Describe the Plasma Homocysteine levels ?
Several studies have investigated the contribution of homocysteine to CVD risk both among immigrant Indians and those living in India. It was observed in two parallel case-control studies to evaluate fasting and post-methionine load homocysteine as risk factors for CAD , one in Europeans and the other in Indians, They found that elevated plasma homocysteine levels were independently associated with CAD in both UK-based Indians and Europeans. In their study, the odds ratio for CAD for a 5 ymol1L increment in plasma homoeysteine was 1.3 in Europeans and, 1.2 in Indians. However, the Indians in this study were not evaluated for the other known associations of CAD characteristic of' Indian ethnicity, namely abnormal WHR, raised Lp(a) and hy perinsulinemia. In the SHARE study which involved newly a thousand participants from three ethnic groups (South Asians, Europeans and Chinese), the presence of clinical Cardiovascular disease and carotid intimae-media thickness measured by B-mode ultrasound were correlated with conventional and nonconventional risk factors.
Even though the South Asians had significantly higher levels of plasma homoeysteine than their European and Chinese counter-parts, this did not translate into an independent association of homocysteine with CAD. Two other comparative studies from southern India also failed to show any differance in plasma homocysteine levels between patients with and without CAD. The case control study by Shastry and colleagues, again confirms that at Indians have higher plasma homocysteine levels, but fails to show any differences in the levels between patients with CAD and those without. The bulk of the evidence therefore suggests that the elevated plasma homocysteine level found in patients of Indian origin is not independently associated with CAD.
Though conventional risk factors are not high in Indians, they remain at least as important in determining the risk of CAD in Indian patients as they are in other populations. In addition to these traditional risk factors, it is clear that there are other known and unknown factors which increase the predilection of Indians to develop premature and severe CAD. The most important set of conditions, which have been unequivocally associated with and are, more prevalent among Indians with CAD, are those constituting the syndrome of insulin resistance. Elevated levels of Lp(a) are seen in Indians irrespective of whether they reside in India or are immigrants to another country, suggesting a genetic predisposition. In the light of current knowledge, adverse interaction between a genetic predisposition and unhealthy lifestyle changes best explains the increased vulnerability of Indians to CAD.
In summary, several factors likely to have contributed to the acceleration of CAD epidemic in India in recent times. These are:
i) Demographic transition to an older population, as a result of increasing life expectancy.
ii) Confluence of both conventional risk factors and non-conventional risk factors in Indians. Conventional factors like Hypertension, diabetes, hypercholesterolaemia, smoking etc., owe their origin to growing urbanization and western 'acculturation' amongst Indians. Non-conventional risk factors like hy perinsulinaeinia, insulin resistance, lipoprotein A etc., are determined by genes or other 'programming' factors and their high prevalence amongst Indians probably explain the malignant, precocious nature of CAD that typically affects Indians.
iii) Recently indicated relationship between low birth-weight which is widely prevalent amongst Indian newborns and enhanced susceptibility to CAD in adult life ('Barker hypothesis').
These multiplicative effects of convictional and emerging risk factors appeal to provide a plausible explanation for the excess burden of CAD among Indians, many of whom are lean, non-smoking, vegetarian, .yoga guru and even marathon athletes.
The excess risk of CAD in Indians appears to be greater at younger ages. When people move from a rural to an urban environment, they become sedentary and/or may adopt western lifestyles. Decreased physical activity and increased consumption of calories and saturated fat result in abdominal obesity, insulin resistance and atherogenic dyslipidaeinia. These acquired metabolic abnormalities appear to have a synergistic effect on the development of CAD in genetically p disposed individuals.