Dietary Fat Intake and the Risk of Coronary Heart Disease in Women
Frank B. Hu, M.D., Meir J. Stampfer, M.D., JoAnn E. Manson, M.D., Eric Rimm, Sc.D., Graham A. Colditz, M.D., Bernard A. Rosner, Ph.D., Charles H. Hennekens, M.D., and Walter C. Willett, M.D.
Background The relation between dietary intake of specific typesof fat, particularly trans unsaturated fat, and the risk ofcoronary disease remains unclear. We therefore studied thisrelation in women enrolled in the Nurses' Health Study.
Methods We prospectively studied 80,082 women who were 34 to59 years of age and had no known coronary disease, stroke, cancer,hypercholesterolemia, or diabetes in 1980. Information on dietwas obtained at base line and updated during follow-up by meansof validated questionnaires. During 14 years of follow-up, wedocumented 939 cases of nonfatal myocardial infarction or deathfrom coronary heart disease. Multivariate analyses includedage, smoking status, total energy intake, dietary cholesterolintake, percentages of energy obtained from protein and specifictypes of fat, and other risk factors.
Results Each increase of 5 percent of energy intake from saturatedfat, as compared with equivalent energy intake from carbohydrates,was associated with a 17 percent increase in the risk of coronarydisease (relative risk, 1.17; 95 percent confidence interval,0.97 to 1.41; P = 0.10). As compared with equivalent energyfrom carbohydrates, the relative risk for a 2 percent incrementin energy intake from trans unsaturated fat was 1.93 (95 percentconfidence interval, 1.43 to 2.61; P<0.001); that for a 5percent increment in energy from monounsaturated fat was 0.81(95 percent confidence interval, 0.65 to 1.00; P = 0.05); andthat for a 5 percent increment in energy from polyunsaturatedfat was 0.62 (95 percent confidence interval, 0.46 to 0.85;P = 0.003). Total fat intake was not significantly related tothe risk of coronary disease (for a 5 percent increase in energyfrom fat, the relative risk was 1.02; 95 percent confidenceinterval, 0.97 to 1.07; P = 0.55). We estimated that the replacementof 5 percent of energy from saturated fat with energy from unsaturatedfats would reduce risk by 42 percent (95 percent confidenceinterval, 23 to 56; P<0.001) and that the replacement of2 percent of energy from trans fat with energy from unhydrogenated,unsaturated fats would reduce risk by 53 percent (95 percentconfidence interval, 34 to 67; P<0.001).
Conclusions Our findings suggest that replacing saturated andtrans unsaturated fats with unhydrogenated monounsaturated andpolyunsaturated fats is more effective in preventing coronaryheart disease in women than reducing overall fat intake.
Low-fat, high-carbohydrate diets have been widely recommendedas a way to reduce the risk of coronary heart disease becausepopulations with low intakes of saturated and total fat tendto be at low risk and because saturated fat increases low-densitylipoprotein (LDL) cholesterol levels.1 However, low-fat, high-carbohydratediets also reduce high-density lipoprotein (HDL) cholesterollevels and raise fasting levels of triglycerides.2 Because lowlevels of HDL cholesterol and high levels of triglycerides independentlyincrease risk, the value of replacing fat in general with carbohydrateshas been questioned.3 Replacing saturated fat and trans unsaturatedfat with unhydrogenated unsaturated fats has clear beneficialeffects on blood lipids2 and thus provides an alternative strategyfor reducing the risk of coronary heart disease.
The results of prospective epidemiologic investigations of dietaryfat and coronary disease have been inconsistent. A significantpositive association between saturated fat and disease was foundin two studies,4,5 but not in others.6,7,8,9,10,11 A significantinverse association between polyunsaturated-fat intake and therisk of disease was found in only one study.9 The interpretationof these findings is complicated by the small size of the studies,inadequate dietary assessment, incomplete adjustment for energyintake, failure to account for trans isomers of unsaturatedfats, and lack of control for other types of fat.12 Repeatedmeasurements of dietary components were rarely obtained duringfollow-up. Moreover, previous research on the relation of dietaryfat to the risk of coronary disease has focused primarily onmen.4,5,6,7,8,9,10,11,13,14,15
We previously reported on the relation of dietary intake oftrans unsaturated fat to the incidence of coronary disease amongwomen in the Nurses' Health Study over an eight-year period.16The present analyses extend those findings to a total of 14years of follow-up to examine the effect of total dietary fatand specific major types of fat and to estimate the effectsof substituting carbohydrates or unsaturated fat for saturatedfat and trans unsaturated fat.
Methods
The Nurses' Health Study Cohort
The Nurses' Health Study was established in 1976, when 121,700female nurses who were then 30 to 55 years of age completeda mailed questionnaire on their medical history and lifestyle.Every two years, follow-up questionnaires have been sent toobtain up-to-date information on risk factors and to identifynewly diagnosed diseases. In 1980, a 61-item food-frequencyquestionnaire was included to assess dietary intake of specificfats and other nutrients. In 1984, the dietary questionnairewas expanded to include 116 items. Similar questionnaires wereused to obtain current information on diet in 1986 and 1990.
After up to four mailings, 98,462 women returned the 1980 dietquestionnaire. We excluded those with 10 or more blank items,those with implausibly high or low scores for total food orenergy intake (<500 kcal or >3500 kcal per day), and thosewith previously diagnosed cancer, angina, myocardial infarction,stroke, or other cardiovascular diseases. Women reporting highserum cholesterol levels or diabetes were excluded from thepresent analyses because these disorders are associated withcoronary heart disease and also could have caused women to changetheir diets. The final 1980 base-line population consisted of80,082 women; over 90 percent responded to the subsequent biennialquestionnaires and about 80 percent completed the food-frequencyquestionnaires during follow-up.
The Semiquantitative Food-Frequency Questionnaires
A detailed description of the food-frequency questionnairesand documentation of their reproducibility and validity havebeen published elsewhere.12 A common unit or portion size foreach food (e.g., one egg or one slice of bread) was specified,and participants were asked how often, on average, they hadconsumed that amount of the item during the previous year. Thenine responses ranged from "never or less than once per month"to "six or more times per day." We also inquired about typesof fat or oil used for frying, for baking, and at the tableand the type of margarine usually used (stick or tub in 1980and 1984 and brand and type in 1986 and 1990).
Nutrient intake was computed by multiplying the frequency ofconsumption of each food by the nutrient content of the specifiedportion, taking into account the type of fat used in preparation.Values for the amounts of dietary fats and other nutrients inthe foods were obtained from the Harvard University Food CompositionDatabase (completed on November 22, 1993), derived from Departmentof Agriculture sources17 and supplemented with information frommanufacturers. Values for total trans isomer contents of foodswere based on analyses by Enig et al.18 and Slover et al.19We included all trans isomers of 18-carbon unsaturated fattyacids. The polyunsaturated fat for which data are reported inthis study was the n – 6 polyunsaturated fat linoleicacid (comprising 81 percent of total polyunsaturated fat inthis population).
