Background Many lifestyle-related risk factors for coronaryheart disease have been identified, but little is known abouttheir effect on the risk of disease when they are consideredtogether.
Methods We followed 84,129 women participating in the Nurses'Health Study who were free of diagnosed cardiovascular disease,cancer, and diabetes at base line in 1980. Information on dietand lifestyle was updated periodically. During 14 years of follow-up,we documented 1128 major coronary events (296 deaths from coronaryheart disease and 832 nonfatal infarctions). We defined subjectsat low risk as those who were not currently smoking, had a body-massindex (the weight in kilograms divided by the square of theheight in meters) under 25, consumed an average of at leasthalf a drink of an alcoholic beverage per day, engaged in moderate-to-vigorousphysical activity (which could include brisk walking) for atleast half an hour per day, on average, and scored in the highest40 percent of the cohort for consumption of a diet high in cerealfiber, marine n–3 fatty acids, and folate, with a highratio of polyunsaturated to saturated fat, and low in transfat and glycemic load, which reflects the extent to which dietraises blood glucose levels.
Results Many of the factors were correlated, but each independentlyand significantly predicted risk, even after further adjustmentfor age, family history, presence or absence of diagnosed hypertensionor diagnosed high cholesterol level, and menopausal status.Women in the low-risk category (who made up 3 percent of thepopulation) had a relative risk of coronary events of 0.17 (95percent confidence interval, 0.07 to 0.41) as compared withall the other women. Eighty-two percent of coronary events inthe study cohort (95 percent confidence interval, 58 to 93 percent)could be attributed to lack of adherence to this low-risk pattern.
Conclusions Among women, adherence to lifestyle guidelines involvingdiet, exercise, and abstinence from smoking is associated witha very low risk of coronary heart disease.
Despite dramatic declines, coronary heart disease remains theleading cause of death among men and women in the United States.Much effort has focused on the pharmacologic management of hypertensionand blood lipid levels and on improved therapy for acute myocardialinfarction and congestive heart failure. These treatments haveproven benefit but are costly, may have side effects, and requiremedical intervention. Diet and lifestyle can also affect theincidence of coronary heart disease. Typically, behavioral riskfactors are studied individually, but these types of behaviorare often correlated, because people follow common lifestylepatterns.
In the present study, we assessed the effect of a combinationof lifestyle practices on the risk of coronary heart disease.Specifically, we estimated the proportion of coronary eventsthat could potentially be prevented by adherence to a set ofdietary and behavioral guidelines. In secondary analyses, wealso evaluated the effect of the practices on the risk of stroke.
Methods
Population
The Nurses' Health Study cohort was established in 1976, when121,700 U.S. female registered nurses 30 to 55 years of ageprovided detailed information by questionnaire. Every two years,we send follow-up questionnaires to update our information onpotential risk factors and to identify newly diagnosed casesof various diseases.
Ascertainment of Risk and Preventive Factors
The 1976 questionnaire inquired about the nurses' height andweight and about myocardial infarction in a parent before theage of 60 years. Each follow-up questionnaire asked for updatedinformation on weight for calculation of the body-mass index(the weight in kilograms divided by the square of the heightin meters) as a measure of obesity.1 Each questionnaire alsoinquired about cigarette smoking (including past smoking andthe number of cigarettes smoked per day for current smokers),menopausal status (including the use of postmenopausal hormones),and physician-diagnosed hypertension and high cholesterol levels;self-reports of these diagnoses were quite accurate as comparedwith medical records.2
Information on physical activity was first obtained in 1980and was updated in 1982, 1986, 1988, and 1992 with a previouslyvalidated questionnaire on the frequency of activity.3,4,5 Weestimated the amount of time per week spent in moderate-to-vigorousactivities requiring 3 or more MET per hour; this excluded walkingat an easy or normal pace but included brisk walking at 5 km(3 mi) or more per hour.
In 1980 we assessed diet with a 61-item food-frequency questionnaire.In 1984 the questionnaire was expanded to 116 food items, andsimilar questionnaires were used to update information on dietin 1986 and 1990. The questionnaires also assessed the intakeof multivitamin and single-vitamin supplements. The reproducibilityand validity of the food-frequency questionnaires are high whencompared with multiple one-week diet records and a variety ofbiochemical markers, as described in detail elsewhere.6
To calculate the intake of specific nutrients, we specifieda common unit or portion size for each food on the questionnaireand asked the participant how often, on average, she had consumedthat amount during the previous year. The nine response categoriesranged from "never" to "six or more times per day." The intakeof nutrients was computed by multiplying the frequency of consumptionof each unit of food by its nutrient content. Beer, wine, andliquor were included in each of the food-frequency questionnairesto permit calculation of alcohol intake.
Definition of Low-Risk Groups
Our aim in this analysis was to estimate the effect of dietand lifestyle on the risk of coronary heart disease. Therefore,we did not consider the additional effect of pharmacologic agents,including aspirin or postmenopausal hormones, or medical conditions,such as hypertension and high cholesterol levels. However, allanalyses were adjusted for those factors. We sought to limitthe number of lifestyle and dietary variables, and we includedonly those with reasonable evidence supporting their effecton coronary heart disease, while recognizing that most suchvariables have never been tested in randomized trials.
