Category — lifestyle

The ends of linear chromosomes have attracted serious scientific study—and Nobel Prizes—since the early 20th century. Called telomeres, these ends serve to protect the coding DNA of the genome. When a cell’s telomeres shorten to critical lengths, the cell senesces. Thus, telomeres dictate a cell’s life span—unless something goes wrong. Work over the past several decades has revealed an active, though limited, mechanism for the normal enzymatic repair of telomere loss in certain proliferative cells.[1. E.H. Blackburn et al., “Telomeres and telomerase: the path from maize, Tetrahymena and yeast to human cancer and aging,” Nat Med, 12:1133-38, 2006.] Telomere lengthening in cancer cells, however, confers an abnormal proliferative ability.

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Background
Psychological stress is suggested to accelerate the rate of biological aging. We investigated whether work-related exhaustion, an indicator of prolonged work stress, is associated with accelerated biological aging, as indicated by shorter leukocyte telomeres, that is, the DNA-protein complexes that cap chromosomal ends in cells.

Methods
We used data from a representative sample of the Finnish working-age population, the Health 2000 Study. Our sample consisted of 2911 men and women aged 30–64. Work-related exhaustion was assessed using the Maslach Burnout Inventory – General Survey. We determined relative leukocyte telomere length using a quantitative real-time polymerase chain reaction (PCR) -based method.

Results
After adjustment for age and sex, individuals with severe exhaustion had leukocyte telomeres on average 0.043 relative units shorter (standard error of the mean 0.016) than those with no exhaustion (p = 0.009). The association between exhaustion and relative telomere length remained significant after additional adjustment for marital and socioeconomic status, smoking, body mass index, and morbidities (adjusted difference 0.044 relative units, standard error of the mean 0.017, p = 0.008).

Conclusions
These data suggest that work-related exhaustion is related to the acceleration of the rate of biological aging. This hypothesis awaits confirmation in a prospective study measuring changes in relative telomere length over time.

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Abstract

Background

It has recently been hypothesized that bipolar disorders are associated with accelerated aging. Telomere dysfunction, a biomarker of aging, is determined by the load of short telomeres, rather than by the mean telomere length. To our knowledge, the load of short telomeres has not been reported in any psychiatric disorder. The aims of the study were to examine the load of short telomeres and the mean telomere length and their relationships with illness duration and lifetime number of depressive episodes in bipolar II disorder (BD-II).

Methods

Twenty-eight patients (mean age = 34.8 ± 7.7) with a DSM-IV diagnosis of BD-II and 28 healthy control subjects (mean age = 34.8 ± 9.2) matched for age, sex, and education participated. The load of short telomeres (percentage of telomeres < 3 kilobases) and mean telomere length in peripheral blood mononuclear cells were measured using high-throughput quantitative fluorescence in situ hybridization.

Results

The load of short telomeres was significantly increased in patients with BD-II relative to healthy controls and may represent 13 years of accelerated aging. The load of short telomeres and the mean telomere length were associated with lifetime number of depressive episodes, but not with illness duration.

Limitations

Modest sample size and cross-sectional design.

Conclusions

Our results suggest that BD-II is associated with an increased load of short telomeres. Depressive episode-related stress may accelerate telomere shortening and aging. However, longitudinal studies are needed to fully clarify telomere shortening and its relationship with clinical variables in BD-II.

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In 1984, University of California, Berkeley biology professor Elizabeth Blackburn and then grad student Carol Greider made the discovery that a quarter century later would win them the Nobel Pnze: They identified telomerase as the enzyme that protects the DNA in our chromosomes, in effect keeping our cells-and, to some degree, us-young. But telomerase is naturally produced only minimally and intermittently in some of our cells-just enough to grt. disposable us a maximum life span of around 120 years. Unless, that is, someone figures out how to increase the telomerase inside our bodies. Such tinkering with the basic machinery of life has been a theoretical possibility since the 1990s, when scientists
at the Bay Area biotech firm Geron and elsewhere identified the human telomerase gene.

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Ramin Farzaneh-Far^1,2*, Jue Lin³, Elissa Epel⁴, Kyle Lapham³, Elizabeth Blackburn³, Mary A. Whooley^2,5,6

1 Division of Cardiology, San Francisco General Hospital, San Francisco, California, United States of America, 2 Department of Medicine, University of California San Francisco, San Francisco, California, United States of America, 3 Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California, United States of America, 4 Department of Psychiatry, University of California San Francisco, San Francisco, California, United States of America, 5 Veterans Affairs Medical Center, San Francisco, California, United States of America, 6 Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, United States of America

Prof Dean Ornish MD, Jue Lin PhD, Jennifer Daubenmier PhD, Gerdi Weidner PhD, Elissa Epel PhD, Colleen Kemp MSN, Mark Jesus M Magbanua PhD, Ruth Marlin MD, Loren Yglecias BA, Prof Peter R Carroll MD and Prof Elizabeth H Blackburn PhD

Telomeres are protective DNA-protein complexes at the end of linear chromosomes that promote chromosomal stability. Telomere shortness in human beings is emerging as a prognostic marker of disease risk, progression, and premature mortality in many types of cancer, including breast, prostate, colorectal, bladder, head and neck, lung, and renal cell. Telomere shortening is counteracted by the cellular enzyme telomerase. Lifestyle factors known to promote cancer and cardiovascular disease might also adversely affect telomerase function. However, previous studies have not addressed whether improvements in nutrition and lifestyle are associated with increases in telomerase activity. We aimed to assess whether 3 months of intensive lifestyle changes increased telomerase activity in peripheral blood mononuclear cells (PBMC).

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