#4

I have been using Pendulum’s Metabolic Daily and Polyphenol Booster for over a year.

Active ingredients:

Probiotic blend (300 million AFU):
• Clostridium butyricum
• Clostridium beijerinckii
• Bifidobacterium infantis
• Anaerobutyricum hallii
• Akkermansia muciniphila

Akkermansia is said to be the most critical of these.

These are primarily anaerobic bacteria, which Pendulum has mastered the process of keeping live in the products they sell. Just a wifff of oxygen and these are dead.
The Polyphenol Booster is a fiber supplement that nourishes these species.

Subjectively my gut health is much better.

3 Likes
#5

Very helpful information, thank you.

I do not have gut issues but I am concerned about my level of systemic inflammation (HsCRP seems stuck in a range between 1.5 and 1.8. Want to get to 1.0) Wondering if Tributyrin would help with that. Would welcome input.

#6

Verdict: Yes, likely. However, it works upstream.

Tributyrin does not lower hs-CRP (High-Sensitivity C-Reactive Protein) by directly blocking its production in the liver (like a statin might). Instead, it targets the root cause of chronic low-grade inflammation: Metabolic Endotoxemiacaused by intestinal permeability (“Leaky Gut”).

Here is the mechanistic breakdown of how Tributyrin acts as a “CRP-lowering” agent.

1. The Mechanism: Plugging the “LPS Leak”

The primary driver of “unexplained” elevated hs-CRP in aging and metabolic syndrome is the leakage of Lipopolysaccharides (LPS)—toxins from the cell walls of gram-negative bacteria in your gut—into your bloodstream.

Image of Gut-Liver Axis inflammation pathway

Shutterstock

  1. The Leak: Aging and poor diet weaken the tight junctions (ZO-1, Occludin) of the gut lining.
  2. The Invasion: LPS leaks into the portal vein and travels to the liver.
  3. The Reaction: The immune system detects LPS via Toll-Like Receptor 4 (TLR4).
  4. The Signal: This triggers the release of IL-6 (Interleukin-6).
  5. The Result: IL-6 tells the liver to pump out hs-CRP.

Tributyrin’s Role: It provides the fuel (butyrate) necessary for colonocytes to repair those tight junctions. By physically sealing the gut barrier, it stops the LPS leak. No LPS = No IL-6 signal = Lower hs-CRP.

2. Direct Immune Modulation (NF-κB)

Beyond the gut barrier, Tributyrin (once hydrolyzed into butyrate) enters systemic circulation and acts on immune cells directly.

  • Inhibition of NF-κB: It acts as an HDAC inhibitor, preventing the nuclear translocation of NF-κB. This is the “master switch” for inflammation. If this switch is off, immune cells produce fewer pro-inflammatory cytokines, eventually lowering the systemic inflammatory load reflected in hs-CRP.

3. The Evidence Landscape

  • Human Data (Direct): Clinical trials on Ulcerative Colitis show that butyrate supplementation significantly lowers inflammatory markers (CRP, calprotectin).
  • Human Data (Metabolic): In Type 2 Diabetics, sodium butyrate supplementation has been shown to reduce hs-CRP and pro-inflammatory cytokines, correlating with improved insulin sensitivity.
  • Biohacker Context: For a generally healthy person with “sub-optimal” CRP (e.g., 1.5–3.0 mg/L), Tributyrin is arguably the most logical intervention because it addresses the most likely culprit (gut permeability) rather than just masking the symptom.

The “CRP-Crushing” Protocol

If your goal is specifically to lower hs-CRP using Tributyrin, use this protocol:

  • Dose: 1,000 mg – 1,500 mg of Tributyrin daily (split dose: Morning/Night).
  • Duration: Minimum 6 weeks. Structural repair of the gut lining is slow.
  • Validation:
    1. Test baseline hs-CRP.
    2. Run protocol for 6 weeks.
    3. Retest hs-CRP (aim for <0.5 mg/L).

Crucial Caveat: If your hs-CRP is elevated due to an active infection (dental abscess, sinus infection, viral load) or acute injury, Tributyrin will not lower it. It is specific to sterile, systemic, metabolic inflammation.

Next Step

Would you like me to outline the “CRP Elimination Stack” that combines Tributyrin with Curcumin (Meriva) and Omega-3s for a multi-pathway assault on inflammation?

