Although progress has been made to understand the association between physiological and lifestyle behaviors with regard to obesity, ethnic differences in markers of obesity and pathways towards obesity remain somewhat unexplained. However, obesity remains a serious growing concern. This paper highlights ethnic differences in African Americans and Caucasians that may contribute to the higher prevalence of obesity among African Americans. Understanding ethnic differences in metabolic syndrome criteria, functioning of the hypothalamic pituitary adrenal axis, variations in glucocorticoid sensitivity and insulin resistance, and physical activity and cardiovascular fitness levels may help to inform practical clinical and public health interventions and reduce obesity disparities. 1. Introduction Overweight and obesity are chronic health illnesses affecting many children and adults in the United States [1, 2]. The health consequences of overweight and obesity are enormous, particularly the risk of developing chronic diseases such as hypertension, Type 2 diabetes mellitus (T2DM), and cardiovascular disease (CVD). Obesity disproportionately affects ethnic minorities, women and individuals from lower socioeconomic groups [3, 4]. In particular, African Americans (AAs) are disproportionately affected by obesity, diabetes, hypertension, and cardiovascular disease, and it is likely that a host of factors interact in complex, and yet unexplained, ways to contribute to these health disparities. The prevalence of overweight or obesity in African women (66%) is 1.4 times that in Caucasian (CA) women (47%) [5], and African American (AA) women may be at greatest risk for the health consequences of obesity and have an almost twofold greater risk of developing diabetes and experiencing hypertension at earlier ages; they also have significantly greater abdominal fat [6] than CA women. The objective of the present paper is to highlight selected ethnic differences associated with obesity by focusing on factors that contribute to obesity: metabolic Syndrome (MS) indicators, regulation of the hypothalamic pituitary adrenal (HPA) axis, glucocorticoid sensitivity (GS), insulin resistance (IR), and physical activity among AAs and Caucasians (CAs). 2. Metabolic Syndrome Metabolic Syndrome (MS) is a constellation of factors used globally for identifying individuals at greatest risk for developing CVD and T2DM [7]. This cluster of interrelated risk factors for CVD and T2DM [8, 9] include glucose intolerance (T2DM, impaired glucose tolerance, impaired fasting glycaemia, or insulin
References
[1]
K. M. Flegal, M. D. Carroll, C. L. Ogden, and L. R. Curtin, “Prevalence and trends in obesity among US adults, 1999–2008,” Journal of the American Medical Association, vol. 303, no. 3, pp. 235–241, 2010.
[2]
T. A. Wadden, K. D. Brownell, and G. D. Foster, “Obesity: responding to the global epidemic,” Journal of Consulting and Clinical Psychology, vol. 70, no. 3, pp. 510–525, 2002.
[3]
G. E. Duncan, S. D. Anton, R. L. Newton Jr., and M. G. Perri, “Comparison of perceived health to physiological measures of health in black and white women,” Preventive Medicine, vol. 36, no. 5, pp. 624–628, 2003.
[4]
D. K. Wilson, H. G. Lawman, M. Segal, and S. Chappell, “Neighborhood and parental supports for physical activity in minority adolescents,” American Journal of Preventive Medicine, vol. 41, no. 4, pp. 399–406, 2011.
[5]
R. L. Weinsier, G. R. Hunter, P. A. Zuckerman et al., “Energy expenditure and free-living physical activity in black and white women: comparison before and after weight loss,” The American Journal of Clinical Nutrition, vol. 71, no. 5, pp. 1138–1146, 2000.
[6]
T. V. Barreira, A. E. Staiano, D. M. Harrington, et al., “Anthropometric correlates of total body fat, abdominal adiposity, and cardiovascular disease risk factors in a biracial sample of men and women,” Mayo Clinic Proceedings, vol. 87, no. 5, pp. 452–460, 2012.
[7]
U. J. Ukegbu, D. C. Castillo, M. G. Knight et al., “Metabolic syndrome does not detect metabolic risk in African men living in the U.S.,” Diabetes Care, vol. 34, no. 10, pp. 2297–2299, 2011.
[8]
K. G. M. M. Alberti, R. H. Eckel, S. M. Grundy et al., “Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity,” Circulation, vol. 120, no. 16, pp. 1640–1645, 2009.
