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Creative Touch Permanent Makeup and Aesthetics

Insulin-like growth factor 1

Protein Growth Factor

Insulin-Like Growth Factor 1 (IGF-1) occupies an unusually central position in and hair biology. It is simultaneously a survival and proliferation signal, a migration stimulus, a -protective ECM factor, and the primary growth factor whose output is reduced in cells in . Its decline with age, driven by two distinct molecular mechanisms, compounds into the impaired regenerative capacity that distinguishes older skin and compromised from younger counterparts. And its interaction with , DHT, and means it sits at the intersection of the hormonal picture that runs through much of the skin and hair knowledge base.

Insulin-like growth factor 1 is a 70- with structural homology to , signalling through the IGF-1 receptor (IGF-1R) – a receptor tyrosine kinase expressed on keratinocytes, dermal fibroblasts, dermal papilla cells, and endothelial cells throughout the skin. [9] In skin, IGF-1 is produced primarily by dermal fibroblasts and secreted in a paracrine fashion toward the , establishing a dermal-to-epidermal IGF-1 axis that supports keratinocyte homeostasis as a routine maintenance function rather than only a wound response. [2] It is also present in alpha granules and released on , making it part of the acute growth factor payload in iPRF and PRP.

IGF-1 activates two primary downstream pathways: PI3K/Akt, which drives fibroblast survival, proliferation, and collagen production; and MAPK/ERK, which supports keratinocyte migration and proliferation. [7] Both pathways decline with age, but through distinct mechanisms that are worth understanding separately.

IGF-1 Decline in Ageing Skin: Two Distinct Mechanisms

The age-related reduction in IGF-1 signalling in skin is not a single process. Two independent mechanisms have been identified that converge on the same outcome: reduced PI3K/Akt activity, impaired fibroblast proliferation, and progressive ECM degradation.

The first is oxidative: age-associated superoxide anion accumulation in fibroblasts directly deregulates the IGF-1 PI3K/Akt pathway, reducing its signalling output independently of IGF-1 ligand availability. [13] The pathway is intact but less responsive to the same stimulus as accumulated oxidative damage impairs the intracellular signalling cascade. The second is transcriptional: age-associated increases in the transcription factor JunB inhibit IGF-1 promoter activation, reducing the amount of IGF-1 produced by fibroblasts and the downstream levels of PI3K/Akt effectors available to support stem cell maintenance and ECM production. [13]

Together, these mechanisms mean that aged is simultaneously producing less IGF-1 and responding less efficiently to the IGF-1 it does produce; a compounding deficit that cannot be fully addressed by exogenous IGF-1 delivery alone, though delivery through meaningfully compensates for the ligand depletion component.

An important calibration note: whilst acute and physiological IGF-1 signalling supports fibroblast proliferation and , prolonged treatment of primary human skin fibroblasts with IGF-1 in vitro has been shown to induce premature senescence. [13] The implication is that IGF-1’s regenerative benefits operate at physiological, intermittent delivery levels – the kind that iPRF provides through fibrin-mediated sustained release over days – rather than through chronic supraphysiological exposure. This nuance reinforces the treatment series logic over continuous daily IGF-1 stimulation.

The “Dual-Hit” of Ageing on IGF-1

MechanismType of DamageBiological ResultTreatment Solution
OxidativeIntracellular (ROS)PI3K/Akt pathway becomes “deaf” to signals.Polynucleotides (reduce ROS/Inflammation).
TranscriptionalGenetic (JunB)Fibroblasts produce less IGF-1 ligand.iPRF (direct ligand delivery).
SynergisticCombined DeficitStalled repair and ECM thinning.The “Creative Touch” Protocol.

IGF-1’s Roles in Skin Maintenance and Repair

IGF-1’s functional contributions to skin biology are broader than any single mechanism:

  • Fibroblast proliferation and survival: IGF-1 supports dermal fibroblast proliferation through PI3K/Akt and protects against apoptosis, maintaining the fibroblast population density that collagen and ECM synthesis depend on [7]
  • Collagen production: IGF-1 directly stimulates collagen synthesis in fibroblasts, and increases production of biglycan and , the small leucine-rich proteoglycans that stabilise collagen fibrils and protect the ECM from degradation [7]
  • Keratinocyte migration and re-epithelialisation: IGF-1 stimulates keratinocyte migration and proliferation during wound healing, including in irradiation-damaged keratinocytes where other growth factor responses may be impaired [10]
  • Wound contraction: in combination with IGF binding protein 1, IGF-1 promotes fibroblast-embedded collagen gel contraction, contributing to wound closure [2]
  • synthesis: IGF-1 stimulates hyaluronic acid production in normal adult skin cells, contributing to ECM hydration and tissue turgor during repair [2]
  • Epidermal homeostasis: IGF-1R signalling maintains normal epidermal and barrier function as a baseline function, not only in response to injury

The aged wound IGF-1 deficit is measurable and clinically significant: in patients undergoing orthopaedic surgery, plasma and wound fluid IGF-1 levels were 25–70% lower in aged patients than younger ones across all postoperative measurement days, correlating directly with delayed wound healing outcomes. [2]

IGF-1 and Oestrogen: A Hormone Interaction That Matters

The oestrogen–IGF-1 relationship in skin adds an important layer to the post-menopausal skin picture. Oestrogen signals through IGF-1 receptors in various tissues, and IGF-1 and oestrogen have overlapping effects on dermal fibroblast collagen synthesis and epidermal thickness maintenance. The 30% increase in dermal thickness produced by one year of oral oestrogen therapy in post-menopausal women [11] is partly mediated through IGF-1R signalling pathways, meaning that at menopause reduces not only direct oestrogen receptor-mediated collagen stimulation but also attenuates IGF-1 receptor signalling in the same fibroblast population. The two deficits compound rather than simply add.

For post-menopausal clients, this IGF-1/oestrogen interaction means that exogenous IGF-1 delivery through iPRF is addressing one part of a multi-mechanism deficit: supporting the PI3K/Akt fibroblast axis that oestrogen withdrawal has partially silenced, alongside the direct oestrogen receptor deficit that topical oestrogen or HRT would address through a different receptor pathway.

IGF-1 in Hair Follicles: AGA and the DPC Connection

IGF-1 has a particularly well-evidenced and clinically direct role in hair follicle biology that goes beyond general growth factor support. Dermal papilla cells are both producers and receivers of IGF-1, using it as an autocrine signal for their own maintenance alongside the paracrine role that supports hair follicle keratinocyte proliferation and promotion. [12]

In androgenetic alopecia, DPCs from balding follicles secrete significantly less IGF-1 than DPCs from non-balding follicles on the same scalp, establishing IGF-1 downregulation as a direct mechanistic contributor to follicle miniaturisation rather than simply a correlate of it. [8] The mechanism connecting to IGF-1 depletion in DPCs has been partially characterised: androgen receptor activation upregulates miR-221, a microRNA that suppresses IGF-1 expression in DPCs, creating a direct molecular pathway from DHT binding to reduced IGF-1 output, shorter anagen cycles, and progressive follicle regression. Restoring IGF-1 in this model rescued DPC proliferation and rescued hair growth, directly confirming IGF-1’s causal role rather than coincidental association.

IGF-1 also promotes expression in hair follicles, enhancing the perifollicular angiogenesis that metabolically active anagen follicles depend on. [4] This creates a connection between declining DPC IGF-1 output in AGA and the concurrent reduction in perifollicular vasculature that miniaturising follicles experience. The vascular support deficit and the growth factor deficit are partially the same event viewed from different angles.

Interestingly, minoxidil – the most widely used topical treatment – promotes hair growth in part through increasing perifolicular IGF-1 signalling alongside its better-known vasodilatory mechanism. This places iPRF-delivered IGF-1 and topical minoxidil on a partially overlapping mechanistic track: both augmenting a signal that DHT-suppressed DPCs are producing inadequately, through different delivery routes.

IGF-1 in the Hair Follicle (The AGA Deficit)

FactorInfluence on DPCOutcome for Hair
DHTUpregulates miR-221.Suppresses IGF-1 production.
IGF-1High in non-balding scalp.Supports Anagen and VEGF output.
MinoxidilIncreases IGF-1 signalling.Vasodilation + Anagen promotion.
iPRFDirect IGF-1 Supplementation.Rescues DPC proliferation from DHT suppression.
Published
Updated

Clinical Application

IGF-1 is relevant across more of the Creative Touch portfolio than its usual framing as “a growth factor in iPRF” suggests, and one of the most clinically significant relationships involves a treatment where IGF-1 isn’t delivered at all, but is restored by the treatment itself.

