Dude, the Far Canadian North is NOT used for smuggling anything in the country, it is just not economical.
Load a pallet of drugs onto a ship. Coast guard can't do anything because it's international waters.
When the coast is clear send in a smaller boat (or rendezvous with one) and dump it on the shore. Then hire a bunch of guys to ride in on snowmobiles and take it down south.
If you're shipping enough drugs or other contraband the low risk could make it economical.
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".
Except we haven't.
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.
My bad, I was thinking statistically valid as a whole, not necessarily those two specific foods. By eye proteins show comparable insulin responses to carbs (and running the numbers would doubtlessly confirm that), which is expected because we know protein stimulates insulin release.
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?
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?
Someone who doesn't like chips probably won't get fat off them. But for berries factors like fibre, flavour, and moisture content might mean berries can reach that same level of addictivness.
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.
No, I've talked extensively about carbs with a high GI and insulin response like rice.
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.
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?
Did you come to this conclusion before or after the evidence the insulin hypothesis didn't work in non-industrial cultures?
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.
1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.
Mostly just in the sense that fat is very energy dense and make foods more palatable leading us to overeat. It may be linked to heart disease in industrial societies but not non-industrial.
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.
Except easily digestible carbs like rice are fine in Japan, and countless non-industrial nations the only real common factor in obesity is industrial societies (though some like Japan avoid this).
That and protein also causes a similar effect on insulin (ie fish).
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.
I agree, but for different reasons
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.
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?:)
One facet of biochemistry, insulin used to store fat, and you've figured out obesity.
But take a statistical test that is a mathematical fact and now you have a problem?!?
If they effed up the stats that's a problem, but if they didn't, and they did the experiment they said they did, then you now have to deal with the fact that porridge triggered a smaller insulin response than fish and you don't understand everything that goes on with insulin responses like insulin release in response to protein.
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.
The sample is too small if the effect size is tiny, but the results were statistically valid so the sample was apparently fine.
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:)
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.
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?
... I seriously have no idea how you think that could be my assertion.
Why not actually simulate social cues in a metabolic ward, or actually maintain a routine in the ward?
Unless your metabolic ward is the friggin Truman Show I don't think that's gonna work.
Lets forget the tribesmen he implied used a fattening ceremony based off carbs, but really did it with fat.
Cite?
One of the first things I posted, I'm tired of constantly re-linking.
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
Even if I agreed with that Lustig assertion (which I don't). Taubes theory is that carbs are bad, refined carbs particularly so, and that the more insulin it releases the more fattening it is.
Even with sugar it's hard to get a bigger insulin spike than white rice or baked potatos, and 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.
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.
You keep claiming I've contradicted myself on the mouse experiment, but I haven't the foggiest idea what you're referring to. Though considering your bizarre statement that I asserted "that social cues and depression and routine somehow stimulate insulin" in my previous post I guess I shouldn't worry too much.
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?
I'm saying that the relationship between blood sugar, insulin release, macronutrients, and other regulatory mechanisms (including glucagon) is a lot more complex than you realize.
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.
It's not about a war. It's about establishing sovereignty, and to maintain control over a territory you need to be police it.
The northwest passage is a big issue over whether it's international waters or Canadian waters. Not just because of potential oil drilling or fishing, but shipping is a big issue. It's a lot easier to ensure the shipping is done safely so a ton of oil isn't dumped on our coastline if we can police the waters. Security is also a concern as there's a lot of unpopulated places for smugglers to drop cargo or illegal immigrants.
A military grade stealth snowmobile is part of the bigger picture, it makes it easier to patrol the territory and search for smugglers or other criminals as well as shows we're taking that part of our territory seriously.
Not a fan of evolutionary psychology, but I think there's a lot of reason to think we do have an aptitude for spoken language. I wouldn't be at all surprised if a well designed voice system left more mental focus available for the task of coding.
I'm not sure if the technology is there yet, and you still don't want to hear your officemates jabbering away, but I could see the theoretical usability of a spoken word interface surpassing that of typing.
None of those starches or sugars is refined at all, which likely reduces the amount of effect that it can have on insulin levels, much less insulin resistance. Hell Baobab is even advertised as low glycemic: (http://baobab-fruit.com)
Using the Hazda to refute the insulin hypothesis, given the low glycemic values of their diet, seems inappropriate.
There's still a lot of berries and starch. And the very low fat content.
You can examine what happens when you eat specific foods in detail and that very valuable. But obesity is caused by our entire lifestyle and can't replicate their lifestyles in a metabolic ward.
"caused by our entire lifestyle?" So for example, if one person watches the news for 30 minutes, and another watches a sitcom, you're going to assert that this lifestyle difference could cause a difference in obesity? By what possible mechanism?
The science of fat accumulation cannot simply be stated as "thou shalt do no measurements, and rely on self reported diet and exercise numbers". Until you get someone in a metabolic ward (where you can test all kinds of hypotheses on what may or may not add to fat accumulation), you're not collecting very good data.
That's a pretty lame reductio ad absurdum. How many times do people go out drinking with friends in a metabolic ward? Go to a potluck, head out for lunch, play a soccer game, go for a walk, have a chat with friends, or work late and hit the snack machine or food stash in their desk? 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.
You can test specific hypotheses in a metabolic ward, but it's not a magic bullet.
You've shown data you believe contradicts him, but doesn't.
Lets forget the tribesmen he implied used a fattening ceremony based off carbs, but really did it with fat. 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. And how injecting insulin into mice doesn't cause obesity, and replacing fat calories with sugar calories 1-1 doesn't cause obesity, and insulin resistance seems to be a mechanism to keep excess glucose out of cells so it doesn't poison cells (don't think I linked this one). And how obesity in the US shows no relationship to carbohydrate consumption.
And lets just concentrate the fact that GI isn't really correlated to insulin after all. So all that carbohydrate evidence he thinks he has doesn't even exist.
You'd have to dig further into the 41 subjects that were a part of that survey. Further, it'd be nice if more than a single subject actually consumed all of the foods listed (http://ajcn.nutrition.org/content/66/5/1264.full.pdf). Even worse that only 15 subjects did more than two food categories.
Always look closely at the data before believing it.
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. If they did it your way you'd be complaining because they either tested fewer foods or did it with fewer volunteers. The only issue is like all studies of their kind it's done on a bunch of western university students.
You've decided the only possible way to get fat is via insulin resistance (well at least for the 70% who have both conditions), so if palatability contributes to obesity you're assuming it must work in this bizarre fashion.
That's correct. We haven't shown any mechanism for fat accumulation outside of insulin resistance and elevated insulin levels, although some MHO data suggests it might be possible for say, 30% of the population.
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. You haven't even accounted for glucagon!
How about this, define palatability. How can you tell one food is more or less palatable than another? Does this vary between individuals? Does it vary over time within individuals? What's your specific definition?
Some people have done some serious research into hyperpalatable foods. There are some characteristics of palatability, crunchiness, low bitterness, sugar, fat, salt. But the fact you don't want to accept a fuzzy definition doesn't mean its not a real thing. 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?
That doesn't mean people haven't tried but you're not going to get a simple story.
Even if you assume an epigenetic factor is at work in western populations you still need to explain why it was activated in western populations and not ancestral populations eating lots of sugar, fructose, and carbs.
I thought you agreed that there is no ancestral population eating lots of sugar (i.e., like comparing sugar comparison between Japan and the US).
Name a single ancestral population eating lots of sugar, fructose and carbs.
No, I'm saying "the study you cited contradicts the other study you cited". Which one is wrong, do you think? Do you think that insulin doesn't cause fat accumulation as shown by study A, or do you believe that insulin does cause fat accumulation by study B?
I'm not sure what this study B you're talking about is. Outside of lipohypertrophy (something different) or insulin used to treat a specific disorder (very specific circumstances and I don't think I posted it anyways) I can't remember posting anything like that.
A metabolic ward is by definition a highly a-typical environment and putting someone in a metabolic ward introduces a pile of confounders that don't show up in the normal population.
So you're asserting that somehow the psychological effect of being in a metabolic ward causes biochemistry to behave differently?
Look, in order to get down to the biomechanisms here, you need to be able to observe things in frightening detail - are you positing some sort of heisenberg uncertainty principle for diet, in that it changes when observed?
You can examine what happens when you eat specific foods in detail and that very valuable. But obesity is caused by our entire lifestyle and can't replicate their lifestyles in a metabolic ward.
Your evidence that two generations of nutritional scientists are complete bunk and someone publishing thousands of papers without actually doing any useful work is largely based on a book by a journalist.
A journalist who has painstakingly cited every finding he's shown. He's just the messenger, the real data is there, and that needs to be contended with.
WTF do you think I've been doing?!? I've shown real data he's misrepresented. I've shown counter examples he's ignored. I've shown how everyone else knows about this 'real data' but also knows the other data that leads to different conclusions!
All Taubes has done is cherrypicked and misrepresented some data and ended up with some fame and a pile of money.
The evidence around low carb diets indicate they work because people spontaneously consume fewer calories (high protein more so).
And isn't it possible that this spontaneous reaction is due to the partitioning of energy? As the body starts getting more energy partitioned to muscle, and less to fat storage, wouldn't whatever "hunger" mechanism kick in and cause a loss of appetite, or "exercise" mechanism kick in and cause a greater expenditure of energy?
Furthermore, wouldn't *any* change in the partitioning in energy (from what ever source), truly be the *cause* of the different behavior?
Except people on low carb diets typically increase their protein consumption (high protein works better than low carb for weight loss).
Low carb also means you need to exclude a bunch of foods including stables like bread, pasta, rice, potatoes, etc. Hunger isn't just a physical reaction. If you exclude a food you tend to overeat then you usually don't replace all those calories with an alternative.
It also means they pay more attention to what they're eating.
So why do fat cells accumulate more fat? Well, insulin resistance and high insulin levels. What are the open questions? What causes insulin resistance, and what causes high insulin levels? Lustig has a possible answer for the first one, and basic biochemistry has already established the second one driven by blood sugar.
A little knowledge is a dangerous thing. You know this one basic fact about metabolism so you assume it must work in a really simple way you understand and be responsible for everything.
If you want to make the claim that "tastiness" drives insulin resistance, which then opens up the door to a susceptibility to high insulin levels (or leptin, which also tracks carbohydrate intake), you've got to show that mechanism.
I don't want to make that claim. You've decided the only possible way to get fat is via insulin resistance (well at least for the 70% who have both conditions), so if palatability contributes to obesity you're assuming it must work in this bizarre fashion.
I think what you've been trying to say (and I could be mistaken), is that "tastiness" is *always* the path to obesity, and that other mechanisms for insulin resistance are bunk. It's also quite possible that what you've heard from me is that fructose is *always* the path to obesity, which I assure you is not my intention.
You are mistaken. I think "tastiness" is often a major contributing factor to obesity. Social cues, sleeping, meal sizes & times, activity levels, satiability and probably a few other things are factors in the modern prevalence of obesity.
Unless the entire western world under went a mutation in the last 100 years and everyone who moves to a western society undergoes the same mutation.
Actually, my understanding is that it's more like Lamarck was correct in some evolutionary cases - prenatal environment (which is passed on by the mother, even though it isn't strictly genetic it shows inheritance), can dramatically change the insulin resistance of offspring. It shows up in generations of natives who have generations get more and more obese as the high blood sugar environment is "passed on" to children in the womb.
So is it necessarily due to a genetic mutation that's isolated to a specific population group? Probably not - all humans are pretty much all humans and race is an imaginary construct.
Even if you assume an epigenetic factor is at work in western populations you still need to explain why it was activated in western populations and not ancestral populations eating lots of sugar, fructose, and carbs.
Claiming insulin works significantly differently in mice is a VERY bold claim, evolutionary biologists would likely be astonished if a shared basic metabolic hormone had different effects between our species (and that nutritionists were so impossibly daft as to never notice it).
That's the claim of the study that insulin injections can cause mice to lose weight.
You're quite literally saying "a study that directly contradicts my theory is wrong because it directly contradicts my theory".
You seem to have this idea that since insulin is the mechanism for fat storage it's a mathematical truth that it drives obesity. Either every mainstream nutrition researcher is a fraud or a complete moron or the picture is a lot more complicated than you realize it is.
By 'metabolic ward' you mean from hospitals?
You could probably construct a metabolic ward anywhere - I mean an isolated environment, where every calorie in and calorie out of the whole environment is controlled, measured, and analyzed. See the report from Peter Attia on his experience going through metabolic ward testing.
That's a useful component for research, and it's done, but it's not nearly as generalizable you think it is. A metabolic ward is by definition a highly a-typical environment and putting someone in a metabolic ward introduces a pile of confounders that don't show up in the normal population.
Yeah, too bad we didn't have some large field of people, dedicated to applying skepticism and falsifiability in investigating these issues.
Yes, it's really too bad. The practice of science has gone from the pursuit of knowledge to a hierarchical grant grubbing factory where toeing the line of current dogma is a prerequisite to success. The fact that someone like Ancel Keys was able to demonize fat to the point that we've raised two whole generations under his misguided nutritional advice and suffered through the worst epidemics of diabetes, heart disease, cancer and other chronic diseases is a testament to the damage one motivated individual can do given the reins of a paternalistic government.
Your evidence that two generations of nutritional scientists are complete bunk and someone publishing thousands of papers without actually doing any useful work is largely based on a book by a journalist. I don't think even Lustig, the one controversial nutrition researcher you've cited a few times, agrees with Taubes.
You can eat pretty much whatever balance of macronutrients you want, but if you're not in a developed economy you're probably not obese.
