{"id":607817,"date":"2026-04-26T17:36:10","date_gmt":"2026-04-26T17:36:10","guid":{"rendered":"https:\/\/www.newsbeep.com\/us\/607817\/"},"modified":"2026-04-26T17:36:10","modified_gmt":"2026-04-26T17:36:10","slug":"scientists-discover-a-surprising-reason-intermittent-fasting-extends-life","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/us\/607817\/","title":{"rendered":"Scientists Discover a Surprising Reason Intermittent Fasting Extends Life"},"content":{"rendered":"

\"Intermittent<\/a>Intermittent fasting has long been linked to longer life, but new research points to an unexpected driver behind its benefits. Credit: Stock<\/p>\n

How the body efficiently shifts metabolism after fasting may be key to improving health, UTSW-led research suggests.<\/p>\n

Cutting calorie intake has long been linked to longer life, and intermittent fasting often appears to work better than maintaining a constant diet. Even so, scientists have struggled to explain exactly why this happens.<\/p>\n

New research from UT Southwestern Medical Center<\/a>, published in Nature Communications, suggests that the key factor is not the fasting period itself, but how the body adjusts its metabolism when food is reintroduced. The experiments were carried out in Caenorhabditis elegans, a type of roundworm commonly used in laboratory studies, and the findings could eventually inform approaches to improving human health.<\/p>\n

\u201cOur discoveries shift the focus toward a neglected side of the metabolic coin \u2013 the refeeding phase. Our data suggest that the health-promoting effects of intermittent fasting are not merely a product of the fast itself, but are dependent on how the metabolic machinery recalibrates during the subsequent transition back to a fed state,\u201d said study leader Peter Douglas, Ph.D., Associate Professor of Molecular Biology and a member of the Hamon Center for Regenerative Science and Medicine at UT Southwestern. Dr. Douglas co-led the study with Lexus Tatge, Ph.D., a former member of the Douglas Lab.<\/p>\n

\"Peter<\/a>Peter Douglas, Ph.D., is Associate Professor of Molecular Biology and a member of the\u202fHamon Center for Regenerative Science and Medicine at UT Southwestern. Credit: UT Southwestern Medical CenterMetabolic switch drives fasting benefits<\/p>\n

During fasting, cells quickly use up limited glucose supplies and then switch to breaking down stored lipids for energy. This shift, known as catabolism, is controlled by a protein called NHR-49. When glucose levels drop, NHR-49 activates and triggers lipid breakdown. Once food is available again, NHR-49 turns off, allowing cells to stop breaking down fats and begin restoring their energy reserves. Earlier work published in 2022<\/a> by Dr. Douglas and colleagues showed that NHR-49 also monitors lipid levels inside cells and helps prevent starvation when those reserves run low.<\/p>\n

To explore whether NHR-49 is responsible for the lifespan benefits of fasting, Dr. Douglas and colleagues removed the gene for this protein in C. elegans and then subjected the worms to a 24-hour fast. The outcome was unexpected. The absence of NHR-49 did not reduce the lifespan benefit. The fasted worms still lived about 41 percent longer on average and showed more youthful behavior, including increased movement, similar to worms with normal NHR-49 function.<\/p>\n

\"Fat<\/a>These images show how three Caenorhabditis elegans roundworms use and restore fat (green) during feeding, fasting, and refeeding: full when fed (left), reduced during fasting (middle), and rebuilt after refeeding (right). UT Southwestern researchers found that short fasting cycles can extend lifespan by over 60%, supporting longer, healthier life. Credit: UT Southwestern Medical CenterRefeeding response determines longevity<\/p>\n

The researchers then turned their attention to what happens after fasting ends, when NHR-49 is normally switched off.<\/p>\n

\"Vincent<\/a>Vincent Tagliabracci, Ph.D., is Associate Professor of Molecular Biology at UT Southwestern and a Howard Hughes Medical Institute Investigator. Credit: UT Southwestern Medical Center<\/p>\n

To understand this process, they examined how NHR-49 is naturally inactivated. Experiments led by Vincent Tagliabracci, Ph.D., Associate Professor of Molecular Biology at UTSW and a Howard Hughes Medical Institute Investigator, along with Victor Lopez, Ph.D., a postdoctoral researcher in the Tagliabracci Lab, showed that an enzyme called protein kinase CK1 alpha 1 (KIN-19) modifies NHR-49 through phosphorylation. When Dr. Douglas and colleagues altered this system so that NHR-49 remained active even after feeding resumed, lipid breakdown continued, and the lifespan-extending effects of fasting disappeared.<\/p>\n

Targeting metabolism could extend life<\/p>\n

Taken together, the findings indicate that the ability to properly shut down NHR-49 after fasting is critical for extending lifespan through calorie restriction. Adjusting this process may offer a way to gain the benefits of fasting without needing to follow strict dietary regimens.<\/p>\n

\u201cOur findings bridge a gap between lipid metabolism and aging research,\u201d Dr. Douglas said. \u201cBy targeting aging, the single greatest risk factor for human disease, we move beyond treating isolated conditions toward a preventive model of medicine that enhances quality of life for all individuals.\u201d<\/p>\n

Reference: \u201cSilencing lipid catabolism determines longevity in response to fasting\u201d by Lexus Tatge, Juhee Kim, Rene Solano Fonseca, Kyle Feola, Jordan M. Wall, Gupse Otuzoglu, Ann C. Johnson, Kielen R. Zuurbier, Jaeyoung Oh, Shaghayegh T. Beheshti, Victor A. Lopez, Anthony J. Daley, Emma G. Werner, Patrick Metang, Sonja L. B. Arneaud, Abigail Watterson, Jeffrey G. McDonald, Vincent S. Tagliabracci, Michael E. French and Peter M. Douglas, 22 January 2026, Nature Communications.
DOI: 10.1038\/s41467-026-68764-y<\/a><\/p>\n

This study was funded by the Clayton Foundation for Research, The Welch Foundation (I-2061-20210327), the American Federation of Aging Research (AFAR 2023), and the National Institutes of Health (R01AG076529, R01GM15385).<\/p>\n

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