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Long-term intake of dietary fat and risk of ulcerative colitis and Crohn's disease.
Ananthakrishnan, AN, Khalili, H, Konijeti, GG, Higuchi, LM, de Silva, P, Fuchs, CS, Willett, WC, Richter, JM, Chan, AT
Gut. 2014;(5):776-84
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Abstract
INTRODUCTION Dietary fats influence intestinal inflammation and regulate mucosal immunity. Data on the association between dietary fat and risk of Crohn's disease (CD) and ulcerative colitis (UC) are limited and conflicting. METHODS We conducted a prospective study of women enrolled in the Nurses' Health Study cohorts. Diet was prospectively ascertained every 4 years using a validated semi-quantitative food frequency questionnaire. Self-reported CD and UC were confirmed through medical record review. We examined the effect of energy-adjusted cumulative average total fat intake and specific types of fat and fatty acids on the risk of CD and UC using Cox proportional hazards models adjusting for potential confounders. RESULTS Among 170,805 women, we confirmed 269 incident cases of CD (incidence 8/100,000 person-years) and 338 incident cases of UC (incidence 10/100,000 person-years) over 26 years and 3,317,338 person-years of follow-up. Cumulative energy-adjusted intake of total fat, saturated fats, unsaturated fats, n-6 and n-3 polyunsaturated fatty acids (PUFAs) were not associated with risk of CD or UC. However, greater intake of long-chain n-3 PUFAs was associated with a trend towards lower risk of UC (HR 0.72, 95% CI 0.51 to 1.01). In contrast, high long-term intake of trans-unsaturated fatty acids was associated with a trend towards an increased incidence of UC (HR 1.34, 95% CI 0.94 to 1.92). CONCLUSIONS A high intake of dietary long-chain n-3 PUFAs may be associated with a reduced risk of UC. In contrast, high intake of trans-unsaturated fats may be associated with an increased risk of UC.
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Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies.
Farvid, MS, Ding, M, Pan, A, Sun, Q, Chiuve, SE, Steffen, LM, Willett, WC, Hu, FB
Circulation. 2014;(18):1568-78
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BACKGROUND Previous studies on intake of linoleic acid (LA), the predominant n-6 fatty acid, and coronary heart disease (CHD) risk have generated inconsistent results. We performed a systematic review and meta-analysis of prospective cohort studies to summarize the evidence regarding the relation of dietary LA intake and CHD risk. METHODS AND RESULTS We searched MEDLINE and EMBASE databases through June 2013 for prospective cohort studies that reported the association between dietary LA and CHD events. In addition, we used unpublished data from cohort studies in a previous pooling project. We pooled the multivariate-adjusted relative risk (RR) to compare the highest with the lowest categories of LA intake using fixed-effect meta-analysis. We identified 13 published and unpublished cohort studies with a total of 310 602 individuals and 12 479 total CHD events, including 5882 CHD deaths. When the highest category was compared with the lowest category, dietary LA was associated with a 15% lower risk of CHD events (pooled RR, 0.85; 95% confidence intervals, 0.78-0.92; I(2)=35.5%) and a 21% lower risk of CHD deaths (pooled RR, 0.79; 95% confidence intervals, 0.71-0.89; I(2)=0.0%). A 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events (RR, 0.91; 95% confidence intervals, 0.87-0.96) and a 13% lower risk of CHD deaths (RR, 0.87; 95% confidence intervals, 0.82-0.94). CONCLUSIONS In prospective observational studies, dietary LA intake is inversely associated with CHD risk in a dose-response manner. These data provide support for current recommendations to replace saturated fat with polyunsaturated fat for primary prevention of CHD.
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The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?
Astrup, A, Dyerberg, J, Elwood, P, Hermansen, K, Hu, FB, Jakobsen, MU, Kok, FJ, Krauss, RM, Lecerf, JM, LeGrand, P, et al
The American journal of clinical nutrition. 2011;(4):684-8
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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.
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Dietary fat is not a major determinant of body fat.
