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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