The stuff about fat, FADH2 & Complex II is discussed at great length on the blog I linked to in my reply to
@Gondwanaland. Wish I had a handy diagram.
I like Peter's Hyperlipid blog. He's extremely smart. But he also tends to address things in a very obscure and minute context without revealing the larger picture to people.
I posted a clear metabolic pathway showing fats in beta oxidation feed the Krebs Cycle. He's clearly addressing an alternative pathway, and he is not trying to say that the pathway he is exposing is the only one. I found a good image that exposes what Peter is talking about here:
http://www.intechopen.com/source/html/45280/media/image2.jpeg
I'll try to study this with others and see if it tells me anything new. If my electron transport chain is impaired by mercury, then presumably my fat would go through beta oxidation to Acetyl-CoA and drive the Krebs Cycle. But it's a really interesting question what happens to a person who eats fat and has no problem with the ETC. How do they convert NADH to NAD+ in sufficient quantity? NAD+ is critical to drive all kinds of cellular processes.
Mercury is certainly bad news. I don't doubt this is an issue for many. Having said that, the symptoms you are describing which coincided with the induction of a low carb diet and that you are attributing to inappropriate ALA supplementation, I've experienced those same symptoms on a low carb diet (long before I took ALA or any other supplement) and I've heard this sort of metabolic breakdown described many times over in the paleo/LC blogosphere and some people on this forum like
@Vegas.
Of course that was the first thought I had as well. I reversed the diet for six months with no effect on my energy levels at all. I have very precise control on what I eat, and I did test more than 150 grams of starchy carbs every day. The condition did not reverse.
Now, could you argue that a low carb diet pushed me over some threshold for some metabolite, and that then started me onto a self-feeding cycle that is not so easily reversed? And could mercury possible work together with this effect to make restarting the aerobic metabolism more difficult? Sure, I can believe all of that. But I assure you have exhaustively tested eating sugar, starchy carbs, and starchy carbs together with fruit, and there is no combination of those things that gets me anywhere close to where I was prior to Nov 2013.
I am curious why do you think sugar is better than starchy carbs + fruit? Metabolically they should be identical.
An immense amount of acrimonious debate has occurred in that community over the last few years as a result of all the people experiencing such symptoms who believe (and have various practitioners telling them) that they have hypothyroidism, not understanding that the low T3/high rT3 issue is a sign of much more profound metabolic problems. As you point out, eating glucose again does NOT fix whatever was broken. In fact, glucose is tolerated less well than before LC and now you find yourself spiking to 160 postprandially. I've been there myself. I ate like that for a year and a half and ended up with a temperature of 94-95 F and a host of very severe symptoms verging on death. You might wanna look into the microbiome stuff as a more likely explanation for these symptoms than mercury.
How did you fix this problem for yourself?
If mankind was so fragile that a change in diet composition was enough to kill us, I don't think we would have made it as a species. I think it was common for our ancestors to eat vastly different diets from one month to the next. You eat what is available on a given day or week. You are ketogenic one week, eating 80% fruit the next week, eating mostly protein and fats when you catch some fish, etc. That kind of metabolic flexibility must be hard wired into our species, and it explains why we have so many metabolic pathways for creating energy. The body has to be able to adjust to such things, and it cannot be so fragile that it requires a specific balance of carb/protein/fats to survive.
Whatever hypothesis you choose, it has to explain both a collapse of aerobic metabolism and a glucose intolerance. Mercury does this very well. It binds to critical proteins in the ETC and breaks it. It binds to insulin receptors and breaks glucose metabolism. And - very important to my case - once you get mercury in a bad compartment of the body, it can take years to get it out. It completely explains the persistence of symptoms despite a wide variety of diets, and more to the point it is actually present in very high amounts in my blood, my urine, and my hair. How can I ignore experimental evidence that the metal is present in me at high levels, when it also explains perfectly every symptom I am having?
Why should I prefer a gut biome diagnosis when my Genova gut test shows fairly normal levels of bacteria, no infections, no pathogens, etc?
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