Thanks for posting. I often find myself defending Jimmy--but in this case, yes, I think he could have been much more gracious to his host. I don't think the perfect health diet is so perfect--probably largely because I did the Zone diet for an extended time, and it really didn't take.
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Ketones substitute for blood glucose in feeding the brain, and it is the brain that controls blood glucose levels. So it is normal for blood glucose readings to be lower when in ketosis. However, what is important for health are total circulating energy levels (glucose + ketones + free fatty acids); elevated circulating energy poisons the pancreatic beta and alpha cells through “glucolipotoxicity.” [4] To be in ketosis, Jimmy has to have elevated levels of free fatty acids and ketones. So it is alarming that his fasting blood glucose levels while in ketosis are as high as 100 mg/dl.
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This part here of Jaminet's post, though, I have a bone to pick with. Glucolipotoxicity has been demonstrated in in vitro studies (tissue or cells in a petri dish etc., for anybody who doesn't know). Yes, elevated free fatty acids paired with elevated glucose causes damage. No, it hasn't been demonstrated with glucose concentrations that would correlate with a blood glucose level of 100, only with one that is considerably higher.
Also, glucose is a good correlate for how much glucose there is in the blood. What it isn't a good correlate for is how much glucose is available to tissues in the body, to be taken up from the blood. It's pretty hard for glucose to participate in glucolipotoxicity in the pancreas, liver, etc. if excess glucose never actually gets delivered to the tissues. I think it's fair to say that this is nonsense. How a person is supposed to suffer from glucose toxicity and 'glucose deficiency' at the same time is beyond me.
Edited to add;
I should probably address what Jaminet said next;
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Note that the loss of pancreatic alpha and beta cells, presumably due to poisoning by glucolipotoxicity, is an observed adverse effect of long-term ketogenic diets [e.g. 5, titled “Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice”].
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First, the "presumably" here is wrong. It isn't presumable that this decrease in alpha and beta cells was due to poisoning by glucolipotoxicity.
How does the system "decide" how many cells of a particular type should be maintained/developed in the first place? How about need? A mouse that is taking in 95 percent fat in its diet, feeding its brain on ketones, doesn't need to produce very much insulin. The need for beta cells is decreased. The same is true of glucagon. Glucagon's action is to ensure that there is enough fuel for the brain, etc. In a low glucose, low insulin setting, the need for glucagon is also greatly reduced. Large counterregulatory surges of glucagon aren't needed where the possibility of hypoglycemia (or at least hypoglycemic crisis, glucose could be quite low safely, if ketones are high enough) isn't an issue.
Bone, muscle, fat, neuronal cells. Differentiation of all of these cell types has been show to be affected by the demands put on the tissue. The liver and gut have a remarkable ability to regenerate themselves according to the demands that are placed on them. The whole system is plastic, I don't see why this should exclude alpha and beta cells.
Scaremongering.