How Many Calories in Your Daily Alcohol?

Booze as food.

Everywhere we turn, the news is packed with stories about the nation’s obesity epidemic. But one little-discussed fact about our daily calorie count is that Americans consume an average of 100 calories each day from alcohol, according to new numbers from the U.S. National Center for Health Statistics (NCHS).

The center, which is part of the Centers for Disease Control and Prevention, said that on a daily basis, about 33 % of men and 18% of women consume alcohol calories daily. Men, who drink more than women, account for 150 daily calories, on average. Women consume a little over 50 calories in the form of alcohol, or roughly half a glass of wine. Predictably, the hardest-drinking cohort was men aged 20-39, who accounted for about 175 calories on daily average.

That may not sound like much—and it is generally within the normal moderation guidelines of one drink per day for women and two drinks for men. However, among members of the study group, about one in five men, and 6% of the women, consumed more than 300 alcohol calories daily—three drinks or more. Considering that the average daily per capita calorie consumption was about 2,500 calories in 2008, according to USDA estimates, this category of drinker can easily end up downing 15% or more of the daily caloric intake in the form of alcohol. The report notes that government dietary guidelines for “solid fats and added sugars”—the  broad category into which alcohol falls—should represent “no more than 5%-15% of calories,” no matter what the overall level of calorie intake.

“A lot of people don’t think about the calories in the alcoholic beverages,” Cynthia Ogden, one of the researchers, told USA Today. “It’s not a diet soda.” Even a shooter of hard liquor, hold the mixer, will run 50-90 calories.  A 12-oz Coke and a 12-oz beer both contain about 150 calories. “We’ve been focusing on sugar-sweetened beverages. This is something new,” said Ogden in an AP article, prompting the unnamed AP writer to ask: “Should New York officials now start cracking down on tall-boy beers and monster margaritas?”

But the Distilled Spirits Council, the lobbying group for hard liquor, saw the silver lining in the research: “The overwhelming majority of adults drink moderately.”

Nonetheless, nutrition policy director Margo Wootan of the Center for Science in the Public Interest told AP she was disappointed that the Obama administration plans to exempt alcoholic drinks from upcoming federal rules mandating calorie labeling on restaurant menus. Customers will be able to see the number of calories in a flavored ice tea drink, but not the calorie count for a Long Island Iced Tea, with easily four times as many calories.

The NCHS Data Brief also found that “no significant differences were observed in average calories per day from alcoholic beverages consumed by non-Hispanic white, non-Hispanic black, and Hispanic persons.” In addition, those in the highest income category drank more than those whose income was at or below the poverty line. Men preferred beer, and women preferred wine.

The study was based on data from the National Health and Nutrition Examination Survey for 2007-2010. Researchers collected data through in-home interviews and at a mobile examination center. The researchers oversampled population subgroups to obtain reliable estimates of nutritional measures in those cohorts.

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

Weight Loss Redux

Why diet pills are problematic.

"Physicians who treat obesity hailed the Food and Drug Administration's recent approval of two new diet drugs—the first in 13 years—as a new era in weight-loss management."
--Wall Street Journal, July 30, 2012

 (The following post was originally published on September 20, 2011)

It took many years to bring depression and its treatment into the rational light of day. Addiction in the mid-1990s was in the process of undergoing a similar medical transformation. Even so, scientists were wary of pronouncing that overeating was in some cases a treatable chemical disorder.

Obesity, in any form other than pituitary cases, was not typically considered a medical disorder at all. In a 1998 interview with MIT’s student newspaper, The Tech, neurology professor Richard Wurtman recalled that ten years earlier, the major drug companies had shown little interest in a drug treatment for obesity: “They thought that if you were obese, it was your fault.” It was the same view that had prevailed concerning depression, alcoholism, and other drug addictions. Bulimia and carbohydrate craving were no different: a simple failure of will was once thought to explain them all. But everything changed when the serotonin-boosting diet pill called Redux (dexfenfluramine) won full FDA approval in 1996. Redux was the first drug ever approved in the U.S. for the long-term treatment of obesity.

In truth, Ely Lilly and Company did move forward with earlier efforts to win approval of high-dose Prozac for weight loss. That petition had been languishing in the FDA pipeline for years under the trade name Lovan. Back in the late 1980s, when Eli Lilly scientists were investigating rats that consumed fewer calories on fluoxetine, the company called upon Dr. Richard Wurtman, the MIT brain scientist who specialized in the connection between serotonin levels and carbohydrate intake. Scientists at Lilly had become increasingly concerned that the weight loss from Prozac was short-lived, and the mechanism of action remained maddeningly imprecise. For more than a decade, Eli Lilly had pursued Prozac along three separate but related lines of development: depression, weight control, and alcoholism. If you took it for depression, and it worked, you might also lose a few pounds, and drink less. If you took it for bulimia or weight loss, you might also feel better emotionally, and drink less. When the FDA made encouraging noises about Prozac as a new front-line treatment for bulimia in 1994, Eli Lilly followed that indication to market, and again chose not to follow up on weight loss or alcoholism.

Eli Lilly was no longer interested, but Richard and Judith Wurtman were undeterred. As it happened, the couple had already patented a serotonin-active drug of their own—dexfenfluramine—which French laboratories had been testing as a weight loss pill. The Wurtmans went public with a new company, Interneuron Pharmaceuticals, and filed with the FDA to market their weight-loss remedy. The Wurtmans became instant millionaires on paper.

“Diet pills” had always had a somewhat unsavory reputation. Typically, they were amphetamines, or the near-beer equivalent, ephedrine—and neither compound was anything like a healthy long-term answer to chronic overeating. The serotonin-active drugs were a new class of medications altogether. Dexfenfluramine wasn’t addictive, any more than Prozac was addictive. Moreover, fenfluramine was specifically intended for use by people suffering from carbohydrate-craving obesity. But would doctors be able to resist the demands of other patients who just wanted to trim off a few pounds?

Initially, the Wurtmans licensed the serotonin-active weight loss drug to several marketers in Europe, where it met with initial success. After a few small-scale studies, Rochester University in New York published a report showing that the weight loss effect was enhanced when fenfluramine was combined with a drug called phentermine. The resulting combination was widely known as “phen-fen.” As with Prozac, dexfenfluramine was tested as an anti-obesity medication at dosages several times higher than the amount typically prescribed for depression.

Early red flags were raised when Johns Hopkins researchers reported some cases of neurological toxicity in monkeys on dexfenfluramine, but MIT, which shared patent rights with the Wurtmans, was understandably enthusiastic when Redux, as dexfenfluramine became known, won full FDA approval in 1996.

And for many people, Redux worked. In the first six months after its approval, physicians wrote at least two million prescriptions for Redux. The phen-fen combination swept the weight loss industry. Estimates of total users of phen-fen ran as high as six million in the U.S. alone. Doctors and weight loss clinics sometimes prescribed Redux, sometimes the phen-fen combination. Initial earnings estimates were running as high as $600 million a year for the Redux portion of phen-fen, netting MIT between one and five per cent of the royalties.

The euphoria didn’t last long. By the time Redux made the cover of Time, researchers were already rumbling about continued reports of high toxicity and hypertension in rat studies. In addition, the serotonin surge associated with the use of dexfenfluramine caused concerns about pulmonary hypertension. In August of 1997, doctors at the Mayo Clinic in Minnesota reported serious heart valve abnormalities in 24 women taking the phen-fen combination.

A month later, at the FDA’s request, phen-fen and Redux were permanently pulled off the market.  In 2002, American Home Products settled a class action suit on behalf of almost 300,000 phen-fen users for $3.75 billion. As class action suits go, this put it right between the $2.4 billion Dalkon Shield settlement and the $4.5 billion breast implant accords.

