Because we joined the UN as a permanent member of the security council. It's our job to protect the rights of foreign people from human rights violations.
I mean I suppose we could resign from our position, supposing you like the idea of China and Russia being in charge the security council.
But is the US capable of protecting them?
The mildest response is to send in a bunch of drones, blow up a bunch of Assad's stuff, and call it a day.
What if Assad then uses more gas? Same response or do you have to escalate? With or without gas what if Assad starts to win? What's the exit strategy?
I'm not completely opposed to a short bombing run from the US, saying "if you use chemical weapons we'll make you regret it". But going further and actually taking a real stake in the conflict, it's not just that I'm not sure the US can win, but I don't know if there's a way to avoid losing. There's no good guys left who are in a position to be a decent government, and any involvement becomes western interference in a Muslim Arab country and destabilizes the surrounding region. It might be that the best thing the US can do for Syrians is nothing.
Then I've failed to communicate that effectively to you:)
You think he meant so say it was merely possible for them to be fat? That vegetarianism could lead to other non-obesity related health problems? Because he didn't say anything remotely like that.
That sounds fair enough, but again, hardly resonating with an actual vegetarian (unless they happened to be one of those fat ones that tried to become vegetarian for health reasons, and weren't seeing success).
My take would be slightly different: "huh, I thought vegetarians were usually healthy, but I guess they must not be because he's done the research and they apparently aren't healthier" - and this, is arguably true.
Unless by "healthy" you mean thin I think your take misses the point.
The book is primarily about obesity. The interview was primarily about obesity. The exchange was primarily about obesity. And the statement in question specifically mentioned obesity.
I guess that's the argument in a nutshell - I'm arguing that psychological processes in the brain aren't primary drivers of appetite, they're secondary or tertiary. To quantify that, I think we're looking at metabolic ward studies, with various controls for macronutrients and a search for quantitative data on biomechanisms rather than subjective surveys.
I think that one thing matabolic ward studies would clear up is that they don't really explain the changes that lead to the small (Yes. You can't rely on getting good results out of bad data.
It's not a binary situation, every dataset has inadequacies, you take that into account with error bars and tempered interpretations, but it's a little too convenient to just throw it out entirely because it's a problem.
What if there wasn't a problem, what if it turned out the records were in fact good? How would you rationalize the data then?
I disagree. The conscious acknowledgement of "tastiness" may occur in some part of the frontal cortex, say, but when it comes to "tastiness as having an effect on actual biomarkers rather than a survey", that's something that is determined by a complex set of tissues and organs, including but not limited to parts of the brain that are not conscious.
I wonder if you would put the brain in a place of primacy if we were talking about say, vertical growth rather than horizontal growth. Would it be possible for the brain to psychologically retard (or accelerate) growth in height? Could it somehow reduce the amount of human growth hormone circulated by the pituitary? More importantly, since vertical growth requires a caloric imbalance (need more calories in than calories out), would the mechanisms you imagine for hunger and appetite be suppressible when trying to avoid vertical growth? Could a teenager reduce their appetite enough to limit their calories enough to stop their vertical growth from happening?
My guess is that you'd admit to the primacy of HGH in determining vertical growth, but that begs the question as to why you wouldn't admit the primacy of insulin in determining horizontal growth.
Well there's one big difference between eating and growing in that eating requires a conscious deliberate action and we know that a strong hunger response can be triggered by brain signals.
And I do agree that HGH is most responsible for height, with the caveat that there's MASSIVE factors I know I'm missing including things that probably counteract, enhance, or regulate HGH, and I don't know how HGH is involved in the feedback mechanism that actually determines how much we grow. We also know the conscious mind doesn't do a lot since vegetative patients still grow to a normal height.
Again, you bring in the messy brain in the example as a point of pride - eventually, every brain response has to culminate in some biomechanism for accumulating fat. You can do a more rigorous and profitable analysis by understanding the basic biomechanisms *first*, and then discovering how the brain might influence those levers. But you can't have a brain doing something magical and unobservable - it eventually needs to get down to the level of accumulating fat in a fat cell.
Wherever you start from you can't go around saying you solved the obesity epidemic when you've left out one of the primary drivers of appetite which you know if being manipulated in modern populations.
Okay, so let's get the test where we measure the biochemical process by which the brain influences say, tastiness. Let's throw away the subjective questionnaires, and measure the actual biochemical signals. Again, first principles, we need to go to the moment of action.
What are you talking about? Tastiness is be determined by signals in the brain, there are feedbacks that occur which changes how we perceive taste, but you're going back to this impractical standard of solving the system instead of analyzing it behaviourally.
Easy. Bad data. They even admit to it: "These numbers are probably not particularly accurate"
So you're throwing it out entirely? The numbers are fuzzy, but if they're even in the ballpark they contradict your allergy theory.
