Astaxanthin boosts some of these
Vera AI: Astaxanthin robustly activates NRF2 and likely engages the SIRT1-FOXOЗA axis in preclinical models, contributing to antioxidant and anti-aging effects. However, human evidence for SIRT1 is inconclusive, and there is no direct evidence that astaxanthin increases Klotho or BDNF. Thus, its strongest and most consistent molecular target is NRF2 activation, with emerging but less definitive roles in SIRT1/ FOXO3A.
In that case it wouldn’t be difficult to find any study with mortality rate or disease on one axis and the alleles on the other for any of these?
Good idea.
I think one still needs to focus on getting it to where one needs it.
Reputable source important.
Blend of bacteria probably important too.
via ChatGPT
Sources of Bifidobacterium available in enteric capsules or with enteric coating:
Jarro-Dophilus EPS: Jarrow Formulas: Proprietary enteric coating. Formulated with 8 strains of probiotic bacteria, including Bifidobacterium longum and Bifidobacterium lactis.
Controlled Delivery Probiotic :Nature’s Bounty: Features delayed-release delivery system.
100 Billion Probiotic: Remedy’s Nutrition. High-potency formula includes several Bifidobacterium species, such as B. lactis, B. bifidum, and B. longum, in coated capsules designed to survive stomach acid.
Probiotics for Women and Men: NATURE TARGET: 30 different probiotic strains, including Bifidobacterium, with the freeze-dried powder wrapped in enteric-coated capsules.
CGM LABS Premium Enteric Coated Probiotics: Blend of bacteria, including Bifidobacterium longum, Bifidobacterium breve, and Bifidobacterium lactis, in enteric-coated capsules that do not require refrigeration.
Life Space Shape B420 Probiotic: Vege-capsules containing Bifidobacterium animalis ssp. lactis (B420™) designed to survive the journey through the stomach.
Another benefit of enteric protection, Increased stability and shelf life, which improves stability of the live bacteria with respect to moisture and heat, extending the product’s shelf life.
Another press story on this, from the Washington Post:
A new study offers insights about what made Maria Branyas Morera exceptional — and what it could mean for the rest of us.
Interest in the physiology of the very old, especially super-agers who remain relatively healthy, isn’t new. Researchers with the Longevity Genes Project at Albert Einstein College of Medicine in the Bronx have been studying the genetics of centenarians since 1998.
But even by the standards of super-aging, Morera was special. Life expectancy for women in Catalonia is 86 years, Esteller said. (In the United States, it’s about 81 years for women and 76 years for men.) Morera outlived that standard by more than 35 years.
“Genetics is certainly a big part” of how we age, Esteller said. And on that count, Morera lucked out. Her cells carried most of the gene variants that past research had found in other long-lived people, including variants that play a role in DNA repair, as well as in the body’s ability to clear away dead or malfunctioning cells, control inflammation and create robust mitochondria, the energy powerhouses inside cells. Her genome also contained seven other variants, Esteller and his colleagues found, that hadn’t been identified in the very elderly before, and which he suspects played a substantial role in her longevity.
Just as important, she didn’t carry any gene variants known to increase risks for cancer, Alzheimer’s, diabetes or most other major chronic illnesses, and never developed any of those conditions. (Her primary physical complaint was arthritis.)
If genes alone explained her lifespan, though, her family tree probably would have been filled with supercentenarians, Esteller felt, and none of her close relatives lived nearly that long.
…
It’s important to point out that Morera’s physiology was hardly perfect, Esteller said. She looked old. Her joints ached, and she had signs of incipient disease, including high levels of the protein amyloid in her bloodstream, which might be a marker of future dementia, as well as issues with abnormal blood cells, which could indicate a risk for blood cancers. But she didn’t have those diseases at the time of her death.
