Weak connection, but this study finds that Testosterone in post-menopausal women will reduce cardiovascular disease (CVD) in women. Their conclusion is based on the rise in CVD in post-menopausal women and the decline in Testosterone levels post-hysterectomy. That is the one instant where Testosterone levels do precipitously decline. Contrast this with natural menopause where Testosterone does not appear to decline as precipitously.
elevated Testosterone found to play role in post menopause breast cancer. No correlation with elevated Testosterone was found in pre menopause--in fact, low estrogen/low Testosterone and elevated prolactin was found in pre menopausal breast cancer patients.
No benefit to memory for post menopause women with estradiol therapy. This study looked at early and late menopause estrogen therapy. The study also found no harm. Only abstract available here. These studies would do more scientific benefit if they would follow hormone levels. This study did not touch on dementia; other studies have shown benefit from estrogen therapy in preventing dementia in women.
Study finds heavy presence of xenoestrogens in obese Portuguese women, both pre menopause and post menopause. This study only looked at obese women; it would be nice to have a control of thin women to contrast the plasma and adipose xenoestrogen levels. The authors found the presence of xenoestrogens in plasma in pre menopause women to be a 10 year predictor of cardiovascular disease risk in these women. The authors also found increased Xenoestrogen levels to be associated with metabolic dysfunction and inflammation.
low SHBG in post-menopausal women correlates with increased risk of metabolic syndrome. More than that, there is an inverse correlation with SHBG in women and metabolic syndrome components. Also, Increasing components of MetS was correlated with Testosterone and free androgen index.
estrogen therapy in surgical menopause preserves memory. Rapid decline in estrogen levels post surgical menopause is associated with cognitive/memory decline. Versus placebo, estrogen therapy preserved memory function.
low vitamin D associated with increased autoimmune thyroid TPO antibodies in women. This association was found in pre menopause women, but not post menopause women.
Female aging is characterized by menopausal change in sex steroid hormones concomitant to increase in aging-related decrements in skeletal muscle performance that can be attenuated by HRT use
The major canonical pathways found to be differentially regulated included mitochondrial dysfunction, oxidative phosphorylation, glycolysis, and TCA-cycle, strong indicators for affected energy metabolism
E2 to exert anti-apoptotic effects in muscle progenitor cells by improving mitochondrial function
E2 is a major regulator of human skeletal muscle signaling in women
After menopause, when ovarian E2 production is ceased, the prevalence of cardio-metabolic diseases increases. Our result that different trajectories of the energy pathways in the skeletal muscle may be regulated by E2 provides candidate molecules as key targets for future interventions to prevent or treat postmenopausal metabolic dysregulation
Study finds Estradiol regulates human skeletal muscle cell signaling (mitochondrial function, oxidative phosphorylation, glycolysis, and TCA cycle) in study of pre/post menopause women through proteome analysis. This study would have been complete if they had carried to search beyond that of protein to epigenetics.
Study finds that Testosterone provided a small anti-inflammatory effect in post-menopausal women and men, whereas Estrogen increased macrophage cytokine production in post-menopausal women with elevated LDL. Now, this study did not differentiate PCOS versus non-PCOS, nor did it look at the effects of adiposity in these hormonal effects in women. Both of which, will effect the outcome.
post menopausal estradiol in women associated with pro-inflammatory state. SHBG was associated with a decrease in the inflammatory cytokine biomarkers. Postmenopausal women were found to have an increased Testosterone to estradiol ratio.
The early post menopause phase is critical for women. This is the phase that requires intensify strategy for exercise. The ER alpha signaling is actually increased and the ability to build muscle is intensified if exercise, particularly resistance training, is employed.
review of the literature finds that Testosterone therapy in women with low libido improves sexual activity without CVD and breast cancer risk in postmenopausal women. Post menopause is a time associated with an increased risk of CVD in women.
2-OH estrogens bind to the estrogen receptor (ER) with affinity equivalent to or greater than estradiol
previous prospective studies have not observed any significant associations with either 2-OH or 16α-OH estrone or the ratio of the two metabolites and breast cancer risk overall.
they may act as only weak mitogens (14, 15), or as inhibitors of proliferation
No significant associations have been observed between 2-OH estrone and breast cancer risk
While 16α-OH estrone binds to the ER with lower affinity than estradiol, it binds covalently (18-20) and once bound, fails to down-regulate the receptor (21). Thus, 16α-OH estrone stimulates cell proliferation in a manner comparable to estradiol in ER+ breast cancer cell lines
In this large prospective study of 2-OH and 16α-OH estrone metabolites and breast cancer risk, we did not observe any significant associations overall with either individual metabolite or with the ratio of the two metabolites
we observed positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with lower BMI and women with ER-/PR-tumors,
To date, several epidemiologic studies have examined the association between the 2-OH and 16α-OH estrogen metabolites and breast cancer risk with inconclusive results.
