Susan's Place Transgender Resources

My blood test results are in, three months after having started hrt. My testosterone level is below 0.5 so that's fine, but my estradiol level is only 125, while it was 101 when I wasn't taking any hormones. I was given half of the standard dose of both cypro en estradiol because of my heart condition and that seems to be sufficient for the t blockers, but I'm a little underwhelmed by my estradiol levels.

Should I ask for the full dose of estradiol, or will that rise gradually?

I put all my test results in a chart (https://docs.google.com/spreadsheets/d/1yayp3PIeQFNQqM8zhfHAGdkmg-bX2bJ4QHENDVZKLqY/edit#gid=0).

Estradiol levels of 125 are over twice what mine are and I am developing. Normal ranges very between 100-200 depending on the doctor so you are within the transition range. Often doctors will bump up estrogen to reach the desired level but you need to have a discussion with the doctor to find out was the plan is. The doctor may want to limit you for some reason or may increases your dosage latter.

In my case, my total estrogen is running about 700 with an estradiol level of 51. I am being held back because the total number is so high. I am running an experiment to see if I can make these numbers work better and if it works, I may not require a dosage change to get lower total and higher estradiol.

Oh? my endo at VU mc (center of expertise on gender dysphoria (https://www.vumc.com/branch/gender-dysphoria/)) here in Amsterdam told me they aim for estradiol levels between 200 and 400?

So can I conclude that I already had high estradiol levels without taking any hormones?

You were already in the feminine range which suggest a possible intersex condition but doesn't prove it. Had your T levels not been present, you should have developed a fairly feminine body without additional HRT. One exception and that is I am assuming that you are using units of pg/ml. If not, then disregard my comments. This table might be helpful

ESTRADIOL LEVELS
SEX                     pg/ml
Women (> 18 years old)   
      Follicular Phase  30-120
      Ovulatory Peak   130-370
      Luteal Phase      70-250
      Post-Menopausal   15-60
Male                    15-60

TOTAL TESTOSTERONE LEVELS
SEX      ng/dl        ng/ml
Females  6 - 86     0.1 - 1.2
Males  270 - 1100   2.4 - 12
Conversion factor: 1 ng/ml = 3.47 nmol/l

Excuse my ignorance, don't have a clue about those measurement units. The clinic is sending me the blood results in an app too, in which it says: "pmol/L". So 125 picomol per liter is 0.125 nanomol per liter, right? Meaning I indeed already was in the feminine range?

(https://s22.postimg.org/89ao8urep/IMG_0415.png)

I do have a lot of physical and character traits that always made me wonder. But I have a son, so my fertility was ok.

It is important to mention units. Since you are from Europe, your estradiol is in pmol/L and T in nmol/L.

Estradiol: 125 pmol/L = 34 pg/ml, in female and male range, they can sometimes overlap. This is low but estradiol levels may fluctuate from one moment to another and aren't very reliable. Mine are anywhere from 1,000 pg/ml to 4,000 pg/ml. Your pretransition E levels were typical of male, 101 pmol/L = 27-28 pg/ml (10-30) but on the high end.

Range in cisfemales during a menstrual cycle is 20-650 pg/ml (73-2,386 pmol/L) and cycling ciswomen suffer less of heart disease than men as estradiol has shown to be cardioprotective, as opposed to non bio-identical estrogen from which all the fear comes. I have gathered, over the years, many studies, showing how bio-identical estradiol can be beneficial for the cardiovascular system and blood pressure.

Cyproterone acetate, in high doses, can be toxic to the liver, has been associated with prolactinomas in transsexual women, tends to stimulate prolactin synthesis, has been associated with meningiomas, depression/anxiety in some, tiredness/lethargy and may affect adrenal (gland) response. It may also (very) slightly increase thromboembolism risks. All, according to studies. Being a glucocorticoid agonist, it can lead to some abdominal weight gain and adversely affect glucose tolerance. It is an anti-androgenic progestin which not only reduces T but also blocks it so that part of the T measured is ALSO blocked by this drug. Your T is low, equivalent to 14 ng/dl (range in women can be anywhere from 8-90 ng/dl).

It's possible for intersex to be fertile so the only way to know for sure is through testing or if there are clear physical signs. The units the lab is returning are different than the ones we discuss so the following document had the table. To convert to the units we tend to use, you need to divide your numbers by 3.67. That explains the doctors targeting 400 as that would put you above 100 pg/ml

https://www.questdiagnostics.com/dms/Documents/test-center/si_units.pdf

Analyte        Gravietric  Conversion International
               Unit        Factor     Unit
Estrone        pg/mL       3.699      pmol/L
Estradiol      pg/ml       3.67       pmol/L
Estriol        pg/ml       3.47       nmol/L

@Dena
Thank you for explaining the measurement units. Basically I find my estradiol value too low. I do experience a lot of changes: my waist became smaller, my ass bigger, breasts started growing, people tell me my face changed, but I feel I could get more out of it when I get the standard dose rather than half. I have a talk with my endo tomorrow and want to convince her of that.

Being intersex or not never manifested as a problem, so it's a nice to know, not a need to know. It doesn't change my gender dysphoria or transition process. It might explain my smooth and hairless skin and other things that were a disadvantage when I was presenting male but now are an advantage, but doesn't change anything.

@KayXo

Yup, read about estradiol being cardioprotective and wonder whether Systen patches contain bio identical estrogen. They do, right? it's phyto estrogens where all the fear comes from? I also get half a dose of Cyproterone acetate, but my testosterone levels already are immeasurable (below 0.5), so probably don't need a higher dose of that.

I didn't gain any weight though. In fact I lost four kilos in three months, without any dieting.

Quote from: Naomi71 on November 10, 2016, 06:26:15 PMYup, read about estradiol being cardioprotective and wonder whether Systen patches contain bio identical estrogen. They do, right?

Right. You can't mention doses on this forum.

Quoteit's phyto estrogens where all the fear comes from?

No. Phytoestrogens are very weak estrogens found in food, for instance. The fear comes from non bio-identical potent/strong estrogens such as conjugated equine estrogens (Premarin), ethinyl estradiol and DES.

Quote from: KayXo on November 10, 2016, 09:58:43 PM
Right. You can't mention doses on this forum.

Really? I did remove the reference, but that sounds like a rule I disagree with. You can  mention your blood levels that are the result of that dose, right?  How can you have a subforum on hrt and have a meaningful conversation, without being allowed to share such basic information? I'm trying to understand why. 

Anyway, Im having a talk with  my endo this morning and the discussion will be about my dose. The risk primarily lies with the t blockers and half the standard dose seems to be doing its job fine, but I feel I could get more physical changes with a higher dose of estradiol and like you write, there isn't any cardiovascular risk in it, quite the contrary. I said the same thing to my doctor, but she told me that the risk for trombosis, or a brain seizure is still there.

When I visited her a few weeks ago, she measured my blood pressure and it turned out to be 182. But I hadn't taken any heart meds that day, a guy on the street had his fighting dog attack me for being trans and then my friend who gave me a ride to the hospital told me her mother had only three months to live. We cried, I was very obset. I had my GP measure it a few days ago and now it's back to 125/70, which is fine. I'm a little nervous about her willingness to prescribe a higher dose

Phew... I feel so relieved... my endo didn't really see the necessity for giving me a larger dose, but went along with it beacuse I insisted :)

Quote from: Naomi71 on November 11, 2016, 01:47:32 AMshe told me that the risk for trombosis, or a brain seizure is still there.

Because she is thinking of studies where non bio-identical estrogens are used. In the case of bio-identical estrogen, especially taken non-orally, studies have shown these risks to be negligible.

Just take the case of men with prostate cancer who were prescribed a very high dose of transdermal patches.

Cancer. 2005 Feb 15;103(4):717-23.

"Patients with prostate carcinoma progressing after primary hormonal therapy received TDE (...) per 24 hours"

TDE = transdermal estradiol

"The mean (+/-95% CI) serum estradiol level increased from 17.2 pg.mL (range, 14.8-19.6 pg/mL) to 460.7 pg/mL
(range, 334.6-586.7 pg/mL)."

"No change in factor VIII activity, F 1.2, or resistance to activated protein C was observed, whereas a modest decrease in the protein S level was observed."

"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."

Median age of patients was 75 (49-91).

J Urol. 2005 Aug;174(2):527-33; discussion 532-3.
Transdermal estradiol therapy for prostate cancer reduces
thrombophilic activation and protects against thromboembolism.

"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."

Prostate 1989;14(4):389-95

"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."

Fertil Steril. 2010 Mar 1;93(4):1267-72.

"Standard MtF cross-sex hormone therapy at our department includes transdermal 17ß-estradiol"

"Activated protein C resistance was detected in 18/251 patients (7.2%), and protein C deficiency was detected in one patient (0.4%). None of the patients developed VTE under cross-sex hormone therapy during a mean of 64.2 +/- 38.0 months."

Biochem Pharmacol. 2013 Dec 15;86(12):1627-42.
Estrogen, vascular estrogen receptor and hormone therapy in postmenopausal vascular disease.

"There was no increase in VTE risk with the use of transdermal estrogen, even in patients with pre-existing thrombophilia [15]."

Climacteric. 2012 Apr;15 Suppl 1:11-7.

"There is a wealth of evidence to suggest that, unlike oral estrogens, transdermal estradiol does not increase the risk of venous thromboembolism, probably due to its lack of effect on the coagulation cascade, including thrombin generation and resistance to activated protein C, and does not increase the risk of stroke. It is cardioprotective, significantly reducing the incidence of myocardial infarction compared with non-users"

Maturitas. 2008 Jul-Aug;60(3-4):185-201.

"Non-orally administered estrogens, minimizing the hepatic induction of clotting factors and others proteins associated with the first-pass effect, are associated with potential advantages on the cardiovascular system. In particular, the risk of developing deep vein thrombosis or pulmonary thromboembolism is negligible in comparison to that associated with oral estrogens. In addition, recent indications suggest potential advantages for blood pressure control with non-oral estrogens."

Am J Obstet Gynecol. 1993 Dec;169(6):1549-53.
Fibrinolytic parameters in women undergoing ovulation induction.

"As serum estradiol levels increased throughout each phase (maximum mean estradiol 739.8 pg/ml)"

"Down-regulation of the fibrinolytic system was observed as estradiol levels increased. However, thrombin formation did not change, thus suggesting that elevated circulating estradiol alone does not predispose to a thromboembolic event."

Pregnant levels have very high levels, up to 75,000 pg/ml (275,000 pmol/L)
http://cebp.aacrjournals.org/cgi/content-nw/full/12/5/452/T1

and yet...

Ann Intern Med. 2005 Nov 15;143(10):697-706.

"Women with deep venous thrombosis or pulmonary embolism first diagnosed between 1966 and 1995, including women with venous thromboembolism during pregnancy or the postpartum period (defined as delivery of a newborn no more than 3 months before the deep venous thrombosis or pulmonary embolism event date, including delivery of a stillborn infant after the first trimester)."

« The relative risk (standardized incidence ratio) for venous thromboembolism among pregnant or postpartum women was 4.29 (95% CI, 3.49 to 5.22;P < 0.001), and the overall incidence of venous thromboembolism (absolute risk) was 199.7 per 100,000 woman-years. The annual incidence was 5 times higher among postpartum women than pregnant women (511.2 vs. 95.8 per 100,000), and the incidence of deep venous thrombosis was 3 times higher than that of pulmonary embolism (151.8 vs. 47.9 per 100,000). Pulmonary embolism was relatively uncommon during pregnancy versus the postpartum period (10.6 vs. 159.7 per 100,000). "

Risk of DVT: 0.1%
Risk of pulmonary embolism: 0.01%

Br J Obstet Gynaecol. 1990 Oct;97(10):917-21.

"There is some anxiety about the possible harmful sequelae of supraphysiological estradiol levels but no data are currently available to show any deleterious effects of these levels on coagulation factors, blood pressure, glucose tolerance or the occurrences of endometrial or breast cancer (Hammond et al. 1974; Thom et id. 1978; Studd B Thom 1981; Armstrong 1988)."

"Supraphysiological oestradiol levels are an uncommon consequence of oestradiol implants occurring most frequently in women with a history of depression or surgical castration. These high serum oestradiol levels were not associated with any deleterious effects and may be necessary for the control of symptoms in specific women"

"The mean serum oestradiol level of the 1388 women attending the clinic in 1988 was 767 pmol/l (range 78-2925 pmol/l), 66% had serum oestradiol levels <1000 pmol/l and 3% (38 women) had levels >1750 pmol/l (Fig 1)."

