There is an opinion among athletes that oral steroids are "softer" than injectable ones and almost do not affect their own hormonal system. Using metandienone as an example, the editors explain why this is not the case: any powerful androgen coming from the outside is perceived by the body as a signal to stop producing its own testosterone - with consequences that can last for months.
How the HPG axis works
Testosterone production in men is regulated by a cascade of three links: the hypothalamus, the pituitary gland, and the testicles (gonads). Hence the name - hypothalamus-pituitary-testicle axis, or HPG axis. The hypothalamus releases in pulses gonadotropin-releasing hormone (GnRH), which stimulates the pituitary gland.
In response, the pituitary gland secretes two hormones. Luteinizing hormone (LH) stimulates the Leydig cells in the testicles to produce testosterone. Follicle-stimulating hormone (FSH) together with a high local concentration of testosterone inside the testicle supports the work of Sertoli cells and, accordingly, spermatogenesis.
The system is self-regulating through negative feedback. When the level of testosterone and its metabolites - oestradiol and DHT - in the blood increases, the hypothalamus and pituitary gland "reduce gas": the frequency of GnRH impulses and the secretion of LH and FSH decrease. When the level drops, the signal is amplified. Thus, a relatively stable hormonal background is maintained.
It is important that the "sensors" in the brain do not distinguish where androgen or oestrogen came from - from one's own testicles or from a pill. They react to the general hormonal load. It is on this principle that suppression of HPG axis by any exogenous anabolic steroids is based.
Mechanism of suppression by metandienone
Metandienone acts on HPG axis in two ways. First, as an androgen, it binds to androgen receptors in the hypothalamus and pituitary gland. Secondly, part of the drug is aromatized to 17α-methyloestradiol, a stable oestrogen, and oestrogens are one of the strongest inhibitors of LH secretion in men.
As a result, the level of LH and FSH decreases, and their own testosterone, which is produced by Leydig cells, also decreases. At the same time, the total testosterone in the tests can be very low, although a person feels a strong androgenic effect - it's just that it is not provided by his own hormone, but by a drug that standard tests for testosterone do not measure.
Depression develops quickly. Studies with various anabolic steroids show that a noticeable decrease in gonadotropins occurs already during the first weeks of taking supraphysiological doses. The short half-life of metandienone (several hours) does not save: with daily intake, the hormonal load remains constant.
Another factor is a decrease in sex hormone-binding globulin (SHBG). 17α-alkylated steroids significantly suppress its synthesis in the liver. This changes the ratio of free and bound testosterone and complicates the interpretation of tests, but does not cancel the main thing: the actual production of the hormone is suppressed.
Testicular and fertility implications
When LH and FSH remain low for a long time, the testicles lose their stimulus to work. The concentration of testosterone inside the testicle, which is normally ten times higher than the concentration in the blood, drops sharply. It is this local testosterone that is needed for sperm maturation, and the high level of androgens in the blood cannot replace it.
Clinically, this is manifested by a decrease in the volume of the testicles (testicular atrophy), a decrease in the number and mobility of spermatozoa, up to their complete absence in the ejaculate - azoospermia. This effect is so predictable that exogenous androgens have been investigated as a potential male contraceptive.
| Index | A typical change in HPG axis suppression | Clinical significance |
|---|---|---|
| LH | Decreased, often to an undetectable level | Leydig cells receive no stimulus |
| FSH | Reduced | Disorders of spermatogenesis |
| Total testosterone (endogenous) | Reduced | After withdrawal — symptoms of hypogonadism |
| SHBG | Reduced (typical for 17α-alkylated) | Makes estimation of free testosterone more difficult |
| Semen analysis | Oligospermia or azoospermia | Temporary or long-term infertility |
| Testicular volume | Decreasing | Visible suppression marker |
For a person who plans to have children, this is the most important argument. A review by Rahnema et al (2014) focuses specifically on steroid-induced hypogonadism and highlights that among men presenting to an andrologist with infertility, the proportion of those who have used anabolic steroids is significant.
Violation of spermatogenesis is often asymptomatic: libido may even be increased while taking it. Therefore, a person learns about the problem only when a couple unsuccessfully tries to have a child.
Recovery after discontinuation
After withdrawal of metandienone, HPG axis should "restart". The drug is removed from the blood relatively quickly, but the hypothalamus and pituitary gland do not immediately restore normal pulsatile secretion. During this period, a person finds himself in a state of secondary hypogonadism: his own testosterone is low, and there is no exogenous testosterone.
Typical symptoms of this period:
- fatigue, reduced work capacity and motivation;
- decreased libido and erectile dysfunction;
- depressed mood, irritability, sometimes clinical depression;
- loss of part of the gained mass and strength;
- sleep disturbance.
It is at this time that the risk of returning to drugs to get rid of unpleasant sensations increases, and this is how the dependence on anabolic steroids, described in the psychiatric literature, is formed.
The duration of recovery is very individual. According to observational studies, many men gradually return to normal within a few months, but some recovery takes a year or more, and some develop persistent hypogonadism. Risk factors — duration and total intensity of use, age, repeated courses.
The editors separately emphasize: independent "recovery schemes" from prescription drugs, which are distributed on forums, are not a substitute for an examination. Diagnosis and treatment of steroid-induced hypogonadism should be carried out by an endocrinologist or andrologist based on tests.
Misconceptions about “mild” oral steroids
The myth of the "softness" of oral drugs is based on the fact that pills are short-acting and can be quickly withdrawn. However, the degree of suppression is determined not by the form of the drug, but by the strength and duration of the androgenic and oestrogenic signal. Metandienone is a powerful androgen with pronounced aromatization, so it suppresses the axis very effectively.
The second mistake is to think that if one feels good, then the hormonal system is fine. As already mentioned, the drug provides a feeling of well-being while taking it. The real state of HPG axis can be seen only by measuring LH, FSH, testosterone and semen analysis.
The third mistake is to think that a short course has no consequences. Even a few weeks of taking it is enough to significantly reduce gonadotropins. Recovery speed after short exposure is usually faster, but there are no guarantees.
Finally, HPG axis suppression occurs regardless of whether a person has exercise, proper nutrition, and sleep. These factors are important for health, but cannot "protect" the hypothalamus from pharmacological feedback.
Editorial conclusions
Metandienone effectively suppresses the HPG axis due to the combination of androgenic action and the formation of a stable oestrogenic metabolite. The result is a drop in LH, FSH, and own testosterone, testicular atrophy, and impaired spermatogenesis.
Recovery after withdrawal takes months and is not always complete. The risk of prolonged hypogonadism and infertility is real and documented in the clinical literature.
The idea of "soft" oral steroids does not correspond to physiology: for the pituitary gland, it does not matter in what form the androgen comes.
We also advise you to read our articles on the oestrogenic activity of metandienone, on the tests that should be monitored and on the risks of virilization in women.
List of used literature
- Rahnema CD, Lipshultz LI, Crosnoe LE, et al. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014;101(5):1271â1279.
- Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341â375.
- Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol. 2008;154(3):502â521.
- Kanayama G, Hudson JI, DeLuca J, et al. Prolonged hypogonadism in males following withdrawal from anabolic-androgenic steroids: an under-recognized problem. Addiction. 2015;110(5):823â831.
- Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715â1744.
- Nieschlag E, Behre HM, Nieschlag S (eds). Testosterone: Action, Deficiency, Substitution. 4th ed. Cambridge University Press; 2012.