…
Lessons on diet and lifestyle
What role did her diet and lifestyle play in all of this? A large one, Esteller and his colleagues believe. “In the last 10 years of her life, she ate three plain yogurts a day,” he said, and otherwise followed a typical Mediterranean diet. “She ate very lightly,” he said, “a lot of fish and olive oil and fruit.” She also walked often and gardened until the final years of her life, he said. The interplay of her lifestyle and genetics probably helped her maintain healthy cholesterol and blood-sugar levels, he said, ensuring her blood chemistry at 116 looked like that of someone decades younger.
…
As for Esteller, the main message he and his colleagues gleaned from studying Morera was that “aging and illness are separable,” he said. She grew old. She did not grow seriously ill. Perhaps she would have, eventually, he said. But something inside of her pushed that eventuality further and further out, until, on Aug. 19, 2024, aged 117 and still mentally and physically well, she peacefully died in her sleep.
Full story: How to live to 117? Researchers find clues in the world’s oldest woman.
Do we have her apoB?
On the authors hypothesis between “excepcional” short telomeres and no cancer: doesn’t it make you wonder about the telomere lengthening protocols?
Telomeres don’t seem to be the limiting factor in longevity generally, as discussed here: Telomeres Testing
Regarding cancer specifically… this is only a single data point, and I haven’t looked into the issue more generally. Perhaps someone who has can comment.
Yep. Telomeres science is still quite confusing like many other “hallmarks of aging” … Regards cancer, I mentioned the investigators hypothesis solely to instigate other hypothesis, I mean, all we have so far.
No - its not available (per CGPT5).
So, I looked a little more deeply into the issue of lipids (LDL-C and APO-B) and centenarians and supercentenarians…
Interesting to note, it seems there are no groups or studies suggesting higher lipid levels are well represented in centenarians and supercentenarian.
Here’s what the peer-reviewed literature says about LDL-C levels in centenarians / super-centenarians, with numeric data where it’s actually reported.
Italy – healthy centenarians (n=75), classic FASEB J cohort (1998)
China – Hainan community centenarians (population cohort)
China – inpatient centenarians (n=121), single-center retrospective (2022)
Okinawa, Japan – long-lived population (reviewed)
Italy – “lipid & lipoprotein subfractions in centenarians,” Very Large Database of Lipids (JACC abstract, 2016)
Mongolia – centenarians vs elderly controls (2024)
Other relevant signals
Supercentenarian (110+) data: direct LDL-C values are rarely published. For María Branyas Morera (117), the Cell Reports Medicine paper emphasizes lipid particle features and metabolomic signatures, not a numeric LDL-C value. (Cell)
| Population | Setting / N | LDL-C (mg/dL) | Notes |
|---|---|---|---|
| Italy (Padova) | Healthy centenarians, n=75 | 115.1 ± 27.8 | LDL similar to young; lower than elderly. |
| China (Hainan) | Community centenarians | ~107 (median) | 2.77 mmol/L; low dyslipidemia prevalence. (Frontiers) |
| China (PLA hospital) | Inpatient centenarians, n=121 | ~79 ± 18 | Heavy statin use (69%); low LDL linked to ↑ all-cause mortality. (Frontiers) |
| Okinawa (historic cohorts) | Population studies (reviewed) | ~102 → 113 | Cohort/time dependent; upward drift over generations. (MDPI) |
| Various (JACC VLDB) | Subfraction profiling | — | Centenarians showed less atherogenic particles (size pattern), not LDL-C per se. (JACC) |
(mmol/L → mg/dL for cholesterol: × 38.67)
Here’s what the published literature actually reports on Apolipoprotein-B (ApoB) in centenarians / super-centenarians. Spoiler: there are only a handful of cohorts with measured ApoB; most “longevity lipid” papers focus on particle size (LDL/HDL) rather than ApoB counts.
