LSD and Alcohol: The History

Back when acid was legal.

After last week’s blitz of coverage concerning studies done in the 60s on the use of LSD for the treatment of alcoholism, I thought it would be useful to provide a bit of background; some pertinent psychedelic history to help put this information in perspective:

It may come as a surprise to many people that throughout the 60s, there were LSD clinics operating in England and Europe. European LSD therapists tended to use very low doses as an adjunct to traditional psychoanalytic techniques. But North American researchers took a different, bolder approach. When “psychedelic” therapy began to catch on in Canada and the United States, therapists typically gave patients only one or two sessions at very high doses. These early efforts were aimed at producing spontaneous breakthroughs or recoveries in alcoholics through some manner of religious epiphany or inner conversion experience. The only other quasi-medical approach of the day, the Schick Treatment Center’s brand of “aversion therapy,” was not seen to produce very compelling long-term recovery rates, and subsequently fell out of favor. In this light, the early successes with LSD therapy, sometimes claimed to be in the 50-75 per cent range, looked noteworthy indeed. However, the design and criteria of the LSD/alcoholism studies varied so widely that it has never been possible to draw definitive conclusions about the work that was done, except to say that LSD therapy seemed to be strikingly effective for certain alcoholics. Some patients were claiming that two or three trips on LSD were worth years of conventional psychotherapy—a claim not heard again until the advent of Prozac thirty years later.

 “I’ve taken lysergic acid several times, and have collected considerable information about it,” Bill Wilson, the co-founder of Alcoholics Anonymous, disclosed in a private letter written in 1958. “At the moment, it can only be used for research purposes. It would certainly be a huge misfortune if it ever got loose in the general public without a careful preparation as to what the drug is and what the meaning of its effects may be.”  Like many others, Wilson was excited by LSD’s potential as a treatment for chronic alcoholism. Even Hollywood was hip to the new therapy. Cary Grant, among others, took LSD under psychiatric supervision and pronounced it immensely helpful as a tool for psychological insight. Andre Previn, Jack Nicholson, and James Coburn agreed. (It could be argued that the human potential movement began here).

No drug this powerful and strange, if American history was any guide, could remain legal for long. Unlike their colleagues in the intelligence agencies, politicians and law enforcement officers didn’t know about Mongolian shamans and their fly agaric mushrooms; about European witches and their use of psychoactive plant drugs like nightshade and henbane; about Persian sheiks with their cannabis water pipes; Latin American brujos with their magic vines.

But for the CIA, the big fish was always LSD.

What interested the Central Intelligence Agency about LSD was its apparent ability to produce the symptoms of acute psychosis. Operation ARTICHOKE was designed to ferret out LSD’s usefulness as an instrument of psychological torture, and as a possible means of destabilizing enemy forces by means of aerosol sprays or contaminated water supplies. (The drug’s overwhelming potency made such parts-per-billion fantasies a possibility.)

The agency knew where to turn for a secure American source of supply. Eli Lilly and Co., the giant drug manufacturer, was already involved in LSD research on behalf of the U.S. government. The trouble was that LSD was expensive, and all roads led to Sandoz Laboratories in Switzerland. Organic LSD had to be painstakingly extracted from ergot, a fungus that grows in kernels of rye. Eventually, Sandoz and Eli Lilly successfully synthesized LSD in their own laboratories. With the advent of a reliable domestic supplier of synthetic LSD, the CIA under Allen Dulles was assured of a steady source for experimental purposes.

When LSD did not pan out as a reliable agent of interrogation, CIA investigators turned their attention to its purported ability to mimic acute psychosis—its “psychomimetic” aspect—which researchers were praising as a new avenue toward a biological understanding of schizophrenia. The CIA funneled grant money for LSD research into the academic and commercial R&D world through a host of conduits. Various experiments with non-consenting subjects—typically military or prison personnel—showed that LSD could sometimes break down established patterns of thought, creating a “twilight zone” during which the mind was more susceptible to various forms of psychological coercion and control. Perhaps, under the influence of LSD, prisoners could be transformed into counter-espionage agents. It also occurred to the CIA that the same drug could be used on their own agents for the same purposes. Numerous CIA agents took LSD trips in order to familiarize them with acid’s Alice-in-Wonderland terrain. Some of these unusual experiments were captured on film for use in military training videos.

