I'm 54. About a year or so ago my periods were very irregular but still appearing every 3 months or so. I was prescribed estradiol patches (with cycling progestin) for vaginal pain and this had the effect that my periods came every month.
In September my doctor changed the estrogen patch to a much lower dose vaginal estradiol tablet and stopped the progestin and I did not have a period. Then in December, on the advice of another doctor, I started to use Serenity progesterone cream in addition to the estrogen. I assumed I was post menopausal and took the cream daily, just stopping for a week at the start of the calendar month. Two days after stopping the cream I bled for 4 days, then that stopped and I started the cream again.
Now, seven days after re-starting the progesterone cream, I'm getting another period! This is not just spotting, it's the real thing.
I assume that I stop the cream now for seven days or maybe more. Does anyone understand what's happening? I have an appointment to see the more clued-up doctor on 3rd February but that seems a long way off at the moment.
I can only assume if you have not stopped cycling for more than 12 months in a row you are still premenopausal. You are cycling P in, which will give you a period. Supposedly from what I have read the Wiley protocol will give post menopausal women a period too because of the way the P is cycled in. Hopefully someone else has a better explanation
Thanks, davinci, I think you may be right. I had hoped I'd be done with all that by now but it seems not. Oh well.
You can be fully menopausal but be supplementing enough estradiol and progesterone to cause a period. You would only really know if you stopped using the hormones, but who wants to do that ? :-)
Fairyhedgehog,
Estrogen causes the lining of your uterus to build-up and progesterone causes it to shed. The shedding of lining of the uterus is a period. If you cycle progesterone 14 days out of the month you will continue to have periods because the lining of your uterus is thickening during the days without progesterone. If you want to stop having a monthly period while still taking hormones, you need to take the estrogen and progesterone continuously throughout the entire month. If you have any questions on how to do this please feel free to call me at the pharmacy at 1-800-728-0288.
Thank you,
Nelly Atallah, PharmD
Estrogen causes the lining of your uterus to build-up and progesterone causes it to shed. The shedding of lining of the uterus is a period. If you cycle progesterone 14 days out of the month you will continue to have periods because the lining of your uterus is thickening during the days without progesterone. If you want to stop having a monthly period while still taking hormones, you need to take the estrogen and progesterone continuously throughout the entire month. If you have any questions on how to do this please feel free to call me at the pharmacy at 1-800-728-0288.
Thank you,
Nelly Atallah, PharmD
QUOTE (Pete Hueseman Hormone Expert @ Jan 22 2009, 10:28 PM) 
Estrogen causes the lining of your uterus to build-up and progesterone causes it to shed. The shedding of lining of the uterus is a period. If you cycle progesterone 14 days out of the month you will continue to have periods because the lining of your uterus is thickening during the days without progesterone. If you want to stop having a monthly period while still taking hormones, you need to take the estrogen and progesterone continuously throughout the entire month. If you have any questions on how to do this please feel free to call me at the pharmacy at 1-800-728-0288.
Thank you for your help. I think I need to talk to my doctor about it but I won't give you a ring as I'm in the UK!
fairyhedgehog, I think davinci is right and you are not yet menopausal and you're just having the normal irregular periods of perimenopause.
I supplemented progesterone only for a while and had the same situation you did, sometimes I would be in the middle of a cycle of P and then get a period. So I did just what you are thinking of doing, I just stopped the P, counted the first day of the period as day 1, and began a new cycle.
I supplemented progesterone only for a while and had the same situation you did, sometimes I would be in the middle of a cycle of P and then get a period. So I did just what you are thinking of doing, I just stopped the P, counted the first day of the period as day 1, and began a new cycle.
Thanks, Sandra.
I really hoped I'd be past all that by now but there you go. My friend and my sister, both a year younger than I am, stopped having periods a couple of year ago with no problems. I suppose we're all different.
I really hoped I'd be past all that by now but there you go. My friend and my sister, both a year younger than I am, stopped having periods a couple of year ago with no problems. I suppose we're all different.
QUOTE (SandraSmith @ Jan 23 2009, 12:27 AM)
fairyhedgehog, I think davinci is right and you are not yet menopausal and you're just having the normal irregular periods of perimenopause.
I supplemented progesterone only for a while and had the same situation you did, sometimes I would be in the middle of a cycle of P and then get a period. So I did just what you are thinking of doing, I just stopped the P, counted the first day of the period as day 1, and began a new cycle.
I supplemented progesterone only for a while and had the same situation you did, sometimes I would be in the middle of a cycle of P and then get a period. So I did just what you are thinking of doing, I just stopped the P, counted the first day of the period as day 1, and began a new cycle.
QUOTE (fairyhedgehog @ Jan 15 2009, 04:50 AM)
I'm 54. About a year or so ago my periods were very irregular but still appearing every 3 months or so. I was prescribed estradiol patches (with cycling progestin) for vaginal pain and this had the effect that my periods came every month.
In September my doctor changed the estrogen patch to a much lower dose vaginal estradiol tablet and stopped the progestin and I did not have a period. Then in December, on the advice of another doctor, I started to use Serenity progesterone cream in addition to the estrogen. I assumed I was post menopausal and took the cream daily, just stopping for a week at the start of the calendar month. Two days after stopping the cream I bled for 4 days, then that stopped and I started the cream again.
Now, seven days after re-starting the progesterone cream, I'm getting another period! This is not just spotting, it's the real thing.
I assume that I stop the cream now for seven days or maybe more. Does anyone understand what's happening? I have an appointment to see the more clued-up doctor on 3rd February but that seems a long way off at the moment.
In September my doctor changed the estrogen patch to a much lower dose vaginal estradiol tablet and stopped the progestin and I did not have a period. Then in December, on the advice of another doctor, I started to use Serenity progesterone cream in addition to the estrogen. I assumed I was post menopausal and took the cream daily, just stopping for a week at the start of the calendar month. Two days after stopping the cream I bled for 4 days, then that stopped and I started the cream again.
Now, seven days after re-starting the progesterone cream, I'm getting another period! This is not just spotting, it's the real thing.
I assume that I stop the cream now for seven days or maybe more. Does anyone understand what's happening? I have an appointment to see the more clued-up doctor on 3rd February but that seems a long way off at the moment.
P-cream made me bleed every 2 weeks, it can be tricky and unpredictable. As natural progesterone can be converted, you never know what hormone it will become, it can easily be converted to estrogen; it also can be too little for you or too much, and/or does not clear fast from your system. May be you can switch to other delivery system, vaginal progesterone based on the records shows the best results, perhaps you can switch?
That's interesting, Iradan. I didn't know that and I'll have to look into it. Thanks!
QUOTE (Iradan @ Jan 23 2009, 07:14 PM)
P-cream made me bleed every 2 weeks, it can be tricky and unpredictable. As natural progesterone can be converted, you never know what hormone it will become, it can easily be converted to estrogen; it also can be too little for you or too much, and/or does not clear fast from your system. May be you can switch to other delivery system, vaginal progesterone based on the records shows the best results, perhaps you can switch?
I'm not finding any scientific sources on the 'net which state that progesterone can be converted into estrogen. Can anyone provide one ? And which estrogen does progesterone convert to ? Estradiol ?
I haven't verified this, but here's a diagram from the wikipedia entry for "estrogen" which shows that progesterone can be converted to estradiol.
One path from progesterone to estradiol is:
progesterone -> 17(alpha)-hydroxyprogesterone -> androstenedione -> testosterone -> estradiol
Another path (the only other one ?):
progesterone -> 17(alpha)-hydroxyprogesterone -> androstenedione -> estrone -> estradiol
Obviously there are going to be limitations. First, you need the proper amounts of enzymes (or whatever they're called !) for the conversions, and only a certain amount at each step will be converted.
So nobody should think that if they supplement progesterone then some huge portion of the progesterone is going to be converted to estradiol. In reality, it's probably a very tiny amount, if the conversion happens at all.
One path from progesterone to estradiol is:
progesterone -> 17(alpha)-hydroxyprogesterone -> androstenedione -> testosterone -> estradiol
Another path (the only other one ?):
progesterone -> 17(alpha)-hydroxyprogesterone -> androstenedione -> estrone -> estradiol
Obviously there are going to be limitations. First, you need the proper amounts of enzymes (or whatever they're called !) for the conversions, and only a certain amount at each step will be converted.
So nobody should think that if they supplement progesterone then some huge portion of the progesterone is going to be converted to estradiol. In reality, it's probably a very tiny amount, if the conversion happens at all.
Sandra,
You are right, and I recently found a study showing that progesterone actually shuts down the E receptors. Some of the purveyors of Progesterone cream on the internet are telling women that even if they might need estrogen, they don't need to use it because it 'wakes up' the E receptors causing an increase in E. That is just not true and I've seen women keep slathering that stuff on and feeling worse, yet the advice is to keep using it.
You are right, and I recently found a study showing that progesterone actually shuts down the E receptors. Some of the purveyors of Progesterone cream on the internet are telling women that even if they might need estrogen, they don't need to use it because it 'wakes up' the E receptors causing an increase in E. That is just not true and I've seen women keep slathering that stuff on and feeling worse, yet the advice is to keep using it.
Also, if any hormone conversion is going to take place it's necessary for the ovaries to be functioning well for that to happen, since they are what drives the conversion, according to Vliet.
One thing about hormonal pathways--everyone's individual biochemistry is different and as such, there is no way to know which conversion pathway will be taken in any given person, or that the conversion process will function properly.
DHEA is a necessary adrenal hormone. I tested low, but when I take it, it is clear to me that it is going down a sex hormone pathway, either E or P, I'm not sure which. If one is low in estrogen, other hormones will be more likely to be used to convert to E to make up for the deficit. If one's E levels are optimal, then it is less likely other hormones will be diverted down that pathway.
One thing about hormonal pathways--everyone's individual biochemistry is different and as such, there is no way to know which conversion pathway will be taken in any given person, or that the conversion process will function properly.
DHEA is a necessary adrenal hormone. I tested low, but when I take it, it is clear to me that it is going down a sex hormone pathway, either E or P, I'm not sure which. If one is low in estrogen, other hormones will be more likely to be used to convert to E to make up for the deficit. If one's E levels are optimal, then it is less likely other hormones will be diverted down that pathway.
QUOTE (Sariah @ Jan 24 2009, 01:12 AM)
Also, if any hormone conversion is going to take place it's necessary for the ovaries to be functioning ...
Not exactly, please, read aon menopausal ovary.
QUOTE
Ovarian changes
The primary basis for the progressive decrease and complete cessation of cyclic function of the female reproductive organs at the time of the menopause appears to lie in the ovary itself. There is continuing loss of the primordial follicles during intrauterine life and throughout the reproductive years until the menopause. After about the age of 35 years, the human ovary begins to decrease in weight and size, and contains much fewer oocytes and follicular structures and more atretic and degenerating follicles [7].
The female fetus starts in utero with approximately 6 million primordial follicles which decrease to 600,000 at birth, 300,000 at menarche and 10,000 or fewer near the time of the menopause. A few immature follicles may continue to undergo maturation and atresia even for a few years after the menopause. There have been some reports of postmenopausal ovulation.
It is important to realize that (1) the feedback mechanisms may cause readjustments between the pituitary and ovary as long as there are follicles remaining in the ovary to respond; (2) over a period of 1 or 2 years, reversal of laboratory findings as well as clinical signs and symptoms may occur.
In the menopausal ovary, although ovarian oestradiol and progesterone secretions are sharply reduced, the ovary is nevertheless capable of substantial steroidogenesis. The ovarian stroma cells as well as the adrenal cells have a steroidogenic capacity for producing androstenedione which is converted by the skin and appendages to oestrone [8].
The primary steroidogenic element of the postmenopausal ovary is the stroma, which frequently contains islands of ‘thecal’ cells and may have the appearance of a generalized bilateral thecal hyperplasia. The steroids secreted by the postmenopausal ovary in response to the stimulus from high concentrations of LH are primarily androgens (androstenedione, testosterone), but some oestradiol may also be produced (Table II). In in vitro studies, hyperplastic stroma, when stimulated, produces oestradiol.
...........................................
Extraglandular source of oestrogen
Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman. Most of the oestrone is formed by the peripheral conversion of androstene-dione. After the menopause, the circulating level of androstenedione is about one-half of that seen prior to the menopause. Most of this postmenopausal androstenedione is derived from the adrenal gland, with only a small amount secreted by the ovary. The conversion rate of androstenedione to oestrone is significantly correlated with obesity (body size), because the peripheral conversion of androstenedione is mostly done at skin appendages, especially fat [3]. The circulating oestradiol level after the menopause is approximately 10–20 pg/ml (40–70 pmol/l), most of which is derived from this conversion [9]. The circulating level of oestrone is higher, the mean level being approximately 30–70 pg/ml (110–260 pmol/l). The average postmenopausal production rate of oestrone is approximately 45 mg/24 h
................................................................................
.................................................................................
.........
Summary
* The postmenopausal ovary exhibits direct secretion of very minimal amounts of oestrone and oestradiol.
* The ovarian stroma continues to be stimulated by LH to produce androstenedione and testosterone.
* Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman, with an
* The levels of oestradiol and oestrone are strongly correlated with the percentage of the ideal body weight.
* Menopausal women have an oestrogen milieu that is lower than necessary for reproductive function.
The menopause could be regarded as a physiologic phenomenon that is protective in nature: protective from undesirable reproduction and the associated growth stimuli by oestrogen deficiency as a consequence of ovarian follicular exhaustion, and by the oestrogen-independent consequences of ageing.
The primary basis for the progressive decrease and complete cessation of cyclic function of the female reproductive organs at the time of the menopause appears to lie in the ovary itself. There is continuing loss of the primordial follicles during intrauterine life and throughout the reproductive years until the menopause. After about the age of 35 years, the human ovary begins to decrease in weight and size, and contains much fewer oocytes and follicular structures and more atretic and degenerating follicles [7].
The female fetus starts in utero with approximately 6 million primordial follicles which decrease to 600,000 at birth, 300,000 at menarche and 10,000 or fewer near the time of the menopause. A few immature follicles may continue to undergo maturation and atresia even for a few years after the menopause. There have been some reports of postmenopausal ovulation.
It is important to realize that (1) the feedback mechanisms may cause readjustments between the pituitary and ovary as long as there are follicles remaining in the ovary to respond; (2) over a period of 1 or 2 years, reversal of laboratory findings as well as clinical signs and symptoms may occur.
In the menopausal ovary, although ovarian oestradiol and progesterone secretions are sharply reduced, the ovary is nevertheless capable of substantial steroidogenesis. The ovarian stroma cells as well as the adrenal cells have a steroidogenic capacity for producing androstenedione which is converted by the skin and appendages to oestrone [8].
The primary steroidogenic element of the postmenopausal ovary is the stroma, which frequently contains islands of ‘thecal’ cells and may have the appearance of a generalized bilateral thecal hyperplasia. The steroids secreted by the postmenopausal ovary in response to the stimulus from high concentrations of LH are primarily androgens (androstenedione, testosterone), but some oestradiol may also be produced (Table II). In in vitro studies, hyperplastic stroma, when stimulated, produces oestradiol.
...........................................
Extraglandular source of oestrogen
Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman. Most of the oestrone is formed by the peripheral conversion of androstene-dione. After the menopause, the circulating level of androstenedione is about one-half of that seen prior to the menopause. Most of this postmenopausal androstenedione is derived from the adrenal gland, with only a small amount secreted by the ovary. The conversion rate of androstenedione to oestrone is significantly correlated with obesity (body size), because the peripheral conversion of androstenedione is mostly done at skin appendages, especially fat [3]. The circulating oestradiol level after the menopause is approximately 10–20 pg/ml (40–70 pmol/l), most of which is derived from this conversion [9]. The circulating level of oestrone is higher, the mean level being approximately 30–70 pg/ml (110–260 pmol/l). The average postmenopausal production rate of oestrone is approximately 45 mg/24 h
................................................................................
.................................................................................
.........
Summary
* The postmenopausal ovary exhibits direct secretion of very minimal amounts of oestrone and oestradiol.
* The ovarian stroma continues to be stimulated by LH to produce androstenedione and testosterone.
* Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman, with an
androstenedione-to-oestrone conversion by the skin and appendages.
* The levels of oestradiol and oestrone are strongly correlated with the percentage of the ideal body weight.
* Menopausal women have an oestrogen milieu that is lower than necessary for reproductive function.
The menopause could be regarded as a physiologic phenomenon that is protective in nature: protective from undesirable reproduction and the associated growth stimuli by oestrogen deficiency as a consequence of ovarian follicular exhaustion, and by the oestrogen-independent consequences of ageing.
http://www.gfmer.ch/Books/bookmp/33.htm
QUOTE
Cholesterol is the precursor to all our steroid hormones which include estrogen, testosterone, progesterone, cortisol, aldosterone, and DHEA. Eighty to ninety percent of cholesterol is made by the liver. Cholesterol is converted into pregnenolone which is then converted into progesterone which is converted into androstanedione which can be converted into estrogen or DHEA or testosterone. If the person has excess body fat, they will make an enzyme called aromatase which will convert testosterone into estrogen increasing estrogen levels. If a person has insulin resistance their body will produce two enzymes, one called 17, 20 lyase and the other17 alpha hydroxylase. These enzymes convert progesterone into testosterone which will can cause polycystic ovary syndrome, hair growth, loss of head hair, and infertility in women. The testosterone could then be converted into estrogen by the aromatase enzyme made in body fat, once again increasing total estrogen levels.
In women high estrogen levels can increase the risk of reproductive cancers as well as uterine fibroids, fibrocystic breast, and endometriosis. According to the “Journal of Carcinogenesis” you can have 10 to 50 times the amount of estrogen in breast tissue than in your blood, therefore blood levels of estrogen may not indicate the tissue levels of estrogen. When you're under stress your body will convert your DHEA into cortisol. This process has been named cortisol steal. When this occurs the body's levels of DHEA, aldosterone, estrogen, progesterone, and testosterone will all decrease. This is how stress can cause hormonal imbalances in people.
There are 11 sites on the estrogen molecule for detoxification, and each has three types of estrogen, therefore the body has 36 different types of estrogen. The three primary detoxification sites are the 2 hydroxylation pathway, the 16 hydroxylation pathway, and the 4 hydroxylation pathway. The 2 hydroxyestrogen's are good for you promote health and actually fight cancer. The 16 hydroxyestrogen's are 30 times more mitogenic (causes cell division), and therefore increase the number of cells to potentially turn into cancer. The 4 hydroxyestrogen's are 30 times more carcinogenic and therefore greatly increase the risk of cancer. In our environment there are thousands of synthetic estrogens, these come in the form of plastics, pesticides and other chemicals. These synthetic estrogens are detoxified through the 16 hydroxylation pathway. Alcohol, smoking and hydrogenated fats are detoxified through the 4 hydroxylation pathway. Indole 3 carbonol which can be found in cruciferous vegetables such as broccoli, cauliflower, cabbage, and brussels sprouts all increase the two hydroxylation pathway and therefore promote hormonal balance. Once an estrogen has been detoxified, if it becomes oxidized, it then becomes a quinone, which is also carcinogenic, and this is why we need good antioxidant status.
In women high estrogen levels can increase the risk of reproductive cancers as well as uterine fibroids, fibrocystic breast, and endometriosis. According to the “Journal of Carcinogenesis” you can have 10 to 50 times the amount of estrogen in breast tissue than in your blood, therefore blood levels of estrogen may not indicate the tissue levels of estrogen. When you're under stress your body will convert your DHEA into cortisol. This process has been named cortisol steal. When this occurs the body's levels of DHEA, aldosterone, estrogen, progesterone, and testosterone will all decrease. This is how stress can cause hormonal imbalances in people.
There are 11 sites on the estrogen molecule for detoxification, and each has three types of estrogen, therefore the body has 36 different types of estrogen. The three primary detoxification sites are the 2 hydroxylation pathway, the 16 hydroxylation pathway, and the 4 hydroxylation pathway. The 2 hydroxyestrogen's are good for you promote health and actually fight cancer. The 16 hydroxyestrogen's are 30 times more mitogenic (causes cell division), and therefore increase the number of cells to potentially turn into cancer. The 4 hydroxyestrogen's are 30 times more carcinogenic and therefore greatly increase the risk of cancer. In our environment there are thousands of synthetic estrogens, these come in the form of plastics, pesticides and other chemicals. These synthetic estrogens are detoxified through the 16 hydroxylation pathway. Alcohol, smoking and hydrogenated fats are detoxified through the 4 hydroxylation pathway. Indole 3 carbonol which can be found in cruciferous vegetables such as broccoli, cauliflower, cabbage, and brussels sprouts all increase the two hydroxylation pathway and therefore promote hormonal balance. Once an estrogen has been detoxified, if it becomes oxidized, it then becomes a quinone, which is also carcinogenic, and this is why we need good antioxidant status.
I can't provide link as it is commercial website.
QUOTE (Sariah @ Jan 24 2009, 01:12 AM)
Also, if any hormone conversion is going to take place it's necessary for the ovaries to be functioning ...
Not exactly, please, read aon menopausal ovary.
QUOTE
Ovarian changes
The primary basis for the progressive decrease and complete cessation of cyclic function of the female reproductive organs at the time of the menopause appears to lie in the ovary itself. There is continuing loss of the primordial follicles during intrauterine life and throughout the reproductive years until the menopause. After about the age of 35 years, the human ovary begins to decrease in weight and size, and contains much fewer oocytes and follicular structures and more atretic and degenerating follicles [7].
The female fetus starts in utero with approximately 6 million primordial follicles which decrease to 600,000 at birth, 300,000 at menarche and 10,000 or fewer near the time of the menopause. A few immature follicles may continue to undergo maturation and atresia even for a few years after the menopause. There have been some reports of postmenopausal ovulation.
It is important to realize that (1) the feedback mechanisms may cause readjustments between the pituitary and ovary as long as there are follicles remaining in the ovary to respond; (2) over a period of 1 or 2 years, reversal of laboratory findings as well as clinical signs and symptoms may occur.
In the menopausal ovary, although ovarian oestradiol and progesterone secretions are sharply reduced, the ovary is nevertheless capable of substantial steroidogenesis. The ovarian stroma cells as well as the adrenal cells have a steroidogenic capacity for producing androstenedione which is converted by the skin and appendages to oestrone [8].
The primary steroidogenic element of the postmenopausal ovary is the stroma, which frequently contains islands of ‘thecal’ cells and may have the appearance of a generalized bilateral thecal hyperplasia. The steroids secreted by the postmenopausal ovary in response to the stimulus from high concentrations of LH are primarily androgens (androstenedione, testosterone), but some oestradiol may also be produced (Table II). In in vitro studies, hyperplastic stroma, when stimulated, produces oestradiol.
...........................................
Extraglandular source of oestrogen
Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman. Most of the oestrone is formed by the peripheral conversion of androstene-dione. After the menopause, the circulating level of androstenedione is about one-half of that seen prior to the menopause. Most of this postmenopausal androstenedione is derived from the adrenal gland, with only a small amount secreted by the ovary. The conversion rate of androstenedione to oestrone is significantly correlated with obesity (body size), because the peripheral conversion of androstenedione is mostly done at skin appendages, especially fat [3]. The circulating oestradiol level after the menopause is approximately 10–20 pg/ml (40–70 pmol/l), most of which is derived from this conversion [9]. The circulating level of oestrone is higher, the mean level being approximately 30–70 pg/ml (110–260 pmol/l). The average postmenopausal production rate of oestrone is approximately 45 mg/24 h
................................................................................
.................................................................................
.........
Summary
* The postmenopausal ovary exhibits direct secretion of very minimal amounts of oestrone and oestradiol.
* The ovarian stroma continues to be stimulated by LH to produce androstenedione and testosterone.
* Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman, with an
* The levels of oestradiol and oestrone are strongly correlated with the percentage of the ideal body weight.
* Menopausal women have an oestrogen milieu that is lower than necessary for reproductive function.
The menopause could be regarded as a physiologic phenomenon that is protective in nature: protective from undesirable reproduction and the associated growth stimuli by oestrogen deficiency as a consequence of ovarian follicular exhaustion, and by the oestrogen-independent consequences of ageing.
The primary basis for the progressive decrease and complete cessation of cyclic function of the female reproductive organs at the time of the menopause appears to lie in the ovary itself. There is continuing loss of the primordial follicles during intrauterine life and throughout the reproductive years until the menopause. After about the age of 35 years, the human ovary begins to decrease in weight and size, and contains much fewer oocytes and follicular structures and more atretic and degenerating follicles [7].
The female fetus starts in utero with approximately 6 million primordial follicles which decrease to 600,000 at birth, 300,000 at menarche and 10,000 or fewer near the time of the menopause. A few immature follicles may continue to undergo maturation and atresia even for a few years after the menopause. There have been some reports of postmenopausal ovulation.
It is important to realize that (1) the feedback mechanisms may cause readjustments between the pituitary and ovary as long as there are follicles remaining in the ovary to respond; (2) over a period of 1 or 2 years, reversal of laboratory findings as well as clinical signs and symptoms may occur.
In the menopausal ovary, although ovarian oestradiol and progesterone secretions are sharply reduced, the ovary is nevertheless capable of substantial steroidogenesis. The ovarian stroma cells as well as the adrenal cells have a steroidogenic capacity for producing androstenedione which is converted by the skin and appendages to oestrone [8].
The primary steroidogenic element of the postmenopausal ovary is the stroma, which frequently contains islands of ‘thecal’ cells and may have the appearance of a generalized bilateral thecal hyperplasia. The steroids secreted by the postmenopausal ovary in response to the stimulus from high concentrations of LH are primarily androgens (androstenedione, testosterone), but some oestradiol may also be produced (Table II). In in vitro studies, hyperplastic stroma, when stimulated, produces oestradiol.
...........................................
Extraglandular source of oestrogen
Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman. Most of the oestrone is formed by the peripheral conversion of androstene-dione. After the menopause, the circulating level of androstenedione is about one-half of that seen prior to the menopause. Most of this postmenopausal androstenedione is derived from the adrenal gland, with only a small amount secreted by the ovary. The conversion rate of androstenedione to oestrone is significantly correlated with obesity (body size), because the peripheral conversion of androstenedione is mostly done at skin appendages, especially fat [3]. The circulating oestradiol level after the menopause is approximately 10–20 pg/ml (40–70 pmol/l), most of which is derived from this conversion [9]. The circulating level of oestrone is higher, the mean level being approximately 30–70 pg/ml (110–260 pmol/l). The average postmenopausal production rate of oestrone is approximately 45 mg/24 h
................................................................................
.................................................................................
.........
Summary
* The postmenopausal ovary exhibits direct secretion of very minimal amounts of oestrone and oestradiol.
* The ovarian stroma continues to be stimulated by LH to produce androstenedione and testosterone.
* Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman, with an
androstenedione-to-oestrone conversion by the skin and appendages.
* The levels of oestradiol and oestrone are strongly correlated with the percentage of the ideal body weight.
* Menopausal women have an oestrogen milieu that is lower than necessary for reproductive function.
The menopause could be regarded as a physiologic phenomenon that is protective in nature: protective from undesirable reproduction and the associated growth stimuli by oestrogen deficiency as a consequence of ovarian follicular exhaustion, and by the oestrogen-independent consequences of ageing.
http://www.gfmer.ch/Books/bookmp/33.htm
QUOTE
Cholesterol is the precursor to all our steroid hormones which include estrogen, testosterone, progesterone, cortisol, aldosterone, and DHEA. Eighty to ninety percent of cholesterol is made by the liver. Cholesterol is converted into pregnenolone which is then converted into progesterone which is converted into androstanedione which can be converted into estrogen or DHEA or testosterone. If the person has excess body fat, they will make an enzyme called aromatase which will convert testosterone into estrogen increasing estrogen levels. If a person has insulin resistance their body will produce two enzymes, one called 17, 20 lyase and the other17 alpha hydroxylase. These enzymes convert progesterone into testosterone which will can cause polycystic ovary syndrome, hair growth, loss of head hair, and infertility in women. The testosterone could then be converted into estrogen by the aromatase enzyme made in body fat, once again increasing total estrogen levels.
In women high estrogen levels can increase the risk of reproductive cancers as well as uterine fibroids, fibrocystic breast, and endometriosis. According to the “Journal of Carcinogenesis” you can have 10 to 50 times the amount of estrogen in breast tissue than in your blood, therefore blood levels of estrogen may not indicate the tissue levels of estrogen. When you're under stress your body will convert your DHEA into cortisol. This process has been named cortisol steal. When this occurs the body's levels of DHEA, aldosterone, estrogen, progesterone, and testosterone will all decrease. This is how stress can cause hormonal imbalances in people.
There are 11 sites on the estrogen molecule for detoxification, and each has three types of estrogen, therefore the body has 36 different types of estrogen. The three primary detoxification sites are the 2 hydroxylation pathway, the 16 hydroxylation pathway, and the 4 hydroxylation pathway. The 2 hydroxyestrogen's are good for you promote health and actually fight cancer. The 16 hydroxyestrogen's are 30 times more mitogenic (causes cell division), and therefore increase the number of cells to potentially turn into cancer. The 4 hydroxyestrogen's are 30 times more carcinogenic and therefore greatly increase the risk of cancer. In our environment there are thousands of synthetic estrogens, these come in the form of plastics, pesticides and other chemicals. These synthetic estrogens are detoxified through the 16 hydroxylation pathway. Alcohol, smoking and hydrogenated fats are detoxified through the 4 hydroxylation pathway. Indole 3 carbonol which can be found in cruciferous vegetables such as broccoli, cauliflower, cabbage, and brussels sprouts all increase the two hydroxylation pathway and therefore promote hormonal balance. Once an estrogen has been detoxified, if it becomes oxidized, it then becomes a quinone, which is also carcinogenic, and this is why we need good antioxidant status.
In women high estrogen levels can increase the risk of reproductive cancers as well as uterine fibroids, fibrocystic breast, and endometriosis. According to the “Journal of Carcinogenesis” you can have 10 to 50 times the amount of estrogen in breast tissue than in your blood, therefore blood levels of estrogen may not indicate the tissue levels of estrogen. When you're under stress your body will convert your DHEA into cortisol. This process has been named cortisol steal. When this occurs the body's levels of DHEA, aldosterone, estrogen, progesterone, and testosterone will all decrease. This is how stress can cause hormonal imbalances in people.
There are 11 sites on the estrogen molecule for detoxification, and each has three types of estrogen, therefore the body has 36 different types of estrogen. The three primary detoxification sites are the 2 hydroxylation pathway, the 16 hydroxylation pathway, and the 4 hydroxylation pathway. The 2 hydroxyestrogen's are good for you promote health and actually fight cancer. The 16 hydroxyestrogen's are 30 times more mitogenic (causes cell division), and therefore increase the number of cells to potentially turn into cancer. The 4 hydroxyestrogen's are 30 times more carcinogenic and therefore greatly increase the risk of cancer. In our environment there are thousands of synthetic estrogens, these come in the form of plastics, pesticides and other chemicals. These synthetic estrogens are detoxified through the 16 hydroxylation pathway. Alcohol, smoking and hydrogenated fats are detoxified through the 4 hydroxylation pathway. Indole 3 carbonol which can be found in cruciferous vegetables such as broccoli, cauliflower, cabbage, and brussels sprouts all increase the two hydroxylation pathway and therefore promote hormonal balance. Once an estrogen has been detoxified, if it becomes oxidized, it then becomes a quinone, which is also carcinogenic, and this is why we need good antioxidant status.
I can't provide link as it is commercial website.
QUOTE (Sariah @ Jan 24 2009, 01:12 AM)
Also, if any hormone conversion is going to take place it's necessary for the ovaries to be functioning ...
Not exactly, please, read aon menopausal ovary.
QUOTE
Ovarian changes
The primary basis for the progressive decrease and complete cessation of cyclic function of the female reproductive organs at the time of the menopause appears to lie in the ovary itself. There is continuing loss of the primordial follicles during intrauterine life and throughout the reproductive years until the menopause. After about the age of 35 years, the human ovary begins to decrease in weight and size, and contains much fewer oocytes and follicular structures and more atretic and degenerating follicles [7].
The female fetus starts in utero with approximately 6 million primordial follicles which decrease to 600,000 at birth, 300,000 at menarche and 10,000 or fewer near the time of the menopause. A few immature follicles may continue to undergo maturation and atresia even for a few years after the menopause. There have been some reports of postmenopausal ovulation.
It is important to realize that (1) the feedback mechanisms may cause readjustments between the pituitary and ovary as long as there are follicles remaining in the ovary to respond; (2) over a period of 1 or 2 years, reversal of laboratory findings as well as clinical signs and symptoms may occur.
In the menopausal ovary, although ovarian oestradiol and progesterone secretions are sharply reduced, the ovary is nevertheless capable of substantial steroidogenesis. The ovarian stroma cells as well as the adrenal cells have a steroidogenic capacity for producing androstenedione which is converted by the skin and appendages to oestrone [8].
The primary steroidogenic element of the postmenopausal ovary is the stroma, which frequently contains islands of ‘thecal’ cells and may have the appearance of a generalized bilateral thecal hyperplasia. The steroids secreted by the postmenopausal ovary in response to the stimulus from high concentrations of LH are primarily androgens (androstenedione, testosterone), but some oestradiol may also be produced (Table II). In in vitro studies, hyperplastic stroma, when stimulated, produces oestradiol.
...........................................
Extraglandular source of oestrogen
Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman. Most of the oestrone is formed by the peripheral conversion of androstene-dione. After the menopause, the circulating level of androstenedione is about one-half of that seen prior to the menopause. Most of this postmenopausal androstenedione is derived from the adrenal gland, with only a small amount secreted by the ovary. The conversion rate of androstenedione to oestrone is significantly correlated with obesity (body size), because the peripheral conversion of androstenedione is mostly done at skin appendages, especially fat [3]. The circulating oestradiol level after the menopause is approximately 10–20 pg/ml (40–70 pmol/l), most of which is derived from this conversion [9]. The circulating level of oestrone is higher, the mean level being approximately 30–70 pg/ml (110–260 pmol/l). The average postmenopausal production rate of oestrone is approximately 45 mg/24 h
................................................................................
.................................................................................
.........
Summary
* The postmenopausal ovary exhibits direct secretion of very minimal amounts of oestrone and oestradiol.
* The ovarian stroma continues to be stimulated by LH to produce androstenedione and testosterone.
* Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman, with an
* The levels of oestradiol and oestrone are strongly correlated with the percentage of the ideal body weight.
* Menopausal women have an oestrogen milieu that is lower than necessary for reproductive function.
The menopause could be regarded as a physiologic phenomenon that is protective in nature: protective from undesirable reproduction and the associated growth stimuli by oestrogen deficiency as a consequence of ovarian follicular exhaustion, and by the oestrogen-independent consequences of ageing.
The primary basis for the progressive decrease and complete cessation of cyclic function of the female reproductive organs at the time of the menopause appears to lie in the ovary itself. There is continuing loss of the primordial follicles during intrauterine life and throughout the reproductive years until the menopause. After about the age of 35 years, the human ovary begins to decrease in weight and size, and contains much fewer oocytes and follicular structures and more atretic and degenerating follicles [7].
