Predisposition towards obesity is genetic

"Ignoramus22273" wrote in message
...
Before people start flaming me without thinking, let me preface this
excerpt from a study with this.

Predisposition towards obesity is genetic. It turns into obesity by
environment (too much food, wrong food and lack of exercise). Pima
indians were not fat 300 years ago (we think). Predisposition can be
overcome, sometimes, by diet and exercise.

But, people blaming their childhood home environment for their
obesity, may be wrong. According to the article, ``a number of studies
have described a closer relationship between the weights of adoptees
and their biological parents rather than their adoptive parents''. So,
environment in adoptive homes did not have nearly as much effect on
adoptees, compared to who was their biological parent.

A question that is open is this. As parents, we try to create some
sort of healthy environment for our children, so that they grow up as
fit people. Are our efforts statistically doomed to be irrelevant to
their final health? It is hard to believe, and does not, strictly
speaking, follow from the adoptee finding, but it is a disconcerting
thought.

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read this and weep...


http://www.med.nus.edu.sg/paed/medic...cs_obesity.htm

``Studies in twins, adoptees and families indicate that as much as 80%
of the variance in the body mass index is attributable to genetic
factors. Twin studies suggest a heritability of fat mass of between
40-70%. Concordance between monozygotic twins is 0.7-0.9, compared to
0.35-0.45 between dizygotic twins. While these associations may in
part be explained by sharing the same childhood environment, a number
of studies have described a closer relationship between the weights of
adoptees and their biological parents rather than their adoptive
parents. These genetic influences are not confined to the extremes of
obesity, but exert their effect across the whole range of body weight
and are consistent with a polygenic inheritance of fat mass.

The potential implication of genetic factors in the development of
human obesity is well demonstrated by the description of six monogenic
forms of the pathological human obesity to date. These genes encode
proteins of the leptin axis and brain-expressed targets of leptin
involved in the melanocortin pathway. They include leptin, the leptin
receptor, pro-opiomelanocortin (POMC), proconvertase 1 (PC1),
Peroxisome-proliferator-activated receptor g2 (PPARg2), and the
melanocortin-4 receptor (MC4-R). Except for MC4-R, mutations in these
genes cause rare, recessive, syndromic forms of obesity, associated
with multiple endocrine abnormalities. ''