Saturday, July 6, 2013

Popular Synthetics: The Class of 2013


Navigating the new alphabet of intoxication.

You don’t have to be a molecular chemist to know which of today’s recreational drugs are safe. Wait, I take that back. You DO have to be a molecular chemist to navigate today’s synthetic drug market with anything like a modest degree of safety.

It’s hard not to get nostalgic: Back in the day, you had your pot, you had your acid, your coke, your speed, and your heroin. And that, with the exception of a few freak outriders like PCP, was about that. Baby boomers of today, already losing touch with leading-edge music—Macklemore? Tame Impala?—can now consider themselves officially out of touch when it comes to illegal drugs.

That is, unless they are familiar with psychoactive chemicals beyond mere methamphetamine “bath salt” knockoffs like mephedrone, and cannabis “Spice” look-alikes such as JWH-018. We’re talking about drugs like Bromo-DragonFly, Benzo Fury, and 2C-B.  As Vanessa Grigoriadis writes in New York Magazine: “These drug users imagine themselves as amateur chemists, proto-Walter Whites, sampling and resynthesizing drugs to achieve exactly the state of consciousness they find most pleasurable. And there are no end of drugs to play with.”

A big piece of the synthetic drugs movement can be traced to the work of the legendary Alexander Shulgin, a Harvard grad who worked for Dow chemical, and who invented more than 100 entirely novel hallucinogenic compounds over the years. Other than the hallucinogens investigated by Shulgin and his coterie of personal friends, who were willing to take new hallucinogens and report back, none of the drugs on this list were meant for, or tested on, human beings.

Many of them are not, technically, new. Nonetheless, writes Grigoriadis, "almost every drug, from pot to GHB to morphine, has been messed with, as chemists find that removing a methoxy group or adding a benzene ring makes a new drug with different properties: body-grooving with a side helping of visuals, euphoric or speedy, long or short, or administering just the right dose of primal fear. Formerly known as “designer drugs,” they have morphed into “synthetic highs.” The tricky precursor chemical problem has become much easier to solve in the present moment, when any budding entrepreneur can send the official chemical designation of a drug, called its CAS number, to any of dozens of manufacturers in China, who will provide them with whatever weird “research” drug they need.


Herewith, a sampling of a few popular drugs of the day:

  • 2C Series
2C-P is an Alexander Shulgin favorite, a hallucinogenic phenethylamine known officially as 2-(2,5-dmethoxy-4-propylphenyl)ethanamine. But your mileage may vary. Phenethylamine is similar in action to amphetamine and acts on dopamine and norepinephrine receptors. Nonetheless, 2C drugs have strong psychedelic effects as well. Other phenethylamine drugs include ephedrine, mescaline, bupropion (Wellbutrin), and venlafaxine (Effexor). There are several drugs in the 2C family, including 2C-B and 2C-I, but 2C-P is considered the strongest in the class, an intense psychedelic with visualizations lasting for up to 16 hours. 2C-B, or 4-bromo-2,5-dimethoxyphenethylamine is another popular hallucinogen, described by some as a cross between LSD and MDMA (Ecstasy)—less “psychedelic” than LSD, with stronger “body effects.” Drugs in this family are generally recognized as non-addictive, but large doses can cause sweating and chills, stomach discomfort, and paranoia or panic. A close cousin, the DOB drugs (2,5-Dimethoxy-4-Bromoamphetamine) are a related family of hallucinogens.

  • Bromo-Dragonfly
This synthetic, sold as 3C-Bromo-Dragonfly and DOB-Dragonfly, is a very strong serotonin agonist, and has effects consistent with serotonin 5-HT hallucinogens such as LSD. This one came out of Purdue Pharmaceuticals as a compound for use in serotonin research, and belongs to a class of drugs called benzodifurans, which are related to the phenethylamines. It has been implicated in several deaths since it was first reported in 2007, says drug site Erowid. Positive effects listed at EROWID  included mood lift, visual changes, and increased energy. Negative effects include short-term memory loss, muscle tension, and “unknown risks due to research chemical status.” This is not a drug to take lightly. Dr. Jeff Lapoint, an attending physician at San Diego’s Kaiser Permanente and an expert in toxicology, recently told Tony O'Neill at The Fix that “Bromo-Dragonfly is probably the scariest thing on the list.”

