High-Fiber Foods May Fight T Cell Senescence

#1

Older people with more blood butyrate have fewer senescent T cells.

Researchers have discovered that butyrate, a short-chain fatty acid with well-documented gut benefits, fights senescence in T cells.

Senescence of the immune system (immunosenescence) is a problem that drives many others. In particular, T cells are known to secrete inflammatory SASP compounds [1] and drive the constant, age-related inflammation known as inflammaging [2]; in essence, the aged immune system overactivates itself. However, instead of being more effective against pathogens, this overactivated system has a degraded ability to effectively respond to threats [3], which is part of why older people have suffered from significantly greater COVID-related mortality [4].

An increase in T cell senescence has been found to drive pathologies in other systems in mice, including the muscles, vasculature, and cognition [5]. In people, this immunosenescence has been linked to arthritis [6] and acute heart failure [7]; unsurprisingly, there is a possible Alzheimer’s link as well [8].

Read the full story:

Related Reading:

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Curcumin, Butyrate, and the Aging Immune System: A Microbiome-Centric Strategy for Longevity
#2

So how do we know how much butyrate we have? I just checked with my local test lab (Quest) and out of 3000+ tests available, none mention butyrate. And how much is optimum?

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#3

Good question. Here is what I can find:

How People Measure Blood Butyrate Levels

There is no standard consumer-grade or routine clinical test for circulating butyrate. It’s a research analyte. But there are established methods used in labs.

Typical Butyrate Concentrations (for context)

Human fasting plasma butyrate is very low:

  • 1–10 µM (rough range in healthy adults)
  • Peaks postprandially if high-fiber or resistant starch intake
  • 15–20 µM is uncommon without supplementation or colonic fermentation spikes

Because the values are so low, only mass spectrometry can detect them reliably.

If You Want to Measure Your Own Butyrate

Here’s the practical path:

Option A: Use a university metabolomics core

Many accept outside samples for a fee.

Search terms:

“university metabolomics core SCFA analysis”

“GC-MS short chain fatty acid quantification service”

Expect:

  • $150–300 per sample
  • Need to send frozen plasma on dry ice
  • Institutional approval sometimes required

Option B: Work with a functional medicine lab that partners with LC-MS services

Ask specifically:

“Do you measure plasma butyrate via LC-MS/MS or GC-MS?”

Most will say no; a few can do it via third-party labs.

Bottom line

To measure blood butyrate, you need GC-MS or LC-MS/MS from a specialty lab.

No mainstream clinic or consumer test offers this.

The concentration is tiny, so only MS methods work.

Realistic Proxies for Blood Butyrate (Clinically Available Today)

1. Fecal Butyrate Percentage (stool SCFA panel)

This is the only direct butyrate-related consumer test.

  • Offered by: Genova GI Effects, Doctor’s Data, Vibrant, some European microbiome labs.
  • They measure butyrate as % of total SCFAs in stool.

Reality check:

Stool butyrate ≠ blood butyrate.

Correlation with plasma is weak to moderate, because colonocytes consume ~95% of butyrate before it reaches circulation.

Useful for:

  • Knowing whether your microbiota produces butyrate.
  • Assessing dietary fiber/RS response.

Not useful for:

  • Estimating actual circulating μM levels.

Still, it’s the best consumer-facing microbiome productivity proxy.

2. Fasting and Post-Prandial GLP-1 (indirect physiology proxy)

Butyrate stimulates L-cells → GLP-1 secretion.

  • GLP-1 can be ordered through many functional labs.
  • A clear post-fiber/post-RS GLP-1 increase suggests strong SCFA signaling (butyrate + propionate).

Correlation is indirect but real in metabolic studies.

3. β-Hydroxybutyrate (BHB) – blood ketone meters

This is not butyrate but behaves as a functional metabolic analog .

  • Rising SCFAs (mainly butyrate) can bump hepatic ketogenesis.
  • People with higher SCFA flux sometimes show slightly elevated BHB despite identical diet.

Not a linear proxy, but if BHB moves consistently after high-fiber/resistant starch meals, it implies increased SCFA availability.

