The actual advice is to eat slower, so the brain has more time to register the food and turn off the hunger, and to eat smaller portions.
1) you're assuming the brain turns off the hunger, not the muscles.
2) you're still telling people to eat smaller portions.
obese people tend to eat beyond what is needed to negate hunger.
The better phrase would be, "obese people tend to hunger beyond what is needed to maintain a normal body weight". Why do they hunger more? The differential insulin hypothesis asserts that muscles are starving even as obese people take in more calories.
I heard them cautioning about saturated fat with things like the atkins diets
Which is provably false. Fat is blamed for making people fat unfairly, but it's par for the course to look down on carnivores in our society.
lots of red meat and saturated fat in a standard western diet will make you fatter (well backed by evidence)
Not so - none of the evidence put forward controls for the role of carbohydrates. I have, and many others have, diets high in red meat and saturated fat that have made us thinner.
My understanding is that insulin resistance is at least partly a mechanism to avoid cells taking in toxic levels of glucose
Well, that goes along with my understanding that obesity is a mechanism to avoid toxic levels of glucose in the blood - everyone you see who is obese is *exactly* obese enough to prevent toxic levels of glucose, i.e., they're as fat as they need to be.
That being said, if they're fat in order to keep glucose levels in check, it would make sense to avoid chronically elevated glucose levels driven by a high glycemic diet, if you wanted to attack the obesity problem.
the trouble with science is that often hypothesis you want to test is not necessarily the hypothesis you can test.
As with many navel gazing theoretical physicists, there is a fine line between real science, and just entertaining science fiction. The line is called falsifiability. If you can't test your hypothesis, or if there is no response to a test that could possibly cause it to fail, you're not doing science, you're doing astrology.
If you want to get specific the nutritionists are counselling people to eat appropriate amounts.
And, if someone is obese, that "appropriate amount" is less than what they eat now - therefore, smaller meals, therefore, the same advice we give to people to make them hungry.
The idea that making fat people hungry will help them lose weight is silly on its face, but that's *exactly* the advice we give when we buy into the "calories in/calories out" hypothesis.
Now, look, I could see someone who believed in the "tastiness" hypothesis giving advice to "don't cook with spices or salt, and drink only bland drinks", and that possibly having some sort of chance (since it doesn't inherently induce hunger), but there's no doubt that the "eat less, exercise more" trope is a gross simplification that is the exactly *wrong* advice for a great many people.
Except they explicitly counsel people that people shouldn't attempt fewer calories by skipping meals.
Yes, yes, I adjusted my statement for you:
"The same advice we use to make people hungry (eat smaller meals, do some vigorous exercise), we use to counsel them for weight loss. Doesn't seem rational to think that inducing hunger will help people lose weight."
And exercise will make you hungrier, and doesn't necessarily help weight loss, but it shouldn't make you hungry beyond the calories you burned.
Whoa, unsupported assertion there - exercise can very easily make you hungry beyond the calories you burned. You're assuming no delay between the input of calories into the mouth and the recognition by the body that it has gotten back all the calories exercised away, for one, but that's an assertion you'll need to show in a metabolic ward.
any diet that restricts food groups will cause weight loss.
I followed the standard low-fat/low-calorie diet/exercise advice of my doc for two years, and gained weight. *Highly* restricted fat that entire time, ran five miles each day, and put on an extra five pounds per year.
It may be that you can find individual cases for specific food restrictions that cause weight loss, but for those of us who are differential insulin resistant, if you don't restrict the carbohydrates, you're not going to get weight loss until you're on starvation rations that finally drop the carbs below the level of your allergy reaction.
There's no other way to interpret that statement other than the vegetarian diet will make kids fat and diabetic.
And that is arguably true in some cases. You can choose to give the benefit of the doubt, or not, but it's not a flat out lie as you propose.
Put another way, eating copious amounts of red meat and saturated fat won't make you fat and diabetic (at least without accompanying carbohydrates) - but nutritionists make that implication all the time. Would you call them out as liars?
Well considering that the consensus view is differential insulin resistance is caused by obesity I'm not sure how you'll get the second test
So, if that's true, we should be able to find a large number of people in the process of getting obese, that don't have differential insulin resistance...unless the consensus view is that differential insulin resistance is caused *immediately* by obesity, with say just a nanosecond delay...
I guess the other thing we could do is implant fat, and see if it causes insulin resistance. I'd be curious to see what the biomechanism is for excess fat causing differential insulin resistance, rather than the other way around...you'd have to be able to isolate some signal or hormone that the fat cell was emitting that caused muscle cells to get insulin resistant quicker than the fat cell...and on top of that, do it without chronically elevated insulin levels.
Sounds like a tough row to hoe.
It's more a slow accumulation of evidence towards a hypothesis.
Voodoo. Popper was right about the requirement of falsifiability as the cornerstone of the scientific method. Astrology has a slow accumulation of evidence towards Cancers and Leos getting along, but it ain't science.
Hey, I'm only arguing about the word "if" not "is":)
As for Taubes, he's not pointing a gun at anyone with his words:) The proper analogy is some guy just saying "if people care about their lives they might want to send me cashiers checks" - the speaker certainly not robbing anyone, nor is making any sort of unambiguous assertion about harm. In fact, the whole *point* of implying something is to *avoid* being unambiguous.