One place where ARTICHOKE research took place was the Addiction Research Centre at the Public Health Service Hospital in Lexington, Kentucky—the same hospital that specialized in the treatment of hardcore heroin addicts. Lexington was part hospital and part penitentiary, which made it perfect for human experimentation. The addict/inmates of Lexington were sometimes given LSD without their consent, a practice also conducted at the federal prison in Atlanta, and at the Bordentown Reformatory in New Jersey. 

In 1953, then-CIA director Allen Dulles authorized Operation MK-ULTRA, which superseded earlier clandestine drug investigations. Under the direction of Dr. Sidney Gottlieb, a chemist, the government began slipping LSD and other psychoactive drugs to unwitting military personnel. During a work retreat in Maryland that year, technicians from both the Army and the CIA were dosed without their knowledge, and were later told that they had ingested a mind-altering drug. Dr. Frank Olson, a civilian biochemist involved in research on biological warfare, wandered away from the gathering in a confused state, and committed suicide a few days later by leaping to his death from an upper floor of the Statler Hilton in New York City. The truth about Olson’s death was kept secret from his family, and from the rest of the nation, for more than twenty years. In 1966, LSD was added to the federal schedule of controlled substances, in the same category as heroin and amphetamine. Simple possession became a felony. The Feds had turned off the spigot, and the research came to a halt. Federal drug enforcement agents began showing up at the homes and offices of well-known West Coast therapists, demanding the surrender of all stockpiles of LSD-25. The original acid elite was being hounded, harassed, and threatened in a rancid atmosphere of pharmaceutical McCarthyism. Aldous Huxley, Humphrey Osmond, even father figure Albert Hoffman, all viewed these American developments with dismay. The carefully refined parameters and preparations, the attention to set and setting, the concerns over dosage, had gone out the window, replaced by a massive, uncontrolled experiment in the streets. Small wonder, then, that the circus atmosphere of the Haight-Ashbury “Summer of Love” in 1967 seemed so badly timed. Countercultural figures were extolling the virtues of LSD for the masses—not just for research, not just for therapy, not as part of some ancient religious ritual—but also just for the freewheeling American hell of it. What could be more democratic than the act of liberating the most powerful mind-altering drug known to man?

It is at least conceivable that researchers and clinicians eventually would have backed away from LSD anyway, on the grounds that the drug’s effects were simply too weird and unpredictable to conform to the rigorous dictates of clinical studies. Nonetheless, researchers had been given a glimpse down a long, strange tunnel, before federal authorities put an end to the research.

—Excerpted from The Chemical Carousel: What Science Tells Us About Beating Addiction

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

Interview with Deni Carise, Chief Clinical Officer of Phoenix House

Why addiction treatment works—if you let it.

This time around, our “Five-Question Interview” series features clinical psychologist Deni Carise, senior vice president and chief clinical officer at Phoenix House, a leading non-profit drug treatment organization with more than 100 programs in 10 states. Chances are, you may have seen or heard her already: Dr. Carise has been a guest commentator about drugs and addiction for Nightline, ABC’s Good Morning America, Fox News, and local New York media outlets. She is frequently quoted in US News and World Report and other periodicals, blogs at Huffington Post, and has also consulted for the U.N. Office on Drugs and Crime.

Dr. Carise earned her doctorate at Drexel University, and served as a post-doctoral fellow at the Center for Studies of Addiction at the University of Pennsylvania. Currently, she is also adjunct clinical professor in the University of Pennsylvania’s Department of Psychiatry. She has been involved with drug abuse treatment and research for more than 25 years, and has worked extensively in developing countries to integrate science-based drug treatments into local programs. She has worked with adults and adolescent populations including dually diagnosed clients, Native Americans, and with medical populations (including spinal cord-injured, cardiac care and trauma patients).

1. As chief clinical officer for Phoenix House Foundation, what's your job description?

Deni Carise: My main responsibility is to ensure that we provide the highest possible standard of care. This means making sure that treatment methods across our programs are consistent with the latest research, represent a variety of evidence-based practices, and are delivered with fidelity. I also collaborate on the implementation and evaluation of Phoenix House’s national and regional strategies to achieve clinical excellence. My home base is New York, but I work directly with all of our programs and regularly travel to our California, New England, Mid-Atlantic, Texas, and Florida regions. I also oversee the activities of our Family Services, Quality Assurance, Research, Workforce Development, and Training initiatives. Finally, I help Phoenix House spread awareness to the public about the need to reduce the stigma of addiction and to increase access to treatment services.

