Prolactin and Progesterone: two hormones that are frequently confused among the anabolic steroid using bodybuilding community. These two hormones start with the letter P, and that’s where the confusion primary comes from, but that’s also where their similarity ends. Let’s first take a look at these two hormones and identify them before moving on. Progesterone is a steroid hormone which holds a purpose in affecting the female menstrual cycle, and pregnancy (promotes gestation), as well as embryogenesis in a vast range of species[1]. Prolactin is (also known as Lactotrope) is a protein hormone secreted by the pituitary gland and is well-known for its role in initiating lactation from the nipples in females after childbirth, however, the initiation and promotion of lactation is but only one of many functions that Prolactin has in vertebrates, and is responsible for a plethora of many other functions in other animals [2].
Progesterone can be a concern for the anabolic steroid user because under some circumstances, anabolic steroids that act as Progestins can be particularly suppressive to the HPTA more so than other compounds, and their interaction with the Progesterone receptor can exacerbate the potential for the development of gynecomastia by increasing the sensitivity of Estrogen receptor to Estrogens. Prolactin can be a concern because elevated Prolactin levels in men will result in lactation from the nipples, as well as suppression of the HPTA and endogenous Testosterone production, as well as libido-reducing effects and anorgasmia (the inability to achieve orgasm).
The two hormones most often associated with Prolactin and Progesterone are: Trenbolone and Deca-Durabolin (Nandrolone). Trenbolone is a derivative of Deca-Durabolin, placing the two in the same category/family of anabolic steroids. Both of these anabolic steroids are Progestins in and of themselves (they are also properly classified as 19-nor steroids). Contrary to a lot of misunderstandings and false claims that are thrown around, Deca and Trenbolone do not convert into Progesterone. They are Progestins, they contain the chemical structure and characteristics that Progesterone does, and they do have a binding affinity to the Progesterone receptors in the body. However, it is very important to understand: they are not Progesterone. They are what we could consider derivatives of Progesterone, much in the same way that Winstrol is a derivative of Dihydrotestosterone (DHT), but you would never refer to Winstrol as being Dihydrotestosterone. The same can be said for Methyltestosterone and Testosterone, or Anavar and Dihydrotestosterone, or Anadrol and Dihydroteststerone (keep that one in mind, I am going to come back to that shortly.
So, where does Prolactin come into play here? Notice I haven’t mentioned the relation that Trenbolone and Deca have with Prolactin just yet. The truth is that they don’t have any real relation with Prolactin that we currently know of. The truth is that what science has already established is that Progesterone is actually an inhibitor of Prolactin not only at the site of breast tissue but at the pituitary gland as well [3] [4] [5] [6]! Furthermore, androgens (especially strong androgens) have a tendency to decrease Prolactin receptors in the body [7] and that rising Estrogen levels will increase prolactin as evidenced by a study subject whose Prolactin levels increased significantly as a result of the aromatization of Testosterone into Estrogen[8].
So, what can we conclude from what we already know about the relation that all of these hormones have with one another? Well, Progesterone does indeed reduce Prolactin levels, so the common claim that 19-nors such as Trenbolone and Deca cause increased Prolactin levels would be valid except for one thing: they are derivatives of Progesterone. In other words, they are modified forms of Progesterone that due to their modifications, might grant these anabolic steroids as of yet unknown effects on the endocrine system. We can best compare this to the relation that Anadrol has with Dihydrotestosterone. We all know that Anadrol is a derivative of DHT. Therefore, Anadrol does share many characteristics of its parent hormone (such as the inability to aromatize into Estrogen). However, we all know that Anadrol 50 exhibits some of the strongest and worst seen Estrogenic effects in users, such as bloating and gynecomastia. But we know that it does not convert into Estrogen, which leads to the belief that Anadrol itself and/or its metabolites exhibit activity with the Estrogen receptors in the body.
This very well could be the case with Trenbolone and Deca. Although they are Progestins and should by all rights express the same or similar characteristics of their parent hormone Progesterone, their modifications may grant them some other strange and quirky mechanisms in the body that result in activity that is contrary to what we might expect. Although it does not occur to everyone who uses Trenbolone or Deca, there are many who have reported increased Prolactin levels as a result of the use of these compounds, as evidenced by bloodwork results these people have shared with others. The only way we can ever know if this is the truth is if further studies are conducted on test subjects with these two compounds. But as a result of the prohibition of anabolic steroids, the social stigma placed upon them, and the criminalization of them in the United States, it is very hard to foresee that we will be able to find answers to these questions any time soon.
