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?
Correct. What I've denied is that it plays a major role in driving obesity.
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*.
I've been slightly overweight and I know the hunger you've talked about. One thing I've learned is it's highly correlated to the tastiness of food. If I have a nice big juicy steak for dinner I'll be ravenously hungry through the next evening.
But that's just me.
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?
So because 'overeating' is a somewhat arbitrary measure depending on multiple factors it doesn't count?
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?
Even when gaining weight there's only a small difference in the average calories we ingest and the average we burn. 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 Taubes think the body regulates fatness? Does he think maintaining blood glucose at X level is the only mechanism?
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.
How are their internal biochemical environments different? If a Japanese or Vietnamese person can be thin with a bunch of calories from white rice why can't I?
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?
Well there's 30% of obesity in Taiwan that doesn't follow Taubes hypothesis on why they're fat, and entire regions of the world (including examples he used) that defy his theory. If mainstream nutrition had this problem I think they'd be in trouble too.
I'd really suggest reading the series on Why Do We Eat? A Neurobiological Perspective. I think you'll be surprised by how complex the picture is and how thorough the literature is.
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?
There's biochemical feedbacks, our bodies learn which foods have more calories and we tend to find those tastier. And there's lots of other stuff going on including a bunch I don't know about. There may even be a small role insulin plays (but nothing like the role Taubes assigns it).
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.
People have different bodies, for some people the lipostat is that much more effective. They either raise their metabolic rate and burn off the calories even being inactive, or they naturally feel full at an equilibrium state.
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.
I don't know a ton about cravings but they can be very specific (an individual food type). If we were simply craving salt or fat or carbs we'd simply be hungry and crave a wide range, but our fixation on specific foods suggests a strong mental component.
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.
Overeat means ingest more calories than is required to maintain your present body mass. It's not a constant number since calories burned is variable, but it is a real number.
Nothing. It means we find the food tasty so we eat more of it.
The system governing appetite isn't trivial
Agreed. And I'd make the assertion that for the vast majority of 400 pound fat people chowing down large pizzas, they're doing so because their muscles are starving, and their appetite is triggered on high, thanks to the partitioning of energy due to insulin into their fat cells.
Further, if we have, say, a model of appetite where one can increase it by reducing caloric intake, and increasing caloric output (as say, when you're told to "bring your appetite", and you skip a meal, or go exercise more to work up your hunger), it seems that focusing on calories in/calories out is going to be self defeating.
Now, imagining that it's all about taste, calorie density, texture, and "filling" begs the question - what are the biochemical processes at work there?
I guess for me it's hard to assert that those particular bits are nearly as important as insulin resistance, and insulin response, especially since we have such a wide variety of response to the same diet.
The insulin hypothesis deals rather neatly with the appetite response observations, since the partitioning of fuel into fat cells starves muscles, driving more eating, which we can then call "overeating" (because it drove fat accumulation - a skinny person, by definition, can never overeat).
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.
If it's all biochemical then how do you explain cravings? How do you explain being completely full, then finding another gear when you realize there's dessert? Do you really think there's no link between hunger and taste?
Note that one factor in low-carb working is that many hyper-palatable foods are high carb (white bread, chips, cake, cookies). It's harder to overeat when you deprive yourself of the starchy base.
You're missing a variable - insulin resistance. If you go by Lustig, if someone eats nothing but starch, but never touches fruit, they never develop insulin resistance.
How can excess fat intake (in the absence of significant carbohydrate intake) raise blood sugar levels? Isn't the problem that they "overeat" carbohydrates?
The ones with insulin resistance are probably overeating carbs (and everything else). But that doesn't mean insulin is driving the hunger.
So, they blame character flaws (gluttony and sloth), and then make observations of "calories in/calories out", without actually asking "what is the metabolic *cause*". Lustig has done some great stuff on that.
No, they blame the diet.
I have, and I've lost weight. In nutritional ketosis, eating 3000+ calories a day, with a sedentary lifestyle, I simply don't gain any weight. You may of course, consider this simply a single anecdote, not data, but you'd have a very difficult time making the case that the insulin hypothesis isn't true in my individual case.
I never disputed that low-carb doesn't work, so does plain rice or potatoes, but that doesn't mean that insulin is the driver of obesity.
What's there to dodge? The question of "look, rice" is like asking "have you stopped beating your wife?" Holding up a country as an example of "look, insulin is wrong" is like the whole race and intelligence crap - you can't start doing your comparison unless you *control* for environment, and in the case of "lots of rice countries", that means controlling for insulin resistance, which might very well vary between populations.
It's funny, it seems as if you're unwilling to entertain the idea that as per the Taiwan study you cited, the vast majority of cases of obesity *support* Taubes' hypothesis. Would you be more forgiving of Taubes if he said simply "in the vast majority of cases", rather than giving you the notion that he believed 100% of the cases followed?
I don't follow....
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.
And only that one simple datapoint is consistent with Taubes, but it's also consistent with mainstream nutrition, as is all the other evidence that disagrees with Taubes.
I think palatablity plays a huge role, in addition to plain taste salt, fat, sugar, calorie density, and crunchiness all make foods more tempting and easier to overeat. Some foods are also more filling per calorie, protein (ie plain chicken), eggs, broccoli, plain potatoes. And some aren't ice cream, pop, cake, chips, butter.
Genetics also play a big part, social cues, eating habits.
I suspect most people get obese from the same factors in different proportions, the ones who do it with more sugar and high GI foods will have tended to have higher insulin, and those people will be more susceptible to insulin resistance.
The system governing appetite isn't trivial and you're unlikely to find a single switch we can easily flip to make people thin without consequences.
That's only with the caveat of a healthy patient with insulin resistance, but it begs the question - if we all agree insulin is a mechanism for fat storage, why *wouldn't* insulin injections cause obesity?
If the regulatory role of insulin is to regulate blood sugar, not fat, then injecting insulin and causing some of that glucose to be turned into fat would draw a response from the actual regulator. This might include reducing appetite to maintain body fat at its current level (but reducing energy), increased hunger to replace blood sugar (which maybe would increase fat), or taking the fat that was just stored by the insulin and using it to replenish the lost blood sugar.
It might cause obesity but the fact you can create obesity by simulating a specific disorder doesn't mean that disorder causes obesity.
But the real measure is to see what their % of calories from carbohydrates is (which I couldn't find)
Not sure what you're driving at here - you think obese native Hawaiians must not be eating much rice? Or that it's not a high enough percentage of their diet?
If Taubes is right there should be a strong correlation between % of calories from carbohydrates, particularly simple ones like rice, and obesity. The correlation isn't there meaning the story is more complex. You say the Hawaiians are fat because they eat a lot of rice. Well do they really eat a lot of rice, more than we eat potatoes and bread? Do they have sauce that is fattening or making the rice particularly palatable and susceptible to overeating? Are they also eating a bunch of mayo and other foods that are really driving the obesity?
