Nov 20Liked by Marc Arginteanu

I'm unsure about the implications of this post, interesting as it is. If I've read correctly, the mix of gut microbes in the test population correlated with the presence or absence of Alzheimer's symptoms (or, perhaps, plaques, if lumbar punctures were involved), and the gut microbes of AD patients generated AD symptoms in rats. So there's reason to link correlation to causation in one direction.

But to be medically significant (as opposed to biologically interesting), wouldn't the question be whether the gut microbes of non-AD patients could ameliorate or arrest those induced AD symptoms in rats--causation in the other direction? After all, there's no interest (or surprise) in learning that a fecal transplant from a C. difficile patient generates C difficile in rats; the interest is in learning that a fecal transplant can arrest and reverse C difficile bacterial growth (first in test rats and then in hospitalized humans) because that growth was originally caused by an abnormal absence of dominant strains that the introduction of normal fecal material reverses--that's the direction of causation that is medically significant.

So my thought is to wonder whether there is now follow-up research on the effect of fecal-normal transplants on induced-AD rats.

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Nov 20·edited Nov 20Liked by Marc Arginteanu

Something for sure to be aware of in our very gut! We sure could learn more of the brain/gut connection. Our dogs have been known to practice this as well. . .🙄! Thanks Marc!

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Great article. Love the wit. I'm sending it to a friend with early stage Alzheimer's. Thanks

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