The very core of LC theory on weight loss is that insulin *causes* fat accumulation through it's action, and basically if we can lower insulin, weight loss occurs. Sounds simple and straight forward.
From Guyton & Hall's Textbook of Medical Physiology, 11th Edition, p. 966
Insulin Deficiency Increases Use of Fat for Energy
All aspects of fat breakdown and use for providing energy are greatly enhanced in the absence of insulin. This occurs even normally between meals when secretion of insulin is minimal, but it becomes extreme in diabetes mellitus when secretion of insulin is almost zero. The resulting effects are as follows.
Insulin Deficiency Causes Lipolysis of Storage Fat and Release of Free Fatty Acids.
In the absence of insulin, all the effects of insulin noted earlier that cause storage of fat are reversed. The most important effect is that the enzyme hormone-sensitive lipase in the fat cells becomes strongly activated. This causes hydrolysis of the stored triglycerides, releasing large quantities of fatty acids and glycerol into the circulating blood. Consequently, the plasma concentration of free fatty acids begins to rise within minutes. This free fatty acid then becomes the main energy substrate used by essentially all tissues of the body besides the brain.
Wow! This is what Gary Taubes and all the LC gurus have been telling us for years now! All along our fat cells have been hoarding these fatty acids and starving our cells of their energy so we go around hungry all the time. Of course most of my readers know this to be the stuff of pure fantasy. In a human with a functioning pancreas, baseline insulin becomes elevated in direct response to increased adiposity to keep from circulating free fatty acid levels in check.
On that same page we find the graphic to the right. (I was thumbing through my 6th edition hard copy and came across this just this morning). Unfortunately, I cannot find the direct reference from which to get actual concentrations/levels, but that isn't really the point. This was what happened when some animal was depancreatized (species not specified either) thereby causing insulin to drop to zero. The first thing that goes awry? The fatty acids. Within minutes. The fatty acids jump right up there and remain elevated. Hyperglycemia develops but levels off. Ketone production is more delayed, slow at first but then accelerates. Note that ketones are produced from the excess fatty acids. From the text:
Excess Usage of Fats During Insulin Lack Causes Ketosis and Acidosis.
Insulin lack also causes excessive amounts of acetoacetic acid to be formed in the liver cells. This results from the following effect: In the absence of insulin but in the presence of excess fatty acids in the liver cells, the carnitine transport mechanism for transporting fatty acids into the mitochondria becomes increasingly activated. In the mitochondria, beta oxidation of the fatty acids then proceeds very rapidly, releasing extreme amounts of acetyl-CoA.A large part of this excess acetyl-CoA is then condensed to form acetoacetic acid, which in turn is released into the circulating blood. Most of this passes to the peripheral cells, where it is again converted into acetyl-CoA and used for energy in the usual manner.
At the same time, the absence of insulin also depresses the utilization of acetoacetic acid in the peripheral tissues. Thus, so much acetoacetic acid is released from the liver that it cannot all be metabolized by the tissues.Therefore, as shown in Figure 78–5, its concentration rises during the days after cessation of insulin secretion, sometimes reaching concentrations of 10 mEq/L or more, which is a severe state of body fluid acidosis.
As explained in Chapter 68, some of the acetoacetic acid is also converted into b-hydroxybutyric acid and acetone. These two substances, along with the acetoacetic acid, are called ketone bodies, and their presence in large quantities in the body fluids is called ketosis. We see later that in severe diabetes the acetoacetic acid and the b-hydroxybutyric acid can cause severe acidosis and coma, which often leads to death.
No ... I'm not going to equate benign ketosis with severe ketoacidosis, but I am going to point out a few things that these short excerpts from a (renowned) physiology text illustrate.
Anything taken out of context can be used to support
a flawed theory on the basis of scientific *facts*
This is what Gary Taubes is so clever at doing. Nobody denies the basic physiological facts that insulin's actions on the adipocyte are to promote fat storage not mobilization. Nobody. But you would have to ask yourself is how it was that the 98-99% of the population with normally functioning pancreata during most of their lives used to manage to remain normal weight, in large proportions, for centuries on end, despite all that Neolithic carbohydrate consumption and corresponding insulin spiking?
I imagine many low carbers gleefully read "this free fatty acid then becomes the main energy substrate used by essentially all tissues of the body" and started breaking out into "I'm a fat burner" chants and cheers. But you will notice that NEFA/FFA become the main energy substrate -- that means burning less glucose and more fat as a proportion. There is NO indication that the body burns more energy in total. And herein lies the problem. Because what you see with these depancreatized animals is that as fatty acid's remain elevated and displace glucose as substrates glucose levels build but so do ketones. Ketones are not being used as energy in this scenario because the animal is awash in its free fatty acids.
Now, thankfully LC diets do not achieve the serious depression in insulin levels that are claimed so as to actually cause this deadly scenario. However, the graphic above shows that the NEFA/FFA levels are the first to go awry and these essentially cause the other two.
But insulin's action to sequester fatty acids in the adipose tissue is not only "healthy" but ultimately required to sustain life. We don't want it going away any time soon. Rather than obsessing over the bulging thighs of an unfortunate Type 1 diabetic who injected herself too frequently in the same locations, one should take note of what would happen to the poor woman were she not to have injected at all. Really folks, otherwise, why not just partially pancreatize the obese and be done with it?