South Asians are at higher risk than White Caucasians for the development of obesity and obesity-related non-communicable diseases (OR-NCDs), including insulin resistance, the metabolic syndrome, type 2 diabetes mellitus (T2DM) and coronary heart disease (CHD). Rapid nutrition and lifestyle transitions have contributed to acceleration of OR-NCDs in South Asians. Differences in determinants and associated factors for OR-NCDs between South Asians and White Caucasians include body phenotype (high body fat, high truncal, subcutaneous and intra-abdominal fat, and low muscle mass), biochemical parameters (hyperinsulinemia, hyperglycemia, dyslipidemia, hyperleptinemia, low levels of adiponectin and high levels of C-reactive protein), procoagulant state and endothelial dysfunction. Higher prevalence, earlier onset and increased complications of T2DM and CHD are often seen at lower levels of body mass index (BMI) and waist circumference (WC) in South Asians than White Caucasians. In view of these data, lower cut-offs for obesity and abdominal obesity have been advocated for Asian Indians (BMI; overweight >23 to 24.9 kg m−2 and obesity ⩾25 kg m−2; and WC; men ⩾ 90 cm and women ⩾80 cm, respectively). Imbalanced nutrition, physical inactivity, perinatal adverse events and genetic differences are also important contributory factors. Other differences between South Asians and White Caucasians include lower disease awareness and health-seeking behavior, delayed diagnosis due to atypical presentation and language barriers, and religious and sociocultural factors. All these factors result in poorer prevention, less aggressive therapy, poorer response to medical and surgical interventions, and higher morbidity and mortality in the former. Finally, differences in response to pharmacological agents may exist between South Asians and White Caucasians, although these have been inadequately studied. In view of these data, prevention and management strategies should be more aggressive for South Asians for more positive health outcomes. Finally, lower cut-offs of obesity and abdominal obesity for South Asians are expected to help physicians in better and more effective prevention of OR-NCDs.
South Asian countries are experiencing a rapid increase in obesity-related non-communicable diseases (OR-NCDs), including type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia and coronary heart disease (CHD).1, 2, 3, 4 Insulin resistance and clustering of proatherogenic, cardiovascular risk factors (the metabolic syndrome) are frequently seen in South Asians, even at a young age.5, 6, 7 Increasing trend of obesity, both in adults and children, is directly responsible for rapid increase in NCDs.7, 8, 9, 10, 11, 12
It has increasingly become apparent that South Asians have a higher risk of NCDs compared with White Caucasians, which may be contributed by a number of factors, discussed subsequently.13, 14, 15, 16 Early onset and heightened risk of OR-NCDs in South Asians as compared with White Caucasians have important implications for prevention and therapy. An understanding of the different mechanisms and factors responsible for increased susceptibility and different outcomes of OR-NCDs would give physicians and scientists a better insight in research and management of these chronic diseases in South Asians.8, 11 This would also be in line with the global strategy of WHO (World Health Organization) to reduce the burden of NCDs through integrated prevention/control of risk factors at individual, family, community and population levels.17
In this review, we attempt to analyze the evidence, possible mechanisms and determinants responsible for increased tendency of OR-NCDs, as well as discuss management issues, in South Asians, as compared with White Caucasians, and also other ethnic groups.
Definition of ‘White Caucasians’ and ‘South Asians’
Natives of first or subsequent generation immigrants originating from the Indian subcontinent (India, Pakistan, Bangladesh, Nepal and Sri Lanka) are referred to as ‘South Asians’. For this ethnic group, ‘Indo-Asians’ has also been used by various authors. ‘White Caucasians’ (henceforth referred as ‘Whites’ in the text) are defined as native Europeans/European immigrants, as well as indigenous White individuals in any other country. However, some studies have not referred ‘Caucasians’ as Whites (though probably implied), and the term ‘Caucasians’ has been used as such there. The term ‘Europeans’ has been retained wherever referred to in the original text.
Methodology for literature search
The literature search has been performed using the key words ‘obesity, insulin resistance, diabetes, hypertension, the metabolic syndrome, cardiovascular risk, coronary artery disease, Asian Indians, South Asians, Indo-Asians, Whites, Caucasians, White Caucasians and Europeans’ from medical search engine Pubmed (National Library of Medicine, Bethesda, MD, USA) from 1966 to December 2009. Manual search for other important references, and medical databases were also performed. Well-designed studies and those published in high impact journals were given preference for citation.
Increasing OR-NCDs in South Asians: lifestyle-driven and multi-factorial origin
Increasing OR-NCDs, including T2DM, hypertension, dyslipidemia and CHD, are seen in urban and even rural South Asian populations due to several reasons, such as increasing urbanization, rural-to-urban migration, mechanization and increased life expectancy (‘epidemiological transition’), ‘westernized lifestyle’ (high carbohydrate, high-fat, low-fiber diet with decreasing trends in physical activity; ‘nutrition and lifestyle transitions’).11, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28
Increase in T2DM, hypertension and CHD in South Asians
In 2000, 44% of the burden of disease in South Asia measured in disability-adjusted life years lost was attributed to NCDs, and these figures are expected to rise, with cardiovascular disease (CVD) being a major contributor to premature mortality and morbidity.17 At present, India has highest global number of patients with diabetes, which is estimated to be 50.8 million in 2010 and 79.4 million in 2030.29, 30, 31, 32, 33 Increasing trend in Asian Indians living in India is more apparent in urban populations (exponential trend R2=0.744) than rural populations (R2=00.289).34 Although the prevalence of diabetes was reported to be 12–14% in urban India, the rural population showed a relatively lower prevalence of 4–5% in 2005–06.34 Neighboring South Asian countries also show a high prevalence of diabetes: Pakistan (8–10% in urban population and 2–10% in rural population),35, 36 Bangladesh (7–9% in urban population),37 Sri Lanka (13–14% in urban areas)38, 39 and Nepal (nearly 19% in urban areas).40 Furthermore, a meta-analysis has shown significant increase in hypertension in India in both urban and rural areas.41 Other South Asian countries also show high prevalence of hypertension: 19% in Pakistani adults (⩾15 years),42 and 19% in 2005 in Sri Lanka.39 It is projected that by 2020 India will have more individuals with CVD than any other region in the world.43 With an estimated 61 million cases in 2015, mortality attributed to CHD in India is expected to rise by 103.1% in men and 90% in women from 1985 to 2015 (approximately one-third of the total mortality).44, 45, 46 Nearly 22% of 1.4 million deaths in Pakistan (2005); 21% of 0.24 million deaths in Nepal (2002); 23% of 1.1 million deaths in Bangladesh (2002) and 34% of 0.15 million deaths in Sri Lanka (2002) were attributed to CVD.47, 48, 49, 50
Obesity and body composition
Prevalence of obesity in South Asian countries is increasing in both urban and in rural areas.7, 11, 12, 27, 28 In urban India, data show a prevalence of 10 and 15.1% (2003);25 20.8 and 32.3% (2004);51 and 43.2 and 47.4% (2007) in men and women, respectively.52 Interestingly, a high prevalence has been reported in economically disadvantaged adults residing in urban slums (14%),22 specifically in postmenopausal women (28%).53 Increase has also been reported in rural areas: from 8% reported in 199754 to 32.4% in men and 41.4% in women in 2007.55 Of concern, childhood obesity is also increasing: from 16% in 2002 to about 24% in 2006 in North India,12 and from 4.9% in 2003 to 6.6% in 2005 in South India.56 Other South Asian countries show similar increasing trend in obesity: 20.3% in men and 36.5% in women (2005) in Sri Lanka39 in contrast to earlier prevalence reported between 15 and 18% (1996).57 It is to be noted that different investigators have used different criteria for diagnosis of obesity; most recent studies have used lower cut-offs for South Asians,11, 27, 28 which may also increase prevalence rates.
BMI and body fat: relationship and definitions
By measurement of body mass index (BMI, a ratio of height and weight), it is not possible to distinguish between fat and fat-free mass.58 Several investigators have shown that BMI systematically underestimated percent body fat in South Asians.58, 59, 60, 61 Asian Indians in Singapore showed lower BMI (∼3 kg m−2) than other ethnic groups at any given percent body fat.24, 62 Furthermore, BMI did not give accurate estimate of body fat distribution, and in particular, significantly underestimated visceral adipose tissue in non-European populations.63 In a recent Consensus Statement for Asian Indians, overweight is defined as BMI between 23 and 24.9 kg m−2 and obesity as ⩾25 kg m−2, values lower than internationally accepted cut-offs (overweight 25–29.9 kg m−2 and obesity ⩾30 kg m−2) (Table 1).64
High prevalence of abdominal obesity is characteristic of South Asians, even at BMI levels <25 kg m−2 and is seen at a young age.14, 20, 22, 24, 65, 66, 67 Both migrant and British-born South Asians had higher waist-to-hip circumference ratio than the Italian/British populations.68 A study on migrant Asian Indians in the United States of America showed that waist circumference (WC) of South Asians was 10 cm lower than Whites with similar percent body fat.69 Similar to BMI, because of higher morbidities seen at lower level of WC in Asian Indians, cut-offs for diagnosis of abdominal obesity have been advocated as ⩾90 and ⩾80 cm, as opposed to international cut-offs of ⩾102 and ⩾88 cm for men and women, respectively (Table 1).64, 70
Truncal and abdominal adipose tissue depots
Overall, South Asians have more fat in various abdominal fat depots (Table 2). In a comparative study of Asian Indians vs Whites of European origin in the United States of America, for similar value of BMI, migrant Asian Indians had significantly greater total abdominal fat and intra-abdominal adipose tissue.71 Some investigators have reported that truncal subcutaneous (SC) adipose tissue (measured by subscapular and suprailiac skinfolds and by abdominal magnetic resonance imaging) is thicker in South Asians than in Whites72, 73, 74, 75 and correlates with the metabolic syndrome.76
Fat deposition in unusual sites
‘Ectopic fat’ (intramyocellular, hepatic and more recently myocardial lipids) represents the deposition of triglycerides within cells of non-adipose tissues, such as liver, muscles and so on. These sites usually contain only a small amount of fat, but recent data have shown that such ‘ectopic’ adipose tissue deposition could potentially disrupt glucose–insulin metabolism. Increasing evidence shows causal relationships between hepatic steatosis (without significant alcohol intake; non-alcoholic fatty liver disease, NAFLD) and hepatic insulin resistance, the metabolic syndrome and even CVD.77, 78, 79 In a recent case–control study, we have reported that urban Asian Indians with NAFLD had significantly higher fasting hyperinsulinemia, the metabolic syndrome and glucose intolerance than those without NAFLD.80 Furthermore, we also showed that normoglycemic, normolipidemic and normotensive subjects with NAFLD had significant derangements of hepatic gluconeogenesis pathway as assessed by 31phosphorous magnetic resonance spectroscopy (31PMRS).81 In an important comparative study in healthy, lean (mean BMI; 21–23 kg m−2) Asian Indians and Whites in the United States of America, hepatic triglycerides content, assessed by proton MRS, was two-fold higher in former (1.94 vs 0.75%, respectively; P<0.001). These authors further showed that increased hepatic triglyceride concentrations in Asian Indians was associated with higher insulin resistance (Table 3), plasma interleukin-6 (1.60 vs 0.78 pg ml−1, respectively; P<0.001), plasma leptin (4.7 vs 2.4 ng ml−1, respectively; P<0.001) and lower adiponectin (6.2 vs 7.3 μg ml−1, respectively; P=0.02) concentrations than Whites.82 These preliminary data suggest that Asian Indians appear to be predisposed to develop hepatic steatosis, associated with hepatic insulin resistance and increased levels of proinflammatory cytokines.82 Interestingly, the prevalence of NAFLD in urban India parallels prevalence of the metabolic syndrome in India.83
Intramyocellular triglyceride deposition, mostly assessed in the soleus muscle, is a potential marker for insulin resistance as shown by the studies carried out in Whites.84, 85 Comparative data show that intramyocellular triglyceride content was higher in Asian Indian men compared with Whites (1.03 vs 0.74%; P=0.001),82 but correlation of intramyocellular triglyceride with percent body fat, waist-to-hip circumference ratio and insulin sensitivity was shown in Europeans, but not in South Asians.86, 87, 88, 89
Anecdotal data suggest that some previously untested phenotypic markers may predict insulin resistance, the metabolic syndrome and even T2DM in Asian Indians. According to our recent study, the presence of excess dorso-cervical fat (mild ‘buffalo hump’ termed as ‘dorso-cervical lipo-hypertrophy’) and excess fat deposition under the chin (‘double chin’) signify heightened risk for the metabolic syndrome in urban Asian Indians, and may be used as novel phenotypic markers.90 Interestingly, ‘buffalo hump’ is a prevalent condition (28.5%) seen in obese NAFLD patients in the United States of America.91 Excess skin and fatty tissues beneath the jaw lead to a ‘double chin’, often seen in obese individuals and is reported to be a significant predictor of diabetes in patients of familial partial lipodystrophy.92
Subcutaneous adipocyte size
Some studies show that increased SC abdominal adipocyte size independently predicts insulin resistance and T2DM. Weyer et al.93 have showed that mean adipocyte size was 11 and 19% higher in subjects with impaired glucose tolerance and T2DM, respectively, as compared with normoglycemic individuals (P<0.001), independent of insulin resistance.93 Furthermore, in normal subjects, 33% of whom developed diabetes, enlarged mean SC abdominal adipocyte size, but not high percent body fat, was an independent predictor of diabetes.93 Interestingly, histological studies of SC adipose tissue have shown South Asians to have larger adipocytes as compared with Caucasians (3491 vs 1648 μm2, respectively; P=0.0001), at comparable levels of total body fat, and comparable intra-abdominal fat and SC abdominal fat (Figure 1). In this study, increased adipocyte size in Asian Indians was inversely correlated to glucose disposal rate (r=−0.57; P=0.0008) and plasma adiponectin concentrations (r=−0.71; P<0.0001).69 These interesting data need further investigation.
