Hello Guru’s
I am on and off the keto diet last 12 months.
I read lot about Keto diet I have below question if any one can throw the light.
I read that Liver converts carbs to glucose and body prefers Glucose, and if cut carbs completely and follow keto diet then liver converts fat into ketones.
So my my question is what happened to all the fat we ate so far with carbs is that liver just trashed the fats or it converted them also into ketones.
Thanks
Eating fat with carbs keeps the body a glucose burner along with storing the fat because the carbs keeps insulin high (i.e. keeps the fat storage hormone high).
Your body doesn’t produce ketones with fat that is accompanied by carbs because of its preference for glucose (i.e. will use glucose when the glucose is available - keeping fat reserves untouched or increasing for survival).
@RobC I used to think burning carbs/fats was pretty much an on/off switch. That is, you’re either burning glucose and storing fat, or burning fat by keeping glucose and insulin below the ‘trigger point’. But apparently it’s not quite that simple. Enter RQ and RER, the direct measure of how much energy is being generated by fats and carbs in real time.
For anyone not familiar with the terms RQ and RER see this.
Here’s a more technical explanation:
Bottom line, depending on the proportions of fat/carbs available as fuel, we burn both simultaneously:
My takeaway: If one eats SAD or some variation, a diminishing amount of fat gets utilized as the amount of available carbs increases. The fats that aren’t utilized are stored. Conversely, the less carbs available the more fat is utilized as fuel. My guess is that keto keeps the RER .73 or below. At .73 one would be getting ~90% of energy from fat.
Makes sense that body burning both fat and carbs simultaneously, if not we would have been more than 10,000 lbs by now.
Welcome back to the forums. Please forgive a slight correction, as I try to explain. The carbohydrate we eat, all except fiber, which is indigestible, is separated into its constituent glucose molecules in the stomach and released into the bloodstream. The rising level of glucose in the blood then triggers the secretion of insulin. The insulin pushes the glucose into muscle cells for them to metabolise, and into fat cells to be stored as fat. If the insulin level remains chronically elevated, much of the carbohydrate we eat keeps getting stored as fat, and we become obese.
When we eat very little or no carbohydrate, the liver makes the small amount of glucose that the body needs, and takes fatty acids, which can now be released from the fat tissue (because there is no extra insulin keeping it in), and turns those fatty acids into ketone bodies. The muscles re-learn to metabolise fatty acids directly, and we start to shed our excess fat.
As you are aware, the body doesn’t use up all our extra fat all at once, but it adjusts our appetite to allow it to use a goodly amount each day, in combination with the fat we eat, until all the excess is gone and we are left with a normal amount of body fat.
Hey, I hope you don’t take this the wrong way about RER and the metabolic breakdown. I have an Exercise Science background.
RER is the breakdown of what percentage of the metabolic pathways you are using during physical activity and exercise. So yes, we do burn fat and carbs at the same time.
Imagine on that chart you are looking at intensity percentages. Replace the .70 on the RER column as 0% and calibrate it to 100%. Zero would be sitting in the recliner and 100% would be sprinting a short distance race with everything you have.
The closer you are to rest and the low intensities you are burning less carbs and more fat, while you are burning more carbs the harder you push yourself. That is if you are a fat burner.
I’ve not looked at research on RER in nutritional ketosis. The text books and college classes I had didn’t cover it. I’m tinkering with the idea of going back and taking a few classes for a Bioenergetics BS and be a pain in the rear of my professors. 
@anon24390425 Keep us posted, please. My interest is primarily what happens in nutritional ketosis after one is relatively well fat adapted and engages in high intensity exercise. In someone not in NK and not fat adapted the metabolism would move into a high glycolytic state, those 1.1 and 1.2 RQs. But presumably in a well fat adapted individual, there would be too low glucose and none or very little glycogen to do that. What happens? And, yes, I am aware of the pretensions of ‘carb cycling’ while in ketosis to replenish glycogen. Is it really necessary?
Do we just ‘hit a wall’ and drop exhausted because we can’t take in enough oxygen? I’m curious about that. Phinney and Volek seem to suggest that after sufficient adaptation and fitness we don’t hit a wall.
Unfortunately, I am 74 years old so my prospects of testing any of this are not good. I bicycle a fair amount and I intend to do what I can cycling. But, that really fits into the oxidative state quite well, slow and steady expenditure of energy over an extended period, except for short sprints. I can still do those.
Also, I presume the simultaneous use of both oxidative and glycolytic pathways only occurs successfully in relatively normal metabolic health. For example, how could a person with a high insulin load and or resistance burn fat and glucose simultaneously? So I’m somewhat interested in that as well.
In sustained high intensity exercise, lactic acid is built up in the active muscles. This is transported to the liver and goes through the Cori Cycle. Basically the liver converts lactic acid to glucose.
Does that happen in fat adapted athletes? I’m not sure. I don’t see why lactic acid wouldn’t be converted to glucose.
Edit-
I would assume that globules of fat in the interstitial spaces inside of the muscle fibers are broken down in order to be put into the Kreb’s Cycle in place of the glucose for energy. It may come from the fat that is inside of the muscle fibers or the source could be from another location.
The goal of the breakdown is to keep attaching the phosphate molecule to ADP to become ATP so the ATP can be used to contract the muscles and the last phosphate be sheared off to wash, rinse, and repeat. ADP = Adenosine di-phosphate and ATP = Adenosine tri-phosphate.
@anon24390425 I’m a CPT and a runner, and have been LCHF for over 5 years. I’ve done RQ tests while running on a treadmill and wearing one of those claustrophobic masks…anyway, what’s interesting in relation to this discussion is that when one is a fat adapted athlete- particularly an endurance athlete- there will be a higher percentage of fat burned in higher HR zones than someone that’s burning glucose. Which is demonstrative of the glucose sparing effect of a Ketogenic diet. Very cool stuff
That does make sense that we would be burning more fat and less glucose at higher intensities as opposed to sugar burners.
@anon24390425 when I had my RQ tested I was utilizing 50% fat in zone 5. The tech doing the test had never seen anything like it- usually zone 5 is fueled nearly 100 % by glucose. So yes, it’s quite amazing what happens when you’re a fat adapted athlete. One major benefit is that when you reduce your utilization of glucose there are fewer inflammatory by products of burning sugar. So recovery is faster and inflammation is lower in general.
As I recall the graph from the latest Volek study, fat-adapted athletes metabolise some glucose during high intensity exercise, but the proportion of glucose to fatty acids is much lower than that in carb-adapted athletes. Phinney says that his fat-adapted athletes loved running or bicycling on fat, because they were effectively bonk-proof. You can only get so many calories out of the limited quantity of muscle and liver glycogen, but there are tens of thousands of calories stored in the fat of even a very lean athlete.