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Healthy People 2010 is the nation's health promotion and disease prevention agenda that has 2 primary goals: (1) to increase the quality and number of years of healthy life and (2) eliminate health disparities.1 During the past few decades, the overall health of the US population has greatly improved. These improvements have largely been due to public health initiatives, programs geared toward health promotion and disease prevention, medical and technologic advances, and increases in the number of health care providers.2,3 Unfortunately, the degree of health status improvement from preventable and treatable diseases has not been as significant among racial/ethnic minorities. In particular, the disparities seen in the burden of cardiovascular disease (CVD) and its related risk factors for African American women (AAW) is quite profound.

CVD Burden

  1. Top of page
  2. CVD Burden
  3. Obesity and the Metabolic Syndrome
  4. Focus on Prevention
  5. References

CVD continues to be the leading cause of death for adult men and women in the United States.4 There has been a consistent downward trend in mortality for men that has not been appreciated in women. AAW are 1.4 times more likely than white women (WW) to die from CVD.4 American Heart Association data from 2005 shows that the prevalence of CVD in AAW is 49% compared with 35% in WW.4 This includes coronary heart disease (7.8% vs 6.0%), high blood pressure (46.6% vs 31.9%), heart failure (3.3% vs 2.1%), and stroke (4.1% vs 2.7%).4 AAW shoulder a considerable amount of the burden for several of the known risks for CVD compared with WW, having a higher prevalence of both type II diabetes mellitus (DM) (13.2% vs 5.6%) and obesity (51.1% vs 30.7%).4 Unfortunately, data suggests that despite multiple educational tools similar to those outlined in Healthy People 2010, AAW are still less aware of their risk for heart disease because many still believe that cancer poses a greater risk of death.5

Obesity and the Metabolic Syndrome

  1. Top of page
  2. CVD Burden
  3. Obesity and the Metabolic Syndrome
  4. Focus on Prevention
  5. References

One of the leading health indicators or high priority focus areas for Healthy People 2010 is overweight (body mass index [BMI] ≥25 kg/m2) and obesity (BMI ≥30 kg/m2). Obesity has been recognized as a public health epidemic in the United States and increasingly so around the world.6 The association between obesity and CVD risk is well-known; prevention of obesity could decrease the risk associated with CVD and other health conditions such as high blood pressure and DM and thereby reduce the racial/ethnic disparities seen in these areas. The projected goal for Healthy People 2010 is to decrease obesity to <15%. Despite efforts of numerous initiatives, obesity rates continue to rise in all groups. The prevalence of overweight in AAW is 79.6% compared with 57.6% in WW; that of obesity is 51.1% compared with 30.7%. These numbers are reflected in an overall increase in obesity for the general adult population, from 23% to 32% based on National Health and Nutrition Examination Survey (NHANES) data from 1988–1994 compared with 2003–2004 data.6

As the prevalence of obesity increases, it is expected that the prevalence of insulin resistance and the metabolic syndrome (MS) will also increase. MS is a clustering of risk factors known to promote the development of coronary heart disease and DM. Although the exact mechanism of MS is not known, many investigators point to insulin resistance as the predisposing factor and suggest that insulin resistance is due to obesity or a genetic defect.7,8 The Third Report of the Adult Treatment Panel National Cholesterol Education Program (NCEP-ATP III)9 clinically defines MS by the presence of ≥3 of the following parameters: (1) abdominal obesity (waist circumference: >102 cm for men, >88 cm for women); (2) triglyceride levels ≥150 mg/dL; (3) high-density lipoprotein cholesterol (HDL-C) (men <40 mg/dL, women <50 mg/dL); (4) blood pressure ≥130/≥85 mm Hg; and (5) fasting glucose ≥100 mg/dL.10 MS affects approximately 22% of the adult US population and 45% of the US population aged 50 years and older.11 What is striking is that the prevalence of MS in AAW is lower than for other groups of women (20.9% compared with 22.9% for WW and 27.2% for Mexican American women).12 These numbers have varied among studies based on geographics, study population characteristics, definition of MS, and study time periods. Because AAW have a high prevalence of obesity, high blood pressure, and diabetes, it would be expected that the prevalence of MS in this population would be much higher. Interestingly, this has not been previously shown. In addition, the current definition of MS underestimates the risk in AAW. Although no single pathogenic mechanism has been identified as the cause of MS, a look at what is known about the pathogenesis may give some clues to the apparent disconnect between MS attributable risk and morbidity/mortality CVD data in AAW.