In the end, while not a guarantee, I heartily agree with the notion that forcing children to be vegan is always harmful to their health, and forcing children to be vegetarian is almost always harmful to their health. I also agree that the standard American diet is always harmful to health, and that a high glycemic diet is always harmful to health (given that the standard american diet is by very definition high glycemic).
Furthermore, I think there's a real bias against understanding the dangers of high glycemic foods. When you tell someone your family is vegetarian, very few people would even consider offering your children meat products...it's just considered impolite. But if you tell someone your family is low-carb, you still have to fend off the friends and relatives offering your kids cookies, candies, cupcakes, french fries, and chicken nuggets. The common apprehension is that vegetarianism is a legitimate health choice, and should not be challenged, but that low-glycemic diets are simply the latest "fad-diet", and should be challenged.
I've never heard nutritionists counsel people to skip meals.
You get my point - fewer calories == skipped meals, or smaller meals. The same advice we use to make people hungry (eat smaller meals, do some vigorous exercise), we use to counsel them for weight loss. Doesn't seem rational to think that inducing hunger will help people lose weight.
And besides, if the cereal, grain, and sugar industry is so powerful why are they letting the government fund all that research into low-carb diets?
Fund all that research into low-carb diets? Really? I'd love to see a breakdown of just how government grants are partitioned in nutrition studies...while low-carb might be moving forward (despite the attempts of keepers of dogma to beat it down), I'd hardly say that this is very common now, or was at all common under the reign of Ancel Keys.
I've consistently agreed with you that low carb diets lead to weight loss
Well, to be specific, I think you've agreed that low carb diets *can* lead to weight loss, but if I'm remembering correctly, the alternate hypothesis to differential insulin resistance you have is "it just makes things taste worse so you spontaneously eat less calories".
I guess from my POV, I can agree that it's possible that for some small fraction of people, the taste factor may in fact be significant (or maybe even dominant), but I'm not convinced as to the exact biomechanism test we could give in a metabolic ward for it, nor am I convinced that it's a common occurrence (arguably based on my own n=1 bias).
So when the population gets fat there's no epigenetic effect, but if they don't become fat there must be a missing epigenetic factor?
That's correct. Two instantiations of the same issue (clouded by the fact that the Tokelau don't have good data, and may in fact show an epigenetic delay if we had better import and health records).
I think what you're really trying to go for, is some *falsifiable* prediction, which is important. To be clear, I'm not making the prediction "there is always a 1 generation delay before obesity arrives in native cultures introduced to the high glycemic western diet", nor am I making the prediction "there is always an immediate effect before obesity arrives in native cultures introduced to the high glycemic western diet." You are behaving as if only one of those may be true, and that's not the case.
The falsifiable prediction I make is actually quite restrained - that under the influence of a high glycemic diet, people with differential insulin resistance will become obese. In both the 1 generation delay, as well as the immediate Tokelau (caveats on data aside), that falsifiable prediction can still be true.
What *cannot* be true, is to have a population with differential insulin resistance, a high glycemic diet, and no obesity...I guess with the further caveat that you're not forcibly starving the population (they'll just be terribly lethargic and hungry at that point).
That's not where this line of argument started. I noted that epigenetic effects could cause a delay in phenotypic expression of carbohydrate poisoning, after you cited a group that apparently hasn't fallen victim to high sugar intake after a short while of having a sweet tooth. You then took that to mean that I meant epigenetic effects must *always* be visible, and then cited the Tokelau example as a native people who started feeling the effects in less than a generation.
At this point, the argument is over whether or not the difference between the Tokelau and the...Zuna I think it was, in any way is a refutation of the differential insulin/chronically elevated insulin hypothesis of obesity.
FWIW, I found the full text of "The Tokelau Island Migrant Study" published in 1974, but it only contains 1968 data, and I believe the reference was for 1968 - 1982 data. I'll keep looking.
It's not ambiguous or open to multiple interpretations
Your actual words - "he directly implies".
Implies: strongly suggest the truth or existence of (something not expressly stated).
The very *purpose* of implying something is to give a suggestion which could be open to multiple interpretations. If we want to make something unambiguous, we simply *say* it, not *imply* it.
You even gloss over the fact that Taubes uses an "if...then..." construction, which by definition is a conditional, not an unambiguous assertion.
Are you so determined to tar Taubes with the "liar" label that you can't actually parse what he really said?
Please don't say allergy since I don't think you really mean it.
Actually, I think it's a pretty accurate term to describe my intention - there are literally some people who cannot eat certain foods without an inflammatory or otherwise adverse effect, and I think this is true as well for carbohydrates. Of course, as with all allergies, it can be on a spectrum, with some able to withstand more of a dose than others, but in my case at least, the level is pretty low...maybe less than 40g or even 30g of carbohydrates per day.
Test foods with salt and bland, see which group eats more over a few weeks.
Well, you also have the other part of that - the output of calories. So it's not just which group eats more, but which group eats more relative to the amount of calories their bodies use.
So I'd run that test with a low-carb regimen, and a high carb regimen. Heck, use twins if you can, and run both tests for everyone (randomize order).
And if it turns out that "salt" vs "bland" only affects fat accumulation in the high carb regimen, then it could be that it's only a second order effect.
Calories in/calories out is correct, it's just that both sides can vary even without exercise.
