Certainly, a rise in glucose from ingesting sugar is expected. But given a specific amount of glucose, wouldn’t the magnitude and duration of that rise be indicative of the degree of insulin response and associated sensitivity?
For the same glucose ingestion burst, wouldn’t a rise from 90 to a peak of, say, 110 suggest greater insulin sensitivity than to a peak of 140?
I’d infer from a more pronounced peak that one’s muscles and organs are growing more resistant to insulin, not more sensitive.
If the spike in glucose went from 90 to 300 would you conclude there’s nothing to infer about one’s insulin resistance? Perhaps we agree on the broader dynamics but differ on the degree?
Again, I have no data to support this (and the individual, amount of glucose, time series response, etc., are all variables that affect one’s pattern of glucose absorption) but my reaction to reading about a spike from 90 to 140 is that this is not a sign of high sensitivity to insulin.
PaulL
(You've tried everything else; why not try bacon?)
#22
The magnitude would depend on the amount of glucose ingested, so far as I understand. The duration is another matter, and my guess is that would likely depend more on the degree of insulin-resistance, given that muscle and adipose would be “reluctant” to take more on board, and more insulin would have to be mobilised to force the issue.
I think saying that implies an almost instantaneous response on the part of the pancreas, and I don’t know how quickly that response can take place. But my impression has always been that the glucose rises, and then the insulin responds. The graphs always show the peak in glucose preceding the peak in insulin, anyway. But you may be right. I suppose this is probably something Dr. Joseph Kraft would have studied, or perhaps his successor, Dr. Catherine Croft. @richard, if you see this, do you know?
Probably, but it’s a moot point, because the patient would most likely be in hyperglycaemic shock, or possibly dead. Something to bear in mind is that even sugar takes a bit of time to digest, and a sugar load capable of raising serum glucose to that level wouldn’t all hit the bloodstream instantaneously. A load of enough carbohydrate big enough to produce that kind of rise would take noticeably longer to digest.
My impression is that the pancreas would do its best, but remember that the amount of insulin that reaches the blood stream is a fraction of what the pancreas produces, because when insulin is secreted, it gets ducted directly from the pancreas to the liver, which metabolises a lot of it, before releasing the remainder to the blood stream. The more insulin-resistant the liver is, the more it will pass into the blood stream, naturally, so that will help the insulin response. But my point is that the detour through the liver has got to be part of what affects the timing of the insulin surge.
Again, I’m only guessing, but my impression is that insulin will start mobilising well before the serum glucose reaches 300, so it will do something to blunt the peak of the glucose spike (which means, actually, that the dietary load of sugar/carbohydrate needed to produce a level of 300 would probably have to be even higher than we might guess), and how much “something” it does will definitely depend on the degree of systemic insulin-resistance.
Now, you could definitely see a spike to 300 in a Type I diabetic who had not taken any insulin, and that’s why doctors worry so much about diabetic ketoacidosis. I don’t know if 300 is a realistic scenario, but elevated serum glucose combined with serum β-hydroxybutyrate of 20.0 or above is a diagnostic for diabetic ketoacidosis. (Actually, the diagnostic specifies a level of 10.0 or above, but symptoms don’t make themselves manifest until 20.0.) The sugar shock, combined with the acidaemia, has been known to kill Type I diabetics, especially in the days before insulin was discovered (which was, I believe, in 1923).
I’ve been fighting a migraine all day and don’t have the energy to go looking for Dr. Kraft’s typical glucose-insulin response graphs, but if you can lay your hands on them, I’d be interested in the conclusions you draw from them.
I buy cases upon cases of Zevia Cola, its a Stevia sweetened cola in caffeinated or not, cost is about $1cdn per can, I mix it with club soda or soda water as its sometimes called. I would like to know the impact that has on me, I need a blood pricked meter thingy, ideally a continuous glucose monitor that measures 24/7 not just 2hrs.
When I was obese and fat, I would drink soda water mixed with pepsi. I learned a lot in the 105lbs I lost in a year and a bit.
With artificial, fake sweeteners, its man made and very unhealthy for you. Kills your good gut bacteria.
Just like vegetable oil thats not even made from vegetables, its made from seeds, is a by product and heavily refined.
I am so sensitive to the real stuff, I would have turned right around.
They could have started on the real stuff then thoughtlessly just finished it the unleaded.
But I will tell you. Drinking soda is maintaining your addiction.
In the beginning it is fine, to help you. But one way to reduce it is to buy regular seltzer.
And mix 10% seltzer in there, then 20%, then 30%… Keep bumping it every week.
Eventually you will be basically drinking seltzer. Dr. Ken Berry used this approach.
I am a fan.
Maintaining that addiction is not great. And my experience is that it can cause you to crave salty foods, and over-eat. (Keep in mind, Pepsi Owns Nabisco for a reason). (And the Tobacco companies own the junk food companies, because they saw more profits in addicting everyone to junk food. That’s why it’s at Lowes, and every store with a register these days!)
