Alcohol and thiamine deficiency together: a dangerous combination?

May 21, 2000

The damaging effects of alcoholism on the body are fairly obvious; the mechanisms by which that damage occurs are less apparent. Researchers and clinicians know that chronic abuse of alcohol may lead to a deficiency in thiamine (also known as Vitamin B1). This deficiency can wreak particular havoc on the brain, causing a wide spectrum of deficits in cognition, behavior, and motor coordination. What researchers now suspect, as noted in a recent study in Alcoholism: Clinical & Experimental Research, is that chronic alcohol consumption and thiamine deficiency combined may have a synergistic and even more devastating effect on the brain and mental capacities.

"We were looking for an interaction between ethanol and thiamine deficiency," explained Philip J. Langlais, professor of psychology at San Diego State University, professor of neurosciences at the University of California - San Diego, and lead author of the study. "We wanted to see if you took thiamine deficiency and combined it with chronic alcohol intake, would you then create a situation that would produce a more severe impairment of cognition and memory than you would with either thiamine deficiency alone, or exposure to chronic alcohol ingestion alone." Using rat subjects, they did indeed find a synergistic effect, sometimes. Learning (for example, figuring out the rules of chess) and reference memory (remembering and consistently applying the rules) appeared the most sensitive to the damaging, synergistic effects of alcohol and thiamine deficiency. Short-term working memory (incorporating the rules of chess into game strategies), on the other hand, was most affected by alcohol alone. Neurological symptoms were most associated with thiamine deficiency.

Alcoholics are at risk for a wide variety of health complications, including brain damage. Alcohol impedes the digestive tract from absorbing needed nutrients. Nerve, muscle and brain tissue are exquisitely sensitive to low levels of vitamins, nutrients and minerals such as thiamine, magnesium, potassium and phosphorus. When nutrients disappear, tissues slowly deteriorate.

Thiamine deficiency contributes to two clinical conditions along the alcoholic's path toward dementia. The first 'phase' is called Wernicke's Encephalopathy (WE), in which people become extremely confused, develop abnormal eye movements, experience muscle weakness, and demonstrate gait disturbances. The second phase is called Wernicke-Korsakoff syndrome (WKS); it is associated with a more severe amnesia, and significant cognitive and reasoning impairments. The first two conditions may respond to, and possibly be reversed by, thiamine treatment. The final and - for all practical purposes, untreatable - phase is dementia.

"This study significantly adds to the database in at least one respect," said David V. Gauvin, psychopharmacologist and drug science specialist at the Drug Enforcement Administration. "It shows that there are unique interactions between alcohol and thiamine deficiency. We don't see that one plus one equals two, rather, one plus one equals three." Gauvin said that he would add a third component to the damaging equation: thiamine supplementation.

"This unique synergism is not just about alcohol and thiamine deficiency," he said, "it's also about thiamine supplementation, and the whole issue of mega-dosing." Gauvin mentioned a study in which he participated where researchers found that thiamine injections made the recipients even more sensitive to the effects of alcohol. He is concerned that the standard practice of giving alcoholics thiamine injections, in order to counteract the progression to symptoms of WE and WKS, may be more detrimental than helpful.

"When you have a surplus of thiamine," he explained, "you have the capacity to induce magnesium deficiencies, which have been linked to a number of alcohol's negative effects." He conjectured that thiamine-induced magnesium deficiency could be the root cause of a new sensitization to alcohol's effects.

Another way of counteracting thiamine deficiency - most often linked to poor nutrition among alcoholics, anorexics and senior citizens - is food supplementation. Both Langlais and Gauvin noted the Australia example (see EurekAlert/A:C&ER October 1999). During the 1980s, Australia had the highest recorded rates of WE in the world, mostly alcoholics, and large numbers of people needing long-term care because of WKS. In 1991, the federal government mandated that bread flour be enriched with thiamin. (In the U.S., most bread flour is enriched but enrichment is not mandatory.) Since then, Australia's WKS rates have significantly decreased. Some policy and health advocates are now calling for thiamine supplementation of alcoholic beverages, primarily beer.

"The Australian practice of food supplementation is okay," said Gauvin, again referring to his earlier study. "When we gave our animals regular food that contained thiamine, they did not develop sensitization to alcohol. The body can naturally absorb and process low-graded doses of thiamine in the gut and the liver. It's the whopping injections that are problematic. Eating enriched Wonder Bread or regular food gives you the thiamine in relatively normal concentrations." Gauvin is less comfortable with the proposition of supplementing alcohol with thiamine: "if you supplement alcohol with mega-doses of Vitamin B, what you may actually be doing is inducing magnesium deficiencies."

Conversely, Langlais believes that we nonetheless need to "re-examine the issue of fortifying alcoholic beverages and perhaps other foods. We also need to seriously think about educating alcoholics with respect to their diet and nutrition."

Gauvin had one final caution. "This study opens the door to a whole other set of questions. For example, what does this say about vitamin supplementation? We have such a benign feeling about vitamins, that we can mega-dose all we want to. Yet there is a physiological result from the overuse or abuse of vitamins. The bowel and the whole digestive system have been developed in such a way to allow for a very unique interaction between food and our needs. Yet bigger is not better, more is not better."
-end-
The co-author of the Alcoholism: Clinical & Experimental Research paper was Rosanne M. Ciccia of the Behavioral Neurobiology Labs, Department of Psychology, San Diego State University. The study was funded in part by Public Health Services and the Department of Veterans Affairs.

Alcoholism: Clinical & Experimental Research

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