- Reaction score
- 3,025
Just a followup regarding the study @bridgeburn posted. Here is the most pertinent excerpt that explains how mast cells play a role in male hair loss, and thus how antihistamines (which deactivate them) can help:
Although androgens are primarily responsible for MPHL [14, 15, 22], the implication of microscopic inflammation in the pathogenesis of MPHL was also suggested from several studies [17, 19, 26, 28]. Sueki, et al. analyzed MC infiltration quantitatively and the ultra-structures of alopecic scalp areas, and suggested that micro-inflammation probably accelerates MPHL by inducing aberrant fibrosis [26].
Mast cells are well known to play a critical role in allergic diseases and to be implicated in inflammatory disorders [24]. In addition, mast cell accumulations are often observed in fibrotic disorders of the skin, e.g., keloid, systemic sclerosis, and during wound healing [9, 18, 21, 23, 30]. The effects of activated mast cells on dermal fibroblast proliferation and collagen and glycosaminoglycans synthesis have been well demonstrated [1, 2]. Moreover, it has also been suggested that mediators and enzymes of mast cells are key initiating agents of perifollicular micro-inflammation and perifollicular fibrosis [19, 26]. MCs may directly or indirectly synthesize and release several mediators capable of modulating extracellular matrix production and degradation [7, 12]. These mediators include TNF-alpha, transforming growth factor (TGF)-beta, prostaglandin (PG)-D2, and basic fibroblast growth factor (bFGF) [1, 7, 12, 13]. TGF-beta is considered a key element in the fibrotic process [3, 29]. Furthermore, tryptase is known to stimulate fibroblast proliferation, to induce mRNAs required for collagen production [5, 13, 25], to increase elastin production in fibroblasts in bladder walls [11]. Therefore, MC accumulations might be responsible for increased collagen and elastic fiber synthesis in MPHL.
Regarding MPHL, Yoo et al. [34], demonstrated that androgen directly stimulated procollagen synthesis in bald scalp skin, and increase in elastic fibers was observed with the progression of alopecia [4], thus some type of dermal matrix remodeling in alopecia lesions appears to contribute to the miniaturization of hair follicles, a well known feature of MPHL.
https://www.ncbi.nlm.nih.gov/pubmed/18286292
Long story short, mast cells are the primary inflammatory cells that are triggered by the androgenic cascade into provoking inflammation and scarring of the skin which is actually what is leading to the destruction of our follicles. Antihistamines tell the mast cells to "stop".
Again, antihistamines should therefore be able to therefore induce positive hair changes without destructive skin changes.
The excerpt above also highlights again why I think seti/fevi will be weak at best. Inflammatory changes in the scalp are so much bigger than just PGD2. There are so many negative inflammatory mediators triggered by the balding process.
Although androgens are primarily responsible for MPHL [14, 15, 22], the implication of microscopic inflammation in the pathogenesis of MPHL was also suggested from several studies [17, 19, 26, 28]. Sueki, et al. analyzed MC infiltration quantitatively and the ultra-structures of alopecic scalp areas, and suggested that micro-inflammation probably accelerates MPHL by inducing aberrant fibrosis [26].
Mast cells are well known to play a critical role in allergic diseases and to be implicated in inflammatory disorders [24]. In addition, mast cell accumulations are often observed in fibrotic disorders of the skin, e.g., keloid, systemic sclerosis, and during wound healing [9, 18, 21, 23, 30]. The effects of activated mast cells on dermal fibroblast proliferation and collagen and glycosaminoglycans synthesis have been well demonstrated [1, 2]. Moreover, it has also been suggested that mediators and enzymes of mast cells are key initiating agents of perifollicular micro-inflammation and perifollicular fibrosis [19, 26]. MCs may directly or indirectly synthesize and release several mediators capable of modulating extracellular matrix production and degradation [7, 12]. These mediators include TNF-alpha, transforming growth factor (TGF)-beta, prostaglandin (PG)-D2, and basic fibroblast growth factor (bFGF) [1, 7, 12, 13]. TGF-beta is considered a key element in the fibrotic process [3, 29]. Furthermore, tryptase is known to stimulate fibroblast proliferation, to induce mRNAs required for collagen production [5, 13, 25], to increase elastin production in fibroblasts in bladder walls [11]. Therefore, MC accumulations might be responsible for increased collagen and elastic fiber synthesis in MPHL.
Regarding MPHL, Yoo et al. [34], demonstrated that androgen directly stimulated procollagen synthesis in bald scalp skin, and increase in elastic fibers was observed with the progression of alopecia [4], thus some type of dermal matrix remodeling in alopecia lesions appears to contribute to the miniaturization of hair follicles, a well known feature of MPHL.
https://www.ncbi.nlm.nih.gov/pubmed/18286292
Long story short, mast cells are the primary inflammatory cells that are triggered by the androgenic cascade into provoking inflammation and scarring of the skin which is actually what is leading to the destruction of our follicles. Antihistamines tell the mast cells to "stop".
Again, antihistamines should therefore be able to therefore induce positive hair changes without destructive skin changes.
The excerpt above also highlights again why I think seti/fevi will be weak at best. Inflammatory changes in the scalp are so much bigger than just PGD2. There are so many negative inflammatory mediators triggered by the balding process.
