Affiliation:
1. Friedman School of Nutrition Science and Policy Tufts University Boston MA
2. Department of Epidemiology Human Genetics and Environmental Sciences University of Texas Health Science Center at Houston TX
3. The George Institute for Global Health Faculty of Medicine University of New South Wales Newtown NSW Australia
4. Fred Hutchinson Cancer Research Center Seattle WA
5. Department of Internal Medicine University of New Mexico Albuquerque NM
6. Department of Medicine, Epidemiology, and Health Services University of Washington Seattle WA
7. Cardiovascular Health Research Unit Department of Medicine University of Washington Seattle WA
8. Kaiser Permanente Washington Health Research Institute Seattle WA
9. Department of Biostatistics University of Washington Seattle WA
10. The New York Academy of Medicine New York City NY
Abstract
Background
Synthesized fatty acids (
FA
s) 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
FA
s 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%
CI
s) 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.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine