Maria Branyas had not escaped aging. Her chromosome ends were worn short, some blood cells carried mutations associated with disease risk, and her immune system bore the marks of more than a century of life. Yet other measurements told a different story: relatively favorable fat metabolism, low levels of certain inflammatory markers and DNA-based age estimates younger than her calendar age.
Branyas died in August 2024 at 117 years and 168 days. A detailed study of her biology, published in Cell Reports Medicine on September 24, 2025, describes this coexistence of molecular wear and apparent resilience. It offers a way to examine how aging and disease can diverge. It does not explain how to live to 117, or prove that researchers can slow human aging.
Many layers of biology, one person
The team, led by Eloy Santos-Pujol and Manel Esteller, used multi-omic profiling. That means measuring several layers of biology together: DNA sequence, gene activity, proteins, small molecules involved in metabolism, microbes and chemical marks on DNA. Each layer answers a different question about how a body is functioning.
Blood, saliva, urine and stool provided material for the analyses. Most blood measurements came from when Branyas was 116 years and 74 days old, which explains the paper’s shorthand name for her, M116. Researchers compared different parts of her profile with different reference populations. Those comparisons add context, but they do not turn the study into a trial or a large study of supercentenarians.
The unmistakable signs of age
Her telomeres, the protective DNA sequences at chromosome ends, were exceptionally short in the sampled blood cells. She also had clonal hematopoiesis: blood-cell populations descended from cells carrying acquired mutations. The researchers identified changes in SF3B1 and TET2, genes implicated in blood-cancer risk.
Neither finding amounted to a diagnosis of cancer. The paper reports that she had not developed cancer or major cardiovascular disease. Why these molecular risks did not produce those outcomes is unresolved.
Her immune profile was also markedly aged. Age-associated B cells, part of the antibody-producing branch of immunity, were expanded. Some T-cell populations showed features of cellular aging, while inexperienced, or naive, T cells were scarce. Describing the entire immune system as youthful would miss much of the evidence.
Genetic clues, without a longevity gene
The genome analysis highlighted rare variants in pathways connected with immunity, brain function, cardiovascular biology and energy production. Variants are differences in DNA sequence; identifying one in a relevant gene does not establish what that particular difference does.
The study also measured features of mitochondria, the structures that help cells produce usable energy. The blood-cell assays were interpreted as evidence of preserved mitochondrial function. They cannot establish that every organ retained the same capacity, or that a particular inherited variant caused the result.
A person selected because of exceptional survival will inevitably have unusual biological features. The scientific challenge is to determine which helped, which merely accompanied survival and which were incidental. That requires comparisons and experiments beyond this case.
An aged immune system with low inflammatory markers
Branyas had low triglycerides and VLDL cholesterol, alongside high HDL cholesterol and a lipoprotein pattern the authors considered favorable. Lipoproteins are particles that transport fats through blood. These measurements describe a metabolic profile, not direct proof of perfectly healthy arteries.
GlycA and GlycB, blood signals reflecting several inflammation-related proteins, were also low. This is the striking contrast: immune-cell features associated with inflammation coexisted with low measured systemic inflammatory activity.
The results were not uniformly reassuring. Some amino-acid levels were low, and lactate and creatinine were elevated. Protein analyses also found mixed signals. The profile therefore resists being compressed into a single score for good health.
A different epigenetic picture
Epigenetics concerns chemical features that influence how DNA is used without changing its sequence. The researchers examined DNA methylation, small chemical marks attached at particular sites. Some patterns were consistent with advanced age, while repetitive stretches of DNA retained marks that may help keep those sequences quiet.
Six epigenetic clocks, algorithms that estimate age from methylation patterns, produced younger estimates across the sampled tissues. A separate ribosomal-DNA clock gave an estimate about 23 years below her chronological age. That figure is an output of one model, not a measurement showing that her entire body was exactly 23 years younger.
Age clocks capture particular statistical patterns. Their interpretation is especially difficult at extreme ages, where people like Branyas are scarce in reference datasets. Different tissues, cell mixtures and clocks can tell different stories. A younger estimate does not erase short telomeres or aged immune cells.
The gut microbiome finding
Her stool samples contained abundant Bifidobacterium, a group of gut bacteria often associated with beneficial functions. The researchers also reported greater microbial diversity than the average in the female comparison group. The gut microbiome is the community of microorganisms living in the digestive tract.
Branyas regularly ate yogurt, and the authors discussed diet as one possible influence. But they could not establish that yogurt produced the bacterial pattern, or that the bacteria caused her longevity. A late-life stool sample cannot reconstruct a century of changing diet, infections, medications and microbial communities.
The study therefore provides no basis for treating a particular yogurt or probiotic as a route to exceptional lifespan.
What one supercentenarian cannot tell us
The central limitation is the sample size: one exceptional individual. Even thousands of measurements remain observations about that person. Reference cohorts varied across analyses, and some comparisons were small. The study cannot reliably separate inherited advantages, environment, chance and the consequences of surviving to extreme age.
Most measurements offer a late-life snapshot rather than a lifelong trajectory. Blood and saliva cannot represent every organ, and telomere measurements in mixed blood-cell populations are not a direct measure of whole-body aging. The authors also call for more detailed functional studies of inflammation, cellular senescence and autophagy, the cell’s recycling process.
No intervention was tested to determine whether reproducing any feature would improve another person’s health. Longitudinal studies, following more people over time, and experiments that test proposed mechanisms are needed before these observations can support treatment claims.
The Lifespan Brief assessment
Branyas’s biology supports a narrower, more useful question than the search for a secret to longevity: which changes reflect accumulated age, and which help determine whether disease develops?
Aging remains strongly connected with disease risk. This case illustrates that the relationship need not be uniform across every molecular system. Understanding how resilience coexists with biological damage could help researchers choose better questions and more informative measurements. It does not yet provide a method for making that resilience transferable.
Sources
Santos-Pujol E, Noguera-Castells A, et al. The multiomics blueprint of the individual with the most extreme lifespan. Cell Reports Medicine (2025). Open full text, figures and study limitations.
Josep Carreras Leukaemia Research Institute: institutional account of the study. University of Leicester: research-team background, September 2025.
Feature image: original AI-generated conceptual illustration of accumulated age and preserved biological function. It is not a portrait of Maria Branyas.