Quote from: Wild Flower on March 29, 2016, 06:01:44 PM
I also do not want to limit my sexual pleasure (need to do more research).
I provided two studies. I can attest to having as much, if not MORE sexual pleasure now than ever before because my body feels right to ME. Sexual pleasure, I think, is also very much influenced by our minds, regardless of hormones, if we are actually doing what we want, have no religious hang-ups, repression, etc.
Quote from: Carrie Liz on March 29, 2016, 07:41:41 PM
For me, it's not even about SRS somehow making me "female," or how I'm seen by anyone else, it's all about that physical dysphoria. I'd want a vagina and labia and clitoris even if I was completely "male" on the outside
Yes! +1
Quote from: warlockmaker on March 29, 2016, 11:46:47 PM
The chance of prostate cancer and any other sex organ cancer is almost eliminated.
The prostate is not removed during SRS and either way, pre or post-op, our androgen levels are very low so it shouldn't make a difference in that respect. Of the 5 (out of overall 6) cases reported in transsexual women in the literature, I have noted 4 being post-op. So, cancer can indeed occur.
Andrologia. 2014 Dec;46(10):1156-60.
Prostate cancer incidence in orchidectomised male-to-female transsexual persons treated with oestrogens.
Gooren L1, Morgentaler A.« When diagnosed in this population, there appears to be a tendency for PCa to behave aggressively. Prostate monitoring should be considered in these individuals beginning at age 50 years."
QuoteIn addition, a slower metabolism and less agressive mental approach encourages long life and less stress related heart attacks.
The same can be said of pre-ops as they have little T. Cardiovascular risks are lessened due to positive effects of estrogen on the cardiovascular system if bio-identical E is taken, preferably non-orally.
QuoteYes, we have a higher exposure to breast cancer
Not quite.
Journal of Clinical & Translational Endocrinology 2 (2015) 55-60"There is no increase in cancer prevalence or mortality due to transgender HT."
"While some guidelines for transgender medical care express concerns for elevated cancer risk with certain hormone regimes, current data suggest that the risk of cancer may not rise."
"Although studies are small, overall cancer incidence in transgender men and transgender women to-date has not been found to be different than their respective male and female controls [5].
There are no reports of change in breast cancer specific risk among transgender individuals on estrogen compared to secular trends of male breast cancer incidence. Rates are lower relative to secular trends of female breast cancer rates."
Breast Cancer Res Treat. 2015 Jan;149(1):191-8.3 cases out of 3,556 transsexual women as is indicated in the full article. An incidence rate of 0.08%.
J Sex Med.2013Dec;10(12):3129-34."We researched the occurrence of breast cancer among transsexual persons 18-80 years with an exposure to cross-sex hormones between 5 to >30 years. Our study included 2,307 male-to-female (MtF) transsexual persons undergoing androgen deprivation and estrogen administration (52,370 person-years of exposure)"
"Among MtF individuals one case was encountered, as well as a probable but not proven second case."
"The number of people studied and duration of hormone exposure are limited but it would appear that cross-sex hormone administration does not increase the risk of breast cancer development, in either MtF or FtM transsexual individuals.
Breast carcinoma incidences in both groups are comparable to male breast cancers.
Cross-sex hormone treatment of transsexual subjects does not seem to be associated with an increased risk of malignant breast development."
"The incidence rate of breast cancer in our MtF cohort was thereby 4.1 per 100,000 person-years (i.e., two cases divided by the total amount of 49,370 person-years of follow-up). The 95% confidence interval of the incidence ranged from 0.8 to 13.0 per 100,000 patient-years. For comparison, the calculated expected incidence of breast cancer in biologic women would be 170.0 per 100,000 person-years of follow-up. In our sample, the one or possibly two incident cases of breast cancer in MtF subjects more closely approximate the expected incidence of breast cancer of 1.2 per 100,000 patient-years that would occur in biologic men."
Quotepossible blood clots which can cause heart issues
Only observed with the use of non bio-identical estrogen and progestogens (as for instance, in the 2003 WHI study).
Journal of Clinical & Translational Endocrinology 2 (2015) 55-60"Other compelling data suggest that
the incidence of venous thromboembolism (VTE) among transgender
women appears associated with the presence of a hypercoaguable
risk factor, including the use of an especially
thrombogenic estrogen (ethinyl estradiol) which is no longer used
[3].
Gooren et al. (2008), reported no increase in VTE among 2236
male-to-female (MTF) transgender individuals on HT from 1975 to
2006 compared with controls, with the exception of those who used
ethinyl estradiol, for which there was a 6-8% incidence [4]."
