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Objective: To evaluate the role of menopause on the regional composition and distribution of fat in women and eventual correlations with the oxidative state., Design: In this observational clinical investigation, 90 women (classified for menopause status according to Stages of Reproductive Aging Workshop criteria) were evaluated for body mass composition and fat distribution by dual-energy x-ray absorptiometry and for oxidative status by determination of serum hydroperoxide levels and residual antioxidant activity., Results: Total body fat mass increases significantly in postmenopause (P < 0.05) by 22% in comparison with premenopause, with specific increases in fat deposition at the level of trunk (abdominal and visceral) (P < 0.001) and arms (P < 0.001). Concomitantly, the antioxidant status increases significantly (P < 0.001) by 17%. When data were adjusted for age by analysis of covariance, statistical significance disappeared for the increase in fat mass, but it was retained for antioxidant status (P < 0.05). Both antioxidant status and hydroperoxide level increased with trunk fat mass, as shown by linear correlation analysis (r = 0.46, P < 0.001 and r = 0.26, P < 0.05, respectively)., Conclusions: The results of our investigation demonstrate that fat content increases in the upper part of the body (trunk and arms) in postmenopause and that age is the main determinant of this increase. During the comparison of premenopausal and postmenopausal women, we also detected a significant increase in antioxidant status. Apparently this change is mainly related to menopausal endocrine and fat changes.

Hormone replacement therapy (HRT) seems to have a favorable influence on the plasma lipid profile. Only a few investigations have examined the effects of HRT versus hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitors. We compared the relative effects of different hypolipidemic strategies on lipoproteins and coagulative parameters in women with recent-onset spontaneous menopause. In this 24-week, placebo-controlled trial, 60 consecutive healthy women aged >/= 45 years, with amenorrhea from 6 to 60 months (mean, 1.9 +/- 1.4 years), serum follicle stimulating hormone (FSH) greater than 40 U/L, and slight to moderate hypercholesterolemia (low-density lipoprotein-cholesterol [LDL-C] 160 to 250 mg/dL, high-density lipoprotein-cholesterol [HDL-C] < 75 mg/dL, and triglycerides < 200 mg/dL) were enrolled and randomized to dietetic advice (placebo group), simvastatin 10 mg, 0.625 mg of conjugated equine estrogen (CEE), or 50 microg estrogen transdermal patch (ETP). In the latter 2 cases, the progestative nomegestrol was added to estrogens (days 17 to 28 of the cicle). Lipoprotein parameters were evaluated after separating very-low-density lipoproteins (VLDLs) by ultracentrifugation, while fasting glucose and insulin, homocysteine, and hemocoagulative parameters were determined in plasma. Fifty-four patients completed the trial. Total cholesterol (TC) and LDL-C significantly decrased in the simvastatin (-62 mg/dL [-20%] and -72 mg/dL [-30%], respectively), CEE (-42 mg/dL [-13%] and -45 mg/dL [-18%]), and ETP (-30 mg/dL [-10%] and -26 mg/dL [-11%]) groups compared to baseline, but only simvastatin showed an effect significantly superior to diet alone. Apolipoprotein (Apo) B was decreased by simvastatin (-25%, P <.001) and by CEE (-10%, P <.05); again, simvastatin was more effective than either diet or ETP. Triglyceride concentration and VLDL-C were unmodified by treatments. HDL-C and Apo A-I significantly increased in the simvastatin group (+18% and +8%, respectively), while HDL-C was unmodified by both HRT regimens and Apo A-I was reduced by ETP treatment (-17%); lipoprotein[a] (Lp[a]) was decreased by both HRTs (-38%, P <.05, and -22%, P =.07, for CEE and ETP, respectively). Among coagulative parameters, plasminogen activator inhibitor-1 (PAI-1) was significantly reduced by CEE (-29%, P <.05) but not ETP treatment (+16%, P = not significant), while fibrinogen, antithrombin, and homocysteine were unaffected by therapy. Thus, HRT, particularly CEE, seems well tolerated and moderately effective in improving the lipid pattern and, perhaps, the coagulative/fibrinolytic balance in postmenopausal hypercholesterolemic women; it may represent a therapeutic option in slightly dyslipidemic subjects. Statins are preferred in case of more severe disease., (Copyright 2002, Elsevier Science (USA). All rights reserved.)

