Turinabol: Dangerous Liver Risks, 10 Studies

Turinabol in three numbers

Three figures frame the drug better than any forum thread. One comes from the secret GDR files, one from the liver injury network, one from the doping laboratory.

Every number on this page comes from one of the 10 papers in the sources list. Liver and lipid figures come from oral 17-alpha-alkylated steroids as a class, and the text says so each time.

What this guide covers

What turinabol is: a chlorinated Dianabol from Jena

Turinabol is the trade name of dehydrochloromethyltestosterone, written 4-chloro-1-dehydro-17-alpha-methyltestosterone in the GDR files (PMID 9216474).

It was produced by VEB Jenapharm in Jena and introduced for clinical use in 1965. Chemically it is a chlorine-substituted version of methandrostenolone, the molecule sold as Dianabol (PMID 9216474).

Developed by Jenapharm in the 1960s and marketed as Oral Turinabol, it is prohibited in sport at all times. Anti-doping laboratories still report several findings every year (PMID 34418529).

The 17-alpha-methyl group is what lets the molecule survive a trip through the liver and work as a tablet. The same group slows clearance in the liver and is the reason oral steroids are more hepatotoxic than injectables (PMID 29521706).

Anabolic steroids remain the most common adverse finding in sport. The damage they can do to health was recorded in detail in the former GDR, which is where its history starts (PMID 18500378).

State Plan 14.25: the turinabol program the GDR kept secret

After the GDR collapsed in 1990, classified theses, reports and Stasi files surfaced. Franke and Berendonk analysed them in Clinical Chemistry in 1997 (PMID 9216474).

From 1966 on, hundreds of physicians and scientists ran doping research and gave athletes prescription and unapproved drugs. Several thousand athletes were treated with androgens every year, including minors of each sex (PMID 9216474).

Oral-Turinabol was the compound used most often. By 1966 it was already being given to male athletes, and before the 1968 Olympics officials began giving androgens to women as well (PMID 9216474).

The program was first called Research Program 08 and later State Plan Research Theme 14.25. The final top secret bill was approved on 23 October 1974 (PMID 9216474).

More than 2000 athletes preparing for international competition were treated each year under that plan. In swimming, girls of 14 or younger were given androgenic hormones (PMID 9216474).

Adolescents were made to swallow the tablets, described as vitamin pills, in front of their coaches. Many of the doctors documented the damaging side effects and called the treatment unethical (PMID 9216474).

What the files recorded: turinabol doses and results

The GDR records are the only large dose dataset for this compound. They are quoted here as history. Nothing in them is a recommendation.

The first documented case is a female shot putter. In 1968 she took two tablets, 10 mg a day, for 11 weeks, and her throws improved by about 2 metres (PMID 9216474).

In 1969 her intake ran from 7 to 21 tablets a week. Without the drug she could not reach 18 metres; on it she set a world record of 20.10 metres (PMID 9216474).

By 1972 she was taking up to 7 tablets a day, 35 mg, in four cycles for a total of 1450 mg that year. Her best reached 20.22 metres (PMID 9216474).

Annual doses for female track and field medal winners ran from 1670 mg in the sprint to 3680 mg in the shot put (PMID 9216474).

Weightlifters took far more. A 1979 Stasi report put upper weight class doses above 10 g a year. One lifter took 11,550 mg of Oral-Turinabol plus 13 injections of testosterone esters and hCG (PMID 9216474).

Swimmers in the mid 1980s started at age 14. They got 670 mg a year in three cycles, with a maximum of 10 mg a day (PMID 9216474).

Virilizing side effects in female athletes were frequent and pronounced. By the 1976 Games, journalists were asking about the deep voices of the GDR women swimmers (PMID 9216474).

Turinabol and the liver: what oral steroid injury looks like

No controlled trial has measured its liver injury on its own. What exists is the literature on oral 17-alpha-alkylated steroids as a class, and turinabol belongs to that class (PMID 29521706).

Hepatotoxicity from these steroids shows up as raised transaminases, acute cholestasis, vascular injury, liver tumours and fatty liver. Most changes reverse after stopping, but some can be life threatening (PMID 29521706).

The US Drug Induced Liver Injury Network described 44 young men with injury from bodybuilding products. Symptoms came a median 73 days after starting. All had jaundice, 84% itched, and 71% were hospitalised (PMID 30934130).

Chemical analysis of their products found anabolic steroids that were not on the label. Nobody died or needed a transplant, but the cholestasis resolved slowly (PMID 30934130).

A review of 52 cases found patients presented 56 days after starting and bilirubin peaked 28 days after stopping. Peak bilirubin was 705 µmol/L while ALT peaked at only 125 U/L (PMID 33214235).

Biopsies showed bland canalicular cholestasis. 43% developed kidney injury alongside the liver. No patient died or needed a transplant (PMID 33214235).

