Berberine has a big effect on TMAO, you need a gram a day I think. My free AI:
Does Berberine use have any effect on TMAO production?
Berberine use
significantly reduces the production of TMAO (trimethylamine N-oxide). Research indicates that berberine acts as a “microbiota remodeler,” specifically targeting the gut-liver axis to inhibit the biosynthesis of this harmful metabolite.
Berberine reduces TMAO levels through several key biological pathways:
Gut Microbiota Remodeling: It significantly alters gut bacterial composition, notably by reducing the Firmicutes/Bacteroidetes ratio. It decreases the abundance of TMA-producing bacteria such as Lachnospiraceae and Ruminococcus while increasing beneficial genera like Lactobacillus and Akkermansia.
Enzyme Inhibition (CutC/D): Berberine and its metabolite, dihydroberberine, directly bind to and inhibit the activity of choline-trimethylamine lyase (CutC/D), the primary bacterial enzyme that converts dietary choline into TMA (the precursor to TMAO).
Hepatic Modulation: In animal models, berberine has been shown to downregulate the expression of flavin-containing monooxygenase 3 (FMO3) in the liver, the host enzyme responsible for oxidizing TMA into TMAO.
[image]Nature +5
Clinical Evidence
Atherosclerosis Patients: In a 4-month clinical study, patients taking 0.5g of berberine twice daily showed a 35% reduction in plasma TMAO and a 37% reduction in plasma TMA.
Hypertension Patients: A study of hypertensive patients found that 0.4g taken three times daily reduced plasma TMAO levels by 16.7% over three months, which correlated with improved vascular function and lower blood pressure.
Thrombosis Risk: By lowering TMAO, berberine has been found to decrease platelet hyperactivity and reduce the potential risk of arterial thrombosis.
Higher fiber intake was associated with a 15 to 30 percent reduction in all-cause mortality and cardiovascular mortality. Lower rates of coronary heart disease, stroke, type 2 diabetes, and colorectal cancer.
The gas increased after I started using the Thorne Fiber Blend supplement. It has lessened since I have started taking the Acarbose separately (not at the same time). I am going to try the Green banana fiber after the Thorne runs out.
I tried Green banana powder before - I tolerated it very well. Will buy again, but Acarbose didn’t work for me. My fasting BG is 90, but it spikes high after meals then goes fast back to the basic reading, but still keeps my HA1c at 5.9 - 6 no matter what I try. I’m not on Metformin or Berberine. Will try again (and again) to modify how I eat, and help me God
People who eat a lot of fibre spend more time in deep sleep
The most comprehensive study to date has revealed what we need to eat throughout the day to sleep well that night
Eating more fibre may help you sleep more deeply, while consuming a wider variety of fruit, vegetables and nuts could help you nod off faster. That’s according to the most comprehensive look yet at how what we eat throughout the day affects our sleep that night.
“Increasing fibre and plant variety is already recommended for overall health, carries low risk for most people and may offer sleep benefits as an additional upside,” says Hagai Rossman at the Weizmann Institute of Science in Israel.
Prior studies have linked eating fibre-rich, plant-based foods to better sleep, but these mostly relied on people recalling their diet in surveys, sometimes weeks or months later. In addition, when sleep has been objectively measured, it has typically been via movement trackers that cannot distinguish between its deeper and lighter phases, which is important for gauging sleep quality.
Now, Rossman and his colleagues have gained the clearest picture to date by analysing sleep and dietary data collected from more than 3500 adults, aged 53, on average. “Previous studies haven’t looked at so many dietary and sleep factors,” says Marie-Pierre St-Onge at Columbia University in New York City.
Over two consecutive days, each participant logged what they ate in a mobile app, either during its consumption or shortly afterwards. At night, they wore a device that has been approved by the US Food and Drug Administration to measure sleep. This is comprised of sensors worn on the chest, a wrist and a finger that track snoring, blood oxygen levels, and heart and breathing rates.
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It is unclear exactly why fibre has these effects, but studies suggest that gut microbes can ferment it into short-chain fatty acids, such as butyrate, that reduce inflammation and alter gut-to-brain signalling in a way that promotes deep sleep, says Rossman.
The researchers also found that those with an above-average fibre intake had a slightly lower heart rate during the night than those who consumed less. A low nocturnal heart rate suggests that a person has entered a state of deep rest and repair, which puts less strain on the heart. “A 1 beat-per-minute difference [as observed between the high- and low-fibre groups] might not be that important for one night, but if that difference is sustained over decades or a lifetime, that could make an important difference [for cardiovascular health],” says St-Onge.
Fascintaing stuff that just validates the gut brain axis and the power of longest information superhighway there exists in our bodies. Its called Vagus nerve.
Butyrate → vagal activation → higher HRV → more stable:
Respiratory sinus arrhythmia
Baroreflex sensitivity
Reduced nocturnal sympathetic spikes
This decreases:
Micro-arousals
Sleep fragmentation
C) Reduces Neuroinflammation
Butyrate is an HDAC inhibitor.
In CNS:
Lowers microglial activation
Reduces inflammatory tone in hypothalamus
Improves circadian gene expression (CLOCK/BMAL1 modulation)
Inflammation disrupts SWS — reducing it improves depth.
Had 29 gm worth of fiber rich supper this evening. Will see how the HR trends and the deep sleep tonight.
Simulations of your gut may predict which probiotics will stick
Tests of “digital gut” simulations hint at personalized probiotics but not a cure‑all yet
Figuring out which bacteria or other nutrients your gut needs may one day be as simple as running detailed computer simulations.
From pills to yogurts to sodas, probiotics are being repackaged and marketed to us more and more, with the promise of boosting our “gut health.” But while commercially available probiotics work for some people, this one-size-fits-all approach hasn’t reliably benefited consumers. Instead, new simulations can predict whether a specific bacterial strain will successfully take up residence in a person’s gut, researchers report February 19 in PLOS Biology.
This is a meandering thread, so please allow me to ask an unrelated question.
If a product says that two capsules have 1020 mg of potassium “as potassium bicarbonate,” does that mean that the capsules have 1020 mg of potassium or 1020 mg of potassium bicarbonate?
I ask because potassium bicarbonate is 40% potassium and 60% bicarb, and I’m not sure what the label is saying.
I’ve learned that citrate is a good alkalizing agent. Just ordered moderate doses of magnesium citrate, calcium citrate, and citric acid, which I will supplement with grapes, nuts, and oatmeal.
Citrate is good for alkanizing. At times my urinary pH is over 9. This obviously affects the solubility of various species. Urate, for example, is not that soluble at 5.5.
My view about sodium citrate is that it is quite distinct from sodium chloride and it is perhaps the anion that is really significant from a BP perspective.
Nutrition Experts are Wrong About Fiber. (Norwitz)
I. Executive Summary
The provided transcript analyzes a high-resolution, multi-omics randomized crossover trial conducted by the Stanford Snyder Lab (2022), comparing the physiological effects of two soluble dietary fibers: arabinoxylan (AX) and long-chain inulin. The core thesis challenges the homogenized public health directive to “eat more fiber,” demonstrating that distinct fiber types yield radically divergent, host-specific biological outcomes. The analysis reveals that AX fiber consistently reduces low-density lipoprotein (LDL) cholesterol in a dose-dependent manner. This reduction is likely mediated via altered bile acid metabolism, enhanced fecal excretion, and systemic polyphenol signaling. Conversely, high-dose inulin supplementation (30 grams/day) paradoxically induced hepatotoxicity—evidenced by elevated alanine aminotransferase (ALT)—and systemic inflammation (IL-6) in a subset of healthy participants, necessitating trial suspension for those individuals.
The speaker correctly emphasizes that dietary fiber is not a monolithic therapeutic agent but a heterogeneous class of bioactive compounds requiring precision application. The transcript identifies the critical interplay among fiber type, dosage, and host microbiome functionality. Additionally, the video posits that high dietary protein intake may synergistically amplify the lipid-lowering effects of AX fiber, though this remains an observational correlation requiring targeted causal investigation to separate verified metabolic interactions from spurious dietary overlaps.
However, the transcript contains a severe translational gap regarding a promoted commercial probiotic (Winnow Labs). The speaker claims this product binds and excretes microplastics from the human gastrointestinal tract. A live clinical search reveals a complete absence of human randomized controlled trials (Level A/B evidence) substantiating this claim. The assertion extrapolates in vitro bacterial screening directly to human clinical efficacy without requisite safety, pharmacokinetic, or longitudinal health outcome data. The actionable intelligence derived from this transcript lies in the precision application of specific functional fibers for targeted metabolic outcomes, while discarding unverified commercial supplementation claims.
II. Insight Bullets
“Dietary fiber” functions as a heterogeneous class of bioactive molecules; prescribing it as a monolithic intervention is scientifically inaccurate.
Arabinoxylan (AX) and inulin are both classified as soluble fibers but trigger diametrically opposed metabolic and hepatic responses.
AX fiber supplementation dose-dependently reduces LDL cholesterol by up to 20 mg/dL in human cohorts.
High-dose long-chain inulin (30 grams/day) induces acute hepatotoxicity in sensitive individuals, indicated by elevated ALT levels.