[9]
A. Rezaianzadeh, S. M. Namayandeh, and S. M. Sadr, “National cholesterol education program adult treatment panel III versus international diabetic federation definition of metabolic syndrome, which one is associated with diabetes mellitus and coronary artery disease?” International Journal of Preventive Medicine, vol. 3, no. 8, pp. 552–558, 2012.
[10]
R. H. Eckel, S. M. Grundy, and P. Z. Zimmet, “The metabolic syndrome,” The Lancet, vol. 365, no. 9468, pp. 1415–1428, 2005.
[11]
S. M. Grundy, J. I. Cleeman, S. R. Daniels et al., “Diagnosis and management of the metabolic syndrome: an American heart association/national heart, lung, and blood institute scientific statement,” Circulation, vol. 112, no. 17, pp. 2735–2752, 2005.
[12]
A. E. Sumner and C. C. Cowie, “Ethnic differences in the ability of triglyceride levels to identify insulin resistance,” Atherosclerosis, vol. 196, no. 2, pp. 696–703, 2008.
[13]
S. A. Zeno, P. A. Deuster, J. L. Davis, S. J. Kim-Dorner, A. T. Remaley, and M. Poth, “Diagnostic criteria for metabolic syndrome: Caucasians versus African-Americans,” Metabolic Syndrome and Related Disorders, vol. 8, no. 2, pp. 149–155, 2010.
[14]
T. Gaillard, D. Schuster, and K. Osei, “Metabolic syndrome in black people of the African diaspora: the paradox of current classification, definition and criteria,” Ethnicity & Disease, vol. 19, no. 2, supplement 2, pp. 1–7, 2009.
[15]
S. J. Kim-Dorner, P. A. Deuster, S. A. Zeno, A. T. Remaley, and M. Poth, “Should triglycerides and the triglycerides to high-density lipoprotein cholesterol ratio be used as surrogates for insulin resistance?” Metabolism, vol. 59, no. 2, pp. 299–304, 2010.
[16]
S. X. Lin, M. Carnethon, M. Szklo, and A. Bertoni, “Racial/ethnic differences in the association of triglycerides with other metabolic syndrome components: the multi-ethnic study of atherosclerosis,” Metabolic Syndrome and Related Disorders, vol. 9, no. 1, pp. 35–40, 2011.
[17]
A. E. Sumner, J. Zhou, A. Doumatey et al., “Low HDL-cholesterol with normal triglyceride levels is the most common lipid pattern in West Africans and African Americans with metabolic syndrome: implications for cardiovascular disease prevention,” CVD Prevention and Control, vol. 5, no. 3, pp. 75–80, 2010.
[18]
B. Frazier, C. W. Hsiao, P. Deuster, and M. Poth, “African Americans and Caucasian Americans: differences in glucocorticoid-induced insulin resistance,” Hormone and Metabolic Research, vol. 42, no. 12, pp. 887–891, 2010.
[19]
L. Razzouk and P. Muntner, “Ethnic, gender, and age-related differences in patients with the metabolic syndrome,” Current Hypertension Reports, vol. 11, no. 2, pp. 127–132, 2009.
[20]
S. A. Zeno, S. J. Kim-Dorner, P. A. Deuster, J. L. Davis, A. T. Remaley, and M. Poth, “Cardiovascular fitness and risk factors of healthy African Americans and Caucasians,” Journal of the National Medical Association, vol. 102, no. 1, pp. 28–35, 2010.
[21]
M. Feinstein, H. Ning, J. Kang, A. Bertoni, M. Carnethon, and D. M. Lloyd-Jones, “Racial differences in risks for first cardiovascular events and noncardiovascular death: the atherosclerosis risk in communities study, the cardiovascular health study, and the multi-ethnic study of atherosclerosis,” Circulation, vol. 126, no. 1, pp. 50–59, 2012.
[22]
E. S. Ford, C. Li, and G. Zhao, “Prevalence and correlates of metabolic syndrome based on a harmonious definition among adults in the US,” Journal of Diabetes, vol. 2, no. 3, pp. 180–193, 2010.
[23]
Y. Wang and Q. J. Wang, “The prevalence of prehypertension and hypertension among US adults according to the new joint national committee guidelines: new challenges of the old problem,” Archives of Internal Medicine, vol. 164, no. 19, pp. 2126–2134, 2004.
