Open Access
Neural vulnerability factors that increase risk for future weight gain.
Author(s) -
Eric Stice,
Sonja Yokum
Publication year - 2016
Publication title -
psychological bulletin
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 10.737
H-Index - 313
eISSN - 1939-1455
pISSN - 0033-2909
DOI - 10.1037/bul0000044
Subject(s) - overeating , weight gain , psycinfo , psychology , vulnerability (computing) , developmental psychology , weight change , clinical psychology , cognitive psychology , neuroscience , obesity , weight loss , medicine , medline , body weight , biology , computer science , biochemistry , computer security
Theorists have proposed several neural vulnerability factors that may increase overeating and consequent weight gain. Early cross-sectional imaging studies could not determine whether aberrant neural responsivity was a precursor or consequence of overeating. However, recent prospective imaging studies examining predictors of future weight gain and response to obesity treatment, and repeated-measures imaging studies before and after weight gain and loss have advanced knowledge of etiologic processes and neural plasticity resulting from weight change. The present article reviews evidence from prospective studies using imaging and behavioral measures reflecting neural function, as well as randomized experiments with humans and animals that are consistent or inconsistent with 5 neural vulnerability theories for excessive weight gain. Extant data provide strong support for the incentive sensitization theory of obesity and moderate support for the reward surfeit theory, inhibitory control deficit theory, and dynamic vulnerability model of obesity, which attempted to synthesize the former theories into a single etiologic model. However, existing data provide only minimal support for the reward deficit theory. Findings are synthesized into a new working etiologic model that is based on current scientific knowledge. Important directions for future studies, which have the potential to support or refute this working etiologic model, are delineated. (PsycINFO Database Record