How does a ketogenic diet actually work, ie how does 'eating fat burn fat'?

(Michael - When reality fails to meet expectations, the problem is not reality.) #1

@David_Stilley started this topic yesterday and it is proving to be quite popular and insightful. Thank you, David, for broaching a controversial topic!

The topic prompted me to ask: How exactly does a ketogenic diet accomplish what at face value seems to be a contradiction? That is, how does eating more fat burn more fat? We have lots of experiential evidence that it does so. But exactly how? That’s what I want to know.

Just to be clear I want to say up front that eliminating carbohydrates as a useful source of energy is obviously the primary prerequisite to the process. So please don’t tell us that you can eat so many carbs and stay in ketosis. That’s a different issue and if you want to talk about that, please start another topic for it. My intention here is to discuss the science of ‘eating more fat to burn more fat’. How exactly that works.

As I find articles/papers/studies, etc that seem pertinent I will post links here along with any comments I think helpful.

OMAD + KETO extreme caloric deficit
Can ketones be stored?
(Michael - When reality fails to meet expectations, the problem is not reality.) #2

There is no doubt that there is strong supportive evidence that the use of ketogenic diets in weight loss therapy is effective [13], however the mechanisms underlying the effects of KDs on weight loss is still a subject of debate. Atkins’ original hypothesis suggested that weight loss was induced by losing energy through excretion of ketone bodies [36], but more recently different hypotheses have been proposed: one hypothesis is that the use of energy from protein in KD is an “expensive” process for the body and so can lead to a “waste of calories” and therefore increased weight loss compared to other “less expensive” diets [37]. During the first phase of a KD 60–65 g of glucose per day are needed by the body, 16% of this is obtained from glycerol whilst the major part is derived via gluconeogenesis from proteins, of either dietary or tissue origin [38]. Gluconeogenesis is an energy-demanding process calculated at approximately 400–600 Kcal/day (due to both endogenous and food source proteins [37]. There is though no direct experimental evidence to support this intriguing hypothesis, on the contrary a recent study reported that there were no changes in resting energy expenditure after a KD [39]. Some authors claim instead that the results obtained with ketogenic diets could be attributed to a reduction in appetite due to higher satiety effect of proteins [38,40] or to some effects on appetite control hormones [41]. Other authors suggest a possible direct appetite suppressant action of the ketone bodies [42] and more in detail by the BHB that it is supposed to act both as a energy/satiety signal (according to Kennedy’s lipostatic theory) and as central satiety signal per se [26]. Over the long term the improvement in fat oxidation mirrored by the decrease of RR (respiratory ratio) could explain the fat loss effect of this kind of diet [39]. Hence we can summarize (listed in order of available evidence) the hypothesized mechanisms of KD’s weight loss effects:
(1) Reduction in appetite due to higher satiety effect of proteins [38,40], effects on appetite control hormones [41] and to a possible direct appetite suppressant action of the ketone bodies [42];
(2) Reduction in lipogenesis and increased lipolysis [33,43];
(3) Greater metabolic efficiency in consuming fats highlighted by the reduction in the resting respiratory quotient [39,44,45];
(4) Increased metabolic costs of gluconeogenesis and the thermic effect of proteins [37,46].

(Robert C) #3

This is easy.
Eating fat doesn’t burn fat.
Instead, eating fat doesn’t cause fat storage.

150+ years ago there were very few obese people.
They were eating things that didn’t cause fat storage.
Then we screwed up and industrialized food.

Want to control weight? Do not eat things make you store fat.
Want to lose weight fast - eat a lot of what makes you store fat least -> fat!

(Full Metal KETO AF) #4

Good posts, In simple terms terms I think it’s like a ball of snow rolling down a slope. The ball being your BMR. When we start at the top our BMR is low (Ball is small) and eating extra fat gets that ball rolling down hill. The ball speeds up picking up snow (body fat), getting bigger (BMR up) and moving faster until you level out with a raised BMR and if you don’t keep eating more and more fat you’re burning a lot of body fat to make that up. I’ll link the one I did yesterday.

:cowboy_hat_face:

(Robert C) #5

Good analogy but not necessarily so automatic.
Just eating lots of fat and no carbs will work for some.
But, bad sleep, high stress, over exercise, zero exercise, artificial sweeteners etc. can slow or reverse the ball’s growth.

(Michael - When reality fails to meet expectations, the problem is not reality.) #6

There is a Michael Eades video popping up here and there in the forum, and I link it here most recently. Part of his video discusses mummy and other evidence of metabolic disease in ancient Egypt. Obesity was common in ancient Egypt, as well as diabetes and coronary heart disease. And these were not limited to the wealthy and royals, but widespread throughout the population as a whole. So we didn’t just screw up by industrializing food during the last 150 years. We screwed up by domesticating, selectively breeding and cultivating grains and other plants beginning 8-10K years ago. Industrialized food only made a bad thing worse. Which is why I contend there are no ‘good’ carbs.

(Michael - When reality fails to meet expectations, the problem is not reality.) #7

I want to know how. And although we might think that ‘burn’ is a little hyperbolic that’s exactly what ‘oxidation’ means in a chemical sense. I know Berry doesn’t like to use ‘burn’ to describe what happens metabolically. But it is a none-the-less accurate chemical description of what occurs.

The “Ketogenic Diet for Obesity: Friend or Foe?” linked above lists ‘energy wasting’ as one of the theories proposed by Atkins to explain why keto works. Bikman proposes this same mechanism here.

(Robert C) #8

Sorry, I don’t know about the actual conversion to energy at the chemical level.

What I focus on is that if insulin is keeping all the fat captured in the cells - that conversion doesn’t matter much and won’t be used.

(You've tried everything else; why not try bacon?) #9

From what I understand, the key is insulin, which among its many other duties, is the main hormone controlling fat storage. The main driver of insulin secretion is the level of glucose in the bloodstream, since hyperglycaemia has toxic effects. The pancreas therefore secretes insulin to drive the glucose out of the bloodstream. The insulin signals the muscles to take up glucose and metabolise it; it signals adipose tissue to take up glucose and store it as triglycerides. As long as insulin levels remain high, these triglycerides are trapped in the adipose tissue.

In the absence of dietary carbohydrate, the resulting low serum glucose allows serum insulin to drop, which frees the fatty acids to leave the adipose and be metabolised. When carbohydrate intake is either low or non-existent, the body’s metabolic needs must be met with some source of calories. Since protein intake is primarily used for building and maintaining bodily structures (protiein metabolism is possible, but it takes far more energy than either glucose or fatty-acid metabolism, so it is not a preferred metabolic pathway), this leaves fat, with its minimal effect on insulin secretion, as the principal source of calories. Thus, eating fat allows the body to burn excess stored fat.

As Jason Fung puts it, “When we eat sugar, we burn sugar; so to burn fat, we have to eat fat.”

(Scott) #10

Short version:
We can get energy from carbs or fat so we must eat one or the other or both.
Carbs spike insulin and will keep it elevated.
Fat does not have the same effect of spiking insulin.
High insulin is the padlock that stores fat and keeps it there.
Low carb high fat diet lowers insulin and unlocks the fat.

(Erin Macfarland ) #11

@amwassil one other component to this is that the lowered insulin levels allow the body to up-regulate the mechanisms that support free fatty acid utilization. A good resource for this is the king of cholesterol, Dave Feldman, of course! He’s very effectively demonstrated how a lipid panel is reflective of energy usage in someone that is fat adapted. So there’s a lot of changes that occur when switching the fuel your body uses. Indeed as others have said here, when you eat mostly fat, you’re telling your body, hey we’re burning fat now!

(Michael - When reality fails to meet expectations, the problem is not reality.) #12

I’m also convinced that insulin plays a key role if not the key role. Still it’s interesting to see scientists who are not particularly ‘keto-oriented’ examine the effects/benefits of very low and no carb eating. There is a lot of info out there. Enough to keep me busy for a while! :slightly_smiling_face:

(BuckRimfire) #13

I was just reading about this in a physiology text 10 hours ago! The key fact is that conversion of tri-acylglycerides (storage fats, aka triglycerides) in cells is done by two enzymes. Without the activity of those enzymes, TAGs can’t be converted to free fatty acids (FFAs) which can get out of the fat cell and into the bloodstream, and in the muscle the TAG can’t enter the citric acid cycle to be “burned” to create ATP.

One of those enzymes is reduced by insulin at the level of mRNA transcription or translation (I forgot which, but the effect is the same: no protein is made from that gene’s code), so the enzyme simply isn’t present in significant amounts when insulin is high.

For the other enzyme, insulin promotes its dephosphorylation by a protein phosphatase and inhibits its phosphorylation by a protein kinase. The phosphorylated form of the enzyme is the active form, so insulin works both sides of that street to keep that enzyme inactive.

So, just from this simple physiology, it’s pretty clear that the “eat six small, carb rich meals a day” is hopeless advice for weight loss. With insulin constantly elevated, you have a fat ratchet: the liver can make FFAs from glucose, adipocytes can take up the FFAs and store them as TAGs, and muscle can even take up some FFA and store it as TAGs (except that they are probably already storing as much TAG as they can), but adipocytes can’t release the fat and the muscles can’t burn it because the enzymes needed to break down the TAGs are absent or inactive. Fats go in, but they can’t get out, except maybe in the middle of the night when the person finally stopped packing their gut with starch for a few minutes and insulin levels dropped.

When insulin is constantly low, TAGs can be converted to FFAs at virtually any time, and most cell types can use those FFAs to make energy (ATP), so any time energy is needed beyond the immediate supply coming from the gut, fat cells can make up the deficit.

