Sunday, October 30, 2011

Book Review of "Drunken Angel"


A hipster gets his shit straight—sort of.

Addiction memoirs remain one of the most popular forms of autobiography on the shelves. But now, when considering a new addition to the genre, it’s impossible not to wonder whether the claims being made by the author are genuine. Since serious drunks often end up visiting the lower circles of hell during the course of their disease, hair-raising and improbable scenes are lamentably common—that is part of the genre’s charm, if that is the right word for it. But how are we to react now? The answer is, you can’t know, and you never really could, that bastard James Frey notwithstanding.

But read them we do. Alan Kaufman, the author of the lively but exasperating autobiography of alcoholism, Drunken Angel, sweetens the pot considerably. He drops so many names, and finds himself involved in so many improbably episodes of transnational mayhem and kinky sex, that the escapades could almost fill a Bond novel. But to be fair, there’s nothing debonair going on here; not from a man who describes himself at one stage as “filthy, nauseous, hungover, astonished at my gargantuan appetite for the abyss.” And a willing suspension of disbelief, an attitude of innocent until proven guilty, must hold sway in the end, else why read them at all?

Alan Kaufman is more Jack Kerouac than James Bond: One of the founding members of California’s Spoken Word scene, editor of The Outlaw Bible of American Poetry, Kaufman bounced through the beat/hippie/downtown scenes in New York, and San Francisco and Israel, writing for Jewish publications, treating his wives shabbily, and blacking out all over whatever town he happened to be in. It’s not pretty, and it’s not meant to be. The deep layer of poverty and grunge that settles over the author’s existence between bouts of the literary high life caused Kirkus Reviews to complain that “Drunken Angels” was marred by the author’s tendency to whip schizophrenically “between manic moments of literary self-aggrandizing and deeply depressive moments of shocking wreckage.” That’s true—but Kaufman is also a classic case of dual diagnosis, an alcoholic who also suffers from delusions, hallucinations, and Post Traumatic Stress Disorder after his time spent in the Israeli Army. (It’s complicated.) Also known as co-morbidity, this combination often makes for complicated, even potentially fatal difficulties, as on a bus ride with his wife one night, when he “realized that certain passengers were Satanists who had singled out Anna and me for human sacrifice.” Not good.

Down and almost out, he is scooped from the gutter by an acceptance letter from the Columbia University Master of Fine Arts program, where he hobnobs with Tama Janowitz and Steve Jobs’ sister, the writer Mona Simpson. But always, there are “the nightmares, the operatives, the unfolding skein of sinister designs” that Kaufman must negotiate as his mental health deteriorated. And the drinking never really stopped.

Finally, in order to both prove he’s sick and to signal his distress, Kaufman slit his wrists, then “staggered to the bathroom, wrapped white towels around the bloody wounds, and with a sense of exhilaration, called 911.” Perhaps the reader may be forgiven for not sharing in the exhilaration at this stage of the narrative, after reading about the author being ejected from crash pads by acid dealers for bad debts, dodging alimony and child support, neglecting a daughter on another continent, veering into sadomasochistic sex (in considerable detail), sleeping in filthy gutters, on warm street grates, on park benches. Kaufman made a habit of sitting down at restaurant tables to finish off the leftovers. “Ate donuts from garbage cans, pizza crusts from sidewalks, half-rotten fruit found in doorways. I kept my cash for booze…” In one excruciating scene, he tracks down an ex-girlfriend in her class at Columbia, calls her a whore in front of the class, and hits her in the face. A roomful of witnesses to that one, presumably. “In all this,” he tells us,” I never once lost my grip on the scotch bottle. Not a drop lost.”

So, that was it for Columbia. “All my life,” Kaufman writes, “ I had been going, fleeing. Leaving. Home, friends, jobs. Cities, countries, armies. Marriages, families—everything…. Anything but this, anyone but you, anywhere but here.” That was also about it for common sense from our anti-hero. We are pretty safe, it seems to me, in assuming that only a blackout alcoholic with severe mental problems is likely to wake up with a cruel hangover, married to the total stranger he finds lying in bed next to him. And then proceed to try and make the marriage work.

