Stress, Food Addiction and Brain: Molecular Determinants and its Neural Networks Using Omics Platform

Abstract

Obesity is a complicated metabolic malfunction linked to disconnected signaling between inter-organs, and inter-molecularly affected by impairment of the neuronal circuit, stemming from environmental stressors in children and adults. Upon environmental intoxication or change in the surrounding environmental stressors; the signaling for hunger could affect regulatory signaling in energy consumption and lead to a wide range of metabolic disruption and sensitivity, cell-to-cell and organ-to-organ. Presently, food addiction is associated with substance-based and behavioral malfunction, which reflects the alteration of molecular and genetic deficiency in animal studies and clinical studies. The prevailing food addiction hypothesis suggest that food types can alter the brain circuitry for a reward compensation which may link to compulsive eating behavior phenotype comparable to drug addiction. Like synthetic drugs, food consumption results in the release of dopamine, which relates to the feelings of being rewarded, and has shown to have similar brain activation patterns. It remains unclear what molecules could engage in the regulatory process, or what are key molecular determinants to control the hormonal secretion. Several interventions such as calorie restriction, exercise, bariatric surgery, and treatments for obesity management have been moderately successful in reducing body fat in the short term, but most fail to maintain long-term weight loss. Herein, we propose the advantage of the molecular-based risk assessment, namely the omics platform, to improve health quality by reviewing the impact of environmental stressors. Bulimia nervosa has received less attention in this regard, despite their regular binge eating symptoms.