Obesity 163and were less efficient at burning it off (such as the Pima Indians discussed
above). According to this analysis, what we have left in today’s world are
those who were best adapted to surviving harsh winters and floods, resulting
in food shortages and periods of famine. However, now that food is plen-
tiful and our lives are far more sedentary, these are the people who overeat,
become obese, and develop health problems, such as Type 2 diabetes, because
the environment no longer requires their thrifty genes.
In summary, there is strong evidence for a genetic basis to obesity. But
how this genetic basis expresses itself remains unclear, as the research on
lowered metabolic rate and high fat cells has mostly been refuted and the
genetics of appetite control remains in its infancy. There are also some pro-
blems with genetic studies which need to be considered. For example, the
sample size of studies is often small, zygosity needs to be confirmed, and
there remains the problem of the environment. Twin studies assume that
the environment for twins is constant and that only the genetic makeup
of nonidentical twins is different. It is possible, however, that identical twins
are brought up more similarly because they are identical whereas parents
of nonidentical twins emphasize their children’s differences. In addition,
adopted children often go to the homes of parents who are similar to their
biological parents. Further, the identification of individual genes respon-
sible for obesity is problematic, as most genes function by interacting either
with each other or with the environment or both. There also remains a
substantial amount of the variance in body fat which is unexplained by
genetics, and the recent increased prevalence of obesity in the West within
populations whose gene pool has remained relatively constant points to a
role for additional factors. This has led to researchers examining the impact
of our changing environment.
The Obesogenic Environment
Physiological models emphasize a number of different mechanisms to
explain obesity onset. They cannot, however, explain why the prevalence of
obesity has increased so rapidly over the past few decades. Our genetics,
neural mechanisms, and metabolic rates take far longer to change than just
years, and yet obesity is now considered an epidemic. To address this change,
researchers have turned their attention to the role of the external world,
which has been labeled an “obesogenic environment” (Hill and Peters, 1998).
For example, they have highlighted the impact of the food industry with
its food advertising, its food labeling, and the easy availability of energy-dense