No, let's be specific - his failure was that he did not speak clearly enough to have his audience understand. That's a failing for someone who is trying to convey a point.
Understand what? I don't know his point.
I mean, honestly, do you think that Taubes' statement in that radio interview convinced a single vegetarian to start on an unhealthy, high glycemic carnivorous diet, as opposed to a healthy low-glycemic carnivorous diet?
I think a lot of listeners went through the program thinking "wow! he's dismantling all these things I knew about nutrition!" and when he got to that bit "huh, I thought vegetarians were usually thin, but I guess they must not be because he's done the research and they apparently weigh more."
His failure was that he was misunderstood. It's not really his fault that in an interview, when discussing in detail the fact that vegetarians were eating foods that by his rules should make them fat and diabetic, he simply claimed that vegetarians were in fact fat and diabetic.
It's clear that he really wanted to say...
After googling the only thing I can find about Taubes and vegitarianism is someone saying that in his book he claimed that Vegetarian Hindus in India were fatter than their non-vegetarian Christian and Muslim counterparts. But I could find no mention of that study, and similar studies, or the actual claim, or even another website saying he said it, so I have no idea what his actual explanation is or if there even is one. But given the obvious relevance to his hypothesis it seems odd that he hasn't dealt with the issue explicitly and directly.
I'm not sure if I quite understand your researcher/other person example.
The point is we can't isolate one variable and hold everything else constant. Other variables can kick in to compensate, the brain responds to the situation, and the factor you're measuring never has a total function as simple as your hypothesis. No matter what you do the data is really messy and the answers can only be guessed at by looking at a lot of different experiments.
And maybe that's the problem I have with your frame - you're asserting that the brain is some massively omnipotent organ that dictates to the rest of the body, and that we can ignore all other factors and concentrate on it as the first order term.
I'm arguing a different frame based on our observations of cellular intelligence (http://www.brianjford.com/w-intelcell.htm, for example). Given the biochemical processes on the *cellular* level is the only way to rationally attack this problem, as far as that frame goes.
No, I'm saying we already know the brain is heavily involved, including decisions made at an abstract level like comfort food or eating in company. Therefore to show a particular biochemical process is active you first need to measure the influence of the brain which we know is there.
So, are you leery of those who say "it's due to eating more calories than those burned!"?
Oversimplification, I'd be leery of those who say "it's all due to palatability", because activity levels, social factors, mental health, advertising, convenience, and a dozen other factors are all probably involved.
Btw, since you think the carb/obesity is only in western populations due to a carbohydrate allergy explain Cuba, during an economic crisis calories dropped from 3,100 to 2,300 and:
"The percentage of dietary fat in the energy intake decreased, while the contribution of carbohydrates (polished rice and refined cereals) increased from 64% in 1990 to 79.4% in 1993. Availability of essential dietary amino acids and fatty acids declined as a consequence of a reduced availability of animal protein and edible oils and fat. Sugar cane, a traditional source of energy in the Cuban diet, rose to 28% of total energy intake, almost three times that of the fat contribution."
Want to guess what happened? Obesity rates dropped by half. So what happened to the carb allergy that caused the initial obesity? Why did they start eating fewer calories? Despite the economic hardship there wasn't actual starvation so surely they could afford 800 of the cheapest calories per day, if your theory about their obesity being caused a carb allergy was correct the extra sugar and refined carbs should have given them uncontrollable hunger and blew them up like a balloon.
That being said, I'm not just talking about discrete simulations (as Wolfram has made particularly interesting finds in cellular automata), I'm talking about real world root cause failures in complex, integrated, man/logic/machine settings (which, do include a biological component of sorts). You cannot hope to find the truth in an analysis of a real-world system (again, not just some pre-programmed simulation, real computers doing real work with real people), without falsifiability.
I agree, but that doesn't mean the system is designed to be easily analyzed via falisifiability. I think a pretty common scenario goes something like this
Researcher: I have a great simple falsifiable hypothesis!
Other person: Awesome! What does it mean if it's true!
Researcher: Uhhh, well I got a list of things that might be happening if it's true.
Other person: Um ok, well you must have a pretty good idea if it's false then?
Researcher: Oh yeah! I got another list!
Other person:.... a lot of the items are the same.
Researcher: Yeah, sorry about that
Certainly hunger would be a complex one, but even in a complex system, you have first, second, third, etc order effects. Furthermore, as you noted, biology generally leads to extremely robust systems, and a system that ignored muscle starvation due to visual stimulation is distinctly *not* robust. The muscle cells can be considered as intelligent actors, just as intelligent as any bit of brain tissue, and they simply cannot be considered a lower order term.
