I have long thought that the Neel "Thrifty Gene" hypothesis is
lacking a compelling physiological basis, just in terms of the
metabolic processes posited. And I find theJenny Brand Miller
"Glucose Sparing" hypothesis more compelling and more surely based
on underlying metabolic processes. Given the lack of evidence of
starvation in the ancient record, the Brand Miller hypothesis gains
more credence.
To a non-linear thinker, there is a defect in the dynamics proposed
by Neel. It is well known (1) that insulin resistance increases
with the accumulation of body fat. Thus, under the Neel hypothesis,
our insulin resistant ancestors who readily gain fat (and selective
advantage) become more insulin resistant and, thus, deposit fat
even more readily. This is an explosive dynamic which we see
culminating in NIDDM among insulin-resistant people (virtually
everyone if the measure is taken against the CHO load imposed by the
modern Western diet).
Were insulin resistance adapted to transitory starvation, it would
have a contracting, not an exploding dynamic. That is to say,
insulin resistance (and the associated rate of fat deposition) would
decrease rather than increase with the accumulation of fat.
The other issue that troubles one about the Neel hypothesis is that
the evidence Loren Cordain and Jenny Brand Miller point to
indicates there was little carbohydrate in the ancestral diet to
trigger the large insulin response assumed by the Neel hypothesis.
A starving ancestor gorging on mammoth would have little insulin
response and would succeed in laying down little fat. The glucose
would have to come from gluconeogenesis, for which humans have small
capacity as Jenny Brand Miller points out. Were the glucose to
trigger a sharp insulin response, the brain would get llittle of it
and an ancestor with low blood sugar would be a "sitting duck" for
predators.
In contrast, if insulin resistance spares glucose for the brain,
then an ancestor lacking CHO in the diet would conserve the limited
glucose derived through gluconeogenesis from the animal-based food
for the brain. As to the consistency of an expansive dynamic in the
mapping from insulin resistance to body fat, I do not see that it
conflicts with the glucose-sparing hypothesis, but I haven't thought
it through.
This reasoning suggests to me, though I haven't filled in the
steps, that few ancients were fat. Obesity is a modern disease
resulting from the CHO load which the modern diet imposes on a
metabolism adapted to low CHO.
Refs.
1. David Bernstein, Dr. Bernstein's Diabetes Solution, 1998.
2. @ARTICLE{ miller:94,
AUTHOR = {Jenny Brand Miller and S. Colagiuri},
TITLE = {The Carnivore Connection - Dietary Carbohdrate
in the Evolution of NIDDM},
JOURNAL = {Diabetologia},
YEAR = 1994,
VOLUME = 37,
NUMBER = 12,
PAGES = {1288-186},
MONTH = {Dec}
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Arthur De Vany
Professor
Institute for Mathematical Behavioral Sciences
3151 Social Science Plaza
Irvine, CA 92697-5100
949-824-5269
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http://www.socsci.uci.edu/mbs/personnel/devany/devany.html
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