Practical: you can measure BHB at home cheaply and repeatedly.

4. Fasting Insulin, HOMA-IR, Matsuda Index

There’s good evidence that higher SCFA flux improves:

  • insulin sensitivity
  • glucose disposal
  • postprandial insulin response

These improvements correlate weakly with plasma butyrate levels in clinical trials of RS2, RS3, AXOS, and butyrogenic diets.

Usefulness:

They’re physiology-level proxies, not molecular proxies.

If your butyrate is rising meaningfully, you usually see:

  • lower fasting insulin
  • improved OGTT curves
  • lower HOMA-IR

But this can also result from many other factors.

Proxies That Are Not Reliable

Even though people claim they are:

:x: Fecal butyrate concentration alone – depends on stool moisture and transit time.

:x: Fecal microbiome sequencing alone – butyrate-producer abundance ≠ actual butyrate production.

:x: Breath hydrogen / methane – measures fermentation, not SCFA absorption.

:x: Urine organic acids like β-hydroxybutyrate – useless for SCFA inference.

If You Need the Closest Practical Approximation

Here’s the best composite proxy approach for a consumer:

Step 1 — Stool SCFA panel

  • Look specifically at butyrate % of total SCFAs
  • A % >15–20% indicates high microbiome butyrate production potential.

Step 2 — GLP-1 response to a standardized resistant starch challenge

  • Measure fasting GLP-1
  • Eat 20–30 g resistant starch
  • Measure GLP-1 at 60 min

A measurable rise indicates strong colonic SCFA signaling.

Step 3 — 2–4 week metabolic markers

  • Fasting insulin
  • HOMA-IR
  • BHB baseline variation

If all three move in the right direction after a butyrate-enhancing intervention, odds are your circulating butyrate went up.

You still don’t know the μM value, but you’re capturing the functional footprint of increased butyrate.

Bottom line

There is no clinically available consumer test that directly approximates blood butyrate.

But you can capture butyrate biology through:

  • stool butyrate %,
  • GLP-1 stimulation,
  • insulin sensitivity changes,
  • subtle shifts in BHB.
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#4

Short version: nobody actually knows the “optimal” blood butyrate level in humans yet. We have typical physiological ranges and associations with better or worse outcomes, but no agreed target like we have for LDL-C or HbA1c.

I’ll break it down.

1. What the Aging Cell paper actually shows

The study you linked (Rees et al., Aging Cell, 2025) looked at stool and serum butyrate and senescent T cells in healthy young vs older adults. Key points:

  • Older adults had lower stool SCFAs and lower serum butyrate than young adults (significant drop with age).
  • In older adults, higher stool butyrate correlated with fewer senescent CD28⁻CD57⁺ T cells (R² ≈ 0.43, p<0.001).
  • In vitro, culturing aged T cells with 0.5–2 mM butyrate reduced senescence markers and SASP cytokines (IL-6, IL-8, IL-1β) without killing the cells, via ↓DNA damage markers, ↓mito ROS, ↓mTOR and ↓NF-κB signalling.
  • In aged mice, faecal supernatant from young donors rich in butyrate reduced accumulation of senescent T-zone cells in spleen.

Important nuance:

  • The correlation with senescent T cells is with stool butyrate , not directly with plasma levels.
  • The paper does not define a specific “optimal” serum butyrate concentration, just that more butyrate (within normal physiological range) is associated with less T-cell senescence .

2. What are “normal” blood butyrate levels?

Most of the literature agrees on very low systemic concentrations compared to colonic lumen:

Colon / portal vs systemic:

  • Colonic lumen: butyrate ≈ 10–20 mmol/L (massive compared to blood).
  • Portal vein: ≈ 15–30 µmol/L.
  • Systemic plasma/serum:
    • Many sources: <10 µM in healthy humans.
    • Some cardiovascular work: “plasma butyrate typically remains below ~1 µM, even after fiber enrichment.”
    • BBB review: states plasma butyrate is <20 µM in general; again, basically low micromolar at most.

