Ecological adaptations and the origin of lactase persistence
March 14, 2014 | James Kohl
Large-scale sequencing effort confirms several mutations that confer lactase persistence in Africans, while haplotype analysis sheds light on the trait’s origins.
By Ashley P. Taylor | March 13, 2014
Excerpt: “Tishkoff and her colleagues identified three known variants…”
My comment: Journalists consistently report that variants are mutations. Experimental evidence and everything currently known about conserved molecular mechanisms in species from microbes to man show that the variants are nutrient-dependent ecological adaptations.
For example, the link from fermented milk products to vitamin D-induced changes in base pairs, amino acid substitutions and epialleles that stablize the organized genome of human populations is clear. Thus, lactase persistence can be considered in the context of the hemoglobin S variant associated with endemic malaria and sickle cell disease.
Otherwise, journalists may continue to ignore what researchers know about the difference between a mutation and an ecological adaptation. Like the variants reported here, hemoglobin S is a nutrient-dependent ecological adaptation.
Variants associated with nutrient-uptake typically result in reproductive fitness, which is why they show up in different populations. Attributing reproductive fitness to mutations is confusing.
The missattribution may also cause people to think that human population-wide differences associated with skin pigmentation are due to mutations, at a time when molecular biologists realize that ecological variation and ecological adaptations are responsible for morphological and behavioral phenotypes.
Only evolutionary theorists, or those who have been taught to believe in the theory, continue to attribute ecological adaptations to mutation-driven evolution.