SARMs and Peptides Bloodwork: The Complete Monitoring Guide

You are running RAD-140 with MK-677 and BPC-157. Your mate did the same stack and "felt fine." But what does your bloodwork actually say?

SARMs and peptides sit in a regulatory grey zone. They are not pharmaceutical-grade medications, they are not dietary supplements, and the quality control on most products is questionable at best. A pharmacovigilance analysis found widespread product mislabelling and contamination among SARM products (Leciejewska et al., 2024). That means your bloodwork is not just monitoring your health; it is the only objective confirmation that whatever you are taking is doing what you think it is doing.

This guide covers what to test, when to test, and what the results actually mean for every major SARM and peptide compound athletes use today.

Why SARMs and peptides need different blood panels

Most bloodwork guides treat SARMs and peptides as interchangeable. They are not. These two compound classes affect your body through completely different mechanisms, and the markers you need to watch reflect that.

How SARMs affect your labs

SARMs bind to androgen receptors selectively, but "selective" does not mean "side-effect free." The three main impacts on bloodwork are:

HPTA suppression. SARMs suppress your hypothalamic-pituitary-gonadal axis the same way anabolic steroids do, just to varying degrees. A 2025 analysis of self-reported lab values from 2,183 SARM users on Reddit found a mean testosterone drop of 38.8% during use (from 585 to 358 ng/dL), with SHBG collapsing 70.8%. Testosterone remained 21.8% below baseline even after the cycle ended (Joshi et al., 2025).

Liver stress. SARMs cause drug-induced liver injury (DILI) more often than most users expect. Multiple case reports document severe cholestatic jaundice, with one Australian man developing dangerously elevated bilirubin after using RAD-140 (Perananthan & George, 2024). The LiverTox database documents ALT and AST elevations across multiple SARM compounds, with RAD-140 showing particularly high rates of hepatocellular stress.

Lipid shifts. Every SARM studied in clinical trials suppresses HDL cholesterol. The mechanism is upregulation of hepatic triglyceride lipase, which accelerates HDL breakdown (Guo et al., 2022). Real-world data shows HDL drops 30% during use and remains 29.7% below baseline post-cycle (Joshi et al., 2025).

How peptides affect your labs

Peptides work through the GH/IGF-1 axis rather than androgen receptors. The primary concern is metabolic, not hormonal.

Insulin resistance. GH secretagogues like MK-677 raise IGF-1 by stimulating growth hormone release. The trade-off is reduced insulin sensitivity. In a two-year randomized trial, MK-677 at 25 mg/day increased fasting glucose by 0.3 mmol/L and raised HbA1c by 0.2% compared to placebo (Nass et al., 2008). That sounds small until you realize 37% of subjects shifted from normal glucose into the pre-diabetic range.

Thyroid effects. Sermorelin carries a documented 6.5% incidence of subclinical hypothyroidism per its FDA prescribing information (Geref label). The mechanism: GH upregulates type II deiodinase, accelerating T4-to-T3 conversion and potentially depleting T4 reserves. The label explicitly requires thyroid function testing before and during sermorelin therapy.

No HPTA suppression. Unlike SARMs, peptides do not suppress LH, FSH, or endogenous testosterone. Ipamorelin showed no effect on FSH, LH, prolactin, or TSH at effective doses. Its selectivity is remarkable: ACTH and cortisol remained unaffected even at doses 200 times the effective GH dose (Raun et al., 1998).

The stacking problem

The real-world issue is that athletes rarely use one compound. RAD-140 plus MK-677 plus BPC-157 is a common stack. That means you are simultaneously dealing with HPTA suppression (from the SARM), insulin resistance (from MK-677), and an unmonitored healing peptide (BPC-157). Your blood panel needs to cover all three risk categories at once.

Compound-by-compound risk matrix

Not every compound needs the same panel. This matrix maps each compound to its specific risk markers, suppression severity, and monitoring priority.