Other factors that might contribute to increased Prolactin levels from the use of Trenbolone or Deca might be the result of adulterated products (usually underground products) on the black market as a result of prohibition. Many products do not contain the labelled hormone, they may contain additional hormones, or even additives of other sorts that might disrupt the endocrine system of the user in many unexpected ways.
This is a topic that could be discussed for days on end, and I will likely continue this discussion in a future blog post, as we haven’t even got through the tip of the iceberg when it comes to the relation between androgens, Progesterone, Prolactin, and Estrogens.
[1] “Metabocard for Hydroxyprogesterone”. Human Metabolome Database. Retrieved 31 July 2013.
[2] Bole-Feysot C, Goffin V, Edery M, Binart N, Kelly PA (June 1998). “Prolactin (PRL) and its receptor: actions, signal transduction pathways and phenotypes observed in PRL receptor knockout mice”. Endocr. Rev. 19 (3): 225–68. doi:10.1210/er.19.3.225. PMID 9626554.
[3] Zinger M, McFarland M, Ben-Jonathan N (February 2003). “Prolactin expression and secretion by human breast glandular and adipose tissue explants”. J. Clin. Endocrinol. Metab. 88 (2): 689–96. PMID 12574200.
[4] Assairi L, Delouis C, Gaye P, Houdebine LM, Olliver-Bousquiet M, Denamur R. 1974. Inhibition by Progesterone of the Lactogenic Effect of Prolactin in the Pseudopregnant Rabbit. Biochem. J. 144, 245-252.
[5] Hall TR, Harvey S, Chadwick A. 1984. Progesterone inhibits prolactin and growth hormone release from fowl pituitary glands in vitro. Br Poult Sci. 25(4):555-9.
[6] C. L. CHEN, and J. MEITES. 1970. Effects of Estrogen and Progesterone on Serum and Pituitary Prolactin Levels in Ovariectomized Rats. Department of Physiology, Michigan State University. Volume 86 Issue 3.
[7]Norstedt G, Mode A 1982. On the primary site of action of estrogens and androgens in the regulation of hepatic prolactin receptors. Endocrinology. 111(2):645-9.
[8] Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F. 1984. Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation. Acta Endocrinol (Copenh). 105(2):167-72.
Progesterone can be a concern for the anabolic steroid user because under some circumstances, anabolic steroids that act as Progestins can be particularly suppressive to the HPTA more so than other compounds, and their interaction with the Progesterone receptor can exacerbate the potential for the development of gynecomastia by increasing the sensitivity of Estrogen receptor to Estrogens. Prolactin can be a concern because elevated Prolactin levels in men will result in lactation from the nipples, as well as suppression of the HPTA and endogenous Testosterone production, as well as libido-reducing effects and anorgasmia (the inability to achieve orgasm).
The two hormones most often associated with Prolactin and Progesterone are: Trenbolone and Deca-Durabolin (Nandrolone). Trenbolone is a derivative of Deca-Durabolin, placing the two in the same category/family of anabolic steroids. Both of these anabolic steroids are Progestins in and of themselves (they are also properly classified as 19-nor steroids). Contrary to a lot of misunderstandings and false claims that are thrown around, Deca and Trenbolone do not convert into Progesterone. They are Progestins, they contain the chemical structure and characteristics that Progesterone does, and they do have a binding affinity to the Progesterone receptors in the body. However, it is very important to understand: they are not Progesterone. They are what we could consider derivatives of Progesterone, much in the same way that Winstrol is a derivative of Dihydrotestosterone (DHT), but you would never refer to Winstrol as being Dihydrotestosterone. The same can be said for Methyltestosterone and Testosterone, or Anavar and Dihydrotestosterone, or Anadrol and Dihydroteststerone (keep that one in mind, I am going to come back to that shortly.