What went wrong? Researchers now believe that the two drugs, which were never offered for sale as a single pill, should never have been combined in the first place. Somehow the fact that the phen part of the combination allegedly acted as an MAO inhibitor, and hence should not have been combined with yet another serotonin-enhancing medication, escaped notice. The combination of the two drugs apparently raised blood plasma levels of serotonin to abnormal levels. Too much serotonin in the bloodstream can damage blood vessels in the heart and lungs. Other suspected MAO inhibitors, like St. John’s Wort, or the Chinese herbal remedy ma huang, would not have combined well with Redux or phen-fen, either. Referring to the casual use of Ecstasy, Dr. Rick Doblin drew a parallel with phen-fen in the autumn 1995 issue of the Multidisciplinary Association for Psychedelic Studies (MAPS):

This use of MDMA, though not conducted in the context of a scientifically controlled experiment, does provide an opportunity for a very large epidemiological study. Similarly, over fifty million people have tried a prescription drug called fenfluramine, a diet aid prescribed for daily use for months or years at a time that causes the same kind of neurotoxicity in animals as does MDMA.

The phen-fen disaster highlighted the need to investigate drug synergies thoroughly before combining them as a pharmacotherapy. The phen-fen heart and lung damage may have been related to a potentially toxic condition known as “serotonin syndrome.”

And the Wurtmans? Ironically, Richard and Judith Wurtman had patented the use of Prozac for severe PMS years earlier, and ultimately sublicensed the rights back to Eli Lilly for several million dollars. Eli Lilly disguised the fact that their PMS drug was a case of old wine in new bottles. As Wellbutrin had become Zyban, so Prozac metamorphosed into Serafem, when prescribed for premenstrual syndrome.

Photo Credit: http://www.drugnet.net/

The Truth About Weight Loss Surgery and Alcohol

Bariatrics and booze don’t always mix.

For many people with obesity, bariatric surgery has proven to be a lifesaver. But for a subset of post-operative patients, the price for losing five pounds every time you step on the scale turns out to be an increased appetite for alcohol.

In a study of almost 2,000 patients who underwent surgery for severe obesity, the patients had either gastric bypass surgery (RYGB) in which a portion of the stomach and small intestine are removed, or gastric banding, a process by which an adjustable “lap band” is tightened around the entrance to the stomach. Those who opted for gastric bypass showed an increase in alcohol consumption two years after surgery, according to a recent study by Wendy C. King and coworkers in the Journal of the American Medical Association.

The notion that weight loss surgery, known as bariatric surgery, was related to increased use of alcohol had been an anecdotal staple among patients with obesity for years. Oprah Winfrey based one of her daytime television shows on the rumor back in 2006. Dr. King and a diverse group of associates concluded last month at the American Society for Metabolic and Bariatric Surgery annual meeting that “a significantly higher prevalence of alcohol use disorder” was associated with the second year following gastric bypass surgery. (During the first postoperative year, patients are strongly advised not to drink at all.)

Moreover, some of the patients who showed high-risk alcohol intake had not been problem drinkers before surgery. Some had not been drinkers at all. But the effects of gastric bypass, coupled with permission to drink a year after surgery, lead to an increase in alcohol abuse and alcoholism. While the overall increase was relatively modest, patients who had gastric bypass surgery were twice as likely to drink heavily than patients who underwent the lap band procedure.

“It’s a great study,” says Dr. Stephanie Sogg, staff psychologist at the Massachusetts General Hospital Weight Center and assistant professor in the Department of Psychiatry at Harvard Medical School, who was not associated with the study group. In an interview for this article, Sogg called the distinction between surgeries “an extremely important finding. They saw changes in alcohol use patterns with gastric bypass, but not with gastric banding. That’s exactly what we would expect.”

