Hair

The follicle is a miniature organ with its own cycle — growth, regression, rest. Most hair complaints are a cycle problem, not a nutrition problem, which is why it wires to hormonal and vascular nodes rather than to intake alone.

Blocks the hormone that shrinks follicles reduces it.

Androgenetic-alopecia mechanism review 2025, Ann Dermatol — DHT binding the dermal-papilla androgen receptor drives progressive follicular miniaturization (suppressing Wnt/β-catenin and inducing TGF-β), shortening anagen. doi:10.5021/ad.25.042. The sensitivity is local, not systemic — which is why baldness is patterned. Elevated DHT and androgen receptor are named the causal factors for androgenetic alopecia, and three things are simultaneously higher in dermal papilla cells from balding scalp and beard than elsewhere: type II 5-alpha-reductase, androgen receptor, and the AR coactivator HIC-5/ARA55. The same circulating androgen therefore produces follicle loss in one scalp region and beard growth in another, because the receiving tissue differs, not the hormone. doi 10.5021/ad.25.042.

Growth factor increases it.

10.3390/cimb47090773. doi 10.3390/cimb47090773

Reduces scarring reduces it.

Foitzik 2000, FASEB J 14:752 — TGF-β1 is an endogenous inducer of catagen (the follicle regression phase), inhibiting keratinocyte proliferation and triggering apoptosis; this is the catagen signal apigenin down-regulates. PMID 10744631. Mechanism is catagen entry — the growth phase is ended, not slowed. The in-vivo paper is titled 'control of murine hair follicle regression (catagen) by TGF-BETA1 in vivo' (Foitzik 2000). Paired human biopsies: in 15 AGA men, balding frontal follicles showed elevated TGF-beta-1 protein and elevated T-beta-RI and T-beta-RII versus their own non-balding occipital follicles — an internally controlled comparison rather than between-subject. PMID 10744631

Quiets the hair-suppressing prostaglandin reduces it.

Garza 2012, Sci Transl Med 4:126ra34 — prostaglandin D2 inhibits hair growth and is elevated (via PTGDS) in the bald scalp of men with AGA, acting through GPR44; this is the mediator luteolin suppresses. doi:10.1126/scitranslmed.3003122. Prostaglandin D2 synthase (PTGDS) is elevated at both mRNA and protein level in bald scalp compared with haired scalp of the same men with AGA, and PGD2 itself is correspondingly elevated. this is an expression difference between scalp regions — direction of causation is supported by the wider literature on PGD2/GPR44 inhibition of hair growth, but the observation itself is correlative. doi 10.1126/scitranslmed.3003122.

Vessel growth signal increases it.

Yano 2001, J Clin Invest 107:409 — VEGF-driven perifollicular angiogenesis controls hair growth and follicle size; VEGF overexpression accelerates regrowth and thickens hair, its blockade inhibits growth. PMID 11181640

Tissue renewal signaling increases it.

Millar 1999, Dev Biol 207:133 — Wnt/β-catenin signaling is required for hair-follicle growth and structure; it is the pro-anagen dermal-papilla pathway lactoferrin engages and DHT suppresses. Wnt10a and LEF1 are down in balding follicles and the reviews name Wnt/beta-catenin as an explicit target for promoting hair growth. the human evidence here is associative (expression in balding vs non-balding scalp) plus inhibitor experiments in cultured dermal papilla cells (XAV939, SB431542) — not an interventional trial in people.

Follicle oxidative stress reduces it.

Trüeb 2009, Int J Trichology — follicular oxidative stress (ROS) drives dermal-papilla senescence and secretion of hair-growth inhibitors (TGF-β1/2), promoting androgenetic alopecia and graying. PMC2929555

Lowers cortisol reduces it.

Cortisol from HPA-axis activation disrupts the hair-growth cycle and pushes follicles toward premature shedding (Thom 2016, J Drugs Dermatol, PMID 27538002) — the stress root of telogen effluvium and an androgenetic-alopecia aggravator. PMID 27538002

Calms inflammation reduces it.

NF-κB-driven perifollicular microinflammation is an established feature of androgenetic alopecia: the chronic low-grade infiltrate secretes cytokines that shorten anagen and drive follicle miniaturization. doi 10.2147/DDDT.S542000

Cell turnover reduces it.

Confirmed from the primary follicle-biology literature. Catagen is not a failure to grow, it is a program to stop: the regression phase is characterized by programmed apoptosis and follicular shrinkage. TUNEL staining localises it precisely — apoptotic cells appeared in the regressing proximal follicle epithelium, the central inner root sheath, the BULGE/ISTHMUS region and the secondary germ, but never in the dermal papilla. The papilla is spared, which is why the follicle can cycle again. The molecular correlate is specific and negative about the obvious candidates: the apoptosis hot spots correlated largely with down-regulation of the Bcl-2/Bax ratio but only poorly with interleukin-1-beta converting enzyme, p55TNFR and Fas/Apo-1. The death-receptor route is not the one. And it is extrinsically driven: intravital microscopy in live mice shows basal cell apoptosis through synergistic action of TGF-beta and mesenchymal-epithelial interactions, in which the basal epithelial cells ARE not internally committed to death and the dermal papilla induces it. PMID 9403711 · PMC12168304

Blood flow (nitric oxide) increases it.

