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Social stress contributes to accelerated aging of the immune system, study finds
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August 04, 2022
Exposure to social stress was associated with accelerated aging of the immune system, according to an NIA-funded study recently published in PNAS. The body’s immune system changes as people age, and there’s large variability in these changes. The study, led by researchers at UCLA, investigated whether social stressors added to immune system decline.
The researchers analyzed data from more than 5,500 people enrolled in the Health and Retirement Study, a long-term, nationally representative study of Americans over age 50. The researchers measured stress by analyzing responses to questions about exposure to various types of social stress, including discrimination, trauma, and other life events, such as unemployment. They also analyzed the participants’ immune profiles — a snapshot of immune system function — by drawing blood and measuring white blood cell levels, specifically T lymphocytes (also called T cells). T cells are an essential part of the immune system and help the body fight off infection.
Results showed that exposure to social stress was associated with a greater proportion of T cells committed only to fighting infections like those already encountered and fewer T cells that could adapt to new challenges, indicative of accelerated immune aging. The association between social stress and T cells was still present even after controlling for education, smoking, drinking, body mass index, and race or ethnicity.
Researchers did find that, after controlling for lifestyle factors such as diet and exercise habits, the connection between stress and accelerated immune aging was not as strong. These findings suggest that improving diet and exercise behaviors in older adults may help offset the immune aging associated with stress.
Increased immune aging is associated with chronic diseases, weakened response to acute infections, increased risk of pneumonia, reduced efficacy of vaccines, and organ system aging. This study provides important insights into the effect of social stress on immune aging, highlighting the key role of health behaviors and social-environmental conditions. It also identifies potential intervention points that may be useful in addressing inequalities in aging.
This research was supported in part by NIA grants U01AG009740 and P30AG017265.
https://www.nia.nih.gov/news/social-stress-contributes-accelerated-aging-immune-system-study-finds
life trauma and chronic stress were associated with a lower percentage of CD4+ naïve T cells, whereas everyday discrimination, lifetime discrimination, and chronic stress were associated with a greater percentage of terminally differentiated CD4+ T cells. Stressful life events, lifetime discrimination and life trauma were associated with a lower percentage of CD8+ naïve T cells, whereas stressful life events, lifetime discrimination, and chronic stress were significantly associated with a higher percentage of terminally differentiated CD8+ T cells. Lifetime discrimination and chronic stress was associated with a lower CD4:CD8 ratio. These effects were all independent of chronological age, sex, and race/ethnicity.
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In the current study we focus on social stressors, that is, difficult or challenging circumstances (18) that arise from social position and experience that are expected to be stressful, that occur in adulthood.
Lifetime exposure to stressful conditions is a known risk factor for poorer health, increasing the risk for early onset of age-related disease and premature death (1–3). Models examining the mechanisms driving these effects have centered on the sequelae of repeated activation and prolonged activation of the sympathoadrenal and hypothalamic pituitary adrenal systems, leading to wear and tear at the biological level (4). Many have postulated that this wear and tear manifests at the cellular level, causing accumulation of DNA damage, increasing inflammation, shortening telomere length, and driving cellular aging (5, 6). Critically short telomere length within immune cells and cellular stress (e.g., DNA damage) can drive cells into a nonreplicating state termed cellular senescence (7, 8). In addition to localized tissue-specific aging (9), age-related changes in immune function contribute to systemic aging, organ failure, and premature mortality, making immunosenescence a critical player in aging and disease (10).
Social stressors associated with age-related T lymphocyte percentages in older US adults: Evidence from the US Health and Retirement Study
June 13, 2022
Significance
As the world’s population of older adults increases, understanding disparities in age-related health is essential. Age-related changes in the immune system play a critical role in age-related morbidity and mortality. This study assesses associations between social stress and immunophenotypes as immune age phenotype markers for the first time in a national sample of older US adults. This study helps clarify mechanisms involved in accelerated development of the immune age phenotype, including socioeconomic and lifestyle factors and cytomegalovirus infection and reactivation. This study also identifies important points of intervention that may be useful in addressing inequalities in aging.
Abstract
Exposure to stress is a risk factor for poor health and accelerated aging. Immune aging, including declines in naïve and increases in terminally differentiated T cells, plays a role in immune health and tissue specific aging, and may contribute to elevated risk for poor health among those who experience high psychosocial stress. Past data have been limited in estimating the contribution of life stress to the development of accelerated immune aging and investigating mediators such as lifestyle and cytomegalovirus (CMV) infection.
This study utilizes a national sample of 5,744 US adults over age 50 to assess the relationship of social stress (viz., everyday discrimination, stressful life events, lifetime discrimination, life trauma, and chronic stress) with flow cytometric estimates of immune aging, including naïve and terminally differentiated T cell percentages and the ratio of CD4+ to CD8+ cells. Experiencing life trauma and chronic stress was related to a lower percentage of CD4+ naïve cells.
Discrimination and chronic stress were each associated with a greater percentage of terminally differentiated CD4+ cells. Stressful life events, high lifetime discrimination, and life trauma were related to a lower percentage of CD8+naïve cells. Stressful life events, high lifetime discrimination, and chronic stress were associated with a higher percentage of terminally differentiated CD8+ cells. High lifetime discrimination and chronic stress were related to a lower CD4+:CD8+ ratio. Lifestyle factors and CMV seropositivity partially reduced these effects. Results identify psychosocial stress as a contributor to accelerating immune aging by decreasing naïve and increasing terminally differentiated T cells.
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