---
canonical_name: sh-Polypeptide-71
alternate_names: Vasoactive Intestinal Peptide, VIP, sh-Polypeptide-65, Synthetic Human Vasoactive Intestinal Peptide
canonical_topic: sh-Polypeptide-71 for Hair Regrowth
short_topic_lc: sh_polypeptide_71_hair
creation_date: 2026-0708-2106
creator_ai_fullname: Opus 4.8
ep_keywords: Neuropeptides, Growth Factor Peptides, Cosmetic Peptides
---

# sh-Polypeptide-71 for Hair Regrowth

Evidence Review created on 07/08/2026 using [AI4L](https://github.com/forever-healthy/AI4L) / Opus 4.8

**Also known as:** Vasoactive Intestinal Peptide, VIP, sh-Polypeptide-65, Synthetic Human Vasoactive Intestinal Peptide

## Motivation

sh-Polypeptide-71 is a laboratory-made copy of a natural body signal called vasoactive intestinal peptide (VIP). The "sh-" label marks it as a synthetic human version — a short chain of amino acids identical to one the body already makes. Inside the body this signal widens blood vessels and calms inflammation. Cosmetic makers now add it to leave-on scalp serums, usually blended with other synthetic growth signals, hoping to wake resting hair follicles and encourage thicker regrowth.

The molecule was first identified in the gut in the early 1970s and has mostly been studied for its effects on blood flow and immunity. Its move into hair care is recent and rides a broader wave of "growth-factor" and peptide serums sold for thinning hair. The interest rests on a simple idea: if a signal improves blood supply and quiets inflammation elsewhere, perhaps it can do the same around a struggling follicle.

This review examines what is known about sh-Polypeptide-71 for hair regrowth: how it is proposed to work, what the laboratory and human evidence does and does not show, its likely benefits and risks, and the practical questions around the serums containing it. Throughout, it separates marketing claims from tested findings.

**[Benefits](#expected-benefits) - [Risks](#potential-risks--side-effects) - [Protocol](#therapeutic-protocol) - [Conclusion](#conclusion)**

## Recommended Reading

This section lists high-level overview material that discusses the mechanism and therapeutic category most relevant to sh-Polypeptide-71 — the role of nerve signals such as VIP in the hair follicle.

* [Neuroendocrinology of the hair follicle: principles and clinical perspectives](https://pubmed.ncbi.nlm.nih.gov/25066729/) - Paus et al., 2014

  A narrative review of how nerve- and hormone-derived signals, including neuropeptides such as VIP, govern the hair growth cycle. It is the best single high-level overview of the biological category that sh-Polypeptide-71 is marketed to act on.

* [Hair-cycle-associated remodeling of the peptidergic innervation of murine skin, and hair growth modulation by neuropeptides](https://pubmed.ncbi.nlm.nih.gov/11179999/) - Peters et al., 2001

  A primary laboratory study showing that nerve-derived peptides actively push the follicle into or out of its growth phase, with the VIP-family marker mapped across the hair cycle. It illustrates why neuropeptides are plausible — but unpredictable — modulators of hair growth.

* [Sequential expression of glutathione-S-transferase isoenzymes during hair growth phases in mice and their relationship to caldesmon, phosphotyrosinase and VIP receptor protein](https://pubmed.ncbi.nlm.nih.gov/7756742/) - Wollina et al., 1995

  The most VIP-specific hair study available: it maps the VIP receptor to the follicle bulge during the growth phase and proposes that VIP signaling may help end, rather than extend, active growth — an important caution for anyone assuming VIP promotes regrowth.

**Note:** Only three eligible high-quality sources could be found, and all are academic rather than consumer-facing, because sh-Polypeptide-71 is an obscure cosmetic ingredient with no dedicated expert commentary. The list was not padded with product-seller blog posts. No relevant content was found from the priority experts (Rhonda Patrick, Peter Attia, Andrew Huberman, Chris Kresser, Life Extension): searches of their platforms returned general hair-loss and peptide material (e.g., Peter Attia's hair-loss Q&A and Andrew Huberman's hair episode) but nothing addressing sh-Polypeptide-71 or VIP for hair.

## Grokipedia

No dedicated Grokipedia article exists for the cosmetic ingredient "sh-Polypeptide-71". A dedicated article does exist for its underlying molecule:

[Vasoactive intestinal peptide](https://grokipedia.com/page/Vasoactive_intestinal_peptide)

The article covers VIP's structure, its VPAC1/VPAC2 receptors, and its vasodilatory and anti-inflammatory actions, providing background on the molecule that sh-Polypeptide-71 replicates — though it does not address the topical hair-regrowth use.

## Examine

No Examine.com article exists for sh-Polypeptide-71. Examine.com focuses on ingestible dietary supplements and does not cover topical cosmetic peptide ingredients.

## ConsumerLab

No ConsumerLab article or product test exists for sh-Polypeptide-71. ConsumerLab evaluates ingestible supplements and does not cover topical cosmetic peptide ingredients.

## Systematic Reviews

No systematic reviews or meta-analyses for sh-Polypeptide-71 were found on PubMed as of 8 July 2026.

## Mechanism of Action

The proposed mechanisms for sh-Polypeptide-71 in hair are extrapolated from the known biology of VIP; none has been demonstrated for hair regrowth in humans.

* **What it is and how it signals.** sh-Polypeptide-71 is synthetic VIP, a 28-amino-acid peptide belonging to the secretin/glucagon family and closely related to PACAP (pituitary adenylate cyclase-activating polypeptide, a sister signaling peptide). It acts on two receptors, VPAC1 and VPAC2 (the two docking proteins for VIP), which are GPCRs (G protein-coupled receptors — cell-surface switches that trigger internal signaling). Binding raises cyclic AMP (cAMP, an internal messenger that turns on downstream enzymes), which in turn can influence cell survival, blood-vessel tone, and inflammation.

* **Proposed hair-relevant actions.** Three overlapping rationales are put forward. First, VIP is a potent vasodilator, so it is proposed to increase blood supply to the dermal papilla (the vascular cluster at the base of each follicle that feeds hair growth) — the same broad rationale used for minoxidil. Second, VIP is anti-inflammatory and shifts immune activity toward tolerance, which is proposed to calm the low-grade inflammation seen around miniaturizing follicles in androgenetic alopecia (AGA — male- and female-pattern hair loss). Third, its cAMP-driven signaling is proposed to support the activity of follicle keratinocytes and dermal papilla cells.

* **Competing mechanistic view.** The assumption that VIP promotes growth is not settled. Follicle mapping shows the VIP receptor appearing in the growth-phase bulge and has led researchers to propose that VIP signaling may help *terminate* the active growth (anagen) phase rather than prolong it. If correct, topical VIP could in theory shorten rather than extend the growth phase — a direct mechanistic conflict with the marketed benefit.

* **Pharmacological properties.** As a peptide, native VIP has a very short half-life in the bloodstream — on the order of one to two minutes — because it is rapidly broken down by peptidases, including DPP-4 (dipeptidyl peptidase-4, a peptide-degrading enzyme). It is not metabolized by the CYP450 system (cytochrome P450 — the liver's main drug-metabolizing enzymes), so classic drug–drug metabolic interactions are not expected. Selectivity is shared between VPAC1 and VPAC2 (and overlaps with PACAP). Tissue distribution and skin penetration of the intact peptide are poorly characterized; its large size and charge make crossing the outer skin barrier difficult, which is why cosmetic products rely on penetration enhancers, encapsulation, or delivery alongside procedures such as microneedling.

## Historical Context & Evolution

* **Original intended use.** VIP was first isolated from the intestine in the early 1970s and named for its ability to widen blood vessels. Its original scientific interest was as a gut hormone, a nerve signaling molecule, and later a regulator of the immune system. A synthetic version, aviptadil, has been investigated as a medicine for conditions unrelated to hair, such as pulmonary blood-vessel disease and acute lung injury.

* **Why it came to be considered for hair.** The move into hair care is recent and commercial rather than clinical. It grew out of the cosmetic industry's broader adoption of "biomimetic" growth-factor and neuropeptide ingredients — synthetic copies of the body's own signaling molecules — marketed for skin and scalp. Under cosmetic ingredient labeling (INCI — the International Nomenclature of Cosmetic Ingredients), synthetic VIP was designated sh-Polypeptide-65 and later renumbered sh-Polypeptide-71. It is typically sold as one component of multi-peptide scalp serums, on the reasoning that its blood-flow and anti-inflammatory effects might help thinning hair.

