A groundbreaking study from the Chinese Academy of Sciences (CAS) suggests that metformin, a widely prescribed drug for type 2 diabetes, may do more than just regulate blood sugar—it could also slow the biological aging process. The study, which involved experiments on primates, found that long-term use of metformin significantly reduced markers of cellular aging, offering the potential to extend the healthy years of human life by up to 18 years.
Published in Cell, the research was a collaborative effort led by Liu Guanghui’s team at CAS, alongside experts from the Beijing Institute of Genomics and other institutes. The study used Cynomolgus monkeys (Macaca fascicularis), which share many physiological similarities with humans, providing valuable insights into aging and metformin’s impact.
Over a 40-month period, the researchers administered metformin to male monkeys and observed its effects on aging across various tissues and organs. Their findings were striking: metformin treatment showed protective effects on critical organs like the liver, heart, lungs, and muscles. Notably, the drug mitigated cerebral cortex atrophy, enhanced cognitive function, and slowed periodontal bone loss—suggesting it may act directly on neurons and other cells, independent of its typical role in blood sugar regulation.
One of the key mechanisms identified was metformin’s activation of the Nrf2-mediated antioxidant gene expression network in the brain, which helped delay cellular aging. This discovery provides strong scientific backing for metformin’s potential as a “geroprotective” agent—offering hope for future treatments that could slow or even reverse the aging process.
In addition to these direct effects, the researchers utilized machine learning models to assess the broader, systemic impact of metformin on aging. These models allowed them to track the aging process across tissues and organs, resulting in a comprehensive understanding of the drug’s benefits.
The results were remarkable. Long-term metformin treatment led to a reduction in biological age markers such as DNA methylation, transcriptome age, and plasma protein and metabolite age. On average, the biological age of the treated monkeys was reduced by five to six years in their brains and livers. When translated to humans, this equates to a significant 15 to 18-year reduction in biological age.
The study’s findings offer a glimpse into a future where aging is not an inevitable decline but a process that can be managed or even reversed. With its profound impact on cellular aging, metformin could be the cornerstone of a new era in geriatric medicine, focusing not just on treating aging-related diseases like Alzheimer’s and heart disease but on targeting the aging process itself.
As life expectancy continues to rise, the potential of metformin to address the root causes of aging offers exciting prospects for improving the quality of life in older adults. The research opens new doors to understanding aging, and may one day lead to therapies that delay aging and enhance the health of future generations.
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