Concrete human data points:

  • Pregnant women with normal glycemia (Mediterranean cohort)
    • First trimester: median butyrate 0.73 µmol/L, reference interval 0.16–1.01 µmol/L.
  • Gestational diabetes cohort (China)
    • Controls vs GDM: butyrate lower in GDM both in T1 and T2 (e.g., 0.37 vs 0.46 µmol/L in T1; 0.54 vs 3.09 µmol/L in T2). Higher butyrate associated with markedly lower GDM risk.
  • Diabetic kidney disease cohort (China, 2025)
    • Mean serum butyrate ≈ 526.6 ± 193.9 ng/mL (UPLC-MS/MS). That’s ~6 µM if you convert from ng/mL using butyrate MW ≈88 g/mol.
    • Higher serum butyrate was linearly associated with higher eGFR in people with diabetes, independent of confounders.

Bottom line: across cohorts and assays, fasting plasma/serum butyrate generally sits in the sub-micromolar to low-micromolar range (roughly ~0.2–6 µM), with huge method-dependent variation.

There is no robust sex-specific reference range; most studies either adjust for sex or don’t stratify, and the kidney-function paper didn’t see interaction by sex.

3. What does the broader human data say about “more vs less” butyrate?

3.1 Conditions where higher butyrate looks favourable

  • T-cell senescence & inflammaging
    • The Aging Cell paper: older adults with higher stool butyrate had fewer senescent CD28⁻CD57⁺ T cells.
    • In vitro millimolar butyrate dampens SASP, DNA damage signalling, mTOR and NF-κB in aged T cells.
  • Gestational diabetes (GDM)
    • Lower plasma butyrate in women who develop GDM vs controls; higher butyrate and higher butyrate/iso-butyrate ratio strongly associated with lower GDM risk and better predictive AUC when added to clinical risk factors.
  • Metabolic health / obesity / insulin resistance
    • Review of obesity: human data show that higher fasting plasma butyrate associates with lower free fatty acids and better metabolic profiles in some cohorts.
    • High-fiber or resistant-starch interventions that raise plasma butyrate modestly (still in the low-µM range) often improve glucose tolerance and lower insulin on the following day.
  • Kidney function in diabetes (2025 dual-cohort analysis)
    • Higher dietary butyrate intake and higher serum butyrate both associated with better eGFR in diabetic adults, in a mostly linear fashion, with no clear toxicity signal at the upper observed levels (~6 µM serum).

Taken together, these support a “more butyrate within the physiological range is probably better” pattern for several age-related or metabolic endpoints.

See the full response here:

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#5

Interesting… prices are not too bad from UCSF, I may try to contact them to discuss:

https://microbiome.ucsf.edu/quantitative-metabolite-analysis-center-colab-plug#below-is-a-summary-of-our-approved-recharge-rates-effective-july-1-2025

#6

One problem could be that it bounces around all day, like blood glucose. And you’d want to take it when?

I started taking my xos more often and it has certainly had an positive impact on my gut. Dysbiosis is gone. I thought I’d be getting SCFA from it, but my AI says not so much. It tells me to take a tablespoon of unmodified potato starch with it. I thought potato starch was digestible but it says no, entirely resistant until cooked. Cooking makes it into glucose, cooling lets some of it crystalize back. Unmodified is food for your gut buddies only.

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#7

This seems to mirror NMR. They consume absurdly high quantitues of fibers. Produce tons of SCFAs. They have
• cancer immunity
• low immune aging
• strong-but-minimalist innate response
• no autoimmune disease

2 Likes
#8

Good point, you are completely right on that.

Short answer: blood butyrate is highly dynamic, changes fast (minutes–hours), and varies a lot day-to-day , especially in people whose fiber/SFCA production fluctuates.

Full analysis:

#9

My Prompt:

What foods or supplements are most effective at raising butyrate levels in people?

CGPT5.1 Response:

Here’s the straight, practical rundown on what actually moves systemic butyrate in humans — based on human data, not microbiome hype.

