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.
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.
I've shown real data he's misrepresented. I've shown counter examples he's ignored.
No, you actually really haven't. You've shown data you believe contradicts him, but doesn't. You've shown examples that you believe contradict him, but don't.
Moreover, you seem to think (although perhaps this isn't what you intend) that the insulin hypothesis simply has no value whatsoever, and must be replaced by a nebulous, undefined "palatability" hypothesis. You then clearly treat this favored hypothesis as immune to the same sort of critique you give to the insulin hypothesis, doing much of what you accuse taubes of - misrepresenting data and ignoring counter examples.
So sure, there certainly is a lot more to be learned about what drives insulin resistance, and perhaps, for some small fraction of obese, what alternative method (MHO) might be causing a hormonal imbalance in fat accumulation. But frankly, Guynet and his wishful thinking about palatability and tastiness just doesn't stand up to the same level of scrutiny that he'd like us to place on the insulin hypothesis.
Except people on low carb diets typically increase their protein consumption (high protein works better than low carb for weight loss).
I don't think that's what the data shows - nutritional ketosis is typically generated through high fat diets.
If you exclude a food you tend to overeat then you usually don't replace all those calories with an alternative.
Let's stay away from the word "overeat", and restate as "if you exclude a food that makes you fat then you usually don't replace all those calories with an alternative". That fits in perfectly with the idea of a food that increases fat accumulation causing abnormal partitioning of energy, which the body recognizes and reacts to.
For instance, given your understanding of this basic biochemistry how do you explain the fact that fish causes higher insulin levels than porridge
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.
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.
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?
You are mistaken. I think "tastiness" is often a major contributing factor to obesity.
Define "tastiness". Be specific, and please, no "overeating" tautologies.
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.
You're quite literally saying "a study that directly contradicts my theory is wrong because it directly contradicts my theory".
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?
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?
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.
One last clarification - yes, it's quite possible that in some cases "tastiness" can create insulin resistance, as well as fructose (as per Lustig). There could be a plethora of pathways to insulin resistance, although some seem more rational than others. There may also be a number of ways to avoid insulin resistance (the magic bullet pharmaceutical for obesity).
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.
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?
Going back to the speeding automobile analogy, yes, in the most trivial sense, a person is speeding because the engine put too much energy into the wheels, and/or the brakes did not take enough energy out of the wheels. This is true in the human body at the level of the fat cell, not the mouth. The question is, *why* wasn't enough energy taken out by the brakes? *Why* was too much energy put into the wheels? Was it because the driver had a pregnant lady in the car and was heading to the hospital? Was it because the road sloped down hill? Was it because the driver was racing someone who cut them off earlier? Was it because the driver was being chased by an active shooter?
The *reason* for the speeding is the *reason* more energy was put in than taken out of the wheels; the *reason* for obesity is the *reason* that more energy was put into than taken out of the fat cells. Simply stating that "more energy was put in than taken out of the wheels" isn't a *reason*, it's simply a statement of the results.
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.
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.
Subsistence hunters or populations using traditional farming techniques.
I'd love to see metabolic ward studies and direct analysis of any subsistence hunter population or "traditional farming" population. My guess is that both would have a significantly lower insulin impact on the insulin resistant.
But I'm still not convinced that insulin resistance itself is a cause, and not a symptom of obesity.
But you can be insulin resistant, stop eating carbohydrates, stop being obese, but still have insulin resistance and an acute allergy to carbohydrate. I suppose you could argue that it is a symptom of obesity that never goes away, even if the obesity itself is transient, but then you've got to find a mechanism for becoming obese and accumulating fat without insulin resistance.
Again, I'd love to see that in a metabolic ward.
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.
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.
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.
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.
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?
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 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.
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.
If low-carb works for people without insulin resistance then clearly insulin resistance isn't the only reason low-carb works.
Insulin resistance is a spectrum. If you have an insulin sensitive person who isn't overweight, and they go low carb and lose five pounds, that's functionally analogous to an insulin resistant person who is 300 pounds, and they go low carb, and lose 140 pounds.
