steroids and progesterone

citystreets

Banned
Ok guys, so im majoring in biology and have good basic knowledge of the human body, but cant figure this out.

19 nors are considered progestins because they act directly on the progesterone receptors. We all know theres drugs out there to control estrogen and prolactin but how do you go about controling progesterone?

2nd question is why some prohormones like epi or superdrol cuz prolactin problems, prolactin is not a problem unless progesterone is present. Any knowledgable folks in here able to answer this?
 
You have to have high levels of circulating estrogen before prolactin becomes a problem. If you can keep estrogen from becoming high in the first place, you have most of the problem solved. Most of the time a low dose AI on cycle will do the trick.
 
dg806 said:
You have to have high levels of circulating estrogen before prolactin becomes a problem. If you can keep estrogen from becoming high in the first place, you have most of the problem solved. Most of the time a low dose AI on cycle will do the trick.
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This is true, prolactin exerts its effects in an estrogen-primed environment. I think too much emphasis is placed on prolactin as a force in gynecomastia.
 
sethroberts said:
This is true, prolactin exerts its effects in an estrogen-primed environment. I think too much emphasis is placed on prolactin as a force in gynecomastia.
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from what i understand when estrogen is high progesterone is low, and vice versa. I dont think estrogen causes prolactin probs its progesterone so how does that work?
 
I found this and am doing a cut and paste. I hope this helps because they say it better here than my awkward explanation would have been...

The presence of progesterone in male bodybuilders is through the use of the progestins, i.e. Oxymetholone (Anadrol, Anapolan50), Trenbolone (Finaject, Parabolan) and Nandrolone (Deca durabolin). A large problem for the bodybuilder is that the symptoms displayed by progesterone are identical to those of oestrogen, but the concurrent use of the typical anti-oestrogens appears to have no effect in controlling or treating it.

Progesterone tends to aggravate oestrogen induced gyno symptoms, making them more difficult to cure. We will look at some methods of avoiding or controlling them, bearing in mind that progesterone actually requires oestrogen presence to activate it in the first place.

Use with non-aromatising steroids
If progesterone requires oestrogen presence to activate it, then one method of avoiding this would be to use the progestins in stacks with non-aromatising steroids. Amazingly heavy androgenic steroids like Anadrol and Trenbolone are exceptionally mild and safe with regard to female characteristics when used in conjunction with non-aromatising steroids like Primobolan or Winstrol. This is great news for the gyno-prone individual who has previously avoided these stronger steroids for fear of gyno development. A simple stack of Anadrol and Primobolan will go along way to packing on some serious mass without the worry of developing gyno.

Competitive Aromatase Inhibitors
If aromatising steroids are to be included in the stack with progestagenic steroids, then the concurrent use of Competitive Aromatase Inhibitors, like Arimidex or Proviron, would also seem a sensible option. These can be incorporated to keep oestrogen levels low and avoid the activation of the progesterone. Although they will not help with already developed progesterone induced gyno, they can certainly be employed to avoid its development. As usual, the amount of aromatase inhibitor required increases with increasing dose of aromatising steroids used, but the best dose is still the minimum amount that can be got away with to produce the desired effect.

Winstrol
The use of Winstrol is also an effective method of controlling progesterone-induced gyno, as it is anti-progestagenic. An effective dose appears to be in the vicinity of 50mg eod (depot) or 30 to 35mg/day (tabs) although this dose may require increasing depending on the doses being employed in the stack.

One important point worth mentioning is, although generally the progestins do not aromatise, there is an exception to this rule: Deca, as well as being a progestin also aromatises, only very slightly, but nevertheless, still does to some extent. Although this is not nearly enough to cause the large majority any problems at all, for those extremely sensitive to gyno, this small amount of aromatisation to oestrogen can be enough of an elevation to activate the progesterone. Very few people are likely to suffer this, but we feel it is a point worth mentioning.
 
so,
my pheraplex/havoc stack is a GREAT idea because havoc is non-aromatizing like winstrol and will provide support against the prolactin inducing effects of pheraplex
 
DetroitHammer said:
I found this and am doing a cut and paste. I hope this helps because they say it better here than my awkward explanation would have been...

