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Review
. 2018 Jan:131:5-13.
doi: 10.1016/j.biopsycho.2017.05.001. Epub 2017 May 4.

Role of addiction and stress neurobiology on food intake and obesity

Rajita Sinha  1
Affiliations
Review

Role of addiction and stress neurobiology on food intake and obesity

Rajita Sinha. Biol Psychol. 2018 Jan.

Abstract

The US remains at the forefront of a global obesity epidemic with a significant negative impact on public health. While it is well known that a balance between energy intake and expenditure is homeostatically regulated to control weight, growing evidence points to multifactorial social, neurobehavioral and metabolic determinants of food intake that influence obesity risk. This review presents factors such as the ubiquitous presence of rewarding foods in the environment and increased salience of such foods that stimulate brain reward motivation and stress circuits to influence eating behaviors. These rewarding foods via conditioned and reinforcing effects stimulate not only metabolic, but also stress hormones, that, in turn, hijack the brain emotional (limbic) and motivational (striatal) pathways, to promote food craving and excessive food intake. Furthermore, the impact of high levels of stress and trauma and altered metabolic environment (e.g. higher weight, altered insulin sensitivity) on prefrontal cortical self-control processes that regulate emotional, motivational and visceral homeostatic mechanisms of food intake and obesity risk are also discussed. A heuristic framework is presented in which the interactive dynamic effects of neurobehavioral adaptations in metabolic, motivation and stress neurobiology may further support food craving, excessive food intake and weight gain in a complex feed-forward manner. Implications of such adaptations in brain addictive-motivational and stress pathways and their effects on excessive food intake and weight gain are discussed to highlight key questions that requires future research attention in order to better understand and address the growing obesity epidemic.

Keywords: Addiction; Food intake; Neurobiology; Obesity; Stress.

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Figures

Fig. 1.
Fig. 1.
A heuristic framework is presented to show the putative effects of highly palatable (HP) food Intake and exposure to their related products (e.g., additives, preservatives, advertisement) on (i) motivation and hunger for specific foods, (ii) metabolic hormones, and (iii) stress and energy regulating peptides to promote HP food motivation and intake (A). Stress-responsive hormones and peptides (e.g., CRF, ACTH, cortisol, NPY) and metabolic factors (e.g., insulin, ghrelin, leptin) influence brain limbic and striatal reward/motivation regions to influence dopaminergic signaling, activate hypothalamic and midbrain arousal regions and prefrontal cortical circuits involved in reward prediction, self control and decision making (B). With activation of metabolic, neuroendocrine and emotion and motivational pathways, there is risk of increased ‘wanting’ and intake of such HP foods (C). Thus HP food intake promotes a sensitized process with increased HP food motivation and intake that would, in turn, also promote weight gain (D), thereby potentiating the cycle of overeating of HP food intake leading to alterations in stress and metabolic pathways that drive weight gain. Increased weight gain would, in turn result in weight related adaptations in brain stress and motivation pathways as well as in metabolic responses to further promote HP food motivation and intake (E). Furthermore, stress and trauma further activate stress and motivation neuroendocrine, metabolic and subjective/behavioral responses and in those with sensitized food motivation circuits may promote increase stress-induced craving and wanting of HP foods, thereby promoting food intake and weight gain (F). Individual difference variables may further moderate these relationships as shown in G.
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