And so in the end, I think you're making the same mistake you're pointing out here - you're treating a large, complex system, as dictated to by a single organ as a first order effect (i.e., it's all in your brain). In fact, biology is *filled* with intelligence, even down to the cellular level, and a robust system simply wouldn't make "tastiness" it's primary directive - that's not robust by any means. It *is* rational to think that cellular intelligence would be concerned with things like protecting from toxic levels of glucose in tissues and the blood stream, and sufficient energy to survive, and the complex failure of the system to maintain a healthy weight (in order to survive in the short term), is quite neatly explained by the insulin and differential insulin resistance mechanism as a *first order* term.
Hunger is a neurological effect so it (probably) all has to end up in the brain at some point, but we don't know the precise inputs, some is undoubtedly largely determined by signals from the body, muscle cells are probably sending some of those signals, but the brain is undoubtedly doing a ton on its own as evidenced by the huge role visual stimuli, social setting, and expectation plays on appetite.
That's why I'm very leery of anyone who stands up and says "I solved the obesity epidemic and it's due to X!" just because we know of so many contributing factors that go in and the number of variables we're changing.
I'm not sure we're going to get any further on this point. Taubes came as close to saying "up is down" as you can possibly get, whatever mental gymnastics or false equivalencies you use to justify it you can't get around that fact. Even if some nutritionists did make an equivalent error Taubes claim is that he's supposed to be better, that he's the only one who took an unbiased look at the evidence. Well here we have a clear example where if you took his at his word you would come away seriously misinformed. At least admit the man is capable of failure.
My contention about the nutritionists disparaging red meat and saturated fat. They are taking a *correlation*, and pretending it's a *causality* - a mistake on their part that is easily verifiable by even the most casual of glances at the references they give.
They take an existing correlation and interpret it as a interpretation (may or may not be right), Taubes does the same, except when he took the correlation he just reversed it. The rationalization is still laughable.
Ah, so in fact, you do "care" in the emotional sense of the word, but have excluded them because you believe they add too much complexity to the picture. Fair enough, although I do think that in order to "do no harm", nutritionists are obligated to understand the *mortality* effects of their advice before giving it. It could be that the safest thing to say to anyone is "your individual body and response to dietary components may vary greatly from someone else's", rather than promote false tropes like "red meat and saturated fat will cause everyone health problems", or "vegetarianism is a healthy lifestyle for anyone"...it's like insisting that everyone should eat 5-6 servings of peanuts a day, even if they're allergic to peanuts.
Maybe, but after probably 100+ comments I don't really want to have that debate.
What this basically says is that audiences have already decided whether or not the movie will be a success before it's been released.
Think about it, sure a preview is somewhat limited by the film its based on, you'll know the actors, director, maybe the writers and producer. And you might get a very rough idea of the characters and plot, but that's about it.
Is there any reason why the previews for Evan Almighty couldn't have been as good as the previews for The 40-Year-Old Virgin?
The film industry is designed to push as much money into the opening weekend as possible to avoid giving audiences a chance to talk about the film and potentially not see the film. This study seems to suggest they're succeeding.
"In total the film made approximately $28.3 million in North American theaters, making it the number 51 highest grossing film of 1994 and the number 21 highest grossing R-rated film of 1994."
What's that say about the correlation between film quality and box office success? Maybe the only reason Evan Almighty flopped is because it was finally a chance for all the people who made Bruce Almighty a hit to make up for their mistake.
Isn't that what you're saying about Taubes in a nutshell? "I think Taubes is wrong, therefore when he disagrees with me he's lying."
More like, "Taubes is explicitly denying an easily verifiable fact. Therefore he's lying or ridiculously incompetent, therefore it's easier to discount his other claims"
Ah, the hobgoblin of correlation again:)
That being said, you really don't care about the health outcomes?
There were so many different measures of health outcomes I never bothered to evaluate them and figured they'd be noisy anyways (they looked pretty noisy by eye). That being said I've tried to keep the discussion narrowly focused on obesity because other health outcomes just make things harder to settle.
There's a saying that if a 'scientist' is in favour of some crank theory they're probably from CS or Engineering.
I'm finishing my masters in CS and I wouldn't call myself a scientist though I do some science. My brother is an assistant prof in a physics dept and he wouldn't call himself a physicist until he finished his PhD. In a way I think us CS/Engineering types are particularly poorly equipped to understand complex system problems like biology and climate since we're used to being given a complex system and having it based on a simple elegant design, and when we want to perform an experiment it's trivial to tweak and repeat it through every variation we can imagine.
