She Lived To 117. Here’s How The World’s Oldest Woman’s Cells Stayed Decades Younger Than Her Age

Maria Branyas, then age four, sitting on a wooden fence with her family in 1911 in New Orleans. (Credit: Arxiu de la família Branyas Morera - Own work, Public Domain / Wikimedia Commons)

Study suggests Maria Branyas Morera’s daily yogurt habit could have shaped her tremendously healthy gut microbiome

* Maria Branyas Morera lived to 117, yet DNA methylation tests showed her cells acting about 23 years younger than her chronological age.

* Her daily yogurt habit coincided with unusually high levels of Bifidobacterium, a gut microbe common in younger people, and extremely low inflammation markers (GlycA and GlycB).

* Blood analysis revealed efficient fat metabolism: very low triglycerides and high HDL cholesterol, patterns linked to heart and brain health.

* Rare protective gene variants and mitochondria that stayed energetically active may have helped her avoid cancer and major diseases despite short telomeres.

BARCELONA — Maria Branyas Morera ate three yogurts every day for the last two decades of her life. It sounds like simple advice from a health-conscious grandmother, but scientists now believe this habit may have been one key to her becoming the oldest verified person in the world.

When Branyas died in August 2024 at 117 years and 168 days old, she left behind more than memories. She left her body to science, and what researchers found has challenged long-held assumptions about aging. Despite her extreme chronological age, her cells told a different story. According to multiple DNA methylation clocks (tests that measure chemical changes to DNA that accumulate with age) her biological age was roughly 23 years younger than the number of candles on her birthday cake.

The finding raises a compelling question: Can we age in years without our cells aging at the same pace?

Branyas’s daily yogurt consumption appears linked to her internal bacterial ecosystem, though proving direct causation would require long-term controlled studies the researchers didn’t conduct. Analysis of her gut bacteria revealed high levels of Bifidobacterium, a beneficial bacterium typically abundant in younger people but known to decline with age. While some centenarians show elevated levels of this microbe, it’s rarely seen in supercentenarians, or those who live past 110.

“This finding contrasts sharply with the typical decline of this bacterial genus in older individuals,” the researchers wrote in Cell Reports Medicine.

Bifidobacterium does more than just exist in the gut. It helps reduce inflammation throughout the body and produces beneficial compounds including short-chain fatty acids, which help regulate metabolism and immune function. Branyas’s gut resembled that of someone decades younger, possibly thanks to the beneficial bacteria in her daily yogurt. The Streptococcus thermophilus and Lactobacillus delbrueckii found in yogurt are known to promote Bifidobacterium growth, and her high Bifidobacterium levels may have contributed to her efficient fat metabolism through pathways connecting gut health to how the body processes cholesterol and triglycerides.

Her microbiome not only looked younger, it appeared to be actively working in her favor. Branyas showed strikingly low levels of systemic inflammation markers called GlycA and GlycB, which are signals from proteins released during inflammatory responses. High levels of these markers predict cardiovascular disease and early death. Hers were extraordinarily low, suggesting her body maintained a state of minimal inflammation even at 117 years old.

Maria Branyas Morera blows out the candles on her 117th birthday. (Credit: Arxiu de la família Branyas Morera – Own work, Public Domain / Wikimedia Commons)

Branyas’ body told two contradictory stories at once, and that contradiction could represent one of the study’s most intriguing findings.

On one hand, she exhibited classic hallmarks of extreme aging. Her telomeres — the protective caps on chromosome ends that shorten each time a cell divides — were among the shortest ever measured in the study’s database of healthy volunteers. She had about 8,000 DNA units of telomere length remaining, with 40% of her telomeres falling below the 20th percentile of all samples studied. For context, telomere shortening is often considered a key driver of aging and age-related diseases.

She also carried clonal hematopoiesis mutations, genetic changes in blood cells where a single mutated cell produces many copies of itself. The mutations occurred in genes called SF3B1 and TET2, changes that typically precede blood cancers and cardiovascular disease in other people. Her immune system showed an expanded population of age-associated B cells, a type of immune cell that accumulates with advancing years and contributes to inflammation.

Yet despite these aging signatures, she maintained good health and never developed cancer or neurodegenerative disease.

The researchers analyzed her genome (DNA sequence), epigenome (chemical modifications to DNA), transcriptome (gene activity), metabolome (small molecules in blood), proteome (proteins), and microbiome (gut bacteria), comparing results with large groups of other people. What emerged was a picture of someone whose cells had found ways to stay functionally young even as chronological age mounted.

