Science, Academia, and Tobacco

A review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition

Part III

Academic collaborations come in many flavors. Just because the money is corporate doesn’t mean the studies that are funded are flawed by definition. But the cigarette industry’s academic philanthropy set new records for hubris, writes Robert Proctor, professor of history at Stanford University, in his new book, The Golden Holocaust. Duke University and Bowman Gray School of Medicine, both in North Carolina, are named for tobacco magnates.

Harvard has a long and dubious history of tobacco largesse.  Harvard’s Tobacco and Health Research Program kicked off in 1972 with a generous tobacco grant from the Tobacco Institute, who dreamed up the program in the first place. “The Harvard project made the industry look good and so was handsomely endowed, absorbing $7 million over an eight-year period.” Also in 1972, Harvard anthropologist Carl Seltzer testified for the industry in numerous public hearings, stating: “We do not know whether or not there is a causal relationship between smoking and heart disease.” In 2002, Harvard’s School of Public Health declared it would no longer undertake research sponsored by the cigarette industry. Many universities had already gone cold turkey, and after Harvard, bans were put in place by the Karolinska Institute, Johns Hopkins University, Emory University, and many others.

Proctor informs us that “Washington University in St. Louis has been another big sponge for tobacco money." In 1971, the university set a new world record for an industry grant to a single institution, and “millions more were eventually funneled into the School of Medicine, turning it into a hotbed of cigarette-friendly activism.” The irony of taking money from Big Tobacco to fund research on lung cancer is not lost on Proctor. A good deal of the research was aimed away from tobacco and toward possible causes like viruses. “The goal was clearly more than cancer cures,” he writes. “The industry also hoped to generate good PR and academic allies.” The industry was able to garner  sympathetic headlines, like “Helping in Fight against Cancer,” in the St. Louis Globe-Democrat.

The other academic hotbed thoroughly penetrated by Big Tobacco was UCLA, according to Proctor. “Tobacco collaborators at UCLA have attracted their fair share of criticism from public health advocates, and for understandable reasons.” The university picked up its own multimillion-dollar grant from cigarette makers for the Program on Tobacco and Health in 1974, and that wasn’t the first tobacco money the university had taken. “As with all such projects,” Proctor writes, “industry lawyers… played a key role in the decision to fund—with the companies also conceding that the decision ‘should be based more on public relations than on purely scientific grounds.’” The end came in 2007, when “UCLA’s dance with the devil” garnered a ton of unwanted press. Reports showed that UCLA had taken more than $6 million from Philip Morris for research “to compare how children’s brains and monkey brains react to nicotine.”

Proctor admits that singling out Harvard, Washington University and UCLA is somewhat misleading, “given that scholars throughout the world have gorged themselves on tobacco money. Indeed it may well be the rare institution that has NOT at one time or another dipped into this pot.”

Including Stanford, where Proctor teaches. Plenty of Stanford researchers have undertaken contract work and served as expert witnesses for the industry right in Proctor’s own backyard, where “at least eighteen faculty members have received monies (in the form of sponsored research) from the Council for Tobacco Research, with at least two of these—Judith Swain and Hugh McDevitt from the medical school—serving on its Scientific Advisory Board. Stanford pharmacologists were assisting the industry with its diethylene glycol studies as early as the 1930s…”

In the conclusion to his densely researched but surprisingly readable work, Proctor returns to the controlling irony of the book: “Our bizarre starting point is the well-stocked shelf of cigarettes, to which we respond by begging people not to purchase them.” He presents the dream of a world in which cigarettes have been abolished. To do so, he admits, would require a leap. “If phasing out tobacco seems out of reach, this is only because our imaginations are impoverished.” And he has scant patience for the “Prohibition failed” argument. It failed, he says, because people like to drink. “Tobacco presents us with a very different situation. Nicotine is not a recreational drug. Most people who smoke wish they didn’t, and most smokers (90 percent) regret ever having started.”

Graphics Credit: http://www.prwatch.org/node/7004

The Tobacco Industry as Disease Vector

A review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition

Part II

The famous Surgeon General’s Report of 1964, officially warning Americans about the dangers of smoking, and publicizing the cancer connection, is typically seen as a triumphal moment in American medical history. But according to Stanford history professor Robert Proctor in his book, The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition, the report was “flawed in a number of interesting respects.” [The author, above, with paraphernalia] For one thing, members of the advisory committee consulting on the report, many of them congressman friendly to the tobacco cause, succeeded in their attempts to have smoking referred to as a “habit” rather than as addiction—a shameful Orwellian turn that went uncorrected for 25 years.

Meanwhile, the industry continued to fund new institutes, and continued to give out research grants for “red herring” research. As an example, the highest-ranking officer of the American Heart Association received money from one of the industry’s fraudulent research arms.

As late as the early 80s, most smokers believed they suffered from a bad habit, rather than an addiction—even though a majority of them wished they didn’t smoke. That is an odd kind of consumer “choice.” Cigarette makers have spent millions to perpetuate this myth. Proctor views tobacco industry executives and lawyers as a unique form of disease vector, spreading the pernicious health consequences of smoking across the globe.

The 2008 World Health Organization (WHO) Report on the Global Tobacco Epidemic fleshes out this metaphor, suggesting that all epidemics have a means of contagion, “a vector that spreads disease and death. For the tobacco epidemic, the vector is not a virus, bacterium or other microorganisms—it is an industry and its business strategy.”

In an email exchange, I asked Professor Proctor to expand on this notion of a disease vector:

“We tend to divide "communicable" from "non-communicable" diseases,” Proctor told me, “when the reality is that many "non-communicable" diseases are in fact spread by communications.”

Examples? “Through ignorance and propaganda, for example, which can spread like a virus,” Proctor wrote. “We don't count the anthropogenic communications, oddly enough, even though these can be just as dangerous, and just as deadly. And just as preventable--by changing our exposure environments.”

In a recent article for Tobacco Control, Proctor laid out how the calculus of the disease vector plays out. We know, for example, that smoking will cause roughly 6 million deaths in 2015. And about a third of those will be from lung cancer. We know that 25 acres of tobacco plants will result in about 10 lung cancer deaths per year, starting 20 or 30 years down the road. Here’s a sick equivalence: “A 40 ft container of the sort shipped overseas or trucked by highway houses 10 million cigarettes, which means that each container will cause about 10 deaths.” Proctor works out the numbers for the value of a human life:

“Cigarette companies make about a penny in profit for every cigarette sold, or about $10,000 for every million cigarettes purchased. Since there is one death for every million cigarettes sold (or smoked), a tobacco manufacturer will make about $10,000 for every death caused by their products…. The value of a human life to a cigarette manufacturer is therefore about $10,000.” 

Proctor has even produced a “factories of death” chart, illustrating that arguably the world’s most lethal production plant is Philip Morris’s Richmond cigarette facility, which churned out 146 billion cigarettes in 2010, which adds up to about 146,000 deaths per year.

By 1964, researchers at Harvard had already identified the presence of radioactivity in the form of polonium 210 in cigarette smoke, and the cry went up for safety. As for the notion of safer cigarettes, Proctor says all cigarette filters function the same way—“basically like drinking through a somewhat thinner straw.” He goes even further, arguing that “filters have reduced smoke particle size, producing cancers deeper in the lungs, making them harder to identify and harder to treat.” (Scientists determined that the radiation source was the newer “superphosphate” fertilizers being used heavily on tobacco plants.)

 Next came mandated “tar and nicotine numbers,” which turned out to be misleading measures obtained from smoking robots. Then, “an opportunity presented itself to game the system, as we find in the brilliant trick of ventilation.” Manufacturers pricked tiny holes in the paper near the mouthpiece of cigarettes brands like Carlton and True, which consumers got around by covering the holes with fingers or with “lipping” behavior. “Low tars were a fraud, just as “lights” would be,” Proctor writes. Smokers just smoked harder, or differently, or more frequently. In 1983, pharmacologist Neal Benowitz at UCSF broke the official news in the New England Journal of Medicine: Smokers got just as much nicotine, whether they smoked high-, low-, filtered, unfiltered, regular, light, or ultra-light.  The industry itself had known this for more than 20 years. “Nicotine in the actual rod was rarely allowed to drop below about 10 milligrams per cigarette,” Proctor asserts, “and no cigarette was ever commercially successful with much less than this amount.” (A Philip Morris psychologist compared nicotine-free cigarettes to “sex without orgasm.”)

Indeed, almost every design modification put in place by tobacco companies over the past century, from flue-curing to filters, has served to make cigarettes deadlier than before. “Talk of ‘safer cigarettes’ is rather like talking about safer terrorism, or safer smallpox, or safer forms of drowning,” Proctor concludes.