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:)
I don't think that self reported eating data is very good, nor is government reported food data very good, nor is indirect measurement by assumption (waist size) very good - and a big part of that is because doing things right and getting good data is expensive.
Honestly, at this point, there's enough data out there of poor quality to argue any point you want, which is why the next steps here have to be direct measurement and a rigorous application of skepticism and falsifiability.
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....
I disagree with the term "overeating" because it is simply defined by the outcome, not the actual act of eating.
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?
The answer is it depends on how those kcal are processed. If 4000 kcal of fat and protein are ingested, 3000 kcal of that is stored as fat, and then you burn 2500 kcal (and are unable to grab the extra 1500 kcal from fat stores because they aren't releasing fat), you lose 1500 kcal of muscle.
If 4000 kcal of fat and protein are ingested, and 0 kcal are stored as fat, and you only burn 2500 kcal, then you've got all kinds of other excretory processes that can take place for the last 1500 kcal, including passing some of those kcal unburned through the intestine, or dumping ketone bodies in urine. Or, if you really pay attention, you may be driven to burn the extra 1500 kcal - just as your body has a "hunger" switch, it certainly also has a "I want to get out and do something physical" switch.
Assuming that every calorie that passes through the lips must be burned or stored as fat is the first misconception here. The second one is that the brain doesn't regulate the burning or dumping of calories if there are any in excess.
I'm sorry, but doing this will kill the universities, they already have problems keeping talent inside.
And it may very well be that like the horse and buggy, universities will become nostalgic rarities.
There are already too few academic jobs
No, there are too many academic jobs and too many academic job seekers.
This turns off many people from academia, and pushed them into the industry jobs.
This is a good thing. We don't need 10,000 professors studying the migration patterns of unladen swallows. It's incredibly unfair to students to pretend that there is any sort of decent career track in academia.
The average attention professors can give to students is diminishing fast
This means that the professors are doing too much besides teaching students.
A university "is supposed" to provide higher education, giving you tools to learn and improve yourself.
It should not take four years and $200,000 to learn how to learn and improve yourself.
An education *should* be about finding a job, period, unless you've got money to burn.
Would an iPad be of higher quality if it was built in the US?
Low-latency video chat is pretty good nowadays, and video chat meetings and presentations regularly include the ability to ask questions.
As for "interactivity", I don't know what you're talking about - that's *exactly* what you would get from a low priced, offshored professor working for 1/10th of the cost in a foreign country over video chat.
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.
Okay, so let's stop using "overeating" since it's simply a synonym for "fat".
So when you say, "the thing that causes insulin to behave in excess" is "overeating" ("all the food we eat"), you're really saying this:
"the thing that causes insulin to behave in excess is being fat"
I'm arguing that its the excess insulin that causes the excess fat accumulation, and you're arguing that somehow the fat is accumulated in excess *first*, and *then* insulin starts misbehaving.
What is the initial accumulation mechanism, if it's insulin that drives fat accumulation?
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.
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.
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.
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?
So as long as you don't become insulin resistant then carbs won't make you fat?
That certainly sounds reasonable, given the biomechanical properties of insulin and fat accumulation.
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.
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:)
Education you are constantly have to upgrade hardware and software to keep up with teaching the newest techniques
But some how these newer techniques haven't improved either outcomes or efficiency.
Even still if you look at how we "innovate" to lower the cost of production for that newest bit density, we typically offshore the process, something you cannot do with education.
Why not? Why not hire professors who literally do live video from another country for 1/10th of the cost? You could even improve the student to teacher ratio that way.
You might not be able to offshore a plumber, but there's not reason you can't offshore a professor.
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.
If multiple different populations stay thin on a high carb diet there's obviously a big piece missing from Taubes' hypothesis.
No, I think you're skipping a piece from his hypothesis - insulin resistance. What we need is better data regarding actual insulin resistance and obesity (rather than say, the proxy of waist size).
What data? You're just making a bald assertion in the face of multiple examples I gave you.
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.
