World’s oldest person had a young microbiome and 'exceptional genome'

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#21

I’ve followed this thread with interest but haven’t had the time to respond until now.

Consuming probiotics doesn’t guarantee that they can get to where you want them.

Via ChatGPT…

1. Survival Through the GI Tract

  • The stomach and upper small intestine present harsh conditions:
    • Low pH (acidic environment in the stomach)
    • Bile salts and digestive enzymes in the small intestine
  • Many microorganisms get killed here, but some probiotic strains (e.g., certain Lactobacillus and Bifidobacterium) demonstrate natural resistance, while others are delivered in protective capsules or formulations designed to improve survival.

2. Evidence of Reaching the Colon

  • Clinical studies have shown that some orally consumed probiotics can indeed be recovered alive from stool samples, which means they survive passage and reach the large intestine.
  • Survival rates vary a lot depending on the strain, dose, and formulation — often estimated in the 1–10% range of what’s ingested.

3. Colonization vs. Transient Effects

  • Most probiotics do not permanently colonize the gut. Instead, they exert effects while passing through, such as producing metabolites (like short-chain fatty acids), competing with pathogens, or modulating immune responses.
  • For sustained benefits, regular intake often becomes necessary.

4. Strength & Dosing

  • Because survival is partial, supplements typically contain high doses (e.g., billions of CFU) to ensure that at least some meaningful number of organisms make it to the colon.
  • Different strains vary widely in effectiveness — Saccharomyces boulardii (a yeast) is quite resilient, while many bacteria need encapsulation to survive transit.

Bottom line: Yes, some orally consumed probiotics do reach the lower intestine in sufficient strength to affect the microbiome, but survival rates are limited, strain-dependent, and usually transient. The clinical effects depend heavily on the specific organism and formulation.

Bacteria with Strong Survival & Evidence

1. Lactobacillus rhamnosus GG (LGG)

  • Survival: Acid- and bile-tolerant. Frequently recovered in stool.
  • Effects: Reduces antibiotic-associated diarrhea, supports immune response, and may protect against some infections.
  • Notes: One of the most clinically tested strains.

2. Bifidobacterium animalis subsp. lactis (BB-12, Bi-07, etc.)

  • Survival: Good survival in GI tract. Detected in fecal samples.
  • Effects: Improves stool consistency, supports lactose digestion, reduces risk of GI infections.
  • Notes: Often combined with LGG in yogurt or capsules.

3. Lactobacillus plantarum (299v)

  • Survival: Can adhere to intestinal mucosa, resisting washout.
  • Effects: Reduces bloating/IBS symptoms, may support iron absorption.
  • Notes: Found in fermented foods and supplements.

4. Bifidobacterium longum (various subspecies)

  • Survival: Strain-dependent, but several survive well with encapsulation.
  • Effects: Supports mood and cognition (“psychobiotic” effects), reduces inflammation.
  • Notes: Some formulations targeted at gut-brain axis.

Yeast with Strong Survival

5. Saccharomyces boulardii CNCM I-745

  • Survival: Excellent; resistant to stomach acid, bile salts, and antibiotics.
  • Effects: Well-proven against antibiotic-associated diarrhea, Clostridioides difficile recurrence, and traveler’s diarrhea.
  • Notes: Acts differently from bacteria — more transient, but very effective.

Important Considerations

  • Formulation matters: Capsules with enteric coating or microencapsulation improve survival.
  • Dose matters: Clinical trials often use 10⁹–10¹¹ CFU/day.
  • Strain specificity: Benefits don’t apply across species — e.g., L. rhamnosus GG ≠ L. rhamnosus generic.

Bottom line: The strains with the best survival and consistent evidence in humans are L. rhamnosus GG, B. animalis lactis, L. plantarum 299v, B. longum, and S. boulardii .

S T R A T E G Y

I have some autoimmune issues I’ve described in the forum and have taken up approaches to address them.

Other than fecal transplants (limited in the USA) I think we have 3 available methods to affect the gut microbiome:

  • Dysbiosis: (i) Identify (sequence gut microbiome) dysbiosis (overgrowth of bad stuff), (ii) knock it down, (iii) Targeted antibiotics have helped me, iv. Maybe other medications could as well (lots of stuff down there other than bacteria that can go wrong.

  • Probiotics: Introduce probiotics to colonize favorable flora and fauna. Getting them to where one needs them presents challenges.

  • Prebiotics: Introduce prebiotics/fiber that (i) can reach the gut, (ii) ferment, and (iii) support colonization of favorable flora and fauna.

More on prebiotics:

  • Resistant starch: I currently take resistant starch (4 tbs potato starch) early in the day.

  • Inulin + psyllium: a combination of inulin (2 tbs) + psyllium seed husks (2 tbs) around 4 PM.

  • Beta-glucan: I want to add soluble beta-glucan to boost butyrate which can in turn address leaky gut associated with autoimmune conditions, although it seems that not all sources of Beta-Glucan do this. As I understand, oat and barley sourced beta glucan do, I just haven’t identified a good source.

  • Fermentation timing: The separation matters as the fibers compete for fermentation in the gut.

Thoughts | comments appreciated.

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#22

Good information. Perhaps it’s more effective to get Bifidobacterium via direct supplementation, than yogurt?

There are many options that seem pretty inexpensive:

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#23

I wonder what would have happened if also took rapamycin, senolytic drug combination and other likely life-extending molecules? Would she have lived to be 130?

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#24

Nick Norwitz has a long commentary on this study. Of interest:

I was looking for her LDL-C levels and didn’t find them - but they are in the supplementary materials… She had an LDL-C of 122, so a little high. Would have been interesting to see her Cleerly scan / CAC scan…

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Source: https://x.com/nicknorwitz/status/1972256509733044400

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#25

I wouldn’t call 122 mg/dl LDL-C low.

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#26

I do find it a little odd that the research paper seems to focus on the other lipids, and not LDL-C. I searched but could find no record of her taking any medications.

Lipid Metabolism

  • Very low VLDL-cholesterol: ~5–10 mg/dL (vs. 20–30 mg/dL typical elderly).
  • Very low triglycerides: ~40–50 mg/dL (normal <150 mg/dL).
  • High HDL-cholesterol: ~80–90 mg/dL (“good” cholesterol; optimal >60 mg/dL).
  • Large HDL and LDL particles: high count (suggesting effective lipid transport).
  • Low small HDL particles: favorable, as small HDL is linked to dysfunction.
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#27

I suppose it was because she was an outlier for those, and around average for the other ones.

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#28

I wanted to dive a little deeper into her superior mitochondrial function. I think it might be interesting to get our own genomes mapped, and then compare the alleles that seem to contribute to her longevity with our own…

Question: When we get our genomes sequenced through the commercial providers like Nucleus, I’m assuming it also includes the genomes of our mitochondria - is that correct?

Perhaps we could get a probability, given the overlap in genetics with a data from a broad enough number of representative supercentenarians, that we will get to the same level of longevity as these people.

The study on María Branyas Morera (M116) provides several explanations for her exceptionally good mitochondrial function:

1. Genetic Variants Supporting Mitochondria

  • Researchers identified rare homozygous variants in multiple genes directly tied to mitochondrial energy metabolism:

    • ND5, COX1 (key components of the electron transport chain).
    • MTG2, MTCH2, MRPS9 (linked to mitochondrial translation and membrane dynamics).

  • These variants are hypothesized to have optimized oxidative phosphorylation, boosting energy production and resilience to age-related decline.

2. Experimental Validation

  • Tests in her peripheral blood mononuclear cells showed preserved mitochondrial membrane potential and low superoxide levels, confirming not just preserved but robust mitochondrial function at age 116–117.

3. Synergistic Protection from Other Pathways

  • The paper emphasizes that no single variant explained her longevity. Instead, multiple protective pathways overlapped:

    • Immune system efficiency and low chronic inflammation.
    • Cardioprotective variants (e.g., LRP1, LRP2).
    • Neuroprotective genes (NSUN5, TTBK1).

  • Together, these helped reduce oxidative stress burden, indirectly preserving mitochondrial integrity.