The female fetus starts in utero with approximately 6 million primordial follicles which decrease to 600,000 at birth, 300,000 at menarche and 10,000 or fewer near the time of the menopause. A few immature follicles may continue to undergo maturation and atresia even for a few years after the menopause. There have been some reports of postmenopausal ovulation.
It is important to realize that (1) the feedback mechanisms may cause readjustments between the pituitary and ovary as long as there are follicles remaining in the ovary to respond; (2) over a period of 1 or 2 years, reversal of laboratory findings as well as clinical signs and symptoms may occur.
In the menopausal ovary, although ovarian oestradiol and progesterone secretions are sharply reduced, the ovary is nevertheless capable of substantial steroidogenesis. The ovarian stroma cells as well as the adrenal cells have a steroidogenic capacity for producing androstenedione which is converted by the skin and appendages to oestrone [8].
The primary steroidogenic element of the postmenopausal ovary is the stroma, which frequently contains islands of ‘thecal’ cells and may have the appearance of a generalized bilateral thecal hyperplasia. The steroids secreted by the postmenopausal ovary in response to the stimulus from high concentrations of LH are primarily androgens (androstenedione, testosterone), but some oestradiol may also be produced (Table II). In in vitro studies, hyperplastic stroma, when stimulated, produces oestradiol.
...........................................
Extraglandular source of oestrogen
Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman. Most of the oestrone is formed by the peripheral conversion of androstene-dione. After the menopause, the circulating level of androstenedione is about one-half of that seen prior to the menopause. Most of this postmenopausal androstenedione is derived from the adrenal gland, with only a small amount secreted by the ovary. The conversion rate of androstenedione to oestrone is significantly correlated with obesity (body size), because the peripheral conversion of androstenedione is mostly done at skin appendages, especially fat [3]. The circulating oestradiol level after the menopause is approximately 10–20 pg/ml (40–70 pmol/l), most of which is derived from this conversion [9]. The circulating level of oestrone is higher, the mean level being approximately 30–70 pg/ml (110–260 pmol/l). The average postmenopausal production rate of oestrone is approximately 45 mg/24 h
................................................................................
.................................................................................
.........
Summary
* The postmenopausal ovary exhibits direct secretion of very minimal amounts of oestrone and oestradiol.
* The ovarian stroma continues to be stimulated by LH to produce androstenedione and testosterone.
* Oestrone accounts for most of the circulating oestrogen in the postmenopausal woman, with an
androstenedione-to-oestrone conversion by the skin and appendages.
* The levels of oestradiol and oestrone are strongly correlated with the percentage of the ideal body weight.
* Menopausal women have an oestrogen milieu that is lower than necessary for reproductive function.
The menopause could be regarded as a physiologic phenomenon that is protective in nature: protective from undesirable reproduction and the associated growth stimuli by oestrogen deficiency as a consequence of ovarian follicular exhaustion, and by the oestrogen-independent consequences of ageing.
http://www.gfmer.ch/Books/bookmp/33.htm
QUOTE
Cholesterol is the precursor to all our steroid hormones which include estrogen, testosterone, progesterone, cortisol, aldosterone, and DHEA. Eighty to ninety percent of cholesterol is made by the liver. Cholesterol is converted into pregnenolone which is then converted into progesterone which is converted into androstanedione which can be converted into estrogen or DHEA or testosterone. If the person has excess body fat, they will make an enzyme called aromatase which will convert testosterone into estrogen increasing estrogen levels. If a person has insulin resistance their body will produce two enzymes, one called 17, 20 lyase and the other17 alpha hydroxylase. These enzymes convert progesterone into testosterone which will can cause polycystic ovary syndrome, hair growth, loss of head hair, and infertility in women. The testosterone could then be converted into estrogen by the aromatase enzyme made in body fat, once again increasing total estrogen levels.
In women high estrogen levels can increase the risk of reproductive cancers as well as uterine fibroids, fibrocystic breast, and endometriosis. According to the “Journal of Carcinogenesis” you can have 10 to 50 times the amount of estrogen in breast tissue than in your blood, therefore blood levels of estrogen may not indicate the tissue levels of estrogen. When you're under stress your body will convert your DHEA into cortisol. This process has been named cortisol steal. When this occurs the body's levels of DHEA, aldosterone, estrogen, progesterone, and testosterone will all decrease. This is how stress can cause hormonal imbalances in people.
There are 11 sites on the estrogen molecule for detoxification, and each has three types of estrogen, therefore the body has 36 different types of estrogen. The three primary detoxification sites are the 2 hydroxylation pathway, the 16 hydroxylation pathway, and the 4 hydroxylation pathway. The 2 hydroxyestrogen's are good for you promote health and actually fight cancer. The 16 hydroxyestrogen's are 30 times more mitogenic (causes cell division), and therefore increase the number of cells to potentially turn into cancer. The 4 hydroxyestrogen's are 30 times more carcinogenic and therefore greatly increase the risk of cancer. In our environment there are thousands of synthetic estrogens, these come in the form of plastics, pesticides and other chemicals. These synthetic estrogens are detoxified through the 16 hydroxylation pathway. Alcohol, smoking and hydrogenated fats are detoxified through the 4 hydroxylation pathway. Indole 3 carbonol which can be found in cruciferous vegetables such as broccoli, cauliflower, cabbage, and brussels sprouts all increase the two hydroxylation pathway and therefore promote hormonal balance. Once an estrogen has been detoxified, if it becomes oxidized, it then becomes a quinone, which is also carcinogenic, and this is why we need good antioxidant status.
In women high estrogen levels can increase the risk of reproductive cancers as well as uterine fibroids, fibrocystic breast, and endometriosis. According to the “Journal of Carcinogenesis” you can have 10 to 50 times the amount of estrogen in breast tissue than in your blood, therefore blood levels of estrogen may not indicate the tissue levels of estrogen. When you're under stress your body will convert your DHEA into cortisol. This process has been named cortisol steal. When this occurs the body's levels of DHEA, aldosterone, estrogen, progesterone, and testosterone will all decrease. This is how stress can cause hormonal imbalances in people.
There are 11 sites on the estrogen molecule for detoxification, and each has three types of estrogen, therefore the body has 36 different types of estrogen. The three primary detoxification sites are the 2 hydroxylation pathway, the 16 hydroxylation pathway, and the 4 hydroxylation pathway. The 2 hydroxyestrogen's are good for you promote health and actually fight cancer. The 16 hydroxyestrogen's are 30 times more mitogenic (causes cell division), and therefore increase the number of cells to potentially turn into cancer. The 4 hydroxyestrogen's are 30 times more carcinogenic and therefore greatly increase the risk of cancer. In our environment there are thousands of synthetic estrogens, these come in the form of plastics, pesticides and other chemicals. These synthetic estrogens are detoxified through the 16 hydroxylation pathway. Alcohol, smoking and hydrogenated fats are detoxified through the 4 hydroxylation pathway. Indole 3 carbonol which can be found in cruciferous vegetables such as broccoli, cauliflower, cabbage, and brussels sprouts all increase the two hydroxylation pathway and therefore promote hormonal balance. Once an estrogen has been detoxified, if it becomes oxidized, it then becomes a quinone, which is also carcinogenic, and this is why we need good antioxidant status.