The findings make biochemical sense: “Gastric bypass surgery bypasses a part of the stomach that secretes alcohol dehydrogenase,”—a primary enzyme of alcohol metabolization, says Sogg. “And in gastric bypass, the alcohol is not coming into contact with the first part of the intestine, the duodenum. That’s going to cause some changes in the way the body processes alcohol that aren’t true of gastric banding. If this were a case of people who are addicted to food having to change their eating and thus becoming addicted to alcohol, we would expect to see the same changes whether the person had gastric bypass or gastric banding.”

It would be natural to assume that people with prior drinking problems would have the most trouble with alcohol control postoperatively. But things are rarely that simple in medicine. “Previous alcohol history sets up people for risk of relapse, but there’s a significant subset of people having trouble with alcohol who never drank at all,” says Dr. Sogg. “That’s where the real story is.”

Dr. David B. Sarwer, associate professor of psychology and director of clinical services for the Center for Weight and Eating Disorders at the University of Pennsylvania, called the King study “the most definitive evidence to date on the prevalence of alcohol use disorders in persons who undergo bariatric surgery.” In an email exchange, Sarwer said: “Individuals with a history of alcohol or substance abuse are informed that the stress of the dietary and behavioral requirements of bariatric surgery, like all major life stressors, could threaten their sobriety or abstinence. However, we simply do not know enough about the use of alcohol and other substances after surgery to predict this with a great degree of certainty.”

Dr. Sogg agrees. For the bariatric surgery population, the pharmacokinetics of alcohol changes. They become more sensitized to its effects—a little now goes a long way. The main problem, she says, is that “we’re not good yet at predicting exactly whom it’s going to happen to.”

But she has some thoughts about vulnerable subsets. “Some people with obesity have poor coping skills,” she says. “And now alcohol is so much more potent and reinforcing for them that alcohol becomes the coping strategy. When this biological change with alcohol happens, they may be the ones who are at higher risk of responding to that change by developing problems with alcohol.”

Warning patients about alcohol risks of weigh-loss surgery is becoming more common, says Dr. Sogg. “It doesn't change my decision-making about whether somebody should or shouldn't have surgery. But we can evaluate people's coping skills before surgery and point out to them that it is important for them to develop other ways of dealing with negative emotions besides eating." 

She also thinks that “people who have a history of actually becoming abstinent after drug or alcohol dependence may be better equipped for surgery. They will be less likely to put themselves in the path of alcohol use, and they have experience at making major successful long-term behavior changes. Basically, we should not consider past encounters with substance abuse as contraindications for surgery. But we should be carefully evaluating whether people are currently using substances at the time of surgery.”

In the end, she said, “I tell every one of my patients before surgery that they need to be aware of the risks of problem drinking after surgery, monitor their alcohol intake, and come back to us immediately at the first sign of any concerns about their drinking.”

King WC, Chen JY, Mitchell JE, Kalarchian MA, Steffen KJ, Engel SG, Courcoulas AP, Pories WJ, & Yanovski SZ (2012). Prevalence of Alcohol Use Disorders Before and After Bariatric SurgeryAlcohol Use Disorders and Bariatric Surgery. JAMA : the journal of the American Medical Association, 1-10 PMID: 22710289

 Photo credit: http://www.treatment4addiction.com/

The Saga of Phen-Fen

How a blockbuster diet pill died.

It took many years to bring depression and its treatment into the rational light of day. Addiction in the mid-1990s was in the process of undergoing a similar medical transformation. Even so, scientists were wary of pronouncing that overeating was in some cases a treatable chemical disorder.

Obesity, in any form other than pituitary cases, was not typically considered a medical disorder at all. In a 1998 interview with MIT’s student newspaper, The Tech, neurology professor Richard Wurtman recalled that ten years earlier, the major drug companies had shown little interest in a drug treatment for obesity: “They thought that if you were obese, it was your fault.” It was the same view that had prevailed concerning depression, alcoholism, and other drug addictions. Bulimia and carbohydrate craving were no different: a simple failure of will was once thought to explain them all. But everything changed when the serotonin-boosting diet pill called Redux (dexfenfluramine) won full FDA approval in 1996. Redux was the first drug ever approved in the U.S. for the long-term treatment of obesity.