SARMs

Ostarine is often marketed as the "mild" SARM, but context matters. The Phase II trial in elderly subjects showed a 57% testosterone drop at just 3 mg/day, and HDL fell 27% (Dalton et al., 2011). Bodybuilders use 10-25 mg.

LGD-4033 has the highest number of DILI case reports of any SARM in the pharmacovigilance literature (Leciejewska et al., 2024). One case developed severe cholestatic jaundice after just two weeks at 10 mg/day (Barbara et al., 2020).

RAD-140 carries the highest hepatic risk per-case. A 24-year-old developed bilirubin of 38.5 mg/dL after five weeks of use (Leung et al., 2022). Its steroidal backbone and oral bioavailability make it behave more like a 17-alpha alkylated oral steroid than a traditional SARM in terms of liver impact.

S-23 has no human clinical trial data. The only published study used it as a male contraceptive model in rats, where it prevented pregnancy in all treated animals and suppressed LH by more than 50% (Jones et al., 2009). If you are using S-23, you are flying without instruments.

YK-11 is a steroidal SARM with a dual mechanism: partial androgen receptor agonism plus follistatin upregulation that indirectly inhibits myostatin (Kanno et al., 2013). Its steroidal backbone means you should treat liver monitoring the same as you would for any methylated oral anabolic.

GH secretagogues

The difference between these compounds comes down to GH release pattern. MK-677 produces continuous, sustained GH elevation over its 24-hour half-life. That non-stop stimulation is what drives insulin resistance. Ipamorelin and CJC-1295 without DAC produce pulsatile GH release, mimicking the body's natural pattern, with recovery windows between pulses that preserve insulin sensitivity.

Tesamorelin is the only FDA-approved GHRH analog and has the strongest evidence base. In its landmark NEJM trial (conducted in HIV patients with lipodystrophy), it reduced visceral fat by 15.2% and lowered triglycerides by 50 mg/dL without significant glucose or HbA1c changes (Falutz et al., 2007). A dedicated trial in type 2 diabetic patients confirmed no worsening of glycemic control (Clemmons et al., 2017).

For a deep dive on the insulin resistance mechanisms of each peptide, see our dedicated guide: GH, MK-677 and Peptides: The Insulin Resistance Guide.

Healing peptides

BPC-157 and TB-500 are effectively invisible on standard bloodwork panels. They do not alter hormones, liver enzymes, glucose, or lipids. The only human safety data for BPC-157 comes from a 2025 pilot study of two subjects receiving IV infusion, which found no measurable effects on heart, liver, kidney, thyroid, or glucose biomarkers (Lee & Burgess, 2025).

The theoretical concern with BPC-157 is its VEGFR2-mediated angiogenesis promotion (Hsieh et al., 2017). Angiogenesis is a hallmark of tumour progression, and no long-term human cancer risk data exists. TB-500 completed a Phase I trial in 40 healthy volunteers with no dose-limiting toxicities (Ruff et al., 2010).

If you are using BPC-157 or TB-500, there is no compound-specific panel to run. Maintain a baseline metabolic and liver panel before starting, and run annual general health checks if using long-term.

The complete testing timeline

Timing matters as much as the markers themselves. Here is a phased testing protocol that covers both SARMs and peptides.

Phase 1: Pre-cycle baseline (2-4 weeks before)

This is the most important blood draw you will do. Every on-cycle and post-cycle result is only interpretable against your personal baseline, not against generic lab reference ranges.

Minimum panel (all users):

• Total testosterone, free testosterone, SHBG
• LH, FSH
• ALT, AST, GGT, bilirubin
• HDL, LDL, triglycerides
• Haematocrit, haemoglobin
• Creatinine, cystatin C

Add for peptide users:

• Fasting glucose, fasting insulin, HbA1c
• IGF-1
• TSH, free T4 (especially for sermorelin/tesamorelin users)

Phase 2: Mid-cycle check (weeks 4-6)

This is when most SARM-induced liver injuries present clinically, typically 4-8 weeks into use. Do not skip this draw.