* **Standing of the underlying research.** The laboratory findings that connect VIP to hair are genuine but sparse and old, and they point in two directions: some neuropeptides accelerate the growth phase while others suppress it, and the VIP receptor's appearance in the growth-phase follicle has been read as a possible "stop" signal. These findings are not debunked; they are simply preliminary and were never designed to test a topical hair product. The evolution here is one of marketing outpacing evidence: an ingredient entered consumer products before controlled hair studies were done, and that gap has not yet been closed on either side.

## Expected Benefits

The benefits below are framed for risk-aware adults actively trying to preserve or regrow hair. A central caveat applies to all of them: the human evidence that exists is for multi-ingredient growth-factor serums and injectable formulations as a class, and much of it is generated or funded by the cosmetic and aesthetic companies that sell these products — a conflict of interest that should be weighed when reading efficacy claims. No controlled human study isolates sh-Polypeptide-71, so no benefit rises above speculative for this specific ingredient.

### High 🟩 🟩 🟩

No benefits reach this evidence level for sh-Polypeptide-71 as an isolated ingredient for hair regrowth.

### Medium 🟩 🟩

No benefits reach this evidence level for sh-Polypeptide-71 as an isolated ingredient for hair regrowth.

### Low 🟩

No benefits reach this evidence level for sh-Polypeptide-71 as an isolated ingredient for hair regrowth.

### Speculative 🟨

#### Improved Follicle Blood Supply

VIP is a genuine and potent vasodilator, so a topical form is proposed to increase micro-circulation to the dermal papilla and thereby improve the delivery of oxygen and nutrients to growing hair. The mechanism is well established for VIP in general circulation, but there is no measurement of scalp blood flow after topical sh-Polypeptide-71, and it is unknown whether enough intact peptide even reaches the follicle. The basis is mechanistic analogy only.

#### Reduced Follicle Inflammation

VIP dampens inflammation and promotes immune tolerance, which is proposed to ease the low-grade inflammation that surrounds shrinking follicles in pattern hair loss and may contribute to it. This is biologically plausible and consistent with VIP's documented immune effects elsewhere, but it has not been tested in human scalp skin for this ingredient. The basis is mechanistic only.

#### Prolonged Hair Growth Phase ⚠ Conflicted

The marketed premise is that sh-Polypeptide-71 helps follicles re-enter and stay in the active growth phase. The evidence directly conflicts: while some nerve-derived peptides accelerate the growth phase, follicle studies place the VIP receptor in the growth-phase bulge and suggest VIP may instead help *end* active growth. Because the same molecule has been proposed both to support and to terminate growth, the net effect on the human hair cycle is genuinely uncertain, and no controlled data resolve it. The basis is conflicting laboratory findings only.

## Benefit-Modifying Factors

* **Genetic factors:** No pharmacogenetic variants are known to change the response to sh-Polypeptide-71 itself. However, the underlying condition it targets — pattern hair loss — is strongly influenced by androgen-receptor (AR) gene sensitivity, which sets how much a follicle miniaturizes and therefore how much room there is for any topical to help.

* **Baseline biomarker levels:** Correctable contributors to shedding — low iron stores (ferritin), low vitamin D, thyroid imbalance, and zinc deficiency — can cap the visible benefit of any topical. A follicle limited by a nutrient or hormone problem is unlikely to respond well until that problem is addressed.

* **Sex-based differences:** Pattern hair loss differs by sex in distribution and hormonal drivers, and women more often have diffuse thinning with treatable causes. Any benefit is likely to track these differences, though no sex-specific data exist for this ingredient.

* **Pre-existing health conditions:** Scalp conditions such as seborrheic dermatitis or psoriasis, and systemic illness or rapid weight loss, independently drive hair loss and can blunt or mask any effect. Active scalp inflammation may also change how much peptide is absorbed.

* **Age-related considerations:** Older follicles that have miniaturized over many years, including in adults at the upper end of the target age range, have less regenerative capacity, so any speculative benefit is likely smaller with advancing age.

## Potential Risks & Side Effects

The risks below are framed for the target audience. Because sh-Polypeptide-71 is applied topically at low cosmetic concentrations with poor skin penetration, serious harm is unlikely; most concerns are local or theoretical.

### High 🟥 🟥 🟥

No risks reach this evidence level for sh-Polypeptide-71.

### Medium 🟥 🟥

No risks reach this evidence level for sh-Polypeptide-71.

### Low 🟥

#### Application-Site Skin Reactions

The most likely adverse effect is local irritation of the scalp — redness, itching, stinging, or dryness — at the site of application. This is a general property of leave-on cosmetic serums and often reflects the excipients, preservatives, and penetration enhancers in the formula rather than the peptide itself. Reactions are typically mild and reversible on stopping. Evidence is class-level, drawn from the general use of topical peptide and growth-factor serums rather than from studies of this specific ingredient.

**Magnitude:** Not quantified in available studies.

### Speculative 🟨

#### Allergic Contact Sensitization

Peptide ingredients and the carriers they are formulated in can occasionally trigger true allergic contact dermatitis, a delayed immune reaction distinct from simple irritation. It would present as persistent redness, swelling, or a rash that worsens with repeated use. No sensitization data exist for sh-Polypeptide-71 specifically; the concern is inferred from topical cosmetics generally and from isolated reports for other peptide actives.

#### Theoretical Stimulation of Unwanted Cell Growth

A recurring theoretical concern for all topical growth signals is that promoting cell proliferation and new blood-vessel formation could, in principle, encourage the growth of pre-existing abnormal or pre-cancerous skin cells. VIP has trophic and blood-vessel-promoting activity, so the concern applies here in theory. There is no evidence that topical sh-Polypeptide-71 causes this, and skin penetration is low, but the possibility cannot be excluded and warrants caution on damaged or lesion-bearing scalp skin.

#### Systemic Effects from Skin Absorption

If a meaningful amount of intact peptide were absorbed, VIP's systemic actions — blood-vessel widening, flushing, or a drop in blood pressure — could theoretically occur. In practice this is very unlikely because the peptide is large, poorly absorbed through intact skin, and rapidly degraded, so any absorbed fraction would be broken down within minutes. The concern rises only with broken skin or delivery-assisting procedures such as microneedling.

## Risk-Modifying Factors

* **Genetic factors:** No genetic variants are known to change the risk profile of sh-Polypeptide-71. General tendencies toward sensitive skin or atopic (allergy-prone) constitution may raise the chance of irritation or sensitization, but this is not specific to this ingredient.

* **Baseline biomarker levels:** No blood marker is established to predict adverse reactions. Individuals with markers of active skin inflammation or barrier disruption may absorb more peptide and experience more local irritation.

* **Sex-based differences:** No sex-specific safety differences are documented. Pregnancy and breastfeeding — discussed under interactions — are the main sex-related precautions, driven by absent safety data rather than known harm.

* **Pre-existing health conditions:** An inflamed, broken, or diseased scalp (eczema, psoriasis, open lesions) increases absorption and irritation risk. A personal history of scalp skin cancer or pre-cancerous scalp lesions is relevant to the theoretical proliferation concern.

* **Age-related considerations:** Older adults, including those at the upper end of the target range, tend to have thinner, drier, more reactive skin and a higher baseline prevalence of scalp sun damage, which may modestly raise both irritation and the theoretical proliferation concern.

## Key Interactions & Contraindications

* **Prescription topical vasodilators (minoxidil):** Caution — potentially additive. Minoxidil (a blood-pressure drug repurposed as a topical hair treatment) shares the blood-flow rationale, and combining the two could increase local vasodilation and scalp irritation. Separating application timing and monitoring for excess redness or scalp discomfort limits this.

* **Prescription hair drugs (finasteride, dutasteride — 5-alpha-reductase inhibitors):** No known negative interaction and plausibly complementary, since they act on hormones while this peptide is proposed to act on blood flow and inflammation. No mitigation needed beyond routine monitoring.

* **Systemic vasodilators and blood-pressure drugs (sildenafil, nitrates, amlodipine):** Caution in theory only. Meaningful systemic absorption of the peptide is unlikely, but if it occurred, additive vasodilation could contribute to flushing or low blood pressure. Monitoring is warranted where the serum is applied to broken skin or over large areas.

* **Over-the-counter topical retinoids and exfoliants (adapalene, glycolic acid):** Caution — these increase skin permeability and can raise both peptide absorption and irritation. Separating them in the routine or alternating days, with attention to stinging or redness, reduces this.

