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Introduction: Mexico ranks second in the global prevalence of obesity in the adult population, which increases the probability of developing dyslipidemia. Dyslipidemia is closely related to cardiovascular diseases, which are the leading cause of death in the country. Therefore, developing tools that facilitate the prediction of dyslipidemias is essential for prevention and early treatment. Methods: In this study, we utilized a dataset from a Mexico City cohort consisting of 2,621 participants, men and women aged between 20 and 50 years, with and without some type of dyslipidemia. Our primary objective was to identify potential factors associated with different types of dyslipidemia in both men and women. Machine learning algorithms were employed to achieve this goal. To facilitate feature selection, we applied the Variable Importance Measures (VIM) of Random Forest (RF), XGBoost, and Gradient Boosting Machine (GBM). Additionally, to address class imbalance, we employed Synthetic Minority Over-sampling Technique (SMOTE) for dataset resampling. The dataset encompassed anthropometric measurements, biochemical tests, dietary intake, family health history, and other health parameters, including smoking habits, alcohol consumption, quality of sleep, and physical activity. Results: Our results revealed that the VIM algorithm of RF yielded the most optimal subset of attributes, closely followed by GBM, achieving a balanced accuracy of up to 80%. The selection of the best subset of attributes was based on the comparative performance of classifiers, evaluated through balanced accuracy, sensitivity, and specificity metrics. Discussion: The top five features contributing to an increased risk of various types of dyslipidemia were identified through the machine learning technique. These features include body mass index, elevated uric acid levels, age, sleep disorders, and anxiety. The findings of this study shed light on significant factors that play a role in dyslipidemia development, aiding in the early identification, prevention, and treatment of this condition.
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Enfermedades Cardiovasculares , Dislipidemias , Masculino , Adulto , Humanos , Femenino , Adulto Joven , Persona de Mediana Edad , Estudios de Cohortes , Dislipidemias/epidemiología , Algoritmos , Enfermedades Cardiovasculares/epidemiología , Aprendizaje AutomáticoRESUMEN
ABSTRACT In individuals with very low high-density lipoprotein (HDL-C) cholesterol, such as Tangier disease, LCAT deficiency, and familial hypoalphalipoproteinemia, there is an increased risk of premature atherosclerosis. However, analyzes based on comparisons of populations with small variations in HDL-C mediated by polygenic alterations do not confirm these findings, suggesting that there is an indirect association or heterogeneity in the pathophysiological mechanisms related to the reduction of HDL-C. Trials that evaluated some of the HDL functions demonstrate a more robust degree of association between the HDL system and atherosclerotic risk, but as they were not designed to modify lipoprotein functionality, there is insufficient data to establish a causal relationship. We currently have randomized clinical trials of therapies that increase HDL-C concentration by various mechanisms, and this HDL-C elevation has not independently demonstrated a reduction in the risk of cardiovascular events. Therefore, this evidence shows that (a) measuring HDL-C as a way of estimating HDL-related atheroprotective system function is insufficient and (b) we still do not know how to increase cardiovascular protection with therapies aimed at modifying HDL metabolism. This leads us to a greater effort to understand the mechanisms of molecular action and cellular interaction of HDL, completely abandoning the traditional view focused on the plasma concentration of HDL-C. In this review, we will detail this new understanding and the new horizon for using the HDL system to mitigate residual atherosclerotic risk.
