Efforts to promote adherence to the Mediterranean dietary pattern appear to be worthwhile in persons aged <80 y, in whom the diet predicts survival, but we do not have any available evidence that such a diet benefits subjects aged > or =80 y.

No abstract

The mechanism for the development of insulin resistance in normal pregnancy is complex and is associated with serum levels of both progesterone and 17 -estradiol. However, it remains unclear whether estrogens alone or progestins alone can cause insulin resistance, or whether it is a combination of both which produces this effect. We attempted to determine the role played by progesterone and/or 17 -estradiol on the phenomena of sensitivity to insulin action that take place during pregnancy in the rat. Ovariectomized rats were treated with different doses of progesterone and/or 17 -estradiol in order to simulate the plasma levels in normal pregnant rats. A euglycemic/ hyperinsulinemic clamp was used to measure insulin sensitivity. At days 6 and 11, vehicle (V)-and progesterone (P)-treated groups were more insulin resistant than 17 -estradiol (E)-and 17 -estradiol+progesterone (EP)-treated groups. Nevertheless, at day 16, the V, EP and E groups were more resistant to insulin action than the P group. On the other hand, the V, EP and E groups were more insulin resistant at day 16 than at day 6, whereas the P group was more insulin resistant at day 6 than at day 16. Our results seem to suggest that the absence of female steroid hormones gives rise to a decreased insulin sensitivity. The rise in insulin sensitivity during early pregnancy, when the plasma concentrations of 17 -estradiol and progesterone are low, could be due to 17 -estradiol. However, during late pregnancy when the plasma concentrations of 17 -estradiol and progesterone are high, the role of 17 -estradiol could be to antagonize the effect of progesterone, diminishing insulin sensitivity.

No abstract

Low selenium levels in humans have been associated with several pathologies; however, an earlier animal investigation found a direct association between Se intake and total plasma homocysteine (tHcy) concentrations. To date, the importance of serum selenium levels in association with tHcy in humans has not been determined. We evaluated the cross-sectional association of blood selenium concentrations with plasma tHcy and other determinants of this cardiovascular disease risk factor. We estimated protein intake and measured the blood status of selenium, tHcy, and several other related factors in serum such as folate, vitamin B-12, and creatinine. Serum selenium was inversely associated with tHcy, explaining 5.8% of tHcy variance with respect to 2.2% accounted for by serum folate. Furthermore, there was a 63% decreased risk of higher tHcy concentrations (>14 micro mol/L) for subjects with serum selenium in the highest tertile (P = 0.013). We also found an inverse association of protein intake with tHcy in men (beta = -0.144; P = 0.036), which disappeared after controlling for serum Se concentrations (beta = -0.055; P = 0.003). In conclusion, selenium should be considered as a potential factor to lower tHcy. In addition, the described association between protein intake and homocysteine levels could be mediated by this trace element.