* **Over-the-counter topical corticosteroids (hydrocortisone):** Monitor — anti-inflammatory creams may blunt or overlap with the peptide's proposed anti-inflammatory action; clinical consequence is minor.

* **Supplement and cosmetic peptide combinations (GHK-Cu copper peptides, other sh-polypeptides):** Caution for cumulative irritation. These are frequently blended in the same serum; the main consequence of stacking is additive scalp irritation rather than a systemic interaction.

* **Additive-effect topicals (minoxidil, niacinamide):** Included because they act on the same blood-flow and anti-inflammatory pathways the peptide targets; using several together increases the chance of local irritation without proven added benefit.

* **Procedural interactions (microneedling, derma-roller, platelet-rich plasma [PRP], low-level laser therapy):** Caution — microneedling and PRP dramatically increase how much peptide and growth-factor signaling reaches the dermis, amplifying both any effect and the theoretical over-stimulation and irritation risks. Low-level laser therapy is complementary with no known negative interaction.

* **Populations who should avoid it:** Absolute avoidance with known hypersensitivity to the peptide or serum excipients, and on broken, inflamed, or lesion-bearing scalp skin. Caution and avoidance is advised in pregnancy and breastfeeding (insufficient safety data), and in anyone with a history of scalp skin cancer or pre-malignant scalp lesions (theoretical growth-signal concern). These are precautionary, driven by absent data rather than demonstrated harm.

## Risk Mitigation Strategies

* **Patch testing before full use:** applying a small amount to a discreet area of scalp or inner forearm for several days before regular use can reveal irritation or allergy early, mitigating application-site reactions and contact sensitization.

* **Application to intact skin only:** keeping the serum off cuts, active dermatitis, sunburn, or freshly microneedled scalp for at least 24 hours limits both excess absorption (systemic effects) and irritation of compromised skin.

* **Introducing one active at a time:** using the serum alone before stacking it with minoxidil, retinoids, or exfoliants allows any reaction to be traced to a single product; this mitigates cumulative irritation and sensitization.

* **Separating timing from permeability-raising products:** keeping retinoids and acids in a different part of the routine (e.g., serum in the morning, retinoid at night) reduces absorption spikes and irritation.

* **Limiting frequency after procedures:** pausing the serum for 24–48 hours after microneedling or PRP avoids amplified delivery, over-stimulation, and irritation of freshly injured skin.

* **Avoidance in defined higher-risk situations:** foregoing use during pregnancy or breastfeeding, or over areas of prior scalp skin cancer or pre-cancerous lesions, mitigates the theoretical proliferation and unknown-safety concerns.

## Therapeutic Protocol

There is no validated clinical protocol for sh-Polypeptide-71; the pattern below reflects how leading cosmetic formulators and hair-focused clinics position multi-peptide scalp serums, alongside conventional and integrative alternatives.

* **Standard cosmetic use:** a few drops of the serum are applied to a clean, dry scalp over thinning areas once or twice daily and massaged in gently. It is a leave-on product and is not rinsed off.

* **Competing approaches.** Conventional hair-loss care leads with proven drugs (minoxidil, finasteride) and does not include this peptide; integrative and aesthetic practitioners position peptide serums as add-ons to minoxidil, microneedling, or platelet-rich plasma. Neither approach is established as superior for this ingredient, and the peptide-serum route rests on far weaker evidence than the drug route.

* **Popularizing sources:** The multi-peptide "growth-factor serum" approach has been popularized largely by cosmetic brands and aesthetic clinics rather than by a single named investigator; no independent expert or clinic has established a signature sh-Polypeptide-71 protocol.

* **Best time of day:** Timing is not evidence-based; morning and/or evening application to a dry scalp is typical. If combined with minoxidil, spacing the two by a couple of hours is commonly advised to limit irritation.

* **Expected half-life:** Native VIP is cleared from the bloodstream within one to two minutes, so any effect depends on how long the formulation keeps the peptide in contact with the skin rather than on lasting circulating levels; this is a core limitation of the approach.

* **Single vs. split dosing:** Because retention is short, products are generally applied once or twice daily rather than as a single dose, on the assumption that repeated contact matters more than a single application.

* **Genetic considerations:** No pharmacogenetic variant is known to guide dosing of this peptide. Variants that drive pattern hair loss (androgen-receptor sensitivity) affect the condition, not the peptide's handling.

* **Sex-based differences:** No sex-specific dosing is established; women with diffuse thinning should first have treatable causes excluded, which influences whether a cosmetic serum is a reasonable choice at all.

* **Age-related considerations:** Older follicles respond less to any stimulus; expectations should be lower for adults at the upper end of the target range, though the application method is unchanged.

* **Baseline biomarker considerations:** Correcting low ferritin, low vitamin D, thyroid imbalance, or low zinc before or alongside use gives any topical its best chance and avoids attributing a nutrient-limited non-response to the product.

* **Pre-existing condition considerations:** Active scalp disease should be treated first, both to improve response and to reduce absorption-related irritation.

## Discontinuation & Cycling

* **Lifelong vs. short-term:** As a cosmetic aimed at an ongoing condition, any effect would require continued use; there is no defined course length and no evidence that a fixed treatment period produces lasting change.

* **Withdrawal effects:** No withdrawal syndrome is known. As with other hair actives, whatever cosmetic benefit accrues is expected to fade gradually after stopping as follicles return to their untreated trajectory.

* **Tapering:** No taper is needed; the product can simply be stopped, since it produces no dependence and no rebound is documented.

* **Cycling:** Cycling has not been studied and is not established as beneficial; there is no mechanistic reason that on-off cycling would maintain efficacy for a topical peptide.

* **Practical framing:** Because benefit is unproven, discontinuation is low-stakes — the main consequence is loss of any cosmetic gain and the cost saved, not a health risk.

## Sourcing and Quality

* **Ingredient identity:** the exact INCI name "sh-Polypeptide-71" appears on the ingredient list; it is almost always one of several peptides in a blend rather than a standalone product, so its position on the list (and thus its concentration) is usually low and undisclosed.

* **Formulation and stability:** peptides degrade with heat, light, and time, so products in opaque, air-restricting packaging (pumps or sealed droppers) with clear storage instructions are preferable; a serum that does not protect its peptides may deliver little intact ingredient.

* **Purity and manufacturing:** Because these are recombinant or synthetic peptides, purity and correct sequence depend on the manufacturer; reputable cosmetic brands that disclose their peptide suppliers and support claims with any testing are preferable to anonymous white-label products.

* **Third-party testing:** Independent verification is uncommon in cosmetics, and there is no established purity certification for this ingredient; in the absence of published data, concentration and "clinically proven" claims warrant skepticism.

* **Reputable sourcing:** No specific brand has independently validated sh-Polypeptide-71 for hair; established cosmetic manufacturers with transparent formulations are preferable to sellers making strong regrowth claims, and compounded or unbranded peptide serums of unknown origin warrant caution.

## Practical Considerations

* **Time to effect:** Hair responds slowly; any cosmetic change would take at least 3–6 months of consistent daily use to become visible, matching the hair cycle, and results may never reach the level of proven drugs.

* **Common pitfalls:** The most common mistakes are expecting drug-level regrowth from a cosmetic, stopping before 3–6 months, using it instead of (rather than alongside) proven options, and not first ruling out treatable causes of shedding.

* **Regulatory status:** sh-Polypeptide-71 is sold as a cosmetic ingredient, not an approved drug; it has not been reviewed by the FDA (U.S. Food and Drug Administration) for hair regrowth, and products may make only limited cosmetic claims. Cosmetic ingredient safety is assessed through bodies such as the CIR (Cosmetic Ingredient Review), not through drug-efficacy trials.

* **Cost and accessibility:** Multi-peptide "growth-factor" serums are typically premium-priced and not covered by insurance; the cost can be substantial over the many months needed to judge any effect, which is a meaningful consideration given the unproven benefit.

* **Setting expectations:** It is best viewed as an experimental cosmetic add-on with a plausible but unproven rationale, not a replacement for evidence-based hair-loss treatment.

## Interaction with Foundational Habits

* **Sleep:** Indirect interaction. VIP is one of the signals in the brain's master clock, and disrupted sleep worsens the stress and inflammation that drive shedding; there is no evidence a topical serum affects sleep, but good sleep supports the follicle environment the product is meant to help.

