EXAMINING HOW NUTRITIONAL HABITS INFLUENCE DNA MARKERS CONNECTED TO HEART FUNCTION AMONG ADULTS IN MIDLIFE LIVING WITH TYPE 2 DIABETES

Abstract

Cardiovascular disease continues to be a causative agent of morbidity and mortality among adults with Type 2 Diabetes Mellitus (T2DM), especially at midlife. While traditional risk factors like obesity, dyslipidaemia, and hypertension are being increasingly understood, there is increasing evidence that nutrition affects cardiovascular health through epigenetic pathways and gene-diet interactions. This research examined the influence of food consumption on DNA methylation of genes important for cardiovascular aspects and investigated the interaction between prevalent genetic variants and food consumption in controlling cardiometabolic threat in adult patients aged 45-60 years with T2DM. 138 patients were included in this study from Nigerian tertiary hospitals. Food intake was measured according to a validated food frequency questionnaire and contrasted with typical dietary advice. Genomic DNA from peripheral blood samples was purified and subjected to methylation status of NOS3, APOE, and PPARG gene promoters by methylation-specific PCR. The SNPs rs1799983 (NOS3), rs429358 (APOE), and rs1801282 (PPARG) were typed. Multivariate logistic regression models were applied to examine cross-sectional association between nutrient intake and gene methylation, and SNP-diet interactions were evaluated with interaction terms. The findings showed that poor nutrition was very common: 84.1% of the participants had inadequate fibber, 79.7% inadequate intake of omega-3 fatty acids, and 68.1% saturated fat intakes over the threshold level. Participants with unhealthy diets exhibited significantly increased rates of methylation of NOS3 (7.9% vs. 4.2%, p<0.001), APOE (6.1% vs. 3.8%, p=0.002), and PPARG (6.5% vs. 5.1%, p=0.011) compared to participants with healthier diets. Consumption of saturated fat was positively associated with gene methylation (β = 0.21–0.38), whereas consumption of fibber and omega-3 was negatively associated (β = –0.24 to –0.35). Gene–diet interaction was also evident: carriers of APOE E4 with high saturated fat consumption had increased LDL-C and increased methylation; carriers of NOS3 rs1799983 with low folate consumption had increased methylation; and carriers of PPARG rs1801282 with low consumption of omega-3 had greater changes in methylation. Increased methylation of NOS3 and APOE were strongly linked with increased blood pressure, LDL cholesterol, and inflammatory biomarkers (hs-CRP). This present research presents new evidence that malnutrition enhances epigenetic silencing of cardiovascular genes in genetically predisposed T2DM patients. The findings demonstrate the basis for precision nutrition that integrates genetic and epigenetic stratification into clinical practice. Tailored diet intervention may be a low-cost and durable approach to minimize cardiovascular risk among middle-aged diabetic patients, especially in low-resource environments.