Are low ketone levels a sign of being keto-adapted or fat-adapted

(Envy Boo) #1

So I’ve been on this WOE for 3-years now. I wanted to know if having low ketone levels is a sign of the body being keto adapted or fat adapted. I suspect that the body will produce less ketones when the body becomes more efficient at using ketones or accessing fat stores as energy. I haven’t given a chance to buy myself a ketone meter in the 3-years of doing this diet. I’ve switched on with Carnivore style diet as well. But thing is how my fasting glucose is at its most optimal range that anyone can ever ask even during dawn phenomenon. Unless my glucose readings are inaccurate… but post exercise my blood sugar stays normal too. You may think that a low blood sugar reading around 60-70mg/dl is outrageously dangerous and have seen it dip as low in the 45’s when prolonging my fast for over 24 hours with no sudden side effects.

So if someone has low ketone levels, been doing keto for over a year long, is it to be assumed this person is fat adapted or keto adapted meaning his or her body uses fat stores, nutritional fats, and ketones as energy?

(Allie) #2

Can be yes, as the body learns to use them more efficiently and makes just what’s needed.

(Envy Boo) #3

Thats interesting thought…so someone who produces more ketones are in a deeper level of ketosis just “hasn’t” been fat adapted or keto adapted… I wonder what about all these ketone tests on youtube… hmm?

(You've tried everything else; why not try bacon?) #4

I wouldn’t exactly call it a “sign” of fat-adaptation, though they tend to associate. Fat-adaptation is a combination of mitochondrial healing and the reactivation of certain cellular pathways related to fatty-acid metabolism. Those processes are not connected with the production of ketone bodies by the liver.

However, it is true that over time, the liver gets better at matching production to consumption. My speculation is that, at the beginning, part of the reason for the over-production is to make sure the muscles are well-supplied with energy, because they are not able at that point to metabolise fatty acids well, so they are limping along with ketones, their glucose supply having been withdrawn. Once they are fat-adapted again, they actually appear to prefer fatty acids to ketones, thus sparing them and glucose for those cells that actually need them.

(Bob M) #5

I also think ketone levels should go down over time. Or at least mine have. (Which makes “0.5 mmol/l = ketosis” to be a bad idea.)

I also think there’s a possible relationship between (animal) fat intake and ketones. In other words, if you go from higher protein, lower fat to animal fat first then meat, you should get higher ketones. What that relationship is, though, is hard to decipher.

#6

I first heard of this phenomenon years ago through Luis Villasenor of Ketogains. I have heard it again more recently through Dr Paul Mason (who I just referenced on another thread). And it certainly chimes with my own experience. I only get higher levels (which I would define as +1 or maybe +1.5 mmol) during extended fasting (or experimenting with MCTs). Most of the time I am under 1 mmol.

(Bob M) #7

This is what happened to me. Started 1/1/14, so 2.5 years later, still had relatively high values:

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(You've tried everything else; why not try bacon?) #8

We do know that eating industrial seed oils, with their extensive PUFA content, does lower serum cholesterol. So, come to think of it, switching to saturated fat might well have an effect on ketones as well as on cholesterol.

#9

I think this came out in a study where KDs were compared using high PUFAs versus higher SF. As hopefully you will see from the graph:

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Source: Differential Metabolic Effects of Saturated Versus Polyunsaturated Fats in Ketogenic Diets. The Journal of Clinical Endocrinology & Metabolism , Volume 89, Issue 4, 1 April 2004

(Bob M) #10

That’s a tough one. They don’t say how they calculated insulin sensitivity, but it was likely HOMA-IR, which has lower values for lower glucose/insulin, and lower values = higher insulin sensitivity.

But they never did a hyperinsulinemic euglycemic clamp (HEC) (see: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8497920/), which measures the actual insulin sensitivity of fat cells.

If Peter D.'s theories are true (from Hyperlipid), then this is exactly as expected, at least for part of it. A higher saturated fat intake causes higher insulin resistance in fat cells, meaning higher insulin in the blood and lower glucose. As for the PUFA version, this is where it gets tricky. I would think PUFAs would cause fat cells to be insulin sensitive, meaning lower insulin in the blood. Where it breaks down – for my knowledge – is the lowered blood glucose for PUFAs. I don’t know how that happens.

This might have been discussed by Peter at his blog, but his site appears to be basically wiped.

Also, they say there are no significant differences between the two groups at baseline, but check this out:

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(a) Who are these people with such low total cholesterol and glucose? (b) a 20+ point difference in total cholesterol is nothing? Depending on how you calculate it, it’s about 15% difference.

I’d love to see this redone with a test of insulin resistance of fat cells via hyperinsulinemic euglycemic clamp (HEC).

Edit: It’s not HOMA-IR, as if you use those glucose and insulin numbers here, you get different results:

https://www.omnicalculator.com/health/homa-ir#what-is-homa-ir-homa-formula-calculation