2. As a clinical psychologist, how did you become involved in drug and alcohol treatment and recovery?

Deni Carise: I actually became involved in the Substance Abuse Treatment (SAT) field prior to becoming a clinical psychologist. When I decided that I wanted to get sober, I got some help from a counselor. This counselor was so helpful to my recovery that I decided to become an SA counselor so that I could assist others on this journey. I was working as a model at that time, and there were a few aspects of that career that I didn’t like: First, it was very clear that I would become less valuable in my career as I got older; secondly, my value was exclusively based on appearance, not knowledge or skills; and finally, my work didn’t contribute to the greater good—that is, no one benefitted by my work. I wanted a new career where I would become more valuable as I got older and more experienced, and where my knowledge and skills would be of value. I also wanted to do something I felt was contributing to society. The SAT field seemed to fit all these criteria.

3. What makes it so difficult for people to accept the disease components of serious drug addiction?

Deni Carise: People have difficulty accepting the disease concept of addiction for three reasons. First, people believe addiction is self-induced; you wouldn’t have it if you didn’t use drugs, right? There is some truth to this, but of all those who try drugs, an estimated 5 to 10% (depending on the drug) will become addicted. There’s a reason why the other 90 to 95% don’t become addicted.

That brings us to reason #2: People generally don’t believe there is a genetic cause. It is now very clear that there is a genetic component to substance use disorders. For example, if a father is an insulin-dependent diabetic, the heritability estimates range from 70 to 90% likelihood that the man’s son will also be diabetic. For hypertension, the heritability estimates are from 25 to 50%, depending which study we look at. For alcohol, the estimates are 55 to 65% likelihood that a young man will be alcohol dependent if his father is. For opiate dependence, it’s 35 to 50%.

The third and probably most important reason is that people think calling addiction a disease absolves the substance abuser of responsibility for his or her actions. Nothing could be further from the truth. Those in recovery see the disease of alcoholism or addiction as a moral obligation to get well. If you know you have this disease and the only way to keep it under control is not to use alcohol or drugs, then that’s what you have to do.

4. Overall, treatment doesn't seem to be that effective. What's missing?

Deni Carise: I believe treatment is effective. We’re just expecting the wrong results. Substance abuse has the same characteristics as any chronic medical disorder. The problem is that we (society, families, even me) want addiction to respond to treatment as though it’s an acute medical problem, like a broken leg or appendicitis. If it were an acute problem, we could send our kids, loved ones, even ourselves to treatment for a set number of days (maybe 7, maybe 28) and leave the hospital or treatment facility with the condition cured—as we would after surgery for an appendicitis! I would love that.

Unfortunately, we’ve been measuring treatment success the same way we would for a surgical problem, even though substance abuse and dependence are, in fact, chronic problems. Think about this—substance abuse treatment success is often measured by symptoms, drug use, and life problems prior to treatment and again six months after treatment ends. Imagine if we measured success of diabetes treatment the same way. We would measure their blood sugar levels, weight, number of diabetic crises, and other related problems before treatment. Then we’d send them off to a treatment program where we would prescribe medications, maybe give them insulin, teach them about a good diet, discharge them (take away that treatment), and measure their blood sugar levels, weight, etc. six months after we stopped the medication. Do we really think that would work with diabetes? Then why would we think it would work with addiction?

As with all chronic disorders, there are no prolonged, symptom-free periods without continued attention and self-management of the illness. Just as some people with diabetes can manage their illness with behavioral changes such as making healthy decisions when offered cakes or cookies, or starting an exercise program, some people with substance abuse problems can control their symptoms by changing their behaviors. This means not being around others who use, making the right decisions when offered alcohol or drugs, etc. For those who can’t do this alone, there’s treatment to teach them how to manage their disease and there are medications to assist them. And I’m talking about the diabetic and the substance abuser.

So treatment can work, but, just like any chronic disease, there’s no quick fix.

5. You're committed to working with developing countries to bring scientifically valid treatment within reach of poorer populations. How is the effort going?

