This article is about prolactin and how it relates to anabolic steroid users.
A long-standing (and still ongoing concern today) is that various anabolic steroids may or may not promote prolactin effects in the body during use, either by stimulating prolactin secretion from the pituitary gland or by expressing prolactin-related activity elsewhere in the body through other mechanisms.
Before moving on, the first thing to note is the importance of clinical studies and data to validate 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 this area.
Studies on the effects of various anabolic steroids used as performance and physique enhancers are very difficult to conduct due to the aforementioned legal status, and there are also other limitations such as the allocation of funding for such studies, the need or requirement for such studies, etc.
At the moment, there is very little data on prolactin and anabolic steroids (especially at the doses and conditions used by humans, especially bodybuilders).
For now, the most sensible thing to do is to acknowledge the current lack of research/information and understand that until such studies are conducted in the future and data is collected, what we can glean from theoretical knowledge and anecdotal evidence is the best we can do to draw logical conclusions.
Anecdotal evidence (as well as evidence in the form of blood test results) from many anabolic steroid users within the bodybuilding community has shown a significant increase in PRL in those using two specific anabolic steroids called progestins: Trenbolone and Nandrolone (Deca-Durabolin).
People who suffer from this hyperprolactinemia usually also experience one or more of the typical prolactin side effects (decreased libido, nipple lactation, etc.).
There are also many people who can use these compounds without hyperprolactinemia blood test results or symptoms. These anabolic steroids are also known and categorized as 19-nor compounds (compounds that lack a carbon atom at the 19th position, which is the carbon that all other anabolic steroids have).
By definition, 19-nor compounds are classified as such.
Additional derivatives of trenbolone or nandrolone (such as methyltrienolone) are also logically progestins.
Due to these facts, it is logical to conclude that individuals experiencing hyperprolactinemia are experiencing problems with trenbolone and/or deca-duabolin because they are progestins.
Research (referenced at the beginning of this article) has shown that progesterone actually acts to inhibit prolactin in several tissues in the body, including the mammary glands.
Therefore, the logical conclusion we can draw is that the use of progesterone and/or progestins should not increase prolactin levels, and in fact should have the opposite effect! However, this is only half of the conclusion.
The other half must be concluded as inconclusive due to the lack of direct evidence regarding the effects of Trenbolone and Deca, especially in bodybuilding doses, on prolactin levels.
An important concept to understand at this point is the fact that trenbolone and nandrolone are derivatives of progesterone and are variations of progesterone.
And because of this modification, these anabolic steroids can have additional unknown effects throughout the body, not only in the endocrine system but also in other tissues.
This is best compared with a similar situation:
Anadrol 50. Anadrol 50 is a derivative of DHT (dihydrotestosterone).
As such, Anadrol shares many similar properties with the parent hormone, as all derivatives of the parent hormone typically do.
Anadrol 50 is therefore unable to interact with the aromatase enzyme and therefore cannot aromatize (convert) into estrogen.
At the same time, however, it is common knowledge that Anadrol has the reputation of being one of the most notorious anabolic steroids for causing estrogen-related side effects in users (bloating, water retention, gynecomastia, etc.).
This doesn't make sense considering that it can't aromatize, but why?
It is hypothesized that it is anadrol itself and/or one or more of its metabolites that bind to estrogen receptors in different tissues of the body to exert these effects.
Unfortunately, this is a hypothesis that has yet to be tested and confirmed through clinical studies, but considering everything we currently know about Anadrol, there must be some activity going on that is inconsistent with conventional logic.
The same conclusion can be drawn about trenbolone and deca durabolin, which are related to prolactin.
These are derivatives of progesterone and should necessarily exhibit the same anti-PRL effects, but their modifications can endow them with other mysterious properties and characteristics that can result in activity contrary to what conventional logic dictates to us (similar to the Anadrol example used).
There are also many users who have used trenbolone and nandrolone without prolactin related issues and then experienced prolactin related issues when they resumed use a few weeks later.
This issue seems to be intermittent across the community and will not be known for certain until further research is conducted that simulates/mimics the exact conditions under which anabolic steroid users use progestins and experience prolactin-related side effects.
In order for studies of this nature to be conducted, these questions will need to be answered in the future:
- Possible mysterious activity of progestin anabolic steroids due to chemical modification.
- It cannot be ruled out that many anabolic steroid users are using illicit products, often purchased on the black market due to the ban.
And many products may not contain the hormone advertised on the label, or may contain additional hormones or other kinds of additives that can disrupt the user's endocrine system in unexpected ways.
The role of estrogen and other hormones essential for breast growth and function while using anabolic steroids such as trenbolone or nandrolone.
Controlling, eliminating, and preventing prolactin
Controlling prolactin is the best first step you can take before taking any other action.
After all, prevention is better than cure, and completely eliminating prolactin levels or allowing them to rise above the normal range is not healthy in any way.
As discussed earlier in this article, estrogen regulation appears to be an important factor in keeping prolactin levels low in the body, as estrogen not only synthesizes prolactin in the pituitary gland, but also has a direct stimulatory effect on promoting mammary tissue function and development.
In fact, in one study in female sheep, a group administered trenbolone plus estradiol (E2) and another group administered estradiol alone, it was found that while the trenbolone + E2 group was able to benefit from the estradiol-induced increase in prolactin, the trenbolone + estradiol group experienced an anti-estrogenic effect of trenbolone that prevented estrogen from stimulating the mammary glands [1].
This is not surprising considering that it is common knowledge that androgens can and do reduce the number of prolactin receptors in the body[2] (especially potent androgens like trenbolone).
Maintaining a high androgen:estrogen ratio is also an important factor in regulating prolactin, and this has been demonstrated in one study where subjects experienced significant prolactin increases during testosterone administration due to the conversion of administered testosterone to estrogen [3].
Therefore, the most important strategy for anabolic steroid users should be to maintain estrogen levels within the normal range while using any anabolic steroid.
If prolactin becomes a serious problem and prevention is no longer a viable option, there are a variety of medications available to directly address the issue.
As mentioned in the introduction to this article, dopamine is the body's natural hormone/neurotransmitter responsible for suppressing prolactin secretion.
Therefore, various drugs known as dopamine agonists have been discovered and developed for the treatment of hyperprolactinemia.
Dopamine agonists (e.g. cabergoline, bromocriptine, pramipexole) inhibit prolactin secretion by binding to the same receptors that dopamine itself binds to, producing similar effects (albeit to different degrees) [4] [5] [6]. Estrogen regulation should also be pursued simultaneously.
Medical references:
[1] Blanco A, Moya L, Flores R, Agüera E, Monterde JG. 2002. Effects of anabolic transplantation on mammary gland microstructure in female sheep with disturbed prolactin secretion under estradiol alone or in combination with trenbolone acetate. J Vet Med Physiol Pathol Clin Med. 2002 Feb 49(1):13-7.
[2] Norstedt G, Mode A 1982. Major sites 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 hyperprolactinemia in a patient with hypothalamic-pituitary dysregulation. Acta Endocrinol (Copenhagen). 105(2):167-72.
[4] Verhelst J, Abs R, Maiter D, et al. (July 1999). "Cabergoline in the treatment of hyperprolactinemia: a study of 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). "Comparison of cabergoline and bromocriptine in the treatment of hyperprolactinemic amenorrhea. Cabergoline Comparison 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/ncpenmet0160. PMID 16932285.
