The neurobiology of food intake in an obesogenic environment

Abstract

The objective of this non-systematic review of the literature is to highlight some of the neural systems and pathways that are affected by the various intake-promoting aspects of the modern food environment and explore potential modes of interaction between core systems such as hypothalamus and brainstem primarily receptive to internal signals of fuel availability and forebrain areas such as the cortex, amygdala and meso-corticolimbic dopamine system, primarily processing external signals. The modern lifestyle with its drastic changes in the way we eat and move puts pressure on the homoeostatic system responsible for the regulation of body weight, which has led to an increase in overweight and obesity. The power of food cues targeting susceptible emotions and cognitive brain functions, particularly of children and adolescents, is increasingly exploited by modern neuromarketing tools. Increased intake of energy-dense foods high in fat and sugar is not only adding more energy, but may also corrupt neural functions of brain systems involved in nutrient sensing as well as in hedonic, motivational and cognitive processing. It is concluded that only long-term prospective studies in human subjects and animal models with the capacity to demonstrate sustained over-eating and development of obesity are necessary to identify the critical environmental factors as well as the underlying neural systems involved. Insights from these studies and from modern neuromarketing research should be increasingly used to promote consumption of healthy foods.

Fig. 1

(colour online) Major neural systems and pathways involved in the control of ingestive behaviour and energy balance regulation with emphasis on interactions between the classical homoeostatic energy regulatory system in the hypothalamus and brainstem (blue boxes and arrows in lower half) and cognitive/emotional brain systems (red boxes and arrows in upper half). Bottom-up modulation of cognitive and emotional processes by metabolic signals and their derivatives is accomplished by (a) circulating hormones and metabolites acting not only on the hypothalamus and brainstem but also on external sensory processing pathways as well as on components of the corticolimbic system (open blue arrows with broken lines), (b) a stream of vagal and spinal sensory information from within the body to all levels of the neuraxis, including the cortex (full blue arrows with solid lines) and (c) neural signals generated by the integrative hypothalamic energy sensor and distributed to areas involved in reward-based decision making (full blue arrows with solid lines). Together, these ascending modulatory influences determine the level of incentive salience directed to specific nutrients. Top-down modulation of food intake and energy expenditure by cognitive and emotional/reward systems is accomplished by (a) direct external (taste and smell) sensory input to the hypothalamic energy sensor and response allocator (dark yellow lines), (b) input from the amygdala, cortex and reward processing systems to mainly the lateral hypothalamus, responsible for conditioned external signals to elicit food intake (full red lines and arrows), (c) inputs from cortex, amygdala and basal ganglia to midbrain extrapyramidal motor pathways (emotional motor system, broken red lines and full arrows) and (d) pyramidal motor system for voluntary behavioural control (broken red lines on the right). N. Accumbens, nucleus accumbens; SMA, supplemental motor area; BLA, basolateral amygdala; CeA, central nucleus of the amygdala; VTA, ventral tegmental area; PAG, periaqueductal gray; GLP-1, glucgon-like-peptide-1; PYY, peptide YY; AT, adipose tissue; SPA, spontaneous physical activity. Adapted from⁽¹²⁾.