I can't provide link as it is commercial website.
QUOTE (Sariah @ Jan 24 2009, 01:05 AM)
I recently found a study showing that progesterone actually shuts down the E receptors. Some of the purveyors of Progesterone cream on the internet are telling women that even if they might need estrogen, they don't need to use it because it 'wakes up' the E receptors causing an increase in E. That is just not true and I've seen women keep slathering that stuff on and feeling worse, yet the advice is to keep using it.
QUOTE
Inhibitory cross-talk between steroid hormone receptors: differential targeting of estrogen receptor in the repression of its transcriptional activity by agonist- and antagonist-occupied progestin receptors.
W L Kraus, K E Weis, and B S Katzenellenbogen
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
Small right arrow pointing to: This article has been cited by other articles in PMC.
Abstract
Although estrogen receptor (ER) and progestin receptor (PR) are members of different steroid hormone receptor subfamilies, there is considerable biological evidence for cross-talk between the estrogen and progestin hormone-receptor signaling pathways. We have developed a model system to analyze the mechanisms underlying this cross-talk, specifically the repression of ER-mediated transcriptional activity by PR complexed with agonistic or antagonistic ligands. Estrogen- and progestin-responsive reporter vectors containing a variety of promoters were transfected into primary cultures of rat uterine cells and 3T3 mouse fibroblasts with expression vectors for PR (the A and/or B isoforms) as well as ER. Our results demonstrate that both PR isoforms can act as potent ligand-dependent repressors of ER activity. The magnitude of the repression was dependent on the PR isoform (i.e., PR A or PR
, ligand type (i.e., agonist or antagonist), PR levels, and ligand concentration but was unaffected by the ER levels. The promoter context was important in determining both the magnitude and PR isoform specificity of the repression for agonist-occupied PR but not for antagonist-occupied PR. Ligand-occupied PR A was a stronger repressor of ER-mediated transcriptional activity than was ligand-occupied PR B, and antagonist-occupied PR was a more effective repressor than agonist-occupied PR. Mechanistic studies suggest that liganded PR represses ER activity by interfering with its ability to interact productively with the transcriptional machinery, a process known as quenching. The data do not support competitive repression, direct repression, or squelching as the mechanism of PR's inhibitory effect. Experiments with ER mutants demonstrated that the N-terminal portion of ER was required for repression by agonist-occupied PR but not by antagonist-occupied PR. These results, as well as other differences between the two PR-ligand complexes, suggest that they differentially target ER when repressing ER transcriptional activity. These findings underscore the mounting evidence for the importance of interactions between members of the steroid hormone receptor family.
W L Kraus, K E Weis, and B S Katzenellenbogen
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
Small right arrow pointing to: This article has been cited by other articles in PMC.
Abstract
Although estrogen receptor (ER) and progestin receptor (PR) are members of different steroid hormone receptor subfamilies, there is considerable biological evidence for cross-talk between the estrogen and progestin hormone-receptor signaling pathways. We have developed a model system to analyze the mechanisms underlying this cross-talk, specifically the repression of ER-mediated transcriptional activity by PR complexed with agonistic or antagonistic ligands. Estrogen- and progestin-responsive reporter vectors containing a variety of promoters were transfected into primary cultures of rat uterine cells and 3T3 mouse fibroblasts with expression vectors for PR (the A and/or B isoforms) as well as ER. Our results demonstrate that both PR isoforms can act as potent ligand-dependent repressors of ER activity. The magnitude of the repression was dependent on the PR isoform (i.e., PR A or PR
, ligand type (i.e., agonist or antagonist), PR levels, and ligand concentration but was unaffected by the ER levels. The promoter context was important in determining both the magnitude and PR isoform specificity of the repression for agonist-occupied PR but not for antagonist-occupied PR. Ligand-occupied PR A was a stronger repressor of ER-mediated transcriptional activity than was ligand-occupied PR B, and antagonist-occupied PR was a more effective repressor than agonist-occupied PR. Mechanistic studies suggest that liganded PR represses ER activity by interfering with its ability to interact productively with the transcriptional machinery, a process known as quenching. The data do not support competitive repression, direct repression, or squelching as the mechanism of PR's inhibitory effect. Experiments with ER mutants demonstrated that the N-terminal portion of ER was required for repression by agonist-occupied PR but not by antagonist-occupied PR. These results, as well as other differences between the two PR-ligand complexes, suggest that they differentially target ER when repressing ER transcriptional activity. These findings underscore the mounting evidence for the importance of interactions between members of the steroid hormone receptor family.http://www.pubmedcentral.nih.gov/articlere...gi?artid=230410
These are very interesting, Iradan, but some of them are way above my head.
What I do understand is that the bodies hormonal system is hugely complex so no wonder it's so difficult to fine tune it and get it right when it goes wrong.
Although I've put on a bit of weight and some of my muscle has turned to fat I am basically reasonably slim and it sounds like that doesn't help in producing enough estrogen for my needs.
I hope my doctor is up to helping me sort this all out.
What I do understand is that the bodies hormonal system is hugely complex so no wonder it's so difficult to fine tune it and get it right when it goes wrong.
Although I've put on a bit of weight and some of my muscle has turned to fat I am basically reasonably slim and it sounds like that doesn't help in producing enough estrogen for my needs.
I hope my doctor is up to helping me sort this all out.
Iradan,
Good studies, I've read these before. Note that they say the hormones 'can' or 'may' convert. As we age, the degree to which that can happen, depending on many variables, can be vastly different from woman to woman. The hormone conversion pathways, as we see on models such as the one Sandra posted, are not guaranteed to happen in the same way and same amounts for each woman. And the conclusions of the studies are based on the presumption that the precursors hormones are present in sufficient quantities to make those conversions.
As for the study about P and E receptors, it seems to confirm what I said, that (in more simplistic language) that P can have an inhibitory effect on E by various mechanisms.
you quoted:
If the person has excess body fat, they will make an enzyme called aromatase which will convert testosterone into estrogen increasing estrogen levels. If a person has insulin resistance their body will produce two enzymes, one called 17, 20 lyase and the other17 alpha hydroxylase. These enzymes convert progesterone into testosterone which will can cause polycystic ovary syndrome, hair growth, loss of head hair, and infertility in women. The testosterone could then be converted into estrogen by the aromatase enzyme made in body fat, once again increasing total estrogen levels.
This says that aromatase is required for that conversion, but also the scenario shown is due to an aberrant condition being present--insulin resistance. However, P is an aromatase inhibitor which this study shows:
The anti-aromatase effect of progesterone and of its natural metabolites 20alpha- and 5alpha-dihydroprogesterone in the MCF-7aro breast cancer cell line.
Pasqualini JR, Chetrite G.