I agree the other 70% have insulin issues, but I challenge that their obesity is caused by those insulin issues instead of insulin issues caused by obesity.
So you think fat accumulation happens *first*, and *then* insulin rises? Given the agreement on insulin as the mechanism for fat storage, exactly how does that jibe together?
They overeat as a result of non-insulin factors. The excess food causes excess blood sugar, this causes an insulin spike and eventual resistance.
My central beef with Taubes is nutritionists already know a huge amount of the story of what causes obesity.
That's categorically untrue. Nutritionists have ignored the basic biochemistry for years, and been driven by misguided government guidelines put out by the USDA (see the 1978 McGovern commission). Like the example of a full dining hall, it is *trivially* true that it is full because more people entered than left, but it that statement gives you *no* information as to *why* people enter and *why* people leave. The typical nutritionist story about obesity is "more calories were stored in fat cells than were removed" - which is simply an observation, not a statement of cause.
From what it looks like the 1978 (77?) guidelines were based on recommendations from nutrition science. And even if they weren't, why would researchers care? Scientists follow the evidence, not government guidelines,
"The typical nutritionist story about obesity is "more calories were stored in fat cells than were removed" - which is simply an observation, not a statement of cause."
This is not the typical nutritionist story. It's a small part, but they spend a lot of time talking about why people eat more calories, how many they burn being active, how many they burn while inactive, metabolic factors, etc....
I'd like to be thinner, but I also ate some cookies when I wasn't really hungry last night. The carbs in the cookies weren't the problem, the problem was that they were cookies.
The cookies are only a problem if they cause fat accumulation. We know that's driven by insulin. If
Lipohypertrophy simply confirms insulin as the mechanism for fat storage which everyone agrees on.
The anorexia link is more compelling but there's an important caveat "AN [anorexia nervosa] may be caused by defects in the evolutionarily conserved response to food and nutrient shortage associated with reduced calorie intake". If there's a defect in the pathway regarding hunger insulin injections might fix that defect, just like fixing a flat tire makes your car go faster. But that doesn't mean that tires regulate your car's speed.
What you'd need to show is insulin injections can cause obesity (not just lipohypertrophy) in healthy patients. And even then it only becomes a potential mechanism since you haven't proven that's what's occurring out in the wild.
Cultures that eat a ton of white rice? They stay thin.
Um, try Hawaii and obesity levels amongst native Hawaiians, who have a *ton* of white rice in their diet.
You have a citation for that? It looks like rice is their staple starch but we don't know their total carb intake.
Some places is asia hit 80% of their calories from rice. But the real measure is to see what their % of calories from carbohydrates is (which I couldn't find)
Inject insulin into rats? Thin
Again, animal model versus human reality. If the rat model was an accurate depiction, anorexics who were treated with insulin would lose weight:)
Insulin plays the same role in their system, I suspect they'd experience lipohypertrophy as well but couldn't find mention either way.
Either way the rat caveat only weakens it as value against the insulin hypothesis, I still haven't seen any evidence for the insulin hypothesis that isn't already consistent with the current state of nutrition research.
Fat people without insulin issues? Significant portion.
As per my other reply, let's say we stipulate to 30% of fat people without insulin issues...are you agreeing that the other 70%, the vast majority, *do* have insulin issues?
Maybe we already have 70% agreement:)
I agree the other 70% have insulin issues, but I challenge that their obesity is caused by those insulin issues instead of insulin issues caused by obesity.
My central beef with Taubes is nutritionists already know a huge amount of the story of what causes obesity. They know a lot of why people get fat and they know how those people can lose weight. The problem is applying that knowledge and getting people to do it in the modern world where we have a bunch of hyper-palatable foods, sedentary lifestyles, tons of fat and salt, numerous social cues, and a bunch of other stuff. I'd like to be thinner, but I also ate some cookies when I wasn't really hungry last night. The carbs in the cookies weren't the problem, the problem was that they were cookies.
Taubes is part of a long line of fad diets, blame obesity on a single cause (which may or may not be part of the big pictu
So you're arguing that the 30% may have still been insulin resistant because they didn't test insulin resistance directly, just blood glucose levels and blood pressure.
Not only that, but they only tested waist size.
As for a writeup of a fat person without insulin resistance or elevated insulin levels, why would someone do that clinical writeup if it's a completely ordinary phenomena?
Always check your premises in science:)
That all being said, let's say we stipulate to 30% of the obese population being driven by say, some odd thyroid problem rather than chronically elevated insulin levels - do you accept that 70% of the obese population has their fat accumulation driven by insulin?
Perhaps I'm driving too hard a bargain, and can convince you that for the overwhelming majority of obese people insulin is a problem, rather than for 100%.
I accept that 70% of the (Taiwanese) obese population, and probably more of our obese people, are obese and insulin resistant.
I think that individual measure would be consistent with insulin driving the obesity, but that other evidence (rat experiments, carb obesity decoupling, other known drivers of obesity, etc) suggests that other causes are at work and the insulin is just along for the ride.
"No data of serum insulin or hs- C-reactive protein (CRP) for further exclusion of metab- olically abnormality in our study was a limitation of re- search; therefore we adopted a metabolic syndrome crite- rion to exclude subjects with insulin resistant characters. It is rare to be insulin-resistant while subject’s blood glu- cose levels were less than 5.6 mmol/L, triglyceride 1.7 mmol/L, HDL-C 1.0 mmol/L in men, 1.3 mmol/L in women and blood pressure 130/85 mmHg."
I did read directly, that's where I got my quotes:P
(well I skimmed)
So you're arguing that the 30% may have still been insulin resistant because they didn't test insulin resistance directly, just blood glucose levels and blood pressure.
But as they said resistance without the glucose is rare, so I really have a tough time believing that it's actually on the order of 30%. So there's definitely insulin sensitive people in that group.
but at 102 cm you're carrying a lot of fat no matter what height you are.
Again, an assertion, not an observation. The study doesn't purport to show what you think it does. What you're looking for is a clinical writeup of a single individual with a fat accumulation problem that doesn't have insulin resistance, or elevated insulin levels. This study clearly has limitations, including the critical statement "To date, there is no uniform definition for MHO."
102 cm at the waist is fat. 200 cm high is tall. Those are assertions I can live with:)
This is also from Taiwan, I have trouble believing that 30% of people in Taiwan with a waist circumference in excess of 102 cm are not obese.
As for a writeup of a fat person without insulin resistance or elevated insulin levels, why would someone do that clinical writeup if it's a completely ordinary phenomena?
Creationist journals are cargo-cult science, nutrition is real science doing real experiments.
A nutritionist who ignores the biochemical role of insulin in fat accumulation, and insists it's all "calories in/calories out" is a creationist then.
I'd agree, but it's sure as hell not Guyenet.
Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".
