OK, I have a doctor that will prescribe HRT on an informed consent basis. This doctor has consulted with my primary care doctor and my cardiologist and both agree that I am old enough to make my decisions and they will not stand in the way. That said they are both concerned about the increased risk of stroke if I go on Estrogen. My primary care doctor was concerned enough that he had me come into his office and discuss this face to face. Read this as he was REALLY concerned.
This has scared the fool out of me. I have no data to assess if the benefit is worth the added risk. Is there some sort of peer reviewed literature that address this issue (specifically stroke) in a comprehensive matter? I know a lot has been said here about specifics of Estrogen therapy to minimize risks - the most repeated one is DVT. DVT might be fatal, a stroke is a lot more likely to be fatal. If anyone has citations for good references, I have acess to a full University library and I can get them.
I don't particularly want to remain male. However, I really do not want to die trying to do something about it. For the moment I am holding off on trying to start HRT. The one doctor suggested going dressed (I really don't pass by any means) to a local trans conference to get more of an idea of how far down the rabbit hole I might go. At the moment I am starting to get cold feet on even trying that. What if I like it? Would I then be willing to risk horrific complications? Would that even be sane?
Good ideas would be appreciated!
Erin - a.k.a. SCARED
People, even young healthy people, keel over and die all the time. Often without sign or warning. That is "life".
If you have a Dr.'s prescription for a hormone regimen, it is going to be within the accepted bounds for your weight and age. It is also very conservative, more so than you are going to want. It should prove to not increase your risk above your baseline potential for disease. You will also be recommended to do blood testing at regular intervals to see if anything is amiss.
To be aware of the reality of risks is one thing, to be paralyses by them is another...
Good luck whatever you decide to do.
This is the reason you get a prescription from a Doctor.
You and the Doctor work together to monitor your health. The Doctor will do blood work on you to monitor your body and how the hormones are affecting it.
Quote from: Sarah Louise on March 21, 2014, 03:52:26 PM
This is the reason you get a prescription from a Doctor.
You and the Doctor work together to monitor your health. The Doctor will do blood work on you to monitor your body and how the hormones are affecting it.
In the German Army when someone strongly disagrees with a direct order (s)he will agree to do as commanded with the words "zum Befehl" - literally "at your order." This may be taken as under strong protest. My Doctor, particularly my primary care Doctor, is taking this approach. Yes dosages will be low. Yes my levels of hormones and other critial things in my blood will be regularly monitored. However, reading my Doctor's body language he doesn't think this is a good idea at all. He is competent and thorough...
Is there a decent publication that will help me to assess risk in a quantitative manner?
I will go to the conference. Then I will see where I go from there.
Erin
I have not started hrt yet as I have not reached my weight goal. From what my doctor says its easier to lose weight before. I brought the same concerns to my doctor about health risks.
The advice given to me was that most forms of estrogen used are in fact VERY bad for your health. That being said, there are forms of estrogen that are in fact good for your health. They are called, not sure if I remember the correct word here but, bio-identical. This is what I will be taking, one to two months from now, when I start hrt.
Hope this helps.
To minimize the risk, don't take anything other than bioidentical hormones and avoid the pills. Patches, creams, gels and pellets are the way to go.
I take bioidentical E and P creams and I'm still here after over a year. ;)
Quote from: ErinWDK on March 21, 2014, 04:06:20 PMHowever, reading my Doctor's body language he doesn't think this is a good idea at all.
Few doctors appreciate when their recommendations and opinions aren't followed.
When push comes to shove, its your decision whether or not the benefits out weigh the risks.
For me the benefits won out, even with my diabetes, age and heart problems. After many years I'm still here.
BMJ. 2012 Oct 9;345:e6409. doi: 10.1136/bmj.e6409.
Effect of hormone replacement therapy on cardiovascular events in recently postmenopausal women: randomised trial.
Bio-identical estradiol was used in this study. With a progestin in women with a uterus.
"In this randomised trial including 1006 women we found a significantly decreased risk of the composite endpoint of death, heart failure, or myocardial infarction when hormone replacement therapy was started early in postmenopause. The beneficial effect occurred in the 10 years randomisation phase and was maintained for an additional six years of non-randomised follow-up. The trend for all components of the endpoint was in the same direction (figs 3 to 6) and this finding was not associated with an increased risk of cancer, stroke, deep vein thrombosis, or pulmonary embolism. Thus this study implies that hormone therapy started in recently menopausal women and continued for a prolonged duration does not increase or provoke adverse cardiovascular events such as mortality, stroke, heart failure, or myocardial infarction."
"For the subgroup of women who had undergone hysterectomy and who received unopposed 17-β-estradiol/control we found a significant reduction in the combined endpoint of mortality or breast cancer in the treatment group. This is in accordance with findings from the Women's Health Initiative, where 10 739 women who had undergone hysterectomy were randomised to conjugated equine oestrogen or placebo 0.625 mg/day; all women (irrespective of age) in the conjugated equine oestrogen arm experienced a reduced risk of breast cancer (hazard ratio 0.77, 95% confidence interval 0.62 to 0.95).35"
"This is the first randomised trial to study healthy women treated early in postmenopause with 17-β-estradiol and norethisterone acetate, and the only study with a 10 year randomised intervention. Additionally the women were followed for a further six years after discontinuation of randomised treatment. Our findings suggest that initiation of hormone replacement therapy in women early after menopause significantly reduces the risk of the combined endpoint of mortality, myocardial infarction, or heart failure. Importantly, early initiation and prolonged hormone replacement therapy did not result in an increased risk of breast cancer or stroke."
The following study from 1998 on 46 male-to-female transsexuals shows that treatment with bio-identical estradiol does not pose risks.
Arch Sex Behav. 1998 Oct;27(5):475-92.
A follow-up study for estimating the effectiveness of a cross-gender hormone substitution therapy on transsexual patients.
"This follow-up study was carried out to validate the effectiveness of cross-gender hormone therapy embedded in a multistep treatment concept for transsexual patients. This therapy described in detail by the authors elsewhere and presented briefly below provides cross-gender hormone substitution to obtain an assimilation of secondary sex characteristics to the desired sex as quickly as possible. Personal and social background data of 46 male-to-female (M-to-F) and 42 female-to-male (F-to-M) patients passing through different stages of the treatment concept were included. In the Endocrinological Outpatient Clinic of the Max-Planck-Institute/Munich the effectiveness of cross-gender hormone replacement therapy as well as frequency and distribution of side effects were examined by follow-up examination of endocrinological parameters. Cross-gender hormones were administered either parenterally or orally. Blood samples were collected routinely after 2 to 6 months depending on the duration of hormone substitution and complication rate. The incidence of hyperprolactinemia in estrogen-treated M-to-F transsexuals lies in the range of studies published before, whereas the number of patients developing galactorrhea is significantly lower in our patients. The incidence of thromboembolic events during the time of cross-gender hormone treatment in our patients is negligible. Changes in hematological parameters are observed under cross-gender hormone therapy. With the cross-gender hormone regimen performed by us it is possible to generate less side effects in the treatment of transsexual patients than described before."
