View Single Post
  #7   ^
Old Fri, May-19-17, 23:23
M Levac M Levac is offline
Senior Member
Posts: 6,498
 
Plan: VLC, mostly meat
Stats: 202/200/165 Male 5' 7"
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
Default

I really can't help myself:
Quote:
The intrauterine environment provides a mechanism that predisposes some people with obesity to develop diabetes later in life. Individuals who were malnourished while in utero may be more prone to weight gain, insulin resistance, beta-cell failure and hence diabetes than those who are well nourished, a hypothesis known as the ‘Developmental Origin of Disease’ or the ‘Barker Hypothesis’ [77]. Maternal undernutrition forces the fetus to adapt during its intrauterine development and drives a reprogramming of its endocrine–metabolic state to produce permanent changes in the structure and the physiology of key organ systems [77, 78]. These changes in low-birth-weight infants (normal range, 3,000–4,000 g) contribute factors to chronic diseases such as type 2 diabetes, coronary heart disease, stroke and hypertension in adult life [79].

The idea is that a mother who starves herself, therefore who is emaciated, will produce an offspring who becomes obese. But that's exactly not what we see, and in fact not how it works. Instead, we see fat mothers give birth to fat babies who grow up into yet fatter adults, who then give birth to even fatter babies who grow up into even fatter adults, and so forth.

Bray calls this epigenetics, but in fact it's called generational epigenetics (I had to correct myself on this point, too). In this phenomenon, each generation manifests the same disorder (because it's the same cause), not opposite disorders. The disorder worsens with each subsequent generation exposed to the same cause.
Reply With Quote