Epidemic of cardiovascular disease in South Asians
BMJ 2002; 324 doi: https://doi.org/10.1136/bmj.324.7338.625 (Published 16 March 2002) Cite this as: BMJ 2002;324:625
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Raj Bhopal’s editorial (1) on CV disease in South Asians pulls
together four main themes in seeking an understanding of this epidemic:
excess exposure to risk factors, greater susceptibility, new risk factors
and competing causes, noting that all the established risk factors are
important.
The effects of risk factors vary, suggesting that their interactions
and the nature of the interactions matter (2,3). Reflecting on such
variety and variability observed in clinical medicine, Maseri suggested
“investigation of the causes of the variable responses of individual
subjects to known pathogenic mechanisms,” and discussed the search for
differences rather than similarities in patients with CV disease (4). The
same risk factors that produce disease in an individual (or population)
may not result in equivalent disease in another. The same extent of
disease may be evident in patients with differing risk factors or
differing levels. Clustering, nonlinear interactions and risk
amplification partly explain such outcomes.
Multiple elements of the factors Bhopal describes come together in
individuals and populations to produce the health or disease state at that
time. These are woven together by the unseen rules of complex dynamics and
hidden biological, social and other effects with emergence of varied
responses, manifest or explainable as susceptibility or sensitivity (2,3).
Two patients or populations with only slightly different apparent risk may
thus have vastly different outcomes, an inherent feature of complex
dynamics.
Averting the epidemic of CV disease in South Asians may thus depend
as much on understanding and identifying the nature of the complex dynamic
interactions involved, and responding to these, in addition to responding
to the risk factors. For example, the amplifying effect of homocysteine
and Lp(a), risk factors found on average at higher levels in South Asians
(5), with multiplicative effects in interaction with conventional risk
factors and with each other, explain some of the excess risk, with
implications for treatment and prevention (3). Such an approach encourages
utilizing the complex dynamics to amplify reduction of global risk, an
untested but not unreasonable hypothesis.
All of the factors Bhopal describes are thus important, but how they
become woven together to produce health or disease may be as important in
figuring out how to achieve desired outcomes and in averting an epidemic.
Modifying their biological, social and behavioral, environmental and other
interactions, as well as modifying their complex dynamics may be as
important as modifying risk factors in reducing global risk and stopping
this epidemic.
References.
1. Bhopal R. Epidemic of cardiovascular disease in South Asians. BMJ
2000; 324:625-626.
2. Rambihar VS. A new mathematical (chaos and complexity) theory of
medicine, health and disease, in A New Chaos Based Medicine Beyond 2000:
the response to evidence. 2000 Vashna Toronto.
3. Rambihar VS. SOUTH ASIAN HEART: Preventing Heart Disease – from
the heart to the edge of the diaspora, from the heart to the edge of
chaos. 1996, 2002. Vashna Toronto.
4. Maseri A. Integration of cellular and molecular biology with
clinical research in cardiology.(ltr) N Eng J Med 1993;328:447.
5. Anand SS, Yusuf S, Vuksan V, Devanesen D, Teo KK, Montague PA, et
al. Difference 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.
Competing interests: No competing interests
Whincup et al have shown that British South Asian children have
greater insulin resistance than white children which cannot be accounted
for by differences in central adiposity.1 The obvious implication of this
is that primary prevention of type 2 diabetes mellitus and CHD should
begin early in childhood.
The possible causes of increased CHD seen in South Asians have been
mentioned in Bhopal’s editorial.2 While insulin resistance and diabetes
mellitus are undoubtedly key factors in causing increased CHD in South
Asians, this cannot account for all the excess burden observed in this
group. The native Pima American Indians have the world’s highest rate of
diabetes mellitus but have the lowest prevalence of coronary artery
disease of all Americans (1%) – the American Indian paradox.
The “lipid tetrad index” is an interesting explanation to explain at
least partly, the excess CHD observed in South Asians.3 This index is much
higher in South Asians and is derived by the product of serum total
cholesterol, triglyceride and lipoprotein (a) concentrations divided by
the high density lipoprotein cholesterol concentration.
Since conventional risk factors like cholesterol, obesity and blood
pressure greatly underestimate the total burden of CHD in South Asians,
separate guidelines incorporating lower thresholds and targets for
treatment are urgently required. Universal cut-off values for BMI to
identify obesity are not appropriate.4 Asians have lower BMI but higher
body fat percentage than age and sex matched Caucasians. Treatment targets
recommended by the Indian Consensus Group for the Prevention of Diabetes
of total cholesterol While prevention is always better than cure, aggressive and effective
treatment is the next best thing.
1. Whincup PH, Gilg JA, Papacosta O, Seymour C, Miller GJ, Alberti
KGMM, Cook DG. Early evidence of ethnic differences in cardiovascular
risk:cross sectional comparison of British South Asian and white children.
.BMJ 2002;324:635-8.
2. Bhopal R. Epidemic of cardiovascular disease in South Asians. BMJ
2002;324:625-6.
3. Enas EA. Rapid angiographic progression of coronary artery disease in
patients with elevated lipoprotein (a). Circulation 1995;92:2353-4.
4. Deurenberg P. Universal cut-off BMI points for obesity are not
appropriate. Brit J Nutr 2001;85:135-6
5. Singh RB, Rastogi SS, Rao PV, Das S, Madhu SV, Das AK, Sahay BK, Fuse
SM, Beegom R, Saini GS, Shah NA, (The Indian Consensus Goup for the
Prevention of Diabetes). Diet and lifestyle guidelines and desirable
levels of risk factors for the prevention of diabetes and its vascular
complications in Indians: a scientific statement of The International
College of Nutrition. J Cardiovasc Risk; 1997:201-8.
Competing interests: No competing interests
To the Editor: In a recent editorial of the British Medical Journal
Bhopal (March 16, p625) 1 pointed towards preventive measures right from
the childhood to tackle the scourge of cardiovascular diseases among those
with a South Asian ancestry. Such measures have been recommended for all
the survivors of acute myocardial infarction. Furthermore, they would be
prescribed a pharmacological recipe, exercise, dietary or smoke
restrictions2. The preventive or post myocardial infarction
recommendations of using dietary products with no aroma, taste leading to
boredom and nausea have not been addressed all the meticulously.
Researchers should emulate initial experiments to produce low-fat
cheese with an aroma, taste and flavor like regular content cheese.
Starting with thermolytic strain of Lactobacillus lactis spp. Cremoris SK
(culture S). L. lactis dactylactis JVI (culture J) and L casei 7A (culture
L) as the starter cultures, it has been possible to produce experimentally
fully palatable cheese with 45% less fat content3. Similar dietary
products would be of immense utility not only during post-myocardial
infarction rehabilitation but would benefit those with hypertension,
diabetes mellitus and thrombosis. They would be an effective component of
dietary intervention to reduce consumption of fat and increase consumption
of fruits and vegetables.
Irrespective of their origin, children, adolescents or adults should
have continuous dietary interventions. Computer-assisted counseling has
been used to reduce diet related risks for cancer. Nutrition intervention
rather than an attention-controlled unrelated to diet in healthy women
aged 40 to 70 years resulted in significantly less fat consumption,
greater consumption of fruits and vegetables along with a significant
reduction in behavioral measure of fat consumption4. Undoubtedly
innovative intervention strategy would be needed for those from China and
India where under nutrition is being reduced rapidly and diet is shifting
toward higher fat and lower carbohydrate. In China, the intake of foods
from animal sources and edible oils is rising sharply. In India, there has
been a phenomenal rise in intake of diary products with added suagar5.
Frequent non-compliance to dietary recipes by those with a South Asian
ancestry of a high-risk profile1 during festivals, feasts or visits to
country on origin could be disastrous and neutralize dietary
interventions. That eventuality could be prevented among those afflicted
with cardiovascular disorders through awareness, through counseling by
clinicians.
Subhash C Arya, MBBS, PhD
Research Physician
Centre for Logistical research and Innovation,
M-122 Greater Kailash- Part 2,
New Delhi- 110048, India
Email subhashji@hotmail.com
References
1. Bhopal R. Epidemic of cardiovascular disease in South Asians. BMJ
2002;324:625-626
2. Cohen JD. ABCs of secondary prevention of CHD: easier said than done.
Lancet 2001; 357:972-973
3. Potera C. Bacterial trio makes tastier low-fat cheese. ASM News 2000;
66(9): 517-519
4. Stevens VJ, Glasgow RE, Toobert DJ, Karanjia N, Smith KS. Randomized
trial of a brief dietary intervention to decrease consumption of fat and
increase consumption of fruits and vegetables. Am J Health Promot 2002;
16(3): 129-134
5. Popkin BM, Horton S, Kim S, Mahal A, Shuigao J. Trends in diet,
nutritional status, and diet-related noncommunicable diseases in China and
India: the economic costs of the nutrition transition. Nutr Rev 2001;
39(12): 379-390
Competing interests: No competing interests
Dear Sir,
This study is a very interesting contribution to the existing confusion in
the field of chronic diseases. While coronary artery disease and diabetes
are major problems, the possibility of "so called" risk factors being the
cause of these seems rather far fetched. At best, as I understand, they
could be associations.
To cite an example, when the fat proflie of an apparently healthy
individual is considered abnormal by the medical fraternity, for the
hapless victim it becomes a serious "doctor-thinks-you-have-a-disease"
problem. The magnitude of the psychological damage done in the long run,
coupled with the known and unknown side effects of the drugs that we give
to set the profile right, might contribute a major share in the final
disease outcome. It has to be seen to be believed in real life situations-
a fact rarely appreciated by the epidemiologist.