Skeletal muscle mass
Whereas body fat is higher, skeletal muscle mass is lower in South Asians than in Whites, particularly so in women.72, 94, 95 Asian Indian males have less muscle mass in the lower extremity than Swedish males.74 Recent study by Unni et al.96 showed that relative increase in BMI and reduced muscle mass were associated with reduced insulin sensitivity in lean Asian Indian men.96 It is possible that low muscle mass in relation to excess adiposity in Asian Indians may have an important role in pathogenesis of insulin resistance and T2DM; however, more studies are needed.
Earlier onset and increased complications of OR-NCDs in South Asians
The following section summarizes the differences (qualitatively and sometimes quantitatively) in clinical and metabolic profiles of OR-NCDs in South Asians, comparing them to other ethnic groups, mostly Whites/Europeans. Phenotypic differences in obesity and body composition between South Asians and Whites are in part responsible for greater metabolic perturbations in the former.97 These and other ethnic differences, as discussed below, have important implications for pathophysiology, management and prevention of OR-NCDs.66, 71, 72, 98, 99
Insulin resistance and the metabolic syndrome
Several studies show that insulin resistance is prevalent and occurs at an early age in South Asians (Table 4).7, 12, 71, 94, 97, 100, 101, 102, 103 Asian Indians had comparative lower insulin sensitivity index and lower rate of glucose disposal than European-origin Whites in the United states of America, even after adjustment for both total body fat and truncal skinfold thickness (P=0.04).99 South Asian children in the United Kingdom also showed higher degree of hyperinsulinemia, correlating with adiposity, than in White children of similar age.97 Similarly, the metabolic syndrome has been seen to be more prevalent in South Asians as compared with Whites (Table 5).94, 104, 105, 106, 107, 108 Furthermore, South Asians having the metabolic syndrome showed higher diastolic blood pressure, plasma triglycerides, fasting insulin and lower high-density lipoprotein-cholesterol (HDL-C) levels compared with UK Whites.109
T2DM and its complications
T2DM manifests nearly a decade earlier,4, 110, 111, 112, 113, 114 and occurs at a lower BMI and WC in South Asians than in Whites.115, 116 Importantly, South Asians are more predisposed to develop microvascular and macrovascular complications than European Whites.117 Several investigators have reported increased predisposition to microalbuminuria and diabetic nephropathy in South Asians (Figure 2).118, 119, 120 Notably, in Sweden, nearly 40-fold increased risk for end-stage renal disease consequent to T2DM was reported in Indo-Asians compared with native Dutch Caucasians, in spite of similar duration of diabetes.121 Nephropathy is reported to occur with shorter duration of diabetes (<10 years) in South Asians than in Whites.122, 123, 124, 125, 126, 127 Furthermore, as compared with White Europeans, South Asian T2DM patients in the United Kingdom were younger at diagnosis and had significantly higher prevalence of diabetic retinopathy, maculopathy, site-threatening retinopathy (45 vs 37%; P=0.059, respectively),128, 129 and specific vascular lesions (for example, arterio-venous nicking; 8.5 vs 7.5%, respectively; P<0.005).130
South Asians with T2DM showed an increased predisposition to CHD as compared with Europeans. Samanta et al.112 showed diabetes to be associated with a higher relative risk of acute myocardial infarction (MI) in UK South Asians than in European Whites (adjusted relative risks being 3.3 and 1.3, respectively).131 T2DM in South Asians causes higher morbidity and mortality than other ethnic groups.3, 132, 133, 134, 135, 136, 137 There are, however, contradictory reports regarding other macrovascular complications, but it appears that the risk of foot ulcers and diabetes-related amputation may be lesser in South Asians than in European Whites/Caucasians.138, 139, 140, 141, 142 A recent report also indicates that Asian Indians with diabetes in the United Kingdom have substantially less large and small fiber neuropathy than European Whites, despite comparable traditional risk factors, possibly due to better skin microvascularization, thus explaining reduced foot ulcer risk.143
Similar to T2DM, dyslipidemia occurs at lower levels of BMI and body fat in South Asians than in Whites.11, 24, 66, 144 Higher triglycerides and lower HDL levels (Table 6) associated with insulin resistance have been consistently shown in Asian Indians/South Asians as compared with Europeans/Whites.14, 71, 99, 109, 114, 137, 145, 146, 147 Interestingly, Asian Indians not only have low levels of protective HDL-C, but also have a preponderance of small-dense dysfunctional HDL-C particles, which are less protective and proinflammatory even at normal HDL levels.148, 149 Furthermore, Kulkarni et al.150 demonstrated higher prevalence of small, dense low-density lipoprotein in Asian Indians compared with Whites in the United States of America (44 vs 21%, respectively; P<0.05) Others have demonstrated similar findings in adult Asian Indians in the United Kingdom,151 and in adolescent (15–16 years) South Asians in the United States of America.152 Overall, a possible explanation of excess CVD risk in South Asians may be due to high prevalence of dysfunctional HDL and small dense low-density lipoprotein as compared with Whites.153
Lipoprotein(a) (Lp(a)), a low-density lipoprotein-like particle (with apolipoprotein B-100 linked to apolipoprotein (a)), is an inherited atherogenic lipoprotein and is thrombogenic.154 Importantly, Lp(a) concentration of South Asians are higher than Whites.155, 156, 157, 158, 159, 160 Some studies show that elevated plasma levels of Lp(a) confer almost three-fold risk of CVD in Asian Indians.161 Physical inactivity, atherogenic diet and abdominal obesity may additionally magnify the effect of high Lp(a) levels in Asian Indians.162 Significance of these findings in South Asians with respect to the development of CHD is not clear, and need further research.
Unlike discussion on other variables shown above, comparative data are not conclusive regarding the prevalence and severity of hypertension between South Asians and Whites. Several investigators from the United Kingdom showed that South Asians tend to have higher prevalence of hypertension than UK-based European Whites.65, 163, 164 However, a meta-analysis comparing hypertension in South Asians and Whites showed mixed results. Out of 12 studies, 7 studies showed lower mean systolic blood pressures, whereas other 7 studies showed higher diastolic pressures in South Asian men compared with Whites.165 Karlsen et al.166 demonstrated age-standardized ratio of mean diastolic blood pressure to be higher in Asian Indian men, but lower in Pakistani and Bangladeshi men than in the general UK population.166 However, this heterogeneity within different South Asian ethnic groups has been reflected in other variables also (such as smoking, physical activity and CHD) and has been ascribed to socioeconomic factors and patient's knowledge and outlook about diseases.167
Higher cardiovascular risk and clustering often at lower levels of adiposity in South Asians than in Whites
Raji et al.71 demonstrated that even at normal BMI, Asian Indians showed clustering of cardiovascular risk factors (insulin resistance, dyslipidemia, procoagulant state).71 Overall, with similar level of weight and obesity even at ‘normal’ BMI and WC levels, South Asians have greater risk of metabolic perturbations (‘metabolically obese’ individuals), T2DM and CVD than Europeans/Whites.9, 14, 68, 168, 169, 170
Earlier onset and higher rates of acute MI and CHD, as well as mortality due to CHD and stroke (Figures 3a, b)171 is higher in South Asians, and is often associated with abdominal obesity, insulin resistance and diabetes than Europeans/Whites.13, 107, 132, 133, 157, 172, 173, 174, 175, 176, 177 Furthermore, South Asians are more likely than Whites to have evidence of CHD in the absence of symptoms or clinical findings.157, 178 Finally, South Asians have more severe angiographic disease (significant left main, distal, along with more diffuse triple vessel disease), and more anterior and larger MI as compared with Europeans/Whites.135, 136, 173, 179
Subclinical inflammation, endothelial dysfunction and procoagulant factors
Subclinical inflammation, denoted by increased levels of high-sensitivity C-reactive protein (hs-CRP), has been reported to correlate with obesity, the metabolic syndrome, T2DM and increased cardiovascular risk.180, 181 Asian Indians have higher hs-CRP concentrations as compared with European/UK Whites, which is strongly associated with obesity and insulin resistance.182, 183, 184 These observations have also been reported in children.185 Chambers et al.182 showed that hs-CRP concentrations significantly predicted the risk of MI, and out of 40% excess risk of CHD reported in Asian Indians compared with European Whites, about two-fifth was thought to be attributable to elevated hs-CRP levels.182 Some investigators have suggested that increased abdominal adiposity may be responsible for subclinical inflammation in South Asians.186
Endothelial dysfunction is believed to be associated with insulin resistance, and may be one of the first event in its pathogenesis.187, 188 Endothelial-dependent dilatation and circulating numbers of endothelial progenitor cells (EPCs) and EPC colony-forming units (indicating dysfunctional endothelium) were significantly lower in South Asian than in White men (Table 7).189 The strongest predictor of flow-mediated dilatation (used for endothelial function assessment) was EPC number. Further, ethnicity was shown to be the strongest predictor of EPC count. In addition to quantitative difference, evidence of lower EPC functional capacity (proliferative capability and migratory response) was also seen in South Asians as compared with Whites.189 Further, Chambers et al.190 showed that Asian Indians with vascular endothelial dysfunction had more visceral and abdominal obesity, insulin resistance and dyslipidemia as compared with European Whites (3.2 vs 5.9%, P=0.03). More importantly, relation between Asian Indian ethnicity and flow-mediated dilatation was independent of insulin resistance and associated metabolic markers, raising the possibility that endothelial function among Asian Indians could be genetically mediated.190 These authors further showed that reduced levels of endothelial nitric oxide in Asian Indians may contribute to vascular injury by facilitating platelet–vascular wall interactions, adhesion of circulating monocytes to the endothelial surface and vascular smooth muscle proliferation.190
Hemostatic and fibrinolytic factors, including plasminogen-activator inhibitor-1 (PAI-1), tissue plasminogen activator and fibrinogen constitute another dimension of insulin resistance and the metabolic syndrome.191, 192 Several studies show that South Asians have higher procoagulant tendency; increased C-3, PAI-1, fibrinogen and decreased tissue plasminogen activator levels as compared with European and North American Whites.71, 109, 157, 160, 193, 194 Importantly, Kain et al.195 showed that significantly higher mean fibrinogen levels were seen in South Asians than UK Whites, even after adjustments for BMI, hypertension, and serum triglycerides. Further, Raji et al.71 showed that PAI-1 levels inversely correlated with glucose disposal rate in Asian Indians but not in Whites.71 Interestingly, South Asians without the metabolic syndrome and UK Whites with the metabolic syndrome had similar plasma levels of C3 and tissue plasminogen activator, as well as comparable degree of insulin resistance.109 Finally, the same authors showed that South Asians with the metabolic syndrome had significantly higher plasma levels of C3, PAI-1 and tissue plasminogen activator, in addition to significantly higher degree of insulin resistance, than UK Whites with the metabolic syndrome.109
Non-esterified fatty acids, leptin and adiponectin
Excess lipolysis, with release of large amounts of non-esterified fatty acids (NEFAs), is believed to increase triglyceride levels in skeletal muscle,196 enhance gluconeogenesis,197 and stimulate triglyceride production,198 thus causing increased triglycerides/lipid overload in non-adipose tissues. This metabolic process, known as ‘lipotoxicity’ causes pancreatic β-cell dysfunction and apoptosis.199, 200, 201 Both fasting and baseline plasma concentrations of NEFAs were reported to be significantly higher in Asian Indians as compared with Whites, along with impaired insulin-mediated plasma NEFA suppression during oral glucose tolerance test.202 Higher fasting plasma NEFAs, despite relative hyperinsulinemia, indicated higher release of NEFAs from adipose tissue of Asian Indians, although reasons for defective insulin action in adipose tissue were not clear.202
Asian Indians have significantly higher fasting serum leptin (5.15 vs 2.3 ng ml−1, respectively; P<0.001), along with lower insulin sensitivity index and lower insulin clearance than Whites.203 Higher leptin concentrations in South Asians as compared with Whites, even after statistical adjustments for body fat, suggest excessive leptin production from adipocytes, independent of overall obesity or abdominal and/or truncal obesity.202 Furthermore, lower serum adiponectin levels, correlating with low HDL-C and central obesity, was seen in Indo-Asians compared with Whites.204 Importantly, thicker truncal skinfolds (indicating high truncal SC fat) in Asian Indians were strongly correlated with low plasma adiponectin levels.202 All these data indicate an intrinsic and yet unknown abnormality in adipose tissue metabolism of Asian Indians, the precise mechanisms of which remain unclear.
