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 

On Harm Reduction and Metabolic Chauvinism

My WebTalk Radio interview for the podcast, “Addicted to Addicts.”
  

 Listen to the podcast at WebTalkRadio HERE.
(Addiction Inbox is now on vacation. Hot fun in the summer sun...)

Amy Winehouse Dies at 27

 

Musicians who died of drug-related causes at the age of 27:

Jimi Hendrix
Brian Jones
Janis Joplin
Jim Morrison
Kurt Cobain
courtesy metro.co.uk.

"Sunday tabloids in the UK have claimed Winehouse was seen buying drugs from a dealer in Camden just after 10.30 pm where she was later found dead in her apartment, according to reports in the Daily Mail."

                                                                                                            Moving tribute from Russell Brand

Drug Links, Various

It’s summer vacation. Did I turn off the stove?


Some recent posts I wrote before ending my run as editor of TheFix.com News Blog:

Drugging the Elderly
Why seniors take too many of the wrong medications at the wrong dose.

Never Heard of Kratom? You Will.
A plant from Thailand with opiate-like properties is the latest "designer drug" speeding its way through America.

How Binge Drinking Causes Fetal Damage
Studies in mice show that alcohol is toxic to DNA in the absence of two specialized enzymes.

Senators Blast Feds for Border Scandal
Botched gun-smuggling scheme put weapons in the hands of Mexican drug thugs, endangered informants, and may have gotten agents killed.

Testimonials to Betty Ford
In the wake of Mrs. Ford’s death, celebrities and politicians tell their personal stories about her work in raising awareness of addiction and recovery.

New Synthetic Marijuana Arrives to Replace Spice, K2
Designers are already busy with the second generation of cannabis-like drugs.

Crack and Coke Will Finally Receive the Same Legal Penalties
Civil rights leaders charged that the legal system's intense obsession with crack amped up minority arrests, but had no scientific basis. Turns out they were right.

Miracle-Gro Goes After the Medical Marijuana Market
It’s just quasi-legal cooperative organic gardening, right? All $1.7 billion of it.

(R.I.P. Amy Winehouse)

An Interview With Research Psychologist Vaughan Bell

An expert on abnormal brain function talks about drugs, hallucinations, and addiction.

Vaughan Bell gets around. The multifaceted clinical and research psychologist, currently a Senior Research Fellow at the Institute of Psychiatry, King’s College, London, is, in fact, down in Colombia right now. He arrived in the country to teach clinical psychiatry at Hospital Universitario San Vicente de Paúl and the Universidad de Antioquia in Medellín, Colombia, where he remains an honorary professor, but right now he works for Médecins sans Frontières (Doctors Without Borders) as mental health coordinator for Colombia, which means he is quite frequently off in the jungle, doing good work under very bad conditions. Bell has written for numerous scientific journals, including Cognitive Neuropsychiatry, Psychiatry Research, and Cortex. He has also written for Slate, The Guardian, Scientific American, and is a contributing editor at Wired. The New York Times ran a fascinating profile of Bell’s work on debunking theories about the Internet as a cause of addiction and psychosis. He is well known online for his contributions to the Mind Hacks blog, which covers unusual and intriguing findings in neuroscience and psychology. He is also working on The Enchanted Window: How Hallucinations Reveal the Hidden Workings of the Mind and Brain, a book for Penguin UK.


Q. You’ve been looking into abnormal brain states of late: delusions, hallucinations, and dissociative disorders.  Do drugs, madness, brain injuries, and religious experiences have anything in common? Is there an underlying cause for seeing or experiencing things that aren’t there?

Vaughan Bell: Apart from involving the brain, often not. Unusual perceptions occur because the normal processes that allow us to generate sensory impressions of the world become distorted. For example, the idea that we see the world as it is, is a bit of a myth, because we experience things that aren’t there all the time. The eye allows light to fall on the retina, two flat areas of photoreceptor cells which provide only patchy and poor resolution coverage of the visual field, and yet we have a very rich visual experience. The brain is filling in the rest. In your blind spots, you receive no visual information and yet we don’t have two black spots in our vision because we ‘hallucinate’ the best guess visual experience.

These are not usually considered hallucinations because the experience remains stable and predictable but these same processes, with just slight instabilities, can lead to spectacular hallucinatory states – such as Charles Bonnet syndrome –where damage to the retina leads to visions of monkeys, rabbits and little men. In other words, there are as many causes for hallucinations as there are causes for our perception of reality. If the same processes are affected through drugs, brain damage, trance states, stress or simply expectation, we can say that a particular experience has a similar basis but we have to think of the interaction to understand them fully. Trying to explain experiences solely by the brain, mind or environment makes little sense.