Sure it is. You refer to some large group (say NASA), and make a baseless assertion without specific attribution. Name the individual, cite the work, or you're simply hand waving.
The NASA example was obviously just for rhetorical purposes. But I've included numerous links to scientific papers, and the Guyenet links I included all used multiple citations.
BOOM!!/me does a rude dance
Wow, if only everything that happens to rats happened to humans:)
Also interesting that you cite a paper "Identification and characterization of metabolically benign obesity in humans", while also citing the other paper that concludes, "Results of the present study indicate that obesity in the absence of the metabolic abnormalities is not such a rare condition in Taiwan. Furthermore, obesity and weight gain are associated with an increased risk for incidences of hypertension, T2DM and the metabolic syndrome in the metabolically healthy, middle-aged population. As such, weight management should continue to be a target for reducing cardiometabolic diseases in all obese indi- viduals."
Good luck getting approval to inject insulin into healthy people to see if it makes them fat.
Smoking causes lung cancer but not all smokers get lung cancer. The fact some people can be obese and metabolically healthy doesn't mean they're not still taking their chances.
The problem is every test of Taubes theories come up negative.
Cultures that eat a ton of white rice? They stay thin.
Inject insulin into rats? Thin
Fat people without insulin issues? Significant portion.
The only thing that agrees with Taubes theories is the low-carb diet, but that's explainable with accepted mechanisms, and there are lots of diets that contradict Taubes that work just as well or better.
Stephan Guyenet seems to have decided to rewrite the Kreb's cycle...seems like wishful thinking in search of evidence:)
I'm not sure I understand this criticism, where is he rewriting the Kreb's cycle?
I don't know what definition they used but quotes from the study clearly indicate the MHO (metabolically healthy obese) had high insulin sensitivity.
"Brochu and Karelis determined that MHO individuals lack most of the metabolic abnormalities, dis-play high levels of insulin sensitivity"
"due to the absence of harmonized criteria, previous studies report MHO subjects to be 20-30% of obese subjects de-pending on the definition. Insulin sensitivity could be the key factor discriminating healthy from at-risk obese subjects."
The other question is "does waist criteria represent obesity"? I knew plenty of people who would've failed on the BMI scale, but did not have a fat accumulation problem. So while it's fairly provocative, I think the study fails to demonstrate what you editorialized in your link text.
A height requirement would be nice, but at 102 cm you're carrying a lot of fat no matter what height you are. I think it's really hard to take any conclusion from that study other than the fact it's possible to be fat and have high insulin sensitivity.
How are they having a debate and presenting evidence about a possible small regulatory role while completely missing the massive regulatory role that Taubes claims?
They're in denial. They have a trope, and even though the data doesn't match it, they refuse to give it up. Very typical of cargo-cult science.
Creationist journals are cargo-cult science, nutrition is real science doing real experiments.
Saying researchers put on blinders and never looked there would be like saying NASA put on blinders and never looked at the sun as the thing holding the solar system together.
Appeal to unnamed authorities fallacy.
Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".
That being said, NASA has put on blinders when it comes to the sun as the thing driving the earth's climate when it comes to the whole catastrophic anthropogenic global warming trope:)
See my 10 foot pole?
It's not even coming close:P
Look, you want to show a single clinical case of an obese person with no insulin resistance, or insulin issues, please, feel free - hopefully whatever happened in that one in a million case is identified and understood. But when it comes to the basic biochemistry of fat accumulation, it is simply incorrect to believe that insulin plays anything but a predominant role.
Actually, no, insulin resistance/sensitivity counts for a lot. Sort of a "square/rectangle" thing - not everyone with elevated insulin levels is going to get obese, but anyone who is obese is so because of elevated insulin levels.
Lustig posits that insulin sensitivity is driven by fructose consumption and its effect on the liver, which seems plausible, but I'm sure a great deal of it has to do with genetics as well. There are bean pole skinny guys out there with high cholesterol and diabetes who don't have any fat accumulation problem, but still get all the other "benefits" of high insulin.
To believe Taubes you need to believe the entire field of nutrition science has been spectacularly incompetent for the past half century
That's not surprising at all. Have you read his book, "Good Calories, Bad Calories"?
No though I've heard/read a number of extended interviews.
Thanks to zealots like Ancel Keys, the direction of government sanctioned research went in a singular direction with blinders, masking and disparaging any divergent opinions.
Look, no matter what your particular axe to grind with Taubes, the fact of the matter is that for every obese person, you've got a combination of insulin resistance and high insulin levels, period. It simply doesn't happen by any other biochemical mechanism.
That's not true, there's a lot of obese people with no insulin issues. And your characterization of nutrition research sounds like climate change denialism. Even if they were looking for something completely different the researchers were researching something.
I read of a recent conference where they were debating whether there was a tiny regulatory role insulin was playing. How are they having a debate and presenting evidence about a possible small regulatory role while completely missing the massive regulatory role that Taubes claims?
Taubes is talking about about one of the three primary sources of calories and one of the most important hormones involving fat storage. Saying researchers put on blinders and never looked there would be like saying NASA put on blinders and never looked at the sun as the thing holding the solar system together. Even if they were studying planets from a completely different perspective every astronomer out there would look at the data and notice something weird was going on with the big yellow thing.
Consider a world where Taubes wasn't being completely fair in his presentation of the evidence, that he was wrong about the history of nutrition science, that he was ignoring critical counter-evidence with Asia and some of his own examples, that he was either unaware of or simply ignoring vast bodies of research that explored his ideas a convincingly debunked them. If we were living on this other world where Taubes was a thorough and well-educated crank would his book look any different?
Having someone who is insulin sensitive semi-starve themselves while eating only potatoes can certainly cause weight loss. Applying an isocaloric potato diet, increasing the % of carbohydrates, to someone who is insulin resistant is going to cause obesity.
I don't know about the insulin resistant population. But for the normal population if Taubes was right the insulin would snatch up all the carbs and put them straight into fat, so even if you were insulin sensitive a potato diet would cause you to get fat and have low energy.
Although Taubes did the seminal work "Good Calories, Bad Calories", which references the undisputed biochemistry I've cited, he isn't the guy who actually did the work - he just reported on it. Calling him a "crank" is to misunderstand how we actually got to understand the Kreb's cycle and the role of insulin in fat accumulation.
Now, Stephan Guyenet has an axe to grind against Taubes, and that's fine, but nothing he's written or cited contraindicates the role of insulin in fat accumulation. There's some question as to what triggers initial insulin resistance (since there are a group of people out there who have no fat accumulation problems despite high carbohydrate intake, although other problems invisible to the naked eye do occur), but there's absolutely no question that the mechanism for fat accumulation in the obese is insulin.
My big beef with Taubes is he basically assumes researchers made a mistake in the 50s, and then... well I'm not sure what.
Have they been doing public advocacy the past 60 years and never bothered to do anymore research?
Are they all such spectacularly bad researchers that no one ever noticed insulin was regulating obesity?