Archives of Sexual Behavior, Vol. 27, No. 5, 1998"The incidence of thromboembolic events during cross-
gender hormone treatment in our patients was zero."
Despite VERY high doses of parenteral bio-identical estradiol and moderate to high doses of oral bio-identical E.
Exp Clin Endocrinol Diabetes. 2005 Dec;113(10):586-92."Sixty male-to-female transsexuals were treated with monthly injections of gonadotropin-releasing hormone agonist (GnRHa) and oral oestradiol-17beta valerate for 2 years to achieve feminisation until SRS."
"Two side effects were documented. One, venous thrombosis, occurred in a patient with a homozygous MTHFR mutation."
Only 1 case with a GENETIC PREDISPOSITION.
J Clin Endocrinol Metab. 2003 Dec;88(12):5723-9.
Venous thrombosis and changes of hemostatic variables during cross-sex hormone treatment in transsexual people"In conclusion, we have shown that treatment of MtF transsexuals with sex steroid hormones (CPA combined with E2 or EE) affects the hemostatic balance with a very pronounced difference in the effects of oral EE compared with the effects of both td E2 or oral E2.
Oral EE induces a clinically relevant prothrombotic state."
J Clin Endocrinol Metab. 2012 Dec;97(12):4422-8."Historically, high-dose estrogen in the form
of ethinyloestradiol or conjugated equine estrogen (CEE) was
used to suppress testicular function and induce feminization.
In
view of the procoagulant nature of these older estrogens and the
inability to use plasma estradiol levels to guide treatment, this
protocol was changed in 2004 to oral estradiol valerate"
BMJ 2012;345After 10 yrs of HRT on bio-identical estradiol:
"Stroke rates did not differ between the groups (
14 in control group v 11 in treated group; 0.77, 0.35 to 1.70; P=0.70).
The rate of venous thromboembolism was low and did not differ significantly between groups. Three women had confirmed deep vein thrombosis (1 in control group v 2 in treated group; 2.01, 0.18 to 22.16) and only one woman (control group) was admitted to hospital with pulmonary embolism."
After 16 yrs follow-up:
"Stroke rates did not differ between groups, with 21 cases in the control group and 19 in the treated group (0.89, 0.48 to 1.65; P=0.71).
The rate of venous thromboembolism and pulmonary embolism was low and there was no significant difference between groups (fig 6⇓). Nine women had confirmed deep vein thrombosis (5 in control group v 4 in treated group; 0.80, 0.22 to 2.99; P=0.74), and
only four women were admitted to hospital with pulmonary embolism (3 in control group v 1 in treated group; 0.33, 0.04 to 3.21; P=0.34)."
"This may be due to the differences in the administered hormones; 17-β-estradiol has been reported to be less thrombogenic than conjugated equine oestrogen.21 22 In human aortic endothelial cells 17-β-estradiol is superior to conjugated equine oestrogen in increasing the production of nitric oxide, partially because of a higher ability to activate the production of endothelial nitric oxide synthase.23"
"The type of progestogen used may be important, as
natural progesterone seems to have more beneficial effects on the cardiovascular system than does medroxyprogesterone acetate.30 31"
Quoteand should check our liver
Liver problems have been associated with a certain anti-androgen (cyproterone acetate) and NON bio-identical estrogens such as ethinyl estradiol and conjugated estrogens.
Exp Clin Endocrinol Diabetes. 2005 Dec;113(10):586-92." Sixty male-to-female transsexuals were treated with monthly injections of gonadotropin-releasing hormone agonist (GnRHa) and oral oestradiol-17beta valerate for 2 years to achieve feminisation until SRS."
"Liver enzymes, lipids, and prolactin levels were unchanged."
J Clin Endocrinol Metab. 2008 May;93(5):1702-10."transdermal E2 exerts minimal effects on CRP and the other inflammation and hepatic parameters."
Am J Obstet Gynecol. 1987 May;156(5):1326-31."None of the doses of transdermal estradiol exerted any measurable action on hepatic markers of estrogen action"
J Clin Endocrinol Metab. 1991 Aug;73(2):275-80."despite the relatively high doses necessary to mimic a hormonally normal cycle, the transdermal route did not significantly alter the hepatic parameters studied"
Hepatol Res. 2007 Apr;37(4):239-47."Our previous studies showed that estradiol suppressed hepatic fibrosis in animal models"
Int J Endocrinol. 2015;2015:294278."In females, estradiol regulates liver metabolism via estrogen receptors by decreasing lipogenesis, gluconeogenesis, and fatty acid uptake, while enhancing lipolysis, cholesterol secretion, and glucose catabolism."
