Background Hypertension is a complex disorder affected by gene-environment interactions. Methylenetetrahydrofolate reductase (MTHFR) gene is one of the genes in One Carbon Metabolic (OCM) pathway that affects both blood pressure and epigenetic phenomenon. MTHFR C677T gene polymorphism leads to reduced methylation capacity via increased homocysteine concentrations. Global DNA methylation (5mC%) also gets affected in conditions such as hypertension. However, no study is found to understand hypertension in terms of both genetics and epigenetics. The present study aims to understand the relation between methylation, MTHFR C677T gene polymorphism and hypertension. It also tries to understand relation (if any) between methylation and anti-hypertensive drugs. Methods This is a cross-sectional study where data were collected from a total of 1634 individuals of either sex in age group 35–65 years. Hypertensives (SBP ≥ 140 mm Hg and DBP ≥ 90 mm Hg) (on treatment/not on treatment) and absolute controls were 236 (cases) and 307 (controls), respectively. All the samples were subjected to MTHFR C677T gene polymorphism screening (PCR–RFLP) and global DNA methylation assay (ELISA based colorimetric assay). Results of both the analyses were obtained on 218 cases, 263 controls. Results Median 5mC% was relatively lower among cases (p > 0.05) compared to controls, despite controlling for confounders (age, sex, smoking, alcohol, diet) (r2-0.92, p-0.08). Cases not on medication had significantly reduced 5mC% compared to controls (p < 0.05), despite adjusting for confounders (r2-0.857, p-0.01). Among cases (irrespective of treatment), there was a significant variation in 5mC% across the three genotypes i.e. CC, CT and TT, with no such variation among controls. Cases (not on medication) with TT genotype had significantly lower methylation levels compared to the TT genotype controls and cases (on medication) (p < 0.01). Conclusion Global DNA hypomethylation seems to be associated with hypertension and antihypertensive drugs seem to improve methylation. Hypertensive individuals with TT genotype but not on medication are more likely to be prone to global DNA hypomethylation. Important precursors in OCM pathway include micronutrients such as vitamin B-12, B-9 and B-6; their nutritional interventions (either dietary or supplement) may serve as strategies to prevent hypertension at population level. However, more epidemiological-longitudinal studies are needed for further validation.
Hypertension is a major contributor to global CVD burden. LMICs including India is challenged with rising hypertension prevalence, yet limited studies are available on temporal change and incidence among community-cohorts. This study aimed to describe trends in hypertension prevalence, awareness, treatment, and control over 8 years among a rural community-cohort from Haryana, India. The study also lends towards an analysis of incidence. Adults ≥ 30 years (N = 1542) recruited during baseline cross-sectional study between 2011 and 2014 were followed up after a median 8.1 years. At endline, demographic/lifestyle characteristics and blood pressure were re-examined. Overall median SBP significantly increased from 120 mmHg at baseline to 125.5 mmHg at endline (p < 0.001), while hypertension prevalence increased from 34.4% (95% CI 32.0–36.9) to 40.4% (95% CI 37.5–43.4) (p = 0.002). Age-standardized hypertension incidence was 30.2% (95% CI 26.7–35.2) over 8 years. Among hypertensive group, awareness, treatment, and control increased from 9.6, 8.8 and 5.0% to 31.8, 27.3 and 9.6% (p < 0.05), respectively. Increasing trend in SBP and hypertension prevalence was observed as the cohort ages. This increase is supported by the high incidence of hypertension. Nevertheless, our study highlights positive trends in hypertension care cascade but poor control, suggesting that this trend may not be adequately impactful to reduce hypertension burden.
Background Anthropogenic air pollution has been implicated in aberrant changes of DNA methylation and homocysteine increase (>15μM/L). Folate (<3 ng/mL) and vitamin B12 (<220 pg/mL) deficiencies also reduce global DNA methylation via homocysteine increase. Although B-vitamin supplements can attenuate epigenetic effects of air pollution but such understanding in population-specific studies are lacking. Hence, the present study aims to understand the role of air pollution, homocysteine, and nutritional deficiencies on methylation. Methods We examined cross-sectionally, homocysteine, folate, vitamin B12 (chemiluminescence) and global DNA methylation (colorimetric ELISA Assay) among 274 and 270 individuals from low- and high- polluted areas, respectively, from a single Mendelian population. Global DNA methylation results were obtained on 254 and 258 samples from low- and high- polluted areas, respectively. Results Significant decline in median global DNA methylation was seen as a result of air pollution [high-0.84 (0.37–1.97) vs. low-0.96 (0.45–2.75), p = 0.01]. High homocysteine in combination with air pollution significantly reduced global DNA methylation [high-0.71 (0.34–1.90) vs. low-0.93 (0.45–3.00), p = 0.003]. Folate deficient individuals in high polluted areas [high-0.70 (0.37–1.29) vs. low-1.21 (0.45–3.65)] showed significantly reduced global methylation levels (p = 0.007). In low polluted areas, despite folate deficiency, if normal vitamin B12 levels were maintained, global DNA methylation levels improved significantly [2.03 (0.60–5.24), p = 0.007]. Conversely, in high polluted areas despite vitamin B12 deficiency, if normal folate status was maintained, global DNA methylation status improved significantly [0.91 (0.36–1.63)] compared to vitamin B12 normal individuals [0.54 (0.26–1.13), p = 0.04]. Conclusions High homocysteine may aggravate the effects of air pollution on DNA methylation. Vitamin B12 in low-polluted and folate in high-polluted areas may be strong determinants for changes in DNA methylation levels. The effect of air pollution on methylation levels may be reduced through inclusion of dietary or supplemented B-vitamins. This may serve as public level approach in natural settings to prevent metabolic adversities at community level.
Background Depression is a highly prevalent mental disorder with complex aetiology. An emerging body of evidence shows that depression tends to co-occur with abnormal blood glucose levels and dyslipidaemia. This study aimed to understand the overall and gender-specific associations of abnormal glucose levels and dyslipidaemia with depression in a single Mendelian population from rural Haryana, India. To achieve the aim, a population-based case-control study, which constituted of 251 depressed (cases) and 251 non-depressed (controls) individuals, was set up. The study was conducted among the Jat community of Palwal District, Haryana (North India). Data collection was done using a pre-tested interview schedule through the household survey method. Depression status was ascertained using Beck Depression Inventory-II. Fasting blood glucose analysis and lipid profiling were done using commercial kits (Randox, USA) through spectrophotometry. Statistical analysis was done using MS-Excel 2010 and SPSS version 16.0. Results In the present study, overall fasting blood sugar level was not found to be associated with depression. However, high blood sugar posed a 3.6-folds elevated risk for depression among females with borderline significance (p = 0.058). Further, higher levels of TC and LDL were found to be inversely associated with depression. In the sex-wise analysis inverse association of TC and LDL with depression remained significant among males but not among females. Instead, high TG and high VLDL showed an increased risk for depression in females. Conclusions This study suggests gender-specific associations of some of the studied biochemical variables with depression. Longitudinal studies are warranted to explicate cause-effect relationships between the studied biochemical variables and depression.
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