* **Nutrition:** Indirect, potentiating. Adequate protein, iron, zinc, and vitamin D are prerequisites for hair growth; a nutrient-limited follicle will not respond to any topical, so correcting deficiencies is likely to determine whether the serum can do anything at all. No specific foods interact with the peptide directly.

* **Exercise:** Indirect, potentiating. Regular exercise improves overall circulation and lowers systemic inflammation, complementing the blood-flow and anti-inflammatory rationale of the ingredient; there is no need to time application around workouts, though applying to a sweat-free, clean scalp aids absorption.

* **Stress management:** Indirect. Psychological stress can trigger diffuse shedding (telogen effluvium) and promote scalp inflammation; since the peptide is proposed to act partly by calming inflammation, reducing stress works in the same direction. Affecting cortisol is not an established action of the topical itself.

## Monitoring Protocol & Defining Success

Because sh-Polypeptide-71 is a cosmetic with unproven benefit, monitoring centers on excluding treatable causes of hair loss before starting and on tracking visible change over time. Baseline laboratory testing is used not to dose the peptide but to find and correct contributors to shedding that would otherwise limit any result. Ongoing review is mainly visual, with standardized photographs at baseline, then at 3 months and 6 months, and every 6 months thereafter, since hair change is slow.

* **Baseline testing:** Before starting, standardized scalp/hairline photographs under consistent lighting are taken, and the blood markers below are checked to rule out reversible drivers of hair loss.

* **Ongoing monitoring cadence:** standardized photographs are repeated at 3 months, 6 months, and then every 6 months; any abnormal baseline blood marker is rechecked after it has been treated, typically at 3 months.

| Biomarker | Optimal Functional Range | Why Measure It? | Context/Notes |
|-----------|--------------------------|-----------------|---------------|
| Ferritin | 40–70 ng/mL (women); 50–150 ng/mL (men) | Low iron stores are a common, reversible cause of shedding | Conventional "normal" can start near 15–30 ng/mL, well below the functional target; ferritin also rises with inflammation, so it is best paired with CRP (C-reactive protein, a general inflammation marker) if unclear |
| Vitamin D (25-hydroxyvitamin D) | 40–60 ng/mL | Low vitamin D is linked to hair thinning and poor follicle cycling | Conventional sufficiency is often set at ≥30 ng/mL; no fasting required |
| TSH | 1.0–2.0 mIU/L | Thyroid imbalance is a reversible cause of diffuse hair loss | TSH = thyroid-stimulating hormone; conventional range extends to ~4.5 mIU/L; best drawn in the morning |
| Serum zinc | 90–120 µg/dL | Zinc deficiency can trigger telogen shedding | Best drawn fasting in the morning; interpreted alongside copper, which zinc can deplete |
| DHEA-S and free testosterone | Lab- and sex-specific reference | Screens for hormone-driven pattern loss, especially in women | DHEA-S = dehydroepiandrosterone sulfate; best drawn in the morning, and in the early cycle for menstruating women |

* **Qualitative markers of success:**

* **Reduced shedding:** Fewer hairs lost during washing and brushing, judged consistently over weeks.
* **Visible density and coverage:** Improvement in standardized photographs at the part line and temples rather than day-to-day impressions.
* **Hair quality:** Subjective sense of thicker, stronger, or faster-growing hair.
* **Scalp comfort:** Absence of irritation, redness, or itching, which also signals good tolerability.

## Emerging Research

* **No trials of the specific ingredient:** A search of clinicaltrials.gov returned no registered clinical trials evaluating sh-Polypeptide-71 (synthetic VIP) for hair regrowth as of 8 July 2026. This absence is itself the central research gap: the ingredient is marketed ahead of any registered human hair study.

* **Category-level human evidence (could strengthen the case):** The closest supporting evidence is for injectable growth-factor and biomimetic-polypeptide formulations in pattern hair loss, summarized in a systematic review — [Effectiveness of minimally invasive injectable modalities in the management of androgenetic alopecia among adults — A systematic review](https://pubmed.ncbi.nlm.nih.gov/39176982/) (Kumar et al., 2024) — which reports satisfactory but low-quality evidence for growth-factor formulations. It does not test sh-Polypeptide-71, so it supports the category, not the ingredient.

* **Mechanistic work that could weaken the case:** Follicle mapping placing the VIP receptor in the growth-phase bulge and proposing a growth-terminating role — [Wollina et al., 1995](https://pubmed.ncbi.nlm.nih.gov/7756742/) — points to a direction in which VIP could fail to help or even hinder regrowth. Confirming whether topical VIP extends or shortens the human growth phase is the single most decisive open question.

* **Delivery science:** Because intact VIP penetrates skin poorly and degrades within minutes, future work on encapsulation, stabilized analogs, and procedure-assisted delivery (microneedling) will determine whether enough active peptide can reach the follicle for any effect to be possible; this is a prerequisite for meaningful efficacy trials.

* **Future direction — controlled topical trials:** The field needs randomized, placebo-controlled studies of the isolated ingredient with objective hair-count and density endpoints, since current claims rest on mechanism and multi-ingredient products rather than on evidence for sh-Polypeptide-71 itself.

## Conclusion

sh-Polypeptide-71 is a synthetic copy of vasoactive intestinal peptide, a natural body signal that widens blood vessels and calms inflammation, now sold as a leave-on ingredient in scalp serums for thinning hair. Its case for hair regrowth rests entirely on plausibility: if better blood flow and less inflammation help elsewhere, perhaps they help the follicle. That reasoning is reasonable but untested. No controlled human study has examined this ingredient for hair, and the limited laboratory work is mixed — some of it hints that this signal may help end, rather than extend, the hair's active growth phase. Much of the supporting material comes from the companies that sell these serums, which is a reason for added caution when reading their claims. The likely downsides are modest, mainly scalp irritation, with only theoretical concerns beyond that because so little of the peptide penetrates the skin. Set against proven options, it should be seen as an experimental, premium-priced add-on with an unproven benefit rather than a treatment one can count on. For now, the gap between a plausible rationale and the absence of any direct human evidence is what most defines its place among hair interventions.

**[Top](#top) - [Benefits](#expected-benefits) - [Risks](#potential-risks--side-effects) - [Protocol](#therapeutic-protocol)**


---
canonical_name: Sh-Polypeptide-7
alternate_names: rh-Polypeptide-7, Synthetic Human IGF-1, Recombinant Human Insulin-like Growth Factor 1, IGF-1, IGF-I, Mechano Growth Factor (related splice variant)
canonical_topic: Sh-Polypeptide-7 for Hair Regrowth
short_topic_lc: sh_polypeptide_7_hair
creation_date: 2026-0629-1353
creator_ai_fullname: Opus 4.8
---

# Sh-Polypeptide-7 for Hair Regrowth

Evidence Review created on 06/29/2026 using [AI4L](https://github.com/forever-healthy/AI4L) / Opus 4.8

**Also known as:** rh-Polypeptide-7, Synthetic Human IGF-1, Recombinant Human Insulin-like Growth Factor 1, IGF-1, IGF-I, Mechano Growth Factor (related splice variant)

## Motivation

Sh-Polypeptide-7 is the cosmetic-industry label (INCI name) for a lab-made copy of insulin-like growth factor 1 (IGF-1), a signaling protein the body normally produces. In the hair follicle, this protein is made by the small cluster of cells at the follicle base that act as its control center, and it helps push follicles into and keep them in their active growing phase. Because scalp follicles affected by pattern hair loss appear to make less of this protein, applying a synthetic version directly to the scalp has become a popular idea in peptide-based hair serums and in-clinic treatments.

Interest grew from a simple observation: balding follicles secrete noticeably less of this growth factor than neighboring healthy ones, and the same protein partly explains why the standard drug finasteride works. This made it an attractive target for products promising to "feed" struggling follicles without hormones.

This review examines what is actually known about applying synthetic IGF-1 to the scalp for hair regrowth — the biological rationale, the human and laboratory evidence, the considerable gap between mechanism and proven topical results, the safety questions that surround growth factors, and how it compares with established options.

**[Benefits](#expected-benefits) - [Risks](#potential-risks--side-effects) - [Protocol](#therapeutic-protocol) - [Conclusion](#conclusion)**

## Recommended Reading

This section lists high-quality, high-level overviews of IGF-1 and hair biology from trusted experts and primary literature, selected to give context beyond the marketing claims.

