Association of Specific Dietary Fats With Total and Cause-Specific Mortality

Abstract

Importance: Previous studies have shown distinct associations between specific dietary fat and cardiovascular disease. However, evidence on specific dietary fat and mortality remains limited and inconsistent.

Objective: To examine the associations of specific dietary fats with total and cause-specific mortality in 2 large ongoing cohort studies.

Design, setting, and participants: This cohort study investigated 83 349 women from the Nurses' Health Study (July 1, 1980, to June 30, 2012) and 42 884 men from the Health Professionals Follow-up Study (February 1, 1986, to January 31, 2012) who were free of cardiovascular disease, cancer, and types 1 and 2 diabetes at baseline. Dietary fat intake was assessed at baseline and updated every 2 to 4 years. Information on mortality was obtained from systematic searches of the vital records of states and the National Death Index, supplemented by reports from family members or postal authorities. Data were analyzed from September 18, 2014, to March 27, 2016.

Main outcomes and measures: Total and cause-specific mortality.

Results: During 3 439 954 person-years of follow-up, 33 304 deaths were documented. After adjustment for known and suspected risk factors, dietary total fat compared with total carbohydrates was inversely associated with total mortality (hazard ratio [HR] comparing extreme quintiles, 0.84; 95% CI, 0.81-0.88; P < .001 for trend). The HRs of total mortality comparing extreme quintiles of specific dietary fats were 1.08 (95% CI, 1.03-1.14) for saturated fat, 0.81 (95% CI, 0.78-0.84) for polyunsaturated fatty acid (PUFA), 0.89 (95% CI, 0.84-0.94) for monounsaturated fatty acid (MUFA), and 1.13 (95% CI, 1.07-1.18) for trans-fat (P < .001 for trend for all). Replacing 5% of energy from saturated fats with equivalent energy from PUFA and MUFA was associated with estimated reductions in total mortality of 27% (HR, 0.73; 95% CI, 0.70-0.77) and 13% (HR, 0.87; 95% CI, 0.82-0.93), respectively. The HR for total mortality comparing extreme quintiles of ω-6 PUFA intake was 0.85 (95% CI, 0.81-0.89; P < .001 for trend). Intake of ω-6 PUFA, especially linoleic acid, was inversely associated with mortality owing to most major causes, whereas marine ω-3 PUFA intake was associated with a modestly lower total mortality (HR comparing extreme quintiles, 0.96; 95% CI, 0.93-1.00; P = .002 for trend).

Conclusions and relevance: Different types of dietary fats have divergent associations with total and cause-specific mortality. These findings support current dietary recommendations to replace saturated fat and trans-fat with unsaturated fats.

Figure 1. Change in total mortality associated with increases in the percentage of energy from specific types of fat

Figure was based on multivariable HRs of total mortality associated with replacing the percentage of energy from total carbohydrate by the same energy form specific types of fat (P for trend <0.001 for all). Model was adjusted for age (in month), Caucasian (yes vs. no), marital status (with spouse, yes or no), body-mass index (<23, 23-24.9, 25-29.9, 30-34.9, ≥35 kg/m2), physical activity (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, ≥27.0 hours of metabolic equivalent tasks per week), smoking status (never, past, current 1-14 cigarettes/d, current 15-24 cigarettes/d, current ≥25 cigarettes/d), alcohol consumption (women: 0, 0.1-4.9, 5.0-14.9, ≥15 g/d; men: 0, 0.1-4.9, 5.0-29.9, ≥30 g/d), multivitamin use (yes vs. no), vitamin E supplementation use (yes vs. no), current aspirin use (yes vs. no), family history of myocardial infarction (yes vs. no), family history of diabetes (yes vs. no), family history of cancer (yes vs. no), history of hypertension (yes vs. no), history of hypercholesterolemia (yes vs. no), intakes of total energy, dietary cholesterol and percentage of energy intake from dietary protein(quintiles), and in women, menopausal status, hormone use (premenopausal, postmenopausal never users, postmenopausal past users, postmenopausal current users) and percentage of energy from remaining specific types of fat (saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids and trans fatty acids, all modeled as continuous variables). Results for NHS and HPFS from the multivariate model were combined using the fixed-effects model.

Figure 2. Multivariable HRs of mortality by isocaloric substitution of specific types of fatty acid for saturated fatty acids

Abbreviations: UFA, unsaturated fatty acid; MUFAs, monounsaturated fatty acids; PUFAs, polyunsaturated fatty acids. Model was adjusted for age (in month), Caucasian (yes vs. no), marital status (with spouse, yes or no), body-mass index (<23, 23-24.9, 25-29.9, 30-34.9, ≥35 kg/m2), physical activity (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, ≥27.0 hours of metabolic equivalent tasks per week), smoking status (never, past, current 1-14 cigarettes/d, current 15-24 cigarettes/d, current ≥25 cigarettes/d), alcohol consumption (women: 0, 0.1-4.9, 5.0-14.9, ≥15 g/d; men: 0, 0.1-4.9, 5.0-29.9, ≥30 g/d), multivitamin use (yes vs. no), vitamin E supplementation use (yes vs. no), current aspirin use (yes vs. no), family history of myocardial infarction (yes vs. no), family history of diabetes (yes vs. no), family history of cancer (yes vs. no), history of hypertension (yes vs. no), history of hypercholesterolemia (yes vs. no), intakes of total energy, dietary cholesterol and percentage of energy intake from dietary protein(quintiles), and in women, menopausal status, hormone use (premenopausal, postmenopausal never users, postmenopausal past users, postmenopausal current users) and percentage of energy from remaining fatty acids (saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids, trans fatty acids, n-6 PUFAs, n-3 PUFAs, linoleic acid, arachidonic acid, α-linolenic acid and marine n-3 fats, all modeled as continuous variables). Results for NHS and HPFS from the multivariate model were combined using the fixed-effects model.