Dianabol (Methandrostenolone)

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Chemical Name: 17a-methyl-17b-hydroxy-1,4-androstadien-3-one
Synonyms: Dianabol (D-bol), Methandienone, Nerobol
Active Half Life: 3 – 6 hours
Anabolic : Androgenic Ratio: 1:1–1:8 (1:1 Testosterone as standard in rodents)

Structural Modification

The addition of a methyl group at the 17α position of the D cyclopentane ring slows First Pass Metabolism in the Liver to allow it to remain in circulation longer than testosterone. The double bond between C1 and C2 of the A cyclohexane ring reduces the androgencity of the compound with a weaker relative binding affinity for the androgen receptor (AR) than testosterone.

Dianabol History

Methandrostenolone was first reported in the literature in 1955; and soon released in 1958 by Ciba Pharmaceuticals to the US prescription market under the drug name Dianabol. A derivative of testosterone, the compound has been modified to reduce the androgenic and preserve the anabolic properties. Historically, it has been the most commonly used C-17a alkylated oral steroid for physique enhancing purposes but does have its history deep rooted in medical prescriptions also.

Originally developed alongside Dr John Ziegler; a physician for US Olympic teams, in hopes of reducing competition to Russia who were already utilizing testosterone with their athletes, Methandrostenolone brought a new dynamic as a compound with lower androgenicity but with retained anabolic properties, soon causing advancements in competitive sports. However, within 5 years the compound was beginning to trend a new wave in steroid abuse in sports with many athletes disregarding the initial prescription guidelines of 5-15mg.

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In 1970, the FDA pushed Ciba for clarification and publiciation of Methandrostenolone’s approved uses and accepted a “probably effective” stance on treating osteoporosis and pituitary deficient dwarfism whilst research continued into its effect on wasting conditions. There are several reports in the literature of its use in childhood dystrophies. By 1983, Ciba withdraw Dianabol from the US market followed by full removal of generic Methandrostenolone by the FDA in 1985. Non-medical use was outlawed in the U.S. under the Anabolic Steroids Control Act of 1990.

Metabolism and Excretion of Methandrostenolone

The metabolism of Methandrostenolone is mainly in the liver by 6β-hydroxylation, 3α- and 3β-oxidation, 5β-reduction, 17-epimerization, and conjugation among other reactions with excretion occurring via urine.

Human mitochondrial steroid hydroxylating enzymes CYP11B1 and CYP11B2 (non liver native) have also been shown to be capable of metabolizing the compound leading to the formation of 11β-hydroxy and 18-hydroxy metabolites. Unconjugated, beta-glucuronidated and sulfated metabolites have also been observed in the urine. Long-term use of Methandrostenolone at high dosages can lead to the appearance of unmetabolized drug in the urine.

Side Effects of Dianabol (Methandrostenolone)

Androgenic
Whilst technically an Anabolic steroid, Methandrostenolone still has androgenic side effects; commonly oily skin and acne (due to sebaceous gland androgenic effects), and body/facial hair growth.

Women should take note of its potential virilizing effects such as deepening on the voice, irregularities in the menstrual cycle, facial hair growth and clitoral enlargement alongside. Clinical history reports of 2 prepubertal girls treated with Dianabol cream by their family physicians during 6 and 8 months because of anal eczema. In both of them, growth velocity and bone maturation was accelerated, and there was hypertrophy of the clitoris and deepening of the voice. All symptoms in one of the girls, with the exception of the deep voice, had disappeared six years after the discontinuation of treatment.

Whilst there is potential for Methandrostenolone to convert via 5-alpha reductase to 5-alpha-dihydroMethandrostenolone, it does so at a very slow rate due to a low binding affinity for the 5-alpha reductase enzyme.

Thyroid
Thyroid Binding Hormone Globulin (THBG) levels have been shown to be effected by as little as 10mg resulting in potentially higher levels of free circulating thyroxine and triiodothyronine.

Estrogenic
Due to this structural modification, Methandrostenolone shares similarity to Boldenone (except for the 17α methyl group); aromatizing at the same extent as Boldenone. However, it is much more estrogenic due to its pathway conversion to a 17α-methylestradiol, a potent estrogen metabolite which is metabolism-resistant and more biologically active than estradiol.

Testosterone Suppression (HPTA)
HPTA suppression is observed at moderate dosage due to negative feedback to the Hypothalmic Pituitary Testicular Axis (HPTA); either as a result of elevated estrogen or elevation in serum testosterone level. Methandrostenolone at a dosage of 15 mg was shown to reduce plasma testosterone levels by 69%. Return of normal HPTA function is normally observed following 6-8 weeks discontinuation provided Secondary or Primary Hypogonadism not developing as a result.

Another important clinical observation is a reduction in Sex Hormone Binding Globuin (SHBG) is observed with Methandrostenolone usage, resulting in higher levels of circulating free testosterone.

In females, Methandrostenolone has been shown to cause menstruation issues, resulting in irregularities of menstrual cycle.

Methandrostenolone is a sperm-suppressive agent. At 15 mg for 2 months, sperm density per ml decreased 46% and 73%. Three of the subjects tested had became azoospermic and one of them had only 1 million sperms/ml after two months use of the drug. The percentage of motile cells decreased in two months about 30%. The percentage of sperms with normal configuration decreased significantly both in one and two months, from 73 ± 8% to 65 ± 5% and 42 ± 23%, respectively. The percentage of sperms with amorphous head increased about 100% during two months use. The changes in sperm morphology and production were however observed to be reversible.

Hepatotoxicity (Liver)
Being a C17-α alkylated compound, this protects the molecule from First Pass Liver Metabolism allowing a very high percentage of the compound to enter the bloodstream following oral administration.

The literature is clear in the association of Methandrostenolone with Hepatic Jaundice, Hepatitis, Cholestasis and Liver Parenchyma cell alterations. Cholestatic Jaundice in rare circumstances can result in renal failure and potentially death.

In rare circumstances, liver carcinoma can develop as a result of liver dysfunction in potential combination with environment factors.

Elevations in bilirubin, Alkaline Phosphatase (ALP), Alanine Transferase (ALT) and Aspartate Transferase (AST) should be closely monitored by bloodwork by a physician during and post use.

A case reports of a 28-year-old body builder who was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking 10-50mg Methandrostenolone by mouth, and 50mg stanozolol intramuscularly every other day. Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. Although the steroids had been discontinued, the patient’s general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient’s state improved simultaneously with the administration of ursodeoxycholic acid (UDCA); a bile acid derivative; and the biochemical values gradually reached normal levels after several weeks. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement. As such TUDCA may be a viable compound as prophylactic treatment.

Cardiovascular (Cholesterol / Lipid)
Methandrostenolone has a reported history of causing elevated serum total cholesterol due to elevations in LDL (bad) cholesterol; as well as causing issues with decreased HDL (good) cholesterol. This reduction in serum HDL is mediated by hepatic triglyceride lipase, an enzyme that regulates serum lipids.

Oral C17-α alkylated AAS stimulate hepatic triglyceride lipase, resulting in decreased serum HDL. Injectable administration of AASs has less profound effects on this enzyme because they enter the circulation without passing through the liver.

Kidney (Renal)
Whilst not directly nephrotoxic, Methandostenolone can increase renal artery BP, probably via potentiating the renin–angiotensin-aldosterone system (RAAS) along with the up-regulation of endothelin. RAAS can increase BP and water retention through promoting tubular sodium and water re-absorption. Acute Kidney Injury (AKI) may also result as a correlation to increases in serum creatinine.

Neurochemistry (Neurotoxicity)
In past literature, it has been attempted to associate violent crime to the use of anabolic steroids but the results are inconclusive in light of other poly substance abuse.

No effect was observed on brain reward-performance of methandrostenlone but a small effect has been observed with Testosterone which may influence the sensitivity of the brain reward system. No effect was observed on changes in hippocampal activity in rats treated with Methandrostenolone.

Reported Clinical Uses

The earliest reports of clinical use have been in pediatrics to treat childhood muscular dystrophy as well as attempting to resolve growth issues in prepubertal male patients.

