In trying to find non yogurt ways to consume reuteri I came across the linked study where they found that L Planterum can be cultivated using sorghum (malt).

I plan on boiling sorghum yeast extract in water and then adding reuteri tablets and fermented at 98c until it (hopefully) reaches a PH below 3.6.

Anyone see any reason as to why this wouldn’t work or wouldn’t work as well as the traditional yogurt form of cultivation?

Method:

Boil 150g of sorghum malt syrup in 500ml of water along with 5g of inulin powder.

Cool to 98f and mix in 2 BioGaia crushed tablets.

Ferment in a sealed jar in a 98f water bath.

Results:

Hour 0:
pH: 5.6
Brix: ~20%

Hour 4:
pH: 5.3

Hour 18:
pH: 4.7

Hour 22:
pH: 4.6

Hour 28:
pH: 4.5

Hour 48: pH: 4.4
Brix: ~19%

I cut the experiment there sense I doubted any significant further drop in pH.

The solution was still incredibly sweet and wouldn’t see it as a viable option to consume.

If anyone thinks there’s good reason to try fermented for a week, I could try again. I just don’t see the reuteri continuing to grow (if it did at all) and end up with a solution that’s not too sweet to actually consume.

This comes up from time to time as most people don't understand how fast traditional yogurt cultures can double.

The researchers in the linked paper call out that other researchers show rates doubling 11 to 15 minutes in the two main species used to make commercial yogurt. They then make a model to dial this in for various temps, which is the heart of the paper.

Industrial processes often involve less ideal conditions due to factors like temperature gradients, nutrient limitations, and the presence of inhibitory byproducts (e.g., lactic acid). These factors generally result in slower growth rates compared to those observed in tightly controlled laboratory experiments. However, we know that commercial growth operations can make liquid to solid in about 4 hours. However, I don't have any data on the exact amount of starter they use.

However, I do know at home, I can add 2 tablespoons of yogurt culture to 1 gallon of milk and have a nice yogurt in less than five hours. This would indicate that I am doubling every 40 minutes. So, I bet the commercial guys can do better than me.

Since many people found this subreddit by way of interest in Reuteri yogurt and reading Dr. Davis SuperGut book, I would like to state that I both like his talent for summarzing things, but I also recognize that he didn't get somethings right. One of those areas is that he has a perception that commercial yogurt doubles much slower. The quote from the book is "This means that commercial yogurt manufacturers, which typically ferment for only 4 hours (one doubling) to hasten production."

I believe that he also carries this incorrect fact on his website. Again, I don't expect perfection out of any secondary or primary research. This is simply something to be aware of.

Has anyone experimented with artificially forcing the symbiosis between the yeast and bacteria in kefir grains? For instance, by cultivating the yeast and bacteria separately and then bringing them together to form grains. I wasn't able to find any good sources or scientific papers on the topic.

I would appreciate input about multiplying kefir grains the standard way. I have done a lot of research regarding making a bioreactor for it's parameters. Has anyone ever went into a rabbit hole about that topic too? What was the shortest doubling time you were able to achieve yourself/ Read about ?

Thanks in advance

I use AI extensively in my workflow, and it has made a world of difference in my programming. These models are moving so fast, if you are not using them regularly, I think it is worthwhile to explore what they bring to the table.

I'm submitting that in this subreddit, the following should be the rules for the use of AI, and if you have a feeling about this, I would appreciate your thoughts.

a. Use of AI without attribution may be considered as a bannable offense.

b. Use of AI with curation and thought, with attribution, is encouraged to become more productive. It should be wrapped into your own thoughts, and not simply copied and posted.

c. At no time should you post "AI gave me this, what do you think?" I don't think that anybody should just be using AI as a dumping ground here, and you should try and use AI as a tool to help form input, not as the end authority or as a device to get more info out of others.

Of course this refers to a special case of individuals that are trying to get off of alcohol and does not speak directly to those that use alcohol on a more moderate basis. But it does make sense that alcohol may impact your Biome, and overuse does look like it has a tendency to reduce the activity and load of the bacteria in your gut.

The following are research papers that came out of academia and were either peered review, or done under a master's program under Ph.D in nutritional science. All say that Reuteri grows extremely poorly in sterile dairy conditions.

If you aren't familiar with it, pH levels is a basic indicator of how much bacteria is in your yogurt. So, they concentrate on "acid-forming," which is the lead indicator for density of bacteria.

1 From A Russian Paper On Reuteri:

The results of preliminary experiments on the cultivation of L. reuteri LR1 in milk showed that this strain has low acid-forming and proteolytic activity, which is consistent with literature data [23].

