Found this, don’t know anything about seller:
https://www.etsy.com/listing/253931752/kefir-fermenter-container-with-kefir
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Main rule is to not use metal. Other than that I like anything that works.
If you read about the origins and the lore, they talk about using bags of leather and hanging it on the door so that it agitates every time somebody uses the door. Obviously plastic is cleaner though I think some of the critters came from leather originally. There is a mold that can cause trouble and I have had it move in on top of the jar, because they say to leave the lid loose. If you shake a couple times (tighten the lid first) as you walk by this is easily solved. It can’t survive.
Long way of saying the kefir grain needs be intimate with the warm milk and not just see it off in the distance. You want to colonize as quickly as possible. Everybody wants the warm milk. There is competition. The floater or the plastic can with holes may be easier and work fine but I think I would increase agitation or maybe use 3 floaters or sinkers. Obviously in this case YMMV.
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The gut microbiome is the great unknown in medical science. We really know very little about it. It’s like a whole separate world of incredible complexity that we have barely scratched the surface of. Puzzles and contradictions abound.
One example is the very fundamental assessment of what makes a beneficial gut microbiome composition in the elderly. As you age, the diversity of your microbiome (bacterial strains) drops. For a long time it was assumed that the greater diversity of youthful biome was beneficial in the elderly, and some FT studies (young to old and old to young) seemed to confirm that. It was thought that the lower diversity in the elderly was driven by less diversity in F&V consumption as the diets of the elderly tend to restrict in diversity. But then, there appeared strong evidence that the opposite is true. In a series of trials in mice it was shown very strongly that far from lower diversity gut microbiome being a negative deterioration in the older physiology, lower diversity was an active adaptation of the gut to age-related changes in the digestive system itself - the gut ages just as do all organs - it undergoes a senescent transition. In these trials, transplanting (FT) from younger to older mice caused negative health consequences, just as transplanting an older biome to younger mice was also a negative. It seems there is such a thing as “age appropriate gut microbiome” and trying to disrupt that by transplantation across age categories has negative consequences.
But it seemed that diverse food - as in more variety in F&V consumption - was still beneficial. All these contradictions have been puzzling me for a long time. Even fiber consumption is not a straightforward issue. Generally it seems more is better, or at least too little is bad, but which fiber when and for whom seems very fraught, and it looks like the wrong fiber can be quite detrimental; worse, the same fiber can be good or bad depending on other factors and the individual involved - few hard and fast rules.
All this has me firmly convinced of the Socratic dictum: “I know that I know nothing”. The whole area strikes me as a great unknown.
Here’s a paper that throws some light on the diversity paradox I described above. More food for thought - but what is actionable?
Increased nutrient diversity can induce loss of microbial diversity through enhanced resource uptake
https://www.nature.com/articles/s41559-026-03111-4
“The origin of biodiversity is a central question in ecology, particularly how numerous microbial species co-exist within a single community. A prevailing hypothesis holds that microbial species co-exist by specializing on different resources, thereby reducing competition. Accordingly, increasing resource diversity is expected to promote species co-existence and boost biodiversity. By integrating high-throughput experiments, ecological analysis of global microbiome data, metabolic profiling and theoretical modelling, we find that the relationship between resource diversity and microbial biodiversity is not consistently positive and can even decline with increasing resource diversity. This unexpected result emerges from a widespread physiological response across diverse microbial taxa, in which more complex environments trigger higher overall resource uptake. This intensifies competition and can lead to biodiversity loss. Updating a central ecological model to include this physiological trait accurately reproduces the observed decline. Our findings suggest that physiological changes at the individual level can substantially alter predicted diversity patterns and scale up to influence community structure.”
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How much pectin do you take?
I noticed nothing. But maybe I wasn’t paying close enough attention. Then again, certinly nothign dramtic.
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Reviving this thread. Has anyone reliably and econimivally sourced Miyarisan Strong from any e-commerce retailer?
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I bought 2 bottles now from the links we gave for ebay. The guy sent this with the bottles:
Rapadmin provided this once but I can’t find it now so this is the one he sent me.
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I bought this one: https://www.ebay.com/itm/225569007871
I was looking to purchase again, but not that thrilled about the added ingredients.
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why do you need that? We just use a fork to pull the large ball out of the kefir
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Abstract only.
Designing fiber–gut microbiome interactions with active learning
https://www.nature.com/articles/s41589-026-02272-4
“Our model-guided approach revealed a highly butyrogenic and robust ecological motif characterized by the copresence of inulin, Bacteroides uniformis and Anaerostipes caccae and a higher-order interaction with Prevotella copri . Human fecal communities invaded with model-designed species–fiber combinations displayed predictable gut-beneficial outputs.”
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I’ve been consuming 30-40g of resistant starch daily for about 6 months now (mostly unmodified potato and green banana). I was worried about TMAO based on these posts and had it checked at LabCorp. Fortunately it came back normal at <3.3. N=1, but wanted to share. Test was not cheap at about $80.
