In a breakthrough that has left scientists and medical researchers buzzing, a series of studies have revealed that blocking the protein IL-11 can extend the lifespan of mice by up to 25%. This discovery could potentially pave the way for anti-aging treatments in humans, although clinical trials are still necessary to confirm the findings.
The team of researchers, hailing from the Medical Research Council Laboratory of Medical Science at Imperial College London and Duke-NUS Medical School in Singapore, embarked on a journey to understand the role of IL-11 in the aging process. Their findings, published in Nature, demonstrate that inhibiting IL-11 not only extends lifespan but also reduces the incidence of cancers and diseases related to aging.
Professor Stuart Cook, one of the lead researchers, commented on the implications of their findings: “The treated mice had fewer cancers and were free from the usual signs of aging and frailty. We also noticed reduced muscle wasting and an improvement in muscle strength. Essentially, the old mice receiving anti-IL11 were healthier.” Cook's enthusiasm is palpable, yet he remains cautiously optimistic. “While these findings are only in mice, it raises the tantalizing possibility that the drugs could have a similar effect in elderly humans.”
The research began with creating mice that lacked the gene responsible for producing IL-11. These genetically engineered mice exhibited a lifespan extension of over 20%. To further test their hypothesis, the scientists administered a drug that blocks IL-11 to 75-week-old mice – approximately the same age as a 55-year-old human. The results were striking: a median lifespan increase of 22.4% in males and 25% in females. Remarkably, these mice lived an average of 155 weeks, compared to just 120 weeks for their untreated counterparts.
The role of IL-11 in the human body has been somewhat misunderstood until now. Initially thought to be anti-inflammatory, this protein has been revealed to be pro-inflammatory and pro-fibrotic, contributing to chronic inflammation and fibrosis, which are hallmark symptoms of aging. These revelations date back to 2018, but the new findings provide even more compelling evidence of IL-11's detrimental effects as we age.
The implications of these discoveries are profound. Professor Cook noted that IL-11 activity increases with age in all tissues of the mouse, leading to a plethora of age-related diseases and declining bodily functions. Multimorbidity and frailty remain among the biggest global healthcare challenges, according to various leading health bodies such as the NHS and WHO. Currently, no treatment effectively addresses multimorbidity; hence, these findings offer a glimmer of hope.
But the journey from mice to humans is fraught with challenges. The safety and effectiveness of IL-11 blocking treatments need to be established through rigorous clinical trials. Nevertheless, the path to human trials is less daunting given that anti-IL-11 treatments are already being tested for other conditions such as lung fibrosis.
Professor Annissa Widjaja from Duke-NUS Medical School, who co-authored the research, stumbled upon the breakthrough quite serendipitously. She shared, “This project started back in 2017 when a collaborator sent us some tissue samples for another project. Out of curiosity, I ran some experiments to check for IL-11 levels and discovered that these levels increased with age.” This accidental discovery set the wheels in motion for what could be a significant leap in understanding and potentially mitigating the aging process in humans.
The researchers hope that their findings will translate to human health, and early indicators from studies on human cells and tissues are promising. “We found these rising levels contribute to negative effects in the body, such as inflammation and preventing organs from healing and regenerating after injury. Although our work was done in mice, we hope that these findings will be highly relevant to human health,” said Assistant Professor Widjaja.
The excitement within the scientific community is palpable. The possibility of extending human healthspan and lifespan by targeting IL-11 offers an attractive alternative to other methods currently under investigation. For instance, treatments like rapamycin have shown promise but come with unwanted side effects. IL-11 inhibitors could provide a more targeted and potentially safer approach.
Professor Cook acknowledges the remaining unanswered questions but is optimistic about the potential impact. “I try not to get too excited, for the reasons you say, is it too good to be true? There’s lots of snake oil out there, so I try to stick to the data and they are the strongest out there.” His cautious optimism is shared by others in the field who see this as a viable avenue for future research and potential therapies.
Of course, translating these findings into practical treatments for humans will require extensive and lengthy clinical trials. There are logistical and ethical challenges to consider, including the long-term effects and potential side effects of blocking IL-11 in humans. Moreover, as Cook pointed out, “Ageing is a tough field, but there are a lot of therapeutic angles, and a lot more biology left to understand.”
Moving forward, the focus is not just on extending lifespan but also on enhancing the quality of life in our later years. The dream is to mitigate age-related frailty, improve muscle strength and metabolism, and reduce the incidence of diseases such as cancer. If successful, this could revolutionize healthcare for the elderly, making the “supermodel granny” scenario not just a lab-based reality but a possibility for future generations.