Deni Carise: I’ve been really lucky to be able to consult for numerous treatment systems, universities, and countries around the world—including training clinicians from Nigeria, Thailand, Egypt, Greece, Iran, Singapore, Brazil, China, Iraq, India, and other countries. It’s fascinating to see how different countries approach local substance abuse problems. Some countries have historically asserted that substance abuse is not a problem in their communities, so for them to offer treatment of any kind means they need to change their socipolitical stance. That doesn’t happen quickly. For one country, the diagnosis of AIDS among 7 substance abusers who had shared needles was the impetus to providing treatment.

Much of what I’ve done internationally involves cultural adaptations of standardized instruments or clinical tools (such as the Addiction Severity Index assessment tool) for use within various cultures. To do this, I typically meet with numerous staff who deliver direct services in the country. We go over each assessment question or worksheet item looking at what would make sense in their culture. Types of things that frequently need adapting are questions about education (not everyone has “high schools”), employment and income, demographic questions such as race categories, and all manner of expressions used to describe drugs and clinical symptoms. Then we pilot the new interview or service with some local clients and get their perspective and make a final version.

Much of this work has been funded by the United Nations Office on Drug Use and Crime, the National Institute on Drug Abuse and Office of National Drug Control Policy.

What is Brain Awareness Week?

Celebrate your sentience March 12-18.

Gather ‘round, children, and the Dana Foundation will tell you an amazing tale about… the You Man Brain…

Well, that is, the HUMAN brain—and the many ways of increasing understanding and awareness of this little three-pound marvel. Officially the brainchild of the Dana Alliance for Brain Initiatives in New York and the European Dana Alliance for the Brain, “Brain Awareness Week (BAW) is the global campaign to increase public awareness of the progress and benefits of brain research,” according to the BAW website.  

Founded in 1996, Brain Awareness Week is designed to unite partner organizations around the world “in a week-long celebration of the brain.” Partners include universities, hospitals, schools, government agencies, and service organizations. Partner organizations come up with creative and innovative community activities to educate people of all ages “about the brain and the promise of brain research.” For example, on Wednesday the Dana Alliance is sponsoring a “brain bee” at The Rockefeller University in New York City, where students from 21 area high schools will go head-to-head on their knowledge of neuroscience.

To see the full list of partnerships, from 41 countries, go HERE. For a list of events planned for the week, take a look HERE.  Events include open houses at neuroscience laboratories, special brain exhibitions at museums, displays and lectures at community centers, and workshops in the classroom.

If you’re feeling cocky, you can test your brain with several challenges at http://www.testmybrain.org/

Sadly, none of this hoopla will necessarily solve certain perennial brain conundrums, such as:

--If you can’t change your mind, how do you know you have one?

--Is that hole in a man’s penis really there to get oxygen to his brain?

--How can we believe that the brain is the most important organ, when the brain is the organ telling us that?

And finally, the one that keeps me awake at night:

-- How did the scarecrow know he didn't have a brain?

What Do Long Distance Running and Marijuana Have in Common?

Maybe it isn't endorphins after all.

[From time to time, I reprint earlier posts that have remained perennial favorites at Addiction Inbox. This one originally ran on August 4, 2010.]

What do long-distance running and marijuana smoking have in common? Quite possibly, more than you’d think. A growing body of research suggests that the runner’s high and the cannabis high are more similar than previously imagined.

The nature of the runner’s high is inconsistent and ephemeral, involving several key neurotransmitters and hormones, and therefore difficult to measure. Much of the evidence comes in the form of animal models. Endocannabinoids—the body’s internal cannabis—“seem to contribute to the motivational aspects of voluntary running in rodents.” Knockout mice lacking the cannabinioid CB1 receptor, it turns out, spend less time wheel running than normal mice. 

A Canadian neuroscientist who blogs as NeuroKuz suggests that “a reduction in CB1 levels could lead to less binding of endocannabinoids to receptors in brain circuits that drive motivation to exercise.” NeuroKuz speculates on why this might be the case. Physical activity and obtaining rewards are clearly linked. The fittest and fleetest obtain the most food. “A possible explanation for the runner’s high, or ‘second wind,’ a feeling of intense euphoria associated with going on a long run, is that our brains are stuck thinking that lots of exercise should be accompanied by a reward.”

In 2004, the British Journal of Sports Medicine ran a research review, “Endocannabinoids and exercise,” which seriously disputed the “endorphin hypothesis” assumed to be behind the runner’s high. To begin with, other studies have shown that exercise activates the endocannabinoid system.

