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Figure 1. Dose-response relationship between red meat intake and risk of all-cause mortality in the Health Professionals Follow-up Study (A) and the Nurses' Health Study (B). The results were adjusted for age (continuous); body mass index (calculated as weight in kilograms divided by height in meters squared) category (<23.0, 23.0-24.9, 25.0-29.9, 30.0-34.9, or ≥35); alcohol consumption (0, 0.1-4.9, 5.0-29.9, ≥30.0 g/d in men; 0, 0.1-4.9, 5.0-14.9, or ≥15.0 g/d in women); physical activity level (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, or ≥27.0 hours of metabolic equivalent tasks per week); smoking status (never, past, or current [1-14, 15-24, or ≥25 cigarettes per day]); race (white or nonwhite); menopausal status and hormone use in women (premenopausal, postmenopausal never users, postmenopausal past users, or postmenopausal current users); family history of diabetes mellitus, myocardial infarction, or cancer; history of diabetes mellitus, hypertension, or hypercholesterolemia; and intakes of total energy, whole grains, fruits, and vegetables, all in quintiles. Broken lines represent 95% CI.

Figure 1. Dose-response relationship between red meat intake and risk of all-cause mortality in the Health Professionals Follow-up Study (A) and the Nurses' Health Study (B). The results were adjusted for age (continuous); body mass index (calculated as weight in kilograms divided by height in meters squared) category (<23.0, 23.0-24.9, 25.0-29.9, 30.0-34.9, or ≥35); alcohol consumption (0, 0.1-4.9, 5.0-29.9, ≥30.0 g/d in men; 0, 0.1-4.9, 5.0-14.9, or ≥15.0 g/d in women); physical activity level (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, or ≥27.0 hours of metabolic equivalent tasks per week); smoking status (never, past, or current [1-14, 15-24, or ≥25 cigarettes per day]); race (white or nonwhite); menopausal status and hormone use in women (premenopausal, postmenopausal never users, postmenopausal past users, or postmenopausal current users); family history of diabetes mellitus, myocardial infarction, or cancer; history of diabetes mellitus, hypertension, or hypercholesterolemia; and intakes of total energy, whole grains, fruits, and vegetables, all in quintiles. Broken lines represent 95% CI.

Figure 2. Hazard ratios and 95% CIs (error bars) for total mortality associated with replacement of other food groups for red meat intake. Adjusted for age (continuous); body mass index (calculated as weight in kilograms divided by height in meters squared) category (<23.0, 23.0-24.9, 25.0-29.9, 30.0-34.9, or ≥35.0); alcohol consumption (0, 0.1-4.9, 5.0-29.9, ≥30.0 g/d in men; 0, 0.1-4.9, 5.0-14.9, or ≥15.0 g/d in women); physical activity level (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, or ≥27.0 hours of metabolic equivalent tasks per week); smoking status (never, past, or current [1-14, 15-24, or ≥25 cigarettes per day]); race (white or nonwhite); menopausal status and hormone use in women (premenopausal, postmenopausal never users, postmenopausal past users, or postmenopausal current users); family history of diabetes mellitus, myocardial infarction, or cancer; history of diabetes mellitus, hypertension, or hypercholesterolemia; total energy intake; and the corresponding 2 dietary variables in the models.

Figure 2. Hazard ratios and 95% CIs (error bars) for total mortality associated with replacement of other food groups for red meat intake. Adjusted for age (continuous); body mass index (calculated as weight in kilograms divided by height in meters squared) category (<23.0, 23.0-24.9, 25.0-29.9, 30.0-34.9, or ≥35.0); alcohol consumption (0, 0.1-4.9, 5.0-29.9, ≥30.0 g/d in men; 0, 0.1-4.9, 5.0-14.9, or ≥15.0 g/d in women); physical activity level (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, or ≥27.0 hours of metabolic equivalent tasks per week); smoking status (never, past, or current [1-14, 15-24, or ≥25 cigarettes per day]); race (white or nonwhite); menopausal status and hormone use in women (premenopausal, postmenopausal never users, postmenopausal past users, or postmenopausal current users); family history of diabetes mellitus, myocardial infarction, or cancer; history of diabetes mellitus, hypertension, or hypercholesterolemia; total energy intake; and the corresponding 2 dietary variables in the models.