You need to understand that natural systems are designed by a completely foreign process. Governing appetite using muscle starvation and a simple insulin feedback mechanism to regulate blood sugar is probably how we'd do it. But the hallmark of evolution is bizarre, extremely complex, though generally robust systems. Maybe muscle starvation isn't linked to hunger at all, maybe the brain has to learn that explicitly, and it sometimes forgets and leads to that feeling of being kinda faint but not actually hungry. A properly designed system wouldn't confuse hunger with thirst, but our bodies do. The data I'm analyzing now comes from people suffering phantom limb pain, would you design a body to continually feel sensation and pain from a missing limb? It shows up in us. The one thing that evolution would predict for hunger is that it wouldn't have a simple solution, it would be a complex one with many different inputs and factors, that's one of the reasons it's hard to manipulate.
1) you're assuming the brain turns off the hunger, not the muscles.
2) you're still telling people to eat smaller portions.
1) The sight of food can trigger hunger, that the brain helps regulate hunger is incontrovertible.
2) Yes. People tend to eat quickly until they're full, instead of eating slowly and stopping when they're less full. This leads to them consuming more calories. Most obese people can lose weight by eating slower and stopping slightly earlier without feeling more hungry in general.
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.
That is a factor as well, but that is not the factor they're addressing with that advice.
Again, you're holding a double standard. Taubes speaks of vegans and vegetarians broadly, when he probably could be more specific.
There's no double standard, if he has some special group of fat vegetarians he's talking about he should specify, but from the context he's clearly talking about all vegetarians, or at least those not eating tons of oil. Don't imagine some imaginary context to let them off the hook.
Status quo nutritionists speak broadly of red meat and saturated fat eaters, when in fact the studies they tout have shown *correlation* not *causation* - so if they were to be more accurate, they'd have to really point out the controlling factor of carbohydrates on insulin, which they quite nearly actively disparage.
Translation: I think nutritionists are wrong, therefore when they disagree with me they're lying.
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. Part of the reason is that obese people tend to eat beyond what is needed to negate hunger.
And yes "eat less, exercise more" is a gross simplification because it's only 4 words, but people have short attention spans so that's often all they hear.
I'm going to take a shot in the dark and assume you're not actually a scientist (I'm not either), just because you seem to have a very odd and buzzword driven idea about what it is that scientists do.
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.
Regardless of your beliefs it is not provably false, even if it had overwhelming evidence is it not provably false. Taubes statement on the other hand makes a specific claim about a specific group of people at it IS provably false.
"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."
If you want to get specific the nutritionists are counselling people to eat appropriate amounts.
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.
a) Oh well.
b) A metabolic ward would suck for that.
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?
There's a big difference between "X will cause Y" and "X generally causes the opposite of Y, but once in a while it can cause Y". Maybe he didn't flat out claim to be the King of Spain but he certainly claimed to be at the front of the Spanish line of succession.
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?
I heard them cautioning about saturated fat with things like the atkins diets (which I think is correct though I don't really know the evidence) and that lots of red meat and saturated fat in a standard western diet will make you fatter (well backed by evidence), but nothing as trivially falsifiable as Taubes' statement.
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.
My understanding is that insulin resistance is at least partly a mechanism to avoid cells taking in toxic levels of glucose, ie the cells can't use up the circulating glucose fast enough so they become resistant and the adipose tissue soaks it up instead. That being said I'm not motivated to go citation diving to figure out more of the mechanism.
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.
You misunderstand. I'm not arguing against falsifiability, but the trouble with science is that often hypothesis you want to test is not necessarily the hypothesis you can test.
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).
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, but if correct you should differential insulin resistance develop in people followed by a spike in obesity.
The problem is that diet is a very complex system, so it's difficult to isolate one mechanism because other mechanism try to compensate. It's more a slow accumulation of evidence towards a hypothesis.
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.
Except they explicitly counsel people that people shouldn't attempt fewer calories by skipping meals. 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. You're inventing a contradiction by deliberately misunderstanding nutritionist advice.
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 I'm not going to look that up, but Guyenet routinely talks about studies finding low-carb leads to spontaneous reductions in appetite, so apparently that research is happening and not being held down by the man.
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".
Also the possibility that people replace the calories with protein (which I think works better than low-carb), and that any diet that restricts food groups will cause weight loss.
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).
Well for me I don't exclude a small role for insulin in hunger, and I don't exclude the possibility of it being a bigger factor in the already obese+diabetic since I haven't seen that specific evidence, but I'm still skeptical.
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Because we joined the UN as a permanent member of the security council. It's our job to protect the rights of foreign people from human rights violations.
I mean I suppose we could resign from our position, supposing you like the idea of China and Russia being in charge the security council.
But is the US capable of protecting them?
The mildest response is to send in a bunch of drones, blow up a bunch of Assad's stuff, and call it a day.
