"We are on the verge of a revolution in medicine: understanding, treating, and ultimately preventing the causes of degenerative aging. But medical revolutions only happen if we all stand up in support of funding and research. We did it for cancer. We're doing it for Alzheimer's. We can do it for aging - and create an era of longer, healthier lives!"

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  • Tuesday, May 5, 2009

    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.

    Posted by Reason

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

    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 6, 2009 12:43 PM]

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

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

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