What happens to carbs/sugars when in keto/fat adapted


#1

Maybe I have it oversimplified. Non-keto oversimplification: consume carbs, they turn into sugars and are used up or stored as fat…insulin reacts differently to broccoli than donuts but still the carbs are used or stored. Oversimplified keto… need fuel but due to lack of carbs body does its thing and lives off fat.

If a seriously ketonian fat adapted person slams down a couple Krispy Kremes where do the carbs (and that wonderful sugar glaze) go? Can he burn it up even though his body is all keto fueled? Surely it isn’t stored as fat and then burnt.

Leading to the real question… if in ketosis, how does the body deal with the various carbs it gets and what makes you stop being in ketosis…

if this has all been answered clearly please send me a link thanks


#2

Never mind…I found some great links that explain it well enough for me…


(Jacqueline Porter) #3

From personal experience, I once ate something a little too carby out of politeness. Suddenly I felt shaky, trembling and faint. Actually symptoms of hypoglycaemia. I believe I had an uncharacteristic shot of insulin, coupled with cells no longer insulin resistant! My blood sugar dropped so dramatically I thought I was going to die! Seriously!
Marvelous excuse to decline carbs in future!


#4

Which explanation did you find?

I’m going to say that if the carbs are glucose digested from starches, they’ll go to being used immediately for fuel or to replenish glycogen in muscle and/or the liver. Once you start storing it in the liver, ketosis is inhibited. If there is enough glycogen to fill hepatic stores then it will be exported as fat. Or, in some cases where there is inadequate choline for example, the fat can’t be completely exported to the rest of the body and some fat will accumulate in the liver.

Now if the source of carbs is a sugar containing glucose and fructose like table sugar or HFCS, then the fructose part does not go to direct energy production or the muscles but goes straight to the liver to be dealt with there.

And then there’s the insulin response and what that may or may not do depending on how high it is and whether the insulin:glucagon ratio is altered. Insulin will cause excess glucose to be stored in fat cells (as triglycrides) along with forcing glycogen storage through insulin dependant transporters. Insulin can also inhibit fat metabolism in cells for energy (carnitine pathway).


(Nasir) #5

@carolT One related question from me that you may be able to answer. Does insulin get involved straight away or only after glycogen has been topped up to full?


#6

Insulin response starts even before you are done digesting. The sweet sensors in your gut send information to the pancreas (and other organs) to potentiate the reponse. But also just injecting glucose into a vein will cause an insulin repsonse, just not as much. And fructose combined with glucose will cause a higher insulin resonse when eaten.

Ketone production however is shut off easily when sufficient oxaloacetate (OAA) is available for the liver to support the Krebs Cycle (TCA). Pretty much any amount of sugar will do this. Of course ketones are stored in the blood, so production being shut off for a short while might go unnoticed unless you’re looking at them under lab conditions.


(Paul H) #7

Dang @carolT… So well said in a understandable nutshell… Thanks for more clarity. :nerd_face:


#8

Aww, geez. Thanks. :slight_smile:

Here’s a diagram I find useful. The typing it into words is the hard part.

[Gotta boot the laptop first …]

KetoneGeneration
SOURCE

P.S.
The diagram is missing the part where hepatic de novo lipogenesis (DNL) occurs with glycogen overload or glycogen storage dysfunction.


(Mark Rhodes) #9

@Fracmeister Yes. You asked the community for assistance and then found your answer but didn’t share. I, for one, find this rude. Please share your link.

Ultimately I think this is a VERY dependant answer. My fasting insulin at 72 hours is under 1.0 uIU/mL. Another prominent member of the forums is still in near 10-14 even though he started keto 2 and a half years before me ( you might know him, he was this week’s podcast interviewee) . This marker alone should be a criteria for how we handle those carbohydrates. I started at 20 g CHO total a day. Currently I can have 70-100 for a week straight with no effect on breath of blood ketones…longer than a week those too will decrease. I rarely do because I cruise towards carnivore lately.

The other factor is people like Danny Vega are using super starches (UCONN) and complex carbs found in sushi rice to jack up their energy for performance with no decrease in ketosis. Is this activity related? insulin related? Both? I am betting both as he never suffered the way some of us have and has greater metabolic flexibility.

The chart Carol T provided is helpful but sometimes analogy works best. The body has learned to use the toxin sugar as fuel. This fuel is akin to rocket fuel but it is so deadly it burns it firsts before, before anything else. If the energy needs do not equal the fuel coming in then this toxin must be detoxified. Going to the more complex metabolic storage and detoxification of the sugar, whatever its source. That it does this is why the assumption was made all those years ago- that sugar is the primary and preferred fuel source rather than say it is a toxin and must be dealt with first.

If we remove the primary assumption which is a filter to how we think about nutrition, that sugar is a PREFERRED fuel source and instead ask why does the body burn fuel sources in the order it does ( Sugar, Fat, Protein) we can look at every single study ever published and derive different answers from the data provided.