  • NBOMe Series
This group of synthetics, now available to underground buyers, is a perfect example of a complicated new series of psychoactive drugs with little or no track record of human use before they appeared online in 2010. When coherently labeled at all, they are sold as 2C-C-NBOMe, 2c-I-NBOMe, 25C-NBOMe, and mescaline-NBOMe, among other designations. The NBOMe series have attributes of both hallucinogens and amphetamines, and are active at very low doses, like LSD. There isn’t even much in the way of animal research on this collection. As with many of these synthetics, reports linking 2C-C-NBOMe to the deaths of young users have surfaced over the past two years.  While hallucinogens always present this Janus-faced aspect, this roll-the-dice-for-a-good-trip-or-a-bad-trip vibe, the ability to actually KNOW what you are taking—always a problem of major significance in the underground drug world—becomes even more acute in the case of research chemicals not intended for human use, let alone Prime Time.  If all goes well, users get a mood lift, visuals, and euphoria. At high doses, the effects can include nausea, paranoia, extreme fear, and panic. It is the essential dilemma at the heart of psychedelic experimentation—there are no guarantees going in, and it is always, at least to a degree, a form of psychic Russian roulette.

  • 6-APB (Benzo Fury)
A lot of different drugs are sold as Benzo Fury, but the name comes originally from 6-APB, or 6-(2-aminopropyl)benzofuran. Like so many other designer amphetamines, 6-APB showed up online in 2010. The online drug discussion site Bluelight notes that vendors also peddle it as 6-APDB, 5-APDB, and 4-D as well. To date it has mostly surfaced as a club drug in the UK, and is chemically similar to MDA, another “entactogen” with strong body effects that was popular in the 60s as the “love drug.” Unfortunately Benzo Fury proved to be such a Euro-smash as a brand that drug sellers started packaging any research chemical at hand as Benzo Fury, so that the brand name has already become meaningless.

  • MDPV
3,4-methylenedioxypyrovalerone, frequently referred to as bath salts, or sometimes as Molly, which is supposed to mean MDMA, is primarily a methamphetamine-style stimulant, but can induce hallucinations at high doses, EROWID reports, as well as tachycardia and elevated blood pressure. As with speed, withdrawal can be extremely problematic, and increased mental and physical energy make this one highly reinforcing. Redosing is common. Recent studies strongly suggest that it is addictive in humans. A report at EROWID states: “Doing/coming off of MDPV is like winning a Mercedes and being told at the last minute they got your name wrong. Uggh.”

  • 5-MeO-DMT
This naturally occurring hallucinogenic tryptamine, 5-methoxy-N,N-dimethyltryptamine by name, has the unfortunate luck of sounding like another drug, simply called DMT. Both have hallucinogenic properties, but vaporized 5-MeO-DMT is active at 5 mg, where DMT is only active at a dosage about 5 times that high. So confusing the two drugs is not wise. High doses of 5-MeO-DMT can cause cardiac problems, convulsions, and mental confusion. Dealers who use them interchangeably are to be avoided. Unlike some of the other drugs in this list, 5-MeO-DMT has a long pedigree, in use since the 1970s, and is thought by some anthropologists to have been an ingredient in “shamanic snuff” used by early civilizations.

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



Tuesday, June 25, 2013

Addiction Trajectories: Book Review


Striving for that elusive middle ground.

