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Allostatic load (AL) manifests from both failed and successful morphological and biological stress responses across physiological systems. Genes, culture, and environment affect adaptive responses to stressors. Associations of AL with age and sex commonly are found across samples; AL is enhanced by senescent processes, predisposes individuals to chronic non-communicable diseases, and predicts future morbidity and mortality. AL represents physical decline from “optimal” physiological function to a more dysfunctional phenotype. Reported research has yet to explore associations of genetic markers with AL. We examined such associations in a sample of 284 American Samoans. Basing AL on seven secondary mediators of allostasis, along with aspects of body habitus and glucose metabolism we examined associations with apolipoprotein E and H, ACE, and ANP genotypes. AL did not differ significantly by apolipoprotein H or ANP genotypes. However, apolipoprotein E and ACE significantly associated with AL. Persons with the apolipoprotein E (3,2) genotype showed significantly lower AL than the (3,3) or (2,2) genotypes. ACE genotypes also demonstrated significant associations with AL (p<.05). As mortality from chronic diseases is a hallmark of the 20th century, genetic predictors of physiological dysfunction may be important modulators of risks for morbidity, senescent biology, and mortality across populations. Examination of such associations provides enhanced understandings of gene-environment-culture interactions across populations.