Blood pressure, glucose, insulin and lipids of young Ethiopian recent immigrants to Israel and in those resident for 2 years

Abstract

To determine influence of residence in Israel on blood pressure, glucose, insulin and lipids levels in recent and resident young Ethiopian immigrants, and to compare them with Israeli students. Young male Ethiopians, resident in Israel for < 3 months and residing in boarding schools, were compared, in a cross-sectional study, with those who had been living under the same conditions for 2 years. The food for both groups was provided from the same kitchen. A group of Israeli students served as an additional comparison group. Body mass index, triceps skinfold width, sitting blood pressure and fasting glucose insulin, lipids and fructosamine levels were measured and a standard oral glucose tolerance test was performed, with glucose and insulin levels being measured 60 and 120 min after the load. Body mass index did not differ by much between the two Ethiopian groups, but was significantly lower in the Ethiopian groups than in the Israeli student group. Systolic (SBP) and diastolic blood pressure (DBP) were significantly higher in the resident immigrants than in the students, but the high-density lipoprotein-cholesterol, triglycerides, fructosamine and insulin response to oral glucose loading were all significantly lower, whereas the blood glucose response was actually higher. Resident immigrants had a significantly higher prevalence of hypertension. SBP and DBP correlated weakly (r = 0.25 and 0.24, respectively) with the sum of insulin after loading among the Ethiopian immigrants but not among the students. After 2 years' residence in Israel, young male Ethiopian immigrants acquire in parallel a rise in blood pressure and an increase in lipidaemia, insulinaemia and glucose response. However, the hypertensive subjects are not hyperinsulinaemic, with increases in insulinaemia accounting for only approximately 6% of blood pressure variability. The increase in the prevalence of hypertension therefore cannot be explained by dietary-induced insulinaemia alone.