Nina Habermann1, Karen W Makar, Clare Abbenhardt, Liren Xiao, Ching-Yun Wang, Heidi K Utsugi, Catherine M Alfano, Kristin L Campbell, Catherine Duggan, Karen E Foster-Schubert, Caitlin E Mason, Ikuyo Imayama, George L Blackburn, John D Potter, Anne McTiernan, Cornelia M Ulrich. 1. 1Division of Preventive Oncology, German Cancer Research Center and National Center for Tumor Diseases, Heidelberg, GERMANY; 2Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA; 3Office of Cancer Survivorship, National Cancer Institute/National Institutes of Health, Bethesda, MD; 4Faculty of Medicine, University of British Columbia, Vancouver, BC, CANADA; 5School of Medicine, University of Washington, Seattle, WA; 6Division of Nutrition, Harvard Medical School, Boston, MA; 7Cancer Prevention Program, Fred Hutchinson Cancer Research Center, Seattle, WA; 8School of Public Health, University of Washington, Seattle, WA; and 9Center for Public Health Research, Massey University, Wellington, NEW ZEALAND.
Abstract
INTRODUCTION: Maintenance of normal weight and higher levels of physical activity are associated with a reduced risk of several types of cancer. Because genomic instability is regarded as a hallmark of cancer development, one proposed mechanism is improvement of DNA repair function. We investigated links between dietary weight loss, exercise, and strand break rejoining in an ancillary study to a randomized-controlled trial. METHODS:Overweight/obese postmenopausal women (n = 439) were randomized to the following: a) reduced calorie weight loss diet ("diet," n = 118), b) moderate- to vigorous-intensity aerobic exercise ("exercise," n = 117), c) a combination ("diet + exercise," n = 117), or d) control (n = 87). The reduced calorie diet had a 10% weight loss goal. The exercise intervention consisted of 45 min of moderate to vigorous aerobic activity 5 d·wk for 12 months. DNA repair capacity was measured in a subset of 226 women at baseline and 12 months from cryopreserved peripheral mononuclear cells using the comet assay. Anthropometric and body composition measures were performed at baseline and 12 months. RESULTS:DNA repair capacity did not change significantly with any of the 12-month interventions compared with control; there were also no significant changes when stratified by changes in body composition or aerobic fitness (V˙O2max). At baseline, DNA repair capacity was positively associated with weight, body mass index, and fat mass (r = 0.20, P = 0.003; r = 0.19, P = 0.004; r = 0.13, P = 0.04, respectively) and inversely with lean body mass (r = -0.14, P = 0.04). CONCLUSION: In conclusion, DNA repair capacity in cryopreserved PBMCs (Comet Assay) did not change with dietary weight loss or exercise interventions in postmenopausal women within a period of 12 months. Other assays that capture different facets of DNA repair function may be needed.
RCT Entities:
INTRODUCTION: Maintenance of normal weight and higher levels of physical activity are associated with a reduced risk of several types of cancer. Because genomic instability is regarded as a hallmark of cancer development, one proposed mechanism is improvement of DNA repair function. We investigated links between dietary weight loss, exercise, and strand break rejoining in an ancillary study to a randomized-controlled trial. METHODS: Overweight/obese postmenopausal women (n = 439) were randomized to the following: a) reduced calorie weight loss diet ("diet," n = 118), b) moderate- to vigorous-intensity aerobic exercise ("exercise," n = 117), c) a combination ("diet + exercise," n = 117), or d) control (n = 87). The reduced calorie diet had a 10% weight loss goal. The exercise intervention consisted of 45 min of moderate to vigorous aerobic activity 5 d·wk for 12 months. DNA repair capacity was measured in a subset of 226 women at baseline and 12 months from cryopreserved peripheral mononuclear cells using the comet assay. Anthropometric and body composition measures were performed at baseline and 12 months. RESULTS: DNA repair capacity did not change significantly with any of the 12-month interventions compared with control; there were also no significant changes when stratified by changes in body composition or aerobic fitness (V˙O2max). At baseline, DNA repair capacity was positively associated with weight, body mass index, and fat mass (r = 0.20, P = 0.003; r = 0.19, P = 0.004; r = 0.13, P = 0.04, respectively) and inversely with lean body mass (r = -0.14, P = 0.04). CONCLUSION: In conclusion, DNA repair capacity in cryopreserved PBMCs (Comet Assay) did not change with dietary weight loss or exercise interventions in postmenopausal women within a period of 12 months. Other assays that capture different facets of DNA repair function may be needed.
Authors: A Hartmann; E Agurell; C Beevers; S Brendler-Schwaab; B Burlinson; P Clay; A Collins; A Smith; G Speit; V Thybaud; R R Tice Journal: Mutagenesis Date: 2003-01 Impact factor: 3.000
Authors: Karen E Foster-Schubert; Catherine M Alfano; Catherine R Duggan; Liren Xiao; Kristin L Campbell; Angela Kong; Carolyn E Bain; Ching-Yun Wang; George L Blackburn; Anne McTiernan Journal: Obesity (Silver Spring) Date: 2011-04-14 Impact factor: 5.002
Authors: David O Kennedy; Meenakshi Agrawal; Jing Shen; Mary Beth Terry; Fang Fang Zhang; Ruby T Senie; Grazyna Motykiewicz; Regina M Santella Journal: J Natl Cancer Inst Date: 2005-01-19 Impact factor: 13.506
Authors: Donna H Ryan; Mark A Espeland; Gary D Foster; Steven M Haffner; Van S Hubbard; Karen C Johnson; Steven E Kahn; William C Knowler; Susan Z Yanovski Journal: Control Clin Trials Date: 2003-10