Documente Academic
Documente Profesional
Documente Cultură
with China showing an increase of > 11% of Obesity prevalence and Great
Britain's prevalence nearly tripling. Prevalence trends differ by race and
ethnic origin for children (Ogden, Carroll, Curtin, Mcdowell, Tabak, et al.,
2006; Wang, Monteiro, & Popkin, 2002).
O'Rahilly and Farooqi (2006) argue that causative mutation in human
genes and the highly heritable nature of obesity is the true cause of the rise
in the prevalence of childhood obesity. Their research finds the mutation to
disrupt the function of hypothalamic integrative centers that leads to
increase food intake. The study finds the estimated heritability of BMI to
range between 64% and 84%. Various studies on the genetics of childhood
obesity also concluded that approximately 25 to 40 percent of BMI is
heritable (Anderson, et al., 2006). Even if mutations in our genes have made
us more susceptible to obesity, the pace at which obesity has been
increasing the past decades is far greater than genes can evolve. A study by
Anderson and Butcher (2006), also demonstrated a correlation between
elevated BMI in children and soda intake. The nutrition empty, ease of
consumption and its replacement of oner, more nutrient laden substances.
This same study identified breast feeding, while not a consistent factor, as
having a lowering affect on children's overall weight. Moreover, the research
found that very young children seem capable of adjusting their food intake to
match their energy outflow. As children grow up their for intake becomes
more reliant on external cues, such as the amount and type of food
presented. Other studies concluded that a child's environment contributes to
obesity. With increased availability of snack foods, less physical education in
schools and increased screen time (computer and television viewing), the
environment promotes imbalance of energy intake and expenditure resulting
in more overweight children (Zhang, Cristoffel, Mason, & Liu, 2006).