Perhaps HFCS in particular encourages LPS bacteria. Or perhaps LPS bacteria particularly stimulates thirst for sweet liquids. It’s impossible to know without (preferably both of) historical LPS and a controlled experiment. Also, your link does not establish a causal link between sugary drink consumption and obesity, merely that they’ve been correlated for a few decades.
In addition, the researchers reviewed a study in schoolchildren that showed an educational program advocating fewer sugary sodas reduced weight gain and obesity among the kids after 12 months.
Which you would expect if the sodas had a causal relationship with obesity, and probably not if they didn’t.
Can you think of any observations, in humans, which favor the LPS bacteria model of obesity, rather than simply being reconcilable with it given enough ad hoc additions?
Perhaps the presence of LPS bacteria and the corresponding immune response provoke a larger appetite.
That’s a possibility, but it’s one under which I would antipredict findings like this.
Perhaps HFCS in particular encourages LPS bacteria. Or perhaps LPS bacteria particularly stimulates thirst for sweet liquids. It’s impossible to know without (preferably both of) historical LPS and a controlled experiment. Also, your link does not establish a causal link between sugary drink consumption and obesity, merely that they’ve been correlated for a few decades.
Well, from that link
Which you would expect if the sodas had a causal relationship with obesity, and probably not if they didn’t.
See also this article.
Can you think of any observations, in humans, which favor the LPS bacteria model of obesity, rather than simply being reconcilable with it given enough ad hoc additions?