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Previous studies have reported that the SIDT2 and ABCA1 genes are involved in lipid metabolism. We aimed to analyze the association-the gene x gene interaction between rs17120425 and rs1784042 on SIDT2 and rs9282541 on ABCA1 and their diet interaction on the HDL-c serum levels-in a cohort of 1982 Mexican adults from the Health Workers Cohort Study. Demographic and clinical data were collected through a structured questionnaire and standardized procedures. Genotyping was performed using a predesigned TaqMan assay. The associations and interactions of interest were estimated using linear and logistic regression. Carriers of the rs17120425-A and rs1784042-A alleles had slightly higher blood HDL-c levels compared to the non-carriers. In contrast, rs9282541-A was associated with low blood HDL-c levels (OR = 1.34, p = 0.013). The rs1784042 x rs9282541 interaction was associated with high blood HDL-c levels (p = 3.4 × 10-4). Premenopausal women who carried at least one rs17120425-A allele and consumed high dietary fat, protein, monounsaturated, or polyunsaturated fatty acids levels had higher HDL-c levels than the non-carriers. These results support the association between the genetic variants on SIDT2 and ABCA1 with HDL-c levels and suggest gene-gene and gene-diet interactions over HDL-c concentrations in Mexican adults. Our findings could be a platform for developing clinical and dietary strategies for improving the health of the Mexican population.
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Dieta , Proteínas de Transporte de Nucleótidos , Humanos , Adulto , Femenino , Estudios de Cohortes , HDL-Colesterol , Alelos , Nutrientes , Transportador 1 de Casete de Unión a ATP/genética , Proteínas de Transporte de Nucleótidos/genéticaRESUMEN
In individuals with very low high-density lipoprotein (HDL-C) cholesterol, such as Tangier disease, LCAT deficiency, and familial hypoalphalipoproteinemia, there is an increased risk of premature atherosclerosis. However, analyzes based on comparisons of populations with small variations in HDL-C mediated by polygenic alterations do not confirm these findings, suggesting that there is an indirect association or heterogeneity in the pathophysiological mechanisms related to the reduction of HDL-C. Trials that evaluated some of the HDL functions demonstrate a more robust degree of association between the HDL system and atherosclerotic risk, but as they were not designed to modify lipoprotein functionality, there is insufficient data to establish a causal relationship. We currently have randomized clinical trials of therapies that increase HDL-C concentration by various mechanisms, and this HDL-C elevation has not independently demonstrated a reduction in the risk of cardiovascular events. Therefore, this evidence shows that (a) measuring HDL-C as a way of estimating HDL-related atheroprotective system function is insufficient and (b) we still do not know how to increase cardiovascular protection with therapies aimed at modifying HDL metabolism. This leads us to a greater effort to understand the mechanisms of molecular action and cellular interaction of HDL, completely abandoning the traditional view focused on the plasma concentration of HDL-C. In this review, we will detail this new understanding and the new horizon for using the HDL system to mitigate residual atherosclerotic risk.
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Aterosclerosis , Lipoproteínas HDL , Humanos , HDL-Colesterol , Aterosclerosis/etiología , Aterosclerosis/terapiaRESUMEN
Dipeptidyl peptidase-4 (DPP4) can influence lipid homeostasis and atherosclerosis progression. We aimed to assess the association of DPP4 gene polymorphisms with hypoalphalipoproteinemia and DPP4 serum levels, in a cohort of Mexican individuals. Five DPP4 polymorphisms (rs12617336, rs12617656, rs1558957, and rs3788979, and rs17574) were genotyped in 748 participants with and 745 without hypoalphalipoproteinemia. The associations were evaluated using logistic regression analyses. Under inheritance models adjusted for confounding variables, the rs12617336 (OR = 0.22, P heterozygote = 0.001) and rs17574 (OR = 0.78, P additive = 0.022; OR = 0.73, P dominant = 0.012; OR = 0.73, P heterozygote = 0.017; OR = 0.72, P codominant 1 = 0.014) minor alleles were associated with a low risk of hypoalphalipoproteinemia. After the correction for multiple comparisons, the associations were marginal except the association of the rs12617336 that remaining significant. Additionally, both DPP4 minor alleles were associated with protection for the presence of insulin resistance (IR) (OR = 0.17, P heterozygote = 0.019 for rs12617336 and OR = 0.75, P additive = 0.049 for rs17574). The rs12617336 minor allele was also associated with a low risk of hyperinsulinemia (OR = 0.11, P heterozygote = 0.006). Differences in DPP4 levels were observed in individuals with rs17574 genotypes, the rs17574 GG genotype individuals had the lowest levels. Our data suggest that rs12617336 and rs17574 DPP4 minor alleles could be envisaged as protective genetic markers for hypoalphalipoproteinemia, IR, and hyperinsulinemia. The rs17574 GG genotype was associated with the lowest DPP4 levels.