And the industry testing continues. The point of tobacco-sponsored research is not simply to discredit an individual researcher’s work, but to create an aggregate bias in the pattern of research—a lot of “noise” in the signal. In other words, “you basically fund lots of research to dispute a hazard, then cite this same research to say that lots of scholars dispute it.” We are told about “mucociliary escalators,” which dredge the tar up and out of smokers’ lungs. We learn that “a rabbit will scream if nicotine is introduced into the eye.” We read excerpts from anguished letters to tobacco companies: “Do you suppose if I continue to smoke Camel Ultra Light Cigarettes and I should develop cancer it will be ‘Ultra Light Cancer?’”

Proctor brings us up to date: Harm reduction, he writes, has become the industry’s new mantra. “The companies now want us to believe that less hazardous products can be and are being made and marketed.” Proctor thinks harm reduction “may end up causing even greater harm” if products touted as “safer” make smokers less likely to quit. As for public health campaigns, “consumers are encouraged to stop consuming,” Proctor writes, “but producers are never discouraged from producing.” Or, as Louis Pasteur once wrote: “When meditating over a disease, I never think of finding a remedy for it, but, instead, a means of preventing it.”

So, what comes next? A glimpse of the future may already be here, in the form of cinnamon- and mint-flavored Camel Orbs, “which look like Tic Tac candy and contain about a milligram of nicotine in a highly freebased form.”

As for the industry’s success in corrupting scientists and academics through various means, the story is just as bad as you think it is: “It would take many thousands of pages to chronicle the full extent of Big Tobacco’s penetration of academia; the scale of such collaborations is simply too vast. From 1995 to 2007 alone, University of California researchers received at least 108 awards totaling $37 million from tobacco manufacturers….”

Part II of III.

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

The Hidden Story of How Big Tobacco Invented Freebasing

Review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition.

Part I

It’s easy to think of cigarettes, and the machinations of the tobacco industry, as “old news.” But in his revealing 737-page book, The Golden Holocaust, based on 70 million pages of documents from the tobacco industry, Stanford professor Robert N. Proctor demonstrates otherwise. He demonstrates how Big Tobacco invented freebasing. He shows how they colluded in misleading the public about “safe” alternatives like filters, “low-tar,” and “ultra-lights.” We discover in Lorillard’s archives an explanation of menthol’s appeal to African Americans: It is all part of a desire by “negroes” to mask a “genetic body odor.” Radioactive isotopes were isolated in cigarette smoke, and evidence of the find was published, as early as 1953. He reveals that the secret ingredient in Kent’s “micronite filter” was asbestos. And he charges that the “corruption of science” lies behind the industry’s drive to continue its deadly trade. “Collaboration with the tobacco industry,” writes Proctor, “is one of the most deadly abuses of scholarly integrity in modern history.”

Half of all cigarette smokers will die from smoking—about a billion people this century, if present trends continue. In the U.S., this translates into roughly two jumbo jets crashing, killing everyone onboard, once daily. Cigarettes kill more people than bullets. The world smokes 6 trillion of them each year. (The Chinese alone account for about 2 trillion). Some people believe that tobacco represents a problem (more or less) solved, at least in the developed West.

All of this represents a continuing triumph for the tobacco industry. The aiders and abettors of tobacco love to portray the tobacco story as “old news.” But as Stanford Professor Robert M. Proctor writes in The Golden Holocaust, his exhaustive history of tobacco science and industry: “Global warming denialists cut their teeth on tobacco tactics, fighting science with science, creating doubt, fostering ignorance.”

Checking in at 737 pages, The Golden Holocaust is nobody’s idea of a light read, and at times its organization seems clear only to the author. But what a treasure trove of buried facts and misleading science Proctor has uncovered, thanks to more than 70 million pages of industry documents now online (http://legacy.library.ucsf.edu) as part of the Master Settlement Agreement of 1998. Once the material was finally digitized and available online, scholars like Proctor could employ full-text optical character recognition for detailed searchability. Ironically, this surreal blizzard of documentation was meant to obscure meaningful facts, not make them readily available, but tobacco executives seem not to have factored in digital technology when they turned over the material.

The single most important technological breakthrough in the history of the modern cigarette was flue-curing, which lowers the pH of tobacco smoke enough to make it inhalable. The reason few people inhale cigars, and very few used to inhale cigarettes, is that without some help, burning tobacco has a pH too high for comfortable inhalation. It makes you cough. But flue-curing lowered pH levels, allowing for a “milder,” less alkaline smoke that even women and children could tolerate.

World War I legitimized cigarettes in a major way. Per capita consumption in the U.S. almost tripled from 1914 to 1919, which Proctor considers “one of the most rapid increases in smoking ever recorded.” After World War II, the Marshall Plan shipped a staggering $1 billion worth of tobacco and other “food-related items.” (The U.S. Senator who blustered the loudest for big postwar tobacco shipments to Europe was A. Willis Robertson of Virginia, the father of televangelist Pat Robertson.)

The military, as we know, has historically been gung-ho on cigarettes. And Proctor claims that “the front shirt pocket that now adorns the dress of virtually every American male, for example, was born from an effort to make a place to park your cigarette pack.” In addition, cigarette makers spent a great deal of time and effort convincing automakers and airline manufacturers to put ashtrays into the cars and planes they sold. Ashtrays were built into seats in movie theaters, barbershops, and lecture halls. There was even an ashtray built into the U.S. military’s anti-Soviet SAGE computer in the 50s.

In the early 50s, research by Ernest Wynder in the U.S. and Angel Roffo in Argentina produced the first strong evidence that tobacco tars caused cancer in mice. Roffo in particular seemed convinced that tobacco caused lung cancer, that it was the tar rather than the nicotine, and that the main culprits were the aromatic hydrocarbons such as benzpyrene. Curiously enough, it was influential members of Germany’s Third Reich in the 40s who first took the possibility of a link seriously. Hans Reiter, a powerful figure in public health in Germany, said in a 1941 speech that smoking had been linked to human lung cancers through “painstaking observations of individual cases.”

In the December 1953 issue of Cancer Research, Wynder, et al. published a paper demonstrating that “tars extracted from tobacco smoke could induce cancers when painted on the skins of mice.” As it turns out, the tobacco industry already knew it. Executives had funded their own research, while keeping a close eye on outside academic studies, and had been doing so since at least the 30s. In fact, French doctors had been referring to cancers des fumeurs, or smokers’ cancers, since the mid-1800s. All of which knocks the first leg out from under the tobacco industry’s classic position: We didn’t know any stuff about cancer hazards until well into the 1950s.

Only weeks after the Wynder paper was published, tobacco execs went into full conspiracy mode during a series of meetings at the Plaza Hotel in New York, “where the denialist campaign was set in motion.” American Tobacco Company President Paul Hahn issued a press release that came to be known as the “Frank Statement” of 1954. Proctor calls it the “magna carta of the American’s industry’s conspiracy to deny any evidence of tobacco harms.” How, Proctor asks, did science get shackled to the odious enterprise of exonerating cigarettes? The secret was not so much in outright suppression of science, though there was plenty of that: In one memorable action known as the “Mouse House Massacre,” R.J. Reynolds abruptly shut down their internal animal research lab and laid off 26 scientists overnight, after the researchers began obtaining unwelcome results about tobacco smoke. But the true genius of the industry “was rather in using even ‘good’ science, narrowly defined, as a distraction, something to hold up to say, in effect: See how responsible we are?”

Entities like the Council for Tobacco Research engaged in decoy research of this kind. As one tobacco company admitted, “Research must go on and on.”

A good deal of the industry’s research in the 50s and 60s was in fact geared toward reverse engineering competitors’ successes. Consider Marlboro. Every cigarette manufacturer want to know: How did they do it? What was the secret to Marlboro’s success?

As it turns out, they did it by increasing nicotine’s kick. And they accomplished that, in essence, by means of freebasing, a process invented by the cigarette industry. Adding ammonia or some other alkaline compound transforms a molecule of nicotine from its bound salt version to its “free” base, which volatilizes much more easily, providing low-pH smoke easily absorbed by body tissue. And there you have the secret: “The freebasing of cocaine hydrochloride into ‘crack’ is based on a similar chemistry: the cocaine alkaloid is far more potent in its free base form than as a salt, so bicarbonate is used to transform cocaine hydrochloride into chemically pure crack cocaine.” Once other cigarette makers figured out the formula, they too began experimenting with the advantages of an “enhanced alkaline environment.”
  
