Adrenalin Gray Hair ? Patterns Unfolding?

Drareg

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Feb 18, 2016
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4,772
I know we have some threads on grey hair already, I was hoping this could be specific to grey/gray hair in relation to excess adrenalin possible being a cause.
Many other things have been implicated in other threads but nobody seems to have had much success thus far in reversal. Research is conflicting showing many ways reversal has occurred,T3 in some cases, reducing hydrogen peroxide in others,rescuing serotonin/tryptophan etc.

Hopefully this thread will allow more patterns to be formed with plenty of speculation.

I know specific genes are not the answer but it's interesting to use them as guides.
IRF4 gene Is latest craze for grey hair solution.

IRF4 is a key thermogenic transcriptional partner of PGC-1α.

IRF4 is a key thermogenic transcriptional partner of PGC-1α. - PubMed - NCBI
Does this imply adrenalin ?


Vitiligo treatment reversed grey hair in some, it was involved with catalse enzyme.
https://www.sciencedaily.com/releases/2013/05/130503132958.htm

C) CATECHOLAMINE IN PIGMENTARY DISORDERS.
Production of the essential cofactor for catecholamines, 6-BH4, is enhanced in lesional and nonlesional skin of vitiligo, leading to the accumulation of the oxidized 6-BH4. This metabolite is toxic to melanocytes in culture (665). High levels of 6-BH4 also lead to upregulation of TH levels (505), perhaps explaining the higher levels of catecholamines in patients with vitiligo in both their skin and plasma (665). Expression of β2-adrenoreceptors in epidermal melanocytes obtained from vitiligo skin may be higher than in healthy controls. Epidermal cells from vitiligo patients also express higher levels of COMT activity (411). COMT is involved in the metabolism of epinephrine, norepinephrine, and dopamine and also prevents the formation of toxic o-quinones during melanin synthesis in melanocytes (765). Indeed, methylation of the melanin precursor molecule DHI by COMT prevents its further incorporation into melanin. Melanocyte “autodestruction” by intermediates of melanin metabolism has been implicated in the etiology of vitiligo (411, 740).

This is implying An excess of dopamine is not always good. Increased ROS. May play a role in vitiligo.

A) DOPAMINE AND MELANOGENESIS.

The specific dopamine receptor D2 agonist (LY 171555) has been reported to inhibit hair follicular melanogenesis in pubertal (eumelanic phase) C3H-HeAvy mice (88); the decrease in tyrosinase activity was reversed by treatment with the D2 receptor antagonists sulpiride. However, no inhibition of hair follicular melanogenesis was observed in adult (pheomelanic phase) mice. Thus different control mechanisms may be operative during periods of eumelanin and pheomelanin synthesis.

Tyrosinase oxidizes dopamine to produce melanin via dopamine quinone (485), although dopamine quinone itself can in turn inactivate tyrosine hydoxylase (908). Dopamine excess generates reactive oxygen species and is associated with toxic effects on catecholaminergic cell lines (396). Viability of the cells is reduced if tyrosinase activity is selectively inhibited by phenylthiourea or 5-hydroxyindole (25, 271). Idiopathic Parkinson's disease is associated with massive cell death in the dopamine-derived neuromelanin-pigmented tyrosinase-positive substantia nigra (281, 826). Indeed, there is a direct correlation between cell loss and percentage of neuromelanin-pigmented neurons remaining in this region with greater relative sparing of nonpigmented than of neuromelanin-pigmented neurons.

The D1B receptor has been implicated in modulating phagocytosis by retinal pigment epithelium while the D4 receptor is thought to be involved in the inhibition of melatonin synthesis in photoreceptors (508). Moreover, movement of photoreceptor cells and migration of melanin granules in retinal pigment epithelial cells as well as synthesis of melatonin in photoreceptors are mediated by D2 receptors (679). Dopamine treatment results in dispersion of black and red pigments within chromatophores in the crab Gecarcinus lateralis, which could be blocked by the dopamine antagonist haloperidol (459).

B) DOPAMINE AND MELANOCYTE DISORDERS.
In vitiliginous skin sections, both epinephrine and dopamine can enhance melanogenesis in dendritic but not in nondendritic melanocytes, suggesting variable responsitivity in melanocytes of different differentiation states (327). D1 receptor mRNA has been demonstrated in mouse melanoma cells, but not in human metastatic melanoma cells (66). Similarly, D2 receptor mRNA was not detected in melanoma cells, and all metastases were receptor negative by immunohistochemistry (67). Thus antitumor effects against melanoma cells are probably mediated by toxic products of dopamine oxidation (888). Because of their cytotoxicity, dopamine and their metabolites may play a role in pathogenesis of vitiligo (135, 495).


Adenosine which stops adrenalin response has been shown to increase hair growth. I haven't found anything on grey hair with it yet.

Does anyone know if DHEA effects adrenalin in any way?
Any thoughts?
 

AlexanderCPPR

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Nov 23, 2019
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Nothing clear in your theory, to be honest, adrenalin is what most if not all guys who do extreme sports, have.

Yet, just some have grey hair
 
M

member 2106

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I have been in a high-adrenaline state (severe anxiety) for about three months, and my hair has become greyer than ever. The growth has also slowed dramatically. I think there could be something in your theory.
 

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