In re-reading this I realize there are a number of redundancies and it is hopelessly long. I don't really have the time/desire to chop it down to a more concise version, so posting it up as is with apologies!
With his English language blog, appearances at various conferences and LLVLC events/cruises, and the apparent rise in popularity of low carbing in Sweden, Andreas Eenfeldt is a rising star promoting low carb diets. Therefore, I think his comments on Stephan's recent debunking of Taubes Wrong Insulin Carbohydrate Hypothesis Of Obesity, TWICHOO, and the post on his blog about same deserve some attention. One of the things that is disturbing about GCBC and Taubes' presentation of the science is that he frequently says "we don't know XYZ because the experiments haven't been done". The "Diet Doc" seems to have taken this to heart as he views TWICHOO as a "working hypothesis" and he seems unaware of the state of knowledge possessed by researchers on various obesity related topics.
Some excerpts of Andreas' first comment in response to Stephan's debunking:
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.
What Stephan said was:
I'd like to begin by emphasizing that carbohydrate restriction has helped many people lose body fat and improve their metabolic health. Although it doesn't work for everyone, there is no doubt that carbohydrate restriction causes fat loss in many, perhaps even most obese people. For a subset of people, the results can be very impressive. I consider that to be a fact at this point, but that's not what I'll be discussing here.
Now Andreas' summary is not horribly misrepresenting what Stephan actually said, but I believe it's indicative of his bias. Stephan did not say that LC diets do work most of the time, he said LC causes fat loss in many, and perhaps even most obese people. Indeed it does seem to work well for most obese, but the results are far less predictable for those who are less overweight. The fact that Stephan didn't speculate on why LC diets work when they do is irrelevant to his debunking of TWICHOO. However does Andreas really believe that nobody can "say for sure why they work" just because Stephan didn't expand on that point? This is the more recent claim by Taubes, his hypothesis that all diets work, when they do, because of carbohydrate restriction. This related hypothesis is also easily debunked, using, again, even the very same studies Taubes and those of like mind use to support it. Indeed in my opinion, this has been demonstrated so many times that it should be considered a fact.
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 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 what they think.
Couldn't we say that bariatric physicians have also failed spectacularly and in epic proportions in treating the obese? It sounds like Andreas is upset the researchers haven't succeeded in creating that magic pill that would reverse obesity effortlessly. Again, why are we talking weight loss here? The TWICHOO is about how a person gets obese. That these researchers haven't found the solution is irrelevant. But since Andreas brought it up and he treats obesity with LC, and at the risk of sounding rude and mean, I ask: Has Andreas ever looked around the room when he gives a presentation on those LC Cruises? The problem with treating obesity is not that folks can't lose weight. Most are able to without even resorting to pharmaceuticals. It is with maintenance and, frankly, part of this is out of the realm of researchers and doctors to solve. There is no drug nor diet that will help a person make a permanent change in their eating habits. It seems that many of those who do with the LC approach, remain significantly overweight.
On to your three so called "falsifications":1: Take a look at Robert Lustig's lecture during AHS. Hyperinsulinemia gives leptin resistance. Problem solved. Moving on.
Huh? I haven't watched this yet. Does Lustig discuss what causes hyperinsulinemia? As far as I can gather, Lustig doesn't believe in TWICHOO.
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".
Is Lustig a proponent of the "starving cells" notion? As I recall, Lustig deals with hypothalamic obesity where hyperinsulinemia results from injury to the hypothalamus following treatment for brain cancer. This is a special case where you actually have a defect in fat metabolism caused by something other than carbohydrate ingestion. How does this support TWICHOO?
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.
I've seen comparison studies that don't demonstrate huge changes in insulin AUC between reducing diets. But even if they do show drastically reduced insulin throughout the day, doesn't the comparable weight loss seen, when protein and calories are controlled for, blow the TWICHOO right out of the water? I'd say so. Grey & Kipnis really put a nail in this coffin.
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 "falsify" a working hypothesis when we have nothing better to replace it with.
I would say that first we have to accept that TWICHOO is a working hypothesis. It should never have been a hypothesis to be tested in the first place. Taubes formulated a hypothesis then cherry picked from the studies and texts for things that supported it. This is not how science works. He ignored vast swaths of information that falsified it. No ... that's not quite true. He even misrepresented some of the research/writings, claiming they supported his hypothesis, when in fact they did not. Taubes is fond of lamenting that "the studies will never be done" to test his hypothesis. It would not be so damning if it were just the newer research he ignored and has no time to look at now. But as it turns out, most of the studies HAD been done. Repeatedly in many cases.
The discussion turns to insulin resistance when Stephan answered some of Andreas' points:
Stephan: "But then we're left with the question: what causes insulin resistance? That factor is not carbohydrate per se, although refined carbohydrate and sugar may contribute."
Andreas: Ah, the million dollar question!My guess: too much refined carbs and sugar for a long time, combined with insufficient exercise (which would have burned the carbs), combined with a genetic vulnerability.Speculation: The chronically elevated insulin combined with already filled-up glycogen deposits makes the cells down-regulate the insulin receptors, as only a few are needed under those circumstances. Thus: The elevation in the insulin levels and the insulin resistance would develop hand in hand. And then we can argue about what is the chicken and what is the egg, while in reality (if this is true) they happen at the same time.
