Anabolic-Androgenic Steroids
Overview & the Anabolic:Androgenic Ratio Concept
Evidence grade 3 of 5, Mixed. Read how the Atlas grades evidence.
The written rationale for this grade is still being prepared.
- FDA
- Schedule III (Anabolic Steroids Control Act, 1990; expanded 2004/2014)
- WADA
- Prohibited at all times (WADA Prohibited List, S1 Anabolic Agents).
Reference only. Not medical advice.
This is something to take to a clinician. The Atlas can tell you what is known about anabolic-androgenic steroids in general. It cannot tell you what is happening in your body, and the difference matters most for exactly the symptoms that bring people to this page.
Anabolic-androgenic steroids (AAS) are testosterone or synthetic derivatives of testosterone that bind the androgen receptor to drive nitrogen retention, muscle protein synthesis (the 'anabolic' effect) and masculinizing 'androgenic' effects. The terms are inseparable in practice: every AAS does both. The historic 'anabolic:androgenic ratio,' derived from a 1950s rodent assay (levator ani muscle vs. ventral prostate/seminal vesicle weight), was used to market compounds as 'tissue-selective,' but it predicts little about human outcomes and nothing about cardiovascular or hepatic harm. This entry is documentary; it does not provide enhancement dosing.
Synthetic derivatives of testosterone, and the marketing fiction of a 'pure anabolic.'
What people take it for
These are the reasons people give for taking it. They are not effects it has been shown to have.
- Narrow medical roles
- A subset of AAS retain or once held FDA/foreign approval for anemia, wasting, hereditary angioedema, severe burns, or delayed puberty, always physician-supervised and dosed far below physique-use levels.
How it is supposed to work
AAS diffuse into cells and bind the cytoplasmic androgen receptor; the hormone-receptor complex translocates to the nucleus and modulates transcription of genes governing muscle protein synthesis, satellite-cell activation, erythropoiesis and secondary sex characteristics. Supraphysiological levels also exert non-genomic and anti-catabolic (anti-glucocorticoid) effects. Because a single receptor mediates both 'anabolic' and 'androgenic' signaling, true separation of the two is not achievable with conventional steroids.
The shared scaffold is the four-ring gonane (steroid) nucleus of testosterone. Modifications define the families: removal of the 19-methyl group yields 19-nortestosterone (nandrolone, trenbolone); 5-alpha reduction in the molecule's design yields DHT-derivatives (drostanolone, stanozolol, oxandrolone, mesterolone); and 17-alpha-alkylation creates orally bioavailable but hepatotoxic compounds.
Why 'the ratio' oversells selectivity
The anabolic:androgenic ratio is a rodent muscle-vs-prostate weight ratio, not a human safety or efficacy measure. It says nothing about hepatotoxicity, lipid changes, hematocrit, cardiac remodeling, or HPTA suppression, the effects that actually injure people. A high 'ratio' compound can still cause hair loss, acne, suppression and cardiovascular harm.
Safety in detail
This intervention involves significant physiological effects and requires evaluation and monitoring by a qualified physician. Self-administration without medical oversight carries documented health risks.
- Cardiovascular: dyslipidemia (suppressed HDL), hypertension, polycythemia, left-ventricular remodeling and documented sudden-death cases.
- Endocrine: suppression of the hypothalamic-pituitary-testicular axis, testicular atrophy and impaired spermatogenesis.
- Hepatic: cholestasis, peliosis hepatis and tumors, concentrated among 17-alpha-alkylated orals.
- Psychiatric: irritability/aggression ('roid rage' in some users), hypomania, and depression on withdrawal.
- Counterfeiting: illicit-market products carry unverified dose, identity and contamination risks.
Replacement is not the same as a cycle
Physiologic testosterone replacement restores a deficient man to a normal reference range under monitoring. AAS physique use is supraphysiological, frequently many multiples of natural production, which is where polycythemia, lipid and cardiac remodeling, and severe HPTA suppression arise. The distinction is central to every entry in this category.
What it does to fertility
As a class, exogenous androgens suppress LH and FSH, shutting down endogenous testosterone production and spermatogenesis. Subfertility or azoospermia is common during use; recovery is variable and, after prolonged use, can be incomplete or prolonged.
What has to be monitored
The bloodwork this needs, and the reason it belongs with a clinician rather than a website.
- Lipid panel
- Hematocrit/hemoglobin
- Blood pressure
- Liver function (especially with orals)
- LH/FSH and total/free testosterone
- Estradiol where relevant
What people get wrong
Often said'Anabolic steroids build muscle without androgenic side effects'
ActuallyNo conventional AAS is purely anabolic. A single androgen receptor mediates both effects; the 'ratio' is a rodent assay artifact, not a guarantee against acne, hair loss, suppression, or cardiovascular and hepatic harm.
Often said'They are basically just extra testosterone, so they are safe'
ActuallySupraphysiological dosing, many multiples of replacement, produces cardiovascular remodeling, polycythemia, lipid derangement and profound HPTA suppression not seen with physiologic testosterone.
Who profits, and who pushes back
Anti-doping science community (e.g., WADA-affiliated researchers)
The anabolic:androgenic ratio derived from the rat Hershberger assay does not translate to humans and should not be read as evidence of tissue selectivity or relative safety.