Environmental, perinatal and genetic factors affecting OR-NCDs
The following section briefly summarizes important differences and observations pertaining to OR-NCDs on environmental, perinatal and genetic role in South Asians. For detailed discussion on these topics, readers should refer to other reviews.10, 100, 205, 206, 207, 208, 209, 210, 211, 212, 213
Higher intakes of carbohydrate, saturated fatty acids, trans fatty acids and ω-6 polyunsaturated fatty acids, along with lower intakes of monounsaturated fatty acids and fiber have been reported in South Asians.10 Burden et al.214 showed higher carbohydrate content (% energy) in South Asian than European diets to be associated with higher fasting glucose, triacylglycerols, higher HDL and post-glucose load insulin levels.215 Another contributory factor to insulin resistance in Asian Indians may be imbalanced dietary ω-6 and ω-3 polyunsaturated fatty acids. Importantly, South Asians consume higher proportion of total fatty acids as ω-6 polyunsaturated fatty acids and a lower proportion of long chain ω-3 polyunsaturated fatty acids as compared with Europeans.216, 217 Furthermore, South Asians, including children, consume less fresh fruits, vegetables and fiber than Whites.97, 218, 219, 220 Many of these imbalanced dietary factors have important implications for OR-NCDs in South Asians. Recent consensus dietary guidelines under preparation have aimed to address some of these issues (Misra A and Indian Dietary Guidelines Consensus Group, unpublished observations, 2010).
Lower level of physical activity in Asian Indian, Pakistani and Bangladeshi adults and children (South Asian populations) than Europeans/Whites are important for the development of OR-NCDs in the former (Table 8).206, 221 Lesser physical activity in Indians, Pakistanis or Bangladeshis than Europeans inversely correlated with BMI, WC, systolic blood pressure, plasma glucose and insulin levels.206 In a recent consensus statement, physical activity guidelines for Asian Indians emphasize 60 min of physical activity daily, and is inclusive of aerobic and resistance exercises, all days of the week.64
Adverse intrauterine milieu is believed to have profound and permanent effect on structure and functional development of fetus, and consequent development of chronic diseases in later life (‘intrauterine fetal programming’).212 Low birth weight of Indian babies (mean <2.7 kg; which is lower by 1 kg than White babies)222 was associated with more adiposity and poorer muscle mass compared with White babies.212 In addition, higher truncal SC fat, insulin and leptin levels in Asian Indian neonates as compared with White neonates have been reported.223 Higher susceptibility of Asian Indians to insulin resistance, T2DM, hypertension and CHD has been attributed to ‘intrauterine programming’ in adverse nutrient milieu, and consequent to low birth weight. Interestingly, most adverse risk profile were seen in children who showed ‘catch-up obesity’ (were small at birth but had a higher weight and fat mass at 8 years).224 Overall, implication of these findings to pathogenesis of OR-NCDs is not clear, given the continued heightened risk to develop these diseases in heterogeneous perinatal conditions and continued risk in Asian Indian children born to affluent families in urban environment.
Several studies show genetic predisposition for development of obesity, diabetes, dyslipidemia and CVD in South Asians. Discussion on this subject is beyond the scope of this article, and could be accessed in original articles and reviews.209, 210, 225, 226, 227, 228, 229, 230, 231, 232, 233 Overall, predominant contribution of gene(s) or gene(s)–environmental interaction(s) in the pathogenesis of OR-NCDs in South Asians remains to be researched.
Problems and barriers to diagnosis and management
South Asian patients have more atypical presentations (for example, discomfort over interscapular region, more diffuse and variable anatomical location of discomfort) than classical chest pain during acute coronary syndromes than Europeans/North American Whites.234, 235, 236, 237, 238, 239, 240, 241, 242 Atypical presentation could be a contributory factor to delayed diagnosis, less aggressive therapy (underutilized thrombolytic therapy) and higher mortality in South Asians.237, 243 Furthermore, British South Asian patients were shown to be less likely to be referred for stress testing, angiography and coronary artery bypass grafting, and were less likely to receive intensive care comparable with European Whites.244 Asian Indians were also less likely to complete the exercise stress test, probably due to poorer exercise tolerance than Europeans.245 Lawrence and Littler246 showed longer mean time from arrival in casualty to admission in coronary care unit with South Asians than European Whites, mostly attributable to communication difficulties.246 Bradley et al.247 also showed that door-to-drug (fibrinolytic) time (in terms of arrival to hospital and reperfusion therapy) was significantly longer for Asian Indian patients with MI than Whites in the United States of America.247
Difficulties in achieving treatment compliance in South Asian patients with diabetes in the United Kingdom are believed to be due to inappropriate or negligible health education, language barriers and lower awareness about disease risk and its complications than Europeans/UK Whites.248, 249, 250, 251, 252, 253, 254 Many South Asian patients could not name any complication of diabetes, were not aware of purpose of attendances at the clinic (screening for early complications) and did not know what a chiropodist did.255
Sociocultural and religious factors influence health beliefs, diet and management in South Asians.256, 257, 258 Cultural factors contribute to higher default from clinic appointments by South Asians than Whites (for example, South Asians having festival/holiday on that day). Furthermore, compliance with therapy (insulin or oral treatment) is less in South Asians during holidays, and control is unsatisfactory due to religious fasting.248, 249, 259 In contrast, an advantageous sociocultural factor seen in South Asians is the extended family structure, often helping patients to cope better with insulin therapy and morbidities.249 South Asian patients with diabetes had a more negative attitude, and believed they were made to wait longer in clinics than the UK Whites.251 Interestingly, cause of diabetes by migrant Bangladeshis in the United Kingdom was believed to lie in taking particular foods, balance of food entering the body and excess emission of body fluids.260 Furthermore, physical exercise was viewed as having a potential to exacerbate illness and physical weakness, instead ritual Muslim prayers (namaz) were cited as worthy and healthy form of exercise.260 Finally, being asymptomatic was interpreted as having well-controlled diabetes, and need for regular surveillance, when asymptomatic was rarely acknowledged.260 A reluctance to start insulin therapy is a frequently encountered problem in Asian Indian Hindus, as it is perceived as a failure of self-care and progression from ‘mild’ to more ‘serious’ diabetes.261 These distorted perceptions may have implications in lesser health-seeking behavior and consequent poor prevention and control of the disease in South Asians than in Whites.
Differences in response to therapy and disease outcomes
Glycemic control is often significantly worse in South Asians than in Whites, in spite of South Asians being younger and having lower BMI.249, 251, 262 South Asians showed smaller improvements in cholesterol and blood pressure compared with Whites.263 Further, South Asians were less likely to receive statins in spite of similar calculated 10-year CHD risk (30% by Framingham algorithm), possibly due to lower average total serum cholesterol concentrations.264 Even when same proportion of patients received lipid-lowering therapy, proportion of patients with uncontrolled total cholesterol and poorly controlled blood pressure were higher in Bangladeshi South Asians than in White Europeans.110 On the contrary, other studies have shown no differences in therapy outcomes in South Asians.265, 266
South Asians, with and without diabetes, not only are more likely to suffer a cardiac event, but are also less likely to survive it than Whites, in spite of intervention. As compared with UK Whites, South Asians with MI had lesser survival possibilities, both at 30 days (82.9 vs 93.2%, respectively, P=0.12) as well as 6 months (89.1 vs 95.0%, respectively, P=0.12), in spite of greater proportion of South Asians receiving thrombolytic drugs (81.2 vs 73.8%, respectively, P=0.12). Importantly, the presence of diabetes was considered to be a likely explanation for therapy differences.134 South Asian ethnicity seems to be an independent predictor of operative and overall mortality after coronary artery bypass grafting.267 Postoperative morbidity (for example, MI, sepsis, sternal wound infection, postoperative hospital stay after coronary artery bypass grafting and use of inotrope drugs) was also higher in South Asians than Whites in Canada.267 Furthermore, revascularization rates at follow-up were also higher for South Asian patients (6.5 vs 3.1%; P=0.001).268 On the other hand, some reports do not show any difference in incidence of MI or long-term adverse survival in South Asians with diabetes than in UK Whites.269, 270
Response to drugs has been suspected to be different in South Asians than Caucasians, but has not been adequately investigated. Increase in rosuvastatin plasma exposure and area under the plasma concentration–time curve from time 0 to the time of last quantifiable concentration was higher in Asian Indians (1.63-fold) as compared with Whites.271 On the basis of these data, it has been suggested that care should be exercised while prescribing rosuvastatin in Asian Indians, and this has led to revised labeling of rosuvastatin.271, 272, 273 Of note, therapy should be started at lower dose (5 mg once daily) and 40 mg per day dose (if needed) should be given with caution in Asian Indians.274 More insulin-resistant Asian Indians as compared with Whites respond more favorably to pioglitazone with marked improvements in insulin sensitivity, cardiovascular/inflammatory risk markers and vascular responses to insulin. A significant 32% increase in glucose disposal in Asian Indians was seen with pioglitazone treatment, whereas the effect was of smaller magnitude in Whites. Importantly, >50% decrease was seen in hs-CRP and PAI-1 levels in Asian Indians with pioglitazone therapy as compared with Whites.275 On the contrary, one report suggests that metformin may be more effective in Whites.276 Importantly, more studies are needed to get clarity on apparent differential response of insulin sensitizers in South Asians than in Whites and the factors responsible for it.
Drug therapy for obesity is presently based on clinical studies based on cut-offs of White population. The current consensus statement for Asian Indians suggest lower cut-offs of BMI for initiation of pharmacotherapy of obesity and for bariatric surgery.64
Increasing disease burden due to obesity and OR-NCDs is being seen in South Asian populations due to rapid industrialization, ‘westernization’ and consequent lifestyle changes. Apart from these environmental factors, genetics, certain innate body composition and differences in metabolic profile are also responsible for higher predisposition and increased prevalence of OR-NCDs in South Asians than in Whites. Higher abdominal and/or truncal obesity in South Asians vs Whites is hypothesized to be responsible for increased morbidity/mortality associated with OR-NCDs. Higher prevalence of insulin resistance, the metabolic syndrome and T2DM and its other components confer South Asians with an increased cardiovascular risk. Poorer nutritional habits and lesser physical activity along with adverse perinatal mileau (low birth weight and ‘catch-up’ obesity) seen in South Asians vs Whites are also believed to be contributory factors. Interestingly, studies in migrant South Asians have shown differences in disease outcomes and therapeutic response than Whites. However, more research is needed in this area so as to optimize the prevention and management strategies, leading to more positive health outcomes. Recent guidelines advocating lower cut-offs of obesity and abdominal obesity for South Asians as compared with international guidelines are expected to help physicians in better and more effective preventive management. However, greater awareness among physicians about the differences in OR-NCDs between South Asians and Whites is needed and would enable them to achieve better treatment outcomes.
King H, Aubert RE, Herman WH . Global burden of diabetes, 1995–2025: prevalence, numerical estimates, and projections. Diabetes Care 1998; 21: 1414–1431.
Reddy KS, Yusuf S . Emerging epidemic of cardiovascular disease in developing countries. Circulation 1998; 97: 596–601.
McKeigue PM, Ferrie JE, Pierpoint T, Marmot MG . Association of early-onset coronary heart disease in South Asian men with glucose intolerance and hyperinsulinemia. Circulation 1993; 87: 152–161.
McKeigue PM, Pierpoint T, Ferrie JE, Marmot MG . Relationship of glucose intolerance and hyperinsulinaemia to body fat pattern in south Asians and Europeans. Diabetologia 1992; 35: 785–791.
Gupta A, Gupta R, Sarna M, Rastogi S, Gupta VP, Kothari K . Prevalence of diabetes, impaired fasting glucose and insulin resistance syndrome in an urban Indian population. Diabetes Res Clin Pract 2003; 61: 69–76.
Gupta R, Misra A, Vikram NK, Kondal D, Gupta SS, Agrawal A et al. Younger age of escalation of cardiovascular risk factors in Asian Indian subjects. BMC Cardiovasc Disord 2009; 9: 28.
Misra A, Khurana L, Vikram NK, Goel A, Wasir JS . Metabolic syndrome in children: current issues and South Asian perspective. Nutrition 2007; 23: 895–910.
Misra A, Misra R, Wijesuriya M, Banerjee D . The metabolic syndrome in South Asians: continuing escalation & possible solutions. Indian J Med Res 2007; 125: 345–354.
Misra A, Vikram NK . Insulin resistance syndrome (metabolic syndrome) and obesity in Asian Indians: evidence and implications. Nutrition 2004; 20: 482–491.
Misra A, Khurana L, Isharwal S, Bhardwaj S . South Asian diets and insulin resistance. Br J Nutr 2009; 10: 465–473.
Misra A, Khurana L . Obesity and the metabolic syndrome in developing countries. J Clin Endocrinol Metab 2008; 93: S9–S30.
Bhardwaj S, Misra A, Khurana L, Gulati S, Shah P, Vikram NK . Childhood obesity in Asian Indians: a burgeoning cause of insulin resistance, diabetes and sub-clinical inflammation. Asia Pac J Clin Nutr 2008; 17 (S1): 172–175.
