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Hair Regrowth and Quality

Hair Regrowth is the goal of either preventing hair loss over time (a condition known as alopecia) or outright stimulating growth, whereas quality refers to enhancing desirable physical properties of the hair.

Our evidence-based analysis on hair regrowth and quality features 34 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
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Research Breakdown on Hair Regrowth and Quality

1Types of Hair Loss

1.1Androgenic Alopecia

Androgenic alopecia is a term used to refer to patterned hair loss starting from the front of the scalp, and working backwards while not significantly affecting the sides of the head; the common term for androgenic alopecia is either 'male pattern hair loss' or a receding hair line.[1] The early stages are associated with thinning of the follicular hair,[2][3] which is thought to be due to less anagen phase relative to telogen phase causing less overall time to grow.

At least in men, androgens are multidirectional regulators of hair growth. While the sides of the head (occipital scalp) and eyebrows/lashes are referred to as androgen insensitive, the frontal and vertex scalp (front and middle) and body hair appeared to be positively regulated;[1] this is evident in androgen insufficiency syndromes, which are not associated with scalp hair loss but a suppression of body hair.[4]

2Hair Growth Cycles



3Positive Regulators of Hair Growth

Positive regulators of hair growth are those that either directly or indirectly (via suppressing negative regulators) promote hair growth and should be sought out during hair growth protocols


Prostaglandins are a subset of eicosanoids, signalling molecules derived from fatty acids of either the omega-3 (fish oil) or omega-6 (arachidonic acid) class. Of these, differing prostaglandins have differing effects on hair growth depending on the receptors they activate.

They are released by the enzyme phospholipase A2 which is expressed on hair follicles.[5] Phospholipase A2per se is neither a positive regulator or negative regulator of hair growth as both eliminating the activity and increasing the activity cause hair loss.[5] This is due to prostaglandins derived from the enzyme being both positive and negative regulators.

Eicosanoids, particularly the prostaglandin classes, appear to be general regulators of hair growth

Prostaglandin E2 (PGE2, of omega-6 origin) is produced locally in a hair follicle[6] and appears to be 2.06-fold higher in the hairy areas of the head of men with androgenic alopecia relative to the balding area.[7] PGE2 does not appear to suppress testosterone production,[8] but there are a class of receptors that respond to both androgens and PGE2 (AKR1C1 to a lesser degree, and both CBR1 and AKR1C3[9] which are expressed in hair follicles[6]) and these receptors, via their posttranslational effects, may mediate hair loss/growth as well.

Interestingly, minoxidil is able to increase PGE2 and this is one of the possible mechanisms underlying its efficacy.[10]

The receptors for PGE2 are numerous, but the two receptors known as EP3 and EP4 have been detected in dermal papillae[11][12] and drugs that act upon these receptors (The PGE2 mimetic Viprostol) can induce hair growth when topically applied[13][14] via increasing anagen phase.[15]

PGE2 signalling through EP3 and EP4 appears to be a positive regulator of hair growth from the omega-3 class

Prostaglandin F2α signalling (of omega-6 origin), via binding to the PGF2α receptor at a concentration of 50-100nM,[16] appears to stimulate hair growth by prolonging anagen phase.[14]

Drugs that mimic PGF2α signalling (Latanoprost) can induce hair growth when topically applied[13][14] via increasing anagen phase.[15] Latanoprost in particular has shown efficacy in primeapes with moderate to advanced levels of androgenic baldness prior to testing, where 500mcg/mL or 0.05% (50mcg/mL barely effective) given at 0.5mL once daily on the frontal scalp (5 days a week) caused 5-10% conversion of vellus hairs to intermediate/terminal hairs,[17] a potency comparable to 5% minoxidil (10% conversion).[18] A subsequent trial in humans using double this dose (0.1% of solution in 50% ethanol; 50µg/L or one drop daily) presenting Hamiltion II-III stages of androgenic hair loss noted that half the group outperformed placebo in hair growth with an average increase (after 22 weeks) of 22% more hair density.[19] The authors made not that this dose is thought to be safe as it is 3.6-fold lower than the dose tolerated well intravenously.