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Obesity, a chronic low-grade inflammation metabolic abnormality, is related to high proinflammatory cytokines concentrations. Epstein-Barr virus-induced gene 3 (EBI3) encodes for the EBI3 beta subunit that constitutes interleukin (IL) 27 and 35. Our objective was to assess the association of three EBI3 single nucleotide polymorphisms (SNPs) with the presence of central obesity in a group of Mexican subjects. The rs428253, rs4740, and rs4905 EBI3 SNPs were genotyped in 1323 individuals (1092 central obese and 231 non-central obese). We also analyzed IL-6, IL-27, and IL-35 concentrations. Under different models, the rs4740 (OR = 0.384, Precessive = 0.010; OR = 0.404, Pcodominant 2 = 0.019) and rs4905 (OR = 0.380, Precessive = 0.009; OR = 0.404, Pcodominant 2 = 0.018) were related with a low risk of central obesity. In central obese subjects, the SNPs were related to lower risk of hypoalphalipoproteinemia (rs4740) and with high IL-6 concentrations (rs428253, rs4740, and rs4905), whereas in non-central obese individuals, the rs428253 was related with low risk of increased visceral abdominal fat and hypertriglyceridemia. Interleukin-6, IL-27 and IL-35 concentrations were similar in both groups and no relation was noticed with the studied genotypes. Our results suggest an association of EBI3 SNPs with a low risk of central obesity and with a few risk factors for cardiovascular disease in individuals with and without central obesity.
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Enfermedades Cardiovasculares/genética , Predisposición Genética a la Enfermedad/genética , Interleucinas/genética , Antígenos de Histocompatibilidad Menor/genética , Obesidad Abdominal/genética , Polimorfismo de Nucleótido Simple/genética , Citocinas/genética , Femenino , Frecuencia de los Genes/genética , Genotipo , Factores de Riesgo de Enfermedad Cardiaca , Humanos , Inflamación/genética , Masculino , Persona de Mediana Edad , Factores de RiesgoRESUMEN
PURPOSE: Type 2 diabetes (T2D) and low serum concentration of high-density lipoprotein cholesterol (HDL-c) are common coexisting metabolic disorders. ABCA1 variants have been shown to be associated to these conditions. We sought to test the combined effect of two ABCA1 gene common variants, rs2422493 (- 565C > T) and rs9282541 (R230C) on HDL-c levels and T2D risk. METHODS: Path analysis was conducted in 3,303 Mexican-mestizos to assess the specific contributions of rs2422493 and rs9282541 ABCA1 variants, insulin resistance, waist-to-height ratio (WHtR), and age on HDL-c levels and T2D risk. Participants were classified into four groups according to their ABCA1 variants carrier status: (i) the reference group carried wild type alleles for both ABCA1 variants (-/-), (ii) +/- were carriers of rs2422493 but non-carriers of rs9282541, (iii) -/+ for carriers of rs9282541 but not carriers of rs2422493 and (iv) carriers of minor alleles for both SNPs (+/+). Principal components from two previous genome-wide association studies were used to control for ethnicity. RESULTS: We identified significant indirect effects on T2D risk mediated by HDL-c in groups -/+ and +/+ (ß = 0.04; p = 0.03 and ß = 0.06; p < 0.01, respectively) in comparison to the -/- reference group. Low concentrations of HDL-c were directly and significantly associated with increased T2D risk (ß = -0.70; p < 0.01). WHtR, male gender, age, and insulin resistance were also associated with T2D risk (p < 0.05). There was no significant direct effect for any of the ABCA1 groups on T2D risk: p = 0.99, p = 0.58, and p = 0.91 for groups +/-, -/+, and +/+ respectively. CONCLUSIONS: The ABCA1 rs9282541 (R230C) allele is associated with T2D in Mexicans through its effect on lowering HDL-c levels. This is the first report demonstrating that HDL-c levels act as an intermediate factor between an ABCA1 variant and T2D.