Microneedling, RF microneedling, and thulium laser: restoring endogenous IGF-1

The most striking finding in the IGF-1 and treatment literature is that controlled wounding therapies – , dermabrasion, and fractional laser resurfacing – restore IGF-1/IGF-1R signalling in aged skin by reversing geriatric fibroblast senescence. [1] At three months post-microneedling, mRNA levels of both collagen I and IGF-1 were measurably increased in previously treated skin, not because IGF-1 was delivered, but because the controlled wounding response reset the senescent fibroblast population toward a more regenerative phenotype that produces more IGF-1 itself. [1]

This reframes how and thulium laser work at the deeper biological level. Beyond stimulating the wound healing cascade that produces collagen through TGF-β1, these treatments are partially restoring the IGF-1 production capacity that aged and photodamaged skin has lost; improving the tissue’s own maintenance signalling rather than simply triggering a repair response. That distinction matters for understanding why a course of RF microneedling produces skin that is progressively more responsive to subsequent treatments: the tissue environment is not just being stimulated, it is being partially rejuvenated at the fibroblast population level.

Applying iPRF alongside RF microneedling or post-thulium laser treatment combines endogenous IGF-1 restoration from the wounding response with exogenous IGF-1 delivery from the platelet payload. Both arriving at the same tissue at the same time, through complementary routes.

iPRF and PRP: direct delivery with synergistic payload

iPRF delivers IGF-1 directly from platelet alpha granules into the treatment zone through fibrin-mediated sustained release – providing the ligand that aged tissue is producing inadequately, to receptors that retain the capacity to respond. [2] But the most important thing about iPRF’s IGF-1 is not what it does alone buts what it does alongside PDGF. The 1986 PNAS wound study established that and IGF-1 together produced a 2.4-fold increase in newly formed connective tissue and a 95% increase in epidermal thickness, whilst neither growth factor alone produced significant morphological change. [6] The synergy is inherent to iPRF’s combined payload, and it is part of why iPRF outperforms single growth factor preparations. The individual components are less important than the coordinated multi-signal environment the full payload creates.

Polynucleotides: improving the environment IGF-1 signals into

don’t deliver IGF-1 and there is no evidence they directly upregulate it. What they do is address the MMP-driven ECM fragmentation and inflammatory cytokine environment that impairs IGF-1 receptor signalling efficiency in damaged tissue. [5] The oxidative impairment of PI3K/Akt signalling described in the full description above – one of the two mechanisms through which aged skin’s IGF-1 responsiveness declines – is partly driven by the chronic low-grade inflammatory environment that polynucleotides moderate. Reducing that inflammatory burden doesn’t directly restore IGF-1 production, but it improves the intracellular signalling environment that IGF-1’s PI3K/Akt pathway operates within, meaning the same IGF-1 signal, delivered through iPRF after polynucleotides have modulated the tissue environment, encounters better downstream signalling conditions than it would in untreated inflammatory tissue.

This is the same environment-first logic that applies across PDGF, , and in the treatment sequencing rationale. Polynucleotides don’t replace iPRF’s IGF-1 delivery; they make the tissue more capable of acting on it.

Red light therapy: independent pathway, genuinely complementary

therapy’s relationship to IGF-1 is distinct. It doesn’t deliver or directly upregulate it, but it modulates the downstream fibroblast signalling pathways that overlap with IGF-1R activation. At therapeutic doses, photobiomodulation drives procollagen secretion and reduces expression in human fibroblasts through cytochrome c oxidase-mediated mitochondrial activation – a route that activates some of the same fibroblast outcomes as IGF-1 but through a completely independent receptor pathway. [3] This makes LED therapy genuinely complementary rather than redundant with IGF-1 delivery: where iPRF provides the ligand to an IGF-1R-mediated signalling cascade, LED therapy stimulates overlapping fibroblast activity through a pathway that doesn’t require IGF-1R at all. This is particularly useful where receptor-level responsiveness is impaired by the oxidative PI3K/Akt deregulation of aged skin.

Hair treatment: AGA, GLP-1 effluvium, and the post-menopausal combined presentation

For AGA clients, iPRF scalp treatment delivers IGF-1 to the dermal papilla zone in follicles where DPCs have reduced their own IGF-1 output through the DHT→AR→miR-221 suppression pathway. This is not blocking DHT (finasteride does that) but supplementing a specific signal that DHT has suppressed, supporting DPC survival and perifollicular vascularisation through a parallel route. For clients already using minoxidil, there is partial mechanistic overlap on the IGF-1 axis since minoxidil also enhances perifolicular IGF-1 signalling, making iPRF a complementary rather than competing approach on this dimension.

For following -driven weight loss, the IGF-1 picture adds a second suppression mechanism beyond the GAS6/cortisol pathway. Significant reduces systemic IGF-1 levels, creating a dual DPC deficit where both the cortisol-suppressed output and the caloric restriction-suppressed IGF-1 are withdrawn simultaneously. iPRF treatment timed to the recovery phase, once weight loss has stabilised, supports both aspects of DPC restoration through the same payload.