As is clear now, time evolution in the human body's working does not
depend on partial intial knowledge of the organism.
The enormous psychological distress that these migrant populations go
through could have major effects on their long term wellness- an area not
taken into consideration in all the studies cited in support of the risk
factor hypotheses. To extrapolate these data wholesale on to all South
Asians would be unfair, to say the least. Medical textbooks have enormous
number of risk factors for coronary disease. Many recent studies have
added hostility to be one of the major risks. Mind/body medicine is
gaining ground, albeit slowly.
If it is as simple as to correct risk factors to keep man healthy, we
should have been able to solve the tricky concerns in the field of
coronary disease where a "risk free" young man, in his 30s, might drop
down dead due to ventricular fibrillation, in contrast to another elderly
person in his 70s who outlives his major three vessel disease with some
anginal pain. I wonder if any of the risk factors have anything to do with
the final assault on the heart muscle, where a clot, suddenly blocks off a
blood vessel which is , at best , marginally obstructed, leaving intact
the major atherosclerotic blocks in other vessels.
"Epidemiology is not an exact science" writes an epidemiologist,
Steven Milloy Ph.D., in his book "Science without Sense," published by the
CATO Institute, Washington DC in 1997. It is not difficult to connect any
two things happening in society concurrently as cause and effect. To cite
an example, after World War II, per capita consumption of fat in Europe
went up directly proportionate to the death rate due to coronary disease,
strengthening the fat hypothesis. Similarly, the sale of trousers also
went up with prosperity. Trosuers should not have anything to do with
coronary disease, although everyone wears them!
Most migrants come from difficult background back home and migrate to
a distant place in search of greener pastures to make it big one day in
their new environment. Naturally, they have many unfathomable stressors
that could contribute to the eventual disease burden. This acculturation
has been the bane of most migrant societies studied in the past as well-
the Wembley Study, Castle's Study of Ploynaesian migrants to the US as
also the studies of Cruz Coke in Chile.
The present study has added one more dimension of insulin resistance.
The latter seems to be the fasion and the be all and end all of major
killer diseases ever since the dawn of the new Syndrome X. I may also add
another dimension of the gene-food mismatch in many of the migrant
populations. Whereas most of them come from a thrify-gene environment back
home, when they get themselves transplanted on to a food-plenty atmosphere
problems start. More food could shorten the life span due to increased
production of oxidants. An elephant lives much more than a rat. The former
eats a very small fraction of its body weight, while the latter eats a lot
more compared to its body weight! Studies have shown that an overfed rat
becomes obese and dies faster than its peers on normal diet.
What follows could be an educated guess! Psychological stress, an
integral part of an immigrant's life, keeps provoking the flight-fight
reaction, resulting in catecholamine secretions. The latter, in turn,
stimulate neo-glucogensis and consequent endogenous hyperinsulin state. In
addition, it could also result in temporary acute extracellular
hypokalaemia. The latter might even precipitate arrhythmias! Insulin
resistence might not be the cause of killer diseases. Rather, it might be
the effect of psychological stress.
Any knotty problem, when looked at from a different perspective, only
becomes knottier! Health and disease do not seem to have simplistic and
linear solutions! Let us keep on searching for the magic solution! While
epidemiology did us a lot of good in infectious disease epidemics, the
story does not seem to repeat in the area of chronic degenerative
diseases. Thinkers, like John Snow, did unravel the mystery of cholera
long before epidemiology and microbilogy did that. Soho residents drawing
water from the Broad Street pump died of cholera while the prison inmates
in Soho, who had their own well, remained healthy. John Snow, therefore,
concluded that cholera did not come from bad air, but came through
contaminated water. Of course, it was later discovered that this pump drew
water downstream of the sewage outlet to the Thames River. Even in the
field of infections, major breakthroughs did come from common sense
observations. The latter is the gretest casualty these days.
Yours ever,
bmhegde
Competing interests: No competing interests
Competing interests: No competing interests
epidemic of chd among young indians.
the spurt of heart disease, primarily coronary heart disease (chd) is
intriguing. indians use excessive amounts of ghee and cooking oils, but
this is not something recent. may be it has become more affordable. in
vogue in the subcontinent is the pernicious habit of chewing betel leaf
(pan) along with nutmeg(sopari),catechu ( katha) and slaked lime (chuna )
+ generous quantities of tobacco.this is available at every conceivable
nook and corner.it is widely advertised and large quantities are consumed
by the young these days, and is fashionable.in the past it was consumed by
older generation. a high incidence of oral leukoplakia and cancer are
found increasing in the young. perhaps this is 'the' risk factor for chd.
Competing interests:
None declared
Competing interests: No competing interests