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Transportador 1 de Casete de Unión a ATP/genética , HDL-Colesterol/sangre , Diabetes Mellitus Tipo 2/epidemiología , Predisposición Genética a la Enfermedad , Polimorfismo de Nucleótido Simple , Adulto , Biomarcadores/análisis , Diabetes Mellitus Tipo 2/sangre , Diabetes Mellitus Tipo 2/genética , Femenino , Estudios de Seguimiento , Estudio de Asociación del Genoma Completo , Humanos , Masculino , México/epidemiología , Persona de Mediana Edad , PronósticoRESUMEN
BACKGROUND: Lecithin-cholesterol acyltransferase (LCAT) is a plasma enzyme that esterifies cholesterol in high- and low-density lipoproteins (HDL and LDL). Mutations in LCAT gene causes familial LCAT deficiency, which is characterized by very low plasma HDL-cholesterol levels (Hypoalphalipoproteinemia), corneal opacity and anemia, among other lipid-related traits. Our aim is to evaluate clinical/biochemical features of a Chilean family with a proband showing clinical signs of familial LCAT deficiency, as well as to identify and assess the functional effects of LCAT mutations. METHODS: An adult female proband with hypoalphalipoproteinemia, corneal opacity and mild anemia, as well as her first-degree relatives, were recruited for clinical, biochemical, genetic, in-silico and in-vitro LCAT analysis. Sequencing of exons and intron-exon boundaries was performed to identify mutations. Site-directed mutagenesis was carried out to generate plasmids containing cDNA with wild type or mutant sequences. Such expression vectors were transfected to HEK-239 T cells to asses the effect of LCAT variants in expression, synthesis, secretion and enzyme activity. In-silico prediction analysis and molecular modeling was also used to evaluate the effect of LCAT variants. RESULTS: LCAT sequencing identified rare p.V333 M and p.M404 V missense mutations in compound heterozygous state in the proband, as well the common synonymous p.L363 L variant. LCAT protein was detected in proband's plasma, but with undetectable enzyme activity compared to control relatives. HEK-293 T transfected cells with vector expression plasmids containing either p.M404 V or p.V333 M cDNA showed detectable LCAT protein expression both in supernatants and lysates from cultured cells, but with much lower enzyme activity compared to cells transfected with the wild-type sequence. Bioinformatic analyses also supported a causal role of such rare variations in LCAT lack of function. Additionally, the proband carried the minor allele of the synonymous p.L363 L variant. However, this variant is unlikely to affect the clinical phenotype of the proband given its relatively high frequency in the Chilean population (4%) and its small putative effect on plasma HDL-cholesterol levels. CONCLUSION: Genetic, biochemical, in vitro and in silico analyses indicate that the rare mutations p.M404 V and p.V333 M in LCAT gene lead to suppression of LCAT enzyme activity and cause clinical features of familial LCAT deficiency.
