Researchers Link Alcoholism and Binge Eating Behavior

Addiction and the role of genetic overlap.

More evidence has arrived, courtesy of Washington University School of Medicine in St. Louis, demonstrating a genetic link between alcoholism and binge eating disorders.

In clinical practice, it is no secret that certain binge eaters and people with bulimia also show high rates of alcoholism. Various reasons have been suggested, but one of the obvious ones is that people prone to alcoholism are also genetically susceptible to certain kinds of eating disorders. A common set of genetic factors may convey these intertwined vulnerabilities to a subset of the population.

In order to examine the matter, Dr. Melissa Munn-Chernoff and coworkers followed the time-honored route: They studied twins, both identical and fraternal, from a database of 6,000 adult twins in Australia. Twin studies have been crucial to medical understanding of comorbid disorders and addiction. In general, while alcoholism and binge/purge disorders were seen as most likely genetic in origin, it was thought that the two disorders were transmitted in families independently. Writing in the Journal of Studies on Alcohol and Drugs, the researchers conclude that “in women, some of the genetic risk factors that influenced vulnerability to alcohol dependence also influenced vulnerability to both binge eating and compensatory behaviors [purging, laxatives, diuretics].”

Previous studies cited by the researchers have pegged the individual heritabilities of alcohol dependence (50-64 percent) and bulimia (28-83%). However, the question of genetic overlap had remained relatively underexplored. Munn-Chernoff and colleagues wanted to evaluate the links between alcohol dependence and binge eating behaviors in women. Among the study group, 6 percent of women had been dependent on alcohol at some point in their lives. As for binge eating, 13% of women had experienced problems with it. 14% of women had engaged in purging or laxative abuse.

The researchers judged the genetic correlation between the two disorders to be statistically relevant: “In women, the multivariate twin model suggested that additive genetic and nonshared environmental effects influenced alcohol dependence, binge eating, and compensatory behaviors, with heritability estimates ranging from 38% to 53%.”(For the specific statistical correlations, see the full-text article. The correlation was stronger for women than for men).

In addition, the study did not find any significant shared environmental influences contributing to covariance between alcoholism and binge behaviors.

Limitations of the study include an older age cohort (mean age 44 in women), higher alcoholism rates in the Australian sample compared with the U.S., and the possibility that other comorbidities, such as depression, might influence the association.

“It appears that some genes that influence alcohol dependence also influence binge eating in men and women,” said Melissa Munn-Chernoff, in a prepared statement. “When you go to an eating disorder treatment center, they don’t often ask questions about alcoholism. And when you go for alcoholism treatment, they don’t generally ask questions about eating disorder symptoms. If centers could be aware of that and perhaps treat both problems at the same time, that would be a big help.”

Women who abuse alcohol have it tough for any number of reasons, and this study gets at one of them: “A combination of pressures to adjust to the changing body at puberty, increased access to alcohol via peer networks, and genetic predispositions for eating disorder symptoms and alcohol problems could result in comorbid alcohol dependence and bulimia symptoms."

Munn-Chernoff M.A., Duncan A.E., Grant J.D., Wade T.D., Agrawal A., Bucholz K.K., Madden P.A.F., Martin N.G. & Heath A.C.  A twin study of alcohol dependence, binge eating, and compensatory behaviors., Journal of studies on alcohol and drugs,    PMID: 23948525

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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.

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