Cohort Studies of Fat Intake and the Risk of Breast Cancer — A Pooled Analysis
David J. Hunter, M.B., B.S., Donna Spiegelman, Sc.D., Hans-Olov Adami, M.D., Lawrence Beeson, M.S.P.H., Piet A. van den Brandt, Ph.D., Aaron R. Folsom, M.D., Gary E. Fraser, M.D., R. Alexandra Goldbohm, Ph.D., Saxon Graham, Ph.D., Geoffrey R. Howe, Ph.D., Lawrence H. Kushi, Sc.D., James R. Marshall, Ph.D., Aidan McDermott, M.A., Anthony B. Miller, M.B., B.Ch., Frank E. Speizer, M.D., Alicja Wolk, Dr.Med.Sci., Shiaw-Shyuan Yaun, M.P.H., and Walter Willett, M.D.
Background Experiments in animals, international correlationcomparisons, and case–control studies support an associationbetween dietary fat intake and the incidence of breast cancer.Most cohort studies do not corroborate the association, butthey have been criticized for involving small numbers of cases,homogeneous fat intake, and measurement errors in estimatesof fat intake.
Methods We identified seven prospective studies in four countriesthat met specific criteria and analyzed the primary data ina standardized manner. Pooled estimates of the relation of fatintake to the risk of breast cancer were calculated, and datafrom study-specific validation studies were used to adjust theresults for measurement error.
Results Information about 4980 cases from studies including337,819 women was available. When women in the highest quintileof energy-adjusted total fat intake were compared with womenin the lowest quintile, the multivariate pooled relative riskof breast cancer was 1.05 (95 percent confidence interval, 0.94to 1.16). Relative risks for saturated, monounsaturated, andpolyunsaturated fat and for cholesterol, considered individually,were also close to unity. there was little overall associationbetween the percentage of energy intake from fat and the riskof breast cancer, even among women whose energy intake fromfat was less than 20 percent. correcting for error in the measurementof nutrient intake did not materially alter these findings.
Conclusions We found no evidence of a positive association betweentotal dietary fat intake and the risk of breast cancer. Therewas no reduction in risk even among women whose energy intakefrom fat was less than 20 percent of total energy intake. Inthe context of the Western lifestyle, lowering the total intakeof fat in midlife is unlikely to reduce the risk of breast cancersubstantially.
The age-adjusted incidence of breast cancer varies more thanfivefold internationally,1 and among descendants of migrantsfrom low-incidence to high-incidence countries, the incidencerates of breast cancer are close to those of the new country.2,3These observations indicate that lifestyle, environment, orboth contribute to the development of breast cancer. Diet maybe a major factor in the international variation in the incidenceof breast cancer.4
In experiments in animals conducted more than 50 years ago,diets high in fat increased susceptibility to mammary tumorsin rodents.5 In the 1970s, a strong positive correlation wasreported between estimates of national per capita fat consumptionand national incidence and mortality rates for breast cancer.4However, the quality of the data on national per capita fatconsumption has been questioned,6 and at least part of the apparentcorrelation is due to a higher prevalence of breast cancer riskfactors related to reproductive history in countries with higherlevels of fat consumption.7,8,9
In the largest case–control study of this relation (2024cases), no appreciable difference in fat intake was observedbetween the case and control patients.10 In a combined analysisof the original data from 12 other case–control studieswith a total of 4312 cases, Howe et al.11 observed a significantpositive association between total- and saturated-fat intakeand the risk of breast cancer. However, case–control studiescan be susceptible to recall and selection biases that can leadto spurious associations.12,13 In a prospective (cohort) study,diet is assessed in a clearly defined sample of subjects beforethe onset of disease in those who become case patients.
The results of several large cohort studies of fat intake andbreast cancer have been variable.14 Possible reasons for thisvariation include chance, errors in assessing diet, the useof various ranges of fat intake, and differences in the statisticalanalyses. Some of these factors can be mitigated in a conventionalmeta-analysis of the published data, but overcoming most ofthem requires a standardized analysis of the primary data. Wetherefore pooled the primary data from seven major cohort studiesof dietary fat and breast cancer.