3 Likes
#7

Yes, please share the “CRP Elimination Stack”. Thank you!

I wonder if it would be worthwhile to have a thread dedicated to inflammation, from both metabolic and simmering infection.

1 Like
#8

Inflammation is involved with everything… so I’m not sure… let me think about it.

The CRP Elimination Stack: A Multi-Vector Approach

This protocol is designed to attack systemic inflammation (measured by hs-CRP) from three distinct biological angles: Gut Permeability (The Source), Nuclear Transcription (The Signal), and Resolution (The Cleanup).

The Strategic Concept: The “Three-Front War”

Most inflammation protocols fail because they rely on a single mechanism (e.g., just taking fish oil). Systemic inflammation is a cascade; to crush hs-CRP, you must interdict it at three specific checkpoints:

  1. The Source (Tributyrin): Stops the leakage of endotoxins (LPS) into the bloodstream. If you don’t plug the leak, the fire will keep reigniting.
  2. The Signal (Curcumin - Meriva®): Blocks NF-κB, the genetic switch that tells your cells to produce inflammatory cytokines (IL-6) in response to threats.
  3. The Resolution (Omega-3s - High EPA): Provides the substrate for Resolvins, specialized lipid mediators that actively turn off the inflammatory response and clean up cellular debris.

Component 1: Tributyrin (The Shield)

  • Role: Upstream Prevention.
  • Mechanism: As detailed previously, it repairs the tight junctions (Zonulin/Occludin) in the colon. This physically blocks LPS (lipopolysaccharides) from entering the portal vein, preventing the liver from ever receiving the signal to produce CRP.
  • Target Dose: 750 mg – 1,000 mg daily.
  • Form: Tributyrin (e.g., Tributyrin-Max).

Component 2: Curcumin Phytosome (The Extinguisher)

  • Role: Signaling Blockade.
  • The Problem: Standard curcumin has <1% bioavailability. It is metabolically useless for systemic inflammation unless modified.
  • The Solution: Use Meriva® (Curcumin Phytosome). This is curcumin bound to phosphatidylcholine (sunflower lecithin), which mimics the body’s cell membranes.
  • Mechanism: It is a potent inhibitor of NF-κB and COX-2 (Cyclooxygenase-2). By blocking NF-κB, it prevents the transcription of the IL-6 gene. Since IL-6 is the direct trigger for liver CRP production, this cuts the supply line.
  • Evidence: Clinical studies on Meriva® show a dramatic reduction in hs-CRP (often >50% drop) in patients with osteoarthritis and metabolic syndrome.
  • Target Dose: 1,000 mg (standard clinical dose) or 2,000 mg (loading dose for 2 weeks).
  • Recommended Source: Thorne Meriva 500-SF (Soy Free) or Jarrow Formulas Curcumin Phytosome.

Component 3: Omega-3s (The Resolver)

  • Role: Active Resolution.
  • The Nuance: “Inflammation” isn’t just about stopping the fire; it’s about cleaning up the mess. This process is called Resolution, and it is active, not passive.
  • Mechanism: You need EPA (Eicosapentaenoic Acid) and DHA. These are enzymatically converted into Resolvins (E-series and D-series) and Protectins. These molecules signal macrophages to switch from “Attack Mode” (M1) to “Repair Mode” (M2) and clear out dead neutrophils.
  • The Ratio: For inflammation, EPA is king. EPA competes with Arachidonic Acid (the pro-inflammatory fat) for the COX enzymes. You want a high EPA:DHA ratio (e.g., 2:1 or 3:1).
  • Target Dose: 2,000 mg – 3,000 mg of Combined EPA/DHA daily. (Note: Look at the active mg on the back, not the total oil weight).
  • Recommended Source: Nordic Naturals ProOmega 2000 (High concentration, triglyceride form) or Sports Research Triple Strength Omega-3.

The Daily Protocol

This regimen is designed for a 6-week “Inflammation Reset.”