Did they have incredible tunnelvision and haven't looked at how insulin reacts with fat at all?
To believe Taubes you need to believe the entire field of nutrition science has been spectacularly incompetent for the past half century, somehow never considering that the hormone that enables fat accumulation also regulates it. Yet some science reporter somehow stumbled on the truth and is giving you a completely unbiased account of it.
Just look at how he responds when asked about the Japanese and their rice consumption. He starts talking about Japanese eating brown rice until 50 years ago and being healthy then. Ok, so what about the Japanese eating white rice now and still being healthy!! He also says that maybe the real problem is sugar. So the goalposts have moved, high carb isn't bad, it has to be high refined carbs, and maybe it isn't even high refined carbs, it has to be actual sugar! So I'm glad that Taubes apparently endorses a primarily brown rice diet as the key to being thin.
Of course, he didn't need to move the goalposts when talking about the Massa, since most people don't really know what the Massa eat it's safe to simply misrepresent their diet.
Guyenet appear to be wedded to his 'food reward' hypothesis which is countered by lots of evidence, including my own personal experience. Food reward is as much a function of the eater as the food and the eater's state of appetite is driven by hormones, which is driven by the food eaten and the state of the mitochondria and probably the feedback circuits in the VMH.
If there's a single criticism I'd level at most nutrition researchers, it is that they don't understand complex, multi-loop feedback systems well. Such systems create lots of statistical associations, but the effects of any intervention become hard to analyze unless you understand how the various feedback systems interact.
Most engineers know very well how feedback works and how it can get out of hand when you meddle with variables in a conditionally stable, complex feedback system. Weight is a classic example, where it is obviously conditionally stable, because some people are stable at 'lean' and some people slowly accumulate fat throughout their lives with higher frequency ups and downs superimposed.
Food reward is just one part and I suspect it's his primary area of research so he probably talks about it disproportionately. But in the first post I link to his 8 part series explaining the neurobiological motivations behind eating. Having read his stuff with a critical eye for a while I've never found him to oversimplify or claim more certainty than is warranted.
Guyenet has an unfortunate obsession with studies that are just short-term observations of extreme behavior.
From your first link:
For example, overfeeding reliably increases fat mass in humans and can produce substantial body fat accumulation, regardless of whether the excess calories come from carbohydrate or fat, and regardless of changes in circulating insulin (49, 50, 51, 52). Similarly, underfeeding reliably decreases fat mass by a predictable amount, also regardless of macronutrients and changes in circulating insulin (53, 54, 55). "Exceptions" to this rule only seem to occur in studies where food intake is not measured accurately.
Of course, studies where food intake is not measured accurately are also known as "real life".
Though in this case I think he was referring to low quality studies with spurious results that Taubes relies on.
The fact that overfeeding or underfeeding someone produces predictable effects on body mass doesn't really tell you anything about what sort of diet will result in sustained weight loss, because chronically underfed people are hungry, and hungry people eventually give in and eat. The potato diet is a perfect example of Guyenet thinking: it demonstrates that smashing food reward behavior to bits by eating only one very bland food is an effective method for losing weight, but he acknowledges from the start that he doesn't advise it (indeed, there's no reason to believe that it could be a complete diet, which animal products can be). Taubes has many mechanisms wrong but provides an effective solution; Guyenet is right on all the pieces but doesn't actually put it together into anything (though he tepidly embraces paleo in one of his linked articles, and he links to some guy who wants to sell you a diet plan for $40 without telling you anything about it).
Well the blog is about giving you the science behind why people overeat and get fat, not about giving you a diet plan. If you read the blog regularly it's not hard to realize what you have to do to lose weight.
As for the diet plan a few months back Guyenet caused a mild controversy on his blog by helping someone else design a diet plan based on nutrition science then endorsing/promoting it in a blog post. The post was fairly tone-deaf and alienated a number of readers though I don't think it influences is writing.
Ultimately, the problem is that people want to know a method that works, and on that, Taubes delivers and Guyenet doesn't. All the rightness in the world can't overcome that.
If you follow Taubes precisely you might be fine. But if you find his rules don't fit your life so you adapt his "science" by avoiding potatoes and eating lots of steak and bacon you're going to be a lot better served by reading someone like Guyenet.
Seth Roberts has an alternative hypothesis of how bland foods affect the brain's set point mechanism (yes, set points are not accepted fact). I don't think it's well established either way, but it works for some and so makes for some interesting data that has to be accounted for in any correct model of the human metabolism.
It worked for me, but low carb works as well and I don't have to drink flax oil, which is one of the least pleasant dietary experiments I've tried.
Seth Roberts has a novel approach, but it mostly relies on the palatability hypothesis. Seth Robets advocates drinking tasteless (or at least unpleasant) calories through oil, which according to the palatability hypothesis is going to make you less hungry in general. I tried it for a while but found the oil weird, then eventually figured out I could replace the tasteless oil with tasteless broccoli or a microwaved potato.
Low carb works, but partially because you replace the carbs with protein instead of fat (high protein works better than low carb), and partially by cutting a big group of tasty foods out of your diet. If you can't eat bread, pasta, rice, or a bunch of other yummy carbs eating becomes less enjoyable so you do less of it.
Guyenet is wedded to a paradigm that keeps his funding flowing.
You sounds like a AGW denialist.
It matters to him that Taubes be wrong not for the health of people, but for his bank account.
Yes, clearly a journalist and author cares only about the truth and health of people, and not about having a best selling book, lucrative speaking career, or being worshipped as a genius who has solved the obesity epidemic.
Taubes isn't wrong. His logic is rigorous, as befits a physicist who casts his eyes over the wasteland that is nutrition research.
From his bio: Born in Rochester, New York, Taubes studied applied physics at Harvard and aerospace engineering at Stanford (MS, 1978).
A BSc (or even a MSc) in physics doesn't make you a physicist. And even if he was it's not hard to find physicists with crank ideas about physics, why is it so hard to think one could have crank ideas about nutrition?
So nutritionists are incompetent to discuss nutrition, even those with a PhD in neurobiology, but a veterinarian is fine. Besides, all I see from Petro is him rambling about a specific physiological phenomena in an extremely obtuse manner, even if he's right diet is far more complicated than that.
If carbs are so bad explain why people going on a exclusive potato diet always loose loads of weight when potatoes have a higher GI than sugar?
Explain why Japan, which eats large amounts of white rice, is virtually the only developed nation to avoid the obesity epidemic?
The research all points to Taubes being wrong.
The diets of entire nations point to Taubes being wrong.
Yet Taubes writing a book that says everyone else is wrong is enough to convince you he's right?
Fat accumulation isn't driven by caloric intake levels, it's driven by insulin.
If you consume calories which drive insulin up, you'll accumulate more fat. Consume calories which don't drive insulin up, and you won't accumulate more fat.
