Maria Branyas at 117: What Her Biology Reveals About Extreme Longevity

Maria Branyas Morera died in 2024 as the world's oldest verified living person, at 117 years and 168 days, outliving the average Catalonian woman by more than three decades. She survived the 1918 influenza pandemic, two world wars, the Spanish Civil War, and COVID-19. Now, in the most comprehensive multi-omics study ever conducted on a supercentenarian, researchers led by Manel Esteller at the Josep Carreras Leukemia Research Institute and the University of Barcelona have mapped her genome, epigenome, proteome, metabolome, transcriptome, and microbiome. What they found defies a simple story about aging.

Maria Branyas Showed Extreme Aging and Robust Health at the Same Time

Esteller describes the results as a "fascinating duality: the simultaneous presence of signals of extreme aging and of healthy longevity." Branyas had very short telomeres, the protective caps on chromosome ends that typically shorten with age. She showed clonal hematopoiesis, a process in which blood stem cells accumulate mutations and gradually dominate the blood supply, a known risk factor for leukemia and cardiovascular disease. Her immune system bore unmistakable signs of decades of wear. Yet she never developed cancer, dementia, or major cardiovascular disease. Her cells, Esteller noted, "seemed younger than her age."

The epigenetic data put a number on that gap. Multiple independent biological clocks placed her biological age at more than 23 years below her chronological age of 117. That is not a rounding error. It suggests that whatever mechanisms drive tissue-level aging in most people were substantially slowed in Branyas, even as her telomeres told a different story. The findings illustrate, as the researchers write in the paper, "how aging and disease can, under certain conditions, become decoupled, challenging the common perception that they are inextricably linked."

Rare Genetic Variants Linked to Immune Fitness, Brain Health, and Heart Protection

Genomic sequencing turned up rare variants that help explain why Branyas aged without the usual catalogue of diseases. The variants clustered around four areas: immune fitness, brain health, heart protection, and mitochondrial function. Her blood lipid profile was consistent with those protective signals: low VLDL and triglycerides, high HDL cholesterol, and exceptionally low systemic inflammation. That combination is a well-recognized shield against cardiovascular disease and metabolic decline.

Earlier research on supercentenarian genetic variants had suggested that extreme survivors may carry some disease-causing mutations like everyone else, but that their advantage likely comes from variants that slow the aging process itself rather than prevent any single disease. The Branyas data fits that picture: the protective variants did not make her immune to cellular damage. They appear to have dampened the rate at which that damage translated into clinical disease.

Broader metabolomics and proteomics work on extreme longevity has flagged high omega-3 polyunsaturated fatty acids, short-chain fatty acids, and specific apolipoproteins as recurring biomarkers in long-lived individuals. Branyas's efficient lipid metabolism aligns with that pattern, lending weight to the idea that metabolic regulation is a shared feature of exceptional survivors.

A Gut Microbiome That Looked Decades Younger

Perhaps the most striking single finding involves bacteria. Branyas's gut microbiome was rich in Bifidobacterium, a genus associated with immune regulation and gut barrier integrity that typically declines steeply in older adults. Her microbiome profile was closer to what you would expect in a much younger, healthier person than in a 117-year-old. The researchers note that her lifelong habit of eating yogurt daily may have contributed, though they are careful to flag that the study cannot establish cause and effect for any single lifestyle factor.

The immune system data reinforced the gut picture. Despite showing the structural marks of an aged immune system, her functional immune profile shared characteristics with substantially younger individuals. Recent research on Brazilian supercentenarians has similarly argued that immune aging in extreme survivors should be read as an adaptation preserving function rather than straightforward decline. Branyas's data supports that reframing.

How a Multi-Omics Approach Made the Study Possible

The researchers collected minimally invasive samples: blood, saliva, urine, and stool. From those, they ran six distinct omics analyses simultaneously, then compared Branyas's results against matched cohorts of non-supercentenarians. The parallel approach matters because any single layer of biology can mislead. Telomere length alone would have predicted catastrophic disease risk. Epigenetic clocks alone might have suggested a moderately healthy elderly person. Only by stacking genomic, proteomic, epigenomic, metabolomic, transcriptomic, and microbiomic data could the team see the full contradiction: a body accumulating damage at the molecular level while somehow insulating its tissues from the consequences.

Advances in single-cell sequencing and cellular atlas technologies are making it increasingly feasible to resolve those contradictions at the individual cell level, observing how different cell types age at different speeds within the same body. The Branyas study relied heavily on bulk tissue analyses, and the researchers acknowledge that single-cell resolution of her samples would be a valuable next step.

What This Means for Aging Research and Its Limits

The obvious caveat is sample size: one person. No matter how thorough the analysis, results from a single individual cannot be extrapolated to broader populations, and the team is explicit about that limitation. Validating these findings will require assembling larger cohorts of supercentenarians, a logistically difficult task given how rare they are globally.

Still, the study is not simply a curiosity about one exceptional woman. It provides a concrete molecular blueprint of what healthy extreme aging looks like, identifying specific genetic variants, microbiome signatures, metabolic patterns, and epigenetic profiles that researchers can now test in wider populations. The goal, as Esteller's group frames it, is to use these findings to develop biomarkers for healthy aging and, eventually, strategies to extend the years of life lived without major disease. Branyas's lifestyle, which included no smoking, no alcohol, regular physical activity, and an active social life, adds a behavioral dimension to that picture, even if the study cannot weight any single factor definitively.

Telomere length, long treated as a proxy for biological age and disease risk, may need rethinking at the extremes of human lifespan. Branyas had very short telomeres and lived to 117 without telomere-associated disease. Clonal hematopoiesis, another marker researchers watch for cardiovascular and cancer risk, also failed to produce its expected consequences in her case. The Branyas data suggests that in supercentenarians, the usual rules governing how molecular damage converts to clinical disease may operate differently, or perhaps not at all.