Horm Metab Res. 1994 Sep;26(9):428-31.

"Six patients were peri- or postmenopausal (49.5 + 4.8 years of age, group A)"

"The duration of the therapy was 6, and in 4 patients 9 months"

"Estradiol increased from 34.8 +/- 7.5 pg/ml to 3226 +/- 393 pg/ml after 3 months and to 2552 +/- 254 pg/ml after 6 months, respectively, in group A."

"Investigations of lipids, liver enzymes and haemostasiology to be published later will show the absence of unwanted metabolic effects of this regimen."

"In conclusion, our data show, that the treatment (...) by means of high parenteral estrogen-progestogen depot injections is effective. Virtually no side effects occurred. The therapy is well accepted by the patients."

In transsexual women...

Archives of Sexual Behavior, Vol. 27, No. 5, 1998

"The incidence of thromboembolic events during cross-gender hormone treatment in our patients was zero."

"None of our patients developed deep vein thrombosis or embolism during cross-gender hormone therapy performed in our clinic."

Despite 17 patients receiving high dose intramuscular estradiol.

Exp Clin Endocrinol Diabetes. 2011 Feb;119(2):95-100

"84 male-to-female transsexuals (MtFs) were treated with (...) oestradiol-17β valerate every 10 days." This was intramuscular.

"We observed one case of deep vein thrombosis in a 49 years old MtF who had uneventful medical history prior hormone therapy. No further side effects or other complications were observed during the study."

Estradiol levels ranged from 340.5 pmol/L to 1,362.4 pmol/L, measured on the last day, just before the next injection so lowest levels (trough).

So, taking these two studies, out of a total of 101 women taking high doses of estrogen intramuscularly (non-orally), there was only one thromboembolic complication (1%) which could be due to just chance, have nothing to do with treatment.

One especially striking is this study in women with advanced breast cancer who were treated with moderate and VERY high dose oral bio-identical estrogen.

JAMA. 2009 August 19; 302(7): 774–780.

"We therefore conducted a randomized phase 2 trial in postmenopausal women with hormone receptor-positive, AI-resistant advanced disease to compare (...) estradiol daily (...) with (...) daily (...)"

"the mean [standard deviation] trough levels of estradiol at one month were 302 [519] pg/mL on the (...) arm and 2403 [2268] pg/mL on the (...) arm (P <.001)"

"The rate of thrombosis was low with one event on each arm of the study." Both Grade 4/5

Median age: 54.7 yrs old (36.3-83.8 ); 59.5 yrs old (39.4-77.7)


Sharing these with your doctor could be helpful. :)

Quote from: Naomi71 on November 11, 2016, 01:47:32 AM
Really? I did remove the reference, but that sounds like a rule I disagree with. You can  mention your blood levels that are the result of that dose, right?  How can you have a subforum on hrt and have a meaningful conversation, without being allowed to share such basic information? I'm trying to understand why. 

You may find someone telling you those are the rules so take it or leave it. But after struggling for a while with the same feeling let me also try and put a positive non-mod perspective on why dosage discussions are wrong.

Everyone reacts differently to the medications. Remember, whether it's the estrogen or the anti-androgens, we're doing things with these drugs that they weren't designed for, particularly in the case of the AA's. No-one can predict how an individual will respond to this or that medication or dosage. I guarantee that if 100 people on this forum took the same dosage of a drug for 6 months their blood levels would show massive variations.

So that relates to an associated issue. The moment dosages were discussed people would take them as gospel. Instead of medicating through an endocrinologist and being professionally prescribed, it could be a carte blanche for unregulated self-medication. Can you just imagine what might happen to Susan and this site if, god forbid, someone died as a result of reading someone else's dosage on here?

And lest you think I'm talking out my hat, I nearly killed myself twice whilst self-medicating, picking up doses from other sites and whacking in pills that I ordered from overseas. It was unbelievably stupid of me, looking back and, yes, I was desperate. But it's so so dangerous.

The only way to do this, and I urge this for anyone on the forum, is through a professional medic with regular blood tests. It took me a long time to realise the importance of that: and I was eventually PM'd by someone senior on this forum. The moment I really and properly listened to her my life transformed.

x

Hugs x

Couldn't have put it better myself

Quote from: Naomi71 on November 10, 2016, 06:26:15 PM
@Dena
Thank you for explaining the measurement units. Basically I find my estradiol value too low. I do experience a lot of changes: my waist became smaller, my ass bigger, breasts started growing, people tell me my face changed, but I feel I could get more out of it when I get the standard dose rather than half. I have a talk with my endo tomorrow and want to convince her of that.

Being intersex or not never manifested as a problem, so it's a nice to know, not a need to know. It doesn't change my gender dysphoria or transition process. It might explain my smooth and hairless skin and other things that were a disadvantage when I was presenting male but now are an advantage, but doesn't change anything.

@KayXo

Yup, read about estradiol being cardioprotective and wonder whether Systen patches contain bio identical estrogen. They do, right? it's phyto estrogens where all the fear comes from? I also get half a dose of Cyproterone acetate, but my testosterone levels already are immeasurable (below 0.5), so probably don't need a higher dose of that.

I didn't gain any weight though. In fact I lost four kilos in three months, without any dieting.

I feel for you as I too have heart disease.  My Total T level is 350   My free T level is 17.9  pg/mL  I do not know the difference but I would suppose the free T level is the benchmark.  Estradiol level is    170 pg/mL As long as I keep monitoring my protyme the risk of thrombosis is greatly reduced. I am amazed of people's knowledge as I am an engineering type and can explain shop efficiency all night long. And no you don't want me to go there. Most people have their eyes roll back in their head once I get started. But dang. I am so clueless about the process. Best of health to you

Dawn

Quote from: DawnOday on November 11, 2016, 07:36:48 PMEstradiol level is    170 pg/mL As long as I keep monitoring my protyme the risk of thrombosis is greatly reduced.

My estradiol levels range anywhere from 1,000-4,000 pg/ml, my prothrombin times are normal. Just goes to show you that levels, in and of themselves, aren't the problem (as confirmed by some studies, as well) but rather the route of administration and the type of estrogen matter. Sadly, as I've realized throughout the years, several doctors are unaware of this. I take estrogen by way of intramuscular injections.

Quote from: Rachel Richenda on November 11, 2016, 02:35:52 PM
So that relates to an associated issue. The moment dosages were discussed people would take them as gospel. Instead of medicating through an endocrinologist and being professionally prescribed, it could be a carte blanche for unregulated self-medication. Can you just imagine what might happen to Susan and this site if, god forbid, someone died as a result of reading someone else's dosage on here?

To me it appears that people self medicating is the actual problem, trying out doses they inevitably find on the interwebs is a symptom of that. If the problem is solved, the symptom disappears too. So on Dutch transfora, people even hinting at self medicating are moderated, while dosage is freely discussed. but I realize the Dutch situation is different. Gendercare is readily available and free, but very regulated by our insurance companies. So basically, if you want it all paid for, you stick to the rules. Those rules were formulated by the VU medical center and everyone on hormones gets the same dose and combination of t blockers and estradiol. Or half of that, as in my case.

Well, I do get the full standard dosage of estradiol now, but I have my psychologist to thank for that, who is also a part of the genderteam treating me. I complained to her that all my trans girlfriends get the full dosage and have way faster boob growth than me, she adviced my endo that prescribing me the full dosage would alleviate my suffering :D

QuoteThe only way to do this, and I urge this for anyone on the forum, is through a professional medic with regular blood tests. It took me a long time to realise the importance of that: and I was eventually PM'd by someone senior on this forum. The moment I really and properly listened to her my life transformed.

I entirely agree with that

hugs,
Naomi

In the United States where the server is located, it's very easy to get sued for providing information that causes harm to to others. We attempt to keep the site clean of dosage information so people who self medicate are unable to use us as a resource. Sites that post dosage information are either unaware of the risk they are taking or they have medical staff which provides them an additional layer of protection.

Board staff is aware of members who self medicate and we do our best to get them in a proper treatment program as it's both safer and cheeper however countries like the UK have long delays for treatment so self medication is often used to get by until treatment is available.

Quote from: KayXo on November 11, 2016, 07:38:38 AM
Because she is thinking of studies where non bio-identical estrogens are used. In the case of bio-identical estrogen, especially taken non-orally, studies have shown these risks to be negligible.

Just take the case of men with prostate cancer who were prescribed a very high dose of transdermal patches.

Cancer. 2005 Feb 15;103(4):717-23.

"Patients with prostate carcinoma progressing after primary hormonal therapy received TDE (...) per 24 hours"

TDE = transdermal estradiol

"The mean (+/-95% CI) serum estradiol level increased from 17.2 pg.mL (range, 14.8-19.6 pg/mL) to 460.7 pg/mL
(range, 334.6-586.7 pg/mL)."

"No change in factor VIII activity, F 1.2, or resistance to activated protein C was observed, whereas a modest decrease in the protein S level was observed."

"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."

Median age of patients was 75 (49-91).

J Urol. 2005 Aug;174(2):527-33; discussion 532-3.
Transdermal estradiol therapy for prostate cancer reduces
thrombophilic activation and protects against thromboembolism.

"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."

Prostate 1989;14(4):389-95

"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."

Fertil Steril. 2010 Mar 1;93(4):1267-72.

"Standard MtF cross-sex hormone therapy at our department includes transdermal 17ß-estradiol"

"Activated protein C resistance was detected in 18/251 patients (7.2%), and protein C deficiency was detected in one patient (0.4%). None of the patients developed VTE under cross-sex hormone therapy during a mean of 64.2 +/- 38.0 months."

Biochem Pharmacol. 2013 Dec 15;86(12):1627-42.
Estrogen, vascular estrogen receptor and hormone therapy in postmenopausal vascular disease.

"There was no increase in VTE risk with the use of transdermal estrogen, even in patients with pre-existing thrombophilia [15]."

Climacteric. 2012 Apr;15 Suppl 1:11-7.

"There is a wealth of evidence to suggest that, unlike oral estrogens, transdermal estradiol does not increase the risk of venous thromboembolism, probably due to its lack of effect on the coagulation cascade, including thrombin generation and resistance to activated protein C, and does not increase the risk of stroke. It is cardioprotective, significantly reducing the incidence of myocardial infarction compared with non-users"

Maturitas. 2008 Jul-Aug;60(3-4):185-201.

"Non-orally administered estrogens, minimizing the hepatic induction of clotting factors and others proteins associated with the first-pass effect, are associated with potential advantages on the cardiovascular system. In particular, the risk of developing deep vein thrombosis or pulmonary thromboembolism is negligible in comparison to that associated with oral estrogens. In addition, recent indications suggest potential advantages for blood pressure control with non-oral estrogens."

Am J Obstet Gynecol. 1993 Dec;169(6):1549-53.
Fibrinolytic parameters in women undergoing ovulation induction.

Kay, I know you're quite rightly a big fan of scientific studies so I found this paper bearing out the above to be very interesting:

"However, there is increasing evidence that the use of transdermal menopausal hormone therapy confers no increase in the risk of venous thromboembolism, in contrast to the use of oral preparations, which are associated with an increased risk. Orally administered hormones are first metabolized by the liver before entering the systemic circulation, and metabolites are excreted in the bile and urine. Transdermally administered estrogen avoids this first-pass metabolism and can therefore be given in lower doses for equivalent physiologic effects. The different doses and concentrations of metabolites may explain the different effects observed with oral and transdermal routes of menopausal hormone therapy and gallbladder disease. For venous thromboembolism, an explanation for the different effects by route of hormone administration is not as clear, although it has been suggested that the metabolites generated from the first-pass metabolism of estrogen may induce thrombogenic changes." [CMAJ. 2013 Apr 16; 185(7): 549–550.]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3626805/

See also: . Canonico M, Oger E, Plu-Bureau G, et al. Hormone therapy and venous thromboembolism among postmenopausal women: impact of the route of estrogen administration and progestogens: the ESTHER Study. Circulation 2007;115:840–5 [PubMed]
Sweetland S, Beral V, Balkwill A, et al. Venous thromboembolism risk in relation to use of different types of postmenopausal hormone therapy in a large prospective study. J Thromb Haemost 2012; September 10 [PubMed]


If that link of DVT to first pass liver metabolism is correct then sublingual administration would also confer a lower risk of DVT. Very interesting.

"Over 5 years, 1 in 660 who had never used HT were admitted to hospital for (or died from) pulmonary embolism, compared with 1 in 475 current users of oral estrogen-only HT, 1 in 390 users of estrogen-progestin HT containing norethisterone/norgestrel, and 1 in 250 users of estrogen-progestin HT containing medroxyprogesterone acetate."

https://www.ncbi.nlm.nih.gov/pubmed/22963114

Quote from: Dena on November 12, 2016, 12:52:27 AM
In the United States where the server is located, it's very easy to get sued for providing information that causes harm to to others.

That's an imaginary legal problem. As long as you don't pretend to be a doctor, just speak for yourself and don't recommend your personal dosage to other people, any judge would consider it freedom of speech. To give you just one extreme example: there are girls idealizing anorexia nervosa, gathering on so called "pro ana/ thinspiration" fora. They constantly share information on how to starve themselves to death and there's not a judge in the world who can do a thing about that. You can't get sued for excercising your first amendmend rights. If people take messages like that out of context and start using that as a guideline for their self medication, that's personal responsibility.

QuoteWe attempt to keep the site clean of dosage information so people who self medicate are unable to use us as a resource.

I  fully agree with that as a moral imperative, because I wish for all transpeople to be careful with their bodies, healthy and have a succesful transition process. I suppose we share the same goals. People self medicating should be discouraged from that every step of the way and one of the (less effective) ways to do that is to keep them away from dosage information. However, that information can be found everywhere, so it seems more effective to me to regulate that information in some way, rather than repressing it. Moderating people mentioning self medication and actively engaging  them seems the best thing to do.

QuoteSites that post dosage information are either unaware of the risk they are taking or they have medical staff which provides them an additional layer of protection.

You seem to implicitly assume here that messages which could be misconstrued as information are information because of that. What you in fact suggest, is that David Chapman, the murderer of John Lennon, could sue JD Salinger, author of The Catcher in the Rye, because the book could be misinterpreted as containing a "trigger for assassination (https://atomicpoet.wordpress.com/2012/01/31/is-catcher-in-the-rye-an-assassination-trigger/)".

It all depends on context. If you pretend to be a medical doctor and start recommending dosages causing damage, that's a legal problem. If you just discuss your own dosage, that's freedom of speech.

QuoteBoard staff is aware of members who self medicate and we do our best to get them in a proper treatment program as it's both safer and cheeper however countries like the UK have long delays for treatment so self medication is often used to get by until treatment is available.

Well, engaging with people self medicating seems an excellent thing to do :)

Your argument about the delays hits home. In Holland, we have the exact same problem with long waiting list, unnecessary diagnostics (we don't have informed consent) and our patient org, Transvisie, recently did a survey (http://www.transvisie.nl/transvisie.nl/images/OnderzoekTransgenderzorgNederland.pdf) about the consequences of that. Turns out that 18% of the people who have to wait fifteen monnths or longer (the average delay before you get any hormones) starts self medicating, 15% loses their job, 18% of the relationships goes off the cliffs, 5% starts using drugs or alcohol and 60% experiences problems in public spaces (violence, looks, etc). So we're fighting for informed consent right now :)

My own diagnostic stage took me a year and it was the worst time of my life. I had already taken the decision to fully transition and to then just talk rather than getting your hormones amplifies the gender dysphoria. I didn't start self medicating though, did lose a job over it, lost my boyfriend, didn't start taking drugs or booze, but did experience violence presenting female and not passing in any way.

Quote from: Naomi71 on November 12, 2016, 12:29:32 AMSo basically, if you want it all paid for, you stick to the rules. Those rules were formulated by the VU medical center and everyone on hormones gets the same dose and combination of t blockers and estradiol.

Despite individuals being different and not all the same. Their protocol, strangely, does not seem to take this into account.

Aust NZ J ObTtet Gvnaecol 1998. 38: 3: 45

"it is difficult to define a therapeutic drug concentration (...) because patients may vary in their oestradiol requirements. In addition, serum oestradiol levels may not necessarily reflect tissue oestradiol levels." The same can be said of doses.

Did you ever bring this issue up with the doctors and if so, what did they say? Is this due to their publishing studies where things must be standardized so findings may be valid? If so, are those women (participants) aware of this and agree to potentially sacrifice their own results (perhaps a regimen other than the standardized one would have produced better results) for a greater understanding of the effects of HRT in transsexual women? Do they need to sign a consent form?

Quote from: Rachel Richenda on November 12, 2016, 03:37:24 AM
"For venous thromboembolism, an explanation for the different effects by route of hormone administration is not as clear, although it has been suggested that the metabolites generated from the first-pass metabolism of estrogen may induce thrombogenic changes."[CMAJ. 2013 Apr 16; 185(7): 549–550.]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3626805/

Orally, there is more estradiol entering the liver and thus triggering estrogen receptors in the portal vein, which leads to a greater change in the production of proteins and factors involved in coagulation.

Obstet Gynecol Clin North Am. 1987 Mar;14(1):269-98.

"The amount of estradiol leaving the liver following oral administration is substantially less than that which enters it through the portal vein. The systemic administration of estradiol avoids this initial hepatic metabolism. Furthermore, only 25 per cent of nonorally administered estrogen will go to the liver at each pass, and nonhepatic tissues would be exposed to a greater extent than after oral administration. Thus, peripheral administration of estradiol reduces the exaggerated hepatic responses in comparison to nonhepatic actions."

Minerva Endocrinol. 1989 Jan-Mar;14(1):41-4.

"Having no first pass effect on the liver, parenteral administrations have less influence than oral ones on the synthesis of certain proteins by the liver (increased SHBG, CBG, TBG, transferrin, ceruloplasmin, angiotensinogen, clotting factors VII, IX, X and X complex; decreased antithrombin III and anti Xa) and on lipid metabolism (increased biliary cholesterol, triglycerides and HDL, especially HDL2; reduced LDL)."

Quotesublingual administration would also confer a lower risk of DVT. Very interesting.

Yes but some will inevitably be swallowed. The route of administration does not seem to be the only important factor, though.

Prz Menopauzalny. 2014 Oct;13(5):267-72.

"Oral estrogens increase the risk of venous thromboembolic complications to varying extents, probably depending on their type and dose used."

J Clin Endocrinol Metab. 2003 Dec;88(12):5723-9.

"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)."

EE = ethinyl estradiol
E2 = estradiol

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"

BMJ. 2012 Oct 9; 345

"17-β-estradiol has been reported to be less thrombogenic than conjugated equine oestrogen.21 22"

The reason being that

Minerva Med. 2013 Apr;104(2):161-7.

"Estradiol itself has a lower impact on estrogen-hepatic proteins, and is more readily metabolized by the liver than ethinyl estradiol, the ethinyl group on which slows down that process. The structure increases the bioavailability of ethinyl estradiol compared with E2, but may also contribute to an increased likelihood of estrogen-related adverse events.40"

Equine (horse) estrogen in Premarin and ethinyl estradiol, being harder to break down by the liver, will pass through the portal vein, again and again, triggering receptors, again and again, hence greatly affecting coagulation whereas estradiol after first going through portal vein, will be strongly metabolized so that much less estradiol will survive and circulate through portal vein, again and again (enterohepatic circulation). Surprisingly, in my discussion with several doctors, few seem to be aware of this. :(

Oral bio estradiol, in very high doses, given to women with advanced breast cancer surprisingly led to a very low incidence of thromboembolic complications, despite their advanced age, as well.

Also this,

J Sex Med. 2016 Nov;13(11):1773-1777.

"From January 1, 2008 through March 31, 2016, 676 transgender women received oral estradiol-based CSHT for a total of 1,286 years of hormone treatment and a mean of 1.9 years of CSHT per patient. Only one individual, or 0.15% of the population, sustained a VTE, for an incidence of 7.8 events per 10,000 person-years."

"93.8% of the transgender women receiving oral estradiol also were prescribed the antiandrogen spironolactone and 16.6% received the antiandrogen finasteride. Conjugated equine estrogens or oral progestins were prescribed to 6.2% and 4.0% of the total study population, respectively. In addition, three patients were prescribed intramuscular medroxyprogesterone acetate in combination with oral estradiol."

"the incidence of VTE observed in the present study is slightly lower than the 8 to 27 events per 10,000 person-years observed in the general population and lower than the 30 events per 10,000 person-years observed in postmenopausal women on unopposed estrogen therapy."

Unopposed estrogen therapy was conjugated equine estrogens so that it is not surprising that incidence was much less in this population which, for the most part, took oral bio-identical estrogen. Also, they were younger, BUT

"our population has a high prevalence of HIV and tobacco use and a large number of African-American individuals, which would be expected to increase the risk of thrombophilia."

There are also limitations of the study which could have lead to underreporting BUT the incidence still remains very low, especially considering a few were taking non bio-identical estrogen or medroxyprogesterone known to increase thromboembolism risks and considering four other factors (demographics) known to increase risks were present to a significant degree. The one incident occurred in someone severely obese (BMI of 37).

Also, this study

Exp Clin Endocrinol Diabetes. 2005 Dec;113(10):586-92.

"Sixty male-to-female transsexuals were treated with monthly injections of gonadotropin-releasing hormone agonist (GnRHa) and oral oestradiol-17beta valerate for 2 years to achieve feminisation until SRS."

"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."

The only DVT complication was seen in an individual with a pre-existing condition/genetic mutation, in a 62 yr old TS woman, oldest of the group. Out of 60 people. This complication could have occurred, regardless.

Estradiol levels ranged from 325-1183 pmol/L, at 12-24 months.

Quote from: Rachel Richenda on November 12, 2016, 03:41:07 AM
"Over 5 years, 1 in 660 who had never used HT were admitted to hospital for (or died from) pulmonary embolism, compared with 1 in 475 current users of oral estrogen-only HT, 1 in 390 users of estrogen-progestin HT containing norethisterone/norgestrel, and 1 in 250 users of estrogen-progestin HT containing medroxyprogesterone acetate."

https://www.ncbi.nlm.nih.gov/pubmed/22963114

The oral estrogen included bio-identical estradiol AND conjugated equine estrogens so despite their different effects on coagulation, they were grouped together as oral estrogen. Interestingly, relative risk of venous thromboembolism is LOWER with higher doses of bio-identical estradiol which suggests something else is at play here (i.e. confounding variables). Relative risk with conjugated equine estrogen is higher at higher doses.

Wow. That's so interesting Kay, or at least it is to me. There are a lot of variables showing up in those studies. It would be good to see surgeons finding consensus about this for MtF's prior to surgery, but that's another issue.

Quote from: KayXo on November 12, 2016, 10:24:31 AM
Despite individuals being different and not all the same. Their protocol, strangely, does not seem to take this into account.

Yes, but fortunately I respond well to that protocol.

QuoteDid you ever bring this issue up with the doctors and if so, what did they say? Is this due to their publishing studies where things must be standardized so findings may be valid? If so, are those women (participants) aware of this and agree to potentially sacrifice their own results (perhaps a regimen other than the standardized one would have produced better results) for a greater understanding of the effects of HRT in transsexual women? Do they need to sign a consent form?

No, never brought it up. Why would I? I'm there for my own transition process and don't feel that's the time and place to make some kind of political point, get into all kinds of conflicts with doctors I need on my side. It's working for me. I did sign a consent form for them to take extra blood  for research purposes. Their protocol is  WPATH6 (outdated) with a few alterations that are the result of negotiations with insurance companies and a few governmental institutions, so I believe the existing protocol is a matter of bureaucracy rather than research. VUmc takes care of the full transition process under one roof and arranges for the diagnosis, hormones and all operations. It has advantages and disadvantages.

I don't think I have the intellectual curiosity to want to know all the research about hormones, what study contradicts the other, etc. Just some basic stuff about my own medication and dosage, measurement units, how my other medicines correlate with my hormones and bloodlevels so I don't do anything stupid, but I trust my doctor to make the right decisions and keep up with that research.

HRT is only a part of the whole transition process and I'm much more concerned with the emotional and physical changes I'm going through than the actual science behind it. That was different before I started taking hormones, but it seems that whole analytical side of me is gone. Although I know it's well intended, it even upsets me to have to go through such a litany of sciency stuff. Maybe I'd engage in all that research when my HRT wasn't working, but fortunately it is.

