> This is basically my thinking, except for the leptin/set point part.
I'm wedded to the set point thing, and I still don't understand why you disagree. I'm not necessarily wedded to the leptin bit.
But leptin sure looks like a 'total fat sensor hormone', and there are several unconvincing studies that show that PUFAs do interfere with leptin signalling, so if that's true that's all we need to explain obesity as a consequence of PUFA poisoning.
If we can nail "PUFAs compete with excess protein in some elimination pathway" I think we've got an explanation for almost everything we've seen.
The thing is, we already have several other things that also independently are enough to explain PUFA poisoning -> obesity. We don't need leptin at all. Maybe it plays a role, not sure.
Do we? Obesity is the one I could never do, because for some reason I thought that leptin as the 'total fat sensor hormone' had turned out not to be true!
> This is basically my thinking, except for the leptin/set point part.
I'm wedded to the set point thing, and I still don't understand why you disagree. I'm not necessarily wedded to the leptin bit.
But leptin sure looks like a 'total fat sensor hormone', and there are several unconvincing studies that show that PUFAs do interfere with leptin signalling, so if that's true that's all we need to explain obesity as a consequence of PUFA poisoning.
If we can nail "PUFAs compete with excess protein in some elimination pathway" I think we've got an explanation for almost everything we've seen.
The thing is, we already have several other things that also independently are enough to explain PUFA poisoning -> obesity. We don't need leptin at all. Maybe it plays a role, not sure.
Do we? Obesity is the one I could never do, because for some reason I thought that leptin as the 'total fat sensor hormone' had turned out not to be true!
What are the other possibilities?
ROS, ECS..