And don't just throw back the Inuit
I paired them with the Masai for good measure:)
So if the data doesn't agree with you you'll just ignore it?
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.
1) open source textbooks - no more fat contracts for minor revisions to a trigonometry text
2) fewer professors - video tape the good lectures, and share them across universities. You'll need significantly fewer profs across the whole industry.
3) prospective salary based tuition - stop funding the use of education dollars into majors that cannot possibly turn into productive, money making jobs.
And that was just from some random goofball on the internet.
That's like saying there's a bit density we'll finally reach that will make ever improving hard drives worthless.
Education institutions need to improve their efficiency. You can't run our modern transportation system on horseback anymore, and education institutions can't simply re-live the practices from the past 100 years either.
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".
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.
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.
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.
There's biochemical feedbacks, our bodies learn which foods have more calories and we tend to find those tastier.
Get down to the individual cells - isn't it that our bodies learn which foods *partition* more calories into fat versus muscles, and learn which foods target the addictive sugar rush/crash cycle, and find them tastier?
There may even be a small role insulin plays (but nothing like the role Taubes assigns it).
You've already agreed that insulin regulates fat accumulation. How is that a small role? You may disagree on what drives insulin (say, a "tastiness" signal from the brain), but you don't deny that it is the biochemical mechanism for fat storage, right?
People have different bodies, for some people the lipostat is that much more effective.
Sounds like insulin resistance versus insulin sensitivity.
I don't know a ton about cravings but they can be very specific (an individual food type).
Question - have you ever been fat? Have you ever had the experience of eating until it feels like you're filled up to the top of your esophagus, and *still* felt hungry?
The difference between a "craving" that may make you feel like noshing on something, and the burning hunger insulin resistant people feel when eating a carbohydrate heavy diet, is *huge*.
Overeat means ingest more calories than is required to maintain your present body mass
So, it means nothing. You can't tell someone "you're overeating" until you see their body mass change. "Overeating" for one person can be "undereating" for another - even if they're the same weight and exercise the same amount!
Rather than blaming fat accumulation on "overeating", isn't it reasonable to think that it could be the opposite way, where fat accumulation is to blame for "overeating", because of the hunger it causes when it steals calories from the muscles?
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?
How does Taubes think the body regulates fatness?
The same way you agreed earlier - insulin. Now, there may be various regulators of insulin (although I'll argue the primary one is carbohydrate intake), but the biochemical mechanism is pretty clear.
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.
I think you'll be surprised by how complex the picture is and how thorough the literature is.
It certainly is complex, but it's hardly thorough:) That being said, it's "what makes us eat more than what we require for leanness?" seems simple - the improper partitioning of incoming energy into fat cells, which starves muscle cells. This improper partitioning is driven by insulin and insulin resistance.
Considering the insulin index of white rice compared to fruit [wikipedia.org] I find this claim pretty dubious.
Lustig makes the point that fructose consumption starts insulin resistance, and *then* the insulin index really matters. Check out his youtube lecture "sugar: the bitter truth" - he goes into serious depth there.
But that doesn't mean insulin is driving the hunger.
If insulin is driving energy into fat cells, and making it unavailable to muscles, and that unavailability is what triggers some sort of hunger response (as we see when say, someone is starving), isn't it simply obvious that in that case insulin is driving the hunger?
I mean, if instead of putting energy into your mouth, and putting it directly into fat storage, you simply didn't put that energy into the body, wouldn't a body get *hungrier*? Isn't that a reasonable assumption?
If you really wanted to compare this to race vs intelligence then note you're the one positing that populations react differently to the same diets.
I'm positing that populations with different internal biochemical *environments* react differently to the same diets, whereas the race and intelligence folk posit that populations differ, *regardless* of environment.
it's also consistent with mainstream nutrition
Would you critique mainstream nutrition with the same tactic, that there are some % of cases that don't follow their hypothesis?
Nothing. It means we find the food tasty so we eat more of it.
So it is purely a mental thing? No biochemical mechanism for being more or less tasty?
