Rachel and Michael: South Asians and their increased cardiovascular risk: A review of risk factors and diet and lifestyle modification.


South Asians (SAs), originating from the Indian subcontinent, are the largest ethnic minority in several European nations. Compared to Caucasian populations, SAs have a higher incidence and severity of cardiovascular disease (CVD) and its complications at a younger age and have a 40-60% higher risk of disease-related mortality1–8. This has prompted the suggestion that SA CVD should be viewed as a separate condition to that found in Caucasians9 or that SA ethnicity is itself a risk factor1. This article discusses the principal challenges in assessing SAs and provides dietary and lifestyle measures to help these patients.

Lowered thresholds for SAs

The guidelines and thresholds for diagnosis, prevention or treatment are largely based on Caucasians, with consequent concern that risks and early disease presentation for SAs may be overlooked. The thresholds principally fail to allow for the SA unique pattern of body fat distribution and abdominal obesity10–11, with higher total body fat percentage and amount of subcutaneous and visceral adipose tissue but less lean body mass for the same BMI as Caucasians12–15. In addition, a higher SA waist-to-hip (WTH) ratio contributes to higher CVD and metabolic syndrome rates15,16. Furthermore, for every level of BMI, SAs are more insulin resistant and more prone to glucose intolerance, T2D and dyslipidaemia than Caucasians1, 17–19. The UK South Asian Health Foundation (SAHF) recommends BMI cut-off levels of 23kg/m2 for overweight adults and 25kg/m2 for obesity (instead of 25kg/m2 and 30kg/m2 respectively) as SA thresholds for dietary and lifestyle intervention20. Other international organisations recommend a waist circumference threshold of 90cm for SA men (94cm in European men), with impaired fasting glucose level at 100mg/dl21–23.

A further concern is that SAs with acute myocardial infarction (MI) may present with atypical symptoms and at a younger age, leading to delay in diagnosis and treatment24,25, while even SA children and neonates are now developing metabolic syndrome and CVD26–28. Additionally, SAs are not a homogeneous population, with Bangladeshis generally having higher risk factors and earlier disease incidence15,29 and considerable differences between other SA ethnicities30. One contributory factor may be ‘foetal origin’, where maternal malnutrition results in low birth weight, with its role in CVD and T2D development31–33, particularly if by age 8 children have a high weight and fat mass33,34.

South Asians and key CVD risk factors

The principal CVD risk factor among SAs is T2D, with up to five times higher disease incidence than Caucasians35,36, and onset occurring up to ten years earlier. SA T2D patients may present with more complications and can suffer a 40% increase in MI incidence and four times higher CV mortality3,37,38. SAs are also likely to have the hallmarks of metabolic syndrome: central obesity, insulin resistance, impaired glucose tolerance, low HDL, high triglycerides and hypertension1,39,40.

Conventional risk factors, even with lowered thresholds, cannot fully predict the increased CVD risk in SAs1,39,41. The INTERHEART study, however, found nine MI risk factors which are valid in all ethnicities, albeit at a younger age in SAs15,42. These include T2D, smoking, hypertension, high WTH ratio, high apoB100/apoA1 ratio, stress/depression, inactivity, high alcohol consumption and low fruit and vegetable consumption15,42,43. In addition, immigrants who adopt western dietary habits and lifestyles could be at even greater risk than those in the Indian subcontinent44,45. Some researchers have also suggested that the smaller coronary arteries found in SAs cause increased stenosis but after correction for body surface area there was no difference in coronary artery diameter between SAs and Caucasians, notwithstanding the potential implications for intervention procedures46.

The SAHF and others recommend that SAs are given routine WTH measurement and testing of fasting glucose and lipids and suggest that a truer adjusted risk can be obtained by multiplying the Framingham risk score by 1.4 or adding 10 years to the SA patient’s age47,48. Diabetes UK and the SAHF also recommend using the total cholesterol to HDL ratio, rather than total cholesterol alone5,49.