Telomeres are found on both ends of chromosomes. Telomere length is affected by lifestyle and has direct impact on human health and lifespan. (3D illustration by nobeastsofierce on Shutterstock)

Six different epigenetic clocks (tests that predict biological age based on chemical modifications to DNA) all reached the same conclusion: Branyas’s tissues were biologically much younger than her years. These clocks work by measuring patterns of methylation, chemical tags that get added to DNA over time in predictable ways.

When researchers used a completely different clock based on ribosomal DNA methylation (a measure of chemical tags on genes that make protein-building machinery), they found her biological age was an astonishing 23 years younger than her chronological age. Her cells were aging at a pace more than 17 years slower than expected.

This wasn’t a fluke of one measurement system. Multiple independent methods, analyzing different tissues including blood, saliva, and urine, all pointed to the same conclusion: her cells had somehow escaped the typical pace of biological aging.

Branyas possessed what researchers described as “one of the most efficient lipid metabolisms reported.” Her blood showed extremely low levels of VLDL cholesterol (the “bad” cholesterol that carries triglycerides) and triglycerides (fats in the blood), while HDL cholesterol (the “good” cholesterol) was very high. Her lipoproteins, the particles that transport fats through the bloodstream, appeared to mature efficiently, with high numbers of large HDL particles and low numbers of small HDL particles.

Studies involving hundreds of thousands of people from the UK Biobank have linked efficient fat metabolism to both extended lifespan and reduced dementia risk. Branyas never showed signs of cognitive decline, remaining mentally sharp until her final days.

Her metabolic advantages extended beyond cholesterol. She had low levels of saturated fatty acids, esterified cholesterol, linoleic acid, and acetone, all biomarkers associated with poor health and increased mortality in population studies. Meanwhile, she showed high levels of free cholesterol, which has been associated with good health and survival.

The combination created what researchers call a favorable cardiometabolic profile, meaning her body processed and managed fats in ways that protected rather than damaged her cardiovascular system.

Bifidobacterium levels in Branyas were extraordinarily high for someone her age. (© Dr_Microbe – stock.adobe.com)

The genetic analysis revealed rare variants that may have contributed to Branyas’s longevity, though the researchers cannot definitively prove these variants caused her exceptional lifespan. She carried unusual versions of genes in areas associated with immune function, cardiovascular protection, brain health, and energy production in cells.

Seven of these genetic variants appeared in a form called homozygous, meaning she inherited the same version from both parents. None of these seven homozygous variants had ever been described in any European control population studied by researchers. Their rarity and the biological processes they affect suggest they may have played a role, but the single-subject nature of the study means these remain associations rather than proven causes.

For example, she had variants in DSCAML1, a gene associated with immune function and maintaining cognitive abilities, and MAP4K3, linked to lifespan regulation in laboratory organisms and tied to autoimmune disease, cancer, and aging in humans. She carried variants in the PCDHA gene cluster related to brain health and heart disease, and in genes called LRP1 and LRP2 involved in fat metabolism and cardiovascular function.

Her mitochondria, the structures inside cells that produce energy, functioned at levels that exceeded even younger women. When researchers measured mitochondrial membrane potential (an indicator of how well mitochondria are working) and chemical signs showing her cells produced energy efficiently, the values in her blood cells were higher than those observed in cells from younger controls.

This was unexpected. Mitochondrial function typically declines with age, contributing to fatigue, muscle weakness, and other aging symptoms. But Branyas’s mitochondria appeared not only preserved but exceptionally robust.

She also had rare variants in genes involved in mitochondrial oxidative phosphorylation, the process cells use to generate energy from nutrients. These variants affected genes including ND5, COX1, MTG2, MTCH2, and MRPS9. While some of these changes might have occurred in her mitochondrial DNA over time, their presence suggests her cells maintained efficient energy production throughout her life.

Perhaps the most intriguing paradox involves those extremely short telomeres. While shortened telomeres are typically considered a sign of cellular aging and often predict health problems, in Branyas’s case they may have served as protection.

Telomeres act like a cellular counting system. Each time a cell divides, its telomeres get shorter. Eventually, they become so short that the cell can no longer divide—it either dies or enters a state called senescence where it stops dividing but doesn’t die. This limit on cell division is actually a built-in cancer prevention mechanism, since cancer requires cells to divide uncontrollably.

The researchers speculate that the severe erosion of Branyas’s telomere sequences could have limited how many times any potential cancer cells could divide, preventing tumors from growing. She was never diagnosed with cancer in her 117 years, despite carrying mutations that typically increase cancer risk.