4. Lifestyle & Microbiome Factors

  • Although not framed as direct mitochondrial interventions, her Mediterranean diet, low systemic inflammation (very low GlycA/GlycB levels), and high Bifidobacterium abundance in the gut likely reduced oxidative load and promoted mitochondrial health.

:white_check_mark: Summary:
M116’s outstanding mitochondrial function likely arose from a synergy of rare protective gene variants (ND5, COX1, MTCH2, etc.), experimentally validated preservation of mitochondrial potential and low ROS, and a favorable systemic environment shaped by efficient immunity, lipid metabolism, and diet. This combination allowed her mitochondria to function youthfully well into extreme old age.

Other Longevity Alleles

Here are the best-supported longevity alleles/variants reported in centenarians and supercentenarians, beyond those highlighted for M116. I’m focusing on signals that (a) recur across cohorts or meta-analyses, or (b) have strong functional data—then noting caveats about supercentenarian-specific evidence.

Well-replicated/common signals

  • FOXO3A (forkhead box O3) — multiple intronic SNPs (e.g., rs2802292 G allele; others in high LD)
    Strongest and most consistent human longevity locus across ancestries; enrichment seen in centenarians and “oldest-old,” with effects on stress resistance/insulin-IGF signaling. (PNAS)

  • APOE — ε2 enrichment and ε4 depletion in centenarians/long-lived; ε3 neutral
    Large GWAS meta-analysis confirms APOE as a major lifespan locus; ε2 associates with survival advantage, ε4 with shorter lifespan/AD risk. (Note: M116 carried a protective APOE-linked genotype but not necessarily ε2.) (Nature)

  • CETP (cholesteryl ester transfer protein) — I405V (rs5882) V allele / VV genotype, and promoter -629A (rs1800775)
    Associated with larger HDL/LDL particle size, higher HDL-C, and enrichment in Ashkenazi centenarians and Japanese cohorts; particle size phenotype tracks with healthy aging in families of centenarians. (Findings are population-specific and not uniformly replicated.) (JAMA Network)

  • IGF1R (insulin-like growth factor-1 receptor) — rare, hypofunctional missense mutations (e.g., A37T, R407H) in some centenarians
    Cells from carriers show reduced IGF-I signaling; carriers tended to be shorter with higher IGF-I—consistent with longevity phenotypes observed in model organisms. (Rare; not a common variant signal.) (PNAS)

Functionally compelling, newer or rarer signals

  • SIRT6 (“centSIRT6”) — rare centenarian-enriched SIRT6 variants
    These increase mono-ADP-ribosylation activity, strengthen interaction with Lamin A/C, and enhance DNA repair/genome stability in functional studies—providing a plausible longevity mechanism. (Enrichment shown in Ashkenazi centenarians; rarity limits population power.) (PMC)

  • Pathway-level signatures (polygenic)
    Work from the New England Centenarian Study indicates polygenic patterns—hundreds of markers—that better predict extreme ages (≥102–105) than single SNPs, consistent with many small-effect protective alleles aggregating in the extremely old. (Boston University Medical Campus)

Additional candidates with mixed or ancestry-specific evidence

  • KLOTHO (KL-VS haplotype), ACE (I/D), IL6 promoter variants: Some meta-analyses report associations with exceptional longevity, but effects vary by cohort/ancestry and are weaker than FOXO3A/APOE. (ScienceDirect)

How this complements the M116 findings

  • M116’s paper emphasized rare protective variants in mitochondrial genes (ND5, COX1, MTG2, MTCH2, MRPS9) and favorable APOE-linked genotype, plus exceptional lipid handling. The broader literature above adds:

    1. FOXO3A as the most consistent longevity locus;
    2. Lipoprotein remodeling genetics (CETP) matching her favorable particle profile;
    3. IGF1R hypofunction and SIRT6 function gains as mechanistic routes to slower aging (reduced IGF signaling; improved genome maintenance).