Maybe your idea of a "developed economy" differs than mine. Obesity is a form of malnutrition, and there are plenty of third world countries where obesity is rampant. Now granted, that's not an "ancestral diet", but I think it's difficult to find, much less define "ancestral diets". Do you have a specific example that would help illustrate what you mean?
In 3rd world countries the fat people are generally just the city dwellers. I guess 'developed economy' was a bad way to put it, populations who's lifestyle hasn't changed significantly in the past 500-1000 years. Subsistence hunters or populations using traditional farming techniques.
r. You think there's something with fructose in particular that causes insulin resistance with the same insulin levels?
Lustig posits (and I think it's fairly reasonable as at least one method) that fructose causes insulin resistance, and that before that point, insulin levels are perfectly well handled (allowing for the high starch/no insulin resistance == not much obesity populations). I think it's also possible that chronically elevated insulin levels in the absence of significant fructose could also be doing something to drive insulin resistance, but that's not as clearly outlined in biomechanical process as Lustig has with his fructose theory. It may be, as with insulin resistance, fructose effect occurs on a spectrum.
So it looks like fructose can be a factor in insulin resistance and it plays a role in abdominal fat. But I'm still not convinced that insulin resistance itself is a cause, and not a symptom of obesity.
So none of those Chinese people are adapted to fat? Is that genetic or environmental?
I'm claiming that any population you identify with a high carb diet and low obesity rates does not have significant allergies to carbohydrates. What triggers an allergy to carbohydrates may be a combination of genetic or environmental factors.
I'd approach the claim of genetic factors with extreme skepticism. Unless the entire western world under went a mutation in the last 100 years and everyone who moves to a western society undergoes the same mutation.
There's a genetic component to obesity obviously, but the smoking gun lies in modern diet and lifestyles.
Are you claiming that mice don't experience lipophypertrophy
I thought that was your claim - insulin given to mice, according to your cite, did not cause fat accumulation.
Lipohypertrophy is a specific form of localized weight gain. The cite said that injecting insulin did not cause total fat gain. Claiming insulin works significantly differently in mice is a VERY bold claim, evolutionary biologists would likely be astonished if a shared basic metabolic hormone had different effects between our species (and that nutritionists were so impossibly daft as to never notice it).
Show me an insulin sensitive person who isn't overweight, and loses 140 pounds on low carb, and then we'll be able to find out if there are any other reasons why low carb works:)
Sure (just a joke in poor taste, I have no idea what her actual diet was).
There might be some bias towards calories from protein being used for muscle, and calories from fat or carbs ending up in lipids, but my understanding is that's not a huge factor. Looking at how gross macronutrients are used I think calories in/calories out is the thing to go by. There probably are foods that are better at providing energy or building muscle, but I suspect that's more complicated than macronutrient categories. Either way I don't know a lot about that area of the science but I'm very skeptical that 4000 kcal of fat and protein will leave you thinner than 4000 kcal of carbs. The evidence around low carb diets indicate they work because people spontaneously consume fewer calories (high protein more so).
I vividly remember seeing something like this once. I was coming home from a hockey practice and saw a large meteor break into two halves before fading out.
Of course I was probably about 8 at the time, and only a couple year earlier I remember seeing a triangular light I thought was a UFO (I tried to get my parents to call the police to report it).
So take my recollection with a tunguska sized grain of salt.
But there's a big before and after period and we don't know how relevant the paleolithic diet is to modern nutrition.
Truth be told, I think it's difficult to make claims about any period that long ago, which was my problem with your contention that ancestral cultures were somehow high carb.
My bad. I meant cultures currently living an ancestral lifestyle (or at least undeveloped). Basically obesity is a disease of civilization. You can eat pretty much whatever balance of macronutrients you want, but if you're not in a developed economy you're probably not obese.
I never said Japan ate a lot of sugar, I said they ate a lot of carbs.
But if it's fructose (found in sugar), as per Lustig, that sets up insulin resistance, then the pattern fits. Once their sugar consumption goes up, their high starch diet will result in more obesity.
What about sugar without fructose? Starch causes a pretty big insulin response, sometimes higher than pure sugar. You think there's something with fructose in particular that causes insulin resistance with the same insulin levels?
If we're all adapted to high fat then why are all those other Chinese communities healthy?
I think perhaps I'm not being clear - I'm not saying we're all adapted to high fat, I'm simply saying that anyone who is obese is. People who swell up after eating peanuts are allergic to peanuts, but that doesn't mean everyone is.
So none of those Chinese people are adapted to fat? Is that genetic or environmental?
I assume you're not referring to the evidence that insulin is the mechanism for fat storage in humans, because it plays the exact same role in mice.
Apparently not if you can inject it into mice and not have fat accumulation. Or is there some biomechanism that you're going to assert interrupts the fat storage capacity of insulin in the experiments you referenced?
Are you claiming that mice don't experience lipophypertrophy, or are you claiming that since mice don't confirm your theory that mice must be different then humans (this would be a very dubious claim).
How do non-insulin resistant people lose weight on low carb diets then?
A non-insulin resistant person isn't someone who needs to lose weight - their fat cells properly store and release fat as intended. Although granted, insulin resistance isn't a switch, it's a spectrum.
It doesn't matter if they don't have to lose weight, the fact is they DO lose weight. If low-carb works for people without insulin resistance then clearly insulin resistance isn't the only reason low-carb works.
Do you have to become insulin resistant before you become obese?
It certainly seems that case in the vast majority of cases, if further investigation in to the MHO doesn't show some problems with the studies you referenced.
Every "assertion" (except the vegetarian thing) I backed up in previous posts, often multiple times, with links to studies, journal articles, or blog posts with extensive citations to journal articles. How is that not data?
It's not a cite if it's not next to your assertion:) Just having a bibliography, and a bunch of assertions based on the bibliography isn't really showing data:)
The Masai and Inuit are famous for showing you can be healthy on a low carb high fat/protein diet, a fact I never argued with.
Excellent, then perhaps I misunderstood your position.
I'd take it a step farther and state that they also give us prominent evidence that ancestral cultures in wildly differing environments tended towards a low carb, high fat/protein diet.
Is a guy selling protein supplements really a reliable source for analysis on whether we're naturally meat eaters?
Even then at best he shows that the European paleolithic population ate a lot of meat. But there's a big before and after period and we don't know how relevant the paleolithic diet is to modern nutrition. Certainly most populations will eat fatty meat when available because it's a great energy source, that doesn't mean doing the same when you have unlimited quantities will keep you thin!
Advanced culture who's high carb and low obesity? Japan.
I never said Japan ate a lot of sugar, I said they ate a lot of carbs.
Primitive cultures who are high carb and low obesity? A bunch of other places in Asia and Africa.
Cite?
I don't know a lot about the site, but here's a bunch of carb heavy communities in China compared with a fat heavy community and there's not much difference. How do you explain that with the paleo evidence? If we're all adapted to high fat then why are all those other Chinese communities healthy? If the Chinese are adapted then how is the high fat community thin?