(Ken) #14

You’re missing a fundamental step in your incomplete knowledge of Lipogenesis. Insulin does not cause the body to convert glucose to triglyceride without one important prerequisite being met first. The recompensation of Glycogen. Up until that time excess glucose converts to Glycogen, and only when levels are full and receptors downgrade do you get the conversion of excess to fat storage.

(You've tried everything else; why not try bacon?) #15

It seems to me that if we are eating carbohydrate below our threshold, there isn’t going to be enough glucose intake to worry about, and gluconeogenesis will take care of recompensating whatever level of glycogen the muscles need (some of that glycogen will already have been stored in the liver, for just this purpose).

Anyone eating carbohydrate over his or her threshold is going to be flooding his or her system with so much glucose that it hardly matters what goes where or in what order. The storage of glucose in muscle and in adipose in such a case happens simultaneously, for all intents and purposes. It’s circulating throughout the entire bloodstream, after all, along with the insulin that tells cells to grab it.

The liver also stores excess glucose as glycogen. The only difference is that muscle glycogen must be metabolised, since it cannot leave the cells; whereas liver glycogen is stored specifically for the benefit of other cells that might need it.

This whole matter of glycogen recompensation seems to me to be simply an excuse to eat carbohydrate, for those who, for some unclear reason, feel judged if they do. They must be judging themselves, because I can’t imagine who else would.

(Ken) #16

Let’s be a little more definitive so we can keep to the science rather that be subjective. The phrase “Seems to me” is not appropriate to a discussion on Science. Neither is the term “Threshold”. Please explain what you think that actually means.

I’m trying to understand what you’re asserting. Are you saying gluconeogenesis within the context of a lipolytic pattern can recompensate glycogen in the muscles as well as the liver?

(You've tried everything else; why not try bacon?) #17

There is a certain level of serum glucose resulting from carbohydrate intake that results in a level of serum insulin that causes glucose to be removed from the bloodstream by being taken up by various organs. The muscles and liver metabolise or store the glucose they take up; the adipocytes store it in the form of triglycerides. The threshold is a particular amount of glucose, not a percentage of caloric intake, which is why recommendations for carbohydrate limits are always couched in terms of grams. Although this limit is idiosyncratic (i.e., you have to discover what your personal limit is), the Dudes recommend a limit of 20 g/day, because that is low enough to be below virtually everyone’s tolerance threshold, except for people whose metabolic damage (i.e., insulin resistance) is particularly severe.

Yes, that’s what I am saying. Volek’s recent study shows that after a period of some months (I don’t remember exactly how long), the glycogen stores of keto-adapted athletes are identical to those of carb-adapted athletes. So the glycogen has to be coming from somewhere, and gluconeogenesis is the only likely mechanism.

(mole person) #18

You’ve made this claim before while suggesting that a fat adapted person doesn’t need to worry about gaining fat from limited excursions from ketogenic principles. That until glycogen stores are filled no actual fat will be gained and subsequent weight losses will occur rapidly as glycogen is drawn back down.

I’ve asked you before if you could provide some evidence that all “excess glucose converts to Glycogen” and “only when levels are full and receptors downgrade do you get the conversion of excess to fat storage.” but your response was that it was “basic science” and that I should go read a biochemistry textbook.

I’d still like to see some evidence for the above claim as I’ve read biochemistry textbooks in university and have no recollection of this. It’s possible I’ve missed something but, to my mind, it’s also possible you are overstating something. The claim is yours however. And it flies in the face of a great deal of experiences that people here have with the rate of weight losses after limited excursions from the diet. So I’ll ask again, have you evidence for the above claims? I’d really like to be able to evaluate it.

(Ken) #19

Ah, I see what happened. You missed my point. My original post dealt with your lack of understanding of Lipogenesis. This was reinforced by your “Threshold” point, as you fail to see that the threshold within your context is that of not dealing with Lipogenesis, but dealing with that of lipolysis, and the need to keep insulin/glucose low enough for that to happen. That is irrelevant to the point I was making, unless you believe that somehow you can switch back into Lipogenesis immediately once you consume enough carbs to stop lipolysis. You somehow seem to think that halting lipolysis immediately switches the body to fat adding Lipogenesis, which it certainly does not. That all depends on Glycogen levels.

(Ken) #20

Here’s a quick one, but I’ll reiterate that it’s very Basic Science. I’ve included another study more specific to athletes. I think I’ve read it, but maybe not so I included it because I thought you might find it interesting.

ketogenic-diet-resource.com/why/we/get/fat.html

The reason why some people do not drop all their glycogen water weight right after their carb event is that muscular glycogen is not immediately depleted like that in the liver. It usually takes some good physical activity to deplete it. (Bodybuilders following CKD have specific protocols, similar to Circuit Training) Muscle glycogen can make up about 2% of muscle weight, while liver glycogen is about 5-6% of liver weight. You’ve got lot’s more weight in muscle than liver, allowing more glycogen storage. Nice thing is, all you have to do is deplete liver glycogen to be back in lipolysis. It does cause a little confusion for those just going by the scale, but in reality is nothing to worry.about.