SARMs users: Repeat liver panel (ALT, AST, GGT, ALP, bilirubin) plus HDL. If liver enzymes are rising, this is your window to catch it before it becomes severe.

Peptide users: Fasting glucose, fasting insulin, IGF-1. Calculate HOMA-IR (fasting glucose in mg/dL x fasting insulin in mIU/L / 405). A HOMA-IR above 2.5 signals developing insulin resistance.

Phase 3: End of cycle / pre-PCT

Draw blood in the final week of your cycle, before starting any PCT compounds. This gives you the maximum-suppression snapshot.

All users: Full hormone panel (testosterone, free T, SHBG, LH, FSH, estradiol), liver panel, lipids, haematocrit.

Phase 4: Recovery confirmation (4-6 weeks post-PCT)

Wait at least 4 weeks after finishing PCT before drawing recovery bloodwork. The LGD-4033 clinical trial showed full hormonal recovery by day 56 (approximately 5 weeks) after cessation of a 21-day, 1 mg/day protocol (Basaria et al., 2013). Recreational doses and longer cycles will take longer.

Target values: LH and FSH within your personal baseline range. Testosterone within 10% of pre-cycle baseline. ALT/AST back to baseline. HDL recovering (lipid recovery typically lags hormonal recovery by several weeks).

For general principles on blood test timing around PED cycles, see: When to Get Bloodwork on TRT: The Complete Timing Guide.

What "normal recovery" actually looks like on bloodwork

Hormonal recovery by suppression tier

Recovery is not instant after stopping SARMs. The HPTA needs time to restart LH and FSH production, which then restarts testosterone synthesis. How long depends on the compound.

Mild suppression (Ostarine, low-dose LGD-4033): LH and FSH reactivate within 2-3 weeks. Testosterone typically returns to baseline in 4-8 weeks without PCT.

Moderate suppression (LGD-4033 at 10+ mg, RAD-140 short cycles): LH recovery takes 3-5 weeks. Full testosterone recovery in 6-10 weeks. PCT with enclomiphene or clomiphene accelerates this by directly stimulating LH and FSH.

Severe suppression (RAD-140 extended cycles, S-23, stacked SARMs): Expect 8-16 weeks for full recovery. LH may take 4-6 weeks to normalize. PCT is strongly recommended. If testosterone remains more than 20% below baseline at 12 weeks post-cycle, see an endocrinologist.

For detailed PCT bloodwork protocols, see: PCT Bloodwork: What to Test and When.

Liver enzyme recovery

The DILI pattern with SARMs is predominantly cholestatic (elevated bilirubin and ALP with moderate transaminase elevation), distinct from the hepatocellular pattern seen with classic oral steroids.

Mild ALT/AST elevations (under 3x upper limit of normal) typically resolve within 4-8 weeks of stopping the compound. Cholestatic presentations with elevated bilirubin can take 2-6 months. The most severe published RAD-140 case took 5 months for bilirubin to normalize.

For a full breakdown of liver enzyme interpretation on PEDs, see: Liver Enzymes on Steroids: A Complete Guide.

Lipid recovery

HDL recovery consistently lags hormonal recovery. Real-world data shows HDL remaining 29.7% below baseline even after testosterone has partially recovered (Joshi et al., 2025). Allow 8-12 weeks post-cycle for lipids to fully normalize. Cardiovascular exercise, omega-3 supplementation, and dietary modifications accelerate HDL recovery.

For lipid management strategies during and after cycles, see: Cholesterol on Steroids: A Complete Guide.

When to worry: action thresholds vs. expected elevations

Not every abnormal result means you need to stop. Here is how to distinguish expected on-cycle changes from genuine red flags.

Liver enzymes

The Hy's Law threshold is non-negotiable. Any combination of transaminases above 3x ULN with bilirubin above 2x ULN (without other causes) predicts serious liver injury and requires immediate medical attention.

Glucose and HbA1c (MK-677 users)

In the two-year MK-677 trial, the clinical protocol reduced the dose from 25 mg to 10 mg when fasting glucose exceeded 140 mg/dL (7.8 mmol/L) (Nass et al., 2008). If you are entering pre-diabetic territory on MK-677, switching to ipamorelin plus CJC-1295 gives you GH stimulation with a fraction of the metabolic cost.