"These recent integrated concepts suggest that sex hormone receptors could be potential promising targets for the prevention of hepatic steatosis."
Am J Physiol Endocrinol Metab. 2014 Aug 1;307(3):E345-54."Diet-induced hepatic steatosis was attenuated by E₂"
Scand J Clin Lab Invest Suppl. 2014;244:90-4."Although not a classical target for estrogens, the liver is a target for their action and is sensitive to their deprivation. The occurrence of menopause is accompanied by a chain of events depending on the progressive estrogen deprivation that eventually leads to a shift from a low inflammatory to a high inflammatory state. This has a series of well-known consequences in many different organs and tissues (bone, heart, brain, body fat etc.) among which the liver is particularly interesting. The consequences are extremely evident in HCV-positive women in whom HCV infection and
menopause cooperate to induce higher necro-inflammatory features, increased hepatic steatosis and eventually faster progression of fibrosis."
Ernst Schering Found Symp Proc. 2006;(1):45-67."These mutations, both natural and experimental, have revealed that estrogen deficiency results in a spectrum of symptoms. These include loss of fertility and libido in both males and females; loss of bone in both males and females; a cardiovascular and cerebrovascular phenotype; development of a metabolic syndrome in both males and females, with truncal adiposity and
male-specific hepatic steatosis. Most of these symptoms can be reversed or attenuated by estradiol therapy."
Gynecol Endocrinol. 1993 Jun;7(2):111-4."Serum concentrations of sex hormone-binding globulin (SHBG), corticosteroid binding globulin (CBG), ceruloplasmin, lipoprotein A and liver enzymes were measured in 30 postmenopausal women treated with (...)
micronized 17 beta-estradiol daily and micronized progesterone (...), as progestogen supplementation. The treatment lasted for 4 months. The serum levels of SHBG and CBG increased during treatment and a weak association between progesterone dosage and CBG was observed.
Levels of lipoprotein A and liver enzymes did not change. It is concluded that micronized natural progesterone is an attractive means of progesterone supplementation in postmenopausal hormone replacement therapy without any liver-related side-effects."
Gynecol Endocrinol. 1996 Feb;10(1):41-7.
Clinical evaluation of near-continuous oral micronized progesterone therapy in estrogenized postmenopausal women "No significant changes were observed in blood glucose or liver enzymes."
Estrogen and progesterone supplementation provide many benefits to the body and mind, regardless if pre or post-op.
QuoteThe orgasmn is much more intense and even not having one is pleasurable.
I have plenty of orgasms post-op, even when I sleep at night, when I dream!
QuoteThen comes reasons many may opt not to have surgery because of the fear of surgery...the pain and the possible complications.
But then, one must weigh this risk which today is quite low vs. the benefits of having the surgery. This will depend on the individual.
QuoteMany cannot afford this surgery
In some countries, it is paid for by the government or insured/covered with certain plans.
Quote from: Ange on March 30, 2016, 03:16:24 AM
20% ?
It would be nice to see the supporting evidence.

For this finding, for the suicide rate post-op.
Quote from: Lucie on March 30, 2016, 07:01:44 AM
Are you sure that the risk of prostate cancer is lower after SRS than before ? How would you explain that ?
Quote from: Laura_7 on March 30, 2016, 08:59:07 AM
Less testo more estro. There are remedies for that based on high doses of estro.
Pre- or post-op, T is low, there is no difference. Same with E. So risks should be similar.
Quote from: jessicats on March 30, 2016, 10:55:45 AM
Some sources say that after removing the gonads you go through the menopause. Yes, with hormones you treat it, but you are already in menopause.
Taking hormones will take you OUT of menopause and you will be no different than a ciswoman who is pre-menopausal except that you have no uterus, fallopian tubes, or ovaries. For me, that is no biggie. I'm ok with that.
QuoteOf course being able to have your own children and give birth would be something that most of us have dreamt of.
Not me. To each their own.

Quote from: Jenna Marie on March 30, 2016, 11:18:55 AM
The difference post-op is that it's permanent, which *is* a big change for anyone who wanted the ability to regain T production if she chose
Then simply take T. It's pretty simple.
Quote from: Lucie on March 30, 2016, 12:24:59 PM
I agree that SRS is not orchidectomy, however I don't see why prostate cancer risk should be higher after orchidectomy than after SRS.
Am I missing something ?
You're perfectly right. It's the same thing. Orchiectomy is removing testicles, thus testicular production of T, same as SRS, except you also get a vagina and the penis removed. From a hormonal standpoint, pre-op and post-op (whether orchiectomy or SRS) are the same.