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Nature/nurture study of type 2 diabetes risk unearths carrots as potential risk reducers

Nature and nurture have long been the 'tomayto' and 'tomahto' of lengthy arguments in both psychology and medicine. At the end of the day, of course, disease is caused neither strictly by genes nor strictly by the environment, but by the interactions between them.

In a new study published in Nature Genetics, Stanford medical-systems expert Atul Butte, MD, PhD (whom I've written about at length in the past), has figured out a sophisticated way to crunch massive amounts of genetic and environmental data and pull faint but important signals out of the noise. Sifting through mountains of data gathered in biennial health-and-nutrition surveys run by the federal government's Centers for Disease Control and Prevention, Butte teased out a gene/environment relationship that may make you want to eat a carrot.

Just over half of us, it's already known, are walking around with two copies - one from dad, one from mom - of a particular version of a gene that seems to very slightly predispose us to developing type 2 diabetes at some point in our lives. Nothing much we can do about that.

Unlike genes, however, our environment is something we can sometimes do something about. The Butte team's new work suggests that in people carrying a double dose of the gene version in question, low blood levels of the micronutrient beta-carotene (a vitamin A precursor found copiously in carrots and many other red, orange and yellow vegetables as well as in many vitamin supplements) are associated with not just a slight risk but a significantly increased risk for type 2 diabetes, whereas in those with high blood levels of the substance, that risk appears to be substantially mitigated.

A bit more offbeat is Butte et al.'s finding that another micronutrient - gamma-tocopherol, one of the eight forms of vitamin E - has the opposite interaction with the exact same gene: High levels of it, in people with two copies of the diabetes-related gene version, substantially boost the risk, while low levels reduce it. Nobody knows yet why that's true, as I explain in our press release:

“We can’t say, based on just this study, that ‘vitamin E is bad for you,’” said [the Human Genetics paper's first author, postdoctoral researcher Chirag Patel, PhD]. He noted that blood levels of alpha-tocopherol - another form of vitamin E that predominates in most supplements - showed no deleterious interaction with the predisposing gene variant in the new study.

But it's not too early to recommend that people who like carrots keep on eating them. And, the authors speculate, it could be that gamma-tocopherol, rather than being bad in itself, may instead just be a marker of a diet rich in the things where vitamin E is found. This includes soybean, corn, or canola oils (which are, unfortunately, ingredients in many processed and fried foods) and trans-fatty-acid-loaded margarine.

Previously: Mining medical discoveries from a mountain of ones and zeroes, Newly identified type-2 diabetes gene's odds of being a false finding equal one in 1 followed by 10 zeroes and Cheap data! Stanford scientists' "opposites attract" algorithm plunders public databases, scores surprising drug-disease hook-ups
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