NBA players offer an interesting insight into the limitations of CICO. They are all millionaires with full time nutritionists/cooks counting their every calorie and macro, yet some of them still struggle with weight gain. Most famously and recently, Luka was porportedly traded by a fitness-obsessed GM for being 30 pounds overweight. The Luka trade has been discussed as one of the worst in sports history, and fat phobia could be an explanation.
Luka's implied daily calorie surplus was around 500 for 7 months out of a daily EE of 4000-5000 calories. That gives us another NBA thought experiment. What's more likely: a millionaire's full time nutritionist can't count to 3500, a hyper competitive player with a single minded lust for dominance can't cut 500 from 4000, or his physiology was causing weight gain regardless of his EI?
Luka has lost weight this summer, either with the help of glp1as or because he's trying a new diet now that he's in LA. His new teammate, LeBron, lost weight a decade ago with Paleo. Perhaps Luka has restricted his carbs now that he's around LA diet culture instead of Texas diet culture.
One of my problems with writing about energy balance thinking is how it leads to absurdity almost anyway you look at it. It's spherically senseless, as Wolfgang Pauli might have called it: it makes no sense from any direction.
Once you start calculating the daily excess of fat added when people start getting fat--say 19 kcal/day for fat gain of 2 excess pounds per year--you end up with absurd concepts, including how any athlete could ever be obese or overweight considering the hundreds and hundreds of calories per day they're burning off through exercise daily. The only way to explain it is physiology, not energy balance, but.... the obesity researchers don't think about these questions so they see no need to explain it.
That said, I will be writing a lot more about this, hoping (wishful thinking probably) that occasionally serious obesity researchers will consider reading one of the posts.
The thing that keeps the CICO theory alive, is that you can lose weight by starving to death, and you die even faster if you exercise. Everyone knows that. So CICO explains what happens in the total absence of food -- you lose weight and die, but is useless to explain gaining weight when food is consumed. (It's interesting to read cases of people who almost starved to death, but didn't. And were never able to gain weight again the rest of their lives. How did their body adapt to survive on almost nothing? Why are they unable to gain weigh? For example: Adrift by Steve Callahan.)
I seem to recall an animal study where genetically obese mice died of starvation, but still obese. (Was this mentioned in GT’s Why We Get Fat? Or Fung’s Diabetes Code?) The implication being that whatever physiological / hormonal environment was coded by the obesity gene prevented fat utilization and weight loss, even in the complete absence of food (Ein = 0).
I don’t know whether we have analogous human studies, but it aligns with my experience in healthcare settings, witnessing overweight or obese who have “starved themselves” on severe calorie restricted diets and still been unable to lose weight.
So, yes, the genetically lean can and do lose weight by eating less — even to the point of starvation and emaciation — but the genetically obese do not. If the CICO model only works sometimes, it can’t be the right model.
Hey Suzie - yes, I've actually written to Gary about the issue you're talking about (which he wrote about in some of his books, if I recall correctly) - the mice who became obese even while practically starving. A mutual acquaintance of ours (mine and Gary's) did a very nice piece on it here: https://farmerversusbanker.substack.com/p/the-rats-who-starved-to-death-while
I did discuss these animal experiments even back in GCBC, and, yes, VeryVer is spot on. When I was doing the research for GCBC I had among the most influential of obesity researchers insisting that fat storage had to be about calories because when people starved they lost weight. And I would say, "well, yes, but starvation inhibits the growth of children and you'd never say their growth is caused by taking in more calories than expend. Same with tumors, for that fact." And they would just insist those are different issues. As I noted in this substack, this kind of thinking was one reason why I was so disparaging to the researchers in the epilog of GCBC. They had come to a conclusion about obesity that seemed common sensical and because they had grown up believing it and everyone they knew thought the same, they were almost cognitively incapable of questioning it. And those of us who did were considered de facto quacks for doing so. Strange world.
Thanks, Suzie. I had to look up "sick burn" to see if it meant what I was hoping it meant.