The concept is pretty simple: to lose weight, don't consume calories that cause fat accumulation. We call these "carbohydrates".
Which is completely consistent with the potato diet, where people eat nothing but potatoes that are pure carbs with a higher glycemic index than sugar, consistently causing people to lose a ton of weight.
Simply put there's a lot of factors of which the author summarized a few with an 8 part series on what motivates people to eat. One of the main hypothesis he pushes is the particularly depressing palatability hypothesis that says the tastier food is the more of it we'll eat.
Diet books are literally a dime a dozen. They generally benefit only the author, publisher and Amazon, leaving the reader frustrated and bloated. With a failure rate of over 99%, diet books are the epitome of a sucker born every minute. One of the few diet books that can offer change
That is where you should stop reading. When someone tells you nearly everything in a category is ineffective, then offers you something in that category as somehow worth your money, something stinks.
If the author is saying that then something stinks, if the reviewer is saying that then the reviewer is probably just ignorant about that category.
It's no mystery how to eat healthy, the mystery is getting people to do it.
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Correct. What I've denied is that it plays a major role in driving obesity.
I've been slightly overweight and I know the hunger you've talked about. One thing I've learned is it's highly correlated to the tastiness of food. If I have a nice big juicy steak for dinner I'll be ravenously hungry through the next evening.
But that's just me.
So because 'overeating' is a somewhat arbitrary measure depending on multiple factors it doesn't count?
Even when gaining weight there's only a small difference in the average calories we ingest and the average we burn. 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 Taubes think the body regulates fatness? Does he think maintaining blood glucose at X level is the only mechanism?
How are their internal biochemical environments different? If a Japanese or Vietnamese person can be thin with a bunch of calories from white rice why can't I?
So it is purely a mental thing? No biochemical mechanism for being more or less tasty?
There's biochemical feedbacks, our bodies learn which foods have more calories and we tend to find those tastier. And there's lots of other stuff going on including a bunch I don't know about. There may even be a small role insulin plays (but nothing like the role Taubes assigns it).
People have different bodies, for some people the lipostat is that much more effective. They either raise their metabolic rate and burn off the calories even being inactive, or they naturally feel full at an equilibrium state.
I don't know a ton about cravings but they can be very specific (an individual food type). If we were simply craving salt or fat or carbs we'd simply be hungry and crave a wide range, but our fixation on specific foods suggests a strong mental component.
Overeat means ingest more calories than is required to maintain your present body mass. It's not a constant number since calories burned is variable, but it is a real number.
What does that mean, biochemically?
Nothing. It means we find the food tasty so we eat more of it.
Agreed. And I'd make the assertion that for the vast majority of 400 pound fat people chowing down large pizzas, they're doing so because their muscles are starving, and their appetite is triggered on high, thanks to the partitioning of energy due to insulin into their fat cells.
Further, if we have, say, a model of appetite where one can increase it by reducing caloric intake, and increasing caloric output (as say, when you're told to "bring your appetite", and you skip a meal, or go exercise more to work up your hunger), it seems that focusing on calories in/calories out is going to be self defeating.
Now, imagining that it's all about taste, calorie density, texture, and "filling" begs the question - what are the biochemical processes at work there?
I guess for me it's hard to assert that those particular bits are nearly as important as insulin resistance, and insulin response, especially since we have such a wide variety of response to the same diet.
The insulin hypothesis deals rather neatly with the appetite response observations, since the partitioning of fuel into fat cells starves muscles, driving more eating, which we can then call "overeating" (because it drove fat accumulation - a skinny person, by definition, can never overeat).
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.
If it's all biochemical then how do you explain cravings? How do you explain being completely full, then finding another gear when you realize there's dessert? Do you really think there's no link between hunger and taste?
Note that one factor in low-carb working is that many hyper-palatable foods are high carb (white bread, chips, cake, cookies). It's harder to overeat when you deprive yourself of the starchy base.
Considering the insulin index of white rice compared to fruit I find this claim pretty dubious.
The ones with insulin resistance are probably overeating carbs (and everything else). But that doesn't mean insulin is driving the hunger.
No, they blame the diet.
I never disputed that low-carb doesn't work, so does plain rice or potatoes, but that doesn't mean that insulin is the driver of obesity.
I don't follow....
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.
And only that one simple datapoint is consistent with Taubes, but it's also consistent with mainstream nutrition, as is all the other evidence that disagrees with Taubes.
I think palatablity plays a huge role, in addition to plain taste salt, fat, sugar, calorie density, and crunchiness all make foods more tempting and easier to overeat. Some foods are also more filling per calorie, protein (ie plain chicken), eggs, broccoli, plain potatoes. And some aren't ice cream, pop, cake, chips, butter.
Genetics also play a big part, social cues, eating habits.
I suspect most people get obese from the same factors in different proportions, the ones who do it with more sugar and high GI foods will have tended to have higher insulin, and those people will be more susceptible to insulin resistance.
The system governing appetite isn't trivial and you're unlikely to find a single switch we can easily flip to make people thin without consequences.
That's only with the caveat of a healthy patient with insulin resistance, but it begs the question - if we all agree insulin is a mechanism for fat storage, why *wouldn't* insulin injections cause obesity?
If the regulatory role of insulin is to regulate blood sugar, not fat, then injecting insulin and causing some of that glucose to be turned into fat would draw a response from the actual regulator. This might include reducing appetite to maintain body fat at its current level (but reducing energy), increased hunger to replace blood sugar (which maybe would increase fat), or taking the fat that was just stored by the insulin and using it to replenish the lost blood sugar.
It might cause obesity but the fact you can create obesity by simulating a specific disorder doesn't mean that disorder causes obesity.
If Taubes is right there should be a strong correlation between % of calories from carbohydrates, particularly simple ones like rice, and obesity. The correlation isn't there meaning the story is more complex. You say the Hawaiians are fat because they eat a lot of rice. Well do they really eat a lot of rice, more than we eat potatoes and bread? Do they have sauce that is fattening or making the rice particularly palatable and susceptible to overeating? Are they also eating a bunch of mayo and other foods that are really driving the obesity?
They overeat as a result of non-insulin factors. The excess food causes excess blood sugar, this causes an insulin spike and eventual resistance.
From what it looks like the 1978 (77?) guidelines were based on recommendations from nutrition science. And even if they weren't, why would researchers care? Scientists follow the evidence, not government guidelines,
"The typical nutritionist story about obesity is "more calories were stored in fat cells than were removed" - which is simply an observation, not a statement of cause."
This is not the typical nutritionist story. It's a small part, but they spend a lot of time talking about why people eat more calories, how many they burn being active, how many they burn while inactive, metabolic factors, etc....
