Quote from: deeiche on March 22, 2016, 05:21:43 PMI have estrogen in my body, adrenal glands also produce estrogen.
Very little.
QuoteI have post-menopause hormone levels.
Post-menopausal levels are very low.
QuoteMy bone density is okay, I'm healthy, my docs acknowledge that. This is after 30 years post SRS with no HRT.
If you feel fine and you are healthy, great! It's a matter of personal choice. But why not take HRT?
QuoteI'd love to read a long term double blind study regarding HRT vs no HRT post SRS in transwomen?
One need only look at what the lack of hormones does in post-menopausal women who only have their adrenal glands producing sex hormones.
Maturitas. 2008 Jul-Aug;60(3-4):185-201."Hormone replacement therapy (HRT) in young postmenopausal women is a safe and effective tool to counteract climacteric symptoms and to prevent long-term degenerative diseases, such as osteoporotic fractures, cardiovascular disease, diabetes mellitus and possibly cognitive impairment."
"In addition, recent indications suggest potential advantages for blood pressure control with non-oral estrogens."
BMJ. 2012 Oct 9;345:e6409."A significant interaction was found between hormone replacement therapy and age at baseline for the composite endpoint mortality or breast cancer (P=0.028) with the younger women (<50 years) receiving hormone therapy having a significantly reduced risk (0.49, 0.28 to 0.87, P=0.015, fig 6). Women who had undergone hysterectomy (n=192) and received oestrogen alone had a decreased risk of death or breast cancer compared with women in the control group (0.42, 0.18 to 0.97; P=0.043; fig 6)."
"After 10 years of randomised treatment, women receiving hormone replacement therapy early after menopause had a significantly reduced risk of mortality, heart failure, or myocardial infarction, without any apparent increase in risk of cancer, venous thromboembolism, or stroke."
Cardiovasc Res. 2006 Mar 1;69(4):777-80."There is an
abundance of scientific evidence for the protective effect of estrogen against atherosclerosis, such as short-term vasodilating effects as well as long-term vascular protective and anti-atherosclerotic effects [2]. Epidemiological evidence shows that pre-menopausal women have a reduced risk for mortality from cardiovascular diseases [3] and that women are at a lower risk for the development of heart failure [4] and have enhanced cognitive function and reduced neurodegeneration associated with Alzheimer's disease and stroke [5]. Further proof for the protective effect of female gender is the fact that post-menopausal women have a similar or even increased risk for cardiovascular disease compared to men [3] and have an increased risk for adverse outcome after myocardial infarction and acute coronary syndromes, despite similar treatment with thrombolysis and percutaneous interventions [6]. It was therefore postulated that estrogen replacement would be beneficial in preventing cardiovascular diseases in post-menopausal females."
"The cardioprotective effect of estrogen is further supported by the findings that ovariectomy caused a loss of cardioprotection, which was regained by chronic estrogen replacement therapy."
"The vascular protective effects of estrogen and their mechanisms are thus fairly well-established."
Volume 64, Number 1
OBSTETRICAL AND GYNECOLOGICAL SURVEY
"Hormone replacement therapy (HRT) studies, in postmenopausal women, demonstrate that it is declining estrogen levels, as opposed to other aspects of aging, that are associated with undesirable skin changes that accompany aging (9)."
"Declines in estrogen in menopause are clearly associated with the thinning of the skin observed as women age. The direct effects of estrogen with regard to skin thickness are confirmed by the observation that estrogen replacement in menopause is consistently associated with a thickening of the skin. HRT has achieved increases in skin thickness of up to 15% (20)."
"The age-associated decline in estrogen is accompanied by drier skin as the water-holding capacity is reduced (20)."
"Estrogen in replacement therapy both prevents collagen loss and stimulates increases in collagen production. A large number of studies have demonstrated an increase, with HRT, of skin thickness associated with higher skin collagen content. Increases in skin collagen as high as 5.1% have been demonstrated with exogenous estrogen through HRT, with increases in dermal collagen as high as 6.5% (20)."
"At the menopause, a rapid decrease in skin elasticity begins (4,14), and this can be slowed or reversed with estrogen replacement therapy (4). Prevention of elasticity loss has also been reported with the use of HRT (14)."
