Intake of individual saturated fatty acids and risk of coronary heart disease in US men and women: two prospective longitudinal cohort studies.
ABSTRACT: 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. Prospective, longitudinal cohort study. Health professionals in the United States. 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. 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. 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. 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.
Project description:Background:Monounsaturated fatty acids (MUFAs) improve blood lipid profiles in intervention studies, but prospective evidence with regard to MUFA intake and coronary heart disease (CHD) risk is limited and controversial. Objective:We investigated the associations of cis MUFA intake from plant (MUFA-P) and animal (MUFA-A) sources with CHD risk separately among 63,442 women from the Nurses' Health Study (1990-2012) and 29,942 men from the Health Professionals Follow-Up Study (1990-2012). Design:Intakes of MUFA-Ps and MUFA-As were calculated by using validated food-frequency questionnaires collected every 4 y. Incident nonfatal myocardial infarction and fatal CHD cases (n = 4419) were confirmed by medical record review. Results:During follow-up, MUFA-Ps and MUFA-As contributed 5.8-7.9% and 4.2-5.4% of energy on average, respectively. When MUFA-Ps were modeled to isocalorically replace other macronutrients, HRs (95% CIs) of CHD were 0.83 (0.68, 1.00) for saturated fatty acids (SFAs; 5% of energy), 0.86 (0.76, 0.97) for refined carbohydrates (5% of energy), and 0.80 (0.70, 0.91) for trans fats (2% of energy) (P = 0.05, 0.01, and 0.001, respectively). For MUFA-As, corresponding HRs (95% CIs) for the same isocaloric substitutions were 1.04 (0.79, 1.38) for SFAs, 1.11 (0.91, 1.35) for refined carbohydrates, and 0.88 (0.77, 1.01) for trans fats (P = 0.76, 0.31, and 0.08, respectively). Given the common food sources of SFAs and MUFA-As (Spearman correlation coefficients of 0.81-0.83 between these groups of fatty acids), we further estimated CHD risk when the sum of MUFA-As and SFAs (5% of energy) was replaced by MUFA-Ps, and found that the HR was 0.81 (95% CI: 0.73, 0.90; P < 0.001) for this replacement. Conclusions:The largely different associations of MUFA-Ps and MUFA-As with CHD risk suggest that plant-based foods are the preferable sources of MUFAs for CHD prevention. These findings are observational and warrant confirmation in intervention settings. This study was registered at clinicaltrials.gov as NCT00005152 and NCT00005182.
Project description:The 2015 Dietary Guidelines for Americans recommend limiting the intake of saturated fatty acids (SFAs) to <10% of energy/d and replacing dietary SFAs with unsaturated fatty acids. A Presidential Advisory from the American Heart Association recently released its evaluation of the relation between dietary fats and cardiovascular disease (CVD), and also recommended a shift from SFAs to unsaturated fatty acids, especially polyunsaturated fatty acids (PUFAs), in conjunction with a healthy dietary pattern. However, the suggestion to increase the intake of PUFAs in general, and omega-6 (n-6) PUFAs in particular, continues to be controversial. This review was undertaken to provide an overview of the evidence and controversies regarding the effects of ?-6 PUFAs on cardiometabolic health, with emphasis on risks and risk factors for CVD (coronary heart disease and stroke) and type 2 diabetes mellitus (T2D). Results from observational studies show that higher intake of ?-6 PUFAs, when compared with SFAs or carbohydrate, is associated with lower risks for CVD events (10-30%), CVD and total mortality (10-40%), and T2D (20-50%). Findings from intervention studies on cardiometabolic risk factors suggest that ?-6 PUFAs reduce concentrations of LDL cholesterol and non-HDL cholesterol in a dose-dependent manner compared with dietary carbohydrate, and have a neutral effect on blood pressure. Despite the concern that ?-6 fatty acids increase inflammation, current evidence from studies in humans does not support this view. In conclusion, these findings support current recommendations to emphasize consumption of ?-6 PUFAs as a replacement of SFAs; additional randomized controlled trials with cardiometabolic disease outcomes will help to more clearly define the benefits and risks of this policy.