Both the original and the revised questionnaires provided areasonable measure of total and specific types of fat when comparedwith four one-week dietary records (correlation coefficientsfor total and specific types of fat assessed by the dietaryrecords and the food-frequency questionnaires ranged from 0.46to 0.58 for the 1980 questionnaire and from 0.48 to 0.68 forthe longer questionnaire used in 1984, 1986, and 1990).12 Thecorrelation between the calculated dietary intake of trans unsaturatedfatty acids and the proportion of trans unsaturated fatty acidsin adipose tissue was 0.51.20
Identification of Cases of Coronary Heart Disease
The primary end point for this study was nonfatal myocardialinfarction or fatal coronary disease occurring after the returnof the 1980 questionnaire but before June 1, 1994. We soughtto review the medical records of all women for whom such eventswere reported. Records were reviewed by study physicians whohad no knowledge of the women's risk-factor status as reportedon their questionnaires. Myocardial infarction was confirmedif it met the World Health Organization's criteria — thatis, symptoms plus either diagnostic electrocardiographic changesor elevated levels of cardiac enzymes.21 Infarctions that requiredhospital admission and for which confirmatory information wasobtained by interview or letter, but for which no medical recordswere available, were designated as probable (17 percent). Weincluded all confirmed and probable cases in our analyses becausethe results were the same when we analyzed only the confirmedcases after excluding probable cases.
Deaths were identified from state vital records and the NationalDeath Index or reported by the women's next of kin or the postalsystem. Follow-up for the deaths was over 98 percent complete.Fatal coronary disease was considered to have occurred if therewas fatal myocardial infarction confirmed by hospital recordsor on autopsy or if coronary disease was listed as the causeof death on the death certificate, if it was the underlyingand most plausible cause, and if evidence of previous coronarydisease was available.
Statistical Analysis
Person-time for each participant was calculated from the dateof return of the 1980 questionnaire to the first end point,death, or June 1, 1994. Women who had reported having cardiovasculardisease or cancer on previous questionnaires were excluded fromsubsequent follow-up; thus, each participant could contributeonly one end point, and the cohort at risk included only thosewho remained free of both a cardiovascular end point and cancerat the beginning of each two-year follow-up interval.
Women were divided into five roughly equal groups accordingto quintiles for the percentage of energy obtained from eachtype of fat. Incidence was calculated by dividing the numberof events by the person-time of follow-up in each quintile.For each type of fat, the relative risk was computed as therate in a specific quintile divided by that in the group withthe lowest intake, with adjustment for five-year age categories.In multivariate nutrient-density models,12 we simultaneouslyincluded energy intake, the percentages of energy derived fromprotein and specific types of fat, and other potentially confoundingvariables. We also considered dietary fats as continuous variables.The coefficients from these models can be interpreted as theestimated effect of substituting a specific percentage of energyfrom fat for the same percentage of energy from carbohydrates.When estimating the effects of substituting one type of fatfor another, using the difference in coefficients from the samemodel, we calculated the percentage reductions in risk and their95 percent confidence intervals.12 To estimate the effects ofsubstituting unhydrogenated unsaturated fat for saturated fator trans unsaturated fat, the model included saturated fat,trans unsaturated fat, and the sum of monounsaturated and polyunsaturatedfats.
In order to represent long-term dietary patterns of individualsubjects as accurately as possible, we used pooled logisticregression22 to model the incidence of coronary disease in relationto the cumulative average fat intake from all available dietaryquestionnaires up to the start of each two-year follow-up interval.For example, the incidence of coronary disease from 1980 through1984 was related to the fat intake reported on the 1980 questionnaire,and incidence from 1984 through 1986 was related to the averageintake reported on the 1980 and 1984 questionnaires. Becausechanges in diet after the development of intermediate end pointssuch as angina, hypercholesterolemia, diabetes, and hypertensionmay confound the associations between diet and disease,23 westopped updating information on diet at the beginning of theinterval during which those intermediate end points developedin an individual subject. We also conducted analyses relatingincidence to fat intake as reported on the base-line (1980)dietary questionnaire. Nondietary covariates, including age,cigarette smoking, body-mass index (defined as the weight inkilograms divided by the square of the height in meters), postmenopausalhormone use, consumption of alcohol, multivitamin use, and useof vitamin E supplements, were updated every two years. Aspirinuse was assessed in 1980, 1982, 1984, and 1988. Whether thewomen engaged in vigorous exercise was assessed in 1980. Allreported P values are two-sided.
Results
During 1,057,269 person-years of follow-up from 1980 through1994, we documented 658 nonfatal infarctions and 281 deathsfrom coronary heart disease. The dietary intakes of specifictypes of fat tended to be positively correlated with one another(Table 1), partly because of shared food sources, but the degreeof correlation was high only between saturated and monounsaturatedfats. The intake of each type of fat at base line was inverselyassociated with the consumption of folate, fiber, and alcohol,use of multivitamin and vitamin E supplements, and vigorousexercise (Table 2).
Table 2. Base-Line Characteristics and Risk Factors for Coronary Heart Disease According to the Intake of Specific Types of Fat at Base Line in 1980.
In age-adjusted analyses, a higher total fat intake was significantlyassociated with increased risk (Table 3). However, the associationvirtually disappeared in the multivariate analysis, primarilybecause of confounding by smoking, but also in part becauseof adjustment for alcohol use, vigorous exercise, and vitaminE supplementation. Adjustment for body-mass index had no furthereffect. When total fat was entered into the multivariate modelas a continuous variable, the relative risk was 1.02 (95 percentconfidence interval, 0.97 to 1.07; P = 0.55) for an increaseof 5 percent in energy obtained from total fat, as comparedwith the equivalent energy obtained from carbohydrates.
Table 3. Relative Risk of Coronary Heart Disease According to Quintiles of Specific Types of Dietary Fat, Dietary Cholesterol, and Keys Score.
The intakes of animal fat, saturated fat, monounsaturated fat,and trans unsaturated fat and the Keys score (which measuresthe projected change in the serum cholesterol concentrationdue to changes in the intakes of specific fats and cholesterol)24were each associated with an increased risk of disease in age-adjustedanalyses (Table 3). After multivariate adjustment, all associationswere attenuated, largely because of control for smoking, butthe trends remained significant for trans unsaturated fats andthe Keys score.
Because major food sources of monounsaturated fat in the UnitedStates (beef, dairy fats, and partially hydrogenated vegetableoil) can also have a high saturated, trans unsaturated, or polyunsaturatedfat content, we included all four types simultaneously in ourmultivariate analyses (Table 3). In the adjusted analyses, theoverall direction of the association for monounsaturated fatreversed, and there was a slight trend toward decreasing riskfrom the second to the fifth quintiles with respect to monounsaturated-fatintake. Because an important source of polyunsaturated fat aswell as trans unsaturated fat is partially hydrogenated vegetableoil, the associations for both polyunsaturated and trans unsaturatedfats in this multivariate analysis became stronger. When thesetwo fats were examined in combination (Figure 1), risk was thelowest among those who had the lowest intake of trans unsaturatedfat and the highest intake of polyunsaturated fat (e.g., thosewho consumed unhydrogenated soybean or corn oil instead of hardmargarine) (relative risk, 0.31; 95 percent confidence interval,0.11 to 0.88; P = 0.01).
Figure 1. Multivariate Relative Risk of Coronary Heart Disease According to Dietary Intake of Trans Unsaturated and Polyunsaturated Fats.
The first and second quintiles for polyunsaturated-fat intake were combined to provide a sufficient number of women in each of the categories. The relative risks have been adjusted for age, time interval, body-mass index, cigarette smoking, menopausal status, parental history of premature myocardial infarction, use of multivitamins, use of vitamin E supplements, alcohol consumption, history of hypertension, aspirin use, physical activity, percentage of energy obtained from protein, saturated fat, and monounsaturated fat, dietary cholesterol, and total energy intake. The reference group for all comparisons was the women with the highest intake of trans unsaturated fat and the lowest intake of polyunsaturated fat.
