This section has reviewed a number of factors in the obesogenic food envi-
ronment that increase food intake in, generally, unaware consumers. Humans are
poor at consumption monitoring, in part because these traits were previously
unnecessary when food selection was less abundant, less reliable and part of the
natural environment. The modern food environment is replete with deceptions in
taste, composition, caloric density, and portion sizes that facilitate increased con-
sumption volume (Wansink2004b, 2010 ). Human psychobiology and neurophys-
iology honed by evolution also operate to increase appetite, decrease satiety, and
facilitate energy storage (Power and Schulkin 2009 ). These largely unseen and
often unsensed hormones, enzymes, neurotransmitters, and other peptides exercise
control over many aspects of appetite and eating behaviors. These biomarkers are
explored in the next section.
The Invisible Regulatory Systems of Appetite and Eating
Behaviors
Obesity is highly heritable (>0.70) and ongoing research on the genetic bases of
obesity has identified approximately 30 rare Mendelian-based syndromes and more
than 40 genes involved in common polygenic obesity and related phenotypes
(Grimm and Steinle 2011 ; Walley et al. 2006 ). Many of these genes and their
products could potentially serve as clinically relevant biomarkers for assessing the
development of obesity and its sequelae (Walley et al. 2006 ). The polymorphic
FTO gene and its AA at-risk genotype have been well studied in numerous pop-
ulations, and genome-wide associations link its diverse pleiotropic effects to fat
mass, abdominal fat mass, BMI, activity patterns, appetite, satiety, hedonic aspects
of taste, ghrelin, and leptin levels (Zdrojowy-Wełna et al. 2014 ). Recently,
experimental results suggest that the noncoding region of FTO interacts with the
promoters of the IRX3 gene and that IRX3 is linked with obesity, influencing body
mass and composition (Smemo et al. 2014 ). IRX3 expression in mice results in
decreased body weight (Smemo et al. 2014 ). Further research is needed to elucidate
the specific roles of these and other obesity-related genes.
Appetite and food intake are regulated by the CNS in response to peptide and
neuronal signals converging from cellular and peripheral organs. Cellular sensors,
primarily AMP-activated protein kinase (AMPK) and the mammalian target of
rapamycin (mTOR), detect energy levels inside the cell (Laplante and Sabatini
2012 ). The peripheral system generates and relays‘hunger’or‘satiety’signals to
the CNS, and the CNS controls autonomic and cognitive decisions regulating when
to start and stop eating, food selection, etc., by integrating signals from the entire
body. The hypothalamus is the primary CNS regulator of appetite, metabolism, and
eating behaviors responding to energy balance. The hippocampus has memory
functions; the thalamus integrates and relays sensory information to the cortex, and
the insular and temporal cortexes receive gustatory signals. In the brain stem the
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