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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Hypertension. Author manuscript; available in PMC 2012 March 1.
Published in final edited form as:
PMCID: PMC3048351


Nicole Redmond, MD, PhD, MPH,1,2,3 Heather J. Baer, ScD,1,3,4 and LeRoi S. Hicks, MD, MPH1,5,6,7


Minorities have a higher prevalence of hypertension, a major risk factor for cardiovascular disease, which contributes to racial/ethnic disparities in morbidity and mortality in the US. Many modifiable health behaviors have been associated with improved blood pressure control, but it is unclear how racial/ethnic differences in these behaviors are related to the observed disparities in blood pressure control.

Cross-sectional analyses were conducted among 21,489 US adults aged >20 years participating in the National Health and Nutrition Examination Survey from 2001–2006. Secondary analyses were conducted among those with a self-reported diagnosis of hypertension. Blood pressure control was defined as systolic values <140 mmHg and diastolic values <90 mmHg (or <130 mmHg and <80 mmHg among diabetics, respectively).

In primary analyses, Non-Hispanic Blacks had 90% higher odds of poorly controlled blood pressure compared to non-Hispanic Whites after adjustment for sociodemographic and clinical characteristics (p <0.001). In secondary analyses among hypertensive subjects, non-Hispanic Blacks and Mexican-Americans had 40% higher odds of uncontrolled blood pressure compared to non-Hispanic Whites after adjustment for sociodemographic and clinical characteristics (p <0.001). For both analyses, the racial/ethnic differences in blood pressure control persisted even after further adjustment for modifiable health behaviors, which included medication adherence in secondary analyses (p <0.001 for both analyses).

Although population-level adoption of healthy behaviors may contribute to reduction of the societal burden of cardiovascular disease in general, these findings suggest that racial/ethnic differences in some health behaviors do not explain the disparities in hypertension prevalence and control.

Keywords: Hypertension, blood pressure, health disparities, minority health, health behavior, exercise, diet


African-Americans and US-born Mexican-Americans, have higher risks for all-cause mortality and cardiovascular disease (CVD) morbidity and mortality compared to Whites.16 A large proportion of excess morbidity and mortality among minorities may be attributable to hypertension.79 As a result, identifying modifiable factors that contribute to racial and ethnic differences in rates of hypertension and blood pressure (BP) control is an essential step toward eliminating disparities in CVD outcomes.

Current literature suggests that some modifiable health behaviors, including moderate alcohol consumption, decreased sodium intake, smoking cessation, increased physical activity, and increased intake of fruits, vegetables, and whole grains may reduce incidence of hypertension and improve BP control among those with and without a prior diagnosis of hypertension.1024 To date, however, data regarding racial and ethnic differences in the distributions of modifiable health behaviors is varied. Prior studies have shown African-Americans and Mexican-Americans as having a higher prevalence of some risk factors (e.g., low rates of physical activity) but similar or lower prevalence of others (e.g., smoking and alcohol intake) when compared to Whites.2530

Despite numerous studies of potential pharmacological and socioeconomic mediators for racial differences in hypertension prevalence and severity, there has been little examination of the possible contribution of racial and ethnic differences in health behaviors to disparities in hypertension prevalence.2, 3133 Therefore, we examined a nationally representative sample of adults participating in the 2001–2006 National Health and Nutrition Examination Survey (NHANES) to assess the relative contribution of racial and ethnic differences in modifiable health behaviors to disparities in hypertension prevalence and control.



NHANES is a complex, stratified multistage probability sample of the non-institutionalized US population with over-sampling for certain groups including African-Americans and Mexican-Americans. Since 1999, NHANES has been conducted continuously with data released every two years. We considered 2001 to 2006 as one time period and generated 6-year sample weights, as recommended in the online survey documentation, for all analyses.34 We limited our analyses to 2001–2006 data because the 2007–2008 survey cycle no longer contains data on individual physical activities needed to calculate total physical activity (MET-hours per week) in the same way as prior cycles and the NHANES 1999–2000 nutrient intakes were calculated using an older version of the USDA Survey Nutrient database compared to the other cycles.35 Detailed descriptions of the history, design, informed consent, data collection, and available data for NHANES are available on the National Center for Health Statistics website.36 Our protocol was approved by the Partners Institutional Review Board.