High-dose inulin drives systemic inflammation, measurable via increased Interleukin-6 (IL-6).
Adverse hepatic and inflammatory responses to inulin are highly individualized, highlighting the necessity of host-microbiome compatibility.
AX fiber operates via multiple pathways: direct bile acid binding/excretion, gut microbiome composition shifts, and systemic receptor signaling.
AX acts as a molecular delivery vehicle for polyphenols, specifically ferulic acid, which subsequently modulate lipid metabolism systemically.
Observational data within clinical trials suggest a high dietary protein intake may amplify AX fiber’s cholesterol-lowering efficacy, but causal mechanisms remain unverified.
Low-to-moderate dose inulin (10 grams/day) may confer metabolic benefits without triggering the hepatotoxicity observed at high doses.
Pre-clinical models suggest gut bacteria utilize inulin to degrade dietary fructose, potentially mitigating hepatic fructose spillover and fatty liver disease.
Current clinical diagnostic tools are insufficiently advanced to accurately prescribe targeted probiotics based on individualized microbiome assays.
Time-restricted eating (TRE) enforcing a feeding window of under 10 hours supports circadian rhythmicity, though human microbiome shifts resulting strictly from TRE remain clinically ambiguous.
Fermented foods introduce transient microbial diversity, but gastrointestinal tolerance is highly variable among individuals with distinct mucosal pathologies.
Claims that specific commercial probiotics bind and neutralize microplastics in the human gut lack in vivo clinical validation and represent a primary safety and efficacy unknown.
Precision nutrition paradigms must replace blanket dietary guidelines, focusing strictly on compound identity, exact dosage, and individual host phenotypes.
III. Adversarial Claims & Evidence Table
Specific Claim
What they cited
Scientific Reality (Current Data) & Link
Evidence Grade
Verdict
AX fiber lowers LDL cholesterol dose-dependently.
Stanford Snyder Lab 2022 Crossover RCT.
Verified. AX supplementation significantly reduced LDL and increased bile acids in humans. Lancaster et al., 2022
Level B
Strong Support
High-dose inulin causes liver damage (ALT) and inflammation.
Stanford Snyder Lab 2022 RCT.
Verified. 30g/day inulin spiked ALT and systemic inflammation in a subset of healthy individuals. Lancaster et al., 2022
Level B
Strong Support
Low-dose inulin protects the liver from fructose.
Prior video / Unseen mechanism data.
Inulin alters gut bacteria to degrade fructose, preventing fatty liver primarily in murine (mouse) models. Human data is mixed. Jang Lab, 2025 / Zheng et al., 2020
Level D
Translational Gap
High protein intake amplifies AX’s cholesterol-lowering effect.
Stanford Snyder Lab 2022 RCT (Correlation).
Verified as an observational finding within the RCT. Causal relationship is unproven and requires dedicated trials. Lancaster et al., 2022
Level C
Speculative
Time-restricted eating (<10 hrs) resets the gut microbiome.
Personal protocol.
Early TRE shows metabolic benefits, but RCTs report small microbiome changes of uncertain clinical significance compared to standard diets. Moro et al., 2022
Level B
Plausible
Winnow Labs probiotic binds and neutralizes microplastics in human gut.
Internal in vitro screening.
Source unverified in live search. Zero Level A/B human clinical data exists proving microplastic neutralization or excretion by probiotics in vivo.
Level E
Safety Data Absent / Unsupported
IV. Actionable Protocol (Prioritized)
This protocol synthesizes verified data into a pragmatic framework, aggressively filtering out speculative commercial claims.
High Confidence Tier (Level A/B Evidence)
Arabinoxylan (AX) for Lipid Management: For individuals targeting LDL cholesterol reduction, AX fiber presents a clinically viable intervention. Titrate dosage slowly from 10 grams to 30 grams per day to assess gastrointestinal tolerance.
Precision Fiber Selection: Discontinue the use of generic “mixed fiber” supplements. Select single-ingredient fibers based on explicit metabolic goals (e.g., AX for lipids, avoiding high-dose inulin for liver preservation).
Experimental Tier (Level C/D Evidence - High Safety Margin)
Low-Dose Inulin: If utilized for metabolic support or glycemic control, strictly limit inulin intake to 10 grams per day to avoid hepatotoxic thresholds. Monitor liver function panels (AST/ALT) if using long-term.
Time-Restricted Eating (TRE): Implement an 8 to 10-hour feeding window aligned with daylight hours (Early TRE). While microbiome alterations are clinically uncertain, the metabolic and glycemic benefits carry a high safety margin and robust secondary support.
Protein-Fiber Co-ingestion: Combine AX fiber supplementation with adequate dietary protein. While the synergistic cholesterol-lowering effect is currently speculative, optimizing protein intake carries independent longevity and lean mass benefits.
