I thought this was pretty interesting for several reasons. First, it seems that in normal weight men there is a very large rise in ketone production in response to a stressful situation. No such reaction in obese men. Interesting that in some circumstances the body produces ketones to handle stress. I didn't know that.

Also, it does make me wonder if some obese people might have a harder time producing ketones in response to other conditions, like carb and calorie restriction. I know some people complain about how hard it is for them to turn those ketone test strips purple. Anyone know of studies showing different capabilities to produce ketones in different people? Could this be the reason some folks lose weight so readily with low carb and others can't lose nearly as well despite going very low carb?

I can get pretty good blood ketones, but not urine ones. But it is the blood ones that are the best kind.

Don't have the full paper, here's the pubmed abstract: http://www.ncbi.nlm.nih.gov/pubmed/24845175

The most interesting is the 454% increase in BHB. If we assume that max blood ketone level is around 8 mmol at baseline, and if we assume that this would rise some degree on demand, and if we assume this rise should track with the BG rise on demand (about 50% for BG during exercise based on Steve Cooksey's experiment), then we can conclude BHB was most likely very low to begin with, probably between 0.5 and 1.5 mmol at baseline.

Since there was no BHB increase in the obese, but BHB was still very low in the lean, this means both lean and obese ketogenesis was significantly inhibited most likely by insulin, and the ability to recover quickly from this was intact in the lean but not in the obese.

If there is an association between stress-related behavior and lean/obesity, then it's likely due in part to the ability or inability to provide enough ketones to the brain during stress.

Taubes explained there's a whole bunch of hormones opposite insulin, so looking only at norepinephrine/epinephrine won't tell us the whole story. I bet if they looked at insulin, it's gonna be much higher in the obese. Actually I bet if they looked at all those hormones, they'd find a global imbalance between insulin and all other hormones. Wait a minute, has anybody ever done something like that? I can't believe I didn't think of that before.

Another paper (don't have full paper either, sorry): http://diabetes.diabetesjournals.or.../8/738.abstract

This paper gives us a plausible reason why it doesn't work properly in the obese. This next paper explains it a bit more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC371414/

My take is that epinephrine shuts down insulin receptors at the liver, resulting in an increase in plasma insulin due to lower insulin clearance rate at the liver (which obviously surpasses the concomitant reduction of insulin secretion by the pancreas), and an increase in ketogenesis and glucogenesis in the liver, but somehow doesn't explain the increase in FFA and glycerol which should indicate lower plasma insulin, so it's more likely that epinephrine also acts directly on fat tissue either by shutting down insulin receptors there too or just having a strong enough effect to overwhelm the effect of insulin (probably through lipoprotein lipase or something).

If it doesn't work properly in the obese, then it's likely that insulin is just too high already, and shutting down insulin receptors in the liver and fat tissue to attempt to increase ketogenesis only bumps insulin even higher. If I use my paradigm, it could be due to too low blood ketones, which the liver interprets as a signal to shut down insulin receptors in an attempt to produce more ketones. But that's not the primary cause, there must be a third factor for insulin resistance and in turn for hyperinsulinemia. It's not obesity, since obesity is the result of hyperinsulinemia. It could be hyperglycemia, but the liver would open up insulin receptors in that situation to take glucose out of the blood and convert it to glycogen. But in doing so, ketogenesis would drop as well, and the liver would then try to shut down insulin receptors later on to produce more ketones. So, the likely primary cause is something that first shuts down ketogenesis, but I can't figure out what comes next. I wonder if fatty liver and fructose has something to do with it.

Got an idea. Fatty liver would promote the liver to shut down insulin receptors in order to use the excess fat for ketogenesis. Until the liver is done with that, it keeps insulin receptors shut. In doing so, it keeps plasma insulin higher than otherwise. Low-carb but most especially low-fructose should hasten the process. So, we have a tentative explanation why it works properly in lean men but not in obese men: A difference in fructose intake and/or fatty liver.

Shoot. Forgot the link. Here it is.

Link

Part of the rise in ketones can probably be ascribed to the rise in free fatty acids with adrenaline etc.'s increase of lipolysis--and as CarbSane has been happy to point out, free fatty acids are generally raised in obesity--with baseline free fatty acids higher than usual, even if free fatty acids go up in stress, they're going from high to higher rather than from low to high, so maybe that's part of the effect.

Some trolls like to use this to criticize low carb--saying the common idea that insulin locks fat into fat cells, causing metabolic starvation is wrong. But it's just an oversimplification, I think. Pennington's "balloon" thesis basically stated not that fat tissue had to grow enough to support normal levels of free fatty acids, but that it had to grow enough to support a level of free fatty acids that allowed a "normal" metabolism. If I remember correctly. If it didn't, then it should have. Higher free fatty acids are blamed on excess fat tissue--what if it's the other way around--something I find likely? High fat storage being necessary to support a higher than usual level of free fatty acids?