This preliminary study addressed the possible associations between dietary, genetic and hormonal factors that are involved in the development of menopausal obesity and its metabolic consequences. We performed anthropometrical, hormonal and biochemical measurements and used a nutritional questionnaire on 43 postmenopausal women who were non-HRT-users (14 obese and 29 non-obese subjects, mean age +/- SD of 52.8 +/- 4.6 years, mean body mass 74.6 +/- 4.6 kg). All of the women also had fat mass assessed by DPX-Lunar. From the 24-h dietary recall, the nutrient intake in daily food rations was calculated using a computer program (Nutritionist IV, San Bruno, CA, USA) based on our own database. Restriction fragment length polymorphism of the estrogen-receptor-alpha gene was determined with the PvuII restriction enzyme. Obese women widely under-reported their daily food intake. The analysis of body fat distribution showed that the total body weight and the percentage of total fat mass were significantly increased in the obese group (p = 0.001). We observed significantly higher leptin (20.56 +/- 11.9 vs. 9.02 +/- 2.8 ng/ml) and total cholesterol (but lower cholesterol HDL), triglycerides levels in the obese subjects (261.89 +/- 48.8 vs. 248.23 +/- 55.9; 52.17 +/- 13.6 vs. 60.92 +/- 13.04; 142.82 +/- 61.02 vs. 106.61 +/- 27.7 mg/dl). Except for diastolic blood pressure, clinical variables were not significantly different between subjects with and without the PvuII ERalpha polymorphism. Allele frequencies of the ERalpha polymorphism did not differ from those previously reported (P-0.48, p-0.52) in our study. In this preliminary study we failed to find dietary and genetic factors involved in the pathogenesis of menopausal obesity. However, our results provide support for the notion that the perimenopausal increase in visceral fat is a significant factor involved in the increased cardiovascular risk in postmenopausal women.