Topical Cetirizine more effective twice a day?

[josh7000]

I currently apply 1ml solution of cetirizine at night, I make my solution so it's around 1 tablet per ml I think. Would this be more effective twice daily?

 

[warner8]

results?

 

[LawOfThelema]

what makes you think its going to be effective at all? the PGD2 in scalp is not due to mast cell degranulation.

 

[josh7000]

Just read success stories on it, and it working in some cases. I don't really know how it works

 

[lickawrist]

What's the mechanistic approach with cetirizine? I've never heard of using it as hair loss treatment.

 

[josh7000]

Crush up cetirizine tablets and do 1 tablet per 1ml roughly, so mix it with water or a vehicle. So 60 tablets with 60ml of water mix it up. Leave it too settle over night then there will be the tablet filler at the bottom and liquid containing the cetirizine at the top. And you can either seperate the filler (I used coffee filters) or you can just draw off the top with pipte and leave the filler there. You apply 1ml to your head exactly the same as you would with minoxidil.

 

[RU serious]

Can't attest to it's actual effectiveness but it feels great on your scalp if you have 'the itch', completely kills it.

 

[josh7000]

You think?

 

[lickawrist]

Crush up cetirizine tablets and do 1 tablet per 1ml roughly, so mix it with water or a vehicle. So 60 tablets with 60ml of water mix it up. Leave it too settle over night then there will be the tablet filler at the bottom and liquid containing the cetirizine at the top. And you can either seperate the filler (I used coffee filters) or you can just draw off the top with pipte and leave the filler there. You apply 1ml to your head exactly the same as you would with minoxidil.

No, I meant what's the pathological reasoning in adding cetirizine to your hair loss regimen? What does it do? I'm not bashing, I'm just curious.

 

[josh7000]

I'm not really fully sure tbh, I think it works in blocking something. A little bit like an anti androgen. But not quite the same. I didn't go into reason much just heard of it working so decided to give it a shot

 

[LawOfThelema]

Well, this is interesting. It may actually be that mast cells are somehow involved in sustaining the baldness pathology:

https://www.researchgate.net/public...r_loss_A_suggestive_implication_of_mast_cells

Dermal fibrosis in male pattern hair loss: A suggestive implication of mast cells


Abstract
A relationship has been suggested between mast cells (MCs) and male pattern hair loss (MPHL), because of histological evidence of perifollicular fibrosis and increased mast cell numbers. Two paired punch biopsies were taken from balding vertexes and non-balding occipital promontory areas of ten patients with MPHL (Ludwig-Hamilton IIIv to IV) and from five normal subjects aged from 20 to 35 years. Masson trichrome and Victoria blue staining were performed to observe collagen frameworks and elastic fiber structures. Numbers of immunoreactive MCs stained with anti-tryptase or anti-chymase antibody were counted. It was found that collagen bundles were significantly increased in balding vertexes than in non-balding occiput scalp skin. A near 4-fold increase in elastic fibers was observed in both vertex and occiput scalp skins with MPHL versus controls. Total numbers of MCs (tryptase-positive) in site-matched scalp samples were about 2-fold higher in MPHL subjects than in normal controls. Percentage elastic fiber (%) was found to be relatively well-correlated with tryptase and chymase-positive MCs. These findings suggest that accumulated MCs might be responsible for increased elastic fiber synthesis in MPHL, and indicate that future investigations are warranted.

And more implication:

J Cutan Pathol. 2014 Apr;41(4):364-9. doi: 10.1111/cup.12286. Epub 2014 Jan 20.
[h=1]A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning.[/h]Larson AR1, Zhan Q, Johnson E, Fragoso AC, Wan M, Murphy GF.
[h=3]Author information[/h]

[h=3]Abstract[/h][h=4]BACKGROUND:[/h]Pattern (androgenetic) alopecia is commonly encountered in scalp biopsies obtained for non-scarring hair loss. Prostaglandin D-synthase is known to be elevated in bald vs. non-alopetic scalp of patients with androgenetic alopecia. We hypothesized that this difference in pattern of prostaglandin D-synthase expression may constitute a developmental pattern inherent to normal as well as alopecic scalp skin, thus defining a 'field' vulnerable to acquired hair loss.
[h=4]METHODS:[/h]We immunohistochemically mapped prostaglandin D-synthase expression from supra-auricular to vertex scalp skin of 11 cadavers.
[h=4]RESULTS:[/h]We found significantly more dermal mast cells immunoreactive for prostaglandin D-synthase in the vertex compared to the lateral aspects of the scalp, with a decrement that spatially approximated the pattern of androgenetic alopecia. This difference was present in both balding and non-balding scalps and was independent of gender. Dual labeling established dermal cells expressing prostaglandin D-synthase as mast cells.
[h=4]CONCLUSIONS:[/h]These data indicate that scalp is spatially programmed via mast cell prostaglandin D-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.
© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

