Examinando por Autor "Cornelis, Marilyn C."
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Ítem Genetic polymorphism of CYP1A2 increases the risk of myocardial infarction(Journal of Medical Genetics, Volumen 41, no. 10, 2004) Cornelis, Marilyn C.; El-Sohemy, Ahmed; Campos Núñez, HanniaThere is growing evidence that DNA damage caused by mutagens found in tobacco smoke may contribute to the development of coronary heart disease (CHD). In order to bind to DNA many mutagens require metabolic activation by cytochrome P450 (CYP) 1A1 or CYP1A2. The objective of this study was to determine the effects of CYP1A1 and CYP1A2 genotypes on risk of myocardial infarction (MI) and whether smoking interacts with genotype to modify risk.Ítem Genetic polymorphism of the adenosine A2A receptor is associated with habitual caffeine consumption(The American Journal of Clinical Nutrition, Volumen 86, no. 1, 2007) Cornelis, Marilyn C.; El-Sohemy, Ahmed; Campos Núñez, HanniaBackground: Caffeine is the most widely consumed stimulant in the world, and individual differences in response to its stimulating effects may explain some of the variability in caffeine consumption within a population. Objective: We examined whether genetic variability in caffeine metabolism [cytochrome P450 1A2 (CYP1A2) −163A→C] or the main target of caffeine action in the nervous system [adenosine A2A receptor (ADORA2A) 1083C→T] is associated with habitual caffeine consumption. Design: Subjects (n = 2735) were participants from a study of gene-diet interactions and risk of myocardial infarction who did not have a history of hypertension. Genotype frequencies were examined among persons who were categorized according to their self-reported daily caffeine intake, as assessed with a validated food-frequency questionnaire. Results: The ADORA2A, but not the CYP1A2, genotype was associated with different amounts of caffeine intake. Compared with persons consuming <100 mg caffeine/d, the odds ratios for having the ADORA2A TT genotype were 0.74 (95% CI: 0.53, 1.03), 0.63 (95% CI: 0.48, 0.83), and 0.57 (95% CI: 0.42, 0.77) for those consuming 100–200, >200–400, and >400 mg caffeine/d, respectively. The association was more pronounced among current smokers than among nonsmokers (P for interaction = 0.07). Persons with the ADORA2A TT genotype also were significantly more likely to consume less caffeine (ie, <100 mg/d) than were carriers of the C allele [P = 0.011 (nonsmokers), P = 0.008 (smokers)]. Conclusion: Our findings show that the probability of having the ADORA2A 1083TT genotype decreases as habitual caffeine consumption increases. This observation provides a biologic basis for caffeine consumption behavior and suggests that persons with this genotype may be less vulnerable to caffeine dependence.Ítem GSTT1 genotype modifies the association between cruciferous vegetable intake and the risk of myocardial infarction(The American Journal of Clinical Nutrition, Volumen 86, no. 3, 2007) Cornelis, Marilyn C.; El-Sohemy, Ahmed; Campos Núñez, HanniaBackground: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are associated with protection against components of the metabolic syndrome, but the role of α-linolenic acid (ALA), the metabolic precursor of EPA and DHA, has not been studied. The Δ6-desaturase enzyme converts ALA into EPA and DHA, and genetic variation in the Δ6-desaturase gene (FADS2) may affect this conversion. Objectives: We hypothesize that high ALA is associated with a lower prevalence of the metabolic syndrome and that genetic variation in FADS2 modifies this association. Design: We studied 1815 Costa Rican adults. Adipose tissue ALA was used as a biomarker of intake, and metabolic syndrome was identified with the definition from the National Cholesterol Education Program, Adult Treatment Panel III. Prevalence ratios (PRs) and 95% CIs were estimated from binomial regression models, and the likelihood ratio was used to test for effect modification. Results: High concentrations of adipose tissue ALA were associated with lower PRs of the metabolic syndrome compared with low ALA (0.81; 95% CI: 0.66, 1.00, for the comparison between the highest and the lowest quintiles; P for trend < 0.02). Higher concentrations of adipose tissue ALA were associated with a lower PR among homozygote (0.67; 95% CI: 0.53, 0.86) and heterozygote (0.84; 95% CI: 0.72, 0.99) carriers of the FADS2 T allele, but not among homozygote carriers of the deletion variant allele (0.99; 95% CI: 0.78, 1.27; P for interaction: 0.08). Conclusions: Elevated ALA concentrations in adipose tissue are associated with lower prevalence of the metabolic syndrome. A lack of association among homozygote carriers of the FADS2 deletion allele suggests that this association may be due in part to the conversion of ALA into EPA.Ítem Microsomal epoxide hydrolase genotype and risk of myocardial infarction(Arch Toxicol, no. 81, march, 2007) Cornelis, Marilyn C.; El-Sohemy, Ahmed; Campos Núñez, HanniaAbstract DNA damage caused by mutagens found in tobacco smoke may contribute to the development of coronary heart disease (CHD). Microsomal epoxide hydrolase (EPHX1) is involved in the metabolism of tobacco smoke mutagens and an amino acid substitution (H139R) in exon 4 of the EPHX1 gene is associated with increased enzyme activity. The objective of this study was to investigate the effect of EPHX1 genotype on risk of myocardial infarction (MI) and to determine whether smoking interacts with genotype to modify risk. Cases (n = 2,022) with a first acute non-fatal MI and population-based controls (n = 2,022) living in Costa Rica, matched for age, sex and area of residence were genotyped by RFLP-PCR. Smoking status was determined by questionnaire. The frequency of the R139 allele was 17% for both cases and controls. EPHX1 genotype was not associated with risk of MI, regardless of smoking status. Compared to individuals with the HH genotype, the multivariate adjusted odds ratio (95% confidence interval) for risk of MI was 0.95 (0.81–1.11) for individuals with the HR genotype and 1.18 (0.79–1.76) for those with the RR genotype. These results suggest that EPHX1 does not play a significant role in the development of CHD