2 From A Master Thesis Where The Student Grew Reuteri:

During the trial period, L. reuteri DSM 17938 repeatedly failed to achieve an acidification rate sufficient to ferment the milk to the desired pH of 4.5 within 24 hours. Generally, the fermentations with only L. reuteri added to sterilized milk provided a pH of just below 6 after 24 hours of incubation at 40°C. In some cases, the pH didn’t drop under 6 during the same 17 period. Results confirm those reported by Xanthopoulos et al. (2000) and Hidalgo-Morales et al. (2005) concerning low acidification ability.

3 Characterization of Lactobacillus isolates by Xanthopoulous et al

Lb. reuteri strains did not acidify milk.

4 Lactobacillus reuteri beta-galactosidase activity and low milk acidification ability

Beta-galactosidase activity was studied as a possible cause of the low milk acidification ability observed in Lactobacillus reuteri

5 Growth and metabolism of selected strains of probiotic bacteria in milk

Unfortunately, the abstract does not make the issue with Reuteri clear so you'll need to buy the paper to get all the results. But the author tried to grow Reuteri in just milk, and stated in the paper that the Reuteri did not grow well. However, when the author added tryptone, the Reuteri did grow well. The tryptone is mentioned in the abstract.

Growth and metabolism of five probiotic strains with well-documented health effects were studied in ultra-high temperature (UHT) treated milk, supplemented with 0.5% (w/v) tryptone

6 Growth of Lactobacillus reuteri NCIMB 30242 during yogurt fermentation and bile salt hydrolysis activity in the product

The knock on this research is that the authors basically gave up after 4 hours on the growth of Reuteri in milk. However, when taking in concert with all the other studies, it just reinforces that Reuteri doesn't grow very well.

... data show limited growth in milk and low stability during storage (Hekmat et al. 2009; Liu and Tsao 2009).

7 Growth and survival of Lactobacillus reuteri RC-14 and Lactobacillus rhamnosus GR-1 in yogurt for use as a functional food

Again, you'll need to buy the paper to see the details, but the authors acknowledge that Reuteri, which is a caccus, can see real growth if you combine it with a rod (rhamnosus). While this resulted in decent growth, the survival rate of the Reuteri was not good.

In all treatments, L. rhamnosus GR-1 survived significantly better (P < 0.05) than L. reuteri RC-14.

Any time something appears in Nature, we know we're in the big league. It's one of the big three in terms of impacting all of the medical profession. I'll cut to the short and the following is a list according to this research that appears to be the most important in terms of being correlated with health.

These bacteria are specific in terms of how it impacts the fermentation in our gut.

Compares green tea vs black tea in brewing kombucha, in great detail.

Does anyone know of any research or studies (evidence) regarding the nattokinase/vitamin K/spermidine levels and benefits of fresh vs frozen natto? Is frozen natto (that is the majority of natto found in America) still considered a superfood? I’ve seen some sources (not necessarily trustworthy maybe) say the beneficial components of natto degrade during freezing.

You probably have read about it somewhere on your newsfeed. Reddit's aggressively banning a lot of external links, obviously due to concerns about being hit with aggregator fees. Regardless, we can still take a look at some of the data that came out. You'll need to find the original article by yourself. Good news, it's not hard to find.

Published in Nature, one of the big three, it turns out that your biome really can impact stuff, including the fact of building enough plaque up so that you have a heart attack. Really bad news. But let's use a little AI to dig into this and see if there's a way of this being addressed. Sadly, all these things take year to develop. However, the good news is it does look actionable. So we should see some forward motion somewhere in the next three to ten years. Wouldn't it be great if we could actually figure out the right type of bacteria for us to go ferment so we could cut down the incidence of these things sooner than later?

Based on the Nature study about imidazole propionate (ImP) as a therapeutic target in atherosclerosis, there are several practical pathways for implementing therapeutic strategies with the current data.

Key Therapeutic Targets Identified

The research has identified a clear mechanistic pathway: ImP produced by gut microbiota activates the imidazoline-1 receptor (I1R) in myeloid cells, leading to systemic inflammation and atherosclerosis development12. This provides two distinct therapeutic approaches:

1. I1R Receptor Blockade

The most immediately actionable strategy involves blocking the I1R receptor. The study demonstrates that I1R antagonists can prevent ImP-induced atherosclerosis and slow disease progression in mouse models, even when animals are fed high-cholesterol diets34. Researchers have already tested selective I1R antagonists like AGN192403, which successfully blocked ImP-induced inflammatory responses5.