From full study (I have access), the most common side-effect was high levels of prolactin (24, probably due to Androcur which is known to increase prolactin). There was NO incidence of deep-vein thrombosis or embolism. There was only 1 single case where blood clotting parameters were pathologically (abnormally) altered under high-dose estrogen (not specified how much or if oral vs injected). Hemoglobin (red blood cells) also decreased which is to be expected in 15 of them.
Interestingly, it is noted further in the study that "single case reports of breast cancers...have been reported", not in the study, but in the general literature, which is to say that breast cancer risk is very rare in transsexual women.
This other study also shows that treatment with bio-identical estradiol poses very little risk as compared to non-bioidentical.
Exp Clin Endocrinol Diabetes. 2005 Dec;113(10):586-92.
Endocrine treatment of male-to-female transsexuals using gonadotropin-releasing hormone agonist.
Dittrich R, Binder H, Cupisti S, Hoffmann I, Beckmann MW, Mueller A.
SourceDepartment of Obstetrics and Gynaecology, Erlangen University Hospital, Universitätsstrasse 21-23, 91054 Erlangen, Germany
"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. There was a significant decline in gonadotropins, total testosterone and calculated free testosterone. In general, the treatment regimen was well accepted. An equal increase in breast size was achieved compared to common hormone therapy. 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."
The only complications were seen in individuals with preexisting conditions or mutations.
A long-term follow-up study of mortality in transsexuals receiving treatment with cross-sex hormones
Eur J Endocrinol April 1, 2011 164 635-642
"The increased risk of cardiovascular mortality was observed only in those who were still using ethinyl estradiol. No increased risk was found in former users who had changed to other formulations and lower doses of estradiol."
"An increased risk of cardiovascular disease was also reported in women using oral contraceptives (OC), in particular if they used OC pills with a higher ethinyl estradiol content, even more so when they were smokers (21, 22, 23). The increased risk, however, disappeared after discontinuing OC use (24). In those MtF who had continued using ethinyl estradiol, subjects had used equally relatively high doses (...) up to advanced age, which could explain our finding of an increased rate of cardiovascular death."
"The total cancer mortality rate was not increased. The statistically significant increase in mortality rate of lung cancer may be related to heavier smoking in the transsexual population."
""The decreased mortality rate for colon cancer, also observed in the Women's Health Initiative (14), is similarly remarkable"
"We did not observe any cases of breast cancer in the population studied, neither in MtF nor in FtM, in agreement with the low prevalence of breast cancer in the literature."
From The TRANSSEXUAL PHENOMENON
Harry Benjamin, M.D. , 1966
"The fear of developing cancer through hormone treatments crops up from time to time, especially if there are irresponsible newspaper reports, for instance, of the results of someone's experiments with mice and rats to produce cancer artificially with estrogen. Such experiments admittedly have no bearing on the reactions of the human organism. Is the attempt to apply experiments with the cancer-susceptible mouse to the human area anything but ludicrous?" asked Dr. Robert A. Wilson, whose extensive work has thoroughly debunked the cancer fear of women receiving estrogen during their change of life.[5]
In my own clinical material of 152 male transsexuals, 141 of whom were treated with medium to fairly large doses of estrogen, some over several years, no incident of breast or any other cancer was observed. One may argue that these are mostly young men, less apt to develop a malignancy. The experiences of urologists, however, who treated elderly and old men with even much larger doses of estrogen for cancer of the prostate, must then be recalled. With the exception of one disputed case of breast cancer (it may have been a metastasis of the prostatic cancer) reported in the medical literature, no such incident was observed in hundreds if not thousands of cases. In a personal communication from Dr. Elmer Belt, one of the outstanding and most experienced urologists in the country, he said:
In regard to the taking of Stilbestrol as a cause for cancer of the breast, we have placed several hundred men on this material (I imagine if we were to search our records we would find the number to be in excess of two thousand) and in all of these cases we have not seen a single occurrence of cancer of the breast, although the dosages we used were of a very high level. "
"Finally, and to conclude the discussion of the nonsurgical therapy for transsexuals, it may be most interesting in future years to watch these patients who have received estrogen over a long period of time. Will they be less prone to develop coronary heart disease and other circulatory ailments that go with the process of aging? A wellknown cardiologist, noted for his research in cholesterol metabolism, who had occasion to see a number of transsexuals under estrogen therapy, remarked jokingly, "These people will probably live forever.""
Quote from: ErinWDK on March 21, 2014, 03:35:52 PM
OK, I have a doctor that will prescribe HRT on an informed consent basis. This doctor has consulted with my primary care doctor and my cardiologist and both agree that I am old enough to make my decisions and they will not stand in the way. That said they are both concerned about the increased risk of stroke if I go on Estrogen. My primary care doctor was concerned enough that he had me come into his office and discuss this face to face. Read this as he was REALLY concerned.
This has scared the fool out of me. I have no data to assess if the benefit is worth the added risk. Is there some sort of peer reviewed literature that address this issue (specifically stroke) in a comprehensive matter? I know a lot has been said here about specifics of Estrogen therapy to minimize risks - the most repeated one is DVT. DVT might be fatal, a stroke is a lot more likely to be fatal. If anyone has citations for good references, I have acess to a full University library and I can get them.
I don't particularly want to remain male. However, I really do not want to die trying to do something about it. For the moment I am holding off on trying to start HRT. The one doctor suggested going dressed (I really don't pass by any means) to a local trans conference to get more of an idea of how far down the rabbit hole I might go. At the moment I am starting to get cold feet on even trying that. What if I like it? Would I then be willing to risk horrific complications? Would that even be sane?
Good ideas would be appreciated!
Erin - a.k.a. SCARED
a lot of factors come into play here here.
what's your age?
do you smoke?
past medical history?
If you have a pretty clean bill of health and don't smoke, chance are he's just trying to talk you out of HRT. It happens.
Pharmacology of estrogens and progestogens: influence of different routes of administration, CLIMACTERIC 2005;8(Suppl 1):3–63
"In women with supraphysiological estradiol levels during treatment with implants, no adverse effects on lipid metabolism, but a reduction in LDL cholesterol and fasting insulin were observed150."