The presence of progesterone in male bodybuilders is through the use of the progestins, i.e. Oxymetholone (Anadrol, Anapolan50), Trenbolone (Finaject, Parabolan) and Nandrolone (Deca durabolin). A large problem for the bodybuilder is that the symptoms displayed by progesterone are identical to those of oestrogen, but the concurrent use of the typical anti-oestrogens appears to have no effect in controlling or treating it.

Progesterone tends to aggravate oestrogen induced gyno symptoms, making them more difficult to cure. We will look at some methods of avoiding or controlling them, bearing in mind that progesterone actually requires oestrogen presence to activate it in the first place.

Use with non-aromatising steroids
If progesterone requires oestrogen presence to activate it, then one method of avoiding this would be to use the progestins in stacks with non-aromatising steroids. Amazingly heavy androgenic steroids like Anadrol and Trenbolone are exceptionally mild and safe with regard to female characteristics when used in conjunction with non-aromatising steroids like Primobolan or Winstrol. This is great news for the gyno-prone individual who has previously avoided these stronger steroids for fear of gyno development. A simple stack of Anadrol and Primobolan will go along way to packing on some serious mass without the worry of developing gyno.

Competitive Aromatase Inhibitors
If aromatising steroids are to be included in the stack with progestagenic steroids, then the concurrent use of Competitive Aromatase Inhibitors, like Arimidex or Proviron, would also seem a sensible option. These can be incorporated to keep oestrogen levels low and avoid the activation of the progesterone. Although they will not help with already developed progesterone induced gyno, they can certainly be employed to avoid its development. As usual, the amount of aromatase inhibitor required increases with increasing dose of aromatising steroids used, but the best dose is still the minimum amount that can be got away with to produce the desired effect.

Winstrol
The use of Winstrol is also an effective method of controlling progesterone-induced gyno, as it is anti-progestagenic. An effective dose appears to be in the vicinity of 50mg eod (depot) or 30 to 35mg/day (tabs) although this dose may require increasing depending on the doses being employed in the stack.

One important point worth mentioning is, although generally the progestins do not aromatise, there is an exception to this rule: Deca, as well as being a progestin also aromatises, only very slightly, but nevertheless, still does to some extent. Although this is not nearly enough to cause the large majority any problems at all, for those extremely sensitive to gyno, this small amount of aromatisation to oestrogen can be enough of an elevation to activate the progesterone. Very few people are likely to suffer this, but we feel it is a point worth mentioning.
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Unfortunately this is incorrect on many levels. Progesterone is actually produced in men and men have similar levels to women during the follicular phase of the menstrual cycle. Progesterone does not act like estrogen.
 
sethroberts said:
Unfortunately this is incorrect on many levels. Progesterone is actually produced in men and men have similar levels to women during the follicular phase of the menstrual cycle. Progesterone does not act like estrogen.
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Thank you, i also found that info misleading. Lets keep this thread going maybe we can shed some light on the issue and reduce the number of gyno threads. Also havoc might be non aromatizing but can still cause gyno like it did me. Just cause estrogen is low, doesnt mean progesterone is too. In fact i believe progesterone would be elevated in a estrogen depraved state, but this theory of mine is coming from looking at women during pregnancy, not men.
 
sethroberts said:
Unfortunately this is incorrect on many levels. Progesterone is actually produced in men and men have similar levels to women during the follicular phase of the menstrual cycle. Progesterone does not act like estrogen.
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As I said, those weren't my words, but I'm not sure I follow what part you feel is inaccurate. Not to defend the author's write up, but I don't believe what you said is contradicted in his statement. The author is a medical doctor, so I felt pretty comfortable posting it, but like I said, I'm not defending what he said and if he's wrong, then please quote the sentence and correct it as you feel fit. Thanks...
 
The presence of progesterone in male bodybuilders is through the use of the progestins, i.e. Oxymetholone (Anadrol, Anapolan50), Trenbolone (Finaject, Parabolan) and Nandrolone (Deca durabolin).

As I stated, progesterone and other progestins occur naturally in males in levels comparable to women during the follicular phase of the mestrual cycle. So, the presence of progesterone is not solely due to the use of any particular steroid.