And, yes, the more I read the German language literature from a century ago--which I couldn't do even five years ago, because I needed AI to translate it for less than exorbitant sums of money--the more I see the parallels with these other failed paradigms. The literature really does document this shift happening, year by year, and the shift is as much the rejection of the energy balance framework as it is the acceptance of something new. And then the Nazi's come to power and World War 2 changes the world significantly and we have this unique situation where the science that was rejected immediately grows back to take over the field. I hope I can do it justice in my book. (I suppose I'm procrastinating by doing the Substack instead. I have to get to writing that book.)
Thank you for another thought-provoking and well-researched piece, Gary.
I've always been fascinated -- and also stupefied, intrigued, and *angered* by two points related to this topic. My apologies for this very long comment, but this has been on my mind for a long time and this post prompted me to finally put it down on paper (or screen, as it were).
1. In "overfeeding" studies, some subjects gain the "expected" amount of weight (or more), while others gain much less than projected. Why? What explains such large discrepancies not only in the total amount that individual subjects gain, but in how different the real-world results are compared to what the researchers (who are, presumably, experts in the field) predicted? Shouldn’t that make the researchers more curious? What is going on in the bodies of the people who gain much less compared to those who gain more? We need to study the people who don’t gain as much as they were “supposed to” and see how we can mimic that or get other people’s bodies to do the same. When people “overeat,” why do some people’s metabolisms rev hotter/faster and simply burn off the excess, while for others (like me), our bodies appear primed to store every last bit of extra? And of course, the amount of body fat subjects were “supposed to” have gained is based on some kind of algorithm, I suppose, or maybe just compared to how many “calories” they were taking in. The fact that there are such large discrepancies in outcomes among individuals should send researchers back to the drawing board, because their “expert” predictions appear to fall pretty far off the mark.
2. Along that same line, something that has always puzzled me: when I was a kid and we had assemblies in school, some kids couldn’t sit still. They were constantly shifting in their seats, fidgeting, etc. (Doing a lot of what researchers today would call NEAT – non-exercise activity thermogenesis.) Contrast that with ME: I was a chubby kid and did an excellent impersonation of a statue during these assemblies: I could sit still for hours and barely move.
“Experts” would tell us those other kids – the fidgety ones, were thin *because* they were fidgeting. Their little bodies were burning off calories by them tapping their feet, wiggling in their seats, etc. But I’ve always suspected it goes deeper than that. These kids were fidgeting because they were bursting with energy—they *couldn’t* sit still. Something in their bodies was prompting them to move to *do something* with all the energy they were producing. And contrast this with me again: I was perfectly content to sit still most of the time. I force myself to work out now, but my favorite activity when I was a kid was—and still is today—sitting with a good book and reading.
What’s the difference in our bodies? I suspect those kids weren’t lean because they were moving more; they were moving more because their bodies *needed* them to move more. They had so much energy, they *had* to dissipate it somehow. (This is something you’ve written about in your books: people don’t lose fat because they move more; they’re driven to move more because they’re burning fat and they *have more energy.*)
No one seems interested in accounting for this. What gives? Is it thyroid hormone? Something to do with thermogenesis? Whatever the mechanisms, some people's bodies just seem to convert food energy into ATP a lot more effectively than others', and the resulting leanness or fatness has nothing to do with willpower and discipline.
This article appeals to me in exactly the way your great book, "Good Calories, Bad Calories," did. It took me awhile (and about four readings) years ago when I happened upon the book at a Barnes & Noble while store driving through Chattanooga, to figure out how your magic worked. I finally figured out that your genius was applying the historical perspective, and it helped that you were talking about my life, my personal history, citing all the books I had read and faithfully followed as I lost tons--OK, not tons, more like 30 pounds each time, but it seemed so--and repeatedly returned to my overweight condition, threatening obesity. You changed the way I read. Now, I look for books that take the time to show the history of a line of thinking in detail, and don't trust the lazier, ahistorical, authors. So I'll be reading all these articles you write with a joyful anticipation of your new book, because with GCBC and this article, you've shown me that, as with archeology, there are layers beneath layers of science.
