For me, my medical condition, and my transition needs, progesterone is something I felt was not needed.  Every individual should work with their care provider to determine if various medications are appropriate or necessary for them and their goals. 

Blanket 'should/should not' statements regarding medical care and best practices are not appropriate for individual care.  What each individual needs is best determined through educated consultation with their care provider.

Quote from: Michelle_P on January 03, 2019, 01:29:18 PM
Blanket 'should/should not' statements regarding medical care and best practices are not appropriate for individual care.  What each individual needs is best determined through educated consultation with their care provider.

This is so true! 

QuoteIm just basing the facts Im telling you through proven researches and from our fellow sisters who have tried it for years including myself.

Hi Chinee,
just curious if you took micronized progesterone or the earlier synthesized variant?

Quote from: chinee on January 03, 2019, 01:14:40 PM

In addition, progesterone increases prolactin in your body which can cause cancer and alarming in high levels. Also, taking progesterone regularly can have masculinizing effect (You can ask your pregnant neighbors, friends, or relatives and see if all of them is enjoying the increase in progesterone in their body). Words can sometimes persuade us but I aint stopping you from trying it. I was one of you back then trying to only open my eyes about the good side of taking progesterone but at the end of the day you have to also look at the negative effects of it and decide wether its for you or not. The debate wether to take the magic P or not has been there for ages and until now the science behind HRT for trans has no solid answer with regards to this.

Im just basing the facts Im telling you through proven researches and from our fellow sisters who have tried it for years including myself.

Anxiety will always be inside of us with or without progesterone.

Cyproterone acetate also increases prolactin and nobody seems to get too fussed by that.

That said, recent trans specific research is showing that a lot of the data currently being used on the effects of HRT on trans women isn't as applicable as previously thought - being that it is almost entirely based on cis women. Recent studies have shown that risk profiles are not directly transferable, such as the apparent risk of stroke/DVT  - apparently, the actual incidence of this in trans women is measurably lower than it is in cis women. This is just one example of what the research is finding.

As Michelle said, progesterone is the precursor for a number of neurosteroids and other related chem, most of which trans women are likely to be deficient in. This is the reason I'm currently looking in to adding P to my protocol, maybe I'll report back with some blood work and actual data, anecdotes are not so useful.

As for anxiety? Speak to your mental health professional, it's not really part of the deal. The only time I've suffered from anxiety since I came out was chemically induced..

Quote from: PurplePelican on January 03, 2019, 03:51:02 PM
Cyproterone acetate also increases prolactin and nobody seems to get too fussed by that.

That said, recent trans specific research is showing that a lot of the data currently being used on the effects of HRT on trans women isn't as applicable as previously thought - being that it is almost entirely based on cis women. Recent studies have shown that risk profiles are not directly transferable, such as the apparent risk of stroke/DVT  - apparently, the actual incidence of this in trans women is measurably lower than it is in cis women. This is just one example of what the research is finding.

The American Association for Clinical Chemistry (AACC) has published several papers this month in their "Mens Health" issue of the AACC Clinical Chemistry Journal that may be of interest on this topic.

HRT is less risky than birth control pills
https://www.aacc.org/media/press-release-archive/2019/01-jan/studies-find-that-transgender-hormone-therapy-is-less-risky-than-birth-control-pills
A team of researchers led by Dina N. Greene, PhD, of the University of Washington in Seattle has now estimated that in transgender women prescribed estrogen, blood clots only occur at a rate of 2.3 per 1,000 person-years. While this is higher than the estimated incidence rate of blood clots in the general population (1.0-1.8 per 1,000 person-years), it is less than the estimated rate in premenopausal women taking oral contraceptives (3.5 per 1,000 person-years), which means that it is an acceptable level of risk. In order to determine this, Greene's team performed a systematic review of all studies that have included the incidence rate of blood clots in transgender women receiving estrogen therapy, identifying 12 that were most relevant. The researchers then used meta-analysis to combine the results of these 12 studies and calculate a risk estimate that is based on all available evidence to date.  

Effects of Gender-Affirming Hormones on Lipid, Metabolic, and Cardiac Surrogate Blood Markers in Transgender Persons
http://clinchem.aaccjnls.org/content/65/1/119
SUMMARY: Studies describing a higher risk for cardiometabolic and thromboembolic morbidity and/or mortality in transgender women (but not transgender men) mainly covered data on transgender women using the now obsolete ethinyl estradiol and, therefore, are no longer valid. Currently, most of the available literature on transgender people adhering to standard treatment regimens consists of retrospective cohort studies of insufficient follow-up duration. When assessing markers of cardiometabolic disease, the available literature is inconclusive, which may be ascribed to relatively short follow-up duration and small sample size. The importance of ongoing large-scale prospective studies/registries and of optimal management of conventional risk factors cannot be overemphasized.

It's so hard to make any direct correlations. Add co-morbidity issues like smoking, weight and genetic variations d it becomes difficult to make sense of any of it. A peri-menopausal woman and a young transwoman share very little physiologically.

lets put the anxiety in another story. I meant by it will always be in us because of we will always be conscious about passing and what would others perceive us in public.

