Association of lifestyle, inflammatory factors, and dietary patterns with the risk of suffering a stroke: A case-control study.

BACKGROUND: Lifestyle, including dietary patterns, could involve specific factors participating in inflammation that confer a higher risk of suffering a stroke. However, little attention has been apparently given to habitual food consumption in patients suffering a cerebrovascular event. OBJECTIVE: To assess the influence of dietary habits as well as other lifestyle-related variables on the risk of suffering a stroke. DESIGN: A case-control study was designed. Fifty-one cases (age: 59.1 ± 9.1y.o; BMI; 30.8 ± 3.4 kg/m2) and 51 controls (age: 61.1 ± 9.1y.o; BMI; 30.4 ± 3.6 kg/m2) were enrolled in the study. Anthropometric and body composition variables were measured. Dietary information was obtained from a validated food frequency questionnaire. Physical activity and lifestyle-related factors were assessed. Blood samples were drawn. RESULTS: Patients suffering a stroke showed higher prevalence of diabetes (30 vs. 7.7%; P = 0.020) and hypertension (74.5 vs. 40.3%; P < 0.001) and were less physically active (36.7 vs. 66.6%; P = 0.024) than controls. Patients registered worse glucose and lipid profiles, higher levels of hepatic biomarkers, and higher blood cell counts than controls. Stroked patients showed lower adherence to a statistically derived healthy dietary pattern than controls (23.5 vs. 42.3%; P = 0.017). A logistic regression model was built up considering hypertension, diabetes, smoking, physical activity, adherence to a 'healthy dietary pattern' and C-reactive protein concentration. The final model strongly associated with the risk of suffering a stroke (R2: 44.6%; Pmodel < 0.0001). CONCLUSION: Lifestyle variables such as physical activity, smoking habit, and a dietary pattern including foods with low inflammatory potential play an important role in the reduction of the risk of suffering a stroke.

Epigenetic Changes in the Methylation Patterns of KCNQ1 and WT1 after a Weight Loss Intervention Program in Obese Stroke Patients.

Ischemic stroke patients often show high concentrations of circulating inflammatory markers that are associated with increased risk of recurrence. Epigenetic mechanisms could be involved in obesity, inflammation and stroke. The objective of this research was to investigate, in obese patients suffering a previous stroke, the effects of a nutritional program on anthropometric and biochemical variables, and on the methylation patterns of two stroke-related genes (KCNQ1: potassium channel, voltage gated KQT-like subfamily Q, member 1; and WT1: Wilms tumor 1). Twenty-two ischemic stroke patients were compared with a control group composed of eighteen obese subjects with similar age and body mass index ranges. Both groups followed a 20-week nutritional program based on an energy-restricted balanced diet with high adherence to the Mediterranean dietary pattern. The intervention significantly improved anthropometric and metabolic variables, such as the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and C-reactive protein concentration, in ischemic stroke patients, and was accompanied by changes in the methylation patterns of both stroke-related genes, which correlated with anthropometric and biochemical variables.

Obesity and ischemic stroke modulate the methylation levels of KCNQ1 in white blood cells.

Obesity and stroke are multifactorial diseases in which genetic, epigenetic and lifestyle factors are involved. The research aims were, first, the description of genes with differential epigenetic regulation obtained by an 'omics' approach in patients with ischemic stroke and, second, to determine the importance of some regions of these selected genes in biological processes depending on the body mass index. A case-control study using two populations was designed. The first population consisted of 24 volunteers according to stroke/non-stroke and normal weight/obesity conditions. The second population included 60 stroke patients and 55 controls classified by adiposity. DNA from the first population was analyzed with a methylation microarray, showing 80 cytosine-guanine dinucleotides (CpG) sites differentially methylated in stroke and 96 CpGs in obesity, whereas 59 CpGs showed interaction. After validating these data by MassArray Epityper, the promoter region of peptidase M20 domain containing 1 (PM20D1) gene was significantly hypermethylated in stroke patients. One CpG site at Caldesmon 1 (CALD1) gene showed an interaction between stroke and obesity. Two CpGs located in the genes Wilms' tumor 1 (WT1) and potassium voltage-gated channel, KQT-like subfamily, member 1 (KCNQ1) were significantly hypermethylated in obese patients. In the second population, KCNQ1 was also hypermethylated in the obese subjects. Two CpGs of this gene were subsequently validated by methylation-sensitive high-resolution melting. Moreover, KCNQ1 methylation levels were associated with plasma KCNQ1 protein concentrations. In conclusion, obesity induced changes in the KCNQ1 methylation pattern which were also dependent on stroke. Furthermore, the epigenetic marks differentially methylated in the stroke patients were dependent on the previous obese state. These DNA methylation patterns could be used as future potential stroke biomarkers.