Sorry.

Even my reason for wanting a higher dose of estrogen was all but scientific. All my friends got a higher dose and I felt left out. Kind of childish. It was my psychologist who recommended it to the genderteam treating me, because not having the standard dose stressed me out. There probably is some science and biochemistry behind my feeling of well being now I'm on a higher dose, but I'm not truly concerned about that.

Understood. Your well-being is of utmost importance.  :angel:

Quote from: Naomi71 on November 13, 2016, 10:04:51 AM
.... There probably is some science and biochemistry behind my feeling of well being now I'm on a higher dose, but I'm not truly concerned about that.

The why doesn't matter, maybe its the higher dose maybe its not...you are happier and not in any danger. Great outcome for you.....fantastic :)

Liz

QuoteUnderstood. Your well-being is of utmost importance. 

The problem with someone random making scientific claims on the interwebs is that it's an extremely unreliable source of information. Quoting all these studies looks very authoritative, but do you have a professional background in that kind of research? How can I tell you're not merely cherrypicking, misinterpreting, or quoting out of context? To find that out, I will have to factcheck all your sources which is a lot of work (too much to bother with)  and to add insult to injury, you seem to have a tendency to quote a lot of sources without making evident what exactly you mean to say by them.

For example: in one of your messages to me on another forum (that i left), you recommended spiro rather than cypro to me, because that would allegedly lower my blood pressure. Beneath that statement you came up with a lot of important sounding quotes, none of them even mentioning spiro. You all of a sudden turn out to be skilled in the field of cardiology as well, even going as far as claiming that certain combinations of hormones could replace the heart meds that I'm taking. Well, i already experimented with that and it nearly killed me. So let's not.

It's just tiring and I really prefer to rely on an actual endocrinologist and cardiologist for this kind of advice. I have both, so I'm good ;) Also, for efficiency's sake, I prefer to just hear their conclusions in their own words instead of  a random bunch of quotes from papers they base those conclusions on.

So that stresses me out to engage with. It's not good for my well being.

I don't recommend, I express my opinions on the matter based on the research I come across, trying to remain objective at all times and not cherry picking because my goal is to get at facts, as much as possible. I have principles I abide by and I try to remain as unbiased as possible for own well-being and that of others. I assure you I'm a honest person that is not interested in winning arguments or pride, I dislike these things. I try to consider all perspectives and I spend tens of thousands of hours researching the matter, reading all possible perspectives on the matter. If I am wrong about something, I will admit it and will change my mind. I try to keep up as much as possible with the latest research without dismissing older research as well. I am not a doctor and I don't pretend to be one. I just quote studies. But, you should indeed question whatever I (or anyone) present and doing all that work of fact checking is indeed tiresome and if it compromises your well-being, then I empathize with your position. :)

I disagree on one point though. Even professionals, doctors are fallible and make mistakes so that double checking, talking to other professionals, reading research material can be useful and in a few instances, life-saving, as I've realized in the past. I no longer blindly follow recommendations after all the wrongdoings I have come across. That is just me, to each their own. But, I also don't let myself get too paranoid and not trust anything anyone says. There is only so much research I can conduct, I have other priorities in my life too. So, there is a point when you have to say to yourself, enough is enough and I'll just cross my fingers and hope these experts are right. Faith!

I don't really see where I may be misinterpreting or quoting out of context but perhaps if you pointed out exactly where I did this, I may realize my own wrongdoing and if so, I apologize in advance. I try to make things as clear as possible but if you have difficulty understanding, I apologize again and would do everything in my power to makes things more understandable.

My goal is to inform so that you may relate this information to your own doctors and incite constructive discussions which may benefit not only you, but the doctor and their own patients. I am open to criticism and always willing to learn. Everyone of us can provide useful feedback and has something important to say and add to the discussion. Every voice is important. :)

Spiro doesn't allegedly lower blood pressure. This is a fact, as many in this forum can attest to. Several studies also confirm this. Whereas cyproterone acetate, as far as I know, doesn't and actually can lead to water retention, I think, due to its glucocorticoid effects. As always, double check with your doctors and available resources but you say you don't have the time or willingness so what am I to do?

I am not a cardiologist either and am neither skilled or had training in that field. But, I report what studies find and then you decide what you want to do with that. Ignore it, or consider it, talk it over with people that ARE skilled and experienced and see what they say.

I am sorry for stressing you out. That was/is not my intention. I hope you will forgive me and truly, you must know that the well-being of each and everyone of you is what matters to me. I care not about my credibility or reputation. My goal is increased awareness, just and respectful treatment of transsexual women and any minority group in this world. I will admit to being stubborn at times and overly persistent. I am far from flawless but every day, I strive to become a better person but I won't ever be perfect. Imperfection is just fine with me.  ;D

Take care and all the best to you, Naomi.

Sincerely,
Kay :)

Quote from: KayXo on November 13, 2016, 09:29:20 PM
I don't recommend, I express my opinions on the matter based on the research I come across, trying to remain objective at all times and not cherry picking because my goal is to get at facts, as much as possible. I have principles I abide by and I try to remain as unbiased as possible for own well-being and that of others. I assure you I'm a honest person that is not interested in winning arguments or pride, I dislike these things. I try to consider all perspectives and I spend tens of thousands of hours researching the matter, reading all possible perspectives on the matter. If I am wrong about something, I will admit it and will change my mind. I try to keep up as much as possible with the latest research without dismissing older research as well. I am not a doctor and I don't preten to be one. I just quote studies. But, you should indeed question whatever I (or anyone) present and doing all that work of fact checking is indeed tiresome and if it compromises your well-being, then I empathize with your position. :)

In an earlier message, I already defended that freedom to express any opinion, as well as my freedom to criticize your way of exercising that right. You can claim to spend tens of thousands of hours researching these matters, but I would have to take your word for that. And even if you did, your knowledge was never tested by other professionals, you never treated patients, never diagnosed anyone, nor does reading a lot of research prove you understood what you just read, let alone your capacity for synthesizing that knowledge in a working hypothesis. You never did any exams testing your knowledge. Reading up on research is an armchair thing. A hobby. I hope you understand the limitations of that.

Contrastingly, my own endocrinologist did her job for almost 25 years at VU university, which actually has the oldest gender clinic worldwide. She treated thousands of transpeople, her knowledge was tested by peers and she and her team don't just read up on research to which she has better access than you do being a part of academia, they also publish their own research. It has a reason that the latest WPATh convention was hosted in Amsterdam.

I'm not willing to research all that medical stuff, I'm a literary scientist. So I spent tens of thousands of hours studying fairy tales (I specialized in the sleeping beauty), oral traditions, James Joyce and the mechanics of interpretation. I speak seven languages, but only had one year of chemistry and biology in highschool. Given my own limitations and general lack of interest in medical issues, I need to trust someone. Would it be wise to trust you, or my endocrinologist?

I don't want to factcheck your claims, these kinds of publications bore me to no end and I hardly uiderstand the language used in it. I intend to keep it that way.

QuoteI disagree on one point though. Even professionals, doctors are fallible and make mistakes so that double checking, talking to other professionals, reading research material can be useful and in a few instances, life-saving, as I've realized in the past.

Of course doctors aren't infallible, but it's reasonable to assume that you're more fallible, not even being qualified as a doctor. Also, when you make a mistake, you cannot be held accountable for that, there are no checks and balances on your dissemination of knowledge. When my endocrinologist makes a mistake, disciplinary hearings will be held and she may even be thrown out of her profession.

When I bring my broken car to a mechanic, there's always a slim chance she made a terrible mistake, causing me to crash and die on the road. But the chance of that happening would be higher when I'd let an unqualified friend fix my car.

QuoteI don't really see where I may be misinterpreting or quoting out of context but perhaps if you pointed out exactly where I did this, I may realize my own wrongdoing and if so, I apologize in advance. I try to make things as clear as possible but if you have difficulty understanding, I apologize again and would do everything in my power to makes things more understandable.

Nope, I leave your claims unchallenged and am entirely unwilling to factcheck. I don't want to be forced to read up on research that bores me and instead choose to trust the professional treating me. How could I presume to falsify medical knowledge if I don't even know the difference between units of measurement?

QuoteMy goal is to inform so that you may relate this information to your own doctors and incite constructive discussions which may benefit not only you, but the doctor and their own patients. I am open to criticism and always willing to learn. Everyone of us can provide useful feedback and has something important to say and add to the discussion. Every voice is important. :)

Look, I have 45 minute meetings with my endo and we have more pressing matters to discuss than the unqualified opinions of some anonymous person on a forum. You seem to assume that she has no knowledge of the things you came up with, which is presumptuous with an aftertaste of narcissism. You may be willing to learn, but who says she's willing to teach? And no, not every voice is important. Relevance depends on qualifications.

QuoteSpiro doesn't allegedly lower blood pressure. This is a fact, as many in this forum can attest to. Several studies also confirm this. Whereas cyproterone acetate, as far as I know, doesn't and actually can lead to water retention, I think, due to its glucocorticoid effects. As always, double check with your doctors and available resources but you say you don't have the time or willingness so what am I to do?

That may or may not be true, but my point was, that you didn't prove that with the quotes you came up with, which didn't even mention spiro. But you went further than that and even claimed that my hormonal treatment could replace my heart meds. Now that's a dangerous claim to make. It may well be an effect of spiro that it lessens one's blood pressure to some extent, but only if the cause of that high blood pressure is an elevated level of aldosterone. Did you read this research paper (http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008169.pub2/abstract;jsessionid=E8223A09C61C83D74266DF60F4D81C2F.f02t03) about it?

Even the Wikipedia page (https://en.wikipedia.org/wiki/Spironolactone#High_blood_pressure) on spiro states:

"...a Cochrane review found adverse effects at high doses and little effect on blood pressure at low doses in the majority of people with high blood pressure."

So I'll just stick with my present medication if you dont mind, which causes a 125/70 heart rate. If it ain't broken, don't fix it.

QuoteI am not a cardiologist either and am neither skilled or had training in that field. But, I report what studies find and then you decide what you want to do with that. Ignore it, or consider it, talk it over with people that ARE skilled and experienced and see what they say.

Yes, you made that abundantyly clear with your ill adviced remarks on spiro that you in fact are not a cardiologist. If I'd follow your advice, I'd be back to a 182 heart rate in no time. Your advice could kill me. You were obviously unaware of the study I just presented to you and instead presented studies as "proof" that didn't evern mention spironolactone. You were just disseminating hot air.

QuoteI am sorry for stressing you out. That was/is not my intention. I hope you will forgive me and truly, you must know that the well-being of each and everyone of you is what matters to me. I care not about my credibility or reputation. My goal is increased awareness, just and respectful treatment of transsexual women and any minority group in this world. I will admit to being stubborn at times and overly persistent. I am far from flawless but every day, I strive to become a better person but I won't ever be perfect. Imperfection is just fine with me.

Yes I forgive you and just hope that you will show a little more modesty in presenting your emphatically unqualified opinions.

Love, hugs and no hard feelings,

Naomi

I agree that reading and studying informations given by Kay and other people about HRT, on Susan's or other discussion panels, takes me a significant amount of time and can be sometimes rather stressful and tiring.
However I have to admit that all these informations have been and still are much much helpful to me for discussing my treatment with doctors and making it as successful and free of adverse effects as possible.

The problem is, that it isn't necessarily information, but might well be misinformation. Like in the spiro example I debunked. Research already proved that high doses of spiro generally have adverse affects on blood pressure and low doses do nothing, but Kay presented spiro as an effective blood pressure medicine, even going as far as claiming the spiro could replace my heart meds. If I had heeded that opinion, it could have killed me.

It's also about the way Kay frames her opinions (I know a little bit more about epistemology than medicine). They're presented as objective, propositional knowledge (knowledge being justified true belief (http://documents.routledge-interactive.s3.amazonaws.com/9781138793934/A2/Epistemologyandmetaphysics/JustifiedTrueBelief.pdf)) instead of opinion, I don't see a shred of doubt or a disclaimer in a statement followed by a set of impressive research quotes. It's presented as fact instead of opinion, which is misleading.

Quote from: Naomi71 on November 14, 2016, 04:25:21 AM
Kay presented spiro as an effective blood pressure medicine, even going as far as claiming the spiro could replace my heart meds. If I had heeded that opinion, it could have killed me.

