Dianabol
Active ingredient: Methandienone (Methandrostenolone). The first serial oral anabolic steroid, since 1958. Two double-blind crossover trials demonstrate weight and potassium gain; in the second, the authors concluded that the increase is not normal muscle.
Auch bekannt als: Dianabol, Dbol, D-Bol, Methandrostenolon, Methandien, Metandienon, Methandienon, Methandrostenolone
What it is
Methandienone is the first anabolic steroid to be mass-produced as a tablet. Ciba brought it to market in 1958 under the name Dianabol, and the trade name has replaced the active ingredient name to this day. The molecular formula is C₂₀H₂₈O₂.
On Testosterone two things have changed. A double bond between C1 and C2 in ring A slows down degradation and dampens the androgenic side. A methyl group on C17 blocks the point where the liver would otherwise render a steroid ineffective, and only then does the substance take effect when swallowed. Bear the same methyl group Superdrol, Methylstenbolone and Norethandrolone, and it is the reason for the same liver burden in everyone.
How it works
What the methyl group really does
A common formulation is that the substance passes through the liver without being metabolized. That is not the case. It passes through the liver like any swallowed substance and is extensively converted there; Doping control works precisely with these degradation products and has described seven of them in the sulfate fraction alone. What the methyl group prevents is a very specific reaction: the oxidation of the hydroxy group at C17, which would render the molecule ineffective. So the material is not spared, it only survives the one attack that matters.
The difference is not academic. Anyone who believes that the substance bypasses the liver has no model for why oral steroids, of all things, put a strain on the liver. The explanation is that he doesn't pass by, but stays there for a long time.
At the receptor
Like any anabolic steroid, methandienone works through the Androgen receptor. It is not completely clear why some derivatives have a stronger effect on the muscle than on the skin and prostate; A review article attributes it to a tissue-dependent control of the amount of receptors, to the metabolism within the cell and to how the loaded receptor fits together with its co-activators. An additional explanation is an anti-catabolic effect via the glucocorticoid receptor; the same review explicitly calls it an attractive hypothesis rather than a finding.
The bond is measured, and the result is unexpected. In a series of replacements in skeletal muscle and prostate, methandienone was one of the weak Binders: its binding strength was less than 5 percent of the comparison substance, in the same group as Stanozolol and fluoxymesterone, while Nandrolone and testosterone were many times higher.
That doesn't fit well with a substance that causes people to measurably gain weight in two controlled trials. Either methandienone works via something other than the pure binding strength, for example via a metabolite or via the amount of the receptor, or the displacement measurement on rat tissue does not reflect the situation in humans. The same work also shows that the ratio of binding in muscle and prostate for all steroids tested was close to one and usually only fluctuated between around 0.4 and 1.7. A ratio of anabolic to androgenic, as is the case with this substance, cannot be read from the receptor at all.
Flavoring
Methandienone is aromatized, and the known estrogenic effects of this substance, i.e. water retention and gynecomastia, are due to this. In the scene there is the sentence that the resulting estrogen is a methylated estradiol, which passes through one aromatase inhibitors can hardly be influenced, which is why SERM is preferable.
No source could be found for this sentence. It is also not conclusive in itself: an aromatase inhibitor blocks the enzyme that carries out the conversion and thus acts before the production of estrogen, regardless of which estrogen is produced. An argument against the aromatase inhibitor would have to explain why aromatase implements this material despite the blockage, and it doesn't.
What the studies show
There are two controlled trials on methandienone in training men, both double-blind, both crossover, both by the same working group, both with 100 mg daily for six weeks. Crossover means: each participant went through both phases and was their own control. This is an unusually clean facility for an anabolic steroid.
In the first trial with eleven training men, the participants on the active ingredient gained 3.3 kg more weight than in their placebo phase and stored 420 mmol more potassium. The increase was in the lean part of the body, the muscles became larger. Strength and performance improved in both phases, and the difference between active substance and placebo was not certain. The active ingredient also increased cortisol in the blood and cortisol excretion in the urine, and testosterone fell. The authors explicitly did not rule out that the increase was due to fluid within the cells and left the question of the anabolic effect open.
The second experiment was built to answer exactly this question. Seven weightlifters in ongoing training, the same dose, the same system, and the body's total nitrogen was also measured. This time weight, potassium, nitrogen, muscle size as well as performance and strength of the legs increased significantly in the active ingredient phase, but not in the placebo phase. The increase was 2.3 kg weight, 436 mmol potassium and 255 g nitrogen.
And then comes the sentence that is not in any advertising: potassium and nitrogen increased too strong in relation to the weight, than it could have been normal muscle tissue or other lean tissue. The authors concluded that this was due to the intake of a substance rich in nitrogen and low in phosphate and wrote that although this could be called anabolic, the weight gain produced was not normal muscle.
Both works are small, eleven and seven participants, and both are over forty years old. The fact that the strength increased in the second attempt and not in the first may be due to the selection of weightlifters or because seven participants are simply too few for a difference of this size. What both studies show is the increase in weight and potassium. What neither of them shows is a gain in strength that goes beyond that of training and can definitely be attributed to the active ingredient.
There are no more recent controlled studies on exercisers. What has appeared on this substance since the 1980s comes almost entirely from doping controls and is concerned with finding it in urine.
Dosage
- The only dose studied is 100 mg daily. This is above what is usually taken today, and at the same time it is the only quantity for which there is any controlled measurement. The common 20 to 50 mg is not a cautious version of a tested dose, it is untested.
- The short duration of action forces division. The substance only lasts a few hours, which is why the daily amount is usually divided into two to three doses. There is no dosage determination for this, it is local practice.