Study Population

Using data from the NHANES 2001–2006, the eligible sample consisted of non-Hispanic White, non-Hispanic Black, and Mexican-American adult participants aged >20 years who were not pregnant, completed the survey questionnaire, had BP measured during the mobile exam center (MEC) evaluation, and reliably completed the dietary recall for the nutrients of interest as defined by NHANES online documentation. Participants reporting race and ethnicity of “Other Hispanic” and “Other” were excluded due to relatively small sample sizes. Secondary analyses were conducted among participants with a prior diagnosis of hypertension.

Study Variables

The primary outcome variable was BP control defined, as a mean systolic BP <140 mmHg (<130 mmHg in diabetic patients) and/or mean diastolic BP <90 mmHg (<80 mmHg in diabetic patients). Mean blood pressure was calculated from four separate measurements obtained by certified examiners during the MEC evaluation according to the study protocol.37 The primary independent variable was self-reported race/ethnicity, coded in NHANES as non-Hispanic White, non-Hispanic Black, or Mexican-American.

Covariates included participants’ self-reported age (continuous) and sex, financial status using the poverty income ratio (PIR), low educational level, and insurance status. Other potential confounders included impaired functional status, self-reported general health status, body mass index, and diabetes.

We included variables related to modifiable health behaviors based on prior literature implicating their role in the incidence and control of high BP.11, 1315, 20, 22, 38, 39 These included: self-reported current smoking status (yes/no), total MET-hours per week calculated from all self-reported individual leisure time physical activities, total energy intake, total daily nutrient intakes of sodium, alcohol, and fiber based on participants’ 24-hour dietary recall. Fiber was used as a proxy for fruit, vegetable, and whole grain intake based on literature suggesting that fiber content mediates their antihypertensive effects.38, 39

Patients with previously diagnosed hypertension may change their health behaviors as a consequence of physician counseling, and thus these factors could have different associations with BP control in this group compared to the general population.40, 41 Therefore, we conducted secondary analyses restricting the sample to subjects with known hypertension. We defined hypertensive participants as those with a positive response to the NHANES survey question “Have you ever been told by a doctor or other health professional that you had…high blood pressure?” Among hypertensives, those responding “no” to “because of your high blood pressure/hypertension, have you ever been told to take prescribed medicine?” were classified as “medication ineligible”. Among medication eligible hypertensives, those who also endorsed current use of these medications by answering “yes” to “Are you now taking prescribed medicine” were classified as “medication adherent”, with the others classified as “non-adherent”.

Statistical Analysis

Bivariable analyses comparing proportions of subjects meeting recommendations for lifestyle behaviors and BP control were conducted by race/ethnicity, age-standardized based on the 2000 US Census Population. Multivariable regression modeling was used to determine the relationship of race with BP control. The base model controlled for age, sex, education, income, insurance status, general health status, functional status, diabetes, and body mass index (Model 1). In the next model, all modifiable health behaviors (smoking status, physical activity, sodium, fiber, and alcohol) were added to the base model (Model 2). Interaction terms between race and each behavior were added separately to Model 2 to evaluate whether associations differed by race/ethnicity. In secondary analyses, these analyses were repeated among known hypertensive participants and, in addition, medication adherence was added to generate a final adjusted model (Model 3). For Model 2 (or Model 3 for hypertensive subpopulation), a greater than 10% change in the estimated odds ratio for race/ethnicity was considered a significant difference compared to their respective Model 1. To account for the complex sampling design of NHANES, we analyzed all data with SAS® version 9.2 (SAS Institute) and SUDAAN version 10.1 (RTI International).


Descriptive Statistics

The final sample for analysis included 21,489 subjects who represent about 37.7 million Americans. Of these, 83.2% were Non-Hispanic Whites, 10.2 % were Non-Hispanic Blacks, and 6.6% were Mexican-Americans. The age adjusted proportion of subjects with the demographic, sociodemographic, or clinical characteristics within each racial/ethnic group is shown in Table 1. Compared to non-Hispanic Whites, a higher proportion of minorities were impoverished, had less than twelve years of education, and were uninsured. Minorities also were more likely to have diabetes and high BMI.