Injecting insulin not causing obesity? Done with mice.
Human evidence contraindicates.
It does? I assume you're not referring to the evidence that insulin is the mechanism for fat storage in humans, because it plays the exact same role in mice.
Replacing x% of calories from fat with pure sugar not causing obesity? Done with people.
Missing the insulin resistance factor.
People losing weight on high carb diets? Tons of vegetarians do this.
Again, insulin resistance factor.
So as long as you don't become insulin resistant then carbs won't make you fat? How do non-insulin resistant people lose weight on low carb diets then? Do you have to become insulin resistant before you become obese? (Assuming we ignore the non-insulin resistant obese)
If none of this data convinces you then what data possibly could?
Those aren't data, those are assertions.
Every "assertion" (except the vegetarian thing) I backed up in previous posts, often multiple times, with links to studies, journal articles, or blog posts with extensive citations to journal articles. How is that not data?
What examples? You simply said "virtually no ancestral cultures", without specifying what an "ancestral culture is", or even dealing with say, the Masai or the Inuit.
The Masai and Inuit are famous for showing you can be healthy on a low carb high fat/protein diet, a fact I never argued with.
The fact you can be healthy on a low carb diet doesn't mean you need a low carb diet. And how can you possibly justify using the Masai and Inuit as evidence while tossing out all of Asia?
No, you look for actual data, rather than rough proxies. The problem with the proxy data given is that it really doesn't show what you think it does.
What does this data look like?
Advanced culture who's high carb and low obesity? Japan.
Primitive cultures who are high carb and low obesity? A bunch of other places in Asia and Africa.
Injecting insulin not causing obesity? Done with mice.
Replacing x% of calories from fat with pure sugar not causing obesity? Done with people.
People losing weight on high carb diets? Tons of vegetarians do this.
Lack of correlation between carb intake and obesity in the US? You think the graphs must by lying because they don't agree with you.
If none of this data convinces you then what data possibly could? You've essentially decided the hormonal role of insulin is obvious and sufficient proof that it drives obesity and researchers are somehow too stupid to realize it.
Actually they did a study, something along these lines: they'd pick a divisive topic, and then show people arguments for and against either side of the topic. The people would also rate the effectiveness of the argument. They also marked down how strongly they believed in their position before and after reading the arguments.
When people read arguments for the side they already agreed with, they would end up agreeing even more strongly - no surprise there. Yet it turned out that when people read arguments against the side they agreed with, they would *still* end up agreeing even more strongly with their own position. In fact, the more well-rated an argument was by people who agreed with that side, the more it would cause someone who already disagreed to disagree even further.
Unfortunately that was a bit laboured and I have no links handy, but I'm pretty sure that's how it went. The net take-away is, you can't convince anybody via textual arguments if they already strongly agree with something. The internet's archives are ample proof of this.
I remember that study but I don't think it shows what most people think it does.
Basically they asked someone how they felt about a topic, showed them an argument that disagreed with them, then asked again and found they were even more convinced of their original position.
But if you think about it in practical terms that's neither surprising nor particularly irrational.
For instance I believe AGW is real. I admit there's some degree of uncertainty, and papers that are wrong, and even researchers or journals not being as unbiased as they should be. But on the balance of evidence I think the evidence for AGW is overwhelming.*
But a true believer who thinks AGW is a mistake or a fraud is going to come to the table with very refined arguments. They'll quote studies, incidents, effects, mistakes, all sorts of things I'll have no answer for. For me to simply switch sides in the face of those arguments would frankly be irrational, since all I'd have to do was wait until I ran into a well educated advocate for the other side and I'd switch back!
Instead I reinforce my opposition to their position and argue back. Push their arguments trying to look for holes or misrepresented facts. This is what I think the study detects, the defensive response when people enter an argument.
What they don't look at is what happens later. When you keep thinking about the good arguments and doing research and the other side still holds up. Eventually if people keep seeing the good arguments they start to reevaluate their position, but it doesn't happen over the course of a single argument where people are trying to defend themselves.
I actually had this happen with regards to nutrition, I'd heard some extended interviews with Gary Taubes explaining how nutrition science had gotten it wrong and carbs and insulin were the true cause of obesity and I was a believer for a time. But then a friend argued with me, presenting some good points, so I dug in and defended Taubes hypothesis. But later I went back, did my own research, and eventually came to the conclusion that Taubes was wrong.**
If that episode was in that study I'd probably been just as sure as before of Taubes in the immediate aftermath of that conversation. But that conversation eventually led me to reverse my position entirely.
* This is just an example, I'm not trying to cause an AGW debate. ** Or a Taubes debate, I've already got one going
Insulin resistance will screw with the regulation but that doesn't mean it started the obesity or is the main driver.
I guess my problem is that we've identified the biochemical driver, and Lustig has an idea of what triggers the insulin resistance, but you're positing some other trigger event or "main driver" that doesn't have a biochemical basis.
I don't know exactly how the brain understands its weight level, but the set point certainly does exist and I can't see how insulin responding to blood sugar alone could be responsible for this.
You forgot the variable "insulin resistance" again - if the brain can tell when muscles are starving (a fair assumption), and insulin resistance causes insulin response to blood sugar to cause a partitioning of energy away from muscles into fat cells (i.e., starving the muscles), then the brain simply needs to know when the muscles are starving for insulin response and insulin resistance to be the root cause.
Show me a country where 2-pack a day smokers have a drastically lower lung cancer rate and we'll talk.
I think we're now arguing individuals versus populations by accident. Your ask was "why can't *I*" do something that another group of people can do. I replaced "group of people" with "a group of 1 that you could be jealous of", and I think what you're trying to say is that you want *more* than a group of one...but that doesn't address the point I was trying to make, that a location where a diet has a different effect cannot be considered something you can extrapolate to everyone.
If multiple different populations stay thin on a high carb diet there's obviously a big piece missing from Taubes' hypothesis.
Virtually no ancestral cultures have high levels of obesity, but tons have high levels of carb intake.
Actually, I think the data on ancestral cultures points in the opposite direction - they had high levels of animal fat intake, and no significant carbs to speak of.
What data? You're just making a bald assertion in the face of multiple examples I gave you.
And don't just throw back the Inuit, your position requires that virtually every ancestral culture for whom we have a good idea of the diet and the obesity levels should show the relation.
And if carbs are responsible for obesity then why did we eat more calories from carbs 100 years ago than we do today
That's simply not true. The USDA data isn't accurate or useful.
If your interpretation of the biochemistry tells you that insulin is driving obesity then your interpretation is wrong because the evidence is pretty overwhelming that carbs are not the culprit.
Again, you've started with incorrect premises, so you've come to an incorrect conclusion.
So if the data doesn't agree with you you'll just ignore it? How do you know Taubes gave you good data? Particularly since I've already given you examples where he gave bad data? What data do you have other than the low carb diet which can be explained by other factors and biochemical facts about a hormone that is only one part of a highly complex system?