“Because the M116 individual presented an overall good health status, it is tempting to speculate that, in this setting, telomere attrition behaves more as a chromosomal clock for aging rather than a predictor of age-linked diseases,” the researchers wrote.

In other words, her shortened telomeres marked the passage of time without necessarily causing disease—though this remains a hypothesis rather than proven fact.

Maria Branyas Morera, 1925 (Credit: Arxiu de la família Branyas Morera – Own work, Public Domain / Wikimedia Commons)

The study reveals that extreme longevity may involve the coexistence of two distinct biological processes within the same individual. Advanced chronological age brought its expected cellular hallmarks: telomere shortening, mutations in blood cells, and aged immune populations. At the same time, Branyas maintained protective genetic variants, low inflammation, an anti-inflammatory gut microbiome, efficient fat metabolism, and chemical tags on DNA associated with chromosomal stability and slower biological aging.

“Aging and disease can, under certain conditions, become decoupled, challenging the common perception that they are inextricably linked,” the researchers concluded.

Branyas wasn’t simply born lucky, though her genetics certainly helped. Her lifestyle choices, particularly her Mediterranean diet rich in yogurt, likely played a role in maintaining her rejuvenated gut ecosystem. She also walked regularly, maintained an active social life, enjoyed reading, played piano, and tended a garden—all activities associated with healthy aging in research studies.

The researchers emphasize that their findings come from a single exceptional individual, and drawing broadly applicable conclusions would be premature. Achieving extreme longevity likely involves a confluence of genetic, environmental, and chance factors unique to each person. What works for one supercentenarian may not work for another.

Still, the study offers tantalizing hints. The observation that Branyas maintained repetitive DNA sequences in a tightly controlled chemical state, like much younger individuals, suggests that protecting these genomic regions from activation could help prevent chromosomal breaks associated with aging. Her efficient fat metabolism and anti-inflammatory microbiome point to potential areas for intervention.

Perhaps most importantly, the research demonstrates that exceptional aging doesn’t require perfection at every biological level. Branyas thrived despite having cellular aging markers that would typically predict poor health outcomes. The right combination of protective factors appears capable of offsetting typical age-related decline, allowing someone to reach an extraordinary age while maintaining quality of life.

Whether that combination can be replicated, enhanced, or encouraged through medical intervention remains to be seen. But for now, the case of Maria Branyas Morera suggests that the relationship between time passed and biological decay is more flexible than previously imagined; and that perhaps, with the right circumstances, our cells can stay decades younger than our years.

Researchers conducted a comprehensive multiomics analysis of Maria Branyas Morera (referred to as M116 in the study), who was the world’s oldest verified living person at the time of sample collection. The team collected peripheral blood, saliva, urine, and stool samples at multiple time points when Branyas was 116 years old. They performed whole genome sequencing, single-cell RNA sequencing of peripheral blood mononuclear cells, whole proton nuclear magnetic resonance metabolomics, proteomics of extracellular vesicles, 16S metagenomic sequencing of gut microbiota, and genome-wide DNA methylation profiling using both microarray and whole genome bisulfite sequencing. Telomere length was measured using high-throughput quantitative fluorescence in situ hybridization. Results were compared with large matched control cohorts, including 75 women from the Iberian population for genetic analysis, over 6,000 individuals for metabolomic comparisons, 445 individuals for microbiome analysis, and 81 individuals aged 21-78 years for epigenetic analysis.

The study found Branyas exhibited extremely short telomeres (about 8 kb, with 40% below the 20th percentile), clonal hematopoiesis mutations in SF3B1 and TET2 genes, and expanded age-associated B cell populations. At the same time, she showed protective features including rare genetic variants in genes related to immune function (DSCAML1, MAP4K3), cardiovascular health (PCDHA1-9, LRP1, LRP2), neuroprotection (NSUN5, TTBK1), and mitochondrial function (ND5, COX1, MTG2, MTCH2, MRPS9). Her mitochondrial membrane potential and superoxide levels exceeded those of younger women. Metabolomic analysis revealed exceptionally efficient lipid metabolism with very low VLDL cholesterol and triglycerides, very high HDL cholesterol, and low inflammation markers (GlycA and GlycB). Microbiome analysis showed high levels of Bifidobacterium, typically seen in younger individuals. Six different DNA methylation clocks indicated her biological age was substantially younger than her chronological age, with the ribosomal DNA clock showing a 23-year difference and an age deceleration pace of more than 17 years.