I have tried progesterone regularly and cycling it... It may help with the mood or sharpness of the mind sometimes but there are so much cons about it.

As I have said, ask the pregnant women you know and see if they are all enjoying it. Progesterone can cause masculinizing effect in the long run and can possibly slow down or make your feminization push back from its previous phase.

Ask your doctors too, there answer about adding P are still divided into two categories, pro and non pro P. But yes at the end of the day theres only one way to find out by trying it.

PS: we can also live with taking E alone not to worry

Quote from: chinee on January 03, 2019, 11:57:46 PM
lets put the anxiety in another story. I meant by it will always be in us because of we will always be conscious about passing and what would others perceive us in public.

I have tried progesterone regularly and cycling it... It may help with the mood or sharpness of the mind sometimes but there are so much cons about it.

As I have said, ask the pregnant women you know and see if they are all enjoying it. Progesterone can cause masculinizing effect in the long run and can possibly slow down or make your feminization push back from its previous phase.

Ask your doctors too, there answer about adding P are still divided into two categories, pro and non pro P. But yes at the end of the day theres only one way to find out by trying it.

PS: we can also live with taking E alone not to worry

I'm really interested as to which P you were on, synthesized or micronized?

Quote from: luckygirl on January 04, 2019, 01:08:39 AM

I'm really interested as to which P you were on, synthesized or micronized?

synthesized and those herbal are lethal if you know what I mean. Of course I used the micronized one.

You may want to try to look at other threads about progesterone among mtf not just in susan. You'll see what I am talking about.

Honestly, I also feel not happy when I stop taking P due to my breast started to shrink.

Thanks, Chinee. I have a love-hate relationship with the stuff, It gets rid of my bloat but doesn't actually do one other positive thing for me. Makes me a little manic and cray, too. Nice to have your shoes all fit nicely and your rings slip off smoothly, but I gotta agree with you that it probably just isn't worth it. I got tired of fighting the boob thing so I just said screw it and got a BA.  Downsides for me with P are ruddier skin, maddening mood swings, masculinizing face and hips and rear fat loss. Overall, from my perspective after 3 years of on off with the stuff, I have to say if it's not doing something you just can't live without, dump it.

When I was first started on micronized P I felt some of the side effects like increased appetite (Felt so hungry) and also sleepy (Great for helping me take naps) Perhaps also moody, but this was less apparent. All the side effects went away once my doctor placed me on Dutasteride. It blocks 5alpha reductace enzyme which converts progesterone into it's other forms such as allopregnanolone and this one has many side effects on the brain. At first I had been placed on Finasteride, but this one did not make much of a change, Dutasteride though did stop the side effects entire. I have experienced fuller breasts on Progesterone and fuller thighs which I like. I have read that progesterone CAN be changed to some forms of testeosterone, but I believe these are the weaker forms of testerone which are mainly formed as 'weak adrenal androgens' and these have far less weaker effects than actual testosterone and dehydrotestosterone. I believe some of the weak adrenal androgens can be converted to dehyrdrotestosterone but it involves the 5 alpha reductace enzyme which is being blocked by dutasteride, so I am not that worried about it. DHT is supposed to be like x10 stronger than T so I am happy to have that covered by Dutasteride.

Also someone keeps mentioning pregnancy and virilization effects and I think this is a bad example to use. Testosterone does increase during pregnancy and I read that when the baby is male the Testosterone levels during pregnancy are higher (If I remember right).

https://www.ncbi.nlm.nih.gov/pubmed/2069866

"Maternal testosterone and fetal sex.
Meulenberg PM1, Hofman JA.
Author information
Abstract

To investigate the influence of fetal sex on maternal testosterone levels throughout pregnancy, blood was sampled from 37 healthy pregnant women from week 14 until term and at 6 weeks postpartum. Testosterone concentrations were measured with a highly specific RIA after chromatographic purification. Mean (+/- SD) testosterone at the end of gestation was significantly higher compared to non-pregnant values (3.10 +/- 2.38 mM/l, n = 32 vs 1.14 +/- 1.06 nM/l, n = 35). It appeared that in women carrying a male fetus testosterone levels gradually increased during pregnancy up to 3.99 +/- 2.72 nM/l. In women carrying a female fetus the levels decreased after the first trimester from 2.44 nM/l to 1.80 nM/l. A statistically significant difference (P less than 0.01) existed in maternal testosterone concentrations between both groups during the second half of pregnancy."

I can't specifically find an article that states higher T is due to increased P during pregnancy. In fact, I read 2 articles that state the increase in T could be due to fetal production from different sources. From the short read it seems to be a little unknown, but they do noted that free T remained similar to no pregnant girls until X time even though total T increased.

https://www.ncbi.nlm.nih.gov/pubmed/7189643

"Total and free testosterone during pregnancy.
Bammann BL, Coulam CB, Jiang NS.
Abstract

Total and free testosterone levels were measured throughout pregnancy and were compared with values found in nonpregnant women to determine whether the increase in plasma testosterone levels during pregnancy can be accounted for entirely by an increase in sex hormone-binding globulin or by an increase in testosterone production that would be reflected by an elevation in plasma free testosterone. The study employed a practical and precise method of determining free testosterone by means of equilibrium dialysis. Even though the testosterone level increased significantly throughout pregnancy, the free testosterone level remained within the range for nonpregnant women until week 28, after which time it was significantly elevated. This indicates that the increase in the total testosterone level before week 28 is due to a decrease in metabolic clearance rate, but after week 28 the production rate is increased. The source of this increase is unknown, but it might be fetal."