Aust N Z J Obstet Gynaecol. 1978 Aug;18(3):198-201.
The effect of oestradiol valerate therapy on coagulation factors and lipid and oestrogen levels in oöphorectomised women
"The effect of oestradiol valerate on levels of blood cholesterol, triglycerides, free oestradiol and coagulation factors, as well as on urinary oestrogens and free cortisol was measured in 10 oöphorectomised women. Despite the very high urinary oestrogen levles obtained, there was no significant change found in the other parameters during and after treatment."
J Sex Med. 2013 Dec;10(12):3129-34. doi: 10.1111/jsm.12319. Epub 2013 Sep 9.
Breast cancer development in transsexual subjects receiving cross-sex hormone treatment.
"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."
Am J Surg Pathol. 2000 Jan;24(1):74-80.
Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men.
"so far, only four cases of breast cancer in male-to-female transsexuals have been documented."
J Clin Endocrinol Metab. 2008 Jan;93(1):19-25. Epub 2007 Nov 6.
Long-term treatment of transsexuals with cross-sex hormones: extensive personal experience.
"There are two reports of M2F who developed breast carcinomas while receiving estrogen treatment (22, 23). Breast fibroadenomas in M2F receiving hormonal treatment have been observed. In our series of approximately 2200 M2F, cumulative over 30 yr, until recently, no single case of breast cancer had been observed, but there is now one case."
Quote from: JordanBlue on March 21, 2014, 04:58:28 PM
a lot of factors come into play here here.
what's your age?
do you smoke?
past medical history?
If you have a pretty clean bill of health and don't smoke, chance are he's just trying to talk you out of HRT. It happens.
I am 60 and will be 61 in a few weeks.
I have never smoked.
General heath is an issue, and will be taken account for in setting dosages.
Thanks for all the replies. I am starting to feel better about eventually going on HRT. I will go to the conference first to see how I do presenting as me to a (hopefully) friendly audience.
Erin
Tidsskr Nor Laegeforen 1993 Mar 10;113(7):833-5
Endocrine treatment of prostatic cancer. A renaissance for parenteral
estrogen.
"38 patients have been treated at Huddinge Hospital in Stockholm, and
14 patients at Aker Hospital in Oslo, with polyoestradiol phosphate
(Estradurin) (...) injected intramuscularly every 4th week"
"Plasma testosterone is reduced to castration level after 2-3 weeks. Liver
function, evaluated by the sexual hormone binding globulin level in
plasma, remains unchanged. Morbidity and mortality from cancer are
the same as may be achieved by surgical orchidectomy. The only side
effect of significance is gynaecomastia. Follow-up of the patients
does not indicate any increased risk of thrombosis or cardiovascular
disease."
Prostate 1991;18(2):131-7
Cardiovascular and all-cause mortality in prostatic cancer patients treated
with estrogens or orchiectomy as compared to the standard population.
"Four hundred and seventy-seven prospectively randomized patients with
prostatic carcinoma were treated with a combination of intramuscular
polyestradiol phosphate (PEP) and oral ethinyl estradiol, with
intramuscular PEP alone, or with orchiectomy. The cardiovascular and
all-cause mortality of the two estrogen therapy modalities and
orchiectomy were compared with those of the Finnish male population
in general. The age-standardized rate ratios (approximately relative
risk) for cardiovascular mortality and for all-cause mortality were
1.51 and 2.31 in the combination estrogen therapy group, 0.17 and
1.50 in the PEP monotherapy group, and 0.78 and 1.78 in the
orchiectomy group, respectively. Further mortality rates by cause for
all three treatment groups were standardized for age using the
age-specific person-years at risk as standard. Age-standardized
mortality from cardiovascular diseases was very low in the PEP group,
as compared to other treatment modalities, and the mortality rates
for prostatic cancer were about equal in all three treatment groups.
It is concluded that intramuscular PEP monotherapy is associated with
low cardiovascular mortality and with an all-cause and prostatic
cancer mortality equal to orchiectomy."
Int J Technol Assess Health Care 1991;7(2):220-5
Cost comparison of parenteral estrogen and conventional hormonal treatment
in patients with prostatic cancer.
"The present study compares the cost of antitumor therapy and adverse
cardiovascular effects during the first year of treatment with oral
estrogens, nonoral estrogens, or surgical castration in patients with
prostatic cancer."
"Twenty-five percent of the patients treated with
oral estrogen suffered cardiovascular complications, compared to none
of the patients treated by orchidectomy or nonoral estrogens."
Prostate 1989;14(4):389-95
Estrogen therapy and liver function--metabolic effects of oral and parenteral
administration.
"Oral estrogen therapy for prostatic cancer is clinically effective
but also accompanied by severe cardiovascular side effects.
Hypertension, venous thromboembolism, and other cardiovascular
disorders are associated with alterations in liver metabolism. The
impact of exogenous estrogens on the liver is dependent on the route
of administration and the type and dose of estrogen. Oral
administration of synthetic estrogens has profound effects on
liver-derived plasma proteins, coagulation factors, lipoproteins, and
triglycerides, whereas parenteral administration of native estradiol
has very little influence on these aspects of liver function."
Prostate 1988;13(3):257-61
Cardiovascular follow-up of patients with prostatic cancer treated with
single-drug polyestradiol phosphate.
"Thirty-eight patients with cancer of the prostate were treated with
strict parenteral estrogen in the form of monthly polyestradiol
phosphate injections(...)in this nonrandomized study.
In contrast to studies with oral estrogens,
there have been no cardiovascular complications at a mean follow-up
of 12.9 +/- 0.7 months (SEM). Twenty-nine of the 38 patients (76%)
have responded to therapy."
Oral estrogens for prostate cancer always include non bio-identical forms such as ethinyl estradiol and diethylbestrol (DES). These affect liver, clotting to a much greater extent than bio-identical estradiol.
Cancer. 2005 Feb 15;103(4):717-23.
Phase II study of transdermal estradiol in androgen-independent
prostate carcinoma
"Oral estrogen therapy has activity in patients with
hormone-naive and androgen-independent prostate carcinoma (AIPC), but
its utility is limited by the associated risk of thromboembolic
toxicity. Parenteral administration may be safer as it avoids "first
pass" liver exposure to estrogen. The authors tested the safety and
efficacy of transdermal estradiol (TDE), as well as the effect of
therapy on hot flashes, sex hormones, the procoagulant cascade, and
bone turnover in patients with AIPC."