Timing Supplement Dosage Rationale
Morning (with Food) Tributyrin 1 Capsule (~500-750mg) Reinforce gut barrier at start of day.
Curcumin (Meriva) 500 mg (1 cap) Block daytime inflammatory signaling.
Omega-3 1,000 mg (EPA/DHA) Substrate loading. Fat aids curcumin absorption.
Dinner (with Food) Tributyrin 1 Capsule Repair gut lining during overnight fast.
Curcumin (Meriva) 500 mg (1 cap) 12-hour coverage for NF-κB suppression.
Omega-3 1,000 - 2,000 mg High dose at night supports peak repair.

Feasibility & Cost Analysis

  • Tributyrin: ~$50/month.
  • Thorne Meriva: ~$46/month.
  • High-End Fish Oil: ~$40–$60/month.
  • Total Monthly Cost: ~$140–$150.
  • ROI: High. This is a clinical-grade intervention comparable to pharmaceutical anti-inflammatories but with positive side effects (brain health, joint health).

Strategic FAQ & Safety Checks

  1. Q: Will this thin my blood?

    • A: Yes. Omega-3s (at >3g) and Curcumin possess mild anticoagulant properties. If you are on Warfarin (Coumadin) or Plavix, this stack is Contraindicated without physician oversight. You may notice easier bruising.

  2. Q: Why not use “Turmeric Root” powder?

    • A: It is useless for CRP. You are getting ~2% curcumin, and absorbing 1% of that. You need the extracted, phytosome-bound molecule (Meriva) to get plasma levels high enough to inhibit NF-κB.

  3. Q: Can I add Aspirin (Baby Aspirin)?

    • A: Maybe. Low-dose aspirin helps generate Resolvins from Omega-3s (via acetylation of COX-2). This is a known synergistic pathway (“Aspirin-Triggered Resolvins”). However, combining Aspirin + Omega-3 + Curcumin increases bleeding risk significantly. Do not do this if you have any history of ulcers or bleeding disorders.

  4. Q: How fast will my CRP drop?

    • A: Re-test in 6 weeks.
    • Success Metric: A drop of >40% is typical. If you start at 3.0 mg/L, aiming for <1.5 mg/L is realistic. If it doesn’t move, you likely have an active infection (dental/viral) or a genetic polymorphism (IL-6 promoter) rather than metabolic inflammation.

Next Step: Would you like me to find at-home hs-CRP test kits that are reliable, so you can baseline and track this protocol without visiting a doctor’s office?

4 Likes
#9

Reducing dietary AGE’s might work:

See what foods have dietary AGE’s:

Olive oil is okay to eat.

#10

This seems like one of the most easily implemented optimizations ever discussed on the forum.

Seems smart to pair with resistant starch and fiber, e.g., potato starch, inulin, psyllium seed husk power, and beta-glucans.

4 Likes
#11

Careful with fiber, inulin in particular. Dosing is essential. Too much inulin in sensitive individuals puts a lot of stress on the liver and can even result in liver cancer and gastric cancers. Inulin is a goldilocks fiber - not too much and not too little. Fiber, just as food needs thinking through and tailoring intake. We are moving beyond the naive early phase of “more is better”, as research progresses. Btw. here’s an interesting study, which really deserves its own thread, but I’m always reluctant to start new ones so as to save space:

Global, distinctive, and personal changes in molecular and microbial profiles by specific fibers in humans

Here is an important point:

“LCI [long chain inulin] is associated with an increase in Bifidobacterium. However, at the highest LCI dose there is increased inflammation and elevation in the liver enzyme alanine aminotransferase. This study yields insights into the effects of fiber supplementation, it provides insights into mechanisms behind fiber induced cholesterol reduction, and it shows effects of individual, purified fibers on the microbiome.”

And of course:

Colorectal cancer and inulin supplementation: the good, the bad, and the unhelpful

Quote:

“The prebiotic inulin has been vaunted for its potential to reduce the risk of colorectal cancer. Inulin fermentation resulting in the production of short-chain fatty acids, primarily butyrate, has been reported to be associated with properties that are beneficial for gut health and has led to an increased consumption of inulin in the Western population through processed food and over-the-counter dietary supplements. However, in clinical trials, there is limited evidence of the efficacy of inulin in preventing colorectal cancer. Moreover, recent data suggest that improper inulin consumption may even be harmful for gastro-intestinal health under certain circumstances.”