Or those fat people eat some pizza, their brains go 'wow! this is so yummy, I want more!', triggers a hunger response, and they eat more.
But what's the biochemical "hunger response"? Just saying "it's yummy" doesn't help much - since there are people who eat all the yummy stuff they want in unlimited quantities and still don't gain weight.
If it's all biochemical then how do you explain cravings?
Shouldn't cravings have biochemical roots? A salt deficiency in your diet, and you'll crave it. An addictive narcotic, messing with your ssi uptake, and you'll crave it.
It's harder to overeat when you deprive yourself of the starchy base.
"Overeat" means nothing, since it's circularly defined. That being said, I believe the insulin hypothesis makes a strong case that when you deprive yourself of a starchy and sugary base, your energy intake is partitioned into use for the muscles rather than storage in the fat cells, so it's harder to accumulate fat if you deprive yourself of carbohydrates.
Slashdot Mirror
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.
"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.
No, you actually really haven't. You've shown data you believe contradicts him, but doesn't. You've shown examples that you believe contradict him, but don't.
Moreover, you seem to think (although perhaps this isn't what you intend) that the insulin hypothesis simply has no value whatsoever, and must be replaced by a nebulous, undefined "palatability" hypothesis. You then clearly treat this favored hypothesis as immune to the same sort of critique you give to the insulin hypothesis, doing much of what you accuse taubes of - misrepresenting data and ignoring counter examples.
So sure, there certainly is a lot more to be learned about what drives insulin resistance, and perhaps, for some small fraction of obese, what alternative method (MHO) might be causing a hormonal imbalance in fat accumulation. But frankly, Guynet and his wishful thinking about palatability and tastiness just doesn't stand up to the same level of scrutiny that he'd like us to place on the insulin hypothesis.
I don't think that's what the data shows - nutritional ketosis is typically generated through high fat diets.
Let's stay away from the word "overeat", and restate as "if you exclude a food that makes you fat then you usually don't replace all those calories with an alternative". That fits in perfectly with the idea of a food that increases fat accumulation causing abnormal partitioning of energy, which the body recognizes and reacts to.
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 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.
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?
Define "tastiness". Be specific, and please, no "overeating" tautologies.
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?
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?
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.
One last clarification - yes, it's quite possible that in some cases "tastiness" can create insulin resistance, as well as fructose (as per Lustig). There could be a plethora of pathways to insulin resistance, although some seem more rational than others. There may also be a number of ways to avoid insulin resistance (the magic bullet pharmaceutical for obesity).
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.
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?
Going back to the speeding automobile analogy, yes, in the most trivial sense, a person is speeding because the engine put too much energy into the wheels, and/or the brakes did not take enough energy out of the wheels. This is true in the human body at the level of the fat cell, not the mouth. The question is, *why* wasn't enough energy taken out by the brakes? *Why* was too much energy put into the wheels? Was it because the driver had a pregnant lady in the car and was heading to the hospital? Was it because the road sloped down hill? Was it because the driver was racing someone who cut them off earlier? Was it because the driver was being chased by an active shooter?
The *reason* for the speeding is the *reason* more energy was put in than taken out of the wheels; the *reason* for obesity is the *reason* that more energy was put into than taken out of the fat cells. Simply stating that "more energy was put in than taken out of the wheels" isn't a *reason*, it's simply a statement of the results.
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.
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'd love to see metabolic ward studies and direct analysis of any subsistence hunter population or "traditional farming" population. My guess is that both would have a significantly lower insulin impact on the insulin resistant.
But you can be insulin resistant, stop eating carbohydrates, stop being obese, but still have insulin resistance and an acute allergy to carbohydrate. I suppose you could argue that it is a symptom of obesity that never goes away, even if the obesity itself is transient, but then you've got to find a mechanism for becoming obese and accumulating fat without insulin resistance.
Again, I'd love to see that in a metabolic ward.
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.
That's the claim of the study that insulin injections can cause mice to lose weight.
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.
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.
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?
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.
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 thought that was your claim - insulin given to mice, according to your cite, did not cause fat accumulation.