Correct. What I've denied is that it plays a major role in driving obesity.
Maybe terminology is hanging you up here - I'm asserting "obesity" == "excess fat accumulation". Since insulin drives fat accumulation, *something* must cause insulin to behave in excess. You seem to be implying that it's not blood sugar, or insulin resistance that causes insulin to behave in excess, but "tastiness" or "craving".
I suppose a simple test would be to see if someone can force themselves to "crave" something, be fed foods that don't raise blood sugar levels, and see if that causes their insulin to drive fat accumulation in the absence of blood sugar spikes.
If I have a nice big juicy steak for dinner I'll be ravenously hungry through the next evening.
Funny, it's rather the opposite for me...although perhaps your juicy steak isn't fatty enough, and you're maxing yourself out on protein (which, does have some minor insulin effect).
So because 'overeating' is a somewhat arbitrary measure depending on multiple factors it doesn't count?
No, I'm not being clear enough - because "overeating" is defined by the outcome, not the action, it's simply a restatement of the outcome. If you're fat, you're "overeating", no matter what your actual eating behavior is. So when you say someone is "overeating", your just saying "you're fat". "Overeating" isn't *why* you got fat, it's simply an assertion that you *are* fat.
So, by that rationale, someone who is speeding on the highway is "over accelerating" - even their foot is on the brake, and the car is out of gas. "Over accelerating" is simply a restatement of the observation that someone is speeding, without any insight into the *cause* of the over acceleration. Perhaps the acceleration is there because the car is being towed, or because the road is going downhill, or someone just hit them from behind - but *that* is what is important, not simply "you're over accelerating".
I'm not confused about terminology or bothered by your issues with "overeating". Yes insulin drives fat accumulation, and the thing that causes insulin to behave in excess is all the food we eat.
Our brain is actively maintaining the level of fatness. If your brain feels it has too much fat and your muscles need energy is will try to take calories from the fat instead of food.
How does the brain actively maintain the level of fatness? Are you saying that even in the presence of insulin resistance, that your brain can override your fat and muscle tissue and make them partition fuel despite the influence of insulin?
Insulin resistance will screw with the regulation but that doesn't mean it started the obesity or is the main driver.
I don't know exactly how the brain understands its weight level, but the set point certainly does exist and I can't see how insulin responding to blood sugar alone could be responsible for this.
If a Japanese or Vietnamese person can be thin with a bunch of calories from white rice why can't I?
If a two pack a day smoker can live until 94 years old without lung cancer, why can't everyone?
In the case of people living in Japan or Vietnam, more things than just their caloric intake of white rice vary - other portions of diet, other environmental factors, all can create a situation that isn't applicable to other locations.
Show me a country where 2-pack a day smokers have a drastically lower lung cancer rate and we'll talk.
Here's the big problem with the Taubes idea.
We weren't always fat. Virtually no ancestral cultures have high levels of obesity, but tons have high levels of carb intake. Some even eat a ton of fruit and honey. You can also swap out a bunch of fat for sugar and not gain weight with modern people.
If your interpretation of the biochemistry tells you that insulin is driving obesity then your interpretation is wrong because the evidence is pretty overwhelming that carbs are not the culprit.
Slashdot Mirror
Dude, the Far Canadian North is NOT used for smuggling anything in the country, it is just not economical.
Load a pallet of drugs onto a ship. Coast guard can't do anything because it's international waters.
When the coast is clear send in a smaller boat (or rendezvous with one) and dump it on the shore. Then hire a bunch of guys to ride in on snowmobiles and take it down south.
If you're shipping enough drugs or other contraband the low risk could make it economical.
I noticed you didn't quite say that insulin causes hunger and extra eating, which is good because it doesn't.
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".
Except we haven't.
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.
My bad, I was thinking statistically valid as a whole, not necessarily those two specific foods. By eye proteins show comparable insulin responses to carbs (and running the numbers would doubtlessly confirm that), which is expected because we know protein stimulates insulin release.
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?
Nope.
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?
Someone who doesn't like chips probably won't get fat off them. But for berries factors like fibre, flavour, and moisture content might mean berries can reach that same level of addictivness.
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.
No, I've talked extensively about carbs with a high GI and insulin response like rice.
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.
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?
Did you come to this conclusion before or after the evidence the insulin hypothesis didn't work in non-industrial cultures?
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.
MHO==MOH==Morbidly Obese Humans?
Insulin resistance is more complicated than you think.
1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.
Mostly just in the sense that fat is very energy dense and make foods more palatable leading us to overeat. It may be linked to heart disease in industrial societies but not non-industrial.
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.
Except easily digestible carbs like rice are fine in Japan, and countless non-industrial nations the only real common factor in obesity is industrial societies (though some like Japan avoid this).
That and protein also causes a similar effect on insulin (ie fish).
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.
I agree, but for different reasons
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.
Maybe they're factors but my BS meter is go
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? :)
One facet of biochemistry, insulin used to store fat, and you've figured out obesity.
But take a statistical test that is a mathematical fact and now you have a problem?!?
If they effed up the stats that's a problem, but if they didn't, and they did the experiment they said they did, then you now have to deal with the fact that porridge triggered a smaller insulin response than fish and you don't understand everything that goes on with insulin responses like insulin release in response to protein.
The sample is too small if the effect size is tiny, but the results were statistically valid so the sample was apparently fine.
What units are you going to measure tastiness in? Even if it's fuzzy, it has to be measured.
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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 :)
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.
I seriously have no idea how you think that could be my assertion.
Unless your metabolic ward is the friggin Truman Show I don't think that's gonna work.
One of the first things I posted, I'm tired of constantly re-linking.
Even if I agreed with that Lustig assertion (which I don't). Taubes theory is that carbs are bad, refined carbs particularly so, and that the more insulin it releases the more fattening it is.
Even with sugar it's hard to get a bigger insulin spike than white rice or baked potatos, and 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.
You keep claiming I've contradicted myself on the mouse experiment, but I haven't the foggiest idea what you're referring to. Though considering your bizarre statement that I asserted "that social cues and depression and routine somehow stimulate insulin" in my previous post I guess I shouldn't worry too much.
So you're now asserting that insulin isn't secreted in response to blood sugar. What, pray tell, is the mechanism you propose?
I'm saying that the relationship between blood sugar, insulin release, macronutrients, and other regulatory mechanisms (including glucagon) is a lot more complex than you realize.
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.
It's not about a war. It's about establishing sovereignty, and to maintain control over a territory you need to be police it.
The northwest passage is a big issue over whether it's international waters or Canadian waters. Not just because of potential oil drilling or fishing, but shipping is a big issue. It's a lot easier to ensure the shipping is done safely so a ton of oil isn't dumped on our coastline if we can police the waters. Security is also a concern as there's a lot of unpopulated places for smugglers to drop cargo or illegal immigrants.
A military grade stealth snowmobile is part of the bigger picture, it makes it easier to patrol the territory and search for smugglers or other criminals as well as shows we're taking that part of our territory seriously.