For post-menopausal women presenting with concurrent hair thinning and skin quality concerns – which is more common than it might appear, given that both involve overlapping IGF-1 deficits alongside oestrogen decline – iPRF addresses shared mechanistic ground in both tissues simultaneously. The same growth factor signal that DPCs need for anagen maintenance is the one dermal fibroblasts need for collagen synthesis and ECM stabilisation. The treatment is addressing the same deficit in two different tissue contexts at once.

The Portfolio “IGF-1 Axis”

TreatmentRelationship to IGF-1Clinical Pairing
iPRFDirect sustained delivery of IGF-1 ligand.RF Microneedling (Reboots receptors + supplies ligand).
RF MicroneedlingResets “Geriatric Fibroblasts” to produce own IGF-1.Thulium Laser (Endogenous IGF-1 reboot).
Oestrogen (HRT)Potentiates IGF-1R sensitivity in the skin.iPRF (Addresses the menopausal skin “gap”).
PolynucleotidesImproves signalling environment by reducing ROS.iPRF (Clears ROS to unblock PI3K/Akt).

Clinical Note: While we acknowledge the significant role of systemic hormones like Oestrogen in maintaining skin density and IGF-1 sensitivity, Creative Touch does not prescribe HRT or hormonal treatments. We focus on the regenerative application of growth factors and polynucleotides to support skin health within the context of these biological changes. For hormonal management, we recommend consulting a specialist or GP.

References

  1. Frommeyer TC, Rohan CA, Spandau DF, et al. (2021). Wounding Therapies for Prevention of Photocarcinogenesis. Front Oncol, 11, 813132 .

  2. Garoufalia Z, Papadopetraki A, Karatza E, et al. (2021). Insulin-like growth factor-I and wound healing, a potential answer to non-healing wounds: A systematic review of the literature and future perspectives. Biomed Rep, 15(2), 66 .

  3. Hernández-Bule ML, Naharro-Rodríguez J, Bacci S, et al. (2024). Unlocking the Power of Light on the Skin: A Comprehensive Review on Photobiomodulation. Int J Mol Sci, 25(8) .

  4. Hsieh WJ, Qiu WY, Percec I, et al. (2025). Insulin-like Growth Factor 1 (IGF-1) in Hair Regeneration: Mechanistic Pathways and Therapeutic Potential. Curr Issues Mol Biol, 47(9) .

  5. Kwon TR, Han SW, Kim JH, et al. (2019). Polydeoxyribonucleotides Improve Diabetic Wound Healing in Mouse Animal Model for Experimental Validation. Ann Dermatol, 31(4), 403-413 .

  6. Lynch SE, Nixon JC, Colvin RB, et al. (1987). Role of platelet-derived growth factor in wound healing: synergistic effects with other growth factors. Proc Natl Acad Sci U S A, 84(21), 7696-700 .

  7. Nan L, Guo P, Hui W, et al. (2025). Recent advances in dermal fibroblast senescence and skin aging: unraveling mechanisms and pioneering therapeutic strategies. Front Pharmacol, 16, 1592596 .

  8. Panchaprateep R, Asawanonda P (2014). Insulin-like growth factor-1: roles in androgenetic alopecia. Exp Dermatol, 23(3), 216-8 .

  9. Sadagurski M, Yakar S, Weingarten G, et al. (2006). Insulin-like growth factor 1 receptor signaling regulates skin development and inhibits skin keratinocyte differentiation. Mol Cell Biol, 26(7), 2675-87 .

  10. Stadelmann N, Horch RE, Schmid R, et al. (2025). Growth factors IGF-1 and KGF and adipose-derived stem cells promote migration and viability of primary human keratinocytes in an in vitro wound model. Front Med (Lausanne), 12, 1516116 .

  11. Thornton MJ (2013). Estrogens and aging skin. Dermatoendocrinol, 5(2), 264-70 .

  12. Trüeb RM (2018). Further Clinical Evidence for the Effect of IGF-1 on Hair Growth and Alopecia. Skin Appendage Disord, 4(2), 90-95 .

  13. Zhang J, Yu H, Man MQ, et al. (2024). Aging in the dermis: Fibroblast senescence and its significance. Aging Cell, 23(2), e14054 .

Also Known As

  • IGF
  • IGF-1
  • IGF1
  • insulin like growth factor 1

Biological Relationships

Biological Interactions

  • Stimulates
  • Stimulates

Influenced By

  • this Interacts with
  • this Produced by
  • this Required by
  • this Required by

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