Quote from: Ritana on March 19, 2016, 04:13:11 PM
I am a few years post op girl. Post srs, i never had my hormones checked until four months ago when my endo thought I was my estrogens were too high. I was on (...) transdermal gel a day. I was advised to reduce (...). I have been on this dose for the last 4 months -except the month of january when I had vfs.
I am due to have my hormones checked next month. During the last 2 months I have been experiencing extreme fatigue and muscle weakness, with daily breathlessness. My gp couldn't find anything wrong with my regular blood test results (not the hormones ones) . My iron levels came back normal and so did the rest.
I am wondering if low estrogen levels could be the culprit? Does anyone know the impact of low estrogen can have in post op girls?
Why did your endo find levels too high? For what reason? Find out as I'm quite certain his reasons for reducing are not supported by actual science but rather by guidelines that don't account for differences in the type of estrogen that is administered, or route of administration or the several studies that show that higher levels of bio-identical estradiol aren't a problem healthwise but have plenty of benefits. I wouldn't be surprised that your symptoms are caused by too low estrogen.
P.S.: you can't post doses in this forum.
1)
Cardiovascular and clotting risks . Ciswomen are reported to be much less affected than men by cardiovascular complications despite pregnancy levels of estradiol and levels of up to 650 pg/ml every menstrual cycle. Their risks increase (and approach that of males) post-menopause when estrogen levels DROP. Studies have strongly suggested a protective role for estrogen. I can provide these studies.
. Randomized controlled trials (the most reliable type of study), the Danish and WHI studies have shown estrogen taken alone or without medroxyprogesterone acetate (known to have deleterious effects on cardiovascular markers and oppose estrogen's beneficial effects on cardiovascular health) to DECREASE the cardiovascular complications (and death from). The Danish study (bio-identical estradiol w/progestin other than medroxyprogesterone acetate) did not observe an increase in stroke nor DVT/PE (deep vein thrombosis/pulmonary embolism) incidence.
. Transdermal and even oral bio-identical estradiol in women have shown to positively impact blood pressure with transdermal having an overall beneficial effect on several cardiovascular markers and negligibly affecting coagulation. Studies to support this.
. Studies in men with prostate cancer (ages 49-91) have shown that estradiol levels up to 700 pg/ml were safe.
There were no cardiovascular complications or incidences of thrombosis. In fact, researchers stated high levels could be PROTECTIVE. Additionally, it was observed that estrogen improved lipid profiles, without cardiovascular deterioration and that it may improve cardiovascular disease and mortality, long-term. These men were treated with high dose injectable or transdermal (patches) estradiol. I can provide you those studies.
. Pregnant women have levels that go as high as 75,000 pg/ml and yet the risk of having a DVT or pulmonary embolism is less than 0.02 % with thromboembolism being 5 times as more likely post-partum (when levels drop) and pulmonary embolism being extremely rare during pregnancy and more common post-partum (when levels drop). I can provide you the evidence as well.
. Four studies show circulating levels of estradiol not to be a useful criterion of risk of thrombosis, as despite high levels, no increased risk was found AND rather the route of administration/type of estrogen is more indicative of the risk.
. Arch Sex Behav. 1998 Oct;27(5):475-92. In this study, transsexual women were given high dose intramuscular E and some were prescribed medium-high doses of oral E. In spite of this, there was not one incidence of thrombosis.
"None of our patients developed deep vein thrombosis or embolism during cross-gender hormone therapy performed in our clinic."
2)
Breast cancer risk. In transsexual women, breast cancer incidence is very low, close to that of men not on HRT and significantly lower relative to ciswomen (as per Dr. Gooren and his team, leading specialists of HRT treatment in transwomen). Only 17 cases reported since 1968 (of which 3 are not likely to be related to estrogen use) despite decades of very aggressive, high doses of oral estrogens and non-oral estrogens (intramuscular). Only one proven case reported in Holland among Gooren's patients in decades of treatment despite high doses of E for several years. Studies to support this.
. In men with prostate cancer treated with high dose estrogen over the years, since the 1960's, breast cancer is extremely rare. Supporting evidence.
. High dose estrogen has actually been used to treat ciswomen afflicted with breast cancer, in one instance, with increased effectiveness relative to tamoxifen, one of the drugs of choice in its treatment.
. In women with previous breast cancer, several different types of studies have shown HRT (with progestin or not) to either not increase recurrence, lead to relatively low rates of recurrences or even improve the rate of recurrence relative to non-HRT users.
. Randomized controlled trials showed estrogen to be either protective of breast cancer incidence or have no effect, even in women who had had breast cancer, when MPA (medroxyprogesterone acetate, linked to breast cancer) was NOT used or sparingly. I can provide studies. One randomized controlled trial, similar to the WHI, undertaken years earlier even showed that breast cancer was less in HRT users.