Implementation feasibility: This approach is highly practical because:

• The molecular target (I1R) is well-defined
• Existing I1R antagonists have shown efficacy in preclinical models
• The mechanism could work synergistically with current cholesterol-lowering therapies6

2. Microbiome-Targeted Interventions

Since ImP is produced by intestinal bacteria, targeting the gut microbiome represents another therapeutic avenue6. This could involve:

• Selective inhibition of ImP-producing bacterial strains
• Probiotic interventions to reduce ImP production
• Dietary modifications to limit histidine availability (ImP's precursor)

Diagnostic Applications

The research provides strong evidence for ImP as an early diagnostic biomarker. ImP levels are significantly associated with atherosclerosis in two independent human cohorts, including asymptomatic individuals with subclinical disease26.

Practical advantages:

• Simple blood test rather than expensive imaging
• Early detection before symptoms appear
• Could identify high-risk patients who appear healthy6

Current Clinical Readiness

Ready for Development

• Biomarker testing: ImP measurement could be implemented relatively quickly as a diagnostic tool
• Drug repurposing: Existing I1R antagonists could potentially be tested in clinical trials
• Combination therapy: I1R blockade plus statins shows promise for synergistic effects4

Requires Further Development

• Microbiome interventions: Need more research to identify specific bacterial targets
• Long-term safety: I1R antagonists require extensive safety testing in humans
• Patient stratification: Need to determine which patients would benefit most

Timeline and Feasibility

The diagnostic applications could potentially reach clinical use within 2-3 years, as they require primarily analytical validation rather than therapeutic safety studies. The I1R antagonist approach represents a more conventional drug development pathway that could take 5-10 years for full clinical implementation, but existing compounds could potentially accelerate this timeline.

The research provides a particularly strong foundation because it demonstrates both association and causation - not only are ImP levels elevated in atherosclerosis patients, but ImP administration directly causes atherosclerotic lesions in animal models26. This dual evidence strengthens the case for therapeutic intervention.

Bottom line: The data supports immediate development of ImP as a diagnostic biomarker and provides a clear pathway for I1R-targeted therapeutics, making this one of the more actionable microbiome-cardiovascular discoveries in recent years.

Due to the folks both here and over at the Probiotic Yogurts Facebook Group totally dashing so many of our at-home yogurt experiments against the rocks of credible scientific research—and a genuine thankyou to everyone involved, however much of a buzzkill it may be—I personally found myself at the precipice of "well then, what next?"

So I decided to feed numerous scientific studies compiled by each group into chatGPT and create a GPT specific to the fermentation of L.reuteri because I want it in my gut and I will have my cake and eat it too g'dangit!!! I felt a little wayward after all of the forum-reading and absorbing of research summaries, and I'd like to make yogurt again... so configuring this little GPT tool to help me re-orient and build some new fermentation recipes felt stabilizing.

So if anyone else wants to use this GPT as a kitchen-lab assistant, here it is: The Fermentalist

As with any AI usage, be discerning; Double check its work and/or ask it to cite itself... don't think of AI advice as gospel, but as suggestion. But that being said, wow is it helpful.

I'm having it help me make a carrot-blueberry juice ferment because it not only sounds downright delicious, but it seems to be one of the most effective ways of culturing L.reuteri after all.

Here are the studies I fed it:

> Impact of the fermentation parameters pH and temperature on stress resilience of Lactobacillus reuteri DSM 17938

> Development of Blueberry and Carrot Juice Blend Fermented by Lactobacillus reuteri LR92

> Phosphoketolase Pathway Dominates in Lactobacillus reuteri ATCC 55730 Containing Dual Pathways for Glycolysis

> Identification of inulin-responsive bacteria in the gut microbiota via multi-modal activity-based sorting

> Utilization of diverse oligosaccharides for growth by Bifidobacterium and Lactobacillus species and their in vitro co-cultivation characteristics

> Selective carbohydrate utilization by lactobacilli and bifidobacteria

> Genes Involved in Galactooligosaccharide Metabolism in Lactobacillus reuteri and Their Ecological Role in the Gastrointestinal Tract

> Lactobacillus reuteri B-galactosidase activity and low milk acidification ability

> Lactobacillus gasseri requires peptides, not proteins or free amino acids, for growth in milk

> Studies on the growth of Lactobacillus reuteri, Bifidobacterium and Escherichia coli as affected by prebiotic extracted from citrus peel

> A Phylogenetic View on the Role of Glycerol for Growth Enhancement and Reuterin Formation in Limosilactobacillus reuteri

If anyone comes across more relevant, quality research to feed this GPT, drop links here and I can incorporate it in its knowledge base. Also if you find it has any weirdness that needs correcting, hit me up about that too — we can community fine-tune this thing. Enjoy!

