![]() Similarly, most deaths observed during follow-up occurred to the oldest NHANES participants, leaving the algorithm’s utility for quantification of aging in younger persons uncertain. Because NHANES participants were all surveyed at one time point, age differences in biomarker levels were not independent of cohort effects measured aging also included secular trends in environmental and behavioral influences on biomarkers. ” In more than 9,000 NHANES participants aged 30–75 y at baseline, Biological Age outperformed chronological age in predicting mortality over a two-decade follow-up ( 26). A promising algorithm is the 10-biomarker US National Health and Nutrition Survey (NHANES)-based measure of “Biological Age. Multibiomarker algorithms have been suggested as a more reliable alternative to single-marker aging indicators ( 23– 25). Candidate biomarkers of aging are numerous, but findings are mixed ( 19– 22). Measuring the aging process is controversial. Results Are Young Adults Aging at Different Rates? We further tested whether, by midlife, young adults who were aging more rapidly already exhibited deficits in their physical functioning, showed signs of early cognitive decline, and looked older to independent observers. We next tested the hypothesis that cohort members with “older” physiologies at age 38 had actually been aging faster than their same chronologically aged peers who retained “younger” physiologies specifically, we tested whether indicators of the integrity of their cardiovascular, metabolic, and immune systems, their kidneys, livers, gums, and lungs, and their DNA had deteriorated more rapidly according to measurements taken repeatedly since a baseline 12 y earlier at age 26. When they were 38 y old, we examined their physiologies to test whether this young population would show evidence of individual variation in aging despite remaining free of age-related disease. We studied aging in a population-representative 1972–1973 birth cohort of 1,037 young adults followed from birth to age 38 y with 95% retention: the Dunedin Study ( SI Appendix). The main obstacle to studying aging before old age-and before the onset of age-related diseases-is the absence of methods to quantify the Pace of Aging in young humans. A solution is to study human aging in the first half of the life course, when individuals are starting to diverge in their aging trajectories, before most diseases (and regimens to manage them) become established. Moreover, whereas animals’ brief lives make it feasible to study animal aging in the laboratory, humans’ lives span many years. The difficulty with these nonhuman models is that they do not typically capture the complex multifactorial risks and exposures that shape human aging. Early interventions to slow aging can be tested in model organisms ( 17, 18). Thus, intervention to reverse or delay the march toward age-related diseases must be scheduled while people are still young ( 16). Age-related changes to physiology accumulate from early life, affecting organ systems years before disease diagnosis ( 12– 15). The difficulty with studying aging in old humans is that many of them already have age-related diseases ( 9– 11). Paradoxically, these seemingly sensible strategies pose translational difficulties. Measured biological aging in young adults can be used to identify causes of aging and evaluate rejuvenation therapies.Īt present, much research on aging is being carried out with animals and older humans. Already, before midlife, individuals who were aging more rapidly were less physically able, showed cognitive decline and brain aging, self-reported worse health, and looked older. Young individuals of the same chronological age varied in their “biological aging” (declining integrity of multiple organ systems). We applied these methods to assess biological aging in young humans who had not yet developed age-related diseases. Our longitudinal measure allows quantification of the pace of coordinated physiological deterioration across multiple organ systems (e.g., pulmonary, periodontal, cardiovascular, renal, hepatic, and immune function). We developed and validated two methods by which aging can be measured in young adults, one cross-sectional and one longitudinal. We studied aging in 954 young humans, the Dunedin Study birth cohort, tracking multiple biomarkers across three time points spanning their third and fourth decades of life. As a result, little is known about aging in young humans. However, most human aging research examines older adults, many with chronic disease. Interventions to slow human aging will need to be applied to still-young individuals. Translation to humans is needed to address the challenges of an aging global population. ![]() Antiaging therapies show promise in model organism research.
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