Which would explain a lower than western prevalence of obesity, but you still need some obesity to start that accumulation.
No, the high blood sugar during gestation in an otherwise non-obese woman can grant differential insulin resistance to her child, who then, under the same diet as her mother, ends up being obese instead of normal weight.
And I don't think many starchy tubors are low GI, they're not all potatoes but they should still have a decent glycemic index.
Let's find a study that actually measures the glycemic index of Hazda foods then.
The system we're interested in has to do with eating, appetite, activity, excretions, as well as fat accumulation.
The problem is that it very well may be that eating, appetite, activity, and even excretions, are driven by fat accumulation. And what I mean by that is that if the *first* order cause is fat accumulation, and that makes you hungrier, and lazier, and makes you eat more, and perhaps even excrete less, we need to be able to discern that.
Put another way, the orders of magnitude here are important, and I don't think that simply because the system is complex that all factors are of equal weight.
Part of this is at the end of the day I've found it's generally not profitable to argue with the textbook.
And it's a good thing that despite that there are some people out there who are willing to argue with textbooks:)
The sad fact, and Taubes exposes this extraordinarily well in GCBC (even if you dismiss his conclusions), is that the nutrition science in this country has not been driven by science, but by pre-determined agendas, be it to sell more cereals and grains, or to demonize meat eating, or to prop up a pet theory by a powerful government science administrator.
Honestly, more than a science book, I found Taubes work to be more interesting on the history side of the equation.
I'd really suggest you follow Guyunet's blog or something similar for a while and approach it with an open mind.
I actually read Guynet quite avidly - especially the comments. He comes off as passionate, but misguided and oddly defensive. Now, perhaps my opinion is colored by the fact that I've got differential insulin resistance, and while the insulin hypothesis matches my anecdotal experience, the "tastiness" hypothesis is actually 100% opposite of my reaction to food. I'm not above imagining that it's *possible* that there's someone out there who is terribly driven by "tastiness", but still doubtful that those urges can result in obesity if there isn't chronic insulin elevation and differential insulin resistance. Again, though, the proper metabolic ward experiment and I could be convinced that it's possible.
"In biology, and specifically genetics, epigenetics is the study of changes in gene expression or cellular phenotype, caused by mechanisms other than changes in the underlying DNA sequence"
The womb environment is a mechanism other than the underlying DNA sequence.
that's a very long way from explaining why the Kuna have no obesity since the obesity has to start somewhere and 25 tsp a week is a good place to start.
Read GCBC. Check it out from a library if you don't want to funnel cash to Taubes. The clear, obvious history of the path of diseases of civilization show a pattern of taking hold as generations pass. The Kuna are in for a rough ride if they continue their habits, and there's no reason to believe they'll be an exception to other native cultures who were introduced to refined carbohydrates - unless you believe they've got some sort of genetic mutation that allows them to be immune to the diseases of civilization.
Except they were also eating a lot of berries, starchy tubors, and fruit.
I find it hard to believe they were actually low glycemic.
But they are. Hell, baobab is *advertised* as low glycemic, and none of them are refined to increase glycemic index.
And the other culture eating white sugar sweetened beverages along with fruits. The model doesn't fit.
The impact of white sugar consumption accumulates over generations, as demonstrated by the gestational diabetes paper.
Sorry, not bothering.
Your loss:)
It's not a caricature, you're convinced insulin resistance is the driver of obesity
Let's be specific. Differential insulin resistance is the driver of obesity. You keep focusing on "look at this group that eats low glycemic, but high starch and fructose, but isn't obese!", while ignoring the necessary factor of differential insulin resistance.
Why do you continue to refuse that factor as part of my position, and simplify it down to "insulin"?
if you want to understand the system you have to actually study the system
Which has been done in depth with the Kreb's cycle, and the basics of fat accumulation biology. Now, perhaps your position is simply "there is no good answer, and I'm annoyed at Taubes for asserting he has one" (ignoring your support of Guynet for the moment) - but you seem to be wilfully ignoring the study of the system that has occurred.
My actual beef is he's ignored decades of very high quality research and knowledge
Odd. You don't seem to hold that research and knowledge up to the same level of scrutiny:)
"You can have type 2 diabetes with or without differential insulin resistance"
Here's the relevant passage from the first quote:
"some tissues might become resistant to insulin while others continued to respond normally, and this would determine how the damage done by the insulin resistance would manifest itself in different individuals"
Here's the relevant passage from the second quote:
"In certain individuals, they suggested, the insulin secretion after eating these carbohydrates would be “disproportionately large.” “The carbohydrate is disposed of in three sites—adipose [fat] tissue, liver and arterial wall,” Stout wrote. “Obesity is produced."
Do you have a cite for the differential insulin resistance?
From GCBC:
"By 1965, Yalow and Berson had suggested why these adult-onset diabetics could appear to be lacking insulin—manifesting the symptoms of diabetes, high blood sugar, and sugar in their urine—while simultaneously having excessive insulin in their circulation: their tissues did not respond properly to the insulin they secreted. They were insulin-resistant, defined by Yalow and Berson as “a state (of a cell, tissue, system or body) in which greater-than-normal amounts of insulin are required to elicit a quantitatively normal response.” Because of their resistance to insulin, adult-onset diabetics had to secrete more of the hormone to maintain their blood sugar within healthy levels, and this would become increasingly difficult to achieve the longer they remained insulin-resistant.*51
A critical aspect of this insulin resistance, Yalow and Berson noted, is that some tissues might become resistant to insulin while others continued to respond normally, and this would determine how the damage done by the insulin resistance would manifest itself in different individuals. So “it is desirable,” they wrote, “wherever possible, to distinguish generalized resistance of all tissues from resistance of only individual tissues.”"
