Faecal transplants 'could reverse ageing', new mouse study suggests

There are dozens of start-ups researching the science of anti-ageing in 2022 — but could faeces hold the secret of eternal youth?

Researchers at the Quadram Institute and the University of East Anglia (UEA) found that transplanting faecal microbiota from young into old mice can reverse hallmarks of ageing in the gut, eyes, and brain.

Even more interestingly, microbes from old mice induced inflammation in the brain of young recipients and depleted a key protein required for normal vision.

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The findings suggest that gut microbes might play a role in some of the negative effects of ageing — and suggest that gut microbe-based therapies could combat age-related decline.

Prof Simon Carding, from UEA's Norwich Medical School and head of the Gut Microbes and Health Research Programme at the Quadram Institute, said: "This ground-breaking study provides tantalising evidence for the direct involvement of gut microbes in ageing and the functional decline of brain function and vision and offers a potential solution in the form of gut microbe replacement therapy."

The research comes at a time when Silicon Valley’s billionaires are investing in a range of well-funded start-ups aiming to reverse ageing.

Amazon’s Jeff Bezos is reported to have invested in Altos Labs, which aims to ‘restore cell health’ and ‘reverse disease’.

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PayPal co-founder Peter Thiel invested in the Methuselah Foundation, which has the goal of making "90 the new 50".

It has been known for some time that the population of microbes that we carry around in our gut, collectively called the gut microbiota, is linked to health.

Most diseases are associated with changes in the types and behaviour of bacteria, viruses, fungi and other microbes in an individual's gut.

Some of these changes in microbiota composition happen as we age, adversely affecting metabolism and immunity, and this has been associated with age-related disorders including inflammatory bowel diseases, along with cardiovascular, autoimmune, metabolic and neurodegenerative disorders.

To better understand the effects of these changes in the microbiota in old age, scientists from the Quadram Institute transferred the gut microbes from aged mice into healthy young mice, and vice versa.

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They then looked at how this affected inflammatory hallmarks of ageing in the gut, brain and eye, which suffer from declining function in later life.

The study, published in the journal Microbiome, found that the microbiota from old donors led to loss of integrity of the lining of the gut, allowing bacterial products to cross into the circulation, which results in triggering the immune system and inflammation in the brain and eyes.

In the eye, the team also found specific proteins associated with retinal degeneration were elevated in the young mice receiving microbiota from old donors.

In old mice, these detrimental changes in the gut, eye and brain could be reversed by transplanting the gut microbiota from young mice.

In ongoing studies, the team are now working to understand how long these positive effects can last, and to identify the beneficial components of the young donor microbiota and how they impact on organs distant from the gut.

Similar pathways exist in humans, and the human gut microbiota also changes significantly in later life, but the researchers caution about extrapolating their results directly to humans until similar studies in elderly humans can be performed.

Lead author of the study, Dr Aimee Parker from the Quadram Institute, said: "We were excited to find that by changing the gut microbiota of elderly individuals, we could rescue indicators of age-associated decline commonly seen in degenerative conditions of the eye and brain.

"Our results provide more evidence of the important links between microbes in the gut and healthy ageing of tissues and organs around the body. We hope that our findings will contribute ultimately to understanding how we can manipulate our diet and our gut bacteria to maximise good health in later life."

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