Researchers here note the results from a study in which a comparatively simple compound biomarker of aging exhibited correlations with the manifestations of aging and age-related disease. The past decade of work on measurement of aging has shown that it is comparatively straightforward to produce metrics that reflect the increasing burden of damage and dysfunction. Making use of the best of these metrics to assess potential approaches to the development of age-slowing and rejuvenating therapies has yet to be carried out in any widespread fashion, however.
As we age, the risk that we will experience chronic diseases (for example, heart disease, diabetes, and cancer) and declining capacities (for example, reduced strength, impaired hearing, and poorer memory) increases. All individuals age chronologically at the same rate, but there is marked variation in their rate of biological aging; this may help explain why some adults experience age-related decline faster than others.
Biological aging can be defined as decline that (1) simultaneously involves multiple organ systems and (2) is gradual and progressive5. Across the lifespan, the consequences of individual differences in genetic endowment, cellular biology, and life experiences accumulate, driving the divergence of biological age from chronological age for some people. Among older adults of the same chronological age, those with accelerated biological aging (as measured by blood and DNA methylation biomarkers) are more likely to develop heart disease, diabetes, and cancer and have a higher rate of cognitive decline, disability, and mortality.
Current disease-management strategies usually treat and manage each age-related chronic disease independently. In contrast, the geroscience hypothesis proposes that many age-related chronic diseases could be prevented by slowing biological aging itself. The geroscience hypothesis states that biological aging drives cellular-level deterioration across all organ systems, thereby causing the exponential rise in multimorbidity across the second half of the lifespan. The implication is that by slowing biological aging directly, instead of managing each disease separately, the risk for all chronic age-related diseases could be simultaneously ameliorated.
We measured biological aging in a population-representative 1972-1973 birth cohort of 1,037 individuals followed from birth to age 45 years in 2019 with 94% retention: the Dunedin Study. Over 20 years - at ages 26, 32, 38 and 45 - we repeatedly collected 19 biomarkers to assess changes in the function of cardiovascular, metabolic, renal, immune, dental, and pulmonary systems, and quantified age-related decline shared among these systems. We call this index of biological aging in the Dunedin Study the 'Pace of Aging'.
At age 45 in 2019, participants with faster Pace of Aging had more cognitive difficulties, signs of advanced brain aging, diminished sensory-motor functions, older appearances, and more pessimistic perceptions of aging. People who are aging more rapidly than same-age peers in midlife may prematurely need supports to sustain independence that are usually reserved for older adults. Chronological age does not adequately identify need for such supports.