Bacteria, both invasive and symbiotic, play their parts in the progression of our biochemistry from young to old. Here I'll point out a couple of interesting recent papers that are representative of the increased level of scientific community interest in what exactly is going on in bacterial populations over the course of aging. In this case the area of focus is the bacteria present in the mouth and the gut.

The first paper suggests that we might blame bacteria for some portion of the damaged or otherwise problematic lipids that contribute to the development of atherosclerosis. This is as opposed to, say, oxidative damage of native lipids as a result of mitochondrial dysfunction or other sources of oxidative stress in tissues. These damaged lipids enter the bloodstream where they can provoke an overreaction in blood vessel walls, leading to a runaway process of inflammation and cell death that over the years produces fatty deposits that narrow and weaken blood vessels. A rational process of walking through the various problem compounds found in atherosclerotic deposits in some order of priority, finding ways to safely break them down, such those of the LysoSENS programs, probably doesn't involve too much introspection about the origins of these compounds. It is more the case that a better understanding of those origins is helpful at this stage to construct the priority list - there are a lot of potential targets.

The second paper is something we're seeing more of these days, the delivery of a young bacterial population to old individuals, or vice versa. The balance of microbial species in the gut changes with age in what are beginning to appear to be fairly characteristic ways, one more secondary consequence of the underlying damage and disruption of aging that is argued to itself go on to create further harms. Raised levels of chronic inflammation are the most likely mediating mechanism for those further harms: inflammation speeds the development of all of the common age-related diseases.

There is, I think, sufficient evidence already to say that changing gut bacteria populations contribute secondary harms in aging. For example, a transplant of gut microbes from young killifish to old killifish extends life. More evidence in mammals rather than fish can't hurt, however. Neither say a great deal about how important this all is in human aging, of course. Short-lived species have very plastic life spans, exhibiting large changes in response to circumstances that, while they certainly impact health in our species, don't do much to human life span. We might imagine that the various effects of exercise, obesity, and calorie restriction place likely bounds on the size of the benefits that might be achieved by maintaining or failing to maintain youthful bacterial populations.

Deposition and hydrolysis of serine dipeptide lipids of Bacteroidetes bacteria in human arteries: relationship to atherosclerosis

Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice