IGF-1
Also known as: Insulin-like Growth Factor 1, Somatomedin C, IGF-1 DES, Des(1-3) IGF-1
Lower numbers = closer to natural. Higher numbers = more enhanced.
Why this rating?
IGF-1 is the primary mediator of GH effects. Per PMC studies, it activates the PI3K/Akt/mTOR pathway for muscle protein synthesis and potentially enables hyperplasia (new muscle fiber creation), an effect beyond what steroids alone can achieve. WADA prohibited (S2 category). Creates supraphysiological anabolic effects with risks including hypoglycemia, organ growth, and cancer associations. IGF-1 LR3 (extended half-life) and DES (10x potency) variants are used for bodybuilding. Rated 7 as a potent growth-promoting peptide with significant enhancement potential.
Overview
A 70-amino acid polypeptide hormone that serves as the primary mediator of Growth Hormone effects. The most commonly used variants in bodybuilding are IGF-1 LR3 (extended half-life, systemic effects) and IGF-1 DES (10x potency, localized site enhancement). Works through the PI3K/Akt/mTOR pathway to stimulate muscle protein synthesis and potentially hyperplasia (new muscle fiber creation).
Important Warnings
- •WADA prohibited - will cause positive drug test
- •Do NOT use if personal or family history of cancer
- •Hypoglycemia risk - always have carbs available
- •Stacking IGF-1 with insulin multiplies the hypoglycemia risk - additive glucose-lowering can be life-threatening
- •Organ growth is a real concern with chronic use
- •IGF-1 LR3: NOT effective for site enhancement (too long half-life)
- •IGF-1 DES: MUST inject into target muscle for local effect
- •Bacteriostatic water may degrade IGF-1 within 24-48 hours - acetic acid preferred
- •Never exceed 100 mcg/day without medical supervision
- •Quality varies significantly between sources - research chemical status
Purpose & Use Cases
Systemic Muscle Growth (LR3)
IGF-1 LR3 provides 20-30 hour half-life for overall muscle growth, enhanced recovery, and improved protein synthesis throughout the body.
Site Enhancement (DES)
IGF-1 DES with its 20-30 minute half-life and 10x potency is injected directly into lagging muscle groups for localized growth stimulation.
Hyperplasia Potential
Unlike steroids which only cause hypertrophy (larger fibers), IGF-1 may stimulate satellite cells to create new muscle fibers (hyperplasia).
Recovery Enhancement
Accelerates recovery from training and injury through enhanced protein synthesis and tissue repair.
Benefits
- Stimulates muscle protein synthesis via mTOR pathway
- Potential for hyperplasia (new muscle fiber creation)
- Anti-catabolic effects (inhibits muscle breakdown)
- Does not suppress natural testosterone - no PCT required
- IGF-1 LR3: Long half-life for systemic effects
- IGF-1 DES: 10x potency for targeted site enhancement
- Works synergistically with HGH and steroids
- Enhances recovery from training
Good to Know
LR3 vs DES are two different tools, don't swap them
IGF-1 LR3 has an arginine substitution plus a 13-amino-acid N-terminal extension that cut IGFBP binding roughly 100-fold, giving a ~20-30 hour half-life for systemic, whole-body effects. IGF-1 DES (des(1-3)IGF-1) is truncated: ~5-10x receptor potency but only ~20-30 minute half-life, so it is used for local site injections directly into a target muscle. Using LR3 for site enhancement (too long-acting to stay local) or DES for systemic growth (clears too fast) is a common and pointless mistake.
It is insulin-like. Hypoglycemia is the acute danger
IGF-1 is ~50% structurally homologous to insulin and activates the insulin receptor at higher concentrations, shuttling glucose out of the blood into cells. That means real hypoglycemia risk: shakiness, sweating, confusion, and in the worst case loss of consciousness, sharply worse if injected fasted. Always eat carbs around the dose and keep fast glucose within arm's reach.
Localized 'site enhancement' is debated, not settled
The popular idea that injecting DES into a lagging muscle makes that specific muscle grow is plausible in principle (local IGF-1 activates satellite cells and local protein synthesis in animal models) but is not well demonstrated to produce meaningful spot-growth in humans at these doses. Treat visible site-specific results as largely anecdotal.
