The possibility that a carbohydrate-rich low-protein meal could raise 5-HT function gave rise to the proposal that some depressed people may self-medicate by eating carbohydrate, so leading to increased 5-HT release in a manner reminiscent of the effects of antidepressant drugs, which enhance aspects of 5-HT function by inhibiting the removal of 5-HT from the synaptic cleft between nerve cells. For the most part, however, early behavioral and pharmacological evidence for such a phenomenon was not very convincing.
Nevertheless, recent research provides some further support for beneficial effects of carbohydrate-rich protein-poor meals on mood and emotion in some people. When participants were divided into high and low stress-prone groups, as defined by a questionnaire, carbohydrate-rich protein-poor meals prior to a stressful task were found to block task-induced depressive feelings and the release of the glucocorticoid stress hormone cortisol, but only in the high stress-prone group. This finding was replicated using high- and low-tryptophan-containing proteins (a-lactalbumin and casein, respectively). It was argued that, because stress increases 5-HT activity, the poor response to stress of the sensitive group might indicate a deficit in 5-HT synthesis that is improved by this dietary intervention.
There is another link between macronutrient intake, stress, and mood. Chronic dysfunction of the stress-sensitive hormone cortisol and its controlling hypothalamic pituitary adrenal (HPA) axis is associated with depression and anxiety and with abdominal obesity. Moreover, protein-rich meals that prevent a meal-induced fall in arousal also stimulate the release of cortisol in unstressed people, and the degree of this effect is positively correlated with the probability of poor psychological well-being. Chronically, a carbohydrate-rich diet is associated with better overall mood state and lower average plasma cortisol than a high-protein diet. Acutely, a carbohydrate preload, but not protein or fat load, enhances cortisol release during stress. This may be related to findings from both human and animal research that suggest that eating carbohydrate-rich and perhaps high-fat foods can help restore normal HPA axis function and gluco-corticoid stress responses. Raised levels of cortisol in stressed people contribute to insulin resistance, which in turn promotes abdominal obesity. However, insulin resistance may increase the likelihood of high-carbohydrate low-protein foods raising brain tryptophan and 5-HT levels, because of increased levels of plasma fatty acids, which result in more unbound tryptophan in plasma. Conversely, it has also been found that high baseline cortisol predicts induction of depression by dietary depletion of tryptophan. This might underlie recent findings that insulin-resistant people are less prone to suicide and depression, both of which are believed to be increased by low 5-HT function. Similarly, patients with seasonal affective disorder show increased insulin resistance in the winter, together with a greater predilection for sugar-rich foods. Unfortunately, despite this protective effect, insulin resistance is a substantial risk to health because of its association with cardiovascular disease.
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