Q: You’ve experimented with “the vine”—ayahuasca, a powerful South American hallucinogenic plant that contains DMT. You obviously lived to tell about it. Did you see any transdimensional machine elves?

Bell: There were no transdimensional machine elves, although the whole experience was quite striking. I was kindly invited to take part in the ceremony by a chap called Romualdo, a Uitito taita (shaman), who I happened to meet in a conference about indigenous culture and I was very grateful for the opportunity.

I suspect the experience of meeting what McKenna called the "machine elves" is more prominent when pure DMT is smoked which gives a more concentrated acute dose. The traditional process of taking ayahuasca, known as yagé in Colombia, involves drinking a potion made from the vine until you start puking. To get a fair dose you need to repeat this process several times, so the absorption is much slower. I managed three or four drink – puke cycles and the psychedelic effects were prominent although I never lost track of reality. I was, however, very struck by the appearance of classic Kluver form constants, geometric patterns that are probably caused by the drug affecting the visual neurons that deal with basic perceptual process (e.g. line detection).

Q. As a research psychologist, you have been critical of the disease model of addiction for being both too simplistic about mind and behavior, and too all-encompassing to be credible. In an article for Slate, you wrote: "Despite the scientific implausibility of the same disease—addiction—underlying both damaging heroin use and overenthusiasm for World of Warcraft, the concept has run wild in the popular imagination. Our enthusiasm for labeling new forms of addictions seems to have arisen from a perfect storm of pop medicine, pseudo-neuroscience, and misplaced sympathy for the miserable." How should we view addiction, and how should we be dealing with it?

Bell: I think we should view addiction as an over-applied label that is distracting us from the fact that not everyone’s difficulties with unhelpful repetitive behavior can be understood and treated in the same way. Often compulsive behaviors do have shared factors. Obsessive-compulsive disorder, impulse control disorders (like pathological gambling or compulsive stealing) and drug addictions are all known to have shared similar behavioral, neurological and genetic features but that does not mean that each disorder is essentially the same.

The idea that playing too many computer games or compulsive use of the Internet is an addiction like any other is really obscuring the fact that different compulsive behaviors also have many different components. It would be like saying that all "mood disorders" are essentially the same—it would neither be scientifically nor clinically helpful and would cause more confusion than insight. This is the situation we have with addiction at the moment.

Q. You’ve been living and working in South America for some time now. How has the drug trade and the drug war changed that part of the world, in your own experience?

Bell: If you don’t mind, I’m going to skip this question. The drug trade is interwoven with the conflict in Colombia and myself and my colleagues in Médecins sans Frontières (Doctors Without Borders) work in areas where the fighting is live and ongoing. One of the things that allows us to do our work in areas controlled by armed groups is that we are a neutral organization solely concerned with providing medical care without getting involved in the politics behind the conflict. Of course, like everyone else, I have a view, but in case it affects either our access to the people we’re trying to treat or the security of our teams in the field, I’ll keep it to myself when I’m mentioned alongside the organization.

Graphics Credit:  http://news.softpedia.com/

There’s No Agreement on DUIC: Driving Under the Influence of Cannabis

The ACLU squares off against law enforcement over how to measure marijuana impairment.

What’s your blood cannabis content? You don’t know, and neither does anybody else, without a fair bit of effort. There’s no device to blow into, no quick chemical field test. You’re impaired by marijuana if the officer says you’re impaired by marijuana, and in most states he or she will decide that matter by using a series of sobriety checks not dissimilar to the well-known alcohol exercises: standing on one foot, walking a line, having your eyeballs and blood pressure checked—and my personal favorite, a test of how well you can guess when 30 seconds is up. Time passes more slowly when you’re about to be arrested for drugs, I’m guessing, since it takes a little while for your life to pass before your eyes. Even the National Highway Traffic Safety Administration admits that it is “difficult to establish a relationship between a person's THC blood or plasma concentration and performance impairing effects. Concentrations of parent drug and metabolite are very dependent on pattern of use as well as dose."

The point is, observable indications of impairment, as they’re called, are really all that law enforcement currently has as a tool for policing the use by drivers of American’s second most popular drug. At one extreme end of the spectrum are the pot enthusiasts who argue that no amount of marijuana significantly impairs you behind the wheel. At the other end of the spectrum stand the zero-tolerance advocates: No amount of marijuana is safe, if you’re planning to get behind the wheel within the next several hours—or at any time during the rest of your life, as some anti-drug advocates seem to be saying.