"In patients with APIC, TDE was well tolerated and produced a modest
response rate, but was not associated with thromboembolic
complications or clinically important changes in several coagulation
factors."
J Urol. 2003 May;169(5):1735-7.
Transdermal estradiol therapy for advanced prostate cancer--forward
to the past?
"A total of 20 patients with advanced prostate cancer were
enrolled in a before and after study
that examined the impact of estradiol patches on hormones, disease,
thrombophilia, vascular flow, osteoporosis and quality of life.
RESULTS: Median followup is 15 months. Estradiol levels greater than
1,000 pmol./l. were achieved (...) and higher levels were
obtained by increasing the number of patches. All patients achieved
castrate levels of testosterone within 3 weeks and had biochemical
evidence of disease regression. One patient died of disease at 14
months and 1 cardiovascular complication occurred. Thrombophilic
activation was avoided and vascular flow improved. Bone mineral
density was significantly increased. Mild or moderate gynecomastia
occurred in 80% of patients but no patient had hot flushes. All other
functional and symptomatic quality of life domains improved."
J Urol. 2005 Aug;174(2):527-33; discussion 532-3.
Transdermal estradiol therapy for prostate cancer reduces
thrombophilic activation and protects against thromboembolism.
"A total of 20 patients with newly diagnosed locally advanced or metastatic
prostate cancer were treated using transdermal estradiol patches and
the coagulation profile was assessed before and during 12 months
therapy."
"Levels of VIIa and XIIa were unaffected by transdermal estradiol therapy.
Although levels of TAT III were
increased in some patients at 12 months, the increase was markedly
less than that observed historically with equivalent doses of oral
estrogens. Levels of the inhibitory and fibrinolytic factors
including protein C, protein S, APC-R, TPA and PAI-1 remained stable.
Reductions in F1+F2, fibrinogen and D-Dimer levels represented a
normalization from increased levels to the physiological range."
"These results suggest that transdermal estradiol reduces
thrombophilic activation in men with advanced prostate cancer, and
protects against the risk of thrombosis."
In the studies involving use of transdermal estradiol, the dose given was much above what is typically prescribed to transsexual women.
In the studies involving use of injectable estradiol, estradiol levels typically reach...
Prostate. 1989;14(2):183-8.
Single-drug parenteral estrogen treatment in prostatic cancer: a study of two maintenance-dose regimens.
"Treatment of 17 patients with prostatic cancer with (...) polyestradiol phosphate (PEP) as intramuscular injections every fourth week suppressed serum testosterone (T) values to orchidectomy levels within 1 month, and serum estradiol-17 beta (E2) rose to a mean level of 2,456 pmol/liter after 6 months."
And yet, no signs of increased cardiovascular toxicity, no increased risks of thrombosis. In men, with a cancer, at an advanced age.
According to CLIMACTERIC 2005;8(Suppl 1):3–63
Ethinyl Estradiol suppresses FSH 120 times stronger than bio-identical estradiol. Remember that number. 120
Then, according to this study
Am J Obstet Gynecol. 1982 Nov 1;144(5):511-8.
"The synthetic estrogens, diethylstilbestrol and ethinyl estradiol, were relatively more potent on a weight basis for every response and produced the most marked response (fourfold to eighteenfold in excess of their FSH suppression) for the hepatic parameters."
Which means that hepatic (liver) parameters such as clotting factors are affected 4-18 x in excess of the effect they have on FSH.
Therefore, if ethinyl estradiol affects FSH 120 times stronger than bio-identical estradiol and if hepatic parameters are affected 4-18x in excess of FSH effect, this means that ethinyl estradiol affects liver 120 times 4-18x stronger than bio-identical estradiol, in other words, 480-2160 x.
Now, consider that doctors quite easily prescribe birth control pills containing ethinyl estradiol to thousands of millions of women worldwide. Consider that the risk on them is...
The Risks of Oral Contraceptive Pills
Semin Reprod Med. 2001;19(4)
"Given a risk of 1 per 10,000 of VTE in the general population, [23] the estimated attributable risk of oral contraceptives currently used in the United States would be 3 per 10,000."
And that these birth control pills have a much larger effect on coagulation/liver than what we typically take orally.
All this being said, one concludes that DVT risk is quite low on bio-identical estradiol.
This study on transsexuals even remarked...
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.
"CPA-only, td-E(2)+CPA, or oral-E(2)+CPA treatment produced rather small effects on hemostatic variables, whereas oral EE treatment resulted in a large increase in APC resistance from 1.2 +/- 0.8 to 4.1 +/- 1 (P < 0.001), a moderate increase in plasma protein C (9%; P = 0.012), and a large decrease in both total and free plasma protein S (30%; P < 0.005). 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)."
"Treatment with CPA-only caused mild APC resistance."
"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."
CPA is cyproterone acetate (Androcur). td E (2) is transdermal estradiol (Estraderm TTS). oral E (2) is oral estradiol valerate (Progynova). EE is ethinyl estradiol.
Also, from
J Clin Endocrinol Metab. 2012 Dec;97(12):4422-8. doi: 10.1210/jc.2012-2030. Epub 2012 Oct 9.
Predictive Markers for Mammoplasty and a Comparison of Side Effect Profiles in Transwomen Taking Various Hormonal Regimens
"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"
"Thromboembolism occurred in 1.2% of individuals,
with a statistically significant increase in the incidence of
thromboembolism in those treated with CEE"
CEE is conjugated equine estrogens, not bio-identical.
"Finally, the important safety finding that the incidence
of thromboembolism is 8 times more common with CEE"
I'm 69 and still going strong, hormones and all.
And finally...
Genetic women have estradiol (the same estradiol we take, bio-identical) coursing through their bodies, for at least 30 years, at levels ranging from 20 to 540 pg/ml (some sources indicate as much as 649 pg/ml) every month, during their menstrual cycle
Am J Med. 1995 Aug;99(2):119-22.
Estrogen acutely increases peripheral blood flow in postmenopausal women.
"normal postmenopausal plasma concentration less than 200 pmol/L (less than 54 pg/ml); normal premenopausal physiologic ranges: luteal 368 to 1,100 pmol/L (100 – 300 pg/ml), midcycle 785 to 1,840 pmol/L (214 – 501 pg/ml), follicular 74 to 368 pmol/L (20 – 100 pg/ml) for estradiol"
Maturitas. 2005 Apr 11;50(4):266-74.
Acute administration of 17beta-estradiol improves endothelium-dependent vasodilation in postmenopausal women.