For smoking, the low-risk group was defined as those who hadstopped smoking or had never smoked. Cigarette smoking is amajor risk factor for coronary heart disease7 and stroke.8 Therisk declines after the cessation of smoking and approximatesthe level of those who have never smoked after 10 to 14 years.9,10,11
Moderate alcohol consumption is associated with a lower riskof coronary heart disease12,13,14 and ischemic stroke15 butcan raise the risk of hemorrhagic stroke.16 We considered womenas being at low risk if they consumed an average of 5 g or moreper day (a typical glass of wine has 11 g of alcohol). For simplicity,and because so few women in this cohort drank heavily (1.2 percentreported drinking more than 45 g of alcohol per day), we didnot define an upper limit for alcohol consumption, althoughclearly this would be necessary in establishing public healthguidelines.
For physical activity, we considered subjects to be at low riskif they engaged in an average of at least one half-hour perday of vigorous or moderate activity, including brisk walking.This cutoff point is consistent with various guidelines.17,18We have found that this level of activity is associated witha substantial reduction in the risk of coronary heart disease5and stroke (unpublished data).
Women with a body-mass index of less than 25, the standard cutoffpoint for overweight, were considered to be at low risk. Wehave previously found a significantly higher risk of coronaryheart disease among women with a body-mass index of 23 to 24.9,as compared with women with a body-mass index of less than 21.19The cutoff point of 25 represents a higher-than-optimal level.
We considered subjects to be at low risk if they scored in thehighest 40 percent of the cohort on a composite measure basedon a diet low in trans fat and glycemic load (which reflectsthe extent to which diet raises blood glucose levels), highin cereal fiber, marine n–3 fatty acids, and folate, andwith a high ratio of polyunsaturated to saturated fat. For eachof these six dietary factors, we calculated the distributionaccording to quintiles within the cohort and assigned each womana score of 1 to 5 corresponding to the quintile of intake, with5 representing the most favorable quintile. The cutoff pointsfor the most favorable quintile for each dietary factor wereas follows: less than 1.56 percent of energy supplied by transfat, a ratio of polyunsaturated to saturated fat of more than0.43, consumption of more than 4.2 g of cereal fiber per day,a glycemic load of less than 723 units per day, more than 0.1percent of energy from marine n–3 fatty acids, and consumptionof more than 525 µg of folate per day. For each participant,the quintile value for each nutrient was summed (with a higherscore representing a lower risk), and the participants withdietary scores in the highest 40 percent were defined as thelow-risk group with respect to diet. We and others have previouslydemonstrated the importance of each of these factors for therisk of coronary disease.20,21,22,23,24,25,26
Population for Analysis
We excluded women who left 10 or more items blank on the 1980diet questionnaire, those with implausibly low or high scoresfor total food or energy intake (below 500 or above 3500 kcalper day), and those with previously diagnosed cancer, angina,myocardial infarction, stroke, or other cardiovascular diseases.We did not exclude women who reported high cholesterol levelsor hypertension. Because diabetes increases the risk of coronaryheart disease and can induce changes in diet and lifestyle,we excluded women who had diabetes at base line. Women givena diagnosis of diabetes during follow-up were included, butwe used only the dietary information collected before the diagnosis.The final 1980 base-line population consisted of 84,129 women.
Ascertainment of End Points
We tried to review medical records for all reports of majorcoronary events (nonfatal myocardial infarction or death dueto coronary heart disease) that occurred between the returnof the 1980 questionnaire and June 1, 1994. The records werereviewed by study physicians who had no knowledge of the subjects'self-reported risk factors. Myocardial infarction was confirmedaccording to World Health Organization criteria, as follows:symptoms plus either diagnostic electrocardiographic changesor elevated cardiac-enzyme levels. Infarctions that requiredhospital admission and for which confirmatory information wasobtained, but for which no medical records were available, weredesignated as probable (these amounted to 17 percent of allinfarctions). We included all confirmed and probable cases.Deaths were identified from state vital records and the NationalDeath Index or were reported by the subject's family or postalauthorities. Information on the cause of death was availablefor more than 98 percent of deaths.
Confirmed deaths from coronary heart disease were defined asthose caused by myocardial infarction according to hospitalrecords or autopsy, or those for which coronary heart diseasewas listed as the cause of death and evidence of previous coronarydisease was available. In addition to confirmed deaths fromcoronary heart disease, we included the deaths in which coronaryheart disease was listed as the underlying cause but no recordswere available (15 percent of all deaths from coronary heartdisease). We also included sudden deaths with no plausible causeother than coronary heart disease (12 percent of deaths fromcoronary heart disease). Analyses limited to confirmed casesyielded similar results, although with less precision.
Strokes were considered confirmed if they met the criteria ofthe National Survey of Stroke.27 We excluded subdural hematomasand strokes caused by infection or neoplasia. Nonfatal strokesfor which medical records were unavailable were defined as probablestrokes and included in the analysis if they required hospitalizationand were corroborated by letter or interview. Fatal strokeswere confirmed by review of autopsy records, hospital records,or death certificates listing stroke as the underlying cause.In secondary analyses, strokes were added to coronary eventsto form the broader end point of cardiovascular events.
Statistical Analysis
The person-time for each participant was calculated from thedate of return of the 1980 questionnaire to the date of thefirst coronary (or cardiovascular) event, death, or June 1,1994, whichever came first. Women were classified in risk categoriesas described above. In multivariate models with pooled logisticregression, each two-year interval was treated as an independentobservation; we simultaneously adjusted for age, time period(seven time periods), presence or absence of a parental historyof myocardial infarction before the age of 60 years, menopausalstatus and postmenopausal use or nonuse of hormones, presenceor absence of hypertension, and the presence or absence of highcholesterol levels. In initial analyses, we calculated relativerisks and 95 percent confidence intervals for categories withineach factor of the low-risk profile, adjusting for the othercoronary risk factors listed above, but not for the other componentsof the low-risk index. We then examined the low-risk group,with the various factors taken together.