My 2 cents anyway.


#10

Sugar consumption via fruit is also the natural way to pack on bodyfat while the food sources are plentiful in anticipation of the oncoming food shortage during winter. Society has made the famine phase undesirable and has rendered it obsolete.


(Mark Rhodes) #11

This has led me to believe that ultimately the “healthiest” diet is one that follows available regional food sources if you are from that region AND your metabolic flexibility has returned. Game in the winter, spring greens in the spring, summer would bring berries. Fat consumption drops throughout as hunting becomes less important. If nothing else we were opportunistic eaters. Why hunt if the other folk can bring you berries? LOL. Eventually root vegetables and game would again become the prevailing food source until the ground froze over and roots were no longer available.

I have no clue how to test this other than begin to experiment with myself once I have stabilized my HOMA-IR for over a year.


#12

So here’s another fun fact that I hesitate to bring up because I’m still trying to wrap my head around certain aspects of it.

There’s this thing called FGF21 which is “Fibroblast growth factor 21 … a liver-derived metabolic regulator induced by energy deprivation.” What’s so cool about it is that it’s secreted by the liver during low insulin, high glucagon conditions (ketosis qualifies as this, as does exercise and starvation) to amplify the insulin response of GLUT4 glucose transporters, which are the insulin dependant ones. GLUT1 on the other hand is a transporter without insulin.

Further reading. Warning: rabbit hole ahead. :hole: :warning:

[DIgging deeper… any effect on glucose uptake is likely in BAT, not WAT or muscle. But it does mediate FFA release.]


#13

Well someone suggested I was being rude for not posting what I found… hmmm… well since I found my answer I really meant to delete the post … that said, @carolT and others more or less posted what I had found… I will add the “just as years of bad eating can’t be corrected by brief ‘good eating’, years of good eating can’t be undone by brief ‘bad eating’” **Not **like the old saying that a little bit of poop messes up a whole bunch of ice cream but even a lot of ice cream doesn’t improve poop.

Anyway the specifics of how much excess carbs get retained and burned vs eventually stored as fat depends on a lot of factors… but someone who is fat adapted may not produce ketones for a while after those krispy kremes but is unlikely to store them as fat… unless you keep at it…

some posters like @Jacqueline_Porter seem hypersensitive to carbs. I have no reason to doubt her response was physiological but I think that eaing a little something “carby” even to the point of a big piece of cake doesn’t give me symptoms of hypoglycemia YMMV


(Bunny) #14

Depends on how much adipose mass you have to muscle mass ratio and choline as Carol mentioned.

The less fat you have on your body the sugar from those donuts would most likely be stored as glycogen if needed then oxidized immediately and not stored as fat by insulin. Insulin only stores it as more fat when there is an abundance of fat to store it in like inflamed adipose fat cells!

So the leaner you are the less likely it is to be stored as fat but could be stored as visceral fat if you are not careful?

If your glycogen storage is depleted enough then that donut or a certain amount of donuts is not going to matter because it may be equal to what is needed to re-stock the glycogen storage facilities.

But donuts are empty calories and really serve no purpose.

It just depends on where your at on the spectrum; are you healthy, TOFI, insulin resistant, pre-insulin resistant, diabetic, pre-diabetic or healthy and fat etc. So many factors to consider and whether or not that box of donuts is going to be stored as fat which is not always the case?

Reference Notes:

[1] Is it time to stop blaming insulin for “fat storage”?

image

[2] Why Insulin Doesn’t Make Us Fat | MWM 2.26


#15

Hmmm, a lot of interesting concepts there. If you have inflamed, overfilled adipose cells they would be harder to fill with more fat, which is one model of how hyperinsulinemia begins. On the other hand, if you have a large number of fat cells but they are healthy, that would make them more insulin sensitive and there would be a large number of them compared to someone with fewer fat cells even though they may both look lean. I’d say fat cell resistance might even make it easier to refill muscle glycogen because of increased insulin levels but sensitive muscle cells.

One of the problems with adipose inflammation is that it can stop new baby progenitor cells from developing correctly, so then you get fat cell turnover but not a proper increase in the number of healthy, effective cells able to respond to normal insulin levels.

Either way, emptying muscle glycogen on a regular basis gives any extra glucose somewhere to go.


#16

I dug into the study that CMJ referenced for his fat vs. lean graphic. They were studying…

Subjects
Thirty obese, nondiabetic women(OB; aged 341 yr, body mass index 47+/-1kg/m2)

^^THAT is the definition of someone who has a large number of insulin sensitive fat cells. Thus increased glucose goes there. The same is likely to be not-true for a diabetic subject with the same BMI.


(Karim Wassef) #17

341yr?


#18

Something got lost in the copy-paste… there was a +/- in there somewhere.
…yes 34 +/-1


(It's all about the bacon, baby) #19

I was going to say that, obese or not, they must be doing something right, to have reached the age of 341! :bacon:


#20

They also had a BMI of 471 but I caught that the first time.