Serial Plasma Phospholipid Fatty Acids in the De Novo Lipogenesis Pathway and Total Mortality, Cause‐Specific Mortality, and Cardiovascular Diseases in the Cardiovascular Health Study

Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Rozenn N. Lemaitre¹  Barbara McKnight²  Marcia C. de Oliveira Otto³  Irena B. King⁴  Bruce M. Psaty⁵  Xiaoling Song⁶  Dariush Mozaffarian⁷  Heidi T.M. Lai⁷  Yujin Lee⁷  Jason H.Y. Wu⁸  David S. Siscovick⁹ 

[1] Cardiovascular Health Research Unit Department of Medicine University of Washington Seattle WA;Department of Biostatistics University of Washington Seattle WA;Department of Epidemiology Human Genetics and Environmental Sciences University of Texas Health Science Center at Houston TX;Department of Internal Medicine University of New Mexico Albuquerque NM;Department of Medicine, Epidemiology, and Health Services University of Washington Seattle WA;Fred Hutchinson Cancer Research Center Seattle WA;Friedman School of Nutrition Science and Policy Tufts University Boston MA;The George Institute for Global Health Faculty of Medicine University of New South Wales Newtown NSW Australia;The New York Academy of Medicine New York City NY;

关键词: cardiovascular disease;    de novo lipogenesis;    fatty acid biomarkers;    longitudinal analysis;    mortality;   

DOI  :  10.1161/JAHA.119.012881

来源: DOAJ

【 摘 要 】

Background Synthesized fatty acids (FAs) from de novo lipogenesis may affect cardiometabolic health, but longitudinal associations between serially measured de novo lipogenesis–related fatty acid biomarkers and mortality or cardiovascular disease (CVD) are not well established. Methods and Results We investigated longitudinal associations between de novo lipogenesis–related fatty acids with all‐cause mortality, cause‐specific mortality, and incident CVD among 3869 older US adults, mean (SD) age 75 (5) years and free of prevalent CVD at baseline. Levels of plasma phospholipid palmitic (16:0), palmitoleic (16:1n‐7), stearic (18:0), oleic acid (18:1n‐9), and other risk factors were serially measured at baseline, 6 years, and 13 years. All‐cause mortality, cause‐specific mortality, and incident fatal and nonfatal CVD were centrally adjudicated. Risk was assessed in multivariable‐adjusted Cox models with time‐varying FAs and covariates. During 13 years, median follow‐up (maximum 22.4 years), participants experienced 3227 deaths (1131 CVD, 2096 non‐CVD) and 1753 incident CVD events. After multivariable adjustment, higher cumulative levels of 16:0, 16:1n‐7, and 18:1n‐9 were associated with higher all‐cause mortality, with extreme‐quintile hazard ratios (95% CIs) of 1.35 (1.17–1.56), 1.40 (1.21–1.62), and 1.56 (1.35–1.80), respectively, whereas higher levels of 18:0 were associated with lower mortality (hazard ratio=0.76; 95% CI=0.66–0.88). Associations were generally similar for CVD mortality versus non‐CVD mortality, as well as total incident CVD. Changes in levels of 16:0 were positively, and 18:0 inversely, associated with all‐cause mortality (hazard ratio=1.23, 95% CI=1.08–1.41; and hazard ratio=0.78, 95% CI=0.68–0.90). Conclusions Higher long‐term levels of 16:0, 16:1n‐7, and 18:1n‐9 and changes in 16:0 were positively, whereas long‐term levels and changes in 18:0 were inversely, associated with all‐cause mortality in older adults.

【 授权许可】

Unknown