But in time, the story arc swings toward redemption, and Kaufmann falls in with AA and the Twelve Steppers.  “You’re allergic to alcohol and obsessed with it at the same time," an AA companion tells him. “The combination is fatal and unstoppable. Once booze hits your system, the jig’s up: you must drink.” And, to his immense credit, at long last, Kaufman gets straight, and eventually stays that way, even if the sordid circumstances of his life do not instantly change for the better. One of the most valuable lessons Kaufman takes away from AA (one of the most valuable lessons many people learn there) is a hoary old maxim called HALT: Don’t get too Hungry, Angry, Lonely, or Tired. All serious trigger conditions for relapse in freshly abstinent alcoholics and other drug addicts.

His book is a reminder that all of an addict’s life problems do not blessedly vanish the instant he or she stops drinking or using, any more than a regular schedule of insulin injections ends all problems for diabetics—the more so in cases where addiction is mixed with diagnosable mental illness. Getting clean and sober does not eliminate Kaufman’s sexual aggression, his tendency to lie to his wives, or bring back his ability to write steadily for a living.

In the end, Kaufman met a lot of famous people, managed to get published in some very hip venues, helped spark a poetry movement in San Francisco—and has now been clean and sober for more than 20 years. So what does he have to say about the prime mover of this amped-up narrative, alcoholism itself? It happened in the usual way—a formative alcohol experience at a young age. In early high school, a football player, Kaufman went out with some school buddies and without much thought began passing around those big gallon jugs of cheap Gallo wine. “I felt the universe swim into view. I stumble, drunk, to the grass and lay with arms and legs akimbo, like an altar sacrifice smiling at the blazing stars. For the first time in my life, I felt connected, happy, sure that life belonged to me and I to it. And I drank myself unconscious.”

Travelling alone in Germany, late in the book, after a nightmarish tableaux of temptation arranged for him by a cadre of Russian soldiers ready to pour vodka down his gullet in the spirit of macho brotherhood, Kaufman breaks away and finds a quiet spot in a deserted train car, and holds his own AA meeting in his head. “My name is Alan, I’m an alcoholic,” he says silently to himself. And then he says the Serenity Prayer, “then the 12 steps, and, appointing myself as guest speaker, shared about the experience I’d just had with Russian soldiers and endless vodka.” The phantom faces of his AA friends “kept me company right until I reached Berlin. And they are always with me, to this day, the meeting that I carry in my soul.”

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

Thursday, October 27, 2011

Drug Fact Not Fiction


National Drug Facts Week is upon us.

Yes, kids, times does fly, and it’s time again to do a CyberShoutout for National Drug Facts Week, which kicks off on Monday, October 31, and runs through November 6. (Check the map for related events in your neck of the woods.)

Sponsored by the National Institute on Drug Abuse (NIDA), National Drug Facts Week is an official health observance designed to shatter myths and spread the facts about drug abuse and addiction. (Information booklet available here). And, okay, let’s face it: Most programs, textbooks, and videos that attempt to instill an anti-drug message in our nation’s youth are lame beyond belief. From “Reefer Madness” to “This is Your Brain on Drugs,” adults have managed to inculcate one overriding message in the nation’s young people: When it comes to drugs and alcohol, you can’t count on older people to tell you what you really need to know.

So, in honor of National Drug Facts Week, it is with pleasure that I point to the Sara Bellum Blog,  maintained by NIDA, and dedicated to the proposition that tweens and teens might just be as interested in straightforward drug facts as anybody else. Here you will find such goodies as Brain Games (my personal favorite), informative videos by actual scientists, and Peerx, a new section about prescription drugs. Not to mention the actual blog for underagers by Sara herself, which is refreshingly science-oriented for that sort of thing, covering everything from alcopops to nanotechnology.

Addiction Inbox is pleased to join the CyberShout again this year, because cigarette smoking among 12th graders reached it’s lowest point in history in 2010—and also because, in the same year, about 10% of high school seniors reported abusing Vicodin. Good things are happening, more truth is being told—but there is a lot of hard work yet to do.