That's been done before, they even have a word for it:
http://en.wikipedia.org/wiki/Lipohypertrophy
http://garytaubes.com/2012/02/on-the-greatly-exaggerated-demise-of-the-insulin-hypothesis/
Heck, they even use it as a therapy for anorexia:
http://www.psychologytoday.com/blog/evolutionary-psychiatry/201206/evolution-and-anorexia-nervosa
Lipohypertrophy simply confirms insulin as the mechanism for fat storage which everyone agrees on.
The anorexia link is more compelling but there's an important caveat "AN [anorexia nervosa] may be caused by defects in the evolutionarily conserved response to food and nutrient shortage associated with reduced calorie intake". If there's a defect in the pathway regarding hunger insulin injections might fix that defect, just like fixing a flat tire makes your car go faster. But that doesn't mean that tires regulate your car's speed.
What you'd need to show is insulin injections can cause obesity (not just lipohypertrophy) in healthy patients. And even then it only becomes a potential mechanism since you haven't proven that's what's occurring out in the wild.
Um, try Hawaii and obesity levels amongst native Hawaiians, who have a *ton* of white rice in their diet.
You have a citation for that? It looks like rice is their staple starch but we don't know their total carb intake.
Some places is asia hit 80% of their calories from rice. But the real measure is to see what their % of calories from carbohydrates is (which I couldn't find)
Again, animal model versus human reality. If the rat model was an accurate depiction, anorexics who were treated with insulin would lose weight :)
Insulin plays the same role in their system, I suspect they'd experience lipohypertrophy as well but couldn't find mention either way.
Either way the rat caveat only weakens it as value against the insulin hypothesis, I still haven't seen any evidence for the insulin hypothesis that isn't already consistent with the current state of nutrition research.
As per my other reply, let's say we stipulate to 30% of fat people without insulin issues...are you agreeing that the other 70%, the vast majority, *do* have insulin issues?
Maybe we already have 70% agreement :)
I agree the other 70% have insulin issues, but I challenge that their obesity is caused by those insulin issues instead of insulin issues caused by obesity.
My central beef with Taubes is nutritionists already know a huge amount of the story of what causes obesity. They know a lot of why people get fat and they know how those people can lose weight. The problem is applying that knowledge and getting people to do it in the modern world where we have a bunch of hyper-palatable foods, sedentary lifestyles, tons of fat and salt, numerous social cues, and a bunch of other stuff. I'd like to be thinner, but I also ate some cookies when I wasn't really hungry last night. The carbs in the cookies weren't the problem, the problem was that they were cookies.
Taubes is part of a long line of fad diets, blame obesity on a single cause (which may or may not be part of the big pictu
Not only that, but they only tested waist size.
Always check your premises in science :)
That all being said, let's say we stipulate to 30% of the obese population being driven by say, some odd thyroid problem rather than chronically elevated insulin levels - do you accept that 70% of the obese population has their fat accumulation driven by insulin?
Perhaps I'm driving too hard a bargain, and can convince you that for the overwhelming majority of obese people insulin is a problem, rather than for 100%.
I accept that 70% of the (Taiwanese) obese population, and probably more of our obese people, are obese and insulin resistant.
I think that individual measure would be consistent with insulin driving the obesity, but that other evidence (rat experiments, carb obesity decoupling, other known drivers of obesity, etc) suggests that other causes are at work and the insulin is just along for the ride.
Read the study directly, it'll be more informative for you than the abstract:
http://apjcn.nhri.org.tw/server/APJCN/21/2/227.pdf
"No data of serum insulin or hs- C-reactive protein (CRP) for further exclusion of metab- olically abnormality in our study was a limitation of re- search; therefore we adopted a metabolic syndrome crite- rion to exclude subjects with insulin resistant characters. It is rare to be insulin-resistant while subject’s blood glu- cose levels were less than 5.6 mmol/L, triglyceride 1.7 mmol/L, HDL-C 1.0 mmol/L in men, 1.3 mmol/L in women and blood pressure 130/85 mmHg."
I did read directly, that's where I got my quotes :P
(well I skimmed)
So you're arguing that the 30% may have still been insulin resistant because they didn't test insulin resistance directly, just blood glucose levels and blood pressure.
But as they said resistance without the glucose is rare, so I really have a tough time believing that it's actually on the order of 30%. So there's definitely insulin sensitive people in that group.
Again, an assertion, not an observation. The study doesn't purport to show what you think it does. What you're looking for is a clinical writeup of a single individual with a fat accumulation problem that doesn't have insulin resistance, or elevated insulin levels. This study clearly has limitations, including the critical statement "To date, there is no uniform definition for MHO."
102 cm at the waist is fat. 200 cm high is tall. Those are assertions I can live with :)
This is also from Taiwan, I have trouble believing that 30% of people in Taiwan with a waist circumference in excess of 102 cm are not obese.
As for a writeup of a fat person without insulin resistance or elevated insulin levels, why would someone do that clinical writeup if it's a completely ordinary phenomena?
A nutritionist who ignores the biochemical role of insulin in fat accumulation, and insists it's all "calories in/calories out" is a creationist then.
I'd agree, but it's sure as hell not Guyenet.
Sure it is. You refer to some large group (say NASA), and make a baseless assertion without specific attribution. Name the individual, cite the work, or you're simply hand waving.
The NASA example was obviously just for rhetorical purposes. But I've included numerous links to scientific papers, and the Guyenet links I included all used multiple citations.
Wow, if only everything that happens to rats happened to humans :)
Also interesting that you cite a paper "Identification and characterization of metabolically benign obesity in humans", while also citing the other paper that concludes, "Results of the present study indicate that obesity in the absence of the metabolic abnormalities is not such a rare condition in Taiwan. Furthermore, obesity and weight gain are associated with an increased risk for incidences of hypertension, T2DM and the metabolic syndrome in the metabolically healthy, middle-aged population. As such, weight management should continue to be a target for reducing cardiometabolic diseases in all obese indi- viduals."
Good luck getting approval to inject insulin into healthy people to see if it makes them fat.
Smoking causes lung cancer but not all smokers get lung cancer. The fact some people can be obese and metabolically healthy doesn't mean they're not still taking their chances.
The problem is every test of Taubes theories come up negative.
Cultures that eat a ton of white rice? They stay thin.
Inject insulin into rats? Thin
Fat people without insulin issues? Significant portion.
The only thing that agrees with Taubes theories is the low-carb diet, but that's explainable with accepted mechanisms, and there are lots of diets that contradict Taubes that work just as well or better.
Stephan Guyenet seems to have decided to rewrite the Kreb's cycle...seems like wishful thinking in search of evidence :)
I'm not sure I understand this criticism, where is he rewriting the Kreb's cycle?
Trying to have your cake and eat it too? :)
Nah, don't wanna get fat.
I don't know what definition they used but quotes from the study clearly indicate the MHO (metabolically healthy obese) had high insulin sensitivity.
