TY - JOUR
T1 - An Analysis of Individual Body Fat Depots and Risk of Developing Cancer
T2 - Insights From the Dallas Heart Study
AU - Gupta, Arjun
AU - Pandey, Ambarish
AU - Ayers, Colby
AU - Beg, Muhammad S
AU - Lakoski, Susan G.
AU - Vega, Gloria L
AU - Grundy, Scott M
AU - Johnson, David H
AU - Neeland, Ian J
N1 - Funding Information:
Grant Support: This work was supported by grant K23DK106520 (I.J.N.) from the National Institute of Diabetes and Digestive and Kidney Diseases, by grants UL1DE019584 and PL1DK081182 from the National Institutes of Health, and by grant UL1TR001105 from the National Center for Advancing Translational Sciences. Dr?Neeland is supported as a Dedman Family Scholar in Clinical Care at the University of Texas Southwestern Medical?Center.
Publisher Copyright:
© 2017 Mayo Foundation for Medical Education and Research
PY - 2017/4/1
Y1 - 2017/4/1
N2 - Objective To examine the association between specific adipose tissue depots and the risk of incident cancer in the Dallas Heart Study. Patients and Methods Individuals without prevalent cancer in the Dallas Heart Study underwent quantification of adipose depots: visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue, and liver fat by magnetic resonance imaging, and subcutaneous lower-body fat (LBF) by dual-energy X-ray absorptiometry from January 1, 2000, through December 31, 2002, and were observed for the development of cancer for up to 12 years. Multivariable Cox proportional hazards modeling was performed to examine the association between fat depots and cancer. Results Of 2627 participants (median age, 43 years; 69% nonwhite race), 167 (6.4%) developed cancer. The most common primary sites of cancer were the breast (in women) and the prostate (in men). In multivariable models adjusted for age, sex, race, smoking, alcohol use, family history of malignancy, and body mass index, a 1-SD increase in VAT was not associated with increased risk of cancer (hazard ratio [HR], 0.94; 95% CI, 0.77-1.14). In contrast, each 1-SD increase in LBF was associated with a reduced incidence of cancer (HR, 0.69; 95% CI, 0.52-0.92) in the fully adjusted model. Conclusions In this study, adiposity-associated cancer risk was heterogeneous and varied by fat depot: VAT was not independently associated with incident cancer, and LBF seemed to protect against cancer development. Further studies of the adiposity-cancer relationship, including serial assessments, are needed to better elucidate this relationship.
AB - Objective To examine the association between specific adipose tissue depots and the risk of incident cancer in the Dallas Heart Study. Patients and Methods Individuals without prevalent cancer in the Dallas Heart Study underwent quantification of adipose depots: visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue, and liver fat by magnetic resonance imaging, and subcutaneous lower-body fat (LBF) by dual-energy X-ray absorptiometry from January 1, 2000, through December 31, 2002, and were observed for the development of cancer for up to 12 years. Multivariable Cox proportional hazards modeling was performed to examine the association between fat depots and cancer. Results Of 2627 participants (median age, 43 years; 69% nonwhite race), 167 (6.4%) developed cancer. The most common primary sites of cancer were the breast (in women) and the prostate (in men). In multivariable models adjusted for age, sex, race, smoking, alcohol use, family history of malignancy, and body mass index, a 1-SD increase in VAT was not associated with increased risk of cancer (hazard ratio [HR], 0.94; 95% CI, 0.77-1.14). In contrast, each 1-SD increase in LBF was associated with a reduced incidence of cancer (HR, 0.69; 95% CI, 0.52-0.92) in the fully adjusted model. Conclusions In this study, adiposity-associated cancer risk was heterogeneous and varied by fat depot: VAT was not independently associated with incident cancer, and LBF seemed to protect against cancer development. Further studies of the adiposity-cancer relationship, including serial assessments, are needed to better elucidate this relationship.
UR - http://www.scopus.com/inward/record.url?scp=85014763284&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85014763284&partnerID=8YFLogxK
U2 - 10.1016/j.mayocp.2016.12.023
DO - 10.1016/j.mayocp.2016.12.023
M3 - Article
C2 - 28291590
AN - SCOPUS:85014763284
SN - 0025-6196
VL - 92
SP - 536
EP - 543
JO - Mayo Clinic Proceedings
JF - Mayo Clinic Proceedings
IS - 4
ER -