Sunday, October 23, 2011

Decoding Dope


Why marijuana gets you high, and hemp doesn’t.

Cannabis sativa comes in two distinct flavors—smokeable weed, and headache-inducing hemp. The difference between hemp and smokeable marijuana is simple: Hemp, used for fiber and seed, contains only a tiny amount of THC, the primary active ingredient in the kind of cannabis that gets you high. I am old enough to recall the sad saga of California hippies driving through my natal state of Iowa, and filling their trunks with “ditch weed”—wild hemp that grows commonly along Iowa rural fencerows, and while it cannot get you high, it could, back then, get you arrested.

But the California hippies who ran afoul of the law in Iowa were not so stupid as it might seem. This post was chosen as an Editor's Selection for ResearchBlogging.orgEven a marijuana connoisseur can have a hard time telling the difference between strong sinsemilla and wild hemp. Both varieties look similar, have similar growth patterns and flowering schedules, and a fresh bud of ditch hemp can look and smell enticingly like the real thing. Even the trichomes—the thousands of sticky, microscopic stalks that grow on the female flowers, each containing a bead of resin, like a crystal golf ball on a tee, containing mostly THC, in the case of pot, and mostly CBD, in the case of hemp—are also similar in appearance and growth behavior.

A study by a group of Canadian researchers, just published in Genome Biology, lays out the draft genome of marijuana, containing all of the plant’s hereditary information as encoded in DNA and RNA.In their article, Timothy Hughes, Jonathan Page and co-workers reported “a draft genome and transcriptome sequence of C. sativa Purple Kush.” (The genome and transcriptome can be browsed or downloaded at The Cannabis Genome Browser.) More than 20 plant genomes have now been sequenced, including corn and rice, but Cannabis sativa marks the first genomic sequencing of a traditional medicinal plant.

So how does it happen that one version of cannabis comes power packed, while the other version shoots blanks, so to speak? The researchers began with the modern facts of the matter: The THC content of medical and recreational marijuana is “remarkably high.” Research shows that median levels of THC in dried female flowers of Purple Kush (the strain used in the study) and other high-end variants now approach 11%, with some strains achieving a stratospheric 23% THC content by dry weight. Why can’t breeders pull any buzz out of ditch weed? How did cannabis split into two distinct subtypes? In an accompanying editorial entitled “how hemp got high,” Naomi Attar calls Cannabis sativa “a plant with a ‘split personality,' whose Dr. Jekyll, hemp, is an innocent source of textiles, but whose Mr. Hyde, marijuana, is chiefly used to alter the mind.” In brief, what are the biological reasons for the psychoactive differences between marijuana and hemp?

Co-lead author Jon Page, a plant biologist at the University of Saskatchewan, along with Tim Hughes of the Department of Molecular Genetics at the University of Toronto, compared the genomic information of Purple Kush, a medical marijuana favorite, with a Finnish strain of hemp called Finola, which was developed for oil seed production and contains less than 1% THC content. That is not enough THC to be mind-altering in any way. Instead, what Finola has in abundance is cannabidiol, or CBD, the other major ingredient in cannabis.

CBD isn’t considered psychoactive, but it does produce a host of pharmacological activity in the body. CBD shows less affinity for the two main types of cannabis receptors, CB1 and CB2, meaning that it attaches to receptors more weakly, and activates them less robustly, than THC.  The euphoric effects of marijuana are generally attributed to THC content, not CBD content. In fact, there appears to be an inverse ratio at work. According to a paper in Neuropsychopharmacology, "Delta-9-THC and CBD can have opposite effects on regional brain function, which may underlie their different symptomatic and behavioral effects, and CBD's ability to block the psychotogenic effects of delta-9-THC."

