Neural controls of human hair growth: Calcitonin gene-related peptide (CGRP) induces catagen

Neural controls of human hair growth: Calcitonin gene-related peptide (CGRP) induces catagen
Department of Dermatology, University of Lübeck, D-23538 Luebeck, Germany; Department of Dermatology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.

J Dermatol Sci 2012 Apr 21.

Calcitonin related-gene peptide (CGRP) induces premature catagen transformation of organ-cultured human scalp hair follicles. (a) Percentage of hair follicles (HFs) in anagen VI, early, mid or late catagen. Note that in the vehicle and phosphoramidon treated groups most HFs are in anagen VI, while in the CGRP treated group the percentage of catagen HFs is greatly increased, and later stages of catagen development have been reached. (b) Hair cycle score (HCS). This score was determined as previously described [4]. After stage determination for each HF (anagen, early catagen, mid catagen, late catagen) anagen VI HFs were arbitrary attributed a score of 100, early catagen – 200, mid catagen – 300 and in late catagen – 400. The sum of scores per group was than divided by the number of investigated HFs. The score thus represents the mean hair cycle stage of all HFs per group. Notice statistically significant higher HCS in the CGRP treated HFs, i.e. it is a catagen inducer.

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Proliferation and apoptosis indices for calcitonin related-gene peptide (CGRP) treated groups compared to controls. (a) Proliferating cells in the hair follicles (HFs) are represented by Ki67 positive (pink) staining. Representative photographs from the vehicle (top), phosphoramidon (middle) and CGRP (bottom) groups. Notice anagen phase HFs with significant cell proliferation in the hair matrix (HM) in the vehicle and phosphoramidon treated HFs. On the contrary, HFs treated with CGRP are in catagen phase with significantly less proliferation in the HM. see (e) for reference areas in the hair bulb. (b) Percentage of Ki-67 positive cells out of all DAPI positive cells. The percentage of proliferating cells is significantly lower in the CGRP treated group compared to control groups. Since terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin Nick end labelling (TUNEL) positive (apoptotic) cells were only rarely documented in the HM of all groups, percentages are not shown. (c) The melanin content of the HFs is documented by the Masson Fontana staining. Representative photographs from the vehicle (top), phosphoramidon (middle) and CGRP (bottom) groups. Notice significant lower melanin content in the CGRP treated group, as those are catagen HFs. (d) Quantitative histomorphometry showing significantly lower melanin content in the CGRP treated group as compared to control. See (f) for reference areas in the hair bulb. (e) Reference area within the hair bulb for the Ki67/TUNEL staining. The white dotted line assigns the Auber's line. In all groups, cells were counted only below that line using the NIH image software cell counter. The white arrow points at a Ki67 positive (pink) cell. (f) Reference areas within the hair bulb for the Masson Fontana staining. White squares assign the measured reference areas in the HM using the NIH image software. Data from one patient (“culture 2”) is shown. n = 5–13 HFs per group; data are mean ± SEM; *P < 0.05, ***P < 0.001, t-test. DP, dermal papilla; HM, hair matrix.

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Caustic, any idea how to avoid this peptide?

angusmojo - One way to look at Calcitonin gene-related peptide (CGRP) is that it is triggered through neurogenic pathways, such as pain or heat signals. For example it is known that cayenne pepper stimulates heat by acting as an TRPV1 agonist. In turn, this increases CGRP and will induce apoptosis in hair follicles.

Like most things, the dose makes a difference, because a small amount of cayenne will actually help stimulate hair growth via activation of CGRP. However, more than a small amount will stimulate too much and cause hair loss.

I should point out that CGRP does not induce neurogenic inflammation. While blocking them can possibly lead to some positive results it isn't efficient and would be better to eliminate the source of the trigger, which is the source of neurogenic inflammation.