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5597951/

"Maternal serum testosterone concentrations increase by 70% during pregnancy (7) and are increased to an even greater degree in women with PCOS (8, 9) and preeclampsia (10). In addition, young maternal age is associated with higher testosterone levels in pregnancy (11, 12, 13). However, the relationship between maternal androgen levels and maternal BMI, weight gain and depression are still less well explored (14).

Generally, maternal testosterone levels are not correlated with the testosterone concentration in the fetal circulation, at least not in conjunction with delivery when the fetal circulation becomes accessible for assessment (15, 16, 17). Presumably, the presence of the aromatase enzyme in the placenta, converting androgens into estrogens, protects the female fetus from direct transfer of maternal testosterone (18). The aromatase enzyme, which is encoded by a gene member of the cytochrome P450 family enzyme, subfamily A, polypeptide 1 (CYP19A1), is about 130 kb long, and located on chromosome 15q21. CYP19A1 tissue-specific expression is regulated by the 5′ flanking region of the gene, which includes multiple tissue-specific promoters (19). Several polymorphisms have been found in the aromatase gene; associations, though sparse, have been found with sex hormones, hyperandrogenism as well as obesity. Among these, the single nucleotide polymorphism (SNP) rs700518 (T > C), located in a coding region of the CYP19A1 gene has been consistently associated with inter-individual differences in estradiol serum levels in men (20, 21, 22), but also with pre-eclampsia (23) and changes in body composition during treatment with aromatase inhibitors (24).

Testosterone levels in the fetus may be assessed at delivery, via the umbilical cord or during pregnancy via the amniotic fluid. From the second trimester and beyond the main source of testosterone into amniotic fluid is via urine from the fetus (25). Mean testosterone levels in the amniotic fluid of male fetuses are significantly higher than those in the amniotic fluid of female fetuses at all stages of gestation (26). It is assumed that the testosterone detected in amniotic fluid of female fetuses is primarily of adrenal origin, where it is partly regulated by adrenocorticotropic-releasing hormone (ACTH) (27)."



Looking at wikipedia the placenta releases levels of HCG and these stimulate testosterone production by the testis in the male fetus which could be a source for increased T if there is amale baby.

https://en.wikipedia.org/wiki/Placenta

"Endocrine function
The first hormone released by the placenta is called the human chorionic gonadotropin hormone. This is responsible for stopping the process at the end of menses when the Corpus luteum ceases activity and atrophies. If hCG did not interrupt this process, it would lead to spontaneous abortion of the fetus. The corpus luteum also produces and releases progesterone and estrogen, and hCG stimulates it to increase the amount that it releases. hCG is the indicator of pregnancy that pregnancy tests look for. These tests will work when menses has not occurred or after implantation has happened on days seven to ten. hCG may also have an anti-antibody effect, protecting it from being rejected by the mother's body. hCG also assists the male fetus by stimulating the testes to produce testosterone, which is the hormone needed to allow the sex organs of the male to grow."

https://www.ncbi.nlm.nih.gov/pubmed/645784

"Maternal peripheral testosterone levels during the first half of pregnancy.
Klinga K, Bek E, Runnebaum B.
Abstract

Peripheral serum testosterone levels were determined in 180 women during weeks 7 to 20 of pregnancy with a specific radioimmunoassay. After a normal pregnancy and delivery 90 serum samples were randomly selected from mothers of boys and 90 serum samples from mothers of girls. The testosterone concentrations were correlated with the sex of the fetuses. The mean testosterone level +/- S.D. in pregnant women with female fetuses was 597 +/- 167 pg. per milliliter. In pregnant women with male fetuses the testosterone concentrations were on the average significantly higher (p less than 0.01), with a mean value of 828 +/- 298 pg. per milliliter. The course of the testosterone concentrations in women with male fetuses showed an increase beginning in week 7, reaching a maximum during weeks 9 to 11, followed by a decrease until weeks 15 to 20. During weeks 9 to 11 of pregnancy fetal sex determination was possible in 28 per cent of the males and in 5 per cent of the females, with a probability of 95.5 per cent."

So I feel that using pregnancy as an example to say Progesterone causes a lot of virilization is not a good example because during pregnancy T is higher in women who have male babies and this is reflected in their blood samples which I feel would have direct effects on possible virilization. The studies have not touched on DHT or other weaker androgens, so who knows if those too increase. I don't think enough evidence has been placed to say Progesterone causes virilization. Progesterone itself I believe does not cause testosterone like virilization.I do believe that certain enzymes could change Progesterone into Testosterone or even DHT, and also weaker androgens, but I need to see which enzymes these are ( I suspect 5 alpha reductase at least) and into what forms of Testosterone these are turned into and if possible into what amouts. I mean, women don't grow a bread during pregnancy right? and..

"Steroid hormone production and uses. Progesterone is largely produced by the corpus luteum until about 10 weeks of gestation. ... When the pregnancy reaches term gestation, progesterone levels range from 100-200 ng/ml and the placenta produces about 250 mg/day.
Hormones in pregnancy - NCBI - NIH
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640235/"

it sounds like the placenta makes really large amounts of progesterone daily. Yet, no full beard on pregnant women or for example start to see FTM injectables like body changes. in IVF they give 50mg of P daily and that is 99% available in the blood due to direct injection into muscle. Micronized P orally is destroyed like 90% + in the gut then what is left goes through a double liver pass that reduces it to lesser forms of P. So what actual little P you get is very little.

I would love to see more data on Progesterone to Testosterone conversion though so if anyone knows please share.

This is a simplified primer on hormones from
https://womeninbalance.org/about-hormone-imbalance/hormones-101/

Hormones You Need to Know
Estrogen
Estrogen stimulates the growth of tissue, such as development of breast and reproductive organs, and ensures their function. In the brain, it boosts the synthesis and function of neurotransmitters that affect sleep, mood, memory, libido, and cognitive factors such as learning and attention span.
Estrogen decreases the perception of pain, preserves bone mass, and increases HDL – the good cholesterol. It also preserves the elasticity and moisture content of the skin, dilates blood vessels, and prevents plaque formation in blood vessel walls.
Estradiol
The most potent form of estrogen made by the ovaries, adrenals and fat cells when older. Estradiol affects the functions of most of the body's organs.
Estriol
The weakest and least active form of estrogen primarily functioning during pregnancy.
Estrone
The primary estrogen after menopause produced mostly by fat cells.
Progesterone
Progesterone is made primarily by the ovaries. The adrenal glands, peripheral nerves, and brain cells produce lesser amounts. Progesterone ensures the development and function of the breasts and female reproductive tract. In the brain, progesterone binds to certain receptors to exert a calming, sedating effect. It improves sleep and protects against seizures.
Progesterone is also a diuretic. It enhances the sensitivity of the body to insulin and the function of the thyroid hormones. It builds bone and benefits the cardiovascular system by blocking plaque formation in the blood vessels and lowering the levels of triglycerides. Progesterone also can increase libido and contribute to the efficient use of fat as a source of energy.
Testosterone
Testosterone is manufactured in women by the ovaries and adrenal glands, enhances libido and sexual response. It strengthens ligaments, builds muscle and bone, assists brain function, and is associated with assertive behavior and a sense of well-being. The level of testosterone influences both stamina and restful sleep. It has a protective effect against cardiovascular disease in both men and women.
Dehydroepiandrosterone (DHEA)
DHEA is made primarily by the ovaries and adrenal gland. Smaller amounts are produced in the skin and brain. DHEA is the most abundant circulating hormone. It provides protection against the effects of physical stress and inflammation.
DHEA can also increase libido and sexual arousal. It improves motivation, engenders a sense of well-being, decreases pain, and enhances immune system function.
DHEA facilitates the rapid eye movement (REM) phase of sleep, enhances memory, and assists in maintaining normal cholesterol levels. DHEA can be converted in into estrogen and testosterone through fat, muscle, bone and liver.
Cortisol
Cortisol is made by the adrenal glands. It regulates the immune response, stimulates the production of glucose, aids short-term memory, and helps the body adapt to stress by increasing heart rate, respiration, and blood pressure.
The level of cortisol increases early in the morning to prepare to meet the demands of the day. It gradually decreases throughout the day and reaches its lowest point late in the evening (a pattern known as "circadian rhythm").
Pregnenalone
Pregnenalone is the precursor (building-block) for all other steroid hormones. It is converted directly into DHEA and/or progesterone. DHEA converts to testosterone and estrogens. Additionally, progesterone converts to estrogens, cortisol, and aldosterone.
It is this succession of conversions that makes human life possible. Without pregnenolone, there can be no human steroid hormone production. Made from cholesterol, pregnenolone is a natural steroid hormone produced primarily in the adrenal glands, but in smaller amounts by many other organs and tissues of the human body, including liver, brain, skin, gonads, and even the retina of the eye. Like many health-promoting hormones, levels of pregnenolone drop with age.

My primary also specializes in gender transition hormone therapy. She is involved in transgender health organizations, follows WPATH protocols, and belongs to a local group of transgender healthcare providers in our city who came together to share best practices. I'm very happy with my results. I take estradiol and spiro (T-blocker) orally and my hormone levels are consistently in the perfect range for females. She asked if I wanted to try progesterone, but I didn't see a need for it, and she said its transitioning benefits are inconclusive. We spend a lot of time discussing med therapies in forums like this, but proper diet, weight management and exercise are overlooked parts of a successful transition to achieve a more female form.

