A study has pointed out that evolution could have increased our vulnerability to certain complex diseases.
Researchers at the Stanford University School of Medicine speculate that at least some of the risky changes may protect carriers against certain viruses and bacteria.
However, whether the beneficial effects arise from the disease-associated mutations themselves, or from neighbouring genes that tag along when DNA is divvied up into sperm and eggs, is not clear.
Many complex diseases are associated with several variants - specific locations in the DNA where the nucleotide "letters" vary between individuals. These locations are known as SNPs, for single nucleotide polymorphisms.
Graduate student Erik Corona found that of the top SNPs associated with type-1 diabetes, 80 have been recently increasing in prevalence.
Similarly, SNPs associated with an increased risk for rheumatoid arthritis were found to be positively selected.
"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 Atul Butte.
Regardless of the reason, some evolutionary tenets still apply. Healthier people are, presumably, more likely to reproduce and pass those same genes - be they protective or risky - to their offspring.
With differences in diet, exposures or location as populations move around the globe, carriers of the risky SNPs began to develop the conditions we struggle with today.
Corona and Butte are now expanding their investigation to include even more SNPs and diseases. They are also looking at the genetic profile of various types of tumours to see if there's evidence for positive evolutionary pressure there as well.
The research will be published Aug. 17 in Public Library of Science ONE.