Next, we treated the percentages of total energy obtained fromspecific types of fat as continuous variables, with adjustmentfor the intake of other types (Table 4). We observed positiveassociations between the incidence of coronary heart diseaseand the intake of saturated fat (P = 0.10) and trans unsaturatedfat (P<0.001) and inverse associations with monounsaturatedfat (P = 0.05) and polyunsaturated fat (P = 0.003). These associationsdid not differ significantly between current smokers and nonsmokers.The positive association for dietary cholesterol intake wasnot significant, whether we used the linear values or the squareroot of cholesterol intake in the analysis. The analyses usingonly base-line diet yielded qualitatively similar but somewhatweaker results (Table 4). Using the model for updated dietaryinformation in Table 4, we estimated the effects of variousisocaloric dietary substitutions on the risk of coronary disease(Figure 2). Replacing 5 percent of energy from saturated fatwith energy from unsaturated fats was associated with a 42 percentlower risk (95 percent confidence interval, 23 to 56 percent;P<0.001), and replacing 2 percent of energy from trans unsaturatedfat with energy from unhydrogenated, unsaturated fats was associatedwith a 53 percent lower risk (95 percent confidence interval,34 to 67 percent; P<0.001).
Table 4. Multivariate Relative Risk of Coronary Heart Disease Associated with Increases in the Percentage of Energy from Specific Types of Fat and Increases in Dietary Cholesterol.
Figure 2. Estimated Percent Changes in the Risk of Coronary Heart Disease Associated with Isocaloric Substitutions of One Dietary Component for Another.
The I bars represent 95 percent confidence intervals.
To examine further the relation of different types of fat tothe risk of coronary disease, we included simultaneously ina multivariate model the intake of vegetable fats and that ofanimal fats, while controlling for the intake of trans unsaturatedfat and other potentially confounding variables. The use ofmore vegetable fat was associated with a reduced risk (relativerisk, 0.84 for each increase of 5 percent of energy, 95 percentconfidence interval, 0.76 to 0.94; P = 0.001), and animal fathad no significant association with disease (relative risk,0.98 for each increase of 5 percent of energy; 95 percent confidenceinterval, 0.92 to 1.03; P = 0.40).
In further analyses, control for diabetes and hypercholesterolemiadiagnosed during follow-up in the multivariate model did notmaterially alter the results. An analysis in which only themost recent dietary data were included yielded qualitativelysimilar results. The results were also similar when we excludedevents that occurred during the first four years of follow-upin order to avoid changes in diet that may have been due tothe presence of preclinical conditions and when we excludedparticipants who failed to complete any one of the dietary questionnairesduring follow-up. Because of the strong correlation betweenthe intakes of saturated and monounsaturated fats, we conductedan analysis in which we eliminated monounsaturated fat fromthe model; the associations for other fats were only slightlyweakened.
Discussion
In this large, prospective study of women, we found that a higherdietary intake of saturated fat and trans unsaturated fat wasassociated with an increased risk of coronary disease, whereasa higher intake of monounsaturated and polyunsaturated fatswas associated with a decreased risk. Because of the oppositeeffects of different fats on incidence, total fat intake wasnot significantly related to the risk of coronary disease. Theobserved relation for saturated fat was much weaker than thatpredicted by international comparisons,1 suggesting that theinternational analysis is seriously confounded by other lifestylefactors.3 However, our findings are consistent with the small-to-negligibleeffect predicted by metabolic studies of the relation of dietand blood lipid levels. For example, Krauss et al.25 have estimatedthat replacing 4 percent of energy from saturated fat with anequivalent amount of energy from carbohydrates would reducethe rate of coronary disease by about 5 percent. If changesin HDL cholesterol are also considered, however, no effect wouldbe anticipated.11 As predicted by metabolic studies,2 the replacementof saturated fat or trans unsaturated fat by cis (unhydrogenated)unsaturated fats was associated with larger reductions in riskthan an isocaloric replacement by carbohydrates. In addition,dietary fats may contribute to risk through other mechanisms— for example, by influencing platelet aggregability,changing the threshold for ventricular fibrillation, or affectingsensitivity to insulin.12
We observed a positive association, albeit not a statisticallysignificant one, between dietary cholesterol intake and therisk of coronary disease. Metabolic studies suggest that theeffect of dietary cholesterol on serum total cholesterol andLDL cholesterol levels in humans is considerably less strongthan that of saturated fat.26 A significant positive associationbetween dietary cholesterol and coronary disease was observedin some studies,4,9 but not in others.10,11,15,27 In a pooledanalysis28 of four studies,4,5,6,9 the relative risk of coronarydisease was 1.30 (95 percent confidence interval, 1.10 to 1.50)for an increase of 200 mg of dietary cholesterol per 1000 kcalof total energy intake; the 95 percent confidence interval includesour estimate.
The inverse association between the dietary intake of polyunsaturatedfat and the incidence of coronary disease is consistent withthe results of numerous metabolic studies that showed strongcholesterol-lowering effects of vegetable oils rich in linoleicacid when they were substituted for saturated fat in the diet.1Also, diets high in polyunsaturated fat have been more effectivethan low-fat, high-carbohydrate diets in lowering total serumcholesterol as well as the incidence of coronary disease.29
Epidemiologic data on monounsaturated fat are sparse. Two prospectivestudies found that the risk of coronary disease increased withhigher intakes of monounsaturated fat in younger but not inolder participants.15,27 However, neither study adjusted forthe intake of other types of fat. In our analyses, after adjustmentfor the intake of other fats, monounsaturated-fat intake wasinversely associated with risk. In metabolic studies, replacingcarbohydrates with monounsaturated fat raises HDL cholesterollevels without affecting LDL cholesterol2 and may also improveinsulin sensitivity.30 In addition, monounsaturated fat is resistantto oxidative modification.31 Ecologic correlations also suggestthat the dietary intake of monounsaturated fat is inverselyassociated with total mortality and mortality due to coronarydisease.32
The positive association of coronary heart disease with theintake of trans unsaturated fat is consistent with the resultsof most previous studies.33 The concentration of trans unsaturatedfatty acids in adipose tissue was not significantly associatedwith the risk of myocardial infarction in the European AntioxidantMyocardial Infarction and Cancer (EURAMIC) study34 or with suddendeath from cardiac causes in a small case–control studyin the United Kingdom.35 However, the 95 percent confidenceintervals for the relative risks in the highest categories ofconsumption of trans unsaturated fatty acids in both studieswere very wide and included our estimate of relative risk. Alsoin the EURAMIC study, after the exclusion of an outlier area(Spain), the relative risk for the highest versus the lowestcategory of dietary intake of trans unsaturated fats was closeto ours (1.44; 95 percent confidence interval, 0.94 to 2.20).
Trans unsaturated fat from foods may adversely affect the riskof coronary disease by raising LDL cholesterol levels and loweringHDL cholesterol levels,36 increasing Lp(a) lipoprotein levels,36raising triglyceride levels,36 and interfering with essential-fatty-acidmetabolism.37 Hence, it is not surprising that the relativerisks in this and other studies are larger than would be predictedsolely on the basis of the effect of trans unsaturated fattyacids on blood lipids.33 Imprecise dietary measurement and residualconfounding have been suggested as alternative explanationsfor the observed positive associations.38 However, errors inmeasuring dietary intake could have accounted for a lack ofassociation, but not for the presence of an association.39 Inthis study, we obtained repeated measurements of dietary intakein an attempt to reduce errors. As expected, the analyses usingrepeated measures yielded stronger effects of trans unsaturatedfat on the incidence of coronary disease than those that includedonly the base-line measures.