Background and Aim: Postmenopausal modification of the lipid profile plays a major role in the risk of ischemic heart disease. Lifestyle counseling and estrogen replacement therapy have all been proposed as first-line measures, but there is no agreement on the best way to treat climacteric dyslipidemia. Soybean-based diet seems particularly attractive in this context, given its cholesterol lowering potential, its hypothetical anticancerous effects and possible modification of climacteric symptoms., Methods and Results: We evaluated the effect of 60 g isolated soy protein (ISP) daily on the lipid profile of 104 postmenopausal women (53.3 +/- 3.3 years) in a double-blind, parallel, placebo-controlled (caseinate) trial, as part of a broader assessment of the effect of ISP on climacteric symptomatology. Serum total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, apo A-I, apo B and lipoprotein (a) were determined before and after a 12-week diet modification. Seventy-seven women completed the trial. Both soy and placebo determined a significant reduction in total cholesterol (-0.42 +/- 0.79 and -0.40 +/- 0.57 mmol/L) and LDL-cholesterol (-0.35 +/- 0.72 and -0.31 +/- 0.54 mmol/L), but only soy had a significant lowering effect on apo B and the LDL-cholesterol/HDL-cholesterol ratio (-6% and -8% from baseline respectively); lipoprotein (a) plasma levels were not significantly changed by either treatment. Forty-four women were dyslipidemic at baseline; those with increased LDL concentrations showed a somewhat greater improvement in their lipoprotein profile (LDL-cholesterol and apo B reduction) with soy rather than placebo. No further information emerged when the subjects were divided into three apo E phenotypes., Conclusions: We conclude that diet supplementation with 60 g ISP is slightly better than caseinate in favorably modifying the lipoprotein metabolism of postmenopausal women; this effect is more evident in hypercholesterolemic subjects.

Objective: To assess the effect of daily dietary supplementation of soy protein isolate powder on hot flushes in postmenopausal women., Methods: We carried out a double-blind, parallel, multicenter, randomized placebo-controlled trial of 104 postmenopausal women. Fifty-one patients (age range 48-61 years) took 60 g of products containing 40 g of isolated soy protein [corrected] daily and 53 patients (age range 45-62 years) took 60 g of placebo (casein) daily. The study lasted 12 weeks. Using analysis of covariance, we analyzed changes from baseline in mean number of moderate to severe hot flushes (including night sweats) during treatment., Results: Soy was significantly superior to placebo (P < .01 in reducing the mean number of hot flushes per 24 hours after 4, 8, and 12 weeks of treatment. In particular, women taking soy had a 26% reduction in the mean number of hot flushes by week 3 and a 33% reduction by week 4 (P < .001 by the Wilcoxon exact test). By the end of the 12th week, patients taking soy had a 45% reduction in their daily hot flushes versus a 30% reduction obtained with the placebo (P < .01). The overall rates of adverse effects were similar for soy and casein-placebo. Twenty-five patients dropped out of the study: 11 in the soy group and 14 in the placebo group. Gastrointestinal side effects were the most common cause of premature withdrawal from the study (seven patients in each group)., Conclusion: Soy protein isolate added daily to the diet substantially reduced the frequency of hot flushes in climacteric women.

Carbocalcitonin spray administered for 12 months at a daily dosage of 80 U MRC according to five schedules has been tested on 150 normal spontaneous postmenopausal women for its influence on bone mineral density (BMD), bone metabolism and osteoarticular pain. BMD was monitored before and at the end of treatment in comparison with BMD of untreated control women. Metabolic markers (serum alkaline phosphatase, serum osteocalcin and urinary hydroxyproline) were also evaluated before and during treatment (at the 9th or 10th month of treatment). Osteoarticular pain was assessed by an analogic visual scale. Intranasal carbocalcitonin, administered according to cyclic schedules at a high frequency dosage, was able to maintain bone mass only in the earlier postmenopausal women. BMD percent increase after 12 months of treatment was 1.10 and 1.31 in women with low (< 0.870 mg/cm2) and high baseline BMD (> or = 0.870 mg/cm2), respectively. In advanced menopause the maintaining effect of carbocalcitonin on BMD seemed evident only if the baseline bone mass was lower than the BMD of the age matched control group. At least six months of treatment/year is necessary for effective therapy. Both systemic and local tolerance were optimal. No significant side-effects were detected.