As an aspiring writer, I also appreciate that, along with the demonstration of quality research and writing, you always show us how to avoid perfectionism, at least in these early drafts. Having practiced law for over 40 years before retiring, I'm an automatic copy editor, which is sometimes a curse. There are so few examples of your kind of writing: great care with the essentials on which few people focus, combined with a blithe disregard for the superficialities. One example: "In those case, wasn’t it reasonable to assume that these people were obese because of their insatiable appetites?"
Thank you for your work, which I believe has saved my life and one day might make me a serious writer if I live that long.
Thanks, Fritz. The kind words are very much appreciated. Re the writing, one of my problems is that I can't stop self-editing also. Once I have a draft done that I think works, I'll run it through AI to catch typos and other obvious issues. But then I'll continue to edit and revise after that, inevitably introducing new typos and issues. Ultimately I have to just force myself to stop. Then I wait with trepidation to find out after it's published what mistakes it contained.
Re the history, it always seemed necessary to me to understand the nature of a controversy. If you ask what evidence is supporting the competing positions, you end up having to go through the references to check the evidence. That, by definition, is a trip back in time. Then the question becomes, when can you stop? When have you gone back far enough? If you tend to be obsessive, or you like to research (as I do) because it also allows you to delay the writing (the hard part), you can go back indefinitely, always ignoring what you do know and trying to fill the holes in what you don't.
Thanks! I do exactly the same thing with late edits, Gary, occasionally leading to embarrassment in court. I'll remember and value your advice on research, because I've been held back by the need to do that work, probably caused by having become a research burn-out in law practice. -- Fritz
Yeah, but as I told Gary, I do it myself. I can't resist late changes that inevitably result in more errors, because I also can't resist making an improvement, on what would have been the last pass, which, as with Gary, I might also have added a slight error. I love being in his company, though--even in terms of mistakes! The solution suggested for this problem is reading out loud; maybe I'm now inspired to do that from now on. Thanks!
I agree that getting fat or not getting fat is related to hormones, and from a clinical perspective we need to ask the question what are the endocrine “influencers” involved.
Eating more to get taller vs. eating more because of increased energy demand vs. eating more to replenish fat stores. Or, for that matter, eating more because you are pregnant. What are the hormones involved? And what signals are involved?
I’m not a researcher, but I would think these things are all measurable.
What I have learned from exercise physiology is that when I exercise at a low level, 99% of skeletal muscle energy production is (supposed to be) from fat. As I exercise more intensely, more glucose is needed until about 65% of capacity, then it is about 50% each, fat and glucose. As exercise intensity continues to increase, like in a fight or flight situation, glucose is then, and only then, the dominant fuel source.
Unfortunately, conventional thinking tells us that glucose is always the preferred fuel source—for the brain and nervous system, yes, but for skeletal muscle, no. So, excess glucose is transformed to fat, and high insulin signals the skeletal muscles to burn glucose, not fat, and we get fat at unhealthy levels.
In addition, if the high carb diet includes excessive fructose, the satiety signal is blocked, so we overeat carbohydrates all the more.
Eventually, the overconsumption of carbs causes Insulin synthesis dysfunction and/or dysfunctional lipogenesis, resulting in diabetes. If these states of dysfunction trigger the sympathetic nervous system, insulin production is further decreased and glucagon is increased and the liver is signaled to release glucose into the bloodstream, making the situation a complete disaster.
Interesting questions and I will do a post on this in the future. One of the problems with writing a book for the lay public that you hope will be read is that you have to leave out complications to the main story that would make a book even longer and more difficult to read (speaking about GCBC primarily in this case). So one thing I left out was the theory of how energy availability in the periphery, particularly the liver, drives hunger and appetite. The gist of it is that the liver is the sense organ of fuel availability in the body and then it sends both neural and endocrine signals to the brain (the hypothalamus) that turn on and off food seeking behavior (i.e., hunger) in response to that fuel availability.
This is how physiological psychologists think of appetite regulation and its very different from how the obesity researchers do. I discussed this to some extent in the last chapter of GCBC but never got into the details. I suppose I will in one of these posts and I'll include links for further reading.
