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I saw this on Peter's Hyperlipid Blog, and I have no idea what would be causing this phenomenon (someone mentioned trans fats in the comments section), but I got that same spooky "oh, that's not good" feeling I got when I first heard about colony collapse in bees.

http://high-fat-nutrition.blogspot.com/

http://4.bp.blogspot.com/-RTIi3ish1Hs/TntAGpDEE4I/AAAAAAAABa8/vSFj23AQdzk/s1600/Slide8.jpg

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a good quote form his recent post : "It is the RESISTANCE of adipocytes to insulin which limits fat gain. And the corollary is??? Sensitivity to insulin drives fat gain. You can't have one conclusion without the other. Anyone telling you that adipocyte insulin resistance limits fat gain and yet insulin per se has nothing to do with fat gain... Well, you decide. I have." – Mallory Oct 6 2011 at 21:25
Hi Mallory, I'm just trying to figure out who he's talking about. I've not heard anyone saying that adipocyte IR limits fat gain. – Evelyn aka CarbSane Oct 7 2011 at 0:47
I deleted my post because Dr. K informed me that I was wrong. it is actually apoptosis. BLAMO! Magnesium deficiency. Bad! Run away run away :( – Stabby Oct 7 2011 at 5:04
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Yikes...The crazy thing, and I guess the magnesium deficiency idea here possibly backs it up, is that these changes are happening long before there are external signs of diabetes or obesity. Which I guess feeds into the Taubes idea that someone "eats too much" because they are getting fat, and not the other way around. Maybe there needs to be a public health campaign encouraging Epsom Salt baths to fight Type 2 Diabetes? Or does the body refuse to take on the magnesium efficiently if it is already in this state? – Happy Now Oct 7 2011 at 6:17

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If I understand correctly, the usual process of metabolic syndrome and obesity is that the muscle cells become insulin resistant at a faster rate than fat cells. Thus insulin starts rising to compensate for the sake of muscle, but the fat cells, which are still sensitive, take this signal at face value and store more fat. It makes sense that adipose tissue insulin resistance would limit fattening.

I'm guessing that what is damaging the mitochondria is ROSs. Cell membranes are made of highly polyunsaturated fatty acids, which are particularly susceptible to such damage.

My current hypothesis is that people who have difficulty with carbohydrate metabolism are not properly coping with the normal ROS production involved in carbohydrate metabolism. So the inflammation is not being cleared, and it is damaging surrounding cells. Why muscle cells would be more susceptible, I don't know.

This could explain, in part, why switching to a ketogenic diet often and stops and reverses the process -- ketones don't generate as much oxidative radicals when used for fuel, and they are also antioxidative.

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