Tips For Your Family's Health

Gene variants that are currently associated with an increased risk of type 1 diabetes may have given previously unknown benefits to their human carriers, say researchers at the Stanford University School of Medicine.  These gene variants may have caused the human race in the recent past to evolve and become more susceptible to some complex diseases, such as diabetes.  Atul Butte, MD, PhD, assistant professor of pediatric cancer biology and bioinformatics expert, pointed out, “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 some of the risky variants may provide protection against certain viruses and bacteria, which made evolutionary sense in the past.  What is unclear is whether the benefits come from the disease-associated mutations themselves, or from neighboring genes that accompany these mutations when DNA is divided into sperm and eggs.  Unlike sickle-cell anemia, which is caused by one gene’s mutation, complex diseases such as type 1 diabetes are associated with several variants located on single-nucleotide polymorphisms (SNPs).  Some of these SNPs are associated with an increased disease risk, others with decreased risk.  The new research shows that of the top SNPs associated with type 1 diabetes, 80 have been increasingly prevalent.  While 58 SNPs are associated with an increased risk of type 1 diabetes, only 22 appear to protect against it.  “It’s possible that, in areas of the world where associated triggers for some of these complex conditions are lacking, carriers would experience only the protective effect against some types of infectious disease,” said Butte.  Butte also noted that the cumulative effect of many SNPs in a person’s genome may provide a buffer against any one variant, even if it did increase the risk for a particular condition such as diabetes.  Whatever the reason for this change in SNPs, some evolutionary tenets still apply, the researchers say.  In theory, healthier people are more likely to reproduce and pass on their genes, whether those genes are protective or risky.  Different diets and other changes may have altered human conditions, exposures, or locations, causing carriers of the risky SNPs to develop the conditions we currently face, including type 1 diabetes.  The research was published in Public Library of Science ONE.

(c)

Similar Posts:

• ADRA2A gene polymorphisms are associated with type 2 diabetes risk and metabolic traits
• Functional HMGA1 gene variants are linked to type 2 diabetes in individuals of white European ancestry
• Type 1 Diabetes Researchers Reach Important Milestone
• Bone mineral density and FRAX scores may predict fracture risk in adults with diabetes
• Bone mineral density and FRAX scores may predict fracture risk in adults with diabetes