"Normal concentrations obtained via a fluorometric method, vary with the phase of the woman's menstrual cycle. During the follicular phase, they range from 35 to 184 pg/mL; during the ovulatory phase, from 191 to 540 pg/mL; and during the luteal phase, from 40 to 228 pg/mL; at menopause, the 17β-estradiol level decreases to about 35 pg/mL. »
And at levels ranging from 1,000 to up to 75,000 pg/ml during pregnancy, which some women go through several times during their lifetime...http://cebp.aacrjournals.org/cgi/content-nw/full/12/5/452/T1
and yet, women are no more at an increased risk of dying from health complications versus men. In fact, women are less likely to be affected by coronary heart disease than men due to estradiol's cardioprotective effects
Volume 15 Suppl 38, 1983, Pages 1-121
Blood pressure and hemodynamics in postmenopausal women during estradiol-17 beta substitution.
"Estradiol-17 beta substitution decreased the systolic and diastolic blood pressure in normotensive, hypertensive and borderline hypertensive postmenopausal women."
"Irrespective of the pretreatment blood pressure levels, heart rate decreased during estradiol-17 beta substitution"
"Estradiol-17 beta substitution caused an increase in the blood volume in all groups of postmenopausal women"
"Cardiac output increased in the normotensive test subjects but decreased in the hypertensive and borderline hypertensive subjects"
J Am Osteopath Assoc. 2011 Mar;111(3):153-64.
Bioidentical hormones: an evidence-based review for primary care providers.
"17β-Estradiol is FDA approved for menopausal symptoms, may have cardioprotective effects, and may have fewer adverse effects on blood pressure than conjugated equine estrogens."
"Bioidentical hormones that are approved by the FDA may be preferred over standard hormone replacement because of their physiologic benefits and safety profile."
Volume 64, Number 1
OBSTETRICAL AND GYNECOLOGICAL SURVEY
Copyright © 2009
by Lippincott Williams & Wilkins
Physiological Changes Associated with the Menstrual Cycle
A Review
"Peripheral vascular resistance is negatively correlated with circulating levels of estradiol, indicating that estradiol may exert a protective influence by alterations of peripheral microvasculature (46)."
Quote from: ErinWDK on March 21, 2014, 05:06:18 PM
I am 60 and will be 61 in a few weeks.
I have never smoked.
General heath is an issue, and will be taken account for in setting dosages.
Thanks for all the replies. I am starting to feel better about eventually going on HRT. I will go to the conference first to see how I do presenting as me to a (hopefully) friendly audience.
Erin
DVT is not a huge risk on HRT if you don't smoke. I'm 59 and certainly not in perfect health. I'm on week 10 of HRT with no problems.
Well, I have actually HAD a stroke before. I discussed what happened with my endo and what they found and what treatment I was on to keep me from having another one. That was good enough from him and I'm on the full tilt boogie strength of HRT now. The last I checked I'm still alive :)
The difficult choice doctors must make in recommending any treatment protocol is whether the benefits outweigh the risks for the individual patient. What may be lifesaving for one person may lead to the death of another. We rely on our doctor's experience and objective third party opinion to weigh the pros & cons to decide what is in each of our best interest. The males in my family have an extremely HIGH risk of heart attack. My OBGYN explained that for me, the small risk associated with estrogen hormone therapy would be more than outweighed by the huge DECREASE in risk women experience compared to men BECAUSE of estrogen.
I am 53, have been on a full transition level estrogen regimen for 4+ years. I lost 2 cousins in their 40's due to heart problems, 2 other under doctors care for problems in their 50's. At 5'10" 146 pounds, I am healthy as a horse half my age. It seems that for me, my doctor made a very good call on the best interest of his patient.
Steroids. 2003 Nov;68(10-13):831-6.
In vitro effects of progesterone and progestins on vascular cells.
"In addition to the regulation of vascular tone, sex steroids have been shown to be tightly involved in the regulation of the atherosclerotic process [4] and [15]. Indeed, animal studies with ovariectomized Cynomolgus monkeys consistently indicate that ovarian ablation is associated with accelerated atherosclerosis, and that administration of hormonal replacement prevents this process, particularly if started in healthy monkeys early after surgical menopause [31] and [32]."
Hence, lack of estrogen increases atherosclerosis. Addition of estrogen prevents it.
Quote from: Virginia on March 22, 2014, 08:49:54 AM
for me, the small risk associated with estrogen hormone therapy
What is the small risk?
Quote from: KayXo on March 22, 2014, 09:49:06 AM
What is the small risk?
I have had three doctors talk to my head saying there is a risk. I have also had the same three doctors agree to go forward with HRT as long as I understand there is a risk and still want to go forward. This becomes a matter of balancing risk. What I am doing now to get estrogen into a normal female range is carry around enough fat cells to aromatize T into E. This has a LOT of risk all on its own.
I am going to do what the doctor who would do the actual prescribing suggested. Go to a (sort of) local trans conference and present as me. She did say this would take a LOT of chutzpah, and I agree. I am pre-everything so I do not pass by a very large margin. To a certain extent I remind people of a large, round, furry animal with tusks and a moustache. But I will see what happens. This may be make or break - so I will see if there is any way to make it work. The group putting this on makes a point to accept everyone.
Once this works then she will start me on a little bit of Spiro and check hormone levels after they stabilize. At that point I may, or may not, still have enough E. If it is not enough we will start a very low dose of E in a gel or cream.
So, thanks everyone for getting me over the tough decision part.
Onward! VERY slowly...
Erin
I wonder if there is any difference in a possible nasty "stroke" whether E is taken oral or from the use of skin patches?
I'm in my mid 50's & use dot patches for E to lower any possible problems from kidneys.
I'm in very good shape, feel great, no health problem issues whatsoever.
Thanks for any advise.
I will throw my 2 cents in. I am 64 started HRT on 12/25/2013 my Christmas present to me.I feel great!! Started with a pretty high dose of spiro and the patch--- sometimes two. Anyway 6'2" 172 lbs very active. Life is good and Francis you should go fishing with us.! One more thing I have HEP C and have since 1969 when I went into the service. Pat
Quote from: ErinWDK on March 22, 2014, 04:48:06 PM
I have had three doctors talk to my head saying there is a risk.
What is the risk? Did they actually tell you what the risks where?
Quote from: ErinWDK on March 22, 2014, 04:48:06 PMWhat I am doing now to get estrogen into a normal female range is carry around enough fat cells to aromatize T into E. This has a LOT of risk all on its own. (...) Once this works then she will start me on a little bit of Spiro and check hormone levels after they stabilize
Taking estrogen is safer than gaining weight and hoping to increase E that way. The female range is quite large, going from as little as 20 to as much as 650 during the menstrual cycle and your levels are already probably in female range!