(End of Part I)

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

What It Means to Say Alcoholism is Genetic

One woman’s journal.

From Insanity to Serenity, by Tommi Lloyd

Excerpts:

"I was born in 1963 in Toronto, Canada, to a family struggling long before I arrived. My dad was an alcoholic, born in Wales in 1921. His father and namesake was also an alcoholic who died at age 28…. My oldest sibling and only brother, Harry, entered a treatment centre at age 36 and has been sober for more than 20 years…. My Uncle Griff died from alcoholism when I was 10 years old…. There were no reprieves by which we spent a day or two in a sober environment. Dad drank from morning until night…. Christmas, Thanksgiving, and Easter—these were some of the worst days of the year…. Santa started leaving a carton of cigarettes next to my stocking at Christmas and I thought it was great.

"I yearned for some quality time before his drinking took center stage for the day… he drank from the minute he got up to the minute he passed out. At the height of his addiction, he was drinking more than 40 ounces of vodka a day…. There were many times when I would walk into the bedroom and see him guzzling the vodka straight from the bottle. It made me feel physical ill and utterly helpless.

"I too, am an alcoholic. In addition to alcohol, my teenage love of marijuana turned into a 30-year affair…. I have two nephews who are addicted to marijuana…. Rather than being sloppy drunks, my nephews opted for the mellow alternative that’s not addictive, (so we like to think) and you can pay for your habit by selling it to your friends.

"By age 11 I tried drinking for the first time…. I recall Susie telling us we could try drinking, but it had to be done quickly so as not to get caught. We poured some very strong rum and cokes and I guzzled mine down by holding my nose with my free hand…. As soon as I lay down on my bed the room started spinning and it wasn’t long before I was throwing up. Mom fussed over me, concluding I had the flu and I recall feeling both happy and guilty at the same time. I loved the attention but felt badly for the cause of my illness. I didn’t drink again for a few years….

"There is nothing more validating for me as a mother than to know I’m an inspiration to my children. I could not have asked for a better gift. This is what sobriety and a renewed spiritual life has brought my children and me…. Intellectually, I recognize how my childhood experiences and the disease of alcoholism molded a lot of my behavior and have been the root of much of my struggle with self-esteem. But self-knowledge does not change our circumstances, action does."

“Addiction Fiction”

Coming-of-Age Drug Novels

Call it “addiction fiction.” In the past few years we have seen a blossoming of this genre, where the private eye goes to 12-Step meetings, and one day your sponsor may just save your life by gunning down a rival in the street. Or, where the wise-beyond-their-years prep school drug addicts engage in Brett Easton Ellis-style sex and ennui.

Fiction readers of a certain age will recall that this is not a new thing under the sun. From Junky to The Man With the Golden Arm, from Naked Lunch to Less Than Zero, drug novels have always been with us. Addiction fiction has two distinct subgenres: addicts with money, and addicts without money. For obvious reasons, the latter genre is the prevailing one—Trainspotting and Requiem for a Dream come to mind. But the wealthy end of the spectrum is not without representation. Consider The Basketball Diaries, or Bright Lights, Big City.

As an example of the first type of book, the one where the addict has no money, we have Spoonful, by first-time author Chris Mendius. As for the upscale second type, there is the recently released novel, No Alternative,  by William Dickerson, a budding film director with an MFA. I would judge both authors to be well south of the age of 40, making both of them pure examples of Generation X. 

Ah, the 90s. As time passes, it seems clear that the death of Kurt Cobain has been added to the touchstones of American youth culture, in a tradition going back to the 60s. Where were you when Kennedy died? When Lennon died? When Cobain died? This last question matters, since Nirvana and Cobain are threaded thematically through both of these new novels. As Chris Willman wrote at Stop the Presses: “April 5 is to many contemporary rock fans what November 22 is to older baby boomers: the day you can almost certainly remember where you were or what you were doing when you heard that ___ died. That's not to say that Kurt Cobain's suicide represented a loss of national innocence in the same way that JFK's assassination did. For one thing, Cobain's whole life and career already symbolized lost innocence, long before he died.”

In Generation X drug novels, lost innocence isn’t lost—there was never any innocence in the first place.

Michael, the narrator of Spoonful, is the kind of drug addict with no money. Michael is forthright, if not one to probe the philosophical ironies of his condition: “Nobody ever says, ‘When I grow up, I want to be a junkie.’” End of story. Well, the beginning, really. In this well-written junky novel, author Chris Mendius brings his tragic characters to life in a manner that calls to mind Hubert Selby, Jr.’s stark New York classics of addiction without redemption.

Set in Chicago’s Wicker Park area, young Michael and his pal Sal find their way to heroin in a hurry. They also quickly learn the flip side of the illness—the sickness of withdrawal, “like having a debilitating combination of food poisoning and the flu, with periodic muscle cramps.” No matter. “Once we made it through all that, we decided to stay off dope. A month passed with no discernible improvement in our lives and we promptly resumed getting high.”

It’s heroin he craves. Michael is no fan of cocaine: “You’re up all night, running your mouth, jaw twitching, nose burning. You might want to fuck but you can’t. All you can do is keep going. Before you know it, the birds are chirping and the garbage trucks are rolling. You’re out hundreds of dollars and for what?” And they scoff at pharmaceutical efforts at non-addictive synthetic opiates, “engineered to not let anyone feel a moment of undeserved pleasure.” One character likens kicking methadone to “getting your skin pulled off with pliers.”

The debate over freely distributing the drug naloxone as an anti-OD safety measure is referred to obliquely: “That’s the thing with smack. It’s a fine line between the time of your life and the end of your life…. More often than not, the difference between life and death was having someone there to revive you or call somebody who could.”

Mendius is good at drawing a picture of the addict’s endless grind: “Finding the ways and means to score is a twenty-four-seven gig. You might get lucky and hit it big now and then but you’re always looking ahead. Plotting. Planning. No matter how much you get or how close the scrape, you always gotta keep at it. Day in and day out.”

Michael never quits for long, and when he is off heroin, he buries himself in marijuana and booze. There is no redemptive ending. He walks off into the sunset.

From seedy Chicago to the upper reaches of Westchester, New York. Like Spoonful, No Alternative by William Dickerson features characters whose collective memory goes back no farther than the 80s. Which sucked, as we all know, and as Thomas, the narrator, never tires of telling us. Thomas and his friends are drug and alcohol abusers with money. The drugs of choice are prescription medications, not heroin or cocaine, for these products of Fordham Prep. 

It is 1994, and the grunge youth of Yonkers, the children of Vietnam vets and hippies, are rootless and confused. “There was no clear-cut path beckoning them. No modus operandi.” It was a generation, Dickerson writes, that “earned a label that was just about as vague as their sense of what to do with their lives: Generation X.” In this version, not much has changed since the crack-crazy L.A. 80s of Brett Easton Ellis. The names and the drugs have been altered, but otherwise the trappings are indistinguishable: high disposable income and excessive ennui.

Thomas supports his crazy little sister Bridget, who becomes a white rapper named Bri Da B. His sister’s drug of choice is cutting herself: “She was determined to be in control. If she was going to bleed, it was going to be a decision, it was going to be controlled, and she was going to bleed everywhere, not just from the abyss between her legs. If pain was to be a constant, might as well get used to it and build up a tolerance.”

No Alternative is readable enough, but it does not carry the campy forward motion of other rich-kid addiction books. It is more measured, dry, and there is an odd hitch in the narration, which is resolved, rather shakily, at the end, with a big Reveal that distracts the reader from the central relationships in the story.

So, two early novels, by promising young writers, about drugs and what they do to you. It will be interesting to find out what becomes of these authors, and what manner of new work they get up to in the future. The story never ends where you think it does.

The Future of Addiction Treatment

Is there some way out of here?

Addictions are chronic diseases. They may require a lifetime of treatment. After a number of severe episodes of alcohol or drug abuse, the brain may be organically primed for more of the same. Long-term treatment is sometimes, if not always, the most effective way out of this dilemma. (The same is true of unipolar depression.)

We will need to learn a lot more about chemicals—the ones we ingest, and the ones that are produced and stored naturally in our bodies—if we plan to make any serious moves toward more effective treatment. What we have learned about the nature of pleasure and reward is a strong start. The guiding insight behind most of the work is that addiction to different drugs involves reward and pleasure mechanisms common to them all. The effects of the drug—whether it makes you sleepy, stimulated, happy, talkative, or delusional—constitute a secondary phenomenon. A good deal of earlier research was directed at teasing out the customized peculiarities of one drug of abuse compared to another. Now most addiction scientists agree that receptor alterations in response to the artificial stimulation produced by the drugs are the biochemical key, and that recovery occurs when the brain’s remarkable “plastic” abilities go to work at the molecular level, re-regulating and adjusting to the new, drug-free or drug-reduced status quo. An addict beats addiction by ceasing the constant and artificial manipulation of neuronal receptors, to be entirely unromantic for a moment about the nature of recovery.

