Testing Life Course Models Whereby Juvenile and Adult Adversity Combine to Influence Speed of Biological Aging.
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ABSTRACT:
SUBMITTER: Simons RL
PROVIDER: S-EPMC7751897 | biostudies-literature | 2019 Sep
REPOSITORIES: biostudies-literature
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Testing Life Course Models Whereby Juvenile and Adult Adversity Combine to Influence Speed of Biological Aging.
Simons Ronald L RL Lei Man-Kit MK Beach Steven R H SRH Simons Leslie Gordon LG Barr Ashley B AB Gibbons Frederick X FX Philibert Robert A RA
Journal of health and social behavior 20190814 3
The present study extends prior research on the links between social adversity and aging by employing more comprehensive measures of adversity and a new gene expression index of aging. Hierarchical regression and 20 years of data from a sample of 381 black Americans were used to test models regarding the impact of social adversity on speed of aging. Consistent with the early life sensitivity model, early adversity continued to predict accelerated aging after controlling for adult adversity. Cont ...[more]
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Project description:Prior research shows that individuals who have exhibited antisocial behavior are in poorer health than their same-aged peers. A major driver of poor health is aging itself, yet research has not investigated relationships between offending trajectories and biological aging. We tested the hypothesis that individuals following a life-course persistent (LCP) antisocial trajectory show accelerated aging in midlife. Trajectories of antisocial behavior from age 7 to 26 years were studied in the Dunedin Multidisciplinary Health and Development Study, a population-representative birth cohort (N = 1037). Signs of aging were assessed at age 45 years using previously validated measures including biomarkers, clinical tests, and self-reports. First, we tested whether the association between antisocial behavior trajectories and midlife signs of faster aging represented a decline from initial childhood health. We then tested whether decline was attributable to tobacco smoking, antipsychotic medication use, debilitating illnesses in adulthood, adverse exposures in childhood (maltreatment, socioeconomic disadvantage) and adulthood (incarceration), and to childhood self-control difficulties. Study members with a history of antisocial behavior had a significantly faster pace of biological aging by midlife, and this was most evident among individuals following the LCP trajectory (β, 0.22, 95%CI, 0.14, 0.28, p ≤ 0.001). This amounted to 4.3 extra years of biological aging between ages 25-45 years for Study members following the LCP trajectory compared to low-antisocial trajectory individuals. LCP offenders also experienced more midlife difficulties with hearing (β, -0.14, 95%CI, -0.21, -0.08, p ≤ 0.001), balance (β, -0.13, 95%CI, -0.18, -0.06, p ≤ 0.001), gait speed (β, -0.18, 95%CI, -0.24, -0.10, p ≤ 0.001), and cognitive functioning (β, -0.25, 95%CI, -0.31, -0.18, p ≤ 0.001). Associations represented a decline from childhood health. Associations persisted after controlling individually for tobacco smoking, antipsychotic medication use, midlife illnesses, maltreatment, socioeconomic status, incarceration, and childhood self-control difficulties. However, the cumulative effect of these lifestyle characteristics together explained why LCP offenders have a faster Pace of Aging than their peers. While older adults typically age-out of crime, LCP offenders will likely age-into the healthcare system earlier than their chronologically same-aged peers. Preventing young people from offending is likely to have substantial benefits for health, and people engaging in a LCP trajectory of antisocial behaviors might be the most in need of health promotion programs. We offer prevention and intervention strategies to reduce the financial burden of offenders on healthcare systems and improve their wellbeing.
