The satiety cascade helps describe the processes
that trigger initial ingestion, terminate intake (satiation), and
prevent subsequent intake after termination (satiety). The regulation
of eating is a function of both homeostatic and hedonic factors
. Homeostatic control helps
ensure that sufficient calories are consumed to meet the body’s
energy needs, and once these needs have been met, ensures that
negative feedback signals help bring the period of eating to an end.
Hedonic factors, in contrast, aremediated by reward. The consumption
of highly palatable foods, for example, can work against
homeostatic control and lead to overconsumption. Poor selfregulation
of eating, therefore, can be a function of homeostatic or
hedonic factors and can be a function of factors at any point in the
satiety cascade. Researchers offer several explanations for the relationships
between executive functioning, emotion regulation, and
childhood obesity. Most argue that, as a group, obese children may
be susceptible to overeating due to inhibitory control deficits, cognitive
inflexibility, and/or overly active food-related reward systems.
As described by Delgado-Rico, , “excessive eating and obesity are
increasingly viewed as a brain-related dysfunction, whereby rewarddriven
urges for pleasurable foods ‘hijack’ context-driven frontalexecutive
control” (p. 1604). These interpretations are consistent
with both Schachter’s externality theory (i.e., that obese individuals
are more responsive to environmental cues to eat) and
Singh’s (1973) inhibition deficit theory (i.e., that obese individuals
have difficulties inhibiting responses to palatable food stimuli).
Verdejo-Garcia et al., however, warn that the correlational
nature of such data “cannot resolve if the association of BMI and
executive function is due to the deleterious effects of increased
weight on prefrontal blood flow and executive competence, or to
the possibility that children with poor executive skills are more likely
to become obese”