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Hipoalfalipoproteinemias/genética , Deficiencia de la Lecitina Colesterol Aciltransferasa/genética , Lípidos/sangre , Fosfatidilcolina-Esterol O-Aciltransferasa/genética , Adulto , Anciano , Chile/epidemiología , Colesterol/sangre , HDL-Colesterol/sangre , Opacidad de la Córnea/genética , Opacidad de la Córnea/patología , Exones/genética , Femenino , Células HEK293 , Humanos , Hipoalfalipoproteinemias/sangre , Hipoalfalipoproteinemias/epidemiología , Hipoalfalipoproteinemias/patología , Deficiencia de la Lecitina Colesterol Aciltransferasa/sangre , Deficiencia de la Lecitina Colesterol Aciltransferasa/epidemiología , Deficiencia de la Lecitina Colesterol Aciltransferasa/patología , Lipoproteínas HDL/sangre , Simulación de Dinámica Molecular , Mutación Missense/genética , Linaje , Fosfatidilcolina-Esterol O-Aciltransferasa/química , Relación Estructura-ActividadRESUMEN
BACKGROUND: Postprandial triglyceridemia may transitory affect the structure of HDL subclasses and probably their antiatherogenic properties but little is known in this field. We analyzed the HDL subclasses lipid content along postprandial period. METHODS: Fifteen metabolic syndrome (MS) patients and 15 healthy controls were enrolled. HDL were isolated from plasma samples obtained at fasting and every 2-h up to 8-h, after a 75-g fat meal. Cholesterol (C), triglycerides (TAG), and phospholipid (Ph) plasma concentrations of five HDL subclasses were determined by densitometry of electrophoresis gels enzymatically stained. RESULTS: The increase of postprandial triglyceridemia expressed as the incremental area under the curve (iAUC) was twice in MS patients than in controls. Only large HDL2b-TAG were higher in MS than controls at 4, 6 and 8h after meal intake, whereas cholesterol of HDL2a, 3a and 3b were lower at 8h. HDL size distribution shifted towards large HDL and HDL3a-, 3b- and 3c-subclasses had a lower content of cholesterol (estimated by the C-to-Ph ratio) in subjects whose iAUC>289.5mgh/dl (n=15) in comparison with those subjects with iAUC below this cutoff point (n=15), independently of the MS status and fasting TAG. Triglycerides content of HDL subclasses changed only discreetly along the postprandial period, whereas paraoxonase-1 remained unchanged. CONCLUSIONS: A high postprandial triglyceridemia conditions the shift of HDL size distribution towards large particles and the decrease of cholesterol in HDL3 subclasses. These data demonstrate that postprandial hypertriglyceridemia contributes to a transitory hypoalphalipoproteinemia that may increase the risk of cardiovascular disease.
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Colesterol , Dieta Alta en Grasa , Hipertrigliceridemia/sangre , Lipoproteínas HDL/sangre , Lipoproteínas HDL/química , Periodo Posprandial , Adulto , Anciano , Dieta Alta en Grasa/efectos adversos , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
INTRODUCTION: Epidemiologic evidence suggests that tomato-based products could reduce the risk of cardiovascular diseases. One of the main cardiovascular risk factors is low levels of high-density lipoprotein cholesterol (HDL-C). This study aimed to prospectively evaluate the effect of tomato consumption on HDL-C levels. SUBJECT AND METHODS: We conducted a randomized, single-blinded, controlled clinical trial. We screened 432 subjects with a complete lipid profile. Those individuals with low HDL-C (men <40 mg/dL and women <50 mg/dL) but normal triglyceride levels (<150 mg/dL) were included. Selected participants completed a 2-week run-in period on an isocaloric diet and then were randomized to receive 300 g of cucumber (control group) or two uncooked Roma tomatoes a day for 4 weeks. RESULTS: A total of 50 individuals (women = 41; 82%) with a mean age of 42 ± 15.5 years and a mean body mass index of 27.6 ± 5.0 kg/m(2) completed the study. A significant increase in HDL-C levels was observed in the tomato group (from 36.5 ± 7.5 mg/dL to 41.6 ± 6.9 mg/dL, P < 0.0001 versus the control group). After stratification by gender, the difference in HDL-C levels was only significant in women. The mean HDL-C increase was 5.0 ± 2.8 mg/dL (range 1-12 mg/dL). Twenty patients (40%) finished the study with levels >40 mg/dL. A linear regression model that adjusted for those parameters that impact HDL-C levels (age, gender, waist-to-hip ratio, body mass index, fasting triglyceride concentration, simple sugars, alcohol, physical activity, and omega-3 consumption) showed an independent association between tomato consumption and the increase in HDL-C (r (2) = 0.69; P < 0.0001). CONCLUSION: Raw tomato consumption produced a favorable effect on HDL-C levels in overweight women.