Also:
"In the late 1960s, Robert Stout of Queen’s University in Belfast published a series of studies reporting that insulin enhances the transport of cholesterol and fats into the cells of the arterial wall and stimulates the synthesis of cholesterol and fat in the arterial lining. Since a primary role of insulin is to facilitate the storage of fats in the fat tissue, Stout reasoned, it was not surprising that it would have the same effect on the lining of blood vessels. In 1969, Stout and the British diabetologist John Vallance-Owen pre-empted Reaven’s Syndrome X hypothesis by suggesting that the “ingestion of large quantities of refined carbohydrate” leads first to hyperinsulinemia and insulin resistance, and then to atherosclerosis and heart disease. In certain individuals, they suggested, the insulin secretion after eating these carbohydrates would be “disproportionately large.” “The carbohydrate is disposed of in three sites—adipose [fat] tissue, liver and arterial wall,” Stout wrote. “Obesity is produced. In the liver, triglyceride and cholesterol are synthesized and find their way into the circulation. Lipid synthesis is also stimulated in the arterial wall and is augmented by deposition of [triglycerides and cholesterol]which in a few decades would reach significant proportions.” In 1975, Stout and the University of Washington pathologist Russell Ross reported that insulin also stimulates the proliferation of the smooth muscle cells that line the interior of arteries, a necessary step in the thickening of artery walls characteristic of both atherosclerosis and hypertension."
And finally:
"“It may be stated categorically,” the University of Wisconsin endocrinologist Edgar Gordon wrote in JAMA in 1963, “that the storage of fat, and therefore the production and maintenance of obesity, cannot take place unless glucose is being metabolized. Since glucose cannot be used by most tissues without the presence of insulin, it also may be stated categorically that obesity is impossible in the absence of adequate tissue concentrations of insulin. Thus an abundant supply of carbohydrate food exerts a powerful influence in directing the stream of glucose metabolism into lipogenesis, whereas a relatively low carbohydrate intake tends to minimize the storage of fat.”"
So that high starch high sugar culture was actually lean off eating a lot of fructose so there goes another mechanism.
I think the question is "what is different from honey than other sources of fructose, like fruit juices without the pulp" - and again, your "high starch high sugar" culture was really a "low glycemic, high fructose culture", so again, the model fits.
When faced with a complex system like biology starting from the ground up is going backwards.
That's the fundamental problem with your position, insulin is basically the one mechanism you know, so everything basically happens as a result of insulin.
You're creating a caricature of my position. Insulin is the mechanism for fat accumulation. Differential insulin resistance is the mechanism for insulin causing obesity, gluttony and sloth. I'm open to the question "where does differential insulin resistance come from?"
Given a complex system with multiple confounders you need to approach it observationally.
I simply can't disagree more. An observational study shows you nothing - you've got to approach it with clear, falsifiable, foundational mechanisms to determine causality.
And I think maybe that's your essential beef - you're angry with Taubes because he's approached the problem from one direction, and you're *positive* that it must be approached from the other.
Sure there is - insulin resistant mothers eating high carbohydrate diets create an interuterine environment that makes their offspring more insulin resistant (differential insulin resistance, of course). So the epigenetic effects are actually well documented.
But only if the gluttony is of the sort that is directed towards foods that continue the improper partitioning of energy. Gluttony may be a necessary factor (caused by improper partitioning of energy), but it is only a second order effect, not in and of itself sufficient.
So now epigenetics are a necessary component in your model?
"First, there's no reason to think that the relationship between sugar(s) consumption and health endpoints is one to one or linear. So maybe a little bit of added sugar pushes us over a threshold, or maybe there's some exponential thing going on due to, say, epigenetic effects."
You can have type 2 diabetes with or without differential insulin resistance - I've known some type 2 diabetics to remain thin and fit, while others are grotesquely obese. I'll assert that for the differential insulin resistance type 2 diabetics, fat is accumulated, and muscles are starved, in a way that overwhelms any hunger suppressing effect high blood sugar levels may have - but that certainly would be an interesting experiment to determine the biological basis of hunger.
I agree that biological systems are filled with feedbacks and confounders, which is why I think that building the knowledge base from the ground up and the actual biological mechanisms is so important.
We've clearly established the role of insulin in fat accumulation, and you can add leptin into the bunch if you'd like (which is quite nearly a proxy for insulin). We've also clearly established the role of carbohydrate intake on blood sugar levels, with all the complexity that entails (high glycemic/low glycemic). We've even demonstrated the differential insulin resistance of fat cells and muscles cells as being a hormonal dysfunction that creates obesity under the influence of insulin.
So what's left?
Perhaps the most interesting stuff - what *causes* differential insulin resistance? What causes differential insulin resistance in the opposite direction than usual (fat more sensitive than muscle)? What may *prevent* differential insulin resistance? Now, perhaps you can design an experiment that narrows it down to fructose intake, or psychological taste factors, or "factor X" whatever it may be...but I don't think any of those experiments or studies has been properly done yet.
maybe the fat prone people find everything tastier
Which would imply to me that it's not about the food, it's about the hormonal imbalance of fat people. Again, gluttony and sloth being *effects* of obesity, rather than causes.
As for the Kuna, I think you've got to watch the population for a few more generations before the diseases of civilization kick in. Differential insulin resistance gets worse generation after generation when ancestral cultures are introduced to refined sugar.
Instead of hunger through muscle starvation insulin resistance could suppress hunger by keeping more sugar in the blood stream
That's not the kind of partitioning you get with differential insulin resistance - the sugar in the blood stream gets pounded to fat, and both the blood stream and the muscles are low in energy.
Now, if you had insulin resistance that was strictly non-differential, you could get what you're proposing, if both fat cells and muscle cells refuse to listen to insulin, and blood sugar stays high...although the toxicity of high blood sugar starts becoming an issue.
I also suppose if you had differential insulin resistance in the *other* direction (where fat cells were more resistant that muscles), you could also have something similar, where fat accumulation is decreased, and blood sugar levels and muscles get most of the energy......do you think maybe that's the disconnect we're having? Your contra-examples could simply be differential insulin resistance in the opposite direction of that which causes obesity?