Important caveats

  • Supercentenarians (110+) are ultra-rare, so many studies pool centenarians (100+) and “oldest-old.” Signals that are rock-solid for 100+ sometimes weaken or shift in 110+ due to tiny sample sizes and survivorship bias. Meta-analyses stress heterogeneity and replication challenges. (PMC)

Here’s a compact table of the main genetic alleles and variants most consistently linked to longevity in centenarians and supercentenarians, beyond those reported for M116:

Genetic Variants Associated with Exceptional Longevity

Gene Key Variant(s) Effect on Longevity Cohorts / Evidence Mechanistic Notes
FOXO3A rs2802292 (G allele), other intronic SNPs Strong enrichment in centenarians; reduced mortality Japan, Hawaii, Italy, Germany, meta-analyses Regulates stress resistance, autophagy, insulin/IGF signaling
APOE ε2 (protective); ε4 (deleterious); ε3 (neutral) ε2 enriched; ε4 depleted in centenarians Multiple populations (Europe, U.S., Japan) Modulates lipid metabolism, CVD, Alzheimer’s risk
CETP I405V (rs5882 V allele); -629A promoter Larger LDL/HDL particles; favorable lipid profiles; enriched in Ashkenazi and Japanese centenarians Ashkenazi Jews, Japanese Enhances cholesterol transport efficiency; lower CVD risk
IGF1R Rare missense mutations (e.g., A37T, R407H) Found in some centenarians with short stature, high IGF-I Ashkenazi Jews Reduces IGF-I signaling, consistent with model organism longevity
SIRT6 centSIRT6 variants (rare, enriched in centenarians) Enhanced DNA repair, genome maintenance Ashkenazi centenarians Increases mono-ADP-ribosylation activity; protects genome stability
KLOTHO (KL) KL-VS haplotype (heterozygous) Mixed evidence; possible cognitive & lifespan benefits U.S., European cohorts Influences FGF23, insulin/IGF, oxidative stress
ACE Insertion/deletion polymorphism (I allele) Some reports of enrichment in centenarians European & Asian cohorts Modulates blood pressure, renin-angiotensin system
IL6 Promoter polymorphisms (e.g., -174G>C) Associations vary by ancestry Italian, Japanese, Northern European Alters inflammatory cytokine levels (CRP, IL-6)

:white_check_mark: Consensus:

  • The most consistent and replicated human longevity loci are FOXO3A and APOE.
  • CETP and IGF1R add metabolic/lipid and IGF signaling dimensions, though effects vary by ancestry.
  • SIRT6 and other rare functional alleles highlight DNA repair and genome stability as additional routes to extreme longevity.
  • Other candidates (KLOTHO, ACE, IL6) show weaker or population-specific signals.
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#29

GREAT find. We may have found the mechanism for why Acarbose comes close to Rapamycin when it comes to extending lifespan in mice.

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#30

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.

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#31

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?

#32

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.

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#33

Another press story on this, from the Washington Post:

How to live to 117? Researchers find clues in the world’s oldest woman.

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.

#34

Do we have her apoB?

#35

On the authors hypothesis between “excepcional” short telomeres and no cancer: doesn’t it make you wonder about the telomere lengthening protocols?

#36

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.

#37

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.

#38

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.

AI Summay:

Here’s what the peer-reviewed literature says about LDL-C levels in centenarians / super-centenarians, with numeric data where it’s actually reported.

What the data show (study-by-study)

Italy – healthy centenarians (n=75), classic FASEB J cohort (1998)

  • LDL-C: 115.1 ± 27.8 mg/dL (calculated by Friedewald).
  • Compared with younger and “elderly” controls, centenarians had LDL similar to young, lower than elderly; HDL was lower and TG higher in centenarians.