What if Assad then uses more gas? Same response or do you have to escalate? With or without gas what if Assad starts to win? What's the exit strategy?
I'm not completely opposed to a short bombing run from the US, saying "if you use chemical weapons we'll make you regret it". But going further and actually taking a real stake in the conflict, it's not just that I'm not sure the US can win, but I don't know if there's a way to avoid losing. There's no good guys left who are in a position to be a decent government, and any involvement becomes western interference in a Muslim Arab country and destabilizes the surrounding region. It might be that the best thing the US can do for Syrians is nothing.
Then I've failed to communicate that effectively to you :)
You think he meant so say it was merely possible for them to be fat? That vegetarianism could lead to other non-obesity related health problems? Because he didn't say anything remotely like that.
That sounds fair enough, but again, hardly resonating with an actual vegetarian (unless they happened to be one of those fat ones that tried to become vegetarian for health reasons, and weren't seeing success).
My take would be slightly different: "huh, I thought vegetarians were usually healthy, but I guess they must not be because he's done the research and they apparently aren't healthier" - and this, is arguably true.
Unless by "healthy" you mean thin I think your take misses the point.
The book is primarily about obesity. The interview was primarily about obesity. The exchange was primarily about obesity. And the statement in question specifically mentioned obesity.
I guess that's the argument in a nutshell - I'm arguing that psychological processes in the brain aren't primary drivers of appetite, they're secondary or tertiary. To quantify that, I think we're looking at metabolic ward studies, with various controls for macronutrients and a search for quantitative data on biomechanisms rather than subjective surveys.
I think that one thing matabolic ward studies would clear up is that they don't really explain the changes that lead to the small (Yes. You can't rely on getting good results out of bad data.
It's not a binary situation, every dataset has inadequacies, you take that into account with error bars and tempered interpretations, but it's a little too convenient to just throw it out entirely because it's a problem.
What if there wasn't a problem, what if it turned out the records were in fact good? How would you rationalize the data then?
I disagree. The conscious acknowledgement of "tastiness" may occur in some part of the frontal cortex, say, but when it comes to "tastiness as having an effect on actual biomarkers rather than a survey", that's something that is determined by a complex set of tissues and organs, including but not limited to parts of the brain that are not conscious.
I wonder if you would put the brain in a place of primacy if we were talking about say, vertical growth rather than horizontal growth. Would it be possible for the brain to psychologically retard (or accelerate) growth in height? Could it somehow reduce the amount of human growth hormone circulated by the pituitary? More importantly, since vertical growth requires a caloric imbalance (need more calories in than calories out), would the mechanisms you imagine for hunger and appetite be suppressible when trying to avoid vertical growth? Could a teenager reduce their appetite enough to limit their calories enough to stop their vertical growth from happening?
My guess is that you'd admit to the primacy of HGH in determining vertical growth, but that begs the question as to why you wouldn't admit the primacy of insulin in determining horizontal growth.
Well there's one big difference between eating and growing in that eating requires a conscious deliberate action and we know that a strong hunger response can be triggered by brain signals.
And I do agree that HGH is most responsible for height, with the caveat that there's MASSIVE factors I know I'm missing including things that probably counteract, enhance, or regulate HGH, and I don't know how HGH is involved in the feedback mechanism that actually determines how much we grow. We also know the conscious mind doesn't do a lot since vegetative patients still grow to a normal height.
Again, you bring in the messy brain in the example as a point of pride - eventually, every brain response has to culminate in some biomechanism for accumulating fat. You can do a more rigorous and profitable analysis by understanding the basic biomechanisms *first*, and then discovering how the brain might influence those levers. But you can't have a brain doing something magical and unobservable - it eventually needs to get down to the level of accumulating fat in a fat cell.
Wherever you start from you can't go around saying you solved the obesity epidemic when you've left out one of the primary drivers of appetite which you know if being manipulated in modern populations.
Okay, so let's get the test where we measure the biochemical process by which the brain influences say, tastiness. Let's throw away the subjective questionnaires, and measure the actual biochemical signals. Again, first principles, we need to go to the moment of action.
What are you talking about? Tastiness is be determined by signals in the brain, there are feedbacks that occur which changes how we perceive taste, but you're going back to this impractical standard of solving the system instead of analyzing it behaviourally.
Easy. Bad data. They even admit to it: "These numbers are probably not particularly accurate"
So you're throwing it out entirely? The numbers are fuzzy, but if they're even in the ballpark they contradict your allergy theory.
No, let's be specific - his failure was that he did not speak clearly enough to have his audience understand. That's a failing for someone who is trying to convey a point.
Understand what? I don't know his point.
I mean, honestly, do you think that Taubes' statement in that radio interview convinced a single vegetarian to start on an unhealthy, high glycemic carnivorous diet, as opposed to a healthy low-glycemic carnivorous diet?