Put another way, they aren't independent variables - which is what the general nutritional advice of today is. The same advice we use to make people hungry (skip a few meals, do some vigorous exercise), we use to counsel them for weight loss. Doesn't seem rational to think that inducing hunger will help people lose weight.
Ya don't think the cattle growers association would give him grants to show a high fat diet is better for you?
Sure they might, but they're no match for the cereal and grain and sugar industry. To imagine that our current nutritional research system is unbiased is very optimistic:)
The fact that low carb is an effective way for you to lose weight doesn't mean carbs are the reason you gained weight.
That's an interesting statement - I'm not sure if you'd accept any refutation of it though. If I added tasty carbs back to my diet, and gained weight, you could blame "tastiness". If I added bland carbs back to my diet, and gained weight, you could blame some personal gluttony of mine.
What would you accept as proof that someone ha a carbohydrate allergy?
Palatability is only part of the puzzle, a significant part but still a part.
I'd argue with the second part of that statement - it may be a part of the puzzle, but it's almost certainly an insignificant part. I'm also not convinced palatability is anything but a circular definition...if there was some additive you could put on anything to increase its palatability, you could test it directly, but because it's a subjective measure, you could have the *exact* same diet for two people, one who finds it more palatable than the other person, and you'd still be left with the question as to whether or not subjective palatibility made the difference, or if it was some other fact.
I suppose if you could find some sort of twins that were equivalent in everything except how tasty they found salt, you could test the palatability hypothesis...but other than that, it seems dubious as a measure.
If he accepted the consensus view he'd become one of many and fall back towards relative obscurity.
Wait, you think that a refutation of the insulin/differential insulin resistance hypothesis would be a fall back to the "consensus view"? We know calories in/calories out is bunk, even if you have doubts about insulin/differential insulin resistance.
Or do you think there is some other consensus view?
He'd get publications in Science, Nature, wherever the hell he wanted. He'd get public speaking engagements, academic job offers, etc.
He can't do that without grants, and he can't get grants without toeing the line on the current dogma.
Seriously, pick up GCBC and read it just as a history lesson on the kind of blackballing that goes on in the nutrition sciences since Ancel Keys.
The actual weight differences required in kids to generate the average effect you're talking about is absurd.
That's not true at all - kids have *huge* variation. Heck, one of my kids didn't even hit the bottom of the height/weight chart until they were 7.
Granted I'm curious about the "nearly" qualifier about the age groups, but that might be something as simple as statistical significance
All published studies should include the raw data, archived for posterity - otherwise you get people arguing like us over how to interpret the one sentence summary of thousands of rows of data:)
Deal with the fact that Taubes is making a statement that is false.
Well, to use your own words, he makes a statement that could "directly imply" something that is false. I read a completely different implication (that vegetarians *can* be obese and diabetic), which I derive from an understanding of the rhetorical point he's trying to make (that there are misguided folk out there who turn to veganism and vegetarianism believing it is inherently healthy, when it is not necessarily so).
Now, you might not care whether or not veganism and vegetarianism is healthy, and you might not even care if people pursue it under false pretenses - but obviously Taubes does, and frankly, that concern resonates with me.
But you can assume it didn't change during that period since there was very little import, the weight gain only started with the jump in imported food.
That's only if we believe the import data is good. Again, too much speculation there, too little data.
I hope you realize there's no way that the youth could in any way significantly impact the 5 kilo average gain. When it's stated "Tokelauans in nearly all age groups gained weight" you can't just speculate it away.
Sure the youth could impact the 5 kilo average gain. If the youngest cohort gained 10 kilos, and was the most numerous, the oldest cohort could have gained much less. Now, if *every* cohort of Tokelauans gained 5kg, from the youngest to the oldest, that's real data, but they didn't state that - they simply said "in *nearly* all age groups" and "gained weight", which leaves open some age groups *not* gaining weight, and some age groups gaining more weight than others.
Data. Need data.
So Japan is fine just by avoiding sugar. So why is Taubes pushing a low carb diet? Why is he obsessed with insulin that has a huge response to white rice and other starches? Why doesn't he simply tell people to eliminate sugar and white flour and they'll be thin like the Japanese?
Well, I'd bet a few things, but for me and my n=1, I've found that once you've been damaged by sugar, and become differential insulin resistant, it's difficult to heal that. I simply do not have the option to eat a high starch diet now that I've damaged my body with sugar. My bet is that many other Americans are in the same boat, so the low carb option as a treatment for carbohydrate allergy is really the only option.
So the advice you'd give to one set of people (say, the japanese, just stop eating more sugar every year), might not be the same advice you'd give to damaged people.
Now, can you show any evidence that the damage done by sugar and refined carbs that induces differential insulin resistance (and other insulin based metabolic syndrome diseases), can be reversed, and then white rice and other starches are fine to eat? Because I do miss my nigiri, and only eat sashimi now:)
And you know what, I can believe that. It's more than possible that your brain has hunger pathways primarily driven by mental "tastiness" properties than mine, and fewer hunger pathways driven primarily by differential insulin resistance and muscle starvation. But I suppose I'd also bet that I've had a worse obesity problem than you ever had...I got up to 250 pounds on about a 5' 11' frame, probably a 44" waist, maybe 46". I'll never be thin and skinny again, but after 7 years of carbohydrate restriction, I've maintained at around 195 and a 34" waist (I also discovered slow burn strength training which greatly increased my relative muscle mass).
the only time he's sure of his knowledge is when dealing with someone who's theories are completely without merit.