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Me too but mine came back at 33, which is clear off the charts high. I stopped taking phosphatidylcholine and Krill. Stopped the RS, what was I thinking. I’ll have it checked again at my next 3 mo.
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Curious if you’ve noted any positive health changes from this protocol.
No, I haven’t noticed any subjective changes or lab/objective changes. But I guess I’m already fairly metabolically healthy–fasting insulin ~2, low trig/HDL ratio, HOMA-IR<1, ALT ~20, A1C 5.2-5.3. I guess I am just trying to optimize as much as possible and hoping the RS does sth.
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Vitamin C Supplementation and Intestinal Microbiome Diversity: A Critical Review of Current Evidence
“Vitamin C supplementation may influence gut microbiome diversity by modulating intestinal oxidative stress, microbial composition, and the production of beneficial metabolites such as short-chain fatty acids. Emerging evidence also points to potential synergies with prebiotics, probiotics, butyrate, and bioflavonoids, although further clinical research is needed to establish optimal doses and long-term effects.“
“Emerging evidence suggests that dietary ascorbic acid plays a pivotal role in shaping microbial community structure by mitigating intestinal oxidative stress and fostering a favourable environment for beneficial taxa1. Clinical studies have shown that targeted vitamin C administration significantly increases microbial alpha diversity and promotes the production of faecal short-chain fatty acids2. This shift is reflected in increased relative abundance of Lachnospiraceae, alongside a corresponding reduction in potentially pathogenic populations such as Enterococci 3. Furthermore, high-dose vitamin C intake is associated with the restoration of essential gut-liver functions, counteracting the depletion of antioxidants4.
This fits with broader nutrition-based approaches to dysbiosis. High-dose supplementation may help regulate metabolic pathways affected by oxidative stress3,5. By neutralising reactive oxygen species, vitamin C may reduce inflammatory signals that promote the growth of pathobionts under oxygen-rich gut conditions6,7. (Figure 1)“
“It may also reduce hydrogen peroxide and other oxidative stressors, thereby supporting the antioxidant defences naturally provided by beneficial bacteria such as Lactobacillus and Bifidobacterium 7. A more stable redox environment could further support certain Clostridiaspecies, which produce antioxidants such as ascorbic acid and glutathione that help protect the intestinal barrier from ongoing stress8. Overall, this antioxidant effect may help stabilise the gut environment and reduce the inflammatory signalling linked to dysbiosis9.
Moreover, by fostering an environment conducive to microbial richness, such supplementation aligns with the broader therapeutic potential of antioxidants—including polyphenols and other vitamins—to rectify dysbiosis and improve long-term host metabolic outcomes10. Beyond these metabolic effects, vitamin C and its oxidation products, including L-dehydroascorbic acid, may inhibit opportunistic pathogens and thereby help commensal bacteria maintain a dominant role in the intestinal community. This synergistic inhibition of enteric bacterial replication, when coupled with the modulation of local redox states, may ultimately promote a resilient ecological profile similar to the high microbial diversity observed in healthy ageing cohorts11,12. Future research should investigate whether these shifts in microbial composition facilitate improved production of short-chain fatty acids, as observed with other antioxidant-rich interventions that enhance host immune signalling and gut barrier integrity13,14. Furthermore, because redox balance is essential for limiting the expansion of virulence factors in pathogens that thrive in oxygen-rich environments, maintaining adequate vitamin C levels may help protect against systemic inflammation. By curbing the oxidative stress that often accompanies dysbiosis, this stabilisation of the gut milieu bolsters the host’s innate immune barrier against pathogen-mediated inflammation15. Moreover, the conversion of vitamin C into reactive metabolites may exert direct bactericidal effects against specific pathogens, complementing the broader metabolic cross-talk that helps stabilise intestinal homeostasis.
Additionally, the antioxidant-rich microenvironment established by ascorbic acid supplementation may act in concert with specific probiotic strains, such as P. freudenreichii, to bolster systemic antioxidant defences and modulate inflammatory pathways like NF-κB16.
Dosage
Daily vitamin C intake strongly affects plasma ascorbic acid levels, but higher oral doses are mostly excreted in urine17. Reaching therapeutic tissue levels may therefore require careful dose adjustment, since the kidneys tightly control plasma vitamin C and help prevent possible pro-oxidant effects at very high doses18.