The slight increase in E from adding fat will probably do nothing to feminize and would only increase the risks associated with being overweight and eating unhealthily to increase weight.
It just makes no sense. E is not toxic (and in fact, quite beneficial), women have it all their lives, in quite high amounts at certain times of their lives and last I checked, the world is still full of women and babies and the world population is greater now than it ever has been!
If anything, Spiro can cause more complications than E as it deregulates electrolyte balance, strongly affects blood pressure and heart rate.
Quote from: FrancisAnn on March 22, 2014, 07:38:16 PM
I wonder if there is any difference in a possible nasty "stroke" whether E is taken oral or from the use of skin patches?
I'm in my mid 50's & use dot patches for E to lower any possible problems from kidneys.
The increase in stroke and cardiovascular problems was found with oral ethinyl estradiol and other oral forms not bio-identical while in the large WHI (Womens' Health Initiative) study of 2003, complications were only found in those women taking Provera (medroxyprogesterone acetate) with oral estrogen, not in those taking oral estrogen (CEE, conjugated equine estrogen) alone (no uterus).
The large Danish study found a decreased risk of cardiovascular complications (and lower death rate) in those women treated with oral bio-identical estrogen and no increase in stroke incidence.
Larger doses of bio-identical estrogen taken orally have been studied in transsexual populations with no increased incidence of cardiovascular or thromboembolic complications.
So far, so good. :) I think the key is to stick to bio-identical estradiol. Kidneys are not affected by estrogen.
Quote from: KayXo on March 23, 2014, 08:25:08 PM
What is the risk? Did they actually tell you what the risks where?
The main risk mentioned was stroke. This is based on statistics that women are more likely to have strokes than men. My primary care doctor did note that taking one baby aspirin a day helps women partially reduce their stroke risk. I am on the aspirin regimen, so that helps.
Quote from: KayXo on March 23, 2014, 08:25:08 PM
If anything, Spiro can cause more complications than E as it deregulates electrolyte balance, strongly affects blood pressure and heart rate.
My primary care doctor was very concerned about a different risk from Spiro that I didn't really understand. He needed to get the full report on my latest echo cardiogram from my cardiologist before he was willling to agree with Spiro.
This is not easy, and does require a doctor (or doctors) to sort it out and make HRT work.
My total E (E1 and E2 combined) was 214 pg/ml at last check. That is well into female range. The very high E level women have during pregnancy is from E3 which is the weakest form of Estrogen. Nature does have a way of making things work.
My doctors are NOT agreeing that generic Estradiol is safer than other forms. This can be argued, but the medical professionals I have a relationship with are not going to go there. This means any dosage of E I get will be really low. I will live with that. This may limit any transition I can make to just becoming more androgynous. I will live with that as well. The key here being I want to live.
Maybe after I get started on HRT and things go well (a big IF as far as my doctors are concerned) the dosage of E can be raised to something approaching a transition level. This is going to be a SLOW start.
Erin
Quote from: ErinWDK on March 24, 2014, 10:23:21 AM
The main risk mentioned was stroke. This is based on statistics that women are more likely to have strokes than men.
Women usually have strokes at an advanced age,
when their estrogen levels are LOW! And as far as I know, women usually live longer than men. Furthermore, I have shown you evidence above indicating that stroke risk was not increased in women taking estrogen and that estrogen actually appeared to reduce cardiovascular incidences.
http://cardiovascres.oxfordjournals.org/content/69/4/777.full
"There is an
abundance of scientific evidence for the protective effect of estrogen against atherosclerosis, such as short-term vasodilating effects as well as long-term vascular protective and anti-atherosclerotic effects [2]. Epidemiological evidence shows that pre-menopausal women have a reduced risk for mortality from cardiovascular diseases [3] and that women are at a lower risk for the development of heart failure [4] and have enhanced cognitive function and reduced neurodegeneration associated with Alzheimer's disease and stroke [5]. Further proof for the protective effect of female gender is the fact that post-menopausal women have a similar or even increased risk for cardiovascular disease compared to men [3] and have an increased risk for adverse outcome after myocardial infarction and acute coronary syndromes, despite similar treatment with thrombolysis and percutaneous interventions [6]. It was therefore postulated that estrogen replacement would be beneficial in preventing cardiovascular diseases in post-menopausal females."
"The cardioprotective effect of estrogen is further supported by the findings that ovariectomy caused a loss of cardioprotection, which was regained by chronic estrogen replacement therapy."
"The vascular protective effects of estrogen and their mechanisms are thus fairly well-established."
The increase in cardiovascular incidences in the Heart and Estrogen/Progestin Replacement Study (HERS) and the WHI (Womens's Health Initiative) study was due to the progestin as no such results were found in women only taking estrogen.
Steroids. 2003 Nov;68(10-13):831-6.
In vitro effects of progesterone and progestins on vascular cells."These pharmacological differences between progestins
are particularly relevant, in light of the first results of the
Women's Health Initiative (WHI) trial [7]. This is a randomized controlled
primary prevention trial, in which 16,608 postmenopausal women
aged 50–79 years with an intact uterus received
conjugated equine estrogens (CEE), plus MPA, or placebo.
The primary outcomes were nonfatal myocardial infarction and coronary
heart disease (CHD) death, with invasive breast cancer as
the primary adverse outcome. While the planned duration of
the treatment was 8.5 years, the CEE+MPA treatment arm
was stopped prematurely after 5.2 years, due to apparent increases
in cardiovascular events and breast cancer incidence
[7].
The evaluation of the CEE-alone treatment arm (women
without a uterus) is still ongoing, due to the absence of such
apparent increases in hazard. This is strongly suggestive
of a potentially harmful effect of the progestin used in the
study (MPA)."
CEE= conjugated equine estrogens
MPA= medroxyprogesterone acetate
Quote from: ErinWDK on March 24, 2014, 10:23:21 AMMy primary care doctor did note that taking one baby aspirin a day helps women partially reduce their stroke risk. I am on the aspirin regimen, so that helps.
Taking an Aspirin can cause ulcers over time. Estrogen is cardioprotective and if you are not genetically predisposed to heart problems (personal or family history), there is no reason to take Aspirin. It might do you more harm than good.
Quote from: ErinWDK on March 24, 2014, 10:23:21 AMThe very high E level women have during pregnancy is from E3 which is the weakest form of Estrogen.
From http://cebp.aacrjournals.org/cgi/content-nw/full/12/5/452/T1
These levels were obtained just before labor/delivery, at the end of pregnancy which lasted on average, 38 weeks.
