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EventsGuyenet, Taubes and why low carb works
After the recent fireworks at AHS, perhaps this should not come as a surprise. Neurobiologist and popular blogger Stephan Guyenet has posted on why he does not believe in (refined) carbohydrates as an important cause of obesity. Although he does acknowledge that a low carb diet is effective for making you lose weight.
Sound complicated? It is:
Whole Health Source: The Carbohydrate Hypothesis of Obesity – a Critical Examination
This makes me think of a common saying regarding forests and trees (thus the illustration). Let’s untangle this mess.
The basic premise
The Carbohydrate Hypothesis, as attacked by Guyenet, looks basically like this:
Excessive amounts of carbohydrates (especially refined carbs / sugar) increases insulin and results in fat gain.
Guyenets argues in his post that carbs are not necessarily the cause of increased insulin, and insulin certainly do not result in gaining weight (maybe the opposite!). Basically he says that while low carb works, the theory to explain it is wrong.
However, as every doctor who has ever treated diabetics with insulin (and their patients) probably knows, injecting insulin certainly does tends to increase fat gain. And in untreated type 1 diabetics, with no insulin, weight plummets. Guyenet does not mention that.
Thin people usually have low insulin levels, obese people usually have high levels of insulin. Guyenet does not believe that is significant.
My answer to Guyenet’s post
Stephen,
Very interesting post (as always), but several surprisingly unconvincing arguments.
First of all: You state that low carb diets do indeed work well for weight loss most of the time, and that you see that as a fact. Kudos to you for acknowledging it. However, you can’t say for sure why they work, if not through insulin, so maybe we should not rush to conclusions yet.
You also claim that obesity and metabolism researchers do not take the carbohydrate theory seriously. Well, as they have so far failed spectacularly to come up with anything useful for obesity I’m not sure that is a bad thing.
In the face of massively increasing obesity rates there is only one drug approved in Europe (where I work as a doctor treating obese patients), orlistat, and everyone pretty much agrees that it sucks. The only solution proposed is to cut away healthy stomachs to stop fat people from eating. Yikes.
The failure of obesity and metabolism researchers (however smart) during the last decades is of epic proportions. It makes the Hindenburg look like a success story. Please don’t tell me we should care about what they believe in.
On to your three so called “falsifications”:
1
You argue that leptin is more important than insulin in obesity. Take a look at Robert Lustig’s lecture during AHS. Hyperinsulinemia results in leptin resistance.
Problem solved. Moving on:
2
Insulin results in fat being pushed into fat cells BUT insulin also signals satiety in the brain… problem? No. Like most hormones (cortisol is a good example) insulin has short term and long term effects:
Short term it increases satiety in the brain. Makes perfect sense as it normally means that we just ate.
Long term hyperinsulinemia, on the other hand, increases fat storage and makes us eat more. At least partly through the resulting leptin resistance, like professor Lustig pointed out.
Again, problem solved. Nothing “falsified”.
3
You claim that not just (especially refined) carbohydrates increase insulin, so does protein to some degree. Sure. But we all need protein and low carb diets are mainly about switching carbs to fat. Carbs release lots of insulin, fats do not.
There are plenty of studies showing that low carb diets drastically reduce insulin levels during the entire day. If you’d like references just say so.
Again, nothing falsified.
To summarize:
Of course not all carbs are evil all the time. But refined carbs (sugar, easily digested starch) can be a huge problem for sensitive people (obese, diabetics). It seems we agree on that, as well as that low carb diets can be most helpful in those conditions.
What is really being questioned here is the explanation behind the way the world works. And perhaps it is not quite so simple as Taubes and others once thought.
However, if we complicate the theory just a little bit it still works fine. Let’s not rush to prematurely “falsify” a working hypothesis when we have nothing better to replace it with.
Thus
Whether we bother to add the step with leptin or not, this still seems to be true:
Excessive amounts of carbohydrates (especially refined carbs / sugar) increases insulin and results in fat gain.
Of course, what “excessive amounts” means vary from person to person, and it also depend on what carbs we are talking about. Two examples: Young fit men often tolerate a lot of carbs, even sugar, without gaining much weight, but middle-aged obese women with type 2 diabetes do not.
Bottom line
Some very smart people disagree why low carb works. But we all seem to agree that it does work.
