“Forever young, I want to be forever young” sang the band Alphaville back in the eighties. In what looks like a paradox, we all want to live to an older age, to celebrate as many birthdays as possible, but at the same time we all want to stay young. No wonder: getting older is often linked to diseases and to a poorer quality of life.
But, what if gut microbiota could help us age more healthily? A group of researchers from McMaster University (Canada) has confirmed previous observations that gut microbes change with age and can cause increased inflammation and premature death, at least in mice. They report their findings in Cell Host & Microbe along with evidence that new strategies, including probiotics and prebiotics, to modify the composition and rebalance the gut microbiota could be used to improve intestinal health and thus stave off diseases linked with old age.
As we get old, we inevitably exhibit constant low levels of inflammation. And it is well known that those with higher markers of inflammation in the blood are likely to be less healthy, die earlier, be less active and frailer, and suffer from more chronic inflammatory diseases, such as dementia or cardiovascular diseases.
Also, individuals with higher levels of inflammation are more often hospitalised and more carer-dependent. Nevertheless, up until now the underlying cause of that increase in inflammation was poorly understood.
This study describes clearly for the first time a causal connection between aging-related changes in the gut microbiota and inflammation levels in mice.
In an experiment with rodents, researchers observed that when gut microbiota composition was altered or unbalanced in older mice, the intestines became leaky and let some bacterial molecules trespass the gut barrier, enter the bloodstream, and trigger inflammation, thus impairing immune function and reducing lifespan.
“To date, the only things you can do to reduce your age-associated inflammation are eat a healthy diet, exercise, and manage any chronic inflammatory conditions to the best of your ability,” states in a press release senior author Dawn Bowdish, a professor of pathology and molecular medicine at McMaster, and member of the Michael G. DeGroote Institute for Infectious Disease Research.
In the experiment they also saw that macrophages from older mice were less able to kill bacteria than those from younger mice. These changes, explained the authors of the article, are due to increased levels of the inflammatory signalling protein tumour necrosis factor (TNF) in the older mice. In this sense, when researchers treated conventional mice with an anti-TNF drug, they saw the animals experienced a reduction in age-related changes in microbiota.
Researchers are now investigating new drugs, some of which are already on the market for other indications, to target age-associated inflammation. In this sense, in the future, not only drugs but also prebiotics and probiotics could be used “to increase the barrier function of the gut to keep the microbes in their place and reduce age-associated inflammation”, according to Bowdish.
Now, the next step would be seeing if the observations made in the rodents can be translated into humans.
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