satiation, and satiety are poor indicators of human ingestive behaviors and
self-reports of appetite. Physical and social factors in the obesogenic environment
are better determinants of eating behaviors even though individuals are not cog-
nizant, and often in denial, of the amount or energy density of what they consume.
Conclusion
Human evolution favored particular anatomical and physiological phenotypes and
behavioral repertories. Our biological legacy of nutritional requirements, metabolic
flexibility, energy storage efficiency or thriftiness, and behaviors involving food
acquisition and processing, once essential for survival, now favor excess adipose
tissue and adverse health outcomes (Lieberman 2003 , 2006 ; Power and Schulkin
2009 ; Turner et al. 2008 ; Ungar 2007 ).
Yet, biomarkers of adiposity, such as leptin and insulin or those of hunger and
satiety, such as CCK and ghrelin, are poorly correlated with subjective reports of
hunger, fullness, satiation, satiety, motivation to eat, frequency and duration of
eating, perceptions of caloric density of foods, portion sizes, and amounts ingested
(de Graaf et al. 2004 ; Kipnis et al. 2014 ; Wansink 2010 ). Former evolutionary
constraints have been relaxed for foraging and food acquisition, and food pro-
cessing has aided (and abetted) ingestion, digestion, absorption, and metabolism,
resulting in adipose tissue accumulation with adverse cardiometabolic sequelae.
Wansink’s‘mindless eating,’of course, does involve the mind at many levels,
and the cortex is involved, consciously and unconsciously responding to visual and
olfactory food cues and socio-environmental triggers causing a cascade of endo-
crine events and motivating eating behaviors (Wansink 2010 ). The processes
involve a complex interplay of dozens of peptides, hormones, neurotransmitters,
enzymes, and receptors in the CNS, peripheral organs, and tissues. The control of
appetite and eating are not top-down or bottom-up processes, but an intricate dance
of coordinated, adaptive, physiological changes at the cellular, tissue, organ, sys-
temic, behavioral and perceptual/cognitive levels. Because these responses now
occur in food abundant, easy access, low effort, hedonically enriched and socially
mediated environments, people do not terminate eating when their stomachs are full
or with other internal signals of positive energy balance. Overweight and obesity
are the result, in part, of the failure to sense the biomarkers of satiation and to
terminate eating. Environmental cues (e.g., large normative serving sizes, large
plate sizes) distorted perceptions of food quantities and food processing deceive the
eater with low-fiber, calorically dense, superdelicious foods (Hermanussen et al.
2008 , 2012 ; Wansink 2010 ).
Although there is agreement among researchers, food manufacturers, pharma-
ceutical companies, and professional health organizations regarding the projections
of increasing global prevalence of overweight and obesity and the monetary and
quality-of-life costs that will ensue, there is much less agreement on the types and
effectiveness of interventions (Swinburn et al. 2011 ; WHO 2000 , 2013 ). The
220 L.S. Lieberman