Question: what keeps ketones within limits when fasting?

(57 yo female started keto Jul '19) #1

From what I read until now I understand this: eating carbs makes insulin rise. And insulin supresses ketone production in the liver. My pancreas is working OK; it produces insulin as needed and that protects me from keto-acidosis.

I am assuming I understood the above right. Please correct me if I am not. But if that is correct, I have a question about how it works when not eating. Say I start a fast. Blood glucose goes low, therefore so does insulin. So ketone production in the liver is not so much suppressed. Ketone levels in the blood go up.

Will in this case the high ketone levels make insulin rise again?
If not: what in this situation protects me from keto-acidosis?

(Jack Bennett) #2

The short answer is that if your body can produce any insulin at all, it will regulate the insulin level in your bloodstream to maintain ketone levels below the ketoacidosis danger zone.

Ketoacidosis represents an unchecked runaway process in which there is literally no insulin present in the blood (frank Type I diabetes with no exogenous insulin, for example).

(Bob M) #3

Glucagon also goes up.

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Plasma glucagon concentrations rose twofold to a peak on the 3rd day of fasting and then declined thereafter to a level maintained at or above postabsorptive. Insulin concentration declined to a plateau by the 3rd day. Thus a persisting altered relationship of glucagon and insulin concentrations characterized the fasted state. A synergism of low insulin and relative or absolute elevation of glucagon levels is viewed as a hormonal mechanism controlling the rate of hepatic substrate extraction for gluconeogenesis.

(57 yo female started keto Jul '19) #4

OK so my body regulates (stears up and down) the insulin. I probably did not state my question very clear, so here is another attempt: what makes the insulin go up? Is it the high ketone concentration that makes the pancreas produce a bit more insulin (thus having a short feedback loop)? If not: what does?

(Bob M) #5

Insulin goes down while fasting, not up. See the curves I posted.

(High) Insulin suppresses gluconeogenesis in the liver, not ketones. A side effect of this is that ketones go down, but that’s an upstream effect, not a direct effect. From the man himself (Dr. Bikman):

Glucagon is basically the opposite of insulin:

(57 yo female started keto Jul '19) #6

OK, I read Dr. Bikmans very nice article.

It does not seem (I can very well be wrong) to answer my question. However it seems to give me a hint: “insuline inhibits ketone production”.

So then somehow there is a mechanism that keeps the insulin from going too low, right? Because otherwise we would have the situation of DB1: no insulin, no inhibiting of ketone production, keto-acidosis. I conclude that somehow the pancreas keeps producing some minimal minimal of insulin. That will inhibit too much ketones and prevent keto-acidosis.

But this does not seem to answer my question; it just shifts it. I therefore, in order to understand why I do not get keto-acidosis, would like to reformulate my question:

In a fast, what ‘tells’ the pancreas to keep producing a minimal amount of insulin?

And a hidden sub-question: is it directly or indirectly the ketone levels themselves? My gut feeling (no pun intended) says it should, otherwise it would be an unstable system. I’d say there is a proper feedback loop somehow.

(Bunny) #7

I think it could be body fat and glucagon, glycogen storage and when that runs out catabolism probably keeps those glucose levels steady as the body eats its own protein…

(Bunny) #8

If you think about it those are ketones you can see or measure in the blood stream or urine, you have no idea what’s actually being used for fuel and how much is being used at the time of the blood draw or urine sample?

The lower the ketone that’s all the more that’s being used so insulin may not matter or have anything to do with ketone production or oxidation of fatty acids, so if your seeing a trace in parts per million that does not mean higher is better?

It is when they are high that it may be a good indication they are not being used but may be therapeutic to kill bad things like cancer cells depending on the type of ketone body we are talking about, like acetone for instance can only be metabolized by the brain but butyrate and acetoacetic acid can be metabolized by all parts of the body and the brain, those are mysteries yet to be unraveled?

Acetone is what you see on a pee stick but your body quits making so much of it after around 6 months so those testing sticks become useless.

Butyrate is what you can see with a blood meter but what about acetoacetic acid?

Associations, correlations and causation is what’s being made with the observing of one but not all three ketone bodies in bodily fluids?

We also have no idea what percentage of the three different ketone bodies are in ratios or combinations that are actually therapeutic or indicate that we are actually burning body fat?

(57 yo female started keto Jul '19) #9

I understand ketone measurements have their limits. I started this thread not because of their potential relation to fat oxidation or therapeutic effects. My question is about the bodily mechanism(s) that prevent ketoacidosis to happen when fasting.

(Bunny) #10

Insulin

(57 yo female started keto Jul '19) #11

Please scroll up and re-read this post.

(Bunny) #12

Endogenous glucose production:

The brain needs glucose even when fasting, it does not exclusively use ketones, so you will be having glucose production from that protein you ate three days ago or up to ten days max (even when fasting) or your own body parts and insulin secretions will follow which will prevent you from going into ketoacidosis.

Insulin prevents ketoacidosis.

(57 yo female started keto Jul '19) #13

I left this for a while, as to me it did not seem logical, but I did not have the words to explain why. As a physicist I’d say it would not be a stable system. But today I found this in “The Ketogenic Diet: A Complete Guide for the Dieter and Practitioner” by Lyle McDonald. To me this is a satisfactory explanation as to why ketoacidosis does not happen when fasting:

[…] in non-diabetic individuals there are at least two feedback loops to prevent runaway ketoacidosis from occurring. When ketones reach high concentrations in the bloodstream (approximately 4-6 mmol), they stimulate a release of insulin (8,12). This increase in insulin has three major effects (24). First, it slows FFA release from the fat cell. Second, by raising the insulin/glucagon ratio, the rate of ketone body formation in the liver is decreased. Third, it increases the excretion of ketones into the urine. These three effects all serve to lower blood ketone body concentration.

In addition to stimulating insulin release, ketones appear to have an impact directly on the fat cell, slowing FFA release (12,22). This would serve to limit FFA availability to the liver, slowing ketone body formation.

Ultimately these two feedback loops prevent the non-diabetic individual from overproducing ketones since high ketone levels decrease ketone body formation.

(Bob M) #14

That’s going to freak people out on this board. High ketones causing increased insulin? What’s next, cats and dogs living together? :yum: