PhilSci Archive

The Childhood Obesity Epidemic as a Result of Nongenetic Evolution: The Maternal Resources Hypothesis

Archer, Edward (2015) The Childhood Obesity Epidemic as a Result of Nongenetic Evolution: The Maternal Resources Hypothesis. In: UNSPECIFIED.

[img] PDF (Non-Genetic Evolution of Obesity)
Archer_MRH_Accepted_all_tables_figures.pdf - Accepted Version

Download (698kB)

Abstract

Over the past century, socioenvironmental evolution (eg, reduced pathogenic load, decreased physical
activity, and improved nutrition) led to cumulative increments in maternal energy resources (ie, body mass
and adiposity) and decrements in energy expenditure and metabolic control. These decrements reduced the
competition between maternal and fetal energy demands and increased the availability of energy substrates
to the intrauterine milieu. This perturbation of mother-conceptus energy partitioning stimulated fetal
pancreatic b-cell and adipocyte hyperplasia, thereby inducing an enduring competitive dominance of
adipocytes over other tissues in the acquisition and sequestering of nutrient energy via intensified insulin
secretion and hyperplastic adiposity. At menarche, the competitive dominance of adipocytes was further
amplified via hormone-induced adipocyte hyperplasia and weight-induced decrements in physical activity.
These metabolic and behavioral effects were propagated progressively when obese, inactive, metabolically
compromised women produced progressively larger, more inactive, metabolically compromised children.
Consequently, the evolution of human energy metabolism was markedly altered. This phenotypic evolution
was exacerbated by increments in the use of cesarean sections, which allowed both the larger fetuses and the
metabolically compromised mothers who produced them to survive and reproduce. Thus, natural selection
was iatrogenically rendered artificial selection, and the frequency of obese, inactive, metabolically
compromised phenotypes increased in the global population. By the late 20th century, a metabolic tipping
point was reached at which the postprandial insulin response was so intense, the relative number of adipocytes
so large, and inactivity so pervasive that the competitive dominance of adipocytes in the sequestering
of nutrient energy was inevitable and obesity was unavoidable.


Export/Citation: EndNote | BibTeX | Dublin Core | ASCII/Text Citation (Chicago) | HTML Citation | OpenURL
Social Networking:
Share |

Item Type: Conference or Workshop Item (UNSPECIFIED)
Creators:
CreatorsEmailORCID
Archer, Edwardarcher1@uab.edu
Keywords: Evolution, genetic, obesity, culture, physiology, diabetes, natural selection, artificial selection, metabolism, energy
Subjects: Specific Sciences > Biology > Developmental Biology
Specific Sciences > Biology > Evolutionary Theory
General Issues > Theory/Observation
Depositing User: Dr Edward Archer
Date Deposited: 06 Jul 2015 20:26
Last Modified: 06 Jul 2015 20:26
Item ID: 11548
Journal or Publication Title: Mayo Clinic Proceedings
Publisher: Elsevier
Official URL: http://www.mayoclinicproceedings.org/article/S0025...
DOI or Unique Handle: 10.1016/j.mayocp.2014.08.006
Subjects: Specific Sciences > Biology > Developmental Biology
Specific Sciences > Biology > Evolutionary Theory
General Issues > Theory/Observation
Date: 2015
Page Range: pp. 77-92
Volume: 90
Number: 1
URI: http://philsci-archive.pitt.edu/id/eprint/11548

Monthly Views for the past 3 years

Monthly Downloads for the past 3 years

Plum Analytics

Altmetric.com

Actions (login required)

View Item View Item