Methylstenbolone

What it is

Methylstenbolone is an anabolic steroid that has never been a drug. It has gone through no approval process, no clinical trial, and no company has ever developed it as a drug. It appeared around 2012 as an ingredient in over-the-counter “food supplements” under names such as M-Sten, Ultradrol or Super DMZ Rx 2.0.

Chemically it is called 2α,17α-dimethyl-17β-hydroxy-5α-androst-1-en-3-one. The framework is that of dihydrotestosterone: a ring A reduced at position 5, plus the keto group at 3 and the hydroxy group at 17. Three things are attached, and each has a task. The double bond between C1 and C2 and the methyl group on C2 are both located in ring A and are considered to be the reason for the striking metabolic stability of the molecule. The methyl group at C17 makes the substance orally effective.

To Superdrol (Methasterone), the distance is very small: there is exactly one double bond missing in ring A, otherwise both molecules are built the same. This is more than just a side note, because in one study a preparation that, according to the label, contained methylstenbolone also contained methasterone.

The sales name “Prohormone” is simply wrong for this substance. A prohormone is a precursor that the body first has to convert. Methylstenbolone is the finished active ingredient and does not need any modification. The term was used to describe an anabolic steroid on the supplement shelf.

How it works

At the androgen receptor

Like any anabolic steroid, it works through the Androgen receptor: it binds inside the cell, the complex migrates to the cell nucleus and switches on genes there, including those involved in muscle protein synthesis. That's the extent of the textbook.

It is not known how tightly methylstenbolone binds. In the literature reviewed here there is no published affinity, neither in the displacement experiment nor in a reporter gene test, nor for the parent substance stenbolone. This means that exactly the number with which one steroid could be classified against another is missing. Any information about the ratio of anabolic to androgenic effects that is circulating for this substance comes from a seller and not from a measurement.

What the 17-alpha-methyl group does and costs

A steroid without this group is oxidized at the hydroxy group at C17 during the first passage through the liver and is therefore finished before it reaches the circulation. The methyl group at C17 blocks this attack. That's why the substance appears to be swallowed and that's why it puts a strain on you Liver. It's not that the oral form is also harmful to the liver: it's the same property, viewed from two sides.

The material is unusually stable. In doping controls it is predominantly found as glucuronide of the unchanged substance, i.e. almost unmetabolized, and that is exactly what the manufacturers advertised. Ten monohydroxylated degradation products were formed on human liver microsomes, In humans, after a single dose to four volunteers, two degradation products were still detectable a week later, while the unchanged substance was only found for around 45 hours.

Why it doesn't turn into estrogen

The aromatase needs a ring A with a keto group on 3 and a double bond between C4 and C5. Methylstenbolone has neither: its ring A is reduced at position 5, the double bond is between C1 and C2, and there is an additional methyl group in the way at C2. Estradiol cannot be produced from this substance.

This is often sold as an advantage and is a half-truth. No estradiol is produced from the substance, but the body's own is still lost because the axis is shut down and there is no longer any testosterone that could be aromatized. If you work with it alone, you will end up with both low. What too low estradiol does to men is below Estrogen.

What the studies show

There is nothing about the effect. No controlled study, no observational series, no dose determination, no measurement of muscle mass, strength or body composition. This is not an oversight of this compilation, but rather the status: searches were made for the name of the substance, for the parent substance stenbolone and for receptor and activity tests, and none of these searches provide any work on the effect on humans.

What there are are two other kinds of work. The first comes from doping control and is only interested in how to find the substance in urine. The second comes from hepatology.

The only published case naming methylstenbolone involves a previously healthy 26-year-old man who took Super DMZ Rx 2.0 exactly as directed by the manufacturer for thirty days and developed jaundice with bile obstruction. In addition to methylstenbolone, the preparation also contained dymethazine, as stated on the label.

The data available for the substance class is broader. The American DILIN network prospectively recorded 44 men who suffered liver damage after taking such preparations: mean age 33 years, mean time from first intake to damage 73 days, all with jaundice, 84 percent with itching, 71 percent in hospital. Nobody died, nobody needed a liver transplant. In the previous evaluation by the same network, the proportion of liver damage caused by nutritional supplements increased from 7 to 20 percent between 2004 and 2013, and the jaundice of bodybuilding cases lasted a median of 91 days.

These series describe the substance class and not this one substance. They are still the best available, and at the same time they show why a clearer classification is difficult: anabolic steroids that were not on the label were found in several of the preparations examined. Those who evaluate the case later often do not know what material they are dealing with, and the user did not know it beforehand either.

Dosage

• There is no tested dose. Every number circulating about this substance comes from a label or a forum. A dose determination never took place, and therefore there is no basis on which one could even speak of a low or high dose.
• “According to package instructions” is not a safe distance. The one documented case did just that, for thirty days, and ended with jaundice. The information on a label that has not undergone an approval process does not provide any information about compatibility.
• The duration is more important than the quantity. It took an average of 73 days for liver damage to occur. A “short course of four weeks” is therefore not outside the risk, but rather within the period in which nothing has happened yet.
• Not next to a second 17-alpha-alkylated preparation. Two of them at the same time do not double the effect, but they attack the same place in the liver. It was exactly this combination that was in the preparation in the case report.
• Without initial values, nothing can be classified later. Who Bilirubin, alkaline phosphatase and did not measure transaminases before the first day, cannot distinguish an elevated value from his own normal value afterwards.
• Anyone who already has a liver test is not an option. This also applies to a known bile flow disorder that runs in the family: variants in the gene ABCB11, which encodes the bile salt pump, were found frequently among those affected in a series.

Side effects

Bile buildup in the liver

What happens: The liver cell pumps bile salts outward via the bile salt export pump at its upper pole. If this pump is inhibited, bile builds up in the cell and in the blood. The result is a build-up of bile without significant cell destruction: the liver is not broken, it is blocked. Liver biopsies from these patients showed mild inflammation with pronounced bile retention, no damage to the bile ducts and no scarring.

What it depends on: About the 17-alpha-alkylation, the duration and the predisposition. In two men with bile stasis after a preparation with a closely related 2α,17α-dimethyl steroid, the bile salt pump in the tissue was visibly reduced, and one carried a known variant in ABCB11. In the larger series, such a variant was found in up to 20 percent. What follows from this is: Is measured Bilirubin and alkaline phosphatase, not just the transaminases. And an important pitfall: both men in the case report had it Gamma-GT normal, although bilirubin was significantly elevated. A normal GGT value doesn't rule anything out here. Things are resolving, but slowly: the jaundice lasted an average of 91 days. What you can do: At the first sign of yellowing or itching, stop using and seek medical advice. Don't wait. For TUDCA There is no controlled study on exactly this clinical picture, but the starting point on the same pump is the most plausible of the available countermeasures. The only measure with proven effectiveness is discontinuation.

Your own axis

What happens: An applied androgen tells the brain that there is enough. GnRH, LH and FSH fall, the testicle stops producing its own, see HPTA axis. Since no estradiol is produced from methylstenbolone and your own testosterone is lost, both hormones drop at the same time.

What it depends on: Of dose and duration, and in recovery from age and how often this has already happened. There are no figures available for this substance; Hypogonadism has been described as a consequence of the class of over-the-counter designer steroids, and steroid use is now considered the most common cause of hypogonadism in men of reproductive age. What follows from this is: Lack of motivation, loss of libido and low mood after stopping are not your imagination, but the expected course and it lasts weeks to months. What you can do: Keep the application short and plan the discontinuation instead of letting it happen. For the restoration of the axis there is with HCG and Clomiphene established approaches, both with their own side effects and both requiring a prescription.

Blood lipids and blood pressure

What happens: Oral 17-alpha-alkylated steroids increase the activity of hepatic lipase, which breaks down HDL particles more quickly. This HDL falls, LDL rises, and both happen within weeks. There is also a tendency towards water and sodium retention with increasing blood pressure, see Cardiovascular risks associated with AAS.

What it depends on: The oral route is the deciding factor here because the substance passes through the liver in high concentrations before it gets anywhere else. There are no figures specifically for methylstenbolone; Renal failure and other serious consequences are reported for the class. What follows from this is: The effect is not noticeable, it is only measurable. If you only pay attention to how you feel, you won't notice anything. What you can do: Measure lipid profile and blood pressure before start and after four weeks. An HDL that drops to single digits is a reason to stop taking fish oil and not continue.

skin and hair

What happens: The molecule is a derivative of dihydrotestosterone and acts directly on the receptor in the skin. Sebaceous glands enlarge, acne appears; With the appropriate predisposition, androgenetic hair loss progresses more quickly, see skin.

What it depends on: Especially from the disposition. Anyone who already gets acne with testosterone will get it here too. What follows from this is: Acne usually disappears after discontinuation, but lost hair does not. What you can do: An inhibitor helps against hair loss 5-alpha reductase Not here, because the substance has already been reduced and is no longer touched by this enzyme. What remains are local remedies and the decision to leave the substance out.

Classification

For most active ingredients, the question is whether the benefits outweigh the disadvantages. This question cannot be asked here because one side of the scale is empty. There is not a single measurement on humans about the effect, nor about binding to the receptor, and the only reliable figures for this group of substances describe liver damage.

This is a different finding than “doesn’t work”. A 17-alpha-alkylated androgen with a DHT framework is very likely to be anabolic, and the reports from use say so. However, this does not say how strong, nor in what quantity, nor in comparison to which other substance. Anyone who takes methylstenbolone is choosing a steroid whose potency they do not know, whose dosage no one has tested and whose liver risk has been documented.

There is also an uncertainty that no other active ingredient in this category has to this extent: what is in the preparation is not reliably stated on the label. In one study, a product sold as methylstenbolone also contained methasterone, In the DILIN series, several preparations contained undeclared steroids. A substance that you do not know cannot be dosed, and an incident cannot be assigned afterwards.

Compared to Superdrol, the closest relative, methylstenbolone is worse off, not because it is more dangerous, but because even less is known about it. Anyone who still wants to go in this direction would be better served with a substance for which there is at least case material and an idea of ​​the dose.

What would decide the matter: a binding measurement on the androgen receptor so that the substance can be classified at all, and an analysis of the purchased preparation before taking it. The first would be work for a laboratory, the second is not available to the buyer. As long as both are missing, any statement about the potency and dosage of this substance is an assertion.

Anyone who still uses it measures bilirubin, alkaline phosphatase, transaminases and the lipid profile before and after four weeks, stops immediately if it turns yellow or itches and knows that a normal gamma GT does not rule out anything. What else is included is below Side effect management.

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