Dear Sir, Hypertension and Type 2 (non-insulin-dependent) diabetes mellitus are associated with obesity [1, 2]. Hypertension is more frequently seen in diabetic than in non-diabetic subjects [3]. In addition, hyperlipidaemia is commonly found in both diabetic [4] and hypertensive subjects [5]. Modan et al.[6] first suggested that hyperinsulinaemia is the common element accounting for obesity, Type 2 diabetes, and hypertension. Since all three conditions are characterized by insulin resistance [7, 8], it has been hypothesized that hyperinsulinism, through insulin resistance, is the key mechanism eventually leading to cardiovascular disease [9, 10]. However, obesity, Type 2 diabetes, and hypertension all have a strong genetic, familial background. To address the possible role of pure, non-genetically determined hyperinsulinaemia in the development of hypertension, we evaluated blood pressure in 13 patients with surgically-confirmed insulinoma and in six patients with non-tumoural hypoglycaemia and hyperinsulinaemia. Insulin resistance (M/I= glucose metabolized divided by prevailing insulin levels) was evaluated during a 24-h fasting period in 16 of the above patients (10 with insulinoma, six with non-tumoural hypoglycaemia)[11] and during a euglycaemic hyperinsulinaemic clamp in three patients with insulinoma [12]. Blood pressure was measured twice a day during the hospitalization period, and for each patient the mean value was calculated. Only three patients were hypertensive, and two of them had family history of hypertension. Figure 1 shows that in the 16 patients studied during the 24-h fasting period there was a direct relationship between serum insulin levels and insulin resistance (p< 0.001); on the contrary, there was no relationship between blood pressure and insulin levels or between M/I index and blood pressure; insulin levels were significantly higher (43.5+ 4.77 vs 10.8+ 1.17 gU/ml, p< 0.01), andtheM/Iindexwas significantly lower (0.04+ 0.003 vs 0.12+ 0.02, p< 0.01) in insulinoma patients than in patients with non-tumoural hypoglycaemia [11]. Thus, only three out of 19 hyperinsulinaemic patients (15.8%) were hypertensive and the percentage is reduced to 1 of 19 (5.3%) if patients with familial history of hypertension are excluded. This figure does not exceed that anticipated for the general population. These results indicate that in the absence of a genetic trait for hypertension or for Type 2 diabetes, pure hyperinsulinaemia is associated with insulin resistance but not with hypertension. This is in agreement with two recent reports [13, 14]. In conclusion, either pure, non-genetically determined hyperinsulinaemia plays little or no role in the genesis of hypertension, or it takes a long time to show an effect.