Mean estradiol levels (E2): 24,000 pg/ml, Range: from 800-75,000 pg/ml
Mean estrone levels (E1): 9,000 pg/ml, Range: from 600-61,000 pg/ml
Mean estriol levels (E3): 18,000 pg/ml, Range: 1,100-34,000 pg/ml
As you can see, the levels of all three estrogens are quite high, the mean levels of estradiol (the strongest estrogen) being the highest of the three, then estriol, then estrone. The range is highest for estradiol (the strongest estrogen), then estrone, then estriol (E3).
Quote from: ErinWDK on March 24, 2014, 10:23:21 AMNature does have a way of making things work.
What do you mean? Male prostate cancer patients were treated with bio-identical estrogen parenterally. Their estradiol levels on average were between 500-700 pg/ml and yet no cardiovascular or thromboembolic complications arose. I have pointed out these studies several times on here.
Quote from: ErinWDK on March 24, 2014, 10:23:21 AMMy doctors are NOT agreeing that generic Estradiol is safer than other forms.
And yet study after study show that bio-identical estradiol is safer than other forms, as it affects liver and clotting to a much lesser extent. The literature on it is quite vast and quite unequivocal. I have provided some of the evidence but there is much more.
Am J Obstet Gynecol. 1982 Nov 1;144(5):511-8.
Comparison of pharmacodynamic properties of various estrogen formulations."On a weight basis, piperazine estrone sulfate and micronized estradiol were equipotent for all responses. Conjugated estrogens suppressed FSH in a fashion equipotent to that of the other nonsynthetic estrogens; however, for all three hepatic parameters, the response was exaggerated twofold to threefold. The synthetic estrogens, diethylstilbestrol and ethinyl estradiol, were relatively more potent on a weight basis for every response and produced the most marked response (fourfold to eighteenfold in excess of their FSH suppression) for the hepatic parameters."
CLIMACTERIC 2005;8(Suppl 1):3–63
Pharmacology of estrogens and progestogens: influence of different routes of administration"EE is much more active than the natural estrogens,
because the 17a-ethinyl group prevents the oxidation
of the 17b-hydroxy group and is able – after
the oxidative formation of a very reactive intermediate
– to inhibit irreversibly cytochrome P450
enzymes, which are involved in the metabolism of
steroids. The potency of conjugated equine estrogens
(CEE) is considerably higher than that of
estradiol, particularly concerning the effect on the
hepatic production of certain serum parameters,
e.g. SHBG, corticosteroid-binding globulin
(CBG), thyroxine-binding globulin (TBG) and
angiotensinogen (Table 3)12–14."
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."
JAMA Intern Med. 2014 Jan 1;174(1):25-31. doi: 10.1001/jamainternmed.2013.11074.
Lower risk of cardiovascular events in postmenopausal women taking oral estradiol compared with oral conjugated equine estrogens."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."
J Am Osteopath Assoc. 2011 Mar;111(3):153-64.
Bioidentical hormones: an evidence-based review for primary care providers"Randomized clinical trial data are sufficient to support the prescription of only estropipate, estradiol, and progesterone for the relief of menopausal symptoms. Estropipate is approved by the FDA for the management of menopausal symptoms. 17β-Estradiol is FDA approved for menopausal symptoms, may have cardioprotective effects, and may have fewer adverse effects on blood pressure than conjugated equine estrogens."
"Bioidentical hormones that are approved by the FDA may be preferred over standard hormone replacement because of their physiologic benefits and safety profile."
Quote from: ErinWDK on March 24, 2014, 10:23:21 AMThis can be argued, but the medical professionals I have a relationship with are not going to go there.
It cannot be argued. The difference in effect and risk has been shown between different estrogens. This is fact, not theory.
Quote from: KayXo on March 24, 2014, 03:15:24 PM
And yet study after study show that bio-identical estradiol is safer than other forms, as it affects liver and clotting to a much lesser extent. The literature on it is quite vast and quite unequivocal. I have provided some of the evidence but there is much more.
Am J Obstet Gynecol. 1982 Nov 1;144(5):511-8.
Comparison of pharmacodynamic properties of various estrogen formulations.
"On a weight basis, piperazine estrone sulfate and micronized estradiol were equipotent for all responses. Conjugated estrogens suppressed FSH in a fashion equipotent to that of the other nonsynthetic estrogens; however, for all three hepatic parameters, the response was exaggerated twofold to threefold. The synthetic estrogens, diethylstilbestrol and ethinyl estradiol, were relatively more potent on a weight basis for every response and produced the most marked response (fourfold to eighteenfold in excess of their FSH suppression) for the hepatic parameters."
CLIMACTERIC 2005;8(Suppl 1):3–63
Pharmacology of estrogens and progestogens: influence of different routes of administration
"EE is much more active than the natural estrogens,
because the 17a-ethinyl group prevents the oxidation
of the 17b-hydroxy group and is able – after
the oxidative formation of a very reactive intermediate
– to inhibit irreversibly cytochrome P450
enzymes, which are involved in the metabolism of
steroids. The potency of conjugated equine estrogens
(CEE) is considerably higher than that of
estradiol, particularly concerning the effect on the
hepatic production of certain serum parameters,
e.g. SHBG, corticosteroid-binding globulin
(CBG), thyroxine-binding globulin (TBG) and
angiotensinogen (Table 3)12–14."
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."
JAMA Intern Med. 2014 Jan 1;174(1):25-31. doi: 10.1001/jamainternmed.2013.11074.
Lower risk of cardiovascular events in postmenopausal women taking oral estradiol compared with oral conjugated equine estrogens.
"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."
J Am Osteopath Assoc. 2011 Mar;111(3):153-64.
Bioidentical hormones: an evidence-based review for primary care providers
"Randomized clinical trial data are sufficient to support the prescription of only estropipate, estradiol, and progesterone for the relief of menopausal symptoms. Estropipate is approved by the FDA for the management of menopausal symptoms. 17β-Estradiol is FDA approved for menopausal symptoms, may have cardioprotective effects, and may have fewer adverse effects on blood pressure than conjugated equine estrogens."
"Bioidentical hormones that are approved by the FDA may be preferred over standard hormone replacement because of their physiologic benefits and safety profile."
It cannot be argued. The difference in effect and risk has been shown between different estrogens. This is fact, not theory.
We sort of come to the bottom line. There are different points of view on this, and the one my doctor has is different. I am not going to argue with my doctor. He will go along with me going on Estrogen - a rather low dose to start - so I will follow his instructions. The actual Estrogen in question will be the "bioidentical."