This is one enduring legacy of GCBC -- misleading folks into thinking that carbohydrates cause insulin resistance. That somehow you've done some irreparable damage to your metabolism by eating carbohydrates. Only amongst the fat metabolism experts Taubes quotes and has interviewed and had discussions with on multiple occasions, there is a working hypothesis. Let's call it the Fatty Acid Hypothesis. Again, one can never name drop the name Keith Frayn enough for my liking in these discussions.
This blog post discusses a 2001 review paper authored by Frayn. That Taubes wrote this in GCBC is journalistic malpractice:
"Over the years, prominent diabetologists and endocrinologists -- from Yalow and Berson in the 1960's through Dennis McGarry in the 1990's -- have speculated on this train of causation from hyperinsulinemia to Type 2 diabetes and obesity. Anything that increases insulin, induces insulin resistance, and induces the pancreas to compensate by secreting still more insulin, will also lead to an excess accumulation of body fat.
He also cites McGarry in GCBC and cites Guenther Boden frequently as well. The fatty acid hypothesis has its roots in a man named Dr. Edwin Bierman who discovered the connection between NEFA and diabetes in the 50's and 60's. And who researched most of his career at .... drum roll please .... Stephan's institution of higher learning with which he is currently affiliated as a post doc: University of Washington. He wrote this classic citation. Those last bits of trivia are, of course, not really relevant to the debate, except it might explain why nobody Stephan works with takes Taubes or his hypotheses seriously.
The FAH is consistent with all observations concerning both hyperinsulinemia and insulin resistance and the relationship to obesity. Tom Naughton's Taubes-inspired adipose-tissue-as-last-glucose-sink schtick is not. That fat cells become insulin resistant last simply is not supported by the evidence.
OK ... so Andreas then moves his discussion over to his blog. Perhaps it's because of a language barrier, but this post really deserves an award for the most misrepresentations and erected strawmen in the fewest words possible.
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:
No .... this does not sound complicated! As I mentioned in my Random Thoughts post, that restricting or eliminating carbs results in fat loss doesn't mean carbohydrates are fattening. Because this logic could be applied to anything. Ultimately we can apply this to all food energy! Restricting calories results in fat loss, therefore calorie are fattening. Well, this is true. What do researchers do to fatten someone in studies? They overfeed them. And what works better for that, fat or carbs? Fat.
Excessive amounts of carbohydrates (especially refined carbs / sugar) increases insulin and results in fat gain.
The Carbohydrate Hypothesis, as attacked by Guyenet, looks basically like this:
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.
First ... must we use the word attacked here? Stephan is clearly referring to fasting insulin levels in this section of his post and that postprandial insulin spikes are not the cause of hyperinsulinemia. Here is where the Grey & Kipnis paper is usually evoked because when they cycled some obese women for 3-4 weeks between essentially iso-protein diets of essentially zero fat and zero carb, their fasting insulin did indeed plummet and shoot up accordingly. But as I've discussed before, you can see that by the end of each phase the fasting insulin levels appear to be normalizing . In any case, the theory put forth by Andreas' and the rest of the Taubesians as to how and why low carb diets work has been falsified by me here before. First, again with Grey & Kipnis, and more recently with the Krauss study evoked by Eades in his AHS presentation.
Under eucaloric (weight maintaining levels) conditions, with protein held constant, weight loss is not seen even with wide variations in the percentages of the remaining calories coming from carbohydrate or fat. Under hypocaloric (energy deficit) conditions, again with protein held constant, weight loss is observed. Further where fat mass is accurately measured, the fat loss is almost invariably consistent with that expected with that rough 3500 cal/lb factor. Therefore:
All weight reducing diets work, when they do,
by reducing caloric intake so as to establish a caloric deficit.
The Carb-Insulin Hypothesis for LC weight loss has been falsified. Carefully controlled studies support the CICO Hypothesis. Or is that a tautology? Andreas continues:
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.
Because the effects of exogenous insulin are irrelevant to TWICHOO. Carbs and proteins elicit a very complicated insulin release and other hormones. Furthermore, when an obese person progresses through type 2 diabetes to the point of requiring insulin, why doesn't their weight plummet?
Thin people usually have low insulin levels, obese people usually have high levels of insulin. Guyenet does not believe that is significant.
What kind of insulin levels does a straw man have? Stephan said no such thing. The correlation does not indicate causality. The FAH is consistent with this observation with the direction of causality being that obesity leads to the hyperinsulinemia not the other way around (absent something like hypothalamic lesion, insulinoma, etc.). Fat cells lose their insulin sensitivity first --> inappropriate NEFA release --> elevated circulating NEFA --> increased basal insulin production. It is not controversial that fasting insulin secretion is stimulated in part by free fatty acids, and I've presented several papers that demonstrate that lowering NEFA decreases insulin and raising them increases it. Two such blog posts here and here. Andreas then published his comments from Stephan's blog which I've already addressed. He concludes with:
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.
He goes on to discuss different carb tolerances. That this must always be explained pretty much falsifies TWICHOO in itself. Those middle aged obese women with T2 diabetes were not always that way. The evidence does not support the hypothesis that eating carbohydrates per se had anything to do with it. Then, the bottom line:
Some very smart people disagree why low carb works. But we all seem to agree that it does work.We don't all agree that it does work, and it is irrelevant if it does or how.
Carbs drives insulin (postprandial) drives fat accumulation is WRONG. It has been thoroughly debunked by yours truly, James Krieger and, now Stephan Guyenet. And I'm sure there have been others. Perhaps it is the dogged insistence that it is a working hypothesis by those who believe it is part and parcel of why no actual researcher in the field takes it seriously.