{"id":770210,"date":"2026-07-18T12:37:21","date_gmt":"2026-07-18T12:37:21","guid":{"rendered":"https:\/\/www.newsbeep.com\/us\/770210\/"},"modified":"2026-07-18T12:37:21","modified_gmt":"2026-07-18T12:37:21","slug":"new-research-reveals-how-humans-could-live-up-to-156-years","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/us\/770210\/","title":{"rendered":"New Research Reveals How Humans Could Live Up to 156 Years"},"content":{"rendered":"

A team of researchers has unveiled a new mathematical model suggesting humans could theoretically live up to 156 years if every reversible hallmark of aging<\/a> were eliminated except one. The finding offers the first quantitative ceiling on human longevity based solely on somatic mutations\u2014the irreversible DNA<\/a> errors that accumulate in our cells over time. <\/p>\n

The work affects both aging science and future therapeutic strategy, signaling that even the most advanced anti-aging interventions may hit a hard biological limit unless genomic damage can be controlled. <\/p>\n

According to the study<\/a>\u2019s authors, the tissues that cannot regenerate\u2014the brain and the heart\u2014are the ones that ultimately set that limit.<\/p>\n

Read More on News<\/p>\n

\"Rear<\/p>\n

The research<\/a>, published in npj Aging<\/a>, uses a multistage model to \u201cswitch on\u201d aging mechanisms one by one and measure how long a human could live if all but somatic mutations\u2014a DNA change that arises in any non\u2011reproductive cell after conception, meaning it affects the body\u2019s tissues but cannot be passed to offspring\u2014were cured.<\/p>\n

The authors found that eliminating every other aging process still leaves a median lifespan capped between 146 and 194 years, with neurons and cardiomyocytes acting as the bottlenecks. \u201cNeurons and cardiomyocytes, which lack the ability to divide, turned out to be the main limiting factors,\u201d said co-author Evgeniy Efimov in a statement.<\/p>\n

Newsweek has reached out to the study’s corresponding author Dmitrii Kriukov via email for comment. <\/p>\n

Somatic Mutations as the Final Barrier<\/p>\n

Unlike other hallmarks of aging\u2014such as mitochondrial decline, epigenetic drift, or loss of proteostasis\u2014somatic mutations cannot be reversed with any existing therapy. They accumulate slowly but relentlessly, and in tissues that cannot replace their cells, the damage becomes permanent. The model shows:<\/p>\n

Liver and other renewing organs can withstand thousands of years of mutation accumulation thanks to continuous cell turnover.Brain and heart cells, which do not divide, cannot dilute their damage and eventually fail.\"GettyImages-71268995\"<\/p>\n

This asymmetry explains why diseases such as dementia and heart failure dominate late\u2011life morbidity: they strike precisely the tissues that cannot regenerate.<\/p>\n

Assistant Professor Jordan Weiss, who studies health span and population\u2011level aging at NYU Grossman School of Medicine, said the model\u2019s tissue\u2011specific insight mirrors real\u2011world patterns.<\/p>\n

\u201cThe conditions that cost people their independent, healthy years\u2014such as dementia and heart failure\u2014fall heavily on precisely the tissues that cannot regenerate,\u201d he told Newsweek. \u201cSo the gap between how long people live and how long they stay well is not one general breakdown of the body. It is concentrated in the organs that have no way to replace worn\u2011out cells.\u201d<\/p>\n

Why the Limit Is 156 Years\"Holding<\/p>\n

The researchers began with a hypothetical \u201cnon-aging human\u201d whose mortality risk never increases with age. In that scenario, the median lifespan would be 1,759 years. Once somatic mutations were added back into the model, the lifespan collapsed to 156 years, entirely due to the vulnerability of non-renewing tissues.<\/p>\n

Even when all other aging processes were removed, the model\u2019s ceiling barely budged. That suggests somatic mutations contribute roughly half of the gap between theoretical immortality and real-world human lifespan.<\/p>\n

Pharmacist and regenerative\u2011medicine researcher Egle Pavyde said the study\u2019s value lies in quantifying what scientists have long suspected. \u201cIt proves that DNA damage accumulating in our cells is one of the reasons we cannot live indefinitely but also shows that our bodies are complex systems and that it is only one piece of a much larger puzzle,\u201d she said.<\/p>\n

What This Means for Aging Research<\/p>\n

The study\u2019s authors and outside experts agree somatic mutations are likely the “highest\u2011hanging” fruit in geroscience. They are difficult to prevent, nearly impossible to reverse, and lack a single druggable pathway.<\/p>\n

As Michael Leone, Assistant Professor in the Division of Precision Medicine at NYU Grossman School of Medicine, told Newsweek: \u201cSomatic mutations are likely among the highest-hanging fruit in targetable geroscience … lower-hanging targets\u2014such as inhibiting mTOR with rapamycin or clearing senescent cells\u2014are far more logical interventions to prioritize.\u201d<\/p>\n

\"Group<\/p>\n

The model does not claim humans will live to 190. Instead, it provides a ranking system for aging mechanisms, showing which ones shorten life the most and where interventions might matter most.<\/p>\n

Pavyde echoed that sentiment, noting that aging is \u201cmore like a machine wearing out in several ways at once,\u201d with mitochondrial dysfunction, protein\u2011quality decline, epigenetic changes and other processes contributing together.<\/p>\n

The Brain and Heart as Longevity Bottlenecks<\/p>\n

The strongest insight from the model is that longevity is not limited by the whole body, but by two specific tissues:<\/p>\n

\"BBQ\"<\/p>\n

These cells cannot divide, cannot replace themselves, and cannot dilute DNA damage. Their failure sets the upper bound on human lifespan\u2014even in a world where every other aging process is cured.<\/p>\n

Weiss said this framing offers a more precise way to think about healthy aging: \u201cIf renewable organs already tolerate decades of DNA damage without much trouble, there is little to gain from protecting them further. The harder and more valuable problem is preserving the DNA of brain and heart cells.\u201d<\/p>\n

What Happens Next<\/p>\n

The researchers plan to expand their model to include other hallmarks of aging, such as:<\/p>\n

mitochondrial dysfunctionepigenetic drifttelomere shorteningloss of proteostasis<\/p>\n

Their goal is a comprehensive quantitative theory of aging\u2014one that can rank every mechanism by how much it shortens life and guide future therapeutic priorities.<\/p>\n

\u201cThe takeaway is not that people might live to 190. It is that researchers now have a way to set priorities,” said Weiss.<\/p>\n","protected":false},"excerpt":{"rendered":"A team of researchers has unveiled a new mathematical model suggesting humans could theoretically live up to 156…\n","protected":false},"author":2,"featured_media":770211,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[34],"tags":[2594,1155,97,19563,35182,5722,1728,79,5497],"class_list":["post-770210","post","type-post","status-publish","format-standard","has-post-thumbnail","category-health","tag-aging","tag-dna","tag-health","tag-health-and-medicine","tag-lifespan","tag-pensions","tag-research","tag-science","tag-study"],"_links":{"self":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/posts\/770210","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/comments?post=770210"}],"version-history":[{"count":0,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/posts\/770210\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/media\/770211"}],"wp:attachment":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/media?parent=770210"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/categories?post=770210"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/tags?post=770210"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}