“In recent years,” according to the authors, “several prominent endorphin researchers—for example, Dr Huda Akil and Dr. Solomon Snyder—have publicly criticised the hypothesis as being ‘overly simplistic,’ being ‘poorly supported by scientific evidence’, and a ‘myth perpetrated by pop culture.’” The primary problem is that the opioid system is responsible for respiratory depression, pinpoint pupils, and other effects distinctly unhelpful to runners.

The investigators wired up college students and put them to work in the gym, and found that “exercise of moderate intensity dramatically increased concentrations of anandamide in blood plasma.” The researchers break the runner’s high into four major components. Exercise, they say, “suppresses pain, induces sedation, reduces stress, and elevates mood.” Some of the parallels with the cannabis high are not hard to tease out: “Analgesia, sedation (post-exercise calm or glow), a reduction in anxiety, euphoria, and difficulties in estimating the passage of time.”

There are cannabinoid receptors in muscles, skin and the lungs. Intriguingly, the authors suggest that unlike “other rhythmic endurance activities such as swimming, running is a weight bearing sport in which the feet must absorb the ‘pounding of the pavement.’” Swimming, the authors speculate, “may not stimulate endocannabinoid release to as great an extent as running.” Moreover, “cannabinoids produce neither the respiratory depression, meiosis, or strong inhibition of gastrointestinal motility associated with opiates and opioids. This is because there are few CB1 receptors in the brainstem and, apparently, the large intestine.”

A big question remains: What about running and the “motor inhibition” characteristic of high-dose cannabis? (An inhibition that may make cannabis useful in the treatment of movement disorders like tremors or tics.) Running a marathon is not the first thing on the minds of most people after getting high on marijuana.  The paper maintains, however, that at low doses, “cannabinoids tend to produce hyperactivity,” at least in animal models. The CB1 knockout mice were abnormally inactive, due to the effect of cannabinoids on the basal ganglia. Practiced, automatic motor skills like running are controlled in part by the basal ganglia. The authors predict that “low level skills such as running, which are controlled to a higher degree by the basal ganglia than high level skills, such as basketball, hockey, or tennis, may more readily activate the endocannabinoid system.”

The authors offer other intriguing bits of evidence. Anandamide, one of the brain’s own cannabinoids, “acts as a vasodilator and products hypotension, and may thus facilitate blood flow during exercise.” In addition, “endocannabinoids and exogenous cannabinoids act as bronchodilators” and could conceivably facilitate breathing during steady exercise. The authors conclude: “Compared with the opioid analgesics, the analgesia produced by the endocannabinoid system is more consistent with exercise induced analgesia.”

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

Night Owls Get a Coffee Break

“Morning people” have more caffeine-related sleep problems.

Let me start by saying that I love this caffeine study for personal reasons. As a lifelong night owl, I have been chastised by wife, family, and friends over the years for my regular habit of drinking coffee after 10 pm. (And falling easily asleep two or three hours later, if I choose to.) Other coffee drinkers have told me how rare and weird this is. If we have a cup, they tell me, or even an afternoon sip, we toss and turn all night.

As it turns out, I was talking to the wrong kind of coffee drinkers. I needed to consult my crowd, and that’s what I did. I checked in with a few confirmed fellow night owls, and yes, a few of them reported that they had no problems going to sleep after a late night cup or two.

Anecdotal, of course—but a recent clinical study published in Sleep Medicine backs me up. The study, “Modeling caffeine concentrations with the Stanford Caffeine Questionnaire: Preliminary evidence for an interaction of chronotype with the effects of caffeine on sleep,” sets out to examine the effects of caffeine on the sleep patterns of college students. Researchers at Stanford told the students to keep sleep logs and to wear an actigraphy wristband to record rest/activity cycles. The students filled out daily questionnaires about their caffeine intake at different times of the day, and gave saliva samples for caffeine assessments.

 The scientists were able to accurately predict salivary caffeine concentrations based on the questionnaires, which was the primary intent of the study. But in the process, they discovered what they believe to be “a novel relationship between the effects of caffeine on sleep and genotype and chronotype.” What the researchers ended up with was some seriously suggestive evidence about the relationship of caffeine and natural sleep rhythms. (Here’s a nifty little test to determine whether you are a lark or an owl, i.e., your chronotype.)