Haematocrit

Peptide-specific haematocrit data does not exist in the peer-reviewed literature. These thresholds are extrapolated from androgen-induced erythrocytosis guidelines (Endocrine Society, ISSAM, and European Association of Urology). IGF-1 and GH both independently stimulate erythropoiesis, so the concern is biologically plausible even without direct evidence.

Practical recommendations

Minimum vs. comprehensive panels

Budget panel (under $100, covers the essentials): Testosterone, LH, ALT, AST, HDL, fasting glucose, HbA1c.

Standard panel ($150-250, recommended for most users): Everything in the budget panel plus free testosterone, SHBG, FSH, estradiol, GGT, bilirubin, LDL, triglycerides, haematocrit, haemoglobin, creatinine, IGF-1.

Comprehensive panel ($300+, for stacked protocols): Everything in the standard panel plus fasting insulin, cystatin C, TSH, free T4, CRP, prolactin.

How to interpret your results

Lab reference ranges are designed for the general population. A 25-year-old bodybuilder at 100 kg of lean mass will have different "normal" values than the average person the range was calibrated against. This is why your personal baseline matters more than the printed reference range.

Exogenous GH and GH secretagogues will push IGF-1 well above the lab reference range. That is the intended effect. The question is whether it is pushed into a range that carries long-term risk. A GH secretagogue safety review notes that long-term cancer incidence data for these compounds does not exist, and that evaluation of cancer risk with sustained IGF-1 elevation remains an open question (Sigalos & Pastuszak, 2017). Epidemiological studies have linked elevated circulating IGF-1 to increased risk of colorectal and prostate cancer. Keep IGF-1 within age-appropriate ranges rather than maximizing it.

For a comprehensive overview of all the markers discussed in this guide, see: The Complete Guide to Blood Work for Bodybuilders.

Key takeaways

• SARMs and peptides affect your bloodwork through completely different mechanisms. SARMs suppress hormones and stress the liver; peptides push the GH/IGF-1 axis and cause insulin resistance. Your panel needs to cover both.
• RAD-140 and LGD-4033 carry real hepatotoxicity risk. Bilirubin is the sentinel marker for SARM-induced cholestatic liver injury, not just ALT/AST.
• MK-677's insulin resistance is dose-dependent and cumulative. Monitor fasting glucose, insulin, and HbA1c. If glucose enters pre-diabetic territory, switch to pulsatile peptides like ipamorelin.
• Test at four time points: pre-cycle baseline, mid-cycle (weeks 4-6), end of cycle, and 4-6 weeks post-PCT.
• Hormonal recovery takes 4-16 weeks depending on the compound and dose. Lipid recovery lags behind hormonal recovery.
• BPC-157 and TB-500 are invisible on standard bloodwork. The monitoring value is in tracking everything else you are stacking them with.
• Your personal baseline is more valuable than any printed reference range. Get bloodwork before you start anything.

---

References

1. Basaria, S., Collins, L., Dillon, E. L., et al. (2013). The safety, pharmacokinetics, and effects of LGD-4033, a novel nonsteroidal oral, selective androgen receptor modulator, in healthy young men. Journals of Gerontology Series A, 68(1), 87-95. PubMed

2. Dalton, J. T., Barnette, K. G., Bohl, C. E., et al. (2011). The selective androgen receptor modulator GTx-024 (enobosarm) improves lean body mass and physical function in healthy elderly men and postmenopausal women. Journal of Cachexia, Sarcopenia and Muscle, 2(3), 153-161. PubMed

3. Joshi, A., Kaune, D. F., Leff, P., et al. (2025). Self-reported side effects associated with selective androgen receptor modulators: social media data analysis. Journal of Medical Internet Research, 27, e65031. PubMed