The study’s primary limitation is that it examines only one individual, making it impossible to determine which findings are generalizable versus unique to this specific person. The researchers acknowledge that extreme longevity likely results from highly individualized combinations of genetic, environmental, and stochastic factors. While the study included comprehensive molecular profiling, it represents snapshots in time rather than longitudinal tracking throughout Branyas’s life, limiting conclusions about cause and effect. The study also could not definitively prove that the high Bifidobacterium levels resulted from yogurt consumption, as this would require a controlled longitudinal study. The research did not extensively investigate all hallmarks of aging such as senescence, autophagy, and inflammation at the cellular level, and did not test potential interventions to explore anti-aging effects of the observed features.

Research in the Manel Esteller group was funded by the CERCA Programme/Generalitat de Catalunya, the European Regional Development Fund, Departament de Recerca i Universitats/Generalitat de Catalunya, European Union THRIVE grant, “La Caixa” Research Foundation, and the Cellex Foundation. Various co-authors received support from Spanish Ministry fellowships, Ramon y Cajal fellowships, Instituto de Salud Carlos III grants, European Research Council grants, and other institutional funding sources. Manel Esteller declared past grants from Ferrer International and Incyte and personal fees from Quimatryx and Eucerin outside the submitted work. All other authors declared no competing interests.

Santos-Pujol E, Noguera-Castells A, Casado-Pelaez M, et al. The multiomics blueprint of the individual with the most extreme lifespan. Cell Reports Medicine. 2025;6:102368. Published online October 21, 2025.

I can’t stand nonfat yogurt. It is chalky. Can I get the same benefits from full-fat yogurt? I kinda doubt the old lady ate nonfat yogurt.

The cheap, easy, and delicious way to get more probiotics in one’s diet is to buy the 3 lb. tub of sour cream at Costco for $4.89 — after picking up the 2 dozen cage-free, free-range eggs for $4.59. That combo is all one needs to have the ultimate keto-diet. It even turns all those chips into a health food. It goes extremely well with eggs (Eggs Benedict), soups, casseroles, etc. It even has a built-in timer requiring you to consume it before it spoils in approximately two weeks — forcing you to eat as much as possible before then. Pretty nearly the perfect food — at a lower price than practically anything else. I tolerate it very well as an ordinarily lactose-intolerant person.

"Branyas’s daily yogurt consumption appears linked to her internal bacterial ecosystem,..."

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Wow, what a fascinating article. I have tended to rather simplistically think aging was just driven by telomeres shortening, like a fuse burning down until nothing was left and cells became unable to viably regenerate. This article shows the relationship between telomeres, cancer and aging is much more complex, and how many other factors there are to consider.

28 posted on 10/13/2025 11:31:12 AM PDT by Red Badger (Homeless veterans camp in the streets while illegals are put up in 5 Star hotels....................)

Studies have shown that all sorts of fermented foods contribute to good health.

I knew an Ethiopian veterinarian who told me that areas where Injera - a bread made of fermented teff batter - was a staple had far less disease than areas where it wasn’t used.

And fermented vegetables like kimchi and sauerkraut have been shown to be healthful.

Most of the microbes that constitute the human immune system are in the gut.

No, but I’ll start eating more sourdough bread and drinking more red wine. Last week, I paired steak with a bottle of GSM wine that was much pricier than I usually buy. Nearly polished off the bottle myself, drank 4 glasses. Notably, I had no hangover the next morning. Blood sugar was up a bit, though. Obviously, more testing is called for.

I don’t think it matters; the fermentation breeds the microbes you need whether it’s whole milk or not.

But I think you need to get a decent starter from a place that specializes in yogurt starters. You’re not going to have good results trying to start it from a supermarket yogurt.

My uncle never had a diet in his life. He’s 102 and is worried about getting his drivers license renewed. Walks1/2 mile day. Good conservative loves Israel

Walking with steepness included appears to be the common deniminator for longer living population pockets around the world. Not what you eat per se.

I’ve posted this before, remembered from when these ads were on TV a lot.

Dannon Yogurt.

https://www.youtube.com/watch?v=J4AAWiNAE8Q

39 posted on 10/13/2025 11:54:55 AM PDT by frank ballenger (There's a battle outside and it's raging. It'll soon shake your windows and rattle your walls. )

The vanilla Greek version is pretty tasty. My husband who never ate yogurt eats this every day. He adds organic honey granola to it. I eat a nontat Chobani fruit yogurt mixed with Dannon nonfat plain yogurt with almonds, cranberries and granola added every day.

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