For a journalist who covers neuroscience, the political and psychoanalytic focus of anthropology sometimes feels like a baffling trip to a foreign land. References to Foucault and Derrida abound, and Freud hovers in the middle distance. The investigative landscape is comprised of socially constructed experiences and environmental processes. Trained to seek out cultural and economic experiences as first causes, many cultural anthropologists have been fighting a rear-guard action against the advances of neuroscience for years now. Which is a shame, because anthropology, importantly, can serve to remind medical scientists of the multi-dimensional nature of addiction. “For psychoactive substances to transform themselves into catalysts for and objects of pleasure and desire,” writes anthropologist Anne M. Lovell, “they must circulate not only through blood, brain, and other body sites but also through social settings.”

It is anthropologists, for example, who have documented that “three-fourths of all state-licensed drug treatment programs in Puerto Rico were faith-based.” This study of faith-based healing in the addiction recovery community forms one chapter of a new volume, Addiction Trajectories, edited by Eugene Raikhel of the University of Chicago and William Garriott of James Madison University.

What anthropologists can do for addiction science is document these sociocultural attributes of addiction. In a chapter on buprenorphine and methadone users in New York City and the five boroughs, Helena Hansen, assistant professor of anthropology and psychiatry at New York University, finds that buprenorphine users live in predominantly white, high-income neighborhoods, tended to have college educations, and get their bupe from a private doctor. However, “others are directed to methadone maintenance programs with requirements for daily attendance, urine drug screens, surveillance, and control,” and there is little overlap between the two recovering populations.

There is a chapter devoted to a punitive form of addiction treatment known in Russia as “narcology,” and another that dwells on the semiotics of meth addiction. There are chapters taking drug counselors to task for their inadequate training and lack of nuanced background. And there is a chapter that views the advent of buprenorphine for heroin addiction as a step backwards, or, at best, a typical step sideways—addictive drugs for addiction, just like the old days when heroin addicts were offered alcohol as a cure.

A chapter by E. Summerson Carr is devoted to the treatment known as motivational interviewing, a technique with which she claims “drug users can talk themselves into sobriety regardless of whether or not they originally believe what they say to be true.” Irrespective of your view on M.I., Carr makes a useful point when she notes that sometimes a client’s refusal to admit drug use, even after a positive drug test, is not because of denial, but because of a logical understanding that their status as credible plaintiffs in legal proceedings could be on the line.

And there is simply no arguing Carr’s central point—while addiction science has been increasingly incorporated within the broad outlines of neuroscientific models, “the project of using talk to treat denial and demonstrate insight remains remarkably consistent” in the treatment practices used by the more than 13,000 outpatient addiction treatment programs across the U.S.

What else can anthropologists bring to the table? An understanding of “the loaded institutional and cultural conditions of clinical assessments, which inevitably and profoundly shape what drug users do and do not say.” Chief among these, Carr writes, is “the distinctly clinical terms of addicted denial, the chief organizing heuristic of mainstream American addiction treatment.”

The gap remains wide between addiction viewed as the neuroscientist’s disease entity, and addiction viewed as the anthropologist’s contingent outcome emerging from specific social settings. It’s easy to see why the attempt at an alliance between anthropologists and neurobiologists is an uphill struggle. Reading Addiction Trajectories, it becomes apparent how frequently the two disciplines are talking past one another. But I like to think there are enough bright and motivated anthropologists and neuroscientists around to forge some manner of middle ground; the elusive third way of viewing addiction, holistically, as a living blend of genetic and environmental influences, sensitive to both, and registering that dual sensitivity in the form of compulsive drug taking. (See, for example, anthropologist Daniel Lende’s recent post.)

The more invigorating contributions in this volume help us to zero in on “the popular representation of drugs as inherently criminogenic,” writes William Garriott, as well as the concomitant “lack of faith in the ability of the criminal justice system—and the state more generally—to address drug problems through the punitive management of the addicted offender population.” It is anthropologists, not neuroscientists, who dwell on the ramifications of this paradox: “The majority of Americans appear committed to fighting a war they feel cannot be won, using a strategy in which they no longer believe.”

