"The electrons that end up clogging the CoQ Couple are carried by the FADH2 coming from beta-oxidation of fat through ETF. More FADH2 means more electrons means more of a traffic jam. Which drives electrons backwards via RET through Complex 1 and pops them off as ROS, driving localized insulin resistance and preventing more fat being moved into the fat cells.
What drives more FADH2 through ETF? Saturated fat.
What drives less through? Polyunsaturated fat (PUFA).
Why does it matter? That’s the question that goes to the heart of the hypothesis.
If you want to keep your fat cells from expanding beyond a certain level, and you want yourself to keep from expanding along with them (i.e., getting fat), then you want to block entry of fat into the fat cells. Which is what localized insulin resistance does. And this localized insulin resistance is driven by FADH2. And what makes more FADH2? Saturated fat. What makes less? PUFA."
“Maybe PUFA is driving the obesity epidemic while saturated fat is protective.”
"By advocating the substitution of PUFA, provided mainly in the form of industrial seed oils, for saturated fat, which we have all eaten for millennia, in a misguided attempt to reduce the rate of heart disease, the nutritional authorities unwittingly set us up for the massive obesity epidemic we’re now in the midst of.
A diet high in PUFA, by the decrease in production of FADH2, inhibits the rate of RET, allowing the fat cells to continue to take up calories beyond a certain set point. Adding saturated fat increases the RET and signals that the fat cells are full.
While the fat cells are open for stuffing, both fat and glucose go in. Since PUFA brings this about, PUFA ends up acting as a sort of supercharged carb in that it continues to flood into the fat cells like glucose, but it has over twice as many calories per gram as glucose."
And with plenty o’ humor woven in among the dizzying array of acronyms!