Wild S, McKeigue P . Cross sectional analysis of mortality by country of birth in England and Wales, 1970–92. Br Med J 1997; 314: 705–710.
Dhawan J, Bray CL, Warburton R, Ghambhir DS, Morris J . Insulin resistance, high prevalence of diabetes, and cardiovascular risk in immigrant Asians. Genetic or environmental effect? Br Heart J 1994; 72: 413–421.
Mansfield MW, Kohler HP, Ariens RA, McCormack LJ, Grant PJ . Circulating levels of coagulation factor XIII in subjects with type 2 diabetes and in their first-degree relatives. Diabetes Care 2000; 23: 703–705.
Kain K, Catto AJ, Grant PJ . Associations between insulin resistance and thrombotic risk factors in high-risk South Asian subjects. Diabet Med 2003; 20: 651–655.
World Health Organization. Health Situation in the South-East Asia Region. 1998–2000. Available at: http://www.searo.who.int/en/Section1243/Section1382/Section1386/Section1898_9439.htm (Last accessed: May 2010).
Khuwaja AK, Qureshi R, Fatmi Z . Noncommunicable diseases and injuries: action needed in South Asia too. PLoS Med 2007; 4: e38.
Yusuf S, Ounpuu S . Tackling the growing epidemic of cardiovascular disease in South Asia. J Am Coll Cardiol 2001; 38: 688–689.
Misra A, Sharma R, Pandey RM, Khanna N . Adverse profile of dietary nutrients, anthropometry and lipids in urban slum dwellers of northern India. Eur J Clin Nutr 2001; 55: 727–734.
Misra A, Pandey RM, Sinha S, Guleria R, Sridhar V, Dudeja V . Receiver operating characteristics curve analysis of body fat & body mass index in dyslipidaemic Asian Indians. Indian J Med Res 2003; 117: 170–179.
Misra A, Pandey RM, Devi JR, Sharma R, Vikram NK, Khanna N . High prevalence of diabetes, obesity and dyslipidaemia in urban slum population in northern India. Int J Obes Relat Metab Disord 2001; 25: 1722–1729.
Misra A, Pandey RM, Sharma R . Non-communicable diseases (diabetes, obesity and hyperlipidaemia) in urban slums. Natl Med J India 2002; 15: 242–244.
Misra A, Athiko D, Sharma R, Pandey RM, Khanna N . Non-obese hyperlipidemic Asian northern Indian males have adverse anthropometric profile. Nutr Metab Cardiovasc Dis 2002; 12: 178–183.
Vikram NK, Pandey RM, Misra A, Sharma R, Devi JR, Khanna N . Non-obese (body mass index <25 kg/m2) Asian Indians with normal waist circumference have high cardiovascular risk. Nutrition 2003; 19: 503–509.
Sethi A, Misra A, Pandey RM, Luthra K, Devi JR, Sharma R et al. Soluble inter-cellular adhesion molecule-1 in urban Asian north Indians: relationships with anthropometric and metabolic covariates. Dis Markers 2002; 18: 111–120.
Misra A, Khurana L . The metabolic syndrome in South Asians: epidemiology, clinical correlates and possible solutions. Int Diabetes Monitor 2009; 21: 92–101.
Misra A, Khurana L . The metabolic syndrome in South Asians: epidemiology, determinants, and prevention. Metab Syndr Relat Disord 2009; 7: 497–514.
International Diabetes Federation. Latest Diabetes Figures Paint Grim Global Picture. Press release: Montreal, Canada, 2009. Available at: http://www.idf.org/latest-diabetes-figures-paint-grim-global-picture (Last Accessed: May 2010).
World Health Organization. Prevalence of diabetes. Available at: http://www.who.int/diabetes/actionnow/en/mapdiabprev.pdf (Last accessed: May 2010).
Wild S, Roglic G, Green A, Sicree R, King H . Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004; 27: 1047–1053.
Ramachandran A, Snehalatha C, Kapur A, Vijay V, Mohan V, Das AK et al. High prevalence of diabetes and impaired glucose tolerance in India: National Urban diabetes survey. Diabetologia 2001; 44: 1094–1101.
World Diabetes Foundation. United Nations Resolution 61/225: World Diabetes Day. Available at: http://www.worlddiabetesfoundation.org/media(3892,1033)/UNR_media_kit_0407.pdf (Last accessed: May 2010).
Gupta R, Misra A . Type 2 diabetes in India: regional disparities. Br J Diabetes Vasc Dis 2007; 7: 12–16.
Shera AS, Jawad F, Maqsood A . Prevalence of diabetes in Pakistan. Diabetes Res Clin Pract 2007; 76: 219–222.
Pappas G, Akhtar T, Gergen PJ, Hadden WC, Khan AQ . Health status of the Pakistani population: a health profile and comparison with the United States. Am J Public Health 2001; 91: 93–98.
Rahim MA, Vaaler S, Keramat Ali SM, Khan AK, Hussain A, Nahar Q . Prevalence of type 2 diabetes in urban slums of Dhaka, Bangladesh. Bangladesh Med Res Counc Bull 2004; 30: 60–70.
Malavige GN, de Alwis NM, Weerasooriya N, Fernando DJ, Siribaddana SH . Increasing diabetes and vascular risk factors in a sub-urban Sri Lankan population. Diabetes Res Clin Pract 2002; 57: 143–145.
Wijewardene K, Mohideen MR, Mendis S, Fernando DS, Kulathilaka T, Weerasekara D et al. Prevalence of hypertension, diabetes and obesity: baseline findings of a population based survey in four provinces in Sri Lanka. Ceylon Med J 2005; 50: 62–70.
Singh DL, Bhattarai MD . High prevalence of diabetes and impaired fasting glycaemia in urban Nepal. Diabet Med 2003; 20: 170–171.
Gupta R . Trends in hypertension epidemiology in India. J Hum Hypertens 2004; 18: 73–78.
Jafar TH, Levey AS, Jafary FH, White F, Gul A, Rahbar MH et al. Ethnic subgroup differences in hypertension in Pakistan. J Hypertens 2003; 21: 905–912.
Murray CJL, Lopez AD eds. The Global Burden of Disease: A Comprehensive Assessment of Mortality and Disability from Diseases, Injuries, and Risk Factors in 1990 and Projected to 2020. Harvard School of Public Health: Boston, Mass, 1996. p 990.
Srikanthan P, Daveb JK, Kamdar VV . Cardiovascular disease in South Asians: a burgeoning epidemic. Curr Cardiovasc Risk Reports 2008; 2: 187–191.
Bulatao RA, Stephens PW . Global Estimates and Projections of Mortality by Cause, 1970–2015. World Bank. Policy Research Working Paper Series; 1007: Washington, DC, 1992. Available at: http://www-wds.worldbank.org/servlet/WDSContentServer/WDSP/IB/1992/10/01/000009265_3961003160329/Rendered/PDF/multi0page.pdf (Last accessed: May 2010).
Indrayan A . Forecasting vascular disease cases and associated mortality in India. NCMH Background Papers: Burden of Disease in India. Available at: http://www.whoindia.org/LinkFiles/Commision_on_Macroeconomic_and_Health_Bg_P2_Forecasting_vascular_disease_cases_and_associated_mortality_in_India.pdf (Last accessed: May 2010).
World Health Organization. Chronic diseases and health promotion. The impact of chronic disease in Pakistan. Available at: http://www.who.int/chp/chronic_disease_report/media/pakistan.pdf (Last accessed: May 2010).
World Health Organization. Chronic diseases and health promotion. The impact of chronic disease in Sri Lanka. Available at: http://www.who.int/chp/chronic_disease_report/sri_lanka.pdf (Last accessed: May 2010).
World Health Organization. Chronic diseases and health promotion. The impact of chronic disease in Nepal. Available at: http://www.who.int/chp/chronic_disease_report/media/impact/nepal.pdf (Last accessed: May 2010).
World Health Organization. Chronic diseases and health promotion. The impact of chronic disease in Bangladesh. Available at: http://www.who.int/chp/chronic_disease_report/bangladesh.pdf (Last accessed: May 2010).
Gupta R, Sarna M, Thanvi J, Rastogi P, Kaul V, Gupta VP . High prevalence of multiple coronary risk factors in Punjabi Bhatia community: Jaipur Heart Watch-3. Indian Heart J 2004; 56: 646–652.
Deepa M, Farooq S, Deepa R, Manjula D, Mohan V . Prevalence and significance of generalized and central body obesity in an urban Asian Indian population in Chennai, India (CURES: 47). Eur J Clin Nutr 2007; 63: 259–267.
Wasir JS, Misra A, Vikram NK, Pandey RM, Luthra K . C-reactive protein, obesity, and insulin resistance in postmenopausal women in urban slums of North India. Diabetes and Metabolic Syndrome: Clinical Research and Reviews 2007; 1: 83–89.
Chadha SL, Gopinath N, Shekhawat S . Urban-rural differences in the prevalence of coronary heart disease and its risk factors in Delhi. Bull World Health Organ 1997; 75: 31–38.
Chow C, Cardona M, Raju PK, Iyengar S, Sukumar A, Raju R et al. Cardiovascular disease and risk factors among 345 adults in rural India—the Andhra Pradesh rural health initiative. Int J Cardiol 2007; 116: 180–185.
Raj M, Sundaram KR, Paul M, Deepa AS, Kumar RK . Obesity in Indian children: time trends and relationship with hypertension. Natl Med J India 2007; 20: 288–293.
World Health Organization. SEARO. Risk factor profile of NCDs in the Region. Available at: http://www.searo.who.int/LinkFiles/NCD_InforBase_risk.pdf (Last accessed: May 2010).
Dudeja V, Misra A, Pandey RM, Devina G, Kumar G, Vikram NK . BMI does not accurately predict overweight in Asian Indians in northern India. Br J Nutr 2001; 86: 105–112.
Jackson AS, Ellis KJ, McFarlin BK, Sailors MH, Bray MS . Body mass index bias in defining obesity of diverse young adults: the Training Intervention and Genetics of Exercise Response (TIGER) study. Br J Nutr 2009; 102: 1084–1090.
Deurenberg-Yap M, Schmidt G, van Staveren WA, Deurenberg P . The paradox of low body mass index and high body fat percentage among Chinese, Malays and Indians in Singapore. Int J Obes Relat Metab Disord 2000; 24: 1011–1017.
Wang J, Thornton JC, Russell M, Burastero S, Heymsfield S, Pierson Jr RN . Asians have lower body mass index (BMI) but higher percent body fat than do whites: comparisons of anthropometric measurements. Am J Clin Nutr 1994; 60: 23–28.
Deurenberg-Yap M, Chew SK, Deurenberg P . Elevated body fat percentage and cardiovascular risks at low body mass index levels among Singaporean Chinese, Malays and Indians. Obes Rev 2002; 3: 209–215.
Lear SA, Humphries KH, Kohli S, Chockalingam A, Frohlich JJ, Birmingham CL . Visceral adipose tissue accumulation differs according to ethnic background: results of the Multicultural Community Health Assessment Trial (M-CHAT). Am J Clin Nutr 2007; 86: 353–359.
Misra A, Chowbey PK, Makkar BM, Vikram NK, Wasir JS, Chadha D et al. Consensus statement for diagnosis of obesity, abdominal obesity and the metabolic syndrome for Asian Indians and recommendations for physical activity, medical and surgical management. J Assoc Physicians India 2009; 57: 163–170.
McKeigue PM, Shah B, Marmot MG . Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet 1991; 337: 382–386.
Misra A, Vikram NK . Clinical and pathophysiological consequences of abdominal adiposity and abdominal adipose tissue depots. Nutrition 2003; 19: 457–466.
Hughes K, Aw TC, Kuperan P, Choo M . Central obesity, insulin resistance, syndrome X, lipoprotein(a), and cardiovascular risk in Indians, Malays, and Chinese in Singapore. J Epidemiol Community Health 1997; 51: 394–399.
Lean ME, Han TS, Bush H, Anderson AS, Bradby H, Williams R . Ethnic differences in anthropometric and lifestyle measures related to coronary heart disease risk between South Asian, Italian and general-population British women living in the west of Scotland. Int J Obes Relat Metab Disord 2001; 25: 1800–1805.
Chandalia M, Lin P, Seenivasan T, Livingston EH, Snell PG et al. Insulin resistance and body fat distribution in South Asian men compared to Caucasian men. PLoS ONE 2007; 2: e812.
International Diabetes Federation. IDF Worldwide definition of the metabolic syndrome. Available at: http://www.idf.org/webdata/docs/MetS_def_update2006.pdf (Last accessed: May 2010).
Raji A, Seely EW, Arky RA, Simonson DC . Body fat distribution and insulin resistance in healthy Asian Indians and Caucasians. J Clin Endocrinol Metab 2001; 86: 5366–5371.
Kamath SK, Hussain EA, Amin D, Mortillaro E, West B, Peterson CT et al. Cardiovascular disease risk factors in 2 distinct ethnic groups: Indian and Pakistani compared with American premenopausal women. Am J Clin Nutr 1999; 69: 621–631.
Misra A . Revision of cutoffs of body mass index to define overweight and obesity are needed for the Asian ethnic groups. Int J Obes Relat Metab Disord 2003; 27: 1294–1296.