The present volume is sometimes inclined to view biology with suspicion, and many of its contributors are quick to point out the hazards of attempting to meld social science and neuroscience. A similar but somewhat less skeptical collection—one that seeks to connect the socioenvironmental influences helping to shape how the biological disorder known as addiction will play out in the real world—was published last year by co-editors Daniel H. Lende and Greg Downey. In The Encultured Brain, Lende and Downey look ahead to a time when field-ready equipment will measure nutritional intake, cortisol levels, prenatal conditions, and brain development in the field. Predicting the future is a fool’s game, but it seems clear that the field of anthropology is aware of, and awake to, the controversial research avenues opened up by advances in contemporary neuroscience.

Graphics credit: http://www.culturalneuroscience.org/

Saturday, June 22, 2013

Smoking and Surgery Don’t Mix


Even routine operations are riskier for smokers.

Smokers who are scheduling a medical operation might want to think seriously about quitting, once they hear the results of a new review of the impact of smoking on surgical outcomes.

A scheduled operation is the perfect incentive for smokers to quit smoking. The fact that smokers have poorer post-surgical outcomes, with longer healing times and more complications, is not a new finding. But the study by researchers from the University of California in San Francisco, and Yale University School of Medicine, published in the Journal of Neurosurgery, spells out the surgicial risks for smokers in graphic detail.

Cellular Injury

The systematic effects of nicotine and carbon monoxide in the blood of cigarette smokers result in tissue hypoxia, which is a lack of adequate blood supply caused by a shortage of oxygen.  When carbon monoxide floods the bloodstream in high concentrations, as it does in smokers, it is capable of binding with hemoglobin and thus lowering the oxygen-carrying capacity of the blood. A cascade of physiological reactions then lead to the possibility of low coagulation levels, vasoconstriction, spasms, and blood clots. 

Wound Healing and Infection

If the circulatory system is dysfunctional, healing will be impaired. “In addition,” the researchers say, “tobacco may stimulate a stress response mediated by enhanced fibroblast activity, resulting in decreased cell migration and increased cell adhesion. The net consequence is inappropriate connective tissue deposition at the surgical site, delayed wound healing, and increased risks of wound infection.”

Blood Loss

 In their review of the neurosurgical literature, the researchers found higher blood loss for smokers particularly following surgery for certain kinds of tumors and for lumbar spine injuries. Smoking causes “permanent structural changes of vessels such as vessel wall thickening,” and there is evidence that smoking is linked to “larger and more vascularized tumors, which may further contribute to intraoperative blood loss during resection.”

Cardiopulmonary Effects

Even smokers who don’t have any chronic conditions associated with smoking are at increased risk during and after surgery. Oxidative damage from smoke can cause “mucosal damage, goblet cell hyperplasia, ciliary dysfunction, and impaired bronchial function,” all of which impedes the ability to expel mucus, which increases the bacterial load, which alters the respiratory immune response, and which ultimately leads to higher rates of postoperative pneumonia in smokers.

The authors of the review note that the evidence is particularly strong in certain specialties: Cranial surgery, spine surgery, plastic surgery, and orthopedic surgery. One randomized clinical trial showed that a 4-week smoking cessation program lead to a 50 relative risk reduction for postoperative complications. Another study showed significant improvement in wound healing when patients abstained from smoking for 6 to 8 weeks prior to surgery. And a third trial of smokers cited in the study showed a major decrease in complications following surgery for the repair of acute bone fractures in patients who quit before surgery.

The authors close by suggesting that the seriousness of surgery can be used to create a “teachable moment” for patients who smoke. Other studies show consistently that “patients tend to be more likely to quit smoking after hospitalization for serious illness.” All of this makes the act of scheduling surgery a perfect point of contact with smokers in medical settings. Clinicians can neutrally lay out the facts of the matter, in a way that truly brings home the health consequences of tobacco.

