Quote from: RebeccaM on April 04, 2016, 02:00:14 PM
i recently had to increase the frequency of my estradiol injections because of an interaction with another medication (Carbamazepine, anti-seizure drug) resulting in estrogen being cleared more quickly.
Have you considered the ketogenic diet for epilepsy? Studies have shown this diet to be safe. I can provide studies.
You can watch the movie "First Do No Harm" (1997), it features the well-known actress Meryl Streep. Also...
Front Pharmacol. 2012 Apr 9;3:59."The most notable example of a dietary treatment with proven efficacy against a neurological condition is the high-fat, low-carbohydrate ketogenic diet (KD) used in patients with medically intractable epilepsy. While the mechanisms through which the KD works remain unclear, there is now compelling evidence that its efficacy is likely related to the normalization of aberrant energy metabolism."
"The ketogenic diet (KD) is now a proven therapy for drug-resistant epilepsy (Vining et al., 1998; Neal et al., 2008), and while the mechanisms underlying its anticonvulsant effects remain incompletely understood (Hartman et al., 2007; Bough and Stafstrom, 2010; Rho and Stafstrom, 2011), there is mounting experimental evidence for its broad neuroprotective properties and in turn, emerging data supporting its use in multiple neurological disease states (Baranano and Hartman, 2008). Even in patients with medically refractory epilepsy who have remained seizure-free on the KD for 2 years or more, it is not uncommon for clinicians to observe that both anticonvulsant medications and the diet can be successfully discontinued without recrudescence of seizures (Freeman et al., 2007). This intriguing clinical observation forms the basis of the hypothesis that the KD may possess anti-epileptogenic properties."
"There is no longer any doubt that the KD is effective in ameliorating seizures in patients, especially children, with medically refractory epilepsy (Vining, 1999; Neal et al., 2008; Freeman et al., 2009). After its introduction in 1920, the KD was used as a first or second-line treatment for severe childhood epilepsy."
"The KD has now become an integral part of the armamentarium of most major epilepsy centers throughout the world (Kossoff and McGrogan, 2005)."
"Kang et al. (2007) reported that the KD was both safe and effective in 14 pediatric patients with established mitochondrial defects in complexes I, II, and IV, all of whom had medically intractable epilepsy. These authors observed that half of these patients became seizure-free on the KD, and only four patients failed to respond."
QuoteFrom working in the field I find that physicians are often quite conservative and will use low estradiol (200 or less as) a a cutoff for a normal level, not recogbizing that in cis women its common to have 10-fold fluctuations in estradiol levels.
Physicians ignore the studies in men with prostate cancer (aged 49-91) where high levels of estradiol, up to 2,500 pmol/L, (patch or injection) were found not to be conducive to increased health risks and where actually the treatment proved to be beneficial. One study in particular in transwomen, from Germany, found high doses of intramuscular estrogen not to be associated with a higher incidence of thrombosis, as opposed to earlier studies which used non-bio-identical estrogens. Pregnant women have very high levels, up to 75,000 pg/ml (275,000 pmol/L) and yet risk of embolism remains VERY low, under 0.2% while the risk increases post-partum, when levels drop abruptly.
Cas Lek Cesk. 1997 Jul 30;136(15):468-72."Incidence of thromboembolism in pregnancy is relatively low regarding to many predisposing factors, inclusively the thrombophilia induced changes in coagulation."
"This data supports the concept that the decreased serum levels of cytoadhesive molecules of sP-selectin and sE-selectin are dependent on serum estrogen levels and together with a new, estrogen induced, equilibrium of the fibrinolytic system suggest an explanation for the relatively low incidence of thromboembolic events in pregnancy. Decrease of cytoadhesive molecules may be one of explanations of favourable effects of estrogens on the development of atherosclerotic vascular changes."
Ann Intern Med. 2005 Nov 15;143(10):697-706."Among pregnant women, the highest risk period for venous thromboembolism and pulmonary embolism in particular is during
the postpartum period." (When estrogen levels drop and are low)
QuoteI also find that most are steadfast opposed to using progesterone as an adjunct to estrogen. There is the thought that there is no conclusive eveidence that it offers any benefits wkth respect to feminization whilst it does have conclusive data showing its potential harms.
There was a study done many years ago showing that progestative agents used in transsexual women were needed for full development of breasts (acini/alveoli and lobules). Also, science, in general, shows quite unequivocally that in women and in mammals, progesterone is required for the stimulation of lobulo-alveolar structures in the breast.