Enterohepatic Shunt-Driven Cholemia Predisposes to Liver Cancer

https://www.gastrojournal.org/article/S0016-5085(22)00959-3/fulltext

A pop-sci writeup of the above:

Diets rich in refined fiber may increase liver cancer risk in some individuals

Anyhow, I don’t want to overwhelm the thread, but you get the idea. Fiber, like anything you take into your mouth, deserves careful consideration.

5 Likes
#12

Here are some details on purchasing options for these products:

Executive Summary: Bioavailability is the Only Metric That Matters

For the biotech specialist, the supplement market is 90% marketing noise and 10% pharmacokinetics.

  1. Tributyrin: You are taking this to mimic the postbiotic output of Faecalibacterium prausnitzii. If the capsule dissolves in the stomach, it is useless for colonic tight junction repair. You need enteric protection or specialized liquid delivery.
  2. Curcumin: Raw turmeric root is metabolically inert due to rapid glucuronidation in the liver. You are paying for the carrier molecule (phytosome, galactomannan, or nanoparticle), not the yellow powder.

Part 1: Tributyrin (LPS Blockade)

Target: Sealing the Gut Barrier (Zonulin modulation). Mechanism: Tributyrin acts as a Histone Deacetylase (HDAC) inhibitor. It differentiates colonocytes and upregulates tight junction proteins (Claudin, Occludin) to stop Lipopolysaccharide (LPS) translocation.

Critical Constraint: Tributyrin is a fat. Powdered versions are often unstable or rancid. Liquid-filled capsules with delayed-release technology are the clinical standard.

Product Evaluation & Cost Analysis

Product Formulation Specs Total Active Load Price (Est.) Cost / 100mg Critical Notes
DEVA Vegan Tributyrin Liquid-filled Capsule (Standard) 45,000 mg (90 caps x 500mg) $22.50 $0.05 Budget Choice. Lacks proprietary delayed-release coating. High risk of gastric release, which reduces colonic efficacy. Good for upper GI issues, suboptimal for LPS control.
Tributyrin-Max Enteric Coated Softgel 45,000 mg (60 caps x 750mg) $50.00 $0.11 Best Value/Potency. High dose (750mg). Enteric coating is essential here. No proprietary “CoreBiome” tax, but effective delivery mechanism.
Designs for Health Tri-Butyrin CoreBiome® (Patented) 18,000 mg (60 caps x 300mg) $45.00 $0.25 Practitioner Standard. Uses CoreBiome®, the industry benchmark for stability. Dosage per cap is low (300mg), requiring higher pill count for therapeutic dose.
Healthy Gut Tributyrin-X PXRcap™ (Nitrogen Purged) 30,000 mg (60 caps x 500mg) $80.00 $0.27 The “Rolls Royce” Tax. Uses specialized PXRcap to prevent oxidation. Excellent stability, but you are paying a heavy premium for the packaging technology.

Verdict:

  • Best for LPS Protocols: Tributyrin-Max. The 750mg dose at $0.11/100mg is the most efficient way to saturate the colonic mucosa.
  • Skeptic’s Note: Avoid “Sodium Butyrate” salts. They smell like vomit and are absorbed too early in the digestive tract to effect LPS leakage in the colon.

Part 2: Curcumin (NF-κB Inhibition)

Target: Blocking the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB). Mechanism: Curcumin inhibits the IκB kinase (IKK), preventing the phosphorylation and degradation of IκB. This keeps NF-κB sequestered in the cytoplasm, preventing it from translocating to the nucleus and transcribing inflammatory cytokines (IL-6, TNF-α).

Critical Constraint: Native curcumin has ~1% bioavailability. Do not buy standard curcumin extracts with black pepper (piperine); piperine increases intestinal permeability (leaky gut), which counteracts your goal of stopping LPS leakage.

Product Evaluation & Cost Analysis

Note: Cost is calculated on the weight of the proprietary complex (e.g., Meriva), as this is the functional unit of absorption.