Table 1
Age-adjusted prevalence (weighted %) of demographic, socioeconomic, clinical characteristics, and health behaviors of total sample, by race/ethnicity*

Health Behaviors

The age-adjusted proportions of subjects with modifiable health behaviors within each racial/ethnic group are shown in Table 1. Compared to non-Hispanic Whites, minorities reported less physical activity, with almost 27% of Non-Hispanic Blacks and about one-third of Mexican-Americans reporting no leisure time physical activity. For sodium intake, more minorities consumed <2000 mg/day when compared to non-Hispanic Whites, who had the largest proportion of subjects consuming >4500 mg/day. Fiber intake was generally low across all racial and ethnic groups; however, a higher proportion of Mexican-Americans achieved the recommended levels of >25 g/day. A higher proportion of African-Americans and Mexican-Americans reported low total energy intake of less than 1400 kcal/day. Rates of smoking were similar across all groups, but a higher proportion of non-Hispanic Whites consumed more than the equivalent of two drinks per day.

Determinants of blood pressure control

In age-adjusted analyses, Non-Hispanic Blacks had a much higher prevalence (27.4%) of uncontrolled BP when compared to other racial/ethnic groups (Non-Hispanic White 17.0%, Mexican-Americans 20.2%). Data from the multivariate regression models is shown in Table 2. In the base model, non-Hispanic Blacks had 90% higher odds of poorly controlled BP when compared to non-Hispanic Whites after adjustment for age, gender, and sociodemographic and clinical characteristics (p <0.001). This difference remained unchanged after addition of self-reported physical activity, smoking status, and dietary intakes of nutrients of interest (p <0.001). Interaction terms between race and each health behavior were added separately to Model 2 for each behavior and were not significant (data not shown).

Table 2
Adjusted Odds Ratios for poorly controlled blood pressure for total sample, by race/ethnicity*

In the final model, age, race, gender, diabetes, and BMI are all strong independent predictors of BP control (please see Table S1 of the Online Supplement Among health-related behaviors, smoking and sodium intake were not significant predictors of BP control. Although there appeared to be trend toward poorer BP control with increasing total daily caloric intake, this was not statistically significant. However, the highest level of physical activity (>50 MET-hours/week) had a 30% lower odds of poorly controlled BP compared to all other levels of activity (p=.02). In addition, those who reported consuming >28 g/day of alcohol had 85% higher odds of poor BP control compared with lower levels of alcohol consumption (p=.006); those consuming less than five grams of fiber per day had 74% higher odds of poor BP control compared with those meeting or exceeding the recommended 25 grams/day (p=.06).

Hypertensive subgroup analyses

The sub-sample of respondents who reported being told by a physician they had high BP included 6043 subjects who represent about 9.2 million Americans, of whom 82.2% were Non-Hispanic Whites, 13.7% were Non-Hispanic Blacks, and 4.1% were Mexican-Americans. Across all racial groups, the sample of known hypertensive respondents had higher proportions of subjects reporting fair/poor general health status, at least one functional limitation, diabetes, smoking, and obesity than the total sample (please see Table S2 of the Online Supplement The racial/ethnic disparity in the prevalence of uncontrolled BP persisted; 36.8% non-Hispanic Black and 37.6% Mexican-American hypertensives had poor control compared to 27.7% non-Hispanic Whites.

In multivariate regression models, known hypertensive non-Hispanic Blacks had 40% higher odds of uncontrolled BP after adjusting for sociodemographic and clinical characteristics when compared to non-Hispanic Whites in the base model (p=.02) (Table 3). Mexican-Americans had a 41% higher adjusted odds compared to Whites (p=.06) of borderline statistical significance. Adjustment for self-reported physical activity, smoking status, dietary intakes of specific nutrients, and medication adherence did not substantially change the estimates in either group.