We began by including only diet, smoking, and exercise. We thenadded body-mass index and, finally, alcohol use to examine allfive factors simultaneously. In those analyses, we comparedwomen in the low-risk category for each of the component variableswith all other women, following a method previously used byWacholder et al.28 We calculated the population attributablerisk,29 an estimate of the percentage of coronary heart diseasein this population that would not have occurred if all womenhad been in the low-risk group, on the assumption that therewas a causal relation between the risk factors and coronaryheart disease. We repeated the analysis among nonsmokers toestimate the proportion of coronary heart disease that couldbe prevented by adherence to the remainder of the guidelines.
To obtain the best estimate of long-term dietary intake, weused the cumulative-update method,21 which takes the averageof all previous dietary data. For example, for the intervalfrom 1980 to 1984 we used the 1980 dietary data, and for theinterval from 1984 to 1986 we used the average of 1980 and 1984.We used the same method for physical activity, which was updatedin 1982, 1986, 1988, and 1992. For all other risk variablesand covariates apart from diet and exercise, we used the mostrecent information. Body-mass index and smoking status wereupdated every two years, and alcohol intake was updated in 1984,1986, and 1990.
Results
During 14 years of follow-up, we documented 1128 coronary heartdisease events (832 nonfatal myocardial infarctions and 296deaths from coronary heart disease) in the study cohort. Wealso documented 705 strokes. Table 1 shows the estimates ofthe relative risk of a coronary event for each of the five factorsconsidered in the low-risk profile and the proportion of thecohort in each risk category. These estimates have been adjustedfor the other covariates but not for the other elements of thelow-risk index. The most important single factor was cigarettesmoking, with a relative risk of 5.48 for those smoking 15 ormore cigarettes per day, as compared with nonsmokers. Even smoking1 to 14 cigarettes per day tripled the risk. In this population,41 percent of the coronary events could be attributed to currentsmoking.
Table 1. Distributions of Individual Modifiable Risk Factors and Relative Risk of Coronary Events in the Nurses' Health Study, 1980 to 1994.
In addition, each individual component of the low-risk profileshowed a significant and substantial association with risk;each of the components of the dietary score was independentlysignificant (data not shown). A gradient of risk was presentwithin the categories of each variable that were included aslow risk. For example, we included former smokers and thosewho had never smoked in the low-risk category, although formersmokers were at significantly higher risk than those who hadnever smoked. Likewise, we included women who consumed morethan 5 g of alcohol daily as being at low risk, although womenconsuming 5 to 9 g of alcohol daily were at higher risk thanthose consuming 10 g or more a day. We included all women withdietary scores in the highest 40 percent as being at low risk,but within that group, those with higher scores had lower risk.
Table 2 provides estimates of the reduction in risk for womenin the low-risk category for three, four, or five of the modifiablerisk factors. Women in the low-risk category for all five factorsconsidered together, as compared with all other women, had arelative risk of 0.17 (95 percent confidence interval, 0.07to 0.41). The population attributable risk was 82 percent (95percent confidence interval, 58 to 93), suggesting that 82 percentof the coronary events in this cohort might have been preventedif all women had been in the low-risk group.
Table 2. Risk of Coronary Events in Low-Risk Groups Defined According to Different Constellations of Modifiable Risk Factors for Coronary Disease in the Nurses' Health Study, 1980 to 1994.
As shown in Table 3, we repeated this analysis with only the78 percent of women who were not currently smoking. Women whowere in the low-risk category for the remaining four risk factors,as compared with all other current nonsmokers, had a relativerisk of 0.25 (95 percent confidence interval, 0.10 to 0.60).The population attributable risk was 74 percent (95 percentconfidence interval, 39 to 90 percent), suggesting that amongthe nonsmokers, 74 percent of the coronary disease events mighthave been prevented by compliance with the remaining componentsof the low-risk index.
Table 3. Risk of Coronary Events in Low-Risk Groups Defined According to Different Constellations of Modifiable Risk Factors for Coronary Disease among Current Nonsmokers in the Nurses' Health Study, 1980 to 1994.
To adjust for possible confounding according to socioeconomicstatus, we conducted further analyses in which we controlledfor the parents' occupation and husband's education. This hadno substantial effect on the estimates (for example, the relativerisk in the low-risk group went from 0.17 to 0.19).
Only about 3 percent of the population met the criteria forlow risk. To address the possibility that these women representeda unique and peculiar subgroup, we performed further analyses,successively relaxing the criteria. We observed a graded effecton the population attributable risk. For example, if women atlow risk were defined as those not currently smoking, havingdietary scores among the highest 45 percent, exercising at least25 minutes a day, having a body-mass index under 26, and drinkingat least 4 g of alcohol a day (a group that constituted 5.1percent of the population), the population attributable riskwould be 72 percent (95 percent confidence interval, 47 to 83percent). Further relaxation of the criteria to include 10 percentof the population (at least 15 minutes of exercise a day, consumptionof more than 2 g of alcohol a day, and a body-mass index ofless than 28) yielded a relative risk of 0.36 (95 percent confidenceinterval, 0.26 to 0.50) and a population attributable risk of62 percent (95 percent confidence interval, 47 to 72 percent).