"Brochu and Karelis determined that MHO individuals lack most of the metabolic abnormalities, dis-play high levels of insulin sensitivity"
"due to the absence of harmonized criteria, previous studies report MHO subjects to be 20-30% of obese subjects de-pending on the definition. Insulin sensitivity could be the key factor discriminating healthy from at-risk obese subjects."
The other question is "does waist criteria represent obesity"? I knew plenty of people who would've failed on the BMI scale, but did not have a fat accumulation problem. So while it's fairly provocative, I think the study fails to demonstrate what you editorialized in your link text.
A height requirement would be nice, but at 102 cm you're carrying a lot of fat no matter what height you are. I think it's really hard to take any conclusion from that study other than the fact it's possible to be fat and have high insulin sensitivity.
Creationist journals are cargo-cult science, nutrition is real science doing real experiments.
Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".
That being said, NASA has put on blinders when it comes to the sun as the thing driving the earth's climate when it comes to the whole catastrophic anthropogenic global warming trope :)
See my 10 foot pole?
It's not even coming close :P
Look, you want to show a single clinical case of an obese person with no insulin resistance, or insulin issues, please, feel free - hopefully whatever happened in that one in a million case is identified and understood. But when it comes to the basic biochemistry of fat accumulation, it is simply incorrect to believe that insulin plays anything but a predominant role.
"Experimentally preventing the increase in circulating insulin that occurs on fattening diets does not alter the course of fat gain in rodents or dogs
Experimentally elevating circulating insulin by creating liver insulin resistance does not lead to fat gain in rodents
Experimentally increasing circulating insulin by infusing it directly into the blood does not cause fat gain in rodents, but instead makes them leaner
Roughly a quarter of obese humans have normal circulating insulin and normal insulin sensitivity ("metabolically healthy" obese)"
BOOM!! /me does a rude dance
Actually, no, insulin resistance/sensitivity counts for a lot. Sort of a "square/rectangle" thing - not everyone with elevated insulin levels is going to get obese, but anyone who is obese is so because of elevated insulin levels.
Lustig posits that insulin sensitivity is driven by fructose consumption and its effect on the liver, which seems plausible, but I'm sure a great deal of it has to do with genetics as well. There are bean pole skinny guys out there with high cholesterol and diabetes who don't have any fat accumulation problem, but still get all the other "benefits" of high insulin.
About 28.5% of obese people are metabolically healthy (ie have normal insulin sensitivity). 70% is a long way from everyone, how'd that 28.5% get fat?
That's not surprising at all. Have you read his book, "Good Calories, Bad Calories"?
No though I've heard/read a number of extended interviews.
Thanks to zealots like Ancel Keys, the direction of government sanctioned research went in a singular direction with blinders, masking and disparaging any divergent opinions.
Look, no matter what your particular axe to grind with Taubes, the fact of the matter is that for every obese person, you've got a combination of insulin resistance and high insulin levels, period. It simply doesn't happen by any other biochemical mechanism.
That's not true, there's a lot of obese people with no insulin issues. And your characterization of nutrition research sounds like climate change denialism. Even if they were looking for something completely different the researchers were researching something.
I read of a recent conference where they were debating whether there was a tiny regulatory role insulin was playing. How are they having a debate and presenting evidence about a possible small regulatory role while completely missing the massive regulatory role that Taubes claims?
Taubes is talking about about one of the three primary sources of calories and one of the most important hormones involving fat storage. Saying researchers put on blinders and never looked there would be like saying NASA put on blinders and never looked at the sun as the thing holding the solar system together. Even if they were studying planets from a completely different perspective every astronomer out there would look at the data and notice something weird was going on with the big yellow thing.
Consider a world where Taubes wasn't being completely fair in his presentation of the evidence, that he was wrong about the history of nutrition science, that he was ignoring critical counter-evidence with Asia and some of his own examples, that he was either unaware of or simply ignoring vast bodies of research that explored his ideas a convincingly debunked them. If we were living on this other world where Taubes was a thorough and well-educated crank would his book look any different?
Consistently?
Having someone who is insulin sensitive semi-starve themselves while eating only potatoes can certainly cause weight loss. Applying an isocaloric potato diet, increasing the % of carbohydrates, to someone who is insulin resistant is going to cause obesity.
I don't know about the insulin resistant population. But for the normal population if Taubes was right the insulin would snatch up all the carbs and put them straight into fat, so even if you were insulin sensitive a potato diet would cause you to get fat and have low energy.
Although Taubes did the seminal work "Good Calories, Bad Calories", which references the undisputed biochemistry I've cited, he isn't the guy who actually did the work - he just reported on it. Calling him a "crank" is to misunderstand how we actually got to understand the Kreb's cycle and the role of insulin in fat accumulation.
Now, Stephan Guyenet has an axe to grind against Taubes, and that's fine, but nothing he's written or cited contraindicates the role of insulin in fat accumulation. There's some question as to what triggers initial insulin resistance (since there are a group of people out there who have no fat accumulation problems despite high carbohydrate intake, although other problems invisible to the naked eye do occur), but there's absolutely no question that the mechanism for fat accumulation in the obese is insulin.
There's a big difference between insulin being required for fat storage and insulin regulating fat storage.
My big beef with Taubes is he basically assumes researchers made a mistake in the 50s, and then... well I'm not sure what.
Have they been doing public advocacy the past 60 years and never bothered to do anymore research?
Are they all such spectacularly bad researchers that no one ever noticed insulin was regulating obesity?
Did they have incredible tunnelvision and haven't looked at how insulin reacts with fat at all?
To believe Taubes you need to believe the entire field of nutrition science has been spectacularly incompetent for the past half century, somehow never considering that the hormone that enables fat accumulation also regulates it. Yet some science reporter somehow stumbled on the truth and is giving you a completely unbiased account of it.
Just look at how he responds when asked about the Japanese and their rice consumption. He starts talking about Japanese eating brown rice until 50 years ago and being healthy then. Ok, so what about the Japanese eating white rice now and still being healthy!! He also says that maybe the real problem is sugar. So the goalposts have moved, high carb isn't bad, it has to be high refined carbs, and maybe it isn't even high refined carbs, it has to be actual sugar! So I'm glad that Taubes apparently endorses a primarily brown rice diet as the key to being thin.
Of course, he didn't need to move the goalposts when talking about the Massa, since most people don't really know what the Massa eat it's safe to simply misrepresent their diet.
Guyenet appear to be wedded to his 'food reward' hypothesis which is countered by lots of evidence, including my own personal experience. Food reward is as much a function of the eater as the food and the eater's state of appetite is driven by hormones, which is driven by the food eaten and the state of the mitochondria and probably the feedback circuits in the VMH.
If there's a single criticism I'd level at most nutrition researchers, it is that they don't understand complex, multi-loop feedback systems well. Such systems create lots of statistical associations, but the effects of any intervention become hard to analyze unless you understand how the various feedback systems interact.
