Intake of individual saturated fatty acids and risk of coronary heart disease in US men and women: two prospective longitudinal cohort studies

Abstract

Objectives: To investigate the association between long term intake of individual saturated fatty acids (SFAs) and the risk of coronary heart disease, in two large cohort studies.

Design: Prospective, longitudinal cohort study.

Setting: Health professionals in the United States.

Participants: 73 147 women in the Nurses' Health Study (1984-2012) and 42 635 men in the Health Professionals Follow-up Study (1986-2010), who were free of major chronic diseases at baseline.

Main outcome measure: Incidence of coronary heart disease (n=7035) was self-reported, and related deaths were identified by searching National Death Index or through report of next of kin or postal authority. Cases were confirmed by medical records review.

Results: Mean intake of SFAs accounted for 9.0-11.3% energy intake over time, and was mainly composed of lauric acid (12:0), myristic acid (14:0), palmitic acid (16:0), and stearic acid (18:0; 8.8-10.7% energy). Intake of 12:0, 14:0, 16:0 and 18:0 were highly correlated, with Spearman correlation coefficients between 0.38 and 0.93 (all P<0.001). Comparing the highest to the lowest groups of individual SFA intakes, hazard ratios of coronary heart disease were 1.07 (95% confidence interval 0.99 to 1.15; Ptrend=0.05) for 12:0, 1.13 (1.05 to 1.22; Ptrend<0.001) for 14:0, 1.18 (1.09 to 1.27; Ptrend<0.001) for 16:0, 1.18 (1.09 to 1.28; Ptrend<0.001) for 18:0, and 1.18 (1.09 to 1.28; Ptrend<0.001) for all four SFAs combined (12:0-18:0), after multivariate adjustment of lifestyle factors and total energy intake. Hazard ratios of coronary heart disease for isocaloric replacement of 1% energy from 12:0-18:0 were 0.92 (95% confidence interval 0.89 to 0.96; P<0.001) for polyunsaturated fat, 0.95 (0.90 to 1.01; P=0.08) for monounsaturated fat, 0.94 (0.91 to 0.97; P<0.001) for whole grain carbohydrates, and 0.93 (0.89 to 0.97; P=0.001) for plant proteins. For individual SFAs, the lowest risk of coronary heart disease was observed when the most abundant SFA, 16:0, was replaced. Hazard ratios of coronary heart disease for replacing 1% energy from 16:0 were 0.88 (95% confidence interval 0.81 to 0.96; P=0.002) for polyunsaturated fat, 0.92 (0.83 to 1.02; P=0.10) for monounsaturated fat, 0.90 (0.83 to 0.97; P=0.01) for whole grain carbohydrates, and 0.89 (0.82 to 0.97; P=0.01) for plant proteins.

Conclusions: Higher dietary intakes of major SFAs are associated with an increased risk of coronary heart disease. Owing to similar associations and high correlations among individual SFAs, dietary recommendations for the prevention of coronary heart disease should continue to focus on replacing total saturated fat with more healthy sources of energy.

Conflict of interest statement

Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf and declare: support from the National Institutes of Health for the submitted work; GZ is supported by a postdoctoral fellowship funded by Unilever R&D, Vlaardingen, Netherlands; AJW, MA, and PLZ are employees of Unilever R&D (Unilever is a producer of food consumer products); FBH has received research support from California Walnut Commission and Metagenics; no other relationships or activities that could appear to have influenced the submitted work.

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Figures

Fig 1 Aged adjusted intake (energy (%)) of individual saturated fatty acids over time in the Nurses’ Health Study (1984-2010) and Health Professionals Follow-up Study (1986-2010). 4:0=butyric acid; 6:0=caproic acid; 8:0=caprylic acid; 10:0=capric acid; 12:0=lauric acid; 14:0=myristic acid; 16:0=palmitic acid; 18:0=stearic acid

Fig 2 Multivariate adjusted hazard ratios of coronary heart disease after substitution of 1% of energy from individual SFAs by alternative nutrients, based on the Nurses’ Health Study (1984-2012) and Health Professionals Follow-up Study (1986-2010). Dots=hazard ratio point estimates; horizontal bars=95% confidence intervals; SFA=saturated fatty acid; 12:0=lauric acid; 14:0=myristic acid; 16:0=palmitic acid; 18:0=stearic acid; PUFA=polyunsaturated fatty acids; MUFA=monounsaturated fatty acids. Hazard ratios were adjusted for age, ethnicity (white, African American, Asian, and other ethnicity), smoking status (never, former, current (1-14, 15-24, or ≥25 cigarettes/day), or missing), alcohol intake (0, 0.1-4.9, 5.0-14.9, and >15.0 g/day in women; 0, 0.1-4.9, 5.0-29.9, and >30.0 g/day in men; or missing), family history of myocardial infarction (yes/no), menopausal status and postmenopausal hormone use (premenopause, postmenopause (never, former, or current hormone use), or missing, for women), physical activity (<3, 3.0-8.9, 9.0-17.9, 18.0-26.9, ≥27.0 metabolic equivalent of task (h/week); or missing), current aspirin use (yes/no), multivitamin use (yes/no), baseline hypertension, baseline hypercholesterolemia, body mass index (<23, 23-24.9, 25-29.9, 30-34.9, >35, or missing), total energy intake as sum of energy from all included macronutrients, energy from trans fat, energy from carbohydrate of non-whole grain sources, and energy from non-plant sources. For PUFA (polyunsaturated fatty acids) replacement, hazard ratios were further adjusted for MUFA (monounsaturated fatty acids), whole grain carbohydrates, plant proteins, and the sum of other SFAs. For MUFA replacement, hazard ratios were further adjusted for PUFA, whole grain carbohydrates, plant proteins, and the sum of other SFAs. For whole grain carbohydrate replacement, hazard ratios were further adjusted for PUFA, MUFA, plant proteins, and the sum of other SFAs. For plant protein replacement, hazard ratios were further adjusted for PUFA, MUFA, whole grain carbohydrates, and the sum of other SFAs. Study estimates from two cohorts were pooled using a fixed effects model