To account for the effects of potential confounding by lifestylefactors, we adjusted for a multitude of dietary and nondietaryrisk factors. The multivariate-adjusted relative risk of coronarydisease associated with the consumption of trans unsaturatedfat was similar to the age-adjusted relative risk, suggestingthat confounding by lifestyle factors had only a small effect.On the other hand, the intake of other fats had more importantconfounding effects, which actually strengthened the associationof trans unsaturated fat with coronary disease. In addition,adjustment for intermediate end points such as hypercholesterolemiaand diabetes did not materially alter the association, suggestingthat confounding by precursors of coronary disease was minimal.Perhaps people with newly diagnosed intermediate end pointssuch as angina might switch from butter to margarine, a changethat could increase their intake of trans unsaturated fat andthus artificially produce an elevated risk. However, our datadid not support this speculation, since women who had intermediateend points actually tended to reduce their intakes of transunsaturated fat. For example, from 1980 to 1984, the mean intakeof trans unsaturated fat declined 13 percent among women inwhom angina developed, as compared with 8 percent among womenwho did not have angina.
Food-consumption patterns in the United States have shiftedconsiderably in the past decade.40 In our study, total fat intakeas a percentage of energy intake declined by about 19 percentfrom 1980 to 1990. Because we incorporated updated dietary information,our analyses took into account changes over time in dietaryhabits and food composition. Although the conclusions drawnfrom the analyses were qualitatively similar whether they werebased on base-line or updated dietary information, the associationswere somewhat stronger in the updated analyses, indicating theadvantage of using the repeated measurements.
Our data provide evidence in support of the hypothesis thata higher dietary intake of saturated fat and trans unsaturatedfat is associated with an increased risk of coronary disease,whereas a higher intake of monounsaturated and polyunsaturatedfats is associated with reduced risk. These findings reinforceevidence from metabolic studies that replacing saturated fatand trans unsaturated fat in the diet with unhydrogenated monounsaturatedand polyunsaturated fats favorably alters the lipid profile,but that reducing overall fat intake has little effect.
Supported by research grants (HL24074, HL34594, CA40356, andDK 46200) and a nutrition training grant (T32DK07703) from theNational Institutes of Health.
We are indebted to the participants in the Nurses' Health Studyfor their continuing outstanding level of cooperation; to AlWing, Mark Shneyder, Gary Chase, Karen Corsano, Lisa Dunn, BarbaraEgan, Lori Ward, and Jill Arnold for their unfailing help; toAlberto Ascherio and Alicja Wolk for helpful comments; and toFrank E. Speizer, principal investigator of the Nurses' HealthStudy, for his support.
Source Information
From the Departments of Nutrition (F.B.H., M.J.S., E.R., W.C.W.), Epidemiology (M.J.S., J.E.M., E.R., B.A.R., W.C.W.), and Biostatistics (B.A.R.), Harvard School of Public Health; and the Channing Laboratory (M.J.S., J.E.M., E.R., G.A.C., B.A.R., C.H.H., W.C.W.) and the Division of Preventive Medicine (J.E.M., C.H.H.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School — all in Boston.
Address reprint requests to Dr. Hu at the Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115.
References
Grundy SM, Bilheimer D, Blackburn H, et al. Rationale of the diet-heart statement of the American Heart Association: report of Nutrition Committee. Circulation 1982;65:839A-854A.
Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins: a meta-analysis of 27 trials. Arterioscler Thromb 1992;12:911-919. [Abstract]
Katan MB, Grundy SM, Willett WC. Beyond low-fat diets. N Engl J Med 1997;337:563-566.
McGee DL, Reed DM, Yano K, Kagan A, Tillotson J. Ten-year incidence of coronary heart disease in the Honolulu Heart Program: relationship to nutrient intake. Am J Epidemiol 1984;119:667-676. [Free Full Text]
Kushi LH, Lew RA, Stare FJ, et al. Diet and 20-year mortality from coronary heart disease: the Ireland-Boston Diet-Heart Study. N Engl J Med 1985;312:811-818. [Abstract]
Kromhout D, de Lezenne Coulander C. Diet, prevalence and 10-year mortality from coronary heart disease in 871 middle-aged men: the Zutphen Study. Am J Epidemiol 1984;119:733-741. [Free Full Text]
Gordon T, Kagan A, Garcia-Palmieri M, et al. Diet and its relation to coronary heart disease and death in three populations. Circulation 1981;63:500-515. [Medline]
Morris JN, Marr JW, Clayton DG. Diet and heart: a postscript. BMJ 1977;2:1307-1314.
Shekelle RB, Shryock AM, Paul O, et al. Diet, serum cholesterol, and death from coronary heart disease: the Western Electric Study. N Engl J Med 1981;304:65-70. [Abstract]
Pietinen P, Ascherio A, Korhonen P, et al. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men: the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Epidemiol 1997;145:876-887. [Free Full Text]
Ascherio A, Rimm EB, Giovannucci EL, Spiegelman D, Stampfer MJ, Willett WC. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States. BMJ 1996;313:84-90. [Free Full Text]
Willett WC. Nutritional epidemiology. New York: Oxford University Press, 1990.
Goldbourt U, Yaari S, Medalie JH. Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees: a 23-year mortality follow-up in the Israeli Ischemic Heart Disease Study. Cardiology 1993;82:100-121. [Medline]
Posner BM, Cobb JL, Belanger AJ, Cupples LA, D'Agostino RB, Stokes J III. Dietary lipid predictors of coronary heart disease in men: the Framingham Study. Arch Intern Med 1991;151:1181-1187. [Abstract]
Willett WC, Stampfer MJ, Manson JE, et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 1993;341:581-585. [CrossRef][Medline]
Department of Agriculture. Composition of foods: raw, processed, prepared, 1963-1991. Agricultural handbook. No. 8-128-21 series. Washington, D.C.: Government Printing Office, 1992.
Enig MG, Pallansch LA, Sampugna J, Keeney M. Fatty acid composition of the fat in selected food items with emphasis on trans components. J Am Oil Chem Soc 1983;60:1788-1795.
Slover HT, Thompson RH Jr, Davis CS, Merola GV. Lipids in margarines and margarine-like foods. J Am Oil Chem Soc 1985;62:775-786.
London SJ, Sacks FM, Caesar J, Stampfer MJ, Siguel E, Willett WC. Fatty acid composition of subcutaneous adipose tissue and diet in postmenopausal US women. Am J Clin Nutr 1991;54:340-345. [Free Full Text]
Rose GA, Blackburn H. Cardiovascular survey methods. Geneva: World Health Organization, 1982.
