Smoking and obesity make a bad problem worse: genetics and lifestyle affect high density lipoprotein levels in Turks.
Low levels of high density lipoprotein cholesterol (HDL-C) are an independent risk factor for coronary heart disease. The Turkish Heart Study revealed very low levels of plasma HDL-C in the Turkish population, a fact confirmed by the Heart Disease and Risk Factors in Turkish Adults study. Low HDL-C levels have also been observed in Turks living in the United States, Germany, and the Netherlands. Dietary habits do not explain the low HDL-C levels, which were found in Turkish Heart Study participants from six regions of Turkey with significant differences in typical diets. Among newborns and pre-pubescent children, plasma HDL-C levels were similar in Turks and western Europeans. After puberty, however, HDL-C levels declined significantly in Turkish boys and girls. These results suggest a genetic basis for the low HDL-C levels. In fact, hepatic lipase activity modulated by sex hormones was 25-30% higher in the Turkish population than in other populations. Elevated hepatic lipase activity is clearly associated with low plasma HDL-C in many studies. Results of a recent genome-wide scan for plasma HDL-C in Turks revealed a linkage on chromosome 15q22 where the hepatic lipase gene is located and that low HDL-C was 80% heritable. In addition, evidence for an interaction between HDL-C levels and modifiable environmental factors, particularly smoking and obesity, came from the study of cholesterol ester transfer protein TaqIB polymorphism. This polymorphism was associated with plasma HDL-C levels in Turks. Subjects with the B2B2 genotype-both smokers and nonsmokers-had higher plasma HDL-C levels. Interestingly, B2B2 subjects were protected from the HDL-C-lowering effect of smoking, whereas B1B1 subjects who smoked had significantly lower HDL-C levels. A similar interaction was observed between TaqIB polymorphism and obesity. In conclusion, low HDL-C levels in Turks were modulated by genetic factors and their interaction with modifiable environmental factors, such as smoking and obesity.
Hodoğlugil
Uğur
U
Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, CA 94158, USA.
Mahley
Robert W
RW
D002318:Cardiovascular Diseases / Q000097:blood / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics; D008076:Cholesterol, HDL / Q000097:blood*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008019:Life Style; D008297:Male; D009765:Obesity / Q000097:blood* / Q000150:complications; D012737:Sex Factors; D012907:Smoking / Q000009:adverse effects / Q000097:blood*; D014421:Turkey / Q000453:epidemiology
D008076:Cholesterol, HDL