Written by Marcia J. Egles, MD. Telomeres, the protected end caps of chromosomes, seemed to be protected during periods of stress by healthy diets, sufficient sleep, and exercise.
Telomeres are the protective end caps of chromosomes. Telomeres consist of repeated sequences of thousands of DNA base pairs. With every cell cycle, telomeres tend to shorten. Short telomeres have been linked to numerous diseases of aging (2, 3). A new prospective study reports that the length of telomeres can be adversely affected by emotionally stressful events, but that healthy diets, exercise and sleep may mitigate the damage (1).
Two hundred and sixty-three healthy female nonsmokers, aged 50 to 65 years, recruited from the San Francisco bay area, were followed for one year. Their telomere lengths, in number of DNA base pairs, were measured at baseline and at the end of 12 months from the DNA of their white blood cells. At four, eight and twelve months, the women answered questionnaires concerning physical activity, dietary practices, and sleep habits.
At the end of 12 months, the women completed a checklist of extreme life stressors such as divorce, death of a close family member, major financial loss, a seriously ill child, or unemployment. Those with extreme health-related stressors on the checklist were considered to be confounded with disease and were excluded from the study. Each stressor on the remaining 13-point checklist was counted as one point. Thirty-seven percent of the women reported no life stressors over the course of the year. Forty seven percent listed 1 or 2, and 16% experienced 3 or more of the major stressful events. A final 239 women completed the study.
Healthy behaviors were not significantly related to life events, except for a marginal trend (p=0.08) that those who tallied more of these events during the year were less likely to be physically active.
Prior studies have shown that telomeres do not normally shorten much over just 12 months of time (1, 2). As expected, the overall telomere length did not change much in this group of women. At baseline, the mean white blood cell DNA telomere length was 5548 base pairs (standard deviation 328.9 base pairs). After 12 months, the lengths were similar with a mean of 5584 base pairs (s.d. 354.9). The majority of women, 68%, did not show an increase or decrease in their telomere length of more than 5% from baseline.
Accelerated telomere shortening, however, was found in the women who reported the highest levels of stressors. For every one event, there was a significantly greater decline in telomere length of 34.7 base pairs (95% confidence interval -62.3 to 6.9).
The study also found that engagement in healthy behaviors during periods of high stress can perhaps attenuate the telomere shortening. For women at the highest self-reported levels of healthy diets, sleep and exercise (one standard deviation above the sample mean of combined healthy behaviors) life stressors were unrelated to telomere shortening. For women which the study considered to have the lowest levels of healthy behaviors, accelerated telomere shortening occurred over the year for an additional 76.5 base pairs (95% confidence interval 123.1 to 30.0) per event.
One of the study authors, Dr. Elizabeth Blackburn, is a recognized authority in telomere research. In 2009 she was awarded the Nobel prize for her discovery of telomerase, an enzyme that lengthens and repairs telomeres. Telomere research is advancing the understanding for the potential of healthy behaviors and nutrition to impact many diseases as well as the aging process itself (1).
Source: Puterman, Eli, Jue Lin, Jeffrey Krauss, Elizabeth H. Blackburn, and Elissa S. Epel. “Determinants of telomere attrition over one year in healthy older women: Stress and health behaviors matter.” Molecular psychiatry 20, no. 4 (2015): 529.
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Posted December 1, 2014.
References:
- Puterman, E and J Lin, J Krauss, EH Blackburn and ES Epel in Molecular Psychiatry (2014), 1-7.
- Blackburn, EH Telomere states and cell fates. Nature; 2000: 408:53-56.
- Sahin E, et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011; 470:359-365.