D'Agostino RB, Lee M-L, Belanger AJ, Cupples LA, Anderson K, Kannel WB. Relation of pooled logistic regression to time dependent Cox regression analysis: the Framingham Heart Study. Stat Med 1990;9:1501-1515. [Medline]
Shekelle RB, Stamler J, Paul O, Shryock AM, Liu S, Lepper M. Dietary lipids and serum cholesterol level: change in diet confounds the cross-sectional association. Am J Epidemiol 1982;115:506-514. [Free Full Text]
Keys A, Parlin RW. Serum cholesterol response to changes in dietary lipids. Am J Clin Nutr 1966;19:175-181. [Abstract]
Krauss RM, Deckelbaum RJ, Ernst N, et al. Dietary guidelines for healthy American adults: a statement for health professionals from the Nutrition Committee, American Heart Association. Circulation 1996;94:1795-1800. [Medline]
Grundy SM, Barrett-Connor E, Rudel LL, Miettinen T, Spector AA. Workshop on the impact of dietary cholesterol on plasma lipoproteins and atherogenesis. Arteriosclerosis 1988;8:95-101. [Medline]
Esrey KL, Joseph L, Grover SA. Relationship between dietary intake and coronary heart disease mortality: Lipid Research Clinics Prevalence Follow-up Study. J Clin Epidemiol 1996;49:211-216. [CrossRef][Medline]
Stamler J, Shekelle R. Dietary cholesterol and human coronary heart disease. Arch Pathol Lab Med 1988;112:1032-1040. [Medline]
Sacks F. Dietary fats and coronary heart disease. J Cardiovasc Risk 1994;1:3-8. [CrossRef][Medline]
Garg A, Grundy SM, Koffler M. Effect of high carbohydrate intake on hyperglycemia, islet function, and plasma lipoproteins in NIDDM. Diabetes Care 1992;15:1572-1580. [Abstract]
Parthasarathy S, Khoo JC, Miller E, Barnett J, Witztum JL, Steinberg D. Low density lipoprotein rich in oleic acid is protected against oxidative modification: implications for dietary prevention of atherosclerosis. Proc Natl Acad Sci U S A 1990;87:3894-3898. [Free Full Text]
Jacobs D, Blackburn H, Higgins M, et al. Report of the Conference on Low Blood Cholesterol: mortality associations. Circulation 1992;86:1046-1060. [Medline]
Willett WC, Ascherio A. Trans fatty acids: are the effects only marginal? Am J Public Health 1994;84:722-724. [Free Full Text]
Aro A, Kardinaal AFM, Salminen I, et al. Adipose tissue isomeric trans fatty acids and risk of myocardial infarction in nine countries: the EURAMIC study. Lancet 1995;345:273-278. [CrossRef][Medline]
Roberts TL, Wood DA, Riemersma RA, Gallagher PJ, Lampe FC. Trans isomers of oleic and linoleic acids in adipose tissue and sudden cardiac death. Lancet 1995;345:278-282. [CrossRef][Medline]
Katan MB, Zock PL. Trans fatty acids and their effects on lipoproteins in humans. Annu Rev Nutr 1995;15:473-493. [Medline]
Kinsella JE, Bruckner G, Mai J, Shimp J. Metabolism of trans fatty acids with emphasis on the effects of trans, trans-octadecadienoate on lipid composition, essential fatty acid, and prostaglandins: an overview. Am J Clin Nutr 1981;34:2307-2318. [Free Full Text]
McKeigue P. Trans fatty acids and coronary heart disease: weighing the evidence against hardened fat. Lancet 1995;345:269-270. [CrossRef][Medline]
Trichopoulos D. Adipose tissue trans fatty acids and coronary heart disease. Lancet 1995;345:1108-1108.
Norris J, Harnack L, Carmichael S, Pouane T, Wakimoto P, Block G. US trends in nutrient intake: the 1987 and 1992 National Health Interview Surveys. Am J Public Health 1997;87:740-746. [Free Full Text]
Bassuk, S. S., Manson, J. E.
(2008). Lifestyle and Risk of Cardiovascular Disease and Type 2 Diabetes in Women: A Review of the Epidemiologic Evidence. AMERICAN JOURNAL OF LIFESTYLE MEDICINE
2: 191-213
[Abstract]
Belfort, M. B, Rifas-Shiman, S. L, Rich-Edwards, J. W, Kleinman, K. P, Oken, E., Gillman, M. W
(2008). Maternal iron intake and iron status during pregnancy and child blood pressure at age 3 years. Int J Epidemiol
37: 301-308
[Abstract][Full Text]
Cardinal, A. J., Dewey, R. E., Burton, J. W.
(2008). Estimating the Individual Effects of the Reduced Palmitic Acid fapnc and fap1 Alleles on Agronomic Traits in Two Soybean Populations. Crop Sci.
48: 633-639
[Abstract][Full Text]
Choi, H. K, Curhan, G.
(2008). Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ
336: 309-312
[Abstract][Full Text]
Halton, T. L, Liu, S., Manson, J. E, Hu, F. B
(2008). Low-carbohydrate-diet score and risk of type 2 diabetes in women. Am. J. Clin. Nutr.
87: 339-346
[Abstract][Full Text]
Esmaillzadeh, A., Azadbakht, L.
(2008). Consumption of Hydrogenated Versus Nonhydrogenated Vegetable Oils and Risk of Insulin Resistance and the Metabolic Syndrome Among Iranian Adult Women. Diabetes Care
31: 223-226
[Full Text]
Merchant, A. T, Kelemen, L. E, de Koning, L., Lonn, E., Vuksan, V., Jacobs, R., Davis, B., Teo, K. K, Yusuf, S., Anand, S. S, for the SHARE and SHARE-AP investigators,
(2008). Interrelation of saturated fat, trans fat, alcohol intake, and subclinical atherosclerosis. Am. J. Clin. Nutr.
87: 168-174
[Abstract][Full Text]
Fehr, W. R.
(2007). Breeding for Modified Fatty Acid Composition in Soybean. Crop Sci.
47: S-72-S-87
[Abstract][Full Text]
Kim, D. H.
(2007). High-Density Lipoprotein and Dietary Fatty Acids. JAMA
298: 2263-2264
[Full Text]
Colon-Ramos, U., Lindsay, A. C, Monge-Rojas, R., Greaney, M. L, Campos, H., Peterson, K. E
(2007). Translating research into action: a case study on trans fatty acid research and nutrition policy in Costa Rica. Health Policy Plan
22: 363-374
[Abstract][Full Text]
Cardinal, A. J., Burton, J. W.
(2007). Correlations between Palmitate Content and Agronomic Traits in Soybean Populations Segregating for the fap1, fapnc, and fan Alleles. Crop Sci.
47: 1804-1812
[Abstract][Full Text]
Eilat-Adar, S., Xu, J., Loria, C., Mattil, C., Goldbourt, U., Howard, B. V., Resnick, H. E.
(2007). Dietary Calcium Is Associated with Body Mass Index and Body Fat in American Indians. J. Nutr.
137: 1955-1960
[Abstract][Full Text]
Chappell, A. S., Bilyeu, K. D.
(2007). The Low Linolenic Acid Soybean Line PI 361088B Contains a Novel GmFAD3A Mutation. Crop Sci.
47: 1705-1710
[Abstract][Full Text]
St-Onge, M.-P., Aban, I., Bosarge, A., Gower, B., Hecker, K. D, Allison, D. B
(2007). Snack chips fried in corn oil alleviate cardiovascular disease risk factors when substituted for low-fat or high-fat snacks. Am. J. Clin. Nutr.
85: 1503-1510
[Abstract][Full Text]
Lin, J., Rexrode, K. M., Hu, F., Albert, C. M., Chae, C. U., Rimm, E. B., Stampfer, M. J., Manson, J. E.
(2007). Dietary Intakes of Flavonols and Flavones and Coronary Heart Disease in US Women. Am J Epidemiol
165: 1305-1313
[Abstract][Full Text]
Sun, Q., Ma, J., Campos, H., Hankinson, S. E., Manson, J. E., Stampfer, M. J., Rexrode, K. M., Willett, W. C., Hu, F. B.
