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In a recent review published in the American Journal of Medicine titled “An Integrative Approach to HPA Axis Dysfunction: From Recognition to Recovery,” the authors provide evidence that, in addition to psychological stress, lifestyle factors, and environmental exposures, there are a number of dietary contributors to HPA axis imbalance, often interfering with sleep patterns. For example, the article cites that diets high in sugar or fat, excessive or insufficient caloric consumption, and micronutrient deficiencies may all impair HPA function.
One concept often used to illustrate the cumulative effects of various stressors, including physical and psychological stressors, is allostatic load. Briefly, stressors wear down the regulatory systems of the body, marked by the secretion of primary stress markers (e.g., cortisol, dehydroepiandrosterone sulfate (DHEA-S), epinephrine and norepinephrine, and C-reactive protein), which promote secondary stress markers (including central adiposity, hypertension, hyperlipidemia, and hyperglycemia) and the development of chronic issues.
In one cross-sectional and nationally representative (NHANES) study, a significant and inverse association between diet quality and allostatic load was observed among people over 30 years old (but not under), with significantly lower risk for an elevated allostatic load among people in the higher quintiles of the Healthy Eating Index 2015 score (calculated to favor whole foods, protein, fruits/vegetables, etc., while minimizing refined foods, sugar, fat, etc.). Similarly, the Dietary Inflammation Index (DII) was shown to partly mediate an association between allostatic load and depressive symptoms in an NHANES population, with DII and allostatic load independently and synergistically increasing the risk for depression. For example, there was a nearly 4-fold risk for depressive symptoms among people with inflammatory diets and high allostatic load, and eliminating both was estimated to prevent 40% of the cases of depression.
The proposed mechanisms are well illustrated in a recent review of the advances in nutritional cognitive neuroscience. A low-quality diet increases inflammation, oxidative stress, and ultimately allostatic load, which changes brain networks involved in stress and emotion regulation (e.g., marked by hyperconnectivity and increased cortical thinning in the default mode network and hypoconnectivity and increased cortical thinning in the salience network). In contrast, a high-quality diet may mitigate an elevated allostatic load by dampening inflammation and oxidative stress. This article also reviews several specific dietary interventions that have been linked to a reduced allostatic load. For example, nutrients such as tryptophan, omega-3 fatty acids, B vitamins, vitamin D, polyphenols, and carotenoids all may play a role in mitigating excessive allostatic load and improving brain health.
Dietary patterns have also been linked to allostatic load, with protective effects observed for the Mediterranean diet, low-glycemic load, and greater plant protein intake, whereas the dietary insulin index is associated with a higher risk for sleep disorders. In addition to dietary components, timing of meals has also been linked to allostatic load and HPA axis dysfunction; for example, eating late at night may drive hyperglycemia, cortisol release, renal sodium retention, and sleep disturbance.
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