But in order for that to happen most effectively, you have to stop taking the drugs.

Comparing our reservoir of pleasure chemicals to money in the bank, Dr. George Koob, Chairman of the Committee On The Neurobiology Of Addictive Disorders at the Scripps Institute in La Jolla, California, draws the following analogy:

We can expend that money over the course of a single weekend’s binge on cocaine or we can expend it over a two-week period in the normal pleasures of everyday life. If you spend these pleasure neurochemicals in one lump sum such as a crack binge, you use up your supply of pleasure for a certain period, and so you pay for it later.

Addicts vividly demonstrate a compulsive need to use alcohol and other drugs despite the worst kinds of consequences—arrest, illness, injury, overdose. What kind of euphoria could be worth such psychic pain? Even stranger, why continue when the drug no longers works as well as it once did due to tolerance? What makes these people eat their words, shred their best intentions, break their promises, and starting using or drinking again and again?

There really is no cheating in this game. The system has to self-regulate. Craving and drug-seeking behavior, once set in motion, disrupt an individual’s normal “motivational hierarchy.” How does this motivational express train come about? It happens at the point where casual experimentation is replaced by the pharmacological dictates of active addiction. It happens when the impulse to try it with your friends transforms itself into the drug-hungry monkey on your back.

 Formal medical treatment and intervention can work, but the results are inconsistent and often little better than no formal treatment at all. Most alcoholics and smokers and other drug addicts, it is frequently asserted, become abstinent on their own, going through detoxification, withdrawal, and subsequent cravings without benefit of any formal programs. Our health policy should not only encourage addicts to heal themselves, but must also help equip them with the medical tools they need in treatment. After all, behavioral habits as relatively harmless as nail biting can be all but impossible to break.

 As detailed by Dr. Mary Jeanne Kreek, a professor and senior attending physician at the Laboratory of the Biology of Addictive Diseases at Rockefeller University:

Toxicity, destruction of previously formed synapses, formation of new synapses, enhancement or reduction of cognition and the development of specific memories of the drug of abuse, which are coupled with the conditioned cues for enhancing relapse to drug use, all have a role in addiction. And each of these provides numerous potential targets for pharmacotherapies for the future.

In other words, when an addiction has been active for a sustained period, the first-line treatment of the future is likely to come in the form of a pill. New addiction treatments will come—and in many cases already do come—in the form of drugs to treat drug addiction. Every day, addicts are quitting drugs and alcohol by availing themselves of pharmaceutical treatments that did not exist twenty years ago. Sometimes medications work, and we all need to reacquaint ourselves with that notion. As more of the biological substrate is teased out, the search for effective medications narrows along more fruitful avenues. This is the most promising, and, without doubt, the most controversial development in the history of addiction treatment.

Fighting fire with fire is not without risk, of course. None of this is meant to deny the usefulness of talk therapy as an adjunct to treatment.  However, consider the risks involved in not finding more effective medical treatments. Better addiction treatment is, by almost any measure, a cost-effective proposition.

Photo: http://www.manorhouserehab.com/

“When Did I Become the Junkie Auntie Mame?”

Courtney Love tells her tangled tale in a new e-book.

Maer Roshan, author of Courtney Comes Clean: The High Life and Dark Depths of Music’s Most Controversial Icon, logged a dozen “exhilarating and exhausting” sessions with the widow of Nirvana’s Kurt Cobain over the course of a year, pulling together a definitive look at Love’s drug addictions and other demons. Roshan taped countless hours of interviews, and received additional written material from the “Tolstoy of texting,” as Love refers to herself. The book is highly readable, almost, one is tempted to say, addictively so. Sure, it’s tabloid stuff—let he or she who has never peeked at Gawker or Jezebel cast the first stone.

Roshan, who has performed editorial duties at Radar, New York, Talk, and Interview, does his best to shape the former rock star’s rambling tales into a coherent narrative. (Disclosure: I have contributed articles and blog posts to Roshan’s online addiction and recovery magazine, The Fix.) But coherence is an uphill struggle with Love, who is clearly a highly intelligent, strong-willed woman; an addict who suffers from comorbid mental disorders, including such possibilities as bipolar disorder, borderline personality disorder, and narcissistic personality disorder. Her brief acting career and string of dramatic financial ups and downs, in the grand tradition of Hollywood stars and superstar musicians dragged down by fame, fate, and drugs, has led to her current “florid obsessions” with financial conspiracies against her, Roshan writes. 

At times she has installed a “sobriety minder” in her New York townhouse; at other times she has tried to bash a Vanity Fair reporter over the head with an Oscar snatched from Quentin Tarantino.  None of this would be of anything but passing interest except for the Keith Richards-style Queen of Drugs role that she has either assumed or has had thrust up on her. As she told Roshan: “Kim Stewart called me up screaming, ‘Courtney, what are we going to do? Kelly [Osbourne] is passed out and is blue on the floor!’ She wasn’t doing too okay back then. For some reason, Kim also called me when Paris Hilton got pulled over for her last DUI. And Lindsay Lohan called me after she was arrested…. And then Lindsay’s father called me for advice every day for weeks. It was weird. I mean, I’m not even friendly with these girls. When did I become the junkie Auntie Mame?”

So, is she a sober or an addicted Auntie Mame? Is she the go-to girl for straight talk on drugs and sobriety, or just another enabler? She has been through formal rehab perhaps a dozen times now. At one point in the book, she crows about the fact that all the drugs she’s currently taking are “entirely legal,” then flies to a posh London Hotel, using a personal physician and a 24-hour nursing staff to kick her addiction to Adderall—prescription speed. Love appears to have the “chronic relapsing” part of addiction down pat.

Roshan notes that, “like many addicts, she has found herself increasingly isolated and withdrawn in recent years.”

 I asked Maer Roshan a few questions about the book, to which he kindly responded:

Q. Has this woman every really been clean and sober for an extended period, or is she just conning everybody about her recovery?

Maer Roshan: She's certainly not sober in any way that would pass muster at A.A., but she's come a long way from the demons that plagued her past… She admits to using prescription pills. (She makes a point to note that they're all legally prescribed.) She also enjoys a few drinks now and again. But she's nothing like the addict she was five years ago, when she was shooting smack five times a day or holed up in her house in L.A, watching for police cars and smoking kilos of crack. For someone like Courtney, that's real progress. In light of all the damage that drugs have inflicted on her life and her family, I think she is serious about sobriety. She's seen first-hand the damage that drugs can do. After all, they killed her husband and ruined her relationship with her daughter. But ultimately sobriety means different things to different people. As they say in A.A., it’s about progress rather than perfection, so even though she's far from a teetotaler, her progress is impressive.

Q. Lindsay and Paris and all the young drug people make pilgrimages to her for advice. Is that a good thing or a bad thing?

Roshan: I think it's neither a good thing nor a bad thing. Obviously, Lindsay or Paris would probably get better advice from a person more grounded in sobriety, or from a therapist or doctor. But, as she notes in the interview, being famous does strange things to people's heads, especially famous women, so in a way it's understandable that younger girls in the same position would relate to her. Believe it or not, Courtney's actually pretty shrill on the subject of drugs. She’s been known to reach out to those women, even if they don't reach out to her.

Q. Courtney seems obviously co-morbid. Has she ever sought psychiatric help?

Roshan: Obviously I'm not qualified to diagnose her. I know she's seen a fair share of psychiatrists throughout her life. In my book, her mother notes that Courtney was agitated and anxious from the time she was a toddler. Her parents built her a special hut attached to their main house in New Zealand, in part to keep her from attacking her brothers and sisters. She was prescribed Valium from the time she was seven. Like most crazy people, she has the capacity to be brilliant and funny and extremely entertaining. But she's also filed with bitterness and unbelievable rage, and you never quite know which Courtney you're gonna get. She's a blast to hang out with, but as I can attest from personal experience, it's kind of scary when her rage is directed at you.
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So what to make of her? “Most people think I dry out at these really posh places,” she told Roshan, “but I’ve landed in some pretty gnarly spots.” And that’s when I began to feel some sympathy for Love, seeing her falsehoods and contradictions and obsessions in the light of her addictions, known that there must have been plenty of horrifying nights, and equally agonizing mornings, and self-loathing, and a lot of time surrounded by people, but always alone. What to make of her? I don’t think we know yet. I hope she gets better, stronger, wiser, and ends up making a fool out of me.

