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Hypertension affects populations globally and is thus a public health and socio-economic problem. Macronutrient and micronutrient deficiencies are common in the general population, and may be even more prevalent in hypertensive patients. This study aimed to determine a possible association between hypertension and intake of fat-soluble vitamins A, D and E. Participants were from the cross-sectional Hortega nutrition study conducted with a random sample of 1514 people (50.3% women, 49.7% men) and two groups: nonhypertensive controls ≥40 years old (n = 429, 28.3%), unknown untreated hypertension cases ≥40 years old (n = 246, 16.2%). Biochemical and anthropometric measurements were taken. Data on dietary intakes, education, socio-economic status, place of residence, health habits, comorbidities, alcohol consumption and smoking were collected and assessed. A descriptive data study was done and compared by ANOVA and Chi-Square. No p value higher than 0.05 was considered significant. The results showed that vitamin A intake was higher in the hypertensive subpopulation (1732.77 ± 962.27 µg vs. 1655.89 ± 902.81 µg), and vitamin D and E intakes were lower (8.13 ± 9.71 µg vs. 8.25 ± 9.52 µg and 18.79 ± 7.84 mg vs. 18.60 ± 8.20 mg, respectively). No statistically significant differences were found in any adjusted model. This study did not significantly associate intake of vitamins A, D and E with hypertension in people aged over 40. Future studies on this topic and a larger sample are necessary.

OBJECTIVE Angiotensin-converting enzyme (ACE) has been related to cardiovascular physiology and bone remodeling. Our aim was to assess the relationship among ACE polymorphisms, cardiovascular risk, and osteoporotic fractures. MATERIAL AND METHODS We prospectively enrolled 71 patients with hypertension from 2001 to 2014. Sociodemographic and medical data were collected. Comorbidity was evaluated with Charlson index. Densitometric studies on lumbar spine were performed. ACE polymorphism was analyzed by polymerase chain reaction. Data were analyzed using SPSS 15.0 (p value

Background ABCG1 mediates cellular cholesterol transport, but there is very little known about the influence of ABCG1 polymorphisms on human plasma lipoprotein cholesterol concentrations or on the interactions of these polymorphisms with diet. Objective Our objective was to investigate whether interactions between PUFA intake and ABCG1 polymorphisms modulate associations with plasma total cholesterol (TC), LDL- and HDL-cholesterol in two Spanish populations. Methods We grounded our investigation on two general population-based studies: the Hortega study (population A) and the Pizarra study (population B). Participants included 1178 individuals (50.0% women, age range 21–85 years) and 763 individuals (66% women, age range 23–73 years) from populations A and B, respectively, without lipid lowering drugs. Subjects were genotyped for ABCG1 variants. Biochemical measurements were taken by standard procedures. Dietary intakes were estimated with a validated questionnaire. Results In population A, the A allele homozygotes of SNP rs4148102 had higher TC and LDLc concentrations in subjects on a high PUFA diet than did the carriers of the G allele (242.1±38.9 vs. 198.0±36.0mg/dL, p =0.003, and 149.8±37.9 vs. 111.4±32.1mg/dL, p =0.005, respectively), and significant gene–diet interactions were observed ( p =0.020 and p =0.013, respectively). In population B, similar differences in TC and LDLc concentrations were also found in association with this SNP under a high PUFA diet (253.2±24.9 vs. 197.7±39.9mg/dL, p =0.009, and 171.8±20.5 vs. 120.4±34.2mg/dL, p =0.004, respectively), but the gene–diet interactions observed were not significant ( p =0.379 and p =0.422, respectively). In the pooled populations, differences in the TC and LDLc concentrations increased (246.8±32.9 vs. 198.0±37.5, p =6×10 −5 , and 159.0±32.6 vs. 114.3±33.1, p =3×10 −5 , respectively), and significant gene–diet interactions were maintained ( p =0.006 and p =0.003, respectively). Conclusion In two Spanish populations, the ABCG1 polymorphism rs4148102 was associated with variations in plasma lipoprotein cholesterol concentrations in subjects with high PUFA intakes. Carriers of the AA genotype consuming high PUFA diet showed higher plasma LDLc concentrations.

Eur J Clin Invest 2011 Abstract Background Increased accumulation of fat results from an imbalance between energy expenditure and intake, being modulated by different environmental and genetic factors. Uncoupling proteins (UCPs) are mitochondrial carrier proteins able to spend energy generating heat. Therefore, variations in these genes are good candidates as potential modulators of body fat accumulation. Our aim was to investigate the possible association of genetic variations of the gene codifying the UCP2 protein with obesity and fat distribution. Design We performed a cross-sectional study in 2367 individuals from two population-based studies from different regions of Spain. The Hortega Study included 1436 individuals (693 women) 21–85 years old, and the Pizarra Study included 931 individuals (584 women) 18–65 years old. We evaluated three polymorphisms of the UCP2 gene. Results The TT genotype of the rs660339 polymorphism and the AA genotype of the rs659366 polymorphism of the UCP2 gene were significantly associated with higher waist circumference in the Hortega Study. Furthermore, subjects carrying both genotypes (TT+AA) also showed higher central adiposity compared with other genotypes. This association was also present in the Pizarra Study. Moreover, in the pooled population, we found a stronger association with waist circumference. Even, we found association with BMI. Furthermore, rs659366 polymorphism was associated with the risk of abdominal obesity (P = 0·04: OR = 1·3; CI = 1·01–1·67). Conclusions Polymorphisms of the UCP2 gene (rs660339 and rs659366) were associated with central obesity. This study shows association between the UCP2 gene and the susceptibility to obesity and body fat distribution in a south European population.

