ABSTRACT
One prominent reason for the prevalence of disease is that the environments we live in are not the same as those in which we evolved: this mismatch illustrates the importance of genotype by environment interaction. We begin the chapter discussing how the rise of allergies, asthma, and autoimmune diseases is partly due to the loss of contact with microbes with which our immune systems evolved. Dietary deficiencies—such as scurvy seen in 18th century sailors and others who have had prolonged lack of access to vitamin C—are also examples of such mismatch. But the idea of mismatch can be taken too far; human populations do have the capacity to evolve reasonably quickly and are not permanently stuck. Examples of such comparatively rapid evolution are adaptions to high altitudes and lactase persistence, which provides the ability to continue consuming the sugar lactose present in dairy products. Also discussed are evolutionary mutant models, the notion that some animals may have phenotypes that are adaptive given their environments but mimic human disease and disorders. Examining these phenotypes and the genes that underlie them could have clinical applications. We conclude with a discussion of the ways that humans are continuing to evolve.