Not a fan of evolutionary psychology, but I think there's a lot of reason to think we do have an aptitude for spoken language. I wouldn't be at all surprised if a well designed voice system left more mental focus available for the task of coding.
I'm not sure if the technology is there yet, and you still don't want to hear your officemates jabbering away, but I could see the theoretical usability of a spoken word interface surpassing that of typing.
Let's take the Hazda:
http://www.epjournal.net/wp-content/uploads/EP07601616.pdf
None of those starches or sugars is refined at all, which likely reduces the amount of effect that it can have on insulin levels, much less insulin resistance. Hell Baobab is even advertised as low glycemic: (http://baobab-fruit.com)
Even honey is a relatively low glycemic index: http://www.livestrong.com/article/270875-honey-vs-sugar-glycemic-index/
Using the Hazda to refute the insulin hypothesis, given the low glycemic values of their diet, seems inappropriate.
There's still a lot of berries and starch. And the very low fat content.
That's a pretty lame reductio ad absurdum. How many times do people go out drinking with friends in a metabolic ward? Go to a potluck, head out for lunch, play a soccer game, go for a walk, have a chat with friends, or work late and hit the snack machine or food stash in their desk? 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.
You can test specific hypotheses in a metabolic ward, but it's not a magic bullet.
Lets forget the tribesmen he implied used a fattening ceremony based off carbs, but really did it with fat. 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. And how injecting insulin into mice doesn't cause obesity, and replacing fat calories with sugar calories 1-1 doesn't cause obesity, and insulin resistance seems to be a mechanism to keep excess glucose out of cells so it doesn't poison cells (don't think I linked this one). And how obesity in the US shows no relationship to carbohydrate consumption.
And lets just concentrate the fact that GI isn't really correlated to insulin after all. So all that carbohydrate evidence he thinks he has doesn't even exist.
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. If they did it your way you'd be complaining because they either tested fewer foods or did it with fewer volunteers. The only issue is like all studies of their kind it's done on a bunch of western university students.
And it's not the only study that decouples insulin and GI.
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. You haven't even accounted for glucagon!
Some people have done some serious research into hyperpalatable foods. There are some characteristics of palatability, crunchiness, low bitterness, sugar, fat, salt. But the fact you don't want to accept a fuzzy definition doesn't mean its not a real thing. 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?
That doesn't mean people haven't tried but you're not going to get a simple story.
I thought you agreed that there is no ancestral population eating lots of sugar (i.e., like comparing sugar comparison between Japan and the US).
Name a single ancestral population eating lots of sugar, fructose and carbs.
Ok
I'm not sure what this study B you're talking about is. Outside of lipohypertrophy (something different) or insulin used to treat a specific disorder (very specific circumstances and I don't think I posted it anyways) I can't remember posting anything like that.
You can examine what happens when you eat specific foods in detail and that very valuable. But obesity is caused by our entire lifestyle and can't replicate their lifestyles in a metabolic ward.
A journalist who has painstakingly cited every finding he's shown. He's just the messenger, the real data is there, and that needs to be contended with.
WTF do you think I've been doing?!? I've shown real data he's misrepresented. I've shown counter examples he's ignored. I've shown how everyone else knows about this 'real data' but also knows the other data that leads to different conclusions!
All Taubes has done is cherrypicked and misrepresented some data and ended up with some fame and a pile of money.
And isn't it possible that this spontaneous reaction is due to the partitioning of energy? As the body starts getting more energy partitioned to muscle, and less to fat storage, wouldn't whatever "hunger" mechanism kick in and cause a loss of appetite, or "exercise" mechanism kick in and cause a greater expenditure of energy?
Furthermore, wouldn't *any* change in the partitioning in energy (from what ever source), truly be the *cause* of the different behavior?
Except people on low carb diets typically increase their protein consumption (high protein works better than low carb for weight loss).
Low carb also means you need to exclude a bunch of foods including stables like bread, pasta, rice, potatoes, etc. Hunger isn't just a physical reaction. If you exclude a food you tend to overeat then you usually don't replace all those calories with an alternative.
It also means they pay more attention to what they're eating.
So why do fat cells accumulate more fat? Well, insulin resistance and high insulin levels. What are the open questions? What causes insulin resistance, and what causes high insulin levels? Lustig has a possible answer for the first one, and basic biochemistry has already established the second one driven by blood sugar.
A little knowledge is a dangerous thing. You know this one basic fact about metabolism so you assume it must work in a really simple way you understand and be responsible for everything.
For instance, given your understanding of this basic biochemistry how do you explain the fact that fish causes higher insulin levels than porridge?
If you want to make the claim that "tastiness" drives insulin resistance, which then opens up the door to a susceptibility to high insulin levels (or leptin, which also tracks carbohydrate intake), you've got to show that mechanism.
I don't want to make that claim. You've decided the only possible way to get fat is via insulin resistance (well at least for the 70% who have both conditions), so if palatability contributes to obesity you're assuming it must work in this bizarre fashion.
I think what you've been trying to say (and I could be mistaken), is that "tastiness" is *always* the path to obesity, and that other mechanisms for insulin resistance are bunk. It's also quite possible that what you've heard from me is that fructose is *always* the path to obesity, which I assure you is not my intention.
You are mistaken. I think "tastiness" is often a major contributing factor to obesity. Social cues, sleeping, meal sizes & times, activity levels, satiability and probably a few other things are factors in the modern prevalence of obesity.
Actually, my understanding is that it's more like Lamarck was correct in some evolutionary cases - prenatal environment (which is passed on by the mother, even though it isn't strictly genetic it shows inheritance), can dramatically change the insulin resistance of offspring. It shows up in generations of natives who have generations get more and more obese as the high blood sugar environment is "passed on" to children in the womb.
So is it necessarily due to a genetic mutation that's isolated to a specific population group? Probably not - all humans are pretty much all humans and race is an imaginary construct.
Even if you assume an epigenetic factor is at work in western populations you still need to explain why it was activated in western populations and not ancestral populations eating lots of sugar, fructose, and carbs.
You're quite literally saying "a study that directly contradicts my theory is wrong because it directly contradicts my theory".
You seem to have this idea that since insulin is the mechanism for fat storage it's a mathematical truth that it drives obesity. Either every mainstream nutrition researcher is a fraud or a complete moron or the picture is a lot more complicated than you realize it is.
That's a useful component for research, and it's done, but it's not nearly as generalizable you think it is. A metabolic ward is by definition a highly a-typical environment and putting someone in a metabolic ward introduces a pile of confounders that don't show up in the normal population.
Your evidence that two generations of nutritional scientists are complete bunk and someone publishing thousands of papers without actually doing any useful work is largely based on a book by a journalist. I don't think even Lustig, the one controversial nutrition researcher you've cited a few times, agrees with Taubes.