One thing, though, that can cause us to be misled in our thinking is any use of the words "over" or "excess", as in "excess fructose" or "overconsumption of carbs". They both assume that somehow the body monitors what is needed and something over that is excess. (They're also tautological because they imply "too much" which implies causing harm.) The alternative is that all these growth systems are taking what they need and the liver (if the physiological psychologists are right) is generating energy from what's left. And if what's left is under some threshold--measured as ATP generation in the liver cells, by this theory--than hunger is uninhibited and the organism starts to eat or seek food.
Re the blockage of the satiety signal with fructose, one reason I always found Rick Johnson's uric acid hypothesis interesting is because he's focusing on the effect of fructose metabolism in liver cells and it actually takes more ATP to metabolize fructose than is produced, hence fitting nicely with that physiological psychology thinking.
Body builders are yoyo dieters in reverse. Our son-in-law routinely loses 40 pounds for competitions and rapidly regains that lost weight afterward. Is he damaging his health? Here is what researchers have learned. https://examine.com/faq/are-bodybuilding-diets-healthy/
Re the unabsorbed calories, it's a possibility but the German metabolism researchers working from 1900-1930 did some ludicrously careful studies trying to understand why some people got fat eating no more than lean folks. The first assumption was that they had a slower metabolism, but when they failed to demonstrate that, they started looking at all the other imaginable possibilities. This was part of that eventual rejection of the paradigm process. In some of the reports of this research they went into great detail about how they measured the caloric content of the various excretions so that they could take this into account. At least back then, they failed to show it made any meaningful difference. I did notice, though, that there was evidence that folks eating very high fat diets excreted some of the fat consumed, which might have explained differential effects between low-carb-very-high-fat diets and higher carb diets. But they weren't interested in those kinds of diet studies back then.
One concept I’ve heard tossed around in the discussion of CICO vs CIM is that the law of energy conservation — foundational to the CICO model — only works in a closed system, and since the human body is an open system, the law (and thus, CICO) doesn’t apply in the same way.
But I’ve also heard physicists claim that the laws of thermodynamics work “well enough” in open systems that this need not be an issue.
I don’t recall hearing you speak to this (please direct me to the right text if I’ve just forgotten). Given your background in physics, I suspect you have an opinion! (as the daughter of an opinionated physicist I’m familiar with the archetype)
Yes, it's true it requires a closed system but it's just irrelevant. The law says nothing about causality. That's the only thing that matters. Once you have a hypothesis of causality, the laws of thermodynamics (like all laws of physics) will constrain the implications to, well, reality, but that's it.
I'm assuming that there are "hormonal treatments" that are known, sure-fire, 100% to make people skinny? It's just that they are dangerous and cause side effects? So, for example, something that blocks insulin? or makes you grow? or revs up your thyroid? So wouldn't that mean that hormones also make you fat?
Well, the GLP1 drugs may be just such "hormonal treatments", although the CW is that they work by getting people to eat less. See my earlier posts on that. And, of course, insulin deficiency, as in type 1 diabetes, is a sure-fire way to make people skinny. The catch is that the energy balance hypothesis always gives you a competing hypothesis because the energy balance hypothesis is just a recapitulation of energy conservation and so it's always true (if always meaningless). So people with uncontrolled type 1 diabetes don't metabolize carbs and tend to pee them all away, so the weight loss that also happens can be blamed on the caloric deficiency from peeing away the glucose. Just as the GLP1 drugs seem to inhibit appetite--as you'd expect from this alternative hypothesis--and so the weight loss can always be blamed on the caloric deficiency from the inhibited appetite. Differentiating between the two hypotheses requires very carefully designed experiments and if the obesity researchers don't want to do them, because, well, they know what the truth is, then we're stuck with making proclamations about what seems more or less likely. Tricky business, this.
NBA players offer an interesting insight into the limitations of CICO. They are all millionaires with full time nutritionists/cooks counting their every calorie and macro, yet some of them still struggle with weight gain. Most famously and recently, Luka was porportedly traded by a fitness-obsessed GM for being 30 pounds overweight. The Luka trade has been discussed as one of the worst in sports history, and fat phobia could be an explanation.
