Guyenet v. Taubes: Thoughts on Stephan's Demolition of the Carbohydrate Hypothesis of Obesity
I've been laying kinda low on Stephan Guyenet's disassembling of Taubes' "Carbohydrate Hypothesis" and just sort of soaking in some of the responses. However as the mood hits, I'll be sharing some thoughts on the reaction in the coming days.
This post, however, relates to his blog post. As I said in the comments on his blog: Well done! Most of the arguments he makes are not new to this blogger, but I think these things need to be stated by as many bloggers as many times as is needed -- and judging from the reactions the work in this regard may never be done!! -- until the following acronym becomes as common in LC circles as acronyms like ACE, OWL and CCL are to Atkins dieters. When Taubes' theories become known as Taubes' Wrong Insulin-Carbohydrate Hypothesis On Obesity - TWICHOO. It kinda rolls off the tongue!
I would first like to highlight what I consider the most important part of Stephan's post: Identifying YET another one of Taubes' GCBC references where he misrepresented what the reference actually stated. Indeed I was just compelled to post GCBC Reference Check ~ Part VI of ? ~ The Massa. I add that to the list of Taubes' own references where he either offers up a misleading interpretation or outright misstates what the reference actually said. I don't care if there were a thousand references, these six -- so far -- and the way in which they were used to support his hypothesis are more than sufficient to dismiss this book as credible. This is not to say he's wrong about everything in the book, but getting it wrong on key points in this manner speaks volumes to the "scholarly incompetence" Gary prefers be used to excuse his professional lapses. We can add this to the previous five:
- GCBC Reference Check ~ Part I of ? ~ Metabolic Adaptability & Energy Balance
- GCBC Reference Check ~ Part II of ? ~ Insulin Resistance (again)
- GCBC Reference Check ~ Part III of ? ~ Is glycerol phosphate rate-limiting?
- GCBC Reference Check ~ Part IV of ? ~ Kipnis
- GCBC Reference Check ~ Part V of ? ~ Insulin Resistance: Taubes v. McGarry
I personally find these transgressions to be far more damning of the man than that his hypothesis has more holes than Swiss cheese. If it weren't for this, I could abide those justifications that GCBC helped so many to lose weight or improve their health. But when one realizes that he was paid almost three-quarters of a million dollars in advance to write a book (that ended up taking five years to deliver) these sorts of "errors" are inexcusable. I'm beginning more and more to think that he didn't even bother to read many of his references which makes all of those mentions of the number of them all the more meaningless.
Back to Stephan's post.
Part I: I would have liked to see Stephan elaborate a bit more on how Taubes does not offer us much in the way of what initiates this defect, but overall solid.
Part II: I have a couple of quibbles with this section. First, Stephan addresses elevated insulin levels and energy expenditure in the obese:
At least two studies have shown that higher fasting insulin is associated with a higher resting energy expenditure, independent of body fatness, not a lower expenditure (14, 15). This is consistent with the idea that elevated fasting insulin opposes body fat accumulation, not that it contributes to it.
Perhaps Stephan got a little caught up in a point/counter-point mindset, so that if elevated fasting insulin doesn't cause fat accumulation per Taubes he's stating it must be consistent with the opposing it. Rather a third option is available: that elevated fasting insulin is not associated with fat accumulation, as I demonstrated here with the scatter plot of change in fasting insulin and weight loss from Kipnis. A little later Stephan states:
Obese people are obese despite having higher fasting insulin, not because of it.
Here I would restate this as I don't really agree that obese people are obese despite the elevated insulin. I believe that there is a clear association between obesity and fasting insulin (on average) and that the obesity is the cause of the increased basal insulin production and not the result. More on that when I address Andreas Eenfeldt's response in a future post.
It appears that Stephan has finally tired of ItsTheWoo2's commentary on his blog and deleted some (all?) of her comments. But I'm presuming she meant the above discussion by Stephan and somewhat misquoted it. She apparently attributed the following quote to Stephan, but I don't find this in my browser search of his post: "This is consistent with the idea that elevated fasting insulin protects against body fat accumulation, not that it contributes to it."
I have commented sparingly over there and in response to this I did add the following:
Here I have a minor quibble. High fasting insulin is the result of obesity and adipose IR not the cause of it. Elevated fasting insulin is not protective against body fat accumulation, it is the body's attempt to protect it from its already accumulated fat! This is what a huge body of post WWII research clearly demonstrates. It's somewhat of a fat cell/pancreatic feedback loop: Overstuffed adipocyte becomes IR -> releases too much NEFA -> stimulates basal insulin production so as to compensate for adipocyte IR and prevent excessive NEFA release.