The kind of cannabis people want to buy has a high THC/low CBD profile, while the hemp chemotype is just the reverse—low THC/high CBD. While the medical marijuana movement has concentrated on Purple Kush and other high-THC breeds, medical researchers have often tilted towards the CBD-heavy variants, since CBD seems to be directly involved with some of the purported medicinal effects of the plant. So, CBD specifically does not produce the usual marijuana high with accompanying euphoria and forgetfulness and munchies. What other researchers have discovered is that pot smokers who suffer the most memory impairment are the ones smoking cannabis low in cannabidiol, while people smoking cannabis high in cannabidiol—cheap, seedy, brown weed—show almost no memory impairment at all. THC content didn't seem to matter. It was the percentage of CBD that controlled the degree of memory impairment, the authors of earlier studies concluded.

 The researchers found evidence in Purple Kush for “upregulation of cannabinoid ‘pathway genes’ and the exclusive presence of functional THCA synthase.” That means the reason hemp doesn’t get you high is because it is lacking the crucial enzyme—THCA synthase—that limits production of CBD and allows the production of THC to go wild. In contrast, cannabis strains producing high levels of THC—the Kushes and Hazes and White Widows and other seriously spendy variants—do have high levels of the enzyme that limits the production of CBD. Purple Kush gets you high because it has a built-in chemical brake on the production of CBD. Hemp doesn’t.

In a press release from the University of Saskatchewan, the researchers explain how they think this divergence came about: “Over thousands of years of cultivation, hemp farmers selectively bred Cannabis sativa into two distinct strains—one for fiber and seed, and one for medicine.” This intensive selective breeding resulted in changes in the essential enzyme for THC production, which “is turned on in marijuana, but switched of in hemp,” as Page put it. Furthermore, says co-leader Tim Hughes of the Department of Molecular Genetics at the University of Toronto, an additional enzyme responsible for removing materials required for THC production was “highly expressed in the hemp strain, but not the Purple Kush.” The loss of this enzyme in Purple Kush eliminated a substance “which would otherwise compete for the metabolites used as starting material” in THC production.

Without knowing the mechanics of it, underground growers and breeders have been steadily maximizing the cultivation of strains of cannabis high in THCA synthase, the result of which is a molecular blocking maneuver that maximizes THC production. This is great for getting high, but may not be the optimal breeding strategy for producing plants with medicinal properties.  Raphael Mechoulam, the scientist who first isolated and synthesized THC, has referred to plant-derived cannabinoids as a “neglected pharmacological treasure trove.”  The authors of this study agree, and have already identified some candidate genes that encode for a variety of cannabinoids with “interesting biological activities.” Such knowledge, they say, will “facilitate breeding of cannabis for medical and pharmaceutical applications.”

But cannabis of this kind may turn out to be low-THC weed. And that may be a good thing, some researchers believe. Marijuana expert Lester Grinspoon told Nature News: "Cannabis with high cannabidiol levels will make a more appealing option for anti-pain, anti-anxiety and anti-spasm treatments, because they can be delivered without causing disconcerting euphoria." (We’ll leave definitional issues about the effects of euphoria for another post.)

Finally, the authors strongly suggest that if it were not for “legal restrictions in most jurisdictions on growing cannabis, even for research purposes,” we would have known all of this stuff years ago, and would have been well on our way to developing “finer tailoring of cannabinoid content in new strains of marijuana,” as Nature News Blog describes it.

van Bakel H, Stout JM, Cote AG, Tallon CM, Sharpe AG, Hughes TR, & Page JE (2011). The draft genome and transcriptome of Cannabis sativa. Genome biology, 12 (10) PMID: 22014239
Photo Credit:http://www.medicinalgenomics.com/

Wednesday, October 19, 2011

An Interview with Neuroscientist Jon Simons


Brain scans, iPhone love, and state-dependent memory.

(Third post in the “Five-Question Interview” series.)

Brain scans have put cognitive neuroscience on the map. They have become a key part of addiction studies as well. In fact, brain scans have put neuroscience on the front page, due to the controversies they have engendered. Cognitive neuroscientist Jon Simons, a lecturer in the Department of Experimental Psychology at the University of Cambridge, UK, and principal investigator at the University’s Memory Laboratory, is attempting to expand our understanding of the specific regions of the brain involved in human memory. His research involves functional neuroimaging of healthy volunteers and examining the effects of neurological and psychiatric disorders, and normal aging, on memory abilities.

