Ladies & Gentlemen, Now playing in the Asylum Theater: Gary Debunks Taubes

Narrated by CarbSane
Starring Gary Taubes as himself
"A delightful drama about the journey from amateur boxer, to physics major turned journalist, to renowned 'expert' on obesity and human metabolism.  The protagonist is befallen by a nasty case of egomonomaniacalis dunshütinfüt but ignores his obesity-researcher-turned-MD's advice when he prescribes digaholedypur arrestin.   This disease is a silent killer of reputations, and left unchecked might do just that.   Will Gary survive the disease?  Or will Gary debunk Taubes?"       or maybe Leptin Man will save the day?

It's really rather amusing when a new Taubes blog post lands in my feed reader, and apparently since he promises a lengthy five part series of posts every few days, I'm guessing there will be no end to my amusement any time soon.  This has inspired another series of posts that from hereon will be dubbed Gary Debunks Taubes.  

What?  Another series?  Yep.  My other GT-inspired series (like the GCBC Reference Checks) have focused on how Taubes cherry picks from. and flat out misrepresents the science contained in many of the references in his book.  Other posts are dedicated to debunking the various facets of TWICHOO.  But in the past few days, between reading his first blog post in a while, composing my latest installment in that series -- GCBC Reference Check ~ Part VII of ? ~ Julius Bauer's Lipophilia Hypothesis, feeling especially self-torturous and listening to a 2007 lecture on YouTube, and finally making it through blog post number two in less than that many months, it dawned on me.  Taubes actually does quite a fine job of debunking himself, and in this regard he does a bang-up job of finding studies that dismantle his hypothesis.

So in the preview, we had Gary citing Julius Bauer stating that nervous centers (some call that the brain) regulate and dominate the metabolism of fat tissue.  Coming up, more quotes from GCBC, but first I'll have at those blog posts.

Each show a different play!  Playing indefinitely in the Theater here at the Asylum.
Admission is free, but please consider a donation towards finding a cure for ED.  Smiley
Conflict Disclosure:  The Theater at the Asylum is really sponsored by Carbsaneuticals Inc., makers of digaholedypur arrestin.


RichieRich said…
"...but first I'll have at those blog posts."

A word (or two) missing?
Looking forward to it. Taubes' smarmy response to Kurt Harris shows the bad behavior at AHS was not a one-time thing. I'm sorry that I gave you grief for your treatment of him (back in the day).
Galina L. said…
I realized in time that just cutting curbs is not enough, although a good start, why shouldn't GT to change something in his views? He already taking into his consideration some comments on his blog, for example. Probably he may start debunking himself. People do it. Obecity problem is so big and complex. Probably, it is not realistic to expect anyone to be right 100%. I know you believe he is more guilty that it sounds in my interpretation. Unfortunately, it is rare when somebody creates masterpiece after masterpiece. GT's masterpiece was that article "What if It's All Been a Big Fat Lie?". It started the more realistic discussion about the treating of obesity without reference to the thermodynamic all the time. I also really like GCBC (together with trigleserol-phosphate and some unavoidable imperfections..) it developed the theme of the complexity in the obesity problem quite nicely, WWGF - not so much, his response to Dr. Kurt G. Harris sounds quite weak. We will see how he will get the fructose, but I am not holding my breath, fructose is a very small part of a huge mosaic, like the FR. I would like to see more research about why different people get fat and what to do about it in every particular case.
CarbSane said…
@RR: I meant it as written: as in "have at it", I'm going to "have at" those blog posts before the GCBC quotes.

@Beth: Thanks!

