Declining fertility rates, aging of the baby-boomers, and increasing life expectancy are leading to population aging. As the population ages, this increases the public-health burden of age-related conditions, such as cardiovascular disease, type 2 diabetes, and dementia. Treating un-prevented diseases in late life has proven costly and ineffective. It is now known that potentially preventable risk exposures and physiological causes of age-related disease emerge in childhood. This recognition lends new scientific significance to studies that have followed cohorts from childhood. It is also now known that the pathogenesis of age-related diseases involves gradually accumulating decline in organ systems, beginning in the first half of the life course. Consequently, new interventions aiming to prevent age-related diseases will have to be applied to individuals while they are yet young, before they reach midlife. Translation of basic-science geronotology discoveries into interventions for young humans is lacking because virtually nothing is known about the process of biological aging during the first half of the life course. This prompts our proposal to study the pace of biological aging from the twenties forward. We will use the Dunedin Multidisciplinary Health & Development Study, a longitudinal study of a birth cohort now entering its fifth decade. This study combines methods of demographic/economic surveys, clinical- quality health assessments, biobanking, and linkage to nationwide administrative records (health, welfare, finances). We propose to administer a full-day data-collection protocol to the 1004 living members of the birth cohort. To assess each cohort member's pace of biological aging we will: (a) measure biomarkers across multiple organ systems, and (b) statistically model correlated change in these biomarkers assessed at ages 26, 32, 38, and 45 years. We will describe individual variation in the pace of aging, plus its developmental origins, genomic signatures, functional consequences, and economic costs. We will identify attributes that set apart individuals whose bodies are months or years younger than their chronological age. The proposed work will improve knowledge by generating findings to support future interventions to slow aging, prevent age-related disease, and improve the quality of longer lives.

Public Health Relevance

As the population ages and life expectancy grows longer, policy makers and citizens are concerned that our extra years should be healthy, productive, and enjoyable, not extra years of disease and disability. Finding new strategies to prevent age-related disease and disability requires research to identify risk factors in early-to- midlife that can be ameliorated or reversed, well before the onset of age-related disease. This recognition lends new scientific significance to studies that have followed cohorts from childhood to midlife, including the Dunedin Study. The proposed work will use biomarker data collected from the same 1000 individuals at ages 26, 32, 38, and 45 to track the pace of their biological aging. We will uncover why some people age faster than peers born in the same year, and why some fortunate people age more slowly than their age-peers. Findings are expected to support interventions to slow aging, prevent age-related diseases, and enhance preparedness for wellbeing in late life.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
5R01AG032282-10
Application #
9687649
Study Section
Behavioral Genetics and Epidemiology Study Section (BGES)
Program Officer
Nielsen, Lisbeth
Project Start
2009-03-01
Project End
2020-03-31
Budget Start
2019-04-01
Budget End
2020-03-31
Support Year
10
Fiscal Year
2019
Total Cost
Indirect Cost
Name
Duke University
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
044387793
City
Durham
State
NC
Country
United States
Zip Code
27705
Belsky, Daniel W; Moffitt, Terrie E; Cohen, Alan A et al. (2018) Eleven Telomere, Epigenetic Clock, and Biomarker-Composite Quantifications of Biological Aging: Do They Measure the Same Thing? Am J Epidemiol 187:1220-1230
Belsky, Daniel W; Domingue, Benjamin W; Wedow, Robbee et al. (2018) Genetic analysis of social-class mobility in five longitudinal studies. Proc Natl Acad Sci U S A 115:E7275-E7284
Caspi, Avshalom; Moffitt, Terrie E (2018) All for One and One for All: Mental Disorders in One Dimension. Am J Psychiatry 175:831-844
Rasmussen, Line Jee Hartmann; Moffitt, Terrie E; Eugen-Olsen, Jesper et al. (2018) Cumulative childhood risk is associated with a new measure of chronic inflammation in adulthood. J Child Psychol Psychiatry :
Wertz, J; Caspi, A; Belsky, D W et al. (2018) Genetics and Crime: Integrating New Genomic Discoveries Into Psychological Research About Antisocial Behavior. Psychol Sci 29:791-803
Rivenbark, Joshua G; Odgers, Candice L; Caspi, Avshalom et al. (2018) The high societal costs of childhood conduct problems: evidence from administrative records up to age 38 in a longitudinal birth cohort. J Child Psychol Psychiatry 59:703-710
Righarts, A; Osborne, L; Connor, J et al. (2018) The prevalence and potential determinants of dysmenorrhoea and other pelvic pain in women: a prospective study. BJOG 125:1532-1539
Elliott, Maxwell L; Belsky, Daniel W; Anderson, Kevin et al. (2018) A Polygenic Score for Higher Educational Attainment is Associated with Larger Brains. Cereb Cortex :
Moffitt, Terrie E (2018) Male antisocial behaviour in adolescence and beyond. Nat Hum Behav 2:177-186
Shearer, Dara M; Thomson, W Murray; Cameron, Claire M et al. (2018) Periodontitis and multiple markers of cardiometabolic risk in the fourth decade: A cohort study. Community Dent Oral Epidemiol 46:615-623

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