One case study has made note that Latanoprost has repigmented white hair in an older woman using eye drops (the normal pharmaceutical usage of Latanoprost is for glaucoma).[20]

PGF2α signalling via its receptor is a positive regulator of hair growth, and applying agonists of this receptor to the scalp (Latanoprost) can induce hair growth in balded states

3.25-alpha reductase inhibitors

5α-reductase inhibitors (5-AR inhibitors) are molecules that inhibit the conversion of testosterone into its more androgenic metabolite known as dihydrotestosteorne (DHT), with the reference drug being finasteride (Propecia). There are two subsets of 5-AR receptors (type 1 and type 2) with the latter being more prevalent in hair follicles.[21][22] Finasteride is a selective inhibitor of 5-AR type 2 while the pharmaceutical known as Dutasteride is a dual inhibitor.[23][24]

Although both testosterone and DHT can bind to the androgen receptor to induce hair loss, DHT is approximately 5-fold more effective at the level of the hair follicle.[1] As signalling through the androgen receptor either causes hair loss or promotes changes that then induce hair loss, reducing signalling through the androgen receptor is thought to confer a preventative effect (reducing the rate of negative regulators, not inherently a hair growth effect).

DHT is furthermore thought to be a therapeutic target as men with a deficiency of the 5α-reductase enzyme have been reported[25][26] and these men appear to be protected from prostate enlargement and androgenic alopecia later in life.

Inhibiting the 5α-reductase enzyme suppresses DHT (and may elevated testosterone), but overall there is less androgenicity and signalling through the androgen receptor which then reduces the negative effects of androgens on hair growth

Binding of androgens to the receptor promote production of TGFβ1 and 2, which promote telogen and dermal papilla cell senescence.[27][28]

4Negative Regulators of Hair Growth

Negative regulator of hair growth are mechanisms or phenomena that are able to suppress the rate of hair growth, and in a hair growth protocol should be avoided


Prostaglandins are a subset of eicosanoids, signalling molecules derived from fatty acids of either the omega-3 (fish oil) or omega-6 (arachidonic acid) class. Of these, differing prostaglandins have differing effects on hair growth depending on the receptors they activate.

Prostaglandin D2 (PGD2) of omega-6 origin and the enzyme that create it (prostaglandin D2 synthase, which is induced by androgens[29][30]) are 10.8-fold higher in the balding area of men (with androgenic alopecia) relative to the non-balding area of the same scalp.[7] PGD2 is thought to be a prime negative regulator of androgenic hair loss as signalling through its receptor (DP2; also known as GPR44 or CRTh2[31][32]) is able to suppress hair growth by shortening anagen phase and overexpressing the synthetic enzyme induces androgenic hair loss in rodents.[7] The other receptor of PGD2 (PGD2 receptor 1) does not appear to be implicated.[7]

Prostaglandin 15-delta J2 (15-ΔPGJ2) also appears to have suppressive effects.[7]

Selective shifting of prostaglandins of omega-6 origin towards PGD2 is able to promote androgenic alopecia


Cyclooxygenase-2 (COX2) is an enzyme that is induced in response to inflammatory stressors.

Genetically overexpressing COX2 is able to induce hair loss, which is restored with COX2 inhibitors.[33][34]