[24]
S. J. Kim-Dorner, C. O. Simpson-McKenzie, M. Poth, and P. A. Deuster, “Psychological and physiological correlates of insulin resistance at fasting and in response to a meal in African Americans and whites,” Ethnicity & Disease, vol. 19, no. 2, pp. 104–110, 2009.
[25]
S. S. Yu, D. C. Castillo, A. B. Courville, and A. E. Sumner, “The triglyceride paradox in people of African descent,” Metabolic Syndrome and Related Disorders, vol. 10, no. 2, pp. 77–82, 2012.
[26]
M. J. Barber, L. M. Mangravite, C. L. Hyde et al., “Genome-wide association of lipid-lowering response to statins in combined study populations,” PloS ONE, vol. 5, no. 3, Article ID e9763, 2010.
[27]
S. M. Grundy, J. I. Cleeman, S. R. Daniels et al., “Diagnosis and management of the metabolic syndrome. An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Executive summary,” Cardiology in Review, vol. 13, no. 6, pp. 322–327, 2005.
[28]
S. Yusuf, S. Hawken, S. ？unpuu et al., “Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study,” The Lancet, vol. 366, no. 9497, pp. 1640–1649, 2005.
[29]
J. F. Carroll, A. L. Chiapa, M. Rodriquez et al., “Visceral fat, waist circumference, and BMI: impact of race/ethnicity,” Obesity, vol. 16, no. 3, pp. 600–607, 2008.
[30]
P. T. Katzmarzyk, G. A. Bray, F. L. Greenway et al., “Ethnic-specific BMI and waist circumference thresholds,” Obesity, vol. 19, no. 6, pp. 1272–1278, 2011.
[31]
P. Deurenberg and M. Deurenberg-Yap, “Differences in body-composition assumptions across ethnic groups: practical consequences,” Current Opinion in Clinical Nutrition and Metabolic Care, vol. 4, no. 5, pp. 377–383, 2001.
[32]
A. E. Sumner, L. K. Micklesfield, M. Ricks et al., “Waist circumference, BMI, and visceral adipose tissue in white women and women of African descent,” Obesity, vol. 19, no. 3, pp. 671–674, 2011.
[33]
S. Agarwal, D. R. Jacobs Jr., D. Vaidya, et al., “Metabolic syndrome derived from principal component analysis and incident cardiovascular events: the multi ethnic study of atherosclerosis (MESA) and health, aging, and body composition (Health ABC),” Cardiology Research and Practice, vol. 2012, Article ID 919425, 9 pages, 2012.
[34]
D. Martins, N. Tareen, G. Ogedegbe, D. Pan, and K. Norris, “The relative risk of cardiovascular death among racial and ethnic minorities with metabolic syndrome: data from the NHANES-II mortality follow-up,” Journal of the National Medical Association, vol. 100, no. 5, pp. 565–571, 2008.
[35]
A. E. Staiano, B. A. Reeder, S. Elliott, et al., “Body mass index versus waist circumference as predictors of mortality in Canadian adults,” International Journal of Obesity, vol. 36, no. 11, pp. 1450–1454, 2005.
[36]
W. Shen, M. Punyanitya, J. Chen, et al., “Waist circumference correlates with metabolic syndrome indicators better than percentage fat,” Obesity, vol. 14, no. 4, pp. 727–736, 2006.
[37]
P. A. Deuster, S. J. Kim-Dorner, A. T. Remaley, and M. Poth, “Allostatic load and health status of African Americans and whites,” American Journal of Health Behavior, vol. 35, no. 6, pp. 641–653, 2011.
[38]
C. Giannini, N. Santoro, S. Caprio, et al., “The triglyceride-to-HDL cholesterol ratio: association with insulin resistance in obese youths of different ethnic backgrounds,” Diabetes Care, vol. 34, no. 8, pp. 1869–1874, 2011.
[39]
S. Arslanian, “Insulin secretion and sensitivity in healthy African-American vs American white children,” Clinical Pediatrics, vol. 37, no. 2, pp. 81–88, 1998.
[40]
E. Ravussin and S. R. Smith, “Increased fat intake, impaired fat oxidation, and failure of fat cell proliferation result in ectopic fat storage, insulin resistance, and type 2 diabetes mellitus,” Annals of the New York Academy of Sciences, vol. 967, pp. 363–378, 2002.
[41]
M. D. DeBoer, M. J. Gurka, and A. E. Sumner, “Diagnosis of the metabolic syndrome is associated with disproportionately high levels of high-sensitivity C-reactive protein in non-hispanic black adolescents: an analysis of NHANES 1999–2008,” Diabetes Care, vol. 34, no. 3, pp. 734–740, 2011.
[42]
A. Kelley-Hedgepeth, D. M. Lloyd-Jones, A. Colvin et al., “Ethnic differences in C-reactive protein concentrations,” Clinical Chemistry, vol. 54, no. 6, pp. 1027–1037, 2008.
[43]
G. P. Chrousos and P. W. Gold, “The concepts of stress and stress system disorders: overview of physical and behavioral homeostasis,” Journal of the American Medical Association, vol. 267, no. 9, pp. 1244–1252, 1992.
[44]
J. P. Herman and W. E. Cullinan, “Neurocircuitry of stress: central control of the hypothalamo-pituitary-adrenocortical axis,” Trends in Neurosciences, vol. 20, no. 2, pp. 78–84, 1997.
[45]
B. M. Kudielka and S. Wüst, “Human models in acute and chronic stress: assessing determinants of individual hypothalamus-pituitary-adrenal axis activity and reactivity,” Stress, vol. 13, no. 1, pp. 1–14, 2010.
[46]
R. C. Hickner, J. Privette, K. McIver, and H. Barakat, “Fatty acid oxidation in African-American and Caucasian women during physical activity,” Journal of Applied Physiology, vol. 90, no. 6, pp. 2319–2324, 2001.
[47]
R. Pasquali, “The hypothalamic-pituitary-adrenal axis and sex hormones in chronic stress and obesity: pathophysiological and clinical aspects,” Annals of the New York Academy of Sciences, vol. 1264, no. 1, pp. 20–35, 2012.
[48]
P. Bj？rntorp and R. Rosmond, “Obesity and cortisol,” Nutrition, vol. 16, no. 10, pp. 924–936, 2000.
[49]
M. S. Johnson, R. Figueroa-Colon, S. L. Herd et al., “Aerobic fitness, not energy expenditure, influences subsequent increase in adiposity in black and white children,” Pediatrics, vol. 106, no. 4, p. e50, 2000.
[50]
S. Cohen, J. E. Schwartz, E. Epel, C. Kirschbaum, S. Sidney, and T. Seeman, “Socioeconomic status, race, and diurnal cortisol decline in the Coronary Artery Risk Development in Young Adults (CARDIA) study,” Psychosomatic Medicine, vol. 68, no. 1, pp. 41–50, 2006.
[51]
R. A. Karb, M. R. Elliott, J. B. Dowd, and J. D. Morenoff, “Neighborhood-level stressors, social support, and diurnal patterns of cortisol: the Chicago community adult health study,” Social Science & Medicine, vol. 75, no. 6, pp. 1038–1047, 1982.
[52]
A. S. DeSantis, E. K. Adam, L. D. Doane, S. Mineka, R. E. Zinbarg, and M. G. Craske, “Racial/ethnic differences in cortisol diurnal rhythms in a community sample of adolescents,” Journal of Adolescent Health, vol. 41, no. 1, pp. 3–13, 2007.
[53]
P. H. Black, “The inflammatory response is an integral part of the stress response: implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X,” Brain, Behavior, and Immunity, vol. 17, no. 5, pp. 350–364, 2003.
[54]
M. S. Kopp and J. Réthelyi, “Where psychology meets physiology: chronic stress and premature mortality—the Central-Eastern European health paradox,” Brain Research Bulletin, vol. 62, no. 5, pp. 351–367, 2004.
[55]
R. Rosmond, “Role of stress in the pathogenesis of the metabolic syndrome,” Psychoneuroendocrinology, vol. 30, no. 1, pp. 1–10, 2005.
[56]
M. F. Dallman, N. C. Pecoraro, S. E. La Fleur et al., “Glucocorticoids, chronic stress, and obesity,” Progress in Brain Research, vol. 153, pp. 75–105, 2006.
[57]
E. A. Lucassen and G. Cizza, “The hypothalamic-pituitary-adrenal axis, obesity, and chronic stress exposure: sleep and the HPA axis in obesity,” Current Obesity Reports, vol. 1, no. 4, pp. 208–215, 2012.