Photo Credit: http://blogs.sfweekly.com

Book Review: Writers On The Edge

A compendium of tough prose and poetry about addiction.

Here’s a book I’m delighted to promote unabashedly. I even wrote a jacket blurb for it. I called it an “honest, unflinching book about addiction from a tough group of talented writers. These hard-hitters know whereof they speak, and the language in which they speak can be shocking to the uninitiated—naked prose and poetry about potentially fatal cravings the flesh is heir to—drugs, booze, cutting, overeating, depression, suicide. Not everybody makes it through. Writers On The Edge is about dependency, and the toll it takes, on the guilty and the innocent alike.”

I am happy to stand by that statement, content to note that this collection of prose and poetry on the subject of addiction and dependency by 22 talented writers, with an introduction by Jerry Stahl of “Permanent Midnight” junky fame, includes a number of names familiar to me. That makes it all the easier to recommend this book—I know some of the talent. Take James Brown, a professor in the M.F.A program at Cal State San Bernardino, the book’s co-editor, who offers an excerpt from his excellent memoir, This River.  James is no stranger to the subject, having pulled out of a drug and alcohol-fueled nosedive that would have felled lesser mortals for good. “Even though you’ll always be struggling with your addiction, and may wind up back in rehab,” Brown writes, “at least for now, if only for this day, you are free of the miracle potions, powders and pills. If only for this day, you are not among the walking dead.” Or my friend Anna David, who is an editor at The Fix, an online addiction and recovery magazine to which I frequently contribute, and author of several books, including Party Girl and Falling for Me. Anna poignantly recalls “my shock over the power than booze had… it was the greatest discovery of my life.” And Ruth Fowler, another Fix contributor and author of Girl Undressed, delivers up a brilliantly detached story of her life as an addict on both coasts and just about everywhere else, which begins with the line, “I gravitated to the fucked up writers.”

Then there are the contributors I don’t know but wish I did, like co-editor Diana Raab, a registered nurse and award-winning poet, as well as co-author of Writers and Their Notebooks, who offers a poem to her grandmother: “Your ashen face and blond bob/disheveled upon white sheets/on the stretcher held by paramedics/lightly grasping each end, and tiptoeing.” Or another poet, B. H. Fairchild, author of the marvelous collection, Early Occult Memory Systems of the Lower Midwest: “When I would go into bars in those days/the hard round faces would turn/to speak something like loneliness/but deeper, the rain spilling into gutters/or the sound of a car pulling away/in a moment of sleeplessness just before dawn.”

And more: Frederick Barthelme, author of Double Down: Reflections on Gambling and Loss. Stephen Jay Schwartz, best-selling crime novelist  and former director of development for filmmaker Wolfgang Petersen. Writers Rachel Yoder, Victoria Patterson, David Huddle, and Scott Russell Sanders. Etc. This collection is a rich brew of essay, poetry, and memoir. A tough book, a brutal book, a real heartbreaker with grit. Some people get stronger and rise; some don’t. It is a thoughtful and creative compendium of addiction stories, and some of them will surprise you. All of them are solidly written, laid out with an unrelenting realism.

Here it is, these authors are saying. This is how it plays out. Unforgettable stuff.

Reward and Punish: Say Hello to Dopamine’s Leetle Friend

  Dopamine recruits a helper to track drug rewards.

Ah, dopamine. Whenever it seems like researchers have finally gotten a bead on how that tricky molecule modulates pleasure and reward, and the role it plays in the process of drug and alcohol addiction, along come new findings that rearrange its role, deepening and complicating our understanding of brain function.

We know that the ultimate site of dopamine activity caused by drugs is the ventral tegmental area, or VTA, and an associated structure, the nucleus accumbens. But dopamine neurons in the VTA actually perform two distinct functions. They discriminate acutely between the expectation of reward, and the actual reward itself. Pavlov showed how these dual functions are linked, but the manner in which dopamine neurons computed and then dealt with the differences between expectation and reward—a controversial concept known as reward prediction error—was not well understood.

We all know about reward and punishment, however. Years ago, behaviorism’s emphasis on positive and negative reinforcement demonstrated the strong connection between reward, punishment, and learning. As Michael Bozarth wrote in “Pleasure Systems in the Brain,” addictive drugs “pharmacologically activate brain reward mechanisms involved in the control of normal behavior. Thus, addictive drugs may be used as tools to study brain mechanisms involved in normal motivational and reward processes.”

But how does the evolutionary pursuit of pleasure or avoidance of punishment that guarantees the survival of an organism—fighting, fleeing, feeding, and… fornicating, in the well-known “4-F” configuration—become a pathological reversal of this function? To begin with, as Bozarth writes, “the direct chemical activation of these reward pathways does not in itself represent any severe departure from the normal control reward systems exert over behavior…. Simple activation of brain reward systems does not constitute addiction!”

What does, then? Bozarth believes addiction results from “motivational toxicity,” defined as deterioration in the “ability of normal rewards to govern behavior.” In an impaired reward system, “natural” rewards don’t alter dopamine function as strongly as drug rewards. “Direct pharmacological activation of a reward system dominates the organism’s motivational hierarchy at the expense of other rewards that promote survival,” Bozarth writes. The result? Drug addicts who prefer, say, methamphetamine to food.

How does an addict’s mind become so addled that the next hit takes precedence over the next meal? A group of Harvard-based researchers, writing in Nature, thinks it may have a handle on how the brain calculates reward expectations, and how those calculations go awry in the case of heavy drug and alcohol use.

The dopamine system somehow calculates the results of both failed and fulfilled expectations of reward, and uses that data in future situations. Cellular biologists, with some exceptions, believe that dopamine neurons effectively signal some rather complicated discrepancies between expected and actual rewards. Dopaminergic neurons were, in effect, computing reward prediction error, according to the theory. They were encoding expectation, which spiked when the reward was better than expected, and fell when the reward was less than expected. As Scicurious wrote at her blog, Neurotic Physiology “If you can’t predict where and when you’re going to get food, shelter, or sex in response to specific stimuli, you’re going to be a very hungry, chilly and undersexed organism.” (See her excellent and very readable post on dopamine and reward prediction HERE. )

But nobody knew how this calculation was performed at the cellular level.

Enter research mice.

As it turns out, dopamine is not the whole story. (A single neurotransmitter rarely is.) Dopaminergic neurons account for only about 55-65% of total neurons on the VTA. The rest? Mostly neurons for GABA, the inhibitory transmitter. “Many addictive drugs inhibit VTA GABAergic neurons,” the researchers note, “which increases dopamine release (called disinhibition), a potential mechanism for reinforcing the effects of these drugs.” By inhibiting the inhibitor, so to speak, addictive drugs increase the dopamine buzz factor.

The researchers used two strains of genetically altered mice, one optimized for measuring dopamine, the other for measuring GABA. The scientists conditioned mice using odor cues, and offered four possible outcomes: big reward, small reward, nothing, or punishment (puff of air to the animal’s face). Throughout the conditioning and testing, the researchers recorded the activity of neurons in the ventral tegmental area. They found plenty of neurons with atypical firing patterns. These neurons, in response to reward-predicting odors, showed “persistent excitation” during the delay before the reward. Others showed “persistent inhibition” to reward-predicting odors.

It took a good deal of sorting out, and conclusions are still tentative, but eventually the investigators believed that VTA dopamine neurons managed to detect the discrepancy between expected and actual outcomes by recruiting GABA neurons to aid in the dendritic computation. This mechanism may play a critical role in optimal learning, the researchers argue.

Furthermore, the authors believe that “inhibition of GABAergic neurons by addictive drugs could lead to sustained reward prediction error even after the learned effects of drug intake are well established.” Because alcohol and other addictive drugs disrupt GABA levels in the brain’s reward circuitry, the mechanism for evaluating expectation and reward is compromised. GABA, dopamine’s partner in the enterprise, isn’t contributing properly. The ability to learn from experience and to accurately gauge the likelihood of reward, so famously compromised in active addiction, may be the result of this GABA disruption.

Naoshige Uchida, associate professor of molecular and cellular biology at Harvard, and one of the authors of the Nature paper, said in a press release that until now, “no one knew how these GABA neurons were involved in the reward and punishment cycle. What we believe is happening is that they are inhibiting the dopamine neurons, so the two are working together to make the reward error computation.” Apparently, the firing of dopamine neurons in the VTA signals an unexpected reward—but the firing of GABA neurons signals an expected reward. Working together, GABA neurons aid dopamine neurons in calculating reward prediction error.