Table 3
Adjusted Odds Ratios for poorly controlled blood pressure among hypertensive subjects

In the final model including health behaviors and adherence to antihypertensive medications, only age, race/ethnicity, diabetes, physical activity and medication adherence were strong independent predictors of BP control (please see Table S3 of the Online Supplement There also appeared to be a non-significant trend toward poorer BP control with higher levels total daily caloric intake and lower levels of fiber intake. Participants reporting non-adherence to anti-hypertensives and diabetes had nearly three times higher odds of uncontrolled BP. Similar to the overall population, the threshold for a statistically significant effect of physical activity occurred at the highest level of activity (>50 MET-hours/week), with the most active known hypertensive patients having 43% lower odds of poorly controlled BP after adjustment for medication adherence.


In our examination of a nationally-representative cohort representing 37.7 million adult individuals in the United States, we found that racial disparities in the prevalence of uncontrolled BP among Non-Hispanic Blacks when compared to Whites persist even after adjustment for demographic, socioeconomic status, clinical characteristics, and modifiable health behaviors in both the overall sample. Among a subsample with self-reported prior diagnoses of hypertension, the disparity in blood pressure control persisted for both Non-Hispanic Blacks and Mexican-Americans after adjustment for all covariates of interest. Further, among known hypertensive subjects, medication adherence was strongly associated with BP control, but did not explain the racial/ethnic disparity in the prevalence of uncontrolled BP. Last, after multivariate adjustment, only participants with self-reported levels of physical activity above 50 MET-hours/week had significantly lower odds of uncontrolled BP. To our knowledge, this is the first study to document the threshold of leisure-time physical activity associated with BP control among a nationally-representative sample utilizing a measure that incorporates duration as well as intensity and frequency of activity.

Differences in hypertension prevalence, treatment, and outcomes between minorities and non-Hispanic Whites have long been noted in the U.S. In a recent study, only 50% of hypertensive participants in NHANES were noted to have controlled hypertension, and Mexican-Americans were found to have higher prevalence of uncontrolled BP compared to non-Hispanic Whites.43 Our findings are consistent with prior literature, showing that age, race/ethnicity, and diabetes were associated with uncontrolled BP overall and among the subsample of known hypertensives.1, 31, 44, 45 We also noted that the minority groups did report lower sodium and alcohol intake as well as lower total energy intake than Whites; however, this did not impact the racial/ethnic disparity in BP control in multivariate regression modeling.

Furthermore, increasing levels of physical activity were associated with improved BP control overall and among hypertensives in NHANES, with extremely high levels of exercise (>50 MET-hrs/week) reaching statistical significance. Although a prior study examining NHANES III showed that greater than five episodes per week of moderate to vigorous activity was associated with decreased hypertension prevalence, frequency of activity was not assessed at that time.31 To put our findings in perspective, the current recommendation for exercise is equivalent to 7.5–12.5 MET-hours per week.46 White men in the highest quartile of leisure activity in the Atherosclerosis Risk in Communities (ARIC) study had 34% lower odds of developing hypertension over six years compared to the least active in multivariate models.10 Further, data from the Nurses’ Health Study, a sample of predominately White professional women, suggest that only the highest levels of activity were associated with decreased risk of incident hypertension.13

None of the self-reported health behaviors, including physical activity, mitigated the disparity in BP control in our study. This is consistent with findings in the ARIC study that although White men who reported high physical activity levels had lower odds of developing hypertension over time, baseline activity was not associated with incident hypertension in white women or blacks, even after controlling for other health behaviors.10 In the Coronary Artery Risk Development in (Young) Adults Study (CARDIA), accounting for lifestyle behaviors narrowed, but did not eliminate, the racial disparity in BP incidence that appeared after seven years of follow-up.47 However, this study did not include sodium intake in the analyses, and utilized a sample of adults who were relatively young (ages 18–30) at study entry. Thus, it is plausible that differences in dietary sodium intake (particularly if higher among Whites as was the case in the current study) may attenuate their findings. Alternatively, the influence of lifestyle behaviors on BP disparities may not persist as these individuals continue to age.

