Peptides vs SARMs vs Steroids vs TRT: A Mechanism-Level Comparison

Four different things, usually argued about as one

The comparison gets searched as though these were points on one scale, from mild to strong. They are not. Two questions separate them cleanly: what does the molecule act on, and what does it do to the testosterone your own body makes?

TRT is prescribed testosterone given to replace a diagnosed deficiency, at doses meant to restore normal levels. Anabolic steroids are testosterone and its synthetic derivatives used above normal levels to build muscle; the molecule class overlaps with TRT, and the purpose and dose do not. SARMs are non-steroidal molecules that bind the same androgen receptor and were designed to favour muscle and bone over other tissues. Peptides, in this market, means two unrelated groups: growth-hormone secretagogues, which raise growth hormone and IGF-1 and do not touch the androgen receptor, and peptides that act on the pituitary to raise the body's own testosterone.

The first three are androgen-receptor drugs. The peptides are not, which is why claims that they are a gentler version of the same thing do not hold up at the level of mechanism.

Side by side

Status columns are as of October 1, 2026. Evidence grades come from our encyclopedia and cover all human evidence for each compound; testosterone, steroids and SARMs have no entries of their own, so their evidence is described in words.

TRT: the one with a guideline and a long-term trial

The Endocrine Society's guideline is narrow about who should be treated. It recommends diagnosing hypogonadism only in men with symptoms and signs of testosterone deficiency and unequivocally and consistently low testosterone, measured in the fasting morning with a reliable assay and confirmed by repeating it. It recommends against starting testosterone in men planning fertility in the near term, and in men with breast or prostate cancer and several other conditions.¹ The fertility line follows directly from the mechanism: testosterone from outside shuts down the signal that drives sperm production.

TRAVERSE is the trial that changed the safety picture. In men with hypogonadism and existing or high cardiovascular risk, testosterone was noninferior to placebo for major adverse cardiac events, with a hazard ratio of 0.96 (95% CI 0.78 to 1.17), over a mean treatment of 21.7 months and follow-up of 33 months. It also found more atrial fibrillation, acute kidney injury and pulmonary embolism in the testosterone group.²

FDA acted on it in February 2025: it required TRAVERSE's results to be added to all testosterone labels, removed the boxed-warning language about an increased risk of adverse cardiovascular outcomes, kept the limitation of use for age-related low testosterone, and added a blood-pressure warning to products that did not carry one.³ So TRT is neither the cardiac danger it was once labelled nor a general-purpose drug: it is approved for men with low testosterone and an associated medical condition, and age-related decline alone is a stated limitation.

Anabolic steroids: the same receptor, used outside any trial

Steroids used for muscle are taken at doses and in combinations no trial has tested, so the evidence on harm comes from following people who use them. A Danish matched cohort followed 545 men who tested positive for steroids in fitness-centre testing between 2006 and 2018 against 5,450 controls. Mortality was three times higher among users (hazard ratio 3.0, 95% CI 1.3 to 7.0), they had more than twice as many hospital contacts a year, and acne, breast tissue growth and erectile dysfunction each affected more than 10% of them.⁴

The effect on the body's own testosterone is the part people most underestimate, because it can outlast the use. A study of former users found a marker of testicular Leydig-cell capacity, INSL3, reduced years after stopping, independently of their testosterone level and lower the longer they had used.⁵ A 2026 community study of men in the first year after stopping found their testosterone no different from non-users, and their depression, anxiety and lower quality of life were tied more strongly to existing psychiatric conditions than to their hormone levels.⁶ Read together: a normal testosterone result after stopping does not mean the testes are back to where they started, and how someone feels after stopping is not only about hormones.

SARMs: selective for tissue, not for your hormones

The selling point of a SARM is selectivity: muscle and bone without the rest of the steroid profile. The trials do not support the version of that claim people care about. In a 21-day trial in healthy young men, LGD-4033 increased lean body mass and caused dose-dependent suppression of total testosterone, sex hormone-binding globulin and HDL cholesterol, with follicle-stimulating hormone and free testosterone suppressed at the highest dose.⁷ A drug can be selective about which tissues grow and still switch off the testes.