Objective To assess the association of single-nucleotide polymorphisms (SNPs) in genes codifying for antioxidant enzymes to blood pressure (BP) values and risk of hypertension. Methods Population-based study including 1388 participants (704 women) older than 18 years in which 300 were untreated hypertensive patients. In 335 untreated hypertensive patients referred to one hypertension clinic, the study was replicated. Thirty-five SNP throughout 13 genes were analyzed using SNPlex. In a subgroup of hypertensive patients, the amount of 8-oxo-deoxyguanosine and GPX activity levels was measured in mononuclear cells. Results In the general population, genotypes with the G allele of the c.172G>A polymorphism in the SOD3 gene and those with the T allele of the c.-20C>T polymorphism in the CAT gene were associated with significant lower values of BP. Likewise, these genotypes were associated with less risk for hypertension after adjusting for confounder variables. Haplotypes in both genes increased the strength of associations. In the hypertensive patients, the same alleles of the two polymorphisms were associated with lower BP values too. In addition, two others, the CT-TT genotypes of the c.*891C>T polymorphism in the GPX1 gene and the CT-CC genotypes of the c.-793T>C polymorphism of the TXN gene were also significantly associated to lower BP values. Furthermore, the CC genotype of the c.*891C>T polymorphism in the GPX1 gene was associated with higher values of 8-oxo-dG and GPX activity levels as compared to those for the CT-TT genotype. Conclusions The results of the present study support the influence of antioxidant enzyme genes in BP values and hypertension risk.

Background: Alterations in the redox balance are involved in the origin, promotion and progression of cancer. Inter-individual differences in the oxidative stress regulation can explain a part of the variability in cancer susceptibility. The aim of this study was to evaluate if polymorphisms in genes codifying for the different systems involved in oxidative stress levels can have a role in susceptibility to breast cancer. Methods: We have analyzed 76 single base polymorphisms located in 27 genes involved in oxidative stress regulation by SNPlex technology. First, we have tested all the selected SNPs in 493 breast cancer patients and 683 controls and we have replicated the significant results in a second independent set of samples (430 patients and 803 controls). Gene-gene interactions were performed by the multifactor dimensionality reduction approach. Results: Six polymorphisms rs1052133 (OGG1), rs406113 and rs974334 (GPX6), rs2284659 (SOD3), rs4135225 (TXN) and rs207454 (XDH) were significant in the global analysis. The gene-gene interactions demonstrated a significant four-variant interaction among rs406113 (GPX6), rs974334 (GPX6), rs105213 (OGG1) and rs2284659 (SOD3) (p-value = 0.0008) with high-risk genotype combination showing increased risk for breast cancer (OR = 1.75 [95% CI; 1.26-2.44]). Conclusions: The results of this study indicate that different genotypes in genes of the oxidant/antioxidant pathway could affect the susceptibility to breast cancer. Furthermore, our study highlighted the importance of the analysis of the epistatic interactions to define with more accuracy the influence of genetic variants in susceptibility to breast cancer. publishedVersion

There is evidence that uncontrolled arterial hypertension (AHT) in patients with metabolic syndrome (MS) increases cardiovascular risks. The renin-angiotensin-aldosterone system (RAAS) and its polymorphisms apparently confer a genetic risk for uncontrolled AHT. This study aims to investigate the influence of RAAS polymorphisms on AHT control in patients diagnosed with MS. This is a two-stage population-based nested case-control pilot study (n=1514). We differentiated between MS-diagnosed patients and non-MS patients (ATP-III criteria) and selected those individuals diagnosed with AHT from each group (n=161 and n=156, respectively). Those who successfully controlled their AHT (controls) and those who did not were compared. In the MS population, the C/G and G/G genotypes of single-nucleotide polymorphism rs1040288 (NR3C2) and A/G and G/G of rs11099680 (NR3C2) were associated with uncontrolled AHT (odds ratio (OR)=2.94 (1.34-6.47) and OR=2.54 (1.09-5.93), respectively). According to Akaike's information criteria, the best adjusted model included gender and age as confounding variables (adjusted OR (ORa)=2.91 (1.31-6.46) and ORa=2.67 (1.13-6.31), respectively). Regarding rs1040288, an ORa of 4.03 (1.44-11.26) was obtained for the saturated model (adjusted for gender, age, waist-to-hip ratio, body mass index, biochemical profile, renal damage, smoking habit and anti-AHT treatment). Yet, when the same analysis was performed on the non-MS population, no association was found between rs11099680 and the failure to control AHT. The results reveal a possible association between the rs11099680 RAAS polymorphism and uncontrolled AHT in MS-diagnosed patients. rs1040288 appears to be associated with uncontrolled blood pressure regardless of MS profile.

Background The objective was to investigate the association between BMI and single nucleotide polymorphisms previously identified of obesity-related genes in two Spanish populations. Forty SNPs in 23 obesity-related genes were evaluated in a rural population characterized by a high prevalence of obesity (869 subjects, mean age 46 yr, 62% women, 36% obese) and in an urban population (1425 subjects, mean age 54 yr, 50% women, 19% obese). Genotyping was assessed by using SNPlex and PLINK for the association analysis. Results Polymorphisms of the FTO were significantly associated with BMI, in the rural population (beta 0.87, p-value 2 in Hortega and 2.0 kg/m2 in Pizarra. Overall, the obesity predictive value was low (less than 1%). Conclusion The risk associated with polymorphisms is low and the overall effect on BMI or obesity prediction is minimal. A weighted genetic risk score based on genes mainly acting through central nervous system mechanisms was associated with BMI but it yields minimal clinical prediction for the obesity risk in the general population.