Biochem Pharmacol. 2013 Dec 15;86(12):1627-42.
Estrogen, vascular estrogen receptor and hormone therapy in postmenopausal vascular disease.
"Cardiovascular disease (CVD), such as coronary heart disease (CHD) and hypertension, is less common in premenopausal women (Pre-MW) than in men of the same age, suggesting vascular benefits of estrogen [1,2]. Also, the risk of CVD increases with age in postmenopausal women (Post-MW) compared with Pre MW, partly due to decreased plasma estrogen levels. Estrogen is the predominant sex hormone in women, affecting the development and function of the female reproductive system. Estrogen is commonly used as a contraceptive, and as a component of menopausal hormone therapy (MHT) for hot flushes, night sweats and vaginal dryness [3]. Earlier observational studies, such as the Nurses' Health Study (NHS) in the mid 1970s, suggested that estrogen therapy in Post-MW reduced the risk of CVD by 35% to 50% [1]. Also, a meta-analysis of observational studies showed 33% reduction in fatal CVD among MHT users compared with nonusers [3]. Experimental studies supported vascular benefits of estrogen. Acute administration of estrogen in female or male patients improves vasodilator responses and ameliorates myocardial ischemia [4]. Also, acute administration of estrogen in dogs and isolated rat and rabbit hearts lowers coronary vascular resistance and enhances coronary blood flow [5]. Estrogen modulates vascular function by targeting estrogen receptor (ER) in endothelial cells (ECs) and vascular smooth muscle (VSM) [1,2]. Estrogen also enhances the release of vasodilator substances such as nitric oxide (NO) and prostacyclin (PGI2), and decreases the production and effects of vasoconstrictors such as endothelin (ET-1) and angiotensin II (AngII) [1,2]."
Thanks to all on this post. I feel great on my level of E, S & Fin. so I'll try to just enjoy life. Have fun girl friends.
It seems there's been plenty of studies on how HRT might effect the chances of stroke or heart related issues, but seems like there aren't many studies that look at those chances if HRT wasn't implemented, i.e., if you didn't take hormones you might have the same risk of something anyway.
Quote from: teeg on April 02, 2014, 08:15:10 AM
It seems there's been plenty of studies on how HRT might effect the chances of stroke or heart related issues, but seems like there aren't many studies that look at those chances if HRT wasn't implemented, i.e., if you didn't take hormones you might have the same risk of something anyway.
An impossible study in humans.
To summarise the latest research studies at the WPATH conference. Ethyl estradiol is a risk for women over 40 who are obese. Contraindications also include smoking.
Women have an increase incidence of breast cancer and it is linked to BRACA1/2 genes as it is in natal females.
The answers, be healthy, a good diet and a good life style and don't worry about it. And do what your medic says.
For men T has very little if any risk.
Cohort sizes >2000
Quote from: teeg on April 02, 2014, 08:15:10 AM
It seems there's been plenty of studies on how HRT might effect the chances of stroke or heart related issues, but seems like there aren't many studies that look at those chances if HRT wasn't implemented, i.e., if you didn't take hormones you might have the same risk of something anyway.
The real risk of not taking HRT is the GID getting so bad that you harm yourself. This is the main reason that the Standards of Care have been updated to ease access to HRT.
Quote from: Cindy on April 02, 2014, 08:28:32 AM
An impossible study in humans.
To summarise the latest research studies at the WPATH conference. Ethyl estradiol is a risk for women over 40 who are obese. Contraindications also include smoking.
Women have an increase incidence of breast cancer and it is linked to BRACA1/2 genes as it is in natal females.
The answers, be healthy, a good diet and a good life style and don't worry about it. And do what your medic says.
For men T has very little if any risk.
Cohort sizes >2000
I will agree with most of what you say. For men T can do a bunch of nasty things; for me it did the following:
1) Destroyed my diabetes control - HbA1C went over 8% regardless how I tried to deal with it.
2) Set my sleep apnea off so that I just plain didn't get any rest (main reason I started phased retirement)
3) Made me retain water like a cistern
4) Ruined my breathing so I couldn't walk a quarter mile, and if I tried my heart rate went out the roof
5) Cranked up my blood pressure
6) Made me even more cranky and mean
7) Set off my GID so badly I am now becoming Erin
All but item 7 are known and accepted "side effects" of T in men. There is now a class action law suit being organized for men who were prescribed T and developed serious heart complications.
All of these hormonal treatments have risks. The reason my doctors are being SO cautious with E is that T did so badly for me. The GID got so bad I have little option but to try E.
Erin
Sorry I didn't explain well, the study was looking at cancer and heart disease.
Quote from: ErinWDK on April 02, 2014, 08:31:24 AM
The real risk of not taking HRT is the GID getting so bad that you harm yourself. This is the main reason that the Standards of Care have been updated to ease access to HRT.
That's certainly one way to put it. Personally I don't think there's much risk at all with anything related to transition - be it HRT, etc. There's risk in everything and you can look at it under a microscope as much as your heart desires.
I can't recall if it was my SRS surgeon, PCP, or Endo who suggested I take, "baby aspirin", and if I actually needed it or if it was simply a suggestion, but I've been just as healthy pre-HRT (with frequent checkups and level checks) as post-HRT.
There are enough studies that show that patches and bioidentical are preferable. Patches don't significantly increase chances of clotting where as tablets do.
Also a recent study of mtf transsexuals involving over a thousand analysed mortality compared to general population and for delay it was raised by 0.51 due to four key factors; in order : suicide, AIDS, drug abuse, cardiovascular disease.
This is why careful counselling, care of yourself and bioidentical hrt with patches and micronised progesterone are the way forward.
I don't think HRT will do you any harm, the problem i think is with the Anti androgen you will have to take in, that's why "Teeg" was suggested to take baby aspirin as that makes the blood thinner and the anti androgen makes it thicker.
Thicker blood means your heart will have to work more, meaning risk for a stoke!
But beware if your blood gets to thin then you could have a cerebral hemorrhage (hope this is the right name in English)
The thing is to keep monitoring your blood, blood pressure, hormone levels.
And there is always a risk.
You can step outside and get run over by a car but you still get outside.
Quote from: Xandra on April 07, 2014, 10:19:56 AM
The thing is to keep monitoring your blood, blood pressure, hormone levels.
Agree 100%. This is the reason to do HRT with full medical supervision.
Erin
I found some handy and helpfull information
http://www.gires.org.uk/assets/DOH-Assets/pdf/doh-hormone-therapy.pdf