Aging and the Role of Your Bacteria

A growing body of research suggests that the bacterial populations existing in symbiosis with your tissues play an important role in how metabolic processes interact to determine longevity. This is yet another good reason not to bet on metabolic engineering as the fast horse in the race to produce engineered longevity - the complexity is staggering.

Here's a little background reading on the topic of aging and your bacteria:

I noticed an interesting paper today that suggests centenarians, in addition to generally having better metabolisms than the rest of us, also have better bacteria:

Generally, there is an age-related decline in the human gut titer of Bifidobacterium species, but the titer in healthy centenarians was previously reported to be comparable to that found in much younger people. We addressed whether elevated Bifidobacterium titers relate positively to immune function.

This study evaluated the immunoactivities of 2 Bifidobacterium strains (B adolescentis BBMN23 and B longum BBMN68) isolated from healthy centenarians in China.


In conclusion, ingestion of B. adolescentis BBMN23 and B. longum BBMN68 can enhance both innate and acquired immunity in healthy specific pathogen-free (SPF) mice and strains of bifidobacteria from healthy centenarians in Bama longevity villages in China may possess potentially valuable immunomodulatory properties.

A immune system in better shape should be enough to raise life expectancy in and of itself, as the immune system not only protects against pathogens, but also destroys damaging senescent cells and cancerous cells, amongst other jobs.

The whole point of a serious program of longevity research, of course, would be to make irrelevant the range of metabolic differences in human populations and the bacteria that inhabit us. These differences are only interesting because we don't yet have a method in hand for reliably adding multiple decades to healthy and maximum life spans - for all that we can clearly and in great detail envisage what that method looks like.


Human bodies exist in a symbiotic relationship with the intestinal bacteria that live within them, with the immune system keeping the bacteria where it does its work. It, therefor, makes sense that if the immune system declines, that the intestinal bacteria (and the bacteria on the skin) is going to spread into other parts of the body. In this case, the bacteria itself is not a cause of aging, but that the changes and the spread of the bacteria is a consequence of the decline of immune function that is, itself, caused by aging.

As such, I fail to see how this relates either to the SENS or the metabolic pathway manipulation approaches to curing aging. The papers you kink to in this posting support this position.

Posted by: kurt9 at May 6th, 2009 12:43 PM

At the moment we can't say for sure how the immune system and symbiotic bacterial populations interact, and the same goes for important metabolic processes and bacterial populations. It's more of an unknown than our own cellular pathways.

That is an example of an additional layer of complexity that makes metabolic manipulation more challenging, but has no impact at all on SENS.

Posted by: Reason at May 6th, 2009 1:04 PM

It may not be possible to ever adequately determine how a microbiota will interact with its host species. Bacterial genomes are in constant flux and their types are theoretically infinite; in fact, some researchers have gone so far as to question the very concept of discrete bacterial species. The picture becomes even more complicated yet when you realize that a microbiota is not the sum of its constituent DNA strains. The organisms involved affect each other as well as the host.

I agree that this phenomenon shows metabolic tinkering to be a suboptimal approach, and I do think it is related to SENS. Our immune systems and resident microbiota affect each other in a cyclic fashion: the more bacteria we harbor, the weaker our immune systems become and the more bacteria we acquire. Killing as many of the bacteria as we can as safely as we can is a big help.

Posted by: shegeek at May 6th, 2009 2:33 PM

Looking at elderly 100 year old people and assuming their gut bacterial fauna have remained the same all their life and or even through earlier critical and typical high stress/mortality periods of the human life span - is absurd. Concluding that their current gut content is responsible for their longevity is equally absurd. The elderly invariably change their eating habits as they age in deference to changes in taste ability/preferences, their general health and dental abilities. With these changes in foods - comes changes in the gut bacterial populations. No doubt their are optimum gut fauna for better health and immunity, however maintaining them through out life is complicated and difficult. Assuming that a commonalty of gut fauna in 100 year old culturally similar people is why they survived to a ripe old ages is really circumstantial - if not very weak science.

Posted by: Durwood M. Dugger at August 7th, 2011 7:14 PM

I agree with the majority of these comments. Your work is certainly flawed. Bacteria causes malfunction to the Immune System and other bodily processes. In Gerentology we understand that aging does not kill you, but rather makes you more killable and more susceptible to malfunction. One would think this is such an elementary statement that it is not worth mentioning, but as Aubrey De Grey said in his work on Mitochondrial Free Radical Theory "gerentologist are forgetting that aging is not what we are trying to cure, we are trying to cure malfunction.... We desire not for people to just live longer, but to also increase the amount of time they are healthy and free of both pain and disease.". Less bacteria means less malfunction, less malfunction means a longer lasting and healthier body. Gerentology has simple concepts, even though the application of these ideas can be difficult. Your concept is not the solution.

Posted by: P.S. Barnes at May 16th, 2018 12:11 PM
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