Methods
We searched for prospective studies that met the following criteria:(1) the study initially included at least 200 incident casesof breast cancer, (2) diet was studied at base line with a comprehensivequestionnaire that studied food and energy intake during theprevious year, and (3) data were available from a validationstudy of the diet-assessment instrument. We identified sevenprospective studies that met these criteria (Table 1).14,15,16,17,18,19,20Follow-up was conducted through questionnaires and the inspectionof medical records,21 through tumor-registry linkage,14,18,19,20or both16,22 and was estimated to be more than 90 percent completein all cohorts. Diet was assessed by food-frequency questionnairesin all studies, and the results were validated by comparingthem with multiple 24-hour–recall interviews23,24 or withdiet records25,26,27,28 (and Ljung H, Wolk A: unpublished data).The Nurses' Health Study was the only study to repeat the dietaryassessment after base line; to take advantage of this and tomake its duration of follow-up similar to those of the othercohorts, we divided the follow-up of this study into two periods— 1980 to the month of return of the 1986 questionnaire(Nurses' Health Study (a)) and 1986 to 1991 (Nurses' HealthStudy (b)).
Table 1. Cohort Studies Included in the Pooled Prospective Analysis of Dietary Fat and the Risk of Breast Cancer.
Exclusion Criteria
In addition to the subjects excluded by the criteria originallyapplied to the individual studies, we excluded those for whomthe estimate of total energy intake was more than 3 SD fromthe loge-transformed mean intake of the base-line populationof each study. We also excluded the small percentage of subjectswho had received diagnoses of cancer (other than nonmelanomaskin cancer) at base line, since their recent diets may havebeen influenced by the cancers or their treatment. Because ofthese exclusions, and because of additional follow-up in theIowa Women's Health Study and the Nurses' Health Study (b),for most studies the size of the base-line cohort and the numberof cases are slightly different in our analysis (Table 1) fromthose in the original published analyses.
Selection of Cases and Sampling of Risk Sets
To reduce the computational burden, we analyzed five cohorts(the Adventist Health Study, the Iowa Women's Health Study,the New York State Cohort, the Nurses' Health Study (a), theNurses' Health Study (b), and the Sweden Mammography Cohort)as nested case–control studies (shown to be efficientand unbiased alternatives to full cohort analysis),29 matching10 controls to each case patient. Case patients were assignedto the calendar year of their diagnoses, and their follow-upceased in that year. For each case patient, from the risk setof women with the same year of birth, 10 controls were selectedwho were alive, were not known to have migrated from the studyarea, and had not received diagnoses of breast cancer beforethe year in which the case patient's cancer was diagnosed. Controlswere selected without replacement within each year but wereeligible to be chosen again or to be reclassified as case patientsin subsequent years. A similar design was used for the CanadianBreast Screening Study,16 but the investigators of that studyselected two controls matched to each case patient on the basisof age (±2 months) and then processed previously administereddietary questionnaires for these case patients and controlsto minimize costs. In the Netherlands Cohort Study,19 the case–cohortdesign was used30; case patients were identified within thecohort, and their dietary and other exposures were comparedwith those of a subcohort of 1812 women randomly sampled atbase line.
Models and Analyses
The basic method used for these analyses was the proportional-hazardsmodel.31 For the six studies for which nested case–controlsampling was used, a conditional logistic-regression analysiswas used to fit this model, with the use of SAS PROC PHREG.32For the Netherlands Cohort Study, the variance was modifiedas required for the case–cohort design with the use ofEpicure software.33 To estimate the rate ratio, or relativerisk, we exponentiated the appropriate conditional logistic-regressioncoefficient multiplied by a nutritionally meaningful incrementfor continuous variables, or we used indicator variables forcategorical analyses. Two-sided 95 percent confidence intervalsare given throughout.
Adjustment for Energy Intake
To provide information on the effect of dietary composition,such as would be obtained in an "isocaloric" metabolic study,we adjusted nutrient intakes for total energy intake in severalways, including the residuals approach34 (in which the loge-transformednutrient is regressed against the loge-transformed energy intake;the residual represents the nutrient intake independent of theenergy intake), the standard multivariate method,14 and theenergy-partition method.35 Since each of these methods of energyadjustment can be transformed to yield an identical relativerisk for the nutrient of interest,36 we present the resultsobtained by the residuals method (standardized to a median energyintake of 1600 kcal) in units chosen to represent an achievablechange in intake. We also modeled the effect of total fat asits "nutrient density" — that is, the ratio of energyfrom total fat intake to total energy intake — since thisis the formulation often used to make dietary recommendations.
