Ludwig has written several high-profile op-ed pieces in recent years, both in the popular press and in scientific journals (1, 2). He argues that our understanding of eating behavior and obesity may be all wrong, and that our focus on calories may be leading us away from the true cause of obesity: hormonal imbalance. And the primary culprit is insulin. You might recognize this idea, because it's similar to the one that science journalist Gary Taubes developed in his book Good Calories, Bad Calories.
According to this view, overeating is irrelevant. We gain fat because our insulin levels are too high, leading our fat tissue to take up too much fat, and other tissues to take up too much glucose, causing our blood energy levels to drop and resulting in fat gain, hunger, and fatigue. The ultimate cause of the problem is the rapidly-digesting carbohydrate and sugar we eat. This idea is encapsulated by Ludwig's quote, "Overeating doesn't make you fat. The process of getting fat makes you overeat" (3).
Here are eleven facts that may make you question this line of reasoning:
- Overeating does make you fat. Randomized controlled trials have shown that eating excess calories causes fat gain, whether the extra calories come from fat or carbohydrate, and regardless of their impact on insulin levels (4, 5). If you eat too many calories, regardless of why you overate, you will gain fat (although some people are intrinsically more resistant to overeating-induced fat gain than others). That's why overeating remains a key concept for understanding body fatness.
- Hunger is only one of the reasons we eat. We don't generally eat dessert because we're still hungry at the end of a meal. We don't drink alcohol or put cream and sugar in our coffee because we're hungry. Much of the eating we do in the affluent world has little to do with hunger-- a phenomenon researchers call "non-homeostatic eating".
- Blood levels of fat and glucose tend to be normal or elevated in people with obesity and high insulin, not lower (6, 7, 8). That's because they're insulin resistant, meaning that insulin isn't doing its job of constraining blood glucose and fat levels as effectively. Since people with obesity/overweight don't have lower circulating energy levels than lean people, this cannot explain why they eat more. Obesity is not a condition of "internal starvation".
- Fat cells do not have an increased affinity for fat in people with obesity and high insulin. In fact, people with obesity and elevated insulin release fat from their fat tissue at a higher rate than lean people with lower insulin (higher total lipolysis rate; 9). Again, this may relate to the fact that they're insulin resistant.
- Body fatness is regulated by the brain, not by fat tissue or the pancreas. There is a vast research literature showing that the brain regulates food intake, energy expenditure, and fat tissue metabolism to regulate the size of body fat stores (10). There is no known mechanism intrinsic to fat tissue or the insulin-secreting pancreas that does this. Genetic differences that impact body fatness tend to be located in genes that affect brain function, not fat tissue or insulin signaling (11, 12).
- High insulin levels do not predict future weight gain (13, 14). This is a basic prediction of the hypothesis that has been tested many times, and the majority of the evidence doesn't support it.
- If high insulin were a major contributor to obesity, weight loss would be a positive feedback process. In other words, the more weight you lost, the easier it would become to lose further weight. This is because weight loss itself reduces insulin levels, both between and after meals (15, 16). Yet what we observe is the opposite: weight loss becomes more difficult the more you lose, despite declining insulin levels (a negative feedback process).
- Foods that lead to higher blood levels of glucose and insulin do not result in greater subsequent hunger. The most comprehensive study examined 38 common foods and found no relationship between glycemic index and subsequent hunger, and an inverse relationship between insulin levels and hunger (i.e., foods that caused greater insulin release tended to be more filling; 17).
- Diets that reduce blood glucose and insulin swings (low-glycemic) are not an effective tool for weight control. This has been shown repeatedly in RCTs lasting longer than two months (18, 19, 20, 21, 22, 23), including an 18-month study by Ludwig's group that found a low-glycemic-load diet to provide the same weight and fat loss, and the same participant satisfaction, as a standard low-fat diet (24). This is despite the fact that these studies often don't control for confounding dietary factors like fiber content, calorie density, protein, and/or palatability (i.e., the "low-glycemic" diet is often a whole-food-based diet).
- Billions of people globally eat high-glycemic diets and remain lean. Many traditional diets are very high in starch and low in fat. If foods that promote large blood sugar and insulin spikes were the primary factor in obesity, shouldn't these people be obese?
- There is no evidence that our appetites increase, and our energy level drops, because our fat cells are hoovering up fat from the bloodstream. You would think, with how often this is repeated, that there would be some kind of evidence that this process is actually happening in common obesity. Yet despite having read a number of works by Taubes and Ludwig, I haven't found anything more concrete than speculation and analogies. The concrete evidence I have encountered (#3 and 4 above) is at odds with the claim.
There are other hypotheses that explain why some of us are "always hungry", but these focus on the brain-- the organ that controls hunger, food motivation, body fatness, and the behaviors of food intake. In my view, these are a better fit for the evidence.
Sort of leaves out the other side of insulin - insulin sensitivity. Insulin is the feedback signal - absolute values are meaningless - it is their value at a particular amount of sensitivity that matter.
Without recognizing the effect of PUFA consumption on insulin sensitivity the analysis is lacking. Add in the following points and it is quite a bit different.
- PUFAs mess up FADH2:NADH ratios causing inappropriate insulin sensitivity in adipocytes - thus weight gain.
- PUFAs reduce ROS thus reduce the production of new mitochondria
- PUFAs generate excess ATP
- SFA generate ROS and switch off glucose metabolism (ie cause insulin resistance) - ROS also tells mitochondria to divide increasing the capability to burn lipids.
I don't even think to buy anymore books that talk about fat, protein and carbs...I'd only like to see comparisons studies of well designed paleo diets, it's about food. Food is much more than starch, fat etc...if you eat cereal grains is far different from eating sweet potatoes as grassfed beef fat is different from seeds oil. If we go on with the dogma of starches, sugar, fat etc.. we'll never go anywhere.
As a boots on the ground primary care MD for over 35 years I would respectfully submit that for the vast majority, "why" is of very little interest. My 3 line diet, developed in desperation 15 years ago works every time and long term
Real food does not have a label. Real food rots
If you have diabetes, eat less empty carbs, they are optional and not required, replace with heathy fats
You cannot outrun your fork. - portions are important for some folks
What the obese, hypertensive diabetic with hip and knee pain desperately wants is practical, doable advice
I would be delighted to see any patient adopt a lifestyle based on any book that encouraged eating real food.
Dr. Guyenet, you are very persuasive.
