I suspect you are right. To call fatburning starvation is to make an assumption that we're not supposed to be burning fat. There's another way to interpret this. Our bodies operate in either a resource rich mode or a resource poor mode. Fat and protein are our bodies' preferred source of fuel and building blocks. When we're eating mostly fat and protein and few carbohydrates, we're in resource rich mode. Our bodies do not need to be economical because there's no shortage of fat and protein.

As soon as the amount of carbohydrates begins to climb, our bodies shift into resource poor mode. The preponderance of carbohydrates means that our preferred fuel source is not available, so it's time to conserve. The insulin stimulated by the carbohydrates prompts our bodies to convert those carbohydrates to saturated fat and store it as adipose tissue as a hedge against continuing poor resource conditions. When we reduce the carbohydrates and go back to eating fat and protein, resource rich conditions,we no longer need those fat stores, so we burn them off.

This idea might also explain why our bodies are efficient at burning glucose--get rid of the stuff as soon as possible and make sure it is completely used up because we have to be economical in resource poor mode.

That's interesting Tom S., and starting to become clearer.... But I thought ketones were only formed in the liver. So does this build up of AcetylCoA happen in the vicinity of each cell's mitochondria, and then get transported back to the liver in the blood so that the ketone thing can happen? Why doesn't the AcetylCoA just hang around each cell and be used when it is needed, much like glycogen? Is it because of the: 'when fat was the more plentiful' hypothesis (fascinating idea)? I realize that glycogen is also stored in the liver as well as the muscle cells. I'm starting to hear the old biochem line: 'fat can only burn in the presence of carbohydrate'. But what I think you are saying is : 'Fat can only burn in the presence of carbohydrate, OR KETONE FORMATION WILL OCCUR (my italics). What's the minimum ratio of glucose to AcetylCoA in the Krebs Cycle before ketone formation starts to happen? And does this ratio change with long term low carbing? In other words, does x amount of burnt FFA result in the formation of y number of ketones in the absence of glucose? Are you saying that the two carbon molecules that form from the complete oxidization of FFA's can't get into the Krebs cycle without some glycolysis too? Or just that without glycolysis a certain number of ketones must be produced. So even after say twenty years of induction levels of carbs, I would still necessarily be producing the same ratio of ketones as a by product of FFA burning . You seem to be saying that the better your cells become at FFA burning the more ketones are produced as well (I mean that [in the absence of glucose] a burnt FFA always produces x no of ketones). But muscles (particularly for instance heart muscle) can burn ketones for energy too can't they? So what are the by products of burning a ketone? I mean if FFA burning (in the absence of glucose) always results in ketone formation, what does ketone burning (presumably also in the absence of glucose) result in? And can the Ketones that are produced when FFA burning produces too much AcetylCoA then be used again by the same muscle cells that just burnt the FFA?
I think I'm totally confused!
Just to use myself as an example. I've been induction lowcarbing for over two years now. I've never been in 'measurable' ketosis. I realize that not being measurable doesn't mean ketone formation, even in large amounts, is not happening. Just that they being used rather than excreted. But then I've never had body fat to lose. I've really upped the fats and actually reduced the protein compared to before low carb. I eat much less food than I did before, because I don't get hungry like I used to, but I suspect that I wasn't even absorbing a lot of the pre - low carb food (not just the carbs either!). But I'm putting muscle on very slowly while working out much less than I did before. My muscles must be getting better at burning FFA's, because my endurance is improving gradually as well. I certainly don't think these strength/endurance improvements will go on indefinitely without at some stage having to up my work rate. Just that at the moment the amazing health benefits of just severe low carbing seem to be enough.
Anyway, so you're saying that I must be producing more ketones also as a result in direct and inviolable proportion to the amount of FFA burnt for energy (without glucose being involved), and then presumably using those ketones perhaps in my brain and heart rather than excreting them?
If all this sounds like total nonsense, perhaps you could simply explain the difference between a ketone and an FFA being burnt in a muscle cell for energy?
Sorry to fire so many questions at you. I'd really like to understand this ketone/ FFA thing properly.

It's important to remember you can burn fat without being in "ketosis". All being in ketosis means is that you have a really high concentration of ketones in the body. This high concentration can be caused by eating an extremely high fat diet, by fasting totally, or by being sick.

Everyone has ketones in their body at any given point, even your friend who eats carbs all day. If you are eating fat at all you will burn fat for fuel and ketone bodies will result. If fat is the smaller percentage of your energy stores (due to lack of energy deficit and low dietary intake), then you will obviously have less ketones in your body than someone who uses fat as a larger percentage of energy (someone creating an energy deficit and/or high percentage of dietary intake of fat).

