Evolutionary change in physiological phenotypes along the human lineage.

Published

Journal Article

Research in evolutionary medicine provides many examples of how evolution has shaped human susceptibility to disease. Traits undergoing rapid evolutionary change may result in associated costs or reduce the energy available to other traits. We hypothesize that humans have experienced more such changes than other primates as a result of major evolutionary change along the human lineage. We investigated 41 physiological traits across 50 primate species to identify traits that have undergone marked evolutionary change along the human lineage.We analysed the data using two Bayesian phylogenetic comparative methods. One approach models trait covariation in non-human primates and predicts human phenotypes to identify whether humans are evolutionary outliers. The other approach models adaptive shifts under an Ornstein-Uhlenbeck model of evolution to assess whether inferred shifts are more common on the human branch than on other primate lineages.We identified four traits with strong evidence for an evolutionary increase on the human lineage (amylase, haematocrit, phosphorus and monocytes) and one trait with strong evidence for decrease (neutrophilic bands). Humans exhibited more cases of distinct evolutionary change than other primates.Human physiology has undergone increased evolutionary change compared to other primates. Long distance running may have contributed to increases in haematocrit and mean corpuscular haemoglobin concentration, while dietary changes are likely related to increases in amylase. In accordance with the pathogen load hypothesis, human monocyte levels were increased, but many other immune-related measures were not. Determining the mechanisms underlying conspicuous evolutionary change in these traits may provide new insights into human disease.

Full Text

Duke Authors

Cited Authors

  • Vining, AQ; Nunn, CL

Published Date

  • January 2016

Published In

Volume / Issue

  • 2016 / 1

Start / End Page

  • 312 - 324

PubMed ID

  • 27615376

Pubmed Central ID

  • 27615376

Electronic International Standard Serial Number (EISSN)

  • 2050-6201

International Standard Serial Number (ISSN)

  • 2050-6201

Digital Object Identifier (DOI)

  • 10.1093/emph/eow026

Language

  • eng