A large problem for the bodybuilder is that the symptoms displayed by progesterone are identical to those of oestrogen, but the concurrent use of the typical anti-oestrogens appears to have no effect in controlling or treating it.

Again, not true, progesterone does not act like estrogen, in fact progesterone acts in many ways as an opposing force to estrogen.

Progesterone tends to aggravate oestrogen induced gyno symptoms, making them more difficult to cure. We will look at some methods of avoiding or controlling them, bearing in mind that progesterone actually requires oestrogen presence to activate it in the first place.
There is little evidence for this. Progesterone agonists (such as medroxyprogesterone) have been used at high doses with few reported cases of gynecomastia. In this second statement he is confusing progesterone with prolactin (a common error on BB message boards) since it is prolactin that requires the presence of estrogen.

The rest of it is pretty much a parroting of standard message board bro-lore.

If this guy is a physician, then I feel sorry for his patients because his understanding of endocrine hormones (as wel las his ability to write above an 8th grade level) is seriously lacking.
 
sethroberts said:
The presence of progesterone in male bodybuilders is through the use of the progestins, i.e. Oxymetholone (Anadrol, Anapolan50), Trenbolone (Finaject, Parabolan) and Nandrolone (Deca durabolin).

As I stated, progesterone and other progestins occur naturally in males in levels comparable to women during the follicular phase of the mestrual cycle. So, the presence of progesterone is not solely due to the use of any particular steroid.

A large problem for the bodybuilder is that the symptoms displayed by progesterone are identical to those of oestrogen, but the concurrent use of the typical anti-oestrogens appears to have no effect in controlling or treating it.

Again, not true, progesterone does not act like estrogen, in fact progesterone acts in many ways as an opposing force to estrogen.

Progesterone tends to aggravate oestrogen induced gyno symptoms, making them more difficult to cure. We will look at some methods of avoiding or controlling them, bearing in mind that progesterone actually requires oestrogen presence to activate it in the first place.
There is little evidence for this. Progesterone agonists (such as medroxyprogesterone) have been used at high doses with few reported cases of gynecomastia. In this second statement he is confusing progesterone with prolactin (a common error on BB message boards) since it is prolactin that requires the presence of estrogen.

The rest of it is pretty much a parroting of standard message board bro-lore.

If this guy is a physician, then I feel sorry for his patients because his understanding of endocrine hormones (as wel las his ability to write above an 8th grade level) is seriously lacking.
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Thanks... This would not be the first time a physician has totally missed the mark on AAS.
 
DetroitHammer said:
Thanks... This would not be the first time a physician has totally missed the mark on AAS.
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I know there was a guy claiming to be a doctor on here before supporting the idea that progesterone causes gyno. Doctors generally know very little about hormones which is why we have specialists called endocrinologists -- and even then their information can be seriously out of date if they do not keep up with the literature.
 
prolactin is a somatotropic hormone!!family with (growth hormone)
it is a single peptide hormone,containing a chain of 199amono acid. most of its physiological value is in women!!apparent in pregnancy!
In men prolactin has not known therapeutic value, and high level are associated with impotence,infertility and gyno.
Gyno is not automatically!!! associated with lactation.
It is caused by an unusual imbalance of hormones(androgens,estrogens,progestins)
 
I think we need to look at progesterone here and its relation, anatomy with estrogen. Problem is theres plenty of info on it but only relating to women..
 
citystreets said:
Ok guys, so im majoring in biology and have good basic knowledge of the human body, but cant figure this out.

19 nors are considered progestins because they act directly on the progesterone receptors. We all know theres drugs out there to control estrogen and prolactin but how do you go about controling progesterone?

2nd question is why some prohormones like epi or superdrol cuz prolactin problems, prolactin is not a problem unless progesterone is present. Any knowledgable folks in here able to answer this?
Click to expand...


dht derivitives will merge with the progesterone receptor, causing estrogen like effects,(gyno, but prolactin related)

and being that its merging there may be an upregulation when stopped.

ie (epi, pplex, mdrol) all have some sort of gyno related to them with no aromatization that occurs, and sometimes its on cycle and sometimes its off cycle,

when it happens off cycle it may be caused by using nolva, which sensitizes the progesterone receptor.

just my theory
 
crazyfool405 said:
dht derivitives will merge with the progesterone receptor, causing estrogen like effects,(gyno, but prolactin related)

and being that its merging there may be an upregulation when stopped.

ie (epi, pplex, mdrol) all have some sort of gyno related to them with no aromatization that occurs, and sometimes its on cycle and sometimes its off cycle,

when it happens off cycle it may be caused by using nolva, which sensitizes the progesterone receptor.

just my theory
Click to expand...