"The consequences of estrogen deficit after menopause include increased wrinkling."
Maturitas. 2012 Mar;71(3):248-56. "Estradiol stimulates the activity of lipoprotein lipase
(LPL) in femoral adipocytes and lipolysis in abdominal adipocytes
[35], thereby promoting accumulation of gluteo-femoral fat. On
the other hand, estrogen deficiency is associated with enhanced
accumulation of abdominal fat [35]."
"HRT actually lowers weight gain and body fat [76,80,81].
In addition, HRT prevents the shift in fat deposition from the normal
female condition to the more unhealthy central fat depots associated
with the menopausal transition (Fig. 5) [76,82,83]."
"treatment of postmenopausal
women with estrogen enhances LPL activity in the
femoral region and at the same time lipolysis in the abdominal
region, which might promote fat accumulation in the former region
and fat loss from the abdomen [84]."
Int J Pharm Compd. 2013 Jan-Feb;17(1):74-85."Administration of compounded transdermal bioidentical hormone therapy in doses targeted to physiologic reference ranges administered in a daily dose significantly relieved menopausal symptoms in peri/postmenopausal women. Cardiovascular biomarkers, inflammatory factors, immune signaling factors, and health outcomes were favorably impacted, despite very high life stress, and home and work strain in study subjects. The therapy did not adversely alter the net prothrombotic potential, and there were no associated adverse events. This model of care warrants consideration as an effective and safe clinical therapy for peri/postmenopausal women especially in populations with high perceived stress and a history of stressful life events prior to, or during the menopausal transition."
Pathol Oncol Res. 2012 Apr;18(2):123-33."Insulin resistance and estrogen deficiency are concomitant disorders with mutual interrelationship. Insulin resistance and the compensatory hyperinsulinemia provoke increased androgen synthesis at the expense of decreased estrogen production. Similarly, a moderate or severe decrease in serum estrogen levels enhances the prevalence of insulin resistant states both in men and women. Healthy premenopausal women enjoy the defensive effect of estrogens against metabolic and hormonal disorders. However, even a slight decrease in their circulatory estrogen levels associated with insulin resistance may increase the risk for cancers, particularly in the organs having high estrogen demand (breast, endometrium and ovary). On the other hand, postmenopausal state with profound estrogen deficiency confers high risk for cancers in different organs with either high or moderate estrogen demand. After menopause, hormone replacement therapy improves insulin sensitivity and decreases the enhanced inclination to malignancies in postmenopausal women."
Diabetologia
June 1997, Volume 40, Issue 7, pp 843-849"Oestrogen replacement therapy is associated with a decreased risk of cardiovascular disease in postmenopausal women. Patients with non-insulin-dependent diabetes mellitus (NIDDM) have an increased cardiovascular risk."
"In a double blind randomized placebo controlled trial we assessed the effect of oral 17 β -estradiol during 6 weeks in 40 postmenopausal women with NIDDM."
"Oestrogen replacement therapy improves insulin sensitivity in liver, glycaemic control, lipoprotein profile and fibrinolysis in postmenopausal women with NIDDM."
J Lipid Res. 2006 Feb;47(2):349-55."This prospective pilot study of 18 men with androgen-independent prostate cancer receiving ADT measured effects of TDE on lipid and inflammatory CVD risk factors before and after 8 weeks of TDE. During treatment, estradiol levels rose 17-fold; total cholesterol, LDL cholesterol, and apolipoprotein B levels decreased. HDL2 cholesterol increased, with no changes in triglyceride or VLDL cholesterol levels. Dense LDL cholesterol decreased and LDL buoyancy increased in association with a decrease in HL activity. Highly sensitive C-reactive protein levels and other inflammatory markers did not worsen. Compared with ADT, short-term TDE therapy of prostate cancer improves lipid levels without deterioration of CVD-associated inflammatory markers and may, on longer-term follow-up, improve CVD and mortality rates."
TDE = transdermal estradiol
ADT = androgen deprivation therapy
Atherosclerosis. 2003 May;168(1):123-9."Both oral and transdermal E2 significantly reduced fasting glucose."