Androgen-receptor-mediated paracrine signaling, mainly TGF-beta, from dermal papilla cells induces apoptosis of microvascular endothelial cells in the dermal papilla of balding scalp. The androgen does not merely shrink the follicle — it kills the follicle’s blood vessels, causing vascular calcification, degeneration of the microvascular network, and an ischemic and hypoxic pilosebaceous unit that suppresses stem cell activity. Why the conditional matters commercially: the vascular loss is downstream of the androgen, not a parallel cause. Raising scalp perfusion in a follicle whose papilla vasculature has already been apoptotically pruned is treating the effect. The authors put it as a clinical rule: early anti-AR treatment is better than late. And it reinforces itself — microcirculatory dysfunction can induce perifollicular fibrosis, and persistent low perfusion drives follicles into catagen. doi 10.1016/j.jid.2022.01.005 · PMC12380480

Calms body-wide inflammation reduces it.

perifollicular fibrosis in the lower infundibulum and isthmus in approximately 76% of bald scalp samples from AGA patients; moderate to dense perifollicular lymphocytic infiltrates were detected in about 33% of patients, whereas no such inflammation was observed in control subjects. PMC12380480

Antioxidant defense increases it.

H2O2 induced premature catagen and hair growth inhibition, whereas Nrf2 activation significantly ameliorated H2O2-dependent hair growth inhibition. Damage and rescue in the same experimental system is what lifts this above an antioxidant marketing claim. The mechanism is specified: activation of Nrf2 signaling enhances cellular resistance to oxidative damage through induction of antioxidant and cytoprotective enzymes. And there is a second route worth noting because it lands on a node already drawn here: growing evidence demonstrates functional crosstalk between Nrf2-mediated antioxidant defenses and Wnt/BETA-CATENIN signaling — Nrf2 activation can stabilize beta-catenin and enhance expression of its downstream targets. the Wnt → Hair Growth link is drawn, so part of this edge may run through it. Cultured human dermal papilla cells throughout; no in vivo Nrf2 manipulation with hair endpoints was retrieved. PMC10181221

Mitochondrial energy increases it.

The claim: once redox balance is broken, the dermal papilla cells that regulate the formation, proliferation and cyclicity of hair follicles show obvious oxidative stress characteristics such as mitochondrial dysfunction, cell apoptosis, and perifollicular inflammation, which is associated with follicle miniaturization. And it is self-reinforcing: mitochondrial dysfunction in HFDPCs can exacerbate ROS production, creating a vicious cycle that impairs hair follicle regeneration. It names three links already on this pathway in one sentence — mitochondrial dysfunction, apoptosis, and perifollicular inflammation — and the route to the executioner is specified: activation of the TGF-BETA1/SMAD pathway by ROS leads to upregulation of TGF-BETA1 and TGF-BETA2, triggering senescence and damage of dermal papilla cells. Review-level synthesis with a mechanistic chain rather than a single decisive experiment. PMC12913381

It increases Mood.

The alopecia literature agrees that the principal consequence of hair loss is psychological. The evidence is a systematic review and meta-analysis across seven databases: 13 studies, 2,737 AGA patients and 17,382 controls, random-effects pooling with sensitivity analysis and publication-bias assessment. Perceived stress SMD -1.09 (-1.43 to -0.74), p < 0.001. Social anxiety -0.50 (-0.84 to -0.16). Depression -0.38 (-0.65 to -0.12). And the conditional is where the honesty is: general distress was null — SMD -0.01 (-0.39 to 0.37), p = 0.97. A point estimate of essentially zero. The effect is specific to appearance-linked dimensions and disappears when the instrument is generic. Anything claiming hair loss causes general psychological harm is claiming the one thing this meta-analysis measured and did not find. Generalized anxiety sits on the boundary at p = 0.05 with an upper bound of exactly 0.00. Worse in women: depression more common in women than men, greater social anxiety and social phobia, and female pattern hair loss reaches 30-40 percent of women aged 60 to 69 while being discussed far less. Observational and cross-sectional throughout — direction is inferred from the clinical context, not from temporal data. PMC12690262

It reduces Calm under stress.

Drawn separately from the Hair Growth → Mood (Positive Affect) link because the meta-analysis separates them and they behave differently. Social anxiety symptoms: SMD -0.50 (95% CI -0.84 to -0.16), p = 0.004 — solid. Generalized anxiety symptoms: SMD -0.50 (95% CI -0.99 to 0.00), p = 0.05 — same point estimate, half the certainty, upper bound touching zero. The qualitative findings point the same way: greater body image dissatisfaction, somatization and interpersonal sensitivity — all social-evaluative rather than free-floating. That simplification is stated rather than hidden. PMC12690262

It increases Nails.

Drawn from reviews of neighboring outcomes rather than from studies of this outcome itself, which is weaker evidence, and the map marks it so. Sources: doi 10.3390/nu18132141; PMC12673670. doi 10.3390/nu18132141 · PMC12673670

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