Butyrate induces HSV/EBV/HHV6 reactivation - Reason why some react negatively to fiber/probiotics?

dannybex

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I have seen that it seems to be quite firmly established that butyrate (butyric acid) is a strong inducer of herpes virus reactivation and replication, including EBV, HHV6 and HSV1.

Studies:

https://www.ncbi.nlm.nih.gov/pubmed/11059774

https://www.ncbi.nlm.nih.gov/pubmed/9753061

https://www.ncbi.nlm.nih.gov/pubmed/17360760

https://www.sciencedirect.com/science/article/pii/0042682286902187

http://grantome.com/grant/NIH/F32-CA165705-03

http://jvi.asm.org/content/88/14/8028.full

https://www.ncbi.nlm.nih.gov/pubmed/220786

Butyrate is produced by probiotic colonic bacteria by fermenting fiber and prebiotics. I have also seen a study which I can't find anymore that butyrate produced by colonic bacteria does enter the blood stream.

I am wondering if this could be the reason why there are many reports of Herxheimer-type reactions to probiotics and also some reports of getting worse with high intake of fiber. I think high fiber intake (10-20g Psyllium husk) might make me worse, but I have been wondering why this is the case.

Could this be an explanation?

I'm late again to the party, but I don't think so. All of the studies you listed have issues.

The first one was based on butyrate being injected in the mice. The 2nd was an in vitro study done using 'Kamata' cell lines, which contain 'integrated HHV-6B'. The third, used HUGE injected doses! The fourth one was also in vitro where the cells were 'treated' with (or saturated with?) butyrate for 24 hours.

The fifth study was a grant proposal that was never completed, the sixth, again cell lines, and there's no abstract for the 7th, but it seems to be connected to the others.

Usually we think of fiber and probiotics as healthy food choices and intake is encouraged, but maybe it should better be limited in order to lower the amount of butyrate.

If people have issues with fiber, etc., it may be due to the levels of so-called 'bad bacteria' or a fungal infection, or some other sort of microbiome imbalance. From what I'm reading, I wish I'd worked on my gut YEARS ago.

Butyrate lowers ammonia levels, it's antifungal, it helps reduce/improve fatty liver, it helps lower histamine and inhibit mast cell activation, it improves insulin sensitivity, it lowers inflammation by inhibiting NF-κB, it's been shown to be helpful for ulcerative colitis, etc., etc..
 
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uglevod

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I herx much more with the minimization of SCFA producing fiber

Short-chain fatty acids produced by anaerobic bacteria inhibit phagocytosis by human lung phagocytes
The effect of short-chain fatty acids on the phagocytic activity of human alveolar macrophages and neutrophils was investigated. These acids, butyric, propionic, and succinic, are produced by anaerobic bacteria. The results indicate that phagocytosis of Staphylococcus aureus by human lung phagocytes is strongly inhibited by the end products of anaerobic catabolism and support the hypothesis that the antiphagocytic activity present in the supernatants of anaerobic cultures may be dependent on the presence of short-chain fatty acids.

All of the short-chain fatty acids tested induced an inhibition of phagocytosis both in absolute numbers of ingested bacteria and in rates of engulfment, which were already significant at 15 min (P < .001;figure IA right).

In the presence of short-chain fatty acids (15:1 bacteria-to PMNL ratio), a proportional decrease in the mean number of ingested bacteria (from 8 ± 0.9 to 4.1 ± 1.4) and of the metabolic activation (from 42.0 ± 2.5 fmol 02/PMNL to 27.1 ± 1.9 fmol 02/PMNL) was observed.

O2 consumption per ingested bacteria in the presence of short-chain fatty acids was not significantly different from a matched control with the same number of phagocytosed bacteria (6.58 ± 0.47 fmol OiPMNLIbacterium with short-chain fatty acids and 6.50 ± 0.52 fmol 02/PMNLIbacterium in the control). These data indicate that short-chain fatty acids did not inhibit PMNL metabolic activation and that the decreased heat effect could be accounted for by the inhibition of the phagocytosis.

Short-chain fatty acid impairment of S. aureus phagocytosis by alveolar macrophages, besides representing a good experimental model in vitro, acquires particular significance in terms of pathogenesis of mixed anaerobic lung infections, from which S. aureusis frequently retrieved [1]. The induced suppression of alveolar macrophage defense could account for the infection by S. aureus, which is normally eliminated by the resident phagocytic population without PMNL recruitment and influx of exudate [2]. From a wider infectivologic point of view, the available evidence indicates that short-chain fatty acids are important virulence factors that inhibit host phagocytic defenses as diverse as PMNLs and macrophages and may contribute to the pathogenesis of anaerobic infections.
 

pattismith

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I remember reading somewhere someone using sodium butyrate + antiviral herbs/etc to draw out virus from the nerves and finish them off. Not sure if it worked though.

Butyrate is an Histone Deacetylase Inhibitor ( HDACi) and
" HDACis have already been used concerning their effect on parasite growth, such as Plasmodium, Leishmania, and Schistosoma [51], as well as to prevent human immunodeficiency virus (HIV) latency [52,53]. "
 
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Although note that viral reactivation may not necessarily be a bad thing in ME/CFS, in the long term; indeed, it could be very beneficial. This is because if you take a virus like EBV, this hides away from the immune system by entering B-cells and then going into latency; but if you could re-awaken all the latent EBV so that it starts replicating, then you would force the immune system to fight and kill EBV, which in theory could entirely eradicate EBV from the body. Similarly for HSV, which goes into latency in peripheral nerve ganglia cells and in other places.

I came into this line of thought after stumbling upon this paper that proposes that latent EBV in B-cells may be causing issues (in some CFS patients) by altering immune signaling.

https://pubmed.ncbi.nlm.nih.gov/34867935/

Also interesting to note that latest Lipkin and other's research found a lack of butyrate-producing bacteria in guts of CFS patients.

If we can induce EBV reactivation with some form of butyrate and take antivirals at the same time to kill off replicating virus, then maybe we can eradicate the latent infection or at least reduce it?

I've seen research where they tried IV butyrate with ganciclovir for EBV associated cancer with some success.
 
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Wonkmonk

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If we can induce EBV reactivation with some form of butyrate and take antivirals at the same time to kill off replicating virus, then maybe we can eradicate the latent infection or at least reduce it?

I thought about this as well, but after years of trying a lot of things, I am now of the opinion that it is best for me to avoid anything that causes symptom flare ups. So if symptom flare ups are in fact reactivations that means that approach won't work (at least for me).

I was on various anti-herpetic drugs for I think 3-4 years with little to no success and while I never deliberately tried to combine the medications with high fiber loads, there were certainly weeks and months when I used both medications and had high fiber or high probiotic diets (including sauerkraut, milk kefir, water kefir, homebrewed kombucha, all of which I tried).

So I do not think this works for me, my best approach is currently to avoid everything that causes symptoms, which I found out is mainly related to some foods or combination of foods.

But again, that's just me. This doesn't meant combining fiber and anti-herpetic drugs won't work for other people. It's generally a great idea.
 
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