Chowdhury B, Lantz H, Sjostrom L . Computed tomography-determined body composition in relation to cardiovascular risk factors in Indian and matched Swedish males. Metabolism 1996; 45: 634–644.
Peters J, Ulijaszek SJ . Population and sex differences in arm circumference and skinfold thicknesses among Indo-Pakistani children living in the East Midlands of Britain. Ann Hum Biol 1992; 19: 17–22.
Goel K, Misra A, Vikram NK, Poddar P, Gupta N . Subcutaneous abdominal adipose tissue is associated with the metabolic syndrome in Asian Indians independent of intra-abdominal and total body fat. Heart 2010; 96: 579–583.
Targher G, Bertolini L, Padovani R, Rodella S, Tessari R, Zenari L et al. Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients. Diabetes Care 2007; 30: 1212–1218.
Petersen KF, Dufour S, Befroy D, Lehrke M, Hendler RE, Shulman GI . Reversal of nonalcoholic hepatic steatosis, hepatic insulin resistance, and hyperglycemia by moderate weight reduction in patients with type 2 diabetes. Diabetes 2005; 54: 603–608.
Seppala-Lindroos A, Vehkavaara S, Hakkinen AM, Goto T, Westerbacka J, Sovijärvi A et al. Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. J Clin Endocrinol Metab 2002; 87: 3023–3028.
Bajaj S, Nigam P, Luthra A, Pandey RM, Kondal D, Bhatt SP et al. A case-control study on insulin resistance, metabolic co-variates & prediction score in non-alcoholic fatty liver disease. Indian J Med Res 2009; 129: 285–292.
Sharma R, Sinha S, Danishad KA, Vikram NK, Gupta A, Ahuja V et al. Investigation of hepatic gluconeogenesis pathway in non-diabetic Asian Indians with non-alcoholic fatty liver disease using in vivo (31P) phosphorus magnetic resonance spectroscopy. Atherosclerosis 2009; 203: 291–297.
Petersen KF, Dufour S, Feng J, Befroy D, Dziura J, Dalla Man C et al. Increased prevalence of insulin resistance and nonalcoholic fatty liver disease in Asian-Indian men. Proc Natl Acad Sci USA 2006; 103: 18273–18277.
Mohan V, Farooq S, Deepa M, Ravikumar R, Pitchumoni CS . Prevalence of non-alcoholic fatty liver disease in urban south Indians in relation to different grades of glucose intolerance and metabolic syndrome. Diabetes Res Clin Pract 2009; 84: 84–91.
Perseghin G, Scifo P, De Cobelli F, Pagliato E, Battezzati A, Arcelloni C et al. Intramyocellular triglyceride content is a determinant of in vivo insulin resistance in humans: a 1H-13C nuclear magnetic resonance spectroscopy assessment in offspring of type 2 diabetic parents. Diabetes 1999; 48: 1600–1606.
Krssak M, Falk Petersen K, Dresner A, DiPietro L, Vogel SM, Rothman DL et al. Intramyocellular lipid concentrations are correlated with insulin sensitivity in humans: a 1 H NMR spectroscopy study. Diabetologia 1999; 42: 113–116.
Forouhi NG, Jenkinson G, Thomas EL, Mullick S, Mierisova S, Bhonsle U et al. Relation of triglyceride stores in skeletal muscle cells to central obesity and insulin sensitivity in European and South Asian men. Diabetologia 1999; 42: 932–935.
Misra A, Sinha S, Kumar M, Jagannathan NR, Pandey RM . Proton magnetic resonance spectroscopy study of soleus muscle in non-obese healthy and type 2 diabetic Asian Northern Indian males: high intramyocellular lipid content correlates with excess body fat and abdominal obesity. Diabet Med 2003; 20: 361–367.
Sinha S, Rathi M, Misra A, Kumar V, Kumar M, Jagannathan NR et al. Subclinical inflammation and soleus muscle intramyocellular lipids in healthy Asian Indian males. Clin Endocrinol (Oxf) 2005; 63: 350–355.
Sinha S, Misra A, Rathi M, Kumar V, Pandey RM, Luthra K et al. Proton magnetic resonance spectroscopy and biochemical investigation of type 2 diabetes mellitus in Asian Indians: observation of high muscle lipids and C-reactive protein levels. Magn Reson Imaging 2009; 27: 94–100.
Misra A, Jaiswal A, Shakti D, Wasir J, Vikram NK, Pandey RM et al. Novel phenotypic markers and screening score for the metabolic syndrome in adult Asian Indians. Diabetes Res Clin Pract 2008; 79: 1–5.
Cheung O, Kapoor A, Puri P, Sistrun S, Luketic VA, Sargeant CC et al. The impact of fat distribution on the severity of nonalcoholic fatty liver disease and metabolic syndrome. Hepatology 2007; 46: 1091–1100.
Haque WA, Oral EA, Dietz K, Bowcock AM, Agarwal AK, Garg A . Risk factors for diabetes in familial partial lipodystrophy, Dunnigan variety. Diabetes Care 2003; 26: 1350–1355.
Weyer C, Foley JE, Bogardus C, Tataranni PA, Pratley RE . Enlarged subcutaneous abdominal adipocyte size, but not obesity itself, predicts type II diabetes independent of insulin resistance. Diabetologia 2000; 43: 1498–1506.
Banerji MA, Faridi N, Alturi R, Chaiken RL, Lebovitz HE . Body composition, visceral fat, leptin and insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999; 84: 137–144.
Rush EC, Freitas I, Plank LD . Body size, body composition and fat distribution: comparative analysis of European, Maori, Pacific Island and Asian Indian adults. Br J Nutr 2009; 102: 632–641.
Unni US, Ramakrishnan G, Raj T, Kishore RP, Thomas T, Vaz M et al. Muscle mass and functional correlates of insulin sensitivity in lean young Indian men. Eur J Clin Nutr 2009; 63: 1206–1212.
Whincup PH, Gilg JA, Papacosta O, Seymour C, Miller GJ, Alberti KG et al. Early evidence of ethnic differences in cardiovascular risk: cross sectional comparison of British South Asian and white children. Br Med J 2002; 324: 635.
Misra A . Overnutrition and nutritional deficiency contribute to metabolic syndrome and atherosclerosis in Asian Indians. Nutrition 2002; 18: 702–703.
Chandalia M, Abate N, Garg A, Stray-Gundersen J, Grundy SM . Relationship between generalized and upper body obesity to insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999; 84: 2329–2335.
Yajnik CS, Lubree HG, Rege SS, Naik SS, Deshpande JA, Deshpande SS et al. Adiposity and hyperinsulinemia in Indians are present at birth. J Clin Endocrinol Metab 2002; 87: 5575–5580.
Ehtisham S, Crabtree N, Clark P, Shaw N, Barrett T . Ethnic differences in insulin resistance and body composition in United Kingdom adolescents. J Clin Endocrinol Metab 2005; 90: 3963–3969.
Kolsgaard ML, Andersen LF, Tonstad S, Brunborg C, Wangensteen T, Joner G . Ethnic differences in metabolic syndrome among overweight and obese children and adolescents: the Oslo Adiposity Intervention Study. Acta Paediatr 2008; 97: 1557–1563.
Ramachandran A, Snehalatha C, Latha E, Satyavani K, Vijay V . Clustering of cardiovascular risk factors in urban Asian Indians. Diabetes Care 1998; 21: 967–971.
Palep-Singh M, Picton HM, Barth JH, Balen AH . Ethnic variations in the distribution of obesity and biochemical metabolic abnormalities in fertility clinic attendees. J Reprod Med 2008; 53: 117–123.
Unwin N, Bhopal R, Hayes L, White M, Patel S, Ragoobirsingh D et al. A comparison of the new international diabetes federation definition of metabolic syndrome to WHO and NCEP definitions in Chinese, European and South Asian origin adults. Ethn Dis 2007; 17: 522–528.
Zoratti R, Godsland IF, Chaturvedi N, Crook D, Stevenson JC, McKeigue PM . Relation of plasma lipids to insulin resistance, nonesterified fatty acid levels, and body fat in men from three ethnic groups: relevance to variation in risk of diabetes and coronary disease. Metabolism 2000; 49: 245–252.
Forouhi NG, Sattar N, Tillin T, McKeigue PM, Chaturvedi N . Do known risk factors explain the higher coronary heart disease mortality in South Asian compared with European men? Prospective follow-up of the Southall and Brent studies, UK. Diabetologia 2006; 49: 2580–2588.
Forouhi N, McKeigue P . How far can risk factors account for excess coronary mortality in South Asians? Can J Cardiol 1997; 13: 47B.
Ajjan R, Carter AM, Somani R, Kain K, Grant PJ . Ethnic differences in cardiovascular risk factors in healthy Caucasian and South Asian individuals with the metabolic syndrome. J Thromb Haemost 2007; 5: 754–760.
Chowdhury TA, Lasker SS, Mahfuz R . Ethnic differences in control of cardiovascular risk factors in patients with type 2 diabetes attending an Inner London diabetes clinic. Postgrad Med J 2006; 82: 211–215.
Mather HM, Keen H . The Southall Diabetes Survey: prevalence of known diabetes in Asians and Europeans. Br Med J (Clin Res Ed) 1985; 291: 1081–1084.
Samanta A, Burden AC, Fent B . Comparative prevalence of non-insulin-dependent diabetes mellitus in Asian and white Caucasian adults. Diabetes Res Clin Pract 1987; 4: 1–6.
Ramachandran A, Jali MV, Mohan V, Snehalatha C, Viswanathan M . High prevalence of diabetes in an urban population in south India. Br Med J 1988; 297: 587–590.
McKeigue PM, Marmot MG, Syndercombe Court YD, Cottier DE, Rahman S, Riemersma RA . Diabetes, hyperinsulinaemia, and coronary risk factors in Bangladeshis in east London. Br Heart J 1988; 60: 390–396.
Ramachandran A, Snehalatha C, Vijay V . Low risk threshold for acquired diabetogenic factors in Asian Indians. Diabetes Res Clin Pract 2004; 65: 189–195.
Nakagami T, Qiao Q, Carstensen B, Nhr-Hansen C, Hu G, Tuomilehto J et al. Age, body mass index and type 2 diabetes-associations modified by ethnicity. Diabetologia 2003; 46: 1063–1070.
Chowdhury TA, Lasker SS . Complications and cardiovascular risk factors in South Asians and Europeans with early-onset type 2 diabetes. QJM 2002; 95: 241–246.
Chandie Shaw PK, Baboe F, van Es LA, van der Vijver JC, van de Ree MA, de Jonge N et al. South-Asian type 2 diabetic patients have higher incidence and faster progression of renal disease compared with Dutch-European diabetic patients. Diabetes Care 2006; 29: 1383–1385.
Fischbacher CM, Bhopal R, Rutter MK, Unwin NC, Marshall SM, White M et al. Microalbuminuria is more frequent in South Asian than in European origin populations: a comparative study in Newcastle, UK. Diabet Med 2003; 20: 31–36.
Mather HM, Chaturvedi N, Kehely AM . Comparison of prevalence and risk factors for microalbuminuria in South Asians and Europeans with type 2 diabetes mellitus. Diabet Med 1998; 15: 672–677.
Chandie Shaw PK, Vandenbroucke JP, Tjandra YI, Rosendaal FR, Rosman JB, Geerlings W et al. Increased end-stage diabetic nephropathy in Indo-Asian immigrants living in the Netherlands. Diabetologia 2002; 45: 337–341.
Lightstone L, Rees AJ, Tomson C, Walls J, Winearls CG, Feehally J . High incidence of end-stage renal disease in Indo-Asians in the UK. QJM 1995; 88: 191–195.
Cruickshank JK . Diabetic renal disease: differences between Asian and white patients. Br Med J (Clin Res Ed) 1986; 293: 696–697.
Cowie CC, Port FK, Wolfe RA, Savage PJ, Moll PP, Hawthorne VM . Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med 1989; 321: 1074–1079.
Burden AC, McNally PG, Feehally J, Walls J . Increased incidence of end-stage renal failure secondary to diabetes mellitus in Asian ethnic groups in the United Kingdom. Diabet Med 1992; 9: 641–645.
Samanta A, Burden AC, Jagger C . A comparison of the clinical features and vascular complications of diabetes between migrant Asians and Caucasians in Leicester, UK. Diabetes Res Clin Pract 1991; 14: 205–213.
Davis TM . Ethnic diversity in type 2 diabetes. Diabet Med 2008; 25 (Suppl 2): 52–56.
Raymond NT, Varadhan L, Reynold DR, Bush K, Sankaranarayanan S, Bellary S et al. Higher prevalence of retinopathy in diabetic patients of South Asian ethnicity compared with white Europeans in the community: a cross-sectional study. Diabetes Care 2009; 32: 410–415.
Pardhan S, Gilchrist J, Mahomed I . Impact of age and duration on sight-threatening retinopathy in South Asians and Caucasians attending a diabetic clinic. Eye 2004; 18: 233–240.
Stolk RP, van Schooneveld MJ, Cruickshank JK, Hughes AD, Stanton A, Lu J et al. Retinal vascular lesions in patients of Caucasian and Asian origin with type 2 diabetes: baseline results from the ADVANCE Retinal Measurements (AdRem) study. Diabetes Care 2008; 31: 708–713.