South Asian knowledge of and attitudes to health risks

A UK National Health Service survey found that many SAs are unaware of their increased risk of CVD and T2D. Even when they have developed disease, SAs are often not aware of related causes and complications or preventive measures, such as healthier foods or cooking methods, despite public health campaigns and publicity14,50,51. An additional problem is that SAs are reluctant to accept that amelioration of their condition is within their control. Diabetics regularly visited by a specialist nurse or dietician showed no significant improvement in diabetes knowledge or self-management52, regardless of the presence of Asian link workers53. They continued with their previous dietary habits despite detriment to glycaemic control54 and even after suffering a cardiac event55. Additionally, South Asian T2D and CVD patients find it difficult to adhere publicly to a healthy dietary or lifestyle programme56, resulting in any glycaemic control which may be achieved in the home being overturned by fasting and festivals14, possibly through fear of alienation from the SA community54. Fasting can result in severe hypoglycaemia while a large sunset meal, often high in fats and sugars, can promote hyperglycaemia, the worst possible combination for SAs56,57.

Dietary and lifestyle recommendations

Most risk factors can be significantly lowered by diet and lifestyle modification and it is worth persevering with attempts to educate SAs as to the protective means which are within their control. In an intervention trial of 1000 SAs with angina, MI or risk factors, those given a diet rich in whole grains, fruits, vegetables and nuts with healthier oils showed significant improvement58.


One key problem is that SAs tend to eat significantly fewer meals per day than Caucasians, with a large late evening meal59. This promotes hypoglycaemia during the day, with the need to snack, followed by hyperglycaemia following the large late night meal, which would also impact adversely on digestion and sleep patterns.

Fruit and vegetables

Although many SAs are vegetarians, their plant intake is low60, with resultant low micronutrient levels, thought to exacerbate risk of atherosclerosis, CHD and T2D27,61-63. Regular high fruit and vegetable consumption is associated with a 30% reduction in acute MI risk among SAs42 and is inversely associated with metabolic syndrome risk factors64. SAs also tend to overcook vegetables, which can destroy 90% of the nutrient content65,66. Many traditional SA vegetables and herbs have hypoglycaemic properties63,67-69 but have recently been abandoned in favour of Western foods45,70. Fruits and root vegetables have a high glycaemic index (GI) and should be eaten sparingly71.


The high carbohydrate content of the typical SA diet increases plasma glucose, insulin and triglyceride levels and lowers HDL and is positively correlated with insulin resistance, insulin levels and T2D development69,72-75. Intake of rice, breads and potato has been found to be particularly high among SA MI patients45,70. Most of the SA energy intake comes from refined (white) flour or rice, which is a risk factor for metabolic syndrome76. Refined grains are lower in dietary fibre, have lost many of their beneficial nutrients and are often high GI foods77. By contrast, the fibre content of complex (unrefined) carbohydrates slows the release of glucose into the blood71,77.

Sugar and sweetened drinks

Sugar intake is positively correlated with insulin resistance72–74, while reduction is associated with higher HDL73. Traditional Indian sweets are predominantly fried sugar and fat, so should be avoided on all counts. Brown sugar (ghor) and honey may mistakenly be considered healthy, but actually have a similar effect on blood glucose as white sugar71. Undiluted fruit juice or sweetened drinks, particularly with high fructose corn syrup, markedly increase T2D risk71.


The principal problem for SAs is the high intake of hydrogenated oils and trans fats78, which are associated with increased incidence of diabetes79 and CVD15,40,42,78 and can interfere with the formation of protective long chain omega-3 polyunsaturated fatty acids (PUFAs), raising LDL and lowering HDL78. SAs regularly use vegetable oils (vanaspati or vegetable ghee) for cooking. When exposed to high temperatures, the cis double bonds in these oils are converted to trans form, creating the dangerous trans fats80. Virtually all SA commercially produced foods and fried snacks have been made with vanaspati heated to very high temperatures and in some foods the trans fat content can be up to 40%56,79. Furthermore, ghee (clarified butter) is more atherogenic than ordinary butter as it contains oxidised lipids56. Frequent use of ghee also leads to increased plasma trans fats and decreased omega-3 PUFAs81,82 and is associated with increased risk of MI60.