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Project description:This study set out to examine the role of different adversities experienced at different life course stages on cognitive aging (i.e., level and change). Data from the longitudinal study: Survey of Health, Ageing, and Retirement in Europe (SHARE) with the selection of participants over 60 years were used (N = 2662, Mdnage = 68, SDage = 5.39) in a Structural Equation Modeling. In early life, the experience of hunger predicted lower delayed recall (β = - 0.10, p < 0.001) and verbal fluency (β = - 0.06, p = 0.001) performance in older age, whereas financial hardship predicted lower verbal fluency (β = - 0.06, p = 0.005) performance and steeper decline in delayed recall (β = - 0.11, p < 0.001). In early adulthood, financial hardship and stress predicted better delayed recall (financial hardship: β = 0.08, p = 0.001; stress: β = 0.07, p = 0.003) and verbal fluency performance (financial hardship: β = 0.08, p = 0.001; stress β = 0.10, p < 0.001), but no adversities were associated with a change in cognitive performance. In middle adulthood, no adversities were associated with the level of cognitive performance, but financial hardship predicted lower decline in delayed recall (β = 0.07, p = 0.048). This study highlights the importance of disentangling the period effect from the specific effect of the adversity experienced in the association between adversity and cognition in older age. Moreover, differential results for delayed recall and verbal fluency measures suggest that it is also important to consider the cognitive outcome domains examined.
| S-EPMC10227009 | biostudies-literature
Project description:BackgroundJuvenile hormone (JH) has been demonstrated to control adult lifespan in a number of non-model insects where surgical removal of the corpora allata eliminates the hormone's source. In contrast, little is known about how juvenile hormone affects adult Drosophila melanogaster. Previous work suggests that insulin signaling may modulate Drosophila aging in part through its impact on juvenile hormone titer, but no data yet address whether reduction of juvenile hormone is sufficient to control Drosophila life span. Here we adapt a genetic approach to knock out the corpora allata in adult Drosophila melanogaster and characterize adult life history phenotypes produced by reduction of juvenile hormone. With this system we test potential explanations for how juvenile hormone modulates aging.ResultsA tissue specific driver inducing an inhibitor of a protein phosphatase was used to ablate the corpora allata while permitting normal development of adult flies. Corpora allata knockout adults had greatly reduced fecundity, inhibited oogenesis, impaired adult fat body development and extended lifespan. Treating these adults with the juvenile hormone analog methoprene restored all traits toward wildtype. Knockout females remained relatively long-lived even when crossed into a genotype that blocked all egg production. Dietary restriction further extended the lifespan of knockout females. In an analysis of expression profiles of knockout females in fertile and sterile backgrounds, about 100 genes changed in response to loss of juvenile hormone independent of reproductive state.ConclusionsReduced juvenile hormone alone is sufficient to extend the lifespan of Drosophila melanogaster. Reduced juvenile hormone limits reproduction by inhibiting the production of yolked eggs, and this may arise because juvenile hormone is required for the post-eclosion development of the vitellogenin-producing adult fat body. Our data do not support a mechanism for juvenile hormone control of longevity simply based on reducing the physiological costs of egg production. Nor does the longevity benefit appear to function through mechanisms by which dietary restriction extends longevity. We identify transcripts that change in response to juvenile hormone independent of reproductive state and suggest these represent somatically expressed genes that could modulate how juvenile hormone controls persistence and longevity.
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Project description:OBJECTIVES:To examine the effect of the relationship between alcohol and cigarette consumption on biological aging using deoxyribonucleic acid methylation-based indices. DESIGN:Hierarchical linear regression modeling followed by fitting of higher-order effects. SETTING:Longitudinal studies of aging and the effect of psychosocial stress. PARTICIPANTS:Participants in two ethnically informative cohorts (n = 656 white, n = 180 black). MEASUREMENTS:Deviation of biological age from chronological age as a result of smoking and alcohol consumption. RESULTS:Greater cigarette consumption was associated with accelerated biological aging, with strong effects evident at even low levels of exposure. In contrast, alcohol consumption was associated with a mixed effect on biological aging and pronounced nonlinear effects. At low and heavy levels of alcohol consumption, there was accelerated biological aging, whereas at intermediate levels of consumption there was a relative decelerating effect. The decelerating effects of alcohol were particularly notable at loci for which methylation increased with age. CONCLUSION:These data support prior epidemiological studies indicating that moderate alcohol use is associated with healthy aging, but we urge caution in interpreting these results. Conversely, smoking has strong negative effects at all levels of consumption. These results also support the use of methylomic indices as a tool for assessing the impact of lifestyle on aging.
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