Originally Posted by Forever Changes:
“i'm not a snitch. I can fight my own battles
now where's your proof that obesity is genetic?”
This review goes into the genetic and epigenetics of obesity. It's incredible that you, having done no actual scientific research in the area, can conclude that obesity has no genetic factors.
Here's the link, I've quoted relevant parts in case you cannot access the document (emphasis is mine).
http://link.springer.com/article/10....438-015-1015-9
Quote:
“Evidence for a genetic component to obesity
Over the last 30 years, the increase in the prevalence of
obesity could be attributed primarily to environmental
changes, or to high-calorie food intake together with the
sedentary lifestyle of modern societies (Xia and Grant
2013). The fact that the prevalence of obesity in many
countries has increased threefold over the last three decades
seems difficult to conjugate with the notion that
genetics are the primary cause of obesity as revealed by
twin and adoption studies (Feinleib et al. 1977; Stunkard
et al. 1986a, b; Silventoinen et al. 2010). Nevertheless, it is
now believed that environmental factors can influence the
genetic background contributing to the increase in obesity
prevalence. Morevover, epigenetic mechanisms, in which
environmental factors cause changes in the expression of
genes, could also help explaining the observed increase in
obesity prevalence.
it is not surprising that one important risk factor
for childhood and adolescent obesity is parental obesity.
Whitaker et al. (1997) found that when both parents are
obese there is an increase of more than double of the risk
for childhood obesity. However, most of the studies found
a small to medium effect of parental obesity as risk factor
for childhood obesity (Danielzik et al. 2002).
Other studies have found a stronger effect for maternal obesity compared
to paternal obesity, which may reflect pre- and postnatal
environmental factors (Magnusson and Rasmussen 2002).
Moreover, maternal weight gain in pregnancy has been
positively associated with BMI of the children into adulthood
(Mamun et al. 2009). Several studies found that environmental
conditions experienced in utero are an important
factor in programming obesity.
Twin studies have been used to model the genetic component
of a given trait, due to the fact that monozygotic
(MZ) twins are genetically identical, while non-identical
dizygotic (DZ) twins share only 50 % of their genetic
material (Xia and Grant 2013). In 1977, Feinleib et al. studied
the correlations for weight in 250 MZ and 264 DZ male
veteran twin pairs, and established for the first time that
familial aggregation for obesity results mainly from genetic
influence. In 1986, Stunkard et al. (1986a) confirmed
these results in a 25-year follow-up study using more
than 4000 MZ and DZ twin pairs. High heritability values
for BMI were observed for the same subjects at 20 years
(h2 = 0.77) and at 45 years (h2 = 0.84). The heritability
of fat mass among MZ twins has been reported to range
from 70 to 90 %, while in DZ twins it is 35–45 %. Adoption
studies have strengthened the evidence of a strong
genetic influence on human body weight. Body corpulence
of adopted children correlates more strongly with BMI of
their biologic parents versus the BMI of their adoptive parents
(Stunkard et al. 1986b). Recently, Silventoinen et al.
(2010), conduct a review of studies in twins and adopted
children, suggesting that genetic factors could have a much
stronger effect than environmental factors on the BMI
trends in children up to the age of 18 years.
The role of maternal nutrition and
stress suffered during pregnancy, mostly due to social disparities
or cultural differences could also influence biological
processes and responses across the life cycle that will
be discussed later. All these factors
affect the intrauterine environment reflecting differences
in birth weight. However, nowadays is still evident that
genetic factors play a considerable role in obesity. Three
distinct forms of obesity could be found: monogenic, syndromic
and polygenic obesity.”