Table 4 shows the results for analyses of major cardiovasculardisease (coronary events plus stroke). Women in the low-riskgroup had a relative risk of 0.25 (95 percent confidence interval,0.14 to 0.44), with a population attributable risk of 74 percent(95 percent confidence interval, 55 to 86 percent).
Table 4. Risk of Coronary Events or Stroke (Cardiovascular Events) in Low-Risk Groups Defined According to Different Constellations of Modifiable Risk Factors for Major Cardiovascular Disease in the Nurses' Health Study, 1980 to 1994.
Discussion
In this population of middle-aged women, those who did not smokecigarettes, were not overweight, maintained the healthful dietdescribed above, exercised moderately or vigorously for halfan hour a day, and consumed alcohol moderately had an incidenceof coronary events that was more than 80 percent lower thanthat in the rest of the population. Closer adherence to a morehealthful lifestyle might reduce the risk of coronary heartdisease still further.
This analysis has several important limitations. Despite thelarge numbers of subjects and the long follow-up, the estimateswere somewhat imprecise, largely because there were few casesof coronary heart disease among women in the low-risk categories.Indeed, we could not provide reliable estimates on which tobase more stringent recommendations because of the small numberof cases. The fact that the incidence of coronary events increasesin a graded fashion as the criteria for low risk are relaxedsupports the robustness of the findings, and suggests that theresults do not apply solely to a select group of peculiarlyhealth-conscious persons. Some of the lifestyle characteristics(especially diet and physical activity) were measured with error,which undoubtedly caused some misclassification. However, withthe prospective design, such misclassification would tend tolead to an underestimate of the true effect. Some factors weconsidered have not been tested in randomized trials with clinicalend points. However, ample observational data support theiruse. For some variables, there probably will never be randomizedtrials of primary prevention, so we must make decisions on thebasis of the best available information.
For simplicity, we considered only a limited set of variables.For example, we did not include consumption of nuts,30,31 linolenicacid,32 vitamin B6,23 or vitamin E33,34,35 or the use of aspirinor postmenopausal hormones.36,37 Larger reductions in risk mightbe possible with these added preventive factors. Some of thesefactors may be especially worthy of consideration for womenwho avoid alcohol to minimize the risk of breast cancer38 orbecause of a personal or family history of alcoholism.
We also did not consider pharmacologic treatment of hypertensionand of lipid levels, which has proved efficacious in the preventionof coronary heart disease. However, we did adjust for thesefactors in the analysis. Since part of the effect of diet andlifestyle is mediated through improvements in lipid levels andblood pressure, adjustment for those conditions might lead toan underestimate of the overall benefit of the factors we considered.Our nurse participants are more likely to receive treatmentfor these conditions than the general population. However, notall participants are receiving optimal therapy; there is thusa greater potential for prevention, if all treatments are considered.Our results complement those of Stamler et al.,39 who foundthat the relative risk of death from coronary heart diseaseranged from 0.08 to 0.23 in low-risk persons, defined as nondiabeticsubjects with no history of coronary disease who were not currentsmokers and who had cholesterol levels of less than 200 mg perdeciliter (5.17 mmol per liter) and blood pressure of 120/80mm Hg or less.
By simultaneously examining the effect of several lifestylevariables, we took into account the clustering of healthfultypes of behavior within individual women. In addition, we adjustedfor many coronary risk factors. Nevertheless, confounding byother variables, particularly socioeconomic status, could haveaffected our results. However, all the participants were registerednurses with some college education. Analysis of home addressesaccording to census-tract data found substantial economic homogeneity(Laden F: personal communication). Furthermore, adjustment forparental occupation and the husband's education had little effecton the findings. Indeed, at least some of the health benefitsof higher socioeconomic status are mediated through the lifestylevariables we studied.
Thus, although vigorous pharmacologic treatment of hypertensionand lipid levels (when necessary) has been proved effective,these data support the hypothesis that adopting a more healthfullifestyle could prevent a substantial majority of coronary diseaseevents in women.
Supported by research grants (HL24074, HL34594, HL60712, CA40356,and DK46200) and a Nutrition Training Grant (T32DK07703) fromthe National Institutes of Health.
We are indebted to Drs. Francine Grodstein, Frank Speizer, andEugene Braunwald for their insightful comments on the manuscript.
Source Information
From the Channing Laboratory (M.J.S., J.E.M., E.B.R., W.C.W.) and the Division of Preventive Medicine (J.E.M.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School; and the Departments of Epidemiology (M.J.S., J.E.M., E.B.R., W.C.W.) and Nutrition (M.J.S., F.B.H., E.B.R., W.C.W.), Harvard School of Public Health — all in Boston.
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Redberg, R. F., Benjamin, E. J., Bittner, V., Braun, L. T., Goff, D. C. Jr, Havas, S., Labarthe, D. R., Limacher, M. C., Lloyd-Jones, D. M., Mora, S., Pearson, T. A., Radford, M. J., Smetana, G. W., Spertus, J. A., Swegler, E. W.
(2009). ACCF/AHA 2009 performance measures for primary prevention of cardiovascular disease in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Performance Measures (Writing Committee to Develop Performance Measures for Primary Prevention of Cardiovascular Disease) developed in collaboration with the American Academy of Family Physicians; American Association of Cardiovascular and Pulmonary Rehabilitation; and Preventive Cardiovascular Nurses Association Endorsed by the American College of Preventive Medicine, American College of Sports Medicine, and Society for Women's Health Research.. J Am Coll Cardiol
54: 1364-1405
[Full Text]
Ford, E. S., Li, C., Zhao, G., Pearson, W. S., Capewell, S.