In other words, if you inhibit GABA neurons through heavy drug use, you screw up a very intricate dopamine feedback loop. When faced with a reward prediction error, such as drug tolerance—a good example of reward not meeting expectations—addicts will continue taking the drug. This seems nonsensical. If the drug no longer works to produce pleasure like it used to do, then why continue to take it? It may be because dopamine-active brain circuits are no longer accurately computing reward prediction errors. Not even close. The research suggests that an addict’s brain no longer registers negative responses to drugs as reward errors. Instead, all that remains is the reinforcing signals from the dopamine neurons: Get more drugs.

[Tip of the hat to Eric Barker (@bakadesuyo) for bringing this study to my attention.]

Cohen, J., Haesler, S., Vong, L., Lowell, B., & Uchida, N. (2012). Neuron-type-specific signals for reward and punishment in the ventral tegmental area Nature DOI: 10.1038/nature10754

Photo Credit: http://www.zazzle.com 

A Few Words About Glutamate

Meet another major player in the biology of addiction.

The workhorse neurotransmitter glutamate, made from glutamine, the brain’s most abundant amino acid, has always been a tempting target for new drug development. Drugs that play off receptors for glutamate are already available, and more are in the pipeline. Drug companies have been working on new glutamate-modulating antianxiety drugs, and a glutamate-active drug called acamprosate, which works by occupying sites on glutamate (NMDA) receptors, has found limited use as a drug for alcohol withdrawal after dozens of clinical trials.

Glutamine detoxifies ammonia and combats hypoglycemia, among other things. It is also involved in carrying messages to brain regions involved with memory and learning. An excess of glutamine can cause neural damage and cell death, and it is a prime culprit in ALS, known as Lou Gehrig’s disease. In sodium salt form, as pictured---> it is monosodium glutamate, a potent food additive. About half of the brain’s neurons are glutamate-generating neurons. Glutamate receptors are dense in the prefrontal cortex, indicating an involvement with higher thought processes like reasoning and risk assessment. Drugs that boost glutamate levels in the brain can cause seizures. Glutamate does most of the damage when people have strokes.

The receptor for glutamate is called the N-methyl-D-aspartate (NMDA) receptor. Unfortunately, NMDA antagonists, which might have proven to be potent anti-craving drugs, cannot be used because they induce psychosis. (Dissociative drugs like PCP and ketamine are glutamate antagonists.) Dextromethorphan, the compound found in cough medicines like Robitussin and Romilar, is also a weak glutamate inhibitor. In overdose, it can induce psychotic states similar to those produced by PCP and ketamine. Ely Lilly and others have looked into glutamate-modulating antianxiety drugs, which might also serve as effective anti-craving medications for abstinent drug and alcohol addicts.

As Jason Socrates Bardi at the Scripps Research Institute writes: "Consumption of even small amounts of alcohol increases the amount of dopamine in the nucleus accumbens area of the brain—one of the so-called ‘reward centers.’ However, it is most likely that the GABA and glutamate receptors in some of the reward centers of the basal forebrain—particularly the nucleus accumbens and the amygdala—create a system of positive reinforcement.”

Glutamate receptors, then, are the “hidden” receptors that compliment dopamine and serotonin to produce the classic “buzz” of alcohol, and to varying degrees, other addictive drugs as well. Glutamate receptors in the hippocampus may also be involved in the memory of the buzz.


Writing in The Scientist in 2002, Tom Hollon made the argument that “glutamate's role in cocaine dependence is even more central than dopamine's.” Knockout mice lacking the glutamate receptor mGluR5, engineered at GlaxoSmithKline, proved indifferent to cocaine in a study published in Nature.

In an article for Neuropsychology in 2009, Peter Kalivas of the Medical University of South Carolina and coworkers further refined the notion of glutamine-related addictive triggers: "Cortico-striatal glutamate transmission has been implicated in both the initiation and expression of addiction related behaviors, such as locomotor sensitization and drug-seeking," Kalivas writes. "While glutamate transmission onto dopamine cells in the ventral tegmental area undergoes transient plasticity important for establishing addiction-related behaviors, glutamatergic plasticity in the nucleus accumbens is critical for the expression of these behaviors."

The same year, in Nature Reviews: Neuroscience, Kalivas laid out his “glutamate homeostasis hypothesis of addiction.”

A failure of the prefrontal cortex to control drug-seeking behaviors can be linked to an enduring imbalance between synaptic and non-synaptic glutamate, termed glutamate homeostasis. The imbalance in glutamate homeostasis engenders changes in neuroplasticity that impair communication between the prefrontal cortex and the nucleus accumbens. Some of these pathological changes are amenable to new glutamate- and neuroplasticity-based pharmacotherapies for treating addiction.

This kind of research has at least a chance of leading in the direction of additional candidates for anti-craving drugs, without which many addicts are never going to successfully treat their disease.


Graphics credit: http://cnunitedasia.en.made-in-china.com/

A Six-Pack of Prior Posts

Don’t fear the chemistry. 

This isn’t a top 10 list, just a compilation of five previous posts here at Addiction Inbox that have continued to draw reader interest since they were first published. If there is a theme running through this set, it is neurochemistry at its most basic level. Take a look, if any of the subjects interests you. (My most popular post of all, on Marijuana Withdrawal, has turned into a self-help message board. I note it here, but leave it off the list, as it has become a blog of its own for all practical purposes.)
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1) Don’t let anyone tell you that the basic notions involved in neurotransmitter action in the brain are over everyone’s head. This post about serotonin and dopamine basics has always been popular, partly because serotonin and dopamine have gone from obscure abstractions to pop buzzwords. But I think it also shows a growing awareness of brain science and its real-world applications among interested readers.

“…. Addictive drugs have molecules that are the right shape for the amine receptors. Drugs like LSD and Ecstasy target serotonin systems. Serotonin systems control feeding and sleeping behaviors in living creatures from slugs to chimps. Serotonin, also known as 5-HT, occurs in nuts, fruit, and snake venom. It is found in the intestinal walls, large blood vessels, and the central nervous system of most vertebrates. The body normally synthesizes 5-hydroxytryptamine, as serotonin is formally known, from tryptophan in the diet….”

Serotonin and Dopamine: A primer on the molecules of reward
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2) Continuing on the chemistry theme, this post on anandamide, the brain’s own form of internal marijuana, has garnered steady attention since 2008. It may be coincidental, but the post also makes mention of serotonin and dopamine.

“…Several years ago, molecular biologists identified the elusive brain receptor where THC, the active ingredient in marijuana, did its work. Shortly after that discovery, researchers at Hebrew University in Jerusalem identified the body’s own form of THC, which sticks to the same receptors, in pulverized pig brains. They christened the internally manufactured substance “anandamide,” after the Sanskrit ananda, or bliss…”

Anandamide, the Brain’s Own Marijuana: Anxiety and the THC receptor.
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3) Interest in the anti-craving drug Topamax, an anti-seizure medication used to treat alcoholism, remains strong with blog readers, although the drug has not become the universal blockbuster many advocates had hoped.

“…Dr. Bankole Johnson, chairman of Psychiatry and Neurobehavioral Sciences at the University of Virginia, told Bloomberg News that Topamax does everything researchers want to see in a pharmaceutical treatment for alcoholism: “First, it reduces your craving for alcohol; second, it reduces the amount of withdrawal symptoms you get when you start reducing alcohol; and third, it reduces the potential for you to relapse after you go down to a low level of drinking or zero drinking…"

Topamax for Alcoholism: A Closer Look. Epilepsy drug gains ground, draws fire as newest anti-craving pill
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4) One of the most popular posts to date was this examination of neurological questions surrounding marijuana and memory loss. Inquiring minds, uh, forget the question. Oh yeah: Does the strain of dope you smoke determine how forgetful you’ll become?

“…As far as memory goes, THC content didn't seem to matter. It was the percentage of cannabidiol (CBD) that controlled the degree of memory impairment, the authors concluded. "The antagonistic effects of cannabidiol at the CB1 receptor are probably responsible for its profile in smoked cannabis, attenuating the memory-impairing effects of THC. In terms of harm reduction, users should be made aware of the higher risk of memory impairment associated with smoking low-cannabidiol strains of cannabis like 'skunk' and encouraged to use strains containing higher levels of cannabidiol..." 


Marijuana and Memory: Do certain strains make you more forgetful?
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5) Finally, a popular post focusing on the biochemistry of nicotine in e-cigarettes, the new, smokeless nicotine delivery system. Are they safe? The latest in harm reduction strategies, or starter kits for youngsters?

