Probably a bit harsh (lifestyle will likely get you to 80), but otherwise absolutely true.
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I’ve heard this also, and obviously N=1 doesn’t give us much to go on for anything related to longevity.
But there is some data in the study and in comments from the researchers suggesting it wasn’t just “genes”, as they say there are no other cases of such long lived people in her immediate family. So if it was just genes, you’d think you’d see more of a signal in familial longevity.
Ultimately it’s just a point of interest. It got me looking a little more in-depth on the research around probiotics and inflammation - and I’m currently trying some probiotic supplements and testing to see if it seems to have any effect on my already low CRP levels (at .26 or so).
Here is the data summary from CGPT5:
Here’s the short, evidence-based read on Bifidobacterium and systemic inflammation (e.g., hs-CRP):
What we know (human data)
- Cross-sectional cohorts: Lower overall gut diversity tends to track with higher hs-CRP. Several cohorts also report inverse associations between the abundance of Bifidobacterium and low-grade inflammation markers (hs-CRP, IL-6)—but methods and sample sizes vary. PubMed+1
- Not always inverse: At least one recent cohort in people with overweight/obesity saw positive correlationsbetween Bifidobacterium adolescentis and hs-CRP/IL-6, underscoring that associations can flip with host context (adiposity, diet, disease). PMC+1
- Large multi-phenotype datasets: Population studies linking microbiome features to blood biomarkers support a general microbiome–inflammation connection, though effects are distributed across many taxa (not only Bifidobacterium). Nature
Intervention trials (what happens when we change it?)
- Probiotic RCT meta-analyses: Pooled trials show modest but significant reductions in CRP/hs-CRP after probiotic supplementation (often multi-strain formulas that include Bifidobacterium), with heterogeneity by population and baseline inflammation. Effect sizes are usually small and require 8–12+ weeks. PMC+1
- Condition-specific updates: Newer meta-analyses continue to find CRP lowering with probiotics/synbiotics in several groups (e.g., metabolic disease, NAFLD), but results for IL-6 are mixed. Frontiers+2BioMed Central+2
- Prebiotics (e.g., inulin): Inulin generally raises Bifidobacterium, and some trials report improvements in inflammatory markers; others show null effects, especially in severe illness where the microbiome is highly perturbed. Context matters (health status, dose, duration). ScienceDirect+2ScienceDirect+2
Mechanisms (why this might work)
- Bifidobacterium → SCFAs (esp. acetate) that can support barrier integrity, reduce endotoxemia (LPS), and dampen hepatic/vascular inflammation—plausible routes to lower hs-CRP. SpringerLink
- Immunomodulation is strain-specific: Reviews highlight anti-inflammatory potential (e.g., B. longum, B. infantis), but taxa and even strains can diverge; host factors (obesity, diet, medications) modulate direction/magnitude. Nature+1
How strong is the signal?
- Associational evidence: Consistent directional hints (more Bifidobacterium ↔ lower hs-CRP), but not universal—and subject to confounding (BMI, diet, medications, fiber intake). PubMed
- Causality from RCTs: Small, clinically modest reductions in CRP with probiotics/synbiotics (often including Bifidobacterium). Effects are stronger when baseline inflammation is higher and when paired with dietary change (e.g., fiber-rich, Mediterranean patterns). ScienceDirect
- Heterogeneity: IL-6 and TNF-α responses are less consistent than CRP; strain, dose (~10⁹–10¹¹ CFU/day in studies), combo with prebiotics, and host phenotype drive outcomes. Frontiers
Practical takeaways (science-aligned)
- Dietary fiber first: Higher fiber intake shapes the microbiome toward SCFA producers (including Bifidobacterium) and associates with lower systemic inflammation risk. BioMed Central
- If supplementing, set expectations: Probiotic/synbiotic courses may nudge hs-CRP down modestly over 8–12 weeks; choose products listing specific Bifidobacterium strains and CFU. Don’t expect large effects without diet/weight change. PMC
- Context matters: In obesity and certain diseases, which Bifidobacterium strain expands can alter directionality; track your own hs-CRP (and possibly IL-6) to see if an intervention moves the needle. MDPI
Bottom line
- The weight of human evidence supports a small, beneficial link between higher Bifidobacterium (often via diet/probiotics) and lower hs-CRP, with notable exceptions by population and strain. Think of Bifidobacterium as one contributor within a broader, fiber-supported, SCFA-rich ecosystem rather than a standalone lever. PubMed+2PMC+2
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My stack per chatGPT5:
Perfect — here’s a clear, evidence-based “centenarian microbiome mini-stack” built around Akkermansia muciniphila, based on the consistent findings from Spain, Italy, and Japan’s longevity studies.