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Las estatinas son el principal tratamiento para la reducción del colesterol LDL habiendo demostrado un claro beneficio en la reducción de enfermedad cardiovascular (ECV). Sin embargo, a pesar de los pacientes alcanzar la meta de colesterol LDL, queda un remanente de riesgo relativo de ECV entre un 60% a 70%, el cual ha sido denominado Riesgo Residual. Por ello, el enfoque actual se inclina sobre objetivos adicionales al colesterol LDL, siendo el colesterol HDL bajo y/o triglicéridos elevados los objetivos terapéuticos para reducir el riesgo residual. Se han empleado diversas combinaciones de hipolipemiantes asociados a las estatinas para optimizar el perfil lipídico. La mayorías de estas drogas clásicas (fibratos, niacina y ácidos grasos omega-3), así como un nuevo grupo de moléculas inhibidoras de la Proteína Transportadora de Esteres de Colesterol, son capaces de mejorar las concentraciones de colesterol HDL y triglicéridos en asociación con estatinas, sin embargo, dichas combinaciones en la mayoría de los casos, no han demostrado beneficios en reducir la presencia de ECV, incluso, en el caso de la niacina, se observan efectos deletéreos en las combinaciones a pesar de la optimización del perfil lipídico. Estos hechos nos hacen replantear el conocimiento que tenemos sobre la dislipidemia y su tratamiento, por lo que se presenta la siguiente revisión.
Statins are the principal treatment for highest levels of LDL cholesterol, with clear benefits in reduction of cardiovascular disease (CVD). However, although patients reach LDL cholesterol goal, 60% to 70% have a relative risk remnant of CVD, named Residual Risk. By this, the discussion is focused in other objectives beside LDL cholesterol, being the low HDL cholesterol and/or elevated triglycerides a relevant therapeutic target to reduce the residual risk. Many combinations of drugs have been associated to statins to optimize lipid profile. Most of these classics drugs (fibratos, niacin, and fatty acids omega-3) and the new drugs of Cholesteryl Ester Transfer Proteins inhibitors, increase HDL cholesterol and reduce triglycerides combined with statins, however, in mostly of cases these combinations have not reduced CVD; in studies with niacin, the combination increase deleterious effects despite the optimization of lipid profile. These facts make us reconsider the knowledge we have on dyslipidemia and its treatment, so we present the following review.
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OBJECTIVE: To describe the prevalence of lipid abnormalities found in the Mexican National Health and Nutrition Survey 2006 (ENSANut 2006). MATERIAL AND METHODS: Information was obtained from 4 040 subjects aged 20 to 69 years, studied after a 9- to 12-hour fast. RESULTS: Median lipid concentrations were: cholesterol 198.5 mg/dl, triglycerides 139.6 mg/dl, HDL-cholesterol 39.0 mg/dl, non-HDL-cholesterol 159.5 mg/dl and LDL-cholesterol 131.5 mg/dl. The most frequent abnormality was HDL-cholesterol below 40 mg/dl with a prevalence of 60.5 percent (95 percentCI 58.2-62.8 percent). Hypercholesterolemia (> 200 mg/dl) had a frequency of abnormality of 43.6 percent (95 percentCI 41.4-46.0 percent). Only 8.6 percent of the hypercholesterolemic subjects knew their diagnosis. Hypertriglyceridemia (> 150 mg/dl) was observed in 31.5 percent (IC 95 percent 29.3-33.9 percent) of the population. CONLUSIONS: The ENSANUT 2006 data confirm that the prevalence of hypoalphalipoproteinemia and other forms of dyslipidemia in Mexican adults is very high.