You're absolutely right - it could be that starving muscles could trigger hunger, or they could trigger sloth...or both, for that matter.
Which means that starving muscles can cause someone to overeat, or be sedentary...which means that by proxy, improper partitioning of energy can cause overeating and sedentary behavior, making the overeating and sedentary behavior *effects* not causes.
For some people maybe they are addictive enough to cause obesity, but for non-industrial cultures this doesn't seem to be a problem
And that would be the kind of thing I would look for - take a food we've seen as generally harmless, find someone who is off the charts on a satiety index with it, and see if it can possibly get them obese. Until that's demonstrated, the whole satiety thing seems more like a 2nd or 3rd order effect than a core reason for obesity.
Except we answered that question and they can eat rice and root crops that are high GI.
And by avoiding sugars, they avoid the path to differential insulin resistance, and don't develop the carbohydrate allergy.
The only plausible mechanism you have left is fructose causing a 'carbohydrate allergy' in industrial populations, but even this is contradicted by non-industrial populations eating a lot of fruit and berries.
I leave it to Lustig to talk further on that, especially regarding the difference between fructose taken in juice form versus whole fruit (he seems to imply there is a difference in digestive process that mitigates the deleterious effects in that case).
Outside of increasing the GI what else does refining do other than making food more palatable?
I just thought of something - we could test this stuff on someone with no taste buds. By the satiety hypothesis, such a person would be unable to overeat, because nothing is tasty. The insulin hypothesis supposes that given insulin resistance, even if the tongue doesn't recognize that something is tasty, the muscles will know if they are being starved or not, and drive hunger.
Exactly what do you think happens to the fat we eat?
It's either broken down into fatty acids, and then processed by the body in various ways, or it slips through the digestive tract unprocessed.
Shouldn't type - 1 diabetes patients, before treatment get fat not thin then?
Why would that follow? Before treatment, type 1 diabetes patients can't produce insulin, therefore cannot signal for fat accumulation, therefore cannot get fat. Your cite makes this observation:
"Insulin in type 1 diabetes is a similar case. You need some basal amount of insulin signaling around for fat cells to store fat properly."
The differential resistance (even in non diabetics) is certainly enough to improperly partition incoming energy through the mouth to fat cells, rather than giving the muscles their due. The movie "Fat Head" has a neat graphic on this, if you get a chance to watch it.
I'm certain that you agree that when muscles don't get enough energy, humans generally experience hunger.
So while you might make the claim that hunger can have other other genesis, it's not clear why you would exclude differential insulin resistance causing an improper partitioning of energy, thereby starving muscles of energy, as a factor that would drive hunger.
So your uncited claim is that insulin only causes hunger when the cells no longer respond to it?
To be specific, I use "insulin resistance" as a shorthand that is perhaps inappropriate - I'm assuming an understanding that I shouldn't.
From GCBC: "A critical aspect of this insulin resistance, Yalow and Berson noted, is that some tissues might become resistant to insulin while others continued to respond normally, and this would determine how the damage done by the insulin resistance would manifest itself in different individuals. "
"Moreover, fat cells remain sensitive to insulin long after muscle cells become resistant to it. Once muscle cells become resistant to the insulin in the bloodstream, as Yalow and Berson explained, the fat cells have to remain sensitive to provide a place to store blood sugar, which would otherwise either accumulate to toxic levels or overflow into the urine and be lost to the body. As insulin levels rise, the storage of fat in the fat cells continues, long after the muscles become resistant to taking up any more glucose. Nonetheless, the pancreas may compensate for this insulin resistance, if it can, by secreting still more insulin. This will further elevate the level of insulin in the circulation and serve to increase further the storage of fat in the fat cells and the synthesis of carbohydrates from fat. It will suppress the release of fat from the fat tissue. Under these conditions—lipid trapping, as the geneticist James Neel described it—obesity begins to look preordained. Weights will plateau, as Dennis McGarry suggested in Science in 1992, only when the fat tissue becomes insulin-resistant as well, or when the fat deposits enlarge to the point where the forces working to release the fat and burn it for fuel—such as the increased concentration of fatty acids inside the fat cells—once again balance out the effect of the insulin itself."
So my apologies for using "insulin resistance" as shorthand for "differential insulin resistance between muscles cells and fat cells".
But for berries factors like fibre, flavour, and moisture content might mean berries can reach that same level of addictivness.
So you're asserting that there is in fact, some universal addictive properties that berries simply don't have? You deny the possibility of someone being addicted to berries because they find them so tasty?
Maybe if there is in fact certain things that cannot possibly be addictive (in this case, taking the Hazda diet, apparently by the tastiness hypothesis, nothing they eat can possibly be addictive since they don't get overweight), we can identify the biological mechanism of addiction.
Surely, my experience has shown sugar to be a particularly addictive substance, and it may be that simple...but I'd be interested in other proposed biomechanisms.
So by eating fructose we've developed some sort of insulin allergy that isn't present in non-industrial (ie ancestral) cultures. And that's why non-industrial cultures can eat any macronutrient balance they want and not get fat?
Well, you can separate the two - Lustig claims that a certain amount of fructose is what develops the carbohydrate allergy (aka, insulin resistance). Whether or not "non-industrial cultures can eat any macronutrient balance they want" begs the question as to the insulin response from those foods. Perhaps it's better to say "non-industrial cultures can eat low glycemic in any macronutrient balance they want".
MHO==MOH==Morbidly Obese Humans?
No, from your original cite, "Metabolically Healthy Obese".
Mostly just in the sense that fat is very energy dense and make foods more palatable leading us to overeat.
So you're saying as a condiment, fat is evil. Taubes is saying in isolation, fat is not evil, but in combination with a high glycemic load, it becomes evil. Looks like simply a restatement of the assertion without really justifying why we should consider calorie density as the real factor.
Except easily digestible carbs like rice are fine in Japan,
You only took a partial quote. The full quote is "The more easily digestible and refined the carbohydrates", and as shown by the lack of sugar consumption in Japan, they don't have more refined carbohydrates.
So again, no disagreement with Taubes except perhaps in the semantics of "easily digestible and refined" versus "easily digestible or refined".
That and protein also causes a similar effect on insulin (ie fish).
Refuted elsewhere - the error bars on both porridge and fish for the 40 out of 41 subjects who didn't actually test all the foods were so large as to easily encompass fish being lower than porridge.
Cancer is higher because of all the carcinogens in our environment
So you don't think that the fact that cancer cells perform particularly well in a high blood sugar environment has anything to do with it?
Correct, the later two are contributing factors.
Okay, so here you have a real disagreement - Taubes insist that "overeating" and "sedentary behavior" are actually *symptoms* of obesity, not causes. And the fact that "overeating" is a tautology makes that hard to refute.
I think for "sedentary behavior", the study that you linked with the notes that the total expended energy (TEE) of the tribesmen was equal to the TEE of sedentary westerners refutes the idea that sedentary behavior really drives that.
What do you think happens to that fat in the fat cells?
In an insulin resistant person, under the influence of insulin, the fat stays in the fat cells. In a normal person, fat cells cycle fat in and out, and don't preferentially store energy as fat.
I noticed you didn't quite say that insulin causes hunger and extra eating
All depends upon insulin resistance - as from the first title, "Elevated postprandial insulin levels do not induce satiety in normal-weight humans." As noted before, obesity is a sign of carbohydrate allergy, and if your body properly partitions energy, you're fine.
If under the influence of insulin, your body partitions more energy to fat than to muscle, you will feel hungry, and you will be driven to eat more.
Unfortunately the abstracts for the second two cites didn't have any note as to the subjects, but my guess is that they were normal weight.
Berries are tasty but not addictive the way potato chips are, I'm not really sure how to measure that but I don't think that insulin is the answer.
What about potoato chip flavored berries, and berry flavored potato chips?
Why *wouldn't* insulin be the answer?
What about someone who *does* think berries are tasty, and potato chips aren't? After all, people can have different addictions. Can someone addicted to berries in the Hazda tribe get fat because of their subjective tastiness?
Taubes theory is that carbs are bad, refined carbs particularly so, and that the more insulin it releases the more fattening it is.
And none of the data you've shown has contradicted that. You might have an example of certain carbs with a low glycemic index being *less* damaging, and therefore possibly negligible in effect, but you've caricatured Taubes into "all carbs must show a high insulin response and cause weight gain", instead of accepting that there is a spectrum of badness.
I don't see you advocating a low in refined sugar but high in starchy foods so it sounds like you're dodging to me.
Not at all. I'm asserting the following - obesity is a sign of a carbohydrate allergy. Regardless of its genesis (say, fructose ala Lustig, or some other hormonal defect), the treatment is carbohydrate restriction. You cannot fix someone's insulin resistance (once they are insulin resistant), by feeding them starchy foods.
And at the end of the day I don't really need to give an alternate mechanism, I just need to show Taubes is wrong.
Granted, let's assume for the moment that you have no alternate mechanism, and that Guynet's assertions are just hand waving. Let's be clear about the important questions still open about the insulin hypothesis:
1) what causes insulin resistance (see Lustig for one option) 2) what other mechanism could account for MHO (if say, further investigation shows that indeed, these large waisted people are able to accumulate fat in the absence of insulin). Perhaps this might end up being some sort of thyroid issue, who knows.
That all being said, I don't think that Taubes has a particular axe to grind on either one of these. Here's his 10 conclusions in GCBC:
"1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.
2. The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis—the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.
3. Sugars—sucrose and high-fructose corn syrup specifically—are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.
4. Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization.
5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.
6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.
7. Fattening and obesity are caused by an imbalance—a disequilibrium—in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.
One facet of biochemistry, insulin used to store fat, and you've figured out obesity.
If you can at least admit that we've narrowed it down to insulin resistance and insulin levels, we could move onto the next step of "what causes insulin resistance".
you now have to deal with the fact that porridge triggered a smaller insulin response than fish
Yes, in a group of 41 subjects, the response of porridge for one of them may have been less than the response for fish in another. Moving from that to a broad claim that fish is always a greater insulin generator than porridge is unjustified.
the results were statistically valid so the sample was apparently fine.
I don't think you understand the term "statistically valid".
Let's look at the data, shall we?
Porridge insulin: 40 +/- 4 (ranging from 36 - 44) Fish insulin: 59 +/- 18 (ranging from 41 - 77)
It is perfectly reasonable, and within their findings, that porridge is at 44, and fish is at 41.
As for measuring "satiety" with a subjective survey, rather than a "satiety-o-mometer", I think you're still in search of a biomechanism. Now, i'd really be interested to see what they saw with their glucose and insulin data that they promised to publish in another paper. Do you have a cite for that follow up?
That's what they have statistics for. Having the same subject consume both lets you run a paired T-test which lets you push the variance lower (I don't know if they did that with the 15) but having the 41 subjects consume foods from different categories is fine.
A study of 41 subjects, of which only one actually sampled everything, and you expect *statistics* to turn that into real data?
I suppose it would've worked even if they had just 2 subjects, right, since you can simply run a paired T-test on a single pair, right?:)
The only issue is like all studies of their kind it's done on a bunch of western university students.
That's one of the problems, but such a tiny sample size is a *huge* issue as well.
We haven't shown any mechanism for fat accumulation outside of insulin. But that doesn't mean you can't get fat without insulin resistance or chronically elevated insulin.
So, in the car analogy, we know the speed is driven by the accelerator and brake, but that doesn't mean you can't pick up speed if you're rolling downhill, or being pulled by a tow truck.
