Lipid and lipoprotein profiles and prevalence of dyslipidemia in Mexican adolescents Rosalinda Posadas-Sánchez a, ⁎ , Carlos Posadas-Romero a , José Zamora-González a , Enrique Mendoza-Pérez a , Guillermo Cardoso-Saldaña a , Liria Yamamoto-Kimura b a Departamento de Endocrinología del Instituto Nacional de Cardiología Ignacio Chávez. Tlalpan, Mexico City, Mexico, D.F. 14080, Mexico b Departamento de Salud Pública, Facultad de Medicina Universidad Nacional Autónoma de México, Ciudad Universitaria, México, D.F. 04510, Mexico Received 12 September 2006; accepted 9 July 2007 Abstract The objective of the study was to determine the prevalence of different forms of dyslipidemia in an urban population of Mexican adolescents. A cross-sectional study was conducted in 1846 students from 8 randomly selected public junior high schools in Mexico City. Anthropometry, blood pressure, and 12-hour fasting lipids and lipoproteins were measured. We studied 770 male and 1076 female adolescents (13.2 ± 1 years). The most prevalent dyslipidemia was low high-density lipoprotein cholesterol (HDL-C) (b35 mg/dL) either combined with other abnormalities (17.5% for male and 12.9% for female subjects, P b .001) or isolated (13.5% and 9.6% for male and female subjects, respectively, P b .001). Obese subjects showed the highest prevalence of low HDL-C (47.2% for male and 34.4% for female subjects) and of high total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) (19.4%, 27.8%, and 36.1%, respectively, for male subjects; 9.8%, 13.1%, and 24.6%, respectively, for female subjects). Multiple regression analysis showed that waist circumference was negatively associated with HDL-C and positively associated with LDL-C and TG levels, whereas Tanner stages were negatively associated but sex was positively associated with total cholesterol, LDL-C, and TG concentrations. As in Mexican adults, low HDL-C and high TG levels were the most prevalent dyslipidemias. Increased blood lipids over long periods suggest that, as adults, these adolescents will be facing a higher risk for atherosclerosis. © 2007 Elsevier Inc. All rights reserved. 1. Introduction Atherosclerotic coronary heart disease (CHD) is a condition of multifactorial origin. A large number of clinical, pathologic, and epidemiologic studies have established that dyslipidemia (DLP) plays an important role in the develop- ment and progression of atherosclerosis. Although clinical CHD usually does not occur until the fourth or fifth decade of life, it is known that atherosclerosis is already present in youth [1]. Autopsy studies in young people have demon- strated a significant association between atherosclerotic lesions and premortem cardiovascular risk factors, including hypercholesterolemia, high blood pressure, obesity, and smoking [2]; and the severity of coronary and aortic atherosclerosis is even higher in youngsters with 3 or more antemortem risk factors [3]. Long-term cohort studies showed that increased carotid intima-media thickness in young and middle-aged adults is associated with total cholesterol (TC) [4] and low-density lipoprotein cholesterol (LDL-C) [5] measured during childhood. It has also been observed that conditions related to lipids and lipoproteins, such as unhealthy dietary habits, tobacco smoking, and physical inactivity, are acquired during childhood and adolescence [6]. Moreover, prospective longitudinal studies have tracked obesity, hyperlipidemia, and hypertension from adolescence into adulthood [7,8]. Data from the Bogalusa Heart Study [9] suggest that more than 70% of children with adverse lipid profiles tend to course with DLP in adult life. Epidemiologic surveys of CHD precursors in children have indicated that differences in lipid and lipoprotein levels among cultures and ethnic groups appear early in childhood [10-12].Therefore, it is not appropriate to extrapolate results from one population to another to esta- blish prevention programs. Available online at www.sciencedirect.com Metabolism Clinical and Experimental 56 (2007) 1666 – 1672 www.elsevier.com/locate/metabol ⁎ Corresponding author. Tel.: +52 55 5573 29 11x1272; fax: +52 55 5573 46 87. E-mail address: rossy_posadas_s@yahoo.it (R. Posadas-Sánchez). 0026-0495/$ – see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.metabol.2007.07.009