“…You may never have heard of it—but it’s the newest drug in town. It’s called an electronic cigarette, or “e-cigarette.” Electronic cigarettes use batteries to convert liquid nicotine into a fine, heated mist that is absorbed by the lungs. No smoke, but plenty of what makes cigarettes go, if you don’t account for taste—or ashtrays and smoke rings….”

E-Cigarettes and Health: Smokeless nicotine comes under scrutiny.

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

The Empty Seat at the Holiday Table

Mothers and the War on Drugs.

Guest post by Gretchen Burns Bergman

Gretchen Burns Bergman is Co-Founder and Executive Director of A New PATH (Parents for Addiction Treatment and Healing) and lead organizer of Moms United to End the War on Drugs.

The Holiday season is upon us. At this time, when the weather turns chilly and we move indoors to enjoy the warmth and safety of our homes and the closeness of family and friends, I am acutely aware of those not so fortunate: people who are out in the elements, either because of dire financial situations or mental and addictive illness.

The Holidays are particularly difficult for those who must navigate the mighty and destructive waves of addiction. It is a painful time for families who are separated because of a loved one’s incarceration, whose young person is lost on the streets due to drug problems, whose children are in danger because of the violence of the drug cartels, or those who have lost a loved one to overdose. Often a family member is missing from the festivities because of stigma and shame.

I don’t remember when I started dreading Thanksgiving. It wasn’t after my father or my nephew died, because they were remembered and celebrated at the table, or even after the breakup of my first marriage. It was all of the times that my older son was absent because he was locked behind bars in that cold, concrete jungle, and I couldn’t figure out where I belonged – with him to somehow nurture and sustain him, or in the bosom of the rest of my family. It is the memories of holidays when one of my sons wasn’t included because he was lost in the maze of his addiction, and his name wasn’t even mentioned because of pain, discomfort, and even judgment. Those omissions widened the hole in my heart.

I weep for the countless families who have been torn apart by discriminatory and destructive drug policies that lock up fathers and remove children from their mothers in the name of the war on drugs, which is really a war waged against families and communities.

This season, mothers are banding together and speaking out with human stories of injustice and devastation, to encourage other mothers to join our voices for change. Moms United to End the War on Drugs is a national movement to end the violence, mass incarceration and accidental overdose deaths that are result of these blundering punitive policies. At a time when 2.3 million people are incarcerated in the United States and overdose is a leading cause of accidental death, mothers must lead the way in demanding harm reduction strategies, health-oriented solutions, and restorative justice.

The following are stories written by mothers who have experienced the ravages of the war on drugs, and who honor that empty seat at the holiday table:

The missing seat at the prison visiting table.

It was Thanksgiving and my family and I drove 4 hrs to visit my young son in his California prison for the holiday. He was serving time for drug possession, celled with a murderer, in one of the state’s highest security prisons, so “processing time” including prison official dysfunction, near total disrobing, endless questioning, metal detectors, sally-ports, and guard escorts, took about 4 hours to complete before we got to the highly secure visiting room. Because of this time consuming process, there was only 45 minutes left to visit. On the other side, my inmate son was being strip searched and waiting in a line moving at glacial speed to enter the visiting area. I cried to the guard that, as time ticked by, I was being left with five minutes to see my son for Thanksgiving…but I wanted those five minutes. He waited in his sally-port on the other side, while we all waited at our assigned table for that precious few minutes with my son. That seat remained empty. Alerts sounded that visiting was over.

--Julia Negron, A New PATH Los Angeles, California

Until this war ends, an extra place at my table.

During the holidays, we reflect as we prepare meals, set our tables, and decorate our homes. As I begin planning, with my daughter and husband’s help, I think back to the time when I was addicted to heroin, and missing from my family’s holiday table. Though it was more than 20 years ago, my family experienced extreme grief over my addiction. My father tells me that he is so grateful that I am alive. He didn’t know, in the midst of my homelessness, whether I’d ever be able to attend, let alone host, a Thanksgiving with my own family. I think how lucky I am, because I had the opportunity to get treatment that worked for me. I know someone waited and despaired over me. Now, I wait for those with substance use disorders to be served by our health care system rather than languishing in prison. Until that wait is over, there will always be an extra place setting at my holiday table for those who are locked up, thrown away or left out. The person in prison for a drug crime might not be able to eat with me this year, but perhaps next year, they will.

--Kathie Kane-Willis, Illinois Consortium on Drug Policy, Roosevelt University

Emptiness is everywhere.

Since our son was born, we always picked out the Christmas tree together. It became a tradition and one of the fun parts of the holiday rush. Dad would put the lights on the tree and make clam chowder, while Jeff and I did the ornaments. As years passed, it was sometimes difficult for us all to be together for this tradition, but we were. Our son had addictive illness, and through the many rehabs, the short county incarcerations, the times where he’d isolate because he was using, we somehow were able to keep that tradition. Christmas Eve was spent with our entire family either in our home or my sister’s. The first year without Jeff – just 3 months after he died of an accidental overdose and 2 days after release from 4 months in county jail, was unreal. Jeff had been so much a part of Christmas, sharing Santa duties and passing out gifts to the little ones with the biggest smile on his face. The emptiness was EVERYWHERE. He should have been there. We haven’t had a Christmas tree or decorations in our home since 2007. I don’t think we ever will again. The Holidays bring nothing but pain.

--Denise Cullen, Broken No More, Orange County, California

Photo Credit: http://sisterjohnpaul.blogspot.com/

What Do We Mean When We Talk About Craving?

An essay on drug addiction and need.

For years, craving was represented by the tortured tremors and sweaty nightmares of extreme heroin and alcohol withdrawal. Significantly, however, the one symptom common to all forms of withdrawal and craving is anxiety. This prominent manifestation of craving plays out along a common set of axes: depression/dysphoria, anger/irritability, and anxiety/panic. These biochemical states are the result of the “spiraling distress” (George Koob’s term) and “incomprehensible demoralization” (AA’s term) produced by the addictive cycle. The mechanism driving this distress and demoralization is the progressive dysregulation of brain reward systems, leading to biologically based craving. The chemistry of excess drives the engine of addiction, which in turn drives the body and the brain to seek more of the drug.

Whatever the neuroscientists wanted to call it, addicts know it as “jonesing,” from the verb “to jones,” meaning to go without, to crave, to suffer the rigors of withdrawal. Spiraling distress, to say the least—a spiraling rollercoaster to hell, sometimes. Most doctors don’t get it, and neither do a lot of the therapists, and least of all the public policy makers. Drug craving is ineffable to the outsider.

As most people know, behavior can be conditioned. From maze-running rats to the “brain-washed” prisoners of the Korean War, from hypnotism to trance states and beyond, psychologists have produced a large body of evidence about behavior change—how it is accomplished, how it can be reinforced, and how it is linked to the matter of reward.

It is pointless to maintain that drug craving is “all in the mind,” as if it were some novel form of hypochondria. Hard-core addicts display all the earmarks of the classical behavioral conditioning first highlighted almost a century ago by Ivan Pavlov, the Russian physiologist. Pavlov demonstrated that animals respond in measurable and repeatable ways to the anticipation of stimuli, once they have been conditioned by the stimuli. In his famous experiment, Pavlov rang a bell before feeding a group of dogs. After sufficient conditioning, the dogs would salivate in anticipation of the food whenever Pavlov rang the bell. This conditioned response extended to drugs, as Pavlov showed. When Pavlov sounded a tone before injecting the dogs with morphine, for example, the animals began to exhibit strong physiological signs associated with morphine use at the sound of the tone alone. Over time, if the bell continued to sound, but no food was presented, or no drugs were injected, the conditioned response gradually lost its force. This process is called extinction.

Physical cravings are easy to demonstrate. Abstinent heroin addicts, exposed to pictures of syringes, needles, or spoons, sometimes exhibit withdrawal symptoms such as runny noses, tears, and body aches. Cravings can suddenly assail a person months—or even years—after discontinuing abusive drug use. Drug-seeking behavior is a sobering lesson in the degree to which the human mind can be manipulated by itself. The remarkable tenacity of behavioral conditioning has been demonstrated in recent animal studies as well. When monkeys are injected with morphine while recorded music is played, the music alone will bring on withdrawal symptoms months after the discontinuation of the injections.  When alcoholics get the shakes, when benzodiazepine addicts go into convulsions, when heroin addicts start to sweat and twitch, the body is craving the drug, and there is not much doubt about it. But that is not the end of the matter.