Lau D., Berger M.S., Khullar D. & Maa J. (2013). The impact of smoking on neurosurgical outcomes, Journal of Neurosurgery,   1-8. DOI:

Graphics Credit:  http://www.ontarioanesthesiologists.ca/

Sunday, June 16, 2013

A Weak Smoker’s Vaccine Might Be Worse Than None


New PET scans show wide responses to antibodies.

One of the brightest hopes of addiction science has been the idea of a vaccine—an antibody that would scavenge for drug molecules, bind to them, and make it impossible for them to cross the blood-brain barrier and go to work. But there are dozens of good reasons why this seemingly straightforward approach to medical treatment of addiction is devilishly difficult to perform in practice.

Last January, health care company Novartis threw in the towel on NicVax, a nicotine vaccine that failed to beat placebos in Phase III clinical trials for the FDA. And back in 2010, a report in the Archives of General Psychiatry demonstrated that a vaccine intended for cocaine addicts only generated sufficient antibodies to dull the effects of the cocaine in 38 percent of the test subjects. Moreover, it proved possible to overcome immunization by upping the cocaine dose, which sounded like an invitation to overdose.

And now, neuroscientists at the Society of Nuclear Medicine and Molecular Imaging annual meeting have presented a new study, the conclusions of which might help researchers understand why the vaccine results have been so mixed. The research “represents one of the first human studies of its kind using molecular imaging to test an investigational anti-nicotine immunization,” lead author Alexey Mukhin, professor of psychiatry and behavioral science at Duke University Medical Center, said in a prepared statement.


Subjects underwent two PET brain scan as they smoked nicotine labeled with radioactive C-11, one before the vaccine was administered, and one after. Ten subjects who developed “high-affinity antibodies” after vaccination showed a slight decrease in nicotine accumulation in the brain, as judged by the scans. However, another group of ten subjects, who showed “intermediate serum nicotine binding capacity and low affinity of antibodies” actually showed an increase in brain nicotine levels. What the PET scans showed was that “strong nicotine-antibody binding, which means high affinity, was associated with a decrease in brain nicotine accumulation. When binding was not strong, an increase in brain accumulation was observed.”

If the bond that holds the antibodies to the nicotine molecules is weak, the bond can break during passage through the blood-brain barrier, potentially allowing excess nicotine to flood in. This result, said Mukhin, tell us “we should care about not only the amount of antibody, but the quality of the antibody. We don’t want to have low-affinity antibodies because that can negate the anti-nicotine effects of the vaccination.”

Back to the drawing board? Not entirely. Another of the study authors, Yantao Zuo of Duke University Medical Center, said that “with reports of new generations of the vaccines showing potentially much higher potencies in animal studies, we are hopeful that our current findings and methodology in human research will facilitate understanding of how these work in smokers.”

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

Monday, June 10, 2013

Seven Questions About Marijuana Legalization


RAND researcher nails it neatly.

I’ve been meaning to offer up the key points from an excellent column on marijuana legalization that appeared in April in USA Today. Beau Kilmer, a senior policy researcher at the RAND Corporation, lists the “new and tricky issues” that Colorado and Washington forgot to consider in depth before passing broad legalization statutes.

Both states are works in progress. What they have passed so far will undoubtedly be revisited. Without further ado, here are Kilmer’s “Seven Ps,” as I call them:

Production. Who gets to grow it, where do they get to grow it, and how much do they get to grow? Will the business model be Starbucks, Jack Daniels, or your local organic family farm? Will it be legal on large commercial operations, indoor growing rooms, backyard gardens? All of this matters economically, since it’s likely that legalization will force down the price of marijuana, as growers will be able to operate in the open, and middlemen won’t have to worry about arrest. Implicit in this category are things like product testing and product safety.

