Gut flora is not much of a hypothesis to start with—it just says “we think the composition of gut flora affects obesity but we have no clue about the mechanism”. It’s a black box with gut flora involved.
For a trivial example, we can substitute “leptin regulation” for “gut flora” and get a similar hypothesis—also black-box and also quite plausible.
Exactly what is the hypothesis that you’re testing? That gut flora affect metabolism and, as a consequence, a variety of things including weight? Sure, I agree. I suspect most everyone will agree.
But that’s a far cry from being the “best hypothesis” as to why some people easily gain weight and some do not.
There are known pathologies of gut bacteria that affect lipid metabolism. That less extreme and thus hard to detect variants exist seems a reasonable claim.
What do you mean, plausible?
Gut flora is not much of a hypothesis to start with—it just says “we think the composition of gut flora affects obesity but we have no clue about the mechanism”. It’s a black box with gut flora involved.
For a trivial example, we can substitute “leptin regulation” for “gut flora” and get a similar hypothesis—also black-box and also quite plausible.
Fecal transplants provide a way of testing the gut flora hypothesis.
Exactly what is the hypothesis that you’re testing? That gut flora affect metabolism and, as a consequence, a variety of things including weight? Sure, I agree. I suspect most everyone will agree.
But that’s a far cry from being the “best hypothesis” as to why some people easily gain weight and some do not.
There are known pathologies of gut bacteria that affect lipid metabolism. That less extreme and thus hard to detect variants exist seems a reasonable claim.