“Craving is a very misunderstood word,” said Dr. Ed Sellers, now with the Centre for Addiction and Mental Health in Toronto. “It’s a shorthand for describing a behavior, but the behavior is more complicated and interesting than that. It’s thought to be some intrinsic property of the individual that drives them in an almost compulsive, mad way. But in fact when you try to pin it down—when you ask people in a general context when they’re exposed to drugs about their desire to use drugs, they generally give rather low assessments of how important it really is.”

While cravings can sometimes drive addicts in an almost autonomic way, drug-seeking urges are often closely related to context, setting, and the expectancy effect. It has become commonplace to hear recovering addicts report that they were sailing through abstinence without major problems, until one day, confronted with a beer commercial on television, or a photograph of a crack pipe, or a pack of rolling papers—or, in one memorable case of cocaine addiction, a small mound of baking powder left on a shelf—they were suddenly overpowered by an onrush of cravings which they could not successfully combat. “If you put them in a setting where the drug is not available, but the cues are,” said Sellers, “it will evoke a conditioned response, and you can show that the desire to use goes up.” Most people have experienced a mild approximation of this phenomenon with regard to appetite. When people are hungry, a picture of a cherry pie, or even the internal picture of food in the mind’s eye, is enough to cause salivation and stomach rumblings. Given the chemical grip which addiction can exert, imagine the inner turmoil that the sight of a beer commercial on television can sometimes elicit in a newly abstinent alcoholic.

When addicts start to use drugs again after a period of going without, they are able to regain their former level of abuse within a matter of days, or even hours. Some sort of metabolic template in the body, once activated, seems to remain dormant during abstinence, and springs back to life during relapse, allowing addicts to escalate to their former levels of abuse with astonishing speed. This fact, and no other, is behind the 12-Step notion of referring to oneself as a “recovering,” rather than recovered, addict—a semantic twist that infuriates some people, since it seems to imply that an addict is never well, never cured, for a lifetime.

Relapse sometimes seems to happen even before addicts have had a chance to consciously consider the ramifications of what they are about to do. In A.A., this is often referred to as forgetting why you can’t drink. It sounds absurd, but it is a relatively accurate way of viewing relapse. Addiction, as one addict explained, “is the only disease that tells you you ain’t got it.”

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The Strange and Secret Keeley Cure for Addiction

“Drunkenness is a disease and I can cure it.”

In America in the late 1800s, curing alcoholism was a serious business—and for Dr. Leslie Keeley, a very lucrative one. Dozens of clinics and cures already existed, and some treatment centers had even experimented with franchising. For the late 19th Century alcoholic in search of treatment, what most of them had on offer was either outright patent medicine fraud, or else well intentioned if ultimately misguided “opium” cures. None of them, writes William L. White in Slaying the Dragon, “was more famous, more geographically dispersed, more widely utilized, and more controversial than Leslie Keeley’s Double Chloride of Gold Cure for the treatment of alcoholism, drug addiction, and the tobacco habit.”

The Irish-born Dr. Keeley served as a surgeon in the Civil War, and, as family lore would have it, started a treatment program for alcoholism in a Union hospital during the war. We do know that in 1879, he opened the first Keeley Institute in Dwight, Illinois, south of Chicago. His sales pitches were colorful and varied, but boiled down to this pledge: “Drunkenness is a disease and I can cure it.” He could cure it with a secret, specific formula, injected four times daily, about which all he would hint publically was that it contained, as one of its ingredients, gold. This was not so outlandish as it may seem. Gold, silver, strychnine, and other potentially poisonous ingredients were already employed in dozens of standard medicines—and, in many cases, still are. But everything else about Dr. Keeley’s magic elixir was as secret as the ingredients in Coke.

Nonetheless, something seemed to be working. He claimed an outlandish 95% success rate, bolstered by legions of enthusiastic followers who formed proto-AA groups with the catchy title of Bi-Chloride of Gold Clubs, better known as the Keeley Leagues. And Keeley himself employed the largest collection of formerly addicted doctors in the known world. There were no counselors at Keeley clinics. There were enough doctors on staff to go around, even though an estimated total of half a million alcoholics and other addicts eventually took the Keeley Cure.

Treatment consisted of the infamous injections, a liquid cordial every two hours, and, according to White, the following modalities: “daily rest, nutrition, mutual sharing, and alternative diversions worked to improve the patient’s physical and psychological health.” We can assume, from this regimen, that some alcoholics and addicts probably improved, regardless of what was in the medicine. And there was the frequent suggestion that, really, it was probably best not to ask too many questions about what was in the medicine, anyway.

“The atmosphere was informal and friendly at the clinics,” White writes, “with a marked absence of the bars and restraints that were typical in most inebriate asylums of the period.” There were, of course, some very vocal detractors. Dr. T. D. Crothers, a leader in the inebriate asylum movement, said: “There is no gold cure for inebriety. There are no facts to show that gold has any value in this disease. All the assertions and statements concerning gold as a remedy are delusions, and will not bear the test of critical examination.”  Perhaps not. But success was success, and soon, the marketplace saw the introduction of Dr. Haines Golden Remedy, the Geneva Gold Cure, the Boston Bichloride of Gold Company, and many other knockoffs. (Keeley proclaimed that his Double Chloride of Gold cured all forms of inebriety by “speeding up the restoration of poisoned cells to their pre-poisoned condition.”)

From 1892 through 1900, the Keeley Company pulled in almost $3 million, including mail-order business. There was a Keeley Day at the 1893 World’s Fair in Chicago. Here is an excerpt from the pamphlet, “To the Keeley Graduate,” given to every patient who completed treatment:

You are now numbered among thousands of men and women who have broken the shackles of alcohol and drug addictions by the Keeley method of treatment. Your cure will be as permanent as your life, you will never have any craving for alcohol or other sedative drugs as long as you live, unless you create it by returning to their use, thus re-poisoning your nerve cells.

But by 1900, the bloom was off the Keeley miracle, as insiders fought for financial control, and congressional investigators looked into the affairs of Keeley League president Andrew J. Smith.

Of course, if Keeley had really possessed a specific, replicable formula that took away the craving for alcohol, it would have been monstrously unethical to hold it a secret. And he was constantly accused of using harmful ingredients, such as codeine, strychnine, and cocaine in his magic injections.

Keeley wouldn’t say. And neither did any of his heirs or business partners. The only thing most court records agree on is that the injection didn’t contain any gold—too many possible side effects. According to the testimony of Keeley’s original business partner, “The only patient who ever received Keeley medicine that actually had gold in it almost died.”

The secret ingredient was probably atropine—a powerful compound belonging to a very weird family of plant drugs known collectively as “anticholinergenic deliriants.”  Atropine is the active ingredient in Belladonna, aka Deadly Nightshade. Along with mandrake, henbane, and jimsonweed, the so-called Belladonna alkaloids are among the primary hallucinatory ingredients found in many a witch’s and sorcerer’s brew throughout the ages. Belladonna can cause terrifying hallucinations, feelings of flight or paralysis, blurred vision, impaired motor control, and other side effects usually experienced as highly unpleasant. It was likely Belladonna, not LSD, that served as the basic rocket fuel for the Manson’s family’s horrific activities, according to some accounts. More mundanely, atropine is familiar to armed forces personnel in the form of a self-injection device for serious wounds. Atropine has the ability to speed up a slowing or overworked heart. In ancient times, it was used as an anesthetic for surgery. Atropine is also a poison. (Scopolamine, used medically for motion sickness, is another.)

But one person’s unpleasant side effect is another’s chemical cure. Did the Keeley concoction just terrify the bejesus out of addicts, as some sort of ad hoc version of aversive therapy, or did it sedate his patients into a semi-catatonic, immobile haze, in which they could pass 3 weeks of detox in relative comfort, or at least immobility and minimal disruption? Probably both, depending on drug dosage, drug combination, and patient metabolism. There were widespread reports of Keeley patients who allegedly died or went insane.

“The pulp image of Dr. Leslie Keeley—that of the country physician who had stumbled onto a revolutionary cure for the inebriety problem that had stumped the best medical scientists,” was key to his success, White believes. “Keeley introduced an approach that carried an aura of scientific truth and all the emotional support and intensity of a revival meeting.”

“The likely ingredients of the Double Chloride of Gold remedy and tonics—alcohol, atropine, strychnia, apomorphine —did aid detoxification,” White concludes. And the graduation pamphlet went on to emphasize the importance of “sustaining the new Keeley habits: regular patterns of sleep, regular and balanced meals, regular consumption of water, abstinence from tobacco and caffeinated drinks, healthy recreation, and care in the selection of personal associates.”

If you skip the atropine injections, that series of admonitions remains the bedrock of drug and alcohol treatment programs everywhere.

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