Intermittent Fasting

[Tincup]

My normal diet has very few carbs (~25 g / day), and so my muscles are running mostly on ketones. My body is already likely converting dietary fat to glucose for the brain. Maybe that is why I'm able to maintain BG...

Your muscles are running on mostly on fat. Your brain is running on a mix of ketones (from the fat metabolism in the liver) and glucose. The glucose is from the glucose you consume as well as converting some of the protein you consume to glucose. There is some glycerol liberated as the fat is metabolised but this is a smaller contribution.

[Tincup]

That's good information to have. I ended up breaking it this morning. Lots of dizziness and just feeling weak. I was ill prepared to do it anyhow. I'd like to try again in the future. For now, I'll be fasting 18/6 and a 24 hour fast once a week. I feel that pretty substantial. And I eat keto with very little "keto" sweeteners as I've learned that they can actually spike insulin more than sugar.

I'm glad you followed Mike's advice to stop the fast if you felt poorly.

Fasting is like exercise, you body get better at it the more you practice. Your 18/6 and 24 hour fasts will help and after a while you can push them a little longer. As I previously noted, it will also allow your liver to process toxins that are liberated from your fat.

My diet would not be considered keto by many in the keto camp as I now consume 100 to 200 g of carbs/day (I originally adapted with 20g/day for a couple of weeks in 2009). However I always test 0.3-0.8 mmol/L BHB ketones on a morning fingerstick. If I fast longer than 24 hours, my glucose will drop quickly into the 50's mg/dL (my all time minimum was 32 mg/dL) and ketones will increase into the 4-7 mmol/L range (though I have maxed the meter at 8.0), depending on the fast length. Adaptation continued for me for a long time.

[mike]

Your muscles are running on mostly on fat. Your brain is running on a mix of ketones (from the fat metabolism in the liver) and glucose. The glucose is from the glucose you consume as well as converting some of the protein you consume to glucose. There is some glycerol liberated as the fat is metabolised but this is a smaller contribution.

You are saying muscles don't use ketones? If protein consumption is less than needed for non-fuel purposes, are you saying if glucose is needed, it would come from dietary protein instead of dietary fat? When I eat pure protein, it barely budges my CGM. I'm curious what you think of the following, which I just found while doing some review. Makes a lot of sense to me.

https://www.marksdailyapple.com/a-metab ... etabolism/

[Tincup]

Your muscles are running on mostly on fat. Your brain is running on a mix of ketones (from the fat metabolism in the liver) and glucose. The glucose is from the glucose you consume as well as converting some of the protein you consume to glucose. There is some glycerol liberated as the fat is metabolised but this is a smaller contribution.

You are saying muscles don't use ketones?

No, muscles can use ketones, but primarily will use fat. In a fasting, very low calorie or keto diet situation, the brain will consume most of the ketones to replace non existent glucose because other cells can use fat (except red blood cells which do not have mitochondria).

If protein consumption is less than nee ... etary fat?
Yes, assuming you are consuming enough protein, otherwise it will come from existing body amino acids. Per your link, the metabolism of fat can contribute up to 20 grams of glycerol. Gluconeogenesis is not only from protein, but primarily from protein.

When I eat pure protein, it barely budges my CGM. Protein will stimulate about 54% of the insulin that carbohydrates will on a gram basis. Also gluconeogenesis is demand driven, not supply driven.

I'm curious what you think of the follo ... etabolism/

It concurs with what I've posted.

[mike]

Gluconeogenesis is not only from protein, but primarily from protein.

I know this is often assumed, but doesn't make a lot of sense to me - why wouldn't the body make it out of fat reserves...seems like that is what they are for. Can you point to something that proves this?

Also gluconeogenesis is demand driven, not supply driven.

I agree, though most places seem to assume if you consume protein your BG will go up, period.

It concurs with what I've posted.

They don't talk about ApoE status, but this seems like it would hold especially true for ApoE4 carriers.

[Tincup]

Gluconeogenesis is not only from protein, but primarily from protein.

I know this is often assumed, but doesn't make a lot of sense to me - why wouldn't the body make it out of fat reserves...seems like that is what they are for. Can you point to something that proves this?