[58]
G. E. Miller, E. Chen, and E. S. Zhou, “If it goes up, must it come down? chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans,” Psychological Bulletin, vol. 133, no. 1, pp. 25–45, 2007.
[59]
M. N. Silverman and E. M. Sternberg, “Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction,” Annals of the New York Academy of Sciences, vol. 1261, pp. 55–63, 2012.
[60]
A. A. Syed and J. U. Weaver, “Glucocorticoid sensitivity: the hypothalamic-pituitary-adrenal-tissue axis,” Obesity Research, vol. 13, no. 7, pp. 1131–1133, 2005.
[61]
A. Islam, Y. Chen, M. Poth, Z. P. Smith, and P. A. Deuster, “Glucocorticoid receptor density correlates with health risk factors and insulin resistance in Caucasian and African American subjects,” Experimental and Clinical Endocrinology & Diabetes, vol. 120, no. 8, pp. 477–481, 2012.
[62]
C. Binnert, S. Ruchat, N. Nicod, and L. Tappy, “Dexamethasone-induced insulin resistance shows no gender difference in healthy humans,” Diabetes & Metabolism, vol. 30, no. 4, pp. 321–326, 2004.
[63]
N. Nicod, V. Giusti, C. Besse, and L. Tappy, “Metabolic adaptations to dexamethasone-induced insulin resistance in healthy volunteers,” Obesity Research, vol. 11, no. 5, pp. 625–631, 2003.
[64]
D. H. van Raalte, K. A. Kwa, R. E. van Genugten, et al., “Islet-cell dysfunction induced by glucocorticoid treatment: potential role for altered sympathovagal balance?” Metabolism: Clinical and Experimental. In press.
[65]
S. S. Fajans and J. W. Conn, “An approach to the prediction of diabetes mellitus by modification of the glucose tolerance test with cortisone,” Diabetes, vol. 3, no. 4, pp. 296–302, 1954.
[66]
J. E. Henriksen, F. Alford, G. M. Ward, and H. Beck-Nielsen, “Risk and mechanism of dexamethasone-induced deterioration of glucose tolerance in non-diabetic first-degree relatives of NIDDM patients,” Diabetologia, vol. 40, no. 12, pp. 1439–1448, 1997.
[67]
P. Bj？rntorp, G. Holm, and R. Rosmond, “Hypothalamic arousal, insulin resistance and type 2 diabetes mellitus,” Diabetic Medicine, vol. 16, no. 5, pp. 373–383, 1999.
[68]
V. Vicennati and R. Pasquali, “Abnormalities of the hypothalamic-pituitary-adrenal axis in nondepressed women with abdominal obesity and relations with insulin resistance: evidence for a central and a peripheral alteration,” The Journal of Clinical Endocrinology and Metabolism, vol. 85, no. 11, pp. 4093–4098, 2000.
[69]
R. Pasquali, L. Gagliardi, V. Vicennati et al., “ACTH and cortisol response to combined corticotropin releasing hormone-arginine vasopressin stimulation in obese males and its relationship to body weight, fat distribution and parameters of the metabolic syndrome,” International Journal of Obesity and Related Metabolic Disorders, vol. 23, no. 4, pp. 419–424, 1999.
[70]
L. P. Palaniappan, M. R. Carnethon, and S. P. Fortmann, “Heterogeneity in the relationship between ethnicity, BMI, and fasting insulin,” Diabetes Care, vol. 25, no. 8, pp. 1351–1357, 2002.
[71]
A. C. Ellis, J. A. Alvarez, W. M. Granger, F. Ovalle, and B. A. Gower, “Ethnic differences in glucose disposal, hepatic insulin sensitivity, and endogenous glucose production among African American and European American women,” Metabolism, vol. 61, no. 5, pp. 634–640, 2012.
[72]
C. J. Tsai and E. L. Giovannucci, “Hyperinsulinemia, insulin resistance, vitamin D, and colorectal cancer among whites and African Americans,” Digestive Diseases and Sciences, vol. 57, no. 10, pp. 2497–2503, 2012.