Samanta A, Woods KL, Burden AC . First myocardial infarction in Asian and white men. Br Med J 1989; 299: 52.
Mather HM, Chaturvedi N, Fuller JH . Mortality and morbidity from diabetes in South Asians and Europeans: 11-year follow-up of the Southall Diabetes Survey, London, UK. Diabet Med 1998; 15: 53–59.
Sheth T, Nair C, Nargundkar M, Anand S, Yusuf S . Cardiovascular and cancer mortality among Canadians of European, south Asian and Chinese origin from 1979 to 1993: an analysis of 1.2 million deaths. CMAJ 1999; 161: 132–138.
Wilkinson P, Sayer J, Laji K, Grundy C, Marchant B, Kopelman P et al. Comparison of case fatality in south Asian and white patients after acute myocardial infarction: observational study. Br Med J 1996; 312: 1330–1333.
McKeigue PM, Marmot MG . Mortality from coronary heart disease in Asian communities in London. Br Med J 1988; 297: 903.
Dhawan J, Bray CL . Angiographic comparison of coronary artery disease between Asians and Caucasians. Postgrad Med J 1994; 70: 625–630.
Enas EA, Garg A, Davidson MA, Nair VM, Huet BA, Yusuf S . Coronary heart disease and its risk factors in first-generation immigrant Asian Indians to the United States of America. Indian Heart J 1996; 48: 343–353.
Abbott CA, Garrow AP, Carrington AL, Morris J, Van Ross ER, Boulton AJ . Foot ulcer risk is lower in South-Asian and African-Caribbean compared with European diabetic patients in the UK: the North-West diabetes foot care study. Diabetes Care 2005; 28: 1869–1875.
UK Prospective Diabetes Study. XII: Differences between Asian, Afro-Caribbean and white Caucasian type 2 diabetic patients at diagnosis of diabetes. UK Prospective Diabetes Study Group. Diabet Med 1994; 11: 670–677.
Abbott CA, Carrington AL, Ashe H, Bath S, Every LC, Griffiths J et al. The North-West Diabetes Foot Care Study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based patient cohort. Diabet Med 2002; 19: 377–384.
Gujral JS, McNally PG, O’Malley BP, Burden AC . Ethnic differences in the incidence of lower extremity amputation secondary to diabetes mellitus. Diabet Med 1993; 10: 271–274.
Chaturvedi N, Abbott CA, Whalley A, Widdows P, Leggetter SY, Boulton AJ . Risk of diabetes-related amputation in South Asians vs Europeans in the UK. Diabet Med 2002; 19: 99–104.
Abbott CA, Chaturvedi N, Malik RA, Salgami E, Yates AP, Pemberton PW et al. Explanations for the lower rates of diabetic neuropathy in Indian Asians versus Europeans. Diabetes Care 2010; 33: 1325–1330.
Forouhi NG . The metabolic syndrome. In: Byrne CD, Wild SH (eds). Chichester: Wiley, 2005. pp 43–84.
Pollard TM, Unwin N, Fischbacher C, Chamley JK . Differences in body composition and cardiovascular and type 2 diabetes risk factors between migrant and British-born British Pakistani women. Am J Hum Biol 2008; 20: 545–549.
Lovegrove JA, Brady LM, Lesauvage SV, Lovegrove SS, Minihane AM, Williams CM . Lack of association between central adiposity and lipaemia in UK Sikh men. Int J Obes Relat Metab Disord 2003; 27: 1373–1382.
Lear SA, Toma M, Birmingham CL, Frohlich JJ . Modification of the relationship between simple anthropometric indices and risk factors by ethnic background. Metabolism 2003; 52: 1295–1301.
Joshi P, Islam S, Pais P, Reddy S, Dorairaj P, Kazmi K et al. Risk factors for early myocardial infarction in South Asians compared with individuals in other countries. JAMA 2007; 297: 286–294.
Dodani S, Kaur R, Reddy S, Reed GL, Navab M, George V . Can dysfunctional HDL explain high coronary artery disease risk in South Asians? Int J Cardiol 2008; 129: 125–132.
Kulkarni KR, Markovitz JH, Nanda NC, Segrest JP . Increased prevalence of smaller and denser LDL particles in Asian Indians. Arterioscler Thromb Vasc Biol 1999; 19: 2749–2755.
Kooner JS, Baliga RR, Wilding J, Crook D, Packard CJ, Banks LM et al. Abdominal obesity, impaired nonesterified fatty acid suppression, and insulin-mediated glucose disposal are early metabolic abnormalities in families with premature myocardial infarction. Arterioscler Thromb Vasc Biol 1998; 18: 1021–1026.
Raschke V, Elmadfa I, Bermingham MA, Steinbeck K . Low density lipoprotein subclasses in Asian and Caucasian adolescent boys. Asia Pac J Clin Nutr 2006; 15: 496–501.
Dodani S . Excess coronary artery disease risk in South Asian immigrants: can dysfunctional high-density lipoprotein explain increased risk? Vasc Health Risk Manag 2008; 4: 953–961.
Hajjar KA, Gavish D, Breslow JL, Nachman RL . Lipoprotein(a) modulation of endothelial cell surface fibrinolysis and its potential role in atherosclerosis. Nature 1989; 339: 303–305.
Chambers JC, Kooner JS . Diabetes, insulin resistance and vascular disease among Indian Asians and Europeans. Semin Vasc Med 2002; 2: 199–214.
Anand SS, Yusuf S, Vuksan V, Devanesen S, Teo KK, Montague PA et al. Differences in risk factors, atherosclerosis and cardiovascular disease between ethnic groups in Canada: the study of health assessment and risk in ethnic groups (SHARE). Indian Heart J 2000; 52: S35–S43.
Anand SS, Yusuf S, Vuksan V, Devanesen S, Teo KK, Montague PA et al. Differences in risk factors, atherosclerosis, and cardiovascular disease between ethnic groups in Canada: the Study of Health Assessment and Risk in Ethnic groups (SHARE). Lancet 2000; 356: 279–284.
Anand SS, Enas EA, Pogue J, Haffner S, Pearson T, Yusuf S . Elevated lipoprotein(a) levels in South Asians in North America. Metabolism 1998; 47: 182–184.
Sandholzer C, Hallman DM, Saha N, Sigurdsson G, Lackner C, Császár A et al. Effects of the apolipoprotein(a) size polymorphism on the lipoprotein(a) concentration in 7 ethnic groups. Hum Genet 1991; 86: 607–614.
Palaniappan L, Anthony MN, Mahesh C, Elliott M, Killeen A, Giacherio D et al. Cardiovascular risk factors in ethnic minority women aged < or =30 yr. Am J Cardiol 2002; 89: 524–529.
Enas EA, Chacko V, Senthilkumar A, Puthumana N, Mohan V . Elevated lipoprotein(a)—a genetic risk factor for premature vascular disease in people with and without standard risk factors: a review. Dis Mon 2006; 52: 5–50.
Enas EA . Dyslipidemia among Indo-Asians: strategies for identification and management. Br J of Diabetes and Vascular Dis 2005; 5: 81–90.
Cappuccio FP, Cook DG, Atkinson RW, Strazzullo P . Prevalence, detection, and management of cardiovascular risk factors in different ethnic groups in south London. Heart 1997; 78: 555–563.
Whitty CJ, Brunner EJ, Shipley MJ, Hemingway H, Marmot MG . Differences in biological risk factors for cardiovascular disease between three ethnic groups in the Whitehall II study. Atherosclerosis 1999; 142: 279–286.
Agyemang C, Bhopal RS . Is the blood pressure of South Asian adults in the UK higher or lower than that in European white adults? A review of cross-sectional data. J Hum Hypertens 2002; 16: 739–751.
Karlsen S, Primatesta P, McMunn A . Blood pressure (Chapter 7). In: Erens B, Primatesta P, Prior G (eds). Health Survey for England¾The Health of Minority Ethnic Groups’99 London. The Stationary Office: London, 2001. pp 175–197.
Bhopal RS . Heterogeneity among Indians, Pakistanis, and Bangladeshis is key to racial inequities. Br Med J 2002; 325: 903.
Misra A, Wasir JS, Vikram NK . Waist circumference criteria for the diagnosis of abdominal obesity are not applicable uniformly to all populations and ethnic groups. Nutrition 2005; 21: 969–976.
Deurenberg-Yap M, Chew SK, Lin VF, Tan BY, van Staveren WA, Deurenberg P . Relationships between indices of obesity and its co-morbidities in multi-ethnic Singapore. Int J Obes Relat Metab Disord 2001; 25: 1554–1562.
Yajnik CS . The lifecycle effects of nutrition and body size on adult adiposity, diabetes and cardiovascular disease. Obes Rev 2002; 3: 217–224.
CHD Statistics 2008: Mortality. Chapter 1 of the BHF Coronary heart disease statistics: Published July 2008. Available at: http://www.heartstats.org/temp/2008.Chaptersp1.pdf (Last accessed: May 2010).
Balarajan R, Bulusu L, Adelstein AM, Shukla V . Patterns of mortality among migrants to England and Wales from the Indian subcontinent. Br Med J (Clin Res Ed) 1984; 289: 1185–1187.
Balarajan R . Ethnic differences in mortality from ischaemic heart disease and cerebrovascular disease in England and Wales. Bmj 1991; 302: 560–564.
Balarajan R . Ethnicity and variations in mortality from coronary heart disease. Health Trends 1996; 28: 45–51.
McKeigue PM, Miller GJ, Marmot MG . Coronary heart disease in south Asians overseas: a review. J Clin Epidemiol 1989; 42: 597–609.
Forouhi NG, Sattar N . CVD risk factors and ethnicity--a homogeneous relationship? Atheroscler Suppl 2006; 7: 11–19.
Hughes LO, Cruickshank JK, Wright J, Raftery EB . Disturbances of insulin in British Asian and white men surviving myocardial infarction. Br Med J 1989; 299: 537–541.
Singh N, Gupta M . Clinical characteristics of South Asian patients hospitalized with heart failure. Ethn Dis 2005; 15: 615–619.
Gupta M, Doobay AV, Singh N, Anand SS, Raja F, Mawji F et al. Risk factors, hospital management and outcomes after acute myocardial infarction in South Asian Canadians and matched control subjects. CMAJ 2002; 166: 717–722.
Tamakoshi K, Yatsuya H, Kondo T, Hori Y, Ishikawa M, Zhang H et al. The metabolic syndrome is associated with elevated circulating C-reactive protein in healthy reference range, a systemic low-grade inflammatory state. Int J Obes Relat Metab Disord 2003; 27: 443–449.
Ford ES . The metabolic syndrome and C-reactive protein, fibrinogen, and leukocyte count: findings from the Third National Health and Nutrition Examination Survey. Atherosclerosis 2003; 168: 351–358.
Chambers JC, Eda S, Bassett P, Karim Y, Thompson SG, Gallimore JR et al. C-reactive protein, insulin resistance, central obesity, and coronary heart disease risk in Indian Asians from the United Kingdom compared with European whites. Circulation 2001; 104: 145–150.
Somani R, Grant PJ, Kain K, Catto AJ, Carter AM . Complement C3 and C-reactive protein are elevated in South Asians independent of a family history of stroke. Stroke 2006; 37: 2001–2006.
Misra A . C-reactive protein in young individuals: problems and implications for Asian Indians. Nutrition 2004; 20: 478–481.
Cook DG, Mendall MA, Whincup PH, Carey IM, Ballam L, Morris JE et al. C-reactive protein concentration in children: relationship to adiposity and other cardiovascular risk factors. Atherosclerosis 2000; 149: 139–150.
Forouhi NG, Sattar N, McKeigue PM . Relation of C-reactive protein to body fat distribution and features of the metabolic syndrome in Europeans and South Asians. Int J Obes Relat Metab Disord 2001; 25: 1327–1331.
Balletshofer BM, Rittig K, Enderle MD, Volk A, Maerker E, Jacob S et al. Endothelial dysfunction is detectable in young normotensive first-degree relatives of subjects with type 2 diabetes in association with insulin resistance. Circulation 2000; 101: 1780–1784.
Wheatcroft SB, Williams IL, Shah AM, Kearney MT . Pathophysiological implications of insulin resistance on vascular endothelial function. Diabet Med 2003; 20: 255–268.
Murphy C, Kanaganayagam GS, Jiang B, Chowienczyk PJ, Zbinden R, Saha M et al. Vascular dysfunction and reduced circulating endothelial progenitor cells in young healthy UK South Asian men. Arterioscler Thromb Vasc Biol 2007; 27: 936–942.
Chambers JC, McGregor A, Jean-Marie J, Kooner JS . Abnormalities of vascular endothelial function may contribute to increased coronary heart disease risk in UK Indian Asians. Heart 1999; 81: 501–504.
Juhan-Vague I, Thompson SG, Jespersen J . Involvement of the hemostatic system in the insulin resistance syndrome. A study of 1500 patients with angina pectoris. The ECAT Angina Pectoris Study Group. Arterioscler Thromb 1993; 13: 1865–1873.