China – Hainan community centenarians (population cohort)

  • LDL-C (median): 2.77 mmol/L ≈ 107 mg/dL; TC 4.60 mmol/L, TG 1.05 mmol/L, HDL-C 1.41 mmol/L.
  • Dyslipidemia prevalence ~19%. (This is the Hainan centenarian cohort referenced in later work.) (Frontiers)

China – inpatient centenarians (n=121), single-center retrospective (2022)

  • LDL-C (mean): 2.05 ± 0.46 mmol/L ≈ 79 ± 18 mg/dL; TC 3.90, TG 1.36, HDL-C 1.14 (all mmol/L).
  • 69% were on lipid-lowering therapy (mostly statins).
  • Lower LDL-C associated with higher all-cause mortality in multivariable models (HR for LDL-C 0.379; p=0.001) — authors caution about “lowest is not best” in this hospitalized, heavily treated group. (Frontiers)

Okinawa, Japan – long-lived population (reviewed)

  • Older report (2001): LDL-C ≈ 102.4 ± 25.1 mg/dL; later cohort: 113.0 ± 27.8 mg/dL; more recent generations show upward drift. (Values summarized in a 2025 review). (MDPI)

Italy – “lipid & lipoprotein subfractions in centenarians,” Very Large Database of Lipids (JACC abstract, 2016)

  • Centenarians had a less atherogenic lipid profile (emphasis on particle subfractions—larger LDL/HDL particles) rather than LDL-C concentration per se. (JACC)

Mongolia – centenarians vs elderly controls (2024)

  • Reported hypercholesterolemia 32.6% in centenarians, but elevated LDL only 4.3%; numerics for mean LDL-C not provided in abstract. (Cajmhe)

Other relevant signals

  • Some centenarian cohorts (e.g., Ashkenazi families) emphasize lipoprotein particle size (larger LDL/HDL) over LDL-C level itself. (Science)
  • In female centenarians, estradiol levels inversely correlated with LDL-C in one Hainan sub-study. (DNB Portal)

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)

Quick comparison table (LDL-C)

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)

How to read this

  • Across community-dwelling centenarians, LDL-C clusters around ~100–115 mg/dL in several cohorts.
  • Hospitalized/treated centenarians can show much lower LDL-C (often due to statins), and in at least one study, lower LDL-C correlated with higher all-cause mortality, likely reflecting illness, frailty, and treatment selection rather than a protective effect of very low LDL in this age stratum. (Frontiers)
  • Many “longevity” papers in the last 10–15 years shifted attention from LDL-C concentration to lipoprotein quality (particle size/composition), which appears more favorable in long-lived families and centenarians—even when LDL-C isn’t exceptionally low. (JACC)

Bottom line

  • Numeric LDL-C in centenarians: typically ~100–115 mg/dL in community cohorts; lower (~80 mg/dL) in hospitalized, heavily treated samples.
  • Supercentenarians: no robust, published LDL-C datasets; case studies focus on efficient lipid metabolism & particle profiles rather than LDL-C numbers. (Cell)

APO-B Summary:

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.

Studies that report ApoB in (or around) centenarians

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.)

What these data suggest (with important caveats)

  • Typical ApoB levels in community centenarians sit around ~90–100 mg/dL in the two most informative cohorts (Italian and Ashkenazi). That’s not “ultra-low” by modern preventive cardiology standards, but not high either. (SpringerLink)
  • There is heterogeneity: selected case series can show very low ApoB (~60 mg/dL), but those are tiny, non-representative samples. (AGs Journals)
  • Many longevity cohorts shift the focus from ApoB amount to lipoprotein quality (especially larger LDL & HDL particles), which repeatedly associates with long life even when absolute LDL-C/ApoB aren’t dramatically different. (PLOS)
  • Some papers in the “oldest-old” (80–99) literature examine ApoB for risk prediction, but they’re not centenarian-only; results often show the usual pattern (higher ApoB → higher ASCVD risk), with possible attenuation in very old age and strong treatment/selection effects. These are helpful context but not direct centenarian ApoB catalogs. (Nature)

Bottom line

  • Direct ApoB measurements in bona fide centenarian cohorts are scarce. Where measured, ApoB ~90–100 mg/dL is common (Italian, Ashkenazi cohorts). Exceptional low values exist in small, selected samples. The strongest and most replicated lipid signature of longevity is large LDL/HDL particle size rather than very low ApoB per se. (SpringerLink)
#39

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.

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#40

Sorry; should have read “lifestyle will get you to 70; after that it’s genetics.”

My bad.

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