We have seen that with the Lap-Band the effect is primarily in the brain. This may indicate that volumetric approach to weight loss might be better.
I wonder what does Ludwig and other proponents of carbohydrate-insulin hypothesis conclude about high protein diets and their effect on insulin levels. Most sources of animal protein are very insulinogenic, for example beef and cheese. They increase postprandial insulin as much as an isocaloric dose of carbohydrates. The insulinogenic response to protein seems to be even more profound in early type 2 diabetes.
The insulinogenic effect of protein was nicely demonstrated by Holt et al. 1992 ( http://ajcn.nutrition.org/content/66/5/1264.full.pdf ) and repetedly reported by other researchers there after. Are high postprandial insulin values induced by protein somehow different according to Ludwig, Taubes etc.? Is postprandial insulin only problematic when it's induced by carbohydrates? Or do they simply keep quite about the effect of protein on postprandial insulin levels?
Protein has been demonstrated to be very satieting despite its ability to drive postprandial insulin peaks. In my opinion, this fact is also (among those 11 presented) against Ludvig's and others' key concept.
Stephan, great thanks for such a detailed post!
I want to ask you one more related question: how does the insulin affect post meal blood sugar level? The common theme on insulin, is that it spikes up after a meal and as result it draws blood sugar level too low which in turn triggers "hunger". As usual, that sounds like a huge oversimplification so perhaps you could please elaborate on this? Thanks!
On the surface, it doesn't sound like he's selling anything that Taubes hasn't said before.
Though interestingly (according to this article https://experiencelife.com/article/hungry-no-more/) it looks like the lower carb intake is just an introductory plan (combined with high protein, standard stuff really) that eventually moves into phase 3 maintenance with a 40% daily carbohydrate intake, definitely not 'low carb'. In fact from what I can recall this approach seems similar to the Ideal Weight program.
I was particularly intrigued when I heard that the book contains meal plans with recipes. Correct me if I'm mistaken, but following a meal plan with measured quantities of food sounds a whole lot like controlling calorie intake to me. He says you're to eat until you're 'comfortably full' in other words, stop before you overeat!
In end what he's really proposing is a full lifestyle intervention, with an introductory reduction in carb intake, exercise, calorie reduction, and a focus on nutrient dense, home-cooked meals with limited refined and processed foods.
To be blunt, he's either just riding the low carb trend in order to sell books, or he's deluding himself into thinking that with all those dramatic lifestyle changes he can confidently say that it all hinges on a moderate reduction in carbohydrates...
I think everyone who talks about/studies weight loss should become obese [if possible for them] and then attempt to lose weight before trying to apply theoretical knowledge to the equation. Everything makes a lot more sense once you've experienced obesity, rather than just talking about and studying it.
A bit more - absolute insulin levels don't matter - it is really the flux of fatty acids into/out of adipocytes that determine weight gain/loss. This is obviously controlled by the combination of insulin levels and insulin sensitivity. To say otherwise means that a whole lot of research is wrong. From wikipedia "insulin is known to activate LPL in adipocytes..." and "hormone sensitive lipase HSL is activated by epinephrine, norepinephrine, ACTH and glucagon, acting via phosphorylation of the enzyme. It is inhibited by insulin "
Most people in biomedical fields don't understand feedback loops - I spent my life in engineering and do understand them - the absolute level of an error signal of a feedback loop is meaningless by it self. The flux of fatty acid into/out off adipocytes is the definition of weight gain/loss. You can't ignore it. And insulin is part of that control loop no matter how many times people try to deny it.
Biological systems are evolved - not engineered - and thus are not intuitive. There are close to a dozen hormones involved it this nested - convoluted control loop. To completely understand the system would require the full evolutionary history of life.
BUT! Blood glucose levels matter - healthy people have postprandials below 110. Today, there is about 40% of the public with elevated BG - which shortens and reduces quality of life. Many of these people can control their BG by reducing carbohydrate intake. Some need medicine (metformin etc). The BG rise from low-carb dieters eating excess protein is easily controlled with a little metformin. Long term, these people tend to even loose that last bit of gut - and metformin lowers insulin. (Actually works on the mitochondria - the insulin goes down due to modulating the system).
Some people may be genetically predisposed - but there is obviously dietary factors that are damaging BG control in a LARGE part of the population. No matter if you are pro or con low-carb - you should care about peoples BG. What people are not talking about here is what is CAUSING the damage to BG control. I don't think we know for sure - but excess PUFA's from vegetable oils and frost resistant farm crops are on my short list.
I agree with the main thrust of your comment, that the insulin signal is determined both by insulin sensitivity and by insulin levels. The absolute value of each is biologically meaningless without the other. It's something I've pointed out on a number of occasions. It's part of the reason why it doesn't make sense to assume a person's lipolysis rate will be suppressed because they have high levels of insulin. I don't understand why prominent carb-insulin advocates cannot grasp that concept.
Insulin does affect fatty acid flux across the adipocyte cell membrane, but this process is widely misunderstood and insulin is not the only factor. For example, noradrenaline released by sympathetic nerve terminals in adipose tissue also plays an important role. But another factor, often overlooked, is equally important (or perhaps more important?): substrate availability. If you know your biochemistry, you know that chemical and cellular processes are often profoundly impacted by the concentration of starting, intermediate, and final compounds. If you ate a fatty meal a few hours ago, there will be a lot of fat in your bloodstream (in chylomicrons). It doesn't matter what your insulin levels are (within the physiological range), fat will be transferred from chylomicrons into your adipose tissue because there is a huge amount of substrate. It may take a bit longer if your insulin signaling is lower, but the net result is the same: whatever you don't oxidize ends up as fat in your fat tissue at the end of the day.
It's not like a low-carb diet makes your adipose tissue refuse the fatty acids, leaving them circulating in the blood: that would be easily observed as massive post-prandial triglyceride levels. Yet we don't see that, demonstrating that the fat carried from the digestive system via chylomicrons is being stored in adipose tissue just fine. There are a lot of things that regulate lipolysis, but that does not change the fact that fat tissue takes up the excess calories we eat, regardless of what insulin is doing (with the exception of extreme states like type 1 diabetes, in which there is no insulin at all).
Appetite is suppressed on low-carb diets. Many studies show this. Mechanisms are becoming better understood. E.g.,:
As far as I understand it, one of the roles of insulin is not so much to take care of blood glucose but to shut down lipolysis as soon as other energy substrates are present. And as Stephan mentioned, there is no need of insulin to store fat, acylation stimulating protein will do it.
Same for excess glucose by the way, insulin helps but glucose uptake by cells only require some gradient. Insulin signals pancreatic alpha-cells to stop glucagon secretion. It is VERY important and pre-diabetic people have the problem that these alpha-cells are not listening. So when they eat carbs, glucagon is not shut down. The dietary carbs are making it to the cells but because the endogenous glucose level is still high due to glucagon not being shutdown, it looks like eating carbs are the problem, when in fact it is not. The problem is down in the pancreas. If alpha-cells become insulin resistant, you have a real problem.
Stephan wrote:"... substrate availability. If you know your biochemistry, you know that chemical and cellular processes are often profoundly impacted by the concentration of starting, intermediate, and final compounds. If you ate a fatty meal a few hours ago, there will be a lot of fat in your bloodstream (in chylomicrons)."
Actually, that is true but you have it backwards. Trygly is disassembled into fatty acids just before they are pulled into a receptive fat cell. It is well known in the low-carb world that trygly goes down on low-carb - typically to about 50. (Vegans run typically about twice that and a typical American gulping down sugar drinks (including so-called healthy fruit drinks) can be pushing 200 )
Doctors that use Low-carb diets use trygly numbers to check compliance. What really spikes trygly are fructose containing sugars - something that has been well known science from the Appollo project. For some reason the excellent work of Winitiz, Greenstien etc was ignored.
(the papers here )These studies were synthetic diets on humans - 100% prison compliance - gold standard stuff. Sat fats don't have the same effect. So if you want to lower trygly - eat low carb.
Now after saying all that I don't think that carbs are the cause of the big problem - I think the big problem is identify what is breaking BG control (which then requires limiting carbs or drugs).
This pandemic of T2D(40% of the public now) is killing people, greatly reducing the quality of the last third of a persons life span. My hunch is it is caused by the over consumption of PUFA - pushed on the public with PSA commercials. Genocide?
Medicine pretends to know a lot of stuff that is speculative - but one thing that is clear - non controversial - is that high BG is harmful (particularly spikes - glycating reactions rates are not linear ). It greatly increases cancer rates (cancers typically have broken mitochondria and depend on glycolysis), Alzheimer's, kidney disease, CAD general aging. It is the most important health issue that we can take interventions to prevent. Being fat is bad - but having high BG is a disaster.
If you could take a drug that would make your body store and retain fat - what would it do to appetite? If that energy is locked up - you think you might feel like eating more?
One last point - insulin resistance (when appropriate) is a good thing - you can't lose weight without it. And eating a meal of complex carbs near bed time prevents it. If you focus on insulin sensitivity - and what changes it - instead of insulin, the picture becomes clearer.
Insulin does MANY things - it is the main feedback loop of glucose control in healthy people. It effects way more than shutting down lipolysis. The point I keep trying to make is it is NOT insulin-resistance(better said low sensitivity) that is the problem - it is that the control system is broken. High BG and ( poor insulin sensitivity(not limited to adipocytes) is the consequence of high BG not the cause).
We do not know with certainty what is causing this damage (apparently permanent - restoring historic diets may improve - but will not return optimal health). The bit I suspect is when peoples in the third world quit cooking in their traditional lards or coconut oil and use artificial fats - that is vegetable oils - loaded with PUFAs - that then - with a lag - we see the spread of T2D.
We do know that PUFA induces weight gain - is carcinogenic ( see this and realize that homocysteine goes up with PUFAs and down with O-3 that likely block some of the bad effects of the O-6). It is likely impossible to get to little PUFA in your diet.
See https://wiki.xtronics.com/images/3/38/Omega-6-consumption-from-seed-oils.jpg and
I also think that the idea summarized as "insulin makes you fat" has done a lot of damages in some nutrition circles. There are so many ample evidence that it is wrong, I can't understand how it is still floating around as some truth. Whether someone eats a high fat diet or high carb diet, 1 meal / day or 10, it does not matter. In the end, it is how much you burn vs how much you ingested. There is no way around. Everybody needs to sleep and if I am not mistaken, this is when there is some serious assessment by the brain re energy status. It is a state when you are not supposed to be heavily digesting, in fact you should be in the fasted state for some few hours every day while at rest and sleeping. Avoiding carbs at daytime is nonsensical unless you are frankly diabetic and need blood sugar control (even then, if type 2, you can reverse it by substantial caloric restriction for a few weeks - this will help your pancreas to restore some healthy islet cells by getting rid of ectopic fat). Taubes has really screwed things up for his personal benefit (I am sure he got tremendously rich from his demonizing of carbs). And a lot of followers are surfing on this idiotic wave, see how many "paleo gurus" started lucrative businesses just by spitting out this nonsense mixed up with the modern fable re what our paleolithic ancestors ate!
You are talking about fasting triglycerides, I was talking about post-prandial trigs as a measure of how well dietary fatty acids are transferred from chylomicrons into adipose tissue. The fact that we don't see massive post-prandial trigs on a low-carb diet means the fatty acids are getting into adipose tissue just fine. As well they should-- it would probably be metabolically disastrous if fatty acids couldn't get into adipose tissue.
You asked if there were a drug that makes the body store and retain fat, what would it do to appetite. Probably reduce it, due to negative feedback from the energy homeostasis system.
But what would happen if we had a drug that reduces circulating FFA levels? Would the brain sense it and increase appetite, as Taubes, Ludwig and others have proposed? Such a drug exists; it's called acipimox. It inhibits hormone-sensitive lipase (and thus FFA levels). Despite reducing fasting FFA by half, it has no effect on calorie intake or BMI. This reminds me that I need to write about this paper.
Chylomicrons are pretty much made up of Trygl (85–92%) not FFA. The Trygl are disassembled just before being transported into adipocytes.
Your second paragraph - I just can not follow the logic - fats are a source of energy - locking them into adipocytes would reduce the available energy - increasing appetite. Perhaps you miss-typed?
I work in electronics - with feedback systems - things like PID loops. The P in PID stands for Proportional control - the signal is proportional to the homeostasis error. Normally the feedback signal stays in a very narrow range - unless the sensor or actuator is broken! Once someone has T2D - carrying too much fat, we see that the BG control loop is broken.
BG control is not that simple - but when we see high BG the assumption is it is the fault of low insulin sensitivity. But if adipocytes are full, there should be low sensitivity - in fact it is needed to return the fats(energy) to the system.