circulating estrogen levels have been associated more strongly with ER+/PR+ tumors than with ER-/PR- tumors
our results do not support the hypothesis that metabolism favoring the 2-OH estrone pathway is more beneficial to breast cancer risk than that favoring the 16α-OH estrone pathway
we observed significant positive associations of both 2-OH estrone and the 2:16α-OH estrone ratio with ER-/PR-tumors
Three (30, 32, 33) of four (30-33) studies observed RRs above 1 for the association between 16α-OH estrone and breast cancer risk (range of RRs=1.23-2.47); none of the point estimates was statistically significant though one trend was suggestive
based on animal studies, 2-OH estrone and the 2:16α-OH estrone ratio have been hypothesized to be inversely associated with breast cancer risk
No significant associations have been observed between 2-OH estrone, 16α-OH estrone, or the 2:16α-OH estrone ratio and breast cancer risk and the direction of the estimates is not consistent across studies.
better worded is no consistent, significant associations. There are some studies that point to the 16 catecholestrogen and increased cancer risk; limited studies show negative effects of 2 catecholestrogens on cancer risk and prospective studies available pretty much dispel the idea that the 2:16 ratio has an risk predictability.
we observed a suggestive inverse association with 16α-OH estrone and a significant positive association with the 2:16α-OH estrone ratio among lean women, suggesting possible associations in a low estrogen environment.
16α-OH estrone increases unscheduled DNA synthesis in mouse mammary cells (27) and hence also may be genotoxic
Although 2-OH estrogens are capable of redox cycling, the semiquinones and quinones (i.e., the oxidized forms) form stable DNA adducts that are reversible without DNA destruction
In our population of PMH nonusers, we observed no associations with ER+/PR+ tumors, but significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with ER-/PR- tumors
one of the few studies to find this association between 2 catecholestrogens and the 2:16 ratio and ER-/PR-tumors
Animal and in vitro studies have shown that hydroxy estrogens can induce DNA damage either directly, through the formation of quinones and DNA adducts, or indirectly, through redox cycling and the generation of reactive oxygen species
genotoxic via directe DNA adducts and indirectly via ROS; this is in addition to the proliferative effect
we observed a significant positive association between the 2:16α-OH estrone ratio and breast cancer risk among lean women
No significant associations have been observed with the 2:16α-OH estrone ratio
In the Danish study, no associations were observed with either ER+ or ER- tumors among PMH nonusers
significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio were observed among PMH users with ER+, but not ER-, tumors
it is possible that the genotoxicity of 2-OH estrone plays a role in hormone receptor negative tumors
4-OH estrogens have a greater estrogenic potential than 2-OH estrogens, given the lower dissociation rate from estrogen receptors compared with estradiol (61), and are potentially more genotoxic since the quinones form unstable adducts, leading to depurination and mutation in vitro and in vivo
the balance between the catechol (i.e., 2-OH and 4-OH) and methoxy (i.e., 2-Me and 4-Me) estrogens may impact risk
The risks of estrogen metabolism are not clear cut. Likely never will be due to the complexity of individual metabolism. This study found no correlation between 2OH-Estrone and 2OH:16alpha-Estrone and breast cancer risk in ER+/PR+ breast cancer. Translated: no benefit in breast cancer risk in 2OH-Estrone metabolism or increased 2OH:16alpha estrone metabolism. There was a positive association between 2OH-Estrone and 2:16alpha-Estrone in women with ER-/PR- tumors and low BMI.
study shows that smoking cessation, physical inactivity, menopause, hysterectomy and energy intake associated with the perimenopause weight gain. What is interesting about it is the energy imbalance is small that results in a big weight gain over time. We need to look closely and be more frank with out clients about the risk that a hysterectomy poses for her health post surgery.
Just an abstract from the Presentation at the 2014 Scientific Session. The abstract points to a 40% reduction in CAD with the onset of BHRT (Estradiol and progesterone topical) within 6 years of menopause compared to women 10 years post-menopause. This points to timing as a critical component of BHRT in women and CAD.
Review finds that low SHBG and higher Testosterone levels are associated with increased CVD risk in post menopausal women. Exact relationship is undetermined.