More
AHS showdown: Gary Taubes vs Stephan Guyenet
78 comments
In my latest post, I had the following to say, which agrees with what you've just said:
"In addition to that, if someone who has wrecked their metabolism for the majority of their life (not someone who is still in their youth - you know, 20s and 30s) discovers a low carb/Paleo/Primal way of living helps them maintain their health and accomplish weight loss, there is nothing saying that they will ever be able to eat the occasional potato or piece of fruit without it being detrimental to their weight or well being. Gary Taubes is right about many things, and so is the low carb movement."
I don't want to comment on Stephan's post as I don't want to get into any heated debates at the moment, but I am glad you have, and have done such a fine job of dismantling his statements. I am following this issue closely. I am interested in any rebuttal he might have. Unfortunately, I don't think Stephen Guyenet can see the forest for those trees right now. :/
Pretty much what I'm hearing from the Paleo/primal camp is something like, "It's not carbohydrates, it's refined and industrial carbohydrates." What do all those carbs have in common? They've had the fiber removed (and usually some or all micronutrients). But what have Taubes--and Atkins--been saying all along? Fiber doesn't matter. It doesn't raise insulin the way the digestible carbs do. So the two camps are actually in AGREEMENT, but you wouldn't know that the way the Paleo folks go on.
Though the truth is, there isn't much dietary requirement for fiber, and even where it *does* help, as with soluble fiber feeding good gut bacteria, you don't need much of it and you can get that from fruit. So at the end of the day it doesn't even matter whether you eat a lot of carbs. You will not die without them.
"Young fit men often tolerate a lot of carbs, even sugar, without gaining much weight, but middle-aged obese women with type 2 diabetes do not." Right. For that matter, middle-aged obese men often can't tolerate carbs as they did in their own youth. I am a great example!
I won't pretend to know who is right about the mechanisms by which low-carb diets work. But both Guyenet and Taubes identify what for me is a key point: people eating low-carb often reduce their caloric intake without even trying to. That is exactly what happened in my case.
On a low-carb plan, I eat 1800 - 2000 calories most days, which is many fewer than I burn. So I lose weight. When I tried to eat at that same caloric level on a standard low-fat diet, I was constantly hungry. I could not do it.
I believe I am a healthier person now than I was before reading Taubes' latest book and starting to eat low-carb. I know I am a lighter, thinner person! You experts can argue about and investigate the precise mechanisms by which low-carb diets succeed for many people. It is fitting and proper that you do so. By all means, share your thoughts with us. But right now, what I care most about is results. I have discovered one thing that works for me -- reducing carbs -- and I will stick with it as long as it continues to work.
Here is my current opinion on this debate:
1. I think Guyenet is totally wrong in claiming that insulin has nothing to do with weight gain.
2. I think the Low Carb Camp needs to acknowledge that not all carbs are the same regarding weight gain and other health issues. We have something to learn from people like Robert Lustig and Staffan Lindeberg. The carbs/starch in tubers does not have the same effect on weight and cardiovascular disease as pure sugars has. Insulin is probebly the major player but the reward theory and emerging neuroscience might explain something about why pure sugars makes it a lot easier to overeat than the slowly digestible starch in tubers.
I also think the glycation factor will turn out to be very important when it comes to explaining why high fructose/sugar consumtion is so much more detrimental to cardivascular health than pure starch is. (fructose and galactose are 10 times more likely to cause glycation than glucose is, and glycation seems to be the key to making LDL smaller and denser).
I do belive that Staffan Lindeberg (and Michael Pollan by the way) is therefore right in his criticism against us in the LCHF/Low Carb community. We are too macronutrient orientated and we need to acknowledge that differnt carbs will be metabolized in radically differnt ways, resulting i highly differnt health and weight outcomes.
Insulin stores fat and prevents fat liberation from fat cells.
Elevated levels of insulin that persist for hours after eating ... store fat, and prevent fat mobilization.
I am filled with regret that I was unable to attend the symposium (I was invited but it coincided with our annual trip to the lake and family time won out).
Here is a comment I posted on Guyenet's blog:
Interesting discussion and remarkably civil, too, which is nice.
My main issue with this debate is that LC works so brilliantly, a virtual magic bullet, for the conditions associated with insulin resistance. Not just overweight, but lipids, BP, PCOS, GERD, etc etc along with a host of inflammatory conditions, too. There is more to this than insulin, LPL and adipocytes. Way more.