In truth, Ely Lilly and Company did move forward with earlier efforts to win approval of high-dose Prozac for weight loss. That petition had been languishing in the FDA pipeline for years under the trade name Lovan. Back in the late 1980s, when Eli Lilly scientists were investigating rats that consumed fewer calories on fluoxetine, the company called upon Dr. Richard Wurtman, the MIT brain scientist who specialized in the connection between serotonin levels and carbohydrate intake. Scientists at Lilly had become increasingly concerned that the weight loss from Prozac was short-lived, and the mechanism of action remained maddeningly imprecise. For more than a decade, Eli Lilly had pursued Prozac along three separate but related lines of development: depression, weight control, and alcoholism. If you took it for depression, and it worked, you might also lose a few pounds, and drink less. If you took it for bulimia or weight loss, you might also feel better emotionally, and drink less. When the FDA made encouraging noises about Prozac as a new front-line treatment for bulimia in 1994, Eli Lilly followed that indication to market, and again chose not to follow up on weight loss or alcoholism.

Eli Lilly was no longer interested, but Richard and Judith Wurtman were undeterred. As it happened, the couple had already patented a serotonin-active drug of their own—dexfenfluramine—which French laboratories had been testing as a weight loss pill. The Wurtmans went public with a new company, Interneuron Pharmaceuticals, and filed with the FDA to market their weight-loss remedy. The Wurtmans became instant millionaires on paper.

“Diet pills” had always had a somewhat unsavory reputation. Typically, they were amphetamines, or the near-beer equivalent, ephedrine—and neither compound was anything like a healthy long-term answer to chronic overeating. The serotonin-active drugs were a new class of medications altogether. Dexfenfluramine wasn’t addictive, any more than Prozac was addictive. Moreover, fenfluramine was specifically intended for use by people suffering from carbohydrate-craving obesity. But would doctors be able to resist the demands of other patients who just wanted to trim off a few pounds?

Initially, the Wurtmans licensed the serotonin-active weight loss drug to several marketers in Europe, where it met with initial success. After a few small-scale studies, Rochester University in New York published a report showing that the weight loss effect was enhanced when fenfluramine was combined with a drug called phentermine. The resulting combination was widely known as “phen-fen.” As with Prozac, dexfenfluramine was tested as an anti-obesity medication at dosages several times higher than the amount typically prescribed for depression.

Early red flags were raised when Johns Hopkins researchers reported some cases of neurological toxicity in monkeys on dexfenfluramine, but MIT, which shared patent rights with the Wurtmans, was understandably enthusiastic when Redux, as dexfenfluramine became known, won full FDA approval in 1996.

And for many people, Redux worked. In the first six months after its approval, physicians wrote at least two million prescriptions for Redux. The phen-fen combination swept the weight loss industry. Estimates of total users of phen-fen ran as high as six million in the U.S. alone. Doctors and weight loss clinics sometimes prescribed Redux, sometimes the phen-fen combination. Initial earnings estimates were running as high as $600 million a year for the Redux portion of phen-fen, netting MIT between one and five per cent of the royalties.

The euphoria didn’t last long. By the time Redux made the cover of Time, researchers were already rumbling about continued reports of high toxicity and hypertension in rat studies. In addition, the serotonin surge associated with the use of dexfenfluramine caused concerns about pulmonary hypertension. In August of 1997, doctors at the Mayo Clinic in Minnesota reported serious heart valve abnormalities in 24 women taking the phen-fen combination.

A month later, at the FDA’s request, phen-fen and Redux were permanently pulled off the market.  In 2002, American Home Products settled a class action suit on behalf of almost 300,000 phen-fen users for $3.75 billion. As class action suits go, this put it right between the $2.4 billion Dalkon Shield settlement and the $4.5 billion breast implant accords.