Dr. Simons obtained his PhD at the MRC Cognition and Brain Sciences Unit in Cambridge, and from there moved to a post-doctoral position at Harvard University. He returned to the UK and took up a research fellowship at University College London before returning to Cambridge. He was recently senior author on a thought-provoking paper published in the Journal of Neuroscience about a brain structure variation that might explain why some people in the general population are better than others at distinguishing real events from those they imagined or were told about. We asked Dr. Simons to help straighten out some of the confusion over scanning data, and to be the third guest in our “Five-Question Interview” series.

1. PET and fMRI scans have stirred up a good deal of debate and heated argument lately. While brain scans have been used to extend our understanding of crucial functions like memory and reward, they’ve also been used to “prove” that we’re addicted to our iPhones. Some scientists put almost no faith in them at all. What’s going on?

Neuroimaging methods like fMRI have certainly become quite common in the media over recent years. Unfortunately, not all the media coverage does the kind of job we might wish in explaining the methods and findings and, importantly, the limitations and caveats that need to be considered when interpreting the data. You mention the recent New York Times op-ed in which it was claimed that people “literally love their iPhones,” on the basis that viewing an iPhone was associated with fMRI activity in a brain region previously linked with “love and compassion.” Unfortunately, the same brain area has also been linked with negative emotions like disgust, as well as many other cognitive functions, seriously undermining the claims in the New York Times story. It may turn out to be true that our feelings about iPhones reflect love, or perhaps more likely a kind of dopamine-driven addiction response, but such simplistic analyses as the one the NYT gave such prominence are unlikely to help with understanding that.

However, I think it’s a mistake to confuse the media representation of fMRI research with the field itself. Many researchers design very careful fMRI experiments in which factors of interest are varied while others are controlled, and resulting patterns of brain activity are analysed with statistical caution and interpreted in the light of a broad range of previous findings. This is the kind of work that is moving the field forward, but, like most good science, it is not particularly sexy, and the researchers involved are less keen to make the kinds of extravagant claims that get you into the New York Times. In my view, it’s up to all of us—scientists and journalists—to make sure that the public get to hear more about the good fMRI work, and less about silly iPhone love stories.

2. Is there a specific role for functional neuroimaging in the diagnosis and treatment of addiction?

This isn’t really my area, but I know from talking with colleagues that neuroimaging has certainly contributed to understanding the neurobiology of addiction. For example, a great deal is known about the brain networks and neurotransmitter systems implicated in impulsivity, compulsions, reward processing and other cognitive functions that are relevant to addiction disorders. Such knowledge is obviously very important for informing clinical practice. Whether neuroimaging can also play a role in diagnosis and treatment is, as far as I can tell, less clear. Making accurate diagnoses in an individual on the basis of neuroimaging data requires characterisation of the specific patterns of brain activity exhibited by that individual, which is difficult to achieve. Similar problems afflict attempts to assess the success of different treatments. However, as imaging technology develops and statistical methods are refined, it may be that neuroimaging will be able to offer new insights that contribute to effective diagnosis and treatment.


3. Please explain the basics of state-dependent memory as it relates to alcohol, using your famous example about remembering Brad Pitt’s or Angelina Jolie’s phone number.

Ha! Glad if the example I used has proven memorable. The basic idea of state-dependent memory is that your recollection of a previous event is likely to be better if you’re in the same physiological state as you were when the event occurred. So, to use alcohol as an example, if you’re at a party and happen to drunkenly strike up conversation with Angelina Jolie (or Brad Pitt, if you prefer) and, bowled over by your charm and witty repartee, she tells you her phone number, you may well not remember it when you wake up sober the next morning. However, the evidence from many state-dependent memory studies suggests that you would have a better chance of recalling the number if you got drunk again. The effect doesn’t just apply to alcohol: any physiological state, any emotion we’re feeling, in fact any aspect of the context we’re in when we try to remember, which was also there when we previously experienced an event, will improve our memory for that event. This was described as the ‘encoding specificity principle’ by a great memory researcher, Endel Tulving.