Study-Specific and Pooled Results
We analyzed the relation between the intake of each nutrientand the risk of breast cancer by treating the energy-adjustednutrient intake (according to the residuals method) as a continuousvariable and categorizing the energy-adjusted nutrient intakein quintiles (Table 2, *). Since the nutrient intakes used inthe Adventist Health Study represent a ranking index ratherthan an estimate of absolute intake, data from that study wereincluded in the categorical analyses only. We used the "randomeffects" method developed by DerSimonian and Laird to combineloge relative risks from multiple studies.37
Table 2. Pooled Relative Risks of Breast Cancer and 95 Percent Confidence Intervals for Quintiles of Energy-Adjusted Nutrient Intake in the Pooled Analysis of Cohort Studies.
Correction of Measurement Error
Error in the measurement of dietary variables can distort relativerisks and confidence intervals; error in prospective studiesis usually nondifferential and attenuates estimates of effecttoward the null. The studies included here had validation studiesavailable from which the measurement error associated with themain cohort questionnaire could be estimated; this informationwas used to estimate the true relative risk and confidence intervalsafter the effect of measurement error was accounted for.38,39Although the measurements regarded as the gold standard or "truth"in these analyses were themselves measured with error, the proceduresused to correct measurement error are valid, provided the errorin the gold standard was unbiased and uncorrelated with theerror in the data from the main cohort questionnaire.40 To theextent that the gold standards used in each study-specific validationstudy are comparable, measurement-error correction will calibratethe studies.41 We adjusted simultaneously for error in the measurementof each nutrient and that of the total intake of energy.
Results
Within-study differences in mean and median nutrient intakebetween case patients and controls were very small.* In no studywas the difference in median intake between case patients andcontrols more than 1 g per day for energy-adjusted total, saturated,monounsaturated, or polyunsaturated fat. The median cholesterolintake was slightly higher among case patients in the AdventistHealth Study, the Iowa Women's Health Study, the Nurses' HealthStudy (b), and the Sweden Mammography Cohort but lower amongthose in the Canadian Breast Screening Study and the New YorkState Cohort; again, these differences were small.
Overall Relative Risks
In Table 2 we show the pooled quintile-specific relative risksof breast cancer as compared with the lowest quintile. Noneof the results of the tests for trend among quintiles approachedstatistical significance, and proportional-hazards assumptionswere satisfied. For comparisons of values in the highest andthe lowest quintiles, the results of the test for heterogeneityamong studies did not indicate a significant difference forany nutrient, suggesting that the pooled relative risks arean appropriate summary of the data. For energy intake, the onlystudy with a significant positive association was the SwedenMammography Cohort; however, the pooled relative risk was notstatistically significant (relative risk, 1.11; 95 percent confidenceinterval, 0.99 to 1.25). For energy-adjusted total fat, womenin the highest quintile in the Iowa Women's Health Study wereat significantly higher risk than those in the lowest quintile(relative risk, 1.34; 95 percent confidence interval, 1.02 to1.76). Similar significant positive associations for saturatedand monounsaturated fat in the Iowa Women's Health Study werenot reflected in the other studies or in the pooled relativerisks. The quintile-specific pooled estimates for other nutrientsdid not suggest departures from linearity in the overall absenceof association (Table 2).
In Table 3, we present relative risks derived by treating eachnutrient as a continuous variable (the Adventist Health Studyis excluded from these analyses, as previously stated). Noneof the tests for heterogeneity indicated statistical significance.Significant positive associations were observed for energy-adjustedtotal and saturated fat in the Iowa Women's Health Study, whereasthe pooled relative risks were close to unity. The only pooledrelative risk that was marginally significant was for cholesterol(relative risk for each 100-mg increase in cholesterol intake,1.04; 95 percent confidence interval, 1.00 to 1.07).
Table 3. Relative Risks and 95 Percent Confidence Intervals for Continuous estimates of Energy-Adjusted Nutrient Intake in the Pooled Analysis of Cohort Studies.
Comparisons of the extreme deciles of the energy-adjusted estimatesof intake of each nutrient yielded similar results. The multivariate-adjustedpooled relative risks comparing the top with the bottom decilewere the following: for energy, 0.96 (95 percent confidenceinterval, 0.79 to 1.16); for total fat, 1.01 (0.82 to 1.25);for saturated fat, 1.11 (0.95 to 1.29); for monounsaturatedfat, 0.96 (0.79 to 1.17); for polyunsaturated fat, 1.06 (0.92to 1.21); for animal fat, 1.06 (0.90 to 1.25); for vegetablefat, 1.14 (0.93 to 1.38); and for cholesterol, 1.15 (1.00 to1.32).
