57 karma · joined September 29, 2018
First, I believe you're correct that gluconeogenesis happens rarely. More specifically, I believe it happens in the absence of carbohydrates in the food you consume. Since I eat a low carb diet, it would make sense that I experience gluconeogenesis.
Second, have I noticed a spike in glucose? Yes! I have to take some amount of insulin if I have a protein shake. The coffee has no effect, so any effect comes from the almond milk and whey. There's maybe half a cup of almond milk in my shakes which is close to negligible. We can probably assume that whey drives most of the glucose effects from my shake.
Third, why is there so much variance in my blood glucose response and insulin requirements? Here, I do not have a defined answer. One aspect may be that whey is quickly digested. The quick digestion may accelerate the effect of gluconeogenesis. Another factor may be the state of the glucose reserves in my liver before I consume the whey. If I'm in a state of ketosis, it may be that my body accelerates gluconeogenesis because it believes it's in a carbohydrate shortage. In this situation, the glucose spike may exceed what would otherwise be expected. There's a few other things such as exercise I'd include here, but I don't have a single definitive answer to this.
A final note: In some sense, I can feel/anticipate my insulin sensitivity during the day. I cannot explain this in writing in any coherent way, but I have decent intuition on what insulin dose between 2 and 4 units I should pick each day. Or, before bed, even if my blood sugar appears constant and in-range, I may anticipate that it'll go up and down as I sleep and eat/inject insulin accordingly. One part of this intuition is "knowing" rather a protein heavy meal will kick into gluconeogenesis while I sleep. Anyways, I can answer more, but as you can perhaps tell, most of my explanations are of the waves hands variety.
Assume a 1:10 insulin to carb ratio (though I don't think insulin dosages have a strictly linear effect) and a meal of 100 carbs. If the meal, in reality, has 80 carbs, you've injected two extra units of insulin. We might expect a unit of insulin to reduce blood glucose by 30-50 mg/dl, so we've reduced our expected blood glucose by 60-80 mg/dl. If you target a blood glucose of 80 mg/dl, this would mean your expected future glucose is 0-20 mg/dl. In that case, you would die.
Now, the problem with this example is that I would 100% take action to avoid dying, so my actual risk of death is still minute despite having a lethal dose of insulin in my body at the time I inject myself. However, it's still a bit strange to know that, conditional on me taking no independent action, I'm hours away from death in certain situations.
My "solution" is to eat low-carb/keto as a "variance reduction" strategy. Still, removing carbs also introduces gluconeogenesis (the production of glucose from protein) as a factor to consider. The synthesis of protein to glucose also occurs on a much time different time horizon than the consumption of carbs themselves which has implications for insulin dosing and insulin type.
I could go on! But long story short, modelling blood glucose is bloody hard.
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