What went wrong? Researchers now believe that the two drugs, which were never offered for sale as a single pill, should never have been combined in the first place. Somehow the fact that the phen part of the combination allegedly acted as an MAO inhibitor, and hence should not have been combined with yet another serotonin-enhancing medication, escaped notice. The combination of the two drugs apparently raised blood plasma levels of serotonin to abnormal levels. Too much serotonin in the bloodstream can damage blood vessels in the heart and lungs. Other suspected MAO inhibitors, like St. John’s Wort, or the Chinese herbal remedy ma huang, would not have combined well with Redux or phen-fen, either. Referring to the casual use of Ecstasy, Dr. Rick Doblin drew a parallel with phen-fen in the autumn 1995 issue of the Multidisciplinary Association for Psychedelic Studies (MAPS):

This use of MDMA, though not conducted in the context of a scientifically controlled experiment, does provide an opportunity for a very large epidemiological study. Similarly, over fifty million people have tried a prescription drug called fenfluramine, a diet aid prescribed for daily use for months or years at a time that causes the same kind of neurotoxicity in animals as does MDMA.

The phen-fen disaster highlighted the need to investigate drug synergies thoroughly before combining them as a pharmacotherapy. The phen-fen heart and lung damage may have been related to a potentially toxic condition known as “serotonin syndrome.”

And the Wurtmans? Ironically, Richard and Judith Wurtman had patented the use of Prozac for severe PMS years earlier, and ultimately sublicensed the rights back to Eli Lilly for several million dollars. Eli Lilly disguised the fact that their PMS drug was a case of old wine in new bottles. As Wellbutrin had become Zyban, so Prozac metamorphosed into Serafem, when prescribed for premenstrual syndrome.

Photo credit:  http://youoffendmeyouoffendmyfamily.com/

The History of Prozac

How a pill for alcoholism became a blockbuster antidepressant.

Back in the 1970s, while doing research on antidepressants at Eli Lilly and Co., several organic chemists had been working on identifying new compounds that showed activity at serotonin receptor sites. The Lilly researchers came across Compound 82816, which very cleanly and very selectively blocked the reuptake of serotonin, and it did so without effecting any other neurotransmitter system at all. Clinical trials of compound 82816, chemically known as fluoxetine, continued into the early 1980s. At the same time, compounds with profiles similar to fluoxetine were being tested at various universities and drug firms.

The new drugs—with names like citalopram, zimelidine, fluoxetine, and fluvoxamine—were extensively investigated in animal models, and along the way, investigators made some unexpected discoveries. European investigators had shown that one serotonin uptake blocker in particular—zimelidine—seemed to reduce the self-administration of morphine and alcohol in addicted rats. A good part of the research began to center on three serotonin-enhancing compounds—zimelidine, citalopram, and fluoxetine.

Since rats decreased their administration of both alcohol and morphine when given zimelidine, and since low serotonin is a strong potential marker for human alcoholics and other addicts, Dr. Claudio Naranjo and Dr. Ed Sellers, along with their colleagues at Toronto’s Addiction Research Foundation, began testing zimelidine on heavy drinkers. Characterized as “early stage problem drinkers,” the test subjects showed a slight but noticeable decrease in the number of drinks consumed per day when they took zimelidine. There was also a consistent increase in the number of days the drinkers were completely abstinent. (Zimelidine was later withdrawn from use worldwide because of immune system side effects.)

As research continued, it became consistently evident that drugs capable of increasing concentrations of brain serotonin tended to cause large numbers of animals and human test subjects to drink less alcohol. But it wasn’t simply an aversive reaction at work, as in the case of Antabuse. People in the clinical trials still drank, but in many cases, the urge to drink seemed to diminish, and while the decrease was modest, it was measurable.

Moreover, rats given serotonin-enhancing drugs selectively cut back on carbohydrates, and lost weight. Ultimately, Lilly’s investment centered on flouxetine. In late 1987, Fortune magazine’s article on fluoxetine reported that “the prospect of making people both happy and thin has helped Lilly stock rise 28 per cent this year.”