SA diets are also low in beneficial omega-3 PUFAs (found as fish oils) and mono-unsaturated fats (mainly olive oil). By contrast, diets high in these fats increase HDL cholesterol and improve insulin sensitivity75,78,83. Several meta-analyses of intervention studies have shown that supplementation of long chain omega-3 PUFAs significantly improved biomarkers of metabolic syndrome and T2D83,84. In addition, breast feeding with a maternal diet high in omega-3s PUFAs can protect against the development of insulin resistance, T2D and hypertension, suggesting that pregnant and lactating women at risk should supplement80.


South Asians often consume little protein and have lower concentrations of haem iron and vitamin B12, putting them at risk of hyperhomocysteinaemia85,86. Protein substituted for carbohydrates can result in a reduction in WTH ratio87, while lean red meat is rich in niacin, which can improve the lipid profile, and vitamin B12, which lowers homocysteine.


Although alcohol consumption is not high among SAs, virtually any intake is associated with increased CV risk, rather than the regular moderate drinking which is protective in Caucasians15,42,74,88. Binge and spirit drinking may be particularly harmful56. The recommended maximum for SAs is one alcoholic drink per day for women and two per day for men, although if serum triglycerides >500mg/dL or the patient has severe liver dysfunction or hypertension, alcohol should be avoided altogether65,71.

Smoking and chewing tobacco and betel nut

Important risk factors for SA CVD include chewing betel quid (paan, gutka), smoking regular cigarettes or bidi (thin cigarettes wrapped in brown tendu leaf) and smoking shisha (water pipe or hookah)1,15,56,66,89. One session of hookah smoking provides the same amount of smoke as more than 100 cigarettes and both contain nicotine, carcinogens and toxic gases, while the CV and respiratory effects of chewing tobacco are similar to those of smoking20,66,90. Chewing of betel nut on its own is highly addictive, inducing a cocaine-like dependency20 and is genotoxic, carcinogenic, mutagenic and associated with hyperglycaemia91. The SAHF points out that imports of smokeless tobacco from the Indian subcontinent are often not adequately labelled and are readily available, even to children, which is both illegal and highly dangerous to health20.


Physical inactivity is an independent CV risk factor for SAs1,42,50,92, who generally take little exercise15,93. A UK study of SA women found that most were unaware that exercise was protective and guidance from health professionals was lacking94. For many, regular physical activity is culturally unacceptable15 and is seen as possibly exacerbating illness and promoting physical weakness14. Most SAs did not feel comfortable in a Western sports centre88. Nevertheless, exercising is protective in SAs15; brisk walking for 35-40 minutes a day was associated with a >50% reduction in CHD risk95, while physical activity improved virtually all CVD and T2D biomarkers92,96,97. Guidelines for SAs vary, with some recommending daily aerobic and anaerobic activity65,71; the NHS recommends 150 minutes of moderate-intensity aerobic exercise every week66.

Vitamin D

Asian Indian immigrants in northern climates have lower serum 25(OH)D than Caucasians and have a tendency to develop rickets and osteomalacia; in the Netherlands over 51% of SAs were vitamin D-deficient (25(OH)D <25nmol/l)98. Low vitamin D concentrations are related to increased risk of T2D, affecting pancreatic insulin secretion and insulin resistance91,99. SAs also appear to have increased vitamin D catabolism, possibly through betel nut chewing and cigarette smoking91,100. However, insulin resistant SA women with serum 25(OH)D <50nmol/l given 4000IU/d or placebo for six months showed significantly improved insulin sensitivity and resistance, particularly when 25(OH)D reached ≥80nmol/l99.