* [The Science of Healthy Hair, Hair Loss and How to Regrow Hair](https://www.hubermanlab.com/episode/the-science-of-healthy-hair-hair-loss-and-how-to-regrow-hair) - Andrew Huberman

  A comprehensive lecture on the biology of hair growth and the mechanical and chemical approaches to slowing loss, including the role of growth factors, blood flow, and follicle stem cells, providing the physiological backdrop against which growth-factor products are positioned.

* [AMA #63: A Guide for Hair Loss — Causes, Treatments, Transplants, and Sex-Specific Considerations](https://peterattiamd.com/ama63/) - Peter Attia

  A practitioner-oriented walkthrough of the evidence tiers for hair-loss interventions, useful for situating unproven growth-factor serums relative to first-line options such as minoxidil and finasteride.

* [How Much Protein Should You Eat? Muscle Growth vs. IGF-1 Longevity Concerns](https://www.foundmyfitness.com/episodes/how-much-protein-should-you-eat-muscle-growth-vs-igf-1-longevity-concerns-rhonda-patrick) - Rhonda Patrick

  A discussion of IGF-1 signaling biology and its double-edged role in growth and aging, which clarifies why raising this growth factor is not automatically benign.

* [Insulin-like Growth Factor 1 (IGF-1) in Hair Regeneration: Mechanistic Pathways and Therapeutic Potential](https://pubmed.ncbi.nlm.nih.gov/41020895/) - Hsieh et al., 2025

  A current narrative review mapping how IGF-1 drives the follicle growth phase through the PI3K/Akt and MAPK/ERK pathways and summarizing the early-stage state of topical delivery, including its limitations.

* [Insulin-like Growth Factor-1: Roles in Androgenetic Alopecia](https://pubmed.ncbi.nlm.nih.gov/24499417/) - Panchaprateep & Asawanonda, 2014

  The primary research letter showing that dermal papilla cells from balding scalp secrete significantly less IGF-1 than non-balding cells, the foundational human finding that motivates the entire therapeutic concept.

*Note: No dedicated content discussing IGF-1, growth factors, or Sh-Polypeptide-7 for hair could be found from two of the prioritized experts — Chris Kresser and Life Extension Magazine — so neither is represented above; the five items shown were selected for direct relevance and depth, with no more than one per source.*

## Grokipedia

No Grokipedia article exists for Sh-Polypeptide-7 (or for synthetic human IGF-1 as a hair-regrowth intervention) as of June 2026.

## Examine

No Examine article exists for Sh-Polypeptide-7. Examine covers orally ingested dietary supplements and does not typically cover topical cosmetic peptide ingredients identified by their INCI (cosmetic-labeling) name.

## ConsumerLab

No ConsumerLab article exists for Sh-Polypeptide-7. ConsumerLab tests ingestible dietary supplements and does not typically cover topical cosmetic peptide ingredients identified by their INCI name.

## Systematic Reviews

This section lists systematic reviews and meta-analyses relevant to growth-factor and regenerative therapies for hair loss, the closest evidence category to topical synthetic IGF-1.

* [The Efficacy of Growth Factor Injection in Androgenic Alopecia: A Systematic Review and Meta-Analysis](https://pubmed.ncbi.nlm.nih.gov/42126441/) - Alali et al., 2026

  Pooling twelve studies (745 patients) of injected growth-factor concentrates and platelet-rich plasma for pattern hair loss, it reports density gains over 12 months but flags high risk of bias, extreme heterogeneity, and non-standardized protocols, judging the evidence hypothesis-generating rather than confirmatory.

* [Regenerative Medicine in the Treatment of Specific Dermatologic Disorders: A Systematic Review of Randomized Controlled Clinical Trials](https://pubmed.ncbi.nlm.nih.gov/38886861/) - Jafarzadeh et al., 2024

  A review of 64 randomized trials (2888 patients) in which androgenetic alopecia was the most-studied condition; growth-factor and platelet-based regenerative methods showed improvement up to 68.4%, but the interventions are injectable concentrates, not standardized single-molecule topical IGF-1.

* [Effectiveness of Minimally Invasive Injectable Modalities in the Management of Androgenetic Alopecia Among Adults — A Systematic Review](https://pubmed.ncbi.nlm.nih.gov/39176982/) - Kumar et al., 2024

  A systematic comparison of injectable modalities including platelet-rich plasma and growth-factor preparations, useful for gauging how isolated growth-factor delivery performs against the broader injectable field.

No systematic review or meta-analysis has yet evaluated Sh-Polypeptide-7 (synthetic human IGF-1) as a standalone topical hair-regrowth ingredient specifically; the reviews above address the adjacent and better-studied category of injected growth-factor and regenerative therapies.

## Mechanism of Action

Sh-Polypeptide-7 is a synthetic, recombinant copy of insulin-like growth factor 1 (IGF-1), a 70-amino-acid protein. Its relevance to hair rests on several converging actions:

* **Anagen induction and maintenance:** In the hair follicle, IGF-1 is produced mainly by dermal papilla cells (the signaling hub at the follicle base) and acts on follicle keratinocytes to drive entry into and prolongation of the anagen (active growth) phase, delaying the regression (catagen) and resting (telogen) phases.

* **Pro-proliferative and anti-apoptotic signaling:** IGF-1 binds the IGF-1 receptor and activates the PI3K/Akt pathway (a master cell-survival and growth cascade — phosphoinositide 3-kinase / protein kinase B) and the MAPK/ERK pathway (mitogen-activated protein kinase / extracellular signal-regulated kinase, which drives cell division). This stimulates keratinocyte proliferation and suppresses programmed cell death in the follicle.

* **Vascular and trophic support:** IGF-1 upregulates VEGF (vascular endothelial growth factor, a signal that builds blood vessels), improving microcirculation and nutrient delivery to the follicle, and its effects are amplified by co-signaling growth factors such as KGF/FGF-7 (keratinocyte growth factor) and PDGF (platelet-derived growth factor).

* **Link to androgen biology:** IGF-1 is partly androgen-regulated. Research indicates that the androgen receptor drives a small regulatory RNA (miR-221) that suppresses IGF-1, and that finasteride's benefit correlates with restored follicular IGF-1 expression — placing IGF-1 downstream of the hormonal cause of pattern hair loss rather than acting on it directly.

Competing mechanistic interpretations exist. The pro-hair view holds that restoring depleted local IGF-1 reactivates dormant follicles. A counter-view, supported by aging biology, holds that chronically elevated skin IGF-1 can instead push hair follicle stem cells into senescence (a dysfunctional, non-dividing state), accelerating follicle aging — so the relationship between IGF-1 level and hair health may be non-linear, with both deficiency and excess being harmful.

**Pharmacological properties (as a topical protein):** Native IGF-1 circulates bound to binding proteins with a complexed half-life of several hours, but free IGF-1 is cleared within minutes. As a large protein, IGF-1 penetrates intact skin poorly, so topical delivery depends heavily on the formulation (liposomal gels, microneedling, or exosome carriers). It is not metabolized by cytochrome P450 enzymes; like other peptides it is broken down by proteases into amino acids. Selectivity is for the IGF-1 receptor, with weaker cross-reactivity at the insulin receptor.

## Historical Context & Evolution

* **Original intended use:** IGF-1 was first characterized as a mediator of growth hormone's effects on body-wide tissue growth; recombinant IGF-1 (mecasermin) was developed as a prescription drug for severe primary IGF-1 deficiency and short stature in children, not for hair.

* **Path to hair optimization:** Dermatology research from the 1990s onward established that IGF-1 is a key positive regulator of the hair cycle. The pivotal human finding came in 2014, when Panchaprateep and Asawanonda showed that dermal papilla cells from balding scalp secrete significantly less IGF-1 than non-balding cells — recasting pattern hair loss partly as a local growth-factor deficiency and motivating the idea of topical replacement.

* **What the historical research actually found:** Animal studies showed exogenous IGF-1 increases follicle number and prolongs anagen; human organ-culture work showed IGF-1 increases the rate at which hair fibers elongate. These are consistent positive signals at the tissue level, distinct from proof that a topically applied serum reaches the follicle and regrows hair in people.

* **Translation into cosmetics:** Because IGF-1 is a prescription biologic when injected systemically, its use in over-the-counter products proceeds under the cosmetic INCI name "Sh-Polypeptide-7" ("sh" = synthetic human), formulated into scalp sprays and serums marketed for hair density rather than as approved drugs.