In my own personal experience, after almost 9 years of VLC, I eat like a horse, I thoroughly enjoy my food, I eat heaps of fat including SFA, but nothing sticks unless I overindulge in carbs. Even nuts can cause me to gain adipose. I do have insulin resistance but since this is endemic in north america now, I am probably in the majority. It would appear that LC is the simple solution to a myriad of medical problems that are draining the collective coffers of society.
I realize n=1 doesn't get a lot of respect, but I have seen the same results in so many others that I have few doubts as to the validity of my observations. I also find lots of supportive literature, especially the carefully executed studies by Jeff Volek et al. In my own research, I have seen remarkable results, unlike anything achieved through other diets or pharmacology.
On balance, I find the explanations put forward by Taubes and Lustig to explain these phenomena more compelling than anything else I have encountered, including the notion of palatability and reward.
Well you missed something, but there is always AHS12! ;)
I have a question about fat storage. I have asked Gary Taubes about this, but his answer was less than satisfying. I’m hoping you can shed some light:
If a person is eating a certain amount of fat, protein and carbs and that person is maintaining their weight, and then suddenly they start eating a lot more fat, just as an experiment, what will happen? I have heard people say that the extra calories will be stored as fat (they call it a “calorie bomb”) and other people will say that it will just cause the metabolism to be revved up to burn off the excess. In my case, it seems to add to my fat and not get burned off.
If it is stored as fat, by what mechanism does this happen? If the “extra” fat is not causing an insulin release (which they say fat cannot do, but carbs and protein can), then how is the fat being stored?
Also, if a person is eating very low carb but not losing weight, then how is that possible? After 2+ years of struggling with weight loss while eating under 20-40 total carbs per day and high fat (70-75%) with moderate protein, my body fat stays around 34%, and I gain weight very easily and lose weight, when I do, very slowly.
I starting checking my blood glucose at home, convinced that I must be really sensitive to carbs, but found that even eating 46 grams of carbs per day is not raising my blood glucose over the 90s. The only time it went high was when I purposely ate ice cream with fudge sauce to see what would happen. My blood glucose shot to 176 after an hour, but went down to 118 an hour later, then back down to my normal mid-80s.
So if it is not insulin that is driving my fat storage, what is? What is the mechanism that will cause fat stores to be “locked up” if it is not excess insulin? By the way, my A1C is 5.1 and my fasting insulin is around 2.
Thanks in advance for any thoughts you have!
Rebecca
If you eat a lot more fat and keep your carbs and protein the same, then you will likely both gain some weight and increase your metabolism.
However most people who increase the amount of fat they eat will feel fuller and eat less of other food, like sugar and starch. Under those circumstances you may lose weight.
Your insulin is never zero so the fat can certainly be stored if you voluntarily overeat. That tends to be hard to do on a strict low carb though, as it will make you feel stuffed and perhaps even nauseous.
Some people, especially some women over 40 y/o, find it hard to reach a perfect weight even on a strict low carb diet. There are some things that may help. Until I put up a translation, here is my older Swedish page on it, weirdly translated by Google:
http://translate.google.com/translate?js=n&prev=_t&hl=en�...
That does look like a great article, Doctor... I look forward to seeing a translation when you have time.
I very much enjoy your blog.
It's like women and testosterone - if she has none, she will not be able to build muscle, regardless of the hours she puts in at the weight room, and she will continue to put on body fat as the muscles she does have waste away.
I guess the younger people would just say that she is not trying hard enough, or she is lying about how much time she spends at the gym!
If I had a 22 year old metabolism, the first thing I would do with it is beat the crap out of jerks like that. :-)
"Stephan Guyenet has posted on why he does not believe in refined carbohydrates as a cause of obesity"
Two fundamental problems I saw in Stephan Guyenet's post was he tried to decouple a coupled system by citing the isolated effects of insulin in the baboon's brain. Any well trained engineer or mathematician will tell you a coupled system has to be solved using eigenvalues and eigenvectors.
The other was his refutation of hypothesis #2 was simply restating the conservation of energy. This is particularly disappointing coming from Guyenet because this is the same mistake calorie counters make. Conservation of energy describes the effects of the problem, not the problem itself.
Nevertheless, your comment sums it up elegantly:
"...if we complicate the theory just a little bit it still works fine. Let’s not rush to prematurely “falsify” a working hypothesis when we have nothing better to replace it with."
Ockham was on to something. :-)
I fear well-meaning diabetics might read his blog and follow his dangerous advice by over-using insulin in the idea that it will make them lose weight.
I now doubt that he has any real understanding of metabolism - it's just such a basic thing. Any diabetic could tell him. Sorry, don't mean to be rude, but he revealed a serious lack of understanding the basics.
I guess you are right. I changed the wording slightly to "important cause".
I posted this on the "Whole Health Source" blog.
When you get a chance, let me know what you think:
@Frank
I take it that the studies you cite show that there is no difference in the rate or amount of fat loss when the amounts of carbohydrate and fat in the diet are varied but protein and total calories are held constant.
Is that correct?
If so, they would not appear to be a refutation of the carbohydrate theory. They only show that in a laboratory, when the subjects are forced to eat the same number of calories, the effect on fat-loss is the same regardless of the macronutrient composition of the diet.
This is nothing more than what anyone would expect: The rate and amount of fat-loss is determined by the total calories in the diet.
The carbohydrate theory of obesity predicts that, in the wild, restricting carbohydrates results in a spontaneous reduction of total calories, and this appears to be the case, based on the studies cited by Andreas.
I have feeling that you are looking for a simple culprit. Obesity and diabetes are effectively treated with high-carb, vegan diets.
When the amount of refined carbohydrates was increased from 45% to 85% (kals of diet) the condition of diabetic enhanced in every measurable way. We have plenty of clinical evidence how high-carb, low-fat veg diets improve the insulin sensitivity of diabetic. However, pay attention to the context, high-carb works when fat intake stays under 15%, which in practise means elimination of vegetable oils and animal products.
“An extremely high carbohydrate-fat ratio improves insulin sensitivity whereas more moderate changes (40-60% carbohydrate) produce less convincing results”
Smith U. Carbohydrates, fat, and insulin action. Am J Clin Nutr. 1994 Mar;59(3 Suppl):686S-689S.”
The Hawaii Diet: ad libitum high carbohydrate, low fat multi-cultural diet for the reduction of chronic disease risk factors: obesity, hypertension, hypercholesterolemia, and hyperglycemia.
“Twenty-two adults recruited from various cultural backgrounds in Hawaii were fed, without calorie or portion size restriction, the Hawaii Diet for 21 days. The Hawaii Diet, based on familiar traditional foods from different cultures, is high in complex carbohydrate (77% of calories), low in fat (12% of calories), and moderate in protein (11% of calories). Participants were encouraged to eat to satiety.”
“The Hawaii Diet consisting of high carbohydrate, low fat ethnic meals appears to have a beneficial influence on weight loss and in decreasing systolic blood pressure, total cholesterol, LDL, and blood glucose values. Marginal improvement occurred for triglyceride levels. There was also a significant drop in HDL levels, however, the Chol:HDL was ratio did not increase. Further studies of longer duration with a control group should be conducted to test the effectiveness of The Hawaii Diet in maintaining these health benefits over a longer period of time.”
To be more precise: in practise this means that 100grams of beef will release more insulin to the blood than 100grams of straight table sugar.
Diabetes care 7, (1984:465)
Diabetic cannot take the protein away from the beef. We all need protein, but is it possible to construct a meal that doesn't meet protein requirements as long sufficient amount of calories are eaten? Hardly. According to WHO biologically we only need 5-6% protein. The same amount of which is supplied in mother's milk. Rice provides 8% protein, potatoes 8%. Why demonize carbs when the reality is way more multifaceted?
"The only data indicating that low-fat high-carbohydrate diets lead to beneficial effects on carbohydrate and lipoprotein metabolism are confounded either by the lack of suitable experimental control, by the fact that diets also differed in the type of dietary fat and amount of dietary cholesterol, or were enormously enriched in dietary fiber. When these factors are taken into consideration, there appears to be little evidence in support of the view that substituting carbohydrate for fat in the diets of individuals with diabetes results in any measurable beneficial effect. Indeed, it could be argued that the most characteristic defects in carbohydrate and lipoprotein metabolism are exacerbated in response to low-fat high-carbohydrate diets."
http://www.ncbi.nlm.nih.gov/pubmed/1959471
Throwing out "beef releases more insulin than table sugar" doesn't even begin to explain why insulin is released and what it is doing.
I actually do not doubt that an extremely low fat vegan diet may also be better for diabetics than todays conventional western industrial diet.