Not all health professionals may be aware of the increased SA prevalence of CVD, T2D and associated mortality, nor of the lowered thresholds for age, BMI and waist circumference. Furthermore SAs may present with atypical symptoms and without some of the conventional risk factors. It has therefore been recommended that thresholds for BMI in SAs should be revised downwards to overweight ≥23kg/m2 and obese ≥25kg/m2, with waist circumference threshold for men of ≥90cm. South Asians are generally poorly informed about their condition and its preventive measures and may not be aware that their disease prevalence and early onset are abnormal or that much of the prevention and management of their condition is within their own control. Moreover, cultural traditions mean that implementation of dietary and lifestyle modification is poor.

The increased risk among SAs may in large part be due to their diet and lifestyle with the high preponderance of food fried in damaging trans fats, low protective omega-3 fats, high sugar intake and little exercise. In addition, many smoke or chew paan, both strong risk factors for cancer and CVD. The radical change that is needed must come with SA community-based initiatives, in which risk factor lowering is freely discussed and the community as a whole is motivated to ensure adherence to diet and lifestyle programmes. Nevertheless, education has to start with information about their condition, an attempt to change the belief that early disease and death are inevitable and encouragement that the means for improvement via dietary and lifestyle modification are in their own hands.



Anand SS, Yusuf S, Vuksan V, Devanesen S 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: 279–84


Yusuf S, Reddy S, Ounpuu S, Anand S ‘Global burden of cardiovascular diseases. II. Variations in cardiovascular disease by specific ethnic groups and geographic regions and prevention strategies’. Circulation. 2001; 104: 2855–64


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: 53–9


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’. BMJ.2003; 327: 526–31


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 to European men? Prospective follow-up of the Southall and Brent. Studies, UK. Diabetologia.2006; 49: 2580–8


Gunarathne A, Patel JV, Gammon B, Gill PS et al ‘Ischemic stroke in South Asians: a review of the epidemiology, pathophysiology and ethnicity-related clinical features’. Stroke. 2009; 40: e415–23


Mathur R, Hull SA, Badrick E, Robson J ‘Cardiovascular multimorbidity : the effect of ethnicity on prevalence and risk factor management’. Br J Gen Pract. 2011; 61(586)e262–70


Zaman MJJ, Patel KCR ‘South Asians and coronary heart disease: always bad news?’. Br J Gen Pract. 2011; 61(582)9–11


Jayasinghe SR, Jayasinghe SH ‘Variant metabolic risk factor profile leading to premature coronary disease: time to define the syndrome of accelerated atherocoronary metabolic syndrome in Asian Indians’. Singapore Med J. 2009; 50(10)949–55


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: 2750–5


Grundy SM ‘Obesity, metabolic syndrome and cardiovascular disease’. J Clin Endocrinol Metab. 2004; 89: 2595–600


Shah A, Hernandez A, Mathur D, Budoff MJ, Kanaya AM ‘Adipokines and body fat composition in South Asians: results of the Metabolic Syndrome and Atherosclerosis in South Asians Living in America (MASALA) study’. Int J Obes. 2011; Epub ahead of print


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: 353–9


Misra A, Khurana L ‘Obesity-related non-communicable diseases: South Asians vs White Caucasians’. Int J Obes. 2011; 35: 167–87


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: 286–94


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: 382–6


Jafar TH, Chaturvedi N, Pappas G ‘Prevalence of overweight and obesity and their association with hypertension and diabetes mellitus in an Indo-Asian population’. CMAJ. 2006; 175(9)1071–7


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(10)1295–1301


Razak F, Anand SS, Shannon H, Vuksan V, Davis B, Jacobs R et al ‘Defining obesity cut points in a multiethnic population’. Circulation. 2007; 115(16)2111–8


www.sahf.org.ukaccessed 10 October2011;


Grundy DM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA et al American Heart Association /National Lung, Heart and Blood Institute. ‘Diagnosis and management of the metabolic syndrome. An American Heart Association /National Lung, Heart and Blood Institute Scientific Statement’. Circulation. 2005; 112: 2735–52