Again - in normal people - when we eat - excess carbs are turned into nice safe 16C SATfats via DNL a one-way process. Then excess dietary fats and these are stored in adipocytes and released later as BG goes down - insulin as well and the flux of FA reverses providing energy.
What is happening is something gets broken - people gain weight - put them on a good diet and they will even catabolize muscle while retaining fat (really bad if that is heart muscle). They have lots of calories in their fat tissue that they can't use. The loop is broken. The people are hungry - burning up muscle fibers to maintain BG instead of burning fat. To release the fat, we need insulin resistance that isn't there. If linoleic acid from over consumption of veg-oils is causing inappropriate insulin sensitivity - we get hotel California of FA.
As far as Taubes and Ludwig - I don't think they get the whole picture, they are only looking at some of the moving parts.
Interesting paper - notice that these were obese people - broken metabolic systems. In your paper, with the changes you list - it is sad they are not losing weight. You once wrote that trygly can block leptin from the brain - I could not find the paper this was based on, but I can see it could explain the fructose-> trygly excess eating pattern seen in some papers.
I said: "One of the roles of insulin ...", not "the sole role of insulin". It is known that insulin has many roles. But consider this:
- how much insulin is required above basal level to shut down lipolysis ? Not much. And that should tell you how important it is to have lipolysis shut down as soon as a slight increase of insulin occurs, more so than clearing away blood glucose from dietary carbs if one looks at the magnitude (and you will also note that in type 2 diabetic people, fat is not trapped easily in adipose tissue during this normal process -> big problem ...)
Moreover, you can't talk about insulin without talking about glucagon and the paracrine effect of insulin on prancreatic alpha-cells. The role(s) of glucagon is (are) as important as insulin and some of them are still poorly understood. In any case, glucagon must shut down when insulin tells alpha cells to stop secreting it. It is very important. The only time when the balance is more nuanced is when you ingest proteins only. Glucagon will ramp up first because insulin is needed for amino acid dealing. If glucagon was shut down as in dietary glucose dealing, we would be hypoglycemic because of protein digestion. That is of course not happening because in this case, the ramping up of glucagon by some amino acids keeps our blood glucose level in the safe range.
So, a lot of these processes are convoluted and can't be isolated. But this is what all the low carb'ers are doing, they isolate one process, namely: insulin increases due to elevated blood glucose from dietary carbs -> lipolysis shutdown -> trapped fat in fat cells. And from there, they conclude that carbs make you fat. This outstandingly stupid.
I realize that chylomicrons are made primarily of triglycerides. The point is that triglycerides are just a storage form of fatty acids, and FFA are the form of fat that is the primary circulating energy substrate. Muscles don't take up triglycerides, they take up FFAs. So FFA and glucose are the primary circulating energy substrates of the body. They are the fat and carbohydrate counterparts of one another, physiologically speaking.
You are assuming that reducing the blood supply of FFAs would induce appetite, based on how you think control theory should apply to the system. What I'm telling you is that reducing FFA levels in humans doesn't appear to stimulate appetite or cause weight gain, regardless of how illogical that might seem. Empirical evidence always trumps theory in biology, because biological systems are too complex to predict accurately and they don't always function optimally.
The brain measures many signals in its efforts to maintain energy homeostasis, and some of them are more important than others. The study I cited in my previous comment suggests that FFA levels may not be an important signal that feeds back on appetite in humans.
The reason I said that sequestering fat in adipose tissue might suppress appetite is that leptin is an important appetite negative feedback signal, and it's secreted in proportion to fat tissue mass. So higher fat mas would increase leptin, and higher leptin would increase negative feedback on appetite. I don't know if this would actually be observed, but you asked me to speculate and that's my guess.
Again - in normal people - when we eat - excess carbs are turned into nice safe 16C SATfats via DNL a one-way process.
Unlike excess dietary fat, carbs entrain their own oxidation. Only when everything that could be burnt was burnt does excess carbs get converted to fat, and that is quite a small fraction overall (and note that it is in the context of overfeeding). Fat overfeeding does not do that, fat oxidation is not ramped up.
There is actually a good simplified summary of how all this works at this link:
It is sort of understandable by a layperson.
Try a low carb diet (as in having micros of 5% or 10% low carb) and then I'll buy your book. Too bad. Very attractive cover art. I was pretty close to buying it till I read these comments.
Thorgal, then how is it I eat 500+ more calories a day "Paleo style" than I did eating the Standard American Diet, yet I lost and have maintained ~25 lbs of weight loss? I also cured my pre-diabetes, and lowered my triglycerides and A1c. Magic?
At one time you made the interesting point that elevated trgly were blocking the BBB for leptin:
It seems if one lowers FFA and trygly as they did in the paper you pointed to that these men should have lost weight if the trygly was blocking the leptin feedback - but they didn't.
I'm not even sure we even have good definitions of appetite - I know I've had times when I felt inappropriately hungry a few hours after eating refined carbs. I also know that if I fast - the initial hunger goes - but is replaced by a different sensation - sort of a weakness that is cured with eating - but not at all the same sensation as the initial hunger. Perhaps some day brain scans can objectively show the difference and I think there could be even more forms of hunger. Some people crave salt - others metal tastes.
Curious where the emerging evidence on gut bacteria fits into this. Some in the press seem to want to push the idea of obesity being caused simply by bad gut bacteria. Stool transplants might be the fix people have been waiting for. I've even read this associated with hunger.
Of course when it comes to this subject the media always seems to want to report a "solve all" solution, so I'm guessing this is overhyped. Still I think it's worth asking the question.
It's worth mentioning that even if this is the case the same simple advice seems to apply. Eating whole foods and not processed foods is the proper diet (whole foods having bacteria in them along with the other benefits that are well documented).
Well-written and backed up by solid research, unlike the questionable theory put forth by Lustig and Taubes. Also of importance is epidemiological evidence, such as number 10 on your list. Traditional Japanese diet is very high in starch and carbohydrates while low in fat. By Lustig's theory, the Japanese should be the fattest people on earth, yet the longest living Japanese and elderly Japanese tend to be slim, and they are the ones who still eat fairly traditional diet low in fat and animal protein, and high in starch. The younger Japanese are not as healthy however, because their diet is starting to mirror Western diets, as in higher in animal protein and fat. I'm part Japanese so I know of that food culture well, and the traditional Japanese diet high in carbs and low in fat and protein, did not/ do not lead to obesity or type 2 diabetes the way that Lustig's theory, if correct, would be a glaring example of a population ravaged by obesity and ill-health.
