Psychological stress— both perceived stress and chronicity of stress—is significantly associated with higher oxidative stress, lower telomerase activity, and shorter telomere length, which are known determinants of cell senescence and longevity, in peripheral blood mononuclear cells from healthy premenopausal women. Women with the highest levels of perceived stress have telomeres shorter on average by the equivalent of at least one decade of additional aging compared to low stress women. These findings have implications for understanding how, at the cellular level, stress may promote earlier onset of age-related diseases. People who are stressed over long periods tend to look haggard, and it is commonly thought that psychological stress leads to premature aging and the earlier onset of diseases of aging. Numerous studies demonstrate links between chronic stress and indices of poor health, including risk factors for cardiovascular disease and poorer immune function. Nevertheless, the exact mechanisms of how such stress exerts these effects are not well known, including whether stress accelerates aging at a cellular level and how cellular aging translates to organismal aging. Recent research points to the crucial roles of telomeres and telomerase in cellular aging and potentially in disease. Telomeres are DNA–protein complexes that cap chromosomal ends, promoting chromosomal stability. When cells divide, the telomere is not fully replicated because of limitations of the DNA polymerases in completing the replication of the ends of the linear molecules, leading to telomere shortening with every replication (3). In vitro, when telomeres shorten sufficiently, the cell is arrested into senescence. In people, telomeres shorten with age in all replicating somatic cells that have been examined, including fibroblasts and leukocytes (4). Thus, telomere length can serve as a biomarker of a cell’s biological (versus chronological) “age” or potential for further cell division.
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