A lot of us take a number of supplements. This thread is to make the case for Butyric Acid - Butyrate.
I started taking it because some guy on another forum said Niacin and Butyrate "cured" his Parkinson's, and then later I noticed he was self diagnosed. This does not mean he was wrong.
So please, anybody else taking Butyrate? Why are we taking it? Any studies? What is the rationale? Is it clearing a-synuclein in the brain? Clearing a-synuclein in the gut? Giving us the energy to fold proteins better?
Thanks, Bolt.
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I found this (it is just something I found): Sodium Butyrate Exacerbates Parkinson's Disease by Aggravating Neuroinflammation and Colonic Inflammation in MPTP-Induced Mice Model
The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson's disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) treated mouse model of PD. Sodium butyrate (NaB; 165 mg/kg/day i.g., 7 days) was administrated from the day after the last MPTP injection. Interestingly, NaB significantly aggravated MPTP-induced motor dysfunction (P < 0.01), decreased dopamine (P < 0.05) and 5-HT (P < 0.05) levels, exacerbated declines of dopaminergic neurons (34%, P < 0.05) and downregulated expression of tyrosine hydroxylase (TH, 47%, P < 0.05), potentiated glia-mediated neuroinflammation by increasing the number of microglia (17%, P < 0.05) and activating astrocytes (28%, P < 0.01). In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1β, 4.11-fold, P < 0.01; IL-18, 3.42-fold, P < 0.01 and iNOS, 2.52-fold, P < 0.05) and NO production (1.55-fold, P < 0.001) in LPS-stimulated BV2 cells. In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice. However, NaB had no effect on NFκB, MyD88 and TNF-α expression in PD mice. Our results indicate that NaB exacerbates MPTP-induced PD by aggravating neuroinflammation and colonic inflammation independently of the NFκB/MyD88/TNF-α signaling pathway.
I recall seeing that study some months ago. It conflicted with what I had read about the benefits of butyrate. Then came that January MIT report we discussed earlier this week that added to the confusion. That's why I paused my inulin prebiotic fiber powder intake for a few months. (I've since resumed it based on the discussion.)
Now look here...
Listed just below the Abstract you just found was this 2021 paper: Neuroprotective effects of short-chain fatty acids in MPTP induced mice model of Parkinson's disease
Gut microbial metabolites, SCFAs, were related with the occurrence and development of Parkinson's disease (PD). But the effects of different short-chain fatty acids (SCFAs) on PD and involving mechanisms are still undefined. In this study we evaluate the effects of three dominant SCFAs (acetate, propionate and butyrate) on motor damage, dopaminergic neuronal degeneration and underlying neuroinflammation related mechanisms in (MPTP)-induced PD mice. High (2.0 g/kg) or low doses (0.2 g/kg) of sodium acetate (NaA), sodium propionate (NaP) or sodium butyrate (NaB) were gavaged into PD mice for 6 weeks. High doses of NaA reduced the turning time of PD mice. NaB significantly reduced the turning and total time in pole test, and increased the average velocity in open field test when compared with PD mice, indicating the most effective alleviation of PD-induced motor disorder. Low and high doses of NaB significantly increased the content of tyrosine hydroxylase (TH) by 12.3% and 20.2%, while reduced α-synuclein activation by 159.4% and 132.7% in the substantia nigra pars compacta (SNpc), compared with PD groups. Butyrate reached into the midbrain SNpc and suppressed microglia over-activation. It inhibited the levels of pro-inflammatory factors (IL-6, IL-1β and TNF-α) (P < 0.01) and iNOS. Besides, butyrate inhibited the activation of NF-κB and MAPK signaling pathways in the SNpc region. Consequently, sodium butyrate could inhibit neuroinflammation and alleviate neurological damage of PD.
With this, and the input of my HU comrades on this topic earlier this week, my confidence in taking measures to boost butyrate has been restored.
In April [2017], researchers also found that Sodium butyrate rescues dopamine-producing cells from alpha synuclein-induced issues. This compound is found in a normal diet, it is produced in large amounts from dietary fiber in the gut and it is present in Parmesan cheese and butter. The most common source of sodium butyrate in the gut, however, is from consumption of legumes.
To read more about the referenced research, go to:
Now that is interesting for a whole other reason. The Wahls Paleo Plus Protocol AND the Specific Carbohydrate Diet (I layer the 2) both outlaw Legumes. Hmmm.
Here are a couple of excerpts from the paper, Impact of Diet-Modulated Butyrate Production on Intestinal Barrier Function and Inflammation found at ncbi.nlm.nih.gov/pmc/articl...
The production of butyrate in the gut and the concentrations in the gut and circulation can be modulated by dietary means, particularly through the content and composition of dietary fiber (DF). There is good evidence that enhanced butyrate production may influence the gut barrier function and level of intestinal inflammation, whereas the effects on peripheral inflammation, in general, are less pronounced and more ambiguous...
...Substrates stimulating the formation of butyrate are starch, arabinoxylan-rich whole grains, and brans from cereals such as wheat, rye and oats. In contrast, cellulose, xylan, pectin and pectin-rich fractions in general all result in relatively low formation of butyrate. In recent studies with pigs it was found that diets high in dietary fiber resulted in substantially higher short-chain fatty acids (SCFA) large intestinal pool size and SCFA absorption than a low DF Western-style diet high in refined carbohydrates from sugar and refined wheat flour...However, it can be assumed that a higher intake of DF will increase SCFA and butyrate production...