This study is subject to some limitations. First, NHANES is a cross-sectional study and thus temporal associations cannot be established. Second, the nutrient intakes were taken from a single 24-hour dietary recall for each subject. Since dietary recalls only cover one 24-hour period, it may not represent an individual’s usual intake if this period is not a typical diet day for the individual. However, the mean of the population’s distribution of usual intake can be estimated from a sample of individuals’ 24-hour recalls without sophisticated statistical adjustment.48 Third, in addition to nutrient intakes, many of the other behavioral and sociodemographic variables were from subject self-report, and therefore misclassification and reporting bias is a concern. Age, sex, obesity, and socioeconomic status have been associated with under-reporting dietary intakes and other self-reported health behaviors; however, it is unclear how this may relate to racial differences in self-reported nutrient intakes.4952 For example, if racial/ethnic minority groups are more likely to under-report their caloric intake compared to non-Hispanic whites, and higher caloric intake is inversely related to blood pressure control, our findings of racial/ethnic disparities in control may underestimate the true magnitude of the racial/ethnic differences. Alternatively, if minorities are less likely to under-report caloric intake compared to non-Hispanic whites, our findings may overestimate the gap between minorities and non-Hispanic whites in rates of blood pressure control. Our findings should be interpreted in light of these limitations.

Last, there may be other variables that were not measured and/or included in our study that may impact the association of race with uncontrolled BP; i.e., occupational-related physical activity53 and/or exposure to psychosocial stressors such as discrimination. A recent study at a single academic medical center reported that Blacks reported more discrimination and concern about antihypertensive medications than Whites; after accounting for these factors, race was no longer a significant predictor of BP control.54 We also could not evaluate differences in health care provider behaviors such as adherence to prescribing guidelines or intensification of antihypertensive medications which may have a role in addressing racial/ethnic health disparities.55 In addition, racial/ethnic differences in genetic susceptibility, gene-environment interactions, and regional/geographic variations also may be more important contributors to the racial disparity in hypertension as well as other metabolic states (i.e., diabetes, obesity) that are associated with poor BP control.11, 56


In this nationally representative cohort of adults, we found that racial/ethnic disparities in BP control were not fully explained by racial/ethnic differences in potentially modifiable health behaviors, including self-reported adherence to anti-hypertensive medications among participants with previously diagnosed hypertension. Our findings suggest that although population-wide adoption of healthy behaviors may be critical to reduce the societal burden of hypertension and its sequelae, interventions targeting racial/ethnic differences in these behaviors may not mitigate disparities in rates of uncontrolled BP. Future research should further assess the potential relationships of gene-environment interactions, job-related stress, racism, and other psychosocial factors to racial/ethnic disparities in the prevalence and outcomes of hypertension in the United States.

Supplementary Material


Drs. Redmond and Hicks conceived and designed the study. Dr. Redmond acquired, analyzed, and interpreted the data and drafted the article. Drs. Hicks and Baer contributed to the interpretation of the data and revised the manuscript critically for important intellectual content. All authors approved the final submitted manuscript. The authors would like to thank Shimon Shaykevich, MS and Lenny Lopez, MD, MDiv, MPH for their advice on statistical programming.

Funding Sources

Dr. Redmond and this study were supported by grant number T32HP10251 from the Health Resources and Services Administration of the Department of Health and Human Services. The study’s contents are solely the responsibility of the authors and do not necessarily represent the official views of the Department of Health and Human Services.

Dr. Hicks was supported by the Health Disparities program of Harvard Catalyst | The Harvard Clinical and Translational Science Center (NIH Grant #1 UL1 RR 025758-01 and financial contributions from participating institutions).


Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.


Dr. Hicks is a scientific advisor to the Health Management Corporation and a member of the Board of Directors to Health Resources in Action. The authors have no other disclosures or conflicts of interest to report.