You managed to shift your caloric balance. If it's not decreased CI, it is increased CO. If you think that a "paleo style" diet is what it takes to get back to normal weight, that's fine too. Whatever works for your energy balance, really.
There is no magic foods or food combo. In the end, it all ends up as nutrients ready to be metabolized. Your health status was probably much poorer in the past and you took some lifetysle decisions that helped improve your health, including boosting your metabolism. You should be glad to have found a way to do so. But don't stick to idiotic dogmas because you are not incontrol of all the variables (sleep quality ? vitamin status ? more unconscious physical activity ? etc). In the end, it's all about the energy balance. And whatever helps it, whether conscious or not, is good. But there is no need to hide under the "paleo" umbrella, there is no magic in it at all. You could have achieved weight loss with the Twinkie diet" : http://www.themarysue.com/twinkie-diet/ which in this case is a CONSCIOUS CI reduction. It is of course not sustainable, one shouldn't be conscious in the long run of how much one eats because it leads to orthorexia. And make no mistake, many in the paleo circles are suffering from it. You can maintain perfect weight and health with proper and regular grain and legume consumption. In fact, dietary constraints (conscious food avoidance for no reason other than fear of weight gain) is a slippery path. I've been on this path myself way back, and in the long run it is absurd.
Today, I eat whatever I want and I don't gain bad weight. I am very active physically and sleep good. I enjoy sunshine whenever I can and don't stress too much about things. The occasional piece of cake remains just that, a piece of cake and not more. If you feel like engulfing a whole cake and more every day, you have a problem. My appetite is well regulated, and I have some occasional periods when I don't eat much (balancing other times like Xmas or birthdays where I won't think twice about eating what is on the table).
I see your point here although I feel like it may be a bit misleading to some. For instance, in #8 you mention that food that caused increased blood levels of insulin were found to be more "filling" thus reducing hunger.. I think it's important to make the distinction that real foods such as sweet potatoes and tubers cause spikes in insulin as well as twinkles and cupcakes. I think it would be helpful for you to include the foods of reference as your points may be taken out of context.
I can definitely attest to the importance of not overeating. I was raised to clean my plate and, when serving myself at the buffet, not to worry about excess quantity since I was young. I believe the reinforcement of those mentalities either inspired or enabled me to FILL my plate and eat every bite...oh, and skip the vegetables and bring on the desserts!
Combined with a sedentary lifestyle, that borderline neurosis led me to incipient obesity. In college, when I wanted to slim down, I still made questionable food choices and had dessert at most meals. Had trouble implementing discipline.
I discovered low carb and lost 20 lbs at 28 years old, and so of course bought into the insulin boogeyman hypothesis. Predictably, that worked until it didn't.
Then I tried a couple of experiments much higher in carbs and lower in fat (as well as calories in general), and reached a considerably lower weight than on low carb. My most recent one involved no fasting, but rather focused on filling up with non-starchy vegetables & fruits, holding the starch down to a few bites per meal (if at all), banishing all but trace amounts of oil/added fat (usually on potatoes...at the mercy of a military dining facility here), and limiting animal foods to only smallish portions eggs and seafood (going full vegan for many meals, when neither was available). The weight loss was effortless & included almost no hunger (the few instances of hunger were mild & typically about four hours after the previous meal...i.e. totally normal). At 72" height, dropped from 175 lbs to 165 in 10 days on that one (a previous experiment with resistant starch & a few 24-hr fasts got me down to 158, but that took two months). It was during this experiment, eating at every meal & feeling plenty satisfied, that I realized just how causal my previous QUANTITY of food was in my higher weight. And it was all psychological...I had only been filling up my plate with more calories due to a mismatch between my body's true energy needs & my brain's conditioned decision making. I had also been living in some willing ignorance about just how calorically dense that fatty meat and those big scoops of rice/potatoes were.
Is weight control determined primarily by CICO, or food quality, or macronutrient quantity? People hate this answer, but it is just not that simple. None of them is solely responsible as if in a vacuum. Elements of all three play a role. You simlly cannot eat processed, highly palatable, addictive garbage and expect your metabolism not to go haywire and scream for more...or your body chemistry WILL sabotage your efforts to manage CICO (must keep stress low for the same reason...plenty of sleep, limit hard exercise, and keep a cool attitude about life). Nor can you gorge on either fats or carbs, even "whole" ones, in biologically (evolutionarily) unadapted quantities & pretend the calories don't add up & the hormones don't go out of whack. And you have to satisfy your appetite with mostly low-density (but high-nutrient!) food choices...just like our ancestors did when they chewed on leaves, roots, & berries after an unsuccessful hunt! If you MUST eat dense food, fill the plate only halfway up & force yourself to wait 10 minutes after the last bite before returning for seconds...at which point you must honestly assess whether you are truly hungry for more or just scratching a psychologically conditioned itch. Restrain yourself enough in this way, and your habits will reset. Weight maintenance will then lose much of its tedium.
I denied the role of CICO for a long time, partially due to my own easy, fleeting weight loss on low carb & previous failure to educate myself and apply dietary discipline. But CICO is ABSOLUTELY applicable, even on a whole foods diet.
(Footnote: my constant second person references of "you" are of course directed at no one in particular...just a product of my sophomoric rhetorical skills) :-)
Correlation does not show causation - several moving parts here - not just insulin. Hard to demonstrate insulin is what makes food seem 'filling'. Insulin has been successfully used to treat anorexia for a long time. Insulin has a complex feedback loop with serotonin - involved in appetite. Insulin effects a lot of things besides BG.
One of the things we(or at least some of us) have known from back in the 1960's is that carbohydrates (and tryptophan) increase serotonin - the feelgood (or at least safe) neurotransmitter. (See Wurtman's old papers).
Like most control systems in the body - nothing is static - the post synaptic serotonin receptors down regulate when serotonin is chronically elevated - and just like discontinuing SSRI antidepressants, there is a rebound effect if one suddenly stops eating carbs - there are some that see excess carb consumption as a form of an addiction (same for the SSRIs - did your doc warn you? $Bs of profit from legal addicts? ).
See - more below...
I still think that if someone takes a drug that changes the fatty-acid flux to fat gain that they will eat more - an increase in appetite. The only other alternative is they would move less - dieting people move less - I think people free to eat will eat instead. Energy-in - energy-out = stored energy. If people store more - they will replace the un-available calories by eating.