I think a lot of listeners went through the program thinking "wow! he's dismantling all these things I knew about nutrition!" and when he got to that bit "huh, I thought vegetarians were usually thin, but I guess they must not be because he's done the research and they apparently weigh more."
Oh yes,
His failure was that he was misunderstood. It's not really his fault that in an interview, when discussing in detail the fact that vegetarians were eating foods that by his rules should make them fat and diabetic, he simply claimed that vegetarians were in fact fat and diabetic.
It's clear that he really wanted to say...
After googling the only thing I can find about Taubes and vegitarianism is someone saying that in his book he claimed that Vegetarian Hindus in India were fatter than their non-vegetarian Christian and Muslim counterparts. But I could find no mention of that study, and similar studies, or the actual claim, or even another website saying he said it, so I have no idea what his actual explanation is or if there even is one. But given the obvious relevance to his hypothesis it seems odd that he hasn't dealt with the issue explicitly and directly.
I'm not sure if I quite understand your researcher/other person example.
The point is we can't isolate one variable and hold everything else constant. Other variables can kick in to compensate, the brain responds to the situation, and the factor you're measuring never has a total function as simple as your hypothesis. No matter what you do the data is really messy and the answers can only be guessed at by looking at a lot of different experiments.
And maybe that's the problem I have with your frame - you're asserting that the brain is some massively omnipotent organ that dictates to the rest of the body, and that we can ignore all other factors and concentrate on it as the first order term.
I'm arguing a different frame based on our observations of cellular intelligence (http://www.brianjford.com/w-intelcell.htm, for example). Given the biochemical processes on the *cellular* level is the only way to rationally attack this problem, as far as that frame goes.
No, I'm saying we already know the brain is heavily involved, including decisions made at an abstract level like comfort food or eating in company. Therefore to show a particular biochemical process is active you first need to measure the influence of the brain which we know is there.
So, are you leery of those who say "it's due to eating more calories than those burned!"?
Oversimplification, I'd be leery of those who say "it's all due to palatability", because activity levels, social factors, mental health, advertising, convenience, and a dozen other factors are all probably involved.
Btw, since you think the carb/obesity is only in western populations due to a carbohydrate allergy explain Cuba, during an economic crisis calories dropped from 3,100 to 2,300 and:
"The percentage of dietary fat in the energy intake decreased, while the contribution of carbohydrates (polished rice and refined cereals) increased from 64% in 1990 to 79.4% in 1993. Availability of essential dietary amino acids and fatty acids declined as a consequence of a reduced availability of animal protein and edible oils and fat. Sugar cane, a traditional source of energy in the Cuban diet, rose to 28% of total energy intake, almost three times that of the fat contribution."
Want to guess what happened? Obesity rates dropped by half. So what happened to the carb allergy that caused the initial obesity? Why did they start eating fewer calories? Despite the economic hardship there wasn't actual starvation so surely they could afford 800 of the cheapest calories per day, if your theory about their obesity being caused a carb allergy was correct the extra sugar and refined carbs should have given them uncontrollable hunger and blew them up like a balloon.
That being said, I'm not just talking about discrete simulations (as Wolfram has made particularly interesting finds in cellular automata), I'm talking about real world root cause failures in complex, integrated, man/logic/machine settings (which, do include a biological component of sorts). You cannot hope to find the truth in an analysis of a real-world system (again, not just some pre-programmed simulation, real computers doing real work with real people), without falsifiability.
I agree, but that doesn't mean the system is designed to be easily analyzed via falisifiability. I think a pretty common scenario goes something like this
Researcher: I have a great simple falsifiable hypothesis!
Other person: Awesome! What does it mean if it's true!
Researcher: Uhhh, well I got a list of things that might be happening if it's true.
Other person: Um ok, well you must have a pretty good idea if it's false then?
Researcher: Oh yeah! I got another list!
Other person: .... a lot of the items are the same.
Researcher: Yeah, sorry about that
Certainly hunger would be a complex one, but even in a complex system, you have first, second, third, etc order effects. Furthermore, as you noted, biology generally leads to extremely robust systems, and a system that ignored muscle starvation due to visual stimulation is distinctly *not* robust. The muscle cells can be considered as intelligent actors, just as intelligent as any bit of brain tissue, and they simply cannot be considered a lower order term.
And so in the end, I think you're making the same mistake you're pointing out here - you're treating a large, complex system, as dictated to by a single organ as a first order effect (i.e., it's all in your brain). In fact, biology is *filled* with intelligence, even down to the cellular level, and a robust system simply wouldn't make "tastiness" it's primary directive - that's not robust by any means. It *is* rational to think that cellular intelligence would be concerned with things like protecting from toxic levels of glucose in tissues and the blood stream, and sufficient energy to survive, and the complex failure of the system to maintain a healthy weight (in order to survive in the short term), is quite neatly explained by the insulin and differential insulin resistance mechanism as a *first order* term.