1. Mensah GA, Mokdad AH, Ford ES, Greenlund KJ, Croft JB. State of Disparities in Cardiovascular Health in the United States. Circulation. 2005;111:1233–1241. [PubMed]
2. Hertz RP, Unger AN, Cornell JA, Saunders E. Racial disparities in hypertension prevalence, awareness, and management. Arch Intern Med. 2005;165:2098–2104. [PubMed]
3. John MF, Keith CF, Samar AN. Epidemiology of Hypertension and Cardiovascular Disease in African Americans. The Journal of Clinical Hypertension. 2003;5:5–11. [PubMed]
4. Hunt KJ, Resendez RG, Williams K, Haffner SM, Stern MP, Hazuda HP. All-cause and cardiovascular mortality among Mexican-American and non-Hispanic White older participants in the San Antonio Heart Study- evidence against the "Hispanic paradox". Am J Epidemiol. 2003;158:1048–1057. [PubMed]
5. Crimmins EM, Kim JK, Alley DE, Karlamangla A, Seeman T. Hispanic paradox in biological risk profiles. Am J Public Health. 2007;97:1305–1310. [PubMed]
6. Wei M, Valdez RA, Mitchell BD, Haffner SM, Stern MP, Hazuda HP. Migration status, socioeconomic status, and mortality rates in Mexican Americans and non-Hispanic whites: the San Antonio Heart Study. Ann Epidemiol. 1996;6:307–313. [PubMed]
7. Wong MD, Shapiro MF, Boscardin WJ, Ettner SL. Contribution of Major Diseases to Disparities in Mortality. New England Journal of Medicine. 2002;347:1585–1592. [PubMed]
8. Fiscella K, Holt K. Racial disparity in hypertension control: tallying the death toll. Ann Fam Med. 2008;6:497–502. [PubMed]
9. Gu Q, Dillon CF, Burt VL, Gillum RF. Association of hypertension treatment and control with all-cause and cardiovascular disease mortality among US adults with hypertension. Am J Hypertens. 2010;23:38–45. [PubMed]
10. Pereira MA, Folsom AR, McGovern PG, Carpenter M, Arnett DK, Liao D, Szklo M, Hutchinson RG. Physical activity and incident hypertension in black and white adults: the Atherosclerosis Risk in Communities Study. Prev Med. 1999;28:304–312. [PubMed]
11. Beilin LJ, Burke V, Cox KL, Hodgson JM, Mori TA, Puddey IB. Non Pharmacologic Therapy and Lifestyle Factors in Hypertension. Blood Pressure. 2001;10:352–365. [PubMed]
12. Krousel-Wood MA, Muntner P, He J, Whelton PK. Primary prevention of essential hypertension. The Medical Clinics of North America. 2004;88:223–238. [PubMed]
13. Forman JP, Stampfer MJ, Curhan GC. Diet and Lifestyle Risk Factors Associated With Incident Hypertension in Women. JAMA. 2009;302:401–411. [PMC free article] [PubMed]
14. Al-Safi SA. Does smoking affect blood pressure and heart rate? Eur J Cardiovasc Nurs. 2005;4:286–289. [PubMed]
15. Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER, Simons-Morton DG, Karanja N, Lin P-H, Aickin M, Most-Windhauser MM, Moore TJ, Proschan MA, Cutler JA. Effects on Blood Pressure of Reduced Dietary Sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet. New England Journal of Medicine. 2001;344:3–10. [PubMed]
16. Bowman TS, Gaziano JM, Buring JE, Sesso HD. A prospective study of cigarette smoking and risk of incident hypertension in women. J Am Coll Cardiol. 2007;50:2085–2092. [PubMed]
17. Halperin RO, Gaziano JM, Sesso HD. Smoking and the risk of incident hypertension in middle-aged and older men. Am J Hypertens. 2008;21:148–152. [PubMed]
18. Narkiewicz K, Kjeldsen SE, Hedner T. Is smoking a causative factor of hypertension? Blood Press. 2005;14:69–71. [PubMed]
19. Beilin LJ, Puddey IB, Burke V. Alcohol and hypertension--kill or cure? J Hum Hypertens. 1996;10 Suppl 2:S1–S5. [PubMed]
20. Fuchs FD, Chambless LE, Whelton PK, Nieto FJ, Heiss G. Alcohol consumption and the incidence of hypertension: The Atherosclerosis Risk in Communities Study. Hypertension. 2001;37:1242–1250. [PubMed]
21. Puddey IB, Beilin LJ. Alcohol is bad for blood pressure. Clin Exp Pharmacol Physiol. 2006;33:847–852. [PubMed]
22. Saremi A, Hanson RL, Tulloch-Reid M, Williams DE, Knowler WC. Alcohol consumption predicts hypertension but not diabetes. J Stud Alcohol. 2004;65:184–190. [PubMed]
23. Sesso HD, Cook NR, Buring JE, Manson JE, Gaziano JM. Alcohol consumption and the risk of hypertension in women and men. Hypertension. 2008;51:1080–1087. [PubMed]
24. Thadhani R, Camargo CA, Jr, Stampfer MJ, Curhan GC, Willett WC, Rimm EB. Prospective study of moderate alcohol consumption and risk of hypertension in young women. Arch Intern Med. 2002;162:569–574. [PubMed]
25. Gao SK, Fitzpatrick AL, Psaty B, Jiang R, Post W, Cutler J, Maciejewski ML. Suboptimal Nutritional Intake for Hypertension Control in 4 Ethnic Groups. Arch Intern Med. 2009;169:702–707. [PubMed]
26. Kurian AK, Cardarelli KM. Racial and ethnic differences in cardiovascular disease risk factors: a systematic review. Ethnicity & disease. 2007;17:143–152. [PubMed]
27. King DE, Mainous Iii AG, Carnemolla M, Everett CJ. Adherence to Healthy Lifestyle Habits in US Adults, 1988–2006. The American Journal of Medicine. 2009;122:528–534. [PubMed]
28. Greenlund KJ, Daviglus ML, Croft JB. Differences in healthy lifestyle characteristics between adults with prehypertension and normal blood pressure. J Hypertens. 2009;27:955–962. [PubMed]
29. Young DR, Aickin M, Brantley P, Elmer PJ, Harsham DW, King AC, Stevens VJ. Physical Activity, Cardiorespiratory Fitness, and their Relationship to Cardiovascular Risk Factors in African Americans and Non-African Americans With Above-Optimal Blood Pressure. Journal of Community Health. 2005;30:107–124. [PubMed]
30. Block G, Rosenberger WF, Patterson BH. Calories, fat and cholesterol: intake patterns in the US population by race, sex and age. Am J Public Health. 1988;78:1150–1155. [PubMed]
31. Bassett DR, Fitzhugh EC, Crespo CJ, King GA, McLaughlin JE. Physical Activity and Ethnic Differences in Hypertension Prevalence in the United States. Preventive Medicine. 2002;34:179–186. [PubMed]
32. Marshall SJ, Jones DA, Ainsworth BE, Reis JP, Levy SS, Macera CA. Race/Ethnicity, Social Class, and Leisure-Time Physical Inactivity. Medicine & Science in Sports & Exercise. 2007;39:44–51. [PubMed]
33. McWilliams JM, Meara E, Zaslavsky AM, Ayanian JZ. Differences in control of cardiovascular disease and diabetes by race, ethnicity, and education: U.S. trends from 1999 to 2006 and effects of medicare coverage. Ann Intern Med. 2009;150:505–515. [PubMed]
34. Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination Survey Data. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2001–2006. National Center for Health Statistics (NCHS)
35. Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination Survey Data. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2001–2002. National Center for Health Statistics (NCHS)
36. Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination Survey Data. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; National Center for Health Statistics (NCHS)
37. Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination Survey Examination Protocol. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2001–2006. National Center for Health Statistics (NCHS)
38. Streppel MT, Arends LR, van 't Veer P, Grobbee DE, Geleijnse JM. Dietary Fiber and Blood Pressure: A Meta-analysis of Randomized Placebo-Controlled Trials. Arch Intern Med. 2005;165:150–156. [PubMed]
39. Whelton SP, Hyre AD, Pedersen B, Yi Y, Whelton PK, He J. Effect of dietary fiber intake on blood pressure: a meta-analysis of randomized, controlled clinical trials. J Hypertens. 2005;23:475–481. [PubMed]
