Curated Citations · The Evidence Behind Every Protocol

The literature, in one page.

Every recommendation we make at Limitless rests on published evidence. This is the bibliography. Send it to your physician. Send it to your skeptical brother-in-law. Send it to yourself, before your next visit.

Curated by Joshua Hare, DO · Last reviewed May 5, 2026

Jump to a protocol

Tesamorelin BPC-157 + TB-500 MOTS-c Ipamorelin / CJC-1295 NAD+ Therapy Daily Tadalafil 5 mg Hormone Optimization Regulatory Reference
Visceral Fat · GHRH Analog

Tesamorelin

The only FDA-approved GHRH analog. Selective visceral-fat reduction with lean-mass preservation — a key advantage over GLP-1 monotherapy.

Falutz J. et al. Effects of tesamorelin on visceral adipose tissue in HIV-associated lipodystrophy. NEJM. 2007;357(23):2359–70.

The original phase III trial demonstrating significant VAT reduction with tesamorelin vs. placebo over 26 weeks. Established the responder threshold (≥8% VAT reduction) used in subsequent literature.

View paper →

Stanley TL et al. Effect of Tesamorelin on Visceral Fat and Liver Fat in HIV-Infected Patients With Abdominal Fat Accumulation: A Randomized Clinical Trial. JAMA. 2014;312(4):380–389.

Demonstrated tesamorelin reduces visceral adiposity and liver fat with concurrent improvement in triglycerides — the metabolic-syndrome triad.

View paper →

Adrian S et al. Tesamorelin Improves Fat Quality Independent of Changes in Fat Quantity. J Clin Endocrinol Metab. 2021.

Even when controlling for VAT volume change, tesamorelin therapy improves fat *density* on imaging — that is, the remaining adipose tissue is metabolically healthier. Implications for NAFLD and cardiometabolic risk.

View paper →

Pooled meta-analysis (2026). Tesamorelin: visceral fat and lean body mass — five RCTs. Reviewed in evergreen and nerds.com synthesis publications, 2026.

Pooled across five RCTs: −27.7 cm² VAT, +1.42 kg lean body mass. The lean-mass preservation is the headline finding for clinicians comparing tesamorelin to GLP-1 monotherapy, where lean-mass loss remains a documented concern.

Read the synthesis →
Recovery · Tissue Repair

BPC-157 + TB-500

A vascular and tissue-repair pair. Hundreds of preclinical studies plus emerging human signal in orthopedic sports medicine.

Mayfield CK, Bolia IK, Feingold CL, Lin EH, Liu JN, Hatch GFR, Gamradt SC, Weber AE. Injectable Peptide Therapy: A Primer for Orthopaedic and Sports Medicine Physicians. Am J Sports Med. 2026.

The most current peer-reviewed clinical primer on injectable peptides for musculoskeletal medicine — covers indications, dosing, evidence base, and physician decision-framework. Anchors physician-led peptide prescribing in mainstream sports-medicine literature.

View paper →

Lentini A et al. Emerging Use of BPC-157 in Orthopaedic Sports Medicine. PMC12313605. 2025.

A clinical review summarizing the orthopedic and sports-medicine signal for BPC-157 — tendinopathy, ligament repair, post-surgical recovery — and outlining open evidence gaps.

View paper →

Sikiric P et al. Stable Gastric Pentadecapeptide BPC 157: Novel Therapy in Gastrointestinal Tract. Curr Pharm Des. 2011;17(16):1612–32.

Foundational mechanism paper — vascular, GI-mucosal, and angiogenic effects in preclinical models. Establishes the rationale for the recovery indication.

View paper →

Goldstein AL, Hannappel E, Kleinman HK. Thymosin β4: actin-sequestering protein moonlights to repair injured tissues. Trends Mol Med. 2005;11(9):421–9.

Mechanism review for TB-500 (thymosin β4 active fragment) — actin-binding and tissue-repair signaling. The biology that pairs TB-500 with BPC-157 in clinical recovery protocols.

View paper →
Mitochondrial · AMPK Activation

MOTS-c

A mitochondrial-derived peptide that activates AMPK — the same energy-sensing pathway hit by exercise and metformin. The inside-the-cell complement to NAD+.

Lee C et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443–54.

The discovery paper. MOTS-c is encoded within the mitochondrial 12S rRNA region and acts on AMPK to improve insulin sensitivity, glucose handling, and exercise capacity in murine models.

View paper →

Reynolds JC et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12:470.

MOTS-c levels rise with exercise; supplementation in aged mice extended physical capacity and improved muscle homeostasis. Anchors MOTS-c as a longevity-relevant intervention.

View paper →
Growth Hormone Optimization

Ipamorelin + CJC-1295

A pulsatile GH-secretagogue stack. The pituitary releases its own GH in physiologic patterns — the regulatory feedback loops that prevent excess remain intact.