Highest-Leverage Ways to Raise Butyrate in Humans

1. Fermentable Fibers (Prebiotics) — The Only Robust, Repeatable Mechanism

Fermentable fibers feed butyrate-producing bacteria (Faecalibacterium prausnitzii, Roseburia, Eubacterium).

Different fibers produce different magnitudes of butyrate rise.

Most Effective (Human Data)

● Resistant Starch Type 2 (RS2)

– Sources: Raw potato starch, green bananas, plantain flour

– Typical effective dose: 15–40 g/day

– Butyrate increase: 25–160% in stool; blood increase modest but real

– Fast onset: 24–72 hours

● Resistant Starch Type 3 (RS3)

– Sources: Cooked-and-cooled potatoes, rice, pasta; Hi-Maize RS3 supplements

– Dose: 20–40 g/day

– Butyrate increase: comparable to RS2, but slower

● Inulin & Fructo-Oligosaccharides (FOS)

– Sources: Chicory root, Jerusalem artichoke, agave, inulin powders

– Dose: 10–20 g/day

– Butyrate increase: typically 20–60%

– Also increases propionate, which indirectly boosts butyrate recycling in colonocytes

● Arabinoxylan-oligosaccharides (AXOS)

– Sources: Wheat bran extracts, psyllium blends with AXOS

– Dose: 5–15 g/day

– Butyrate rise: 30–100% in stool

– Supports Faecalibacterium strongly

● Partially Hydrolyzed Guar Gum (PHGG)

– Extremely well-tolerated

– Dose: 5–10 g/day

– Butyrate increase: moderate, but reliably increases butyrate producers

2. Classic Food Sources

Not all fibers behave similarly; real-world meals matter.

Best Natural Foods

● Cooked-and-cooled potatoes / rice / pasta (RS3)

The “cooling” increases retrograded starch → more substrate for butyrate.

● Legumes

Lentils, chickpeas, white beans — high fermentable starch and arabinoxylans.

● Whole grains high in AXOS

Wheat bran (the good kind), barley, rye.

● Green bananas & green banana flour

Massive RS2 content.

● High-polyphenol foods

Berries, pomegranate, red grapes; they support SCFA producers indirectly by modulating microbiota.

3. Probiotics That Actually Increase Butyrate (Human Evidence)

Most “butyrate probiotics” are marketing fiction — but a few have real data.

Probiotics with Human Butyrate-Increase Evidence

● Clostridium butyricum MIYAIRI 588 (CBM 588)

– Strongest human evidence

– Increases fecal butyrate 20–40%

– Shown to increase butyrate producers and lower inflammation

– Widely sold in Asia (Miyarisan)

● Bifidobacterium longum + inulin synergy

Not directly a butyrate producer, but cross-feeds butyrate bacteria.

● Certain multi-strain synbiotics

Only when paired with RS or inulin substrates.

Probiotics alone rarely move blood butyrate meaningfully — prebiotics do the heavy lifting.

4. Direct Butyrate Supplements

These exist, but the truth is:

Sodium butyrate / tributyrin / glycerol-tributyrate

  • Do not significantly raise colon butyrate (absorbed too early)
  • Can raise plasma butyrate modestly
  • Better for systemic signaling than gut-level SCFA production
  • Tribunalin/tributyrin is the most bioavailable form

Typical dosing:

  • Sodium butyrate: 600–1500 mg/day
  • Tributyrin: 500–1500 mg/day

If your goal is blood butyrate (like in the senescent T-cell study you mentioned), tributyrin works better than sodium butyrate, and far better than butyrate salts.

5. Polyphenols That Boost Butyrate (Microbiome-Mediated)

These don’t contain fiber but shift the microbiome toward butyrate production.

Strongest human data:

  • Grape seed extract (proanthocyanidins) — increases Faecalibacterium
  • Green tea catechins
  • Pomegranate extract (urolithin precursors)
  • Curcumin + piperine
  • Black raspberries / anthocyanins

Effects are modest but synergistic with fiber.

What Raises Blood Butyrate the Fastest?