Quote from: Asakawa on January 04, 2019, 06:40:40 PM
When I was first started on micronized P I felt some of the side effects like increased appetite (Felt so hungry) and also sleepy (Great for helping me take naps) Perhaps also moody, but this was less apparent. All the side effects went away once my doctor placed me on Dutasteride. It blocks 5alpha reductace enzyme which converts progesterone into it's other forms such as allopregnanolone and this one has many side effects on the brain. At first I had been placed on Finasteride, but this one did not make much of a change, Dutasteride though did stop the side effects entire. I have experienced fuller breasts on Progesterone and fuller thighs which I like. I have read that progesterone CAN be changed to some forms of testeosterone, but I believe these are the weaker forms of testerone which are mainly formed as 'weak adrenal androgens' and these have far less weaker effects than actual testosterone and dehydrotestosterone. I believe some of the weak adrenal androgens can be converted to dehyrdrotestosterone but it involves the 5 alpha reductace enzyme which is being blocked by dutasteride, so I am not that worried about it. DHT is supposed to be like x10 stronger than T so I am happy to have that covered by Dutasteride.

Also someone keeps mentioning pregnancy and virilization effects and I think this is a bad example to use. Testosterone does increase during pregnancy and I read that when the baby is male the Testosterone levels during pregnancy are higher (If I remember right).

https://www.ncbi.nlm.nih.gov/pubmed/2069866

"Maternal testosterone and fetal sex.
Meulenberg PM1, Hofman JA.
Author information
Abstract

To investigate the influence of fetal sex on maternal testosterone levels throughout pregnancy, blood was sampled from 37 healthy pregnant women from week 14 until term and at 6 weeks postpartum. Testosterone concentrations were measured with a highly specific RIA after chromatographic purification. Mean (+/- SD) testosterone at the end of gestation was significantly higher compared to non-pregnant values (3.10 +/- 2.38 mM/l, n = 32 vs 1.14 +/- 1.06 nM/l, n = 35). It appeared that in women carrying a male fetus testosterone levels gradually increased during pregnancy up to 3.99 +/- 2.72 nM/l. In women carrying a female fetus the levels decreased after the first trimester from 2.44 nM/l to 1.80 nM/l. A statistically significant difference (P less than 0.01) existed in maternal testosterone concentrations between both groups during the second half of pregnancy."

I can't specifically find an article that states higher T is due to increased P during pregnancy. In fact, I read 2 articles that state the increase in T could be due to fetal production from different sources. From the short read it seems to be a little unknown, but they do noted that free T remained similar to no pregnant girls until X time even though total T increased.

https://www.ncbi.nlm.nih.gov/pubmed/7189643

"Total and free testosterone during pregnancy.
Bammann BL, Coulam CB, Jiang NS.
Abstract

Total and free testosterone levels were measured throughout pregnancy and were compared with values found in nonpregnant women to determine whether the increase in plasma testosterone levels during pregnancy can be accounted for entirely by an increase in sex hormone-binding globulin or by an increase in testosterone production that would be reflected by an elevation in plasma free testosterone. The study employed a practical and precise method of determining free testosterone by means of equilibrium dialysis. Even though the testosterone level increased significantly throughout pregnancy, the free testosterone level remained within the range for nonpregnant women until week 28, after which time it was significantly elevated. This indicates that the increase in the total testosterone level before week 28 is due to a decrease in metabolic clearance rate, but after week 28 the production rate is increased. The source of this increase is unknown, but it might be fetal."


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5597951/

"Maternal serum testosterone concentrations increase by 70% during pregnancy (7) and are increased to an even greater degree in women with PCOS (8, 9) and preeclampsia (10). In addition, young maternal age is associated with higher testosterone levels in pregnancy (11, 12, 13). However, the relationship between maternal androgen levels and maternal BMI, weight gain and depression are still less well explored (14).

Generally, maternal testosterone levels are not correlated with the testosterone concentration in the fetal circulation, at least not in conjunction with delivery when the fetal circulation becomes accessible for assessment (15, 16, 17). Presumably, the presence of the aromatase enzyme in the placenta, converting androgens into estrogens, protects the female fetus from direct transfer of maternal testosterone (18). The aromatase enzyme, which is encoded by a gene member of the cytochrome P450 family enzyme, subfamily A, polypeptide 1 (CYP19A1), is about 130 kb long, and located on chromosome 15q21. CYP19A1 tissue-specific expression is regulated by the 5′ flanking region of the gene, which includes multiple tissue-specific promoters (19). Several polymorphisms have been found in the aromatase gene; associations, though sparse, have been found with sex hormones, hyperandrogenism as well as obesity. Among these, the single nucleotide polymorphism (SNP) rs700518 (T > C), located in a coding region of the CYP19A1 gene has been consistently associated with inter-individual differences in estradiol serum levels in men (20, 21, 22), but also with pre-eclampsia (23) and changes in body composition during treatment with aromatase inhibitors (24).