Maybe my problem is that the alternatives he poses ("tastiness" for example) simply don't hold up to the scrutiny he poses to others - it seems a peculiar myopia. And for many of the refutations he tries to make, just a little scratching on the surface makes you realize that it's not nearly as clean a refutation as he supposes (i.e., the low glycemic nature of the Hazda diet).
If Taubes stood up tomorrow and said "Sorry folks, I messed up interpreting the data and it turns out my big insulin hypothesis is wrong" what do you think would happen to his income?
It'd probably increase. He'd write the book that refutes the insulin hypothesis, and laugh his way to the bank! After all, he's just a science reporter - he could write about *anyone's* hypothesis (even Guynet's), and make money because he's a good writer.
Guynet, on the other hand, probably couldn't get a grant to show that the past 40 years of dietary advice by the USDA has actually caused epidemics of diabetes, cancer, obesity, hypertension, heart disease, and other chronic diseases. Too many people in power with vested interests in the status quo would quash such investigation flat.
You know the really sad part though - there really are interests on both sides. It just so happened that in the 1950s, with Ancel Keys, the cereal and grain lobby won out over the meat and poultry lobby - but I can imagine a counterfactual that went the other way, where cereals and grains lost out to meat and poultry. We might be healthier today if meat and poultry had won, but as a large interest group they'd have opportunities to abuse their position as well, I'm sure.
What do you mean? It's empirically true if the vegetarian or vegan diet is high glycemic enough, and their children are, or become differential insulin resistant.
The point he's trying to make is that you can have an ethical and moral reason to be a vegetarian or vegan (although Lierre Keith would disagree), but don't pretend it's a health choice - or at least don't pretend that it's some universally healthy choice (which maybe you could agree with). If anything, his snark against vegetarians and vegans is tame compared to the vitriol spewed against meat eaters.
So yeah, Taubes is snarky, but I think he makes a valid point with his rhetoric - there are people who would make a different choice about veganism or vegetarianism if the only way they could justify it to themselves was on a moral or ethical basis.
BTW, Lierre Keith's "The Vegetarian Myth" is a *must* read on the whole vegan/vegetarian thing.
You'd also need to explain one of Taubes own favourite examples The Tokelau Island Migrant Study [blogspot.ca] who started getting fat in less then a generation.
"Tokelau's troubles began in 1765 with its 'discovery' by British commodore John Byron. "
Where's the evidence that they got fat in less than a generation? I see the graph starting from the 1960s...but where's the data on diet from 1765 - 1960?
Furthermore: "Between 1968 and 1982, Tokelauans in nearly all age groups gained weight, roughly 5 kilograms (11 pounds) on average."
11 pounds doesn't seem like rampant obesity...although I'd like to see the age breakdown (my suspicion is that younger cohorts increased more (say, someone pregnant in 1968, with a high blood sugar uterus, might produce a 4 year old child in 1972 that was significantly more obese than a 4 year old child in 1968).
Why could I listen to an hour long interview with him talking about the dangers of carbs, sugars particularly, but also starches, and I never heard him mention Japan or China?
A few excerpts from GCBC:
"By the mid-1990s, however, the Japanese contingent of the Seven Countries Study, led by Yoshinori Koga, reported that fat intake in Japan had increased from the 6 percent of calories they had measured in the farming village of Tanushimaru thirty-five years earlier, to 22 percent of calories. “There have been progressive increases in consumption of meats, fish and shellfish and milk,” they reported. Mean cholesterol levels rose in the community from 150 mg/dl to nearly 190 mg/dl, which is only 6 percent lower than the average American values (202 mg/dl as of 2004). Yet this change went along with a “remarkable reduction” in the incidence of strokes and no change in the incidence of heart disease. In fact, the chance that a Japanese man of any particular age would die of heart disease had steadily diminished since 1970. “It is suggested that dietary changes in Tanushimaru in the last thirty years have contributed to the prevention of cardiovascular disease,” Koga and his colleagues concluded."
"When Keys linked the low-fat, high-carbohydrate diet of the Japanese in the late 1950s to the extremely low incidence of heart disease, he paid no attention to sugar consumption. Fat consumption in Japan was extremely low, as were heart-disease rates, and so he concluded that the lower the fat the better. But the consumption of sugars in Japan was very low, too—less than forty pounds per person per year in 1963, and still under fifty pounds in 1980—equivalent to the yearly per-capita consumption recorded in the United States or in the United Kingdom a century earlier."
"And these investigators, too, concluded that differences in cancer rates could be explained by differences in fat consumption and animal-fat consumption, particularly between Japan and the United States. They did not serve science well by ignoring sugar consumption and the difference between refined and unrefined carbohydrates."
"This model also explains, as Pete Ahrens suggested in 1961, why high-carbohydrate diets appear innocuous in populations that are chronically undernourished. This was inevitably the case with those Southeast Asian populations extolled by Keys and others for their low total-cholesterol levels and apparent absence of heart disease. Such populations lived on carbohydrate-rich diets out of economic necessity rather than choice. Their diets were predominantly unrefined carbohydrates because that’s what they cultivated and it was all they could afford. As Ahrens had noted, the great proportion of individuals in such populations barely eked out enough calories to survive. This was true not only of Japan in the year
Surround yourself with bland foods like raw veggies and plain baked potatoes. When that's what you have to choose from see how not hungry you are.
