I don't know if this theory has been posted yet or not. I haven't read every post in the forum, though I've read quite a few.
I've seen pieces of this theory in places, but not the whole thing.
It does seem to me that insulin should be one of the key parts to the theory. And user NTB has tried to push this point in another thread.
However, I'm not sure NTB accommodates all of Seth's observations in his report:www.sethroberts.net/about/whatmakesfoodfattening.pdf
I know NTB has read this, and, by the way, I would encourage everyone to read this document before spinning theories. It's a good guide to all the things a theory should try to accommodate.
The "perhaps-missed" observation is the appearance of a "set point".
Now, I know that Seth and Gary Taubes had a little exchange about "set point" versus "settling point", and I don't want to put words in Seth's mouth, but it seems to me that this debate, contrary to what Taubes says, might not be that important in this case.
Taubes portrays the two concepts soemthing like this:
Set point: some brain-mediated, thermostat-like thingy.
Settling point: some point at which a homeostatic process, largely mediated by the fat cells, happens to settle at, for who knows what reason.
I'm not sure Seth is really committed to the definition of "set point" as Taubes characterizes it. When I first read Seth's article, I took him to be describing something of a "black box". We observe that people who lose weight tend to go back to their original weight, and it's as if there's some sort of "set point" mechanism at play. But who knows if it's mediated in the brain or in the fat cells.
Anyway, whether Seth is committed to some brain-mediated thermostat-like thingy or not, I'm not sure he needs to be. I think his theory could work regardless of how the "set point" or "settling point" is mediated.
So, what makes us seem to go back quickly to our original weight, and perhaps overshoot a bit, when we lose our grip on a typical diet? And what makes us stop putting the weight on so quickly after that point?
One simplistic suggestion would be that our fat cells can only stretch so far. They have only so much capacity, and when they get full, they begin pushing back, making us less hungry. They can stretch over time, but it's a relatively slow process. However, when we take fat out of them, they retain their capacity and, if they shrink over time, it's very slowly. So our "set point" would be determined by the capacity of our fat cells. I know I've heard this theory in the past, but I'm not sure where --- maybe it's nothing more than some pseudo-explanation made up by some Cosmo writer rushing to get the latest "top ten reasons you can't lose weight" kind of article :-D Or maybe there's something to it . . .
Now, on to insulin.
I read somewhere, maybe it was in Taubes, that when we eat a meal there is often more than one insulin spike. There's often an insulin spike that occurs right as we begin eating, before we even start digesting the calories. And more insulin is triggered, as needed, as macronutrients begin to make their way into the bloodstream.
And, it could be that the initial insulin spike is a trained response, much as Seth describes. It's trained by the association of flavor with the calories that repeatedly come a little later. It could be there are sensors in the nose that trigger this response. It takes some time to make the association, but once it's there, when we experience a certain insulin-associated flavor, the flavor triggers an initial release of insulin.
So, given all these wild untested assumptions (which seem plausible, but might be wildly wrong), here's why the SLD would work, and why we see the phenomena reported in Seth's PDF:
1. When we eat flavorless calories, or plug our noses, it prevents the flavor molecules from reaching the sensors in the nose that initiate the preliminary insulin spike.
2. We wind up producing less insulin in a given day, because we have fewer anticipatory insulin secretion events, and thereby store less fat, and lose weight. In this way the SLD would work for much the same reason a low carb diet works. Less insulin = weight loss.
3. And the set-point type phenomena are produced by the twin factors of insulin always trying to store more fat (once the muscles and liver are full), and fat-cells pushing back once full.
This is a little "off the hip". If others are interested, I might take a closer look, try to itemize the phenomena in need of explaining from Seth's article, and making a chart comparing how the main live theories in play here accommodate them. (Or if Seth wants to do that . . .