Evolution May Have Pushed Humans Toward Greater Risk for Type 1 Diabetes

http://www.sciencedaily.com/releases/2010/08/100817171603.htm

ScienceDaily (Aug. 18, 2010) — Gene variants associated with an increased risk for type-1 diabetes and rheumatoid arthritis may confer previously unknown benefits to their human carriers, say researchers at the Stanford University School of Medicine. As a result, the human race may have been evolving in the recent past to be more susceptible, rather than less, to some complex diseases, they conclude.

"At first we were completely shocked because, without insulin treatment, type-1 diabetes will kill you as a child," said Atul Butte, MD, PhD, assistant professor of pediatric cancer biology and a bioinformatics expert. "Everything we've been taught about evolution would indicate that we should be evolving away from developing it. But instead, we've been evolving toward it. Why would we have a genetic variant that predisposes us to a deadly condition?"

The researchers speculate that at least some of the risky changes may protect carriers against certain viruses and bacteria -- a trade-off that may have made evolutionary sense in the not-too-distant past when infectious diseases were devastating and largely untreatable. It's not clear, however, whether the beneficial effects arise from the disease-associated mutations themselves, or from neighboring genes that tag along when DNA is divvied up into sperm and eggs.

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The idea that disease-causing genes can be beneficial is not new. The most clear-cut case involves a gene variant that, when present in two copies, causes sickle cell anemia, which can result in severe pain, organ damage and death. Although it seems that natural selection would work to eliminate the disorder, the variant remains prevalent in some areas of Africa because people with just a single copy are less susceptible to malaria. Evolutionarily the trade-off is worth it: Far more people are protected from malaria than ever develop sickle cell anemia even in today's environment.

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"Now we're starting to see little hints as to why this might be the case," said Butte. For example, a recent study in another lab showed that genetic variations in an antiviral response gene called IFIH1 that improve its ability to protect against enterovirus infection (and the resulting severe, potentially deadly, abdominal distress) also increase a carrier's risk for type-1 diabetes. And scientists who study global disease patterns have long noted that the prevalence of tuberculosis varies inversely with that of rheumatoid arthritis.

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