40. Lopez L, Cook EF, Horng MS, Hicks LS. Lifestyle modification counseling for hypertensive patients: results from the National Health and Nutrition Examination Survey 1999–2004. Am J Hypertens. 2009;22:325–331. [PubMed]
41. Halm J, Amoako E. Physical activity recommendation for hypertension management: does healthcare provider advice make a difference? Ethnicity & disease. 2008;18:278–282. [PubMed]
42. Helping Patients Who Drink Too Much: A Clinician’s Guide: U.S. Department of Health and Human Services. National Institutes of Health National Institute on Alcohol Abuse and Alcoholism. 2005
43. Egan BM, Zhao Y, Axon RN. US trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008. JAMA. 2010;303:2043–2050. [PubMed]
44. Flack JM, Ferdinand KC, Nasser SA. Epidemiology of hypertension and cardiovascular disease in African Americans. J Clin Hypertens (Greenwich) 2003;5:5–11. [PubMed]
45. de Simone G, Devereux RB, Chinali M, Roman MJ, Best LG, Welty TK, Lee ET, Howard BV. for the Strong Heart Study I. Risk Factors for Arterial Hypertension in Adults With Initial Optimal Blood Pressure: The Strong Heart Study. Hypertension. 2006;47:162–167. [PubMed]
46. Haskell WL, Lee IM, Pate RR, Powell KE, Blair SN, Franklin BA, Macera CA, Heath GW, Thompson PD, Bauman A. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Circulation. 2007;116:1081–1093. [PubMed]
47. Liu K, Ruth KJ, Flack JM, Jones-Webb R, Burke G, Savage PJ, Hulley SB. Blood Pressure in Young Blacks and Whites: Relevance of Obesity and Lifestyle Factors in Determining Differences : The CARDIA Study. Circulation. 1996;93:60–66. [PubMed]
48. Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination Survey Examination Protocol. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2001–2006. National Center for Health Statistics (NCHS)
49. Briefel RR, Sempos CT, McDowell MA, Chien S, Alaimo K. Dietary methods research in the third National Health and Nutrition Examination Survey: underreporting of energy intake. Am J Clin Nutr. 1997;65:1203S–1209S. [PubMed]
50. Poslusna K, Ruprich J, de Vries JH, Jakubikova M, van't Veer P. Misreporting of energy and micronutrient intake estimated by food records and 24 hour recalls, control and adjustment methods in practice. Br J Nutr. 2009;101 Suppl 2:S73–S85. [PubMed]
51. Westerterp KR, Goris AH. Validity of the assessment of dietary intake: problems of misreporting. Curr Opin Clin Nutr Metab Care. 2002;5:489–493. [PubMed]
52. Newell SA, Girgis A, Sanson-Fisher RW, Savolainen NJ. The accuracy of self-reported health behaviors and risk factors relating to cancer and cardiovascular disease in the general population: a critical review. American Journal of Preventive Medicine. 1999;17:211–229. [PubMed]
53. Folsom AR, Cook TC, Sprafka JM, Burke GL, Norsted SW, Jacobs DR. Differences in leisure-time physical activity levels between blacks and whites in population-based samples: The Minnesota heart survey. Journal of Behavioral Medicine. 1991;14:1–9. [PubMed]
54. Kressin NR, Orner MB, Manze M, Glickman ME, Berlowitz D. Understanding Contributors to Racial Disparities in Blood Pressure Control. Circ Cardiovasc Qual Outcomes. 2010;3:173–180. [PMC free article] [PubMed]
55. Hicks LS, Fairchild DG, Horng MS, Orav EJ, Bates DW, Ayanian JZ. Determinants of JNC VI guideline adherence, intensity of drug therapy, and blood pressure control by race and ethnicity. Hypertension. 2004;44:429–434. [PubMed]
56. Hicks LS, Fairchild DG, Cook EF, Ayanian JZ. Association of region of residence and immigrant status with hypertension, renal failure, cardiovascular disease, and stroke, among African-American participants in the third National Health and Nutrition Examination Survey (NHANES III) Ethnicity & disease. 2003;13:316–323. [PubMed]