| Study / cohort | Who was measured | ApoB (units as reported → mg/dL) | Key takeaways |
|---|---|---|---|
| Malaguarnera et al., 1996 (Clinical Drug Investigation) | Italian centenarians vs. controls | 0.92 ± 0.26 g/L → 92 ± 26 mg/dL | Centenarians had lower TC, LDL-C, TG and ApoB, and higher HDL-C/ApoA-I vs. controls. (SpringerLink) |
| Barzilai et al., 2003 (Ashkenazi “exceptional longevity”, JAMA) | Long-lived probands (centenarians), their offspring, age-matched controls | ApoB (all probands): 96 ± 22 mg/dL; men: 91 ± 19 mg/dL (controls ~100–104 mg/dL depending on subgroup) | Longevity phenotype emphasized larger LDL/HDL particle sizes; ApoB similar or modestly lower than controls. Table shows ApoB alongside LDL/HDL and particle metrics. (JAMA Network) |
| Hazzard, 2001 (J Am Geriatr Soc commentary/series) | 9 very old “long-livers” | ApoB ~61 mg/dL (LDL-C ~65 mg/dL) | Small, selective sample with very low ApoB and LDL-C; not population-representative, but shows the lower tail exists. (AGs Journals) |
| Atzmon et al., 2006 (PLoS Biology) | Ashkenazi centenarians & offspring (genetic study) | ApoB measured (with ApoA1/ApoC3), but paper centers on APOC3/CETP variants and particle size; no single cohort-wide ApoB mean is highlighted | Confirms favorable lipoprotein profile in long-lived families; emphasis is genetics & particle size, not ApoB concentration per se. (PLOS) |
| Heijmans et al., 2006 (PLoS Medicine) | Long-lived siblings (men ≥ 89, women ≥ 91) & population peers | Focus on LDL/HDL particle size & concentrations; ApoB not the headline metric | Shows larger LDL & HDL particles track with longevity in families and in sporadic 90-year-olds. (PLOS) |
| Italian Multicentric Study on Centenarians, 1998 (Arch Gerontol Geriatr) | Large Italian centenarian sample | Paper tables include TC/HDL/TG & ApoA-I (ApoB data discussed in references to standardization but not tabulated in this report) | Confirms broadly benign lipid panels in healthy centenarians; this particular report doesn’t list ApoB means. (Air Unimi) |
Super-centenarians (110+): I could not find any peer-reviewed study reporting ApoB concentrations specifically in super-centenarians. The recent multi-omics case on the 117-year-old (M116) reported lipid particle features/metabolomics but not ApoB. (Your uploaded paper also omits ApoB.)
Don’t wish to rain on BBC anybody’s parade but people seem to be losing their minds because the lady ate yogurt 3 times per day.
Can you imagine how many millions of people eat yogurt every day? How many eat it 3 times per day? Less; but still a significant number I imagine.
I just don’t buy it that yogurt was responsible for her extreme age.
Someone once said that “genes will get you to 70-odd, but after that, it’s genetics.” I agree.
Sorry; should have read “lifestyle will get you to 70; after that it’s genetics.”
My bad.
Probably a bit harsh (lifestyle will likely get you to 80), but otherwise absolutely true.
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):
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 !
It would be interesting to test your inflammation (HS-CRP, etc.) pre and post use of this stack.
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.
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!
Every time you eat a meal, you’re hosting a dinner party. Your guests are the trillions of microbes that live in your gut.
These hungry microbes, collectively known as your gut microbiome, directly affect your long-term health for better or for worse depending on what you feed them. Eat the right foods, and your gut microbes will churn out beneficial compounds that protect and improve your health. Feed them the wrong foods, and they can wreak havoc on your gut, setting off inflammation and increasing your risk of chronic diseases.
That’s according to Karen Corbin, an associate investigator at the AdventHealth Translational Research Institute of Metabolism and Diabetes in Orlando who has published groundbreaking studies on nutrition and the microbiome.
You can make your gut microbes happy by doing the following, Corbin said: Limit your intake of ultra-processed foods, and try to eat items that contain plenty of fiber, particularly those that contain a special type of fiber called resistant starch. These include plant foods such as beans, peas, lentils, bananas (especially green bananas), apples, pears, and whole grains like barley, brown rice and oats. Health authorities recommend that adults eat around 28 grams of fiber daily — yet most people eat far less than that. If you make an effort to eat more fiber-rich foods, you’ll invariably end up eating a lot of resistant starch.
