I look back on a previous attempt to do Atkins in 2004 and after the initial 20 lbs I stalled for 3 months. I didn’t know about fasting or limiting my eating windows and not snacking because none of these are addressed in Atkins. I also never increased my carbs above the induction phase.
I did not eat any additional fat so the fat I got was in the meat/cheese/dairy I ate. This should have been better, right? Less plate fat/burn body fat. Except I didn’t.
There was no limit on protein - just carbs - and I ate a LOT of protein. I wonder now if I am one of those whose blood sugar rises more than typical with protein?
With keto I don’t eat as much protein nor get sick of the food since I am eating a lot more fat, including my sacred BPC!
It was probably a combination of things back in 2004 and I had no support community like this one to help me figure it out.
Protein is the last resort energy source. It’s also the hardest macro to convert as well as the only macro your body doesn’t store… So, as long as your body has the required fat intake the amount of protein you intake is pretty irrelevant because there is no reservoir for your body to pull from.
Limansky’s is covered in excruciating detail in the KetohackingMD podcast - the only thing you mention that isn’t covered is the insulin/glucagon ration, but glucagon is discussed.
New research suggests, apparently, that gluconeogenesis is determined, not by supply, but by demand. It is stimulated by a low insulin/glucagon ratio. Ketogenesis, likewise. So excess protein in a high-carb diet has quite an effect on insulin, raising the insulin/glucagon ratio significantly, whereas increased protein in a low-carb diet leaves the insulin/glucagon level unchanged, so it stays low. Thus, gluconeogenesis can continue at the necessary rate, ketogenesis is not inhibited, and the increased insulin level has no effect, because it is matched by an increased glucagon level.
Paul, that makes sense - the body needs to tightly regulate blood glucose, so why be pumping out sugar if it’s not needed? Higher blood sugar would in theory (and with hormonal things working well) feature higher insulin and lower glucagon, which should reduce gluconeogenesis, and the reverse of that should stimulate it, as you say above.
Yet some things don’t add up for me here. One is that gluconeogenesis is fairly stable and doesn’t go up and down fast, from everything I’ve read. Some theorize that if there’s “extra” glucose from the process, then it doesn’t get absorbed into the blood as much as when there’s a need for it.
Another is the “raise blood sugar or not” question when eating protein. Some people report higher blood sugar after doing that, even while eating ketogenically. I have to believe them. Yet for many (most?) people that appears not to be true.
a number of researchers showed that the ingestion of protein by subjects with and without diabetes did not result in an increase in blood glucose levels.
As an example, as early as 1936, Conn and Newburgh reported no effect on blood glucose levels after a meal containing a large amount of protein in the form of lean beef. Fifteen subjects with diabetes and three control subjects were fed breakfasts of glucose or carbohydrate or protein foods calculated to yield equal amounts of glucose (2 g protein/kg compared to 1 g carbohydrate/kg). The blood glucose response after carbohydrate or glucose was as expected. However, there was no increase in blood glucose levels after the protein meal even though there was a consistent rise in blood urea nitrogen indicating protein utilization. The finding that protein did not raise blood glucose levels seems to have been lost or misinterpreted over the years.
This is fairly strongly and flatly saying that protein doesn’t increase blood sugar. So, how to reconcile it with accounts from individuals where it does appear to raise it?
My question would be what was going on with insulin at the same time? Did they do multiple tests (baseline before ingestion and values at 30, 60, 90, 120 mins after)? Since we can’t test insulin at home (yet), that would have been the only way to understand what was going on. I would also love to know such people’s HbA1C level, as well. Peter at Hyperlipid sets great store by physiological insulin resistance, and he is on record as not being concerned by higher serum glucose numbers as long as HbA1C remains low.
I would think the high serum glucose would need to be of relatively short duration, then - in order for the A1C to stay down.
The physiological insulin resistance aspect makes enormous sense here - if the liver is making glucose but the body doesn’t need it (I realize this is not in line with it being totally ‘demand-driven’ - but I don’t think it comes to a complete stop) then for the liver to store glucose as glycogen is no big trick - it’s fast and easy. A glycogen is like 4 glucose molecules minus 6 hydrogens and 3 oxygens.
So yes - one’s insulin state would have bearing, as well as insulin resistance - right down to “Is there room to store the glucose or not?” If not, then higher blood sugar could well result.