Further clinical uses for Methandrostenolone focused on reporting increases in nitrogen retention and subsequent decrease in nitrogen excretion (30 % lower) and increase in serum protein values aiding in tissue repair and decrease healing time after surgery, burns, fractures or skin grafts.

There are several reports on its use in geriatric states, debilitation, and after chronic infections (tuberculosis) as well as aiding in calcium retention in osteoporosis and increasing red blood cell count in anemic patients.

Steroid hormone interactions are not just limited to the Androgen Receptor and many published reports have exhibited the interaction of Methandrostenolone with the glucocorticoid receptor; blocking their activation and subsequent anti-inflammatory effect.

Methandrostenolone has also been shown to diminish the rate of production of adrenocortical steroid by inhibiting corticotrophin production or release; resulting in lower circulating cortisol levels.

There is research to also suggest Methandrostenolone can augment insulin resistance in Diabetic patients but further research is required as well as former AAS users potentially through increase in Visceral Adipose Tissue (VAT).

Athletes and Strength Training

The earliest report of Methandrostenolone being used for physical enhancement was of a dosage of 5mg taken for 3 weeks resulting in a 2.48 kg (5.45 lb) increase in lean muscle mass tissue and has been demonstrated to support maintenance and recovery of strength following a 12 week de-trained period.

Anti – Doping / Fake Supplements

As of the mid 2000s, dietary supplements have come under scrutiny due to the potential illegal containment of AAS; most specifically the Prohormones which were readily available at the time. Out of a study of 103 supplements, 3 were found to contain illegal amounts of undisclosed Methandrostenolone within. Consumers are advised from an Anti-Doping perspective to be aware of what is contained within the products they buy, and as such, particular interest has been paid as of late to the detection of AAS in dietary supplements with new methods of detection constantly being developed and improved upon.

Reported Deaths
The majority of reported deaths in the literature causatively to Methandrostenolone use are in association with myocardial infarctions or progression of cardiovascular disease. However, the majority of cases note this as a response to polydrug use and not one particular substance.

Health Supplementation to consider when using Methandrostenolone

As Methandrostenolone is a hepatoxic C17-α alkylated compound, particular attention should be paid to the management of prevention of cholestatic injuries to the liver and management of bile metabolism. Bile acids such as Tauroursodeoxycholic acid (TUDCA) and synthetic bile derivatives such as Ox-Bile should be considered to aid in bile flow; as well as lipotrophic compounds such as Choline and Inositol to aid in fat metabolism within the liver. Supplement Needs Dr Dean St Mart Liver Stack (https://www.supplementneeds.co.uk/products/supplement-needs-liver-stack-240-capsules) is a combination of 1000mg Ox Bile, 800mg TUDCA, 800mg Choline and 800mg Inositol. Care should be taken to not co-administer TUDCA alongside Methandrostenolone due to a plausible ability to increase hepatocyte uptake of Methandrostenlone resulting in enhanced hepatotoxicity.

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Administration Of Dianabol (Doses)

Originally dosages of 0.1-0.3 mg/kg were prescribed for children in the treatment of muscular dystrophies.

In males, 5mg as a daily dose was the initial prescribing guidelines with no more than 6 weeks consecutive use. This was initially an effective dose but today, in physique enhancement and performance, a dosage of 30-50 mg is commonly observed producing very noticeable and rapid results. A 1981 published athletic performance paper showed a dosage of 100mg was well tolerated for 6 weeks although health markers were not closely monitored. Several other reports in early literature have shown dosages of 0.6mg / kg.

For females, a dosage of 2.5mg was originally prescribed for osteoporosis. However, females should be mindful of the potential virilizing side effects as outlined previously.

Availability Of Dianabol
Methandrostenolone is a controlled substance in the United States and Western Europe, but still remains popular among bodybuilders sourced via the Underground Black Market. However, Methandrostenolone is readily available without a prescription in certain countries as well as also being manufactured in Asia and many East European countries in Black Market Underground Pharmaceutical Facilities such as Alpha Pharma (India) and Balkan Pharmaceuticals (Moldova).

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