Misra A, Vikram NK, Gupta R, Pandey RM, Wasir JS, Gupta VP ‘Waist circumference cutoff points and action levels for Asian Indians for identification of abdominal obesity’. Int J Obes (Lond). 2006; 30(1)106–11


Alberti KG, Zimmet P, Shaw J ‘The metabolic syndrome – a new worldwide definition’. Lancet. 2005; 366: 1059–62


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: 183–8


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: 276–9


Whincup PH, Gilg JA, Owen CG, Odoki K, Alberti KG, Cook DG ‘British South Asians aged 13-16 years have higher fasting glucose and insulin levels then Europeans’. Diabet Med. 2005; 22(9)1275–7


Whincup PH, Gilg JA, Papacosta O et al ‘Early evidence of ethnic differences in cardiovascular risk: cross-sectional comparison of British South Asian and white children’. BMJ. 2002; 324(7338)635


Yajnik CS, Lubree HG, Rege SS et al ‘Adiposity and hyperinsulinemia in Indians are present at birth’. J Clin Endocrinol Metab. 2002; 87(12)5575–80


Bhopal R, Unwin N, White M et al ‘Heterogeneity of coronary heart disease risk factors in Indian, Pakistani, Bangladeshi and European origin populations: cross-sectional study’. BMJ. 1999; 319(7204)215–20


The Health Survey for England. The health of Ethnic Minority Groups. Available from http://www.ic.nhs.uk/pubs. 2005-March 2006 Accessed 13 October 2011


Barker DJ Fetal origins of coronary heart disease’. BMJ.1995; 311: 171–4


Yajnik CS, Yudkin JS ‘The Y-Y paradox’. Lancet. 2004; 363: 163


Yajnik CS ‘Early life origins of insulin resistance and type 2 diabetes in India and other Asian countries’. J Nutr. 2004; 134: 205–10


Bavdekar A, Yajnik CS, Fall CH et al ‘Insulin resistance syndrome in 8-year-old Indian children: small at birth, big at 8 years, or both?’. Diabetes. 1999; 48: 2422–9


Unwin N, Alberti KG, Bhopal R et al ‘Comparison of the current WHO and new ADA criteria for the diagnosis of diabetes mellitus in three ethnic groups in the UK’. Diabet Med. 1998; 15: 554–7


Enas EA, Garg A, Davidson MA et al ‘Coronary heart disease and its risk factors in first generation immigrant Asian Indians to the United states of America’. Indian Heart J. 1996; 48: 343–53


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: 211–5


Chaturvedi N, Fuller JH ‘Ethnic differences in mortality from cardiovascular disease in the UK: do they persist in people with diabetes?’. J Epidemiol Community Health. 1996; 50: 137–9


Lyratzopouos G, McElduff P, Heller RF, Hanily M, Lewis PS ‘Comparative levels and time trends in blood pressure, total cholesterol, body mass index and smoking among Caucasian and South Asian participants of a UK primary-care based cardiovascular risk factor screening programme’. BMC Public Health. 2005; 5125


Misra A, Luthra K, Vikram NK ‘Dyslipidemia in Asian Indians: determinants and significance’. J Assoc Physicians India. 2004; 52: 137–42


Cappuccio FP, Oakeshott P, Strazzullo P, Kerry SM ‘Application of Framingham risk estimates to ethnic minorities in United Kingdom and implications for primary prevention of heart disease in general practice: cross sectional population based study’. Need remainder of Ref.