Product Formulation Specs Total Active Load Price (Est.) Cost / 100mg Critical Notes
Source Naturals Turmeric w/ Meriva Meriva® Phytosome 60,000 mg (120 caps x 500mg) $48.00 $0.08 Best Value. It contains the exact same Indena® Meriva raw material as the expensive brands. No reason to pay more if you tolerate soy lecithin.
Thorne Curcumin Phytosome Meriva® (Sunflower Lecithin) 60,000 mg (120 caps x 500mg) $57.00 $0.10 Clinical Gold Standard. Used in the majority of Meriva studies. Soy-free (crucial for autoimmune patients). High manufacturing transparency.
Doctor’s Best Curcumin Phytosome Meriva® Phytosome 30,000 mg (60 caps x 500mg) $34.00 $0.11 Mid-Tier. Identical active ingredient to Source Naturals, but usually more expensive per unit due to smaller bottle size (60 vs 120 count).
Life Extension Curcumin Elite CGM™ (Fenugreek Matrix) 30,000 mg (60 caps x 500mg) $36.00 $0.12 The Competitor. Uses galactomannans instead of phospholipids. Claims 45x bioavailability (vs Meriva’s 29x). Good alternative if phytosomes fail you.
Integrative Tx Theracurmin HP Colloidal Nanoparticles 36,000 mg (60 caps x 600mg) $56.00 $0.16 Acute Care. Nanoparticle dispersion creates the highest peak plasma levels quickly, but has a shorter half-life than Meriva. Best for acute flare-ups, not daily maintenance.

Verdict:

  • Best for Daily NF-κB Suppression: Thorne Curcumin Phytosome. The $0.02 premium over Source Naturals is worth it for the sunflower lecithin (soy-free) sourcing and NSF Certified for Sport purity (lower heavy metal risk).
  • Skeptic’s Note: Many brands claim “95% Curcuminoids.” This is irrelevant if it isn’t dissolved in a lipid or nanoparticle matrix. You will excrete 99% of it.
1 Like
#13

I asked Gemini to review the literature and identify the specific scenarios or situations where inulin may be harmful. Here is what it says:

Specific Circumstances of Harm (From Provided Text & Context)

The “recent data” referencing harmful effects on gastrointestinal health primarily points to active intestinal inflammation and specific metabolic defects, where inulin consumption can drive disease progression rather than health.

  • Circumstance 1: Inflammatory Bowel Disease (IBD) & Colitis Exacerbation
    • Mechanism: In individuals with active colitis or specific gut microbiome “signatures” (characterized by reduced fermentative capacity or dysbiosis), inulin may remain unfermented or be fermented into pro-inflammatory metabolites (such as increased bile acids or succinate) rather than beneficial short-chain fatty acids (SCFAs).
    • Outcome: This can trigger an excessive immune response (e.g., IL-33, IL-5, IL-18 production), worsening intestinal inflammation, tissue damage, and symptoms like diarrhea and weight loss, as observed in preclinical models (DSS-induced colitis) and human ex vivo IBD studies.
  • Circumstance 2: Hepatocellular Carcinoma (Liver Cancer) with High Bile Acids
    • Mechanism: In mice with portosystemic shunts (vascular defects) or cholestasis (impaired bile flow) that result in high systemic bile acids, inulin consumption caused a rapid progression to liver cancer (HCC).
    • Outcome: The fermentation of inulin in this specific high-bile-acid environment promoted liver inflammation and immunosuppression, leading to 100% cancer incidence in affected mice (Singh et al., Cell 2018), whereas control mice remained cancer-free.

Full response here: https://gemini.google.com/share/480e0588330b

1 Like
#14

I would encourage people to read that first study I posted above, in humans. It’s crossover design, and quite eye opening.

1 Like
#15

Not All Fibers Are Created Equal: Your “Healthy” Gut Supplement Might Be Inflaming Your Liver

In a landmark multi-omics study from Stanford University, researchers have dismantled the monolithic view of “dietary fiber,” revealing that specific fiber types trigger distinct, personalized biological programs that can either optimize health or, surprisingly, stress the liver. Published in Cell Host & Microbe, the study moves beyond generic advice to eat more roughage, demonstrating that Arabinoxylan (found in whole grains and psyllium) and Long-Chain Inulin (found in chicory) are not interchangeable fuel sources but rather distinct signaling molecules.

The “Big Idea” here is specificity. While Arabinoxylan successfully lowered LDL cholesterol by hijacking bile acid metabolism, Inulin—often touted as the gold standard prebiotic—showed a dark side. At high doses (30g/day), Inulin triggered a spike in inflammation and elevated the liver enzyme ALT in a subset of participants, suggesting that for some, this “healthy” fiber acts as a metabolic stressor. The study underscores a new paradigm in longevity nutrition: fiber supplementation is not a volume game but a precision medicine intervention requiring personalized validation.