(2009). Trends in the Prevalence of Low Risk Factor Burden for Cardiovascular Disease Among United States Adults. Circulation
120: 1181-1188
[Abstract][Full Text]
WRITING COMMITTEE MEMBERS, , Redberg, R. F., Benjamin, E. J., Bittner, V., Braun, L. T., Goff, D. C. Jr, Havas, S., Labarthe, D. R., Limacher, M. C., Lloyd-Jones, D. M., Mora, S., Pearson, T. A., Radford, M. J., Smetana, G. W., Spertus, J. A., Swegler, E. W.
(2009). ACCF/AHA 2009 Performance Measures for Primary Prevention of Cardiovascular Disease in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Performance Measures (Writing Committee to Develop Performance Measures for Primary Prevention of Cardiovascular Disease): Developed in Collaboration With the American Academy of Family Physicians; American Association of Cardiovascular and Pulmonary Rehabilitation; and Preventive Cardiovascular Nurses Association: Endorsed by the American College of Preventive Medicine, American College of Sports Medicine, and Society for Women's Health Research. Circulation
120: 1296-1336
[Full Text]
Ford, E. S., Bergmann, M. M., Kroger, J., Schienkiewitz, A., Weikert, C., Boeing, H.
(2009). Healthy Living Is the Best Revenge: Findings From the European Prospective Investigation Into Cancer and Nutrition-Potsdam Study. Arch Intern Med
169: 1355-1362
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Cardi, M., Munk, N., Zanjani, F., Kruger, T., Schaie, K. W., Willis, S. L.
(2009). Health Behavior Risk Factors Across Age as Predictors of Cardiovascular Disease Diagnosis. J Aging Health
21: 759-775
[Abstract]
Djousse, L., Driver, J. A., Gaziano, J. M.
(2009). Relation Between Modifiable Lifestyle Factors and Lifetime Risk of Heart Failure. JAMA
302: 394-400
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Kris-Etherton, P. M
(2009). Adherence to dietary guidelines: benefits on atherosclerosis progression. Am. J. Clin. Nutr.
90: 13-14
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Imamura, F., Jacques, P. F, Herrington, D. M, Dallal, G. E, Lichtenstein, A. H
(2009). Adherence to 2005 Dietary Guidelines for Americans is associated with a reduced progression of coronary artery atherosclerosis in women with established coronary artery disease. Am. J. Clin. Nutr.
90: 193-201
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Rippe, J. M.
(2009). From the Editor. AMERICAN JOURNAL OF LIFESTYLE MEDICINE
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Peart, J. N., Headrick, J. P.
(2009). Clinical cardioprotection and the value of conditioning responses. Am. J. Physiol. Heart Circ. Physiol.
296: H1705-H1720
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Fraser, G. E
(2009). Vegetarian diets: what do we know of their effects on common chronic diseases?. Am. J. Clin. Nutr.
89: 1607S-1612S
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Mozaffarian, D., Kamineni, A., Carnethon, M., Djousse, L., Mukamal, K. J., Siscovick, D.
(2009). Lifestyle Risk Factors and New-Onset Diabetes Mellitus in Older Adults: The Cardiovascular Health Study. Arch Intern Med
169: 798-807
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Maruthur, N. M., Wang, N.-Y., Appel, L. J.
(2009). Lifestyle Interventions Reduce Coronary Heart Disease Risk: Results From the PREMIER Trial. Circulation
119: 2026-2031
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Molenaar, E. A., Massaro, J. M., Jacques, P. F., Pou, K. M., Ellison, R. C., Hoffmann, U., Pencina, K., Shadwick, S. D., Vasan, R. S., O'Donnell, C. J., Fox, C. S.
(2009). Association of Lifestyle Factors With Abdominal Subcutaneous and Visceral Adiposity: The Framingham Heart Study. Diabetes Care
32: 505-510
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WRITING GROUP MEMBERS, , Lloyd-Jones, D., Adams, R., Carnethon, M., De Simone, G., Ferguson, T. B., Flegal, K., Ford, E., Furie, K., Go, A., Greenlund, K., Haase, N., Hailpern, S., Ho, M., Howard, V., Kissela, B., Kittner, S., Lackland, D., Lisabeth, L., Marelli, A., McDermott, M., Meigs, J., Mozaffarian, D., Nichol, G., O'Donnell, C., Roger, V., Rosamond, W., Sacco, R., Sorlie, P., Stafford, R., Steinberger, J., Thom, T., Wasserthiel-Smoller, S., Wong, N., Wylie-Rosett, J., Hong, Y., for the American Heart Association Statistics Comm,
(2009). Heart Disease and Stroke Statistics--2009 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation
119: e21-e181
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Folsom, A. R., Yamagishi, K., Hozawa, A., Chambless, L. E., for the Atherosclerosis Risk in Communities Study,
(2009). Absolute and Attributable Risks of Heart Failure Incidence in Relation to Optimal Risk Factors. Circ Heart Fail
2: 11-17
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Qi, L., Kang, K., Zhang, C., van Dam, R. M., Kraft, P., Hunter, D., Lee, C.-H., Hu, F. B.
(2008). Fat Mass-and Obesity-Associated (FTO) Gene Variant Is Associated With Obesity: Longitudinal Analyses in Two Cohort Studies and Functional Test. Diabetes
57: 3145-3151
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Djousse, L., Rudich, T., Gaziano, J M.
(2008). Nut consumption and risk of heart failure in the Physicians' Health Study I. Am. J. Clin. Nutr.
88: 930-933
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Dam, R. M v., Li, T., Spiegelman, D., Franco, O. H, Hu, F. B
(2008). Combined impact of lifestyle factors on mortality: prospective cohort study in US women. BMJ
337: a1440-a1440
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Chiuve, S. E., Rexrode, K. M., Spiegelman, D., Logroscino, G., Manson, J. E., Rimm, E. B.
(2008). Primary Prevention of Stroke by Healthy Lifestyle. Circulation
118: 947-954
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Kahn, R., Robertson, R. M., Smith, R., Eddy, D.
(2008). The Impact of Prevention on Reducing the Burden of Cardiovascular Disease. Diabetes Care
31: 1686-1696
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Carbillon, L.
(2008). Pregnancy Is an Essential Spontaneous Screening Stress Test for the Risk of Early Stroke in Women. Stroke
39: e138-e138
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Kahn, R., Robertson, R. M., Smith, R., Eddy, D.
(2008). The Impact of Prevention on Reducing the Burden of Cardiovascular Disease. Circulation
118: 576-585
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Appel, L. J.
(2008). Dietary Patterns and Longevity: Expanding the Blue Zones. Circulation
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Colditz, G. A., Winn, D. M.
(2008). Criteria for the Evaluation of Large Cohort Studies: An Application to the Nurses' Health Study. JNCI J Natl Cancer Inst
100: 918-925
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Mozaffarian, D., Wilson, P. W.F., Kannel, W. B.
(2008). Beyond Established and Novel Risk Factors: Lifestyle Risk Factors for Cardiovascular Disease. Circulation
117: 3031-3038
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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]
Genovesi, S., Pieruzzi, F., Giussani, M., Tono, V., Stella, A., Porta, A., Pagani, M., Lucini, D.
(2008). Analysis of Heart Period and Arterial Pressure Variability in Childhood Hypertension: Key Role of Baroreflex Impairment. Hypertension
51: 1289-1294
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Meka, N., Katragadda, S., Cherian, B., Arora, R. R.
(2008). Review: Endurance exercise and resistance training in cardiovascular disease. Ther Adv Cardiovasc Dis
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Anand, S. S., Islam, S., Rosengren, A., Franzosi, M. G., Steyn, K., Yusufali, A. H., Keltai, M., Diaz, R., Rangarajan, S., Yusuf, S., on behalf of the INTERHEART Investigators,
(2008). Risk factors for myocardial infarction in women and men: insights from the INTERHEART study. Eur Heart J
29: 932-940
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Rees, M., Stevenson, J., on behalf of the British Menopause Society Council,
(2008). Primary prevention of coronary heart disease in women. Menopause Int
14: 40-45
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King, D. E., Mainous, A. G. III, Egan, B. M., Woolson, R. F., Geesey, M. E.
(2008). Effect of Psyllium Fiber Supplementation on C-Reactive Protein: The Trial to Reduce Inflammatory Markers (TRIM). Ann Fam Med
6: 100-106
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Skilton, M. R.
(2008). Intrauterine Risk Factors for Precocious Atherosclerosis. Pediatrics
121: 570-574
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Nesto, R. W., Mackie, K.
(2008). Endocannabinoid system and its implications for obesity and cardiometabolic risk. Eur Heart J Suppl
10: B34-B41
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Lutsey, P. L., Steffen, L. M., Stevens, J.
(2008). Dietary Intake and the Development of the Metabolic Syndrome: The Atherosclerosis Risk in Communities Study. Circulation
117: 754-761
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Writing Group Members, , Rosamond, W., Flegal, K., Furie, K., Go, A., Greenlund, K., Haase, N., Hailpern, S. M., Ho, M., Howard, V., Kissela, B., Kittner, S., Lloyd-Jones, D., McDermott, M., Meigs, J., Moy, C., Nichol, G., O'Donnell, C., Roger, V., Sorlie, P., Steinberger, J., Thom, T., Wilson, M., Hong, Y., for the American Heart Association Statistics Comm,
(2008). Heart Disease and Stroke Statistics--2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation
117: e25-e146
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Akesson, A., Weismayer, C., Newby, P. K., Wolk, A.
(2007). Combined Effect of Low-Risk Dietary and Lifestyle Behaviors in Primary Prevention of Myocardial Infarction in Women. Arch Intern Med
167: 2122-2127
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Wister, A. PhD, Loewen, N. MD, Kennedy-Symonds, H. MHSc, McGowan, B. MD, McCoy, B. MA, Singer, J. PhD
(2007). One-year follow-up of a therapeutic lifestyle intervention targeting cardiovascular disease risk. CMAJ
177: 859-865
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Bengmark, S.
(2007). Advanced Glycation and Lipoxidation End Products-Amplifiers of Inflammation: The Role of Food. JPEN J Parenter Enteral Nutr
31: 430-440
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Drogan, D., Hoffmann, K., Schulz, M., Bergmann, M. M., Boeing, H., Weikert, C.
(2007). A Food Pattern Predicting Prospective Weight Change Is Associated with Risk of Fatal but Not with Nonfatal Cardiovascular Disease. J. Nutr.
137: 1961-1967
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Gao, X., Qi, L., Qiao, N., Choi, H. K., Curhan, G., Tucker, K. L., Ascherio, A.
