- Jun 25, 2006
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Estrogen Rebound?
You’ve probably heard the term “estrogen rebound” so often that its existence is a given for you. Certainly, this phrase has become ingrained in the lore of the hard-core bodybuilding subculture, and the need for dealing with this phenomenon post-cycle, with anti-estrogens or aromatase inhibitors, is almost second nature. We are referring, of course, to the belief that estrogen levels become elevated for a period of time after steroids have been discontinued. The first several weeks post-cycle is undoubtedly a delicate window of time, with gynecomastia symptoms being a recurring problem for some people. This would seem to lend solid support for the belief that estrogen levels are becoming elevated. After all, when puffy nipples start poking out of your shirt, isn’t this just common sense? But how do we know that estrogen levels are actually running out of control in the post-cycle period, and by what mechanism would this occur? It turns out that a little investigation into the subject reveals some surprising answers, with the theory of estrogen rebound turning out to be less than entirely accurate.
The Source of Estrogen
To understand what’s going on post-cycle, it is first important to understand where estrogen comes from in men. This hormone is produced in our bodies largely through the aromatization of precursor steroids such as androstenedione and testosterone (these two steroids convert to the estrogens estrone and estradiol, respectively). It’s a process that takes place in both glandular (testes[1]) and extra glandular tissues (including adipose,[2] liver,[3] central nervous system[4] and skeletal muscle[5] tissue). Extraglandular tissues are actually the primary source for circulating estrogens in the male body, with a much smaller amount being accounted for by testicular secretion of this hormone.[6] As a result of this precursor/target hormone relationship, the availability of plasma androstenedione and testosterone are dominating factors controlling the level of estrogens in the body. That means, obviously, that if the levels of these precursor hormones drop, circulating estrogen levels will directly decline as a result.
Post-Cycle Estrogen
During the post-cycle window, of course, testosterone levels are suppressed. This restricts one of the main substrates used for the formation of estrogen in the body, which means we most certainly should not expect estrogen levels to be higher than they are normally. In fact, until testosterone production is restored to normal, estrogen levels should actually be a little lower than they were before the cycle. Studies published in 1993 with testosterone enanthate show the absence of a true “estrogen rebound” well.[7] In this male contraception trial, 28 subjects aged 22-40 years were given weekly injections of testosterone (200mg). Their hormonal profiles, including testosterone, estradiol, LH and FSH, were measured before, during, and after a 12-month period of steady therapy. Only the data from those men who had reached a state of azoospermia (suppressed sperm production) were actually included in the presented final data, giving us a good inside view of what your hormones should look like when recovering from strong endogenous testosterone suppression. The recovery period included in the investigation was six months, which was more than an ample window to chart hormonal parameters after drug withdrawal. The investigators noted that both estrogen and testosterone actually returned to pre-treatment values within the first month, and reported no unusual elevation in serum estrogen levels at all. In fact, the recovery pattern of estrogen mirrored that of testosterone very closely.
Androgen/Estrogen Imbalance
So, if estrogen levels are not elevated post-cycle, then what accounts for the individual who swears he is prone to symptoms of gyno during this period? The possible answer lies in the fact that it’s the ratio of estrogens to androgens that is most relevant to the formation of gynecomastia, not necessarily the total amount of estrogen present.[8] It turns out that androgens and estrogens play opposing roles in the growth of mammary tissue, and simply lowering the level of androgenic activity can be a trigger of this condition. Additionally, when looking at the two main sources of estrogens in the body, we find an interesting situation. Androstenedione is a hormone largely of adrenal origin,[9] which means that even as testicular steroidogenesis is diminished and testosterone suppressed, the body may still be left with pretty ample amounts of estrogen precursor hormones. Our extragonadal source of estrogen may therefore not be as drastically inhibited, causing an important and unwelcome shift in the estrogen to androgen ratio. With androgen levels not sufficient to counter estrogen’s activity in the breast, gyno could be triggered, even if levels of estrogen itself are normal or slightly suppressed. This possibility is illustrated well in a report published in the Journal of Clinical Endocrinology and Metabolism in 1980, concerning the spontaneous occurrence of gynecomastia in three elderly men one to 30 years after suffering from the mumps.[10] The men had serum testosterone concentrations of only about 20 percent of what is normal for men of their age, demonstrating a clear impairment of their bodies’ abilities to produce testosterone. Concentrations of androstenedione, estradiol and estrone, however, were within the range considered normal for healthy young men, with peripheral aromatization said to account for virtually all the estrogen produced in these subjects. The researchers suggested that the capacity of Leydig cells in the testes to secrete testosterone was impaired after mumps in the three men, but the capacity to form estrogen was not similarly impaired, since most estrogen is formed in extraglandular tissues. The resulting imbalance of androgen to estrogen ratio was likewise believed to be responsible for the onset of gynecomastia, which occurred even without high estrogen levels.
Drawing Conclusions
The above information suggests that estrogen rebound is, in fact, just another in a long line of misunderstandings in the bodybuilding world, an explanation quite off the mark of what is really happening in our bodies. If we want to be accurate, we are looking instead, of course, at a possible rebound imbalance in hormone levels. But what does this really mean to the average bodybuilder preparing to conclude his most recent steroid cycle? High estrogen levels or imbalanced estrogen/androgen ratio are going to be very similar to those in the individual prone to gynecomastia in a practical sense, so it should certainly not be interpreted as a recommendation to abandon anti-estrogens or aromatase inhibitors. These agents are indeed effective in preventing gynecomastia in either case, and well worth the money for that purpose. It does, however, allow us to look at the post-cycle window from a slightly different perspective. No longer are we to assume that estrogen is the main enemy during post-cycle recovery. In fact, we could logically conclude that this hormone may be offering less inhibition in the average post-cycle window than it does in normal physiological conditions. While there still may be reasons to include anti-estrogens in a well-thought-out recovery program, there no longer seems to be any reason to think estrogen suppression should be the sole focus of post-cycle therapy.
References
[1] Aromatase expression in the human male. Brodie A, Inkster S, Yue W. Mol Cell Endocrinol 2001 Jun 10;178(1-2):23-8
[2] Aromatization of androgens by muscle and adipose tissue in vivo. Longcope C, Pratt JH, Schneider SH, Fineberg SE. J Clin Endocrinol Metab 1978 Jan;46(1):146-52
[3] The aromatization of androstenedione by human adipose and liver tissue. J Steroid Biochem. 1980 Dec;13(12):1427-31.
[4] A review of brain aromatase cytochrome P450. Lephart ED. Brain Res Brain Res Rev 1996 Jun;22(1):1-26
[5] Aromatization by skeletal muscle. Matsumine H, Hirato K, Yanaihara T, Tamada T, Yoshida M. J Clin Endocrinol Metab 1986 Sep;63(3):717-20
[6] Origin of estrogen in normal men and in women with testicular feminization. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK. J Clin Endocrinol Metab 1979 Dec;49(6):905-16
[7] Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. I: Plasma luteinizing hormone, follicle stimulating hormone, testosterone, estradiol, and inhibin concentrations EM Wallace, SM Gow, and FC Wu. J. Clin. Endocrinol. Metab. 77: 290-293
[8] Gynecomastia. Leung AK. Am Fam Physician 1989 Apr;39(4):215-22
[9] Proceedings: Adrenal androgens. 11. Blood androst-4-ene-3, 17-dione. Akane Y, Nawada S, Aiba H, Ueda T, Motomatsu T. Nippon Naibunpi Gakkai Zasshi 1974 Feb 20;50(2):34
[10] Androgen and estrogen production in elderly men with gynecomastia and testicular atrophy after mumps orchitis. Aiman J, Brenner PF, MacDonald PC. J Clin Endocrinol Metab 1980 Feb;50(2):380-6
Black Market Update
Bodybuilders have been reeling with the news that individuals involved with the Mexican veterinary drug firm Ttokkyo labs were arrested October 3rd in what is being called the largest ketamine smuggling ring in North America. Ketamine is not an anabolic steroid, but an anesthetic drug commonly sold on the black market and used recreationally for its ability to produce a numbing and introspectively focused high. Ketamine, or Special K, became a controlled substance in 1999, resulting in severe penalties on the illegal distribution of this drug in the U.S. Ttokkyo owner Dr. Francisco Molina was among those arrested, having been first detained by police in Panama and thereafter turned over to authorities in the U.S. to face charges. In total, 10 individuals have been indicted, seven of which have been arrested. These arrests are the culmination of a two-year investigation into the operation, which charted the distribution of Ttokkyo’s ketamine product from a Tijuana-based supply company to drug dealers in San Diego, San Bernardino, San Francisco, New York, Orlando, Philadelphia and Boston. Bodybuilders who have come to rely on Ttokkyo’s extensive and quality line of anabolic steroids are, of course, very concerned right now about what, if any, impact this will have on future steroid availability in the U.S. Pictured here is one of the few testosterone cypionate preparations you will find outside of North America. It seems that in the rest of the world, the enanthate ester is by far the most dominant, with cypionate-containing preparations coming few and far between. Deposteron is one of the few standouts, which is produced by the Brazilian drug firm Novaquimica. Each ampoule contains 200 milligrams of this long-acting testosterone ester, and has been made out of both clear and amber (light resistant) glass. The latter appearance seems the most recent. Each ampoule contains two milliliters of solution, so what we have is a modest, but acceptable, 100mg/ml steroid. Contained in each box are three ampoules or 600 milligrams of steroid in total, which usually sells for a very modest price in this area of the world. By the time it is found in the U.S., however, the box has usually been discarded and the ampoules sold separately for as much as $15-20 each. When located on the black market, this item can be trusted, especially if the ampoules are accompanied by the appropriate box. —WL
You’ve probably heard the term “estrogen rebound” so often that its existence is a given for you. Certainly, this phrase has become ingrained in the lore of the hard-core bodybuilding subculture, and the need for dealing with this phenomenon post-cycle, with anti-estrogens or aromatase inhibitors, is almost second nature. We are referring, of course, to the belief that estrogen levels become elevated for a period of time after steroids have been discontinued. The first several weeks post-cycle is undoubtedly a delicate window of time, with gynecomastia symptoms being a recurring problem for some people. This would seem to lend solid support for the belief that estrogen levels are becoming elevated. After all, when puffy nipples start poking out of your shirt, isn’t this just common sense? But how do we know that estrogen levels are actually running out of control in the post-cycle period, and by what mechanism would this occur? It turns out that a little investigation into the subject reveals some surprising answers, with the theory of estrogen rebound turning out to be less than entirely accurate.
The Source of Estrogen
To understand what’s going on post-cycle, it is first important to understand where estrogen comes from in men. This hormone is produced in our bodies largely through the aromatization of precursor steroids such as androstenedione and testosterone (these two steroids convert to the estrogens estrone and estradiol, respectively). It’s a process that takes place in both glandular (testes[1]) and extra glandular tissues (including adipose,[2] liver,[3] central nervous system[4] and skeletal muscle[5] tissue). Extraglandular tissues are actually the primary source for circulating estrogens in the male body, with a much smaller amount being accounted for by testicular secretion of this hormone.[6] As a result of this precursor/target hormone relationship, the availability of plasma androstenedione and testosterone are dominating factors controlling the level of estrogens in the body. That means, obviously, that if the levels of these precursor hormones drop, circulating estrogen levels will directly decline as a result.
Post-Cycle Estrogen
During the post-cycle window, of course, testosterone levels are suppressed. This restricts one of the main substrates used for the formation of estrogen in the body, which means we most certainly should not expect estrogen levels to be higher than they are normally. In fact, until testosterone production is restored to normal, estrogen levels should actually be a little lower than they were before the cycle. Studies published in 1993 with testosterone enanthate show the absence of a true “estrogen rebound” well.[7] In this male contraception trial, 28 subjects aged 22-40 years were given weekly injections of testosterone (200mg). Their hormonal profiles, including testosterone, estradiol, LH and FSH, were measured before, during, and after a 12-month period of steady therapy. Only the data from those men who had reached a state of azoospermia (suppressed sperm production) were actually included in the presented final data, giving us a good inside view of what your hormones should look like when recovering from strong endogenous testosterone suppression. The recovery period included in the investigation was six months, which was more than an ample window to chart hormonal parameters after drug withdrawal. The investigators noted that both estrogen and testosterone actually returned to pre-treatment values within the first month, and reported no unusual elevation in serum estrogen levels at all. In fact, the recovery pattern of estrogen mirrored that of testosterone very closely.
Androgen/Estrogen Imbalance
So, if estrogen levels are not elevated post-cycle, then what accounts for the individual who swears he is prone to symptoms of gyno during this period? The possible answer lies in the fact that it’s the ratio of estrogens to androgens that is most relevant to the formation of gynecomastia, not necessarily the total amount of estrogen present.[8] It turns out that androgens and estrogens play opposing roles in the growth of mammary tissue, and simply lowering the level of androgenic activity can be a trigger of this condition. Additionally, when looking at the two main sources of estrogens in the body, we find an interesting situation. Androstenedione is a hormone largely of adrenal origin,[9] which means that even as testicular steroidogenesis is diminished and testosterone suppressed, the body may still be left with pretty ample amounts of estrogen precursor hormones. Our extragonadal source of estrogen may therefore not be as drastically inhibited, causing an important and unwelcome shift in the estrogen to androgen ratio. With androgen levels not sufficient to counter estrogen’s activity in the breast, gyno could be triggered, even if levels of estrogen itself are normal or slightly suppressed. This possibility is illustrated well in a report published in the Journal of Clinical Endocrinology and Metabolism in 1980, concerning the spontaneous occurrence of gynecomastia in three elderly men one to 30 years after suffering from the mumps.[10] The men had serum testosterone concentrations of only about 20 percent of what is normal for men of their age, demonstrating a clear impairment of their bodies’ abilities to produce testosterone. Concentrations of androstenedione, estradiol and estrone, however, were within the range considered normal for healthy young men, with peripheral aromatization said to account for virtually all the estrogen produced in these subjects. The researchers suggested that the capacity of Leydig cells in the testes to secrete testosterone was impaired after mumps in the three men, but the capacity to form estrogen was not similarly impaired, since most estrogen is formed in extraglandular tissues. The resulting imbalance of androgen to estrogen ratio was likewise believed to be responsible for the onset of gynecomastia, which occurred even without high estrogen levels.
Drawing Conclusions
The above information suggests that estrogen rebound is, in fact, just another in a long line of misunderstandings in the bodybuilding world, an explanation quite off the mark of what is really happening in our bodies. If we want to be accurate, we are looking instead, of course, at a possible rebound imbalance in hormone levels. But what does this really mean to the average bodybuilder preparing to conclude his most recent steroid cycle? High estrogen levels or imbalanced estrogen/androgen ratio are going to be very similar to those in the individual prone to gynecomastia in a practical sense, so it should certainly not be interpreted as a recommendation to abandon anti-estrogens or aromatase inhibitors. These agents are indeed effective in preventing gynecomastia in either case, and well worth the money for that purpose. It does, however, allow us to look at the post-cycle window from a slightly different perspective. No longer are we to assume that estrogen is the main enemy during post-cycle recovery. In fact, we could logically conclude that this hormone may be offering less inhibition in the average post-cycle window than it does in normal physiological conditions. While there still may be reasons to include anti-estrogens in a well-thought-out recovery program, there no longer seems to be any reason to think estrogen suppression should be the sole focus of post-cycle therapy.
References
[1] Aromatase expression in the human male. Brodie A, Inkster S, Yue W. Mol Cell Endocrinol 2001 Jun 10;178(1-2):23-8
[2] Aromatization of androgens by muscle and adipose tissue in vivo. Longcope C, Pratt JH, Schneider SH, Fineberg SE. J Clin Endocrinol Metab 1978 Jan;46(1):146-52
[3] The aromatization of androstenedione by human adipose and liver tissue. J Steroid Biochem. 1980 Dec;13(12):1427-31.
[4] A review of brain aromatase cytochrome P450. Lephart ED. Brain Res Brain Res Rev 1996 Jun;22(1):1-26
[5] Aromatization by skeletal muscle. Matsumine H, Hirato K, Yanaihara T, Tamada T, Yoshida M. J Clin Endocrinol Metab 1986 Sep;63(3):717-20
[6] Origin of estrogen in normal men and in women with testicular feminization. MacDonald PC, Madden JD, Brenner PF, Wilson JD, Siiteri PK. J Clin Endocrinol Metab 1979 Dec;49(6):905-16
[7] Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. I: Plasma luteinizing hormone, follicle stimulating hormone, testosterone, estradiol, and inhibin concentrations EM Wallace, SM Gow, and FC Wu. J. Clin. Endocrinol. Metab. 77: 290-293
[8] Gynecomastia. Leung AK. Am Fam Physician 1989 Apr;39(4):215-22
[9] Proceedings: Adrenal androgens. 11. Blood androst-4-ene-3, 17-dione. Akane Y, Nawada S, Aiba H, Ueda T, Motomatsu T. Nippon Naibunpi Gakkai Zasshi 1974 Feb 20;50(2):34
[10] Androgen and estrogen production in elderly men with gynecomastia and testicular atrophy after mumps orchitis. Aiman J, Brenner PF, MacDonald PC. J Clin Endocrinol Metab 1980 Feb;50(2):380-6
Black Market Update
Bodybuilders have been reeling with the news that individuals involved with the Mexican veterinary drug firm Ttokkyo labs were arrested October 3rd in what is being called the largest ketamine smuggling ring in North America. Ketamine is not an anabolic steroid, but an anesthetic drug commonly sold on the black market and used recreationally for its ability to produce a numbing and introspectively focused high. Ketamine, or Special K, became a controlled substance in 1999, resulting in severe penalties on the illegal distribution of this drug in the U.S. Ttokkyo owner Dr. Francisco Molina was among those arrested, having been first detained by police in Panama and thereafter turned over to authorities in the U.S. to face charges. In total, 10 individuals have been indicted, seven of which have been arrested. These arrests are the culmination of a two-year investigation into the operation, which charted the distribution of Ttokkyo’s ketamine product from a Tijuana-based supply company to drug dealers in San Diego, San Bernardino, San Francisco, New York, Orlando, Philadelphia and Boston. Bodybuilders who have come to rely on Ttokkyo’s extensive and quality line of anabolic steroids are, of course, very concerned right now about what, if any, impact this will have on future steroid availability in the U.S. Pictured here is one of the few testosterone cypionate preparations you will find outside of North America. It seems that in the rest of the world, the enanthate ester is by far the most dominant, with cypionate-containing preparations coming few and far between. Deposteron is one of the few standouts, which is produced by the Brazilian drug firm Novaquimica. Each ampoule contains 200 milligrams of this long-acting testosterone ester, and has been made out of both clear and amber (light resistant) glass. The latter appearance seems the most recent. Each ampoule contains two milliliters of solution, so what we have is a modest, but acceptable, 100mg/ml steroid. Contained in each box are three ampoules or 600 milligrams of steroid in total, which usually sells for a very modest price in this area of the world. By the time it is found in the U.S., however, the box has usually been discarded and the ampoules sold separately for as much as $15-20 each. When located on the black market, this item can be trusted, especially if the ampoules are accompanied by the appropriate box. —WL