Here was my experience with that - I'd wake up in the middle of the night, starving. I'd eat the bland food (raw carrots, plain baked potatoes) until my stomach was so full that I felt like it was overflowing into my esophagus. I'd still be desperately hungry.
Now, the insulin/differential insulin resistance hypothesis models this well - most of the calories sent to my stomach were being shunted to my fat cells, starving my muscles. I suffered through competing "hunger" signals - the stomach feeling so bloated that I was nauseous, but my muscles feeling so starved I was ravenous.
I think the defensiveness comes from being a professional researcher who keeps having to argue with highly dedicated amateurs who don't realize the gaps in their knowledge.
And that's definitely something Guynet needs to work on - his apparent attitude precludes there being gaps in *his* knowledge, which means it's hard to trust that he's been thorough in critiquing himself. It doesn't help either that his financial interests are aligned with the status quo, and gaining study grants that must pass through the hoops of bureaucrats with a vested interest in maintaining a certain narrative.
Again, it's obvious that vegans have serious health problems, and that vegetarians can be both high glycemic and low glycemic, not to mention whatever variations of lacto-ovo cheats they may have.
So how do we tell if Taubes is right, and that universally acclaimed "healthy" diets such as veganism (which kills babies), and vegetarianism aren't in fact, universally healthy?
We go back to first principles, and study the issue from the ground up:)
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1) you're assuming the brain turns off the hunger, not the muscles.
2) you're still telling people to eat smaller portions.
The better phrase would be, "obese people tend to hunger beyond what is needed to maintain a normal body weight". Why do they hunger more? The differential insulin hypothesis asserts that muscles are starving even as obese people take in more calories.
Which is provably false. Fat is blamed for making people fat unfairly, but it's par for the course to look down on carnivores in our society.
Not so - none of the evidence put forward controls for the role of carbohydrates. I have, and many others have, diets high in red meat and saturated fat that have made us thinner.
Well, that goes along with my understanding that obesity is a mechanism to avoid toxic levels of glucose in the blood - everyone you see who is obese is *exactly* obese enough to prevent toxic levels of glucose, i.e., they're as fat as they need to be.
That being said, if they're fat in order to keep glucose levels in check, it would make sense to avoid chronically elevated glucose levels driven by a high glycemic diet, if you wanted to attack the obesity problem.
As with many navel gazing theoretical physicists, there is a fine line between real science, and just entertaining science fiction. The line is called falsifiability. If you can't test your hypothesis, or if there is no response to a test that could possibly cause it to fail, you're not doing science, you're doing astrology.
And, if someone is obese, that "appropriate amount" is less than what they eat now - therefore, smaller meals, therefore, the same advice we give to people to make them hungry.
The idea that making fat people hungry will help them lose weight is silly on its face, but that's *exactly* the advice we give when we buy into the "calories in/calories out" hypothesis.
Now, look, I could see someone who believed in the "tastiness" hypothesis giving advice to "don't cook with spices or salt, and drink only bland drinks", and that possibly having some sort of chance (since it doesn't inherently induce hunger), but there's no doubt that the "eat less, exercise more" trope is a gross simplification that is the exactly *wrong* advice for a great many people.
Yes, yes, I adjusted my statement for you:
"The same advice we use to make people hungry (eat smaller meals, do some vigorous exercise), we use to counsel them for weight loss. Doesn't seem rational to think that inducing hunger will help people lose weight."
Whoa, unsupported assertion there - exercise can very easily make you hungry beyond the calories you burned. You're assuming no delay between the input of calories into the mouth and the recognition by the body that it has gotten back all the calories exercised away, for one, but that's an assertion you'll need to show in a metabolic ward.
I followed the standard low-fat/low-calorie diet/exercise advice of my doc for two years, and gained weight. *Highly* restricted fat that entire time, ran five miles each day, and put on an extra five pounds per year.
It may be that you can find individual cases for specific food restrictions that cause weight loss, but for those of us who are differential insulin resistant, if you don't restrict the carbohydrates, you're not going to get weight loss until you're on starvation rations that finally drop the carbs below the level of your allergy reaction.
And that is arguably true in some cases. You can choose to give the benefit of the doubt, or not, but it's not a flat out lie as you propose.
Put another way, eating copious amounts of red meat and saturated fat won't make you fat and diabetic (at least without accompanying carbohydrates) - but nutritionists make that implication all the time. Would you call them out as liars?
So, if that's true, we should be able to find a large number of people in the process of getting obese, that don't have differential insulin resistance...unless the consensus view is that differential insulin resistance is caused *immediately* by obesity, with say just a nanosecond delay...
I guess the other thing we could do is implant fat, and see if it causes insulin resistance. I'd be curious to see what the biomechanism is for excess fat causing differential insulin resistance, rather than the other way around...you'd have to be able to isolate some signal or hormone that the fat cell was emitting that caused muscle cells to get insulin resistant quicker than the fat cell...and on top of that, do it without chronically elevated insulin levels.
Sounds like a tough row to hoe.
Voodoo. Popper was right about the requirement of falsifiability as the cornerstone of the scientific method. Astrology has a slow accumulation of evidence towards Cancers and Leos getting along, but it ain't science.