Yusuf S, Hawken S, Ounpuu S et al INTERHEART Study Investigators. ‘Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case control study’. Lancet. 2004; 364: 937–52


Karthikeyan G, Teo KK, Islam S, McQueen MJ et al ‘Lipid profile, plasma apolipoproteins and risk of a first myocardial infarction among Asians: an analysis from the INTERHEART study’. J Am Coll Cardiol. 2009; 53: 244–53


World Health Organisation. ‘The World Health Report. 2003; Shaping the future’. Geneva: WHO 2003


Patel JV, Vyas A, Cruickshank JK et al ‘Impact of migration on coronary heart disease risk factors: comparison of Gujaratis in Britain and their contemporaries in villages of origin in India’. Atherosclerosis. 2006; 185: 297–306


Dhawan J, Bray CL ‘Are Asian coronary arteries smaller than Caucasian? A study on angiographic coronary artery size estimation during life’. Int J Cardiol. 1995; 49: 267–9


South Asian Health Foundation. Consensus Statement. 2006; Dyslipidaemia management in South Asians. 2006


Aarabi M, Jackson PR ‘Predicting coronary risk in UK South Asians: an adjustment method for Framingham-based tools’. Eur J Cardiovasc Prev Rehabil. 2005; 12: 46–51


Patel KCR, Satter N ‘Dyslipidaemia’ in. Khunti K, Kumar S ‘Diabetes UK and South Asian Health Foundation Recommendations on Diabetes Research Priorities for British South Asians’. 1st Ed.Diabetes UKLondon, UK.2009; pp83–90


Lip GY, Luscombe C, McCarry M, Malik I, Beevers G ‘Ethnic differences in public health awareness, health perceptions and physical exercise: implications for heart disease prevention’. Ethn Health. 1996; 1(1)47–53


Bedi US, Singh S, Syed A, Aryafar H, Arora R ‘Coronary artery disease in South Asians: an emerging risk group’. Cardiol Rev. 2006; 14: 74–80


Vyas A, Haidery AZ, Wiles PG, Gill S, Roberts C, Cruickshank JK ‘A pilot randomised trial in primary care to investigate and improve knowledge, awareness and self-management among South Asians with diabetes in Manchester’. Diabet Med. 2003; 20(12)1022–6


Bellary S, O’Hare JP, Raymond NT, Gumber A, Mughal S, Szczepura A, Kumar S Barnett AH: UKADS Study Group’. Lancet. 2008; 371(9626)1769–76


Lawton J, Ahmad N, Hanna L, Douglas M, Bains H, Hallowell N ‘We should change ourselves but we can’t: accounts of food and eating practices amongst British Pakistanis and Indians with type 2 diabetes’. Ethn Health. 2008; 13(4)305–19


Mohan S, Wilkes L, Jackson D ‘Lifestyle of Asian Indians with coronary heart disease: the Australian context’. Collegian. 2008; 15(3)115–21


Hill J ‘Management of diabetes in South Asian communities in the UK’. Nurs Stand. 2006; 20(25)57–64


Mian SI, Brauer PM ‘Dietary education tools for South Asians with diabetes’. Can J Diet Pract Res. 2009; 70(1)28–35


Singh RB, Dubnov G, Niaz MA, Ghosh S, Singh R, Rastogi SS et al ‘Effect of an Indo-Mediterranean diet on progression of coronary artery disease in high risk patients (Indo-Mediterranean Diet Heart Study): a randomised single-blind trial’. Lancet. 2002; 360(9344)1455–61


Simmons D, Williams R ‘Dietary practices among Europeans and difference South Asian groups in Coventry’. Br J Nutr. 1997; 78(1)5–14


Ismail J, Jafar TH, Jafary FH et al ‘Risk factors for non-fatal myocardial infarction in young South Asian adults’. Heart. 2004; 90: 259–63


Joshipura KJ, Hu FB, Manson JE et al ‘The effect of fruit and vegetable intake on risk for coronary heart disease’. Ann Intern Med. 2001; 134: 1106–14


Panagiotakos DB, Pitsavos C, Kokkinos P et al ‘Consumption of fruits and vegetables in relation to the risk of developing acute coronary syndromes: the CARDIO. 2000 case control study’. Nutrition.2003; 2: 2


Nahas R, Moher M ‘Complementary and alternative medicine for the treatment of type 2 diabetes’. Can Fam Physician. 2009; 55(6)591–6


