Longevity researchers have good reason to suspect a causal rather than bystander role for age-related microbiome changes.

A unifying theme arising from some of the best-studied models of aging is the central role of the intestines

as a critical determinant in lifespan. In C. elegance, the expression of a longevity gene

in the animal's nerves produced a modest 10% life extension, and in their muscles had no effect

on lifespan at all. Expressed in their intestines, however, it increased lifespan by 50 to 60 percent.

In fruit flies, age-related changes in their gut microbiomes precedes a loss of intestinal barrier function

that ultimately leads to death.

The lifespan of individual flies can be predicted by this gut leakiness.

How do we know their microbiomes have anything to do with it? Because if you give 10-day-old

flies, the equivalent of a fecal transplant from a 30-day-old fly, their young gut starts to leak,

and they die sooner compared to getting microbiota

from another 10-day-old.

We suspect the driver is the acquisition of bad bugs from the older flies, rather than the

loss of good bugs, since antibiotic treatment significantly increases their lifespan, too.

Invertebrates are one thing. What about an animal with a backbone?

African turquoise killifish are a popular aging model, since they naturally only live a few months,

allowing for rapid experimental turnarounds.

What happens when you recolonize the guts of middle-aged fish with bacteria from younger fish?

They live longer lives.

They were also significantly more active later in life in terms of spontaneous exploratory behavior.

So at least in the African turquoise killyfish, age-related microbiome changes appeared not to just be a passive

consequence of getting older, but an active driver of the aging process. When they just gave antibiotics

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