GOT ECZEMA? IT MAY JUST BE BAD EVOLUTIONARY LUCK, STUDY FINDS

A new study probes the evolutionary history of eczema, and finds no evidence that a genetic disposition for this disorder has helped humans.

Some genetic diseases persist for generation after generation because the genes that cause them can benefit human health.

Sickle cell anemia is one example: This disorder compels red blood cells to take on a crescent moon shape, leading to anemia. But carrying a copy of the sickle cell gene can guard against malaria.

Not all ancient diseases come with such a blessing, however.

The research examines a genetic variant strongly associated with the most common form of eczema, atopic dermatitis.

This skin condition can cause a slew of unpleasant symptoms, including extreme itchiness and dry, scaly rashes, but there doesn't seem to be a tradeoff for this discomfort: The genetic variant studied appears to be a random vestige of evolution. We present a complex evolutionary history of this disease variant, and it seems to be just bad luck that it has endured for so long. Unlike other disease variants, such as those linked to sickle cell anemia or psoriasis, the one we studied is just not that important from the standpoint of evolution. It doesn't appear to affect what biologists call 'fitness,' which is another word for reproductive success, says the lead author.

The gene at the heart of the research is the filaggrin gene, which tells the body how to make a protein of the same name in skin cells.

In some people, inherited genetic mutations cause the filaggrin gene to stop working, impairing healthy skin function and creating an increased risk for developing eczema.

The study found that "loss of function" mutations are significantly more common in filaggrin than in other human genes. However, despite this prevalence, the variants don't appear to serve an adaptive purpose. The loss of function creates a susceptibility to eczema, but it does not appear to have an effect on the reproductive success of modern humans.

Thanks to: sciencedaily.com