Project description:We used data-driven approaches to identify independent diet exposures among 45 candidate variables, for which we then probed cross-sectional associations with cardiometabolic risk (CMR). We derived average daily caloric intake and macronutrient composition, daily meal frequencies, and irregularity of energy and macronutrient intake from 7-day food diaries in the Airwave Health Monitoring Study participants (N = 8090). We used K-means and hierarchical clustering to identify non-redundant diet exposures with representative exposures for each cluster chosen by silhouette value. We then used multi-variable adjusted logistic regression to estimate prevalence ratios (PR) and 95% confidence intervals (95%CI) for CMR (?3 criteria: dyslipidemia, hypertension, central adiposity, inflammation and impaired glucose control) across diet exposure quartiles. We identified four clusters: i) fat intake, ii) carbohydrate intake, iii) protein intake and intake regularity, and iv) meal frequencies and energy intake. Of these clusters, higher carbohydrate intake was associated with lower likelihood of CMR (PR = 0.89, 95%CI = 0.81-0.98; ptrend = 0.02), as was higher fiber intake (PR = 0.76, 95%CI = 0.68-0.85; ptrend < 0.001). Higher meal frequency was also associated with lower likelihood of CMR (PR = 0.76, 95%CI = 0.68-0.85; ptrend < 0.001). Our results highlight a novel, data-driven approach to select non-redundant, minimally collinear, primary exposures across a host of potentially relevant exposures (including diet composition, temporal distribution, and regularity), as often encountered in nutritional epidemiology.
Project description:Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ?2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.
Project description:Dietary recommendations for adults with diabetes are to follow a healthy diet in appropriate portion sizes. We determined recent trends in energy and nutrient intakes among a nationally representative sample of US adults with and without type 2 diabetes.Participants were adults aged ?20 years from the cross-sectional National Health and Nutrition Examination Surveys, 1988-2012 (N = 49 770). Diabetes was determined by self-report of a physician's diagnosis (n = 4885). Intake of energy and nutrients were determined from a 24-h recall by participants of all food consumed. Linear regression was used to test for trends in mean intake over time for all participants and by demographic characteristics.Among adults with diabetes, overall total energy intake increased between 1988-1994 and 2011-2012 (1689 kcal versus 1895 kcal; Ptrend < 0.001) with evidence of a plateau between 2003-2006 and 2011-2012. In 2007-2012, energy intake was greater for younger than older adults, for men than women, and for non-Hispanic whites versus non-Hispanic blacks. There was no change in the percentage of calories from carbohydrate, total fat or protein. Percentage of calories from saturated fat was similar across study periods but remained above recommendations (11.2% in 2011-2012). Fibre intake significantly decreased and remained below recommendations (Ptrend = 0.002). Sodium, cholesterol and calcium intakes increased. There was no change in energy intake among adults without diabetes and dietary trends were similar to those with diabetes.Future data are needed to confirm a plateau in energy intake among adults with diabetes, although the opportunity exists to increase fibre and reduce saturated fat.
Project description:Dietary n-3 PUFAs are inversely associated with risk of sudden cardiac death (SCD); however, little is known about other fats and SCD. Furthermore, concerns have been raised that high n-6 PUFA intake may attenuate the benefits of n-3 PUFAs.We examined associations and selected interactions between dietary fatty acids, expressed as a proportion of total fat and SCD.We conducted a prospective cohort study among 91,981 women aged 34-59 y from the Nurses' Health Study in 1980. Over 30 y, we documented 385 SCDs.In multivariable models, women in the highest compared with the lowest quintile of SFA intake had an RR of SCD of 1.44 (95% CI: 1.04, 1.98). Conversely, women in the highest compared with the lowest quintile of PUFA intake had an RR of SCD of 0.57 (95% CI: 0.41, 0.78). Intakes of n-6 and n-3 PUFAs were both significantly associated with a lower risk of SCD, and n-6 PUFAs did not modify the association between n-3 PUFAs and SCD. MUFAs and trans fats were not associated with SCD risk. After further adjustment for coronary heart disease (CHD) and CHD risk factors potentially in the causal pathway, the association between PUFAs and SCD remained significant, whereas the association for SFAs was no longer significant.Intake of PUFAs as a proportion of fat was inversely associated with SCD risk, independent of traditional CHD risk factors. These results support dietary guidelines to improve dietary fat quality by replacing intake of SFAs with n-6 and n-3 PUFAs.