Profit. If the history of cigarette and alcohol regulation have any bearing on the matter (and they do), it’s likely that marijuana marketers will want to concentrate promotional efforts on the heaviest smokers. States might decide to limit production to mom-and-pop home producers—or try to, at least. Or they could throw the door open to marijuana in the free market, and attempt to regulate the for-profit corporations that flock to the new opportunity. Monopolistic practices, collusion, price-fixing, bribes, payoffs to government officials—the whole panoply of corporate malpractice would be available to Big Pot if things go that way.

Promotion. The California medical marijuana movement got itself in hot water straightaway by hiring sign pointers to stand on Los Angeles street corners and advertise the cheapest Ozs in the neighborhood. Not smart. States that legalize will likely need to pursue some form of restriction on advertising for institutions or storefronts selling marijuana. However, as the cigarette industry has shown in its successful effort to block mandatory graphic warnings on packaging, companies are availing themselves of 1st Amendment defenses as a way of demolishing attempts to restrict advertising and promotional activities. Since corporations are now officially people, it looks, so far, like a winning strategy in court.

Prevention. States will obviously enact some age restrictions, which haven’t been terribly effect with cigarettes and alcohol. In addition, the decades-old message to America’s schoolchildren about staying “chemical-free,” starting with the evil weed, will have to be revisited and revised. The pioneering states have expended much time and verbiage on the subject of how much to tax marijuana sales, and a good deal less time on whether any of that tax money will go for prevention efforts, or for addiction treatment. Yes, pot is addictive for some people, and pot smokers who are lucky enough not to have this problem cannot seem to summon much sympathy for those who do. This will have to change, as marijuana addiction and withdrawal enter the public sphere with legalization.

Potency. If you count butane hash oil, or “dabbing,” the potency of modern seedless marijuana ranges from about 15 per cent to as high as 90 per cent THC. Yes, that’s quite a bit higher than the shoebox full of Mexican from the good old days. Arguments rage in the research community over the effect of strong pot, and whether it increases cognitive deficits, general anxiety, panic attacks, and even mental illnesses. Beer, wine and alcohol have mandated strength levels, printed right there on the bottle. Something similar will likely have to be crafted for marijuana.

Price. How elastic is the price of pot? Could heavy taxation push the whole game back underground? What’s a fair market price for a quarter of Train Wreck? “Retail prices will largely be a function of consumer demand, production costs and tax rates,” writes Kilmer. “The way taxes are set will also have an effect on what’s purchased and consumed—that is, whether pot is taxed by value, total weight, THC content, or other chemical properties.”

Permanency. With legalization, we are likely to see a pioneer penalty: “The first jurisdictions to legalize pot will probably suffer growing pains and want to make changes later on,” Kilmer believes. He envisions a powerful lobbying organization putting the arm on legislators on behalf of a newly legal and seriously profitable line of business. It would be best if legislation comes with maximum flexibility to make future changes, so states can adapt their operations as the thing plays out on the ground for the first time.


I personally understand and sympathize with the drive for legalization. I also think that Colorado and Washington have jumped first, and plan to think later, sorting it all out in freefall. That seems like a possible recipe for disasters large and small. Moving a popular drug across the legal/illegal line is a bit like getting molecules through the blood-brain barrier: It can be done, but it had better be done with sufficient care and forethought.

Graphics Credit: http://thebottomline.as.ucsb.edu/

Thursday, June 6, 2013

What We Talk About When We Talk About Drugs


Some number crunching at bluelight.ru.


A fantastic set of interactive graphics tracking conversational trends in drugs at the chat board bluelight.ru reveals some surprises, to the delight of data journalists everywhere. Virostatiq, a software package authored by Marko Plahuta, was put to the task of analyzing traffic at the drug discussion site. Various kinds of plots are available, with endless variables to permutate. Bear in mind that the data that got crunched dealt with the subject of messages, and cannot be directly correlated with drug use, trends, distributions, etc. But it is a fascinating glimpse at what illegal drug users are talking about, and from that, some inferences can be hazarded.