Harrison Pope
Long-term AAS use is associated with underappreciated cardiovascular, hepatic, and psychiatric harms, and a growing aging cohort of former users faces consequences that were never adequately studied.
Systematic reviewers of AAS cardiovascular effects
Causal long-term harm is hard to quantify because most human evidence is observational, confounded by polypharmacy, and drawn from self-selected users rather than controlled trials.
How we got here
The androgenic and anabolic activity of testosterone was characterized after its 1935 isolation and synthesis (Butenandt, Ruzicka). Through the 1950s and 1960s, pharmaceutical chemists synthesized hundreds of derivatives seeking the elusive 'pure anabolic' for catabolic illness; the levator-ani rat assay generated the ratio figures still quoted in gym culture. The performance-use era began when these agents reached competitive sport, culminating in the 1990 US Anabolic Steroids Control Act placing them in Schedule III.
- 1935Testosterone isolated and synthesized
- 1950s-60sHundreds of synthetic AAS created; anabolic:androgenic ratios catalogued
- 1976IOC bans anabolic steroids; testing introduced
- 1990US Anabolic Steroids Control Act, Schedule III
- 2004 & 2014US law expanded to add designer steroids and prohormones
Set against the alternatives
The four classes differ mainly in metabolism and route. Testosterone esters are bioidentical and aromatize to estradiol, so they carry estrogenic effects but also a more familiar safety profile. The 19-nor compounds resist aromatization but have progestogenic activity that drives distinct sexual and mood side effects. DHT-derivatives do not aromatize and are favored for a 'lean/dry' look, but several strain lipids and the heart. The 17-alpha-alkylated orals survive first-pass liver metabolism, making them orally active at the cost of marked hepatotoxicity and steep HDL suppression. Across all classes the same androgen receptor mediates both anabolic and androgenic effects, so the historic claim that any class is meaningfully 'tissue-selective' in humans is not supported; the differences are of degree and side-effect pattern, not a clean separation of muscle-building from masculinizing action.
| Class | Examples | Key trait | Notable risk |
|---|---|---|---|
| Testosterone esters | Cypionate, enanthate, undecanoate | Bioidentical; aromatizes | Polycythemia, estrogenic effects |
| 19-nortestosterone (19-nor) | Nandrolone, trenbolone | Progestogenic; less aromatization | Sexual dysfunction, mood effects |
| DHT-derivatives | Stanozolol, oxandrolone, drostanolone | Non-aromatizing, 'dry' | Lipid/cardiac strain, hair loss |
| 17-alpha-alkylated orals | Methandrostenolone, oxymetholone | Orally active | Hepatotoxicity, severe HDL drop |
What we do not know
- What are the true long-term cardiovascular and mortality risks of chronic AAS use, given the absence of controlled trials?
- How reversible are HPG-axis suppression, cardiac remodeling, and metabolic changes after cessation?
- Can any androgen, including SARMs, achieve clinically meaningful anabolic-androgenic dissociation in humans?
- What is the prevalence and trajectory of AAS dependence as a distinct disorder?
- How should the large aging cohort of former high-dose users be screened and managed?
What could change
SARMsInvestigational nonsteroidal AR ligands marketed as selective, but none approved and several flagged for liver and cardiac signals.Designer/novel steroidsUnlisted analogs engineered to evade detection and scheduling, complicating both testing and safety.Harm-reduction clinicsSpecialized services emerging to monitor and support nonmedical AAS users rather than only deter them.Advanced detectionLongitudinal steroidal-passport and isotope-ratio methods improving anti-doping sensitivity.
At a glance
- Receptor
- Androgen receptor (AR)
- Reference assay
- Hershberger / levator ani rat assay (1950s)
- Legal status (US)
- Schedule III controlled substances
- Classes
- Testosterone esters, 19-nortestosterone (19-nor), DHT-derivatives, 17-alpha-alkylated orals
What this entry does not yet cover
What follows is unfinished work on our side, not a finding about Anabolic-Androgenic Steroids. A short entry is not a safe entry.
- Cost and market. We have not documented what it sells for or who sells it.
- Supply chain. We have not mapped where it is made.
- Who uses it. We have not documented the user groups.
- Children and teenagers. We have not checked what is known about younger people.
- What can go wrong. We have not written the risk line for this one. Read the safety section below rather than treating its absence as reassurance.
Sources
The studies below are named and described, but not linked. You cannot open them from here and check our reading against them, which means this page is our summary of the literature rather than a document you can verify. Weigh it accordingly until the links exist.
The studies that matter
Pope, Kanayama et al., 'Adverse Health Consequences of Performance-Enhancing Drugs: An Endocrine Society Scientific Statement' (Endocrine Reviews)2014
Comprehensive synthesis concluding AAS misuse carries cardiovascular, endocrine, hepatic and psychiatric harms; lifetime US prevalence estimated in the millions.
Pope et al., 'The Lifetime Prevalence of AAS Use and Dependence in Americans' (Am J Addict)2014
Estimated roughly 2.9-4 million Americans had used AAS, with about 1 million developing dependence.
Kuhn, 'Anabolic Steroids' (Recent Prog Horm Res)2002
Reviewed the limits of the levator-ani ratio for predicting human tissue selectivity.