If there is less trygl, ketones, and FFA available, cells burn more glucose thus inducing appetite - Clearly people have to consume more calories to gain weight. What causes people to consume more is appetite. Stored fat does send a signal via leptin(which isn't strong enough to stop the obesity pandemic) - but if the fat is stored due to a drug - there is an immediate energy imbalance that indirectly reduces BG - inducing more appetite.
A drug that induces fat gain - exists - called PUFA - particularly bad if it is linoelic acid(Look up AA ).
Back to appetite - I don't think it is well defined - there is the urge to eat 'comfort foods' - high carb foods that up serotonin - there is the urge to eat when blood sugar falls, leptin, serotonin, ghrelin,NPY -- and more - see
https://en.wikipedia.org/wiki/Orexigenic (hmm - that list includes insulin ) - the subjective experience from different causes may vary by cause - what matters is if that experience leads one to eat - and what they eat.
I can imagine that insulin as an indirect appetite stimulant - I think of it more as a BG feed-back signal - and switching from burning carbs to fats(in healthy people). The key is that this signal increases fat storage relative to insulin sensitivity (which varies all over the place over the course of a day). There is clear research that shows it's effect on LPL and HSL.
Eating food is really important - if appetite does get people to eat - death is the result. Thus, I think there is little surprise that multiple systems have evolved that prevent a single point mutation from being lethal. The urge to eat is not a single factor control loop. Thus I think Taubs and Lustig have over simplified why low-carb works - insulin is involved, but so are a list of other things.
Eating purified vegetable oils does cause weight gain - thus effects appetite.
Dietary linoleic acid elevates the endocannabinoids 2-AG and anandamide and promotes weight gain in mice fed a low fat diet.
Not only that but CAD:
18:2 ω-6 linoleic acid increases LDL oxidation (oxLDL ( not regular LDL) is the bad lipoprotein that stimulates the inappropriate immune response that causes CAD )
A high linoleic acid diet increases oxidative stress in vivo and affects nitric oxide metabolism in humans
A very small amount of Linoleic Acid is needed in ones diet - but not huge amounts being consumed.
while you can get a strong insulin response from fat-and-protein mixes such as beef or cheese, comparable to those from pure carbohydrate (and greater than seen with isocaloric pure protein) this is balanced with a glucagon response, which is lipolytic, and of course insulin plays a role in protein synthesis - an insulin molecule bound to a receptor on one type of cell may not be available afterwards for use by another. You will only get a noticeable glucagon response from pure carbohydrate in decompensated diabetes.
There seems to be very little to no insulin response to feeding pure fat in the fasted state, yet the strongest response is probably to fat and carbohydrate combinations.
These differential insulin responses to components of weight loss or fattening diets are thus probably not so paradoxical once the effects of the other hormones released in response to the nutrients are factored in, and once the divergent fate of insulin in different contexts is considered.
Why do you think low carb diets are so effective? If our food infrastructure became LC friendly, making LC easy to follow, would food companies make hyper-rewarding sugar-free foods thus resulting in just as much obesity? Can you make a hyper-rewarding LC diet that produces obesity as readily and a high carb one?
Ludwig posted a response to this on Medium. I think he clearly hasn't read a lot of your work as he misses a whole lot of data and topics you have discussed (i.e. insulin action, the difference between overfeeding studies and our actual food environment). I wish he had done some more digging and been more thorough before he published this.
It has been my feeling that sugar is, believe it or not, being ignored in all of this.
The Japanese don't eat ANYTHING like the amount of sugar Americans eat.
Excess protein can be problematic too, particularly for the insulin resistant. http://optimisingnutrition.com/2015/07/06/insulin-index-v2/
Why does it have to be so black or white one way or the other? Insulin versus calories?
The recent study by Chris Gardner showed that everyone benefits from a whole food, nutrient dense high fiber diet and naturally decreases calories leading to weight loss and better blood markers. However if you were insulin resistant you did even better on a reduced carbohydrate approach that stabilised blood glucose and reduced insulin.
How about a nutrient dense, whole foods, high fibre approach with an tailored to your insulin resistance / ability to achieve normal blood glucose? e.g. http://wp.me/p5VAQF-64
Whilst I do not agree with your flexibility (if that's the right word) on carbs YMWV you are absolutely spot on in relation to why we overeat. HF foods can be just as rewarding. Yes maybe I can't scoff down as much cheese/nuts as opposed to a junky carby sugary treat, but the energy density excess will still park on my gut regardless. Even eating bland foods is not the solution, for instance adding boiled, cooled potatoes created some kind of inflammation reaction that set me off on a binge. Meat and veggies, adequate fat seems to be best bet, complete avoidance of problem foods (people like me can't do moderation). I'm looking forward to your book. If you can address the reason/solution to why I can eat a full wholesome meal to satiety and then continue to be hungry and white knuckle the rest of the day then you can offer some hope to us binge eaters. Is it insulin driving me to keep eating and eating or my brain.
@ Genia and those who think that CICO is relevant
You need to read the rebuttal that is posted by Dr. Ludwig at https://medium.com/@davidludwigmd/ludwig-responds-to-whole-health-source-article-93d8e1667477#.9navn9kbt
What may seem obvious and well researched might seem less so.
Re your reference "Dietary linoleic acid elevates the endocannabinoids 2-AG and anandamide and promotes weight gain in mice fed a low fat diet", there is a recent post over at Hyperlipid (Peter Dobromylskij)in which he writes about this paper. Thought you might not have seen it.
Why do you think there is so much emphasis on insulin-carbs in these irrelevant debates when chylomicrons and ASP are what drives fat storage even in the absence of insulin ?
I don't get it. In all this internet noise produced by all the LCHF nonsense, we never hear about these fat storage drivers. P. Attia even formerly called his website "The War on Insulin". How can you get more ludicrous ? Why not "War on ASP" ? Read the review linked above, ASP deficient mice do not get obese and yet eat more than mice without the deficiency. So WTF are these low-carb gurus talking about ?? Insulin is definitely a master hormone for nutrient transport and all sorts of signalling in relation to metabolism. But fat storage is chylomicrons and ASP more than insulin. I also fail to hear these guys talk about glucagon. Always insulin, it's like there is nothing else in all the complexity of our biochemistry and energetics.
To a large extent, the attempt to conclude this stuff based on isolated observations of singled out hormones is going to end up leading down endless rabbit holes of complexity, and moreover never settle the issue. Yes, scientists can observe correlations with insulin in the ways Lustig, Taubes, et al describe. And yes, that seems to make a case for the carb boogeyman hypothesis.