Plahuta writes:

I thought it would be nice to visualize these drug groups based on what users of harm-reduction forums say, so I analyzed around 1.2 million posts on bluelight.ru and constructed a simple diagram that tells a lot…. My whole database contains posts from 2010 until March 2013. Here’s an analytical tool to better understand what’s going on in the recreational drug community. Time is on horizontal axis, while the proportion of posts mentioning specific drug relative to all posts in that month is on the vertical axis. Play around with interactive chart to discover emerging trends, or simply to behold the wax and wane of specific chemicals as they compete for users’ neurological apparatuses, while their manufacturers are temporarily evading ever stricter analog laws.

The chart above represents a graphic created for Addiction Inbox using the visual data provided by Virostatiq. I have singled out six drugs of abuse for discussion. Bear in mind that the trend lines for common drugs like LSD, Ecstasy, marijuana, and methamphetamine all show much higher usage than the ones I have chosen to chart.

Mephedrone, arguably the most common “bath salt” stimulant, was mentioned at bluelight.ru a lot during 2010, when it came to the U.S. in a major way. But comments have been tailing off pretty steeply ever since. This suggests that mephedrone was sampled and found wanting by those who knew what drug they were taking. Or it could simply be old news by now, and less of a topic for discussion. But if the graph is suggestive of interest levels in the drug-using community, mephedrone seems to have a PR problem.

—Surprisingly, at least to me, a hallucinogen name 2c-e was one of the most talked-about designer drugs of all. 2c-e is a research chemical similar to mescaline but with a spotty track record. Linked to deaths and hospitalizations in Oklahoma and Minnesota, it isn’t known for certain whether the medical problems were due to the pure drug or contaminants. 2c-e is one of the drugs to come out of Alexander Shulgin’s infamous laboratories, and has been around for 20 years. As Tony O’Neill wrote at The Fix: “All in all, it doesn’t sound like the best bet for a recreational Saturday night at the dance club.” As with mephedrone, 2c-e was less talked bout in the last year of the graph.

Kratom retained a steady popularity over the full 3-year period. Kratom has always been hovering in the background of the opiate family, but seems to have undergone an unprecedented surge in underground popularity of late. From a tree native to Southeast Asia, and often used as a tea, Kratom is powered by an active ingredient called mitragynine—a substance capable of partially activating the mu- and delta-opioid receptors. Kratom serves as a weak opium, and some opiate enthusiasts swear by it for use as a withdrawal aid.

—One of the popular synthetic cannabis products to come out of the Huffman labs at Clemson University, jwh-018 seems to have pretty much cratered as a topic of discussion among drug cognoscenti. Perhaps some of the news about synthetic cannabis and correlations with serious liver problems has taken the shine off that apple. Or simply the fact that, over the few years that synthetic cannabis has been available, users have learned that they prefer the real thing, drug tests notwithstanding.

Hydrocodone, otherwise known as Vicodin, may have lost some popularity lately due to the popularity of oxycontin and other new synthetic opiate formulations. This is the drug that may have cost Rush Limbaugh his hearing. As a legitimate pain drug, it suffers in comparison with oxycontin, aka Percodan.

Ketamine is a major topic of discussion, which makes sense. Lately it has rebounded as a party drug, and also scored highly in clinical testing of its efficacy as a short-acting treatment for depression. Unfortunately, use of the drug has been linked to bladder problems  lately.


Sunday, June 2, 2013

Will Marijuana “Dabbing” Harm the Legalization Movement?


“Relax, bro—it’s just a blowtorch.”

It is called dabbing, and it is something the marijuana legalization movement would rather you didn’t know about. As crack is to powdered cocaine, so a dab is to a joint of marijuana: the same drug, in a much more concentrated form. But butane hash oil, or BHO, the end product of dabbing, is seen by many in the movement as a potential public relations disaster.