Thogersen AM, Jansson JH, Boman K, Nilsson TK, Weinehall L, Huhtasaari F et al. High plasminogen activator inhibitor and tissue plasminogen activator levels in plasma precede a first acute myocardial infarction in both men and women: evidence for the fibrinolytic system as an independent primary risk factor. Circulation 1998; 98: 2241–2247.
Kain K, Catto AJ, Grant PJ . Impaired fibrinolysis and increased fibrinogen levels in South Asian subjects. Atherosclerosis 2001; 156: 457–461.
Markovitz JH, Kulkarni K, Goldschmidt-Clermont P, Kiefe CI, Rustagi P, Sekar P et al. Increased platelet activation and fibrinogen in Asian Indians. Potential implications for coronary risk. Eur Heart J 1998; 19: 720–726.
Kain K, Blaxill JM, Catto AJ, Grant PJ, Carter AM . Increased fibrinogen levels among South Asians versus Whites in the United Kingdom are not explained by common polymorphisms. Am J Epidemiol 2002; 156: 174–179.
Sinha R, Dufour S, Petersen KF, LeBon V, Enoksson S, Ma YZ et al. Assessment of skeletal muscle triglyceride content by (1)H nuclear magnetic resonance spectroscopy in lean and obese adolescents: relationships to insulin sensitivity, total body fat, and central adiposity. Diabetes 2002; 51: 1022–1027.
Groop LC, Bonadonna RC, DelPrato S, Ratheiser K, Zyck K, Ferrannini E et al. Glucose and free fatty acid metabolism in non-insulin-dependent diabetes mellitus. Evidence for multiple sites of insulin resistance. J Clin Invest 1989; 84: 205–213.
Aitman TJ, Godsland IF, Farren B, Crook D, Wong HJ, Scott J . Defects of insulin action on fatty acid and carbohydrate metabolism in familial combined hyperlipidemia. Arterioscler Thromb Vasc Biol 1997; 17: 748–754.
Shimabukuro M, Zhou YT, Levi M, Unger RH . Fatty acid-induced beta cell apoptosis: a link between obesity and diabetes. Proc Natl Acad Sci USA 1998; 95: 2498–2502.
Zhou YP, Grill V . Long term exposure to fatty acids and ketones inhibits B-cell functions in human pancreatic islets of Langerhans. J Clin Endocrinol Metab 1995; 80: 1584–1590.
Prentki M, Vischer S, Glennon MC, Regazzi R, Deeney JT, Corkey BE . Malonyl-CoA and long chain acyl-CoA esters as metabolic coupling factors in nutrient-induced insulin secretion. J Biol Chem 1992; 267: 5802–5810.
Abate N, Chandalia M, Snell PG, Grundy SM . Adipose tissue metabolites and insulin resistance in nondiabetic Asian Indian men. J Clin Endocrinol Metab 2004; 89: 2750–2755.
Liew CF, Seah ES, Yeo KP, Lee KO, Wise SD . Lean, nondiabetic Asian Indians have decreased insulin sensitivity and insulin clearance, and raised leptin compared to Caucasians and Chinese subjects. Int J Obes Relat Metab Disord 2003; 27: 784–789.
Valsamakis G, Chetty R, McTernan PG, Al-Daghri NM, Barnett AH, Kumar S . Fasting serum adiponectin concentration is reduced in Indo-Asian subjects and is related to HDL cholesterol. Diabetes Obes Metab 2003; 5: 131–135.
Isharwal S, Misra A, Wasir JS, Nigam P . Diet & insulin resistance: a review & Asian Indian perspective. Indian J Med Res 2009; 129: 485–499.
Hayes L, White M, Unwin N, Bhopal R, Fischbacher C, Harland J et al. Patterns of physical activity and relationship with risk markers for cardiovascular disease and diabetes in Indian, Pakistani, Bangladeshi and European adults in a UK population. J Public Health Med 2002; 24: 170–178.
Abate N, Chandalia M, Satija P, Adams-Huet B, Grundy SM, Sandeep S et al. ENPP1/PC-1 K121Q polymorphism and genetic susceptibility to type 2 diabetes. Diabetes 2005; 54: 1207–1213.
Radha V, Mohan V . Genetic predisposition to type 2 diabetes among Asian Indians. Indian J Med Res 2007; 125: 259–274.
Naran NH, Chetty N, Crowther NJ . The influence of metabolic syndrome components on plasma PAI-1 concentrations is modified by the PAI-1 4G/5G genotype and ethnicity. Atherosclerosis 2008; 196: 155–163.
Chandak GR, Ward KJ, Yajnik CS, Pandit AN, Bavdekar A, Joglekar CV et al. Triglyceride associated polymorphisms of the APOA5 gene have very different allele frequencies in Pune, India compared to Europeans. BMC Med Genet 2006; 7: 76.
Waterworth DM, Talmud PJ, Humphries SE, Wicks PD, Sagnella GA, Strazzullo P et al. Variable effects of the APOC3–482C >T variant on insulin, glucose and triglyceride concentrations in different ethnic groups. Diabetologia 2001; 44: 245–248.
Yajnik CS . Obesity epidemic in India: intrauterine origins? Proc Nutr Soc 2004; 63: 387–396.
Yajnik CS, Fall CH, Coyaji KJ, Hirve SS, Rao S, Barker DJ et al. Neonatal anthropometry: the thin-fat Indian baby. The Pune Maternal Nutrition Study. Int J Obes Relat Metab Disord 2003; 27: 173–180.
Burden ML, Samanta A, Spalding D, Burden AC . A comparison of the glycaemic and insulinaemic effects of an Asian and a European meal. Practical Diabetes Int 1994; 11: 208–211.
Merchant AT, Anand SS, Kelemen LE, Vuksan V, Jacobs R, Davis B et al. Carbohydrate intake and HDL in a multiethnic population. Am J Clin Nutr 2007; 85: 225–230.
McKeigue PM, Marmot MG, Adelstein AM, Hunt SP, Shipley MJ, Butler SM et al. Diet and risk factors for coronary heart disease in Asians in northwest London. Lancet 1985; 2: 1086–1090.
Miller GJ, Kotecha S, Wilkinson WH, Wilkes H, Stirling Y, Sanders TA et al. Dietary and other characteristics relevant for coronary heart disease in men of Indian, West Indian and European descent in London. Atherosclerosis 1988; 70: 63–72.
Mitra SR, Mazumder DN, Basu A, Block G, Haque R, Samanta S et al. Nutritional factors and susceptibility to arsenic-caused skin lesions in West Bengal, India. Environ Health Perspect 2004; 112: 1104–1109.
Pushpamma P, Geervani P, Rani MU . Food intake and nutrient adequacy of rural population of Andhra Pradesh, India. Hum Nutr Appl Nutr 1982; 36A: 293–301.
Panwar B, Punia D . Food intake of rural pregnant women of Haryana State, northern India: relationship with education and income. Int J Food Sci Nutr 1998; 49: 243–247.
Rogers A, Adamson JE, McCarthy M . Variations in health behaviours among inner city 12-year-olds from four ethnic groups. Ethn Health 1997; 2: 309–316.
Sachdev HP . Low Birth Weight in South Asia. Int J Diab Dev Ctries 2001; 21: 13–33.
Fall CHD, Yajnik CS, Rao S, Coyaji KJ, Shier RP . The effects of maternal body composition before birth on fetal growth: the Pune Maternal nutrition and Fetal Growth Study. In: O’Brien PMS, Wheeler T, Barker DJP (eds). Fetal Programming; Influences on Development and Disease in Later Life. RCOG Press: London, 1999.
Sachdev HS, Fall CH, Osmond C, Lakshmy R, Dey Biswas SK, Leary SD et al. Anthropometric indicators of body composition in young adults: relation to size at birth and serial measurements of body mass index in childhood in the New Delhi birth cohort. Am J Clin Nutr 2005; 82: 456–466.
Renges HH, Wile DB, McKeigue PM, Marmot MG, Humphries SE . Apolipoprotein B gene polymorphisms are associated with lipid levels in men of South Asian descent. Atherosclerosis 1991; 91: 267–275.
Saha N, Tay JS, Heng CK, Humphries SE . DNA polymorphisms of the apolipoprotein B gene are associated with obesity and serum lipids in healthy Indians in Singapore. Clin Genet 1993; 44: 113–120.
Cassell PG, Saker PJ, Huxtable SJ, Kousta E, Jackson AE, Hattersley AT et al. Evidence that single nucleotide polymorphism in the uncoupling protein 3 (UCP3) gene influences fat distribution in women of European and Asian origin. Diabetologia 2000; 43: 1558–1564.
Shen H, Qi L, Tai ES, Chew SK, Tan CE, Ordovas JM . Uncoupling protein 2 promoter polymorphism -866G/A, central adiposity, and metabolic syndrome in Asians. Obesity (Silver Spring) 2006; 14: 656–661.
Vimaleswaran KS, Radha V, Mohan V . Thr54 allele carriers of the Ala54Thr variant of FABP2 gene have associations with metabolic syndrome and hypertriglyceridemia in urban South Indians. Metabolism 2006; 55: 1222–1226.
Miller M, Rhyne J, Khatta M, Parekh H, Zeller K . Prevalence of the APOC3 promoter polymorphisms T-455C and C-482 T in Asian-Indians. Am J Cardiol 2001; 87: 220–221, A8.
Abate N, Carulli L, Cabo-Chan Jr A, Chandalia M, Snell PG, Grundy SM . Genetic polymorphism PC-1 K121Q and ethnic susceptibility to insulin resistance. J Clin Endocrinol Metab 2003; 88: 5927–5934.
Chiu KC, Chuang LM, Yoon C, Saad MF . Hepatic glucokinase promoter polymorphism is associated with hepatic insulin resistance in Asian Indians. BMC Genet 2000; 1: 2.
Miller M, Rhyne J, Chen H, Beach V, Ericson R, Luthra K et al. APOC3 promoter polymorphisms C-482 T and T-455C are associated with the metabolic syndrome. Arch Med Res 2007; 38: 444–451.
Teoh M, Lalondrelle S, Roughton M, Grocott-Mason R, Dubrey SW . Acute coronary syndromes and their presentation in Asian and Caucasian patients in Britain. Heart 2007; 93: 183–188.
Lear JT, Lawrence IG, Pohl JE, Burden AC . Myocardial infarction and thrombolysis: a comparison of the Indian and European populations on a coronary care unit. J R Coll Physicians Lond 1994; 28: 143–147.
Laakso M, Lehto S . Epidemiology of macrovascular disease in diabetes. Diabetes Rev 1997; 5: 294–315.
Barakat K, Wells Z, Ramdhany S, Mills PG, Timmis AD . Bangladeshi patients present with non-classic features of acute myocardial infarction and are treated less aggressively in east London, UK. Heart 2003; 89: 276–279.
Patel DJ, Winterbotham M, Sutherland SE, Britt RG, Keil JE, Sutton GC . Comparison of methods to assess coronary heart disease prevalence in South Asians. Natl Med J India 1997; 10: 210–213.
King KM, Khan NA, Quan H . Ethnic variation in acute myocardial infarction presentation and access to care. Am J Cardiol 2009; 103: 1368–1373.
Gupta M, Tabas JA, Kohn MA . Presenting complaint among patients with myocardial infarction who present to an urban, public hospital emergency department. Ann Emerg Med 2002; 40: 180–186.
Fischbacher CM, Bhopal R, Unwin N, White M, Alberti KG . The performance of the Rose angina questionnaire in South Asian and European origin populations: a comparative study in Newcastle, UK. Int J Epidemiol 2001; 30: 1009–1016.
Goldberg R, Goff D, Cooper L, Luepker R, Zapka J, Bittner V et al. Age and sex differences in presentation of symptoms among patients with acute coronary disease: the REACT Trial. Rapid early action for coronary treatment. Coron Artery Dis 2000; 11: 399–407.
Canto JG, Shlipak MG, Rogers WJ, Malmgren JA, Frederick PD, Lambrew CT et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. JAMA 2000; 283: 3223–3229.
Shaukat N, de Bono DP, Cruickshank JK . Clinical features, risk factors, and referral delay in British patients of Indian and European origin with angina matched for age and extent of coronary atheroma. Br Med J 1993; 307: 717–718.
Lear JT, Lawrence IG, Burden AC, Pohl JE . A comparison of stress test referral rates and outcome between Asians and Europeans. J R Soc Med 1994; 87: 661–662.
Lawrence RE, Littler WA . Acute myocardial infarction in Asians and whites in Birmingham. Br Med J (Clin Res Ed) 1985; 290: 1472.
Bradley EH, Herrin J, Wang Y, McNamara RL, Webster TR, Magid DJ et al. Racial and ethnic differences in time to acute reperfusion therapy for patients hospitalized with myocardial infarction. JAMA 2004; 292: 1563–1572.
Hawthorne K, Mello M, Tomlinson S . Cultural and religious influences in diabetes care in Great Britain. Diabet Med 1993; 10: 8–12.
Mather HM . Diabetes in elderly Asians. J R Soc Med 1994; 87: 615–616.
Wrightson KJ, Wardle J . Cultural variation in health locus of control. Ethn Health 1997; 2: 13–20.
Hawthorne K . Asian diabetics attending a British hospital clinic: a pilot study to evaluate their care. Br J Gen Pract 1990; 40: 243–247.