I do not self-medicate and I'd never consider as prescriptions advices given about HRT here or elsewhere. I take them only as elements (among others) to be discussed with my doctors.

Quote from: Naomi71 on November 14, 2016, 04:25:21 AM
Research already proved that high doses of spiro generally have adverse affects on blood pressure and low doses do nothing, but Kay presented spiro as an effective blood pressure medicine

Spironolactone COULD perhaps be an effective blood pressure medicine (as well as having anti-androgenic actions) and an option given your situation (to be ultimately determined by doctor) at typical doses prescribed to transsexual women. Doctors will usually start low (but not too low) to see how patient reacts.

Quote from: Lucie on November 14, 2016, 04:42:57 AM
I take them only as elements (among others) to be discussed with my doctors.

Exactly that. I present information others may or may not be aware so that it may be critically examined with health experts. There is a chance it could be helpful or not. Experts don't always know everything, as I've several times realized and may benefit from their own patient's research and feedback. Mine did and she thanked me. My doctor welcomes and even encourages me to share any pertinent studies I come across with her. Working together with one's doctor is, I believe, the optimal and most effective approach instead of the traditional, he/she says and I follow.

I once went to see a doctor who held a prestigious position in endocrinology, who treated many transsexual patients before and who knew nothing about cyproterone acetate's effects on prolactin going as far as denying it when studies (and plenty of anecdotal evidence) clearly show otherwise. Another very reputable endocrinologist claimed HRT in transsexual women would increase the risk of breast cancer when it was found and concluded in studies that this was not the case so I corrected him and he finally agreed.

My point here is not to put down doctors and I don't blame them for not knowing everything (they are busy, they can only do so much) but to simply say that on occasion, being armed with extra knowledge in the matter puts you at an advantage, where you can share information with your doctor that he/she may not be aware of. Help them become better informed, is what I'm saying and protect yourself of potential mistreatment or increase your odds of getting the best treatment possible. My endocrinologist even admitted that what he valued most was his patient's feedback and that is how he learned the most, not what he was taught at school (i.e. Cambridge University). HRT treatment of transsexual individuals is certainly not something you learn about in medical school but on the field, through your patients and by reading as much on the research pertinent to the matter, as possible, the latter being somewhat of a problem for doctors that just don't have the time, sometimes, to keep up and read all that stuff.

Ah yes. All those wretched ignorant doctors who know next to nothing about their own profession. Lay people should help them!

Quote from: KayXo on November 14, 2016, 07:02:40 AM
Spironolactone COULD perhaps be an effective blood pressure medicine (as well as having anti-androgenic actions) and an option given your situation (to be ultimately determined by doctor) at typical doses prescribed to transsexual women. Doctors will usually start low (but not too low) to see how patient reacts.

No Kay, please. It could not. Did you even read the research I linked to in my reply to you? I already tried to explain to you, that spiro only works as a high blood pressure inhibitor if that pressure is caused by a thyroid disorder (http://universityhealthnews.com/daily/heart-health/unexpected-symptoms-of-thyroid-issues-include-high-blood-pressure/), resulting in elevated levels of aldosterone  (https://en.wikipedia.org/wiki/Aldosteronel)in your body. Spiro is an aldosterone inhibitor and definitely doesn't work as a high blood pressure inhibitor in general like you continue to falsely suggest, notwithstanding evidence to the contrary, that you for some reason choose to ignore. Thing is, my aldosterone levels are just fine, the high blood pressure has other causes. In my case, it's a hereditary thing.

I also showed you, that even with people who have that thyroid disorder, it's not working in low doses and has adverse effects in high doses. So no. in my case it could not have that effect under any circumstance.

More importantly, you're trying to solve a nonexistent problem. With the heart medication I'm presently taking, my blood pressure levels are just fine and I get half the standard dose of cypro, that already made my testosterone unmeasurable (below 0.5).

So no, I will not bother my cardiologist and endocrinologist with this. It's nonsens.

p.s. You still failed to come up with research proving all the wonderful workings of spiro as a general high blood pressure inhibitor. You don't have to come up with lengthy quotes, but why don't you provide me with a few links to all that great research you're referring to?

Obstet Gynecol. 2015 Mar;125(3):605-10.

"In transgender women, estrogen therapy, with or without antiandrogen therapy, was associated with lower BP."

"Transgender women were treated with estrogens. Fourteen (88%) were given sublingual micronized 17-beta estradiol (...). One subject was given (...) estradiol via transdermal patch, and one subject received estradiol valerate (...) intramuscular every 2 weeks. All but one transgender woman (who wished to retain erectile function) were administered spironolactone"

"Transgender women (persons assigned male at birth, but who identify as females and who use estrogens with or without an anti-androgen to develop female secondary sex characteristics) had normal median baseline and 6 month body mass index (24.8 kg/m2 (IQR=4.3) and 23 kg/m2 (IQR=4.5) respectively). Both systolic and diastolic median blood pressures in this group dropped significantly from baseline to 6 months (130.5 mmHg (IQR 11.5) to 120.5 mmHg (IQR 15.5) p=.006; 78 mmHg (IQR 21) to 67 mmHg (IQR 12), p=.001 respectively)."

"All transgender women had estradiol levels at least in the physiologic female – range at 6 months, with 3/16 (19%) having supraphysiologic levels > 1000pg/dl (including the one transgender woman using intramuscular estradiol valerate). At 6 months, free testosterone was in the female physiologic range in 14/15 (93%), however only 10/15 (66%) had total testosterone levels in the female physiologic range (Table 4)."

Arch Sex Behav. 1989 Feb;18(1):49-57.

"The clinical and hormonal response to 12-month therapy with the antiandrogen, spironolactone, in conjunction with near-physiologic doses of female gonadal steroids in 50 transsexual males, is presented."

"The antihypertensive medication, spironolactone, is an effective therapy for androgen excess in women (Cummings et al., 1982; Shapiro and Evron, 1980; Messina et al., 1983). Although it was created as a mineralocorticoid antigonist, it is a true antiandrogen since it interferes with dihydrotestosterone action in the pilosebaceous unit. Spironolactone has multiple other actions including lowering testosterone (T) production by reduction of cytochrome P450, decreasing sex hormone binding thereby increasing free T clearance, and lowering gonadotrophins (Givens, 1985)."

"This study reports three changes to conventional therapy for transsexual men: (i) near-physiologocal doses of cyclic oral conjugated estrogen, (ii) cyclic or continuous medroxyprogesterone, and (iii) spironolactone."

"Systolic blood pressure dropped (128 +/- 14 to 121 +/- 14 mm Hg, p less than 0.05). The clinical response, including decreased male pattern hair, breast development, feminization, and lack of erections was excellent in most subjects."


Interesting study I came across...

J Sex Med. 2016 Nov;13(11):1765-1772.

"Eighty-two patients were included in the spironolactone group and 31 patients were included in the CPA group. Baseline HDL and prolactin levels were not significantly different between the two groups. At 12 months, HDL increased by 0.10 mmol/L (SD = 0.24) in the spironolactone group but decreased by 0.07 mmol/L (SD = 0.21) in the CPA group (P = .002). The difference remained significant after adjusting for baseline HDL, use of lipid-lowering drugs, and age. The change in prolactin was +3.10 μg/L (SD = 5.70) in the spironolactone group and +11.8 μg/L (SD = 8.63) in the CPA group (P < 0.001). This difference also remained significant after adjusting for baseline prolactin level."

"These data suggest that spironolactone use in transgender women increases HDL levels and that CPA has the opposite effect. CPA also is associated with a larger increase in prolactin. These factors should be considered when choosing between these two antiandrogen agents."

I know several transsexual women who changed their blood pressure medication to Spironolactone after starting transition and had positive outcomes. Not only did it lower blood pressure but it inhibited androgen significantly. This needs to be discussed with a physician, of course as each case is different so while, it may be doable and beneficial for some, it may not for others. There is no harm in simply bringing it up with doctors and see what they say.

You've only managed to come up with research that really doesn't prove your point about spiro, although you present the information deceptively to make it look like it does if one takes a superficious look at it. A little intellectual integrity would be nice.  All of the papers you quote from show combinations with other substances that lower blood pressure too and your first paper even explicitly states, that the lower blood pressure was also accomplished without antiandrogen therapy (that is, spiro).

In an earlier reply I mentioned cherrypicking, misinterpreting and taking out of context. You did all of that.

Quote from: KayXo on November 14, 2016, 10:27:14 AM
Obstet Gynecol. 2015 Mar;125(3):605-10.

"In transgender women, estrogen therapy, with or without antiandrogen therapy, was associated with lower BP."

"Transgender women were treated with estrogens. Fourteen (88%) were given sublingual micronized 17-beta estradiol (...). One subject was given (...) estradiol via transdermal patch, and one subject received estradiol valerate (...) intramuscular every 2 weeks. All but one transgender woman (who wished to retain erectile function) were administered spironolactone"

That doesn't prove its because of the spiro these women have lower blood pressure. In fact it was proven that estradiol protects against hypertension, so this is a misrepresentation. Are you now taking research results out of context to create the false suggestion it was all because of the spiro? To wit (from "estrogen and hypertension (https://www.ncbi.nlm.nih.gov/pubmed/16965722)")

" Both animal experimental and human clinical investigations suggest that estrogen engages several mechanisms that protect against hypertension, such as activation of the vasodilator pathway mediated by nitric oxide and prostacyclin and inhibition of the vasoconstrictor pathway mediated by the sympathetic nervous system and angiotensin."

Additionally, the lower blood pressure was also accomplished without the spiro, like you quoted yourself.

QuoteThe clinical and hormonal response to 12-month therapy with the antiandrogen, spironolactone, in conjunction with near-physiologic doses of female gonadal steroids in 50 transsexual males, is presented."

"Systolic blood pressure dropped (128 +/- 14 to 121 +/- 14 mm Hg, p less than 0.05). The clinical response, including decreased male pattern hair, breast development, feminization, and lack of erections was excellent in most subjects."

Doesn't prove anything either about spiro, because gonadol steroids already have beneficial cardiovascular effects. To wit (from "Effects of Gonadal Steroids and Their Antagonists on DNA
Synthesis in Human Vascular Cells (https://www.researchgate.net/profile/Fortune_Kohen/publication/13609689_Effects_of_Gonadal_Steroids_and_Their_Antagonists_on_DNA_Synthesis_in_Human_Vascular_Cells_Dalia_Somjen_Fortune_Kohen_Anat_Jaffe_Yehudit_Amir-Zaltsman_Esther_Knoll_and_Naftali_Stern/links/0046353a68fce7067e000000.pdf)"):

"Gonadal steroid–dependent inhibition of VSMC proliferation and stimulation of endothelial
replication may contribute to vascular protection and remodeling responses to vascular injury."

The "interesting study" you came across doesn't even look at blood pressure.

So no, you didn't prove anything, but just took some research out of context that doesn't  prove a causal relationship between spiro and lower blood pressure.

QuoteI know several transsexual women who changed their blood pressure medication to Spironolactone after starting transition and had positive outcomes.

Anecdotal "evidence" doesn't prove a thing either.

Quote from: Naomi71 on November 14, 2016, 11:12:10 AMAll of the papers you quote from show combinations with other substances that lower blood pressure too and your first paper even explicitly states, that the lower blood pressure was also accomplished without antiandrogen therapy (that is, spiro).

Indeed, you are right. I was pressed for time so didn't manage to mention the other studies but they are nonetheless interesting although not showing unequivocally that spironolactone alone reduces blood pressure.

QuoteThe "interesting study" you came across doesn't even look at blood pressure.

Indeed, you are right again. It does not pertain to the matter at hand but came across it so thought it was interesting to mention it since these anti-androgens are typically prescribed to us, pre-op.

QuoteSo no, you didn't prove anything, but just took some research out of context that doesn't  prove a causal relationship between spiro and lower blood pressure.

Hypertension. 2007;49:839-845

"We evaluated the effect among 1411 participants in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm who received spironolactone mainly as a fourth-line antihypertensive agent for uncontrolled blood pressure and who had valid BP measurements before and during spironolactone treatment."

