanding that potent painkillers are not being offered in sufficient amounts to patients suffering intractable and agonizing pain.

“There’s a certain amount of hysteria about narcotics among doctors,” maintains one researcher. At least half of all cancer patients seen in routine practice report inadequate pain relief, according to the American College of Physicians. For cancer patients in pain, adequate relief is quite literally a flip of the coin.

At least 6 million cancer and AIDS patients currently receive no appropriate pain treatment of any kind. In addition, WHO estimates that four out of five patients dying of cancer are also suffering severe pain. The numbers of untreated patients suffering intractable, unrelieved pain from nerve damage, burns, gunshots, sickle cell anemia, and a host of other medical conditions can only be guessed at.

Figures gathered by a different U.N. agency, the International Narcotics Control Board, make clear that “citizens of rich nations suffer less.” To put it starkly, the use of morphine per person in the United States is 17,000 times higher than per person usage in Sierra Leone. Doctors in Africa paint a grim picture of patients hanging themselves or throwing themselves in front of trucks as an alternative to life without pain relief. The U.S., Canada, Britain, France, Germany, and Australia together account for roughly 80 per cent of the world’s medicinal morphine use. Other countries, particularly the poor and undeveloped nations, scramble for what’s left.

In many cases, pain relief is the one thing doctors can offer their patients, and the one thing they withhold.

--Adapted from The Chemical Carousel, by Dirk Hanson

Photo Credit: http://www.eurac.edu