Obesogens: epigenetics and obesity

he debate between nature and nurture has persisted through history. Both
have long been considered for their influence on incidence rates of
diseases like obesity. While technologies have improved our ability to
examine the underlying genetic causes, both have failed to sufficiently
account for the observed incidence of obesity. Such rapid changes in
incidence produces an apparent disparity between genetic and
environmental factors. Although the most widely accepted cause of
obesity is overconsumption of calorically dense food coupled with
diminished physical activity, emerging evidence indicates that
environmental factors can predispose individuals to gain weight,
irrespective of diet and exercise. In line with this, there is a high
rate of obesity in very young children, including infants .
Whereas one can argue that adolescents, and adults may be consuming more
and exercising less than in the past, it is implausible that this would
apply to infants. A more probable explanation is that obesity results
from prolonged disturbances in the homeostatic regulation of energy
metabolism that favors triglyceride storage and adipocyte hypertrophy.
This could occur through the prenatal environment causing these infants
to be born with an increased level of fat and predisposing them to
accumulate fat more readily, or through significant changes in the
postnatal environment. In support of the later, animals living in close
proximity to humans (e.g. dogs, cats, and laboratory animals such as
mice, rats, and primates) have exhibited pronounced increases in obesity
over the past few decades .