I've personally benefited from it, in terms of helping mood, sleeping, softening my skin/hair (progesterone increases sebum/oil production, estrogen decreases it), increasing fat deposition in the female areas (buttocks), plumped up my face and my breasts, made my breasts rounder. Progesterone can also counter water retention due to its antimineralocorticoid effects and this may benefit people with high blood pressure. Many transwomen have seen a clear benefit from it too.
About conclusive data showing its potential harms, this is false. Ask the doctors to provide you the studies and you will notice those studies always include the use of a progestogen called medroxyprogesterone acetate, different in molecular structure than the bio-identical progesterone that women produce in great quantity during the luteal phase and during pregnancy (up to 200-300 ng/ml). If indeed progesterone caused great harm, then how does one explain ciswomen getting away with such high levels during pregnancy or during the second half of their menstrual cycle? Wouldn't the fetus be harmed as well? Progesterone is also prescribed to pregnant women, sometimes in quite high doses, to prevent miscarriage or preterm abortion.
Studies have shown the differences between progesterone and other progestogens, especially the one that has shown to cause harm ( increase breast cancer risk, clotting and cardiovascular problems), to be significant.
. Progesterone has shown to NOT be to associated with an increase in breast cancer risk.
. Progesterone does not adversely affect liver or increase coagulation, as opposed to medroxyprogesterone acetate (MPA), which due to its significant glucocorticoid action, can increase the risk of thrombosis.
. Progesterone's byproduct, allopregnanolone (not present with medroxyprogesterone acetate) has shown to have anti-depressive and anxiolytic properties versus medroxyprogesterone acetate, shown to sometimes cause depression in some.
. Progesterone is neither androgenic nor does it lead to increased androgen levels as opposed to medroxyprogesterone acetate which somewhat "triggers" androgen receptors, which explains why it opposes oral estradiol's beneficial effects on HDL while progesterone doesn't.
. Progesterone has been shown to either not affect vasculature or add to the beneficial effect that estradiol exerts on blood vessels, being a vasodilator as well. It can reduce blood pressure. On the other hand, medroxyprogesterone acetate can negatively impact on cardiovascular health and was associated with an increased risk of coronary heart disease in women taking it in the WHI study of 2003.
You need to explain to those doctors that medroxyprogesterone acetate is NOT the same as progesterone, apart from both having progestogenic effects and that the studies they refer to as showing conclusively the harms associated with "progesterone" did not actually comprise of progesterone but rather an analogue with very differents effects on the body.
Maturitas 46S1 (2003) S7–S16"Basically all progestins do have only one effect in common, the progestogenic effect on the estrogen-primed endometrium of the rabbit, but there are large differences between progestins in the multitude of other biological effects elicited."
Clin Ther. 1999 Jan;21(1):41-60; discussion 1-2."All comparative studies to date conclude that the side effects of synthetic progestins can be minimized or eliminated through the use of natural progesterone, which is identical to the steroid produced by the corpus luteum."
"The results of published clinical studies show minimal or no changes in lipid profile, blood pressure, or carbohydrate metabolism during treatment with oral micronized progesterone.28 This safety profile contrasts with the reported negative effects of some synthetic progestins, including adverse effects on lipid metabolism and glucose tolerance. Several studies, including the 3-year prospective PEP1 study, 4, 28 have shown that oral micronized progesterone significantly improves metabolic tolerance compared with such progestins as MPA.52,54,58"
CLIMACTERIC 2005;8(Suppl 1):3–63"As progestogens differ in their hormonal pattern, e.g. glucocorticoid, androgenic or antiandrogenic, or antimineralocorticoid activity, there may be differences between the various progestogens regarding the clinical response to HRT."
Experimental and Clinical Psychopharmacology 2007, Vol. 15, No. 5, 427–444"It is important to note that although progesterone and synthetic progestins are used for similar purposes, these may not exert similar modulatory effects on target organs, and each progestin molecule may have specific effects on neuroendocrine action (Bernardi et al., 2006)."
Med Hypotheses. 2001 Feb;56(2):213-6."natural progesterone--now available in micronized oral preparations--does
not oppose the hepatic effects of oral estrogen, and moreover may be
preferable to androgenic progestins with respect to vascular
function."
Many doctors unfortunetaly have not taken the time to thoroughly investigate the matter but rather repeat what they have been told. I can, if you wish, send you a summary of findings with progesterone with its benefits, risks, etc. showing all what I've asserted above, in much more detail with supporting evidence. You can then show this to your doctors.
QuoteAnyhow, all that to say I finally obtained avRx for Profmgesterone last week and am hoping this will help with the weight loss, energy, sex drive, and facial/breast fullness. A lot to pin on a little spherical orb I realize but fingers crossed.