What is your downhill and tow truck for getting fat? "Tastiness"?
Are you seriously going to claim that we can't look at tastiness because I can't prove why icecream tastes better than a block of vegetable shortening?
What units are you going to measure tastiness in? Even if it's fuzzy, it has to be measured.
There's still a lot of berries and starch. And the very low fat content.
Remember the mechanism we're talking about - insulin response to carbohydrate intake plus insulin resistance. If you have lots of berries and starch in a form that isn't as insulin stimulating (and you haven't popped into insulin resistance), you're still in support of the insulin hypothesis.
I'd also argue that berries are tasty:)
Social cues and depression both affect eating. Routine is a huge factor in eating habits and is something that's probably impossible to maintain in a metabolic ward.
So is your assertion that social cues and depression and routine somehow stimulate insulin?
Why not actually simulate social cues in a metabolic ward, or actually maintain a routine in the ward?
Lets forget the tribesmen he implied used a fattening ceremony based off carbs, but really did it with fat.
Cite?
And how he just changes the subject when it comes to Japan and tons of other places that are high carb and even starch without being obese.
Insulin resistance? Sugar consumption which triggers insulin resistance ala Lustig? You're simply ignoring the response to the asserted paradox.
And how injecting insulin into mice doesn't cause obesity
Does insulin drive fat accumulation in mice or not? You seem to be claiming both.
And lets just concentrate the fact that GI isn't really correlated to insulin after all
So you're now asserting that insulin isn't secreted in response to blood sugar. What, pray tell, is the mechanism you propose?
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No, the high blood sugar during gestation in an otherwise non-obese woman can grant differential insulin resistance to her child, who then, under the same diet as her mother, ends up being obese instead of normal weight.
Let's find a study that actually measures the glycemic index of Hazda foods then.
The problem is that it very well may be that eating, appetite, activity, and even excretions, are driven by fat accumulation. And what I mean by that is that if the *first* order cause is fat accumulation, and that makes you hungrier, and lazier, and makes you eat more, and perhaps even excrete less, we need to be able to discern that.
Put another way, the orders of magnitude here are important, and I don't think that simply because the system is complex that all factors are of equal weight.
And it's a good thing that despite that there are some people out there who are willing to argue with textbooks :)
The sad fact, and Taubes exposes this extraordinarily well in GCBC (even if you dismiss his conclusions), is that the nutrition science in this country has not been driven by science, but by pre-determined agendas, be it to sell more cereals and grains, or to demonize meat eating, or to prop up a pet theory by a powerful government science administrator.
Honestly, more than a science book, I found Taubes work to be more interesting on the history side of the equation.
I actually read Guynet quite avidly - especially the comments. He comes off as passionate, but misguided and oddly defensive. Now, perhaps my opinion is colored by the fact that I've got differential insulin resistance, and while the insulin hypothesis matches my anecdotal experience, the "tastiness" hypothesis is actually 100% opposite of my reaction to food. I'm not above imagining that it's *possible* that there's someone out there who is terribly driven by "tastiness", but still doubtful that those urges can result in obesity if there isn't chronic insulin elevation and differential insulin resistance. Again, though, the proper metabolic ward experiment and I could be convinced that it's possible.
"In biology, and specifically genetics, epigenetics is the study of changes in gene expression or cellular phenotype, caused by mechanisms other than changes in the underlying DNA sequence"
The womb environment is a mechanism other than the underlying DNA sequence.
Read GCBC. Check it out from a library if you don't want to funnel cash to Taubes. The clear, obvious history of the path of diseases of civilization show a pattern of taking hold as generations pass. The Kuna are in for a rough ride if they continue their habits, and there's no reason to believe they'll be an exception to other native cultures who were introduced to refined carbohydrates - unless you believe they've got some sort of genetic mutation that allows them to be immune to the diseases of civilization.
But they are. Hell, baobab is *advertised* as low glycemic, and none of them are refined to increase glycemic index.
The impact of white sugar consumption accumulates over generations, as demonstrated by the gestational diabetes paper.
Your loss :)
Let's be specific. Differential insulin resistance is the driver of obesity. You keep focusing on "look at this group that eats low glycemic, but high starch and fructose, but isn't obese!", while ignoring the necessary factor of differential insulin resistance.
Why do you continue to refuse that factor as part of my position, and simplify it down to "insulin"?
Which has been done in depth with the Kreb's cycle, and the basics of fat accumulation biology. Now, perhaps your position is simply "there is no good answer, and I'm annoyed at Taubes for asserting he has one" (ignoring your support of Guynet for the moment) - but you seem to be wilfully ignoring the study of the system that has occurred.
Odd. You don't seem to hold that research and knowledge up to the same level of scrutiny :)
Here's the relevant passage from the first quote:
"some tissues might become resistant to insulin while others continued to respond normally, and this would determine how the damage done by the insulin resistance would manifest itself in different individuals"
Here's the relevant passage from the second quote:
"In certain individuals, they suggested, the insulin secretion after eating these carbohydrates would be “disproportionately large.” “The carbohydrate is disposed of in three sites—adipose [fat] tissue, liver and arterial wall,” Stout wrote. “Obesity is produced."
I'm not sure though, what your problem with the assertion that type 2 diabetes can have different manifestations - here's another paper that discusses this: http://www.plosone.org/article/info:doi/10.1371/journal.pone.0018284
From GCBC:
"By 1965, Yalow and Berson had suggested why these adult-onset diabetics could appear to be lacking insulin—manifesting the symptoms of diabetes, high blood sugar, and sugar in their urine—while simultaneously having excessive insulin in their circulation: their tissues did not respond properly to the insulin they secreted. They were insulin-resistant, defined by Yalow and Berson as “a state (of a cell, tissue, system or body) in which greater-than-normal amounts of insulin are required to elicit a quantitatively normal response.” Because of their resistance to insulin, adult-onset diabetics had to secrete more of the hormone to maintain their blood sugar within healthy levels, and this would become increasingly difficult to achieve the longer they remained insulin-resistant.*51
A critical aspect of this insulin resistance, Yalow and Berson noted, is that some tissues might become resistant to insulin while others continued to respond normally, and this would determine how the damage done by the insulin resistance would manifest itself in different individuals. So “it is desirable,” they wrote, “wherever possible, to distinguish generalized resistance of all tissues from resistance of only individual tissues.”"