Hawthorne K . Effect of culturally appropriate health education on glycaemic control and knowledge of diabetes in British Pakistani women with type 2 diabetes mellitus. Health Educ Res 2001; 16: 373–381.
Hawthorne K, Tomlinson S . Pakistani moslems with Type 2 diabetes mellitus: effect of sex, literacy skills, known diabetic complications and place of care on diabetic knowledge, reported self-monitoring management and glycaemic control. Diabet Med 1999; 16: 591–597.
Baradaran H, Knill-Jones RP . Assessing the knowledge, attitudes and understanding of type 2 diabetes amongst ethnic groups in Glasgow, Scotland. Pract Diab Int 2004; 21: 143–148.
Hawthorne K . South Asian diabetic patients need more education about their illness. Br Med J 1997; 314: 1486.
Chowdhury AM, Helman C, Greenhalgh T . Food beliefs and practices among British Bangladeshis with diabetes: implications for health education. Anthropol Med 2000; 7: 209–226.
Samanta A, Campbell JE, Spaulding DL, Neogi SK, Panja KK, Burden AC . Eating habits in Asian diabetics. Diabet Med 1986; 3: 283–284.
Macaden L, Clarke CL . Risk perception among older South Asian people in the UK with type 2 diabetes. Int J Older People Nursing 2006; 1: 177–181.
Aslam M, Healy MA . Compliance and drug therapy in fasting Moslem patients. J Clin Hosp Pharm 1986; 11: 321–325.
Greenhalgh T, Helman C, Chowdhury AM . Health beliefs and folk models of diabetes in British Bangladeshis: a qualitative study. Br Med J 1998; 316: 978–983.
Patel V, Morrissey J, Goenka N, James D, Shaikh S . Diabetes care in the Hindu patient: cultural and clinical aspects. Br J Diabetes Vasc Dis 2001; 1: 132–135.
Allawi J, Rao PV, Gilbert R, Scott G, Jarrett RJ, Keen H et al. Microalbuminuria in non-insulin-dependent diabetes: its prevalence in Indian compared with Europid patients. Br Med J (Clin Res Ed) 1988; 296: 462–464.
Mukhopadhyay B, Forouhi NG, Fisher BM, Kesson CM, Sattar N . A comparison of glycaemic and metabolic control over time among South Asian and European patients with Type 2 diabetes: results from follow-up in a routine diabetes clinic. Diabet Med 2006; 23: 94–98.
Martin SC, Jones AF . South Asians with diabetes mellitus do not receive lipid-lowering treatment despite an identical calculated risk of coronary heart disease compared with Caucasians. Pract Diabet Int 2000; 17: 77–80.
Close CF, Lewis PG, Holder R, Wright AD, Nattrass M . Diabetes care in South Asian and white European patients with type 2 diabetes. Diabet Med 1995; 12: 619–621.
Gupta M, Braga MF, Teoh H, Tsigoulis M, Verma S . Statin effects on LDL and HDL cholesterol in South Asian and white populations. J Clin Pharmacol 2009; 49: 831–837.
Brister SJ, Hamdulay Z, Verma S, Maganti M, Buchanan MR . Ethnic diversity: South Asian ethnicity is associated with increased coronary artery bypass grafting mortality. J Thorac Cardiovasc Surg 2007; 133: 150–154.
Blackledge HM, Newton J, Squire IB . Prognosis for South Asian and white patients newly admitted to hospital with heart failure in the United Kingdom: historical cohort study. Br Med J 2003; 327: 526–531.
Mukhtar HT, Littler WA . Survival after acute myocardial infarction in Asian and white patients in Birmingham. Br Heart J 1995; 73: 122–124.
UK Prospective Diabetes Study Group. The incidence of myocardial infarction in White, south Asian and Afro-Caribbean patients with type diabetes (UKPDS 32). Diabetes Care 1998; 21: 1271–1277.
Lee E, Ryan S, Birmingham B, Zalikowski J, March R, Ambrose H et al. Rosuvastatin pharmacokinetics and pharmacogenetics in white and Asian subjects residing in the same environment. Clin Pharmacol Ther 2005; 78: 330–341.
Kim K, Birmingham BK . Increased Systemic Exposure to Rosuvastatin in Asian Subjects Residing in the United States as Compared to Caucasians. Poster presented at: American Society for Clinical Pharmacology and Therapeutics, 2–5 April Orlando, Florida, USA, 2008.
Helfand M, Carson S, Kelley C . Drug Class Review on HMG-CoA Reductase Inhibitors (Statins). Oregon Health & Science University: Portland, Oregon. Final report 2006. Available at: http://www.ncbi.nlm.nih.gov/bookshelf/picrender.fcgi?book=statins&blobtype=pdf (Last accessed: May 2010).
CRESTOR (rosuvastatin) European Prescribing Information. Available at: http://www.crestor.info/_mshost586501/content/resources/media/607780/607782. (Last accessed: May 2010).
Raji A, Gerhard-Herman MD, Williams JS, O’Connor M E, Simonson DC . Effect of pioglitazone on insulin sensitivity, vascular function and cardiovascular inflammatory markers in insulin-resistant non-diabetic Asian Indians. Diabet Med 2006; 23: 537–543.
Emott M, Freemark M . Treatment of Insulin Resistance in Youth: the Role of Metformin; Energy Metabolism and Obesity. Chapter 13. Humana Press: Springer Link, 2008, pp 247–267.
Earle KK, Porter KA, Ostberg J, Yudkin JS . Variation in the progression of diabetic nephropathy according to racial origin. Nephrol Dial Transplant 2001; 16: 286–290.
World Health Organization. Obesity and overweight. Available at: http://www.who.int/mediacentre/factsheets/fs311/en/ (Last accessed: May 2010).
Grundy SM, Brewer Jr HB, Cleeman JI, Smith Jr SC, Lenfant C . Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation 2004; 109: 433–438.
Williams ED, Kooner I, Steptoe A, Kooner JS . Psychosocial factors related to cardiovascular disease risk in UK South Asian men: a preliminary study. Br J Health Psychol 2007; 12: 559–570.
Smith J, Al-Amri M, Sniderman A, Cianflone K . Leptin and adiponectin in relation to body fat percentage, waist to hip ratio and the apoB/apoA1 ratio in Asian Indian and Caucasian men and women. Nutr Metab (Lond) 2006; 3: 18.
Razak F, Anand S, Vuksan V, Davis B, Jacobs R, Teo KK et al. Ethnic differences in the relationships between obesity and glucose-metabolic abnormalities: a cross-sectional population-based study. Int J Obes (Lond) 2005; 29: 656–667.
Tillin T, Forouhi N, McKeigue P, Chaturvedi N . Microalbuminuria and coronary heart disease risk in an ethnically diverse UK population: a prospective cohort study. J Am Soc Nephrol 2005; 16: 3702–3710.
Stoney CM, Hughes JW, Kuntz KK, West SG, Thornton LM . Cardiovascular stress responses among Asian Indian and European American women and men. Ann Behav Med 2002; 24: 113–121.
Dickinson S, Colagiuri S, Faramus E, Petocz P, Brand-Miller JC . Postprandial hyperglycemia and insulin sensitivity differ among lean young adults of different ethnicities. J Nutr 2002; 132: 2574–2579.
Patel S, Unwin N, Bhopal R, White M, Harland J, Ayis SA et al. A comparison of proxy measures of abdominal obesity in Chinese, European and South Asian adults. Diabet Med 1999; 16: 853–860.
Pomerleau J, McKeigue PM, Chaturvedi N . Factors associated with obesity in South Asian, Afro-Caribbean and European women. Int J Obes Relat Metab Disord 1999; 23: 25–33.
Tillin T, Forouhi N, Johnston DG, McKeigue PM, Chaturvedi N, Godsland IF . Metabolic syndrome and coronary heart disease in South Asians, African-Caribbeans and white Europeans: a UK population-based cross-sectional study. Diabetologia 2005; 48: 649–656.
Anand SS, Razak F, Yi Q, Davis B, Jacobs R, Vuksan V et al. C-reactive protein as a screening test for cardiovascular risk in a multiethnic population. Arterioscler Thromb Vasc Biol 2004; 24: 1509–1515.
Gerstein HC, Anand S, Yi QL, Vuksan V, Lonn E, Teo K et al. The relationship between dysglycemia and atherosclerosis in South Asian, Chinese, and European individuals in Canada: a randomly sampled cross-sectional study. Diabetes Care 2003; 26: 144–149.
Kalhan R, Puthawala K, Agarwal S, Amini SB, Kalhan SC . Altered lipid profile, leptin, insulin, and anthropometry in offspring of South Asian immigrants in the United States. Metabolism 2001; 50: 1197–1202.
Shaukat N, de Bono DP, Jones DR . Like father like son? Sons of patients of European or Indian origin with coronary artery disease reflect their parents’ risk factor patterns. Br Heart J 1995; 74: 318–323.
Knight T, Smith Z, Lockton JA, Sahota P, Bedford A, Toop M et al. Ethnic differences in risk markers for heart disease in Bradford and implications for preventive strategies. J Epidemiol Community Health 1993; 47: 89–95.
McKeigue PM, Laws A, Chen YD, Marmot MG, Reaven GM . Relation of plasma triglyceride and apoB levels to insulin-mediated suppression of nonesterified fatty acids. Possible explanation for sex differences in lipoprotein pattern. Arterioscler Thromb 1993; 13: 1187–1192.
Mohan V, Sharp PS, Cloke HR, Burrin JM, Schumer B, Kohner EM . Serum immunoreactive insulin responses to a glucose load in Asian Indian and European type 2 (non-insulin-dependent) diabetic patients and control subjects. Diabetologia 1986; 29: 235–237.
Anand SS, Yi Q, Gerstein H, Lonn E, Jacobs R, Vuksan V et al. Relationship of metabolic syndrome and fibrinolytic dysfunction to cardiovascular disease. Circulation 2003; 108: 420–425.
Chandalia M, Mohan V, Adams-Huet B, Deepa R, Abate N . Ethnic difference in sex gap in high-density lipoprotein cholesterol between Asian Indians and Whites. J Investig Med 2008; 56: 574–580.
Bhalodkar NC, Blum S, Rana T, Kitchappa R, Bhalodkar AN, Enas EA . Comparison of high-density and low-density lipoprotein cholesterol subclasses and sizes in Asian Indian women with Caucasian women from the Framingham Offspring Study. Clin Cardiol 2005; 28: 247–251.
Merchant AT, Anand SS, Vuksan V, Jacobs R, Davis B, Teo K et al. Protein intake is inversely associated with abdominal obesity in a multi-ethnic population. J Nutr 2005; 135: 1196–1201.
Mohanty SA, Woolhandler S, Himmelstein DU, Bor DH . Diabetes and cardiovascular disease among Asian Indians in the United States. J Gen Intern Med 2005; 20: 474–478.
Riste L, Khan F, Cruickshank K . High prevalence of type 2 diabetes in all ethnic groups, including Europeans, in a British inner city: relative poverty, history, inactivity, or 21st century Europe? Diabetes Care 2001; 24: 1377–1383.
Shaukat N, Douglas JT, Bennett JL, de Bono DP . Can physical activity explain the differences in insulin levels and fibrinolytic activity between young Indo-origin and European relatives of patients with coronary artery disease? Fibrinolysis 1995; 9: 55–63.
Rudat K . Black and Minority Ethnic Groups in England: Health & Lifestyles. Health Education Authority: London, 1994. Available at: www.nice.org.uk/nicemedia/documents/black_minorities_england94.pdf (Last accessed: May 2010).
Williams R, Bhopal R, Hunt K . Coronary risk in a British Punjabi population: comparative profile of non-biochemical factors. Int J Epidemiol 1994; 23: 28–37.
Knight TM, Smith Z, Whittles A, Sahota P, Lockton JA, Hogg G et al. Insulin resistance, diabetes, and risk markers for ischaemic heart disease in Asian men and non-Asian in Bradford. Br Heart J 1992; 67: 343–350.
Owen CG, Nightingale CM, Rudnicka AR, Cook DG, Ekelund U, Whincup PH . Ethnic and gender differences in physical activity levels among 9–10-year-old children of white European, South Asian and African-Caribbean origin: the Child Heart Health Study in England (CHASE Study). Int J Epidemiol 2009; 38: 1082–1093.
Duncan EK, Scott Duncan J, Schofield G . Pedometer-determined physical activity and active transport in girls. Int J Behav Nutr Phys Act 2008; 5: 2.
Bettiol H, Rona RJ, Chinn S . Variation in physical fitness between ethnic groups in nine year olds. Int J Epidemiol 1999; 28: 281–286.
Williams R, Shams M . Generational continuity and change in British Asian health and health behaviour. J Epidemiol Community Health 1998; 52: 558–563.
We are grateful to Mr Amit Kumar, who helped us in reproducing the figure from the data.
The authors declare no conflict of interest.
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Misra, A., Khurana, L. Obesity-related non-communicable diseases: South Asians vs White Caucasians. Int J Obes 35, 167–187 (2011). https://doi.org/10.1038/ijo.2010.135
- coronary heart disease
- South Asians
- White Caucasians
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