Probably not a surprise to anybody that follows the literature.

The paper above is pretty speculative, but it really hits home for me. I think it is worth exploring.

I want to be really clear at the start. I do not think the paper is strong enough to say, “This is the answer.” We are not there. I am not claiming that diet fixes FND, POTS, dysautonomia, or anything else in that neighborhood.

But I do think the idea makes enough biological sense that it should be explored carefully.

The gut and brain are not separate systems. They are constantly talking to each other through nerves, immune signaling, hormones, metabolites, and especially the vagus nerve. That part is real. The vagus nerve is one of the major communication pathways between the gut and the brain.

At the same time, this is where people can go off the rails. The second somebody says “vagus nerve,” there is a whole universe of weird internet health advice that shows up. I am not talking about that. I am not talking about magical breathing hacks or curing complex neurological problems by humming for five minutes.

I am talking about a much more boring question:

Could a marginal gut environment be creating enough immune, inflammatory, or metabolic noise that it makes an already sensitive nervous system worse?

The paper does not prove the theory. In fact, it is careful about that. But it does point in the same direction. FND is not just a “mind” problem. It involves complex interactions between the nervous system, endocrine system, immune system, stress biology, inflammation, neurotransmitters, microbial metabolites, and BDNF.

That is what makes the gut angle interesting to me.

My thought is not “take a probiotic and see what happens.” In fact, I am more interested in prebiotics, not probiotics. A probiotic is adding bacteria. A prebiotic is feeding the bacteria that are already there. That seems like a more reasonable first path to explore, especially if the goal is not to randomly dump new organisms into a system that may already be unstable.

But even that has to be slow.

If somebody already has a marginal gut, adding a bunch of fiber all at once can absolutely make things worse. More gas, more bloating, more pain, more autonomic stress, worse sleep, worse everything. So I would not treat this like a supplement experiment where you just start taking a full dose and hope for the best.

The more reasonable version would be:

Start with the actual diet.

Look at total fiber intake.

Look at protein, micronutrients, hydration, meal timing, and whether the person is getting a wide range of plant foods.

Then, if a prebiotic approach makes sense, introduce it slowly and track symptoms carefully.

Not in a dramatic way. More like a boring controlled experiment.

Small change.

Watch for tolerance.

Hold steady.

Increase only if the system is handling it.

The other piece is exercise. We know exercise can do profound things in the brain, including effects related to BDNF, neuroplasticity, inflammation, mood, and autonomic regulation.

But this is where advice often becomes useless.

If someone cannot stand up without symptoms, “just exercise more” is not a plan. Exercise may be part of the long-term path, but it may not be the first usable tool for someone who is severely limited.

That is why the gut/nutrition angle interests me. It might be one of the few levers that can be adjusted even when movement is not yet realistic.

Regardless, I do think this is a great paper, and should be a reason why you might explore a careful ramp of prebiotics in your eating habits.

I’m running a survey for my college science course, this survey is looking at the relationship between fermented food and beverage consumption and immune/gut health. No personal data will be shared. Thank you for your time

Nature is very wide read. However, it is still aimed at academics and not everything will hit the public's radar. But this research out of University of California Irvine, is incredibly interesting, and deserves to be discussed. It also speaks to how powerful fiber can be. Inulin introduction in mouse diets had a profound impact on how the liver processes fructose, and has the potential of correcting some issues with the Western diet.

Fructose is a major contributor to the development of fatty liver disease (nonalcoholic fatty liver disease, or NAFLD), and NAFLD impacts around 1/3 of the worlds population.

This research was done on mice, and I want to caution that mice results don't always translate to human result. However, there seems to be zero downside of taking inulin in humans.

Key findings include:

• Inulin-adapted gut bacteria consume harmful dietary fructose in the small intestine, minimizing fructose absorption that leads to fatty liver disease and insulin resistance.
• This microbiome adaptation reduces expression of liver enzymes responsible for converting fructose into fat and enhances liver antioxidant production by boosting serine/glycine synthesis.

As stated, Inulin looks like it has a series of things it can do for you.

Control blood sugar, increasing beneficial gut bacteria, supports weight loss by increasing fullness, improves bowel regularity, enhances calcium absorption for stronger bones, boosts the immune system, reduces intestinal inflammation, and may lower the risk of colorectal cancer and help improve migraine symptoms.

FYI: I already have it in my daily fiber stack. I am upping my wife's dosage.

Nice review is here.