Stress, diet, and aging: a comprehensive analysis of allostatic load in biological aging.

Abstract

Background: As the global population continues to age, biological aging has emerged as a significant public health challenge. It is imperative to identify modifiable factors and underlying mechanisms that can promote healthy aging. Allostatic load (AL), a comprehensive indicator of chronic stress, is linked to numerous adverse outcomes in behavioral health. However, there is a paucity of comprehensive analyses and mechanistic investigations regarding the relationship between AL and biological aging across the entire population. This study seeks to elucidate the relationship between AL and biological aging, with a particular focus on examining the mediating role of the Dietary Inflammatory Index (DII).

Method: This study analyzed data from NHANES (2001-2010 and 2015-2018) with 25,775 U.S. adults, excluding those with missing data. It measured AL using 8 biomarkers and assessed biological aging with four indicators: Phenotypic Age, Biological Age, GOLD BioAge, and Light BioAge. The DII was calculated from 24-h dietary recall of 45 food items. Sociodemographic and clinical factors were covariates. Weighted linear and logistic regressions examined the complex relationship between AL, DII, and biological aging, with subgroup and mediation analyses exploring mediating role of DII in the AL-aging link.

Result: A total of 21.56% of participants were in the high AL group, showing significantly higher DII scores and elevated biological aging indicators compared to the low AL group (P < 0.001). After adjusting for confounders, high AL was linked to faster biological aging, with a 2.08-year increase in Phenotypic Age and a 9.06-year increase in Biological Age. Odds ratios for elevated GOLD BioAge and Light BioAge were 1.60 and 2.16, respectively (P < 0.001). The AL-aging link was stronger in young/middle-aged adults, females, and non-obese individuals. DII was positively linked to all aging indicators, and exploratory mediation analysis suggested that DII may statistically account for a small proportion of the AL-aging association, with mediation proportions ranging from 0.33% to 5.45% (P < 0.001).

Conclusion: In a nationally representative sample of U.S. adults, elevated AL is significantly associated with accelerated biological aging assessed by multiple complementary indicators, and exploratory mediation analysis suggested that DII may partly account for part of this association. These findings underscore the importance of mitigating chronic physiological stress and reducing the inflammatory potential of the diet as strategies to promote healthy aging. Clinical assessment of AL and DII may provide valuable insights for identifying individuals at risk of accelerated biological aging and guiding targeted intervention measures to improve long-term health outcomes.