When María Branyas Morera turned 116, scientists asked if they could take a peek under the hood. She agreed, cheerfully. Blood, saliva, urine, stool — they wanted it all. What they found was nothing short of astonishing: a multi-layered biological blueprint for surviving 117 years and 168 days.
“She had an exceptional genome enriched in variants in genes that are associated with enhanced lifespan in other species, such as dogs, worms and flies,” Manel Esteller of the Josep Carreras Leukaemia Research Institute in Barcelona told New Scientist.
The Genetics of Living to 117
The research team, led by Eloy Santos-Pujol and Aleix Noguera-Castells, dug into every “-omics” you can imagine: genome, metabolome, proteome, microbiome, epigenome. The paradox they faced was simple: how did someone who had all the classic molecular hallmarks of aging — shredded telomeres, clonal mutations in blood cells, an aged immune landscape — manage to stay so healthy?
The answer, it turns out, is balance.
Her genome carried rare protective variants that seemed to guard her against cardiovascular disease, dementia, and diabetes. Unlike most of us, she lacked the usual culprits: no risky Alzheimer’s mutations and no metabolic-disorder genetic signatures. She even had a mitochondrial system that functioned better than women decades younger.
And yet, her chromosomes told a different story. Branyas’s telomeres were shredded — “the shortest mean telomere length among all healthy volunteers” in the study.
Telomeres are like the plastic tips on shoelaces, capping the ends of our chromosomes and keeping our genetic code from fraying every time cells divide. The problem is, they shrink with age — and when they get too short, cells either stop dividing or start malfunctioning, which has been tied to cancer, heart disease, and dementia. That’s why scientists usually treat short telomeres as a bad omen, a molecular clock ticking down toward disease and death.
In most of us, that would spell cancer or neurodegeneration. But not for María Branyas Morera — and perhaps other edge cases like hers. “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 authors wrote in Cell Reports Medicine.
The Microbes and Meals That Kept Her Young
While her DNA provided the foundation, her daily habits likely built on it. Branyas never smoked, never drank alcohol, and ate a Mediterranean diet rich in fruits, legumes, olive oil—and most famously, yogurt. Three servings a day, plain and unsweetened.
Her love for yogurt could explain her unusually high levels of Bifidobacterium, a probiotic bacterium linked to reduced inflammation and gut health. These microbes usually decline with age. In her case, they flourished.
“It shows that maybe a dietary intervention can be associated not only with avoiding obesity and other pathologies, but also with prolonged life, acting through the microbiome gut landscape,” Esteller told New Scientist.
Her microbiome, when mapped against 445 controls aged 61–91, looked shockingly young. Less inflammation, more diversity. The kind of gut you’d expect in someone half her age.
And this microbial youthfulness radiated through her body. Blood analyses showed ultra-low “bad” cholesterol, sky-high “good” cholesterol, and inflammation markers so low they looked practically engineered. She had one of the most efficient lipid metabolisms ever recorded.
Her immune system, too, refused to give up. At 113, she survived COVID-19, making her the oldest known survivor in Spain.
Additionally, she reportedly surrounded herself with family and friends, avoided stress, and stayed active both mentally and physically. These habits, supported by scientific evidence, are known to stave off dementia and other age-related declines.
The Lottery and the Lesson
Still, we shouldn’t get carried away. Richard Faragher, a biogerontologist at the University of Brighton, cautioned against reading too much into one case. “There is a danger that a slightly unusual variant in, for example, a gene can be turned into a scientific ‘just-so story’ about its relevance to ageing,” he told New Scientist. Sometimes, he added, survival to extreme old age is simply “luck.”
Branyas herself saw it that way. “She said: ‘My only merit is that I’m alive’,” Esteller recalled.
Yet the study offers something larger than a just-so story. It shows that aging and disease are not always in lockstep. The Spanish team put it bluntly in their paper: “The picture that emerges from our study, although derived only from this one exceptional individual, shows that extremely advanced age and poor health are not intrinsically linked.”
That’s revolutionary. We’ve been told that aging inevitably means decline. But Branyas’s biology split the two apart. Yes, her cells carried the scars of time. But her body’s systems — lipids, microbiome, immunity — stayed astonishingly resilient.
Her life suggests a radical possibility for most of us: that the future of longevity medicine isn’t about erasing aging, but about decoupling it from disease. Genes dealt her an unusually good hand, but diet, microbes, and low inflammation kept her in the game.
