Prevalence of Selected Intermediate Risk Factors for Non-communicable Diseases in an Apparently Healthy Indian Community in KwaZulu-Natal, South Africa.

South Africa, burdened with the emerging chronic diseases, is home to one of the largest migrant Indian population, however, little data exists on the risk factors for non-communicable diseases in this population. The aim of this study was to determine the prevalence of yet undiagnosed selected intermediate risk factors for non-communicable diseases among the Indian population in KwaZulu-Natal. We randomly selected 250 apparently healthy Indians, aged 35-55 years, living in KwaDukuza to participate in this study. Clinical and anthropometric measurements were taken under prescribed clinical conditions using Asian cut-off points. Pearson correlations was used to detect associations between anthropometric and clinical risk markers. A large percentage of participants' systolic blood pressure fell within the normal range. Diastolic blood pressure was >85 mmHg for 61 % of the participants and triglyceride levels were >1.69 mmol/L for 89 % of the participants'; 94 % of the women and 87 % of the men were classified as centrally obese. Raised fasting blood glucose was seen in 39 % of participants'. Waist circumference and body mass index showed statistically significant associations with all clinical risk markers except for diastolic blood pressure. Our findings suggest that the use of ethno specific strategies in the management of the disease profile of South African Indians, will enable the South African health system to respond more positively towards the current trend of increased metabolic and physiological risk factors in this community. Moreover, key modifiable behaviours such as increased physical activity and weight reduction may improve most of these metabolic abnormalities.

Nutritional genetics: the case of alcohol and the MTHFR C677T polymorphism in relation to homocysteine in a black South African population.

BACKGROUND/AIMS: It is unknown whether the effect of alcohol consumption on homocysteine (Hcy) is modulated by the methylenetetrahydrofolate reductase (MTHFR) C677T. We explored this hypothesized effect by analyzing cross-sectional data of 1,827 black South Africans. METHODS: Total Hcy concentrations were determined by fluorescence polarization immunoassay and the genotype through polymerase chain reaction-based RFLP analysis. RESULTS: Subjects harboring the 677 TT genotype had the highest Hcy. Among subjects harboring the 677 CC genotype, men had higher Hcy (p = 0.04). Age and gamma-glutamyltransferase (GGT) correlated best (r = 0.26 and r = 0.27; p < 0.05), while the percentage carbohydrate-deficient transferrin and the B vitamins correlated weakly (r < 0.1; p < 0.05) with Hcy. Hcy was positively associated with the reported alcohol intake (p ≤ 0.01). There was no interaction between alcohol consumption and the MTHFR 677 CC or CT genotypes (p > 0.05) for Hcy concentrations; however, an interaction was determined for GGT and the MTHFR genotype (p = 0.02). Age, GGT, gender, MTHFR and vitamin B6 explained 16.8% of the variation in Hcy (p < 0.01). CONCLUSION: The determined interactions might result in differences in the risk conveyed through Hcy with regard to disease development in those with unfavorable GGT concentrations.

The effect of ethanol and its metabolism on fibrinolysis.

The role of ethanol metabolism in possible haemostatic cardioprotective effects has not yet been determined. To this end, we investigated the effect of a moderate dose of ethanol (35 g) and its metabolism, on haemostatic variables over 14 hours (h). Eighteen Caucasian males participated in a placebo-controlled, randomised, cross-over study. Blood was collected prior to alcohol consumption, and at 10 time points for 14 h. Blood ethanol peaked at 1 h and was cleared after 8 h following ethanol consumption, significantly increasing plasma acetate (p=0.0028). Ethanol did not influence the coagulation factors significantly. PAI-1act increased (p<0.0001) and tPAact (p=0.047) decreased following alcohol consumption, reaching maximum (0.69 to 22.2 IU/ml) and minimum (0.88 to 0.33 IU/ml) levels at 5 h, respectively. Significantly increased plasma clot lysis times (46.8 to 67.6 minutes) and reduced global fibrinolytic capacity of whole blood, measured as D-dimer production during incubation of blood clots (2.26 to 0.29 µg/ml), were found at 5 h. Except for PAI-1act (borderline significance; p=0.05), there was no significant difference in the fibrinolytic markers between the two groups the following morning. Moderate ethanol consumption resulted in a significant temporary fibrinolysis inhibition. Any protective effects of moderate ethanol consumption on cardiovascular disease do not appear to be due to improvement in fibrinolytic potential within the first 14 h following consumption. The use of global fibrinolytic assays is recommended for determining the true effect of ethanol on fibrinolysis.