If the goal is systemic butyrate (your target):

Fastest → Slowest

  1. Tributyrin supplement (20–40 minutes)
  2. Large RS2/RS3 bolus (12–24 hours)
  3. Inulin/FOS (1–3 days)
  4. Probiotics (3–14 days)
  5. Diet pattern shift (whole grains/legumes) (1–4 weeks)

Best Practical Stack for Maximum Butyrate

This combination has clinical evidence and covers multiple mechanisms.

Daily stack

  • RS2: 20 g raw potato starch OR 20 g green banana flour
  • Inulin: 10 g
  • PHGG: 5 g (improves tolerability, reduces bloating)
  • Polyphenols: 300 mg grape seed extract or pomegranate extract
  • Probiotic: Clostridium butyricum (if available)
  • Tributyrin: 500–1000 mg if you want a guaranteed plasma bump

This is the most potent, evidence-backed approach to raising both colonic and blood butyrate in humans.

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#10

Related:

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#11

I can confirm that inulin in coffee works well. I’ll have to try the green banana powder in smoothies at some point.

Prompt: Which of the best sources of fiber for butyrate can mix well in coffee or smoothies without disrupting the taste too much?

Response:

:mag: Best picks for minimal taste disruption

If I were to pick the top two for your coffee/smoothie regime (given your interest in longevity / data-driven biomarker work), I’d recommend:

  1. Inulin (chicory‐root powder) – blends almost invisibly into coffee or smoothie, doesn’t change flavour too much, and has strong mechanistic backing for butyrate via targeted fibre.
  2. Green banana flour (resistant starch) – in smoothies this works nicely, adds a neutral-to-slightly banana note, good for colon health and butyrate production.

Between them you’ll cover good “butyrate-friendly” fibre intake while keeping taste and texture manageable.

:warning: Things to watch / practical tips

  • Introduce fiber gradually. Sudden increases can cause gas, bloating. Especially resistant starch and high inulin.
  • Hydration is key. More fibre means you’ll want more water so transit stays smooth.
  • The amount of butyrate produced depends on your gut microbiome’s composition. The paper from 2024 shows that response to inulin or RS depends significantly on pre-intervention microbiota. So expect individual variation.
  • Coffee: if you add fibre powder, consider whether it affects mouthfeel (slick texture, slight grit). Use finely milled powder and blend if needed.
  • Smoothies: better place for fibre mix – banana, spinach, yoghurt + fibre supplement = good vehicle.
  • Keep overall diet diverse: multiple fibre types = more diverse microbiome = better support for butyrate producers.

:fire: If your goal is butyrate → what actually works in coffee

If you specifically want something that disappears into coffee and meaningfully supports butyrate production, use:

1. Inulin (chicory root fiber)

  • Dissolves almost fully
  • Slight sweetness
  • Real butyrate-enhancing evidence
  • Works perfectly in coffee

2. Partially hydrolyzed guar gum (PHGG / Sunfiber)

  • Nearly completely dissolves
  • Zero taste
  • Very well tolerated
  • Good data for SCFA production (including butyrate)

3. Acacia fiber

  • Very mild taste
  • Dissolves reasonably well (better in hot liquids)
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#12

Doesn’t Acarbose also increase SCFA such as butyrate? This could be the mechanism that increases lifespan for Acarbose users.

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#13

Yes. Acarbose does increase SCFAs — including butyrate — and the evidence is strong.

Acarbose blocks α-glucosidase in the small intestine → carbohydrates are not absorbed → they pass into the colon → the gut microbiota ferments them → SCFAs rise (acetate, propionate, butyrate).

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#14

I was looking more at fibers I can easily add to my coffee in the morning so did a comparison between Inulin and PHGG / Sunfiber. I currently use about 15g to 20g of inulin, and it’s ok. I think I will add some PHGG and try that out.

Here’s a straight, evidence-based, non-sugar-coated comparison of PHGG (Sunfiber) vs Inulin—what each actuallydoes in humans and where one is clearly superior to the other.

This is grounded in published RCTs, systematic reviews, and mechanistic data. No hype.

