Post-Menopausal Estrogen Production

Author(s):  
P. K. Siiteri
Author(s):  
Vijay Zutshi ◽  
Shreshtha Gupta ◽  
Charanjeet Ahluwalia ◽  
Monica R.

Endometriosis is an estrogen dependant disorder of reproductive-age women. It is uncommon after menopause, however, peripheral estrogen production may account for endometriosis in post-menopausal women. We reported a case of a 68 year old post-menopausal woman with an adnexal mass suspected malignant ovarian tumor on imaging and normal serum CA 125 levels. Total hysterectomy with bilateral salpingo-oophorectomy was done. The final histopathology revealed the diagnosis of ovarian endometriosis. Rarely, ovarian endometrioma can mimic ovarian malignancy in a post-menopausal woman.


2014 ◽  
Vol 9 ◽  
pp. IMI.S15682 ◽  
Author(s):  
Jim R. Sliwinski ◽  
Aimee K. Johnson ◽  
Gary R. Elkins

Cognitive decline is a frequent complaint during the menopause transition and among post-menopausal women. Changes in memory correspond with diminished estrogen production. Further, many peri- and post-menopausal women report sleep concerns, depression, and hot flashes, and these factors may contribute to cognitive decline. Hormone therapy can increase estrogen but is contraindicated for many women. Mind–body medicine has been shown to have beneficial effects on sleep, mood, and hot flashes, among post-menopausal women. Further, mind–body medicine holds potential in addressing symptoms of cognitive decline post-menopause. This study proposes an initial framework for how mind–body interventions may improve cognitive performance and inform future research seeking to identify the common and specific factors associated with mind–body medicine for addressing memory decline in peri- and post-menopausal women. It is our hope that this article will eventually lead to a more holistic and integrative approach to the treatment of cognitive deficits in peri- and post-menopausal women.


2009 ◽  
Vol 22 (2) ◽  
pp. 332-335 ◽  
Author(s):  
Mark A. Rodrigues ◽  
Jonathan K. Foster ◽  
Giuseppe Verdile ◽  
Karen Joesbury ◽  
Richard Prince ◽  
...  

Alzheimer's disease (AD) is the major form of age-related dementia worldwide, accounting for more than two-thirds of all dementia cases. The disease is characterized by a progressive loss of cognitive and intellectual functioning (Gilman, 1997). A number of risk factors for AD have been identified. The prevalence of AD increases with age, diabetes, depression, family history of Parkinson's disease and following head injury or exposure to solvents (Jorm et al., 1991; van Duijn et al., 1991; Ott et al., 1995; Yoshitake et al., 1995; Devanand et al., 1996). Published research further suggests that low education levels are associated with increased prevalence of clinical AD (Gatz et al., 2001; Qiu et al., 2001; Ravaglia et al., 2002). Women also have a higher risk for developing the disease than men, with the risk being markedly increased following menopause (Sherwin, 2002; Sherwin 2003). Additionally, slightly more severe cognitive deficits have been reported in AD in women compared to men (Buckwalter et al., 1993, Henderson and Buckwalter, 1994). These epidemiological trends may be a consequence of reproductive hormonal changes. Specifically, menopause results in a marked diminution in gonadal estrogen production in women (see Sherwin, 2003, for a review). Estrogen plays a pivotal role in the maintenance and function of neuronal circuits in the brain and in resistance to neuronal damage (McEwen, 2001). The neuroprotective properties of estrogen are thought to be mediated at least in part by anti-amyloidogenic, anti-oxidative and ant-inflammatory mechanisms (reviewed in Barron et al., 2006a). However, limited and somewhat mixed data exist regarding the association between endogenous levels of estrogen and cognitive decline (Manly et al., 2000; Schupf et al., 2003). Based on some of our own findings, we here consider the factors that may be useful in predicting memory decline as a risk factor for Alzheimer's disease in older post-menopausal women.


1976 ◽  
pp. 25-28 ◽  
Author(s):  
J. H. H. Thijssen ◽  
C. Longcope

2008 ◽  
Vol 28 (01/02) ◽  
pp. 85-88 ◽  
Author(s):  
D. Fuchs ◽  
H. Daniel ◽  
U. Wenzel

SummaryEpidemiological studies indicate that the consumption of soy-containing food may prevent or slow-down the development of cardiovascular disease. In endothelial cells application of a soy extract or a combination of the most abundant soy isoflavones genistein and daidzein both inhibited apoptosis, a driving force in atherosclerosis development, when applied in combination with oxidized LDL or homocysteine. Proteome analysis revealed that the stressorinduced alteration of protein expression profile was reversed by the soy extract or the genistein/daidzein mixture. Only few protein entities that could be functionally linked to mitochondrial dysfunction were regulated in common by both application forms of isoflavones. A dietary intervention with isoflavone-enriched soy extract in postmenopausal women, who generally show strongly increased cardiovascular risk due to diminished estrogen production, led to significant alterations in the steady state levels of proteins from mononuclear blood cells. The proteins identified by proteome analysis revealed that soy isoflavones may increase the anti-inflammatory response in blood mononuclear cells thereby contributing to the atherosclerosispreventive activities of a soy-rich diet. Conclusion: By proteome analysis protein targets were identified in vitro in endothelial cells that respond to soy isoflavones and that may decipher molecular mechanisms through which soy products exert their protective effects in the vasculature.


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