* **Evolving and unsettled opinion:** The early framing of "more IGF-1 = more hair" has been complicated by 2025 aging-biology findings that excess epidermal IGF-1 can drive follicle stem-cell senescence and hair loss. Rather than overturning the deficiency hypothesis, this suggests the field is moving toward a dose- and context-dependent understanding that is not yet resolved.

## Expected Benefits

A dedicated search of clinical, mechanistic, and expert sources was performed for the complete benefit profile of synthetic/topical IGF-1 in hair. The evidence is dominated by laboratory and injectable-concentrate data; direct evidence for the topical cosmetic ingredient is minimal, which is reflected in the conservative grades below.

### High 🟩 🟩 🟩

(No benefits of topical Sh-Polypeptide-7 meet the High evidence bar, which requires consistent randomized controlled trials or meta-analyses of the specific topical intervention. None exist.)

### Medium 🟩 🟩

(No benefits meet the Medium bar for the specific topical intervention.)

### Low 🟩

#### Promotion and prolongation of the hair growth phase ⚠ Conflicted

IGF-1 is one of the most consistently identified positive regulators of the anagen (growth) phase. In animal models, exogenous IGF-1 increases follicle number and extends anagen, and in human follicle organ culture it increases the hair-fiber elongation rate. The proposed mechanism is PI3K/Akt and MAPK/ERK activation in follicle keratinocytes. The evidence is graded Low because it derives almost entirely from preclinical and ex-vivo models rather than controlled trials of the topical ingredient in people; it is flagged conflicted because aging-biology data indicate excess IGF-1 can instead drive follicle stem-cell senescence and hair loss.

**Magnitude:** In human follicle organ culture, IGF-1 increased fiber elongation to roughly 0.10 mm/day versus about 0.08 mm/day in controls (≈25% relative increase); no validated regrowth magnitude exists for the topical product in humans.

#### Adjunctive density gains within growth-factor / regenerative protocols

When growth factors are delivered as injected concentrates (platelet-rich plasma, growth-factor concentrate) for pattern hair loss, pooled analyses report measurable density and thickness gains, and IGF-1 is one component of these mixtures. This provides indirect support that locally delivered growth-factor signaling can influence hair density. The grade is Low and the relevance is indirect: these are multi-factor injectable preparations, not standardized topical Sh-Polypeptide-7, and the underlying trials carry high risk of bias and extreme heterogeneity.

**Magnitude:** Across pooled injectable growth-factor studies, hair-density increases of roughly 20–57 hairs/cm² over 12 months have been reported, but these are not attributable to topical Sh-Polypeptide-7 specifically.

### Speculative 🟨

#### Replacement of follicular IGF-1 deficiency in pattern hair loss

Because balding-scalp dermal papilla cells secrete less IGF-1 than healthy follicles, topically restoring local IGF-1 is hypothesized to reactivate underperforming follicles. The basis is mechanistic and correlational (the 2014 deficiency finding plus the finasteride–IGF-1 correlation); no controlled human study demonstrates that a topical serum restores follicular IGF-1 or regrows hair, and skin penetration of an intact protein is a major unresolved barrier.

#### Synergy with co-applied growth factors and microneedling

Formulations pair Sh-Polypeptide-7 with other growth factors (VEGF, KGF, PDGF) and with microneedling to enhance delivery, and the combined signaling could plausibly outperform IGF-1 alone. This is supported only by mechanistic reasoning and the broader regenerative-injectable literature, with no isolated evidence for the specific topical combination.

## Benefit-Modifying Factors

* **Androgen status and hormonal cause:** Because pattern hair loss is androgen-driven and IGF-1 sits downstream of androgen receptor signaling, any benefit may be limited if the upstream hormonal driver (dihydrotestosterone activity) is not also addressed; IGF-1 replacement does not block the cause.

* **Genetic polymorphisms (androgen-receptor sensitivity):** The strongest genetic predictor of pattern hair loss is variation in the *AR* gene (androgen receptor, the protein that binds dihydrotestosterone); shorter CAG-repeat lengths increase receptor sensitivity and tend to drive more aggressive miniaturization. Because IGF-1 acts downstream of this receptor, individuals with high-sensitivity AR variants may see less benefit from growth-factor signaling unless the upstream androgen driver is also lowered.

* **Baseline follicular IGF-1 / miniaturization stage:** The deficiency rationale predicts greater potential benefit in follicles that are underperforming but not yet fully miniaturized; long-dormant or scarred follicles are unlikely to respond to growth-factor signaling regardless of dose.

* **Delivery and formulation:** Benefit is gated by whether the intact protein actually reaches the dermal papilla. Liposomal encapsulation, exosome carriers, or microneedling substantially change the realistic benefit relative to a simple topical solution.

* **Sex-based differences:** The foundational deficiency data derive from male balding scalp. Female pattern hair loss has a different hormonal context and a less-defined relationship to follicular IGF-1, so benefit cannot be assumed equivalent across sexes.

* **Age-related considerations:** In older individuals, skin IGF-1 tends to rise with age and has been linked to follicle stem-cell senescence; adding exogenous IGF-1 in this setting may yield diminishing or even counterproductive effects, making age a meaningful modifier at the older end of the target range.

## Potential Risks & Side Effects

A dedicated search of drug-reference, pharmacovigilance, and primary literature was performed for the side-effect profile of IGF-1 and topical growth-factor products. Most documented systemic risks derive from injected/systemic IGF-1; for the topical cosmetic ingredient, the principal concern is theoretical proliferative risk plus formulation-related local effects.

### High 🟥 🟥 🟥

(No risks of topical Sh-Polypeptide-7 meet the High evidence bar from controlled study of the topical ingredient.)

### Medium 🟥 🟥

#### Theoretical proliferative and oncological concern from a growth factor

IGF-1 is a potent mitogen and anti-apoptotic signal, and elevated systemic IGF-1 is epidemiologically associated with increased risk of several cancers. Applying a proliferation-promoting growth factor to skin raises a theoretical concern about stimulating unwanted cell growth, particularly over precancerous lesions or in individuals with a personal cancer history. The evidence is graded Medium because the carcinogenic association of IGF-1 systemically is well established, even though topical penetration and local risk are unproven; this is the most-cited safety argument in the cosmetic-safety literature on growth-factor products.

**Magnitude:** Not quantified in available studies for topical scalp use; systemic epidemiology shows higher-tertile IGF-1 associates with modestly increased risk for certain cancers, but topical exposure magnitude is unknown.

### Low 🟥

#### Local scalp irritation, redness, and folliculitis

As with most scalp serums, the vehicle (preservatives, solubilizers, alcohols) and any accompanying microneedling can cause irritation, redness, itching, or superficial folliculitis. The mechanism is direct local irritation or barrier disruption rather than the peptide itself. The grade is Low because these effects are common to topical scalp products generally and are typically mild and reversible.

**Magnitude:** Not quantified in available studies.

#### Paradoxical follicle aging from IGF-1 excess

Aging-biology research shows that ectopic, elevated epidermal IGF-1 can push hair follicle stem cells into senescence, accelerating graying and hair loss in animal models. This raises the possibility that overdosing local IGF-1 could be counterproductive for hair. The grade is Low for the topical product because the finding comes from transgenic-overexpression and mouse models rather than human topical use.

**Magnitude:** Not quantified in available studies.

### Speculative 🟨

#### Endocrine effects from systemic absorption

If a topical IGF-1 product were absorbed in meaningful quantity, systemic IGF-1 elevation could theoretically affect blood sugar (hypoglycemia) and other endocrine endpoints, as seen with injected IGF-1 therapeutics. This is speculative for cosmetic topicals because intact-protein skin penetration is generally very low and no systemic levels have been demonstrated from such products.

#### Unknown effects of contaminants or mislabeled potency

Because these are unregulated cosmetic products rather than approved biologics, the actual IGF-1 content, activity, and purity may differ from label claims, introducing unquantified risk from degradation products or contaminants. The basis is the general regulatory gap for cosmetic growth-factor products, not specific incident reports.

## Risk-Modifying Factors

* **Personal or family cancer history:** Given IGF-1's mitogenic profile, a personal history of skin or hormone-sensitive cancers, or active precancerous scalp lesions, amplifies the theoretical proliferative concern and is the most relevant risk modifier.

* **Genetic polymorphisms (IGF-1 axis and cancer susceptibility):** Common variants in the *IGF1* gene and its receptor (*IGF1R*) influence circulating IGF-1 levels and signaling strength, and certain alleles are associated with higher baseline IGF-1 or greater cancer susceptibility; individuals carrying high-IGF-1 or proliferation-prone variants are theoretically the least suitable candidates for adding an external growth-factor signal, particularly where systemic absorption is plausible.