4. Leciejewska, N., Jedrejko, K., et al. (2024). Selective androgen receptor modulator use and related adverse events including drug-induced liver injury. European Journal of Clinical Pharmacology, 80(3), 371-381. PubMed

5. Leung, K., Yaramada, P., Goyal, P., et al. (2022). RAD-140 drug-induced liver injury. Ochsner Journal, 22(4), 371-374. PubMed

6. Barbara, M., Dhingra, S., & Mindikoglu, A. L. (2020). Ligandrol (LGD-4033)-induced liver injury. ACG Case Reports Journal, 7(6), e00370. PubMed

7. Perananthan, V., & George, J. (2024). Severe liver injury following use of RAD-140. Australian Prescriber, 47(1). PubMed

8. Singam, N. S. V., et al. (2023). Idiosyncratic drug-induced liver injury related to RAD140: a case report. Journal of Medical Case Reports, 17(1), 120. PubMed

9. Bedi, H., et al. (2021). Drug-induced liver injury from enobosarm (Ostarine). ACG Case Reports Journal, 8(1), e00518. PubMed

10. Vignali, J. D., et al. (2023). Systematic review of safety of selective androgen receptor modulators in healthy adults. Journal of Xenobiotics, 13(2), 218-236. PubMed

11. Guo, W., et al. (2022). Effect of selective androgen receptor modulator on cholesterol efflux capacity. Journal of the Endocrine Society, 6(8), bvac099. PubMed

12. Jones, A., et al. (2009). Preclinical characterization of S-23 as a selective androgen receptor modulator for hormonal male contraception. Endocrinology, 150(1), 385-395. PubMed

13. Kanno, Y., et al. (2013). YK11 regulates myogenic differentiation of C2C12 myoblasts by follistatin expression. Biological and Pharmaceutical Bulletin, 36(9), 1460-1465. PubMed

14. Chapman, I. M., et al. (1996). Stimulation of the GH-IGF-I axis by daily oral MK-677 in healthy elderly subjects. Journal of Clinical Endocrinology and Metabolism, 81(12), 4249-4257. PubMed

15. Nass, R., et al. (2008). Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults. Annals of Internal Medicine, 149(9), 601-611. PubMed

16. Raun, K., et al. (1998). Ipamorelin, the first selective growth hormone secretagogue. European Journal of Endocrinology, 139(5), 552-561. PubMed

17. Teichman, S. L., et al. (2006). Prolonged stimulation of growth hormone and IGF-I secretion by CJC-1295 in healthy adults. Journal of Clinical Endocrinology and Metabolism, 91(3), 799-805. PubMed

18. Ionescu, M., & Frohman, L. A. (2006). Pulsatile secretion of growth hormone persists during continuous stimulation by CJC-1295. Journal of Clinical Endocrinology and Metabolism, 91(12), 4792-4797. PubMed

19. Falutz, J., et al. (2007). Metabolic effects of a growth hormone-releasing factor in patients with HIV. New England Journal of Medicine, 357(23), 2359-2370. PubMed

20. Clemmons, D. R., et al. (2017). Safety and metabolic effects of tesamorelin in patients with type 2 diabetes. PLoS One, 12(6), e0179538. PubMed

21. Sigalos, J. T., & Pastuszak, A. W. (2017). The safety and efficacy of growth hormone secretagogues. Sexual Medicine Reviews, 6(1), 45-53. PubMed

22. Hsieh, M. J., et al. (2017). Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation. Journal of Molecular Medicine, 95(3), 323-333. PubMed

23. Lee, E., & Burgess, K. (2025). Safety of intravenous infusion of BPC157 in humans: A pilot study. Alternative Therapies in Health and Medicine, 31(5), 20-24. PubMed

24. Ruff, D., et al. (2010). A randomized, placebo-controlled study of intravenous thymosin beta4 in healthy volunteers. Annals of the New York Academy of Sciences, 1194, 223-229. PubMed

25. Bond, P., et al. (2024). Testosterone therapy-induced erythrocytosis: Can phlebotomy be justified? Endocrine Connections, 13(10), e240283. PubMed