Maybe your idea of a "developed economy" differs than mine. Obesity is a form of malnutrition, and there are plenty of third world countries where obesity is rampant. Now granted, that's not an "ancestral diet", but I think it's difficult to find, much less define "ancestral diets". Do you have a specific example that would help illustrate what you mean?
In 3rd world countries the fat people are generally just the city dwellers. I guess 'developed economy' was a bad way to put it, populations who's lifestyle hasn't changed significantly in the past 500-1000 years. Subsistence hunters or populations using traditional farming techniques.
So it looks like fructose can be a factor in insulin resistance and it plays a role in abdominal fat. But I'm still not convinced that insulin resistance itself is a cause, and not a symptom of obesity.
I'd approach the claim of genetic factors with extreme skepticism. Unless the entire western world under went a mutation in the last 100 years and everyone who moves to a western society undergoes the same mutation.
There's a genetic component to obesity obviously, but the smoking gun lies in modern diet and lifestyles.
Lipohypertrophy is a specific form of localized weight gain. The cite said that injecting insulin did not cause total fat gain. Claiming insulin works significantly differently in mice is a VERY bold claim, evolutionary biologists would likely be astonished if a shared basic metabolic hormone had different effects between our species (and that nutritionists were so impossibly daft as to never notice it).
Sure (just a joke in poor taste, I have no idea what her actual diet was).
There might be some bias towards calories from protein being used for muscle, and calories from fat or carbs ending up in lipids, but my understanding is that's not a huge factor. Looking at how gross macronutrients are used I think calories in/calories out is the thing to go by. There probably are foods that are better at providing energy or building muscle, but I suspect that's more complicated than macronutrient categories. Either way I don't know a lot about that area of the science but I'm very skeptical that 4000 kcal of fat and protein will leave you thinner than 4000 kcal of carbs. The evidence around low carb diets indicate they work because people spontaneously consume fewer calories (high protein more so).
I vividly remember seeing something like this once. I was coming home from a hockey practice and saw a large meteor break into two halves before fading out.
Of course I was probably about 8 at the time, and only a couple year earlier I remember seeing a triangular light I thought was a UFO (I tried to get my parents to call the police to report it).
So take my recollection with a tunguska sized grain of salt.
I can see why you disagree with the term 'overeating' if you don't believe calories from protein or fat ever end up in our fat....
But if that's the case, and you eat 4000 kcal of fat and protein and burn only 2500 kcal, then what do you think happens to the extra 1500 kcal?
Truth be told, I think it's difficult to make claims about any period that long ago, which was my problem with your contention that ancestral cultures were somehow high carb.
My bad. I meant cultures currently living an ancestral lifestyle (or at least undeveloped). Basically obesity is a disease of civilization. You can eat pretty much whatever balance of macronutrients you want, but if you're not in a developed economy you're probably not obese.
What about sugar without fructose? Starch causes a pretty big insulin response, sometimes higher than pure sugar. You think there's something with fructose in particular that causes insulin resistance with the same insulin levels?
So none of those Chinese people are adapted to fat? Is that genetic or environmental?
Are you claiming that mice don't experience lipophypertrophy, or are you claiming that since mice don't confirm your theory that mice must be different then humans (this would be a very dubious claim).
A non-insulin resistant person isn't someone who needs to lose weight - their fat cells properly store and release fat as intended. Although granted, insulin resistance isn't a switch, it's a spectrum.
It doesn't matter if they don't have to lose weight, the fact is they DO lose weight. If low-carb works for people without insulin resistance then clearly insulin resistance isn't the only reason low-carb works.
It certainly seems that case in the vast majority of cases, if further investigation in to the MHO doesn't show some problems with the studies you referenced.
It's not a cite if it's not next to your assertion :) Just having a bibliography, and a bunch of assertions based on the bibliography isn't really showing data :)
Well what would you accept as data?
AGW == Anthropocentric Global Warming.
It basically means the planet is getting warmer and humans are the cause, it's essentially the climatology consensus in 3 letters.
Excellent, then perhaps I misunderstood your position.
I'd take it a step farther and state that they also give us prominent evidence that ancestral cultures in wildly differing environments tended towards a low carb, high fat/protein diet.
http://www.proteinpower.com/drmike/low-carb-diets/are-we-meat-eaters-or-vegetarians-part-iii/
Is a guy selling protein supplements really a reliable source for analysis on whether we're naturally meat eaters?
Even then at best he shows that the European paleolithic population ate a lot of meat. But there's a big before and after period and we don't know how relevant the paleolithic diet is to modern nutrition. Certainly most populations will eat fatty meat when available because it's a great energy source, that doesn't mean doing the same when you have unlimited quantities will keep you thin!
http://www.wolframalpha.com/input/?i=sugar%20consumption%20per%20capita%20in%20USA%20and%20Japan
I never said Japan ate a lot of sugar, I said they ate a lot of carbs.
Cite?
I don't know a lot about the site, but here's a bunch of carb heavy communities in China compared with a fat heavy community and there's not much difference. How do you explain that with the paleo evidence? If we're all adapted to high fat then why are all those other Chinese communities healthy? If the Chinese are adapted then how is the high fat community thin?
Human evidence contraindicates.
It does? I assume you're not referring to the evidence that insulin is the mechanism for fat storage in humans, because it plays the exact same role in mice.
Missing the insulin resistance factor.
Again, insulin resistance factor.
So as long as you don't become insulin resistant then carbs won't make you fat? How do non-insulin resistant people lose weight on low carb diets then? Do you have to become insulin resistant before you become obese? (Assuming we ignore the non-insulin resistant obese)
Those aren't data, those are assertions.
Every "assertion" (except the vegetarian thing) I backed up in previous posts, often multiple times, with links to studies, journal articles, or blog posts with extensive citations to journal articles. How is that not data?
What examples? You simply said "virtually no ancestral cultures", without specifying what an "ancestral culture is", or even dealing with say, the Masai or the Inuit.
The Masai and Inuit are famous for showing you can be healthy on a low carb high fat/protein diet, a fact I never argued with.
The fact you can be healthy on a low carb diet doesn't mean you need a low carb diet. And how can you possibly justify using the Masai and Inuit as evidence while tossing out all of Asia?
No, you look for actual data, rather than rough proxies. The problem with the proxy data given is that it really doesn't show what you think it does.
What does this data look like?
Advanced culture who's high carb and low obesity? Japan.
Primitive cultures who are high carb and low obesity? A bunch of other places in Asia and Africa.
Injecting insulin not causing obesity? Done with mice.
Replacing x% of calories from fat with pure sugar not causing obesity? Done with people.
People losing weight on high carb diets? Tons of vegetarians do this.
Lack of correlation between carb intake and obesity in the US? You think the graphs must by lying because they don't agree with you.
If none of this data convinces you then what data possibly could? You've essentially decided the hormonal role of insulin is obvious and sufficient proof that it drives obesity and researchers are somehow too stupid to realize it.
