alterations in the most basic aspects of the human experience (where and how we feel, sleep, and feed) provide the conduit through which unequal exposure to behavioral social stressors (e.g., poverty, social isolation, discrimination, and racism) culminates in disparate disease frequency and outcome. Though its linkage to specific diseases is beyond the scope of this chapter, the influence of allostatic load is one of the major gateways to chronic disease and disease conditions (cardiovascular, metabolic, and cancer). Understanding these biological physiological pathways identifies important areas for future investigation that will augment strategies for intervention, reveal mechanisms of differential disease susceptibility, and elucidate how these factors interact with behavioral, social, and environmental determinants to influence disease incidence and outcome.
2.9 Key Points
The domains that have the greatest impact on health disparities include environmental, social, behavioral, and biological determinants. These domains are inextricably linked and their combinations may have synergistic impacts on health disparities.
The concept of allostatic load provides a conceptual framework from which to understand the root or fundamental causes of health disparities in sleep, diet/nutrition, and depression.
The concept of allostatic load provides the mechanistic underpinnings revealing the biological factors that link the influence of societal conditions (e.g., socioeconomic status, social isolation, racism) to disparities in health and disease outcomes.
Understanding the biological pathways through which environmental and behavioral determinants affect health disparities will provide scientific insights that could inform interventions to decrease health disparities.
Sleep is an essential human need for maintaining biological homeostasis.
Poor sleep is a gateway to higher allostatic load and numerous mental and physical health conditions such as anxiety and depression, obesity, hypertension, type 2 diabetes, cardiovascular disease, and premature mortality.
Large racial/ethnic disparities in sleep and sleep disorders exist. Therefore, preventing or minimizing the impact of modifiable environmental and social disturbances on sleep duration, quality, and timing could help mitigate racial/ethnic and socioeconomic disparities in common chronic health conditions associated with rising levels of allostatic load.
Addressing sleep disparities to prevent subsequent poor health outcomes will require more racial/ethnic minority inclusion in scientific studies.
Disparities in the consumption of nutritious food are associated with disparities in health and well‐being.
Food deserts and food insecurity are more likely to be concentrated in neighborhoods with a high proportion of minority and low‐income populations, which likely contributes to health disparities.
While racial and ethnic disparities in many physical illnesses have been clearly established, the depression disparities have not been clearly delineated.
Individuals of low SES and racial/ethnic minorities (especially Blacks, Hispanics/Latinos, and Native Americans) usually live and work in environments with limited material and social resources and increased probability of exposure to threats—and, thus, report higher levels of stressors and stress than high‐SES and White individuals. Nonetheless, Blacks and Hispanics/Latinos have been less frequently given depression diagnoses than Whites.
Research should focus on identifying key developmental periods in the life course to target the antecedents of allostatic load which, in addition to delineating key areas of vulnerability and resilience, may yield effective interventions to decrease depression rates among vulnerable populations.
Disclaimer
The views and opinions expressed in this chapter are those of the authors only and do not necessarily represent the views, official policy, or position of the U.S. Department of Health and Human Services or any of its affiliated institutions or agencies.
References
1 1 Gardner, K. (2018). The science of cancer health disparities: a young discipline with an old heritage. The American Journal of Pathology 188 (2): 268–270.
2 2 Sterling, P. and Eyer, J. (1981). Biological basis of stress‐related mortality. Social Science & Medicine Part E 15 (1): 3–42.
3 3 Seeman, T.E., McEwen, B.S., Rowe, J.W. et al. (2001). Allostatic load as a marker of cumulative biological risk: MacArthur studies of successful aging. Proceedings of the National Academy of Sciences of the United States of America 98 (8): 4770–4775.
4 4 Chrousos, G.P. and Gold, P.W. (1992). The concepts of stress and stress system disorders. Overview of physical and behavioral homeostasis. Journal of the American Medical Association 267 (9): 1244–1252.
5 5 Nicolaides, N.C., Kyratzi, E., Lamprokostopoulou, A. et al. (2015). Stress, the stress system and the role of glucocorticoids. Neuroimmunomodulation 22 (1‐2): 6–19.
6 6 Geronimus, A.T., Hicken, M., Keene, D. et al. (2006). “Weathering” and age patterns of allostatic load scores among blacks and whites in the United States. American Journal of Public Health 96 (5): 826–833.
7 7 McEwen, B. and Lasley, E.N. (2003). Allostatic load: when protection gives way to damage. Advances in Mind‐Body Medicine 19 (1): 28–33.
8 8 Williams, D.R. and Sternthal, M. (2010). Understanding racial‐ethnic disparities in health: sociological contributions. Journal of Health and Social Behavior 51 (Suppl): S15–S27.
9 9 Spencer, R.L. and Deak, T. (2017). A users guide to HPA axis research. Physiology & Behavior 178: 43–65.
10 10 Nicolaides, N.C., Charmandari, E., Kino, T. et al. (2017). Stress‐related and circadian secretion and target tissue actions of glucocorticoids: impact on health. Frontiers in Endocrinology (Lausanne) 8: 70.
11 11 Le Thuc, O., Stobbe, K., and Cansell, C. (2017). Hypothalamic inflammation and energy balance disruptions: spotlight on chemokines. Frontiers in Endocrinology (Lausanne) 8: 197.
12 12 Saper, C.B., Scammell, T.E., and Lu, J. (2005). Hypothalamic regulation of sleep and circadian rhythms. Nature 437 (7063): 1257–1263.
13 13 Huang, W., Ramsey, K.M., Marcheva, B. et al. (2011). Circadian rhythms, sleep, and metabolism. The Journal of Clinical Investigation 121 (6): 2133–2141.
14 14 Plano, S.A., Casiraghi, L.P., Moro, P.G. et al. (2017). Circadian and metabolic effects of light: implications in weight, homeostasis and health. Frontiers in Neurology 8: 558.
15 15 de Quervain, D., Schwabe, L., and Roozendaal, B. (2017). Stress, glucocorticoids and memory: implications for treating fear‐related disorders. Nature Reviews Neuroscience 18 (1): 7–19.
16 16 Kino, T. (2015). Stress, glucocorticoid hormones, and hippocampal neural progenitor cells: implications to mood disorders. Frontiers in Physiology 6: 230.
17 17 Sheline, Y.I., Wang, P.W., Gado, M.H. et al. (1996). Hippocampal atrophy in recurrent major depression. Proceedings of the National Academy of Sciences of the United States of America 93 (9): 3908–3913.
18 18 Spijker, A.T. and van Rossum, E.F.C. (2012). Glucocorticoid sensitivity in mood disorders. Neuroendocrinology 95 (3): 179–186.