Raun K et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552–61.

The introductory pharmacology paper. Ipamorelin selectively stimulates GH release without significantly elevating cortisol, prolactin, or ACTH — distinguishing it from earlier secretagogues.

View paper →

Teichman SL et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295. J Clin Endocrinol Metab. 2006;91(3):799–805.

Demonstrated sustained GH/IGF-1 elevation with CJC-1295 administration, with preservation of pulsatile pattern. Foundation for the modern Ipamorelin/CJC-1295 stacking rationale.

View paper →
Longevity · Cellular Energy

NAD+ Therapy

The substrate that powers DNA repair, mitochondrial output, and sirtuin signaling. Levels decline measurably with age. Restoration is the most evidence-based longevity intervention currently available outside lifestyle.

Rajman L, Chwalek K, Sinclair DA. Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metab. 2018;27(3):529–47.

Comprehensive review of NAD+ precursor and substrate strategies — NR, NMN, and direct NAD+ — with the in vivo evidence that anchors the longevity rationale.

View paper →

Yoshino J, Baur JA, Imai SI. NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR. Cell Metab. 2018;27(3):513–28.

The biology of NAD+ decline with age and the therapeutic logic for substrate restoration. Required reading for the patient who wants the mechanism behind the IV.

View paper →
Endothelial · Standing Adult-Male Protocol

Daily Tadalafil 5 mg

FDA-approved for BPH and ED. The unifying mechanism — sustained nitric oxide signaling — extends benefit across cardiovascular, urinary, sexual, exercise-tolerance, and likely cognitive domains.

Roehrborn CG et al. Tadalafil administered once daily for lower urinary tract symptoms secondary to benign prostatic hyperplasia. J Urol. 2008;180(4):1228–34.

The pivotal trial supporting daily tadalafil 5 mg for BPH-LUTS — the indication on which the FDA approval rests.

View paper →

Vlachopoulos C et al. PDE5 inhibitors and the endothelium: a meta-analysis. J Am Coll Cardiol. 2013;62(23):2236–43.

The endothelial-function case for chronic PDE5 inhibition — improvement in flow-mediated dilation across pooled trials. Supports the cardiovascular preventative rationale beyond ED.

View paper →

Public clinical advocacy. Stanford Medicine — Dr. Mike Eisenberg, Head of Male Sexual Health, Department of Urology.

Dr. Eisenberg has publicly recommended daily tadalafil 2.5–5 mg for most men over 40 on the basis of the cross-domain endothelial benefit. Echoed in mainstream longevity media (Andrew Huberman, others).

Read the full Limitless protocol →
Hormone Optimization

BHRT — Standard Anchors

The hormone literature is vast. These are the two papers we most often hand to patients who want the evidence behind functional ranges and TRT.

Bhasin S et al. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018;103(5):1715–44.

The current endocrine society guideline. We use this as the floor; the Limitless protocol layers functional ranges and biomarker monitoring on top.

View paper →

The 2022 Hormone Therapy Position Statement of The North American Menopause Society. Menopause. 2022;29(7):767–94.

Foundation for the perimenopausal/menopausal BHRT framework — estradiol, progesterone, and the modern risk-benefit framing that supports physician-supervised hormone replacement.

View paper →
Regulatory Reference

The 2026 FDA Reclassification

The April 23, 2026 reclassification restored 503A compounding for twelve peptides. The PCAC formal review meeting is July 23–24, 2026.

FDA Pharmacy Compounding Advisory Committee — July 23–24, 2026 Meeting Notice.

Day 1 covers BPC-157, KPV, TB-500, and MOTS-c. Day 2 covers Emideltide (DSIP), Semax, and Epitalon. Public docket FDA-2025-N-6895; comment deadline July 9, 2026.

View FDA notice →

Limitless internal: 503A pharmacy audit checklist and compliance statement.

Our internal sourcing standard, two qualified 503A pharmacy partners on file by 2026-06-01, and the patient-facing compliance statement that documents how we source.

Read the compliance statement →
A standing rule
If a protocol is on a Limitless page, it is on this page. If it is not on this page, it is not on a Limitless page.

Bring this to your visit.

If a question on this page is your question, bring it. If a paper here changes your read, bring that too. The whole point of publishing the bibliography is that you and I can have an evidence-based conversation about your protocol — not a marketing one.

Schedule a Consultation
Note on the citations. All papers are linked to the public PubMed, journal, or PMC abstract page. Citations are summarized for accessibility; readers are encouraged to read the primary source. This page is updated as new evidence accumulates and as the Limitless standing protocols evolve. Curated by Joshua Hare, DO. Last reviewed May 5, 2026.