To examine further the risk of breast cancer at the lowest fatintakes, we calculated the percentage of energy from fat andcompared 5 percent increments of this scale, using the levelrepresenting 30 to less than 35 percent of energy from fat asthe reference category (Figure 1). Above the reference categorywe saw little evidence of an increase in risk, and below itlittle evidence of a decrease in risk. In the lowest category(<20 percent of calories from fat), the pooled relative riskwas 1.06 (95 percent confidence interval, 0.83 to 1.37). Forwomen reporting less than 15 percent energy from fat, relativerisks were above 1.5 in all four of the studies that contributeddata (the New York State Cohort, the Nurses' Health Study (a),the Nurses' Health Study (b), and the Sweden Mammography Cohort);the pooled relative risk was 2.12 (95 percent confidence interval,1.34 to 3.36), on the basis of 26 case patients and 134 controlswith levels of energy from fat below 15 percent.
Figure 1. Pooled Relative Risks and 95 Percent Confidence Intervals for Various Levels of Energy from Fat.
Relative risks are adjusted for the variables listed in the first footnote to Table 2. A level of 30 to less than 35 percent of total energy from fat was designated as the reference category. N denotes the number of cases in each category.
Separate results for postmenopausal women (3465 case patients),in whom an association between breast cancer and dietary fatintake has been hypothesized to be strongest, were similar tothose for the entire population; the pooled estimate of theenergy-adjusted relative risk for a change of 25 g in totalfat intake was 1.01 (95 percent confidence interval, 0.91 to1.12). The results for premenopausal women were similar, aswere the results when case patients receiving diagnoses in thefirst year of follow-up were excluded. Excluding 480 case patientswith carcinoma in situ or an unknown degree of invasion hadlittle influence on the results.
Influence of Measurement Error
Correlation coefficients between total fat intake estimatedon the basis of the food-frequency questionnaires and that estimatedby the reference methods (diet records or multiple 24-hour–recallinterviews) were 0.34 in the Adventist Health Study, 0.45 inthe Canadian Breast Screening Study, 0.54 in the Iowa Women'sHealth Study, 0.48 in the Netherlands Cohort Study, 0.40 inthe New York State Cohort, 0.52 in the Nurses' Health Study(a), 0.51 in the Nurses' Health Study (b), and 0.49 in the SwedenMammography Cohort.
Pooled relative risks corrected for measurement error were 1.07for total fat (per 25 g; 95 percent confidence interval, 0.86to 1.34), 1.08 for saturated fat (per 10 g; 0.93 to 1.26), 1.01for monounsaturated fat (per 10 g; 0.80 to 1.28), 1.05 for polyunsaturatedfat (per 10 g; 0.83 to 1.34), and 1.07 for cholesterol (per100 mg; 1.01 to 1.14).
Discussion
Epidemiologic evidence of an association between dietary fatand breast cancer has been contradictory. Ecologic studies,4,42,43a pooled analysis of some case–control studies,11 anda meta-analysis of case–control studies44 have suggesteda positive association, whereas the results of cohort studieshave tended to be null or only weakly positive. The deficienciesof dietary analyses in ecologic and case–control studieshave been reviewed,8 and the prospective data have been criticizedas misleading because of the lack of statistical power of individualstudies, the limited range of fat intake in the populationsstudied, and the misclassification of fat intake, which tendsto attenuate associations.45,46 To address these problems, wepooled the available prospective data to increase the statisticalpower, examined effects between the extremes of intake in thevarious studies, and incorporated information on the validityof each diet-assessment method to account for measurement error.These prospective data are not susceptible to the recall andselection biases that may arise in conventional case–controlstudies.29
We observed no positive association between total dietary fatintake and the incidence of breast cancer among seven independentpopulations from four countries. These seven studies involvedalmost 5000 incident cases among more than 335,000 women withprospectively collected dietary information and follow-up periodsof up to seven years. Before and after adjustment for knownrisk factors for breast cancer, these data suggested that therisk among women with high fat intake is the same as the riskamong those with low fat intake. This conclusion holds whetherwe consider total, saturated, monounsaturated, or polyunsaturatedfat or animal or vegetable fat. The method of adjustment forenergy intake had relatively little effect on these results.Analyses that were limited to postmenopausal women and thatexcluded women whose disease was diagnosed in the first yearof follow-up yielded equivalent results. we included cases ofcarcinoma in situ, since there is little evidence that nutritionalrisk factors for these early lesions are different from thosefor invasive disease; excluding the 9 percent of case patientswho had carcinoma in situ did not materially alter the results.The results of other prospective studies with too few casesto meet the criteria for this pooled analysis47,48,49,50 arecompatible with these results.