Also:
"In the late 1960s, Robert Stout of Queen’s University in Belfast published a series of studies reporting that insulin enhances the transport of cholesterol and fats into the cells of the arterial wall and stimulates the synthesis of cholesterol and fat in the arterial lining. Since a primary role of insulin is to facilitate the storage of fats in the fat tissue, Stout reasoned, it was not surprising that it would have the same effect on the lining of blood vessels. In 1969, Stout and the British diabetologist John Vallance-Owen pre-empted Reaven’s Syndrome X hypothesis by suggesting that the “ingestion of large quantities of refined carbohydrate” leads first to hyperinsulinemia and insulin resistance, and then to atherosclerosis and heart disease. In certain individuals, they suggested, the insulin secretion after eating these carbohydrates would be “disproportionately large.” “The carbohydrate is disposed of in three sites—adipose [fat] tissue, liver and arterial wall,” Stout wrote. “Obesity is produced. In the liver, triglyceride and cholesterol are synthesized and find their way into the circulation. Lipid synthesis is also stimulated in the arterial wall and is augmented by deposition of [triglycerides and cholesterol]which in a few decades would reach significant proportions.” In 1975, Stout and the University of Washington pathologist Russell Ross reported that insulin also stimulates the proliferation of the smooth muscle cells that line the interior of arteries, a necessary step in the thickening of artery walls characteristic of both atherosclerosis and hypertension."
And finally:
"“It may be stated categorically,” the University of Wisconsin endocrinologist Edgar Gordon wrote in JAMA in 1963, “that the storage of fat, and therefore the production and maintenance of obesity, cannot take place unless glucose is being metabolized. Since glucose cannot be used by most tissues without the presence of insulin, it also may be stated categorically that obesity is impossible in the absence of adequate tissue concentrations of insulin. Thus an abundant supply of carbohydrate food exerts a powerful influence in directing the stream of glucose metabolism into lipogenesis, whereas a relatively low carbohydrate intake tends to minimize the storage of fat.”"
I think the question is "what is different from honey than other sources of fructose, like fruit juices without the pulp" - and again, your "high starch high sugar" culture was really a "low glycemic, high fructose culture", so again, the model fits.
So we start with God, and work backwards from there? Watch this series, especially lecture 2 regarding cells: https://itunes.apple.com/us/itunes-u/cognitive-ubiquity-evolution/id464839816
You're creating a caricature of my position. Insulin is the mechanism for fat accumulation. Differential insulin resistance is the mechanism for insulin causing obesity, gluttony and sloth. I'm open to the question "where does differential insulin resistance come from?"
I simply can't disagree more. An observational study shows you nothing - you've got to approach it with clear, falsifiable, foundational mechanisms to determine causality.
And I think maybe that's your essential beef - you're angry with Taubes because he's approached the problem from one direction, and you're *positive* that it must be approached from the other.
Sure there is - insulin resistant mothers eating high carbohydrate diets create an interuterine environment that makes their offspring more insulin resistant (differential insulin resistance, of course). So the epigenetic effects are actually well documented.
http://www.ncbi.nlm.nih.gov/pubmed/23000698
But only if the gluttony is of the sort that is directed towards foods that continue the improper partitioning of energy. Gluttony may be a necessary factor (caused by improper partitioning of energy), but it is only a second order effect, not in and of itself sufficient.
Sure, why not?
And yes, Tabues has mentioned this before, in both his examples of increasing obesity over generations during the spread of the "diseases of civilization", as well as explicitly: http://www.motherjones.com/blue-marble/2012/10/gary-taubes-sugar-reddit-ama-halloween-candy
"First, there's no reason to think that the relationship between sugar(s) consumption and health endpoints is one to one or linear. So maybe a little bit of added sugar pushes us over a threshold, or maybe there's some exponential thing going on due to, say, epigenetic effects."
You can have type 2 diabetes with or without differential insulin resistance - I've known some type 2 diabetics to remain thin and fit, while others are grotesquely obese. I'll assert that for the differential insulin resistance type 2 diabetics, fat is accumulated, and muscles are starved, in a way that overwhelms any hunger suppressing effect high blood sugar levels may have - but that certainly would be an interesting experiment to determine the biological basis of hunger.
http://www.sciencedaily.com/releases/2013/07/130730101715.htm
I agree that biological systems are filled with feedbacks and confounders, which is why I think that building the knowledge base from the ground up and the actual biological mechanisms is so important.
We've clearly established the role of insulin in fat accumulation, and you can add leptin into the bunch if you'd like (which is quite nearly a proxy for insulin). We've also clearly established the role of carbohydrate intake on blood sugar levels, with all the complexity that entails (high glycemic/low glycemic). We've even demonstrated the differential insulin resistance of fat cells and muscles cells as being a hormonal dysfunction that creates obesity under the influence of insulin.
So what's left?
Perhaps the most interesting stuff - what *causes* differential insulin resistance? What causes differential insulin resistance in the opposite direction than usual (fat more sensitive than muscle)? What may *prevent* differential insulin resistance? Now, perhaps you can design an experiment that narrows it down to fructose intake, or psychological taste factors, or "factor X" whatever it may be...but I don't think any of those experiments or studies has been properly done yet.
There's always hope for the future though! :)
Which would imply to me that it's not about the food, it's about the hormonal imbalance of fat people. Again, gluttony and sloth being *effects* of obesity, rather than causes.
