Obesity is complex and not fully understood. However, recent advances in the nutritional sciences have shown that the ‘eat-too-much, do-too-little’ paradigm of weight gain is erroneous. The new paradigm suggests that abdominal obesity is the result of overloading the liver with high fructose low fibre foods, which induces hepatic insulin resistance and metabolic dysfunction. The driving force of this behaviour is complex, but may involve a myriad of other factors that can influence food choices and nutritional motivation. Stress is one such component that has been identified by researchers being suspected of increasing the risk of abdominal obesity, through activation of high levels of cortisol. Lifestyles in developed nations are conductive to the development of chronic long-term stress which may explain the high rates of obesity in such regions. In particular chronic stress is known to increase intakes of sugary foods perceived by the consumer as comforting.
Chronic stress is particular damaging because of the way it interacts with the brain. High levels of circulating cortisol interact with the amygdala in the temporal lobes of the brain, through a feedback mechanism. In this way, cortisol is thought to cause a positive feedback signal in the amygdala which increases the sensitivity of this part of the brain to future stress. Because the amygdala is involved in the motivation to eat, chronic stress may therefore prime the brain for this sort of behaviour. In particular, this motivation may be targeted at consumption of high fat and sugar foods, which may be the sort of foods to contain high concentrations of fructose and low concentrations of dietary fibre. Those individuals consuming high intakes of sugar due to their stress reaction may therefore overload their livers and increase risk of developing metabolic syndrome. This explains the association between circulating cortisol and abdominal obesity reported in some studies.
Recent evidence shows that activation of the amygdala in inversely associated with satiety in normal weight individuals. For example, in a study published in the American Journal of Clinical Nutrition1, 23 healthy subjects underwent magnetic resonance imaging of the brain while being shown pictures of various types of food. The results showed that fasting amygdala activation was negatively associated with perceived fullness, supporting evidence that activation of the amygdala may be high in those with uncontrolled eating patterns. Following consumption of breakfast, those subjects with higher activation of the amygdala chose buffet foods with a higher fat content. This was supported by data from the imaging of the brain that showed that hunger correlated with higher personal appeal ratings for fattening foods. The motivation to eat energy dense food therefore reflects activation of the amygdala region of the brain and this may explain the motivation for uncontrolled eating patterns.
The amygdala assesses emotional and motivational stimuli and determines the level of response from these stimuli. Therefore behaviour reflect the perceived value of these emotional and motivational events. Activation of the amygdala is this high when motivation to eat is high and low in the post absorptive phase when the motivation to eat is diminished through satiety. Satiety may therefore be characterised by a lower appeal for fattening or calorie dense foods. This is likely the normal homeostatic condition in humans. Alteration of this physiological parameter away from satiety and towards the motivation for eating high calories foods may involve stress induced activation of the amygdala. Activation of the amygdala by chronic high levels of circulating cortical increase the motivation to find and consume foods with low nutritional but high energy contents. This may explain the driving force behind the desire of those living in developed countries to eat modern Western food.
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