Hey, I'm only arguing about the word "if" not "is" :)
As for Taubes, he's not pointing a gun at anyone with his words :) The proper analogy is some guy just saying "if people care about their lives they might want to send me cashiers checks" - the speaker certainly not robbing anyone, nor is making any sort of unambiguous assertion about harm. In fact, the whole *point* of implying something is to *avoid* being unambiguous.
In the end, while not a guarantee, I heartily agree with the notion that forcing children to be vegan is always harmful to their health, and forcing children to be vegetarian is almost always harmful to their health. I also agree that the standard American diet is always harmful to health, and that a high glycemic diet is always harmful to health (given that the standard american diet is by very definition high glycemic).
Furthermore, I think there's a real bias against understanding the dangers of high glycemic foods. When you tell someone your family is vegetarian, very few people would even consider offering your children meat products...it's just considered impolite. But if you tell someone your family is low-carb, you still have to fend off the friends and relatives offering your kids cookies, candies, cupcakes, french fries, and chicken nuggets. The common apprehension is that vegetarianism is a legitimate health choice, and should not be challenged, but that low-glycemic diets are simply the latest "fad-diet", and should be challenged.
One day, I hope that changes.
You get my point - fewer calories == skipped meals, or smaller meals. The same advice we use to make people hungry (eat smaller meals, do some vigorous exercise), we use to counsel them for weight loss. Doesn't seem rational to think that inducing hunger will help people lose weight.
Fund all that research into low-carb diets? Really? I'd love to see a breakdown of just how government grants are partitioned in nutrition studies...while low-carb might be moving forward (despite the attempts of keepers of dogma to beat it down), I'd hardly say that this is very common now, or was at all common under the reign of Ancel Keys.
Well, to be specific, I think you've agreed that low carb diets *can* lead to weight loss, but if I'm remembering correctly, the alternate hypothesis to differential insulin resistance you have is "it just makes things taste worse so you spontaneously eat less calories".
I guess from my POV, I can agree that it's possible that for some small fraction of people, the taste factor may in fact be significant (or maybe even dominant), but I'm not convinced as to the exact biomechanism test we could give in a metabolic ward for it, nor am I convinced that it's a common occurrence (arguably based on my own n=1 bias).
That's correct. Two instantiations of the same issue (clouded by the fact that the Tokelau don't have good data, and may in fact show an epigenetic delay if we had better import and health records).
I think what you're really trying to go for, is some *falsifiable* prediction, which is important. To be clear, I'm not making the prediction "there is always a 1 generation delay before obesity arrives in native cultures introduced to the high glycemic western diet", nor am I making the prediction "there is always an immediate effect before obesity arrives in native cultures introduced to the high glycemic western diet." You are behaving as if only one of those may be true, and that's not the case.
The falsifiable prediction I make is actually quite restrained - that under the influence of a high glycemic diet, people with differential insulin resistance will become obese. In both the 1 generation delay, as well as the immediate Tokelau (caveats on data aside), that falsifiable prediction can still be true.
What *cannot* be true, is to have a population with differential insulin resistance, a high glycemic diet, and no obesity...I guess with the further caveat that you're not forcibly starving the population (they'll just be terribly lethargic and hungry at that point).
That's not where this line of argument started. I noted that epigenetic effects could cause a delay in phenotypic expression of carbohydrate poisoning, after you cited a group that apparently hasn't fallen victim to high sugar intake after a short while of having a sweet tooth. You then took that to mean that I meant epigenetic effects must *always* be visible, and then cited the Tokelau example as a native people who started feeling the effects in less than a generation.
At this point, the argument is over whether or not the difference between the Tokelau and the...Zuna I think it was, in any way is a refutation of the differential insulin/chronically elevated insulin hypothesis of obesity.
Sad news, looks like Guynet's reference is a book, not an peer reviewed article:
http://books.google.com/books/about/Migration_and_health_in_a_small_society.html?id=dZwPAQAAMAAJ
Couldn't find data there with a casual search, but maybe someone has it somewhere.
FWIW, I found the full text of "The Tokelau Island Migrant Study" published in 1974, but it only contains 1968 data, and I believe the reference was for 1968 - 1982 data. I'll keep looking.
If you manage to get the full text, please, let me know.
Your actual words - "he directly implies".
Implies: strongly suggest the truth or existence of (something not expressly stated).
The very *purpose* of implying something is to give a suggestion which could be open to multiple interpretations. If we want to make something unambiguous, we simply *say* it, not *imply* it.
You even gloss over the fact that Taubes uses an "if...then..." construction, which by definition is a conditional, not an unambiguous assertion.
Are you so determined to tar Taubes with the "liar" label that you can't actually parse what he really said?
Actually, I think it's a pretty accurate term to describe my intention - there are literally some people who cannot eat certain foods without an inflammatory or otherwise adverse effect, and I think this is true as well for carbohydrates. Of course, as with all allergies, it can be on a spectrum, with some able to withstand more of a dose than others, but in my case at least, the level is pretty low...maybe less than 40g or even 30g of carbohydrates per day.
Well, you also have the other part of that - the output of calories. So it's not just which group eats more, but which group eats more relative to the amount of calories their bodies use.
So I'd run that test with a low-carb regimen, and a high carb regimen. Heck, use twins if you can, and run both tests for everyone (randomize order).
