When University of Virginia neuroscientist Bankole Johnson first introduced the idea two decades ago that alcoholism lends itself to pharmacological treatment in just the same way other diseases do, he was regarded as something of a rogue by his peers. Now, Johnson finds himself at the forefront of a large body of research.
Johnson, a medical doctor with two additional doctorate degrees, was at Oxford when he proposed that the type 3 5-hydroxytryptamine (serotonin) receptor was responsible for intersubject differences in euphoric stimulation resulting from drinking alcohol, or even the idea of drinking it. In English, this means that some people are wired to derive a big old buzz from toping, whereas others simply aren’t. This should not come as a surprise; we’re all subject to the whims of our various chemoreceptors. Take taste: Some people like lobster and shrimp (like my dad), and other people would just as soon eat cardboard (like his son).
From a strict reductionist perspective, all behaviors can be broken down into neurochemical elements. So whether a mental or brain disorder is overtly “organic” (e.g., epilepsy, schizophrenia) or seemingly rooted in morality or choice (addictions, radically impulsive behaviors surrounding appetitive stimuli such as sex and food), there is, in theory, a way to guide symptom reduction through biochemical intervention. But clearly, this is much easier with respect to some illnesses than it is in others.
Presently, Johnson is heading up a study that will examine the anti-alcohol-dependence efficacy of a combination of two drugs already used to treat other disorders: topiramate (used to treat seizures and migraine headaches) and ondansetron (used to reduce chemotherapy-induced nausea in cancer patients). Topiramate alone has already been found to “ameliorate the turbulence of anxiety and mood instability that accompanies cessation from alcohol” and produce “a robust effect on improving maintenance of abstinence and reduced alcohol use” (Robert Malcolm, M.D., of the Center for Drug and Alcohol Programs at the Medical University of South Carolina). Similarly, ondansetron alone may reduce cravings. So in simple terms, the two drugs together in theory address both the before and the after of a bender. The value of reducing cravings needs to explanation, and the utility of reducing withdrawal symptoms is obvious when considering the fact that the first thing someone in alcohol withdrawal is likely to do is seek out more to drink in order to get rid of the shakes, anxiety, guilt, sweats, insomnia, night terrors, and whatever else might accompany a post-binge state. (Not that I would know.)
Left out of this interesting discussion are medications that are intended not to prevent cravings or deal with the aftermath of boozing it up, but to blunt the high of drinking itself. Already on the market for this is naltrexone, long known as an opioid antagonist and therefore a comprehensive, unapologetic buzz-kill. Also ignored is the fact that regardless of genetics, if people who abuse alcohol fail to address underlying problems in their lives–and virtually no one drinks to excess in a vacuum–all of the creative pharmacology in the world probably won’t amount to a piss-warm, half-full can of Pabst Blue Ribbon.
(Apologies for the non-religion-mocking post.)