* **Baseline IGF-1 and metabolic status:** Individuals with already-high systemic IGF-1 (e.g., acromegaly) or insulin-resistant states represent a context where added IGF-1 signaling is least desirable; baseline metabolic biomarkers are relevant where systemic absorption is plausible.

* **Sex-based differences:** Hormonal milieu differs by sex; women who are pregnant or breastfeeding are routinely advised to avoid growth-factor cosmetics because effects on the fetus or infant are untested.

* **Pre-existing scalp conditions:** Active dermatitis, psoriasis, infection, or a disrupted scalp barrier increases both irritation risk and the likelihood of greater-than-expected absorption.

* **Age-related considerations:** Older adults already exhibit rising skin IGF-1 linked to follicle senescence; adding exogenous growth factor in this group may shift the balance toward the paradoxical-aging risk noted above.

## Key Interactions & Contraindications

* **Topical minoxidil (over-the-counter vasodilator):** Commonly stacked in hair routines. No documented harmful interaction; both increase follicular activity and the combination is additive rather than antagonistic. Severity: caution only. Mitigation: introduce one product at a time to attribute any irritation.

* **5-alpha-reductase inhibitors (finasteride, dutasteride — prescription DHT blockers):** Mechanistically complementary, since these drugs restore follicular IGF-1 by lowering dihydrotestosterone. No adverse interaction is described. Severity: monitor; consequence: potential additive benefit, not harm.

* **Other topical growth factors and peptides (VEGF, KGF/FGF-7, PDGF, copper peptides):** Frequently co-formulated; additive proliferative signaling. Severity: caution. Consequence: amplified local growth-factor load, which is also the basis of the theoretical proliferative concern.

* **Microneedling and other barrier-disrupting procedures:** These deliberately increase penetration, raising both efficacy and systemic-absorption potential. Severity: caution. Mitigation: separate aggressive procedures from application and avoid on broken or infected skin.

* **Retinoids and exfoliating acids on the scalp:** May increase irritation and barrier disruption when layered with a growth-factor serum. Severity: caution; mitigation: time-separate applications.

* **Populations who should avoid this intervention:**

  - Anyone with a current or recent malignancy, especially skin or hormone-sensitive cancers, or active precancerous scalp lesions (theoretical proliferative risk).
  - Pregnant or breastfeeding individuals (untested; growth-factor cosmetics are routinely contraindicated here).
  - People with acromegaly or other states of pathologically elevated IGF-1.
  - Individuals with active scalp infection, open wounds, or uncontrolled inflammatory scalp disease.

## Risk Mitigation Strategies

* **Patch test before scalp-wide use:** Apply a small amount to a limited area for several days to screen for irritation or allergic reaction before broader application, mitigating local irritation, redness, and folliculitis.

* **Avoid use over lesions and in cancer-risk contexts:** Do not apply over moles, precancerous keratoses, or recent surgical sites, and avoid entirely with a personal history of skin or hormone-sensitive cancer, directly addressing the theoretical proliferative/oncological concern.

* **Keep the lowest effective frequency and avoid layering multiple growth factors:** Using a single growth-factor product at the manufacturer's recommended (typically once- or twice-daily) frequency, rather than stacking several, limits total proliferative signaling and the paradoxical follicle-senescence risk.

* **Separate from barrier-disrupting steps:** Apply away from same-session microneedling, retinoids, or acids, and never on broken or infected skin, to limit excess absorption and irritation.

* **Prefer products with transparent sourcing and third-party verification:** Choosing serums from manufacturers that disclose peptide source and provide independent purity/potency testing mitigates the unregulated-cosmetic risk of mislabeled potency or contaminants.

* **Discontinue on adverse signs:** Stopping at the first sign of persistent irritation, new or changing scalp lesions, or unexpected systemic symptoms limits harm from both local and (theoretical) systemic effects.

## Therapeutic Protocol

There is no validated, evidence-based clinical protocol for topical Sh-Polypeptide-7; the points below describe how leading hair-restoration practitioners and product manufacturers typically position growth-factor serums, which remain adjunctive rather than first-line.

* **Standard practitioner positioning:** Hair-restoration physicians (e.g., the approach discussed by Alan Bauman in Peter Attia's hair-loss content) generally treat growth-factor topicals as an add-on to evidence-based first-line therapy (minoxidil, finasteride/dutasteride), not as a replacement, given the weak standalone evidence.

* **Competing approaches without a default:** Two broad strategies coexist — topical application (serums/sprays containing Sh-Polypeptide-7, often with other growth factors) and in-office injectable delivery (platelet-rich plasma or growth-factor concentrate, sometimes with microneedling). The injectable route has more (though still low-quality) clinical data; the topical route is more convenient but faces the protein-penetration barrier. Neither is established as superior for the isolated ingredient.

* **Delivery enhancement:** Because intact IGF-1 penetrates skin poorly, protocols frequently combine the serum with microneedling or use liposomal/exosome carriers to improve follicular delivery; this is the single most important practical variable.

* **Best time of day:** No circadian advantage is established; products are typically applied once or twice daily to a clean, dry scalp consistent with general topical-serum practice.

* **Half-life consideration:** Free IGF-1 is cleared from circulation within minutes and as a protein is rapidly degraded by skin proteases, which is the rationale for repeated daily application and for delivery systems that protect and slowly release the peptide.

* **Single vs. split dosing:** Given rapid local degradation, manufacturers favor twice-daily split application over a single daily dose to sustain follicular exposure.

* **Genetic considerations:** Androgen-receptor sensitivity (the principal genetic driver of pattern hair loss) sits upstream of IGF-1; individuals with strong androgenic miniaturization may need concurrent DHT-lowering therapy for any growth-factor approach to matter.

* **Sex-based differences:** Protocols derived from male-pattern data may not transfer to female pattern hair loss, where the hormonal context and the IGF-1 relationship are less defined; dosing in women is empirical.

* **Age-related considerations:** In older users with already-elevated skin IGF-1, a conservative frequency is reasonable given the senescence concern.

* **Baseline biomarkers:** No specific biomarker gates topical use, but documenting baseline scalp density (global photography, phototrichogram) is the practical way to judge response.

* **Pre-existing conditions:** Active scalp inflammation or infection should be treated before starting, since it alters both response and absorption.

## Discontinuation & Cycling

* **Lifelong vs. short-term:** Like other hair-density interventions, any benefit is presumed to depend on continued use; pattern hair loss is progressive, so stopping is expected to allow gradual return toward the untreated trajectory. No data define a durable post-treatment effect.

* **Withdrawal effects:** No specific withdrawal syndrome is documented for topical IGF-1; the main consequence of stopping is loss of any maintained density over subsequent months, paralleling discontinuation of minoxidil.

* **Tapering:** No tapering protocol is established or necessary; abrupt discontinuation has no known rebound effect beyond loss of effect.

* **Cycling:** No evidence supports cycling for efficacy. A theoretical argument for periodic breaks exists only in the context of limiting cumulative growth-factor exposure given the proliferative and senescence concerns, but this is not data-driven.

* **Practical framing:** Because efficacy itself is unproven, discontinuation decisions are typically driven by lack of visible benefit, cost, or emergence of irritation rather than by a defined schedule.

## Sourcing and Quality

* **Recombinant source and purity:** Sh-Polypeptide-7 is produced by recombinant DNA technology ("sh" denotes synthetic human). Because it is sold as a cosmetic ingredient rather than an approved biologic, manufacturing standards vary; look for disclosure of expression system, purity, and peptide concentration.

* **Third-party testing and stability:** Prefer products that provide independent verification of identity, potency, and absence of contaminants, and that address cold-chain or stability handling, since IGF-1 is a labile protein that degrades with heat and time.

* **Formulation and delivery system:** What to look for is an explicit delivery strategy (liposomal encapsulation, exosome carriers, or paired microneedling), because an unencapsulated protein in a simple solution is unlikely to penetrate to the follicle.

* **Reputable product categories:** Clinic-dispensed growth-factor systems (e.g., KeraFactor-type in-office serums) and established peptide hair sprays (e.g., KERAVIVE-type peptide sprays, Saturday Skin scalp peptide treatments) list Sh-Polypeptide-7 among their ingredients; clinic-channel products generally carry more formulation accountability than anonymous marketplace serums.