:brain: Executive Summary (Bottom Line)

Question Winner Why
GI tolerance (gas, bloating, cramping) PHGG Inulin is notoriously gas-producing via rapid fermentation; PHGG ferments slowly and produces far fewer symptoms. Excellent tolerability in IBS RCTs.
Solubility / texture in coffee PHGG Fully dissolves, no thickness, zero flavor. Inulin adds sweetness + slight body, and doesn’t fully dissolve in hot liquids at higher doses.
Clinical evidence for reducing constipation PHGG Very strong RCT data in chronic constipation and IBS-C. Inulin has modest benefit but symptom flares are common.
Clinical evidence for diarrhea / loose stools PHGG PHGG normalizes stool consistency in both constipation and diarrhea. Inulin can worsen diarrhea.
Butyrate production Inulin(slightly) Inulin boosts Bifidobacteria and saccharolytic fermentation → somewhat more butyrate in responders. PHGG still increases SCFAs but more mildly.
Blood glucose stabilization Tie Both slow glucose absorption; PHGG may edge out due to better tolerance at effective dissolvable doses.
Lipid reduction (LDL) Inulin Consistent 5–10% LDL reductions at 10–15 g/day. PHGG: smaller but present effect.
FODMAP compatibility PHGG (Sunfiber) PHGG is Low FODMAP certified. Inulin is a high-FODMAP fermentable oligosaccharide.
Reducing bloating PHGG RCTs show decreased bloating. Inulin often causes bloating.

Overall:

If your goal is butyrate → Inulin.

If your goal is actually tolerability, daily use, GI stability, and mixability → PHGG wins by a mile.

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#16

May be inulin with AM coffee and PHGG with dinner/supper and you reach the 35 gm/d fiber goal and blunt glucose variability with dinner. I might as well try that for month and a half till New Year😀

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#17

I find it very easy to overdo inulin (which I get from bake believe chocolate chips…could be the erythritol though) XOS for me can be done at 2 or 3 times the normal dose of 3 grams and I feel nothing. It selectively feeds bifido and lacto in the gut and helps lower the ph to fight the bad guys.

XOS is expensive in the little tub, pretty cheap in the big bag.

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#18

Well, ChatGPT (Thinking model) suggests PHGG in AM and Inulin in PM withRS2 incorporation:

  1. Big picture rules

  2. PHGG = base layer (gentle, all-day, low gas)

  3. Inulin = targeted weapon (small dose, only with food, only PM)

  4. Green banana (RS2) = butyrate booster (evening, titrated slowly)

  5. Never introduce all three at full dose like a maniac. You ramp.

  1. Week-by-week ramp

Week 1: Lock in PHGG

Morning (with protein shake):

PHGG 5 g (about 1 heaping teaspoon / measured scoop depending on product)

Mix into shake or water. Let it fully dissolve.

Why AM PHGG stays:

Sets up second-meal effect → reduces the spike from your PM carbs

Gives low, steady SCFAs without drama

Zero reason to waste inulin here on a low-carb shake

If gut feels fine by end of week (no noticeable bloating / cramping), go to week 2.

Week 2: Add green banana powder (RS2)

Keep PHGG 5 g AM, unchanged.

Evening (with or right after dinner):

Green banana powder: 1 teaspoon (not tablespoon)

Stir into a small portion of your meal, or into water / non-dairy yogurt / smoothie-like mix.

If no major gas, cramps, or urgency after 4–5 days → increase to 2 teaspoons.

End of week: you can sit at 2 tsp or push to 1 tablespoon if very well tolerated.

Why PM RS2:

Butyrate production deeper in the colon, mostly overnight

Helps overnight glucose and next-day postprandial response

Doesn’t screw with your fasted window

If things are behaving (i.e. you’re not writing me angry texts from the bathroom), move on.

Week 3: Layer in inulin

PHGG stays. Green banana stays at whatever dose your gut tolerated (ideally 2 tsp–1 tbsp).

Dinner (this is the carb bomb):

Start inulin at 2 g (usually ~½–1 tsp depending on product)

Mix into food (soup, curry, dal, whatever) or a drink taken with dinner.