Progesterone tends to be inhibitory as opposed to excitatory (i.e. estrogen) and thus can have a significant impact on seizure activity. Do realize that you may need to take a higher dose of it than normal (your doctors should be aware of this) as the anti-seizure medication you are taking increases its metabolization and rate of elimination.
Progesterone should help, hopefully but you need enough of it to have a significant effect. Food increases its absorption two-fold.
Neurology. 2014 Jul 22;83(4):345-8."To determine whether allopregnanolone (AP) may mediate seizure reduction in progesterone-treated women with epilepsy."
"The findings support AP as a mediator of seizure reduction in progesterone-treated women who have a substantial level of perimenstrually exacerbated seizures."
Neurol Sci. 2011 May;32 Suppl 1:S31-5."Oestrogen and progesterone have specific receptors in the central nervous system and are able to regulate neuronal development and plasticity, neuronal excitability, mitochondrial energy production, and neurotransmitter synthesis, release, and transport. On neuronal excitability, estradiol and progesterone seem to have an opposite effect, with estradiol being excitatory and progesterone and its derivative allopregnanolone being inhibitory. Estradiol augments N-methyl-D-aspartate-mediated glutamate receptor activity, while progesterone enhances gamma-aminobutyric acid-mediated chloride conductance. Sex steroid regulation of the balance of neuroexcitatory and neuroinhibitory activities may have a role in modulating clinical susceptibility to different neurological conditions such as migraine, catamenial epilepsy, premenstrual dysphoric disorder, and premenstrual syndrome."
Curr Neurol Neurosci Rep. 2011 Aug;11(4):435-42."Reproductive hormones have been found to have a role in the pathogenesis and treatment of seizures by also altering neuronal excitability, especially in women with catamenial epilepsy. The female reproductive hormones have in general opposing effects on neuronal excitability; estrogens generally impart a proconvulsant neurophysiologic tone, whereas the progestogens have anticonvulsant effects. It follows then that fluctuations in the levels of serum progesterone and estrogen throughout a normal reproductive cycle bring about an increased or decreased risk of seizure occurrence based upon the serum estradiol/progesterone ratio. Therefore, using progesterone, its metabolite allopregnanolone, or other hormonal therapies have been explored in the treatment of patients with epilepsy."
Methods Find Exp Clin Pharmacol. 2004 Sep;26(7):547-61."Generally, progesterone has antiseizure effects, while estrogens facilitate seizure susceptibility. The progesterone metabolite allopregnanolone has been identified as a key endogenous neurosteroid with powerful antiseizure activity. Allopregnanolone is a potent, positive allosteric modulator of GABA(A) receptors. Progesterone and allopregnanolone exposure and withdrawal affects GABA(A) receptor plasticity. In animal models, withdrawal from chronic progesterone and, consequently, of allopregnanolone levels in brain, has been shown to increase seizure susceptibility. Natural progesterone therapy is proven to be effective in women with epilepsy."
Epilepsia. 2001 Feb;42(2):216-9."These data are consistent with a role for allopregnanolone in the control of neuronal excitability and seizures."
J Pharmacol Exp Ther. 1999 Feb;288(2):679-84.
Finasteride, a 5alpha-reductase inhibitor, blocks the anticonvulsant activity of progesterone in mice."Progesterone is an effective anticonvulsant against pentylenetetrazol (PTZ) seizures. This action is hypothesized to require the metabolic conversion of progesterone to the gamma-aminobutyric acidA receptor potentiating neuroactive steroid allopregnanolone by 5alpha-reductase isoenzymes followed by 3alpha-hydroxy oxidoreduction."
"The anticonvulsant activity of progesterone against PTZ-induced seizures can be blocked by 5alpha-reductase inhibition, providing strong evidence that the anticonvulsant effect of the steroid in this model is mediated by its active metabolite allopregnanolone."
For this reason, finasteride/dutasteride would perhaps not be best for you.
QuoteAnyhow, back to the topic at hand - REASONS FOR FFS:
It sounds like folks have a diverse array of reasons and that mine are not entirely unique. Prior to having surgery I will be certain to discuss the specific risks as I do NOT wantt to feel/look worse post-operatively than i did before (the immediate period obviously excluded).
I would contend that our sense of dysphoria is real regardless and exists independent (thoigh often closely intertwined it can be hard to parse apart) of gender attribution by others. Even if we lived in a society where cissexism and transphobia did not exost I believe many of us would still experience dysphoria at the features of our bodies that undergone change in response to testosterone, as is the case for me.
I wouldn't resort to FFS just yet. The right hormones in the right amounts might help.
