Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis1234

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Background: Although dietary recommendations have focused on restricting saturated fat (SF) consumption to reduce cardiovascular disease (CVD) risk, evidence from prospective studies has not supported a strong link between total SF intake and CVD events. An understanding of whether food sources of SF influence these relations may provide new insights.

Objective: We investigated the association of SF consumption from different food sources and the incidence of CVD events in a multiethnic population.

Design: Participants who were 45–84 y old at baseline (n = 5209) were followed from 2000 to 2010. Diet was assessed by using a 120-item food-frequency questionnaire. CVD incidence (316 cases) was assessed during follow-up visits.

Results: After adjustment for demographics, lifestyle, and dietary confounders, a higher intake of dairy SF was associated with lower CVD risk [HR (95% CI) for +5 g/d and +5% of energy from dairy SF: 0.79 (0.68, 0.92) and 0.62 (0.47, 0.82), respectively]. In contrast, a higher intake of meat SF was associated with greater CVD risk [HR (95% CI) for +5 g/d and a +5% of energy from meat SF: 1.26 (1.02, 1.54) and 1.48 (0.98, 2.23), respectively]. The substitution of 2% of energy from meat SF with energy from dairy SF was associated with a 25% lower CVD risk [HR (95% CI): 0.75 (0.63, 0.91)]. No associations were observed between plant or butter SF and CVD risk, but ranges of intakes were narrow.

Conclusion: Associations of SF with health may depend on food-specific fatty acids or other nutrient constituents in foods that contain SF, in addition to SF.

Abbreviations:

CHD
coronary heart disease
CVD
cardiovascular disease
FFQ
food-frequency questionnaire
MESA
Multi-Ethnic Study of Atherosclerosis
SF
saturated fat

Cited by (0)

1

From the Division of Epidemiology, Human Genetics and Environmental Sciences, The University of Texas School of Public Health, Houston, TX (JAN and MCOO); the Department of Epidemiology, Harvard School of Public Health, Boston, MA (DM and MCOO); the Division of Human Nutrition, Wageningen University, Wageningen, Netherlands (DK); the Department of Public Health Sciences, Wake Forest University, Winston-Salem, NC (AGB); the NIH, Bethesda, MD (CTS); the Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN (DRJ); and the Department of Nutrition, University of Oslo, Oslo, Norway (DRJ).

2

The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the Cancer Prevention and Research Institute of Texas.

3

Supported by a University of Texas Health Innovation for Cancer Prevention Research Postdoctoral Fellowship, The University of Texas School of Public Health – Cancer Prevention and Research Institute of Texas (grant RP101503; to MCOO); a K01 from the NIH, National Institute of Diabetes and Digestive and Kidney Diseases (5K01DK082729-04; to JAN); and the National Heart, Lung, and Blood Institute (contracts N01-HC-95159 through N01-HC-95166).

4

Address correspondence to M Otto, Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Kresge Building, Room 913, Boston, MA 02115. E-mail: [email protected].

Copyright © 2012 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.