- The duration is the size at which the liver hangs. Six weeks is the length tested in both experiments. What goes beyond this is unproven, and the best-known case of severe liver damage on anabolic steroids involved an athlete after 18 months.
- Not next to a second oral steroid. Two 17-alpha-alkylated preparations attack the same site, and the case series of these liver injuries regularly mention preparations with more than one steroid.
- The substance is not an option for tested athletes. A breakdown product from a single dose of 5 mg was still detectable 26 days later. Five milligrams, once.
- Initial values before the first tablet. transaminases, Bilirubin, lipid profile and blood pressure, otherwise a value cannot be classified after four weeks.
Side effects
Liver
What happens: The 17-alpha-alkylation disrupts the removal of bile salts from the liver cell, resulting in a build-up of bile with jaundice and itching. In the American DILIN network's prospective series, 44 men developed liver damage after bodybuilding supplements, a mean of 73 days after onset, all with jaundice, 84 percent with itching and 71 percent in the hospital. In addition, there are rare but severe structural damage: peliosis hepatis, nodular changes and malignant degeneration have been described for anabolic steroids, and a 30-year-old bodybuilder presented with bleeding esophageal varicose veins after 18 months of use.
What it depends on: On alkylation, on the duration and on the predisposition in bile salt transport. What follows from this is: Not only ALT and AST are measured, but also Bilirubin and alkaline phosphatase: the bile buildup runs with little cell destruction and can exist with almost normal transaminases. Elevated transaminases alone are often muscle origin in exercisers. What you can do: If yellow discoloration, dark urine or itching occurs, stop using immediately and seek medical advice. For TUDCA there is no controlled study on this clinical picture; the only measure with a proven effect is discontinuation.
water and blood pressure
What happens: A large part of the rapid increase under this substance is retained fluid. In addition to weight, both controlled experiments found disproportionate potassium storage, and in the second, the ratio of potassium and nitrogen to weight was the reason for not classifying the increase as normal muscle tissue. Blood pressure increases with water.
What it depends on: From the dose, from the salt intake and from the extent of flavoring, which increases with body fat percentage. What follows from this is: Some of the increase on the scale disappears after discontinuation, and this is not a surprise, but the expected course. Anyone who thinks this part is muscle is planning their next treatment based on the wrong number. What you can do: Measure blood pressure in the morning under the same conditions and measure the circumference at a fixed point instead of just the weight. A dehydrator, on the other hand, treats the display, see Drainage.
Your own axis, and the cortisol next to it
What happens: Supplied androgen drives the HPTA axis down; In the first experiment, the testosterone in the blood fell accordingly under the active ingredient. The second finding of the same measurement is noteworthy: cortisol in the blood and cortisol excretion in the urine rose under methandienone.
What it depends on: The finding comes from a study with eleven participants and has not been repeated. What follows from this is: It fits poorly with the popular idea that anabolic steroids have an anti-catabolic effect by displacing cortisol. The review article explicitly lists this anti-catabolic effect as a hypothesis. What you can do: Planning the exit instead of letting it happen. For restarting the axis HCG and Clomiphene the established remedies, both requiring a prescription.
Blood lipids
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 this happens within a few weeks.
What it depends on: The oral route is the decisive factor here because the substance passes through the liver in high concentrations. What follows from this is: No figures specifically on methandienone could be found in the literature reviewed; the two controlled experiments did not measure blood lipids. This is a gap and not an all-clear: the mechanism applies to the substance class and is well documented. What you can do: Lipid profile before the start and after four weeks, and use a significantly fallen HDL as a reason for discontinuation, see Cardiovascular risks associated with AAS.
Classification
Dianabol is the best-known anabolic steroid of all and at the same time one of the worst proven. What we have are two small crossover attempts from 1976 and 1981, and they're better built than almost anything that came after them. Your result can be said in two sentences. The weight gain is real, confirmed and found in both experiments. In the second attempt, the authors tested whether it was muscle and answered in the negative.
That doesn't make the substance ineffective. Muscles became measurably larger in both experiments, and participants gained weight in the lean portion of their bodies. It is said that part of what appears to be a quick success on the scales and in the mirror is retained fluid, and that exactly this part disappears after stopping. The role of a stimulus at the start of a treatment depends to a large extent on this visible but fleeting effect.
The price is the same as any oral steroid and this one is particularly well documented because it has been around since 1958: bile stasis with jaundice as the common problem, Peliosis and nodular tags as the rare and severe. In addition, there is a traceability that excludes the substance for every athlete tested: 26 days after a single 5 mg tablet.
What would decide the matter is a repetition of the Hervey experiment using today's means: the same crossover system, but with magnetic resonance instead of potassium counting and with a muscle biopsy that separates water content and contractile protein. The crucial question about this material has been precisely posed since 1981 and has not been taken up again since then.
Sources
- Hervey GR et al. Anabolic effects of methandienone in men undergoing athletic training. Lancet. 1976. PubMed
- Hervey GR et al. Effects of methandienone on the performance and body composition of men undergoing athletic training. Clin Sci (Lond). 1981. PubMed
- Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol. 2008. PubMed
- Winwood PJ et al. Bleeding oesophageal varices associated with anabolic steroid use in an athlete. Postgrad Med J. 1990. PubMed
- Stolz A et al. Severe and protracted cholestasis in 44 young men taking bodybuilding supplements: assessment of genetic, clinical and chemical risk factors. Aliment Pharmacol Ther. 2019. PubMed
- Gomez C et al. A new sulphate metabolite as a long-term marker of metandienone misuse. Steroids. 2013. PubMed
- Saartok T, Dahlberg E, Gustafsson JA. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin. Endocrinology. 1984. PubMed
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