[73]
S. A. Arslanian, R. Saad, V. Lewy, K. Danadian, and J. Janosky, “Hyperinsulinemia in African-American children: decreased insulin clearance and increased insulin secretion and its relationship to insulin sensitivity,” Diabetes, vol. 51, no. 10, pp. 3014–3019, 2002.
[74]
J. White and R. Jago, “Prospective associations between physical activity and obesity among adolescent girls: racial differences and implications for prevention,” Archives of Pediatrics & Adolescent Medicine, vol. 166, no. 6, pp. 522–527, 2012.
[75]
C. J. Lavie, T. Kuruvanka, R. V. Milani, A. Prasad, and H. O. Ventura, “Exercise capacity in adult African-American referred for exercise stress testing: is fitness affected by race?” Chest, vol. 126, no. 6, pp. 1962–1968, 2004.
[76]
H. W. Kohl III, C. L. Craig, E. V. Lambert, et al., “The pandemic of physical inactivity: global action for public health,” The Lancet, vol. 380, no. 9838, pp. 294–305, 2012.
[77]
G. R. Button, P. D. Martin, M. A. Welsch, and P. J. Brantley, “Promoting physical activity for low-income minority women in primary care,” American Journal of Health Behavior, vol. 31, no. 6, pp. 622–631, 2007.
[78]
J. C. Lovejoy, C. M. Champagne, S. R. Smith, L. de Jonge, and H. Xie, “Ethnic differences in dietary intakes, physical activity, and energy expenditure in middle-aged, premenopausal women: the healthy transitions study,” American Journal of Clinical Nutrition, vol. 74, no. 1, pp. 90–95, 2001.
[79]
S. Lee and S. A. Arslanian, “Fat oxidation in black and white youth: a metabolic phenotype potentially predisposing black girls to obesity,” Journal of Clinical Endocrinology and Metabolism, vol. 93, no. 11, pp. 4547–4551, 2008.
[80]
H. K. Kuo, C. J. Yen, J. H. Chen, Y. H. Yu, and J. F. Bean, “Association of cardiorespiratory fitness and levels of C-reactive protein: data from the National Health and Nutrition Examination Survey 1999–2002,” International Journal of Cardiology, vol. 114, no. 1, pp. 28–33, 2007.
[81]
T. Naidoo, K. Konkol, B. Biccard, K. Dudose, and A. J. McKune, “Elevated salivary C-reactive protein predicted by low cardio-respiratory fitness and being overweight in African children,” Cardiovascular Journal of Africa, vol. 23, no. 9, pp. 501–506, 2012.
[82]
R. V. Brown, B. G. Kral, L. R. Yanek, et al., “Ethnic-specific determinants of exercise capacity in a healthy high-risk population,” Medicine and Science in Sports and Exercise, vol. 44, no. 6, pp. 1150–1156, 2012.
[83]
A. L. Willig, G. R. Hunter, K. Casazza, D. C. Heimburger, T. M. Beasley, and J. R. Fernandez, “Body fat and racial genetic admixture are associated with aerobic fitness levels in a multiethnic pediatric population,” Obesity, vol. 19, no. 11, pp. 2222–2227, 2011.
[84]
T. R. Gaillard, W. M. Sherman, S. T. Devor, T. E. Kirby, and K. Osei, “Importance of aerobic fitness in cardiovascular risks in sedentary overweight and obese African-American women,” Nursing Research, vol. 56, no. 6, pp. 407–415, 2007.
[85]
T. S. Church, C. E. Barlow, C. P. Earnest, J. B. Kampert, E. L. Priest, and S. N. Blair, “Associations between cardiorespiratory fitness and C-reactive protein in men,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 22, no. 11, pp. 1869–1876, 2002.
[86]
B. Gutin, R. A. Harris, C. A. Howe, M. H. Johnson, H. Zhu, and Y. Dong, “Cardiometabolic biomarkers in young black girls: relations to body fatness and aerobic fitness, and effects of a randomized physical activity trial,” International Journal of Pediatrics, vol. 2011, Article ID 219268, 7 pages, 2011.
[87]
R. R. Wing, R. F. Hamman, G. A. Bray et al., “Achieving weight and activity goals among diabetes prevention program lifestyle participants,” Obesity Research, vol. 12, no. 9, pp. 1426–1434, 2004.
[88]
Prevention CfDCa, Obesity Still a major problem, 2006.