Radhika G, Sudha V, Mohan Sathya R, Ganesan A, Mohan V ‘Association of fruit and vegetable intake with cardiovascular risk factors in urban south Indians’. Br J Nutr. 2008; 99(2)398–405


Singh RB, Mori H, Chen J et al ‘Recommendations for the prevention of coronary artery disease in Asians: a scientific statement of the International College of Nutrition’. J Cardiovasc Risk. 1996; 3: 489–94


www.nhs.uk/Livewell/SouthAsianhealthaccessed 10 Oct2011;


Ansari NM, Houlihan L, Hussain B, Pieroni A ‘Antioxidant activity of five vegetables traditionally consumed by South-Asian migrants in Bradford, Yorkshire, UK’. Phytother Res. 2005; 19(10)907–11


Prabhakar PK, Doble M ‘Mechanism of action of natural products used in the treatment of diabetes mellitus’. Chin J Integr Med. 2011; 17(8)563–74


Mohan V, Radhika G, Sathya RM, Tamil SR, Ganesan A, Sudha V ‘Dietary carbohydrates, glycaemic load, food groups and newly detected type 2 diabetes among urban Asian Indian population in Chennai, India (Chennai Urban Rural Epidemiology Study 59)’. Br J Nutr. 2009; 9: 1–9


Wandel M, Raberg M, Kumar B, Holmboe-Ottesen G ‘Changes in food habits after migration among South Asians settled in Oslo: the effect of demographic, socio-economic and integration factors’. Appetite. 2008;


Misra A, Sharma R, Gulati S, Joshi SR, Sharma V, Ghafoorunissa et al ‘Consensus dietary guidelines for healthy living and prevention of obesity, the metabolic syndrome. Diabetes and related disorders in Asian Indians’. Diabetes Technology Therapeutics. 2011; 13(6)683–94


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: 208–11


Merchant AT, Anand SS, Kelemen LE, Vuksan V, Jacobs R, Davis B et al ‘Carbohydrate intake and HDL in a multi-ethnic population’. Am J Clin Nutr. 2007; 85: 225–30


Sevak L, McKeigue PM, Marmot MG ‘Relationship of hyperinsulinemia to dietary intake in south Asian and European men’. Am J Clin Nutr. 1994; 59: 1069–74


Mensink RP, Zock PL, Kester AD, Katan MB ‘Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials’. Am J Clin Nutr. 2003; 77: 1146–55


Radhika G, Van Dam RM, Sudha V, Ganesan A, Mohan V ‘Refined grain consumption and the metabolic syndrome in urban Asian Indians (Chennai Urban Rural Epidemiology Study 57)’. Metabolism. 2009; 58(5)675–81


Radhika G, Sumathi C, Ganesan A, Dudha V, Jeya Kumar Henry C, Mohan V ‘Glycaemic index of Indian faltbreads (rotis) prepared using whole wheat flour and ‘atta mix’-added whole wheat flour’. Br J Nutr. 2010; 103(11)1642–7


Teng KT, Voon PT, Cheng HM, Nesaretneam K ‘Effects of partially hydrogenated, semi-saturated and high oleate vegetable oils on inflammatory markers and lipids’. Lipids. 2010; 45(5)385–92


Ghafoorunissa G ‘Role of trans fatty acids in health and challenges to their reduction in Indian foods’. Asia Pac J Clin Nutr. 2008; 17 Suppl1: 212–5


Das UN ‘Metabolic syndrome X is common in South Asians, but why and how?’. Nutrition. 2002; 18(9)774–6


Jacobson MS ‘Cholesterol oxidises in Indian ghee: possible cause of unexplained high risk of atherosclerosis in Indian immigrant populations’. Lancet. 1987; 2: 656–8


Shankar SR, Bijlani RL, Baveja T et al ‘Effect of partial replacement of visible fat by ghee (clarified butter) on serum lipid profile’. Indian J Physiol. Pharmacol. 2002; 46: 355–60