So, if you are creating a demand on body fat by exercise, that body fat will be burned the exact same way as any other lipids. Ketone bodies will result.

Using ketones for energy is a perfectly natural process. Detractors seem to think there is something unhealthy or unnatural about using ketones as a preferential/primary fuel source, however, which is why people will say Atkins (induction) isn't good for you. There's a lot of misconceptions about a fat based metabolism, namely some "experts" are afraid of mineral problems on a low carb intake which could theoretically lead to ketoacidosis. The claims are largely unfounded, if someone is eating a nutritionally adequate high fat diet ketoacidosis is not a risk or concern for a healthy person anymore than hyperglycemia is a concern for a healthy person eating a high carb diet. Healthy bodies can keep our ketones in check, just as a healthy body doesn't become hyper/hypoglycemic from sugar.

Interesting theory... so you believe that your body can get better at using FFAs for fuel over time. This adaption to burning fat makes it harder to lose weight on LC, because direct FFA usage can make your body use fat more like sugar (instantly without lengthy conversion processes (into ketones), processes which hog energy and increase total metabolic rate making it easier to lose weight). Am I correct?

If this is what you believe, what is responsible for your body "learning" to use fats more efficiently? I imagine it must have something to do with hormones and enzymes etc... is this just a theory up in the air or is there real evidence to support it?

Wooo, although I know of no specific studies dealing with metabolic adaptations to a low carb diet, it is certainly easy to believe that our metabolisms adapt to this way of eating. Control theory tells us that nearly all the enzymes in a pathway are feedback regulated, so as to maintain a steady throughput and avoid buildup of a particular intermediate. If a buildup of acetyl CoA was a consequence of an abnormal dietary situation (ie, eating too much fat to where glycolysis is not "keeping up"), you would quickly see glycolytic enzymes activated to work faster, and/or activation of the genes encoding the enzyme proteins resulting in more enzymes. This is how the pathways adapt to varying levels of substrates. The regulatory mechanisms are quite sophisticated, and the pathways are interconnected at multiple steps. The result being, everything affects everything else and you have a system that can deal with a great variety of inputs (everything from an apple to a zuchini) with the same output (a healthy functioning individual).

The fact that we can be in ketosis and have elevated levels of ketones in our systems for a prolonged period, just proves that it is normal for such chemicals to be present in our systems. Otherwise, our biochemical pathways would quickly adjust to eliminate thes intermediates from our systems. The ketones are there for a reason, to supply the brain with an energy source in the absence of glucose.

I'm still trying to review my biochem to see just where all this stuff happens.

OK I went and did a little review (its been a long time since biochem class).

First of all, ketone bodies ARE only formed in the liver (yeah you were right, get over it). They are formed from acetyl CoA, which is the breakdown product of fatty acid degradation. Ketone bodies are formed when carbs are low, because when carbs are low so is an intermediate in the Krebs cycle (oxaloacetate, it is used for making glucose). Without OAA, the acetylCoA can't get burned on up in the Krebs cycle. So the liver turns this into ketone bodies and ships them out in the blood. The ketone bodies are then carried to other tissues for use as energy.

The info I read said muscle could use ketone bodies, but the brain requires glucose (also heard this is not entirely the case but haven't researched this yet). Supposedly, when glucose is low the ketone bodies are made to feed muscle and thereby spare what glucose there is, for the brain. Don't know if thats true, but we ARE making glucose via gluconeogenesis. I think our blood glucose levels are on the low side but measurable (and stable, which is nice.) The liver lacks the enzymes to metabolize ketone bodies, which is why it can make them for export.

Fatty acids are oxidized to acetyl CoA in other tissues like muscle. In these tissues, acetyl CoA feeds into the Krebs cycle and electron transport and is used to generate energy (ATP). The ketone bodies are also broken back down to acetyl CoA and fed back into the Krebs cycle for energy. How much of each a muscle uses, I don't know. I'm supposing ketone bodies make a significant contribution to muscle energy needs, otherwise why have the pathway?

Since we still have glucose in our systems (although not a large store of glycogen in our livers), I'm assuming our muscles still utilize glucose as an energy source to some degree. So we have some glycolysis going in our muscles, in addition to the Krebs cycle/electron transport.

One thing I'm realizing, is that the liver is a key organ in energy storage and metabolism. It is the place where glucose is stored in times of plenty, where it is made in times of little carbs, where fatty acids are converted to ketone bodies in times of fat but no carb, and where glucogenic amino acids are converted to glucose in times of protein but no carb. Theres a lot going on in the liver. Makes me ashamed I periodically pickle it with liquor.

