CROSS-SECTIONAL VERSUS PROSPECTIVE ASSOCIATIONS OF SELENIUM STATUS WITH CARDIOVASCULAR RISK FACTORS: AN 8-YEAR FOLLOW-UP ANALYSIS OF THE OLIVETTI HEART STUDY: PP.7.292

Abstract

AB Background: Recent findings raise concern about the possible association of high selenium (Se) exposure with adverse cardio-metabolic outcomes in the US population, characterized by a high Se status. In populations with lower Se status, such as the Italian one, there is little epidemiological evidence about the possible association of Se with cardio-metabolic risk factors. We therefore examined cross-sectional and prospective relationships of serum Se levels with cardio-metabolic risk factors including blood pressure (BP), diabetes and blood lipids in the Olivetti Heart Study. Methods: The study population consisted of 650 adult male individuals for whom baseline serum Se measurement and cardio-metabolic risk factors were available both at baseline (1994-95) and follow-up examination (2002-04 - average follow-up=8 years) (age: 50.8 +/- 6.8 yr; BMI: 26.9 +/- 3.9 kg/m2; systolic BP: 129.8 +/- 17.2 mm Hg; total cholesterol: 221.06 +/- 38.7 mg/dL). Serum Se was measured by atomic absorption spectroscopy (AAS). Results: Average serum selenium concentration at baseline was 77.5 +/- 19.2 [mu]g/L. In cross-sectional analyses, the serum Se level was not associated with BP, hypertension or diabetic status while it was significantly and directly associated with serum total cholesterol (r = 0.189, 0=0.001). In prospective analysis, serum Se at baseline was likewise a strong predictor of total serum cholesterol (p < 0.001) and LDL-cholesterol (p < 0.001) after adjustment for age, BMI, cigarette smoking, and physical activity. The association was no longer statistically significant after additional adjustment for baseline blood lipids. Se status was not prospectively associated with BP, hypertension or diabetes. Conclusions: These findings corroborate previous cross-sectional associations of high Se status with adverse blood lipid profile. However, prospective analyses do not support the causality of this relation. Randomized and mechanistic evidence is necessary to clarify the causal mechanisms underlying the associations observed. (C) 2010 Lippincott Williams & Wilkins, Inc.