Luka's implied daily calorie surplus was around 500 for 7 months out of a daily EE of 4000-5000 calories. That gives us another NBA thought experiment. What's more likely: a millionaire's full time nutritionist can't count to 3500, a hyper competitive player with a single minded lust for dominance can't cut 500 from 4000, or his physiology was causing weight gain regardless of his EI?
Luka has lost weight this summer, either with the help of glp1as or because he's trying a new diet now that he's in LA. His new teammate, LeBron, lost weight a decade ago with Paleo. Perhaps Luka has restricted his carbs now that he's around LA diet culture instead of Texas diet culture.
Hi EP,
One of my problems with writing about energy balance thinking is how it leads to absurdity almost anyway you look at it. It's spherically senseless, as Wolfgang Pauli might have called it: it makes no sense from any direction.
Once you start calculating the daily excess of fat added when people start getting fat--say 19 kcal/day for fat gain of 2 excess pounds per year--you end up with absurd concepts, including how any athlete could ever be obese or overweight considering the hundreds and hundreds of calories per day they're burning off through exercise daily. The only way to explain it is physiology, not energy balance, but.... the obesity researchers don't think about these questions so they see no need to explain it.
That said, I will be writing a lot more about this, hoping (wishful thinking probably) that occasionally serious obesity researchers will consider reading one of the posts.
Best,
gt
Confirmed: Luka has lost weight with a low carb diet
https://www.menshealth.com/fitness/a65511720/luka-doncic-nutrition-diet/
Great comment 👍
Thank you!!! I think I finally understand this now. Your analogies were spot on.
The thing that keeps the CICO theory alive, is that you can lose weight by starving to death, and you die even faster if you exercise. Everyone knows that. So CICO explains what happens in the total absence of food -- you lose weight and die, but is useless to explain gaining weight when food is consumed. (It's interesting to read cases of people who almost starved to death, but didn't. And were never able to gain weight again the rest of their lives. How did their body adapt to survive on almost nothing? Why are they unable to gain weigh? For example: Adrift by Steve Callahan.)
I seem to recall an animal study where genetically obese mice died of starvation, but still obese. (Was this mentioned in GT’s Why We Get Fat? Or Fung’s Diabetes Code?) The implication being that whatever physiological / hormonal environment was coded by the obesity gene prevented fat utilization and weight loss, even in the complete absence of food (Ein = 0).
I don’t know whether we have analogous human studies, but it aligns with my experience in healthcare settings, witnessing overweight or obese who have “starved themselves” on severe calorie restricted diets and still been unable to lose weight.
So, yes, the genetically lean can and do lose weight by eating less — even to the point of starvation and emaciation — but the genetically obese do not. If the CICO model only works sometimes, it can’t be the right model.
Hey Suzie - yes, I've actually written to Gary about the issue you're talking about (which he wrote about in some of his books, if I recall correctly) - the mice who became obese even while practically starving. A mutual acquaintance of ours (mine and Gary's) did a very nice piece on it here: https://farmerversusbanker.substack.com/p/the-rats-who-starved-to-death-while
Thanks Amy — I’ll check it out.
Hi all,
I did discuss these animal experiments even back in GCBC, and, yes, VeryVer is spot on. When I was doing the research for GCBC I had among the most influential of obesity researchers insisting that fat storage had to be about calories because when people starved they lost weight. And I would say, "well, yes, but starvation inhibits the growth of children and you'd never say their growth is caused by taking in more calories than expend. Same with tumors, for that fact." And they would just insist those are different issues. As I noted in this substack, this kind of thinking was one reason why I was so disparaging to the researchers in the epilog of GCBC. They had come to a conclusion about obesity that seemed common sensical and because they had grown up believing it and everyone they knew thought the same, they were almost cognitively incapable of questioning it. And those of us who did were considered de facto quacks for doing so. Strange world.
gt
Also, as someone with a background in the history of science, I just want to say what a sick burn it is to compare CICO to phlogiston.
Thanks, Suzie. I had to look up "sick burn" to see if it meant what I was hoping it meant.
And, yes, the more I read the German language literature from a century ago--which I couldn't do even five years ago, because I needed AI to translate it for less than exorbitant sums of money--the more I see the parallels with these other failed paradigms. The literature really does document this shift happening, year by year, and the shift is as much the rejection of the energy balance framework as it is the acceptance of something new. And then the Nazi's come to power and World War 2 changes the world significantly and we have this unique situation where the science that was rejected immediately grows back to take over the field. I hope I can do it justice in my book. (I suppose I'm procrastinating by doing the Substack instead. I have to get to writing that book.)
https://open.substack.com/pub/sensiblemed/p/the-nutritional-cold-war?utm_source=share&utm_medium=android&r=7n6vy
Thank you for another thought-provoking and well-researched piece, Gary.
I've always been fascinated -- and also stupefied, intrigued, and *angered* by two points related to this topic. My apologies for this very long comment, but this has been on my mind for a long time and this post prompted me to finally put it down on paper (or screen, as it were).
1. In "overfeeding" studies, some subjects gain the "expected" amount of weight (or more), while others gain much less than projected. Why? What explains such large discrepancies not only in the total amount that individual subjects gain, but in how different the real-world results are compared to what the researchers (who are, presumably, experts in the field) predicted? Shouldn’t that make the researchers more curious? What is going on in the bodies of the people who gain much less compared to those who gain more? We need to study the people who don’t gain as much as they were “supposed to” and see how we can mimic that or get other people’s bodies to do the same. When people “overeat,” why do some people’s metabolisms rev hotter/faster and simply burn off the excess, while for others (like me), our bodies appear primed to store every last bit of extra? And of course, the amount of body fat subjects were “supposed to” have gained is based on some kind of algorithm, I suppose, or maybe just compared to how many “calories” they were taking in. The fact that there are such large discrepancies in outcomes among individuals should send researchers back to the drawing board, because their “expert” predictions appear to fall pretty far off the mark.
2. Along that same line, something that has always puzzled me: when I was a kid and we had assemblies in school, some kids couldn’t sit still. They were constantly shifting in their seats, fidgeting, etc. (Doing a lot of what researchers today would call NEAT – non-exercise activity thermogenesis.) Contrast that with ME: I was a chubby kid and did an excellent impersonation of a statue during these assemblies: I could sit still for hours and barely move.
“Experts” would tell us those other kids – the fidgety ones, were thin *because* they were fidgeting. Their little bodies were burning off calories by them tapping their feet, wiggling in their seats, etc. But I’ve always suspected it goes deeper than that. These kids were fidgeting because they were bursting with energy—they *couldn’t* sit still. Something in their bodies was prompting them to move to *do something* with all the energy they were producing. And contrast this with me again: I was perfectly content to sit still most of the time. I force myself to work out now, but my favorite activity when I was a kid was—and still is today—sitting with a good book and reading.
What’s the difference in our bodies? I suspect those kids weren’t lean because they were moving more; they were moving more because their bodies *needed* them to move more. They had so much energy, they *had* to dissipate it somehow. (This is something you’ve written about in your books: people don’t lose fat because they move more; they’re driven to move more because they’re burning fat and they *have more energy.*)
No one seems interested in accounting for this. What gives? Is it thyroid hormone? Something to do with thermogenesis? Whatever the mechanisms, some people's bodies just seem to convert food energy into ATP a lot more effectively than others', and the resulting leanness or fatness has nothing to do with willpower and discipline.
Superlative work, Gary!
This article appeals to me in exactly the way your great book, "Good Calories, Bad Calories," did. It took me awhile (and about four readings) years ago when I happened upon the book at a Barnes & Noble while store driving through Chattanooga, to figure out how your magic worked. I finally figured out that your genius was applying the historical perspective, and it helped that you were talking about my life, my personal history, citing all the books I had read and faithfully followed as I lost tons--OK, not tons, more like 30 pounds each time, but it seemed so--and repeatedly returned to my overweight condition, threatening obesity. You changed the way I read. Now, I look for books that take the time to show the history of a line of thinking in detail, and don't trust the lazier, ahistorical, authors. So I'll be reading all these articles you write with a joyful anticipation of your new book, because with GCBC and this article, you've shown me that, as with archeology, there are layers beneath layers of science.
As an aspiring writer, I also appreciate that, along with the demonstration of quality research and writing, you always show us how to avoid perfectionism, at least in these early drafts. Having practiced law for over 40 years before retiring, I'm an automatic copy editor, which is sometimes a curse. There are so few examples of your kind of writing: great care with the essentials on which few people focus, combined with a blithe disregard for the superficialities. One example: "In those case, wasn’t it reasonable to assume that these people were obese because of their insatiable appetites?"
Thank you for your work, which I believe has saved my life and one day might make me a serious writer if I live that long.
-- Fritz
Thanks, Fritz. The kind words are very much appreciated. Re the writing, one of my problems is that I can't stop self-editing also. Once I have a draft done that I think works, I'll run it through AI to catch typos and other obvious issues. But then I'll continue to edit and revise after that, inevitably introducing new typos and issues. Ultimately I have to just force myself to stop. Then I wait with trepidation to find out after it's published what mistakes it contained.
Re the history, it always seemed necessary to me to understand the nature of a controversy. If you ask what evidence is supporting the competing positions, you end up having to go through the references to check the evidence. That, by definition, is a trip back in time. Then the question becomes, when can you stop? When have you gone back far enough? If you tend to be obsessive, or you like to research (as I do) because it also allows you to delay the writing (the hard part), you can go back indefinitely, always ignoring what you do know and trying to fill the holes in what you don't.
Thanks! I do exactly the same thing with late edits, Gary, occasionally leading to embarrassment in court. I'll remember and value your advice on research, because I've been held back by the need to do that work, probably caused by having become a research burn-out in law practice. -- Fritz
Actually, as a former copy editor myself, I noticed that this article of Gary's had more typos than usual.
Yeah, but as I told Gary, I do it myself. I can't resist late changes that inevitably result in more errors, because I also can't resist making an improvement, on what would have been the last pass, which, as with Gary, I might also have added a slight error. I love being in his company, though--even in terms of mistakes! The solution suggested for this problem is reading out loud; maybe I'm now inspired to do that from now on. Thanks!
I agree that getting fat or not getting fat is related to hormones, and from a clinical perspective we need to ask the question what are the endocrine “influencers” involved.
Eating more to get taller vs. eating more because of increased energy demand vs. eating more to replenish fat stores. Or, for that matter, eating more because you are pregnant. What are the hormones involved? And what signals are involved?
I’m not a researcher, but I would think these things are all measurable.
What I have learned from exercise physiology is that when I exercise at a low level, 99% of skeletal muscle energy production is (supposed to be) from fat. As I exercise more intensely, more glucose is needed until about 65% of capacity, then it is about 50% each, fat and glucose. As exercise intensity continues to increase, like in a fight or flight situation, glucose is then, and only then, the dominant fuel source.
Unfortunately, conventional thinking tells us that glucose is always the preferred fuel source—for the brain and nervous system, yes, but for skeletal muscle, no. So, excess glucose is transformed to fat, and high insulin signals the skeletal muscles to burn glucose, not fat, and we get fat at unhealthy levels.
In addition, if the high carb diet includes excessive fructose, the satiety signal is blocked, so we overeat carbohydrates all the more.
Eventually, the overconsumption of carbs causes Insulin synthesis dysfunction and/or dysfunctional lipogenesis, resulting in diabetes. If these states of dysfunction trigger the sympathetic nervous system, insulin production is further decreased and glucagon is increased and the liver is signaled to release glucose into the bloodstream, making the situation a complete disaster.
Hi Gary,
Interesting questions and I will do a post on this in the future. One of the problems with writing a book for the lay public that you hope will be read is that you have to leave out complications to the main story that would make a book even longer and more difficult to read (speaking about GCBC primarily in this case). So one thing I left out was the theory of how energy availability in the periphery, particularly the liver, drives hunger and appetite. The gist of it is that the liver is the sense organ of fuel availability in the body and then it sends both neural and endocrine signals to the brain (the hypothalamus) that turn on and off food seeking behavior (i.e., hunger) in response to that fuel availability.
This is how physiological psychologists think of appetite regulation and its very different from how the obesity researchers do. I discussed this to some extent in the last chapter of GCBC but never got into the details. I suppose I will in one of these posts and I'll include links for further reading.
One thing, though, that can cause us to be misled in our thinking is any use of the words "over" or "excess", as in "excess fructose" or "overconsumption of carbs". They both assume that somehow the body monitors what is needed and something over that is excess. (They're also tautological because they imply "too much" which implies causing harm.) The alternative is that all these growth systems are taking what they need and the liver (if the physiological psychologists are right) is generating energy from what's left. And if what's left is under some threshold--measured as ATP generation in the liver cells, by this theory--than hunger is uninhibited and the organism starts to eat or seek food.
Re the blockage of the satiety signal with fructose, one reason I always found Rick Johnson's uric acid hypothesis interesting is because he's focusing on the effect of fructose metabolism in liver cells and it actually takes more ATP to metabolize fructose than is produced, hence fitting nicely with that physiological psychology thinking.
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Body builders are yoyo dieters in reverse. Our son-in-law routinely loses 40 pounds for competitions and rapidly regains that lost weight afterward. Is he damaging his health? Here is what researchers have learned. https://examine.com/faq/are-bodybuilding-diets-healthy/
Another consideration is unabsorbed calories. https://www.bmj.com/rapid-response/2011/10/31/unabsorbed-calories-important-consideration
Hi David,
Re the unabsorbed calories, it's a possibility but the German metabolism researchers working from 1900-1930 did some ludicrously careful studies trying to understand why some people got fat eating no more than lean folks. The first assumption was that they had a slower metabolism, but when they failed to demonstrate that, they started looking at all the other imaginable possibilities. This was part of that eventual rejection of the paradigm process. In some of the reports of this research they went into great detail about how they measured the caloric content of the various excretions so that they could take this into account. At least back then, they failed to show it made any meaningful difference. I did notice, though, that there was evidence that folks eating very high fat diets excreted some of the fat consumed, which might have explained differential effects between low-carb-very-high-fat diets and higher carb diets. But they weren't interested in those kinds of diet studies back then.
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Typo: "In those case, wasn’t it reasonable to assume that these people were obese because of their insatiable appetites?"
Thanks. Fixed now online.
One concept I’ve heard tossed around in the discussion of CICO vs CIM is that the law of energy conservation — foundational to the CICO model — only works in a closed system, and since the human body is an open system, the law (and thus, CICO) doesn’t apply in the same way.
But I’ve also heard physicists claim that the laws of thermodynamics work “well enough” in open systems that this need not be an issue.
I don’t recall hearing you speak to this (please direct me to the right text if I’ve just forgotten). Given your background in physics, I suspect you have an opinion! (as the daughter of an opinionated physicist I’m familiar with the archetype)
Hi Suzie,
Yes, it's true it requires a closed system but it's just irrelevant. The law says nothing about causality. That's the only thing that matters. Once you have a hypothesis of causality, the laws of thermodynamics (like all laws of physics) will constrain the implications to, well, reality, but that's it.
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I'm assuming that there are "hormonal treatments" that are known, sure-fire, 100% to make people skinny? It's just that they are dangerous and cause side effects? So, for example, something that blocks insulin? or makes you grow? or revs up your thyroid? So wouldn't that mean that hormones also make you fat?
Well, the GLP1 drugs may be just such "hormonal treatments", although the CW is that they work by getting people to eat less. See my earlier posts on that. And, of course, insulin deficiency, as in type 1 diabetes, is a sure-fire way to make people skinny. The catch is that the energy balance hypothesis always gives you a competing hypothesis because the energy balance hypothesis is just a recapitulation of energy conservation and so it's always true (if always meaningless). So people with uncontrolled type 1 diabetes don't metabolize carbs and tend to pee them all away, so the weight loss that also happens can be blamed on the caloric deficiency from peeing away the glucose. Just as the GLP1 drugs seem to inhibit appetite--as you'd expect from this alternative hypothesis--and so the weight loss can always be blamed on the caloric deficiency from the inhibited appetite. Differentiating between the two hypotheses requires very carefully designed experiments and if the obesity researchers don't want to do them, because, well, they know what the truth is, then we're stuck with making proclamations about what seems more or less likely. Tricky business, this.
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