Unlike the World Health Organization definition of MS, the ATP-III does not require evidence of insulin resistance, which is believed by many investigators to be a major pathogenic factor. Instead, the ATP-III relies on the strength of the association between insulin and dyslipidemia (ie, high triglyceride levels and low HDL-C), maintaining that a separate maker for insulin resistance is not necessary.9 Unfortunately, several investigators have reported that the association between insulin resistance and lipids in AAW may be much weaker because African Americans (AAs) show differing patterns of dyslipidemia compared with other groups.13–15 Typically, triglyceride levels are lower and the higher HDL-C levels tend not be atheroprotective.16,17

A recent report from the Jackson Heart Study (JHS),18 a large AA population-based investigation of the predictors and outcomes of CVD and related disorders, addresses some of the discrepancies found in the literature regarding MS in AAs. The prevalence of MS was found to be 39.4% in the cohort ages 21 to 94 years. Age-adjusted prevalence among those 35 to 84 years was 44.8% for women, higher than corresponding national rates.18,19

Large percentages of participants in JHS were found to have elevated blood pressure levels and abdominal obesity but also low HDL-C concentrations (37.2%), which is contrary to previous reports. However, recent analysis of NHANES data from 1999–2000 showed a trend of increasing rates of low HDL-C.18,19 In JHS, reciprocal elevations of triglyceride levels were not seen as would be expected in the setting of lower HDL-C concentrations.18 The frequency of elevated glucose was also substantial.

JHS also showed a high prevalence of CVD, the odds of which were increased in the setting of MS. This suggests a higher attributable risk for MS in AAW. A similar association between MS and CVD death in women was previously shown in the San Antonio Heart Study,18,20 where the increased risk was attributed to a stronger association between DM and CVD. In JHS, the association appeared to be strongest between obesity and low HDL-C level; this may imply a sex-specific impact of obesity on glucose, lipids, and atherosclerosis.18,21

The relationship between obesity and CVD mortality in AAs is not as clear as the relationship seen with hypertension and DM. AAW are almost 3 times more likely to die from a complication related to hypertension than WW (40.9% vs 14.9%).22 Similarly, the death rate from diabetes for AAW is 2 times higher than for WW.4 Although the link between obesity and CVD morbidity has been established, the relationship between CVD mortality and obesity in AAs is much more difficult to characterize. Data have shown that the mortality rates for CVD by ethnicity are not parallel to the prevalence of obesity at the population level.23 There are also inconsistencies across datasets and in comparison with data for white populations regarding the within-population association of obesity with mortality in AAs.

For example, previous analysis of data from the Black Pooling Project24 has shown that obesity is associated with increased CVD mortality in WW but not in AAW. Subsequent analysis of the dataset looking at the effect of age on the association between BMI and CVD mortality again showed no associated increased risk in AAW, but a statistically significant association in older and younger WW. Similarly, other data estimating the difference between the number of years of life expected based on whether an individual were obese or not (designated years of life lost) showed lesser number of years of life lost in AAs across the spectrum of BMIs and age ranges when compared with whites.25 This means that the impact of obesity was lesser in AAs than whites in decreasing life expectancy, again an apparent paradox.

Therefore, these and other data suggest that the contribution of obesity to CVD mortality is very complex. The predictive value of obesity in relation to CVD mortality is probably lost given the high prevalence of obesity in AAW. It is likely that the association is an indirect one reflected through the burden obesity imposes on traditional cardiovascular risk factors. Even more so, the strong influence of other variables on obesity, such as lifestyle, quality of care, access to care, social constraints, and genetics, cannot be ignored.23

Focus on Prevention

  1. Top of page
  2. CVD Burden
  3. Obesity and the Metabolic Syndrome
  4. Focus on Prevention
  5. References

Clinical trial data suggest that lifestyle modifications and weight loss can be very effective in lowering blood pressure, preventing hypertension and DM, and thereby reducing CV risk. In the Diabetes Prevention Program26 where a large number of AAs were participants, it was clearly shown that lifestyle modifications and weight loss resulted in substantial reductions in diabetes risk. The effect of this intervention on cardiovascular risk is being evaluated in the Diabetes Prevention Program—Ongoing Study. Other trials like the Dietary Approaches to Stop Hypertension (DASH)27 and Premier28 studies have shown the benefit of modest degrees of dietary and lifestyle modifications in reducing hypertension-related risks in AA participants.