Hormones and Cancer Research Unit, Institut de Puériculture et de Périnatalogie, Paris, France. jorge.pasqualini@wanadoo.fr
BACKGROUND: Progesterone is metabolized in the normal breast mainly into 4-ene-pregnenes (e.g. 20alpha-dihydroprogesterone, 20alphaDHP) but, in contrast, in breast cancer tissue the 5alpha-dihydropregnanes (e.g. 5alpha-dihydroprogesterone, 5alphaDHP) are prevalent. In the present study the effect of progesterone and its main metabolites 20alphaDHP and 5alphaDHP on the aromatase activity in a stable aromatase-expressing estrogen receptor-positive human breast cancer cell line, MCF-7aro, was explored. MATERIALS AND METHODS: The MCF-7aro cells were stripped of endogenous steroids and incubated with physiological concentrations of [3H]-testosterone ([3H]-testos: 5 x 10(-9)M) alone or in the presence of progesterone, 20alphaDHP or 5alphaDHP (5 x 10(-6) or 5 x 10(-8)M) for 24 h at 37 degrees C. The cellular radioactivity uptake was determined in the ethanolic supernatant and the DNA content in the remaining pellet. [3H]-Estradiol (E2), [3H]-estrone (E1) and [3H]-testos were characterized by thin layer chromatography and quantified using the corresponding standard. RESULTS: Aromatase activity was present at a high level in the MCF-7aro cells after incubation with [3H]-testos when the concentration of [3H]-E2 was 3.70 pmol/mg DNA; 20alphaDHP at concentrations of 5 x 10(-6)M or 5 x 10(-8)M significantly inhibited this conversion by 50.3% and 36.5%, respectively. No significant effect was found with the metabolite 5alphaDHP or the parent hormone, progesterone. CONCLUSION: The MCF-7aro cell line shows high detectable aromatase activity. The present data indicate that the progesterone metabolite 20alphaDHP, found mainly in normal breast tissue, can act as an anti-aromatase agent.
So I'm not sure how any of this shows that P will convert to E., only that it MAY if many variables are present. When I said "Also, if any hormone conversion is going to take place" I thought it understood I meant the conversion of P to E. I did not mention testosterone at all.
And my point was that those who say that using P will fulfill the needs of any woman for both E and P have no scientific basis for making these claims.
I think we can still safely say that P converting to E requires many enzymes and other variables and even then, the amounts won't be significant. So women should not be expecting P to fulfill any E deficiencies they might have, which I believe was the original point Sandra was trying to make.
Good studies, I've read these before. Note that they say the hormones 'can' or 'may' convert. As we age, the degree to which that can happen, depending on many variables, can be vastly different from woman to woman. The hormone conversion pathways, as we see on models such as the one Sandra posted, are not guaranteed to happen in the same way and same amounts for each woman. And the conclusions of the studies are based on the presumption that the precursors hormones are present in sufficient quantities to make those conversions.
As for the study about P and E receptors, it seems to confirm what I said, that (in more simplistic language) that P can have an inhibitory effect on E by various mechanisms.
you quoted:
If the person has excess body fat, they will make an enzyme called aromatase which will convert testosterone into estrogen increasing estrogen levels. If a person has insulin resistance their body will produce two enzymes, one called 17, 20 lyase and the other17 alpha hydroxylase. These enzymes convert progesterone into testosterone which will can cause polycystic ovary syndrome, hair growth, loss of head hair, and infertility in women. The testosterone could then be converted into estrogen by the aromatase enzyme made in body fat, once again increasing total estrogen levels.
This says that aromatase is required for that conversion, but also the scenario shown is due to an aberrant condition being present--insulin resistance. However, P is an aromatase inhibitor which this study shows:
The anti-aromatase effect of progesterone and of its natural metabolites 20alpha- and 5alpha-dihydroprogesterone in the MCF-7aro breast cancer cell line.
Pasqualini JR, Chetrite G.
Hormones and Cancer Research Unit, Institut de Puériculture et de Périnatalogie, Paris, France. jorge.pasqualini@wanadoo.fr
BACKGROUND: Progesterone is metabolized in the normal breast mainly into 4-ene-pregnenes (e.g. 20alpha-dihydroprogesterone, 20alphaDHP) but, in contrast, in breast cancer tissue the 5alpha-dihydropregnanes (e.g. 5alpha-dihydroprogesterone, 5alphaDHP) are prevalent. In the present study the effect of progesterone and its main metabolites 20alphaDHP and 5alphaDHP on the aromatase activity in a stable aromatase-expressing estrogen receptor-positive human breast cancer cell line, MCF-7aro, was explored. MATERIALS AND METHODS: The MCF-7aro cells were stripped of endogenous steroids and incubated with physiological concentrations of [3H]-testosterone ([3H]-testos: 5 x 10(-9)M) alone or in the presence of progesterone, 20alphaDHP or 5alphaDHP (5 x 10(-6) or 5 x 10(-8)M) for 24 h at 37 degrees C. The cellular radioactivity uptake was determined in the ethanolic supernatant and the DNA content in the remaining pellet. [3H]-Estradiol (E2), [3H]-estrone (E1) and [3H]-testos were characterized by thin layer chromatography and quantified using the corresponding standard. RESULTS: Aromatase activity was present at a high level in the MCF-7aro cells after incubation with [3H]-testos when the concentration of [3H]-E2 was 3.70 pmol/mg DNA; 20alphaDHP at concentrations of 5 x 10(-6)M or 5 x 10(-8)M significantly inhibited this conversion by 50.3% and 36.5%, respectively. No significant effect was found with the metabolite 5alphaDHP or the parent hormone, progesterone. CONCLUSION: The MCF-7aro cell line shows high detectable aromatase activity. The present data indicate that the progesterone metabolite 20alphaDHP, found mainly in normal breast tissue, can act as an anti-aromatase agent.
So I'm not sure how any of this shows that P will convert to E., only that it MAY if many variables are present. When I said "Also, if any hormone conversion is going to take place" I thought it understood I meant the conversion of P to E. I did not mention testosterone at all.
And my point was that those who say that using P will fulfill the needs of any woman for both E and P have no scientific basis for making these claims.
I think we can still safely say that P converting to E requires many enzymes and other variables and even then, the amounts won't be significant. So women should not be expecting P to fulfill any E deficiencies they might have, which I believe was the original point Sandra was trying to make.
QUOTE (Sariah @ Jan 24 2009, 12:04 PM)
Iradan,
Good studies, I've read these before. Note that they say the hormones 'can' or 'may' convert. [...] I think we can still safely say that P converting to E requires many enzymes and other variables and even then, the amounts won't be significant. So women should not be expecting P to fulfill any E deficiencies they might have, which I believe was the original point Sandra was trying to make.
Good studies, I've read these before. Note that they say the hormones 'can' or 'may' convert. [...] I think we can still safely say that P converting to E requires many enzymes and other variables and even then, the amounts won't be significant. So women should not be expecting P to fulfill any E deficiencies they might have, which I believe was the original point Sandra was trying to make.
That's it. 'Can' or 'may', very important to note this.
I don't think anyone, the scientists included, can tell someone exactly how much of their P will convert to estradiol. And look, one of the transformation paths goes through testosterone, so if someone is worried about P turning into E2, they should also be worried about P turning into T.
Hey, is that where my facial hair is coming from ????? But then again, I couldn't care less about the Superbowl, so I guess I'm safe. :-)
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