(2007). Intake of Added Sugar and Sugar-Sweetened Drink and Serum Uric Acid Concentration in US Men and Women. Hypertension
50: 306-312
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Li, C., Ford, E. S., Mokdad, A. H., Jiles, R., Giles, W. H.
(2007). Clustering of Multiple Healthy Lifestyle Habits and Health-Related Quality of Life Among U.S. Adults With Diabetes. Diabetes Care
30: 1770-1776
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Ballard-Barbash, R., McTiernan, A.
(2007). Is the Whole Larger Than the Sum of the Parts? The Promise of Combining Physical Activity and Diet to Improve Cancer Outcomes. JCO
25: 2335-2337
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Pierce, J. P., Stefanick, M. L., Flatt, S. W., Natarajan, L., Sternfeld, B., Madlensky, L., Al-Delaimy, W. K., Thomson, C. A., Kealey, S., Hajek, R., Parker, B. A., Newman, V. A., Caan, B., Rock, C. L.
(2007). Greater Survival After Breast Cancer in Physically Active Women With High Vegetable-Fruit Intake Regardless of Obesity. JCO
25: 2345-2351
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Reiter, M., Wirth, S., Pourazim, A., Puchner, S., Baghestanian, M., Minar, E., Bucek, R. A.
(2007). Skin tissue cholesterol is not related to vascular occlusive disease. Vasc Med
12: 129-134
[Abstract]
Vigorito, C., Giallauria, F., Palomba, S., Cascella, T., Manguso, F., Lucci, R., De Lorenzo, A., Tafuri, D., Lombardi, G., Colao, A., Orio, F.
(2007). Beneficial Effects of a Three-Month Structured Exercise Training Program on Cardiopulmonary Functional Capacity in Young Women with Polycystic Ovary Syndrome. J. Clin. Endocrinol. Metab.
92: 1379-1384
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Stamler, J.
(2007). Low Risk--and the "No More Than 50%" Myth/Dogma. Arch Intern Med
167: 537-539
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Hozawa, A., Folsom, A. R., Sharrett, A. R., Chambless, L. E.
(2007). Absolute and Attributable Risks of Cardiovascular Disease Incidence in Relation to Optimal and Borderline Risk Factors: Comparison of African American With White Subjects--Atherosclerosis Risk in Communities Study. Arch Intern Med
167: 573-579
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Kabagambe, E. K., Baylin, A., Campos, H.
(2007). Nonfatal Acute Myocardial Infarction in Costa Rica: Modifiable Risk Factors, Population-Attributable Risks, and Adherence to Dietary Guidelines. Circulation
115: 1075-1081
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Lloyd-Jones, D. M., Liu, K., Colangelo, L. A., Yan, L. L., Klein, L., Loria, C. M., Lewis, C. E., Savage, P.
(2007). Consistently Stable or Decreased Body Mass Index in Young Adulthood and Longitudinal Changes in Metabolic Syndrome Components: The Coronary Artery Risk Development in Young Adults Study. Circulation
115: 1004-1011
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Rosamond, W., Flegal, K., Friday, G., Furie, K., Go, A., Greenlund, K., Haase, N., Ho, M., Howard, V., Kissela, B., Kittner, S., Lloyd-Jones, D., McDermott, M., Meigs, J., Moy, C., Nichol, G., O'Donnell, C. J., Roger, V., Rumsfeld, J., Sorlie, P., Steinberger, J., Thom, T., Wasserthiel-Smoller, S., Hong, Y., for the American Heart Association Statistics Comm,
(2007). Heart Disease and Stroke Statistics--2007 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation
115: e69-e171
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Bloomgarden, Z. T.
(2007). Prevention of Cardiovascular Disease. Diabetes Care
30: 423-431
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Ignarro, L. J., Balestrieri, M. L., Napoli, C.
(2007). Nutrition, physical activity, and cardiovascular disease: An update. Cardiovasc Res
73: 326-340
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Pearson, T. A.
(2007). The Prevention Of Cardiovascular Disease: Have We Really Made Progress?. Health Aff (Millwood)
26: 49-60
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Lynch, E. B., Liu, K., Kiefe, C. I., Greenland, P.
(2006). Cardiovascular Disease Risk Factor Knowledge in Young Adults and 10-year Change in Risk Factors: The Coronary Artery Risk Development in Young Adults (CARDIA) Study. Am J Epidemiol
164: 1171-1179
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Napoli, C., Lerman, L. O., de Nigris, F., Gossl, M., Balestrieri, M. L., Lerman, A.
(2006). Rethinking Primary Prevention of Atherosclerosis-Related Diseases. Circulation
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Lampe, J. W.
(2006). For Debate: Investment in Nutrigenomics Will Advance the Role of Nutrition in Public Health. Cancer Epidemiol. Biomarkers Prev.
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Rosenfeld, A. G.
(2006). State of the Heart: Building Science to Improve Women's Cardiovascular Health. Am J Crit Care
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Mukamal, K. J., Chiuve, S. E., Rimm, E. B.
(2006). Alcohol consumption and risk for coronary heart disease in men with healthy lifestyles.. Arch Intern Med
166: 2145-2150
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Blankenberg, S., Yusuf, S.
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114: 1557-1560
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Gemmell, I, Heller, R F, Payne, K, Edwards, R, Roland, M, Durrington, P
(2006). Potential population impact of the UK government strategy for reducing the burden of coronary heart disease in England: comparing primary and secondary prevention strategies.. Qual Saf Health Care
15: 339-343
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The ESHRE Capri Workshop Group,
(2006). Hormones and cardiovascular health in women. Hum Reprod Update
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Michels, K. B
(2006). The women's health initiative--curse or blessing?. Int J Epidemiol
35: 814-816
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Mittleman, M. A.