So, where does Prolactin come into play here? Notice I haven’t mentioned the relation that Trenbolone and Deca have with Prolactin just yet. The truth is that they don’t have any real relation with Prolactin that we currently know of. The truth is that what science has already established is that Progesterone is actually an inhibitor of Prolactin not only at the site of breast tissue but at the pituitary gland as well [3] [4] [5] [6]! Furthermore, androgens (especially strong androgens) have a tendency to decrease Prolactin receptors in the body [7] and that rising Estrogen levels will increase prolactin as evidenced by a study subject whose Prolactin levels increased significantly as a result of the aromatization of Testosterone into Estrogen[8].
So, what can we conclude from what we already know about the relation that all of these hormones have with one another? Well, Progesterone does indeed reduce Prolactin levels, so the common claim that 19-nors such as Trenbolone and Deca cause increased Prolactin levels would be valid except for one thing: they are derivatives of Progesterone. In other words, they are modified forms of Progesterone that due to their modifications, might grant these anabolic steroids as of yet unknown effects on the endocrine system. We can best compare this to the relation that Anadrol has with Dihydrotestosterone. We all know that Anadrol is a derivative of DHT. Therefore, Anadrol does share many characteristics of its parent hormone (such as the inability to aromatize into Estrogen). However, we all know that Anadrol 50 exhibits some of the strongest and worst seen Estrogenic effects in users, such as bloating and gynecomastia. But we know that it does not convert into Estrogen, which leads to the belief that Anadrol itself and/or its metabolites exhibit activity with the Estrogen receptors in the body.
This very well could be the case with Trenbolone and Deca. Although they are Progestins and should by all rights express the same or similar characteristics of their parent hormone Progesterone, their modifications may grant them some other strange and quirky mechanisms in the body that result in activity that is contrary to what we might expect. Although it does not occur to everyone who uses Trenbolone or Deca, there are many who have reported increased Prolactin levels as a result of the use of these compounds, as evidenced by bloodwork results these people have shared with others. The only way we can ever know if this is the truth is if further studies are conducted on test subjects with these two compounds. But as a result of the prohibition of anabolic steroids, the social stigma placed upon them, and the criminalization of them in the United States, it is very hard to foresee that we will be able to find answers to these questions any time soon.
Other factors that might contribute to increased Prolactin levels from the use of Trenbolone or Deca might be the result of adulterated products (usually underground products) on the black market as a result of prohibition. Many products do not contain the labelled hormone, they may contain additional hormones, or even additives of other sorts that might disrupt the endocrine system of the user in many unexpected ways.
This is a topic that could be discussed for days on end, and I will likely continue this discussion in a future blog post, as we haven’t even got through the tip of the iceberg when it comes to the relation between androgens, Progesterone, Prolactin, and Estrogens.
[1] “Metabocard for Hydroxyprogesterone”. Human Metabolome Database. Retrieved 31 July 2013.
[2] Bole-Feysot C, Goffin V, Edery M, Binart N, Kelly PA (June 1998). “Prolactin (PRL) and its receptor: actions, signal transduction pathways and phenotypes observed in PRL receptor knockout mice”. Endocr. Rev. 19 (3): 225–68. doi:10.1210/er.19.3.225. PMID 9626554.
[3] Zinger M, McFarland M, Ben-Jonathan N (February 2003). “Prolactin expression and secretion by human breast glandular and adipose tissue explants”. J. Clin. Endocrinol. Metab. 88 (2): 689–96. PMID 12574200.
[4] Assairi L, Delouis C, Gaye P, Houdebine LM, Olliver-Bousquiet M, Denamur R. 1974. Inhibition by Progesterone of the Lactogenic Effect of Prolactin in the Pseudopregnant Rabbit. Biochem. J. 144, 245-252.
[5] Hall TR, Harvey S, Chadwick A. 1984. Progesterone inhibits prolactin and growth hormone release from fowl pituitary glands in vitro. Br Poult Sci. 25(4):555-9.
[6] C. L. CHEN, and J. MEITES. 1970. Effects of Estrogen and Progesterone on Serum and Pituitary Prolactin Levels in Ovariectomized Rats. Department of Physiology, Michigan State University. Volume 86 Issue 3.
[7]Norstedt G, Mode A 1982. On the primary site of action of estrogens and androgens in the regulation of hepatic prolactin receptors. Endocrinology. 111(2):645-9.
[8] Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F. 1984. Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation. Acta Endocrinol (Copenh). 105(2):167-72.