Insulin resistance is a spectrum. If you have an insulin sensitive person who isn't overweight, and they go low carb and lose five pounds, that's functionally analogous to an insulin resistant person who is 300 pounds, and they go low carb, and lose 140 pounds.
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 :)
Well, I think the gold standard is the whole metabolic ward stuff. Peter Attia shares some of his experiences there: http://www.youtube.com/watch?v=NqwvcrA7oe8&feature=player_embedded
I don't think that self reported eating data is very good, nor is government reported food data very good, nor is indirect measurement by assumption (waist size) very good - and a big part of that is because doing things right and getting good data is expensive.
Honestly, at this point, there's enough data out there of poor quality to argue any point you want, which is why the next steps here have to be direct measurement and a rigorous application of skepticism and falsifiability.
I disagree with the term "overeating" because it is simply defined by the outcome, not the actual act of eating.
The answer is it depends on how those kcal are processed. If 4000 kcal of fat and protein are ingested, 3000 kcal of that is stored as fat, and then you burn 2500 kcal (and are unable to grab the extra 1500 kcal from fat stores because they aren't releasing fat), you lose 1500 kcal of muscle.
If 4000 kcal of fat and protein are ingested, and 0 kcal are stored as fat, and you only burn 2500 kcal, then you've got all kinds of other excretory processes that can take place for the last 1500 kcal, including passing some of those kcal unburned through the intestine, or dumping ketone bodies in urine. Or, if you really pay attention, you may be driven to burn the extra 1500 kcal - just as your body has a "hunger" switch, it certainly also has a "I want to get out and do something physical" switch.
Assuming that every calorie that passes through the lips must be burned or stored as fat is the first misconception here. The second one is that the brain doesn't regulate the burning or dumping of calories if there are any in excess.
And it may very well be that like the horse and buggy, universities will become nostalgic rarities.
No, there are too many academic jobs and too many academic job seekers.
This is a good thing. We don't need 10,000 professors studying the migration patterns of unladen swallows. It's incredibly unfair to students to pretend that there is any sort of decent career track in academia.
This means that the professors are doing too much besides teaching students.
It should not take four years and $200,000 to learn how to learn and improve yourself.
An education *should* be about finding a job, period, unless you've got money to burn.
Why does offshoring have to mean lower quality?
Would an iPad be of higher quality if it was built in the US?
Low-latency video chat is pretty good nowadays, and video chat meetings and presentations regularly include the ability to ask questions.
As for "interactivity", I don't know what you're talking about - that's *exactly* what you would get from a low priced, offshored professor working for 1/10th of the cost in a foreign country over video chat.
Okay, so let's stop using "overeating" since it's simply a synonym for "fat".
So when you say, "the thing that causes insulin to behave in excess" is "overeating" ("all the food we eat"), you're really saying this:
"the thing that causes insulin to behave in excess is being fat"
I'm arguing that its the excess insulin that causes the excess fat accumulation, and you're arguing that somehow the fat is accumulated in excess *first*, and *then* insulin starts misbehaving.
What is the initial accumulation mechanism, if it's insulin that drives fat accumulation?
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.
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.
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.
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?
That certainly sounds reasonable, given the biomechanical properties of insulin and fat accumulation.
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 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 :)
But some how these newer techniques haven't improved either outcomes or efficiency.
Why not? Why not hire professors who literally do live video from another country for 1/10th of the cost? You could even improve the student to teacher ratio that way.
You might not be able to offshore a plumber, but there's not reason you can't offshore a professor.
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/
But it could mean that fat people need a low carb diet.
http://www.wolframalpha.com/input/?i=sugar%20consumption%20per%20capita%20in%20USA%20and%20Japan
Cite?
Human evidence contraindicates.
Missing the insulin resistance factor.
Again, insulin resistance factor.
Those aren't data, those are assertions.
No, I think you're skipping a piece from his hypothesis - insulin resistance. What we need is better data regarding actual insulin resistance and obesity (rather than say, the proxy of waist size).
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.