Typically, clinical trials with caffeine are limited to the basic question: How much coffee did you drink today? But the Stanford researchers wanted to include the many variables that modulate caffeine intake—things like the timing of ingestion, the variations in the amount of caffeine among beverages, individual variations in caffeine metabolism, and the wide differences in half-life that caffeine can exhibit under various circumstances. They attempted to establish the students’ genotypes for adenosine receptors, where caffeine does most of its work, and to select volunteers who had “statistically indistinguishable” differences in adenosine receptor gene frequencies.

As you might expect, even among students, caffeine intake progressively decreased throughout the day in the study group. However, a small number of participants continued their intake of caffeine well into the night. The metric known as “wake after sleep onset,” or WASO, was used as the primary measurement of sleep disruption. “Our data indicate caffeine strongly influences WASO in those who self-identify as morning-type,” the researchers found. “It affects WASO less so in those who are neither type, and does not appear to affect WASO in those who are evening-type. To our knowledge, there have been no previous reports linking the effects of caffeine and chronotype.”

Some warnings on the study: It involved only 50 college students. And they were students, meaning their schedules were highly erratic by definition, and they were chronically sleep-deprived by habit. The study authors attempted to turn this defect into a virtue, noting that “the students were under such homeostatic pressure that their mood had little effect on their sleep.” Nonetheless, we will need to see if the findings hold up using less, er, unpredictable subjects.

If they do hold up, it will make it easier for people to understand the homily delivered by the coffee-drinking grandmother of a friend of mine: “The only time coffee ever kept me awake was when I knew there was another cup in the pot.”

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

Nova, P., Hernandez, B., Ptolemy, A., & Zeitzer, J. (2012). Modeling caffeine concentrations with the Stanford Caffeine Questionnaire: Preliminary evidence for an interaction of chronotype with the effects of caffeine on sleep Sleep Medicine DOI: 10.1016/j.sleep.2011.11.011

The Black Bag: Odds and Ends

Drug news from the world of science and medicine.


--How Marijuana Impairs Memory

Mo Costandi at the UK Guardian expands on his Nature article about the mechanisms that result in memory impairment when people smoke marijuana. Memory formation depends on the neurotransmitter glutamate. What goes wrong when you smoke pot? Enter the astrocyte…

--Coffee Will Disrupt Your Sleep—Unless You’re a Night Owl

From Scientific American comes the news that your “chronotype”—the chronological patterns you naturally favor—may determine whether or not caffeine keeps you tossing and turning and night. Morning people, or “larks,” had more periods of wakefulness during sleep hours than night people, or “owls.” The findings, published in the journal Sleep Medicine, show that “for the early risers, the more caffeine in their bodies, the more time they spent awake during the night after initially falling asleep. This was not seen in the night owls.”

--Brain Scans Get Better

You wouldn’t know it from all the bad press about moving heads and specious interpretations, but fMRI technology continues to improve. Time Healthland reports that new machines will be able to do a better job spotting traumatic brain injury in military personnel, athletes, and accident victims. High-definition fiber tracking, as this article in the Journal of Neurosurgery explains, will allow medical staff to better assess damage to nerve fibers deep in the brain, due to technological improvements in “assessing white matter injuries that are not apparent in standard anatomical imaging.”

--Cig Makers Trump FDA on Free Speech Grounds

The FDA maybe didn’t think this one through quite as thoroughly as they should have. Reuters reports  that a U.S. judge “sided with tobacco companies on Wednesday, ruling that regulations requiring large graphic health warnings on cigarette packaging and advertising violate free-speech rights under the U.S. Constitution.” Evidently, FDA officials didn’t see the 1st Amendment argument coming. By mandating grisly pictures of diseased lungs, rotting teeth, and dying smokers on cigarette packs, “the government has failed to carry both its burden of demonstrating a compelling interest and its burden of demonstrating that the rule is narrowly tailored to achieve a constitutionally permissible form of compelled commercial speech," U.S. District Judge Richard Leon said.

--Meth Head Burns Down Tree Older Than Jesus

And finally, as if we needed any more evidence, here’s a story about bad decision-making among the meth head crowd: WFTV reports that a female meth addict in Seminole County, Florida, burned down a historic cypress believed to have been the world’s 5th oldest tree. Authorities learned that the woman and a friend had been cooking methamphetamine under the 3,500 year-old tree. Officials said the woman took pictures of the disaster with her cell phone, and was quoted saying: "I can't believe I burned down a tree older then Jesus."