  1. ^ a b c Kaufman KD. Androgens and alopecia. Mol Cell Endocrinol. (2002)
  2. ^ Price VH. Testosterone metabolism in the skin. A review of its function in androgenetic alopecia, acne vulgaris, and idiopathic hirsutism including recent studies with antiandrogens. Arch Dermatol. (1975)
  3. ^ Whiting DA. Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male pattern androgenetic alopecia. J Am Acad Dermatol. (1993)
  4. ^ Androgen resistance syndromes.
  5. ^ a b Yamamoto K, et al. Hair follicular expression and function of group X secreted phospholipase A2 in mouse skin. J Biol Chem. (2011)
  6. ^ a b Colombe L, et al. Prostaglandin metabolism in human hair follicle. Exp Dermatol. (2007)
  7. ^ a b c d e Garza LA, et al. Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia. Sci Transl Med. (2012)
  8. ^ Chen W, et al. Human sebocytes express prostaglandin E2 receptors EP2 and EP4 but treatment with prostaglandin E2 does not affect testosterone production. Br J Dermatol. (2009)
  9. ^ Bauman DR, Steckelbroeck S, Penning TM. The roles of aldo-keto reductases in steroid hormone action. Drug News Perspect. (2004)
  10. ^ Kvedar JC, Baden HP, Levine L. Selective inhibition by minoxidil of prostacyclin production by cells in culture. Biochem Pharmacol. (1988)
  11. ^ Torii E, et al. Expression of prostaglandin E(2) receptor subtypes in mouse hair follicles. Biochem Biophys Res Commun. (2002)
  12. ^ Müller-Decker K, et al. Expression of cyclooxygenase isozymes during morphogenesis and cycling of pelage hair follicles in mouse skin: precocious onset of the first catagen phase and alopecia upon cyclooxygenase-2 overexpression. J Invest Dermatol. (2003)
  13. ^ a b Roenigk HH Jr. New topical agents for hair growth. Clin Dermatol. (1988)
  14. ^ a b c Johnstone MA, Albert DM. Prostaglandin-induced hair growth. Surv Ophthalmol. (2002)
  15. ^ a b Sasaki S, Hozumi Y, Kondo S. Influence of prostaglandin F2alpha and its analogues on hair regrowth and follicular melanogenesis in a murine model. Exp Dermatol. (2005)
  16. ^ Samuelsson B, et al. Prostaglandins and thromboxanes. Annu Rev Biochem. (1978)
  17. ^ Uno H, et al. Effect of latanoprost on hair growth in the bald scalp of the stump-tailed macacque: a pilot study. Acta Derm Venereol. (2002)
  18. ^ Uno H, Kurata S. Chemical agents and peptides affect hair growth. J Invest Dermatol. (1993)
  19. ^ Blume-Peytavi U, et al. A randomized double-blind placebo-controlled pilot study to assess the efficacy of a 24-week topical treatment by latanoprost 0.1% on hair growth and pigmentation in healthy volunteers with androgenetic alopecia. J Am Acad Dermatol. (2012)
  20. ^ Bellandi S, et al. Repigmentation of hair after latanoprost therapy. J Eur Acad Dermatol Venereol. (2011)
  21. ^ Russell DW, Wilson JD. Steroid 5 alpha-reductase: two genes/two enzymes. Annu Rev Biochem. (1994)
  22. ^ Thigpen AE, et al. Tissue distribution and ontogeny of steroid 5 alpha-reductase isozyme expression. J Clin Invest. (1993)
  23. ^ Kaufman KD, Dawber RP. Finasteride, a Type 2 5alpha-reductase inhibitor, in the treatment of men with androgenetic alopecia. Expert Opin Investig Drugs. (1999)
  24. ^ Arif T, et al. Dutasteride in Androgenetic Alopecia: An Update. Curr Clin Pharmacol. (2017)
  25. ^ Walsh PC, et al. Familial incomplete male pseudohermaphroditism, type 2. Decreased dihydrotestosterone formation in pseudovaginal perineoscrotal hypospadias. N Engl J Med. (1974)
  26. ^ Imperato-McGinley J, et al. Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science. (1974)
  27. ^ Winiarska A, et al. Effect of 5alpha-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells. Skin Pharmacol Physiol. (2006)
  28. ^ Inui S, Itami S. Molecular basis of androgenetic alopecia: From androgen to paracrine mediators through dermal papilla. J Dermatol Sci. (2011)
  29. ^ Zhu H, et al. Expression and regulation of lipocalin-type prostaglandin d synthase in rat testis and epididymis. Biol Reprod. (2004)
  30. ^ Treister NS, et al. Influence of androgens on gene expression in the BALB/c mouse submandibular gland. J Dent Res. (2005)
  31. ^ Nagata K, et al. Selective expression of a novel surface molecule by human Th2 cells in vivo. J Immunol. (1999)
  32. ^ Hirai H, et al. Prostaglandin D2 selectively induces chemotaxis in T helper type 2 cells, eosinophils, and basophils via seven-transmembrane receptor CRTH2. J Exp Med. (2001)
  33. ^ Neufang G, et al. Abnormal differentiation of epidermis in transgenic mice constitutively expressing cyclooxygenase-2 in skin. Proc Natl Acad Sci U S A. (2001)
  34. ^ Bol DK, et al. Cyclooxygenase-2 overexpression in the skin of transgenic mice results in suppression of tumor development. Cancer Res. (2002)