Can that be fixed taking p5p and/or vitex?
 
crazyfool405 said:
dht derivitives will merge with the progesterone receptor, causing estrogen like effects,(gyno, but prolactin related)

and being that its merging there may be an upregulation when stopped.

ie (epi, pplex, mdrol) all have some sort of gyno related to them with no aromatization that occurs, and sometimes its on cycle and sometimes its off cycle,

when it happens off cycle it may be caused by using nolva, which sensitizes the progesterone receptor.

just my theory
Click to expand...


I also believe in nolva upregulation on the pgr as well.
 
crazyfool405 said:
dht derivitives will merge with the progesterone receptor, causing estrogen like effects,(gyno, but prolactin related)

and being that its merging there may be an upregulation when stopped.

ie (epi, pplex, mdrol) all have some sort of gyno related to them with no aromatization that occurs, and sometimes its on cycle and sometimes its off cycle,

when it happens off cycle it may be caused by using nolva, which sensitizes the progesterone receptor.

just my theory
Click to expand...

Can you tell me where I can find the pharmacological term "merging". Regurgitated bro-telligence with some original wording. Wow. I think I will go merge my estrogen receptors with some nolvadex.
 
crazyfool405 said:
would BIND work better for you? or attach...

look at ALRs Chemical muscle enhancement PDF
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Unfortunately for me I guess, I don't consider Alri to be an expert in steroid hormone biochemistry. However, if you look in a much less reliable source (sarcasm) like the Williams Textbook of Endocrinology on page 86 it reads "...progesterone lowers cytosolic estrogen receptor levels even when estradiol is present." Furthermore "..progesterone induces estrogen sulfotransferase, an enzyme that inactivates estradiol, thus interfering with the estrogen-dependent replenishment of the estrogen receptor. Therefore, progesterone acts by several mechanisms to decrease the level of estrogen receptor and reduce the response to estrogen."
 
sethroberts said:
Unfortunately for me I guess, I don't consider Alri to be an expert in steroid hormone biochemistry. However, if you look in a much less reliable source (sarcasm) like the Williams Textbook of Endocrinology on page 86 it reads "...progesterone lowers cytosolic estrogen receptor levels even when estradiol is present." Furthermore "..progesterone induces estrogen sulfotransferase, an enzyme that inactivates estradiol, thus interfering with the estrogen-dependent replenishment of the estrogen receptor. Therefore, progesterone acts by several mechanisms to decrease the level of estrogen receptor and reduce the response to estrogen."
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im not that good on termonology, so if you would like to explain your qouted info, ill be like a sponge and soak it up reall good.
 
crazyfool405 said:
im not that good on termonology, so if you would like to explain your qouted info, ill be like a sponge and soak it up reall good.
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What it says is that progesterone reduces estrogenic stimulation by actually decreasing receptor quantity and also byspeeding up the metabolism of estrogen. In essence it does exactly the opposite of what you (and nearly everyone else) were quoting above. This is recognized by experts in the field to be strong enough to be included in a well-known endocrinology text.
 
sethroberts said:
What it says is that progesterone reduces estrogenic stimulation by actually decreasing receptor quantity and also byspeeding up the metabolism of estrogen. In essence it does exactly the opposite of what you (and nearly everyone else) were quoting above. This is recognized by experts in the field to be strong enough to be included in a well-known endocrinology text.
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gotcha.

hmm misleading information like that kinda annoys me, but i probably should get that text and read from it.

whne progest is high, estrogen receptor quantity is low.

so when progesterone is raised, it induces an unfavorable ratio of PR to ER and that may be the leading cause of prolactin? along with low test?
 
crazyfool405 said:
gotcha.

hmm misleading information like that kinda annoys me, but i probably should get that text and read from it.

whne progest is high, estrogen receptor quantity is low.

so when progesterone is raised, it induces an unfavorable ratio of PR to ER and that may be the leading cause of prolactin? along with low test?
Click to expand...