I'm going the route of dietary fiber instead of butyrate supplements. It's my understanding that butyrate is produced in the colon from prebiotic fiber, especially inulin. So I'm taking pure "It's Just" [brand name] inulin prebiotic fiber in the form of chicory root powder. I tolerate it well (unlike my 5-month trial of mannitol). I also eat legumes.
I'm slowing working my way back up to 12 grams a day. According to the package, that's 3 teaspoons. I dissolve the first dose in my morning tea. Other later doses are mixed with water. Dosage suggestions were gleaned from here:
Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson’s disease
This part: "These discrepancies could reflect differences in microbiota composition between patients and controls; Bacteroides is more abundant in controls, and Bifidobacterium is more abundant in PD patients in this cohort [32], which could increase their functional impacts within their respective microbial communities. This could explain the positive association between SCFAs and Bacteroides, a producer of SCFAs, in controls, but not necessarily the inverse relationship between Bifidobacterium and butyric acid in PD patients. Increases in Bifidobacterium are considered butyrogenic due to cross-feeding of butyrate-producing bacteria [50], but the opposite association was found in our PD cohort, suggesting an altered function or strain profile of the Bifidobacterium genus in the metabolic network of the PD microbiota. Further evidence that Bifidobacterium may not be performing a homeostatic function in PD is its positive correlation with the inflammatory marker NGAL in patients only."
Particularly this part: "Increases in Bifidobacterium are considered butyrogenic due to cross-feeding of butyrate-producing bacteria [50], but the opposite association was found in our PD cohort, suggesting an altered function or strain profile of the Bifidobacterium genus in the metabolic network of the PD microbiota."
I need to research this more, but it seems to be saying, maybe (to my High School educated mind) that our bacteria strain may be altered and what seems good for a normal person may not be good for us. But it is a maybe. FMT seems like a good addition to this formula.
I just got suckered in by an infomercial. A dude named Horton says taking butyrate fixed his sarcopenia (muscle wasting) without any need for exercise. Always a sucker for anything too good to be true. At least it was cheap; $10 for 3 months worth of capsules.
Here is a recent paper that discusses, in the context of Parkinson's Disease, interactions of niacin and butyrate with a gut protein called GPR109A. This protein plays an important role in controlling gut permeability and inflamamtion.
Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and
Dysbiosis is implicated by many studies in the pathogenesis of Parkinson’s disease (PD). Advances in sequencing technology and computing have resulted in confounding data regarding pathogenic bacterial profiles in conditions such as PD. Changes in the microbiome with reductions in short-chain fatty acid (SCFA)-producing bacteria and increases in endotoxin-producing bacteria likely contribute to the pathogenesis of PD. GPR109A, a G-protein coupled receptor found on the surface of the intestinal epithelium and immune cells, plays a key role in controlling intestinal permeability and the inflammatory cascade. The absence of GPR109A receptors is associated with decreased concentration of tight junction proteins, leading to increased intestinal permeability and susceptibility to inflammation. In inflammatory states, butyrate acts via GPR109A to increase concentrations of tight junction proteins and improve intestinal permeability. Niacin deficiency is exacerbated in PD by dopaminergic medications. Niacin supplementation has been shown to shift macrophage polarization from pro-inflammatory to an anti-inflammatory profile. Niacin and butyrate, promising nutrients and unique ligands for the G protein-coupled receptor GPR109A, are reviewed in this paper in detail.
Butyrate interacts with the GPR109A receptor and exhibits anti-inflammatory and anti-carcinogenic properties [12]. Butyrate is also the intestinal epithelial cells’ most-utilized SCFA for energy, making its investigation of the utmost importance for intestinal well-being [15]. In the study led by Feng et al., 24 piglets weaned at 21 days with diarrhea were divided into two groups. One group was fed with the basal diet and the other with basal diet plus 2000 mg/kg sodium butyrate. This experiment lasted a total of 21 days in which the diarrhea rate, frequency, and index were decreased compared to control. It was determined that intestinal permeability also was influenced by the addition of sodium butyrate, with upregulation of occludin and claudin-3 in the ileum and occludin, claudin-3, and ZO-1 expression in the colon. Using Western Blot analysis, ERK1/2, Akt, and P38 were phosphorylated, which indicated activation of the GPR109A pathway. Pro-inflammatory markers such as TNF-α were found to be significantly decreased with the administration of butyrate [12]. In another study, Yan et al. investigated the effects of butyrate on tight junction proteins on an LPS-induced inflammation model. They found that butyrate increased concentrations of claudins-3 and 4 and their mRNA expression in a dose-dependent manner, as well as prevented downregulation of Akt by LPS [57]. These studies suggest that butyrate may enhance tight junction expression through the Akt/mTOR pathway.
I've settled on taking butyrate, but only taking two pills a day (instead of 6) as they have magnesium in them and I don't want to cut out my Magnesium l-threonate.
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Why should I take extra vitamins
Butyrate , TUDCA or UDCA : trials for PD, ALS, ALZ - Slows ALS decline 
I am now a B1 Believer :-) +* 6/21/22 day 36 of taking TTDF: 
