Lipoprotein(a) as a marker of coronary artery disease and its association with dietary fat.

OBJECTIVE: The main objectives of the study were to evaluate the effect of dietary fat on plasma lipoprotein(a) [Lp(a)] levels and to study the potential of Lp(a) as a more reliable marker for CAD compared to other lipids and lipoproteins. METHODS: Twenty CAD patients and 20 healthy controls were recruited for the study. Their fasting plasma Lp(a) levels and complete lipid profile were assayed. The fat intake was calculated using 24 hours dietary recall method. The patients and controls were each divided into two subgroups: Group A consuming dietary fat > 30% and Group B consuming dietary fat < or = 30% of the total kilo-calories/day. RESULTS: Results indicated that plasma Lp(a), total serum cholesterol (TC), tryglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and LDL-C/HDL-C ratio of CAD patients were significantly higher than the controls. High fat intake was found to be associated with higher plasma Lp(a) levels (p<0.05) in patients only. No significant correlation was found between Lp(a) levels and other conventional lipoproteins. CONCLUSION: The lack of correlation between Lp(a) and other lipoproteins indicates its potential as an independent risk factor for CAD. High fat intake led to higher plasma Lp(a) levels in patients; hence it would be worthwhile to evaluate the effect of quality and quantity of fat intake on plasma Lp(a) levels in a larger sample size.

Knowledge amongst adult population regarding vectors of malaria in 21 states of India.

Malaria is the world's most important tropical disease which kills more people than any other disease except tuberculosis. It is a public health problem in more than 90 countries, inhabited by a total of some 2400 million people, 40% of the world's population. More than 90% of all malaria cases are in sub Saharan Africa, with two thirds of the remainder concentrated in six countries viz. India, Brazil, Sri Lanka, Afghanistan, Vietnam and Columbia in decreasing order of prevalence. Even now the problem of malaria in India is grossly underestimated. A rough estimate of morbidity due to malaria made on the basis of consumption of antimalarials comes to 35.5 million episodes in addition to malaria cases treated by the National Anti Malaria Programme (NAMP). In addition to large scale morbidity and mortality, it affects agricultural and industrial produce causing great socioeconomic losses.

Does moderate alcohol intake protect against coronary heart disease?

There is abundant epidemiological and clinical evidence to show that light-to-moderate drinking is associated with a reduced risk of coronary heart disease (CHD), total and ischemic stroke, and total mortality in middle-aged and elderly men and women. The evidence suggests a J- or U-shaped relationship between alcohol and CHD. Alcohol reduces the risk of coronary heart disease both by inhibiting the formation of atheroma and by decreasing the rate of blood coagulation. It appears that for most conditions, other than cardiovascular diseases and cholelithiasis, moderate alcohol consumption has either none or only an intermediate type of risk as compared with the risk of either abstinence or excessive drinking. It is now fully recognized and accepted that drinking alcohol regularly for years is toxic to almost every tissue of the body. However, most people who choose to drink alcohol have little or no problem limiting their consumption to amounts that do not generally cause serious health or social consequences. Moreover, a given dose of alcohol may affect different people differently. It is, therefore, imperative that a critical evaluation, based on the observations made hitherto, be done of both the harmful and the protective effects of alcohol consumption on various organs/systems of the body. This article reviews epidemiological evidence for the protective effects of alcohol on the cardiovascular system and discusses how alcohol might lower the risk of CHD.

Apolipoprotein(a) polymorphism and its association with plasma lipoprotein(a) levels: a north Indian study.

Elevated levels of lipoprotein(a) has been regarded as an independent risk factor for coronary, peripheral and cerebral atherosclerosis. The enormous intra-personal variation in the plasma concentration of lipoprotein(a) is almost entirely controlled by the apolipoprotein(a) i.e. gene locus on the chromosome 6q 26-27. The apolipoprotein(a) molecule is highly polymorphic and is known to exist in multiple, genetically determined isoforms. These polymorphisms may be responsible for difference in promoter activity, variable size of apolipoprotein(a) and thereby variation in plasma lipoprotein(a) concentration. We studied the effect of two types of polymorphisms, (i) variation in length of the pentanucleotide repeat in the 5' flanking region starting -1373 bp upstream of AUG codon, and (ii) the Kringle-4 type 2 size polymorphism, on plasma lipoprotein(a) levels in North Indian population. The study group consisted of 88 angiographically assessed male coronary artery disease patients (age range 30-70 years) and 83 age- and sex-matched healthy controls. The pentanucleotide repeat polymorphism was analysed using polymerase chain reaction. In all, 8/11 pentanucleotide repeat isoforms were observed. Using SDS-agarose gel electrophoresis and immunoblotting isoforms having 12-50 Kringle-4 type 2 repeats were detected. Our study indicates a strong association of elevated plasma lipoprotein(a) concentration with coronary artery disease. An inverse correlation was seen between lipoprotein concentration and isoform size for both the pentanucleotide repeat polymorphism and the Kringle-4 type 2 polymorphisms; statistically significant difference (p = 0.001) was, however, observed only for the later.

Genetic Contributribution to Alcohol Consumption and Alcohol Dependence.

Although the use of alcoholic beverages is found in virtually all societies, certain socio-economic, cultural, biobehavioural factors and ethnic / gender differences are among strongest determinants of drinking pattern in a society. The legacy of alcoholism among certain ethnic groups suggests that genetic factors can increase an individual's vulnerability for this disease. Although some of the putative environmental and genetic factors remain obscure in their character, there is a strong evidence that a crucial interplay of nature and nurture, heredity and environment, and biology and culture is responsible for the development of alcoholism across ethnic groups and gender.