Androstenedione (4-andro)

Cameron

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@haidut would you be interested in some people to raise money to help fund a study of 4-androstenedione and raising testosterone. No studies using less then 50mgs to increase testosterone without to much estrogen conversion.


Androstendedione and androstenediol are the direct pre-cursors of testosterone in mammals. These exist naturally in the 4- position structurally. There are also many analogs of these in-cluding 5- position, 19- position and nor- analogs. The only ones that have any science at all behind them are plain old, regular 4- positioned androstenedione or androstenediol. There has been an endless parade of junk science studies that purport to show how “dangerous” androstenedione is and how “ineffective” it is in raising testosterone in humans. In nearly every single one of these “studies” young men with naturally high testosterone are given huge overdoses of hundreds of milligrams of androstenedione. Even the few “studies” that used middle aged men, they were not hypogonadal and were still heavily overdosed. Since men cannot normally have high levels this overdose simply raises estrogen and estrone. Testosterone is not raised - just estrogens!!! Amazingly there have been no published studies on the responsible low-dose (i.e. 50 mg or less) use of androstenedione in hypogonadal men anywhere in the world, much less on testosterone deficient women. Women have ovaries rather than testicles and metabolize androstenedione (and androstenediol) into testosterone more efficiently than men. It may well be possible for women to take oral androstenedione to raise their testosterone, but we will need studies to see if their blood levels of androstenedione go up too much and if any excess estrone and estradiol are formed as by-products. Since one third of American women are castrated without cause and their testosterone levels are cut in half, this would certainly be much needed research.


The University of Ontario was about the only institution in the world to even address this issue (Canadian Journal of Applied Physiology v. 27, 2002, pp. 628-45). They pointed out that sublingual administration of the androstenedione family is far more effective in hypogonadal men. It is very difficult to solubilize androstenedione and it must be complexed in cyclodextrin sus-pension to dissolve under the tongue. They referred to Blacquier et al back in 1967 (Acta Endocrinologica v. 55, pp.697-704) who found that androstenediol was almost three times as effective in transforming into testosterone than androstenedione. If this is true we should be studying androstenediol rather than androstenedione primarily in both men and women. They also referred to Horton et al back in 1955 (Journal of Clinical Investigation v. 45, pp. 301-13) who was one of the only researchers in the world to show that women transform the androstenedione family into testosterone more efficiently than men. They found that about 60% of plasma testosterone is derived from androstenedione biologically in women, while only about 37% is derived in men. They referred to Mahesh et al back in 1962 (Acta Endocrinologica v. 41, pp. 400-6) where women were given completely irresponsible 100 mg doses of oral androstenedione and then 100 mg of DHEA! They also found orally administered androstenedione family hormones were very poorly absorbed by either sex, and intravenously administration was far more effective. Of course, injecting people with anything is always a poor idea unless absolutely necessary in a medical emergency. We must always remember that women only make about 300 mcg (less than one third of one milligram) of testosterone daily and a general rule is to get about 150 mcg into their blood if they are proven to be deficient.


While this is the best review ever published on testosterone prohormones, they still just didn’t comprehend that high dose oral supplementation, especially in young men, is completely irrational and merely produces estrogens. They continually referred to previous studies where healthy men with normally high testosterone levels were given irrational amounts of oral androstenedione. Again, men only produce about 6-8 mg a day of testosterone and men with normal levels should not take any at all. King et al in 1999 gave healthy young men 300 mg of oral androstenedione. Of course their estradiol and estrone levels rose dramatically, but not their testosterone. Wallace et al gave middle aged men both 100 mg of DHEA and 100 mg of androstenedione, but did not even test them to see if they were deficient in either hormone! Leder et al in 2000 gave healthy men 300 mg of androstenedione and got huge rises in both estradiol and estrone, but not testosterone. Earnest et al in 2000 gave men either 200 mg of androstenedione or androstenediol who were not low in testosterone. At least Earnest found out that the androstenediol was more effective than the androstenedione. Ballantyne et al gave healthy men 200 mg of oral androstenedione with the usual bad effects. Brown et al in 2000 gave men 300 mg of oral androstenedione and got estrogens. The list goes on. There has not been one single study giving hypogonadal middle aged or elderly men a reasonable 50 mg oral dose of any of the androstenedione prohormones, much less using the more promising androstenediol, much less using this sublingually in suspension. These completely unscientific “studies” will now be used to ban all the andro-stenedione family and make mere possession a felony punishable by five years in federal prison under the Steroid Hormone Act.


When androstenedione first became available in the marketplace in the mid-1990’s many older men successfully used this to raise testosterone levels by simply taking an inexpensive 50 mg tablet. At the time this seemed like a practical and effective means of raising testosterone without seeing a doctor to get a prescription. It should be mentioned that unreputable companies tried to promote supposedly transdermal androstenedione creams which were claimed to penetrate the skin and bypass the liver to make it more effective. These were plain and simple frauds, yet you still see them offered from time to time. Androstenedione and androstenediol are not metabolized into testosterone very effectively whether taken orally, or used transdermally. Injections are more effective but very ill advised. If you used, for example, a ridiculous 5 grams of 10% androstenedione cream (which would be 500 mg of actual androstenedione), you would only be getting about 50 mg of actual hormone into your bloodstream (a 10% absorption rate is reasonably expected here). With an 8% conversion rate you would be getting a mere 4 mg of actual testosterone in your body. That means at best that 500 mg of androstenedione would end up as a mere 4 mg of available testosterone in your blood - ideally and theoretically that is. We simply don’t know what would happen with women. Since women only produce about 300 mcg (one third of one mg) of testosterone a day it would be reasonable to experiment with using a half gram of 10% androstenedione cream on women who are low in testosterone. This might not work at all, however. Again, the research on women is ignored.


One possible answer here that has gotten almost no attention or research is to use the sublingual route especially with androstenediol rather than androstenedione. It is very difficult to dissolve any of the androstenedione family unfortunately. This can be done by cyclodextrin suspension, but only in a laboratory and not at home. Research into low dose sublingual administration of androstenediol for both men and women might turn out to be very beneficial.
 

LeeLemonoil

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When androstenedione first became available in the marketplace in the mid-1990’s many older men successfully used this to raise testosterone levels by simply taking an inexpensive 50 mg tablet. At the time this seemed like a practical and effective means of raising testosterone without seeing a doctor to get a prescription.


So it’s Test raising properties have already been demonstrated? Any records of that? Was that in the US?
 
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Cameron

Cameron

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So it’s Test raising properties have already been demonstrated? Any records of that? Was that in the US?
No studies in low dose most responsible use of andro has just been in claims that it’s increased performance and individual blood tests. Science of how it works is overwhelming just no actually studies besides high dose that show to high of estrogen increase of hundreds off mgs a day
 

haidut

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@haidut would you be interested in some people to raise money to help fund a study of 4-androstenedione and raising testosterone. No studies using less then 50mgs to increase testosterone without to much estrogen conversion.


Androstendedione and androstenediol are the direct pre-cursors of testosterone in mammals. These exist naturally in the 4- position structurally. There are also many analogs of these in-cluding 5- position, 19- position and nor- analogs. The only ones that have any science at all behind them are plain old, regular 4- positioned androstenedione or androstenediol. There has been an endless parade of junk science studies that purport to show how “dangerous” androstenedione is and how “ineffective” it is in raising testosterone in humans. In nearly every single one of these “studies” young men with naturally high testosterone are given huge overdoses of hundreds of milligrams of androstenedione. Even the few “studies” that used middle aged men, they were not hypogonadal and were still heavily overdosed. Since men cannot normally have high levels this overdose simply raises estrogen and estrone. Testosterone is not raised - just estrogens!!! Amazingly there have been no published studies on the responsible low-dose (i.e. 50 mg or less) use of androstenedione in hypogonadal men anywhere in the world, much less on testosterone deficient women. Women have ovaries rather than testicles and metabolize androstenedione (and androstenediol) into testosterone more efficiently than men. It may well be possible for women to take oral androstenedione to raise their testosterone, but we will need studies to see if their blood levels of androstenedione go up too much and if any excess estrone and estradiol are formed as by-products. Since one third of American women are castrated without cause and their testosterone levels are cut in half, this would certainly be much needed research.


The University of Ontario was about the only institution in the world to even address this issue (Canadian Journal of Applied Physiology v. 27, 2002, pp. 628-45). They pointed out that sublingual administration of the androstenedione family is far more effective in hypogonadal men. It is very difficult to solubilize androstenedione and it must be complexed in cyclodextrin sus-pension to dissolve under the tongue. They referred to Blacquier et al back in 1967 (Acta Endocrinologica v. 55, pp.697-704) who found that androstenediol was almost three times as effective in transforming into testosterone than androstenedione. If this is true we should be studying androstenediol rather than androstenedione primarily in both men and women. They also referred to Horton et al back in 1955 (Journal of Clinical Investigation v. 45, pp. 301-13) who was one of the only researchers in the world to show that women transform the androstenedione family into testosterone more efficiently than men. They found that about 60% of plasma testosterone is derived from androstenedione biologically in women, while only about 37% is derived in men. They referred to Mahesh et al back in 1962 (Acta Endocrinologica v. 41, pp. 400-6) where women were given completely irresponsible 100 mg doses of oral androstenedione and then 100 mg of DHEA! They also found orally administered androstenedione family hormones were very poorly absorbed by either sex, and intravenously administration was far more effective. Of course, injecting people with anything is always a poor idea unless absolutely necessary in a medical emergency. We must always remember that women only make about 300 mcg (less than one third of one milligram) of testosterone daily and a general rule is to get about 150 mcg into their blood if they are proven to be deficient.


While this is the best review ever published on testosterone prohormones, they still just didn’t comprehend that high dose oral supplementation, especially in young men, is completely irrational and merely produces estrogens. They continually referred to previous studies where healthy men with normally high testosterone levels were given irrational amounts of oral androstenedione. Again, men only produce about 6-8 mg a day of testosterone and men with normal levels should not take any at all. King et al in 1999 gave healthy young men 300 mg of oral androstenedione. Of course their estradiol and estrone levels rose dramatically, but not their testosterone. Wallace et al gave middle aged men both 100 mg of DHEA and 100 mg of androstenedione, but did not even test them to see if they were deficient in either hormone! Leder et al in 2000 gave healthy men 300 mg of androstenedione and got huge rises in both estradiol and estrone, but not testosterone. Earnest et al in 2000 gave men either 200 mg of androstenedione or androstenediol who were not low in testosterone. At least Earnest found out that the androstenediol was more effective than the androstenedione. Ballantyne et al gave healthy men 200 mg of oral androstenedione with the usual bad effects. Brown et al in 2000 gave men 300 mg of oral androstenedione and got estrogens. The list goes on. There has not been one single study giving hypogonadal middle aged or elderly men a reasonable 50 mg oral dose of any of the androstenedione prohormones, much less using the more promising androstenediol, much less using this sublingually in suspension. These completely unscientific “studies” will now be used to ban all the andro-stenedione family and make mere possession a felony punishable by five years in federal prison under the Steroid Hormone Act.


When androstenedione first became available in the marketplace in the mid-1990’s many older men successfully used this to raise testosterone levels by simply taking an inexpensive 50 mg tablet. At the time this seemed like a practical and effective means of raising testosterone without seeing a doctor to get a prescription. It should be mentioned that unreputable companies tried to promote supposedly transdermal androstenedione creams which were claimed to penetrate the skin and bypass the liver to make it more effective. These were plain and simple frauds, yet you still see them offered from time to time. Androstenedione and androstenediol are not metabolized into testosterone very effectively whether taken orally, or used transdermally. Injections are more effective but very ill advised. If you used, for example, a ridiculous 5 grams of 10% androstenedione cream (which would be 500 mg of actual androstenedione), you would only be getting about 50 mg of actual hormone into your bloodstream (a 10% absorption rate is reasonably expected here). With an 8% conversion rate you would be getting a mere 4 mg of actual testosterone in your body. That means at best that 500 mg of androstenedione would end up as a mere 4 mg of available testosterone in your blood - ideally and theoretically that is. We simply don’t know what would happen with women. Since women only produce about 300 mcg (one third of one mg) of testosterone a day it would be reasonable to experiment with using a half gram of 10% androstenedione cream on women who are low in testosterone. This might not work at all, however. Again, the research on women is ignored.


One possible answer here that has gotten almost no attention or research is to use the sublingual route especially with androstenediol rather than androstenedione. It is very difficult to dissolve any of the androstenedione family unfortunately. This can be done by cyclodextrin suspension, but only in a laboratory and not at home. Research into low dose sublingual administration of androstenediol for both men and women might turn out to be very beneficial.

No interest in 4-andro on my end. Quite a few studies have been done, even with lower doses. If you search the medical databases of other countries (Russia, India, UK, Germany, Brazil, etc) you will find other studies.
4-androstenedione is about as effective an estrogenic precursor as you can get. T is a lot LESS estrogenic despite being 1 step away from estradiol because T is itself a relatively good aromatase inhibitor (AI) while 4-andro is not. In fact, some studies suggest that the pathway through which T raises estrogens is by converting back to 4-andro and then 4-andro gets converted into estrone, estradiol, estriol, etc. DHEA is less estrogenic than 4-andro simply because it is one step earlier in the cascade and we all know how easily DHEA can raise estrogen if more than 15mg are taken daily (and in some people even less than that). T levels are pretty tightly controlled, mostly by estrogen and cortisol and just adding a precursors is not a very reliable way as it would favor the estrogenic pathway if something is blocking the conversion into T (lack of cofactors, high cortisol, prolactin, estrogen, serotonin, etc). Using an AI, especially combined with a cortisol blocker is probably the best way to raise endogenous levels without giving any precursors. If precursors have to be used, then an AI and pregnenolone is probably a good way, and progesterone (estrogen/cortisol blocker) + DHEA would be another good option.
 
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Cameron

Cameron

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No interest in 4-andro on my end. Quite a few studies have been done, even with lower doses. If you search the medical databases of other countries (Russia, India, UK, Germany, Brazil, etc) you will find other studies.
4-androstenedione is about as effective an estrogenic precursor as you can get. T is a lot LESS estrogenic despite being 1 step away from estradiol because T is itself a relatively good aromatase inhibitor (AI) while 4-andro is not. In fact, some studies suggest that the pathway through which T raises estrogens is by converting back to 4-andro and then 4-andro gets converted into estrone, estradiol, estriol, etc. DHEA is less estrogenic than 4-andro simply because it is one step earlier in the cascade and we all know how easily DHEA can raise estrogen if more than 15mg are taken daily (and in some people even less than that). T levels are pretty tightly controlled, mostly by estrogen and cortisol and just adding a precursors is not a very reliable way as it would favor the estrogenic pathway if something is blocking the conversion into T (lack of cofactors, high cortisol, prolactin, estrogen, serotonin, etc). Using an AI, especially combined with a cortisol blocker is probably the best way to raise endogenous levels without giving any precursors. If precursors have to be used, then an AI and pregnenolone is probably a good way, and progesterone (estrogen/cortisol blocker) + DHEA would be another good option.
Thank you that makes a lot of sense. Have you considered using low dose testosterone in studies to increase levels to a point without suppressing endogenous levels and raising estrogen too high. It seems unlikely as any amount would suppress lh but doctors giving young men small amounts in the form of drops is likely impossible without showing some studies on testosterones ability to be promising in low and higher dosages. Like your dht study a bio identical testosterone study should show promising findings unlike a unfavorable ester based testosterone study.
 
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