And if it turns out that "salt" vs "bland" only affects fat accumulation in the high carb regimen, then it could be that it's only a second order effect.
Put another way, they aren't independent variables - which is what the general nutritional advice of today is. The same advice we use to make people hungry (skip a few meals, do some vigorous exercise), we use to counsel them for weight loss. Doesn't seem rational to think that inducing hunger will help people lose weight.
Sure they might, but they're no match for the cereal and grain and sugar industry. To imagine that our current nutritional research system is unbiased is very optimistic :)
That's an interesting statement - I'm not sure if you'd accept any refutation of it though. If I added tasty carbs back to my diet, and gained weight, you could blame "tastiness". If I added bland carbs back to my diet, and gained weight, you could blame some personal gluttony of mine.
What would you accept as proof that someone ha a carbohydrate allergy?
I'd argue with the second part of that statement - it may be a part of the puzzle, but it's almost certainly an insignificant part. I'm also not convinced palatability is anything but a circular definition...if there was some additive you could put on anything to increase its palatability, you could test it directly, but because it's a subjective measure, you could have the *exact* same diet for two people, one who finds it more palatable than the other person, and you'd still be left with the question as to whether or not subjective palatibility made the difference, or if it was some other fact.
I suppose if you could find some sort of twins that were equivalent in everything except how tasty they found salt, you could test the palatability hypothesis...but other than that, it seems dubious as a measure.
Wait, you think that a refutation of the insulin/differential insulin resistance hypothesis would be a fall back to the "consensus view"? We know calories in/calories out is bunk, even if you have doubts about insulin/differential insulin resistance.
Or do you think there is some other consensus view?
He can't do that without grants, and he can't get grants without toeing the line on the current dogma.
Seriously, pick up GCBC and read it just as a history lesson on the kind of blackballing that goes on in the nutrition sciences since Ancel Keys.
That's not true at all - kids have *huge* variation. Heck, one of my kids didn't even hit the bottom of the height/weight chart until they were 7.
All published studies should include the raw data, archived for posterity - otherwise you get people arguing like us over how to interpret the one sentence summary of thousands of rows of data :)
Well, to use your own words, he makes a statement that could "directly imply" something that is false. I read a completely different implication (that vegetarians *can* be obese and diabetic), which I derive from an understanding of the rhetorical point he's trying to make (that there are misguided folk out there who turn to veganism and vegetarianism believing it is inherently healthy, when it is not necessarily so).
Now, you might not care whether or not veganism and vegetarianism is healthy, and you might not even care if people pursue it under false pretenses - but obviously Taubes does, and frankly, that concern resonates with me.
That's only if we believe the import data is good. Again, too much speculation there, too little data.
Sure the youth could impact the 5 kilo average gain. If the youngest cohort gained 10 kilos, and was the most numerous, the oldest cohort could have gained much less. Now, if *every* cohort of Tokelauans gained 5kg, from the youngest to the oldest, that's real data, but they didn't state that - they simply said "in *nearly* all age groups" and "gained weight", which leaves open some age groups *not* gaining weight, and some age groups gaining more weight than others.
Data. Need data.
Well, I'd bet a few things, but for me and my n=1, I've found that once you've been damaged by sugar, and become differential insulin resistant, it's difficult to heal that. I simply do not have the option to eat a high starch diet now that I've damaged my body with sugar. My bet is that many other Americans are in the same boat, so the low carb option as a treatment for carbohydrate allergy is really the only option.
So the advice you'd give to one set of people (say, the japanese, just stop eating more sugar every year), might not be the same advice you'd give to damaged people.
Now, can you show any evidence that the damage done by sugar and refined carbs that induces differential insulin resistance (and other insulin based metabolic syndrome diseases), can be reversed, and then white rice and other starches are fine to eat? Because I do miss my nigiri, and only eat sashimi now :)
And you know what, I can believe that. It's more than possible that your brain has hunger pathways primarily driven by mental "tastiness" properties than mine, and fewer hunger pathways driven primarily by differential insulin resistance and muscle starvation. But I suppose I'd also bet that I've had a worse obesity problem than you ever had...I got up to 250 pounds on about a 5' 11' frame, probably a 44" waist, maybe 46". I'll never be thin and skinny again, but after 7 years of carbohydrate restriction, I've maintained at around 195 and a 34" waist (I also discovered slow burn strength training which greatly increased my relative muscle mass).
Maybe my problem is that the alternatives he poses ("tastiness" for example) simply don't hold up to the scrutiny he poses to others - it seems a peculiar myopia. And for many of the refutations he tries to make, just a little scratching on the surface makes you realize that it's not nearly as clean a refutation as he supposes (i.e., the low glycemic nature of the Hazda diet).
It'd probably increase. He'd write the book that refutes the insulin hypothesis, and laugh his way to the bank! After all, he's just a science reporter - he could write about *anyone's* hypothesis (even Guynet's), and make money because he's a good writer.
Guynet, on the other hand, probably couldn't get a grant to show that the past 40 years of dietary advice by the USDA has actually caused epidemics of diabetes, cancer, obesity, hypertension, heart disease, and other chronic diseases. Too many people in power with vested interests in the status quo would quash such investigation flat.