Photo Credit: http://www.squidoo.com 

Is Gambling the Opiate of the Masses?

 
Two new books tackle gambling’s addictive mysteries.

Charles Fey, the American who invented the three-reel slot machine in 1898, is a well-known part of gambling history. But few people have heard of Inge Telnaes, the mathematician credited with the invention of the “virtual reel” almost 90 years later, in 1984. The virtual reel worked like this: The Telnaes patent allowed slot machine makers to store the various symbols on the spinning reels as digital data on microprocessor chips. After that, random number generating software produced the actual results in the form of three-symbol sets. So far so good. But inherent in the process was another step—the “virtual stop.” And this idea was a real killer. As gambling guru Donald Catlin wrote at Casino City Times:

Virtual reels contained more stops than were contained on the real reels, which meant that the probability of a particular symbol appearing on the pay line had nothing to do with its frequency on the real reels and everything to do with its frequency on the virtual reels.  If this seems deceptive to you, consider the following quote taken from the Telnaes patent submission: "Thus, it is important to make a machine that is perceived to present greater chances of payoff than it actually has within the legal limitations that games of chance must operate."

Pretty straightforward. You could program a thousand stops per reel, if you wanted to. The advantage was that you could post huge jackpots without the fear of anyone hitting them very often, because when gamblers thought about a line of 7s on those three reels, they were in fact facing many more spin combinations than they realized.

But I digress. We all know the house wins. Gamblers know it, too. Gambling can be defined as an activity in which something of value is put at risk in a situation where the outcome is uncertain. That’s really all there is to it. And for most people, it all adds up to little more than an evening of escapist fun.

So how do pathological gamblers gets so turned around? Viewing their behavior from the outside, it’s hard to have sympathy with them—the same way it can be hard to have sympathy for alcoholics. Willful self-destruction often looks like the only way to account for it. 

Heavy gamblers, the kind of gamblers who get into major debt, are people who get an unnatural buzz out of winning and losing money. Like most things having to do with addiction, it’s complicated, and involves a spiral of negative, damaging behavior that transcends bad habits or lack of self-control. They’re the ones in the casinos well past midnight, drink in hand, cigarette burning in the ashtray, and perhaps making the occasional sprint to the restroom for a snort of cocaine or meth. Slot attendants tell stories about gamblers who would rather urinate in their clothes than leave a machine. What, exactly, accounts for that kind of behavior?

For one thing, gambling and alcohol go together like…. cigarettes and alcohol. Gambling is being proposed as an addition to the bible of psychiatry, the DSM-5. All three habits often function together as a set of multiple addictions. The reason for this may be biological. Consider the unexpected side effects caused by certain dopamine-active medications for Parkinson’s. Some seniors who take the drugs begin to feel an uncontrollable urge to, that’s right, go to the casino and gamble. They prefer slot machines, and sometimes lose a lot of money. When they go off the medications, they lose interest in their new hobby—which lends a certain weight to the argument that some compulsive gamblers act the way they do because of innate biochemical dysfunctions. They do it, Howard Shaffer believes, because gambling is one manifestation of the disease he calls “addiction syndrome.”

Howard J. Shaffer and Ryan Martin, writing in the Annual Review of Clinical Psychology, note that just as there are divisions between alcoholic drinking, heavy drinking, and social drinking, there are also differences between pathological gambling, excessive gambling, and social gambling. Pathological gambling has proven to be “a more complex and unstable disorder than originally and traditionally thought.” Once the neurophysiology of the gambling state of mind came under scrutiny, the parallels with addiction cropped up everywhere. Shaffer, a professor of psychiatry at Harvard Medical School and director of the Division on Addiction at Cambridge Health Alliance  (see my interview with him here), notes that “the rate of pathological gambling in America has remained relatively constant for the past 35 years, despite a huge expansion in the opportunities on offer.” 

Change Your Gambling, Change Your Life, by Howard Shaffer, written with Ryan Martin, John Kleschinsky, and Liz Neporent, follows a relaxed workbook approach to problem gambling. Perhaps the most useful aspect of the book’s organization is its division into what we could call co-morbid chapters. Gamblers with anxiety, mood disorders, impulse control problems, or drug addictions each warrant their own section of the book, in order to personalize the advice. Organized in this way, the authors explicitly recognize the likelihood that problem gamblers do not normally suffer the condition in isolation from other mental health and substance use issues.

