Prolactin & Anabolic Steroids


This is what it all boils down to concerning Prolactin and how it relates to the anabolic steroid using community. The concern for a very long time (and still continues today) is that various anabolic steroids may or may not promote Prolactinergic effects on the body during use, either through stimulating Prolactin secretion from the pituitary gland or perhaps expressing Prolactin-related activity elsewhere in the body through other mechanisms. What should be noted first before moving on is the importance of having clinical research and data in order to verify claims. Unfortunately due to the current general legal status of anabolic steroids in the Western world (especially in the United States), clinical research and data is limited in the scope of this area. Research on the effects of various anabolic steroids in their use as performance and physique enhancers is very difficult to conduct because of the aforementioned legal status, and furthermore there are other limitations as well, such as: the allocation of funding for said research, the perceived need or requirement for such research, and so on and so forth. At this point in time, there is very little data to go by when the question of Prolactin and anabolic steroids is concerned (specifically in humans, and specifically at bodybuilding doses, and specifically under the conditions that a bodybuilder would use them).

For the time being, the best logical conclusions to make are diligent ones that acknowledge the lack of current research/information, and to understand that until such research is (hopefully) done in the future and data is gathered, theoretical knowledge and what we can discern from anecdotal evidence is the best we can do to form logical conclusions. Anecdotal evidence (as well as evidence in the form of blood test results) from many anabolic steroid users within the bodybuilding community have demonstrated significant PRL increases from those who use two particular anabolic steroids that are Progestins by nature: Trenbolone and Nandrolone (Deca-Durabolin). These hyperprolactinaemic afflicted individuals do also typically experience one or more of the typical Prolactin side effects: anrogasmia, lactation from the nipples, etc. There are also numerous individuals who can utilize these compounds without any hyperprolactinaemic blood results or symptoms. These anabolic steroids are also known and classified as 19-nor compounds (designating that these compounds lack a carbon atom at the 19th position, which is a carbon held by all other anabolic steroids). This is, by definition, what any 19-nor compound is. Further derivatives of Trenbolone or Nandrolone (such as Methyltrienolone) are logically also Progestins. By virtue of this fact, it is logical that individuals experiencing hyperprolactinaemia would come to the conclusion that because Trenbolone and/or Deca-Duabolin are Progestins, they must be causing the problem.

The truth is that as research has shown (referenced in the introduction of this article), Progesterone is in fact an inhibitor of Prolactin in numerous tissues throughout the body, including at the mammary gland. Therefore, the logical conclusion we can make is that the use of Progesterone and/or Progestins should not cause an increase in Prolactin levels, but should in fact have the opposite effect! However, this is only half of the total conclusion. For the other half, we must conclude that this is inconclusive due to a lack of direct evidence concerning Trenbolone and Deca and their effects, especially at bodybuilding dosages, on Prolactin levels.

The important concept to grasp at this point is the fact that Trenbolone and Nandrolone are derivatives of Progesterone, they are modifications of it. And these anabolic steroids can very well have unknown additional effects throughout the body in different tissues (as well as the endocrine system) due to these modifications. This is best compared to a similar situation: Anadrol 50. Anadrol 50 is a derivative of DHT (Dihydroteststerone). As such, Anadrol shares many similar characteristics with its parent hormone, as all derivatives of parent hormones normally do. Therefore, Anadrol 50 does possess the inability to interact with the aromatase enzyme and is therefore unable to aromatize (convert) into Estrogen. However, at the same time it is common knowledge that Anadrol carries with it a reputation for being one of the most notorious anabolic steroids to afflict Estrogen-related side effects on the user (bloating, water retention, gynecomastia, etc.). This doesn’t make sense considering it is unable to aromatize, so why is this the case? It is hypothesized that it is Anadrol itself and/or one or more of its metabolites that binds to the Estrogen receptor in different tissues in the body to exert these effects. Unfortunately this is a standing hypothesis that is yet to be tested and confirmed via clinical study, but considering everything we do currently know about Anadrol, there must be activity ongoing that does not conform to conventional logic here.

This is the same conclusion we must make with Trenbolone and Deca-Durabolin as they relate to Prolactin. They are derivatives of Progesterone and by all means should express the same anti-PRL effects, but their modifications possibly grant them other mysterious characteristics and qualities that might result in seemingly contrary activity to what conventional logic dictates to us (akin to the Anadrol example used). Furthermore, there are plenty of users who have used Trenbolone and Nandrolone with no Prolactin-related issues, and upon resuming use several cycles later, they experienced the Prolactin-related issues. The problem seems to be intermittent across the community, and until further research can be conducted that simulate/mimic the exact conditions under which anabolic steroid users use Progestins and experience Prolactin-related side effects, we will never know for sure.

These are the questions that need to be answered in the future if studies of this nature are to be conducted:

– The possibility of mysterious activity of Progestin anabolic steroids due to their chemical modifications.
– Ruling out the possibility that many anabolic steroid users are utilizing adulterated products (usually underground products) purchased on the black market as a result of prohibition. Many products do not contain the hormone that is advertised on the label, or they may contain additional hormones, or even additives of other sorts that might disrupt the endocrine system of the user in many unexpected ways.
– The role of Estrogens and other hormones that are vital to mammary growth and function in the midst of the use of anabolic steroids such as Trenbolone or Nandrolone.

Control, Elimination, and Prevention Prolactin

Control of Prolactin would ideally be the first and best possible course of action before any other measures are taken. An ounce of prevention is worth a pound of cure, after all, and it is not healthy in any way to completely eliminate Prolactin levels or allow them to rise above the normal range. As evidenced previously in this article, the control of Estrogen seems to be the key factor in maintaining low levels of Prolactin in the body, as Estrogen has a direct stimulatory effect on not only the synthesis of Prolactin at the pituitary gland, but also in facilitating mammary tissue function and development. As a matter of fact, one study conducted on female lambs involved the administration of Trenbolone along with Estradiol (E2) and another group of lambs with Estradiol-only, which resulted in the expected effect of Prolactin increases as a result of Estradiol, but the Trenbolone + E2 group experienced an anti-Estrogen effect from Trenbolone, preventing the mammary stimulus of Estrogen[1]. This is hardly surprising, considering it is common knowledge that androgens can and do decrease the number of Prolactin receptors in the body as well[2] (especially strong androgens such as Trenbolone). Maintaining an high androgen:estrogen ratio is a key factor in controlling Prolactin as well, as evidenced by one study in which a subject experienced significant Prolactin increase during Testosterone administration as a result of the aromatization of the administered Testosterone into Estrogen[3].

Therefore, the first and foremost strategy for the anabolic steroid user should be to merely maintain Estrogen levels within the normal range during the use of any and all anabolic steroids, period.

If Prolactin has become a significant concern and prevention is no longer a viable course of action, various medications can be sought after in order to directly tackle the problem. As mentioned in the introduction of this article, dopamine is the body’s natural hormone/neurotransmitter that is responsible for the suppression of Prolactin secretion. As such, various medications known as dopamine agonists have been discovered and developed in the treatment of hyperprolactinaemia. Dopamine agonists (such as Cabergoline, Bromocriptine, and Pramipexole among many others) bind to the same receptors that dopamine itself binds to, and initiates similar effects (to different degrees), resulting in an inhibition of Prolactin secretion[4] [5] [6]. Estrogen control should be sought after simultaneously as well.


Medical References:

[1] Blanco A, Moya L, Flores R, Agüera E, Monterde JG. 2002. Effects of anabolic implants of oestradiol alone or in combination with trenbolone acetate on the ultrastructure of mammary glands in female lambs regarding their interference in prolactin secretion. J Vet Med A Physiol Pathol Clin Med. 2002 Feb;49(1):13-7.

[2] 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.

[3] 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.

[4] Verhelst J, Abs R, Maiter D, et al. (July 1999). “Cabergoline in the treatment of hyperprolactinemia: a study in 455 patients”. J. Clin. Endocrinol. Metab. 84 (7): 2518–22. doi:10.1210/jc.84.7.2518. PMID 10404830.

[5] Webster J, Piscitelli G, Polli A, Ferrari CI, Ismail I, Scanlon MF (October 1994). “A comparison of cabergoline and bromocriptine in the treatment of hyperprolactinemic amenorrhea. Cabergoline Comparative Study Group”. N. Engl. J. Med. 331 (14): 904–9. doi:10.1056/NEJM199410063311403. PMID 7915824.

[6] Colao A, Di Sarno A, Guerra E, De Leo M, Mentone A, Lombardi G (April 2006). “Drug insight: Cabergoline and bromocriptine in the treatment of hyperprolactinemia in men and women”. Nat Clin Pract Endocrinol Metab 2 (4): 200–10. doi:10.1038/ncpendmet0160. PMID 16932285.