Consequently, pharmacokinetic studies indicate[…]”
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Fiber supplementation protects from antibiotic-induced gut microbiome dysbiosis by modulating gut redox potential
https://www.nature.com/articles/s41467-023-40553-x
“Antibiotic-induced gut dysbiosis (AID) is a frequent and serious side effect of antibiotic use and mitigating this dysbiosis is a critical therapeutic target. We propose that the host diet can modulate the chemical environment of the gut resulting in changes to the structure and function of the microbiome during antibiotic treatment. Gut dysbiosis is typically characterized by increases in aerobic respiratory bacterial metabolism, redox potential, and abundance of Proteobacteria. In this study, we explore dietary fiber supplements as potential modulators of the chemical environment in the gut to reduce this pattern of dysbiosis. Using defined-diets and whole-genome sequencing of female murine microbiomes during diet modulation and antibiotic treatment, we find that fiber prebiotics significantly reduced the impact of antibiotic treatment on microbiome composition and function. We observe reduced abundance of aerobic bacteria as well as metabolic pathways associated with oxidative metabolism. These metatranscriptomic results are corroborated by chemical measurements of eH and pH suggesting that fiber dampens the dysbiotic effects of antibiotics. This work indicates that fiber may act as a potential therapeutic for AID by modulating bacterial metabolism in the gut to prevent an increase in redox potential and protect commensal microbes during antibiotic treatment.“
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Synergy between Enterobacteriaceae and diet mediates competition between dominant Bacteroidales in the human gut
https://www.nature.com/articles/s41564-026-02500-6
“Healthy human gut microbiota is dominated by Bacteroidaceae in industrialized populations and by Prevotellaceae in those with traditional lifestyles, but diet alone is insufficient to explain this dominance of different Bacteroidota. Here we screened 94 dietary components in synthetic gut communities and find that these two bacterial families compete for overlapping nutritional niches. Segatella copri , a key member of Prevotellaceae-rich communities, outcompeted Bacteroidaceae when preferred polysaccharides such as arabinan were available, but this advantage depended on community composition, particularly the presence of Enterobacteriaceae. Metatranscriptomics and targeted metabolomics further revealed that Enterobacteriaceae synergized with dietary components to promote Segatella dominance in human and mouse gut communities. These interactions were validated by using multiple E. coli and Segatella isolates. Analyses of global metagenomes also showed a positive correlation between Segatella -rich non-industrialized microbiomes and Enterobacteriaceae abundance. Our results establish an ecosystem-level dynamic interplay between dietary components and key gut commensals that favour the dominance of Prevotellaceae.”
“We next investigated whether S. copri and the Bacteroidaceae species compete within the community. We chose arabinan supplementation as a model, as arabinan promotes S. copri over the Bacteroidaceae species, and the PUL specific for arabinan utilization is known for S. copri and B. thetaiotaomicron , and is predicted for P. vulgatus 19,23. Moreover, B. thetaiotaomicron , P. vulgatus and S. copri grow efficiently on arabinan (Extended Data Fig. 2a,b). Compared to mGAM, supplementation of arabinan led to a ~35-fold increase in S. copri relative abundance (1.7% vs 59.6%) and >6-fold decrease in overall Bacteroidaceae (47% vs 7.3%) (Fig. 2a). Thus, S. copri has a clear advantage within the community in the presence of arabinan and shows a negative correlation with most members of the Bacteroidaceae (Fig. 2a,e and Extended Data Fig. 2c). Metatranscriptome analysis revealed that the SusC/D-like gene pairs in the S. copri arabinan-specific PUL14 are upregulated up to ~16-fold compared to mGAM alone, suggesting active arabinan metabolization by S. copri within the community (Fig. 2b and Supplementary Table 3). Of note, genes in the B. thetaiotaomicron arabinan PUL were also upregulated (Supplementary Table 3). Deletion of SusC1 in the arabinan PUL14 renders S. copri unable to utilize arabinan19 (Extended Data Fig. 2d). Unlike S. copri WT, the S. copri ΔsusC1 mutant strain was unable to expand within the community in the presence of arabinan (Fig. 2c). These results show that S. copri gains a competitive advantage within the community by directly utilizing arabinan.”
“Our findings reveal that besides its specific preference for plant-derived fibres, S. copri also exhibited expansion in response to most fibres derived from microbial and algal sources. As previously noted, only a small portion of animal or host-derived glycans enhanced the abundance of S. copri in the community20,42. This suggests that S. copri possesses a broad preference for complex glycans from various sources despite having a significantly smaller number of glycan-processing enzymes when compared with B. thetaiotaomicron and B. ovatus 19,20,47. This may imply a greater versatility of S. copri ’s PULs and CAZymes or indicate the existence of additional unknown loci involved in diverse complex glycan utilization. This provides an important resource for future studies on Segatella carbohydrate utilization and its effects on colonization. In addition to dietary glycans, vitamin B3 and B5 promote S. copri expansion while decreasing Bacteroidaceae abundance within the community in an E. coli -dependent manner (Figs. 1 and 4). S. copri and various Bacteroidaceae species are predicted to synthesize most B vitamins, which are essential for their colonization48,49,50. It has been shown that dietary supplementation with these vitamins increases the relative abundance of Prevotella and decreases that of Bacteroides in lactating women51. However, the mechanisms underlying vitamin-mediated interactions and the concentrations available in the distal gut, particularly those from dietary intake, remain poorly understood.”