This post covers the relationship between prolactin and users of anabolic-androgenic steroids.
A long-standing concern is that various anabolic steroids might stimulate prolactin secretion from the pituitary gland or induce prolactin-related activity through other mechanisms.
First, it is crucial to note the importance of clinical research and data to verify any claims.
Currently, research in this field is limited due to the legal status of anabolic steroids in the Western world, especially in the United States.
Studies on the effects of anabolic steroids as performance and physique-enhancing agents are difficult to conduct due to legal issues.
Limitations such as funding allocation and the perceived need for research also exist.
Currently, there is very little data on prolactin and anabolic steroids.
Specifically, research at the dosages and conditions used by bodybuilders is non-existent.
Acknowledging the lack of research, a realistic approach is to draw logical conclusions from theoretical knowledge and anecdotal evidence until future studies can be conducted.
According to a large body of anecdotal evidence and blood work results within the bodybuilding community, significant increases in PRL are seen in users of two specific anabolic steroids: Trenbolone and Nandrolone (Deca-Durabolin).
These possess progestogenic properties.
Those who experience hyperprolactinemia show typical side effects such as decreased libido and lactation from the nipples.
On the other hand, many people use them without any symptoms or abnormalities in their blood work.
These compounds are classified as 19-nor compounds, characterized by the absence of a carbon atom at the 19th position.
Derivatives of Trenbolone or Nandrolone (e.g., Methyltrienolone) are also logically progestins.
Therefore, it is reasonable for an individual experiencing hyperprolactinemia to conclude that Trenbolone or Deca-Durabolin is causing the problem due to its progestogenic nature.
Research findings (referenced at the beginning of this article) have shown that progesterone actually acts to suppress prolactin in various tissues of the body, including the mammary glands.
Therefore, the logical conclusion is that the use of progesterone and/or progestins should not increase prolactin levels but should, in fact, have the opposite effect.
However, this is only half of the overall conclusion.
The other half must be deemed inconclusive due to the lack of direct evidence regarding the effects of Trenbolone and Deca on prolactin levels, especially at bodybuilding dosages.
An important concept to understand at this point is that Trenbolone and Nandrolone are derivatives of progesterone, meaning they are modified forms of progesterone.
Because of these modifications, these anabolic steroids may possess additional, unknown effects throughout the body, not only in the endocrine system but in other tissues as well.
This is best illustrated by comparing it to a similar situation.
Anadrol-50 is a derivative of DHT (Dihydrotestosterone).
Anadrol shares many similar characteristics with its parent hormone, as is generally the case with all derivatives.
Therefore, Anadrol-50 cannot interact with the aromatase enzyme and thus cannot aromatize (convert) into Estrogen.
However, at the same time, Anadrol has a reputation as one of the most notorious anabolic steroids for causing Estrogen-related side effects in users (e.g., bloating, water retention, gynecomastia).
This makes no sense, considering its inability to aromatize.
Why is this?
It has been hypothesized that it is Anadrol itself and/or one or more of its metabolites that bind to Estrogen receptors in different tissues in the body to exert these effects.
Unfortunately, this is a hypothesis that has not yet been tested and confirmed through clinical research, but considering everything we currently know about Anadrol, there must be some activity occurring that defies conventional logic.
The same conclusion can be drawn for Trenbolone and Deca Durabolin in relation to prolactin.
They are derivatives of progesterone and should exhibit the same anti-PRL effects, but their modifications might grant them other properties that could result in activity contrary to what conventional logic dictates (similar to the Anadrol example).
Furthermore, many users have used Trenbolone and Nandrolone without any prolactin-related issues, only to experience them weeks later upon resuming their use.
This issue appears to be intermittent throughout the community, and it is impossible to know for certain until further studies are conducted that simulate the exact conditions under which progestins are used and prolactin-related side effects are experienced.
For research of this nature to be conducted, answers to the following questions must be sought in the future:
- The potential for mysterious activity from progestogenic anabolic steroids due to their chemical modifications
- The influence of unexpected additives in illicit products purchased from the black market
- The role of Estrogen and other hormones
Controlling, Eliminating, and Preventing Prolactin
Controlling prolactin is the best first course of action to take before any other measures.
Prevention is more important than treatment, and it is unhealthy to either completely eliminate prolactin levels or allow them to rise above the normal range.
Estrogen control appears to be a crucial factor in keeping prolactin levels low in the body, as Estrogen not only synthesizes prolactin in the pituitary but also has a direct stimulatory effect in promoting breast tissue function and development.
A study on female sheep showed that the group administered both Trenbolone and Estradiol (E2) experienced anti-estrogenic effects from Trenbolone, which blocked the breast stimulation from Estrogen[1].
This is not surprising, considering that androgens (especially a powerful androgen like Trenbolone) can reduce the number of prolactin receptors in the body.[2]
Maintaining a high androgen-to-estrogen ratio is also a critical factor in controlling prolactin, as demonstrated in a study where administered testosterone converted to estrogen, causing subjects to experience a significant increase in prolactin[3].
Therefore, the most crucial strategy for anabolic steroid users is to maintain Estrogen levels within the normal range while using any anabolic steroid.
If prolactin becomes a significant problem and prevention is no longer a viable option, various drugs can be sought to address the issue directly.
Dopamine is the body’s natural hormone/neurotransmitter responsible for inhibiting prolactin secretion.
Therefore, various drugs known as dopamine agonists (such as Cabergoline, Bromocriptine, Pramipexole, etc.) have been developed to treat hyperprolactinemia[4][5][6].
Estrogen control should also be pursued concurrently.
Medical References
[1] Blanco A, Moya L, Flores R, Agüera E, Monterde JG. 2002. Effects of anabolic implantation on mammary gland microstructure in female lambs interfering with prolactin secretion with estradiol alone or with trenbolone acetate. J Vet Med A Physiol Pathol Clin Med. 2002 Feb;49(1):13-7.
[2] Norstedt G, Mode A 1982. Major site of action of estrogens and androgens in the regulation of the hepatic prolactin receptor. 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 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/ncpenmet0160. PMID 16932285.