There is glycerol in triglycerides that is liberated when they are broken apart. In this chapter abstract

Gluconeogenesis occurs in the liver and kidneys. Gluconeogenesis supplies the needs for plasma glucose between meals. Gluconeogenesis is stimulated by the diabetogenic hormones (glucagon, growth hormone, epinephrine, and cortisol). Gluconeogenic substrates include glycerol, lactate, propionate, and certain amino acids. PEP carboxykinase catalyzes the rate-limiting reaction in gluconeogenesis. The dicarboxylic acid shuttle moves hydrocarbons from pyruvate to PEP in gluconeogenesis. Gluconeogenesis is a continual process in carnivores and ruminant animals, therefore they have little need to store glycogen in their liver cells. Of the amino acids transported to liver from muscle during exercise and starvation, Ala predominates. b-Aminoisobutyrate, generated from pyrimidine degradation, is a (minor) gluconeogenic substrate.

Note that only glycerol in the gluconeogenic substrates comes from fat. No fatty acids are substrates. That is why. The fatty acids can be used to make ketones and the muscles and most of the non cerebral cells (except red blood cells) can use fatty acids for fuel, so use them without any conversion. I'm not a biochemist. If memory serves, BYU prof Ben Bikman talks about it in this talk, but it was 4 years ago when I was at this talk.

[Quantifier]

Gluconeogenesis is not only from protein, but primarily from protein.

I know this is often assumed, but doesn't make a lot of sense to me - why wouldn't the body make it out of fat reserves...seems like that is what they are for. Can you point to something that proves this?

Humans can't convert fatty acids back to glucose, we can only burn them in the mitochondria. Some species can, but not humans. I saw it explained more mechanistically here - I hope this clarifies it.

[Tincup]

Thanks! As a heads up, when posting a link, don't enclose the link in "". I took the liberty of using my mod powers to edit your link and remove them.

Also this

Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.

This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).

The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)

So triglyceride is a poor source of glucose in starvation, and that is not its primary function. Some Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate) in starvation, which can replace part — but not all — of the brain’s requirement for glucose.

Plants and some bacteria can convert fatty acids to glucose because they possess the glyoxylate shunt enzymes that allow two molecules of Acetyl-CoA to be converted into malate and then oxaloacetate. This is generally lacking in mammals, although it has been reported in hibernating animals (thanks to @Roland for the last piece of info).

Source

If protein consumption is less than needed for non-fuel purposes, are you saying if glucose is needed, it would come from dietary protein instead of dietary fat?

I would also suggest that eating less protein than required for non-fuel purposes is suboptimal when in ketosis for a long duration. Sarcopenia would be the predicted outcome.

[mike]

Humans can't convert fatty acids back to glucose, we can only burn them in the mitochondria. Some species can, but not humans. I saw it explained more mechanistically here - I hope this clarifies it.

This would suggest otherwise. Energy inefficient, but if you need glucose for the brain, still seems to make sense over breaking down muscle...

https://en.wikipedia.org/wiki/Gluconeogenesis

[mike]

Note that only glycerol in the gluconeogenic substrates comes from fat. No fatty acids are substrates. That is why. The fatty acids can be used to make ketones and the muscles and most of the non cerebral cells (except red blood cells) can use fatty acids for fuel, so use them without any conversion. I'm not a biochemist. If memory serves, BYU prof Ben Bikman talks about it in this talk, but it was 4 years ago when I was at this talk.

This would suggest if need be, glucose can also be made from fatty acids... Requires energy, but possible.
https://en.wikipedia.org/wiki/Gluconeogenesis
https://www.livestrong.com/article/4958 ... -the-body/

It is my understanding that the brain uses about 20% of our energy and ketones can provide up to 60% of that. So the brain needs about 8% of our energy in the form of glucose. So about 92% (red blood cells?) of our energy needs can be in the form of fatty acids and ketones. If a person has body fat to spare, then even if less efficient than creating glucose from amino acids, it seem like it would still be more efficient than breaking down muscle and then having to rebuild it later... Though the autophagy in the muscle cells might be worth it.