Context:

  • Institution: Stanford School of Medicine, USA

Full Gemini Analysis: https://gemini.google.com/share/4cdc0f15ba4e

3 Likes
#16

Does this mean Butyrare supplementation is non necessary and irrelevant to those that have “normal” NLR’s (neutrophil to lymphocyte ratio), apparently between 1 and 2 (which is my case)?

#17

From Gemini (in the same prompt and the paper that started this thread):

Verdict: No, it is not irrelevant.

But claiming it is “necessary” for everyone is also an overstatement.

Here is the “Tell it like it is” breakdown. If your NLR is between 1 and 2, your systemic immune balance is currently excellent. You are not in a state of acute “inflammaging” or immune exhaustion.

However, dismissing Butyrate based solely on a normal NLR is a strategic error for a longevity biohacker. Here is why reliance on NLR alone is a “False Negative” for aging.

1. The “Lagging Indicator” Fallacy

NLR is a systemic fire alarm. It spikes after inflammation has spilled over into the bloodstream and disrupted bone marrow production of immune cells.

  • The Reality: Senescence begins locally in tissues (specifically the gut and skin) years before it registers on a systemic blood panel.
  • The Butyrate Role: In this context, Butyrate is fireproofing, not a fire extinguisher. You take it to keep your NLR at 1.5 as you age, preventing the inevitable “gut barrier drift” that occurs in your 40s and 50s.

2. The “Local vs. Systemic” Gap

You can have a “rotten” gut environment without a systemic spike in neutrophils—yet.

  • The Mechanism: Colonocytes (colon cells) rely on butyrate for 70% of their energy. Without it, they undergo autophagy (self-eating) and eventually senescence.
  • The Risk: A normal NLR does not tell you if you have pre-cancerous polyps or weak tight junctions. It only tells you that your body isn’t currently fighting a massive war.
  • Relevance: Butyrate is the primary chemopreventative for Colon Cancer. This benefit is completely independent of your current inflammation levels.

3. The Epigenetic “Bonus” (HDAC Inhibition)

This is the “Longevity” value proposition that has nothing to do with inflammation.

  • Neuroprotection: Butyrate crosses the Blood-Brain Barrier and increases BDNF (Brain-Derived Neurotrophic Factor) via histone acetylation. This promotes neuroplasticity and memory.
  • Metabolic Defense: It stimulates GLP-1 secretion from L-cells in the gut. Even if you aren’t inflamed, optimizing insulin sensitivity and satiety is a core longevity pillar.

The Adjusted Protocol: “Maintenance vs. Repair”

Since your NLR is optimal (1–2), you do not need the “Repair Protocol” (High dose, expensive, aggressive). You shift to the “Optimization Protocol.”

Metric Repair Protocol (High NLR / High CRP) Optimization Protocol (Normal NLR)
Goal Extinguish Inflammation / Plug Leaky Gut Maintain Barrier / Neuroprotection / Cancer Prevention
Dose ~1.2g active Butyrate (High) ~300–500 mg active Butyrate (Low/Medium)
Frequency Daily, Split Dose Daily or Every Other Day
Necessity Critical Optional but Strategic
Sourcing Supplements (Tributyrin) mandatory Dietary Fiber First (resistant starch), Supplement secondary

Actionable Intelligence

If your NLR is 1.5:

  1. Do not waste money on high-dose Tributyrin-Max protocols. You are diminishing your ROI.
  2. Focus on Fiber: Your microbiome is likely healthy enough to produce butyrate if you feed it. Eat Resistant Starch (cooked and cooled potatoes/rice, green bananas, inulin).
  3. Low-Dose Insurance: If you want the epigenetic benefits, take a standard low-dose Tributyrin (e.g., Designs for Health or Healthy Gut) 3–4 times a week, rather than daily loading.

Bottom Line: A normal NLR means you don’t need a paramedic (High Dose). It doesn’t mean you stop eating nutritious food (Maintenance Dose). Butyrate is food for your gut.

