Can Products That Stimulate Vascular Endothelial Growth Factor (VEGF) Improve Blood Flow to Hair Follicles?

When we begin to lose hair, one of the first ideas we encounter is that “poor circulation” is the problem. From there, it is a short leap to products that claim to stimulate Vascular Endothelial Growth Factor, commonly known as VEGF. If VEGF builds blood vessels, and hair follicles need blood, then stimulating VEGF should improve hair growth. That logic is attractive. But does the science support it?

To answer this properly, we need to understand what VEGF actually does, whether blood flow is truly impaired in common hair loss, and whether increasing VEGF meaningfully changes long-term outcomes.

What VEGF Actually Is and Why It Matters

VEGF is a signaling protein that regulates angiogenesis, the formation of new blood vessels from existing ones. Angiogenesis is a tightly controlled biological process essential for wound healing, embryonic development, and tissue repair. According to the National Institutes of Health, VEGF binds to specific receptors on endothelial cells, which are the cells lining blood vessels. Once activated, these cells proliferate and form new capillaries.

Hair follicles are metabolically active mini-organs. During the anagen phase, the active growth phase of the hair cycle, follicles require oxygen and nutrients delivered by capillaries in the surrounding dermal papilla. VEGF expression naturally increases during anagen and declines during telogen, the resting phase. This pattern suggests VEGF participates in normal hair cycling. However, association does not prove causation. The fact that VEGF increases during growth does not automatically mean artificially increasing VEGF will override the biological mechanisms driving hair loss.

Experimental Evidence: What Happens When VEGF Is Increased?

One of the most cited studies examining VEGF and hair growth was conducted by Yano, Brown, and Detmar in 2001. This research, published in The Journal of Clinical Investigation, used genetically modified mice engineered to overexpress VEGF in their skin. The investigators assessed hair growth visually and examined skin samples under microscopy to quantify blood vessel density around follicles. The mice showed increased perifollicular vascularization and accelerated hair regrowth compared to control mice. The study followed animals across hair cycles and evaluated tissue histologically.

The critical limitation is obvious: this was an animal model with genetic overexpression. Overexpressing VEGF in mice through genetic engineering is not equivalent to applying a topical cosmetic product in humans. Animal hair cycles are also shorter and biologically different from human scalp hair cycles. Therefore, while the study demonstrated that VEGF can enhance vascular networks around follicles, it did not establish that topical VEGF stimulation reverses human androgenetic alopecia.

Is Blood Flow Actually Reduced in Pattern Hair Loss?

Before assuming that increasing VEGF will help, we must ask whether reduced blood supply is the primary problem.

Goldman and colleagues in 1997 examined scalp biopsy specimens from men with androgenetic alopecia. Using histological analysis, they compared vascularization around miniaturized follicles with that of non-miniaturized follicles. They observed reduced perifollicular vascular structures in miniaturized follicles. However, the study was observational and cross-sectional. It did not measure blood flow in living tissue, nor did it determine whether reduced vascularization caused miniaturization or resulted from it.

This distinction is crucial. In androgenetic alopecia, dihydrotestosterone, or DHT, binds to androgen receptors in genetically susceptible follicles. This hormonal interaction shortens the anagen phase and progressively shrinks follicles in a process called miniaturization. As follicles shrink, their metabolic demand decreases. It is biologically plausible that blood supply decreases secondarily because the follicle requires fewer nutrients.

In other words, reduced vascularization may be a consequence rather than a cause of hair loss.

Minoxidil: A VEGF-Modulating Drug with Regulatory Approval

Minoxidil is the only widely used hair loss treatment with strong evidence of VEGF upregulation. Originally developed as an oral antihypertensive drug due to its vasodilatory effects, it was later formulated as a topical treatment and approved by the U.S. Food and Drug Administration for androgenetic alopecia.

Lachgar and colleagues in 2002 investigated the effects of minoxidil on cultured human dermal papilla cells. Dermal papilla cells regulate hair growth signaling. In this in vitro study, VEGF expression was measured after exposure to minoxidil using molecular assays. The researchers observed increased VEGF production. The limitation is that cell culture models cannot replicate the complex environment of living scalp tissue, including immune interactions and hormonal signaling.

Human evidence is more clinically relevant. While minoxidil consistently demonstrates modest increases in hair density in controlled trials, these trials do not isolate VEGF as the sole mechanism. Minoxidil also opens potassium channels, prolongs anagen duration, and may influence prostaglandin signaling. Therefore, even in the case of an FDA-approved drug, VEGF stimulation appears to be one mechanism among several, not a standalone solution.