Actually they did a study, something along these lines: they'd pick a divisive topic, and then show people arguments for and against either side of the topic. The people would also rate the effectiveness of the argument. They also marked down how strongly they believed in their position before and after reading the arguments.
When people read arguments for the side they already agreed with, they would end up agreeing even more strongly - no surprise there. Yet it turned out that when people read arguments against the side they agreed with, they would *still* end up agreeing even more strongly with their own position. In fact, the more well-rated an argument was by people who agreed with that side, the more it would cause someone who already disagreed to disagree even further.
Unfortunately that was a bit laboured and I have no links handy, but I'm pretty sure that's how it went. The net take-away is, you can't convince anybody via textual arguments if they already strongly agree with something. The internet's archives are ample proof of this.
I remember that study but I don't think it shows what most people think it does.
Basically they asked someone how they felt about a topic, showed them an argument that disagreed with them, then asked again and found they were even more convinced of their original position.
But if you think about it in practical terms that's neither surprising nor particularly irrational.
For instance I believe AGW is real. I admit there's some degree of uncertainty, and papers that are wrong, and even researchers or journals not being as unbiased as they should be. But on the balance of evidence I think the evidence for AGW is overwhelming.*
But a true believer who thinks AGW is a mistake or a fraud is going to come to the table with very refined arguments. They'll quote studies, incidents, effects, mistakes, all sorts of things I'll have no answer for. For me to simply switch sides in the face of those arguments would frankly be irrational, since all I'd have to do was wait until I ran into a well educated advocate for the other side and I'd switch back!
Instead I reinforce my opposition to their position and argue back. Push their arguments trying to look for holes or misrepresented facts. This is what I think the study detects, the defensive response when people enter an argument.
What they don't look at is what happens later. When you keep thinking about the good arguments and doing research and the other side still holds up. Eventually if people keep seeing the good arguments they start to reevaluate their position, but it doesn't happen over the course of a single argument where people are trying to defend themselves.
I actually had this happen with regards to nutrition, I'd heard some extended interviews with Gary Taubes explaining how nutrition science had gotten it wrong and carbs and insulin were the true cause of obesity and I was a believer for a time. But then a friend argued with me, presenting some good points, so I dug in and defended Taubes hypothesis. But later I went back, did my own research, and eventually came to the conclusion that Taubes was wrong.**
If that episode was in that study I'd probably been just as sure as before of Taubes in the immediate aftermath of that conversation. But that conversation eventually led me to reverse my position entirely.
* This is just an example, I'm not trying to cause an AGW debate.
** Or a Taubes debate, I've already got one going
I guess my problem is that we've identified the biochemical driver, and Lustig has an idea of what triggers the insulin resistance, but you're positing some other trigger event or "main driver" that doesn't have a biochemical basis.
You forgot the variable "insulin resistance" again - if the brain can tell when muscles are starving (a fair assumption), and insulin resistance causes insulin response to blood sugar to cause a partitioning of energy away from muscles into fat cells (i.e., starving the muscles), then the brain simply needs to know when the muscles are starving for insulin response and insulin resistance to be the root cause.
I think we're now arguing individuals versus populations by accident. Your ask was "why can't *I*" do something that another group of people can do. I replaced "group of people" with "a group of 1 that you could be jealous of", and I think what you're trying to say is that you want *more* than a group of one...but that doesn't address the point I was trying to make, that a location where a diet has a different effect cannot be considered something you can extrapolate to everyone.
If multiple different populations stay thin on a high carb diet there's obviously a big piece missing from Taubes' hypothesis.
Actually, I think the data on ancestral cultures points in the opposite direction - they had high levels of animal fat intake, and no significant carbs to speak of.
What data? You're just making a bald assertion in the face of multiple examples I gave you.
And don't just throw back the Inuit, your position requires that virtually every ancestral culture for whom we have a good idea of the diet and the obesity levels should show the relation.
That's simply not true. The USDA data isn't accurate or useful.
Again, you've started with incorrect premises, so you've come to an incorrect conclusion.
So if the data doesn't agree with you you'll just ignore it? How do you know Taubes gave you good data? Particularly since I've already given you examples where he gave bad data? What data do you have other than the low carb diet which can be explained by other factors and biochemical facts about a hormone that is only one part of a highly complex system?
Maybe terminology is hanging you up here - I'm asserting "obesity" == "excess fat accumulation". Since insulin drives fat accumulation, *something* must cause insulin to behave in excess. You seem to be implying that it's not blood sugar, or insulin resistance that causes insulin to behave in excess, but "tastiness" or "craving".
I suppose a simple test would be to see if someone can force themselves to "crave" something, be fed foods that don't raise blood sugar levels, and see if that causes their insulin to drive fat accumulation in the absence of blood sugar spikes.
Funny, it's rather the opposite for me...although perhaps your juicy steak isn't fatty enough, and you're maxing yourself out on protein (which, does have some minor insulin effect).
I'd be curious to see what bulletproof coffee would do to your appetite: http://www.bulletproofexec.com/how-to-make-your-coffee-bulletproof-and-your-morning-too/
No, I'm not being clear enough - because "overeating" is defined by the outcome, not the action, it's simply a restatement of the outcome. If you're fat, you're "overeating", no matter what your actual eating behavior is. So when you say someone is "overeating", your just saying "you're fat". "Overeating" isn't *why* you got fat, it's simply an assertion that you *are* fat.
So, by that rationale, someone who is speeding on the highway is "over accelerating" - even their foot is on the brake, and the car is out of gas. "Over accelerating" is simply a restatement of the observation that someone is speeding, without any insight into the *cause* of the over acceleration. Perhaps the acceleration is there because the car is being towed, or because the road is going downhill, or someone just hit them from behind - but *that* is what is important, not simply "you're over accelerating".
I'm not confused about terminology or bothered by your issues with "overeating". Yes insulin drives fat accumulation, and the thing that causes insulin to behave in excess is all the food we eat.
How does the brain actively maintain the level of fatness? Are you saying that even in the presence of insulin resistance, that your brain can override your fat and muscle tissue and make them partition fuel despite the influence of insulin?
Insulin resistance will screw with the regulation but that doesn't mean it started the obesity or is the main driver.
I don't know exactly how the brain understands its weight level, but the set point certainly does exist and I can't see how insulin responding to blood sugar alone could be responsible for this.
Show me a country where 2-pack a day smokers have a drastically lower lung cancer rate and we'll talk.
Here's the big problem with the Taubes idea.
We weren't always fat. Virtually no ancestral cultures have high levels of obesity, but tons have high levels of carb intake. Some even eat a ton of fruit and honey.
You can also swap out a bunch of fat for sugar and not gain weight with modern people.
And if carbs are responsible for obesity then why did we eat more calories from carbs 100 years ago than we do today? And why isn't there a correlation between that macronutrient graph and obesity rates over the same period
If your interpretation of the biochemistry tells you that insulin is driving obesity then your interpretation is wrong because the evidence is pretty overwhelming that carbs are not the culprit.