Quote from: Tamika Olivia on February 16, 2016, 05:09:51 PM
He isn't comfortable prescribing orals due to their risks of DVT and liver problems.
Studies have shown that bio-identical estradiol, when given to transsexual women, does not harm liver nor does it significantly increase risk of DVT. This is because it is BIO-IDENTICAL, is quickly metabolized, unlike other forms of estrogen which he is likely thinking about and does not pass through the portal vein, again and again, triggering clotting factors and harming liver.
Archives of Sexual Behavior, Vol. 27, No. 5, 199824 transsexual women in this study were on oral estradiol, low to high doses.
"The incidence of thromboembolic events during cross-gender hormone treatment in our patients was zero."
"None of our patients developed deep vein thrombosis or embolism during cross-gender hormone therapy performed in our clinic."
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"
"Two side effects were documented. One, venous thrombosis, occurred in a patient with a
homozygous MTHFR mutation. One patient was found to be suffering from symptomatic
preexisting gallstones. No other complications were documented. Liver enzymes, lipids, and prolactin levels were unchanged. Significantly increased oestradiol and SHBG serum levels were detectable. In addition, an increase in bone mass density, in the femoral neck and lumbar spine, was recorded. We conclude that cross-sex hormone treatment of male-to-female transsexuals using GnRHa and oestradiol-17beta valerate is effective, and side effects and complication rates can be reduced using the treatment regimen presented here."
Hence, only two complications in two people with pre-existing problems (mutation and gallstones).
Estradiol valerate is the same as estradiol.
Maturitas. 1982 Dec;4(4):315-24."After oral or parenteral administration, oestradiol valerate, the synthesis compound contained in various commercially available preparations, is completely converted into the natural substances 17 beta-oestradiol and valeric acid. The 17 beta-oestradiol produced on cleavage of the ester behaves in the organism like the endogenous steroid hormone. Oestradiol valerate and 17 beta-oestradiol are virtually dose-equivalent. No differences in the spectrum of action of the oestrogen and its ester have been found either in animal experiments or man. The pharmacokinetic behaviour and the biotransformation of the 17 beta-oestradiol originating from oestradiol valerate are no different from those of natural 17 beta-oestradiol."
J Clin Endocrinol Metab. 2003 Dec;88(12):5723-9. (In transsexual women)
"The large differential effect of oral EE and oral E(2) indicates that the prothrombotic effect of EE is due to its molecular structure rather than to a first-pass liver effect (which they share)."
"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."
J Clin Endocrinol Metab. 2012 Dec;97(12):4422-8. (In transsexual women)
"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"
JAMA Intern Med. 2014 Jan 1;174(1):25-31. "In an observational study of oral hormone therapy users, CEEs use was associated with a higher risk of incident venous thrombosis and possibly myocardial infarction than estradiol use. This risk differential was supported by biologic data. These findings need replication and suggest that various oral estrogen drugs may be associated with different levels of cardiovascular risk."
Biochem Pharmacol. 2013 Dec 15;86(12):1627-42."In effect, the term CEE may obscure the fact that it does not contain E2. CEE and E2 have different chemical structures, pharmacological properties, metabolic products, and ER binding affinity, selectivity, and agonistic properties [1]. Because both ER-dependent and ER-independent mechanisms play a role in mediating the cardiovascular actions of E2, CEE may not mimic the cardiovascular effects of E2."
J Thromb Haemost. 2014 Mar 15."Compared with E2 users, CEE users had greater thrombin generation peak values, endogenous thrombin potential, and lower total protein S (multivariate adjusted differences of 49.8 nM (95%CI: 21.0, 78.6); 175.0 nMxMin (95%CI: 54.4, 295.7); and -13.4% (95%CI: -19.8, -6.9), respectively). Factor VII and antithrombin levels were not different between E2 and CEE users. Results were similar in subgroups of users of unopposed HT, opposed HT, low-dose estrogen and standard dose estrogen. »
"The hemostatic profile of women using CEE is more prothrombotic than that of women using E2. These findings provide further evidence for a different thrombotic risk for oral CEE and oral E2."
Maturitas. 2015 Mar 9. "In an observational study of oral HT users, CEE was associated with a significantly higher risk of incident venous thrombosis (OR, 2.08; 95% CI, 1.02–4.27), significantly higher activated protein C resistance (OR 1.68; 95% CI, 1.24–2.28), and a nonsignificant elevation in myocardial infarction risk (OR, 1.87; 95% CI, 0.91–3.84) when compared with estradiol use [56]."
"The hemostatic profile of women taking CEE was shown to be more prothrombotic than that of women using oral estradiol, including significantly higher thrombin generation peak value and decreased total protein S (P = 0.001 and P ≤ 0.001, respectively) [57]. In an oophorectomized pig model, both estradiol and CEE reduced aggregation of platelets, but only estradiol increased platelet secretion of nitric oxide, and platelets from estradiol-treated animals caused relaxation of coronary arteries [58]. »
Minerva Med. 2013 Apr;104(2):161-7."Estradiol itself has a lower impact on estrogen-hepatic proteins, and is more readily metabolized by the liver than ethinyl estradiol, the ethinyl group on which slows down that process. The structure increases the bioavailability of ethinyl estradiol compared with E2, but may also contribute to an increased likelihood of estrogen-related adverse events.40 »
"Agren et al evaluated multiple coagulatory and thrombolytic indices over six cycles of oral contraceptive use in a randomized study comparing NOMAC-E2 with levonorgestrel–ethinyl estradiol. They reported that NOMAC-E2 had minimal influence on markers of hemostasis, and caused less change in these parameters than the pill containing ethinyl estradiol »
Minerva Ginecol. 2014 Feb;66(1):91-102."Micronized estradiol (E2) and its estere valerate (EV), is more easily metabolized by the liver than ethynylestradiol (EE). This causes minimal metabolic impact »
"In comparison to EE/levonorgestrel (LNG), EV/DNG is more neutral on metabolism and coagulation"
"E2/NOMAc is more neutral than EE/LNG on metabolism and more neutral than EE/DRSP on coagulation"
Maturitas. 1980 Jul;2(2):95-100."The material consisted of 32 patients, 12 of whom were selected for control. All were cases approaching the menopause and had been subject to oophorectomia bilateralis and hysterectomia for myomas. All 20 investigation patients received estradiol valerianate orally"
"In the liver enzymes no changes occurred."
And yet, contraceptive pills are prescribed to millions of women worldwide by doctors, often without any blood tests before.