 

[RU serious]

My understanding is that cet works by inhibiting pgd2, but the downside is that it also inhibits pge2, which is good for hair growth. Starving your hair of pge2 is definitely not a good idea, a load of people on a german forum tried cet and it made their hair worse. So in theory, using it along with a pge2 agonist might counteract that?

 

[LawOfThelema]

I thought the PTGDS upregulation in Androgenetic Alopecia was NOT due to mast cell degranulation, but we really don't know the full role of the mast cells in this pathology. I was going back over the original Translational Medicine paper, and they DID note increased mast cell proliferation. They write:

Quote

Follicle miniaturization is accompanied by a decrease in the duration of the growing phase of the follicle (anagen), which normally lasts several years to produce hair more than 1 m long, but which decreases to only days or weeks in Androgenetic Alopecia. This results in an increase in the percentage of resting (telogen) hair follicles containing microscopic hairs in bald scalp (4). In addition to these intrinsic changes to the hair follicle, infiltrating lymphocytes and mast cells have been identified around the miniaturizing follicle (9), especially in the area of the stem cell–rich bulge area (10).
​

And within the mouse hair cycling:

QuoteWe also noted a unique peak of PGD2 production within hours of depilation, which was not seen in the spontaneous hair cycle in Fig. 3B. This coincides with degranulation of mast cells observed previously after depilation (21). The more narrow peaks of markers in the depilated hair cycle likely reflect tighter synchronization of the hair follicle cycle after depilation. To better define expression of Ptgds, we performed immunohistochemistry on tissue sections from skin of the animals used for the time course in Fig. 3C. Ptgds was evident in late anagen in the keratinocytes of the outer root sheath below the stem cell–r​

And other studies have shown that the PTGDS identified actually COINCIDES with mast cells, and that the gradient of mast cells could be contributing to the "baldness field" commonly observed in Androgenetic Alopecia:

QuoteJ Cutan Pathol. 2014 Apr;41(4):364-9. doi: 10.1111/cup.12286. Epub 2014 Jan 20.
[h=1]A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning.[/h]Larson AR1, Zhan Q, Johnson E, Fragoso AC, Wan M, Murphy GF.
[h=3]Author information[/h]


[h=3]Abstract[/h][h=4]BACKGROUND:[/h]Pattern (androgenetic) alopecia is commonly encountered in scalp biopsies obtained for non-scarring hair loss. Prostaglandin D-synthase is known to be elevated in bald vs. non-alopetic scalp of patients with androgenetic alopecia. We hypothesized that this difference in pattern of prostaglandin D-synthase expression may constitute a developmental pattern inherent to normal as well as alopecic scalp skin, thus defining a 'field' vulnerable to acquired hair loss.
[h=4]METHODS:[/h]We immunohistochemically mapped prostaglandin D-synthase expression from supra-auricular to vertex scalp skin of 11 cadavers.
[h=4]RESULTS:[/h]We found significantly more dermal mast cells immunoreactive for prostaglandin D-synthase in the vertex compared to the lateral aspects of the scalp, with a decrement that spatially approximated the pattern of androgenetic alopecia. This difference was present in both balding and non-balding scalps and was independent of gender. Dual labeling established dermal cells expressing prostaglandin D-synthase as mast cells.
[h=4]CONCLUSIONS:[/h]These data indicate that scalp is spatially programmed via mast cell prostaglandin D-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.
© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.