The problem is, countless anecdotes of people gaining weight on a low-carb, low-insulin diet (often in a reversal of initial weight loss following a plateau) "prove" that hypothesis incorrect. I use the quotation marks because I know people think anecdotes are useless, but they aren't. Anecdotes tell us whether an attractive, even seemingly perfect, hypothesis works in real life, where real choices are made in a living context.
Lustig & the others should not waste their time in such vigorous and steadfast denial of CICO, because doing so destroys their credibility. When you honestly assess this beast of CICO & hormones, it is a real chicken or egg conundrum, with virtually infinite confounding variables...not a black and white situation. A serious researcher who wants to find the truth--rather than proselytize and ignore contrary views--will frame his data and observations in such a context.
I'm well aware of glucagon - this post was about insulin. Also - ASP levels appear dependent on, once again, insulin.
But - I actually in a way agree: I repeat, looking at insulin levels by themselves is meaningless - it is a feedback signal.
But of course it is much more complicated than what either side of the low-fat/low-carb debate is talking about - a huge number of moving parts.
IMO long term weight loss via low-carb seems more likely than low-fat - but all types of diets don't work very well - and people on higher carb diets don't start out gaining weight - my hunch is it takes the excess consumption of PUFA (particularly linoleic acid?) to break the control system - and the damage appears permanent. But I could be wrong.
Many of these signals have non linear effects, - some are released in pulses - the control is sometimes under-damped(slightly oscillating) - pulses of hormones are released(thyroid). The control loops are nested and interconnected. Most of the researchers do not have a good understanding of control loops - and evolution has created an amazingly complex system that humans tend to think of as 'designed' when biology does not take engineering approaches - it is evolved. To tease out which link in this system gets broken and why is very hard - might require the development of AI to sort it out.
Here is a drawing I once made trying to sort out thyroid regulation - I'm sure it has errors and is incomplete - lacks magnitude effects/nonlinear features - but there are lots of moving parts - weight balance is also this complex.
That being said - if I have high BG - I'm going to avoid carbs - The level of BG has exponentially increasing bad effects - glycation of lipids - leading to oxlipids. The best single way to reduce my cancer rate is to keep my BG low (cancers depend on sugars to out grow the immune-system).
The study you cited is referenced in the review I linked to. What you read in it is like "insulin's influence on ASP prod is minimal", the real driver is the concentration of chylomicrons by far. I don't recall that the latter transport carbs ...
Moreover, from the abstract of the same study:
"As with ASP, glucose, oleate, insulin, and hepatic lipoproteins (VLDL, LDL, and HDL) had little or no effect on C3 secretion. In contrast, CHYLO had an even greater effect on C3 secretion than on ASP generation. Finally, the effects of CHYLO on generation of ASP and C3 were not dependent on lipolysis of CHYLO by lipoprotein lipase (LPL). These results are consistent with the changes in plasma ASP seen postprandially, and suggests a role of ASP as a positive feedback regulator of triacylglycerol synthesis in adipose tissue"
Basically: eat fat and it goes straight into storage.
And that's fine. It says nothing about weight loss or gain. This goes back to CICO, the most "useless among all explanations" but a rather good pratical guide for weight maintenance if you don't stress too much about food labels.
If in doubt, don't forget to feel real hunger once in a while ...
For those interested in control systems, see the following two free papers:
Mathematical models of energy homeostasis
Ratchada Pattaranit and Hugo Antonius van den Berg*
J R Soc Interface. 2008 Oct 6; 5(27): 1119–1135.
Published online 2008 Jul 8. doi: 10.1098/rsif.2008.0216
Modelling adipose tissue production and the development of obesity
Problem proposed by Jim Maas1 and James Smith1,
report by John Ward2, Jonathan Wattis3 and Jan Bouwe van den Berg4,
additional work by John Fozard3, Natasha Li5, Eleanor Norris2,
Colin Please6, Derek Tan5, and Henry Winstanley4.
It amazes me how easily we're taken in by the same magic tricks over and over. This is the day I hit the Powerball jackpot. Same logic applies to carb insulin theory: this is the day that eating a plate of bacon and eggs with a cube of butter will fix my obesity.
The next day the sun comes up. Back to 7-11 for another Powerball ticket. This is the day Dr. Oz will fix the obesity, with this maple bar, a can of Monster and ayurvedic herbs.
We're sleepwalking through history.
If that's true then LC is just a trick to reduce eating. No magic, but further confirmation that CI is fundamentally correct. Unfortunately CO goes down eating butter sticks instead of the carby foods that will get you through the 1000 calories a day of activity Cordain recommends.
I have thought about creating an index of Paleo compliance, giving 75% weight to CO and 25% to eating the optimal CI. For CO I cite Cordain's estimate of 1000 kcal/day expenditure for HG's.
So a person could be 75% paleo eating wine, pasta and bread (like Ancel Keys) if they put forth the Paleo effort. Few do.
Personally, I'm at about 800 calories a day activity and eating 25% Paleo-Approved foods, so would self-score around 65% Paleo. Jack Lalanne would score higher - at least 85%. Robert Atkins would score well under 50%. Sedentary HFLC dieters would be lucky to score above 25%.
The same could be done for Med or Okinawan diet compliance, but I'd still give higher weight to CO than CI.
What is Real is a question for storybook rabbits. There are better and worse foods, but they all metabolize. Muscles don't care whether it's cake or steak.
@thorgal @bret Ancel Keys' starvation study might be instructive at this point, because the effects of controlled CI and CO are so well documented over a 6 month period. For CI, 1500 kcal per day of potatoes and cabbage, with unlimited chewing gum. A moderately low calorie HCLF European post-war starvation diet, with very poor nutrient quality. For CO, 22 miles a day walking. I estimate this to be about 1500 calories per day effort over and above BMR. Net/net, a sustained deficit of 1000-2000 kcal per day.
The psychological and physiological effects on the participants are fascinating. The extreme obsession with food. The lethargy. The guy that threatened to kill Keys. The insatiable hunger which continued for a long period post-study. In losing a lot of weight over a short period, going from obesity to normal weight, I could identify with much of what they experienced.