* **Realistic expectation of labeled content:** Because potency is unregulated, treat label claims cautiously; the actual active IGF-1 content and bioactivity may differ substantially from what is stated.

## Practical Considerations

* **Time to effect:** Hair interventions generally require 3–6 months of consistent use before any density change is visible, reflecting the hair cycle; there is no validated timeline for topical Sh-Polypeptide-7 specifically.

* **Common pitfalls:** The most common mistakes are expecting a standalone growth-factor serum to match drug therapy, neglecting the delivery problem (applying an intact protein with no penetration strategy), and stacking multiple growth-factor products without regard to cumulative exposure.

* **Regulatory status:** In most markets, Sh-Polypeptide-7 is used in cosmetic products that make appearance claims, not approved drug claims; topical/injected IGF-1 for hair is off-label and unapproved as a therapy. Systemic recombinant IGF-1 (mecasermin) is a regulated prescription drug for unrelated indications.

* **Cost and accessibility:** Growth-factor serums and especially in-office growth-factor or platelet treatments can be substantially more expensive than first-line topical drugs, with uncertain incremental benefit; this cost-to-evidence mismatch is the main accessibility consideration.

## Interaction with Foundational Habits

* **Sleep:** The interaction is indirect. Growth hormone, the upstream driver of systemic IGF-1, is secreted predominantly during deep sleep, so chronic sleep deprivation lowers endogenous IGF-1; while this concerns systemic rather than scalp IGF-1, adequate sleep supports the body's own growth-factor milieu. No direct effect of the topical product on sleep is known.

* **Nutrition:** The interaction is indirect and bidirectional. Protein and overall energy intake regulate endogenous IGF-1 (severe restriction lowers it), and insulin/IGF-1 signaling is linked to dietary carbohydrate and protein load. Practically, very low-protein or severely calorie-restricted diets reduce the body's own IGF-1 environment; no specific food needs to be paired with or avoided around topical application.

* **Exercise:** The interaction is indirect and generally potentiating. Resistance and high-intensity exercise transiently raise systemic and local IGF-1 and improve scalp microcirculation, which is mechanistically aligned with follicular support. There is no need to time topical application around workouts, though applying to a clean scalp after sweating is sensible.

* **Stress management:** The interaction is indirect. Chronic stress elevates cortisol, which can shift follicles toward the resting phase and is associated with stress-related shedding; managing stress supports the hair cycle generally and counteracts a catabolic hormonal state that opposes growth-factor signaling. No direct effect on cortisol from the topical product is established.

## Monitoring Protocol & Defining Success

Because topical Sh-Polypeptide-7 is an unapproved cosmetic intervention with no validated biomarker, monitoring centers on objective hair measures plus screening labs only where systemic IGF-1 exposure or metabolic risk is a concern. Baseline assessment should be performed before starting, with standardized scalp photography documented at the outset.

Ongoing monitoring follows the hair cycle: reassess at roughly 3 months, 6 months, then every 6–12 months, since visible density change requires multiple months. Laboratory monitoring is optional and reserved for individuals where systemic absorption or metabolic status is a consideration.

* Baseline testing is introduced here as a deliberate first step: capture standardized global scalp photographs and, where available, a phototrichogram before any product use, so that later change can be judged objectively rather than by impression.

| Biomarker | Optimal Functional Range | Why Measure It? | Context/Notes |
|-----------|--------------------------|-----------------|---------------|
| Hair density (phototrichogram, hairs/cm²) | Stable or increasing vs. baseline | Objective measure of response | Same scalp region, lighting, and device each visit; reassess at 3, 6, then every 6–12 months |
| Fasting serum IGF-1 (ng/mL) | Age- and sex-adjusted mid-normal range | Screens for systemic elevation if absorption is a concern | Optional; relevant mainly with microneedling-enhanced delivery or pre-existing IGF-1 disorders; draw fasting, morning |
| Fasting glucose / HbA1c | Glucose <90 mg/dL; HbA1c <5.4% | IGF-1 signaling overlaps insulin signaling; screens metabolic context | HbA1c (hemoglobin A1c, a measure of average blood sugar over ~3 months); optional baseline; conventional reference (glucose <100, HbA1c <5.7%) is broader than the functional target shown |
| Ferritin | 40–70 ng/mL (functional target for hair) | Low iron stores independently impair hair growth and confound results | Conventional "normal" extends much lower (>15–30 ng/mL); fasting not required; pairs well with a full iron panel |
| TSH (thyroid-stimulating hormone) | 0.5–2.5 mIU/L (functional) | Thyroid dysfunction is a common, treatable cause of hair shedding that confounds results | Conventional upper limit (~4.0–4.5) is higher; best drawn in the morning, paired with free T4 |

* **Qualitative markers to track:**

  - Reduced daily shedding (hairs on pillow, in shower, on brush)
  - Subjective scalp coverage and styling ease
  - Visible regrowth of short, fine "vellus-to-terminal" hairs at the hairline or part
  - Absence of scalp irritation, redness, or new/changing lesions

## Emerging Research

* **No registered hair-specific trials of Sh-Polypeptide-7:** A search of ClinicalTrials.gov returned no interventional trials evaluating Sh-Polypeptide-7 (synthetic human IGF-1) as a topical hair-regrowth treatment as of June 2026; registry activity around IGF-1 concerns endocrine, oncologic, and growth-disorder indications rather than hair.

* **IGF-1 mimetic peptides as a strengthening direction:** [Self-assembling peptide inspired by insulin and type 1 insulin-like growth factor for the treatment of androgenetic alopecia](https://pubmed.ncbi.nlm.nih.gov/40822304/) (Hu et al., 2025) reports that a small IGF-1-mimetic self-assembling peptide (Ac-GFFY-IGF) promoted hair regrowth more effectively than minoxidil and native IGF-1 in a preclinical model, with better stability and skin permeability — a line of work that could strengthen the case for IGF-1-pathway targeting while sidestepping the delivery limits of the full protein.

* **Mechanistic consolidation:** The 2025 review by [Hsieh et al.](https://pubmed.ncbi.nlm.nih.gov/41020895/) maps remaining gaps in topical IGF-1 delivery (liposomal gels, exosome carriers) and calls for controlled long-term human studies, directly framing where the topical concept must be tested.

* **Aging-biology counter-evidence:** [Targeting IGF1-Induced Cellular Senescence to Rejuvenate Hair Follicle Aging](https://pubmed.ncbi.nlm.nih.gov/40159808/) (Wang et al., 2025) shows that excess epidermal IGF-1 drives follicle stem-cell senescence and hair loss in mice — research that could weaken the "more IGF-1 is better" rationale and reframe optimal dosing.

* **Androgen-pathway mechanism:** [The AR/miR-221/IGF-1 pathway mediates the pathogenesis of androgenetic alopecia](https://pubmed.ncbi.nlm.nih.gov/37496996/) (Li et al., 2023) clarifies how androgens suppress follicular IGF-1, identifying upstream targets (miR-221) that future therapies might address instead of supplementing IGF-1 directly.

* **Future research areas:** The decisive open questions are whether an intact topical protein can reach the dermal papilla in humans, the dose at which benefit turns to senescence-driven harm, and whether randomized controlled trials of standardized Sh-Polypeptide-7 (versus vehicle and versus minoxidil) show real-world regrowth. Until such trials exist, the intervention's standing remains mechanistic and hypothesis-generating.

## Conclusion

Sh-Polypeptide-7 is a lab-made copy of the natural growth factor IGF-1, sold as a cosmetic ingredient in scalp serums and clinic treatments aimed at thinning hair. Its appeal is well-grounded in biology: this growth factor helps keep hair in its active growth phase, balding follicles make less of it, and it sits along the same hormonal pathway that the standard hair-loss drug finasteride works through. Laboratory and animal studies consistently show that adding IGF-1 can lengthen the growth phase and boost follicle activity.

The gap between this promise and proof, however, is wide. There are no controlled human trials of the topical product itself, the related evidence comes from injected growth-factor mixtures of uneven quality, and a large protein like this struggles to penetrate the scalp at all without special delivery methods. Newer aging research adds an important caution: too much of this growth factor may push follicle stem cells into a worn-out state and worsen hair loss, so more is not reliably better. There are also unresolved safety questions, since growth factors encourage cells to multiply and the products are largely unregulated. Overall, the idea is mechanistically reasonable but the human evidence is thin and uncertain, placing this firmly in the experimental category rather than among established options.

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