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


Senior Member
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.









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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Senior Member
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.


Senior Member
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]. "