. Some epidemiological studies show no increased risk of cancer with the use of oral contraceptives, duration proving to not be a factor in one instance, while being a factor in another.
. The incidence of breast cancer from one country to another were not found to be correlated with levels of estrogens. In fact, the only significant finding was a higher level of estradiol in a subpopulation (adolescents) of the country (during the luteal phase) with the least incidence of breast cancer.
. The more childbirths a woman (hence, the more pregnancies when levels of E are sky high), the lower the risk of breast cancer. On the other hand, celibate nuns are historically known to have a higher incidence of breast cancer risk, going as far back as the 1700's.
. Breast cancer risk is highest in women over the age of 40 and especially 50,
when estrogen levels drop.
. Studies in mice and observations that carcinoma incidence is increased post-pregnancy suggest high levels of estradiol are protective.
. Based on all the evidence so far, we still cannot establish causation between HRT and breast cancer as there are too many conflicting data. Studies with estrogen taken alone or without MPA combined (and other observations) have so far been actually more suggestive of a protective effect while those with bio-identical progesterone or dydrogesterone suggest no increased risk.
3)
Uterine cancer risk. YOU HAVE NO UTERUS
4)
Prolactinoma. Ciswomen have very high levels of prolactin, up to 600 ng/ml (ug/L), during pregnancy and continue to have high levels during breastfeeding which can sometimes last a few years. Despite this, the fact that estradiol levels can also peak quite high during a menstrual cycle (up to 650 pg/ml) and women's history of taking birth control pills or HRT involving estrogens that strongly affect pituitary gland, the prevalence of prolactinoma has been estimated to be 0.1% in women. Doctors/health authorities do not ask mothers to stop breastfeeding their children or not become pregnant again due to risk of prolactinoma.
. Causation has not been established between the use of estrogen or pregnancy and prolactinoma in women. Association between OC/HRT use and prolactinoma may have more to do with the increased likelihood that women with prolactinoma use treatment to regulate menstrual cycle disrupted by prolactinoma.
. There is a negligible impact of either birth control pills, HRT or pregnancy (when E levels are very high) on small pituitary adenoma in women. Pregnancy has even shown to have a favorable effect on microadenomas with spontaneous remission ranging from 17-35% (Presse Med, 17 (1998), pp. 2117–2119) vs. 13-15% in those who have not undergone pregnancy. From J Clin Endocrinol Metab. 2007 Aug; 92( 8 ):2861-5.
"Changes in tumor vasculature resulting in pituitary necrosis, microinfarction, or hemorrhage have been suggested as potential mechanisms to explain how pregnancy might lead to normalization of prolactin (21)."
. Breastfeeding, despite higher than normal prolactin levels, has not been shown to cause or worsen prolactinomas.
. Arch Sex Behav. 1998 Oct;27(5):475-92. In this study, transsexual women were given high dose intramuscular E and some were on medium-high dose oral E. In spite of this, there was not one incidence of prolactinoma.
"we detected no prolactinoma as described by other authors (Asscheman et al., 1988, 1989; Kovacs et al., 1994; Gooren et al., 1980)."
. In my extensive search through incidences of prolactinoma in transsexual women, the only incidences reported were found to be in those women who took high doses of non bio-identical forms of estrogen orally (ethinyl estradiol, equine estrogens) most often with high doses of cyproterone acetate, OR a combination of estradiol enanthate and dihydroxyprogesterone acetophenide, all known to
abnormally elevate prolactin levels (in the last case due to progestogen component). Incidences in women taking bio-identical estradiol without the above mentioned agents taken simultaneously have NEVER been reported to date. Incidences in male to female transsexuals are also RARE, only 8 cases reported in the literature as of 2015 despite sometimes very high doses of estrogen taken during several decades. Studies to support.
. All of the above therefore suggests that high doses of non-bio-identical estrogens and/or some progestogens may be slight risk factors for prolactinoma but causation has yet to be established.
I urge you to ask endo to provide
studies (not statements made by an association) to support their assertions.
I'm POST-OP and on a high dose of intramuscular E. Supervised by three doctors who approve, one of whom is an author of a book on female hormones, another a trans-specialist endocrinologist from the University of Cambridge. My blood tests results show no change in clotting factors, or liver enzymes, or lipids, insulin, glucose, c-reactive protein. Nothing is out of range given my high levels of E2, which are in the range of 1,000-4,000 pg/ml. I've also been on high doses of oral bio-identical estradiol for several years. I started HRT in 2004.
I read from many other transwomen pre and post-op who have taken high doses E and their blood test results always came back normal. Most were above 40 yrs old.