Basically I think any other diet is a step in the right direction.
As I understand it, there is only _one_ kind of cholesterol.
There are different carrier proteins though, bad ones that increase on a high carb diet and good ones that increase when eating a high fat diet.
Cholesterol in itself is extremely important to the body since its needed to make basically all hormones, and also to repair and build cells.
And finally, ingested cholesterol seem to have very little effect on total cholesterol levels since the body produces the most of it anyway.
Thats my understanding anyways, picked up from lurking in the paleo/lchf domains for far too long. :-)
Good that you clarified your standpoint.
However, one thing puzzless me. You've concluded that young & lean people handle starches well. Why do you personally adhere to a strict LCHF? Do you have a history with obesity?
Zepp, pay attention to the context. The study you recited merely addressed that official recommendations work poorly. Moderation does not work, we need aggressive nutritional intervention. The study was published in 1991 and we have indeed plenty of accumulated clinical evidence showing that 'overly' high-carb, vegeterian diets are succesfull in treating diseases of affluence, obesity, diabetes, rheumatoid arthritis, hypertension, etc.
But for sure we don't know everything about food and obesity until we can explain how the Shangri-La diet works too and I think the food-reward angle is a very interesting one which has the potential to add to our knowledge.
We are not going to resolve this one by talking about the Pima of 1902. It is today´s Americans who are fat and rapidly getting fatter, with the rest of the world following behind them.
Q 1 How did (most) fat people get fat ?
A 1 They got fat because they ate too much carbs
I think Gary T nailed this one in GCBC, no need for further discussion
Q 2 Why did they eat too much carbs ?
A 2.1 Because they were taught that carbs are good for them, and they didn´t know to question what they were taught
A 2.2 Because carbs have an addictive quality, you eat some and then you want to eat some more (positive feedback)
Actually both of these answers could be correct, and the second answer is a narrow form of the food-reward hypothesis. My experience is that when I stopped eating carbs, in a few weeks I stopped wanting to eat them,and I just followed my new low carb habits. I have also found, if I break out of low-carb and for example have a cinnamon bun with my mid-morning coffee, the next day I will find myself thinking about having another one.
Q 3 Why is it getting worse in recent decades ?
A 3.1 Because hard physical work increases carb tolerance and in recent decades fewer and fewer people do this.
A 3.2 Because high-carb food availability both in terms of supply and the ordinary persons purchasing power is higher than ever.
A 3.3 Because food manufacturers have learnt to profit from formulating more addictive foods, which also happen to be high in carbs (positive feedback as the higher profit allows more research into increasing addictivity and allows wider advertising and distribution)
Again, all three could be correct, maybe in different proportions, and none of them contradict A 1 Where Stefan has gone wrong in my view is a) putting food-reward forward as ´a dominant factor´in obesity, which I can´t see as justified in the current state of knowledge and b) challenging A1
BTW, moving from England to Sweden, I was struck by how few massively obese people you see on the streets here, compared with England.
I just don't. You know, I'm boring in this way - I think calories count if you have the genes that make them count, just as milk will be your problem is you lack those genes too. Until we talk about the genes, we can't really help people.
For example, we know from studies like Bouatia-Naji N et al. (2008) . “A Polymorphism Within the G6PC2 Gene Is Associated with Fasting Plasma Glucose Levels.” Science. that it's possible to lose the blood glucose genetic lottery. There are folks who natively are born with genes that give them different "setpoints."
We need to ID the people who had bad luck with that gene situation and work with them intensely when they are younger.
We also know from other studies like Loos RJ et al. (2008) . “Common variants near MC4R are associated with fat mass, weight and risk of obesity.” Nat Genet. that there are folks who are just born to have high BMIs. There are even genes discovered that are significantly associated with the ability to gain fat at waist based on a low-fat or high-fat diet.
Folks need to know where they fall in the BMI/diet gene situation. What works for Lance Armstrong isn't gonna work for Oprah. Different diets are going to be more likely to work based on a person's genes. We are now in a place in history where we can answer what diet is more likely to work for a person - because now we can look at people's genes.
So forgive if I find the whole Guyenet point-of-view irrelevant.
Please don't forget that associations do not prove causality. Those are nice theories but they are not tested as far as I know.