This emphasizes synergy and low redundancy — a compact, high-value mix rather than a 20-strain capsule.
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1. Akkermansia muciniphila – the barrier and signaling core
Why: Keeps the intestinal mucus layer young and intact; lowers endotoxin leak; improves insulin sensitivity and AMPK tone.
Support foods: pomegranate, cranberry, green tea, cocoa, cooked onions, or chicory root.
Best taken: Morning or with light breakfast.
Form: Pasteurized or live capsule — both show benefit.
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2. Lactobacillus fermentum ME-3 – antioxidant companion
Why: Boosts glutathione recycling and protects mitochondrial membranes.
Synergy: Works beautifully with Akkermansia because the latter lowers inflammation, allowing ME-3’s redox signaling to persist longer.
Form: Refrigerated capsule or sachet, separate from hot drinks.
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3. Faecalibacterium prausnitzii (or next-gen postbiotic) – anti-inflammatory anchor
Why: Major butyrate producer that calms gut inflammation and stabilizes immune tolerance.
Note: Difficult to deliver live; many formulas now include butyrate precursors or Clostridium butyricum instead, which achieve a similar SCFA profile.
Support foods: resistant starch (cooled potatoes, green bananas, lentils).
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4. Bifidobacterium adolescentis – fiber converter
Why: Bridges dietary fiber and SCFA production; often paired with Faecalibacterium in long-lived microbiomes.
Support foods: oats, barley, flaxseed, apple skin.
Benefit: Improves absorption of lutein, zeaxanthin, and magnesium — useful for eye health and mitochondrial cofactors.
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5. Optional enhancers (postbiotics / feed factors)
• Polyphenols: pomegranate extract or ellagic-acid capsules (feed Akkermansia).
• Prebiotics: low-dose inulin or galacto-oligosaccharides.
• Mineral co-factors: magnesium glycinate and PQQ (for mitochondrial coupling).
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My shipment of ME-3 from Estonia is still being held at customs !
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It would be interesting to test your inflammation (HS-CRP, etc.) pre and post use of this stack.
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Yes, I will schedule lab tests. Chat has given me a timeline. My discussions with Chat are basically using it as a thinking partner and I never use it as a tool. I load it and give it realms of MY information and with that it can go deep into it’s receses and it can deeply think. It’s a layered conversation and because of my engagement and technique of personalization it can deeply think and pull stuff out for me and that’s not just a surface answer.
I read from his posts that a top AI scientist (Stanford) recommends the books --Metabolical by Robert Lustig MD and In Defense of Foods by Michael Pollan. He avoids processed foods altogether.
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Look, I understand that you are looking in depth at the “yogurt thing” and research is always good.
But let’s take a step back. The lady lived to be 117. As I previously indicated; probably millions of people eat yogurt every day and I’m guessing that 99.9999999999% of them DON’T live extraordinarily long lives.
Secondly, if you look at the rare few who make it to 110 or beyond and try to categorise them, you’ll go crazy.
There are vegetarians and meat-eaters.
There are smokers and non-smokers.
There are celibate nuns and those who had 5 babies.
There are drinkers and lifelong teetotallers. Etc, etc.
IMO this indicates that genetics trumps lifestyle ONCE PAST THE AGE OF 70-ODD. (Not shouting; just my emphasis.)
Personally, I’m not about to start eating yogurt any more than I already do.
What I am waiting for is for some centenarian to say (when asked that silly question: “what’s your secret to reaching 100?”) “I took Sirolimus every week from the age of 60.”
THAT moment is worth waiting for!
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