Testosterone levels in the fetus may be assessed at delivery, via the umbilical cord or during pregnancy via the amniotic fluid. From the second trimester and beyond the main source of testosterone into amniotic fluid is via urine from the fetus (25). Mean testosterone levels in the amniotic fluid of male fetuses are significantly higher than those in the amniotic fluid of female fetuses at all stages of gestation (26). It is assumed that the testosterone detected in amniotic fluid of female fetuses is primarily of adrenal origin, where it is partly regulated by adrenocorticotropic-releasing hormone (ACTH) (27)."



Looking at wikipedia the placenta releases levels of HCG and these stimulate testosterone production by the testis in the male fetus which could be a source for increased T if there is amale baby.

https://en.wikipedia.org/wiki/Placenta

"Endocrine function
The first hormone released by the placenta is called the human chorionic gonadotropin hormone. This is responsible for stopping the process at the end of menses when the Corpus luteum ceases activity and atrophies. If hCG did not interrupt this process, it would lead to spontaneous abortion of the fetus. The corpus luteum also produces and releases progesterone and estrogen, and hCG stimulates it to increase the amount that it releases. hCG is the indicator of pregnancy that pregnancy tests look for. These tests will work when menses has not occurred or after implantation has happened on days seven to ten. hCG may also have an anti-antibody effect, protecting it from being rejected by the mother's body. hCG also assists the male fetus by stimulating the testes to produce testosterone, which is the hormone needed to allow the sex organs of the male to grow."

https://www.ncbi.nlm.nih.gov/pubmed/645784

"Maternal peripheral testosterone levels during the first half of pregnancy.
Klinga K, Bek E, Runnebaum B.
Abstract

Peripheral serum testosterone levels were determined in 180 women during weeks 7 to 20 of pregnancy with a specific radioimmunoassay. After a normal pregnancy and delivery 90 serum samples were randomly selected from mothers of boys and 90 serum samples from mothers of girls. The testosterone concentrations were correlated with the sex of the fetuses. The mean testosterone level +/- S.D. in pregnant women with female fetuses was 597 +/- 167 pg. per milliliter. In pregnant women with male fetuses the testosterone concentrations were on the average significantly higher (p less than 0.01), with a mean value of 828 +/- 298 pg. per milliliter. The course of the testosterone concentrations in women with male fetuses showed an increase beginning in week 7, reaching a maximum during weeks 9 to 11, followed by a decrease until weeks 15 to 20. During weeks 9 to 11 of pregnancy fetal sex determination was possible in 28 per cent of the males and in 5 per cent of the females, with a probability of 95.5 per cent."

So I feel that using pregnancy as an example to say Progesterone causes a lot of virilization is not a good example because during pregnancy T is higher in women who have male babies and this is reflected in their blood samples which I feel would have direct effects on possible virilization. The studies have not touched on DHT or other weaker androgens, so who knows if those too increase. I don't think enough evidence has been placed to say Progesterone causes virilization. Progesterone itself I believe does not cause testosterone like virilization.I do believe that certain enzymes could change Progesterone into Testosterone or even DHT, and also weaker androgens, but I need to see which enzymes these are ( I suspect 5 alpha reductase at least) and into what forms of Testosterone these are turned into and if possible into what amouts. I mean, women don't grow a bread during pregnancy right? and..

"Steroid hormone production and uses. Progesterone is largely produced by the corpus luteum until about 10 weeks of gestation. ... When the pregnancy reaches term gestation, progesterone levels range from 100-200 ng/ml and the placenta produces about 250 mg/day.
Hormones in pregnancy - NCBI - NIH
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640235/"

it sounds like the placenta makes really large amounts of progesterone daily. Yet, no full beard on pregnant women or for example start to see FTM injectables like body changes. in IVF they give 50mg of P daily and that is 99% available in the blood due to direct injection into muscle. Micronized P orally is destroyed like 90% + in the gut then what is left goes through a double liver pass that reduces it to lesser forms of P. So what actual little P you get is very little.

I would love to see more data on Progesterone to Testosterone conversion though so if anyone knows please share.

It took me years to finish reading your post kidding! Anyways Im intrigued about taking dutasteride together with progesterone to counter its bad effects.

May I ask if you are already post op? I was wondering because Im not sure if dutasteride and DHT are applicable to post ops but I may be wrong too.

Hi Chinee,

I am not. After castration Testosterone levels drop significantly. The specific range from what I have read online is that after Castration T is left somewhere around 20ng/dl or less. From what I read the left over Testosterone is adrenal in origin. These are the Weak Adrenal Hormones.

https://en.wikipedia.org/wiki/Adrenal_gland#Androgens

"Androgens

Cells in zona reticularis of the adrenal glands produce male sex hormones, or androgens, the most important of which is DHEA. In general, these hormones do not have an overall effect in the male body, and are converted to more potent androgens such as testosterone and DHT or to estrogens (female sex hormones) in the gonads, acting in this way as a metabolic intermediate.[34] "

https://en.wikipedia.org/wiki/Zona_reticularis

"Cells in the zona reticularis produce precursor androgens including dehydroepiandrosterone (DHEA) and androstenedione from cholesterol.[2] DHEA is further converted to DHEA-sulfate via a sulfotransferase, SULT2A1.[3] These precursors are not further converted in the adrenal cortex if the cells lack 17Beta Hydroxysteroid dehydrogenase. Instead, they are released into the blood stream and taken up in the testis and ovaries to produce testosterone and the estrogens respectively. "