Microneedling and Platelet-Rich Plasma: Indirect VEGF Stimulation

Microneedling induces controlled micro-injury to the scalp. Tissue injury triggers wound healing pathways, including growth factor release. In a 2013 randomized evaluator-blinded study, Dhurat and colleagues compared minoxidil alone with minoxidil plus weekly microneedling in 100 men over 12 weeks. Hair counts were assessed using standardized photography and dermoscopy. The combination group showed greater increases in hair count.

The study’s strength lies in its randomized design and objective evaluation method. However, the duration was only 12 weeks, relatively short for hair growth studies, and VEGF levels were not directly measured in participants. The proposed mechanism involves growth factor induction, including VEGF, but this was inferred rather than directly quantified.

Platelet-rich plasma contains multiple growth factors, including VEGF. However, PRP preparation methods vary widely between studies. While several small clinical trials report improvement in hair density, methodological inconsistencies, small sample sizes, and short follow-up periods limit definitive conclusions. Regulatory agencies have not approved PRP as a standardized treatment for androgenetic alopecia.

The Safety Dimension of VEGF Stimulation

VEGF is not a benign growth signal. It plays a role in tumor angiogenesis, which is the formation of blood vessels that supply tumors. For this reason, oncology treatments often aim to block VEGF activity. This does not mean topical hair treatments are carcinogenic, but it underscores that VEGF is part of a tightly regulated biological system. Artificially increasing VEGF in a controlled, localized manner may enhance follicular blood supply. However, long-term data evaluating sustained VEGF stimulation in the scalp are limited. The body regulates angiogenesis carefully for a reason.

What Do We Actually Need to Know?

If we are evaluating VEGF-stimulating products critically, several points become clear. First, VEGF plays a legitimate biological role in supporting hair follicles during growth phases. Second, increasing VEGF can increase perifollicular vascularization in animal models. Third, in humans, the best evidence comes indirectly through minoxidil, which modestly improves hair density and increases VEGF expression.

However, androgenetic alopecia is primarily a hormonally driven condition. DHT-mediated miniaturization remains the central mechanism. Increasing blood supply does not remove DHT sensitivity. Therefore, VEGF stimulation may improve the follicular environment but does not address the underlying hormonal trigger. If we are considering VEGF-targeted approaches, we must understand that they may support growth but are unlikely to reverse advanced miniaturization without concurrent hormonal management.

user experiences

Within the Tressless community, discussions about VEGF are rarely isolated from broader treatment strategies. Users frequently report visible thickening with consistent minoxidil use, which aligns with laboratory findings of increased VEGF expression. Many also describe improved outcomes when microneedling is combined with topical therapies.

At the same time, experienced members often emphasize that blood flow alone does not halt progression. Reports repeatedly note that without addressing DHT through medications such as finasteride or dutasteride, improvements may plateau or regress. Community sentiment tends to reflect what controlled studies suggest: VEGF stimulation may enhance results but is rarely sufficient on its own.

Conclusion

Products that stimulate VEGF can improve blood flow around hair follicles. Experimental animal data and in vitro human cell studies support this biological effect. Clinical evidence, particularly from minoxidil use, suggests that VEGF upregulation contributes to modest hair density improvements.

However, the available research does not support the idea that VEGF stimulation alone reverses androgenetic alopecia. Reduced blood flow appears more likely to be a secondary feature of follicle miniaturization rather than the primary cause. Therefore, while VEGF-stimulating approaches may enhance the follicular environment, they do not replace therapies targeting hormonal drivers.

Understanding this distinction is essential before investing in products marketed primarily on circulation claims.

References

Dhurat, R., Sukesh, M., Avhad, G., Dandale, A., Pal, A., & Pund, P. (2013). A randomized evaluator blinded study of effect of microneedling in androgenetic alopecia. International Journal of Trichology, 5(1), 6–11. https://pubmed.ncbi.nlm.nih.gov/23960389/

Goldman, B. E., et al. (1997). Vascular changes in androgenetic alopecia. Dermatology, 195(2), 123–128. https://pubmed.ncbi.nlm.nih.gov/9406824/

Lachgar, S., Charveron, M., Gall, Y., & Bonafé, J. L. (2002). Minoxidil upregulates the expression of vascular endothelial growth factor in human hair dermal papilla cells. Journal of Investigative Dermatology, 119(2), 345–350. https://pubmed.ncbi.nlm.nih.gov/12174053/

National Institutes of Health. (n.d.). Vascular endothelial growth factor (VEGF) overview. https://www.nih.gov/

U.S. Food and Drug Administration. (n.d.). Minoxidil topical solution information. https://www.fda.gov/

Yano, K., Brown, L. F., & Detmar, M. (2001). Control of hair growth and follicle size by VEGF-mediated angiogenesis. Journal of Clinical Investigation, 107(4), 409–417. https://pubmed.ncbi.nlm.nih.gov/11181642/

Tressless community discussions on VEGF and hair growth. (n.d.). https://tressless.com/