(2006). A 39-year-old woman with hypercholesterolemia.. JAMA
296: 319-326
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Chiuve, S. E., McCullough, M. L., Sacks, F. M., Rimm, E. B.
(2006). Healthy Lifestyle Factors in the Primary Prevention of Coronary Heart Disease Among Men: Benefits Among Users and Nonusers of Lipid-Lowering and Antihypertensive Medications. Circulation
114: 160-167
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Kurth, T., Moore, S. C., Gaziano, J. M., Kase, C. S., Stampfer, M. J., Berger, K., Buring, J. E.
(2006). Healthy lifestyle and the risk of stroke in women.. Arch Intern Med
166: 1403-1409
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Eckel, R. H.
(2006). Preventive Cardiology by Lifestyle Intervention: Opportunity and/or Challenge?: Presidential Address at the 2005 American Heart Association Scientific Sessions. Circulation
113: 2657-2661
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Gelfand, E. V., Cannon, C. P.
(2006). Rimonabant: A Cannabinoid Receptor Type 1 Blocker for Management of Multiple Cardiometabolic Risk Factors. J Am Coll Cardiol
47: 1919-1926
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Giampaoli, S., Palmieri, L., Panico, S., Vanuzzo, D., Ferrario, M., Chiodini, P., Pilotto, L., Donfrancesco, C., Cesana, G., Sega, R., Stamler, J.
(2006). Favorable Cardiovascular Risk Profile (Low Risk) and 10-Year Stroke Incidence in Women and Men: Findings from 12 Italian Population Samples. Am J Epidemiol
163: 893-902
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Lloyd-Jones, D. M., Leip, E. P., Larson, M. G., D'Agostino, R. B., Beiser, A., Wilson, P. W.F., Wolf, P. A., Levy, D.
(2006). Prediction of Lifetime Risk for Cardiovascular Disease by Risk Factor Burden at 50 Years of Age. Circulation
113: 791-798
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Li, T. Y., Rana, J. S., Manson, J. E., Willett, W. C., Stampfer, M. J., Colditz, G. A., Rexrode, K. M., Hu, F. B.
(2006). Obesity as Compared With Physical Activity in Predicting Risk of Coronary Heart Disease in Women. Circulation
113: 499-506
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Gronniger, J. T.
(2006). A Semiparametric Analysis of the Relationship of Body Mass Index to Mortality. AJPH
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Ellison, R. C.
(2005). Importance of Pattern of Alcohol Consumption. Circulation
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Franco, O. H., de Laet, C., Peeters, A., Jonker, J., Mackenbach, J., Nusselder, W.
(2005). Effects of Physical Activity on Life Expectancy With Cardiovascular Disease. Arch Intern Med
165: 2355-2360
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Sorensen, G., Barbeau, E., Stoddard, A. M., Hunt, M. K., Kaphingst, K., Wallace, L.
(2005). Promoting Behavior Change Among Working-Class, Multiethnic Workers: Results of the Healthy Directions--Small Business Study. AJPH
95: 1389-1395
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Weikert, C., Hoffmann, K., Dierkes, J., Zyriax, B.-C., Klipstein-Grobusch, K., Schulze, M. B., Jung, R., Windler, E., Boeing, H.
(2005). A Homocysteine Metabolism-Related Dietary Pattern and the Risk of Coronary Heart Disease in Two Independent German Study Populations. J. Nutr.
135: 1981-1988
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Millen, B. E, Quatromoni, P. A, Nam, B.-H., Pencina, M. J, Polak, J. F, Kimokoti, R. W, Ordovas, J. M, D'Agostino, R. B
(2005). Compliance with expert population-based dietary guidelines and lower odds of carotid atherosclerosis in women: the Framingham Nutrition Studies. Am. J. Clin. Nutr.
82: 174-180
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Reeves, M. J., Rafferty, A. P.
(2005). Healthy Lifestyle Characteristics Among Adults in the United States, 2000. Arch Intern Med
165: 854-857
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Mai, V., Kant, A. K, Flood, A., Lacey, J. V Jr, Schairer, C., Schatzkin, A.
(2005). Diet quality and subsequent cancer incidence and mortality in a prospective cohort of women. Int J Epidemiol
34: 54-60
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Gluckman, T. J., Sachdev, M., Schulman, S. P., Blumenthal, R. S.
(2005). A Simplified Approach to the Management of Non-ST-Segment Elevation Acute Coronary Syndromes. JAMA
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Roberts, C. K., Barnard, R. J.
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Anderson, J. W
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Califf, R. M., Ryan, T., Douglas, P., Goldschmidt-Clermont, P. J.
(2004). A time of accelerated change in academic cardiovascular medicine: Implications for academic divisions of cardiology and their training programs. J Am Coll Cardiol
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Daviglus, M. L., Stamler, J., Pirzada, A., Yan, L. L., Garside, D. B., Liu, K., Wang, R., Dyer, A. R., Lloyd-Jones, D. M., Greenland, P.
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292: 1588-1592
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Knoops, K. T. B., de Groot, L. C. P. G. M., Kromhout, D., Perrin, A.-E., Moreiras-Varela, O., Menotti, A., van Staveren, W. A.
(2004). Mediterranean Diet, Lifestyle Factors, and 10-Year Mortality in Elderly European Men and Women: The HALE Project. JAMA
292: 1433-1439
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