Lovegrove JA, Lovegrove SS, Lesauvage SV, Brady LM, Saini N, Minihane AM et al ‘Moderate fish oil supplementation reverses low-platelet, long-chain N-3 polyunsaturated fatty acid status and reduces plasma triacylglycerol concentrations in British Indo-Asians’. Am J Clin Nutr. 2004; 79: L 974–82


Abeywardena MY, Patten GS ‘Role of w3 Longchain polyunsaturated fatty acids in reducing cardio-metabolic risk factors’. Endocr Metab Immune Disord Drug Targets. 2011; 11(3)232–46


Donin AS, Nightingale CM, Owen CG, Rudnicka AR, McNamara MC, Prynne CJ et al ‘Nutritional composition of the diets of South Asians, black African-Caribbean and white European children in the United Kingdom: the Child Heart and Health Study in England (CHASE)’. Br J Nutr. 2010; 104(2)276–85


Yajnik CS, Deshpande SS, Lubree HG, Naik SS, Bhat DS, Uradey BS et al ‘Vitamin B12 deficiency and hyperhomocysteinaemia in rural and urban Indians’. J Assoc Physicians India. 2006; 54: 775–82


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(5)1196–201


Farooqi A, Nagra D, Edgar T, Khunti K ‘Attitudes to lifestyle risk factors for coronary heart disease amongst South Asians in Leicester: a focus group study’. Family Practice. 2000; 17(4)293–7


Teo KK, Ounpuu S, Hawken S, Pandey MR et al ‘Tobacco use and risk of myocardial infarction and 52 countries in the INTERHEART study – a case-control study’. Lancet. 2006; 368: 647–58


NICE Public Health Guidance 10.‘Smoking cessation services in primary care, pharmacies, local authorities and workplaces, particularly for manual working groups, pregnant women and hard to reach communities’. NICE, London, UK.2008;


Ogunkolade WB, Boucher BJ, Bustin SA, Burrin JM, Noonan K, Mannan N, Hitman GA ‘Vitamin D metabolism in peripheral blood mononuclear cells is influenced by chewing ‘Betel Nut’ (Areca catechu) and vitamin D status’. J Clin Endocrinol Metab. 2006; 91: 2612–7


Hayes L, White M, Unwin M 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: 170–8


Fischbacher CM, Hunt S, Alexander L ‘How physically active are South Asians in the United Kingdom? A literature review’. J Public Health (Oxf). 2004; 26: 250–8


Sriskantharajah J, Kai J ‘Promoting physical activity among South Asian women with coronary heart disease and diabetes: what might help?’. Fam Pract. 2007; 24: 71–6


Rastogi T, Vaz M, Speigelman D et al ‘Physical activity and risk of coronary heart disease in India’. Int J Epidemiol. 2004; 33: 759–67


National Institutes of Health.‘Physical activity and cardiovascular health. NIH Consensus Development Panel on Physical Activity and Cardiovascular Health’. JAMA. 1996; 276: 241–6


Bhalodkar NC, Blum S, Rana T, Bhalodkar A, Kitchappa R, Enas EA ‘Effect of leisure time exercise on high-density lipoprotein cholesterol, its subclasses and size in Asian Indians’. Am J Cardiol. 2005; 96: 98–100


Van der Meer IM, Boeke AJ, Lips P, Grootjans-Geerts I, Wuister JD, Deville WL et al ‘Fatty fish and supplements are the greatest modifiable contributors to the serum 25-hydroxyvitamin D concentration in a multi-ethnic population’. Clin Endocrinol (Oxf). 2008; 68(3)466–72


Von Hurst PR, Stonehouse W, Coad J ‘Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient – a randomised placebo-controlled trial’. Br J Nutr. 2010; 103(4)549–55


Awumey EM, Mitra DA, Hollis BW, Kumar R, Bell NH ‘Vitamin D metabolism is altered in Asian Indians in the Southern United States: a clinical research centre study’. J Clin Endocrinol Metab. 1998; 83(1)169–73

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