(2007). A Prospective Study of Trans Fatty Acids in Erythrocytes and Risk of Coronary Heart Disease. Circulation
115: 1858-1865
[Abstract][Full Text]
Sheridan, M. J., Cooper, J. N., Erario, M., Cheifetz, C. E.
(2007). Pistachio Nut Consumption and Serum Lipid Levels. J. Am. Coll. Nutr.
26: 141-148
[Abstract][Full Text]
Esposito, K., Ciotola, M., Giugliano, D., Hrdy, D. B., Halton, T. L., Willett, W., Hu, F. B.
(2007). Low-carbohydrate diet and coronary heart disease in women.. NEJM
356: 750-750
[Full Text]
Cardinal, A. J., Burton, J. W., Camacho-Roger, A. M., Yang, J. H., Wilson, R. F., Dewey, R. E.
(2007). Molecular Analysis of Soybean Lines with Low Palmitic Acid Content in the Seed Oil. Crop Sci.
47: 304-310
[Abstract][Full Text]
Chavarro, J. E, Rich-Edwards, J. W, Rosner, B. A, Willett, W. C
(2007). Dietary fatty acid intakes and the risk of ovulatory infertility. Am. J. Clin. Nutr.
85: 231-237
[Abstract][Full Text]
Halton, T. L., Willett, W. C., Liu, S., Manson, J. E., Albert, C. M., Rexrode, K., Hu, F. B.
(2006). Low-Carbohydrate-Diet Score and the Risk of Coronary Heart Disease in Women. NEJM
355: 1991-2002
[Abstract][Full Text]
Colon-Ramos, U., Baylin, A., Campos, H.
(2006). The Relation between Trans Fatty Acid Levels and Increased Risk of Myocardial Infarction Does Not Hold at Lower Levels of Trans Fatty Acids in the Costa Rican Food Supply. J. Nutr.
136: 2887-2892
[Abstract][Full Text]
Xu, J., Eilat-Adar, S., Loria, C., Goldbourt, U., Howard, B. V, Fabsitz, R. R, Zephier, E. M, Mattil, C., Lee, E. T
(2006). Dietary fat intake and risk of coronary heart disease: the Strong Heart Study.. Am. J. Clin. Nutr.
84: 894-902
[Abstract][Full Text]
Litonjua, A. A, Rifas-Shiman, S. L, Ly, N. P, Tantisira, K. G, Rich-Edwards, J. W, Camargo, C. A Jr, Weiss, S. T, Gillman, M. W, Gold, D. R
(2006). Maternal antioxidant intake in pregnancy and wheezing illnesses in children at 2 y of age.. Am. J. Clin. Nutr.
84: 903-911
[Abstract][Full Text]
Zaloga, G. P., Harvey, K. A., Stillwell, W., Siddiqui, R.
(2006). Trans Fatty Acids and Coronary Heart Disease. Nutr Clin Pract
21: 505-512
[Abstract][Full Text]
Willett, W. C., Hu, F. B.
(2006). Not the Time to Abandon the Food Frequency Questionnaire: Point. Cancer Epidemiol. Biomarkers Prev.
15: 1757-1758
[Full Text]
Kostikas, K., Papaioannou, A. I., Gourgoulianis, K. I., Etzel, C. J., Kachroo, S., Yanai, H., Yoshida, H., Tada, N., Jacobson, B. C., Camargo, C. A. Jr.
(2006). BMI and Gastroesophageal Reflux in Women. NEJM
355: 848-850
[Full Text]
Giugliano, D., Ceriello, A., Esposito, K.
(2006). The Effects of Diet on Inflammation: Emphasis on the Metabolic Syndrome. J Am Coll Cardiol
48: 677-685
[Abstract][Full Text]
Lichtenstein, A. H.
(2006). Thematic review series: Patient-Oriented Research. Dietary fat, carbohydrate, and protein: effects on plasma lipoprotein patterns. J. Lipid Res.
47: 1661-1667
[Abstract][Full Text]
Vega-Lopez, S., Ausman, L. M, Jalbert, S. M, Erkkila, A. T, Lichtenstein, A. H
(2006). Palm and partially hydrogenated soybean oils adversely alter lipoprotein profiles compared with soybean and canola oils in moderately hyperlipidemic subjects. Am. J. Clin. Nutr.
84: 54-62
[Abstract][Full Text]
Bischoff, H. A., Staehelin, H. B., Willett, W. C.
(2006). The effect of undernutrition in the development of frailty in older persons.. J. Gerontol. A Biol. Sci. Med. Sci.
61: 585-589
[Full Text]
Katan, M. B
(2006). Alternatives to low-fat diets. Am. J. Clin. Nutr.
83: 989-990
[Full Text]
Halton, T. L, Willett, W. C, Liu, S., Manson, J. E, Stampfer, M. J, Hu, F. B
(2006). Potato and french fry consumption and risk of type 2 diabetes in women. Am. J. Clin. Nutr.
83: 284-290
[Abstract][Full Text]
Prepared by: British Cardiac Society, British Hype,
(2005). JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice. Heart
91: v1-v52
[Full Text]
Appel, L. J., Sacks, F. M., Carey, V. J., Obarzanek, E., Swain, J. F., Miller, E. R. III, Conlin, P. R., Erlinger, T. P., Rosner, B. A., Laranjo, N. M., Charleston, J., McCarron, P., Bishop, L. M., for the OmniHeart Collaborative Research Group,
(2005). Effects of Protein, Monounsaturated Fat, and Carbohydrate Intake on Blood Pressure and Serum Lipids: Results of the OmniHeart Randomized Trial. JAMA
294: 2455-2464
[Abstract][Full Text]
He, J., Gu, D., Wu, X., Chen, J., Duan, X., Chen, J., Whelton, P. K.
(2005). Effect of Soybean Protein on Blood Pressure: A Randomized, Controlled Trial. ANN INTERN MED
143: 1-9
[Abstract][Full Text]
Riedel, M. J., Light, P. E.
(2005). Saturated and cis/trans Unsaturated Acyl CoA Esters Differentially Regulate Wild-Type and Polymorphic {beta}-Cell ATP-Sensitive K+ Channels. Diabetes
54: 2070-2079
[Abstract][Full Text]
Nestel, P. J, Baghurst, K., Colquhoun, D. M, Simes, R J., Mehalski, K., White, H. D, Tonkin, A. M, Kirby, A., Pollicino, C., for the Long-Term Intervention with Pravastatin in,
(2005). Relation of diet to cardiovascular disease risk factors in subjects with cardiovascular disease in Australia and New Zealand: analysis of the Long-Term Intervention with Pravastatin in Ischaemic Disease trial. Am. J. Clin. Nutr.
81: 1322-1329
[Abstract][Full Text]
Keogh, J. B., Grieger, J. A., Noakes, M., Clifton, P. M.
(2005). Flow-Mediated Dilatation Is Impaired by a High-Saturated Fat Diet but Not by a High-Carbohydrate Diet. Arterioscler. Thromb. Vasc. Bio.
25: 1274-1279
[Abstract][Full Text]
Choi, H. K., Willett, W. C., Stampfer, M. J., Rimm, E., Hu, F. B.
(2005). Dairy Consumption and Risk of Type 2 Diabetes Mellitus in Men: A Prospective Study. Arch Intern Med
165: 997-1003
[Abstract][Full Text]
Oh, K., Hu, F. B., Manson, J. E., Stampfer, M. J., Willett, W. C.