"During spironolactone therapy, mean blood pressure fell from 156.9/85.3 mm Hg (SD: ±18.0/11.5 mm Hg) by 21.9/9.5 mm Hg (95% CI: 20.8 to 23.0/9.0 to 10.1 mm Hg; P<0.001); the BP reduction was largely unaffected by age, sex, smoking, and diabetic status. Spironolactone was generally well tolerated; 6% of participants discontinued the drug because of adverse effects. The most frequent adverse events were gynecomastia or breast discomfort and biochemical abnormalities (principally hyperkaliemia), which were recorded as adverse events in 6% and 2% of participants, respectively. In conclusion, spironolactone effectively lowers blood pressure in patients with hypertension uncontrolled by a mean of ≈3 other drugs. Although nonrandomized and not placebo controlled, these data support the use of spironolactone in uncontrolled hypertension."

The dose used was lower than what is typically prescribed to transsexual women. Adverse effects, as expected. Among those, some we don't mind at all like gynecomastia. :)

Addition of spironolactone very effective in resistant hypertension
31-8-2015 • ESC - London 2015

The principal results of the Prevention And Treatment of Hypertension With Algorithm based therapY (PATHWAY) - Optimal treatment of drug resistant hypertension - PATHWAY 2
Presented at the ESC Congress 2015 by: Bryan Williams (London, UK)

"PATHWAY 2 examined whether additional diuretic therapy with spironolactone would be the most effective at reducing BP compared to treatment with two other antihypertensives that have different mechanisms of action: doxazosin which acts to reduce arterial resistance, and bisoprolol which acts to reduce cardiac output.
The study included patients with resistant hypertension who were already treated with maximally tolerated doses of a combination of three drugs"

"In 314 patients, spironolactone had superior HSBP control compared to placebo (a reduction of 8.70 mmHg, P<.001); doxazosin (a reduction of 4.03 mmHg, P<0.001), and bisoprolol (a reduction of 4.48 mmHg, P<0.001); as well as the mean of doxazosin and bisoprolol (a reduction of 4.26 mmHg, P<0.001)."

"Overall, almost three quarters of patients with uncontrolled blood pressure saw a major improvement in their blood pressure on spironolactone, with almost 60% meeting a stringent measure of blood pressure control (P<0.001)."

"Spironolactone was the best drug at lowering blood pressure in 60%, whereas bisoprolol and doxazosin where the best drug in only 17% and 18% respectively."

"Spironolactone was well tolerated with no significant excess adverse effects with the caveat that serum potassium levels and renal function should be monitored on treatment and treatment duration was too short to assess incident gynecomastia (~6% in longer-term studies)"

"Spironolactone unequivocally showed to be the most effective treatment for resistant hypertension."

"According to prof. Williams, the findings "challenge the concept that that resistant hypertension cannot be treated adequately with drug therapies, and suggest that treatments which have a natriuretic action, in that they promote sodium excretion, are likely to be the most effective"

Methodist Debakey Cardiovasc J. 2015 Oct-Dec;11(4):235-9.

"Spironolactone and eplerenone both affect reductions in blood pressure either as mono- or add-on therapy; moreover, they each afford survival benefits in diverse circumstances of heart failure and the probability of renal protection in proteinuric chronic kidney disease."

"Hyperkalemia should always be considered a possibility in patients receiving either of these medications; therefore, anticipatory steps should be taken to minimize the likelihood of its occurrence if long-term therapy of these agents is being considered."

Nephrology (Carlton). 2015 Aug;20( 8 ):567-71.

"At 6 months, systolic BP decreased by 24 ± 9.2 mmHg (from 163.6 ± 8.6 to 139.6 ± 8.1 mmHg) in the spironolactone group, compared with 13.8 ± 2.8 mmHg (from 162 ± 7.9 to 148 ± 6.4 mmHg) in the furosemide group (P < 0.01). Diastolic BP fell 11 ± 8.1 mmHg in the spironolactone group compared with 5.2 ± 2.2 mmHg in the furosemide group (P < 0.01)."

"Spironolactone is more effective than furosemide for control of BP in RHT patients, with a positive added effect on albuminuria. Spironolactone is safe in patients with mild kidney impairment, although serum potassium should be closely monitored, especially in diabetics."

Medicine (Baltimore). 2014 Dec;93(27)

"This study was designed to assess the effect of the addition of low-dose spironolactone on blood pressure (BP) in patients with resistant arterial hypertension. Patients with office systolic blood pressure (SBP) >140 mm Hg or diastolic blood pressure (DBP) >90 mm Hg despite treatment with at least 3 antihypertensive drugs, including a diuretic, were enrolled in this double-blind, placebo-controlled, multicentre trial."

"One hundred sixty-one patients in outpatient internal medicine departments of 6 hospitals in the Czech Republic were randomly assigned to receive (...) spironolactone (N = 81) or a placebo (N = 80) once daily as an add-on to their antihypertensive medication, using simple randomization."

"At 8 weeks, BP values were decreased more by spironolactone, with differences in mean fall of SBP of -9.8, -13.0, -10.5, and -9.9 mm Hg (P < 0.001 for all) in daytime, nighttime, and 24-hour ambulatory BP monitoring and in the office. The respective DBP differences were -3.2, -6.4, -3.5, and -3.0 mm Hg (P = 0.013, P < 0.001, P = 0.005, and P = 0.003). Adverse events in both groups were comparable. The office SBP goal <14 mm Hg at 8 weeks was reached in 73% of patients using spironolactone and 41% using placebo (P = 0.001). Spironolactone in patients with resistant arterial hypertension leads to a significant decrease of both SBP and DBP and markedly improves BP control."

Med J Aust. 1980 Feb 9;1(3):124-5.

"Once-a-day therapy with spironolactone has been compared with a twice-a-day regimen in an open crossover trial in patients with essential hypertension. When compared with placebo, both treatments significantly lowered blood pressure. Twice-a-day therapy provided slightly better blood pressure control than the once-a-day dosing schedule. There were only minor differences in biochemical findings between the two regimens. Three of the 17 patients developed reversible gynaecomastia."

J Hypertens. 2013 Oct;31(10):2094-102.

"Low dose spironolactone exerts significant BP and urinary albumin creatinine ratio lowering effects in high-risk patients with resistant hypertension and type 2 diabetes mellitus"

Am J Cardiol. 1990 Jun 19;65(23):36K-38K.

"In a double-blind, randomized, multicenter study of 194 patients with moderate hypertension, spironolactone and nifedipine were found to reduce blood pressure (BP) to about the same extent and in the same percentage of patients after 45 days of treatment (47 and 50%, respectively)."

Am J Cardiol. 1987 Oct 1;60(10):820-5.

"Despite limitations inherent in the interpretation of data banks, it is concluded that spironolactone administered in daily practice reduced BP without inducing adverse metabolic adverse effects"

Eur J Clin Pharmacol. 1982;21(4):263-7.

"Since there is only scanty, indirect information about the mechanism of the hypotensive effect of spironolactone, 9 patients with essential hypertension were studied according to a randomised double-blind, cross-over protocol."

"After spironolactone there was a significant decrease in the systolic and diastolic blood pressures in the supine, sitting and standing positions; the sitting systolic and diastolic blood pressure decreased by (mean +/- SE) 27 +/- 4mm Hg (p less than 0.001) and 11 +/- 4mm Hg (p less than 0.02), respectively."

"The present data confirm the hypotensive properties of spironolactone and show that this effect is associated with dilatation of muscle and skin arteries in many but not in all the patients."

Hypertension. 1980 Sep-Oct;2(5):672-9.

"In a prospective, double-blind, intraindividual, cross-over, placebo-controlled multicenter study, clinical and biochemical effects of once daily postprandial dose regimens of (...) spironolactone were investigated in 45 outpatients with primary hypertension"

"All three spironolactone doses resulted in statistically significant blood pressure (BP) reductions independent of initial pretreatment levels and yielded satisfactory BP control in more than half of the patients."

"Spironolactone therapy resulted in decreased serum sodium and magnesium values; potassium, creatinine, urate, and triglyceride levels were increased. However, all treatment values were within normal ranges. Side effects were infrequent and mainly of endocrine nature."

J Endocrinol Invest (2015) 38:269–282

"Spironolactone is the anti-androgen most
widely used in the United States. It has similar properties to
those of cyproterone acetate, as it directly inhibits testosterone
secretion and blocks the binding of testosterone to its
receptors. When it is used, blood pressure and electrolytes
need monitoring to avoid hypotension and/or hyperkalemia."

J Sex Reprod Med Vol 1 No 1 Summer 2001
Towards optimal hormonal treatment of male to female
gender identity disorder

"Spironolactone's hypotensive effect
is an advantage in many cases, but in a small minority of
patients, particularly in the leaner and very physically
active individual, the hypotensive effects necessitate a
change in therapy"

Ok, that's better. However, this long list isn't conclusive at all and actually consistently shows a small blood pressure reduction at best. these numbers are not good enough to actually replace beta blockers, like you suggested (i take metoprolol). It proves I would still have high blood pressure on spiro, if anything.

Hypertension. 2007;49:839-845 - nonrandomized and not placebo controlled. Next.

The principal results of the Prevention And Treatment of Hypertension With Algorithm based therapY (PATHWAY) - - Bingo! That's the first relevant paper you came up with. Unfortunately it only focuses on patients with resistant hypertension, which is a tiny percentage of the people suffering from high blood pressure.

Methodist Debakey Cardiovasc J. 2015 Oct-Dec;11(4):235-9. - I should know a little more about methodology before I can properly weigh it. But sounds promising.

Nephrology (Carlton). 2015 Aug;20( 8 ):567-71. - It's considered effective to reduce blood pressure relative to the other medicines that were part of this research. However, compared with my medication, the results reported are laughable. On spiro they went from 163 to 139, while I went from 182 to 125 in less than a week on beta blockers

Medicine (Baltimore). 2014 Dec;93(27) In this study, spiro was used as an add-on to other medication, so it's hard to tell to what extent reduced blood pressure can be attributed to that.

Med J Aust. 1980 Feb 9;1(3):124-5. - A study consisting of 17 patients? Next.

J Hypertens. 2013 Oct;31(10):2094-102. - Only focuses on resistant hypertension and diabetes patients. Next.

Am J Cardiol. 1990 Jun 19;65(23):36K-38K. - only 47% of the patients had reduced blood pressure after a whopping 45 days? ? Not good enough.

Am J Cardiol. 1987 Oct 1;60(10):820-5.  - "limitations inherent in the interpretation of data banks" next.

Eur J Clin Pharmacol. 1982;21(4):263-7. - a study consisting of nine patients? next.

Hypertension. 1980 Sep-Oct;2(5):672-9. - "statistically significant". How much is that? a blood pressure reduction of one already is statistically significant.

J Endocrinol Invest (2015) 38:269–282 - A risk for hypotension (I suppose in people who dont have high blood pressure) is not the same as a reduction of high blood pressure.

OK, anecdotal drive here...  I had sodium-sensitive prehypertension; typically 135/90.  I followed an extremely low sodium diet, 700 mg/day, and got consistent 115/75 to 120/80 readings, in looking over my old logs.  If I went off the wagon one evening, say, dinner out, there was a systolic pressure spike about 20 hours later.  Pretty standard for the sodium sensitive variation.

So, I start on spiro, teeny tiny unprintable dose.  Bang, 100/70.  OK, better raise my salt intake. OK, 110/75.  Proceed to double the dose?  OK, Eeeep!  95/65!  Raise sodium intake to ful 2300 mg/day.

Phew!  I settled out at about 105/70, and considering that I was doing an hour of cardio a day, and no dizziness, that's OK.

My conclusion?  For certain types of hypertension, measured across a population of 1, there is a correlation between spiro and blood pressure.

:D

Quote from: Naomi71 on November 14, 2016, 05:15:02 PM
Ok, that's better. However, this long list isn't conclusive at all and actually consistently shows a small blood pressure reduction at best. these numbers are not good enough to actually replace beta blockers, like you suggested (i take metoprolol). It proves I would still have high blood pressure on spiro, if anything.

You wanted proof for a causal effect between spironolactone and lower blood pressure. I believe the studies I provided, taken together, strongly suggest there is indeed a causal relationship. I spent 12 yrs reading reports from transsexual women who took spironolactone and I know how much it can affect blood pressure, to what extent and that sometimes, it can even cause too much of a drop, resulting in lowering of the dose or withdrawal of the drug. Personally, I don't need further proof but should I come across more studies, I will share them with you. :)

QuoteHypertension. 2007;49:839-845 - nonrandomized and not placebo controlled.