To answer some of your specific questions, when a ketone body (which is acetoacetic acid, hydroxybutyrate or acetone) is burned in a cell, it is first converted back to acetyl CoA (which is what it was made form in the first place). This is then turned into energy (ATP and/or reducing power) and carbon dioxide in the Krebs cycle.

As for you not testing positive for ketone bodies, as I understand it the strips only detect one of the three ketones I mentioned. Maybe you happen to produce more of the others. Or maybe as you suggest, you are using most of your ketone bodies for energy, which would be the case if you are not eating a whole lot of calories.

I'll quit now, before I get in any deeper. Hope this adds to your understanding of whats going on at the molecular level.

Here are a few references I googled up to brush up on my biochem. Don't know how this reads but have at it.

http://www.rpi.edu/dept/bcbp/molbio...1/MB1index.html

http://www.mun.ca/biochem/courses/1430/lipmethints.html

http://web.indstate.edu/thcme/mwkin...-oxidation.html

Thank you, Tom Sawyer. Your explanations are lucid and helpful. I especially appreciated your discussion of self-regulating enzymatic pathways. I have learned a good deal by participating in this thread.

Yeah Tom S. , many thanks. This thread is fascinating. I too have learnt a great deal. I really should apologize for sounding a bit sure of my facts a few posts earlier. I think I'm beginning to appreciate just how complex this whole short/medium and long term adaption of lipolysis to low carbing is. I do want to understand why I feel so amazingly well the lower and the longer I spend low carbing. It's starting to be a bit intoxicating. I think I've spent most of my life in a kind of carb induced stupor. Everything, and I mean everything - body wellness, memory , mood , relationships , sleep, dental, and (yes I have to say it , even sex) - it's ALL getting better. If this was as good as it gets, I'd be a happy man. But low carb bliss seems to be becoming a journey, not a destination. I keep hoping it's even half as good for all you other low carbers as it is for me. It would be truly appalling if I was the only one....

Moving right along, you said that cells can re-use the ketones that the liver has made from the excess AcetylCoA that the mitochondria have made from the FFA. And when a ketone gets sent out by the liver and is converted into AcetylCoA in this kind of 'secondary burn' , presumably this secondary acetylCoA also needs some glucose involvment for the Krebs cycle to work? I'm still wondering wether the amount of glucose the Krebs cycle needs per unit of AcetylCoA reduces with long term low carbing, so that (a) more of the AcetylCoA that mitochondria make from FFA's is used for creating energy and not redirected to the liver to be converted into ketones ; and (b) the only ketones the liver really needs to make are those for the brain and heart. And I presume the liver can make it's own ketones directly from FFA's rather than waiting for excess AcetylCoA to arrive back from other mitochondria?
As you said, the liver's role in making ketones from the excess AcetylCoA from FFA burning is pretty central to lipolysis, at least early on in low carbing. But I'm really curious about whether the mitochondria actually get better at using the AcetylCoA they make from FFA's without needing as much glucose if their ongoing supply of glucose is limited by long term lowcarbing? I'm afraid I get a bit impatient with most of the biochem texts, because they treat carb restriction as short term 'starvation' and not a desirable long term transition. I think we need some Inuit Biochemists!

Questions, Questions , Questions.
Btw. Be nice to your liver!

And Woo. I was hoping that this was well established biochemical fact. I noticed in another thread somebody mentioned that competitive athletes become much better at burning FFA's directly in muscle mitochondria. That is presumably not even a low carbing adaption, but a training one. My speculation is that prolonged low carbing probably has the same effect. It certainly has with me, and I'm not a competitive athlete ;) , but I was hoping one of this forum's biochem gurus could explain it a bit. Most people say their weightloss slows as they approach goal. But I wonder whether this is the same process as somebody who is still nowhere near goal but has been low carbing for an extended period and finds the weightloss slows. It's worth repeating that even if this is in fact the case, the amazing health benefits of low carbing, would make it a sensible lifestyle choice anyway, even if you only lose slowly. Not that any of this will be generally accepted for a long time. Professional opinion still hasn't worked out that low carbing is the most effective, (regardless of wether it is the healthiest way to eat, period) way to lose weight. Sigh!
I think the thread that is discussing moderate carb cycling (LCanita et al)is very interesting in this regard. Maybe some of their success in keeping the weightloss on the boil is because the gentle carb cycling stops their mitochondria getting too efficient at burning FFA's. Rivetting stuff, isn't it?