@Galina: Oh if only Gary Taubes was actually rethinking. He hasn't done any such thing, pretty much the new book is a "carbs make you fat" period mess. All he's changed is where he has been shown wrong in areas where there is no room for nuance (e.g. the G3P, can't store fat w/o dietary carb nonsense he perpetuated for years), he's just left those parts out. What this series is going to do is use Gary's own words and references and show that he has inadvertantly provided data/information that debunks his own hypothesis while trying to counter others.
RichieRich said…

A case of my English English not comprehending your American English! I'm now with the program...or should that be programme!?
John said…

The fructose monkeys had lower metabolic rate per unit mass. I'm going to look past the lack of control group and assume there would have been little change after a year. At first it looks to weakly support Taubes, as I would side with the insulin hypothesis vs a seemingly unfalsifiable fat "setpoint," but note that the fasting insulin decreased from months 6 to 12, while the fat mass increased. Did you pick up on that? So, this counters his hypothesis, at least in that it is solely insulin; it doesn't counter the hypothesis of obesity being a "disorder of fat accumulation" though. I don't see any reason to think the monkeys at month 6 had an increase in adipose insulin signaling.

Taubes throws around "insulin resistance" such that it makes it difficult to know exactly what he is saying, especially with recent talk about LIRKO and tissue specificity, which is kind of annoying.
John said…
Wait, sorry...from months 6 to 12, fat mass increased a bit; insulin decreased; energy expenditure increased; overall weight increased a bit; so it actually does somewhat look like insulin is negatively affecting energy expenditure (I think that's more likey than energy expenditure affecting insulin, though both could be oppositely affected by something else). Why does fasting insulin decrease from months 6 to 12?
Anonymous said…

"Taubes throws around "insulin resistance" such that it makes it difficult to know exactly what he is saying, especially with recent talk about LIRKO and tissue specificity, which is kind of annoying."

I am not sure he really knows what it means when he says it. He seems to use the term as synonymous with "metabolically damaged" Look at his reply to me where he claims my initial fat loss was due to decreased insulin resistance. Anyone eating VLC and starting with no diabetes ( and a fasting insulin of 6!) could likely have MORE whole body IR after the fat loss, rather than less.

Can IR improve as a consequence of fat loss? Yes, of course it can. But this is an EFFECT of successful fat loss, not the cause of it.

At the very least, one should specify which organ or the whole body when using the term insulin resistance.

It requires blinders to ignore all the evidence contrary to the CIH - especially the evidence that fat loss is basically independent of insulin levels, and insulin levels fall as a consequence of fat loss rather than being required to lose fat....

Evelyn is correct in that GT has abandoned crucial bricks in the CIH wall without replacing them or explicitly building a new one.

He seems to grant now that starch per se may not be a problem, but sugar and "refined carbohydrates" are. But sugar has a lower GI than starch, and fructose in excess causes IR independent of its effects on insulin - insulin is not mediating the IR due to fructose, it may be an effect of fructose in excess.

If refined carbohydrates are bad because they have easily digestible starch, why aren't white potatoes with their high GI bad? And if refinement is the issue, why is white rice not bad?

The reason he does not articulate a new theory that is still a CIH is that it falls apart while still on the back of the envelope.

You can't salvage a CIH with fructose and "refined carbohydrates" that has insulin as a mediator because there is no such theory that makes physiologic sense, and this would be obvious the moment such a theory is articulated, as I hope I have demonstrated just now....
Kurt, if you think GT's theory re IR makes no physiologic sense, wait until you get ahold of Mercola's recent comments re Rosedale/Jaminet and safe starches: "Raising blood glucose raises insulin, which increases insulin and leptin resistance."

Yee gads. We're not going to get anywhere re obesity if this is what folks are putting out there!
Anonymous said…

I'd not seen Mercola on that but the "IR is a result of high insulin" idea indeed seems to live on.
John said…

Isn't he trying to simply salvage the theory with fructose's supposed long term effects on fasting insulin? He's all over the place, but that's besides the point. I'm just trying to figure out what's going on...

Do you have any idea as to why the monkeys'* average fasting insulin decreased from month 6 to 12, despite a slight increase in fat (and overall weight)? Up until 6 months or so, the fructose-insulin hypothesis actually looked pretty good, with the monkeys gaining fat, increasing fasting insulin, and lowering expenditure.

CarbSane said…
Hi John, I haven't had a chance to take a whack at the monkey study question. Reading other interesting human stuff at the moment.