Table 1. Baseline Age-Standardized Characteristics of Participants in the 2 Cohorts According to Quintiles of Total Red Meat Consumption
Table 1. Baseline Age-Standardized Characteristics of Participants in the 2 Cohorts According to Quintiles of Total Red Meat Consumption
Table 2. All-Cause Mortality According to Red Meat Intake in the Health Professionals Follow-up Study and the Nurses’ Health Study
Table 2. All-Cause Mortality According to Red Meat Intake in the Health Professionals Follow-up Study and the Nurses’ Health Study
Table 3. Cardiovascular Mortality According to Red Meat Intake in the Health Professionals Follow-up Study and the Nurses’ Health Study
Table 3. Cardiovascular Mortality According to Red Meat Intake in the Health Professionals Follow-up Study and the Nurses’ Health Study
Table 4. Cancer Mortality According to Red Meat Intake in the Health Professionals Follow-up Study and the Nurses’ Health Study
Table 4. Cancer Mortality According to Red Meat Intake in the Health Professionals Follow-up Study and the Nurses’ Health Study
1.
Pan A, Sun Q, Bernstein AM,  et al.  Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis.  Am J Clin Nutr. 2011;94(4):1088-1096PubMedArticle
2.
Micha R, Wallace SK, Mozaffarian D. Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis.  Circulation. 2010;121(21):2271-2283PubMedArticle
3.
Zheng W, Lee SA. Well-done meat intake, heterocyclic amine exposure, and cancer risk.  Nutr Cancer. 2009;61(4):437-446PubMedArticle
4.
Fraser GE. Associations between diet and cancer, ischemic heart disease, and all-cause mortality in non-Hispanic white California Seventh-day Adventists.  Am J Clin Nutr. 1999;70(3):(suppl)  532S-538SPubMed
5.
Key TJ, Fraser GE, Thorogood M,  et al.  Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies.  Am J Clin Nutr. 1999;70(3):(suppl)  516S-524SPubMed
6.
Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. Meat intake and mortality: a prospective study of over half a million people.  Arch Intern Med. 2009;169(6):562-571PubMedArticle
7.
van Dam RM, Willett WC, Rimm EB, Stampfer MJ, Hu FB. Dietary fat and meat intake in relation to risk of type 2 diabetes in men.  Diabetes Care. 2002;25(3):417-424PubMedArticle
8.
Fung TT, Schulze M, Manson JE, Willett WC, Hu FB. Dietary patterns, meat intake, and the risk of type 2 diabetes in women.  Arch Intern Med. 2004;164(20):2235-2240PubMedArticle
9.
Hu FB, Rimm E, Smith-Warner SA,  et al.  Reproducibility and validity of dietary patterns assessed with a food-frequency questionnaire.  Am J Clin Nutr. 1999;69(2):243-249PubMed
10.
Salvini S, Hunter DJ, Sampson L,  et al.  Food-based validation of a dietary questionnaire: the effects of week-to-week variation in food consumption.  Int J Epidemiol. 1989;18(4):858-867PubMedArticle
11.
Rich-Edwards JW, Corsano KA, Stampfer MJ. Test of the National Death Index and Equifax Nationwide Death Search.  Am J Epidemiol. 1994;140(11):1016-1019PubMed
12.
Hu FB, Stampfer MJ, Rimm E,  et al.  Dietary fat and coronary heart disease: a comparison of approaches for adjusting for total energy intake and modeling repeated dietary measurements.  Am J Epidemiol. 1999;149(6):531-540PubMedArticle
13.
Qiu W, Rosner B. Measurement error correction for the cumulative average model in the survival analysis of nutritional data: application to Nurses' Health Study.  Lifetime Data Anal. 2010;16(1):136-153PubMedArticle
14.
Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC. Major dietary protein sources and risk of coronary heart disease in women.  Circulation. 2010;122(9):876-883PubMedArticle
15.
Spiegelman D, Hertzmark E, Wand HC. Point and interval estimates of partial population attributable risks in cohort studies: examples and software.  Cancer Causes Control. 2007;18(5):571-579PubMedArticle
16.
Willett WC. Nutritional Epidemiology. 2nd ed. New York, NY: Oxford University Press; 1998
17.
Ascherio A, Willett WC, Rimm EB, Giovannucci EL, Stampfer MJ. Dietary iron intake and risk of coronary disease among men.  Circulation. 1994;89(3):969-974PubMed