As for the Kuna, I think you've got to watch the population for a few more generations before the diseases of civilization kick in. Differential insulin resistance gets worse generation after generation when ancestral cultures are introduced to refined sugar.
That's not the kind of partitioning you get with differential insulin resistance - the sugar in the blood stream gets pounded to fat, and both the blood stream and the muscles are low in energy.
Now, if you had insulin resistance that was strictly non-differential, you could get what you're proposing, if both fat cells and muscle cells refuse to listen to insulin, and blood sugar stays high...although the toxicity of high blood sugar starts becoming an issue.
I also suppose if you had differential insulin resistance in the *other* direction (where fat cells were more resistant that muscles), you could also have something similar, where fat accumulation is decreased, and blood sugar levels and muscles get most of the energy... ...do you think maybe that's the disconnect we're having? Your contra-examples could simply be differential insulin resistance in the opposite direction of that which causes obesity?
You're absolutely right - it could be that starving muscles could trigger hunger, or they could trigger sloth...or both, for that matter.
Which means that starving muscles can cause someone to overeat, or be sedentary...which means that by proxy, improper partitioning of energy can cause overeating and sedentary behavior, making the overeating and sedentary behavior *effects* not causes.
Okay, so let's have three imaginary buckets:
1) fat cells
2) muscle cells
3) blood glucose
You might be able to add a 4th for ketone bodies but let's simplify for now.
Type 1 diabetics have an empty #1, and struggle to keep #3 from killing them. #2 can probably deal with it mostly.
Differential insulin resistant people (carbohydrate allergy), have a partitioning error where #1 gets full, and #2 and #3 mostly don't.
My guess is that if you have #1 full, and #3 full, but #2 running on empty, you'll have hunger.
And that would be the kind of thing I would look for - take a food we've seen as generally harmless, find someone who is off the charts on a satiety index with it, and see if it can possibly get them obese. Until that's demonstrated, the whole satiety thing seems more like a 2nd or 3rd order effect than a core reason for obesity.
And by avoiding sugars, they avoid the path to differential insulin resistance, and don't develop the carbohydrate allergy.
I leave it to Lustig to talk further on that, especially regarding the difference between fructose taken in juice form versus whole fruit (he seems to imply there is a difference in digestive process that mitigates the deleterious effects in that case).
I just thought of something - we could test this stuff on someone with no taste buds. By the satiety hypothesis, such a person would be unable to overeat, because nothing is tasty. The insulin hypothesis supposes that given insulin resistance, even if the tongue doesn't recognize that something is tasty, the muscles will know if they are being starved or not, and drive hunger.
It's either broken down into fatty acids, and then processed by the body in various ways, or it slips through the digestive tract unprocessed.
Why would that follow? Before treatment, type 1 diabetes patients can't produce insulin, therefore cannot signal for fat accumulation, therefore cannot get fat. Your cite makes this observation:
"Insulin in type 1 diabetes is a similar case. You need some basal amount of insulin signaling around for fat cells to store fat properly."
The differential resistance (even in non diabetics) is certainly enough to improperly partition incoming energy through the mouth to fat cells, rather than giving the muscles their due. The movie "Fat Head" has a neat graphic on this, if you get a chance to watch it.
I'm certain that you agree that when muscles don't get enough energy, humans generally experience hunger.
So while you might make the claim that hunger can have other other genesis, it's not clear why you would exclude differential insulin resistance causing an improper partitioning of energy, thereby starving muscles of energy, as a factor that would drive hunger.
To be specific, I use "insulin resistance" as a shorthand that is perhaps inappropriate - I'm assuming an understanding that I shouldn't.
From GCBC: "A critical aspect of this insulin resistance, Yalow and Berson noted, is that some tissues might become resistant to insulin while others continued to respond normally, and this would determine how the damage done by the insulin resistance would manifest itself in different individuals. "
"Moreover, fat cells remain sensitive to insulin long after muscle cells become resistant to it. Once muscle cells become resistant to the insulin in the bloodstream, as Yalow and Berson explained, the fat cells have to remain sensitive to provide a place to store blood sugar, which would otherwise either accumulate to toxic levels or overflow into the urine and be lost to the body. As insulin levels rise, the storage of fat in the fat cells continues, long after the muscles become resistant to taking up any more glucose. Nonetheless, the pancreas may compensate for this insulin resistance, if it can, by secreting still more insulin. This will further elevate the level of insulin in the circulation and serve to increase further the storage of fat in the fat cells and the synthesis of carbohydrates from fat. It will suppress the release of fat from the fat tissue. Under these conditions—lipid trapping, as the geneticist James Neel described it—obesity begins to look preordained. Weights will plateau, as Dennis McGarry suggested in Science in 1992, only when the fat tissue becomes insulin-resistant as well, or when the fat deposits enlarge to the point where the forces working to release the fat and burn it for fuel—such as the increased concentration of fatty acids inside the fat cells—once again balance out the effect of the insulin itself."
So my apologies for using "insulin resistance" as shorthand for "differential insulin resistance between muscles cells and fat cells".
So you're asserting that there is in fact, some universal addictive properties that berries simply don't have? You deny the possibility of someone being addicted to berries because they find them so tasty?
Maybe if there is in fact certain things that cannot possibly be addictive (in this case, taking the Hazda diet, apparently by the tastiness hypothesis, nothing they eat can possibly be addictive since they don't get overweight), we can identify the biological mechanism of addiction.
Surely, my experience has shown sugar to be a particularly addictive substance, and it may be that simple...but I'd be interested in other proposed biomechanisms.
Well, you can separate the two - Lustig claims that a certain amount of fructose is what develops the carbohydrate allergy (aka, insulin resistance). Whether or not "non-industrial cultures can eat any macronutrient balance they want" begs the question as to the insulin response from those foods. Perhaps it's better to say "non-industrial cultures can eat low glycemic in any macronutrient balance they want".