4. Some researchers maintain that mental illness and addiction to drugs and alcohol are not, properly speaking, diseases at all. What’s your stance on the continual battles over the “disease model” of addiction and other disorders like depression?

There are both advantages and disadvantages to the “disease model” of cognitive disorders. For some people, it might be helpful to receive a clinical disease diagnosis and, perhaps, an idea of the therapeutic interventions through which they might go about “recovering” from their condition. Among the disadvantages are that labelling people as “addicts”, for example, can stigmatise those struggling with dependence and might lead to them avoiding responsibility for changing their addictive behaviour because they see diseases as requiring expert intervention. It’s a difficult area, and I can see both sides of the debate.

5. You’ve done neuroscience at Cambridge in the U.K., and at Harvard in the U.S. Is science conducted differently in the two countries?

My experience was that science in the US at that time (in 2000-2001) was different from in the UK. There seemed to be many more opportunities to get involved in interesting projects and to gain access to advanced technical equipment like fMRI scanners than was the case in the UK then. I also noted a difference in the willingness of people who were experts in techniques like fMRI, or in research involving patients with rare brain lesions, to share their expertise and resources in a collaborative way. Fortunately, I’ve found since I’ve been back in the UK a similarly friendly and collaborative environment, particularly in Cambridge now. I think this is partly a result of initiatives to bring researchers together across traditional scientific boundaries, such as Cambridge Neuroscience. However, I think the biggest US/UK difference now is the prevalent feeling that science is valued much more in the US than it is over here. Despite the best efforts of campaigns like Science is Vital, successive UK governments have failed to invest in science to the same degree as other nations, including the US. Particularly in the current financial climate, when significant cuts to science funding have been threatened, this means that morale is low, uncertainty is high, and significant numbers of scientists are deciding to move abroad. I don’t know that I’m ready to join them yet, but if the situation gets much worse, it would have to be something I’d consider.

Photo Credit: http://www.neuroscience.cam.ac.uk

Wednesday, October 12, 2011

Prohibition in Perspective


An essay on the Harrison Narcotic Act of 1914.

As the 20th Century began, America’s drinking habits were undergoing a thorough review. But In late 1914, five years before the prohibition of alcohol became the law of the land, the government also took aim at other drugs. The legal status of heroin and cocaine changed overnight with the passage of the Harrison Narcotic Act. The U.S. Congress, with the vociferous backing of William Jennings Bryan, the prohibitionist Secretary of State, voted to ban the “non-medical” use of opiates and derivatives of the coca plant.

Under the Harrison Act, physicians could be arrested for prescribing opiates to patients. “Honest medical men have found such handicaps and dangers to themselves and their reputation in these laws,” railed an editorial in the National Druggist, “that they have simply decided to have as little to do as possible with drug addicts...” The Harrison Act did have the effect of weeding out casual users, as opium became dangerous and expensive to procure. Housewives, merchants, salesmen, and little old ladies who had been indulging in the “harmless vice” now gave it up.

By 1919, continued pressure from the alcohol temperance movement culminated in Congressional passage of the Volstead Act, which provided for federal enforcement of alcohol prohibition. The temperance activists had pulled it off, though there is nothing very “temperant” about total prohibition. A year later, the states ratified the 18th Amendment. Within a five-year period, morphine, cocaine, and alcohol had all been banned in America. The Prohibition Era had begun. At roughly the same time, alcohol prohibition movements were sweeping across Europe, Russia, and Scandinavia, as evidenced by this 1921 news photograph of Chinese Maritime Officers with 300 lbs of smuggled morphine confiscated in cylinders shipped from Japan.