FDA's position is unambiguous. It states that SARMs have not been approved, that products containing them are illegally marketed, and that life-threatening reactions including liver injuries requiring hospitalisation have occurred; it lists heart attack or stroke, liver failure, infertility and testicular shrinkage among their potential harms, and says it has issued warning letters and pursued criminal actions against distributors.⁸ Case reports continue to add to that: a 2026 report describes severe cholestatic liver injury in a previously healthy young man after a supplement containing RAD-140 and andarine,⁹ and a 2025 report describes the first known case in an adolescent.¹⁰

WADA names them outright: andarine, enobosarm (ostarine), LGD-4033, RAD140, S-23 and YK-11 are listed as examples under S1.2, other anabolic agents.¹¹

Growth-hormone peptides: a different axis entirely

CJC-1295, sermorelin and tesamorelin act like growth-hormone-releasing hormone; ipamorelin and MK-677 act on the ghrelin receptor. Both routes raise growth hormone and then IGF-1. Neither involves the androgen receptor, and neither replaces testosterone.

What has been measured is the hormone response. In healthy adults, CJC-1295 produced sustained, dose-dependent rises in growth hormone and IGF-1, with an estimated half-life of 5.8 to 8.1 days and IGF-1 staying above baseline for up to 28 days after repeated doses.¹² What has not been measured is the outcome people buy it for: no trial has shown that these peptides build muscle or improve body composition in healthy people using them the way they are marketed. Our CJC-1295 and ipamorelin entries set out exactly what has and has not been studied.

Tesamorelin is the exception that proves the rule: it is an approved drug, for reducing excess abdominal fat in adults with HIV-associated lipodystrophy, with trials behind that one use and not others.

The peptides that raise your own testosterone

A second group is marketed directly against TRT: gonadorelin, a copy of the hypothalamic hormone that tells the pituitary to release LH; kisspeptin, which sits above that; and hCG, which acts like LH on the testis. All three work by stimulating the body's own production rather than replacing it, which is why they are pitched to men worried about fertility or about shutting down their own testosterone.

Two facts belong beside that pitch. First, they depend on the testes being able to respond: they amplify a working system rather than replace a failed one, so they are not an alternative for men whose deficiency starts in the testis. Our comparison of kisspeptin, gonadorelin and hCG covers where each acts and what the human studies measured. Second, they are not a way round anti-doping rules. WADA's 2027 list bans testosterone-stimulating peptides in males in a section of their own — chorionic gonadotrophin, LH, gonadorelin and its analogues, and kisspeptin and its analogues — at all times.¹¹

If you are tested

Every class in this article is prohibited at all times, in and out of competition, under the 2027 list: testosterone and other anabolic steroids under S1.1, SARMs under S1.2, testosterone-stimulating peptides under S2.2.1, and growth-hormone-releasing peptides and secretagogues under S2.2.4.¹¹ A prescription does not change that for a tested athlete; only a therapeutic use exemption does. Our regulatory tracker gives the WADA section for every compound on this site, dated at the source.

The short version

TRT, steroids and SARMs are androgen-receptor drugs, and all three switch off your own testosterone to some degree; only TRT has a guideline, an approved indication and a long-term safety trial. SARMs are unapproved, suppress testosterone in trials and carry a growing record of liver injury. The growth-hormone peptides work on a different axis and have hormone data rather than outcome data. The testosterone-stimulating peptides need working testes, and in sport they are banned in their own section.

None of that is a recommendation for or against any of them. It is the frame that makes the comparison answerable: decide what problem you are actually trying to solve, because these four do not solve the same one.

Frequently asked questions

Are peptides safer than steroids?

They are not the same kind of drug, so the comparison is not like-for-like. Steroids act on the androgen receptor and have cohort evidence of harm, including a threefold higher mortality in one Danish study. The growth-hormone peptides act on a different axis and have hormone-response data but no outcome data, so their long-term safety is unknown rather than shown to be good.

