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JAK/STAT pathway and hair loss

Discussion in 'Antivirals, Antibiotics and Immune Modulators' started by Changexpert, Oct 26, 2015.

  1. Changexpert

    Changexpert Senior Member

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    Along with CFS, I have been suffering from hair loss for a while at a such young age, so hair loss research has been one of my primary focus lately. The idea of inhibiting JAK pathway stems from a theory that hair loss is caused by autoimmune response creating unnecessary inflammation.This experimental success for hair regrowth was an accidental finding, which was confirmed by a rat study recently. The first accidental finding was noticed with a rheumatoid arthritis patient, taking JAK inhibitor drug orally. However, researchers concluded that inhibiting JAK can create a new host of problems, so oral ingestion is not suitable for hair loss purpose. As a result, the rat experiment was done topically, not orally.

    http://www.belgraviacentre.com/blog...s-drug-xeljanz-may-have-serious-side-effects/
    http://www.nbcnews.com/health/health-news/cancer-drug-could-be-baldness-remedy-too-n450256

    The difference among JAK1, 2, and 3 is really subtle, as all of them are involved in many pathways as shown in the diagram attached below.

    A diagram that shows differecne among different JAK (1,2,3) pathways
    http://www.ebioscien...tat-pathway.jpg

    I think inhibiting JAK-2 is not as beneficial because it will result in HGH inhibition, but that's just my guess.


    On the other hand, here is an interesting blog post about how STAT is involved in immune system mediation. The post focuses on CFS/ME instead of hair loss.

    http://optimalprediction.com/wp/ori...e-immune-system/comment-page-1/#comment-81716

    I personally think CFS and hair loss are closely related because I think both of them happen from immune system dysfunction, whether it be due to overstimulation, lack of suppression, deficiency, or too much suppression. Unfortunately, there has not been much study to back up such claim. Keep in mind that correlation is not equal to causation, and I am not saying one causes another.

    The post discusses how CFS/ME patients (mainly ME) are more prone to infection due to decreased function of STAT1 that leads to Th2 dominance, resulting in decreased level of IL-22, IFN gamma, AND INCREASED LEVEL OF TGF-B. Many studies concluded that TGF-B is elevated in the scalp of hair loss patients. This theory seems very fitting, but its conclusion is the OPPOSITE of what researchers have been conducting (first two articles).

    If dysfunctional STAT1 is the cause of increased TGF-B, it would not make much sense from TGF-B perspective to inhibit JAK pathway. Since JAK is a precursor of STAT pathway, JAK inhibition would decrease the available reactants for STAT1 process, which would ultimately increase TGF-B even more. From all this, we can see that there are at least two schools of thought.

    1. Immune system deficiency (Th1) causes Th2 dominance, resulting in increased TGF-B, allowing infections to occur/proliferate more easily. (what the blog post suggests)
    2. Immune system overdrive causes autoimmune response, which can be mediated by inhibiting JAK pathway (what the researchers are working on)

    I can see both theories being plausible, but my experience agrees more with second theory. I have never tolerated any immune booster supplements like IP6, beta glucan, mushroom extracts (reishi, shiitake, maitake, chaga, cordyceps, etc), and even vitamin C; they always caused more body rashes, scalp bumps, and acne.Other therapeutic supplements like methyl B12 and iodine (kelp, Lugol's, nascent) always resulted in side effects mentioned above, along with insomnia and muscle cramps.

    It's always tough when two great sounding theories are contradictory of each other. I would love to hear different opinions on this topic. Thank you so much!

    @Hip @adreno @heapsreal
     
    Last edited: Oct 26, 2015
    wastwater likes this.

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