Indeed, randomized double blind placebo controlled trials are the most reliable of the studies BUT do you really think blood pressure would have fallen to such an extent in a placebo group, by 21.9/9.5 mm Hg? I know your answer but it's doubtful.

QuoteThe principal results of the Prevention And Treatment of Hypertension With Algorithm based therapY (PATHWAY) - - Bingo! That's the first relevant paper you came up with. Unfortunately it only focuses on patients with resistant hypertension, which is a tiny percentage of the people suffering from high blood pressure.

Circulation. 2012 Apr 3; 125(13): 1594–1596.

"Using data collected from 2003 through2008, Persell estimated that the prevalence of resistant hypertension was 8.9% of all US adults with hypertension"

"Looking at trends in blood pressure control as measured by NHANES, Egan et al found that the estimated prevalence of resistant hypertension has been increasing progressively over the last several decades.4 Between 1988-1994 the estimated prevalence of resistant hypertension was 5.5% of all US hypertensive adults. Between 1999-2004, the rate was 8.5%, and most recently, between 2005-2008, the estimated prevalence was 11.8%. With an estimated 76 million adult Americans with hypertension, a prevalence rate of almost 12% would translate into an estimated 9 million Americans with resistant hypertension.5"

Not that tiny but still, I agree, a small portion of that population.

QuoteNephrology (Carlton). 2015 Aug;20( 8 ):567-71. - It's considered effective to reduce blood pressure relative to the other medicines that were part of this research. However, compared with my medication, the results reported are laughable. On spiro they went from 163 to 139, while I went from 182 to 125 in less than a week on beta blockers

What I wonder is what would happen if you took estrogen and spiro and progesterone (also shown to have antimineralocorticoid effects and hypotensive action, the latter being confirmed in small scale studies)? Would you need as much of the other medications that you took for control of your blood pressure? This is something I personally would discuss with my doctors and ask if it could be tried, gradually, under their supervision. What's the harm in just proposing this course of action to your doctors? You've never tried this particular approach. Spiro, in addition to estradiol and progesterone, would help further reduce blood pressure and exert anti-androgenic action. Double whammy! 

Food for thought. Take it or leave it. ;)

QuoteMedicine (Baltimore). 2014 Dec;93(27) In this study, spiro was used as an add-on to other medication, so it's hard to tell to what extent reduced blood pressure can be attributed to that.

It isn't because a placebo group WAS present.

"One hundred sixty-one patients in outpatient internal medicine departments of 6 hospitals in the Czech Republic were randomly assigned to receive (...) spironolactone (N = 81) or a placebo (N = 80) once daily as an add-on to their antihypertensive medication, using simple randomization."

"At 8 weeks, BP values were decreased more by spironolactone, with differences in mean fall of SBP of -9.8, -13.0, -10.5, and -9.9 mm Hg (P < 0.001 for all) in daytime, nighttime, and 24-hour ambulatory BP monitoring and in the office. The respective DBP differences were -3.2, -6.4, -3.5, and -3.0 mm Hg (P = 0.013, P < 0.001, P = 0.005, and P = 0.003)."

"The office SBP goal <14 mm Hg at 8 weeks was reached in 73% of patients using spironolactone and 41% using placebo (P = 0.001). Spironolactone in patients with resistant arterial hypertension leads to a significant decrease of both SBP and DBP and markedly improves BP control."

QuoteMed J Aust. 1980 Feb 9;1(3):124-5. - A study consisting of 17 patients? Next.

I see this study as additional proof, additional confirmation, even if the sample was small. It's important to look at the whole picture, I think.

QuoteAm J Cardiol. 1990 Jun 19;65(23):36K-38K. - only 47% of the patients had reduced blood pressure after a whopping 45 days? ? Not good enough.

The dose was somewhat low, had it been slightly higher, perhaps the effect would have been greater/faster. I do however realize that studies found a plateau after which, further increasing dose didn't provide additional reduction in BP. But, that plateau was not fully reached in this particular study as slightly higher doses were found to be more effective in other experiments.

Blood pressure also continued to fall after 90 days. An extra 15-16 for systolic and 8-9 for diastolic.

QuoteAm J Cardiol. 1987 Oct 1;60(10):820-5.  - "limitations inherent in the interpretation of data banks" next.

See how I don't cherrypick and instead mention everything. I could have quoted:

"it is concluded that spironolactone administered in daily practice reduced BP without inducing adverse metabolic adverse effects"

You don't know me. You've made quick personal judgments about me without giving me a chance, a second chance. I seek facts and I care more about that than being right. I will readily admit when I am wrong about something and reconsider after enough proof is provided. Always! These are principles that matter very much to me and that I force myself to abide by, at all times.


"Despite limitations inherent in the interpretation of data banks, it is concluded that spironolactone administered in daily practice reduced BP without inducing adverse metabolic adverse effects"

In addition, in full study,

"Besides those induced by the nonrandom choice of
the therapy, the main bias of such interrogation of a
data bank when used to determine treatment efficacy
are those introduced by the patients lost to follow-up.1°
Indeed, when a patient is not followed-up at the clinic,
it is almost impossible in such a retrospective study to
analyze the reason for his outcome: decision of the
clinic, voluntary choice of the patient or of the general
practitioner, high quality of the results, drug's side effects,
complications due to the disease or the treatment.
However, we already showed the validity of
retrospective analysis of data in the ARTEMIS system
in a study of the cost effectiveness of different methods
of investigating hypertension, which provided the
same results as a simultaneously performed randomized
trial.ll Other authors have also shown that such
pragmatic retrospective analysis could provide results
similar to those obtained in randomized trials in areas
as different as the results of aortocoronary bypass12
or the efficacy of tonsillectomy for recurrent throat
infection.13"

"The results confirm the efficacy of spironolactone
in treating moderate essential hypertension on a long
term basis. Indeed, 60% of the patients had a diastolic
BP of 90 mm Hg or less on treatment, and in only 10%
was it more than 100 mm Hg with this monotherapy."

"These results are in agreement with the reports of randomized studies that concern a small number of patients.14J5"

I know...SMALL. But it ADDS up.

QuoteEur J Clin Pharmacol. 1982;21(4):263-7. - a study consisting of nine patients? next.

But adding yet to the pool of evidence. Small samples here and there eventually become bigger and bigger sample. The whole picture.

QuoteHypertension. 1980 Sep-Oct;2(5):672-9. - "statistically significant". How much is that? a blood pressure reduction of one already is statistically significant.

Looking at the actual results from the study (full article), a difference of 16-22 for systolic between placebo and spironolactone at low and high doses AND a difference of 8-11 for diastolic between placebo and spiro, in supine position. In the upright position, 19-27 for systolic and 8-10 for diastolic. The only thing I take issue with is that results with placebo are only available before Spiro use and not after so that blood pressure was taken pre and post in all Spiro group but only pre for placebo. That is not right and objective. And you say I cherrypick. Pfff...LOL. I thank you though for for making these remarks and helping me look closer at the ways in which I report findings. I am extra careful now. :)

QuoteJ Endocrinol Invest (2015) 38:269–282 - A risk for hypotension (I suppose in people who dont have high blood pressure) is not the same as a reduction of high blood pressure.

If there is a risk of hypotension in people who don't have high blood pressure, then that means that a reduction in blood pressure can occur in normotensive people as well, confirming spironolactone's blood pressure lowering effects which was what you wanted proof of. In other words, even in normotensive individuals, spironolactone can potentially lower blood pressure.

You didn't mention the last study I provided for some reason which states:

J Sex Reprod Med Vol 1 No 1 Summer 2001
Towards optimal hormonal treatment of male to female
gender identity disorder

"Spironolactone's hypotensive effect
is an advantage in many cases, but in a small minority of
patients, particularly in the leaner and very physically
active individual, the hypotensive effects necessitate a
change in therapy"

So that they did notice an improvement in blood pressure in many transsexual patients and even to the point that in a small group of people, blood pressure dropped TOO MUCH.

Really, do you need more proof for spironolactone's effects on blood pressure?

Others:

J Am Geriatr Soc. 2010 Jul;58(7):1327-32.

"To determine the efficacy of spironolactone (SPIRO) and hydrochlorothiazide (HCTZ) as monotherapy in older patients with hypertension in blood pressure (BP) control and measures of vascular stiffness."

"Randomized double-blind trial."

"Forty-five subjects with hypertension (24 men, 21 women, mean age 69)."

"Six months of HCTZ and SPIRO treatment was associated with significant decreases in 24-hour and nocturnal SBP and diastolic BP (DBP) (analysis of variance (ANOVA) P<.001). At 6 months, average 24-hour and nocturnal SBP were lower in the SPIRO than the HCTZ group (P<.001)."

142/81 to 126/74 for Spiro at 6 months (24 hour BP)
130/73 to 116/67 for Spiro at 6 months (nocturnal BP).
Moderate to typically prescribed amount for TS women.

(Remember, it's adding up).

Hypertension. 2010 May;55(5):1217-23.

"Aldosterone receptor blockade and thiazide therapy effectively lower blood pressure in geriatric hypertension. Their impact on sympathetic nervous system function has not been evaluated. In a double-blind, randomized study, 36 patients with stage 1 hypertension underwent 6 months of therapy with either aldosterone receptor blockade (spironolactone, n=19; 68+/-1 years) or hydrochlorothiazide (n=17; 68+/-2 years)."

"Arterial blood pressure decreased significantly with both spironolactone (160+/-3 to 134+/-2 mm Hg; 77+/-2 to 68+/-2 mm Hg) and hydrochlorothiazide (161+/-4 to 145+/-4 mm Hg; 78+/-2 to 73+/-2 mm Hg) treatment."

"These findings demonstrate a beneficial effect of aldosterone receptor blockade on reducing sympathetic nervous system activity and blood pressure in hypertensive older patients."

Clin Exp Hypertens. 2009 Nov;31( 8 ):648-56.

"This study was performed to investigate the additional anti-hypertensive effects and safety of low-dose thiazide diuretic, trichlormethiazide (TCTZ), and a mineralocorticoid receptor blocker, spironolactone (SPI), as add-on therapy in 64 patients whose blood pressure (BP) at office were over 140/90 mmHg, while receiving anti-hypertensive medication including an angiotensin-converting enzyme inhibitor or angiotensin II type I receptor antagonist. After 6 months, we observed a decrease of office and home BP."

From full study,

"After 6 months of treatment, we observed a significant decrease of office BP (systolic BP/ diastolic BP), 140 ± 7/77 ± 10 mmHg to 122 ± 14/71 ± 9 mmHg in the SPI-treated group"

"and of home BP (systolic BP/diastolic BP), 139 ± 6/79 ± 10 mmHg to 124 ± 8/71 ± 9 mmHg in the SPI-treated group"

"In conclusion, low-dose thiazide diuretic or SPI provided a significant additional anti-hypertensive effect in patients in whom hypertension was not controlled by medication"

Clin Cardiol. 2005 Oct;28(10):484-7.

"The study was a prospective, double-blind, randomized, placebo-controlled trial. Thirty elderly subjects between 60 and 85 years of age with isolated diastolic dysfunction and no contraindications for spironolactone were randomized to (...)spironolactone or placebo for 4 months."

Very low dose of Spiro.

"Spironolactone may improve diastolic function in the elderly."

Hypertension. 2005 Sep;46(3):481-7.

"In a prospective, randomized, placebo-controlled, double-blind clinical trial, we used a 2-by-2 factorial design with 4 treatment groups: amiloride (a direct inhibitor of ENaC), spironolactone (an aldosterone receptor antagonist), the combination of both drugs, and placebo. The subjects (n=98) had an elevated blood pressure despite treatment that included a diuretic and a calcium channel blocker; the level of plasma renin activity was < or =0.56 ng/L per second."

"The reductions in systolic and diastolic blood pressures (mm Hg) were, respectively, 9.8+/-1.6 (SE) and 3.4+/-1.0 for amiloride (P<0.001) and 4.6+/-1.6 (P=0.006) and 1.8+/-1.0 for spironolactone (P=0.07)."

"In conclusion, treatment with either amiloride or spironolactone can provide an additional reduction in blood pressure in blacks already receiving conventional antihypertensive therapy."

LOW DOSE spironolactone.

Contraception. 1991 Aug;44(2):113-24.

"Fifty-one hirsute women were randomly treated for nine months with ethinyl estradiol (...) plus norethindrone (...) or (...) ethinyl estradiol plus (...) norethindrone acetate if they needed contraception or spironolactone (...) daily if they did not."

