Quote from: Joanne Feliz on November 10, 2016, 02:59:56 PMIn regards to the health risks millions of woman use microgynon daily and it seems in australianat least that is what they seem to prescribe. But I'll talk to my ends about it, I should be seeing a new endrinologist shortly anyhow. Thanks for your concern.
I just don't see the rationale behind using ethinyl estradiol over bio-identical estradiol when the latter has an even lesser risk of thromboembolism and is EQUALLY EFFECTIVE for feminization purposes.
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."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). Moreover, these differences may explain why M-->F transsexuals treated with oral EE are exposed to a higher thrombotic risk than transsexuals treated with td E(2)."
"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."
EE = ethinyl estradiol
td = transdermal
E2 = bio-identical estradiol
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"
Minerva Med. 2013 Apr;104(2):161-7."New kinds of COC without EE but with Estradiolvalerat or Estradiol showed a much lower degree of coagulation activation than "classical" COC containing EE."
"
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 »
"Gaussem et al41 studied markers of coagulation and fibrinolysis in women randomized to take three cycles of either levonorgestrel–ethinyl estradiol (...) or NOMAC-E2.
The authors reported a procoagulatory shift in levels of these markers in women taking levonorgestrel–ethinyl estradiol. In contrast, they reported significantly smaller changes from baseline in these markers among women taking NOMAC-E2. One outcome was a change in activated protein C resistance. This marker, which has been proposed as an independent risk factor for venous thromboembolism, increased to a greater degree in levonorgestrel–ethinyl estradiol users than in NOMAC-E2 users (0.46 versus 0.20, P < 0.01). »
"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"
Andrologia. 2014 Sep;46(7):791-5."
Ethinyl oestradiol, due to its chemical structure, was in 2003 identified as a major factor in the occurrence of VTE. Most clinics do not prescribe ethinyl oestradiol any longer"
"Cessation of use of ethinyl oestradiol and peri-operative thrombosis prophylaxis for surgery have reduced prevalence rate of VTE."
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]."
Gynecol Obstet Invest. 1986;22(4):198-205."the marked influence of ethinyl estradiol on liver protein synthesis should make estradiol valerate the first choice in clinical replacement therapy."
The progestin, levonorgestrel, is also ANDROGENIC and thus can prove to be counterproductive. It reduces SHBG which binds androgens strongly.
Maturitas 46S1 (2003) S7–S16"Levonorgestrel causes a decrease of SHBG of 50% [8,9,16]."
"some of the older-generation progestins such as MPA, norethindrone acetate, norethindrone, and
levonorgestrel, which bind with relatively high affinity to the AR,
have been reported to act as agonists or partial agonists in some contexts, unlike progesterone (Table 4) (77–86)"
"MPA, norethindrone,
levonorgestrel, and gestodene, but not dienogest,
exhibit strong to weak partial agonist activity for AR-mediated transactivation via androgen response elements (77, 105, 178–180), whereas dienogest, trimegestone, drospirenone, and progesterone, but not MPA or norethindrone, can antagonize DHT-mediated
transactivation via the AR (97, 178, 179)."
"
The findings that some progestins like MPA, norethindrone, levonorgestrel, and gestodene bind to the AR with
relatively high affinity and exhibit partial agonist activity via the AR in cell lines, and androgenic effects in rats, suggest that these progestins may result in AR-mediated androgenic genomic effects in women on HT. In particular, AR-mediated genomic effects by MPA or other AR partial agonists have been suggested to play a role in
increasing the risk of breast cancer by disrupting some androgen signaling in the breast that may be protective for breast cancer (182)."
Also,
"unlike progesterone and dienogest, it was found that
MPA, norethindrone acetate, and levonorgestrel increase expression of two markers of vascular inflammation, intracellular adhesion molecule-1 (ICAM-1) and vascular cell
adhesion molecule-1 (VCAM-1)"
You can discuss these with your doctor. This is why it's important, if possible, to be proactive in one's health management and do a little a bit of research.