1 Like
#18

Yes, been takin tributyrate for multiple sclerosis for a while once I discovered a deficiency of buyterate in the pathology

2 Likes
#19

The other thing to keep in mind is that there is inconsistent use of the term “inulin”. Inulin is not one molecule. There is a whole range of inulins, with disparate effects. It’s a collection of polysaccharides. The degree of polymerization of inulin is anywhere from 2 to 60 depending on the process of production.

When you buy inulin as a supplement, powder or capsule, you really have no idea what you’re getting, unless it’s specified. Some better companies acually specify whether it’s a short chain or long chain inulin and label it differently, for example NOW markets short chain inulin as NutraFlora FOS (Fructooligosaccharides), and then long chain as Organic Inulin. But many others don’t and these fibers are distinct with distinct characteristics and impact.

Differential effects of inulin and fructooligosaccharides on gut microbiota composition and glycemic metabolism in overweight/obese and healthy individuals: a randomized, double-blind clinical trial

Quote:

“Practically, inulin may be more suitable for managing glycemic dysregulation in overweight or obese individuals, while FOS may be considered for HCY reduction in individuals with normal glycemic status. Such targeted use of prebiotics could complement existing dietary and pharmacologic strategies in personalized metabolic care.”

This should be part of the consideration:

Response differences of gut microbiota in oligofructose and inulin are determined by the initial gut Bacteroides/Bifidobacteriumratios

And so on. This is a rich topic, and again, it needs a lot of consideration. We shouldn’t blithly talk about “inulin” without specifying which inulin we mean, and we should be mindful of dosages, because it can be very dire for people with IBD and also in people without gastric morbidities but who are sensitive to the impact on the liver among others. Remember the rule: if a molecule has powerful effects, it can also be powerful in ways that are not desirable, it cuts both ways. So with any powerful molecule we should be extra considerate. YMMV.

2 Likes
#20

@CronosTempi Thank you for this. I recently ordered my second bottle of Inulin and I noticed the various forms and found it confusing. I ultimately just assumed they were all the same thing!

Based on the post, I’m considering tributyrate.
I read the AI analysis, but I’m curious what the group is actually buying, if you even are. Ty

1 Like
#21

I’m taking inulin - 1/4 or little less of teaspoon. Is it a healthy dose or too much?

#22

You’re taking a very low dose. I’ve taken 20 grams to 30 grams in my coffee for the past 6 months+ with no issues, but lately have scaled it back to around 10 grams and about 20 grams of sun fiber, which works out better for me, zero gas (vs. a little gas).

The research study above said 30 grams + sometimes causes issues for people. You’re well below that.

Here, from Gemini:

30 grams of inulin powder is approximately 7.5 to 11 level teaspoons.

Because inulin powder density varies significantly by brand (fluffy vs. packed), volume is an inaccurate way to measure 30 grams.

The Conversion Breakdown

  • Denser Powder (Packed): ~4 grams per teaspoon → 7.5 teaspoons for 30g.
  • Lighter Powder (Fluffy): ~2.7–3 grams per teaspoon → 10–11 teaspoons for 30g.

Practical Notes

  • Use a Scale: For precise dosing—especially for longevity or gut health protocols—a digital kitchen scale is the only accurate method.
  • Dosing Caution: 30 grams is a high daily dose. Most clinical protocols start at 2–5g daily and titrate up to avoid severe gastrointestinal distress (gas, bloating, cramping). Taking 30g at once without prior adaptation will likely cause significant discomfort.
1 Like
#23

I’ve been buying Chicory root inulin and using it for the past year or two and it’s been good. I was vaguely aware of the other types. It seems most people probably want the Chicory root version, though it depends on what you’re trying to do:

=========
Here is the breakdown of commercially available inulin types, classified by chemical structure and source. This classification is critical because “inulin” is a broad umbrella term; the metabolic effects (and side effects) depend entirely on the chain length and fermentation profile.

1. Classification by Degree of Polymerization (DP)

The most scientifically relevant classification is the Degree of Polymerization (DP), which refers to the number of fructose units in the chain. Chain length dictates how far the molecule travels in the gut before being fully fermented.

