[KempyKolibri]

Sorry, I summarised what I thought was your goalpost earlier in the exact same words and you didn’t correct me, so I made the assumption in subsequent replies. I’m not interested in straw manning your argument, just trying to understand.

I’m going to pass on the crash test dummies bit. You’ve misunderstood the point I was making, but it could be poor communication by me and I think the point is becoming increasingly tangential.

> When it comes to pharmaceutics and food additives, our mechanistic understanding is insufficient so we often have to resort to empirical studies on humans, including RCTs

> It does, because again, mechanism is provided. You could say that the study has weak evidence for the mechanism and it works like that perhaps only for sugar. Because that some mechanism is found in mice does not mean it is also found in humans, and it would be a fair point. This is why many species are tested and so far the results held up (testing humans takes too long for obvious reasons).

So you don’t feel you’re being straw manned again, can I get a clear answer to this: is your argument that if we stack together sufficient numbers of mechanistic animal studies we can be sufficiently confident enough in the translation rate of such studies to humans that we can roll out public health interventions without any evidence of efficacy in human populations?