Do SARMs shut down your testosterone?

In a 21-day trial in healthy young men, LGD-4033 caused dose-dependent suppression of total testosterone, with free testosterone and FSH suppressed at the highest dose. SARMs are selective about tissue, not about the hormone axis.

Can peptides replace TRT?

Not in the sense the question usually means. Growth-hormone peptides do not raise testosterone at all. Peptides such as gonadorelin or hCG stimulate the body's own production, which depends on the testes being able to respond, so they are not an alternative for men whose deficiency starts in the testis.

Is TRT bad for your heart?

In the TRAVERSE trial of men with hypogonadism and cardiovascular risk, testosterone was noninferior to placebo for major adverse cardiac events, though atrial fibrillation, acute kidney injury and pulmonary embolism were more common. FDA removed the cardiovascular-outcomes language from the boxed warning in February 2025 and added a blood-pressure warning.

Are SARMs legal?

FDA states they are not approved and that products containing them are illegally marketed, including those sold as dietary supplements; it has issued warning letters and pursued criminal actions against distributors.

Are any of these allowed in sport?

No. Under WADA's 2027 list, steroids and testosterone (S1.1), SARMs (S1.2), testosterone-stimulating peptides (S2.2.1) and growth-hormone-releasing peptides (S2.2.4) are all banned at all times.

Related on Grey Peptides

• CJC-1295
• Ipamorelin
• Regulatory tracker: FDA, 503A/503B and WADA
• Peptide encyclopedia

Sources

1. Bhasin, S. et al. (2018). Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. The Journal of Clinical Endocrinology and Metabolism, 103(5), 1715-1744. PMID: 29562364
2. Lincoff, A. M. et al. (2023). Cardiovascular Safety of Testosterone-Replacement Therapy. The New England Journal of Medicine, 389(2), 107-117. PMID: 37326322
3. US Food and Drug Administration. FDA issues class-wide labeling changes for testosterone products. Content current as of February 28, 2025; read October 1, 2026. FDA
4. Horwitz, H. et al. (2019). Health consequences of androgenic anabolic steroid use. Journal of Internal Medicine, 285(3), 333-340. PMID: 30460728
5. Rasmussen, J. J. et al. (2021). Serum Insulin-like Factor 3 Levels Are Reduced in Former Androgen Users, Suggesting Impaired Leydig Cell Capacity. The Journal of Clinical Endocrinology and Metabolism, 106(7), e2664-e2672. PMID: 33693710
6. Grant, B. et al. (2026). Clinical features of androgen abuse withdrawal in men during the first year of cessation: a community dwelling cohort. The Journal of Clinical Endocrinology and Metabolism, 111(9), 2649-2663. PMID: 41818709
7. Basaria, S. et al. (2013). The safety, pharmacokinetics, and effects of LGD-4033, a novel nonsteroidal oral, selective androgen receptor modulator, in healthy young men. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 68(1), 87-95. PMID: 22459616
8. US Food and Drug Administration. Certain bodybuilding products put consumers at risk for heart attack, stroke, serious liver damage and more. Content current as of December 2, 2025; read October 1, 2026. FDA
9. Dao, D. et al. (2026). Unregulated gains: a case of RAD-140-induced liver injury. Proceedings (Baylor University. Medical Center), 1-3. PMID: 42417499
10. Katibian, D. J. et al. (2025). Drug-induced liver injury associated with selective androgen receptor modulators in an adolescent patient. JPGN Reports, 6(4), 515-518. PMID: 41245032
11. World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2027, sections S1.1, S1.2, S2.2.1 and S2.2.4. Dated August 26, 2026; in force January 1, 2027. WADA
12. Teichman, S. L. et al. (2006). Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. The Journal of Clinical Endocrinology and Metabolism, 91(3), 799-805. PMID: 16352683

This article is for education. It is not medical advice and it is not a guide to obtaining or using any of these drugs. Testosterone deficiency is a diagnosis made by a clinician on repeated tests; if you are considering any treatment, start there.