I paired them with the Masai for good measure :)
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.
1) open source textbooks - no more fat contracts for minor revisions to a trigonometry text
2) fewer professors - video tape the good lectures, and share them across universities. You'll need significantly fewer profs across the whole industry.
3) prospective salary based tuition - stop funding the use of education dollars into majors that cannot possibly turn into productive, money making jobs.
And that was just from some random goofball on the internet.
That's like saying there's a bit density we'll finally reach that will make ever improving hard drives worthless.
Education institutions need to improve their efficiency. You can't run our modern transportation system on horseback anymore, and education institutions can't simply re-live the practices from the past 100 years either.
Innovate or die.
Investing is great, if you're doing a good job of it.
There is such thing as a bad investment, and the failure to recognize those can turn a good intention into a bad thing.
You forgot "or gets more efficient at educating students".
Universities need to figure ways use fewer resources per student, so they can have more students and lower tuitions.
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 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.
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.
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.
Get down to the individual cells - isn't it that our bodies learn which foods *partition* more calories into fat versus muscles, and learn which foods target the addictive sugar rush/crash cycle, and find them tastier?
You've already agreed that insulin regulates fat accumulation. How is that a small role? You may disagree on what drives insulin (say, a "tastiness" signal from the brain), but you don't deny that it is the biochemical mechanism for fat storage, right?
Sounds like insulin resistance versus insulin sensitivity.
Question - have you ever been fat? Have you ever had the experience of eating until it feels like you're filled up to the top of your esophagus, and *still* felt hungry?
The difference between a "craving" that may make you feel like noshing on something, and the burning hunger insulin resistant people feel when eating a carbohydrate heavy diet, is *huge*.
So, it means nothing. You can't tell someone "you're overeating" until you see their body mass change. "Overeating" for one person can be "undereating" for another - even if they're the same weight and exercise the same amount!
Rather than blaming fat accumulation on "overeating", isn't it reasonable to think that it could be the opposite way, where fat accumulation is to blame for "overeating", because of the hunger it causes when it steals calories from the muscles?
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?
The same way you agreed earlier - insulin. Now, there may be various regulators of insulin (although I'll argue the primary one is carbohydrate intake), but the biochemical mechanism is pretty clear.
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.
It certainly is complex, but it's hardly thorough :) That being said, it's "what makes us eat more than what we require for leanness?" seems simple - the improper partitioning of incoming energy into fat cells, which starves muscle cells. This improper partitioning is driven by insulin and insulin resistance.
Lustig makes the point that fructose consumption starts insulin resistance, and *then* the insulin index really matters. Check out his youtube lecture "sugar: the bitter truth" - he goes into serious depth there.
If insulin is driving energy into fat cells, and making it unavailable to muscles, and that unavailability is what triggers some sort of hunger response (as we see when say, someone is starving), isn't it simply obvious that in that case insulin is driving the hunger?
I mean, if instead of putting energy into your mouth, and putting it directly into fat storage, you simply didn't put that energy into the body, wouldn't a body get *hungrier*? Isn't that a reasonable assumption?
I'm positing that populations with different internal biochemical *environments* react differently to the same diets, whereas the race and intelligence folk posit that populations differ, *regardless* of environment.
Would you critique mainstream nutrition with the same tactic, that there are some % of cases that don't follow their hypothesis?
So it is purely a mental thing? No biochemical mechanism for being more or less tasty?
But what's the biochemical "hunger response"? Just saying "it's yummy" doesn't help much - since there are people who eat all the yummy stuff they want in unlimited quantities and still don't gain weight.
Shouldn't cravings have biochemical roots? A salt deficiency in your diet, and you'll crave it. An addictive narcotic, messing with your ssi uptake, and you'll crave it.
"Overeat" means nothing, since it's circularly defined. That being said, I believe the insulin hypothesis makes a strong case that when you deprive yourself of a starchy and sugary base, your energy intake is partitioned into use for the muscles rather than storage in the fat cells, so it's harder to accumulate fat if you deprive yourself of carbohydrates.