A. Short-Chain Inulin (Oligofructose / FOS)

  • Definition: Inulin that has been enzymatically hydrolyzed (chopped) into shorter chains.
  • Chain Length (DP): < 10 (Average DP ~4).
  • Physiology: Highly soluble and sweet. It undergoes rapid “flash” fermentation in the proximal (upper) colon.
  • Critical Assessment: Because it ferments instantly upon entering the large intestine, it produces a rapid spike in gas. As noted in your previous analysis, this form failed to improve glucose metrics in the referenced study. It is often used as a sugar substitute rather than a metabolic therapeutic.
  • Common Labeling: FOS, Oligofructose, Fructooligosaccharides.
  • Reference: FDA GRAS Notice for Oligofructose

B. Native Inulin (Standard)

  • Definition: The unrefined extraction from the plant root. It is a heterogeneous mix containing short, medium, and long chains.
  • Chain Length (DP): Range of 2 to 60 (Average DP ~10–12).
  • Physiology: “Broad spectrum” fermentation. The short chains ferment early (proximal colon), and the longer chains ferment later (transverse colon).
  • Critical Assessment: This is the default “Inulin” found in most supplements. It balances solubility with functionality. It is effective for general gut health but lacks the specific distal-colon targeting of isolated long-chain fractions.
  • Common Labeling: Chicory Root Fiber, Native Inulin.

C. Long-Chain Inulin (High Performance / HP)

  • Definition: Native inulin that has been physically processed to remove the short-chain fraction (sugar/oligomers).
  • Chain Length (DP): Range of 10 to 60+ (Average DP > 23).
  • Physiology: Low solubility and no sweetness. It resists early fermentation and reaches the distal (lower) colon.
  • Critical Assessment: This is the specific fraction associated with potent metabolic effects (GLP-1 secretion, systemic glucose blunting) and distal gut repair. It ferments slowly, often resulting in better GI tolerance (less immediate gas pressure) but sustained SCFA production.
  • Common Labeling: HP Inulin, Long-Chain Inulin.
  • Reference: Study on Chain Length and Fermentation

D. Synergized Inulin (Oligofructose-Enriched)

  • Definition: A formulated blend of Long-Chain HP Inulin and Short-Chain Oligofructose, typically at a specific ratio (often 50/50).
  • Physiology: Designed to maximize calcium absorption by ensuring acidification occurs across the entire length of the colon.
  • Critical Assessment: While effective for bone density, this blend re-introduces the rapid gas production of FOS. If the goal is strictly metabolic/glucose control (as per the BMC Medicine study), pure Long-Chain is likely superior to this blend.
  • Common Labeling: Orafti Synergy1, Enriched Inulin.

2. Classification by Botanical Source

While chemically similar, the source plant dictates the branching structure, which influences microbial access and fermentation speed.

A. Chicory Root (Standard)

  • Structure: Linear chains with beta(2-1) linkages.
  • Verdict: The clinical gold standard. 90%+ of all safety and efficacy data (including the BMC Medicine paper) is derived from chicory inulin. It is the most reliable choice for replicating study results.

B. Agave Inulin (Branched)

  • Structure: Branched chains containing both beta(2-1) and beta(2-6) linkages.
  • Verdict: Highly soluble even in cold water, making it popular for beverage manufacturing. However, the branched structure alters the fermentation rate and may select for different bacterial clusters than the linear chicory inulin used in most metabolic studies.
  • Reference: Structural differences between Agave and Chicory Inulin

C. Jerusalem Artichoke

  • Structure: Similar to chicory but often sold as “whole tuber powder.”
  • Verdict: Often less processed, meaning lower purity (~90% inulin) with residual micronutrients. It is functionally similar to Native Inulin but harder to dose precisely due to batch variability.

Summary Table for Decision Making

Type Classification Avg Chain Length Fermentation Site Primary Utility
Oligofructose (FOS) Short-Chain DP ~4 Proximal (Start) Sweetener / Bifido boost
Native Inulin Mixed DP ~12 Mixed General Maintenance
HP Inulin Long-Chain DP >23 Distal (End) Metabolic / Glucose Control
Agave Inulin Branched Mixed Variable Solubility / Cold Drinks

The Bottom Line: To replicate the “Inulin” group effects from the research report (glucose blunting, HCY reduction), you require Chicory-derived Long-Chain (HP) Inulin or Native Inulin. You must avoid “FOS” or “Oligofructose,” as the study explicitly confirmed these short-chain versions failed to produce the desired metabolic phenotype.

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