Manganese is also needed by insulin-producing beta cells. Endocrine cells are very sensitive to oxidative stress, because they make large amounts of proteins for export that have to be properly folded. Oxidative stress prevents proper folding. Stephan does not talk about this because of something that happened a while ago when he was discussing leptin resistance. A recent paper had suggested the Unfolded Protein Response as the cause, and he thought the work was sloppy. In fact the UPR has been linked to insulin resistance as well as to leptin resistance, and is itself linked to inflammation, which becomes necessary if the misfolded proteins cannot be cleared by UPR mechanisms.
Obviously, if your endocrine cells are struggling to clear misfolded proteins, they cannot do their job properly. So if your diet is very low in manganese, your metabolism is likely to be 'broken'. White flour has not only had nearly all its manganese removed, it also has added iron and calcium, which can both prevent absorption of what little manganese is left. Worse, excess iron is apparently the cause of oxidative stress. I expect you have seen the recent paper 'Iron behaving badly'.
If beta cells cannot respond fast enough to a rise in blood glucose, it will go on rising, and then they will go into panic mode and overshoot. This means hyperinsulinemia and fluctuating blood glucose, with anxiety, fatigue and hunger.
Why do you think only the obese will benefit from HFLC? I have been lean and training hard all my life, so I can handle carbs very well. But I am a high fat eater for a last 5 years and it seems there is no turning back! Why?
I maintain my 3-5% bodyfat with half the training volume,
I eat 2-3 times instead of 4-6 times a day, enjoying (!) every meal,
I have steady energy level,
I have more time,
I do not feel I am a slave to eating and training anymore.
So I am much more efficient and healthier human being now.
Can't see it, sorry.
Good to hear about all the positive stuff you've experienced. If you used to eat a Bic-Mac meal a day and now skip the fries and coke that would make up an actual improvement in your diet. I have no idea of your past dietary history, impossible to tell. Someone asked Gary Taubes once howcome vegeterians are lean despite of their high carb diets, Taubes said that its because they avoid processed foods. You figure. With all the evidence available it's very likely that you will prematurely age yourself with a diet high in animal fat and protein and risk the health of your heart in the process.
Abstract 3610: Comparative Effects of 3 Popular Diets on Lipids, Endothelial Function and Biomarkers of Atherothrombosis in the Absence of Weight Loss
http://circ.ahajournals.org/cgi/content/meeting_abstract/116/16_Meeti...
“..a recent study by Foo and colleagues shows that HPLC diets may accelerate atherosclerosis through mechanisms that are unrelated to the classic cardiovascular risk factors”.
Clinical Implications of Basic Research. A Look at the Low-Carbohydrate Diet (2009)
PS. The chubby Atkins himself had a progressed coronary heart disease, which he lied about, but which his wife revealed to the public after his death.
It is not widely known that one starts to reap the benefits of LCHF when over 65% of overall calories comes from fat, mostly from animal fats. The study used 50% fat, which means carbs and protein were too high to detect positive results. And total LDL does not mean anything as long as triglycerides are not measured.
In chapter 16 of GCBC Taubes mentions a couple of studies showing that there are individual variations to weight gain in a caloric surplus context and recently this documentary was aired on the BBC Why Thin People Aren't Fat, they did an overeating experiment and the results were that some students got fat easily while others didn't. The energy balance theory doesn't explain those results.
The fact that a calorie deficit leads to weight loss does not necessarily means that a calorie surplus is the cause of weight gain. In my experience the type of food I overeat makes a big difference. Perhaps some people put on fat easily even in a low insulin context but I'm not one of them.
Instead of studying fat loss the obesity researchers should be studying fat gain and find out what's the best way to get fat. Put thin people in a lab for two weeks, overfeed them different types of diets and see which group gets fatter the faster.
@Chris, It's fine to be a reductionist. But, you can't reduce a coupled system by magically decoupling all the potential variables. As I pointed out in my previous response, coupled systems have to be solved using eigenvalues and eigenvectors. So, while the science models aren't fully understood yet, the more they figure out, the more complicated and coupled it gets, the less likely that it won't be an eigenvalue problem. Dr. Eenfeldt explained succinctly the time response of insulin.
Guyenet unfortunately bit off more than he could chew. Taubes with his physics and engineering training knows better. And, I kind of saw that with Dr. Eades' presentation as well. At the end when asked about fermented foods, he simply said he didn't know enough about fermentation to comment. Youthful exuberance, perhaps. Guyenet is much younger than Taubes or Eades.