The liver is a primary site for fatty acid oxidation, and it makes ketone bodies out of fatty acids (via acetyl CoA) when there is plenty of fat but not much carbs. It must be the case, that muscle cells do not have the same biochemistry going on, otherwise they would be pumping out ketone bodies too. I don't think muscle makes ketone bodies. It simply is able to burn free fatty acids via oxidation/Krebs, and ketone bodies from the liver via the same basic mechanisms. Obviously low glucose does not inhibit acetyl CoA from being used in the Krebs cycle, in muscle. Part of this, may be due to the fact that low carbing does NOT cause extremely low blood glucose levels. I assume this is because the amount of carbs you eat isused to maintain blood glucose levels, and also the protein is converted to glucose in the liver (some amino acids can be converted to glucose). I still haven't researched whether the brain can use ketone bodies, I guess it doesn't have to since we low carbers still have blood glucose in our systems. I also haven't seen what sort of blood glucose levels we typically run on induction level carbs. It must be on the low side of normal, but my guess is its well above zero. Healthy blood glucose is like 100mg/dcl right? My diabetic friend tries to get hers below 110.

On the subject of feeling better, I think that is due to not carrying around as much extra weight. It is a LOT of work to tote around an extra 40+ lbs. I beleive diet allows you to lose weight, to a point that you are then able to be more physically active without it being too taxing to yur system. A snowball effect in the right direction. This is my personal experience. I know others think exercise is more fundamental to their weight loss.

On the subject of slowing of weight loss, I've thought a bit about this and here's where I'm at. We all start our diet program from a different point. Our pre-diet eating habits have stretched our stomachs to different degrees, and we are used to eating a certain amount of food. We are also used to eating a certain composition of food. I think that the more carbs you were eating before starting your diet, the better you'll respond to the diet initially. This is because your apetite will change most drastically, and you will consume a lot fewer calories than you were before. At some point though, you will get used to eating an amount of calories that is enough to stall your weight loss. At this point, you can get used to eating this amount of calories, and then work on portion control as phase 2 of your weight loss. Since you are now a smaller person, you SHOULD be able to train yourself to eat less with less effort than when you were supersized.

I admit that there is probably also a metabolic advantage to a low carb diet, and you are probably right that this advantage is attnetuated with time. Might always be a small advantge, but my guess is that the body adapts and becomes more efficient over a matter of months. Stands to reason, although when you consdier that we are eating a diet that signals a time of plenty, we may never have the need to be as efficient.

I think there is merit to the idea that carb cycling may allow a replenishing of intermediates in the Krebs cycle (or other metabolic processes), so that optimum fatty acid oxidation may proceed. Its also possible taht carb cycling is the most satisfying way of eating for these people, such that their consumption is the lowest. Yes, I'm still someone who believes thta calories count. Although, I realize that a calorie is ot a calorie, given the differences in digestion, absorption and utilization.

It is fun to pretend that we know why low carb works. Almost as fun as hearing the experts trying to reconcile our success with their wrong dogma.

Tom S. I'm reasonably sure that your brain can adapt fairly quickly to about 85% ketones 15% glucose. I wonder if anyone ever tested a traditional diet Inuit for neurological ketone/glucose utilization?
cheers

I'd just like to know what an Atkins induction dieter runs for blood sugar. I'll see if I can find out. Just because we don't eat carbs, doesn't mean we aren't making them as we need them. Gotta do something with the protein anyway.

BTW, there are glucogenic amino acids and ketogenic amino acids. Meaning some can be converted to pyruvate and then to glucose (gluconeogenesis), and others can be made into Krebs cycle intermediates.

Wow, this if true is pretty insightful. I've never heard anybody put things that way... it's been more of the 'body switches into emergency mode with ketosis' line of thinking. :rolleyes:

If you go way back historically, it could make sense in a hunter-gatherer paradigm. (Of course, everything's a theory.) In essence it's suggesting that if you were in a rich hunting ground with adequate meats and the animals themselves were well fed, then life was good. But that early on in evolutionary terms (at least for some populations) resorting to making breads out of grains and eating mostly roots and other non-meat non-fish items meant you were scrounging and life was not good.

Heh, thanks for the nicely-put daily dose of cynicism borne of burgeoning incredulity. :D

Very good stuff, Tom Sawyer. According to Dr Mary Enig, short and medium chain fatty acids can be broken down directly in the mitochondria, only long chain fatty acids go through the whole ketone cycle. Our bodies store fat as long chain faty acids. Atkins cites studies done on brain tissue at Harvard Medical as showing that most of the brain can not only function well on ketones, be actually seems to function better than on glucose. Nyah Levi