Hunger is a neurological effect so it (probably) all has to end up in the brain at some point, but we don't know the precise inputs, some is undoubtedly largely determined by signals from the body, muscle cells are probably sending some of those signals, but the brain is undoubtedly doing a ton on its own as evidenced by the huge role visual stimuli, social setting, and expectation plays on appetite.
That's why I'm very leery of anyone who stands up and says "I solved the obesity epidemic and it's due to X!" just because we know of so many contributing factors that go in and the number of variables we're changing.
I'm not sure we're going to get any further on this point. Taubes came as close to saying "up is down" as you can possibly get, whatever mental gymnastics or false equivalencies you use to justify it you can't get around that fact. Even if some nutritionists did make an equivalent error Taubes claim is that he's supposed to be better, that he's the only one who took an unbiased look at the evidence. Well here we have a clear example where if you took his at his word you would come away seriously misinformed. At least admit the man is capable of failure.
My contention about the nutritionists disparaging red meat and saturated fat. They are taking a *correlation*, and pretending it's a *causality* - a mistake on their part that is easily verifiable by even the most casual of glances at the references they give.
They take an existing correlation and interpret it as a interpretation (may or may not be right), Taubes does the same, except when he took the correlation he just reversed it. The rationalization is still laughable.
Ah, so in fact, you do "care" in the emotional sense of the word, but have excluded them because you believe they add too much complexity to the picture. Fair enough, although I do think that in order to "do no harm", nutritionists are obligated to understand the *mortality* effects of their advice before giving it. It could be that the safest thing to say to anyone is "your individual body and response to dietary components may vary greatly from someone else's", rather than promote false tropes like "red meat and saturated fat will cause everyone health problems", or "vegetarianism is a healthy lifestyle for anyone"...it's like insisting that everyone should eat 5-6 servings of peanuts a day, even if they're allergic to peanuts.
Maybe, but after probably 100+ comments I don't really want to have that debate.
What this basically says is that audiences have already decided whether or not the movie will be a success before it's been released.
Think about it, sure a preview is somewhat limited by the film its based on, you'll know the actors, director, maybe the writers and producer. And you might get a very rough idea of the characters and plot, but that's about it.
Is there any reason why the previews for Evan Almighty couldn't have been as good as the previews for The 40-Year-Old Virgin?
The film industry is designed to push as much money into the opening weekend as possible to avoid giving audiences a chance to talk about the film and potentially not see the film. This study seems to suggest they're succeeding.
Just look at the top movie on IMDB, The Shawshank Redemption
"In total the film made approximately $28.3 million in North American theaters, making it the number 51 highest grossing film of 1994 and the number 21 highest grossing R-rated film of 1994."
What's that say about the correlation between film quality and box office success? Maybe the only reason Evan Almighty flopped is because it was finally a chance for all the people who made Bruce Almighty a hit to make up for their mistake.
Isn't that what you're saying about Taubes in a nutshell? "I think Taubes is wrong, therefore when he disagrees with me he's lying."
More like, "Taubes is explicitly denying an easily verifiable fact. Therefore he's lying or ridiculously incompetent, therefore it's easier to discount his other claims"
Ah, the hobgoblin of correlation again :)
That being said, you really don't care about the health outcomes?
There were so many different measures of health outcomes I never bothered to evaluate them and figured they'd be noisy anyways (they looked pretty noisy by eye). That being said I've tried to keep the discussion narrowly focused on obesity because other health outcomes just make things harder to settle.
Surely, the brain can help regulate hunger, but the idea that slow eating will override starving muscle signals is dubious.
I'm not going to look but I'm certain if you looked for literature some study shows that people told to eat slower will spontaneously eat less.
I still wonder - if the brain can trigger hunger on the sight of food, is there any visual that can suppress hunger?
Goatse?
There's a saying that if a 'scientist' is in favour of some crank theory they're probably from CS or Engineering.
I'm finishing my masters in CS and I wouldn't call myself a scientist though I do some science. My brother is an assistant prof in a physics dept and he wouldn't call himself a physicist until he finished his PhD. In a way I think us CS/Engineering types are particularly poorly equipped to understand complex system problems like biology and climate since we're used to being given a complex system and having it based on a simple elegant design, and when we want to perform an experiment it's trivial to tweak and repeat it through every variation we can imagine.