From full study:

"Spironolactone, unlike the two OC preparations, caused a lowering of the systolic blood pressure (Fig. 2)."

79 to 77 after 3 months to 72 after 9 months with Spiro. No real change in other groups.

Br J Clin Pharmacol. 1981 Oct;12(4):585-8.

"All were caucasian, fully ambulant and on an unrestricted
diet. Their ages ranged from 17.6 to 70.7
years, mean 50.3 + 13.2 years"

"Their previous maximum
mean systolic and diastolic blood pressure was 186 +
22/119 + 12 mm Hg (mean + s.d.), with a mean
duration of hypertension 4.9 ± 4.8 years"

"At entry into the study
all patients were taking spironolactone (...).
Their mean supine systolic and diastolic blood
pressure was 153 ± 19/93 + 10 mm Hg. Three of the
patients were receiving another antihypertensive
drug (debrisoquine, propranolol and metoprolol)."

"In this admittedly small group of 13 patients with
moderate hypertension, spironolactone(...) produced effective blood
pressure control when used in once a day or divided
daily dose schedules, either alone or in combination
with other antihypertensive drugs."

Schweiz Med Wochenschr. 1977 Sep 3;107(35):1228-32.

"The blood pressure lowering effects of spironolactone have been studied in 40 subjects with benign essential hypertension in an attempt to determine the optimum starting dose for the drug. The trial was carried out by the double blind method. In almost all patients (...) spironolactone caused a signnificant decrease in diastolic and systolic arterial pressure."

"In conclusion, it would appear that spironolactone--in association with other antihypertensive regiments--may improve the treatment of essential hypertension, especially in patients showing a tendency to hypokalemia and uricemia, and may offer an additional possibility or alternative in the therapy of hypertensive diseases."

Am J Cardiol. 1976 Mar 31;37(4):642-9.

"Twenty-seven patients with hypertension were randomly allocated to a 10 month crossover study. Treatment consisted of spironolactone (...) for 2 months, propranolol (...) for 2 months and combined administration of both drugs at half the dosage. Between treatment periods placebo was given for 2 months. Fourteen patients were previously untreated. The average pretreatment blood pressure for the entire group was 188/114 +/- 16/7(mean +/- standard deviation) mm Hg supine and 188/118 +/- 20/9 mm Hg standing. Both spironolactone and propranolol reduced blood pressure significantly in both the supine and standing positions."

"There was a close correlation between plasma renin activity and the effects of the drugs: With increasing renin level the response to propranolol was better whereas the opposite was true for spironolactone."

"All patients achieved a normal supine pressure. Blood pressure and plasma renin activity returned toward pretreatment values during placebo administration."

From full study,

"During treatment with spironolactone
blood pressure decreased by 34/15 mm Hg in
the recumbent and by 38/12 mm Hg in the standing
positions (P <O.OOl for all) from pretreatment
values. At the end of the corresponding placebo period,
blood pressure again increased to almost pretreatment
values with differences of 11/6 mm Hg supine
and 7/4 mm Hg standing (P <O.Ol for difference
of supine systolic pressure, all other differences P
<0.05)."

"Spironolactone has been reported
to reduce blood pressure in patients with primary
hypertension. In addition, it has been
found especially effective in patients with primary aldosteronisms7,a8
and low renin hypertension.ls,"s Our
study confirms that spironolactone has a clinically
useful antihypertensive effect in patients with primary
hypertension with low and normal plasma renin
activity levels."

Arch Inst Cardiol Mex. 1975 Jul-Aug;45(4):487-94.

"Spironolactone is a diuretic, selective aldosterone, antagonist with its own antihypertensive action which prevents body loss of potassium. Its clinical use has been documented on the treatment of essential arterial hypertension; however, there does not seem to be enough information to form a solid chemical criterion. This work is a clinical evaluation of the antihypertensive effect of the drug using double-blind technic with 41 patients with essential arterial hypertension, all external patients from the Instituto de Cardiología. They were divided in two groups, selected at random, to be able to observe their tensional range with spironolactone every two weeks, during 16 weeks; and using a placebo for the next 16 weeks. On group following this order; and the other one viceversa. After 32 weeks, the results observed show the effect of placebo, as well as spironolactone on arterial pressure and the statistic comparison, states the real antihypertensive effect of the drug on this group of patients."

"The authors suggest that this drug is useful in cases of essential hypertension although its pathway isn't deeply known. Apparently, the antihypertensive effect of spironolactone is not solely on patients with hypertension due to primary aldosteronism."

Eur J Obstet Gynecol Reprod Biol. 2007 Mar;131(1):61-7.

"Thirty-two women with PCOS were divided into two groups: 16 received (...) spironolactone and 16 spironolactone plus (...) licorice"

"Mean blood pressure was significantly reduced during spironolactone treatment, while it was unchanged in women receiving spironolactone plus licorice."

Full study,

"Systolic blood pressure was significantly reduced after 1 and 2 months of therapy with SP, but not during the combination therapy, while diastolic blood pressure was unchanged."

In the range of typical dose for transsexual women. 118 ± 5/82 ± 4 at baseline, 115 ± 4/80 ± 2 at day 4, 115 ± 6/78 ± 3 at day 7, 114 ± 5/75 ± 3 at 1 month (p < 0.05), 113 ± 4/72 ± 5 at month 2 (p < 0.05), with spironolactone treatment. 

Quote from: KayXo on November 14, 2016, 09:17:31 PM
You wanted proof for a causal effect between spironolactone and lower blood pressure. I believe the studies I provided, taken together, strongly suggest there is indeed a causal relationship. I spent 12 yrs reading reports from transsexual women who took spironolactone and I know how much it can affect blood pressure, to what extent and that sometimes, it can even cause too much of a drop, resulting in lowering of the dose or withdrawal of the drug. Personally, I don't need further proof but should I come across more studies, I will share them with you. :)

No, I just pointed out that your earlier message didn't even prove that causal relationship. Of course I know that it exists, I even explained to you how it reduces blood pressure, by functioning as an aldosterone inhibitor, which also shows why it isn't a very effective blood pressure medicine. Most people don't have a high blood pressure because of their high aldosterone levels (one out of a hundred to be precise). You chose to ignore that whole message, but that argument still stands.

You should really stop trying to impress me with the amount of years you spent reading things. I don't care. Whatever you read, It's quite obvious that you just learnt the word "hypertension" from my replies to you, combined that with the search term "spirolacton" in google scholar or science.io, took a superficious look at the search results and cherrypicked a few research quotes you thought fitted your argument, but without truly understanding them. Parrotting research results like that doesn't constitute an actual argument.

I get it. You like to self medicate, want to propagate self medication to others (even set up a forum for it) and believe yourself to be far more knowledgable than an average doctor. The way you deal with research you preselect to fit your "argument" already shows you're not.

QuoteIndeed, randomized double blind placebo controlled trials are the most reliable of the studies BUT do you really think blood pressure would have fallen to such an extent in a placebo group, by 21.9/9.5 mm Hg? I know your answer but it's doubtful.

No, such results are patently unreliable. One should ignore them.

QuoteNot that tiny but still, I agree, a small portion of that population.

A lot of the research of the blood pressure  effects of spiro focuses on that "medicine resistant" group, because it's that part of the population actually benefitting from it. Other blood pressure medicines don't work for that group, beacuse the aldosterone keeps raising the blood pressure, even when taking beta blockers.

those standard blood pressure meds yielding much better results than spiro work just fine for me though.

QuoteWhat I wonder is what would happen if you took estrogen and spiro and progesterone (also shown to have antimineralocorticoid effects and hypotensive action, the latter being confirmed in small scale studies)? Would you need as much of the other medications that you took for control of your blood pressure? This is something I personally would discuss with my doctors and ask if it could be tried, gradually, under their supervision. What's the harm in just proposing this course of action to your doctors? You've never tried this particular approach. Spiro, in addition to estradiol and progesterone, would help further reduce blood pressure and exert anti-androgenic action. Double whammy!

Keep wondering! In the mean time, I'll just continue taking my beta blockers and cypro, if you don't mind. Why did you ignore my notion that the blood pressure reduction on spiro is tiny compared with my beta blockers? Going from 163 to 139 is nothing compared with 182 to 125. Again, if it ain't broken, don't fix it. I'm not a labrat and I'm just fine with my present regimen. You should respect that. I didn't ask you to come up with all kinds of proposals for new regimens and don't see you as sufficiently knowledgeable to even remotely understand what medication would or would not be useful for me. Keep me out of it, I really don't want you to cross that line anymore. even if I had questions or doubts about my regimen, I sure as hell wouldn't ask you for advice.

QuoteFood for thought. Take it or leave it. ;)

I'll leave it and no, it didn't make me think about anything.

QuoteIt isn't because a placebo group WAS present.

My argument wasn't about placebos. What I tried to say, is that in this study, the intake of spiro was combined with other blood pressure meds, so you can't attribute the test results to spiro. It doesn't prove anything exactly like the research you showed in an earlier posting, i which spiro was combined with the intake of estrogen.

QuoteI see this study as additional proof, additional confirmation, even if the sample was small. It's important to look at the whole picture, I think.

You don't see the whole picture if you only study 17 people. It doesn't prove a thing.

etc.

Ok, I've had enough from your pseudoscience now. Like I stated before, I really don't want to have to deal with all that research.

Quote from: Michelle_P on November 14, 2016, 06:34:19 PM
My conclusion?  For certain types of hypertension, measured across a population of 1, there is a correlation between spiro and blood pressure.

I never negated that relationship and even explained what the relationship is (aldosteron etc), just stated that the research Kay came up with didn't even prove that correlation, which she acknowledged herself too.  For some reason she wants to push spiro down my throat and experiment with all sorts of exciting combinations of meds, while I'm doing fine on my beta blockers.

I just need her to respect that and call it a day.

I'm dropping out of this thread and going to leave you two to it  ;)

x

Quote from: Rachel Richenda on November 15, 2016, 02:16:57 AM
I'm dropping out of this thread and going to leave you two to it  ;)

x

I'm sorry about this whole debate, my initial question was about my estradiol blood levels, nothing else. I got carried away in a whole discussion I didn't ask for and even pointed that out halfway. I really don't want to have to deal with Kay's long and dreary lists of search engine results, my hospital doesn't even prescribe spiro (standard t blocker across the ocean but not over here), I wouldn't get it even if I asked for it. Self medication is not an option for me either, so there's no way in hell I will ever take spiro.

I'm not questioning the heart meds and hormones I'm taking, am not open for a change of my regimen (except for upping my estradiol so I have the same dosage as my friends do) and don't feel like having to defend that either.

I trust the judgment of my doctors and really don't feel like second guessing that, it's all working fine for me. It seems Kay is just interested in her own points using my topic as a vehicle for that and it was my mistake to engage. Never again wil I publically discuss my medication, that's the lesson I learnt.

Quote from: Naomi71 on November 15, 2016, 01:43:59 AM
You should really stop trying to impress me with the amount of years you spent reading things. I don't care. Whatever you read, It's quite obvious that you just learnt the word "hypertension" from my replies to you, combined that with the search term "spirolacton" in google scholar or science.io, took a superficious look at the search results and cherrypicked a few research quotes you thought fitted your argument, but without truly understanding them. Parrotting research results like that doesn't constitute an actual argument.

I get it. You like to self medicate, want to propagate self medication to others (even set up a forum for it) and believe yourself to be far more knowledgable than an average doctor. The way you deal with research you preselect to fit your "argument" already shows you're not.

Whatever you or KayXo are right or not, I find your recriminations against her absolutely unfair, they are quite insulting and full of bad faith.

Quote from: Lucie on November 15, 2016, 03:06:24 AM
Whatever you or KayXo are right or not, I find your recriminations against her absolutely unfair, they are quite insulting and full of bad faith.

They're not unfair at all and I stand by them. It already became evident that she isn't pulling these studies from her personal archive after having given them long and deep consideration. That became clear when she came with a list of research quotes that didn't even prove the point she was trying to make, making certain sentences bold as to create the false impression they did. And if you read back the discussion, you will find that she often doesn't even understand the quotes she came up with herself.

In the byline of her own forum she writes that she wants to take her treatment into her own hands, self medication is actively propagated.

A little knowledge is a dangerous thing (http://www.phrases.org.uk/meanings/a-little-knowledge-is-a-dangerous-thing.html) is all I'm saying.