A birth cohort that has been tracked from childhood is now entering its fifth decade, and researchers will measure how fast each person’s body is ageing across multiple organ systems. Age-related diseases such as cardiovascular disease, type 2 diabetes, and dementia are costly to treat once they appear, and prevention efforts have been hampered because almost nothing is known about how biological ageing unfolds during the first half of life. This study fills that gap by using decades of biomarker data—collected repeatedly from the same individuals—to model the pace of ageing from the twenties onward. If the research succeeds, it will reveal why some people’s bodies remain biologically younger than their chronological age, and identify the developmental origins, genomic signatures, and functional consequences of faster or slower ageing. These findings could eventually support interventions applied before midlife to slow ageing and prevent age-related disease, improving the quality of longer lives. The work is fundamental science—it does not test a treatment or intervention—but it provides the missing evidence base needed to translate gerontology discoveries into preventive strategies for younger humans.
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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 gerontology discoveries into preventive 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, associated cognitive changes, 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 during midlife or earlier, to slow aging, prevent age-related disease, and improve the quality of longer lives.
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