It’s easy to find instructions on the Internet for making butane hash oil. (Not to be confused with the hash oil of the 1970s produced, most commonly, using sieves, ice, naphtha, or acetone to separate the THC-rich trichomes from the rest of the plant material.) Butane hash oil, produced by “blasting”  butane through top-quality marijuana, then “purging” away the butane, looks a bit like beeswax and allegedly boosts THC content to a mind-blowing 70 to 90 per cent. The most potent of today’s varietals rarely reach or exceed 20 per cent. The result is known as wax, shatter, honey oil, and about a dozen other monikers. It is smoked using a glass tube and a red-hot piece of metal, not unlike the hippie “hot knives” method of smoking.

As Andrew Sullivan wrote at his blog, The Dish: “Going on the basis of such super high purity alone, even the funkiest colored trichome crystal encased high-grade leaf starts to look like steam punk technology in a fossil fuel world.”

Or, in the pithy phrasing favored by High Times: “A quantum leap forward in stoner evolution.”

In a High Times magazine article last year, author Bobby Black wrote about the central problem, namely that “the techniques used to make and consume BHO bear an eerie resemblance to those used for harder drugs like meth and crack.” This creates “a fear that seeing teenagers wielding blowtorches or blowing themselves up on the evening news might incite a new anti-pot paranoia that could set the legalization movement back decades.”

It happened when wine and ale became whiskey and gin, according to one school of thought. It happened again when hand dried, hand rolled tobacco became the machine rolled cigarette. And it happened when powdered cocaine became crack. Increasingly concentrated forms of plant drugs became more potent, more addictive, more expensive—and more socially disruptive. Has it happened in a high-tech way with good old friendly organic backyard marijuana?

And is BHO any more dangerous to users than regular weed? The butane technique is controversial, and the effects of ingesting marijuana that has previously been supersaturated with that particular solvent are intensely debated in the weed world. Marijuana collectives in California have been selling “butane honey oil” to qualified medical marijuana customers for some time now. There are tasting parties called “Wax Wednesdays.” But the state has made it illegal to produce BHO. David Downs, writing last month in Oakland’s East Bay Express, reported on a state appellate courting hearing in San Francisco, “in which an attorney for defendant Ryan Schultz worked to overturn the San Francisco resident’s three-year probation sentence for operating a BHO ‘drug lab.’ Meanwhile, several blocks away at permitted pot dispensaries, the fruits of such drug labs are on sale for upwards of $50 per gram.”

The defendant’s case was not helped when, in January, “two blasters blew themselves up in a San Diego motel, resulting in hospitalization, followed by drug lab charges.” And just to confuse the matter a bit more, BHO production is legal in Colorado, and other medical marijuana states are considering it.

The health verdict on all this isn’t in yet. The primary danger of BHO may be its manufacture, and in all the Richard Pryor-type explosions that lie ahead. Even High Times seems to be a bit wary of it. The magazine “strongly discourages anyone who has not been professionally trained from making BHO on their own.” Ventilation, it seems, is the key.

It’s unlikely, but not impossible, that the amount of residual butane inhaled could constitute a health threat. Cheap butane contains various impurities, and there has been at least one reported case of chemical epiglottitis, a condition in which inflammation caused by a chemical blocks off the windpipe. But as one marijuana backer told High Times, “you can actually get epiglottitis from hot coffee if you swallow it incorrectly.”

In February, The Federal Emergency Management Agency (FEMA) was moved to issue a formal bulletin on the matter: “Butane is highly explosive, colorless, odorless and heaver than air and therefore can travel along the floor until it encounters an ignition source…. Reported fires and explosions have blown out windows, walls, and caused numerous burn injuries.”

Bob Melamede, an associate professor of biology at the University of Colorado and the CEO of Cannabis Science Inc., told High Times: “If you have contaminants (i.e., pesticides, herbicides, fungi) on your plant, that’s going to come off into the extract. Then, when you evaporate the solvent, you’ll actually be concentrating those things—and THAT’S the real danger.”

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

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