Project description:OBJECTIVES:The aim of this study was to examine whether magnesium intake is associated with coronary artery calcification (CAC) and abdominal aortic calcification (AAC). BACKGROUND:Animal and cell studies suggest that magnesium may prevent calcification within atherosclerotic plaques underlying cardiovascular disease. Little is known about the association of magnesium intake and atherosclerotic calcification in humans. METHODS:We examined cross-sectional associations of self-reported total (dietary and supplemental) magnesium intake estimated by food frequency questionnaire with CAC and AAC in participants of the Framingham Heart Study who were free of cardiovascular disease and underwent Multi-Detector Computed Tomography (MDCT) of the heart and abdomen (n = 2,695; age: 53 ± 11 years), using multivariate-adjusted Tobit regression. CAC and AAC were quantified using modified Agatston scores (AS). Models were adjusted for age, sex, body mass index, smoking status, systolic blood pressure, fasting insulin, total-to-high-density lipoprotein cholesterol ratio, use of hormone replacement therapy (women only), menopausal status (women only), treatment for hyperlipidemia, hypertension, cardiovascular disease prevention, or diabetes, as well as self-reported intake of calcium, vitamins D and K, saturated fat, fiber, alcohol, and energy. Secondary analyses included logistic regressions of CAC and AAC outcomes as cut-points (AS >0 and AS ?90th percentile for age and sex), as well as sex-stratified analyses. RESULTS:In fully adjusted models, a 50-mg/day increment in self-reported total magnesium intake was associated with 22% lower CAC (p < 0.001) and 12% lower AAC (p = 0.07). Consistent with these observations, the odds of having any CAC were 58% lower (p trend: <0.001) and any AAC were 34% lower (p trend: 0.01), in those with the highest compared to those with the lowest magnesium intake. Stronger inverse associations were observed in women than in men. CONCLUSIONS:In community-dwelling participants free of cardiovascular disease, self-reported magnesium intake was inversely associated with arterial calcification, which may play a contributing role in magnesium's protective associations in stroke and fatal coronary heart disease.
Project description:Epicardial adipose tissue (EAT) inflammation is implicated in the development and progression of coronary atherosclerosis. Dietary saturated and polyunsaturated fatty acids (SFAs and PUFA) can influence adipose tissue inflammation. We investigated the influence of dietary patterns, with emphasis on dietary fat type, and statin therapy, on EAT fatty acid (FA) composition and inflammatory gene expression. Thirty-two Ossabaw pigs were fed isocaloric amounts of a Heart Healthy (high in unsaturated fat) or Western (high in saturated fat) diets +/- atorvastatin for 6 months. EAT FA composition reflected dietary fat composition. There was no significant effect of atorvastatin on EAT FA composition. Total and long-chain SFAs were positively associated with inflammatory signaling (TLR2) and a gene involved in lipid mediator biosynthesis (PTGS2) (P<.0003). Medium-chain SFAs capric and lauric acids were negatively associated with IL-6 (all P<.0003). N-6 and n-3 PUFAs were positively associated with anti-inflammatory signaling genes (PPARG, FFAR4 and ADIPOQ) and long-chain n-3 PUFAs were positively associated with a gene involved in lipid mediator biosynthesis (ALOX5) (all P<.0003). These data indicate that dietary patterns, differing in fat type, influence EAT FA composition. Associations between EAT SFAs, PUFAs, and expression of genes related to inflammation provide a link between dietary quality and EAT inflammation.
Project description:Dairy products are a major contributor to dietary SFA. Partial replacement of milk SFA with unsaturated fatty acids (FAs) is possible through oleic-acid rich supplementation of the dairy cow diet. To assess adherence to the intervention of SFA-reduced, MUFA-enriched dairy product consumption in the RESET (REplacement of SaturatEd fat in dairy on Total cholesterol) study using 4-d weighed dietary records, in addition to plasma phospholipid FA (PL-FA) status.In a randomised, controlled, crossover design, free-living UK participants identified as moderate risk for CVD (n?=?54) were required to replace habitually consumed dairy foods (milk, cheese and butter), with study products with a FA profile typical of retail products (control) or SFA-reduced, MUFA-enriched profile (modified), for two 12-week periods, separated by an 8-week washout period. A flexible food-exchange model was used to implement each isoenergetic high-fat, high-dairy diet (38% of total energy intake (%TE) total fat): control (dietary target: 19%TE SFA; 11%TE MUFA) and modified (16%TE SFA; 14%TE MUFA).Following the modified diet, there was a smaller increase in SFA (17.2%TE vs. 19.1%TE; p?<?0.001) and greater increase in MUFA intake (15.4%TE vs. 11.8%TE; p?<?0.0001) when compared with the control. PL-FA analysis revealed lower total SFAs (p?=?0.006), higher total cis-MUFAs and trans-MUFAs (both p?<?0.0001) following the modified diet.The food-exchange model was successfully used to achieve RESET dietary targets by partial replacement of SFAs with MUFAs in dairy products, a finding reflected in the PL-FA profile and indicative of objective dietary compliance.ClinicalTrials.gov Identifier: NCT02089035 , date 05-01-2014.