To assess the risk of breast cancer associated with fat intakesthat are very low by Western standards, we used the large samplemade available by pooling multiple studies and saw no evidenceof lower risk with a fat intake of less than 20 percent of caloriesfrom fat. In most individual studies, even the lowest decilesof fat intake correspond to about 25 to 30 percent of caloriesfrom fat, a level still above the targeted group average of20 percent of energy from fat for the intervention group inthe Women's Health Initiative clinical trial,51 and substantiallyabove the 15 percent of energy from fat consumed by some womenin Asian countries with low breast cancer rates. A recent case–controlstudy conducted in two populations in China, with 834 case patientsand controls whose diets supplied an interquartile range of15 to 35 percent of energy from fat, did not show a significantrelation between dietary-fat intake and the risk of breast cancer.52These data provide no support for the hypothesis that a verylow fat intake protects against breast cancer.
Nondifferential error in measuring fat intake in epidemiologicstudies could obscure an association with breast cancer risk.42,46However, we corrected relative-risk estimates for measurementerror using data from study-specific validation studies; theuncorrected relative risks were still close to unity for totalfat and subtypes of fat. More important, even when the 95 percentconfidence intervals were expanded to account for measurementerror, they remained narrow and excluded substantial positiveassociations.
It has been suggested that it is the type of fat, rather thanthe total amount of fat, that is relevant; specifically, monounsaturatedfats may be inversely associated with the risk of breast cancerafter other types of fat are accounted for.53 Distinguishingthe associations of various types of fat with the risk of breastcancer is difficult because of multicollinearity among the typesof fat; we are currently investigating this issue and otheraspects of diet that may influence the risk of breast cancer.
In the analyses treating nutrients as continuous variables,we did observe a small increase in the pooled estimate amongwomen consuming more dietary cholesterol; the only study inwhich this was independently significant was the Nurses' HealthStudy (b). Several large prospective studies54,55 have observedno relation between serum cholesterol and the incidence of breastcancer, suggesting that the weak positive association that weobserved may be due to chance.
The possibility that aspects of diet during childhood or adolescence,including energy intake and total fat intake, may be associatedwith the risk of breast cancer decades later cannot be ruledout on the basis of the results of prospective studies of adultwomen. Nonetheless, it appears unlikely that a reduction intotal fat consumption by middle-aged and older women will substantiallyreduce their risk of breast cancer.
Supported by grants from the National Institutes of Health (CA55075and CA50597) and by a Faculty Research Award (FRA-455) fromthe American Cancer Society (to Dr. Hunter).
We are indebted to Tracey Corrigan for preparation of the manuscript,to Diane Feskanich for assisting with data analysis, and toLaura Newcomer and Walkyria Pas de Almeida for computer programming.
* See NAPS document no. 05272 for 5 pages of supplementary material.To order, contact NAPS c/o Microfiche Publications, 248 HempsteadTpk., West Hempstead, NY 11552.
Source Information
From the Departments of Epidemiology (D.J.H., D.S., W.W.), Nutrition (W.W.), and Biostatistics (D.S.), and the Center for Cancer Prevention (D.J.H.), Harvard School of Public Health, Boston; the Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston (D.J.H., A.M., F.E.S., S.-S.Y., W.W.); the Center for Health Research, Loma Linda University School of Medicine, Loma Linda, Calif. (L.B., G.E.F.); the National Cancer Institute of Canada Epidemiology Unit, Department of Preventive Medicine and Biostatistics, Faculty of Medicine, University of Toronto, Toronto (G.R.H., A.B.M.); the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis (A.R.F., L.H.K.); the Department of Epidemiology, University of Limburg, Maastricht, the Netherlands (P.A.B.); the Department of Nutrition, TNO Nutrition and Food Research Institute, Zeist, the Netherlands (R.A.G.); the Department of Social and Preventive Medicine, State University of New York, Buffalo (S.G., J.R.M.); and the Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden (H.-O.A., A.W.).
Address reprint requests to Dr. Hunter at the Channing Laboratory, 180 Longwood Ave., Boston, MA 02115.
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Dietary Fat and the Risk of Breast Cancer
Blackburn G. L., Ishikawa M., Smith J. A., Flynn M., Walker A. R.P., Walker B. F., Hunter D. J., Spiegelman D., Willett W.
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N Engl J Med 1996;
334:1606-1607, Jun 13, 1996.
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