Author: Carroll JE, Diez Roux AV, Fitzpatrick AL, Seeman T.
Division of Geriatrics (T.S.), The Cousins Center for Psychoneuroimmunology, UCLA Semel Institute of Neuroscience and Human Behavior (J.E.C.), David Geffen School of Medicine, University of California, Los Angeles, CA; Department of Epidemiology (A.V.D.R.), Center for Integrative Approaches to Health Disparities, University of Michigan, Ann Arbor, MI; and Department of Epidemiology (A.L.F.), School of Public Health, University of Washington, Seattle, WA.
Conference/Journal: Psychosom Med.
Date published: 2013 Jan 31
Other: Word Count: 206
ObjectiveThe primary goal was to test the hypothesis that limited social support (SS) is related to shorter leukocyte telomere length (LTL), particularly in an older adult population.MethodsCross-sectional analyses were performed on 948 participants aged 45 to 84 years at Examination 1 of the Multi-Ethnic Study of Atherosclerosis (18.4% white, 53.1% Hispanics, and 28.5% African American). LTL was determined by using quantitative polymerase chain reaction, and SS was measured with the Enhancing Recovery in Coronary Heart Disease SS inventory.ResultsAcross the entire sample, SS was not associated with LTL (p = .87) after adjusting for demographic (age, sex, race/ethnicity, socioeconomic status), age × sex, age × race, health (body mass index, diabetes, pulse pressure), and life-style factors (smoking, physical activity, diet); however, the interaction term age (dichotomized) × SS was significant (p = .001). Stratification by age group revealed a positive association between SS (score range, 5-25) and LTL in the older (65-84 years; B[SE] = .005[.002]; p = .007) but not younger participants (45-64 years; p = .12) after adjusting for covariates.ConclusionsThese results from a racially/ethnically diverse community sample of men and women provide initial evidence that low SS is associated with shorter LTL in adults aged 65 years and older and is consistent with the hypothesis that social environment may contribute to rates of cellular aging, particularly in late life.