The myonuclei / hyperplasia angle (and why it matters for the natty scale)
IGF-1 activates satellite cells that fuse into muscle fibers and add myonuclei, and it may promote hyperplasia (new fibers) rather than just hypertrophy (bigger fibers). Extra myonuclei are the cellular basis of 'muscle memory', so in theory an IGF-1 phase can nudge the long-term natural ceiling upward even after you stop, though robust human hyperplasia evidence is still limited. This is part of why it is rated well above the pure healing peptides.
A growth factor, not a sex hormone
IGF-1 is the main downstream mediator of growth hormone, not an androgen. It does not suppress the HPTA or need PCT on its own. But 'not hormonal' does not mean benign: it grows all tissues, so chronic high-dose use raises concerns about organ growth (visceromegaly / 'GH gut') and, theoretically, acceleration of existing or dormant tumors, since elevated IGF-1 is associated with several cancers.
Dosage Guidelines
| Experience Level | Dosage Range |
|---|---|
| Beginner | 20 – 40 mcg/day |
| Intermediate | 40 – 70 mcg/day |
| Advanced | 70 – 100 mcg/day |
IGF-1 LR3: 20-100 mcg/day, inject SubQ or IM anywhere. IGF-1 DES: 20-80 mcg per injection, must inject IM into target muscle for localized effect. Cycle 4-6 weeks on, equal time off to prevent receptor desensitization. Best timed post-workout when muscle is most receptive. Always have carbs available for potential hypoglycemia. These ranges are community-derived (bodybuilding/research-chemical forum consensus), not clinical dosing guidance; the one published self-report data point (US weightlifters surveyed on IGF-1 use) found a median of ~50-75 mcg/day for a median lifetime duration of 9 weeks, though the authors cautioned self-reported doses may be unreliable.
The ~20 hour base figure is for unmodified rhIGF-1 given subcutaneously in healthy adults; it is shorter (~6h) in GH-receptor-deficient states. The LR3 and DES variants differ by design: LR3 escapes IGFBP binding for a long systemic half-life, while DES clears in minutes for localized use.
Side Effects
Hypoglycemia
commonIGF-1 mimics insulin and increases glucose uptake. Can cause low blood sugar symptoms: shakiness, sweating, confusion, weakness.
Consume carbohydrates before and after injection. Never inject fasted. Have fast-acting glucose available.
Organ Growth (Visceromegaly)
uncommonIGF-1 stimulates growth in ALL tissues, including heart, liver, kidneys, intestines, and lymphoid tissue (tonsils/adenoids, documented in clinical IGF-1 therapy, sometimes causing snoring or sleep apnea). Can contribute to "HGH gut" / Palumboism. May be irreversible with chronic use.
Use conservative doses. Limit cycle length. This is a long-term concern with chronic high-dose use.
Cancer Risk Concerns
rareIGF-1 promotes cell proliferation and inhibits apoptosis. Meta-analyses link higher circulating IGF-1 to increased risk of prostate and premenopausal breast cancer; a colorectal cancer association has also been proposed historically but is less consistent in newer studies. Does not cause cancer but may accelerate growth of existing/dormant tumors.
Do not use if you have personal or family history of cancer. Regular health screenings.
Joint/Muscle Pain
uncommonRapid tissue growth can cause temporary discomfort.
Usually temporary. NSAIDs if needed.
Water Retention
uncommonSodium retention can cause mild bloating.
Reduce sodium intake if problematic.
Headaches / Intracranial Pressure
uncommonIGF-1 (like GH) can raise intracranial pressure, causing headaches and, less commonly, vision changes, nausea, or vomiting. Documented with therapeutic recombinant IGF-1 (mecasermin) and typically resolves with dose reduction.
Stay hydrated. Reduce dose if persistent. Seek medical evaluation if headaches come with vision changes, nausea, or vomiting.
Injection Site Reactions (Lipohypertrophy)
commonRepeated injections at the same spot can cause local fat tissue buildup (lipohypertrophy) at the injection site.
Rotate injection sites.