18.
Klipstein-Grobusch K, Grobbee DE, den Breeijen JH, Boeing H, Hofman A, Witteman JC. Dietary iron and risk of myocardial infarction in the Rotterdam Study.  Am J Epidemiol. 1999;149(5):421-428PubMedArticle
19.
van der A DL, Peeters PH, Grobbee DE, Marx JJ, van der Schouw YT. Dietary haem iron and coronary heart disease in women.  Eur Heart J. 2005;26(3):257-262PubMedArticle
20.
Qi L, van Dam RM, Rexrode K, Hu FB. Heme iron from diet as a risk factor for coronary heart disease in women with type 2 diabetes.  Diabetes Care. 2007;30(1):101-106PubMedArticle
21.
Menke A, Muntner P, Fernández-Real JM, Guallar E. The association of biomarkers of iron status with mortality in US adults [published online ahead of print February 15, 2011].  Nutr Metab Cardiovasc DisArticle
22.
Bibbins-Domingo K, Chertow GM, Coxson PG,  et al.  Projected effect of dietary salt reductions on future cardiovascular disease.  N Engl J Med. 2010;362(7):590-599PubMedArticle
23.
Smith-Spangler CM, Juusola JL, Enns EA, Owens DK, Garber AM. Population strategies to decrease sodium intake and the burden of cardiovascular disease: a cost-effectiveness analysis.  Ann Intern Med. 2010;152(8):481-487, W170-W173PubMed
24.
Kleinbongard P, Dejam A, Lauer T,  et al.  Plasma nitrite concentrations reflect the degree of endothelial dysfunction in humans.  Free Radic Biol Med. 2006;40(2):295-302PubMedArticle
25.
Pereira EC, Ferderbar S, Bertolami MC,  et al.  Biomarkers of oxidative stress and endothelial dysfunction in glucose intolerance and diabetes mellitus.  Clin Biochem. 2008;41(18):1454-1460PubMedArticle
26.
World Cancer Research Fund/American Institute for Cancer Research.  Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global Perspective. Washington, DC: American Institute for Cancer Research; 2007
27.
Hughes R, Cross AJ, Pollock JRA, Bingham S. Dose-dependent effect of dietary meat on endogenous colonic N-nitrosation.  Carcinogenesis. 2001;22(1):199-202PubMedArticle
28.
Skog K, Steineck G, Augustsson K, Jägerstad M. Effect of cooking temperature on the formation of heterocyclic amines in fried meat products and pan residues.  Carcinogenesis. 1995;16(4):861-867PubMedArticle
29.
Sinha R, Rothman N, Salmon CP,  et al.  Heterocyclic amine content in beef cooked by different methods to varying degrees of doneness and gravy made from meat drippings.  Food Chem Toxicol. 1998;36(4):279-287PubMedArticle
30.
Cross AJ, Sinha R. Meat-related mutagens/carcinogens in the etiology of colorectal cancer.  Environ Mol Mutagen. 2004;44(1):44-55PubMedArticle
31.
Cross AJ, Pollock JR, Bingham SA. Haem, not protein or inorganic iron, is responsible for endogenous intestinal N-nitrosation arising from red meat.  Cancer Res. 2003;63(10):2358-2360PubMed
32.
Sesink AL, Termont DS, Kleibeuker JH, Van der Meer R. Red meat and colon cancer: the cytotoxic and hyperproliferative effects of dietary heme.  Cancer Res. 1999;59(22):5704-5709PubMed
33.
Huang X. Iron overload and its association with cancer risk in humans: evidence for iron as a carcinogenic metal.  Mutat Res. 2003;533(1-2):153-171PubMedArticle
Original Investigation
Apr 9, 2012

Red Meat Consumption and MortalityResults From 2 Prospective Cohort Studies

Author Affiliations

Author Affiliations: Departments of Nutrition (Drs Pan, Sun, Bernstein, Stampfer, Willett, and Hu) and Epidemiology (Drs Manson, Stampfer, Willett, and Hu), Harvard School of Public Health, and Channing Laboratory (Drs Sun, Stampfer, Willett, and Hu) and Division of Preventive Medicine (Dr Manson), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; Wellness Institute of the Cleveland Clinic, Lyndhurst, Ohio (Dr Bernstein); and Department of Molecular Epidemiology, German Institute of Human Nutrition, Nuthetal, Germany (Dr Schulze).

Arch Intern Med. 2012;172(7):555-563. doi:10.1001/archinternmed.2011.2287
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