Never one to miss an opportunity to portray me as being incapable of understanding plain English (let alone all that science stuff), and fresh off of slagging me over at Paleo Hacks, Kurt Harris donned his white knight outfit and posted up this:
CS (me): "Elevated fasting insulin is not protective against body fat accumulation, it is the body's attempt to protect it from its already accumulated fat!"
S.G.: "This is consistent with the idea that elevated fasting insulin protects against body fat accumulation, not that it contributes to it."
KGH: I actually took Stephan to mean "protects (the body) against the already accumulated fat" as in, " a defense against that fat and the NEFA it contains". And the fat storage itself can be conceptualized as a defense in the first place. So I think all three of us are actually in agreement. It was just awkward wording.
Not wanting to be accused of spamming SG's blog, I responded "fair enough". Now perhaps Stephan has changed the wording from "protects" in the intervening days, but I contend that the new wording is equally incorrect. In any case, however, it is clear that SG did not mean what KGH tries to make it seem he meant so that for a change of pace I was in agreement with the big boys with higher degree lettering after their names.
On the topic of "starving cells" I only wish Stephan had done a little name dropping. And no, I don't mean yours truly as it appears Taubesians far and wide are already a little miffed at him for posting his comment here and making them feel all dirty landing at my blog from the various obscured links to it around the web. No, I'm talking about Keith Frayn whom Gary is now quoting in his lectures in addition to his frequent references to having discussions with him, some seemingly rather recent. Frayn's body of material is extensive, but he's also of the habit of writing (or coauthoring) comprehensive and comprehensible review/summary articles. That by this late date Taubes has not availed himself of these is inexcusable when they so definitively refute this notion of rogue fat cells hoarding energy and starving the rest of the body. Why We Got Fat was released in Dec. 2010 and he has to keep the schtick up long enough until at least to the point where those book sales taper off. If we ever get an acknowledgement from Taubes of his errors, it won't be coming much sooner than that.
Stephan puts quite a few nails in the coffin of TWICHOO, but his next section on genetics (it should perhaps have been Part Ib instead of IIb?) I think is his strongest argument yet. In fact, while all that came before is damning, this perhaps cuts more to the core. If obesity is a result in a defect in fat tissue regulation, then genetic obesity should result in a defect in something in the fat tissue regulatory process. As Stephan points out, every genetic cause of obesity identified to date involves leptin signaling. I do believe it's a bit unfair for him to state "body fatness is normally regulated by the brain, not by fat tissue". After all, this leptin acting on the brain is produced by fat tissue, but clearly leptin signalling between fat and brain is key. Nora Gedgaudas, to name just one other hopelessly mired in flawed dogma speaker at AHS describes leptin as controlling the other hormones if I understand correctly.** In any case, for TWICHOO to be TRICHOO (R = right), the genetics would have to point to something involving insulin and triglyceride/fatty acid cycle regulation and this does not appear to be the case. Game, set, match Stephan Guyenet.
On to the remainder ...
I don't really have much to say about the rest other than that Stephan dismantles Taubes' new tack which is to stress the degree of refinement of the carbs as a factor. He did this in one interview (no link handy) by first claiming that the Japanese eat brown rice, but he's been ratcheting up the insulinogenic argument quite a bit lately. He told Fat Head that he wanted each and every one of us to forget about calories, thus there must be something particularly insulinogenic about nuts and cheeses. He has dug his trench deeper and deeper that "carbs make you fat" ... and yet he also says that it's quite possible that w/o sugar it may be impossible to get obese. Ummmm.... In any case, this section does a good job of undermining any validity to that argument. His graphic on the macronutrient distribution through the years is also compelling.
More to come with commentary on the commentary ....
** 1. Please correct me if I've misstated Nora's position on leptin
2. Sorry, but it's impossible for me to take someone seriously who can write that all body fat comes from glucose and defend that statement to me in an email. Indeed whenever I read her name it goes something like Nora Good-Gawd-help-us if folks are learning human metabolism from her. It even seems from this that she said something similar in her book. I'll not waste money or a trip to the library for that book, but if anyone has an ebook to donate to the cause, I'd be grateful.