(2005). Dietary Fat Intake and Risk of Coronary Heart Disease in Women: 20 Years of Follow-up of the Nurses' Health Study. Am J Epidemiol
161: 672-679
[Abstract][Full Text]
Lopez-Garcia, E., Schulze, M. B., Meigs, J. B., Manson, J. E., Rifai, N., Stampfer, M. J., Willett, W. C., Hu, F. B.
(2005). Consumption of Trans Fatty Acids Is Related to Plasma Biomarkers of Inflammation and Endothelial Dysfunction. J. Nutr.
135: 562-566
[Abstract][Full Text]
Schmidely, P., Morand-Fehr, P., Sauvant, D.
(2005). Influence of Extruded Soybeans With or Without Bicarbonate on Milk Performance and Fatty Acid Composition of Goat Milk. J DAIRY SCI
88: 757-765
[Abstract][Full Text]
Laaksonen, D. E., Nyyssonen, K., Niskanen, L., Rissanen, T. H., Salonen, J. T.
(2005). Prediction of Cardiovascular Mortality in Middle-aged Men by Dietary and Serum Linoleic and Polyunsaturated Fatty Acids. Arch Intern Med
165: 193-199
[Abstract][Full Text]
Oh, K., Hu, F. B., Cho, E., Rexrode, K. M., Stampfer, M. J., Manson, J. E., Liu, S., Willett, W. C.
(2005). Carbohydrate Intake, Glycemic Index, Glycemic Load, and Dietary Fiber in Relation to Risk of Stroke in Women. Am J Epidemiol
161: 161-169
[Abstract][Full Text]
Roberts, C. K., Barnard, R. J.
(2005). Effects of exercise and diet on chronic disease. J. Appl. Physiol.
98: 3-30
[Abstract][Full Text]
Desroches, S., Paradis, M.-E., Perusse, M., Archer, W. R., Bergeron, J., Couture, P., Bergeron, N., Lamarche, B.
(2004). Apolipoprotein A-I, A-II, and VLDL-B-100 metabolism in men: comparison of a low-fat diet and a high-monounsaturated fatty acid diet. J. Lipid Res.
45: 2331-2338
[Abstract][Full Text]
Mozaffarian, D., Rimm, E. B, Herrington, D. M
(2004). Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am. J. Clin. Nutr.
80: 1175-1184
[Abstract][Full Text]
Baylin, A., Campos, H.
(2004). Arachidonic Acid in Adipose Tissue Is Associated with Nonfatal Acute Myocardial Infarction in the Central Valley of Costa Rica. J. Nutr.
134: 3095-3099
[Abstract][Full Text]
Gillman, M. W., Rifas-Shiman, S. L., Kleinman, K. P., Rich-Edwards, J. W., Lipshultz, S. E.
(2004). Maternal Calcium Intake and Offspring Blood Pressure. Circulation
110: 1990-1995
[Abstract][Full Text]
Jakobsen, M. U., Overvad, K., Dyerberg, J., Schroll, M., Heitmann, B. L.
(2004). Dietary Fat and Risk of Coronary Heart Disease: Possible Effect Modification by Gender and Age. Am J Epidemiol
160: 141-149
[Abstract][Full Text]
Tanasescu, M., Cho, E., Manson, J. E, Hu, F. B
(2004). Dietary fat and cholesterol and the risk of cardiovascular disease among women with type 2 diabetes. Am. J. Clin. Nutr.
79: 999-1005
[Abstract][Full Text]
Willett, W. C.
(2004). Reduced-Carbohydrate Diets: No Roll in Weight Management?. ANN INTERN MED
140: 836-837
[Full Text]
Rastogi, T., Reddy, K S., Vaz, M., Spiegelman, D., Prabhakaran, D, Willett, W. C, Stampfer, M. J, Ascherio, A.
(2004). Diet and risk of ischemic heart disease in India. Am. J. Clin. Nutr.
79: 582-592
[Abstract][Full Text]
Mozaffarian, D., Pischon, T., Hankinson, S. E, Rifai, N., Joshipura, K., Willett, W. C, Rimm, E. B
(2004). Dietary intake of trans fatty acids and systemic inflammation in women. Am. J. Clin. Nutr.
79: 606-612
[Abstract][Full Text]
Meksawan, K., Pendergast, D. R., Leddy, J. J., Mason, M., Horvath, P. J., Awad, A. B.
(2004). Effect of Low and High Fat Diets on Nutrient Intakes and Selected Cardiovascular Risk Factors in Sedentary Men and Women. J. Am. Coll. Nutr.
23: 131-140
[Abstract][Full Text]
Clifton, P. M., Keogh, J. B., Noakes, M.
(2004). Trans Fatty Acids in Adipose Tissue and the Food Supply Are Associated with Myocardial Infarction. J. Nutr.
134: 874-879
[Abstract][Full Text]
Choi, H. K., Atkinson, K., Karlson, E. W., Willett, W., Curhan, G.
(2004). Purine-Rich Foods, Dairy and Protein Intake, and the Risk of Gout in Men. NEJM
350: 1093-1103
[Abstract][Full Text]
Weinberg, S. L.
(2004). The diet-heart hypothesis: a critique. J Am Coll Cardiol
43: 731-733
[Abstract][Full Text]
Gregg, E. W., Gerzoff, R. B., Thompson, T. J., Williamson, D. F.
(2004). Trying to Lose Weight, Losing Weight, and 9-Year Mortality in Overweight U.S. Adults With Diabetes. Diabetes Care
27: 657-662
[Abstract][Full Text]
Salazar-Martinez, E., Willett, W. C., Ascherio, A., Manson, J. E., Leitzmann, M. F., Stampfer, M. J., Hu, F. B.
(2004). Coffee Consumption and Risk for Type 2 Diabetes Mellitus. ANN INTERN MED
140: 1-8
[Abstract][Full Text]
Jiang, R., Ma, J., Ascherio, A., Stampfer, M. J, Willett, W. C, Hu, F. B
(2004). Dietary iron intake and blood donations in relation to risk of type 2 diabetes in men: a prospective cohort study. Am. J. Clin. Nutr.
79: 70-75
[Abstract][Full Text]
Ravnskov, U.
(2003). Dietary fat intake and risk of stroke: Allegations about dietary fat are unfounded. BMJ
327: 1348-1348
[Full Text]
He, K., Willett, W. C, Ascherio, A.
(2003). Dietary fat intake and risk of stroke: Authors' reply. BMJ
327: 1348-1349
[Full Text]
Seddon, J. M., Cote, J., Rosner, B.
(2003). Progression of Age-Related Macular Degeneration: Association With Dietary Fat, Transunsaturated Fat, Nuts, and Fish Intake. Arch Ophthalmol
121: 1728-1737
[Abstract][Full Text]
Newby, P., Hu, F. B, Rimm, E. B, Smith-Warner, S. A, Feskanich, D., Sampson, L., Willett, W. C
(2003). Reproducibility and validity of the Diet Quality Index Revised as assessed by use of a food-frequency questionnaire. Am. J. Clin. Nutr.
78: 941-949
[Abstract][Full Text]
He, K., Merchant, A., Rimm, E. B, Rosner, B. A, Stampfer, M. J, Willett, W. C, Ascherio, A.