This one is a good article to read:

https://www.ncbi.nlm.nih.gov/books/NBK278929/

"INTRODUCTION

The adrenal androgens (AAs), normally secreted by the fetal adrenal zone, the zona fasciculata and the zona reticularis of the adrenal cortex are steroid hormones with weak androgenic activity. The adrenal androgens are DHEA, DHEA sulfate and androstenedione. DHEA and DHEA sulfate are secreted in greater quantities, although androstenedione is more important, because it is more readily converted peripherally to testosterone. Production of testosterone (T) by these glands is minimal (1). Although AAs do not appear to play a major role in the fully androgenized adult man, they seem to play a role in the adult woman and in both sexes before puberty. Girls, women, and prepubertal boys may be negatively affected by AA hypersecretion in contrast to adult men. This capter reviews AA biosynthesis, regulation, physiology and biological action."

"CIRCULATION, PERIPHERAL CONVERSION AND METABOLISM

Adrenal androgens are secreted from the adrenal cortex in an unbound state. Bound steroids are biologically inactive. Androstenedione, DHEA and DHEA sulfate bind mainly to albumin. About 90% of adrenal androgens are bound to albumin and 3% approximately is bound to sex hormone-binding globulin (SHBG). The binding globulins have high affinity and low capacity, whereas, albumin has low affinity and high capacity for steroids.

Adrenal androgens can lead to two different pathways after entering the circulation. Their metabolism can result either in degradation and inactivation or the peripheral conversion to their more potent derivatives testosterone and dihydrotestosterone.

The AAs and their metabolites are inactivated or degraded in various tissues, including the liver and kidneys (69). Major biochemical routes for inactivation and excretion are conjugation of androgens to glucuronate or sulfate residues to produce hydrophilic glucuronides or sulfates that are excreted in the urine (figure 6A).

DHEA, DHEA-S, and 4-A are converted to the potent androgens T and DHT in peripheral tissues. Major conversions are those of 4-A to T and T to DHT by the enzymes 17β -hydroxysteroid dehydrogenase (17β-HSD) and 5-reductase, respectively. Major peripheral sites of androgen conversion are the hair follicles, the sebaceous glands (fig.6A), the prostate,the external genitalia and the adipose tissue. (70,71). DHEAS is the sulfated version of DHEA. This conversion is catalyzed by sulfotransferase (SULT2A1) primarly in the adrenals, the liver, the kidney and small intestine. The levels of DHEAS in the circulation are about 300 times higher than those of free DHEA. DHEAS levels show no diurnal variation, whereas DHEA levels reach their peak in the early morning hours. DHEA secreted by the adrenal gland can be also converted to Δ4-androstenedione. Both DHEA and DHEAS are also metabolized to 7α and 16α – hydroxylated derivatives and by 17β reduction to Δ5-androstenediol and its sulfate. Androstenedione is converted either to testosterone or by reduction of its 4,5 double bond to etiocholanolone or androsterone. Testosterone is converted to DHT in androgen-sensitive tissues by 5β reduction. The product is mainly metabolized by 3α reduction to androstanediol. The metabolites of these androgens are conjugated either as glucuronides or sulfates and excreted in the urine.

Active uptake of androgens and in situ estrogen synthesis occur in peripheral adipose tissue (figure 6B) through the enzymes 17β-HSD and aromatase, respectively (72-75). Peripheral conversion contributes significantly to circulating T levels in women, but not in men, in whom T is largely produced by the testis.

Three main enzyme complexes are involved in the synthesis of estrogens in peripheral tissues (76-78):

    Aromatase for the aromatization of androstenedione to estrone.
    Estrone sulfatase (E1-STS), which catalyses the formation of estrone from estrone sulfate.
    Estradiol-17-β-hydroxysteroid dexydrogenase (17β-HSD) Type 1 which is responsible for the reduction of estrone to the biologically active estrogen, estradiol."

So as you can see enzymes 17β -hydroxysteroid dehydrogenase (17β-HSD) and 5-reductase do the major conversions of these androgen hormones to T and DHT.

It also mentions "Major peripheral sites of androgen conversion are the hair follicles, the sebaceous glands (fig.6A), the prostate,the external genitalia and the adipose tissue."  If I remember right the prostate and external genitalia, which I believe is the scrotum, have a high concentration of 5alpha reductase (if I remember right).

But back to your question! Well, the amount of adrenal hormones released by the adrenals is small and the conversion should also be small. I would say their effect on the body would be small too .  So in terms of effects from these hormones after being converted should be... small! Still they are there and do take effect. The additional possible benefit of taking Dutasteride if you are taking progesterone is that you might see a reduction in the progesterone side effects, maybe. It depends. You'd have to talk to your  doctor about it, but I have a feeling they might not exactly know. Progesterone and Dutasteride relation and effect do not seem to be too well discussed. How often do you see it brought up here? Also, you'd have to be on progesterone already and feel the side effects from it first to see if you get any reduction after being placed on Dutasteride. Otherwise comparing the two would be kind of hard.