Unfortunately, that misleading information is repeated over and over again until it becomes dogma.
 
crazyfool405 said:
this thread may be a good thing to un brainwash.

is what i said sounding correct though?

oh and this is just some thing i have on PR expression
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The paper is basically useless because it is looking at pre/perinatal expression patterns - not really applicable to what we are discussing
 
crazyfool405 said:
Invalid Link Removed
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This one is pretty good and actually shows the antagonizing effect of progesterone on prolactin and possibly the reduction in prolectin receptors in a high progesterone environment. This makes sense because women genrally don't start lactating in ernest until after birth and the high progesterone environment subsides.
 
Here is the abstract for the second one. Shows the expected increase in prolactin levels with increased estradiol. So this all fits together. Progesterone decreases estrogen, progesterone decreases prolactin, estrogen increases prolactin, and it is known that estrogen increases progesterone receptors.

1: Andrologia. 1991 Sep-Oct;23(5):373-9.Links
Effects of progesterone administration on follicle-stimulating hormone and prolactin release in estrogen treated eugonadal adult men.Mancini A, De Marinis L, Fiumara C, Saporosi A, Fabrizi ML, Menini E, Turchi P, Menchini-Fabris GF.
Instituti di Endocrinologia, Università Cattolica del S. Cuore, Roma, Italy.

In order to investigate the modulatory effect of steroids on FSH secretion in vivo, we studied 16 human males, aged 51-81 years, affected by prostatic carcinoma. They were given estradiol or E2 plus progesterone (P), added at different times during E2 treatment. Daily blood samples were collected in order to determine LH, FSH, and PRL levels; moreover, blood samples were collected at 2 h intervals for 12 h on the day of P administration. We observed the expected biphasic effect on LH secretion, whereas daily basal FSH levels, during E2 treatment, decreased gradually and progressively from the first day until the end of the study. FSH levels exhibited, after P administration, wide fluctuations, with peak levels observed from 2 to 6 h after P in 4 of 6 patients studied (at 72 h during E2 treatment). A clear trend toward FSH increase was also observed in 3 out of 5 patients in whom P was administrated 96 h after starting E2 administration. In this case, FSH increases were delayed, becoming evident between 8th and 10th h after P injection. Finally, during E2 administration basal PRL levels showed a progressive increase, which was significant in all three groups. In conclusion, these data confirm the biphasic effects of estrogen administration on LH secretion in eugonadal adult human males; while estrogens alone showed an inhibitory effect on FSH secretion, the addition of P induced also a positive action, resulting in a clear FSH peak in some patients tested. The time course of E2 and P administration seems to be critical for the hormone response pattern.(ABSTRACT TRUNCATED AT 250 WORDS)
 
sethroberts said:
This one is pretty good and actually shows the antagonizing effect of progesterone on prolactin and possibly the reduction in prolectin receptors in a high progesterone environment. This makes sense because women genrally don't start lactating in ernest until after birth and the high progesterone environment subsides.
Click to expand...


i think there was one on 5a R antagonizing progesterone receptors, which would mean prolactin would raise?
 
yes, androgens (especially DHT) are known to have antagonistic effects on estrogens -- that is why the androgen/estrogen balance is important. if you disrupt this balance it can cause gyno. No need to invoke all kinds of complicated mechanisms. That is not to say that gyno can be caused through other mechanisms -- it can.
 
sethroberts said:
yes, androgens (especially DHT) are known to have antagonistic effects on estrogens -- that is why the androgen/estrogen balance is important. if you disrupt this balance it can cause gyno. No need to invoke all kinds of complicated mechanisms. That is not to say that gyno can be caused through other mechanisms -- it can.
Click to expand...


so can we think (for the sake of better visualization) that DHT based AAS acts like AI where the 'rebound' occurs after cessation? the body will try to normalize by making more estrogen and once the 'block' is gone then thats why we see delayed or rebound of gyno after cycle?

or is it more like SERM in terms of its antagonistic behavior?
 
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