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December 2013 - Issue 2
South Asians and their increased
cardiovascular risk: A review of risk factors
and diet and lifestyle modification
Rachel Nicoll BSc and Michael Henein MD, PhD
Department of Public Health and Clinical Medicine, Umea University Heart Centre, Umea, Sweden
Canterbury Christ Church University, Kent, UK
Abstract
South Asians (SAs) have a significantly higher incidence and severity of type 2 diabetes and cardiovascular disease (CVD)
than Caucasians and can present with atypical ischaemic symptoms. This can present a challenge for health professionals
who may not be aware of the lowered thresholds recommended for SA body mass index, waist circumference and age.
Although SAs are likely to have all the hallmarks of metabolic syndrome: central obesity, insulin resistance, impaired glucose
tolerance, reduced high density lipoprotein, high triglycerides and hypertension, conventional risk factors alone do not fully
predict the increased CVD risk among this community. Furthermore, SAs themselves may not be aware of their increased
predisposition to disease nor of the dietary and lifestyle modifications which could reduce the risk and severity of their
condition. Even where some modification has been attempted, there may be cultural pressure to conform to a traditional
diet and the requirements for fasting and feasting. Principally, SAs should avoid large late meals, reduce sugary sweets and
drinks, alcohol and foods fried in plant oils which create damaging transfats, while increasing protein and non-fried vegetables
to help glycaemic control. Chewing paan, with or without added tobacco, is a particular risk factor for both CVD and cancer,
on a par with the dangers of smoking. Although not in the culture, exercise would also be of great benefit.
Introduction
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
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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.
Mealtimes
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.
Carbohydrates
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.
Fats
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.
Protein
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.
76
Alcohol
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.
Exercise
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.
Conclusion
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
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December 2013 - Issue 2
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.
Correspondence to:
Michael Henein MD MSc PhD FESC FACC FRCP
Professor of Cardiology
Department of Public Health and Clinical Medicine, Umea
University, Umea
Sweden
[email protected]
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