Turinabol and cholesterol: the oral steroid lipid effect

Oral anabolic steroids produce striking reductions in HDL cholesterol. The cleanest test of this is a crossover trial in 11 weightlifters, using oral stanozolol against injectable testosterone (PMID 2915439).

Stanozolol is not turinabol, but both are oral 17-alpha-alkylated steroids. The authors tied the effect to that route rather than to androgenic potency (PMID 2915439).

Six weeks of oral stanozolol cut HDL by 33% and the HDL2 subfraction by 71%. Apolipoprotein A-I fell 40% and LDL rose 29% (PMID 2915439).

The same men on injectable testosterone lost 9% of HDL, with LDL falling 16%. Hepatic lipase activity rose 123% on the oral and 25% on the injectable (PMID 2915439).

Significant changes in lipoproteins are listed among the liver related effects of anabolic steroids, because hepatic lipase is a liver enzyme (PMID 29521706).

Turinabol and the adrenal enzymes: a 2016 finding

A 2016 study tested whether the human enzymes that build cortisol and aldosterone also act on this steroid. The mitochondrial enzymes CYP11A1, CYP11B1 and CYP11B2 all metabolised it (PMID 26658226).

CYP11B2, the aldosterone synthase, converted turinabol most efficiently, at 3338 per minute per millimolar, in the same range as its natural substrates (PMID 26658226).

All three enzymes were inhibited by it in their natural function. The microsomal steroid hydroxylases did not convert it at all (PMID 26658226).

The products included 11-beta-hydroxy turinabol and, from CYP11B2, 18-hydroxylated metabolites. These were made in milligram amounts in an E. coli system and identified by NMR (PMID 26658226).

Turinabol detection time: why old samples keep testing positive

Turinabol detection changed in 2012. Sobolevsky and Rodchenkov fractionated pooled positive urines and found about 50 metabolites (PMID 22142641).

Six new long term metabolites were characterised. The one named M3 outlasted every previously known metabolite in most cases (PMID 22142641).

Those metabolites were put into the re-test programme. Samples from the 2008 and 2012 Olympics produced adverse findings years after the Games (PMID 34418529).

In 2021 a controlled trial gave five men a single 5 mg oral dose and collected urine for 60 days. M3 served as the long term marker in four of the five (PMID 34418529).

In one volunteer M3 was detectable for 45 days after that single tablet. The last positive sample across the group fell between 9.9 and 44.9 days (PMID 34418529).

Across IOC re-tests of 2004, 2008 and 2012, exogenous steroids were present in 90% of 142 athlete samples. Turinabol and stanozolol accounted for 79% of the substances found (PMID 33835351).

Of 134 Olympic medals affected by doping violations, only 26% were caught at the Games. Re-test cases took a mean of 6.8 years to announce (PMID 33835351).

Turinabol vs Dianabol vs Anavar: what the sources support

Turinabol vs Dianabol is a comparison between a molecule and its chlorinated version. The GDR files describe turinabol as a chlor-substituted methandrostenolone (PMID 9216474).

Both are oral 17-alpha-alkylated steroids, so both carry the slower liver clearance and the hepatotoxicity that goes with it (PMID 29521706).

Turinabol vs Anavar is the same story on the liver side. Oxandrolone is also 17-alpha-alkylated, and the class effects on lipids and liver apply to it (PMID 29521706, 2915439).

No head to head trial of turinabol against Dianabol or Anavar exists in PubMed. Claims about which gives more gains or less water rest on user reports, not on measurement.

Five turinabol mistakes the sources rule out

Verdict: turinabol in 10 studies

1. It is chlorinated Dianabol, made by Jenapharm from 1965. Oral and 17-alpha-alkylated (PMID 9216474).

2. It was the GDR workhorse. Over 2000 athletes a year, girls from age 14 (PMID 9216474).

3. Recorded doses ran 670 to 3680 mg a year. One lifter took 11,550 mg (PMID 9216474).

4. The oral class injures the liver by cholestasis. Jaundice in 100% of 44 men, two months in (PMID 29521706, 30934130).

5. Recovery is slow but nobody died in the series. Bilirubin peaked 28 days after stopping (PMID 33214235).

6. Oral steroids cut HDL by a third in six weeks. Injectable testosterone cut it 9% (PMID 2915439).

7. It competes with adrenal enzymes. CYP11B2 converts and is inhibited by it (PMID 26658226).

8. Fifty metabolites, six of them long term. M3 outlasts the rest (PMID 22142641).

9. One 5 mg tablet shows for up to 45 days. Controlled trial, five men (PMID 34418529).

10. It is the Olympic re-test steroid. With stanozolol, 79% of substances found (PMID 33835351).

Anabolic steroid risks should not be exaggerated, but an attitude of personal invulnerability is misguided (PMID 18500378).