The prospect of making alcoholics drink less, or stop drinking altogether, was a less publicized but equally attractive notion. Lilly already had a trade name picked out for fluoxetine. They were calling it Prozac.

A year after its introduction as an antidepressant, Prozac was a runaway success. Prozac quickly proved the existence of a huge potential market for serotonin reuptake inhibitors. Research continued on the diminished craving response that the serotonin uptake blockers seemed to produce in certain drinkers. The drug’s allure as an anti-craving medication for alcoholism and other possible addictions remained an open secret among researchers. Lilly wasn’t saying much in public about it, and with sales booming for fluoxetine as an antidepressant, the company could afford to concentrate on that indication. In the end, Lilly chose not to pursue further investigation of Prozac’s ability to reduce drinking and initiate weight loss.

Excerpted from The Chemical Carousel: What Science Tells Us About Beating Addiction by Dirk Hanson © 2008

Photo Credit: http://bryanking.net/prozac-fluoxetine

addiction drugs

Drug for Cocaine Addicts Causes Weight Loss

Is Vigabatrin the next big diet pill?

The U.S. Department of Energy's Brookhaven National Laboratory announced that obese rats lost weight on the experimental anti-cocaine drug vigabatrin, reinforcing the idea that certain forms of obesity--particularly binge eating--result from the same kinds of neurotransmitter disturbances that underlie vulnerability to addictive drugs like cocaine.

Amy DeMarco, lead author of the study, said in a press release from Brookhaven that the results "appear to demonstrate that vigabatrin induced satiety in these animals."

Earlier, the U.S. Food and Drug Administration (FDA) had given Fast Track designation to vigabatrin, an anticonvulsant, for evaluation as an anti-craving drug for cocaine and methamphetamine addiction. If successful, it would be the first medication ever approved for the treatment of addiction to stimulants. The FDA has yet to approve the drug for use in the U.S., citing concerns about reports of retinal damage in patients overseas.

First synthesized as a drug treatment for epilepsy in 1974, vigabatrin increases brain levels of the neurotransmitter GABA, an inhibitory compound also implicated in alcoholism. According to a press release from Ovation Pharmaceuticals, a marketer of the drug under the trade name Sabril, “Sabril may block the euphoria associated with cocaine administration in humans and may suppress craving by increasing brain levels of gamma-aminobutyric acid (GABA).” Increased brain levels of GABA, an inhibitory transmitter, result in higher levels of dopamine and serotonin. Catalyst Pharmaceutical Partners is also testing a version of vigabatrin called CPP-109.

The weight loss study involved 50 genetically obese lab animals, and 50 normal animals. Each of the animals was given doses of vigabatrin or placebo for forty days. At the end of that period, the obese animals had lost 19 per cent of their body weight, while the non-obese animals lost from 12 to 20 per cent of their weight.

Brookhaven senior scientist Stephen Dewey, who did much of the early work on vigabatrin, said: "The fact that these results occurred in genetically obese animals offers hope that this drug could potentially treat severe obesity." In the lab press release, Dewey also observed that "This would appear to be true even if the obesity results from binge eating, as this disorder is characterized by eating patterns that are similar to drug-taking patterns in those with cocaine dependency."

Perhaps. But ten years ago, the research community was just as enthusiastic when a serotonin-boosting diet pill called Redux (dexfenfluramine) won full FDA approval in 1996. Redux was the first drug ever approved in the U.S. for the long-term treatment of obesity. But the euphoria didn’t last long. By the time Redux made the cover of Time, researchers were already rumbling about continued reports of high toxicity and hypertension in rat studies. Concerns about pulmonary hypertension arose, and in August, 1997, doctors at the Mayo Clinic in Minnesota reported serious heart valve abnormalities in 24 women taking the "phen-fen" combination.

A month later, at the FDA’s request, phen-fen and Redux were permanently pulled off the market.

Graphics Credit: SheKnows.com