The intake of RJ 150 mg for three months is associated with significant improvements of the lipid profile of postmenopausal women. RJ supplementation may offer an alternative method of controlling the menopause - associated dyslipidemia.

Cardiovascular disease (CVD) represents the leading cause of morbidity and mortality in the Western World. 1 The increasing prevalence of CVD and the related mortality are affected mainly by the aging of the population, which is strongly associated with impaired arterial hemodynamics, vascular aging, and inactivity. 1,2 Indeed, arterial stiffening and endothelial dysfunction, through degradation of elastin fibers, increased vascular oxidative stress and chronic low-grade inflammation, are biological events that take place along

Background Accumulating evidence suggests that circulating amyloidβ 1–40 (Αβ1–40), a proatherogenic aging peptide, may serve as a novel biomarker in cardiovascular disease (CVD). We aimed to explore the role of plasma Αβ1–40 and its patterns of change over time in atherosclerosis progression in postmenopausal women, a population with substantial unrecognized CVD risk beyond traditional risk factors (TRFs). Methods In this prospective study, Αβ1–40 was measured in plasma by enzyme-linked immunosorbent assay and atherosclerosis was assessed using carotid high-resolution ultrasonography at baseline and after a median follow-up of 28.2 months in 152 postmenopausal women without history or symptoms of CVD. Results At baseline, high Αβ1–40 was independently associated with higher carotid bulb intima-media thickness (cbIMT) and the sum of maximal wall thickness in all carotid sites (sumWT) (p < 0.05). Αβ1–40 levels increased over time and were associated with decreasing renal function (p < 0.05 for both). Women with a pattern of increasing or persistently high Αβ1–40 levels presented accelerated progression of cbIMT and maximum carotid wall thickness and sumWT (p < 0.05 for all) after adjustment for baseline Αβ1–40 levels, TRFs, and renal function. Conclusion In postmenopausal women, a pattern of increasing or persistently high Αβ1–40 was associated with the rate of progression of subclinical atherosclerosis irrespective of its baseline levels. These findings provide novel insights into a link between Αβ1–40 and atherosclerosis progression in menopause and warrant further research to clarify the clinical value of monitoring its circulating levels as an atherosclerosis biomarker in women without clinically overt CVD.

Endometriosis is one of the most frequent gynecological disorders defined as the existence and growth of endometrial tissue outside the uterine cavity. Aim of this study was to evaluate the level of six oxidative stress markers in the serum of patients with and without endometriosis. This study included 46 women who were undergoing laparoscopy. The participants were divided into two groups based on their laparoscopic results. Thirty-one women had visually and histopathologically confirmed endometriosis, whereas 15 did not. The serum level of ADMA (asymmetric dimethylarginine), MCP1 (monocyte chemoattractant protein 1), MMP2 (matrix metalloproteinases 2), MMP9 (matrix metalloproteinases 9), RANTES (regulated upon activation, normal T cell expressed and presumably secreted), and VEGF-A (vascular endothelial growth factor) as oxidative stress markers were measured and compared between the two groups. No significant difference in the ADMA, MCP1, MMP2, MMP9, RANTES, and VEGF-A serum levels was detected between the entometriosis patients and controls. The disease stage did not affect any of the markers' level either. Women with endometriosis had menarche at an earlier age compared to controls [11.7 (SD 1.09) vs 12.6 (SD 1.4), p = 0.04)]. These results suggest that there is no association between endometriosis and increased oxidative stress. The elevation and possible role of oxidative stress markers in the diagnosis and pathogenesis of endometriosis should be evaluated in more extended studies.