And somewhere in between, according to the American Civil Liberties Union (ACLU) of Washington State, lies a possible compromise for gauging marijuana impairment. “Adding a science-based threshold for likely impairment to the mix and providing educational information that allows people to estimate their personal level of intoxication can be effective strategies for preventing impaired driving in the first place and improving public safety,” the  ACLU asserts.

The ACLU favors the so-called Pennsylvania Model, which sets that state’s legal limit for cannabis in whole blood at 5 nanograms per milliliter (ng/mL). Why 5, and not some other number? Because a legal cut-off of 5 ng/mL is also what the National Organizaton for the Reform of Marijuana Laws (NORML) recommends, based in turn on an analysis of scientific studies of marijuana’s effect on driving skills. Specifically, NORML recommends a limit in the range of 3.5-5.0 ng/mL, which the group says will “clearly separate unimpaired drivers with residual THC concentrations of 0-2 ng/mL from drivers who consumed cannabis within the last hour or so.” Levels under that range tend to indicate that the driver smoked at least 1 to 3 hours ago. Anyone testing over that range, says NORML is “likely to be impaired.”

But it’s not quite that simple, of course. First, you have to rule out a whole roster of cannabis metabolites that stay in the system for days or weeks, but have no impact on driving skills. And the metabolism of cannabinoid by-products varies so widely from person to person (this is just beginning to be understood scientifically), that the results of testing are not foolproof. The iron law of metabolic diversity makes that claim unlikely. Moreover, there is currently no reliable way of testing blood in the field for THC concentrations. But there will be. Introducing the Vantix Biosensor, a device that looks, ironically, like a portable vaporizer for marijuana. Open your mouth, please, as the officer politely swabs the inside of your cheek with a plastic wand, and inserts the wand in the handheld machine. Sensors on a microchip react with telltale antibodies, and you test positive for cocaine, or marijuana, or, soon, synthetic marijuana. Or perhaps it will be some other company’s device. But rest assured it is being looked upon as a growth market.

And then there is, as the ACLU points out, the wrong way to go about it: zero tolerance. At least 11 states have now set the requisite cut-off level for illegal drugs at zero. That may raise a cheer in certain quarters of the anti-drug movement, but it is a decision “based not in science but on convenience,” says the ACLU. It establishes a crime wholly “divorced from impairment” behind the wheel. Put simply, zero tolerance “does not differentiate between a dangerously incapacitated driver and an individual who may have smoked the past Monday but was pulled over as a sober ‘designated driver’ on Saturday night.” Furthermore, “even a statute excluding cannabis metabolites but criminalizing trace amounts of THC” could result in the arrest of drivers several days after they last smoked pot. It’s pretty simple, really. “If science dictates that the presence of a trace amount of cannabis or a cannabis metabolite in an individual’s blood has NO ‘influence’ on his capacity to drive, it should not constitute per se evidence of ‘driving under the influence.’” But toxicologist Marilyn Huestis, at the National Institute on Drug Abuse, disagrees. She believes that there is no safe level of marijuana consumption, where driving is concerned. Paul Armentano, deputy director for NORML, scoffs at that, telling the Los Angeles Times that individual states “are not setting a standard based on impairment, but one similar to saying that if you have one sip of alcohol you are too drunk to drive for the next week.”

 One abiding problem is that for car accidents, it’s not necessarily a pure play. Alcohol mixed with one or more additional drugs is common, and if it’s difficult to set limits for alcohol and marijuana alone, imagine the permutations involved in creating legal limits for a combination of both. A 2007 survey of experimental studies, published in Addiction by a group of researchers in six countries, concluded that a rule of thumb police might want to consider is based on the finding that “a THC concentration in the serum of 7–10 ng/ml is correlated with an impairment comparable to that caused by a blood alcohol concentration (BAC) of 0.05%. Thus, a suitable numerical limit for THC in serum may fall in that range.” Considering that we allow drivers to exhibit blood alcohol limits as high as 0.08, NORML’s 5 ng/mL limit looks downright conservative.

There’s no simple solution. Maybe that’s because cannabis is not a simple drug. We’re still teasing apart its effects, and nailing down the particulars of driving under the influence of cannabis is one of them. As Jeffrey P. Michael of the National Highway Traffic Safety Adminstration refreshingly disclosed to the Los Angeles Times, “We don’t know what level of marijuana impairs a driver.” But they are trying to find out. A federal study in Virginia intends to round up more than 7,000 blood samples by showing up at the scene of car accidents and asking drivers to provide random, anonymous  samples to compare with control samples.

Other studies of a similar nature are underway. Driving under the influence of drugs could become as common a criminal charge as classic DUIs and DWIs.

Photo credit: http://www.janisian.com/