A calorie ≠ a calorie, but is a carb = a carb?

(Carpe salata!) #21

Generally insulin resistance means chronically high levels of insulin.

(Sjur Gjøstein Karevoll) #22

As a consequence, yes but you can’t attribute that as a direct cause although it is often found alongside the real causes.

You know how in japan they (at least used to) employ “train stuffers”, people who would help push people into overcrowded trains? As the trains fill up it becomes harder and harder to stuff more people into them, they become “train stuffer resistant” and you need more train stuffers to help push people in. However, it’s not the presence of train stuffers that make the trains train stuffer resistant, it’s the overcrowding. If there wasn’t overcrowding then it doesn’t matter how many train stuffers there are. Without overcrowding maybe they only need to help old ladies with heavy bags enter the train. It wouldn’t matter if it was one train stuffer and one old lady, or 50 of each, or 500 of each, as long as there is no overcrowding there is zero “train stuffer resistance” going on no matter how many train stuffers.

Insulin resistance is somewhat similar. The ultimate biochemical mechanism that determines if a cell responds to insulin or not is the cell’s ability to handle the incoming energy. This is determined by the amount of oxidative stress present in the cell.

When mitochondria generate energy they generally break down larger hydrocarbon structures in the presence of oxygen to end up with CO2 + H2O + free energy. However, chemistry being what it is there’s not just one reaction possible given the same starting point, and sometimes you get reactions you don’t want, like the creation of superoxide (O2-). This is a really powerful oxidant that can very easily cause damage to the mitochondrion, and therefore it is very quickly taken care of to produce hydrogen peroxide (H2O2). Hydrogen peroxide is also a powerful oxidant (it is also used as rocket fuel), but much less so than superoxide and therefore a safer “storage” form of reactive oxygen species (ROS) until the anti-oxidant defense system can pacify them and you eventually pee them out.

However, when you are generating large amounts of energy you are accumulating dangerous levels of H2O2 and therefore you need a governor to slow down energy production before the cell becomes damaged. This mechanism is cleverly H2O2 itself, as it will inhibit various receptors and enzymes that are needed for energy production, first in the mitochondrion as it becomes overloaded, then as more mitochondria become overloaded a larger amount of H2O2 is going to leak out into the cytosol (the liquid inside the cell) and inhibit receptors in the cell membrane proper.

Among the receptors affected by high levels of cytosolic H2O2 are insulin receptors. The insulin couples with the receptor, but the working end has been deactived. Insulin is sitting there and stepping on the gas, but H2O2 has disengaged the clutch so nothing’s happening. This is actually pretty good design because it allows overworked cells to wind down a bit and clean out their dangerous waste products before they become a danger. It also allows the energy that would otherwise go into the overstressed cell to instead pass on to other, unstressed cells that can make use of that energy. As long as only a small number of cells are refusing insulin signaling this is beneficial. The problem is when a majority of cells become overstressed because you end up with too few cells doing actual work and too much energy in the blood where it can become damaging, and that’s when we say you have insulin resistance.

It is not actually the high levels of insulin that cause insulin resistance, it is widespread oxidative stress in tissues. This widespread stress can be caused by a lot of things and many of them also cause an increase in insulin so attempting to lower insulin as much as possible isn’t entirely stupid, but it’s not entirely accurate either. Some sources of oxidative stress that don’t increase insulin are smoking and other oxidative toxins, malfunctioning mitochondria (damaged or genetic) and an inadequate anti-oxidant defense system (which may be remedied by eating more carbs, depending on why it is inadequate).

Obesity can also cause increased oxidative stress and therefore insulin resistance. It is not actually the amount of fat you have on you that determines this, but your inability to become even more fat. Adipose tissue, like every other tissue, requires a framework of supporting structures and blood vessels, and at some point you are unable to support more fat growth, either because you have too much already or because it’s growing too fast. Insufficient blood flow decreases the cells’ ability to cleanly produce energy so the produce more waste products and also the clearing of those waste products is worse so you get an environment of high oxidative stress. White blood cells are sent to investigate thinking it might be an infection and their response is to produce even more oxidants as oxidants are highly effective at defeating infections and toxins. Because of the high amount of oxidative stress your adipose become insulin resistant. Fat starts leaking into other cells where it doesn’t belong and they too start becoming insulin resistant as a result and now you start developing all the symptoms of metabolic syndrome.

This doesn’t mean obesity always precedes insulin resistance, it can also be the other way around. If for examples your muscles (or other organ tissues) have few and old mitochondria (because they keep getting damaged or growth of new ones is not being stimulated through exercise) or if their environment is especially toxic e.g. in a smoker their ability to handle oxidation is being overloaded and they become insulin resistant. Because the muscles refuse to take up energy the metabolic rate goes down, which also further reduces your ability to handle the excessively toxic environment, and the extra energy available becomes stored in your adipose instead. This time it was insulin resistance that caused obesity.

Once you delve into these things it quickly becomes very complicated which is a major reason why obesity is such a contested topic. Keto is not the right answer, it is a hypothesis (or maybe I should say antithesis) that has a lot of science and medicine going for it, but also has quite a few unanswered questions as well as some commonly held wisdoms and implications that are demonstrably wrong. The same goes for conventional wisdom and other dietary hypothesis. For example when people lose weight and improve every measured marker of health on the Ornish diet (which is what, 70-80% carbs?) I have no doubt that is true and therefore the wisdom that carbs cause obesity has to be wrong. On the other hand the conclusion of Ornish that fat and animal foods cause obesity is also wrong because of the people who reverse obesity and metabolic syndrome on high-animal food keto diets. It’s also very clear that in some contexts a calorie is just a calorie, but it’s also true that there’s no such thing as just a calorie and that context is really important.

Science is trying its best to resolve all these different data points and produce a theory free of paradoxes and inconsistencies but the process takes a lot of work and a lot of time. As an individual the best course of action is to keep doing what works for you, experiment when it doesn’t work as well as you think it should and don’t judge other people when what works for them is different from what you do.

(Damon Chance) #23

Where did you find that explanation on Insulin resistance? I’ve seen the over-full adipocytes mentioned but never the science on it. If love to read more.

(Carpe salata!) #24

Thanks for that interesting writeup.

I had been painting the laundry on the weekend and felt like I did on carbs - your post made me think it was the paint fumes causing oxidative stress like carbs do. Taking some ALA and going to bed early now :slight_smile:

(Sjur Gjøstein Karevoll) #25

This podcast gives a very good overview of the topic. The entire podcast series is very good if you’re into the nitty gritty of nutrition and biochemistry.

(Edith) #26

Wow!!! What a great explanation! This should be saved somewhere on the site to be used as reference material. Thank you for taking the time to make that lengthy explanation!

(Sjur Gjøstein Karevoll) #27

Thanks, but the real credit goes to the podcast I linked. I just rewrote it in my own words, probably adding a bunch of errors in the process.

#28

The author of the podcasts is Chris Masterjohn. While he presents some interesting ideas, he is ultimately a fan of CICO. He has been widely discussed on here, if you put his name into the search you will find many other posts an opinions

(You've tried everything else; why not try bacon?) #29

A very little thought can answer the question posed by the title of this thread. We know that not all calories are handled by the body in the same way, and that is equally true of carbohydrates. Most fiber is not digestible, for example. And most other carbohydrates are easily broken down into their constituent glucose molecules, which the body has evolved effective ways of utilizing, in practically all its cells. Ethanol, sucrose, and fructose require special handling in the liver, and consuming high quantities of them cause liver damage and other problems. (The glucose component of sucrose is, of course, no problem; it is the fructose moiety that causes the trouble.)

From all this it seems clear, to me at least, that a carb is not a carb.

(Ross) #30

white potatoes were recently moved to the Banting orange list (i.e. OK on Keto in smaller quantities).
Turns out, upon further testing, they are pretty much the same as eating a sweet potato.
The original testing by LC used a specific type of potato made for McDonald’s french fries and that screwed the results.

#31

Oh yes - potatoes would be a slippery slope for me - as they are one of my fave foods! Fortunately, steamed and mashed cauliflower with lots of butter and salt/pepper hits the spot. Potato chips/french fries are easy for me to pass on with a high fat lifestyle, but baked and mashed potatoes are another thing.

(Todd Allen) #32

I agree with Rian the types of carbs matter tremendously.

Many track net carbs, carbs minus fiber. Insoluble fiber is largely indigestible though bacteria in the large intestine can convert it to short chain fatty acids. https://www.sciencedaily.com/releases/2015/09/150929070122.htm. Soluble fiber encompasses a wide range of types of varying digestibility. But even when it is digestible the process is slow minimizing the rise in blood sugar and the spiking of insulin.

When you eat an apple which is fairly high in sugars the fiber and the structure with much of the sugar inside cells behind cell walls of indigestible cellulose slow the release and digestion of those sugars reducing their impact. If you eat processed food with the same amount of refined sugar added to the food that structure is missing. Even if the food has fiber added to it the fiber isn’t as effective in slowing access to the sugar and the food will spike your blood sugar more resulting in a bigger insulin response.

The other carbs vary tremendously too. Starch comes in many forms and sometimes is highly digestible and sometimes is nearly indigestible. For example instant mashed potatoes were found to have a glycemic index of 88 (pure refined glucose = 100) while baby potatoes boiled and served cold as potato salad had a glycemic index of about 40 which varied quite a bit depending on the variety of potato - ones with waxy texture being lowest.

And sugar comes in many types with differing properties. Fructose digests very differently from glucose. Some people are lacking in an enzyme for digesting lactose. Ribose is far more reactive than glucose making it a much bigger contributor to glycation, cell dysfunction and cell death.
http://www.sciencedirect.com/science/article/pii/S2352396417303936
http://www.sciencedirect.com/science/article/pii/S0304416512000062

It is difficult to get detailed info on the mix of carbs in the foods we eat. For the most part I’ve stopped trying to track and count carbs. Instead I regularly monitor my breath ketones (cheap and easy), sometimes monitor blood sugar (would do more except for cost) and rarely check blood ketones (would love to do more if it wasn’t crazy expensive). And I’m developing a sense of what foods I can eat in what quantities and how I can prepare them. Raw salad greens I ignore the carbs and eat without constraint but I’ve completely stopped making smoothies even green smoothies as then the carbs are an issue for me.

(jilliangordona) #33

Totally anecdotal, but I found after I was fat adapted if I had something with sugar (such as ice cream or cake) I would immediately get a headache. If I ate something else equally carby (a sandwich, for example) I would not get a headache.

#34

I like your statement a lot. It made me think more. I’m still not clear- though.

From the posted responses it seems to me we all agree a “carb” is not a “carb”.

In my mind- similar to the way you state it: “a calorie” really should always be a “a calorie”; because- it is a unit of measurement. Like an inch = an inch. Google definition follows. But “context” is important to us. But this would only applies to the molecules(?macros, type of carb…).

Dictionary

calorie
cal·o·rie
ˈkal(ə)rē/Submit
noun
either of two units of heat energy.
the energy needed to raise the temperature of 1 gram of water through 1 °C (now usually defined as 4.1868 joules).
noun: small calorie; plural noun: small calories
the energy needed to raise the temperature of 1 kilogram of water through 1 °C, equal to one thousand small calories and often used to measure the energy value of foods.
noun: large calorie; plural noun: large calories

I’m not trying to split hairs with you. I just want to be sure I am thinking about this right. Please correct me if this doesn’t make sense to you.

Thanks

(Todd Allen) #35

A calorie is a measure of energy in a food released by completely burning it. But not all of the food we eat is completely burned for energy. Some doesn’t get absorbed, either it is excreted or consumed by bacteria in our large intestine. Some gets absorbed but isn’t burned such as amino acids and fats used for structural purposes. Some is partially processed with metabolites excreted in urine, feces, breath & sweat, etc.

(You've tried everything else; why not try bacon?) #36

The smaller unit is the scientific one. The larger unit, properly called a kilocalorie and sometimes written with an upper-case ‘C’, is used in nutrition, because of the amount of energy involved. The tendency to measure quantities of foodstuffs by their energy content is analogous to the tendency to say things along the lines of “Chicago is eighteen hours from New York.” We could, of course, be pedantic and insist that people say that such-and-such a food “contains 500 calories’ worth of energy” and “it takes eighteen hours to drive between New York and Chicago,” but the value of the convenient locutions is plain to everyone.

So basically, when we in the LCHF/keto world insist that “a calorie is not a calorie,” we are really saying that there are other considerations involved when considering the foods we eat, in addition to their energy content. Indigestible fiber can be burned and its caloric content measured, but those calories are irrelevant to the human diet. Not even the most ardent adherent of “calories in, calories out” would insist on counting those calories!

And, of course, the whole notion of ketogenic eating holds that it is important to eat as little carbohydrate as possible, given that carbohydrate stimulates the secretion of insulin, which in turn causes the body to store fat rather than metabolising it. So by minimising the secretion of insulin, we are permitting our bodies to use their stored fat as energy, rather than continuing to store it. And this only works because, (a) the body has no minimum requirement for carbohydrate intake, and (b) the fat we eat has (almost) no effect on insulin secretion.

#37

Ok! Thanks for explaning that, Paul and Todd; I think I got it, now.

I’m relatively new to Keto- and still learning a lot; especially from this forum.

With regard to your last paragraph Paul- could you help me follow that through.

Ok- carbs stimulate insulin, leading to fat storage rather than metabolism.

Ok- when insulin is low the body does metabolize stored fat.

Ok- works because…

Question-

Assuming weight loss with LCHF comes from the metabolism of stored fat, and when done properly, protein is spared.

Is it true, at least for the most part, that for me to metabolize my stored fat, while eating the proper LCHF diet; I will have to keep my “caloric intake” and now I am thinking about only those that are getting absorbed and burned- lower than my energy requirements?

Alternatively, if I consumed a large amount of calories (but within LCHF parameters (mostly fat/minimal to moderate protein/say no carbs)); and this amount of calories was higher than my energy expenditure- would the body take that excess energy up and store it, as fat; even though insulin levels remain low?

Thanks again for your previous reply- it really helped me clarify the concept!

(Adam Kirby) #38

I think this article is useful, particularly the quotes by Michael Eades (in red). The interesting paradox seems to be, while a calorie deficit is required to draw on body fat, a calorie surplus in a low-insulin environment doesn’t necessarily result in fat storage.

(Damon Chance) #39

This is a really good post and the conclusions align to what I’ve been coming up with the more I look at it. While i may in theory be able to tell how much to eat based on satiety, I don’t know that my signaling is up to par yet for that. So I put my diet on rails so to speak… i track the calories and try to stay within a range daily that is, according to calculators, at a deficit. And then I see how I feel there. I find I do better that way.
I’m sure getting insulin down, allowing fat to be burned, is a requirement to this working at all otherwise you will just be at too great a deficit and start to see BMR issues.

(Todd Allen) #40

Type 1 diabetics with negligible insulin production were desperately thin prior to the availability of insulin, despite often eating far in excess of their likely caloric needs.

Plenty of people have attested to gaining weight while eating a strict keto diet.

My take on this is eating keto is not a guarantee of insulin falling low enough to allow eating to excess and make weight loss easy. Thus one desiring weight loss might still be inclined to not press their luck overeating. With luck your insulin will fall low enough that you’ll have easy access to stored body fat and reduce your appetite to a level that some weight loss occurs effortlessly.

My personal view is relying on satiety to avoid overeating is a hit or miss affair. It works for many at least for a while but there are many circumstances where it doesn’t get results or at least not as fast as wanted. On the plus side satiety driven effortless weight loss is the most sustainable path. So try it and cross your fingers. And if it isn’t sufficient explore fasting. For me the power of keto has been to make fasting possible. And fasting makes attaining my goals possible - but not easy.