Accelerated Biological Age Measures Correlate With Cardiometabolic Disease Risk
If measures of biological age are in fact reflections of the burden of damage and dysfunction making up degenerative aging, then we should expect there to be correlations between an accelerated biological age greater than chronological age and risk of conditions such as diabetes that are already known to be associated with increased mortality and reduced life span. The study here shows that to be the case for two aging clocks that are derived from blood chemistry measures rather than omics data.
Cardiometabolic diseases (CMDs) have emerged as the most significant health challenges. Cardiometabolic multimorbidity (CMM) refers to the coexistence of two or more CMDs, including conditions such as stroke, ischemic heart disease (IHD), and type 2 diabetes (T2D). Populations with CMM have a two-fold increased mortality risk and a 12-15 year reduced life expectancy than those with single CMDs. Biological aging, which is associated with decreased metabolic rates, vascular stiffening, chronic inflammation, and oxidative stress, as well as the interplay of comorbidities, may underlie the progression of CMDs to CMM.
The ideal measurement strategy for biological aging should include as many system indicators as possible. For predicting disease, the PhenoAge and Klemera-Doubal method Biological Age (KDM-BA) are the best-validated algorithms according to blood-chemistry-derived measures in multi-ethnic cohorts of older adults. Accelerated aging refers to the phenomenon where an individual's biological age advances more rapidly than their chronological age. This concept goes beyond the mere passage of time, as it emphasizes the underlying biological processes and pathological changes. Thus, this study used both algorithms to test the association between biological aging and CMM.
The study included 415,147 individuals with an average age of 56.5 years. During the average 11-year follow-up period, CMD-free individuals with accelerated aging had a significantly greater risk of CMD (KDM-BA, hazard ratio [HR] 1.456; PhenoAge, HR 1.404), CMM (KDM-BA, HR 1.952; PhenoAge, HR 1.738), dementia (KDM-BA, HR 1.243; PhenoAge, HR 1.212), and mortality (KDM-BA, HR 1.821; PhenoAge, HR 2.047) in fully-adjusted Cox regression models. Accelerated aging had adjusted HRs of 1.489 (KDM-BA) and 1.488 (PhenoAge) for CMM, 1.434 (KDM-BA) and 1.514 (PhenoAge) for dementia, and 1.943 (KDM-BA) and 2.239 (PhenoAge) for mortality in participants with CMD at baseline.