Willett, WC, Leibel, RL
The American journal of medicine. 2002;:47S-59S
Abstract
The percentage of energy from fat in diets has been thought to be an important determinant of body fat, and several mechanisms have been proposed. Comparisons of diets and the prevalence of obesity between affluent and poor countries have been used to support this relationship, but these contrasts are seriously confounded by differences in physical activity and food availability. Within areas of similar economic development, regional intake of fat and prevalence of obesity have not been positively correlated. Randomized trials are the preferable method to evaluate the effect of dietary fat on adiposity and are feasible because the number of subjects needed is not large. In short-term trials, a modest reduction in body weight is typically seen in individuals randomized to diets with a lower percentage of calories from fat. However, compensatory mechanisms appear to operate, because in randomized trials lasting >or=1 year, fat consumption within the range of 18% to 40% of energy appears to have little if any effect on body fatness. The weighted mean difference was -0.25 kg overall and +1.8 kg (i.e., less weight loss on the low-fat diets) for trials with a control group that received a comparable intensity intervention. Moreover, within the United States, a substantial decline in the percentage of energy from fat during the last 2 decades has corresponded with a massive increase in the prevalence of obesity. Diets high in fat do not appear to be the primary cause of the high prevalence of excess body fat in our society, and reductions in fat will not be a solution.
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Dietary fat plays a major role in obesity: no.
Willett, WC
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2002;(2):59-68
Abstract
The percentage of dietary energy from fat has been suggested to be an important determinant of body fat, and this presumed effect has been invoked to justify the general promotion of low-fat diets. Dietary fat and the prevalence of obesity are lower in poor countries than in affluent countries. However, these contrasts are seriously confounded by differences in physical activity and food availability; within areas of similar economic development, per capita intake of fat and the prevalence of obesity have not been positively correlated. Randomized trials are the preferable method for evaluating the effect of dietary fat on adiposity because they avoid problems of confounding that are difficult to control in other studies. In short-term trials, a small reduction in body weight is typically seen in individuals randomized to diets with a lower percentage of calories from fat. In a meta-analysis of these trials, it was estimated that a decrease in 10% of energy from fat would reduce weight by 16 g d-1, which would correspond to a 9-kg weight loss by 18 months. However, compensatory mechanisms appear to operate because in trials lasting one year or longer, fat consumption within the range of 18-40% of energy has consistently had little, if any, effect on body fatness. Moreover, within the United States (US), a substantial decline in the percentage of energy from fat during the last two decades has corresponded with a massive increase in obesity, and similar trends are occurring in other affluent countries. Diets high in fat do not account for the high prevalence of excess body fat in Western countries; reductions in the percentage of energy from fat will have no important benefits and could further exacerbate this problem. The emphasis on total fat reduction has been a serious distraction in efforts to control obesity and improve health in general.
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Dietary fat and risk of lung cancer in a pooled analysis of prospective studies.
Smith-Warner, SA, Ritz, J, Hunter, DJ, Albanes, D, Beeson, WL, van den Brandt, PA, Colditz, G, Folsom, AR, Fraser, GE, Freudenheim, JL, et al
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 2002;(10 Pt 1):987-92
Abstract
Lung cancer rates are highest in countries with the greatest fat intakes. In several case-control studies, positive associations have been observed between lung cancer and intakes of total and saturated fat, particularly among nonsmokers. We analyzed the association between fat and cholesterol intakes and lung cancer risk in eight prospective cohort studies that met predefined criteria. Among the 280,419 female and 149,862 male participants who were followed for up to 6-16 years, 3,188 lung cancer cases were documented. Using the Cox proportional hazards model, we calculated study-specific relative risks that were adjusted for smoking history and other potential risk factors. Pooled relative risks were computed using a random effects model. Fat intake was not associated with lung cancer risk. For an increment of 5% of energy from fat, the pooled multivariate relative risks were 1.01 [95% confidence interval (CI), 0.98-1.05] for total, 1.03 (95% CI, 0.96-1.11) for saturated, 1.01 (95% CI, 0.93-1.10) for monounsaturated, and 0.99 (95% CI, 0.90-1.10) for polyunsaturated fat. No associations were observed between intakes of total or specific types of fat and lung cancer risk among never, past, or current smokers. Dietary cholesterol was not associated with lung cancer incidence [for a 100-mg/day increment, the pooled multivariate relative risk was 1.01 (95% CI, 0.97-1.05)]. There was no statistically significant heterogeneity among studies or by sex. These data do not support an important relation between fat or cholesterol intakes and lung cancer risk. The means to prevent this important disease remains avoidance of smoking.