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Gut and Digestion inflammation by foods —> AGA?

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Gut and Digestion inflammation by foods —> AGA?

Post  Kazbar on Thu Dec 06, 2018 5:02 pm

Has anyone looked into gut / digestion inflammation as the possible cause of AGA?
1) Particularly inflammation caused by foods you eat.
2) Gut fungus or bacteria infections of the gut again being fed by foods you eat.
I think there is a strong link here.

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Re: Gut and Digestion inflammation by foods —> AGA?

Post  YARO on Fri Dec 07, 2018 3:02 pm

I have experience with those symptoms. After eating, especially a carb heavy meal, bloating and bad digestion ensues. After i feel bad, acid reflux and i feel like something is definitely wrong with my gut.

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Re: Gut and Digestion inflammation by foods —> AGA?

Post  CausticSymmetry on Fri Dec 07, 2018 3:16 pm

Kazbar wrote:Has anyone looked into gut / digestion inflammation as the possible cause of AGA?
1) Particularly inflammation caused by foods you eat.
2) Gut fungus or bacteria infections of the gut again being fed by foods you eat.
I think there is a strong link here.

Not a cause, but absolutely makes it much worse. However, it is linked to autoimmune based alopecia and since most of the food has been compromised, most of us to an extent suffer from both forms.


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Re: Gut and Digestion inflammation by foods —> AGA?

Post  CausticSymmetry on Fri Dec 07, 2018 3:35 pm

Here's some thing one could call iatrogenic induced alopecia (from an antibiotic)

Cell Rep. 2017 Aug 15;20(7):1513-1524. doi: 10.1016/j.celrep.2017.07.057.
Intestinal Dysbiosis and Biotin Deprivation Induce Alopecia through Overgrowth of Lactobacillus murinus in Mice.
Hayashi A1, Mikami Y2, Miyamoto K1, Kamada N3, Sato T2, Mizuno S2, Naganuma M2, Teratani T2, Aoki R4, Fukuda S5, Suda W6, Hattori M7, Amagai M8, Ohyama M9, Kanai T10.

Metabolism by the gut microbiota affects host physiology beyond the gastrointestinal tract. Here, we find that antibiotic-induced dysbiosis, in particular, overgrowth of Lactobacillus murinus (L. murinus), impaired gut metabolic function and led to the development of alopecia. While deprivation of dietary biotin per se did not affect skin physiology, its simultaneous treatment with vancomycin resulted in hair loss in specific pathogen-free (SPF) mice. Vancomycin treatment induced the accumulation of L. murinus in the gut, which consumes residual biotin and depletes available biotin in the gut. Consistently, L. murinus induced alopecia when monocolonized in germ-free mice fed a biotin-deficient diet. Supplementation of biotin can reverse established alopecia symptoms in the SPF condition, indicating that L. murinus plays a central role in the induction of hair loss via a biotin-dependent manner. Collectively, our results indicate that luminal metabolic alterations associated with gut dysbiosis and dietary modifications can compromise skin physiology.

https://www.cell.com/cell-reports/fulltext/S2211-1247(17)31036-7?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124717310367%3Fshowall%3Dtrue


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Mechanisms of tolerance and potential therapeutic interventions in Alopecia Areata

Post  CausticSymmetry on Sat Dec 08, 2018 9:22 am

Mechanisms of tolerance and potential therapeutic interventions in Alopecia Areata

https://doi.org/10.1016/j.pharmthera.2017.05.008

This review aims to address the mechanisms of compromised immune tolerance contributing to the development and maintenance of Alopecia Areata (AA). Our goal is to also highlight future treatment opportunities and therapeutics that will safely and efficiently restore hair growth and maintain patients in remission.

AA is a presumptive autoimmune disorder that coincides and genetically clusters to several other autoimmune diseases. In this review, we pay attention to the learnings from the mechanistic research and drug development in these other autoimmune conditions. Interestingly, most of these diseases have been linked to compromised central and peripheral tolerance, and increased intestinal inflammation with enhanced gut permeability. Break of tolerance and priming of the autoreactive T-cells to attack antigenic epitopes in the hair follicle most likely requires several steps which include escape from negative selection and compromised peripheral tolerance. Local skin-related changes are also of importance due to the patchy manifestation of the skin areas with loss of hair, particularly in the early disease. Here, we discuss the defective mechanisms of tolerance, both central and peripheral, and hypothesize that the disease is driven by areas of tolerance break, and that these could be targeted for successful therapeutic interventions.

https://www.sciencedirect.com/science/article/pii/S0163725817301274?via%3Dihub

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