OBJETIVO: Presentar la prevalencia de las dislipidemias observada en la Encuesta Nacional de Salud y Nutrición 2006 (ENSANUT 2006). MATERIAL Y MÉTODOS: Se incluyeron 4040 individuos con edad entre 20 y 69 años estudiados bajo un ayuno de 9 a 12 horas. RESULTADOS: Las concentraciones medias de los lípidos sanguíneos fueron colesterol 198.5 mg/dl, triglicéridos 139.6 mg/dl, colesterol HDL 39.0 mg/dl, colesterol noHDL 159.5 mg/dl y colesterol LDL 131.5 mg/dl. La anormalidad más común fue la hipoalfalipoproteinemia (colesterol HDL< 40 mg/dl); su prevalencia fue 60.5 por ciento (IC95 por ciento 58.2-62.8 por ciento). La hipercolesterolemia (colesterol > 200 mg/dl) fue la segunda anormalidad en frecuencia, con 43.6 por ciento (IC95 por ciento 41.4-46.0 por ciento). Sólo el 8.6 por ciento de los casos conocía su diagnóstico. La hipertrigliceridemia (> 150 mg/dl) fue observada en 31.5 por ciento (IC95 por ciento 29.3-33.9 por ciento) de la población en estudio. CONCLUSIONES: Los datos de la ENSANUT 2006 confirman que la prevalencia de hipoalfalipoproteinemia y otras formas de dislipidemia es muy alta en los adultos mexicanos.
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Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Masculino , Persona de Mediana Edad , Adulto Joven , Dislipidemias/epidemiología , Encuestas Epidemiológicas , Encuestas Nutricionales , Dislipidemias/sangre , Ayuno/sangre , Hipercolesterolemia/sangre , Hipercolesterolemia/epidemiología , Hipertrigliceridemia/sangre , Hipertrigliceridemia/epidemiología , Hipoalfalipoproteinemias/sangre , Hipoalfalipoproteinemias/epidemiología , México/epidemiología , Prevalencia , Factores de Riesgo , Muestreo , Factores Socioeconómicos , Adulto JovenRESUMEN
OBJECTIVE: To estimate the percentage of Mexican adults that may require lipid-lowering treatment according to National Cholesterol Education Program-III guidelines, using data from the National Health and Nutrition Survey 2006 (ENSANut 2006). MATERIAL AND METHODS: Information was obtained from 4 040 subjects aged 20 to 69 years, studied after a 9 to 12 hours fast. RESULTS: A cardiovascular risk equivalent was found in 13.8 percent and >2 risk factors were present in 31.5 percent of the population. LDL-C concentrations were above the treatment goal in 70 percent of the high-risk group and in 38.6 percent of subjects with >2 risk factors. Nearly 12 million Mexicans should be taught how to change their lifestyles and close to 8 million individuals require drug therapy to decrease their cardiovascular risk. CONCLUSIONS: Thirty percent of Mexican adults require some form of lipid-lowering treatment (lifestyle modifications in 36.25 percent, drug therapy in 24.19 percent).
OBJETIVO: Calcular el porcentaje de adultos que requiere tratamiento hipolipemiante de acuerdo con las recomendaciones del Programa Nacional de Educación en Colesterol-III, usando los datos de la Encuesta Nacional de Salud y Nutrición 2006. MATERIAL Y MÉTODOS: Se incluyeron 4040 individuos con edad entre 20 y 69 años estudiados bajo un ayuno de 9 a 12 horas. RESULTADOS: Un equivalente de enfermedad cardiovascular fue identificado en 13.8 por ciento de los participantes. El 31.5 por ciento de la población tenía >2 factores de riesgo cardiovascular. La concentración de colesterol LDL estuvo arriba de la meta terapéutica en 70 por ciento de los casos con alto riesgo cardiovascular y en el 38.6 por ciento de los sujetos con >2 factores de riesgo. Cerca de 12 millones de mexicanos deben modificar su estilo de vida para reducir su concentración de colesterol LDL. Casi 8 millones califican para recibir tratamiento farmacológico. CONCLUSIONES: Una tercera parte de los adultos requiere alguna forma de tratamiento hipolipemiante (cambios en el estilo de vida: 36.25 por ciento, medicamentos: 24.19 por ciento).
