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These three categories are routinely discussed as though they were points on a single scale of strength. They are not. They differ in chemical class, in how they interact with the androgen receptor, in whether they are converted into other active hormones inside the body, and in their liver profile. This guide separates them properly, because the differences that matter to a research buyer are the ones that never appear in a ranking table.
What each class is
Anabolic androgenic steroids are synthetic derivatives of testosterone. Testosterone itself, nandrolone, trenbolone, oxandrolone and the rest share the four-ring steroid nucleus and act as full agonists at the androgen receptor in every tissue that expresses it. Several are licensed medicines with genuine clinical indications.
Prohormones is a marketing term rather than a chemical class. It has been applied to compounds that are converted in the body to an active androgen, and to related compounds studied for other reasons, such as Arimistane, which is researched as an aromatase inhibitor rather than an androgen.
Selective androgen receptor modulators are non-steroidal molecules with entirely different chemical scaffolds that bind the same receptor. Ostarine, LGD-4033, RAD-140 and the rest fall here. They are not steroids, they are not converted into steroids, and they were designed to act as tissue-selective partial agonists.
Receptor selectivity versus full agonism
This is the central pharmacological difference and it is worth understanding properly.
Testosterone is a full agonist at the androgen receptor everywhere the receptor is expressed: skeletal muscle, bone, prostate, skin, hair follicle, liver and brain. The muscle effects and the prostate and skin effects are the same signalling event in different tissues, which is why they cannot be separated.
SARMs bind the same receptor but produce a different conformational change in it, recruiting a different set of co-regulator proteins. Because the available co-regulators differ between tissues, the result is more transcriptional activity in muscle and bone and less in prostate, skin and hair follicle. That is the entire meaning of selective, and it is demonstrated in animal models, where anabolic effects on muscle occur at doses with much less effect on prostate weight than testosterone. Selectivity is relative and dose-dependent. It is not an on and off switch, and no human trial has characterised where it breaks down.
Aromatisation and 5-alpha reduction
Testosterone is a substrate for two enzymes that change what it does. Aromatase converts it to oestradiol, which is responsible for the oestrogenic effects of steroid use including gynaecomastia and fluid retention, and is also why aromatase inhibitors are discussed alongside steroids and prohormones. 5-alpha reductase converts testosterone to dihydrotestosterone in skin, scalp and prostate, and DHT is a more potent receptor agonist, which drives androgenic effects including hair loss in those genetically predisposed.
Steroidal compounds enter these same pathways, and what each one converts into determines its profile in the literature. Arimistane is researched as an aromatase inhibitor.
SARMs are non-steroidal and are not substrates for either enzyme. They do not aromatise and are not 5-alpha reduced. That is the most concrete mechanistic difference between the classes and the one most often stated correctly in marketing.
Liver profile
Many oral steroids and prohormones are 17-alpha-alkylated, a chemical modification that lets them survive first-pass metabolism in the liver and reach the circulation intact. That modification is the established cause of the cholestatic liver injury associated with oral androgens. The Drug-Induced Liver Injury Network prospective study reported by Navarro and colleagues in Hepatology in 2014 found bodybuilding supplements to be a leading cause of liver injury attributed to herbal and dietary supplements in the United States, with a characteristic prolonged cholestatic pattern.
SARMs are not alkylated in this way and liver enzymes were largely unremarkable in the trials, with the exception of RAD-140, whose first-in-human trial reported by LoRusso and colleagues in Clinical Breast Cancer in 2022 was limited by raised transaminases. The published case series of liver injury associated with SARM-labelled products, including Flores and colleagues in Hepatology Communications in 2020, shows the class is not exempt, particularly where products were unverified.
Suppression
All three classes suppress the hypothalamic pituitary gonadal axis, because all three supply androgen receptor signalling that the body reads as sufficient. The phase I LGD-4033 study by Basaria and colleagues in the Journals of Gerontology in 2013 showed falls in testosterone, LH and FSH during the 21 day study that returned to baseline after the study drug was stopped. Anabolic steroids suppress more completely and for longer, and prohormones suppress in a similar way because they are metabolised into active androgens.
How to check a supplier
The standard is the same across all three classes. Require a batch-specific certificate of analysis, identity confirmed by HPLC or LC-MS, a stated purity percentage and a batch number matching the bottle, together with UK manufacture, a clear amount per capsule, a capsule count and a research-only notice. The JAMA 2017 analysis by Van Wagoner and colleagues, which found that only 52 per cent of 44 products sold as SARMs contained any SARM at all, applies to every category sold online.
Frequently asked questions
Are SARMs steroids? No. They are non-steroidal molecules that bind the same receptor and are not converted to oestrogen or DHT.
Are SARMs safer than steroids? No head to head human trial exists. Steroids have far more long-term data, SARMs have none, so the comparison is theoretical.
Do prohormones aromatise? It depends on the compound. Arimistane is researched as an aromatase inhibitor.
Related reading
- Are SARMs legal in the UK? 2026 update
- Are SARMs safe? What the evidence says about side effects
- PCT after SARMs: what the studies show
Sources
Primary papers and official guidance cited in this guide, linked so each one can be checked directly.
- Basaria S et al., J Gerontol A Biol Sci Med Sci 2013;68:87-95. PubMed 22459616
- LoRusso P et al., Clin Breast Cancer 2022;22:67-77. PubMed 34565686
- Navarro VJ et al., Hepatology 2014;60:1399-1408. PubMed 25043597
- Flores JE et al., Hepatol Commun 2020;4:450-452. PubMed 32140660
- Van Wagoner RM et al., JAMA 2017;318:2004-2010. PubMed 29183075
- WADA Prohibited List 2026.