If tolerated after 4–5 days → increase to 3–4 g max.

Most people do not need more than 4–5 g. Above that is where the brass band in your colon starts.

Why only PM inulin:

Ferments fast → SCFA surge when you actually have carbs present

Strong bifido stimulation, but you buffer the GI hit by co-ingesting with your legume/grain bowl

Zero point taking it with low-carb shake and sitting on gas all day

  1. Steady-state “mature” protocol (after 3–4 weeks)

Assuming your gut is okay with everything:

Morning

Coffee

Protein shake + collagen

PHGG 5–7 g

If you still see big post-dinner spikes even after weeks, you can go up to 10 g PHGG total per day by adding a small PM dose (see below).

Fasting window

Water, electrolytes, black coffee / plain tea

No fibers here; let your system rest.

Dinner (carb-heavy vegetarian bowl)

Your usual legumes / quinoa / veg

Inulin 3–4 g mixed into the meal or drink

Optional: extra PHGG 3–5 g if CGM/glucose still spikes higher than you like and your gut tolerates it

After dinner / pre-bed

Green banana powder (RS2): 2 tsp to 1 tbsp

Mixed into water / almond milk / small snack portion

This is your deep-colon butyrate & overnight support dose

  1. What each piece is doing for you

PHGG (AM ± small PM top-up)

Flattens glucose curves through the day & especially at that PM meal

Minimal gas

Steady, background SCFA, mild GLP-1/PYY support

Makes your whole system less reactive

Inulin (PM only, with food)

Strong bifidobacteria stimulation

Fast SCFA surge around your biggest carb load

Enhances satiety and post-meal metabolic signaling

Needs to be kept on a leash dose-wise

Green banana powder (RS2, PM)

Deep-colon butyrate production

Overnight gut-barrier and anti-inflammatory support

Subtle next-day improvement in glucose handling

Needs slow titration, but once you tolerate it, it’s a long-game asset

  1. When to dial things back

Back off inulin first if:

Bloating gets >3/10

You feel pressure/cramping after dinner

Gas becomes socially… problematic

Back off RS2 if:

You get delayed gas / cramping several hours after dinner or overnight

Stools suddenly get much looser

Only back off PHGG if:

You notice clear correlation with looser stools even at 5 g
(rare, but possible; in that case, drop to 3 g for a bit)

  1. Red-flag category (don’t ignore)

If you ever:

Have known IBD, SIBO, significant gut disease, or

Are on diabetes meds with risk of hypoglycemia

…then this kind of aggressive fiber stacking really should be sanity-checked with your doc / GI / endocrinology brain.

2 Likes
#19

So is this the same guar gum used as a thickener in various products such as nut milks etc. ?
People were vilifying guar gum as “unhealthy additive”.
I checked my organic almond milk from Costco and I think they changed the thickener to gellan gum.

#20

Yes and no…
Regular guar gum (food additive)

Extracted from guar beans, then ground into a powder.

Used mainly as a thickener and stabilizer in foods: ice cream, sauces, gluten-free baking, etc.

Very viscous in water. Forms a gel.

Not specifically processed for gut tolerance. It’s fiber, but that’s not its main design goal.

PHGG (Partially Hydrolyzed Guar Gum)

Same starting material (guar), but then it’s enzymatically broken down (partially hydrolyzed) into smaller chains.

Result: a low-viscosity, soluble prebiotic fiber powder that mixes like nothing is there.

Designed specifically as a GI-friendly, fermentable fiber for IBS, constipation, gut health, etc.

Think:

Guar gum = glue

PHGG = invisible fiber in your water

  1. Viscosity & mixing

Guar gum (additive)

Thickens fast. A small amount can turn liquid into slime if you’re not careful.

Can clump, feel gummy, and change texture big time.

High viscosity in the gut can slow gastric emptying and affect how fast things move through.

PHGG

Very low viscosity. You can put 5–10 g in a glass of water and it’ll still look and feel like water.

Doesn’t really change taste or mouthfeel when dosed reasonably.

Much easier to take daily without hating your life.

1 Like
#21

Who is NMR?