Among the arguments in favor of Metenolone Acetate is often the thesis that it "almost does not suppress" its own testosterone production. This opinion moves from forum to forum, but does it have a physiological basis? The editors explain how the hypothalamic-pituitary-gonadal axis works, why any androgen in sufficient quantity inhibits it, and what is known about recovery.
How the hormonal axis is arranged
Testosterone production in men is regulated by the hypothalamic-pituitary-gonadal (HPG) axis, also called the hypothalamic-pituitary-testicular axis. The hypothalamus releases gonadotropin-releasing hormone (GnRH) in pulses, stimulating 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 within the testes supports spermatogenesis in the Sertoli cells.
The system works on the principle of negative feedback, like a thermostat. When there are enough androgens and estrogens in the blood, the hypothalamus and pituitary gland reduce the production of GnRH, LH and FSH. When there are few of them, the stimulation increases.
The key point: the hypothalamus and the pituitary "don't know" where the androgen came from. They respond to general androgenic and estrogenic effects. Therefore, external androgen, which activates androgen receptors, is perceived as a signal "hormones are enough".
Why metenolone suppresses the axis
Metenolone is a full-fledged androgen receptor agonist. Androgen receptors are in the hypothalamus and pituitary gland, so their activation reduces the secretion of GnRH and gonadotropins. This mechanism is independent of aromatization: non-aromatized androgens such as DHT are also able to suppress LH.
True, testosterone has an additional "lever" - estradiol, which also inhibits the axis, moreover, very effectively. Metenolone is deprived of this lever, and theoretically, per unit of androgenic action, it can suppress the axis somewhat milder. However, there are no quantitative comparisons in humans to confirm this.
The degree of inhibition depends on the dose, duration of use and probably on individual sensitivity. A review by Rahnema et al (2014) describes that with supraphysiological androgen loading, LH and FSH are often reduced to very low, sometimes undetectable levels.
When LH falls, the production of own testosterone in the testicles also falls. After some time, this is manifested by a decrease in their volume. Data from HAARLEM—a prospective cohort study of 100 men using androgens (Smit et al., 2021)—showed that gonadal suppression was one of the most common effects.
| Index | What happens during the use of androgens | What does it mean |
|---|---|---|
| LH | Decreasing | The testicles stop receiving the signal to synthesize testosterone |
| FSH | Declining | The maintenance of spermatogenesis is disturbed |
| Endogenous testosterone | Decreasing | Androgenic action is supported only by an external drug |
| Testicular volume | May decrease | External sign of prolonged suppression |
Implications for fertility
Spermatogenesis requires a very high concentration of testosterone inside the testicles — much higher than in the blood. External androgen raises the level of androgens in the blood, but not inside the testicles, because there testosterone is produced locally under the action of LH.
Therefore, it is paradoxical: with an excess of androgens in the blood inside the testicles, they become insufficient. Together with a decrease in FSH, this leads to a decrease in the number of spermatozoa up to azoospermia. This effect is so reliable that androgens have been investigated as potential male contraceptives.
Anawalt (2019) notes that the use of anabolic steroids is one of the causes of infertility in young men, which is often undiagnosed by doctors unless the patient discloses taking the drugs.
For people planning to have children, this is especially important: recovery of spermatogenesis may take longer than recovery of testosterone and require specialized testing.
Restoration after stopping treatment
After cessation of androgen use, the axis gradually "wakes up". First, the secretion of GnRH and LH is restored, then the production of testosterone, and then, the slowest, spermatogenesis. The full cycle of sperm maturation lasts about three months, so you should not expect a faster recovery of the sperm count.
During the transition period, a person may experience symptoms of androgen deficiency: fatigue, decreased libido, depressed mood, erectile dysfunction. Kanayama and Pope associate this particular period with the risk of returning to steroid use and forming an addiction.
- The speed of recovery depends on the duration and intensity of suppression.
- For some people, recovery takes months.
- Cases of persistent hypogonadism after long-term use have been described.
- The initial state of the hormonal system before the start of use is also important.
Medical recovery is a separate medical topic that requires diagnosis and prescription. The editors deliberately do not provide any schemes: the choice of tactics depends on the analyzes and should be carried out by an andrologist or endocrinologist.
If several months after withdrawal symptoms persist, and testosterone and LH remain low, this is a reason for examination, and not for independent experiments.
Where does the myth of "weak suppression" come from?
The notion that metenolone has "virtually no effect" on its own testosterone probably arose from several sources. The first is the absence of the estrogenic component of suppression, which we wrote about above. The second is that the drug has historically been used in moderate medical doses.
The third source is subjective feelings. Since metenolone is itself an androgen, a person does not experience androgen deficiency during use, even if their own testosterone is suppressed. Problems appear only after stopping treatment.
The fourth is the lack of analyses. Without determination of LH, FSH and testosterone, it is impossible to tell how suppressed the axis is. Subjective "everything is fine" is not a reliable criterion here.
Finally, it is worth remembering that the analytical test of testosterone during the use of metenolone will show exactly your own testosterone, because metenolone is not determined by standard tests for testosterone. A low result in such a situation directly reflects the degree of oppression.
Editorial conclusions
Metenolone acetate, like any androgen receptor agonist, inhibits the hypothalamic-pituitary-gonadal axis. The lack of aromatization can slightly change the intensity of this effect, but does not cancel it.
The consequences are a decrease in one's own testosterone, a decrease in the volume of the testicles and a violation of spermatogenesis up to infertility. Recovery from withdrawal can take months, and in some people it is incomplete.
Subjective well-being during use does not reflect the state of the hormonal axis; it can only be assessed in a laboratory.
We also advise you to read the editorial materials about the tests that are monitored when using metenolone acetate, about its estrogenic activity and about the myths surrounding this drug.
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.
- Smit DL, Buijs MM, de Hon O, den Heijer M, de Ronde W. Positive and negative side effects of androgen abuse. The HAARLEM study: a one-year prospective cohort study in 100 men. Scand J Med Sci Sports. 2021;31(2):427â438.
- Anawalt BD. Diagnosis and management of anabolic androgenic steroid use. J Clin Endocrinol Metab. 2019;104(7):2490â2500.
- 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.
- Kanayama G, Pope HG Jr. History and epidemiology of anabolic androgens in athletes and non-athletes. Mol Cell Endocrinol. 2018;464:4â13.
- Nieschlag E, Behre HM, Nieschlag S (eds). Testosterone: Action, Deficiency, Substitution. 4th ed. Cambridge University Press; 2012.