Shaffer gives a variety of useful advice concerning triggers, and methods for controlling urges. He believes that the risk of developing addiction syndrome involves “a complex interaction of genetic, psychological, social, and other factors.” Shaffer estimates that about two million Americans suffer from some level of addictive gambling disorder, with another 3.5 million gamblers with problem behaviors that don’t meet the addictive threshold.

In fact, the overlap between problem gambling, mental health problems, and other forms of addiction is staggering. According to numbers from the National Epidemiologic Survey on Alcohol and Related Conditions cited in the book, more than 11 percent of heavy gamblers suffer from generalized anxiety disorder; up to 50 percent have exhibited mood disorders; 40 percent qualified for an impulse control disorder; and 50 percent can be classified as “alcohol dependent."

Professor Shaffer takes a nonjudgmental stance on the question of moderation versus abstinence, while cautioning the problem gambler about the realities of having “the self-control to bet a little when he has the urge to bet a lot.” To attempt moderation, a gambling addict (or alcoholic for that matter) must be willing to accept the consequences of being unsuccessful. However, some research shows that those who engaged in disordered gambling “move on from excessive gambling to less gambling over time,” according to Shaffer. There may be a simple explanation for this: “Many people with gambling disorders eventually run out of money.” (Back when I used to gamble regularly in casinos, I often joked that there was nothing quite like the uneasy thrill of risking money you really couldn’t afford to lose.)

But if you are serious about quitting, warns Shaffer, “you also need to be prepared for people who, for their own selfish reasons, deliberately entice you to gamble.” Really? This may sound unlikely, but I recall that in my own case, when I first stopped drinking, an older friend used to pour me drinks and leave them nearby—just in case I came to my senses. If you are a gambling addict, and know it, there are self-exclusion programs at most casinos, designed to allow gamblers to bar themselves for a specified period, in an arrangement rather like Linus and his blanket.

Shaffer also points to continuing work on various drugs for problem gamblers. Naltrexone, used for opiate and alcohol addiction, is one such candidate. (A University of Minnesota study showed that 40 percent of pathological gamblers abstained from gambling for at least a month while taking naltrexone.) So is nalmefene, which also operates on opiate brain receptors. Other medications under study include common SSRI antidepressants like Prozac and Celexa.

Change Your Gambling, Change Your Life is a structured, clearly written, nonjudgmental approach for motivated people wishing to deal seriously with their “disordered gambling.”
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Another book on gambling turned up in the book bag recently. In his e-book called Slots: Praying to the God of Chance, David V. Forrest, M.D., notes that casinos can clear as much as $2,500 per day from a popular slot machine. Not considered sexy or the domain of the high roller, slot machine action accounts for roughly 70 to 80 % of casino income. To attract young players, who tend to favor table games, slot machine manufacturers are experimenting with joysticks and a dollop of skill-based play—but it’s not clear, says Forrest, that older, established slot players want to substitute “a competitive mind-set for the meditative trance induced by the random spinning and stopping of the reels.” (Note: The last time your humble narrator played the slots in Las Vegas, the spinning induced an attack of intense vertigo and dizziness due to a chronic ear disorder. Talk about negative conditioning.)

How do you know if you’re a slot addict, like former Drug Czar William Bennett? “Looking forward to slot playing as the best thing in your future is not a good sign,” Forrest helpfully suggests. One casino on the East Coast uses the ominous advertising tag line: “You’ll Come Back.” Forrest mischievously notes that both “the American Psychiatric Association and the American College of Psychiatrists have traditionally refused to hold their annual conventions in Las Vegas for fear of seeming to endorse a behavior that can become pathological.”

Here are some of Dr. Forrest’s suggestions for the problem gambler:

-- Avoid playing alone.

--Play out your time, not your money.

--Break the hypnotic spell through thought and activity.

--Beware the dangers of comorbidity.

With this final admonition, Dr. Forrest lines up squarely with Howard Shaffer: “In my psychiatric experience,” he writes, “some of the most defenseless to the excesses of gambling have been bipolar patients in the manic phase of their illness.”

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