Nice comment Kurt. I do think we all talk past each other on IR to a degree because of the lack of a clear definition or specifying what we mean. That's not really anyone's fault as the literature doesn't clarify either. It would probably make for a ton of different definitions, but both tissue and mechanism must be addressed. For example MIRKO lacks insulin receptors, and yet the impaired glucose disposal by the LIRKO is described as these mice being insulin resistant despite normal glucose transport/utilization by the muscles.

@Beth, I just saw that Mercola piece. His article made little sense. We're all going to be damaged by starch, but if you want a healthy diet, check out PHD. Seems contradictory, like he didn't want to step on anyone's toes. Came off more like him reading a few blogs for his readers as if they couldn't decipher for themselves. Kinda condescending IMO.
P2ZR said…
'You can't salvage a CIH with fructose and "refined carbohydrates" that has insulin as a mediator....'

Well, the hallmark of a fundamentally flawed theory is that never-say-die proponents do all sorts of weird sh*t to it to keep it afloat. Ptolemaic astronomy and epicycles of epicycles of...epicycles of...?

Sugar is bad because it's a disaccharide that is half fructose, and fructose is the devil because GI doesn't actually matter, or maybe it really does, but anyway, some subset of the macro known as 'carbs' will lead to insulin resistance, which in turn will lead to catapulting over epigenetic levees into leptin resistance, which will then flip some more rogue switches in the body to cause even poorer tolerance of carbs, and...somewhere in all of this, we'll have acknowledged that the FRH was correct all along, but at the end of the day, it's still the CARBS, stupid!
Galina L. said…
There is a lot of data about groups of people transitioning from their tradition diets to the western diet and getting western deceases. Looks like in the proses they all started eating in big quantities food made out of refined wheat and food that contained a lot of sugar. May be Dr. Davis is right after all, despite some lapses with "buttery acid"?
I don't know for sure what is causing the big increase in hunger, which is a common complain for people who have a cluster of conditions associated with so called "metabolic syndrome", but it is the main obstacle that prevents such people from just eating less. Lets not forget that a carbohydrate restriction (different degree for different people) is the remedy for appetite control for if not all, but for big portion of such people.
CarbSane said…
Hi Galina, The problem with the transition from traditional to Western/SAD diet being pinned on refined wheat and sugar are twofold: 1. My generation had access to a lot of refined wheat and sugar as children but did not get fat. Indeed it could be argued that the normal diet of that day was Wonder (white) bread, not even brown wheat bread. 2. More than just the nature of the carbs change, the amount and nature of the fats change as well.

I'm constantly bothered by those who look at fries and mega burgers with bacon and cheese, pizza and whatnot and assume it's the carbs in those foods that are fattening. These are the folks eating meatzahs and cream cheese and almond meal concoctions with sugar free syrups and chocolate and wondering why they aren't losing weight!
Anonymous said…

"Hi Galina, The problem with the transition from traditional to Western/SAD diet being pinned on refined wheat and sugar are twofold: 1. My generation had access to a lot of refined wheat and sugar as children but did not get fat"

I think Galina is referring to the diseases of civilization that were identified by investigators like Price, Yudkin and Cleave that were seen in nutritional transitions that may be independent of obesity or were identified long before our current obesity epidemic.

Cancer, coronary disease, diverticulutis. These were more common with western diets than native diets long before there were big differences in obesity.

There are reasons to be suspicious of wheat flour and excess sugar besides obesity, even if we are not sure of the mechanisms yet.
Evelyn, I'm completely with you that it's not just the refined carbs/sugars. That said, as someone who grew up around the time you did, I think it's also fair to say that our access to these foods was very different than it is today.
CarbSane said…
I agree Beth -- could it be we eat more of these foods simply because we can? It can't be that simple, can it?

Speaking of access, kids these days have far more control over what they eat than my friends and I did. Even those friends who were fed junk did not have access to virtually unlimited amounts.
CarbSane said…
Sarah, you better climb down off that 30,000 foot levee or I'm going to re-reset your leptin!