Prohibition and the passage of the Harrison Narcotics Act coincided, as well, with a short-lived effort to prohibit cigarettes. Leaving no stone unturned in the battle to eliminate drugs and alcohol from American life, Henry Ford and Thomas Edison joined forces to wage a public campaign against the “little white slavers.” Edison had shown an earlier fondness for Vin Mariani, a French wine laced with prodigious amounts of cocaine, but he and Ford wanted to stamp out cigarette smoking in the office and the factory. Although that effort would have to wait another 75 years or so, and may yet become the next large-scale test of federal prohibition, New York City did manage to pass an ordinance prohibiting women from smoking in public.  Fourteen states eventually enacted various laws prohibiting or restricting cigarettes. By 1927, all such laws had been repealed.

As Prohibition continued, police and federal law enforcement budgets soared, and arrest rates skyrocketed, but no legal maneuvers served to make alcohol prohibition effective, once “respectable” citizens had chosen not to give up drinking. The experience was so repellent that even today, when drug legalization is considered a legitimate topic of debate, most American reformers are unwilling to argue the case for neo-prohibitionism. (America’s ambivalence over alcohol is still evident in some states, where “dry” counties have made the sale of liquor illegal from time to time.)

As the temperance crusaders faded away, politicians and the public turned their attention back to heroin addiction, as the opiates became the official villains again. However, one practice that remained quietly popular with an older generation of physicians well into the 1940s was the conversion of alcoholics into morphine addicts. The advantages of alcohol-to-morphine conversion were spelled out  by Lawrence Kolb, the Assistant Surgeon General of the U.S. Public Health Service at the time:  “...Drunkards are likely to be benefited in their social relations by becoming addicts. When they give up alcohol and start using opium, they are able to secure the effect for which they are striving without becoming drunk or violent.” Perhaps so, but there were plenty of doctors who did not believe that addiction of any kind fell within the scope of medical practice in the first place.

Subsequent laws tightened up the strictures of the Harrison Act. Mandatory life sentences were imposed in several states for simple possession of heroin. The first addict sentenced to life imprisonment under the new laws was a twenty-one year-old Mexican-American epileptic with an I.Q. of 69, who sold a small amount of heroin to a seventeen year-old informer for the FBI. (In 1962, the U.S. Supreme Court ruled that imprisonment for the crime of simply being an addict, in cases where the arrest involved no possession of narcotics, was cruel and unusual punishment in violation of the Bill of Rights.) 

The Prohibition Years also sparked a rise in marijuana use and marijuana black marketeering. To checkmate the migration toward that drug, Congress passed the Marihuana Tax Act of 1937, modeled closely after the Harrison Act. The American Medical Association opposed this law, as it had opposed the Harrison Act, but to no avail. The assault on marijuana was led by Harry J. Anslinger, the indefatigable U.S. Commissioner of Narcotics who served a Hoover-like stretch from 1930 to 1962. At one point, Anslinger announced that marijuana was being taken by professional musicians. “And I’m not speaking about good musicians,” he clarified, “but the jazz type.” Due in no small part to Anslinger’s tireless public crusade against “reefer madness,” additional state and federal legislation made marijuana penalties as severe as heroin penalties. The most famous early victim of Anslinger’s efforts was screen actor (and reputed jazz fan) Robert Mitchum, who was busted in 1948 and briefly imprisoned on marijuana charges.

One highly addictive drug that did not immediately fall under the proscriptions of the Harrison Act was a cocaine-like stimulant called amphetamine. Originally intended as a prescription drug for upper respiratory ailments and the treatment of narcolepsy (sleeping sickness), the drug was first synthesized in 1887 by a German pharmacologist. It was a British chemist named Gordon Alles, however, who showed everyone just what amphetamine could really do. There was no direct analog in the plant kingdom for this one. Alles, who also worked at UCLA and Caltech, documented the remarkable stimulatory effect of “speed” on the human nervous system—research that led directly to the commercial introduction of amphetamines in the late 1930s under the trade name Benzedrine. Once it became widely available over the counter in the form of Benzedrine inhalers for asthma and allergies, it quickly became one of the nation’s most commonly abused drugs, and remained so throughout the late 1950s and 1960s—with periodic comebacks.

