Biological age is increased by stress and restored upon recovery

The activation of stress-related neuroendocrine systems helps to maintain homeostasis, but excessive stress can damage body functions. We review current evidence from basic sciences and epidemiology linking stress to the development and progression of metabolic disorders throughout life. Findings from rodents demonstrate that stress can affect features of metabolic dysfunction, such as insulin resistance, glucose and lipid homeostasis, as well as ageing processes such as cellular senescence and telomere length shortening. In human studies, stressors in the home, workplace and neighbourhood are associated with accelerated ageing and metabolic and immune alterations, both directly and indirectly via behavioural risks. The likelihood of developing clinical conditions, such as diabetes mellitus and hepatic steatosis is increased in individuals with adverse childhood experiences or long-term (years) or severe stress at work or in private life. The increased risk of metabolic disorders is often associated with other stress-related conditions, such as mental health disorders, cardiovascular disease and increased susceptibility to infections. Equally, stress can worsen prognosis in metabolic diseases. As favourable modifications in stressors are associated with reductions in incidence of metabolic disorders, further investigation of the therapeutic value of targeting stress in personalized medicine is warranted. 

/pdf/the-multiple-roles-of-life-stress-in-metabolic-disorders-3ngn73iq.pdf

The multiple roles of life stress in metabolic disorders

Significance In a nationally representative US adult population, measures of epigenetic age acceleration are associated with concurrent cognitive dysfunction, functional limitations and chronic conditions measured 2 y after DNA methylation measurement, and 4-y mortality. PC-based clocks do not significantly change the relationship between DNAm-based age acceleration and health outcomes. These findings suggest that along with demographic measures, SES, mental health, and health behaviors, epigenetic age acceleration serves as a useful tool to facilitate investigation into the biology of aging and helps in the prediction of later life morbidity and mortality.

Epigenetic-based age acceleration in a representative sample of older Americans: Associations with aging-related morbidity and mortality

Research on maternal-fetal epigenetic programming argues that adverse exposures to the intrauterine environment can have long-term effects on adult morbidity and mortality. However, causal research on epigenetic programming in humans at a population level is rare and is often unable to separate intrauterine effects from conditions in the postnatal period that may continue to impact child development. In this study, we used a quasi-natural experiment that leverages state-year variation in economic shocks during the Great Depression to examine the causal effect of environmental exposures in early life on late-life accelerated epigenetic aging for 832 participants in the U.S. Health and Retirement Study (HRS). HRS is the first population-representative study to collect epigenome-wide DNA methylation data that has the sample size and geographic variation necessary to exploit quasi-random variation in environments, which expands possibilities for causal research in epigenetics. Our findings suggest that exposure to changing economic conditions in the 1930s had lasting impacts on next-generation epigenetic aging signatures that were developed to predict mortality risk (GrimAge) and physiological decline (DunedinPoAm). We show that these effects are localized to the in utero period specifically as opposed to the pre-conception, postnatal, childhood, or early adolescent periods. After evaluating changes in mortality rates for Depression-era birth cohorts, we conclude that these effects likely represent lower bound estimates of the true impacts of the economic shock on long-term epigenetic aging.

https://doi.org/10.1101/2022.05.18.22275258

In utero exposure to the Great Depression is reflected in late-life epigenetic aging signatures

Key Points Question As a biomarker of biological aging, does DNA methylation (DNAm) adequately assess the rate of change in aging over time among socioeconomically diverse middle-aged African American and White adults? Findings In this cohort study of 470 socioeconomically diverse middle-aged African American and White adults, household income below poverty level and African American race were associated with a higher DNAm-based pace of aging. Meaning These findings suggest that the DNAm-based pace of aging may provide insight into how social constructs such as race play a role in healthy aging.

/pdf/association-of-race-and-poverty-status-with-dna-methylation-2cwcttpt.pdf

Association of Race and Poverty Status With DNA Methylation–Based Age

Acceleration of biological processes of aging is hypothesized to drive excess morbidity and mortality in socially disadvantaged populations. DNA methylation measures of biological aging provide tools for testing this hypothesis.Next-generation DNA methylation measures of biological aging developed to predict mortality risk and physiological decline are more predictive of morbidity and mortality than the original epigenetic clocks developed to predict chronological age. These new measures show consistent evidence of more advanced and faster biological aging in people exposed to socioeconomic disadvantage and may be able to record the emergence of socially determined health inequalities as early as childhood. Next-generation DNA methylation measures of biological aging also indicate race/ethnic disparities in biological aging. More research is needed on these measures in samples of non-Western and non-White populations. New DNA methylation measures of biological aging open opportunities for refining inference about the causes of social disparities in health and devising policies to eliminate them. Further refining measures of biological aging by including more diversity in samples used for measurement development is a critical priority for the field. 

Integrating DNA Methylation Measures of Biological Aging into Social Determinants of Health Research

Lower socioeconomic status is associated with faster biological aging, the gradual and progressive decline in system integrity that accumulates with advancing age. Efforts to promote upward social mobility may, therefore, extend healthy lifespan. However, recent studies suggest that upward mobility may also have biological costs related to the stresses of crossing social boundaries. We tested associations of life-course social mobility with biological aging using data from participants in the 2016 Health and Retirement Study (HRS) Venous Blood Study who provided blood-chemistry (n = 9,255) and/or DNA methylation (DNAm) data (n = 3,976). We quantified social mobility from childhood to later-life using data on childhood family characteristics, educational attainment, and wealth accumulation. We quantified biological aging using 3 DNAm "clocks" and 3 blood-chemistry algorithms. We observed substantial social mobility among study participants. Those who achieved upward mobility exhibited less-advanced and slower biological aging. Associations of upward mobility with less-advanced and slower aging were consistent for blood-chemistry and DNAm measures of biological aging, and were similar for men and women and for Black and White Americans (Pearson-r effect-sizes ∼0.2 for blood-chemistry measures and the DNAm GrimAge clock and DunedinPoAm pace-of-aging measures; effect-sizes were smaller for the DNAm PhenoAge clock). Analysis restricted to educational mobility suggested differential effects by racial identity; mediating links between educational mobility and healthy aging may be disrupted by structural racism. In contrast, mobility producing accumulation of wealth appeared to benefit White and Black Americans equally, suggesting economic intervention to reduce wealth inequality may have potential to heal disparities in healthy aging. 

Social mobility and biological aging among older adults in the United States

Decision letter: Assessing the causal role of epigenetic clocks in the development of multiple cancers: a Mendelian randomization study

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Integrating DNA Methylation Measures of Biological Aging into Social Determinants of Health Research

Social mobility and biological aging among older adults in the United States

Decision letter: Assessing the causal role of epigenetic clocks in the development of multiple cancers: a Mendelian randomization study