(2003). Dietary fat intake and risk of stroke in male US healthcare professionals: 14 year prospective cohort study. BMJ
327: 777-782
[Abstract][Full Text]
Duggirala, M. K., Mundell, W. C., Mikkilineni, P., Aziz, I., Garrido, J. A., Roberts, C. K., Barnard, R. J., Samaha, F. F., Stern, L., Iqbal, N., Foster, G. D., Hill, J. O., Klein, S.
(2003). Low-Carbohydrate Diets as Compared with Low-Fat Diets. NEJM
349: 1000-1002
[Full Text]
Hu, F. B
(2003). Plant-based foods and prevention of cardiovascular disease: an overview. Am. J. Clin. Nutr.
78: 544S-551
[Abstract][Full Text]
Bilyeu, K. D., Palavalli, L., Sleper, D. A., Beuselinck, P. R.
(2003). Three Microsomal Omega-3 Fatty-acid Desaturase Genes Contribute to Soybean Linolenic Acid Levels. Crop Sci.
43: 1833-1838
[Abstract][Full Text]
Merchant, A. T., Hu, F. B., Spiegelman, D., Willett, W. C., Rimm, E. B., Ascherio, A.
(2003). The Use of B Vitamin Supplements and Peripheral Arterial Disease Risk in Men Are Inversely Related. J. Nutr.
133: 2863-2867
[Abstract][Full Text]
McCullough, M. L, Willett, W. C
(2003). Reply to JE Lincoln. Am. J. Clin. Nutr.
78: 349-350
[Full Text]
Osganian, S. K., Stampfer, M. J., Rimm, E., Spiegelman, D., Hu, F. B., Manson, J. E., Willett, W. C.
(2003). Vitamin C and risk of coronary heart disease in women. J Am Coll Cardiol
42: 246-252
[Abstract][Full Text]
Osganian, S. K, Stampfer, M. J, Rimm, E., Spiegelman, D., Manson, J. E, Willett, W. C
(2003). Dietary carotenoids and risk of coronary artery disease in women. Am. J. Clin. Nutr.
77: 1390-1399
[Abstract][Full Text]
Seymour, J. D., Calle, E. E., Flagg, E. W., Coates, R. J., Ford, E. S., Thun, M. J.
(2003). Diet Quality Index as a Predictor of Short-term Mortality in the American Cancer Society Cancer Prevention Study II Nutrition Cohort. Am J Epidemiol
157: 980-988
[Abstract][Full Text]
Chen, H., Zhang, S. M., Hernan, M. A., Willett, W. C., Ascherio, A.
(2003). Dietary Intakes of Fat and Risk of Parkinson's Disease. Am J Epidemiol
157: 1007-1014
[Abstract][Full Text]
Foster, G. D., Wyatt, H. R., Hill, J. O., McGuckin, B. G., Brill, C., Mohammed, B. S., Szapary, P. O., Rader, D. J., Edman, J. S., Klein, S.
(2003). A Randomized Trial of a Low-Carbohydrate Diet for Obesity. NEJM
348: 2082-2090
[Abstract][Full Text]
Mensink, R. P, Zock, P. L, Kester, A. D., Katan, M. B
(2003). Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am. J. Clin. Nutr.
77: 1146-1155
[Abstract][Full Text]
Hu, F. B., Cho, E., Rexrode, K. M., Albert, C. M., Manson, J. E.
(2003). Fish and Long-Chain {omega}-3 Fatty Acid Intake and Risk of Coronary Heart Disease and Total Mortality in Diabetic Women. Circulation
107: 1852-1857
[Abstract][Full Text]
Kark, J. D, Kaufmann, N. A, Binka, F., Goldberger, N., Berry, E. M
(2003). Adipose tissue n-6 fatty acids and acute myocardial infarction in a population consuming a diet high in polyunsaturated fatty acids. Am. J. Clin. Nutr.
77: 796-802
[Abstract][Full Text]
Baylin, A., Kabagambe, E. K., Ascherio, A., Spiegelman, D., Campos, H.
(2003). High 18:2 Trans-Fatty Acids in Adipose Tissue Are Associated with Increased Risk of Nonfatal Acute Myocardial Infarction in Costa Rican Adults. J. Nutr.
133: 1186-1191
[Abstract][Full Text]
Soinio, M., Laakso, M., Lehto, S., Hakala, P., Ronnemaa, T.
(2003). Dietary Fat Predicts Coronary Heart Disease Events in Subjects With Type 2 Diabetes. Diabetes Care
26: 619-624
[Abstract][Full Text]
Lemaitre, R. N, King, I. B, Mozaffarian, D., Kuller, L. H, Tracy, R. P, Siscovick, D. S
(2003). n-3 Polyunsaturated fatty acids, fatal ischemic heart disease, and nonfatal myocardial infarction in older adults: the Cardiovascular Health Study. Am. J. Clin. Nutr.
77: 319-325
[Abstract][Full Text]
Morris, M. C., Evans, D. A., Bienias, J. L., Tangney, C. C., Bennett, D. A., Aggarwal, N., Schneider, J., Wilson, R. S.
(2003). Dietary Fats and the Risk of Incident Alzheimer Disease. Arch Neurol
60: 194-200
[Abstract][Full Text]
Yancy, W. S. Jr, Westman, E. C., French, P. A., Califf, R. M.
(2003). Diets and Clinical Coronary Events: The Truth Is Out There. Circulation
107: 10-16
[Full Text]
Muller, H., Lindman, A. S., Brantsaeter, A. L., Pedersen, J. I.
(2003). The Serum LDL/HDL Cholesterol Ratio Is Influenced More Favorably by Exchanging Saturated with Unsaturated Fat Than by Reducing Saturated Fat in the Diet of Women. J. Nutr.
133: 78-83
[Abstract][Full Text]
Engelhart, M. J., Geerlings, M. I., Ruitenberg, A., van Swieten, J. C., Hofman, A., Witteman, J. C.M., Breteler, M. M.B.
(2002). Diet and risk of dementia: Does fat matter?: The Rotterdam Study. Neurology
59: 1915-1921
[Abstract][Full Text]
McCullough, M. L, Feskanich, D., Stampfer, M. J, Giovannucci, E. L, Rimm, E. B, Hu, F. B, Spiegelman, D., Hunter, D. J, Colditz, G. A, Willett, W. C
(2002). Diet quality and major chronic disease risk in men and women: moving toward improved dietary guidance. Am. J. Clin. Nutr.
76: 1261-1271
[Abstract][Full Text]
Jiang, R., Manson, J. E., Stampfer, M. J., Liu, S., Willett, W. C., Hu, F. B.
(2002). Nut and Peanut Butter Consumption and Risk of Type 2 Diabetes in Women. JAMA
288: 2554-2560
[Abstract][Full Text]
Hu, F. B., Willett, W. C.
(2002). Optimal Diets for Prevention of Coronary Heart Disease. JAMA
288: 2569-2578
[Abstract][Full Text]
Renaud, S. C, Lanzmann-Petithory, D.
(2002). The beneficial effect of {alpha}-linolenic acid in coronary artery disease is not questionable. Am. J. Clin. Nutr.
76: 903-904
[Full Text]
Dashti, N., Feng, Q., Freeman, M. R., Gandhi, M., Franklin, F. A.
(2002). Trans Polyunsaturated Fatty Acids Have More Adverse Effects than Saturated Fatty Acids on the Concentration and Composition of Lipoproteins Secreted by Human Hepatoma HepG2 Cells. J. Nutr.
132: 2651-2659
[Abstract][Full Text]
A correction has been published: N Engl J Med 1998;338(13):917.
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