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Increased telomerase activity and comprehensive lifestyle changes: a pilot study - 26/09/12

Doi : 10.1016/S1470-2045(08)70234-1 
Dean Ornish, ProfMD a, e, , Jue Lin, PhD b, , Jennifer Daubenmier, PhD a, , Gerdi Weidner, PhD e, Elissa Epel, PhD c, Colleen Kemp, MSN e, Mark Jesus M Magbanua, PhD d, Ruth Marlin, MD e, Loren Yglecias, BA e, Peter R Carroll, ProfMD d, Elizabeth H Blackburn, ProfPhD b
a Department of Medicine, University of California, San Francisco, CA, USA 
b Department of Biochemistry and Biophysics, University of California, San Francisco, CA, USA 
c Department of Psychiatry, University of California, San Francisco, CA, USA 
d Department of Urology, The Helen Diller Family Comprehensive Cancer Center, School of Medicine, University of California, San Francisco, CA, USA 
e Preventive Medicine Research Institute, Sausalito, CA, USA 

* Correspondence to: Prof Dean Ornish, Preventive Medicine Research Insitute, Sausalito, CA 94965, USA

Summary

Background

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).

Methods

30 men with biopsy-diagnosed low-risk prostate cancer were asked to make comprehensive lifestyle changes. The primary endpoint was telomerase enzymatic activity per viable cell, measured at baseline and after 3 months. 24 patients had sufficient PBMCs needed for longitudinal analysis. This study is registered on the ClinicalTrials.gov website, number NCT00739791.

Findings

PBMC telomerase activity expressed as natural logarithms increased from 2·00 (SD 0·44) to 2·22 (SD 0·49; p=0·031). Raw values of telomerase increased from 8·05 (SD 3·50) standard arbitrary units to 10·38 (SD 6·01) standard arbitrary units. The increases in telomerase activity were significantly associated with decreases in low-density lipoprotein (LDL) cholesterol (r=−0·36, p=0·041) and decreases in psychological distress (r=−0·35, p=0·047).

Interpretation

Comprehensive lifestyle changes significantly increase telomerase activity and consequently telomere maintenance capacity in human immune-system cells. Given this finding and the pilot nature of this study, we report these increases in telomerase activity as a significant association rather than inferring causation. Larger randomised controlled trials are warranted to confirm the findings of this study.

Funding

US Department of Defense (US Army Medical Research Acquisition Activity W81XWH-05-1-0375, Fort Detrick, Frederick, MD, USA); Henry M Jackson Foundation for the Advancement of Military Medicine (contract 56422; Rockville MD, USA) from the National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (grant number K01AT004199; Bethesda, MD, USA); Bahna Foundation (Stamford, CT, USA); DeJoria Foundation (Los Angeles, CA, USA); Kerzner Foundation (New York, NY, USA); Bernard Osher Foundation (San Francisco, CA, USA); Walton Family Foundation (Bentonville, AK, USA); Jeff Walker Family Foundation (Wilton, CT, USA); Safeway Foundation (Pleasanton, CA, USA).

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Vol 9 - N° 11

P. 1048-1057 - novembre 2008 Retour au numéro
Article précédent Article précédent
  • Prediagnostic body-mass index, plasma C-peptide concentration, and prostate cancer-specific mortality in men with prostate cancer: a long-term survival analysis
  • Jing Ma, Haojie Li, Ed Giovannucci, Lorelei Mucci, Weiliang Qiu, Paul L Nguyen, J Michael Gaziano, Michael Pollak, Meir J Stampfer
| Article suivant Article suivant
  • Time to biochemical failure and prostate-specific antigen doubling time as surrogates for prostate cancer-specific mortality: evidence from the TROG 96.01 randomised controlled trial
  • James W Denham, Allison Steigler, Chantelle Wilcox, David S Lamb, David Joseph, Chris Atkinson, John Matthews, Keen-Hun Tai, Nigel A Spry, David Christie, Paul S Gleeson, Peter B Greer, Catherine D’Este, on behalf of the Trans-Tasman Radiation Oncology Group 96.01 Trialists ‡

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