You know the really sad part though - there really are interests on both sides. It just so happened that in the 1950s, with Ancel Keys, the cereal and grain lobby won out over the meat and poultry lobby - but I can imagine a counterfactual that went the other way, where cereals and grains lost out to meat and poultry. We might be healthier today if meat and poultry had won, but as a large interest group they'd have opportunities to abuse their position as well, I'm sure.
What do you mean? It's empirically true if the vegetarian or vegan diet is high glycemic enough, and their children are, or become differential insulin resistant.
The point he's trying to make is that you can have an ethical and moral reason to be a vegetarian or vegan (although Lierre Keith would disagree), but don't pretend it's a health choice - or at least don't pretend that it's some universally healthy choice (which maybe you could agree with). If anything, his snark against vegetarians and vegans is tame compared to the vitriol spewed against meat eaters.
So yeah, Taubes is snarky, but I think he makes a valid point with his rhetoric - there are people who would make a different choice about veganism or vegetarianism if the only way they could justify it to themselves was on a moral or ethical basis.
BTW, Lierre Keith's "The Vegetarian Myth" is a *must* read on the whole vegan/vegetarian thing.
What?
http://wholehealthsource.blogspot.com/2009/01/tokelau-island-migrant-study-background.html
"Tokelau's troubles began in 1765 with its 'discovery' by British commodore John Byron. "
Where's the evidence that they got fat in less than a generation? I see the graph starting from the 1960s...but where's the data on diet from 1765 - 1960?
Furthermore: "Between 1968 and 1982, Tokelauans in nearly all age groups gained weight, roughly 5 kilograms (11 pounds) on average."
11 pounds doesn't seem like rampant obesity...although I'd like to see the age breakdown (my suspicion is that younger cohorts increased more (say, someone pregnant in 1968, with a high blood sugar uterus, might produce a 4 year old child in 1972 that was significantly more obese than a 4 year old child in 1968).
A few excerpts from GCBC:
"By the mid-1990s, however, the Japanese contingent of the Seven Countries Study, led by Yoshinori Koga, reported that fat intake in Japan had increased from the 6 percent of calories they had measured in the farming village of Tanushimaru thirty-five years earlier, to 22 percent of calories. “There have been progressive increases in consumption of meats, fish and shellfish and milk,” they reported. Mean cholesterol levels rose in the community from 150 mg/dl to nearly 190 mg/dl, which is only 6 percent lower than the average American values (202 mg/dl as of 2004). Yet this change went along with a “remarkable reduction” in the incidence of strokes and no change in the incidence of heart disease. In fact, the chance that a Japanese man of any particular age would die of heart disease had steadily diminished since 1970. “It is suggested that dietary changes in Tanushimaru in the last thirty years have contributed to the prevention of cardiovascular disease,” Koga and his colleagues concluded."
"When Keys linked the low-fat, high-carbohydrate diet of the Japanese in the late 1950s to the extremely low incidence of heart disease, he paid no attention to sugar consumption. Fat consumption in Japan was extremely low, as were heart-disease rates, and so he concluded that the lower the fat the better. But the consumption of sugars in Japan was very low, too—less than forty pounds per person per year in 1963, and still under fifty pounds in 1980—equivalent to the yearly per-capita consumption recorded in the United States or in the United Kingdom a century earlier."
"And these investigators, too, concluded that differences in cancer rates could be explained by differences in fat consumption and animal-fat consumption, particularly between Japan and the United States. They did not serve science well by ignoring sugar consumption and the difference between refined and unrefined carbohydrates."
"This model also explains, as Pete Ahrens suggested in 1961, why high-carbohydrate diets appear innocuous in populations that are chronically undernourished. This was inevitably the case with those Southeast Asian populations extolled by Keys and others for their low total-cholesterol levels and apparent absence of heart disease. Such populations lived on carbohydrate-rich diets out of economic necessity rather than choice. Their diets were predominantly unrefined carbohydrates because that’s what they cultivated and it was all they could afford. As Ahrens had noted, the great proportion of individuals in such populations barely eked out enough calories to survive. This was true not only of Japan in the year
Here was my experience with that - I'd wake up in the middle of the night, starving. I'd eat the bland food (raw carrots, plain baked potatoes) until my stomach was so full that I felt like it was overflowing into my esophagus. I'd still be desperately hungry.
Now, the insulin/differential insulin resistance hypothesis models this well - most of the calories sent to my stomach were being shunted to my fat cells, starving my muscles. I suffered through competing "hunger" signals - the stomach feeling so bloated that I was nauseous, but my muscles feeling so starved I was ravenous.
And that's definitely something Guynet needs to work on - his apparent attitude precludes there being gaps in *his* knowledge, which means it's hard to trust that he's been thorough in critiquing himself. It doesn't help either that his financial interests are aligned with the status quo, and gaining study grants that must pass through the hoops of bureaucrats with a vested interest in maintaining a certain narrative.
Again, it's obvious that vegans have serious health problems, and that vegetarians can be both high glycemic and low glycemic, not to mention whatever variations of lacto-ovo cheats they may have.
But beyond that any observational study is essentially worthless other than for speculation - http://www.marksdailyapple.com/will-eating-red-meat-kill-you/#axzz2chiATIP6
So how do we tell if Taubes is right, and that universally acclaimed "healthy" diets such as veganism (which kills babies), and vegetarianism aren't in fact, universally healthy?
We go back to first principles, and study the issue from the ground up :)