I personally think it would not hurt if you are under a doctor's care and have blood work done and are healthy. I believe it took me about a month or so to see a reduction in effects from progesterone after starting Dutasteride. While on Finasteride I did not experience any reduction. Prior to being placed on Finas I was on Dutasteride on my own, but doctor said they only give out Finas at the clinic and it was covered by insurance (I am poor) so I switched. I actually saw a small increase in libido at first while on finas then was placed on Progesterone and felt the side effects from it. Once I brought up the libido to my doctor (and a little hair shedding) he was able to place me back on dutasteride and I saw the difference. Libido also went down which was great. That is just my experience.

Ima not gonna post a tl;dr post but regarding being post op and need or negated need for a dht inhibitor like finasteride or dutasteride, the reality is that ciswomen in important numbers, lacking comorbidities like PCOS, still face androgenic hair loss and I believe 66 to 75 percent of these women regained their hair on finasteride or dutasteride. This would indicate to me that post op women with hair loss may benefit from taking those drugs and it may well negate the negatives from Progesterone for us. I have just added Finasteride back into my protocol of EV and P and will report back with anecdotal feelings in about 30 days regarding my personal efficacy.

true true... but when i searched about dutasteride here, i see negative effects like speech problems and brain fog... Oh well i guess all have its own pros and cons

Quote from: chinee on January 06, 2019, 12:25:01 PM
true true... but when i searched about dutasteride here, i see negative effects like speech problems and brain fog... Oh well i guess all have its own pros and cons

I have been on dutasteride for almost two years and I don't ...  Ummm...  Ah... What was I talking about again?   

Quote from: chinee on January 06, 2019, 12:25:01 PM
true true... but when i searched about dutasteride here, i see negative effects like speech problems and brain fog... Oh well i guess all have its own pros and cons

Well,  I guess almost all medications have some side effect for some people.
You read about the side effects of Finasteride all over the place.  I'm on the strongest dose for many years now, and I am still waiting for the first side effects to show up!

Quote from: chinee on January 06, 2019, 12:25:01 PM
true true... but when i searched about dutasteride here, i see negative effects like speech problems and brain fog... Oh well i guess all have its own pros and cons

Ok, I searched online about dutasteride and speech problems (Because I had never herd that before) and (There really isn't much talk about it)  it eventually links back to propecia/hair loss men forums. The hottest topic there is, of course, hair loss and often the guys are on propecia/finasteride/dutasteride/etc. I have looked into the forums before and always a hot topic is allopregnanolone. These drugs block different forms of 5a-reductase which is the enzyme I mentioned earlier. The enzyme does other things other than turning T into DHT. One of these is when Progesterone is eventually turned into allopregnanolone. The big concern is that allopregnanolone is beneficial for the brain and other areas, and from what I recall, this one is also a big topic in blaming a lot of the bad sexual side effects and emotional sides on the drugs.

Some of the talk (Started by 1 guy in 2009 that then disappeared) sounds like allopregnanolone helps protect neurons in the spinal cord over long term damage (Years worth) that could lead to speech problems and other things.

https://forum.propeciahelp.com/t/finasteride-and-neurological-damage/2187/6

The Dutas insert doesn't mention this and I can't find a formal warning online from like FDA or formal authority? so take this form of speculated damage as a grain of salt. I am not familiar with the spinal topic, but often times inside those hairloss forums people always talk about ways to increase allopregnanolone. Some mention supplements other mention cannabis (Apparently is increases allopregnanolone) and others mention drinking beer/alcohol and other things lol. Also, I have read that some suggest progesterone cream and progesterone supplements because progesterone is eventually turned into allopregnanolone via enzyme action 5a-reductase. So, increasing circulating levels of progesterone could increase levels of allopregnanolone.

There is a number of 5a-reductase enzymes in the body. Dutasteride/Finasteride have a certain amount of enzyme blocking molecules that are released after absorption into the blood which then bind to the enzyme. When the enzyme is bound it is not available for other steroids like for example T which turns into DHT and progesterone like steroids that turn into allopregnanolone. Increasing Progesterone levels means higher levels of circulating Progesterone which means higher chances for the Progesterone to bind to a free 5a-reductase enzyme and be turned into allopregnanolone then released. The enzyme is not bound forever. If it was you'd only take one pill of dutas and be done with it. Instead, you take it daily to keep blocking the enzymes. So, increasing circulating levels of progesterone would increase the chances of it binding first to a not yet bound 5a-reductase and creating allopregnanolone. So, taking progesterone this way might not be bad to keep up the reduced production of allopregnanolone.

I'm not a doctor! And you should talk about this to your doctor, but if you research the subject and logically follow how it works this is essentially it. The enzyme is not bound forever and eventually either gets free or new enzymes come up. It takes some time to get bound again so higher levels of circulating progesterone could possibly yield higher levels of allopregnanolone.

I'd say take the speculative damage with a grain of salt . Take everything the same way! Talking to your doctor is the best thing to do.