No abstract

Many postmenopausal women live with diabetes mellitus; however, little information is available about how the changes that occur around the time of menopause might uniquely affect management of diabetes mellitus in this population. Although the weight gain that commonly occurs during the menopausal transition is largely attributable to aging rather than the transition itself, changes in body composition have been independently associated with menopausal status. These changes in body composition have, in turn, been associated with alterations in insulin sensitivity and glucose metabolism in postmenopausal women. Hormone therapy seems to have neutral or beneficial effects on the adverse changes in body composition associated with menopause. Whether menopausal status independently influences diabetes risk remains controversial. Nevertheless, consistent findings from large clinical trials suggest that postmenopausal hormone therapy decreases the risk of developing diabetes mellitus. Similarly, many studies suggest that postmenopausal hormone therapy has neutral or beneficial effects on glycemic control among women already diagnosed as having diabetes mellitus. Future studies are needed to elucidate the mechanisms that underlie these relationships and to determine how these observations should influence recommendations for the care of postmenopausal women with diabetes mellitus.

In women, urinary and serum aldosterone levels are significantly higher during the luteal phase in high- but not low-sodium balance, whereas PRA and AngII do not differ between phases. Progesterone may directly contribute to increased luteal phase aldosterone production, independent of the renin-angiotensin system.

Objective-Emerging evidence suggests that women with menopausal vasomotor symptoms (VMS) have increased cardiovascular disease (CVD) risk as measured by surrogate markers. We investigated the relationships between VMS and clinical CVD events and all-cause mortality in the Women's Health Initiative Observational Study (WHI-OS).* Corresponding author and address reprint requests to: Emily D. Szmuilowicz, MD, MS Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University 211 E. Chicago Ave., #1050 Chicago, IL 60611 edszmuilowicz@post.harvard.edu Phone: (312) 944-6677 x318, fax: (312) 944-3346. Financial disclosure/conflicts of interest Dr. Szmuilowicz reported that she was previously a sub-investigator in a clinical trial of a diabetes treatment (GLP-1 agonist) sponsored by Sanofi-aventis, and she received no financial compensation. Dr. Seely reported that she received a Bayer Health Care investigator-initiated grant. Dr. Howard reports: consultant for Merck/Schering-Plough; research support from donation of drugs from Merck/Shering-Plough; lectures for Merck/Schering-Plough. None of the other authors reported financial disclosures. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptMenopause. Author manuscript; available in PMC 2012 June 1. Conclusions-Early VMS were not associated with increased CVD risk. Rather, early VMS were associated with decreased risk of stroke, total CVD events, and all-cause mortality. Late VMS were associated with increased CHD risk and all-cause mortality. The predictive value of VMS for clinical CVD events may vary with onset of VMS at different stages of menopause.Further research examining the mechanisms underlying these associations is needed. Future studies will also be necessary to investigate whether VMS that develop for the first time in the later postmenopausal years represent a pathophysiologic process distinct from classical perimenopausal VMS.