Metabolic Profile Of Individuals Research Articles

The “Good Cholesterol”

Atherosclerosis is an insidious and dangerous disease: a progressive chemical and structural injury to the blood vessels in such critical organs as the heart, brain, and kidney. The hallmark feature of atherosclerosis is the buildup of cholesterol into lesions called plaques that can reduce the flow of blood. When the delivery of blood to heart muscle drops enough, this can result in the development of chest pain or angina. Angina indicates that the heart muscle is not receiving enough oxygen to carry out its pumping functions. Atherosclerotic plaques can also suddenly rupture, develop a blood clot on their surface, and completely choke off a portion of heart muscle. This chain of events frequently results in heart attack or sudden death without warning. Atherosclerotic disease also predisposes people to stroke, peripheral vascular disease, lower-extremity amputation, and loss of kidney function, among other devastating outcomes. Despite all that we have learned in the past 50 years, atherosclerosis remains the No. 1 killer of men and women and the chief reason for loss of quality of life in Western countries. We are, however, gaining ground. Considerable research has revealed the importance of factors that increase an individual’s risk for developing this disease. Among the most important of these risk factors are elevated blood pressure, diabetes mellitus, obesity, inactivity, smoking, and cholesterol levels. When your physician measures your cholesterol level, he or she is looking at your lipid profile, which comprises low-density lipoprotein cholesterol (LDL-C, or the “bad” cholesterol), triglycerides (blood fats), and high-density lipoprotein cholesterol (HDL-C, or the “good” cholesterol). In a general way, when it comes to measurement of your LDL-C and triglyceride values, a lower value is better because these lipids drive the development and progression of atherosclerosis. In sharp contrast, when it …

Differential Impact of Obesity in Related Populations

To search for genetic and environmental determinants of obesity, we compared the prevalences and the impact of obesity in three populations from two cities: Mexican Americans (n = 820) and non-Hispanic whites (n = 1112) from San Antonio, Texas, and Mexicans from Mexico City (n = 1878). In the age range examined, 35-64 years, only Mexican men and women showed a significant increase in the prevalence of obesity with age. On the other hand, genetic ancestry, especially in women, made significant differences in the rates of obesity. Mexican Americans showed relatively high, and non-Hispanic whites low, rates of obesity. To discriminate between genetic and environmental influences mediating the impact of obesity on a set of hemodynamic and metabolic variables, we compared this impact between Mexican Americans and both non-Hispanic whites (same macro-environment, different gene pools), and Mexicans (same gene pool, different environments). We found that obesity always worsens the hemodynamic and metabolic profiles of individuals, but the magnitude of the effects may be variable. We showed that the levels of insulin concentrations for a given level of obesity were similar in Mexicans and Mexican Americans, suggesting that genetic influences predominate in determining insulin levels; the levels of triglycerides and HDL for a given level of obesity were similar in Mexican Americans and non-Hispanic whites, suggesting predominant environmental influences on lipid levels. On the other hand, the levels of glucose and systolic blood pressure for a given level of obesity were usually different between Mexican Americans and either of the other two populations, suggesting that these levels may result from genotype-by-environment interactions.