​

So the pattern of the mast cells is the same in both balding AND non balding scalps, but the question is now why is mast cell degranulation and release of ptgds occuring in balding scalp


Studies as far back as the 70s (props to Danny Roddy for finding this one) have documented the role of mast cells in hair cycling, noting a correspondence between histamine level and the phase the hair follicle is in

1. QuoteMorettie, G., et al. The Hair Cycle Re-Evaluated. International Iournal Of Dermatology (1976). "The skin content of histamine and heparin contained in the mast-cell granules is high at this time [ANA 4].” "The rise in heparin in the first week of anagen probably helps to maintain normal blood fluidity in the simultaneously increased perifollicular vessel networks, which are dilated and made more permeable by histamine.” "When follicles have reached ANA 6, however, a gradual but radical decrease in mast cells, histamine and heparin begins. This continues through the rest of ANA 6 and the whole of catagen. The mast cell population diminishes by a third, when it retreats to the lower dermis and hypodermis."During telogen the mast cells, histamine, and probably heparin, increase again and continue rising in the subsequent anagen, as we know from studies on consecutive hair cycles. The final stage of telogen probably prepares the hair for the next growth phase. This stage and anagen, until the point when the follicles are differentiated and emerge, are characterized by an increase in mast cell population and in their secretory activity.” "During telogen, hair survival is dependent on energy (ATP), mainly produced by anaerobic glycolysis,” "Thyroxine shortens the resting phase, whereas estradiol, adrenal hormones and testosterone prolong telogen."​

But the problem here is Other studies show that Ceterizine simply does not inhibit or prevent mast cell degrantulation, and some show that it has an effect on what is secreted, but that it varies by tissue. As noted in In vitro effects of H[SUB]1[/SUB]-antihistamines on histamine and PGD[SUB]2[/SUB] release from mast cells of human lung, tonsil, and skin:

Quote This drug showed concentration-dependent inhibition of IgE-dependent mediator release from lung and tonsil mast cells only. Our results show that human mast cells are heterogeneous with respect to modulation of mediator release by these H[SUB]1[/SUB]-antihistamines. In particular, differences were observed between skin mast cells and those dispersed from lung and tonsils.​

Continuing on, we find that human skin cells express H2, H4 receptors, but that H1 receptors likely have no functionality vis a vis the degranulation of mast cells and the secretion of inflammatory mediators:

Quote[h=3]Abstract[/h]Mast cells generate and release histamine during anaphylactic reactions, and there is pharmacological evidence that histamine regulates this process via specific receptors. Therefore, we examined human leukemic (HMC-1) and normal skin mast cells for the expression of all four currently known histamine receptors. Both cell types expressed H2 and H4 receptors at mRNA and protein levels, whereas H3 receptor specific mRNA and receptor protein was undetectable. Similarly, immunohistochemistry of cutaneous tissue showed an absence of H3 receptor in these cells. Despite transcription of mRNA, H1 receptor protein was only moderately expressed in HMC-1 cells and was virtually absent in skin mast cells. Furthermore, only H1, H2, and H4 receptors were detectable by Western blot analysis of HMC-1 cells. Radiolabeled histamine binding was strongly inhibited only by H2 (ranitidine)- and H3/H4 (FUB 108)-specific antagonists. Histamine-induced increase of cAMP was inhibited by the H2 receptor antagonist famotidine, whereas induction of IP3 was not observed, making signaling via the H1 receptor unlikely. These data show that human mast cells constitutively express primarily H2 and H4 receptors and that H2 receptors are functionally linked to cellular processes. They provide new insights into the mechanisms that govern auto- and paracrine histamine-induced mast cell functions.

​

To me this all supports the unlikelihood that ceterizine does anything as an Androgenetic Alopecia treatment, but it is actually not conclusive since histamine fluctuation is observed in the induction of different hair phases.

So, the question becomes what are the H1 receptors doing in the skin and what are they doing in the hair, and what is the histamine concommitant with the mast cell degranulation and hair cycling doing to the scalp, and can h1 receptor blockage have any effect, and would this effect be positive.

Frankly I dont think anyone knows.

But I think we can now say that the ptgds in the scalp is associated with mast cells.

In the past I denied this assertion, but now I stand corrected.

 

[josh7000]

So what's the summary of this? Does Cet help or not? I now know it can have some sort of action involved and I think that was sort of what I was guessing is it was involved in blocking something contributing too hairloss

 

[LawOfThelema]

no one knows and everyone has more or less moved on from this, now that actual crth2 receptor blockers are available

 

[josh7000]

Like what?

 

[parisienne]

setipiprant

 

[josh7000]

setipiprant

Where can I obtain this and how do I take it? What are the doses?

 

[MindfluX]

Cetirizine can grow hair, but it has a negative effect on the quality of your hair. I advice you not to use it.

 

[josh7000]

Cetirizine can grow hair, but it has a negative effect on the quality of your hair. I advice you not to use it.

What do you mean, how?