Healthy People 2010 outlines a strategy for decreasing health disparities centered around preventive measures.1 Controlling weight and preventing obesity in children and adults is a leading initiative. It is important to acknowledge that behavioral and dietary changes are often difficult to implement and even more difficult to maintain. Successful strategies must address cultural attitudes and perceptions regarding weight, exercise, diet, and body image.29 As health care professionals, we must aggressively promote CVD prevention and risk factor screening, evaluation, and treatment in populations at greatest risk.

References

  1. Top of page
  2. CVD Burden
  3. Obesity and the Metabolic Syndrome
  4. Focus on Prevention
  5. References
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    American Heart Association. Heart Disease and Stroke Statistics—2008 Update. Dallas, TX: American Heart Association; 2008.
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    Christian AH, Rosamond W, White AR, et al. Nine-year trends and racial and ethnic disparities in women's awareness of heart disease and stroke: an American Heart Association national study. J Women's Health. 2007;16(1):6881.
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    DeFronzo RA, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care. 1991;14:173194.
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    Haffner SM, D'Agostino R, Goff D, et al. LDL size in African Americans, Hispanics, and non-Hispanic whites: the insulin resistance atherosclerosis study. Arterioscler Thromb Vasc Biol. 1999;19(9):22342240.
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    Sumner AE, Finley KB, Genovese DJ, et al. Fasting triglyceride and the triglyceride-HDL cholesterol ratio are not markers of insulin resistance in African Americans. Arch Intern Med. 2005;165(12):13951400.
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    Taylor H, Liu J, Wilson G, et al. Distinct component profiles and high risk among African Americans with the metabolic syndrome: the Jackson Heart Study. Diabetes Care. 2008 Mar 10 [Epub ahead of print].
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    Ford ES. Prevalence of the metabolic syndrome in US populations. Endocrinol Metab Clin North Am. 2004;33:333350.
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    Hunt KJ, Resendez RG, Williams K, et al. National Cholesterol Education Program versus World Health Organization metabolic syndrome in relation to all-cause and cardiovascular cardiovascular mortality in the San Antonio Heart Study. Circulation. 2004;110:12511257.
  • 21
    Lonnqvist F, Thorne A, Large V, et al. Sex differences in visceral fat lipolysis and metabolic complications of obesity. Arterioscler Thromb Vasc Biol. 1997;17:14721480.
  • 22
    Thom T, Haase N, Rosamond W, et al. Heart Disease and Stroke Statistics—2006 Update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2006;113:e85e151.
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    Smith SC Jr, Clark LT, Cooper RS, et al. Discovering the full spectrum of cardiovascular disease, minority health summit 2003, report of the obesity, metabolic syndrome and hypertension writing group. Circulation. 2005;111:e134e139.
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    Abell JE, Egan BM, Wilson PW, et al. Age and race impact the association between BMI and CVD mortality in women. Public Health Rep. 2007;122(4):507512.
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    Fontaine KR, Redden DT, Wang C, et al. Years of life lost due to obesity. JAMA. 2003;289:187193.
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    Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention of metformin. N Engl J Med. 2002;346:393403.
  • 27
    Appel LJ, Moore TJ, Obarzanek E, et al; DASH Collaborative Research Group. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med. 1997;336:11171124.
  • 28
    Elmer PJ, Obarzanek E, Vollmer WM, et al; PREMIER Collaborative Research Group. Effects of comprehensive lifestyle modification on diet, weight, physical fitness, and blood pressure control: 18-month results of a randomized trial. Ann Intern Med. 2006;144:485495.
  • 29
    Boyington JE, Carter-Edwards L, Piehl M, et al. Cultural attitudes toward weight, diet, and physical activity among overweight African American girls. Prev Chronic Dis. 2008;5(2):A36.