You need to understand that natural systems are designed by a completely foreign process. Governing appetite using muscle starvation and a simple insulin feedback mechanism to regulate blood sugar is probably how we'd do it. But the hallmark of evolution is bizarre, extremely complex, though generally robust systems. Maybe muscle starvation isn't linked to hunger at all, maybe the brain has to learn that explicitly, and it sometimes forgets and leads to that feeling of being kinda faint but not actually hungry. A properly designed system wouldn't confuse hunger with thirst, but our bodies do. The data I'm analyzing now comes from people suffering phantom limb pain, would you design a body to continually feel sensation and pain from a missing limb? It shows up in us. The one thing that evolution would predict for hunger is that it wouldn't have a simple solution, it would be a complex one with many different inputs and factors, that's one of the reasons it's hard to manipulate.
1) you're assuming the brain turns off the hunger, not the muscles.
2) you're still telling people to eat smaller portions.
1) The sight of food can trigger hunger, that the brain helps regulate hunger is incontrovertible.
2) Yes. People tend to eat quickly until they're full, instead of eating slowly and stopping when they're less full. This leads to them consuming more calories. Most obese people can lose weight by eating slower and stopping slightly earlier without feeling more hungry in general.
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.
That is a factor as well, but that is not the factor they're addressing with that advice.
Again, you're holding a double standard. Taubes speaks of vegans and vegetarians broadly, when he probably could be more specific.
There's no double standard, if he has some special group of fat vegetarians he's talking about he should specify, but from the context he's clearly talking about all vegetarians, or at least those not eating tons of oil. Don't imagine some imaginary context to let them off the hook.
Status quo nutritionists speak broadly of red meat and saturated fat eaters, when in fact the studies they tout have shown *correlation* not *causation* - so if they were to be more accurate, they'd have to really point out the controlling factor of carbohydrates on insulin, which they quite nearly actively disparage.
Translation: I think nutritionists are wrong, therefore when they disagree with me they're lying.
Think about all the b.s. that came out of the China Study, that denise minger so thoroughly dissected - http://rawfoodsos.com/2011/07/31/one-year-later-the-china-study-revisited-and-re-bashed/
I didn't care about the health outcomes, I figured those would be messy. I cared about the obesity correlation which seems to have held up.
May I ask what kind of science?
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. Part of the reason is that obese people tend to eat beyond what is needed to negate hunger.
And yes "eat less, exercise more" is a gross simplification because it's only 4 words, but people have short attention spans so that's often all they hear.
I'm going to take a shot in the dark and assume you're not actually a scientist (I'm not either), just because you seem to have a very odd and buzzword driven idea about what it is that scientists do.
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.
Regardless of your beliefs it is not provably false, even if it had overwhelming evidence is it not provably false. Taubes statement on the other hand makes a specific claim about a specific group of people at it IS provably false.
"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."
If you want to get specific the nutritionists are counselling people to eat appropriate amounts.
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.
a) Oh well.
b) A metabolic ward would suck for that.
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.
I'm not going to argue with anecdotal evidence.
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?
There's a big difference between "X will cause Y" and "X generally causes the opposite of Y, but once in a while it can cause Y". Maybe he didn't flat out claim to be the King of Spain but he certainly claimed to be at the front of the Spanish line of succession.
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?
I heard them cautioning about saturated fat with things like the atkins diets (which I think is correct though I don't really know the evidence) and that lots of red meat and saturated fat in a standard western diet will make you fatter (well backed by evidence), but nothing as trivially falsifiable as Taubes' statement.
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.
My understanding is that insulin resistance is at least partly a mechanism to avoid cells taking in toxic levels of glucose, ie the cells can't use up the circulating glucose fast enough so they become resistant and the adipose tissue soaks it up instead. That being said I'm not motivated to go citation diving to figure out more of the mechanism.
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.
You misunderstand. I'm not arguing against falsifiability, but the trouble with science is that often hypothesis you want to test is not necessarily the hypothesis you can test.
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).
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, but if correct you should differential insulin resistance develop in people followed by a spike in obesity.
The problem is that diet is a very complex system, so it's difficult to isolate one mechanism because other mechanism try to compensate. It's more a slow accumulation of evidence towards a hypothesis.
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.
Except they explicitly counsel people that people shouldn't attempt fewer calories by skipping meals. 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. You're inventing a contradiction by deliberately misunderstanding nutritionist advice.
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 I'm not going to look that up, but Guyenet routinely talks about studies finding low-carb leads to spontaneous reductions in appetite, so apparently that research is happening and not being held down by the man.
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".
Also the possibility that people replace the calories with protein (which I think works better than low-carb), and that any diet that restricts food groups will cause weight loss.
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).
Well for me I don't exclude a small role for insulin in hunger, and I don't exclude the possibility of it being a bigger factor in the already obese+diabetic since I haven't seen that specific evidence, but I'm still skeptical.