Photo Credit: www.newworldencyclopedia.org

Thursday, October 6, 2011

Feds Go “Passive-Aggressive” in Fight Against Medical Marijuana


Sending in the IRS instead of knocking down doors.

It’s official: The Obama administration has thrown off the gloves, repudiating Attorney General Eric Holder’s vow of two years ago that the federal government was not interested in prosecuting “state-legal” cannabis activity. Instead, a flurry of action is underway, intended to signal that the DOE and DEA are out to put a stake through the heart of the medical marijuana industry as a whole. Marijuana, however it is used, remains wholly illegal under federal statutes, and federal law enforcement officials insist such laws trump any state laws aimed at allowing the sale and use of cannabis.

During the last 30 days:

-- The DEA raided medical marijuana clinics in Tempe, Arizona.

--The Rhode Island governor reneged on an earlier pledge to okay medical marijuana in his state, saying that any such activity would make the state a target for federal prosecution. 

-- Federal prosecutors seized the bank accounts of medical marijuana shops in Sacramento, claiming a series of “irregular deposits.”

--The IRS decreed that the biggest marijuana dispensary in California cannot deduct ordinary business expenses on its taxes.

--A study of marijuana for posttraumatic stress disordered descended into “regulatory limbo,” as Brian Vastag reported for the Washington Post, after the National Institute on Drug Abuse (NIDA), the only legal source of cannabis for researchers, refused to hand over government marijuana to the study authors because of “a number of concerns” about research protocol.

--A California Appellate Court ruled that the statute allowing  marijuana dispensaries in Long Beach is in violation of federal law, which will force a long and arduous rewrite of the permitting laws for that city, and presumably other cities as well.

 The irony is that California’s medical marijuana industry, the first in the nation, may have survived the SWAT team attacks of the Bush years, only to fall victim to renewed regulatory fervor under President Obama’s watch. And, as I reported earlier at The Fix: “Britain’s giant GW Pharmaceuticals received U.S. patent approval for the use of Sativex, its nasal spray for treatment of advanced cancer pain composed of—yes, that’s right—a combination of the two primary chemicals found in cannabis. Since then, Sativex has made it all the way to Phase III clinical testing in a bid for FDA approval. At the moment, the company’s chances of producing a cannabis based pill are looking very good.” Meanwhile, so-called “whole-plant” marijuana research is getting squeezed out.

And now comes word that federal prosecutors are following up with a giant crackdown on all California dispensaries. Associated Press reports that U.S. attorneys sent letters this week to at least 16 pot dispensaries, “warning the stores they must shut down in 45 days or face criminal charges and confiscation of their property even if they are operating legally under the state’s 15-year-old medical-marijuana law.”

Sources say that cease-and-desist letters from U.S. Attorney Melinda Haag in California had been received by some dispensaries, stating the “violations of the federal law referenced…. is a federal crime,” and further stipulating that the penalties could include property forfeitures and 40 years of prison time, reports Chris Roberts at SF Weekly.

And the Associated Press obtained copies of letters sent to San Diego dispensaries, in which federal prosecutors claim that marijuana shops are illegal and subject to criminal prosecution and civil enforcement actions. “Real and personal property involved in such operations are subject to seizure by and forfeiture to the United States… regardless of the purported purpose of the dispensary.”

The action follows warning letters that were sent to dispensary owners and state officials by federal prosecutors in June, which strongly hinted that state employees might be liable for prosecution as well. A California attorney told SF Weekly that the feds were now embarking on a more effective “passive-aggressive” approach to shutting down the medical marijuana industry. “They’ve systematically changed their approach,” said the attorney. “Probably after talking to a PR professional.”

Graphics Credit:  http://www.shouselaw.com/

Wednesday, October 5, 2011

Bath Salts, Graphically

What you need to know about mephedrone.

The Pat Moore Foundation has put together this nifty chart as a primer on mephedrone, the amphetamine-type stimulant marketed as "bath salts." Thanks PMF! 

 Bath Salt Abuse Infographic, created by Pat Moore Foundation, a drug rehabCreated by Pat Moore Foundation
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