No, from your original cite, "Metabolically Healthy Obese".
So you're saying as a condiment, fat is evil. Taubes is saying in isolation, fat is not evil, but in combination with a high glycemic load, it becomes evil. Looks like simply a restatement of the assertion without really justifying why we should consider calorie density as the real factor.
You only took a partial quote. The full quote is "The more easily digestible and refined the carbohydrates", and as shown by the lack of sugar consumption in Japan, they don't have more refined carbohydrates.
So again, no disagreement with Taubes except perhaps in the semantics of "easily digestible and refined" versus "easily digestible or refined".
Refuted elsewhere - the error bars on both porridge and fish for the 40 out of 41 subjects who didn't actually test all the foods were so large as to easily encompass fish being lower than porridge.
So you don't think that the fact that cancer cells perform particularly well in a high blood sugar environment has anything to do with it?
Okay, so here you have a real disagreement - Taubes insist that "overeating" and "sedentary behavior" are actually *symptoms* of obesity, not causes. And the fact that "overeating" is a tautology makes that hard to refute.
I think for "sedentary behavior", the study that you linked with the notes that the total expended energy (TEE) of the tribesmen was equal to the TEE of sedentary westerners refutes the idea that sedentary behavior really drives that.
In an insulin resistant person, under the influence of insulin, the fat stays in the fat cells. In a normal person, fat cells cycle fat in and out, and don't preferentially store energy as fat.
All depends upon insulin resistance - as from the first title, "Elevated postprandial insulin levels do not induce satiety in normal-weight humans." As noted before, obesity is a sign of carbohydrate allergy, and if your body properly partitions energy, you're fine.
If under the influence of insulin, your body partitions more energy to fat than to muscle, you will feel hungry, and you will be driven to eat more.
Unfortunately the abstracts for the second two cites didn't have any note as to the subjects, but my guess is that they were normal weight.
What about potoato chip flavored berries, and berry flavored potato chips?
Why *wouldn't* insulin be the answer?
What about someone who *does* think berries are tasty, and potato chips aren't? After all, people can have different addictions. Can someone addicted to berries in the Hazda tribe get fat because of their subjective tastiness?
And none of the data you've shown has contradicted that. You might have an example of certain carbs with a low glycemic index being *less* damaging, and therefore possibly negligible in effect, but you've caricatured Taubes into "all carbs must show a high insulin response and cause weight gain", instead of accepting that there is a spectrum of badness.
Not at all. I'm asserting the following - obesity is a sign of a carbohydrate allergy. Regardless of its genesis (say, fructose ala Lustig, or some other hormonal defect), the treatment is carbohydrate restriction. You cannot fix someone's insulin resistance (once they are insulin resistant), by feeding them starchy foods.
Granted, let's assume for the moment that you have no alternate mechanism, and that Guynet's assertions are just hand waving. Let's be clear about the important questions still open about the insulin hypothesis:
1) what causes insulin resistance (see Lustig for one option)
2) what other mechanism could account for MHO (if say, further investigation shows that indeed, these large waisted people are able to accumulate fat in the absence of insulin). Perhaps this might end up being some sort of thyroid issue, who knows.
That all being said, I don't think that Taubes has a particular axe to grind on either one of these. Here's his 10 conclusions in GCBC:
"1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.
2. The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis—the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.
3. Sugars—sucrose and high-fructose corn syrup specifically—are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.
4. Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization.
5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.
6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.
7. Fattening and obesity are caused by an imbalance—a disequilibrium—in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.
8. Insulin
Oh wait, interesting, the insulin data is the 41 subject study you referenced before!
Okay, same caveats apply - small sample size and huge swings (error bars larger than the effect you're trying to show).
If you can at least admit that we've narrowed it down to insulin resistance and insulin levels, we could move onto the next step of "what causes insulin resistance".
Yes, in a group of 41 subjects, the response of porridge for one of them may have been less than the response for fish in another. Moving from that to a broad claim that fish is always a greater insulin generator than porridge is unjustified.
I don't think you understand the term "statistically valid".
Let's look at the data, shall we?
Porridge insulin: 40 +/- 4 (ranging from 36 - 44)
Fish insulin: 59 +/- 18 (ranging from 41 - 77)
It is perfectly reasonable, and within their findings, that porridge is at 44, and fish is at 41.
As for measuring "satiety" with a subjective survey, rather than a "satiety-o-mometer", I think you're still in search of a biomechanism. Now, i'd really be interested to see what they saw with their glucose and insulin data that they promised to publish in another paper. Do you have a cite for that follow up?
A study of 41 subjects, of which only one actually sampled everything, and you expect *statistics* to turn that into real data?
I suppose it would've worked even if they had just 2 subjects, right, since you can simply run a paired T-test on a single pair, right? :)
That's one of the problems, but such a tiny sample size is a *huge* issue as well.
So, in the car analogy, we know the speed is driven by the accelerator and brake, but that doesn't mean you can't pick up speed if you're rolling downhill, or being pulled by a tow truck.
What is your downhill and tow truck for getting fat? "Tastiness"?
What units are you going to measure tastiness in? Even if it's fuzzy, it has to be measured.
Remember the mechanism we're talking about - insulin response to carbohydrate intake plus insulin resistance. If you have lots of berries and starch in a form that isn't as insulin stimulating (and you haven't popped into insulin resistance), you're still in support of the insulin hypothesis.
I'd also argue that berries are tasty :)
So is your assertion that social cues and depression and routine somehow stimulate insulin?
Why not actually simulate social cues in a metabolic ward, or actually maintain a routine in the ward?
Cite?
Insulin resistance? Sugar consumption which triggers insulin resistance ala Lustig? You're simply ignoring the response to the asserted paradox.
Does insulin drive fat accumulation in mice or not? You seem to be claiming both.
So you're now asserting that insulin isn't secreted in response to blood sugar. What, pray tell, is the mechanism you propose?