Receptor Desensitization
commonProlonged use can downregulate IGF-1 receptors, reducing effectiveness.
Cycle 4-6 weeks on, equal time off. IGF-1 DES has lower desensitization risk due to short half-life.
General Mitigation Strategies
Always have fast-acting carbohydrates available for hypoglycemia. Cycle use to prevent receptor desensitization (4-6 weeks on, equal time off). Do not use if history of cancer. IGF-1 LR3 has higher systemic side effect potential; IGF-1 DES has lower systemic effects but must be injected into target muscle. Avoid use within 2 hours of bedtime as it may suppress natural GH release during sleep.
Support Supplements
Ancillary supplements commonly run alongside IGF-1 to manage side effects, support the target tissue, or fill nutrient demands it creates.
Fast-acting carbohydrates / glucose (dextrose, juice, glucose tabs)
KeyDirect countermeasure for hypoglycemia. IGF-1 shares ~50% homology with insulin and drives glucose into cells, so blood sugar can crash, fast carbs both prevent and rescue a hypo. This is the single most important thing to have on hand.
- Dose
- Carbs around each injection; keep 15-20g fast glucose within reach for a hypo (shakiness, sweating, confusion)
- Timing
- Eat carbs before and after the injection. NEVER inject fasted.
- When
- Mandatory, not optional: treat it as core equipment for using IGF-1, not a bonus supplement.
Adequate protein and calories
IGF-1 amplifies protein synthesis; the anabolic signal needs substrate and a caloric surplus (for growth) to translate into tissue.
- Dose
- ~1.6-2.2 g/kg/day protein
- Timing
- Spread across the day
Post Cycle Therapy (PCT)
IGF-1 does not suppress natural testosterone production. No PCT required for IGF-1 alone. However, if stacking with suppressive compounds (steroids), PCT is required for those compounds.
How It Works
IGF-1 binds to IGF-1R receptor, triggering autophosphorylation and activating two major pathways: (1) PI3K/Akt/mTOR for protein synthesis and anti-catabolism, and (2) RAS/MAPK for cell proliferation. It inhibits FoxO transcription factors and suppresses E3 ubiquitin ligases (MuRF1, MAFbx), reducing protein breakdown. Stimulates satellite cell proliferation and myoblast fusion, potentially enabling hyperplasia. IGF-1 LR3 has poor binding to IGFBPs, allowing extended circulation. IGF-1 DES binds the IGF-1R with similar affinity to native IGF-1, but its N-terminal truncation removes the primary IGFBP-binding domain. This loss of IGFBP sequestration (not higher receptor affinity) is what gives it roughly 10x greater bioavailable potency for localized effects.
Fundamentals
Reference on the practices relevant to IGF-1: how they are done and where they go wrong. Not a recommendation to use it.
Common Stacks
- IGF-1 LR3 + HGH - Upstream (HGH) + downstream (IGF-1) growth stimulation
- IGF-1 LR3 + Testosterone - Multiple anabolic pathways
- IGF-1 DES for site enhancement during any cycle
- IGF-1 + Insulin (advanced/dangerous) - Maximum nutrient shuttling
Legal Status
Sold as an unregulated "research chemical" (USA) for bodybuilding use. WADA prohibited (S2 category). The only FDA-approved form (mecasermin/Increlex) is approved solely for severe primary IGF-1 deficiency in children, not for enhancement.
Legal status varies by country and changes over time. This is a general summary, not legal advice.
WADA Status
IGF-1 and all its analogues (including IGF-1 LR3 and IGF-1 DES) fall under WADA's S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) category and have been explicitly prohibited at all times since the original 2003 WADA Code.
References
- PMC - Mechanisms of IGF-1-Mediated Regulation
- PMC - Use of GH, IGF-I, and Insulin for Anabolic Purpose
- Oxford Academic - IGF-1 and Cancer Risk
- PubMed - Pharmacokinetics of rhIGF-I
- Renehan et al. 2004 - IGF-I, IGFBP-3, and Cancer Risk: Systematic Review and Meta-Regression (The Lancet, PMID 15110491)
- DailyMed - INCRELEX (mecasermin) Prescribing Information