Most engineers know very well how feedback works and how it can get out of hand when you meddle with variables in a conditionally stable, complex feedback system. Weight is a classic example, where it is obviously conditionally stable, because some people are stable at 'lean' and some people slowly accumulate fat throughout their lives with higher frequency ups and downs superimposed.
Food reward is just one part and I suspect it's his primary area of research so he probably talks about it disproportionately. But in the first post I link to his 8 part series explaining the neurobiological motivations behind eating. Having read his stuff with a critical eye for a while I've never found him to oversimplify or claim more certainty than is warranted.
Guyenet has an unfortunate obsession with studies that are just short-term observations of extreme behavior.
From your first link:
For example, overfeeding reliably increases fat mass in humans and can produce substantial body fat accumulation, regardless of whether the excess calories come from carbohydrate or fat, and regardless of changes in circulating insulin (49, 50, 51, 52). Similarly, underfeeding reliably decreases fat mass by a predictable amount, also regardless of macronutrients and changes in circulating insulin (53, 54, 55). "Exceptions" to this rule only seem to occur in studies where food intake is not measured accurately.
Of course, studies where food intake is not measured accurately are also known as "real life".
Though in this case I think he was referring to low quality studies with spurious results that Taubes relies on.
The fact that overfeeding or underfeeding someone produces predictable effects on body mass doesn't really tell you anything about what sort of diet will result in sustained weight loss, because chronically underfed people are hungry, and hungry people eventually give in and eat. The potato diet is a perfect example of Guyenet thinking: it demonstrates that smashing food reward behavior to bits by eating only one very bland food is an effective method for losing weight, but he acknowledges from the start that he doesn't advise it (indeed, there's no reason to believe that it could be a complete diet, which animal products can be). Taubes has many mechanisms wrong but provides an effective solution; Guyenet is right on all the pieces but doesn't actually put it together into anything (though he tepidly embraces paleo in one of his linked articles, and he links to some guy who wants to sell you a diet plan for $40 without telling you anything about it).
Well the blog is about giving you the science behind why people overeat and get fat, not about giving you a diet plan. If you read the blog regularly it's not hard to realize what you have to do to lose weight.
As for the diet plan a few months back Guyenet caused a mild controversy on his blog by helping someone else design a diet plan based on nutrition science then endorsing/promoting it in a blog post. The post was fairly tone-deaf and alienated a number of readers though I don't think it influences is writing.
Ultimately, the problem is that people want to know a method that works, and on that, Taubes delivers and Guyenet doesn't. All the rightness in the world can't overcome that.
If you follow Taubes precisely you might be fine. But if you find his rules don't fit your life so you adapt his "science" by avoiding potatoes and eating lots of steak and bacon you're going to be a lot better served by reading someone like Guyenet.
Seth Roberts has an alternative hypothesis of how bland foods affect the brain's set point mechanism (yes, set points are not accepted fact). I don't think it's well established either way, but it works for some and so makes for some interesting data that has to be accounted for in any correct model of the human metabolism.
It worked for me, but low carb works as well and I don't have to drink flax oil, which is one of the least pleasant dietary experiments I've tried.
Seth Roberts has a novel approach, but it mostly relies on the palatability hypothesis. Seth Robets advocates drinking tasteless (or at least unpleasant) calories through oil, which according to the palatability hypothesis is going to make you less hungry in general. I tried it for a while but found the oil weird, then eventually figured out I could replace the tasteless oil with tasteless broccoli or a microwaved potato.
Low carb works, but partially because you replace the carbs with protein instead of fat (high protein works better than low carb), and partially by cutting a big group of tasty foods out of your diet. If you can't eat bread, pasta, rice, or a bunch of other yummy carbs eating becomes less enjoyable so you do less of it.
Guyenet is wedded to a paradigm that keeps his funding flowing.
You sounds like a AGW denialist.
It matters to him that Taubes be wrong not for the health of people, but for his bank account.
Yes, clearly a journalist and author cares only about the truth and health of people, and not about having a best selling book, lucrative speaking career, or being worshipped as a genius who has solved the obesity epidemic.
Taubes isn't wrong. His logic is rigorous, as befits a physicist who casts his eyes over the wasteland that is nutrition research.
From his bio:
Born in Rochester, New York, Taubes studied applied physics at Harvard and aerospace engineering at Stanford (MS, 1978).
A BSc (or even a MSc) in physics doesn't make you a physicist. And even if he was it's not hard to find physicists with crank ideas about physics, why is it so hard to think one could have crank ideas about nutrition?
Petro Dobromylskyj will set set your thinking straight. http://high-fat-nutrition.blogspot.com/
So nutritionists are incompetent to discuss nutrition, even those with a PhD in neurobiology, but a veterinarian is fine. Besides, all I see from Petro is him rambling about a specific physiological phenomena in an extremely obtuse manner, even if he's right diet is far more complicated than that.
If carbs are so bad explain why people going on a exclusive potato diet always loose loads of weight when potatoes have a higher GI than sugar?
Explain why Japan, which eats large amounts of white rice, is virtually the only developed nation to avoid the obesity epidemic?
The research all points to Taubes being wrong.
The diets of entire nations point to Taubes being wrong.
Yet Taubes writing a book that says everyone else is wrong is enough to convince you he's right?
Fat accumulation isn't driven by caloric intake levels, it's driven by insulin.
If you consume calories which drive insulin up, you'll accumulate more fat. Consume calories which don't drive insulin up, and you won't accumulate more fat.
The concept is pretty simple: to lose weight, don't consume calories that cause fat accumulation. We call these "carbohydrates".
Which is completely consistent with the potato diet, where people eat nothing but potatoes that are pure carbs with a higher glycemic index than sugar, consistently causing people to lose a ton of weight.
Fat accumulation is driven by the hormone insulin. Undisputed biochemistry.
Insulin levels are driven by blood sugar levels. Undisputed biochemistry.
Blood sugar levels are driven by carbohydrate intake. Undisputed biochemistry.
I'm sorry to inform you but Gary Taubes is a crank.
Stop eating carbohydrates. It's simple.
Low carb diets work, but not for the reason you think they do.
One thing people might want to check out is a blog by an actual obesity researcher
Simply put there's a lot of factors of which the author summarized a few with an 8 part series on what motivates people to eat. One of the main hypothesis he pushes is the particularly depressing palatability hypothesis that says the tastier food is the more of it we'll eat.
He also takes down the nonsense of Gary Taubes.
Diet books are literally a dime a dozen. They generally benefit only the author, publisher and Amazon, leaving the reader frustrated and bloated. With a failure rate of over 99%, diet books are the epitome of a sucker born every minute. One of the few diet books that can offer change
That is where you should stop reading. When someone tells you nearly everything in a category is ineffective, then offers you something in that category as somehow worth your money, something stinks.
If the author is saying that then something stinks, if the reviewer is saying that then the reviewer is probably just ignorant about that category.
It's no mystery how to eat healthy, the mystery is getting people to do it.