Red Flag Zone (Debunked / Safety Data Absent)
High-Dose Inulin (>20-30 grams/day): Contraindicated. Carries a verified risk of inducing hepatocellular injury and systemic inflammation.
Anti-Microplastic Probiotics: Avoid. Translating in vitro bacterial binding of plastics to human gastrointestinal efficacy ignores complex gut motility, pH degradation, and mucosal immunity. Safety data is entirely absent.
V. Technical Mechanism Breakdown
Arabinoxylan (AX) Lipid Modulation via Enterohepatic Circulation: AX increases the viscosity of the intestinal lumen, mechanically binding bile acids. The liver compensates for this continuous fecal bile acid loss by upregulating the enzyme cholesterol 7 alpha-hydroxylase (CYP7A1). This enzyme catalyzes the rate-limiting step in converting circulating endogenous cholesterol into new bile acids, effectively draining the systemic LDL pool.
Polyphenol Systemic Signaling: AX acts as a structural matrix for polyphenols. Ferulic acid, covalently bound to the arabinose branches of AX, is liberated by microbial esterases in the lower gastrointestinal tract. Once absorbed into systemic circulation, ferulic acid functions as a signaling molecule, reducing hepatic oxidative stress and modulating lipid metabolism pathways.
Inulin-Induced Hepatotoxicity (High Dose): Rapid and excessive fermentation of long-chain inulin alters the osmotic balance and microbial ecology of the colon. This dysbiosis can degrade the mucin layer, increasing intestinal permeability (“leaky gut”). The resulting translocation of lipopolysaccharides (LPS) from the gut lumen into the portal vein activates hepatic Kupffer cells via Toll-like receptor 4 (TLR4). This cascade drives the overproduction of pro-inflammatory cytokines, specifically IL-6, resulting in hepatocellular stress and the subsequent leakage of intracellular ALT into the bloodstream.
Bile Acid Receptor Signaling: Beyond mere excretion, specific fibers shift the microbial conversion of primary bile acids into secondary bile acids, such as ursodeoxycholic acid (UDCA) and lithocholic acid (LCA). These secondary bile acids escape the gut and act as potent endocrine hormones. They bind to the Farnesoid X Receptor (FXR) in the liver and the Takeda G-protein Receptor 5 (TGR5) in systemic tissue, fundamentally altering whole-body glucose and lipid homeostasis. Additional multi-omics data is required to map the exact secondary bile acid profiles generated by individual fiber subtypes.
A comprehensive market analysis indicates that sourcing 10 distinct, consumer-direct suppliers of pure arabinoxylan powder is currently impossible. The commercial market for this compound is highly consolidated. Most arabinoxylan is either restricted to B2B wholesale supply chains (e.g., Comet Bio), compounded into proprietary encapsulated formulas, or sold as research-grade reagents at prohibitive costs.
Below are the only three verifiable, in-stock sources for arabinoxylan explicitly labeled and sold as a powder available for shipping to the United States.
Note: For the BioBran/Lentin Plus products, each packet/bag contains 1.4 grams of total powder (yielding 1000 mg of active MGN-3 arabinoxylan compound). The total weight calculated above relies on the gross powder weight (1.4 g per sachet) to ensure accurate comparative density pricing.
Shipping Cost Summary:
Rank 1 (Walmart): Free shipping.
Rank 2 (eBay - happy japanese): Free shipping (import fees included in the listing price).
Rank 3 (eBay - Minoxidil Wholesale): $30.00 flat rate for economy shipping from outside the US.
Pharmacological and Longevity Context
For applications in healthcare and longevity, arabinoxylan is primarily investigated for its capacity to delay immunosenescence and regulate metabolic homeostasis.
Data indicates that enzymatically modified arabinoxylan (such as the MGN-3/BioBran variant) directly upregulates Natural Killer (NK) cell cytotoxicity and enhances T and B lymphocyte proliferation. This is achieved through the modulation of critical cytokines, including TNF-alpha and IFN-gamma. Furthermore, as a complex hemicellulose polysaccharide, its degradation by gut microbiota yields highly bioavailable short-chain fatty acids (SCFAs), predominantly butyrate and propionate. These metabolic byproducts are critical in downregulating systemic inflammation pathways (such as NF-kappa B) and improving glucose homeostasis, mechanisms that are central to extending healthspan.
Its very questionable, how they managed to keep this bacteria alive in capsules.
I found a way cheaper product, it’s japanese. Miyarisan. Contains only Clostridium butyricum, which is not aerofobic as akkermansia. But its should be enough to get butyric acid with inulin, and especcialy resistant starch.
