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.
I'd almost imagine you were trolling if you hadn't responded to evidence in other places.
There's no other way to interpret that statement other than the vegetarian diet will make kids fat and diabetic. This isn't parsing some old study of some obscure tribe, it's basic english.
So if I follow for the population eating sugar and not getting fat you say it's delayed because of epigenetic effects.
So I counter with a population switching to a western diet and getting fat, and you eventually concede that that population shows no epigenetic delay.
So when the population gets fat there's no epigenetic effect, but if they don't become fat there must be a missing epigenetic factor?
Ya'll hear about the geometer who went to the beach to catch some rays and became a tangent ?
