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alcohol intolerance may indicate risk of alzheimer's

new research suggests alcohol increases injury to brain cells and accelerates signs of alzheimer's disease

getty images/istockphoto
as if alcohol intolerance reactions weren’t uncomfortable enough, it turns out having the inherited deficiency that causes it can put you at risk of something much more harmful than a flushed face.a new study from stanford university shows this mutation can put you at a greater risk of alzheimer’s disease.for those with an alcohol intolerance, the effects after just a few sips of a drink are all too familiar: itchy skin, bloodshot eyes, racing heartbeat, pounding headache, and the giveaway: tomato-red skin all over the face, neck, and chest. if that sounds like an allergic reaction, it’s because, in a way, it is.often called the ‘asian flush’ or ‘asian glow’ because of its prevalence in east asian populations, alcohol intolerance occurs in people who have an inherited deficiency on aldehyde dehydrogenase 2 (aldh2), one of the enzymes involved with breaking down alcohol.because this key enzyme has a mutation, instead of breaking alcohol down into acetate (a harmless component of vinegar and easy for the body to eliminate), it is converted into a toxic chemical called acetaldehyde—which has also been shown to increase risk of esophageal cancer.

study conducted on mice and cell cultures

in this new study, stanford researchers looked at genetically engineered mice with the mutated gene and gave them an alcoholic equivalent to two drinks per day in humans for 11 weeks. they also studied the cell cultures from 20 people with alzheimer’s disease.they found that both the mice and cell cultures with the mutated gene had more free radicals, which form toxic chemicals.  normally, these are eliminated, but in people who have a mutated gene, the buildup of these toxic chemicals damages the enzyme that gets rid of them. in the case of alzheimer’s disease, this can lead to brain cell damage.“our data suggest that alcohol and alzheimer’s disease-prone genes may put humans at greater risk of alzheimer’s onset and progression,” said daria mochly-rosen, senior author of the study and professor of chemical and systems biology, in a news release from stanford.“this is based on our patient-derived cell studies and our animal studies, so an epidemiological study in humans should be carried out in the future.”

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