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Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Enfermedades Cardiovasculares/prevención & control , Necesidades y Demandas de Servicios de Salud/estadística & datos numéricos , Hiperlipidemias/tratamiento farmacológico , Salud Pública , Hipolipemiantes/uso terapéutico , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/etiología , Estudios Transversales , Diabetes Mellitus/epidemiología , Ayuno/sangre , Objetivos , Encuestas Epidemiológicas , Hiperlipidemias/sangre , Hiperlipidemias/complicaciones , Hiperlipidemias/epidemiología , México/epidemiología , Encuestas Nutricionales , Educación del Paciente como Asunto , Prevalencia , Factores de Riesgo , Población Rural , Muestreo , Población UrbanaRESUMEN
Las lipoproteínas de alta densidad (HDL) son una familia de partículas que difieren en tamaño, densidad y composición química. La heterogeneidad de las HDL resulta de la velocidad de síntesis y de catabolismo de las partículas, y de la acción de enzimas y proteínas de transporte que las remodelan continuamente. Los bajos niveles de colesterol HDL correlacionan con un riesgo elevado de desarrollar enfermedad aterosclerosa coronaria. La disminución de las HDL afecta el transporte reverso de colesterol, que es la vía metabólica responsable de la remoción del colesterol excedente de la células periféricas y su transporte hacia el hígado para reciclarlo o eliminarlo. Las HDL poseen además propiedades antiinflamatorias, antioxidativas, antiagregatorias, anticoagulantes y profibrinolíticas in vitro . Algunas de estas propiedades potencialmente antiaterosclerosas, también se han puesto de manifiesto in vivo con infusiones de HDL. Estas evidencias, además de la protección que se logra en modelos animales genéticamente modificados, permite plantear a las HDL como un objetivo primario en la prevención de la aterosclerosis coronaria. Algunos estudios epidemiológicos han demostrado una reducción importante en el riesgo cardiovascular asociado a elevaciones del colesterol HDL, principalmente en prevención secundaria. En consecuencia, elevar las concentraciones de las HDL a través de medidas higiénicas como el ejercicio aeróbico, la pérdida de peso y eliminar el tabaquismo, es ampliamente recomendado para reducir el riesgo coronario. Cuando las medidas higiénicas fallan, la intervención farmacológica con niacina o fibratos debe ser considerada en ciertos pacientes con niveles bajos de HDL. Por último, las diferentes subclases de HDL no poseen las mismas propiedades antiaterogénicas, lo que sugiere que las intervenciones tanto higiénicas como farmacológicas se deberán enfocar en el futuro hacia incrementos de la funcionalidad de las HDL, más que a incremento en la concentración del colesterol HDL.
High density lipoproteins (HDL) are a family of heterogeneous particles that vary in size, density and chemical composition, as a result of their synthesis and catabolism rates, and a continuous intravascular remodeling by the action of enzymes and transport proteins. Low plasma levels of HDL correlate with a high risk of atherosclerotic heart disease. Such a diminished concentration of HDL affect reverse cholesterol transport, which is the metabolic pathway responsible for the movement of cholesterol excess from peripheral tissues to the liver for recycling or excretion. In addition, HDL possess anti-inflammatory, anti-oxidative, anti-aggregatory, anti-coagulant, and pro-fibrinolytic properties, as has been demonstrated by in vitro studies. Some of those potentially anti-atherosclerotic in vitro-properties has been corroborated by HDL infusion in vivo. Such evidences and the protection of susceptible animals from atherosclerosis by transgenic manipulation of HDL metabolism, raise the possibility to focus the HDL plasma levels as a main target in coronary hearth disease prevention. Intervention trials have shown an important reduction in coronary events by rising HDL-cholesterol, mainly in the secondary prevention. Increasing HDL plasma levels by hygienic intervention such as aerobic exercise, weight loss and stop smoking is strongly recommended to reduce coronary risk in primary prevention. Pharmacological intervention to rise the HDL plasma levels with niacin or fibrates, should be considered in some patients as an alternative when hygienic intervention fails. Finally, it most be taken into account that the different HDL subclasses does not possess the same anti-atherosclerotic properties, suggesting that hygienic and pharmacological interventions should focus to increase HDL functionality rather than HDL-cholesterol plasma levels. (Arch Cardiol Mex 2004; 74:53-67).