I have a lot of respect for Keys' rigor in controlling his experiments. Unfortunately he also established a pattern for many of the "soldier nutritionists" of the future. Atkins, vegans, the Med, Paleos, etc. etc. etc. all follow this rigorous "you can eat this, but you can't eat that" form. This methodology jams normal square peg omnivores into round unsustainable diet hellholes. CICO (or as Keys called it Scientific Reducing) is one of the few methods that allows unlimited food choices.
@karl. The easiest way for me to lower blood glucose is to go for a walk. Weight loss, bike riding and carb elimination work too. Each has drawbacks compared to walking, which is effective immediately.
From the paper Karl posted,
"Insulin increased ASP production up to 2-fold (208% IS%, P< 0.01). However, the most profound increase in ASP was generated by the addition of chylomicrons to the cell culture medium. Chylomicrons (CHYLO) obtained from postprandial plasma increased ASP production in a time- and concentration dependent manner, producing up to a 150-fold increase in ASP at the highest concentration of CHYLO tested (500 yg triacylglycero1,"L medium ( P < 0.001))."
When is your book coming out, Stephan? I plan on buying it.
@Bret as an N=1 who lost 50 pounds using CICO I found Lustig's and Taubes' assertions offensive. I'm sure that carb avoidance benefits people greatly in weight loss. But IMO any food avoidance strategy which accomplishes a reduction in CI is effective, whether it involves carbs or fats, or more simply reducing the consumption of both.
Despite the fact that I still eat grains, sugar, saturated fats and processed foods, I have measurably better health than I had 9 years ago. My blood pressure is lower and HDL is higher, resulting in a very low Framingham CVD risk score. My triglycerides are under 50. My previously out-of-control blood glucose is under 100. I exercise more, eat more, and maintain the weight loss by continuing to use the CICO model.
Today I will eat a basket of fries and drink a glass of red wine while watching the Super Bowl. None of my health factors will vary as a result, because most of those calories will be metabolized while I ride my bike home. My bike is essential to CICO. But carb insulin theory is as relevant to me as my bike would be to a fish. It may be relevant if you're obese and sedentary, but weight loss and activity render it meaningless.
That Keys starvation study is interesting indeed. I have read abundant anecdotes of folks whose metabolisms seemed to erode and ultimately sabotage their resolve, the more extreme the energy deficit. Leads me to believe the CICO-based approach likeliest to work for the most people is one that takes things slowly and steadily, like investing for retirement or paying off a mortgage. Perhaps a 10% daily deficit under baseline is where I would start if I were to be very meticulous about it. But then again I like to think less about numbers and instead let my own hunger signals guide me, which is why I gravitate towards high-volume, low-density whole foods (high-density/processed food have always correlated with disaster for me... I always run out of time or motivation to enforce appetite discipline on myself for prolonged periods). But everyone's mileage varies, as in anything else.
Now, I'm not an Atkins apologist or activist, but my understanding of his protocol is to spend the first couple of weeks filling up on fat to the exclusion of sugar and starch, and thereafter eat normally, but with firm restriction of starch and fruit to mild doses. No restriction or discouragement of low-density vegetables that I am aware of, and no exhortation to gorge on animal products (I'll humbly admit to being wrong if someone produces contrary evidence). Not exactly what I would call a carnivorous extreme. I think the Atkins diet got that reputation due to merciless misrepresentation in the media and academia.
I've eaten PUFA's for 9 years and have regained 5 lbs of a 50 lb weight loss. For me PUFA's are food. They're not a weight gain drug.
Of course you can make LC hyper rewarding. Put cream or butter in your coffee. Eat bacon and eggs with lots of salt. Do you think Atkins got plump and jowly eating boiled beef liver?
My bad again...starvation study walking was 22 miles a week, not per day. So daily calorie deficits were probably under 1000. Typical high rate weight loss, though pretty extreme for men starting at a healthy weight.
Well you can control your blood sugar with either low carb or low fat high carb, I have done both. Both have their merits and it depends on the individuals response.
I am not a scientist, so I can just respond to this as a longtime fat person.
I like the Always Hungry Diet because it worked for me when most diets didn't.
I'd lost about 40 pounds over 16 years by slight calorie restriction and activity increase. But once I went through menopause, it didn't matter that I was walking 2-3 miles a day - I very rarely lost weight and actually gained a little. I also craved carbohydrates all the time.
Since starting the Always Hungry diet, I've lost about 15 pounds. Granted, that's less than a pound a week, but the trend is continuing downward. I'm walking about 3 miles a day and I am counting calories (though I expect younger people on Always Hungry might not need to be as careful about that). And I'm not craving carbs the way I used to and can usually by satisfied by snacks like an apple or a piece of cheese.
I happened to have my annual physical five weeks after starting the Always Hungry? diet. While my blood sugar was unchanged over last year (95), all of my cholesterol levels had improved by about 20%. That was the first time in about six years that my cholesterol levels hadn't creeped upward.
Dieting isn't a "one size fits all." I know there are people on the Always Hungry diet who report no weight loss, but most people report some and a few report quite a lot of weight loss. I always hated the tiny pieces of meat, no cheese and lots of salad diets and could never stay on them. But I've learned how to eat better this year and plan to stick with Always Hungry until I lose about another 45 pounds.
Here's Dr. Ludwig's response: https://medium.com/@davidludwigmd/ludwig-responds-to-whole-health-source-article-93d8e1667477#.hfz7isyht
10. Billions of people globally eat high-glycemic diets and remain lean. Many traditional diets are very high in starch and low in fat. If foods that promote large blood sugar and insulin spikes were the primary factor in obesity, shouldn’t these people be obese?
"So-called “ecological” studies comparing different populations comprise the lowest quality epidemiological data. The white rice consumed by peasants in China may keep them from starvation — but that says nothing about effects in other populations. Now that those individuals are moving to the cities, taking their high carbohydrate diets, but leaving behind the high levels of physical activity, rates of obesity and diabetes are skyrocketing."
The first problem with that argument is that many cultures eat (or ate) high-carb, high-glycemic diets and are (or were) not on the brink of starvation. These cultures are (or were) among the leanest in the world. All you have to do is look at the diets of high-income Asian countries like South Korea. South Koreans have plenty of food, so why are they so lean eating a diet that's based around white rice?
The second problem with the argument is that these high-carb cultures eat less carb and more fat as they urbanize/industrialize. So the increase in obesity and chronic disease is associated with decreasing carb intake, decreasing glycemic load, and increasing fat intake in these cases. See this paper for example:
I responded to other points in his response here:
The subjects we're required to walk 22 miles per week, not 22 miles per day.
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