Stick a Toothpick in It? Taubes' 4-pronged Carb/Insulin "Fork" Loses its Tines

I'm bumping this today, because in the weeks to come I hope to update, flesh out, and reference it fully.  Looking back at something written almost 2 and a half years ago it seems rough, but nonetheless it  still summarizes what I call TWICHOO and the arguments against it pretty well.  

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This post updated slightly 6/22/2012.   Original publication date 1/23/11

In the comments at Jimmy's blog on my interview podcast, several comments either directly or by inference say I failed to make my case against Taubes.  Well, I think I did pretty much get to what I consider the four prongs of Taubes carb/insulin hypothesis, but I've decided to try and summarize this in a blog post.  Another common comment is that I'm somehow nit-picking at minutia, basically if folks lose weight on low carb, it doesn't matter the details of why.  To those, if they are reading this, I would say that any objective view of my arguments would lead to the conclusion that these are NOT minor details, they are the sum total of Taubes' evidence in support of his hypothesis.  Not only has he NEVER debunked the calorie-based theories on obesity, but almost all evidence in support of his "alternate" theory HAS been.  

I will not be referencing this post, it's all been done before here, and I don't have the time to trace down every link etc.  

So, what do the four prongs of the fork stuck in the potato above represent?  

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The Triglyceride/Fatty Acid CycleS and the role of Glyceroneogenesis

Thanks to a certain journalist, much of the discussion of fat tissue metabolism on the internet presents a very myopic view of things taken out of context.  One example of this, is that in Chapter 22 of GCBC, Taubes lists all of the hormones acting on adipocytes.  The caption on the graphic reads:

In 1965, hormonal regulation of adipose tissue looked like this: at least eight hormones that worked to release fat from the adipose tissue and one, insulin, that worked to put it there.

Let's leave aside for a moment that in the four subsequent decades preceding the writing and publication of his book, probably the most potent regulatory hormone of fat mass, leptin, was discovered.  Let's also leave aside all of the other adipokines (the term for the collection of hormones and peptides produced by adipocytes most of which appear to be secreted).   There's a lesson to be learned solely from Taubes' narrow, outdated view.  Under the title "Hormones that promote fat mobilization", Taubes lists:   Epinephrine, Norepinephrine, Adrenocorticotropic hormone (ACTH), Glucagon, Thyroid-stimulating hormone, Melanocyte-stimulating hormone, Vasopressin, and Growth hormone.  In the opposing column under the title "Hormones that promote fat accumulation", he lists only one:  Insulin.  He precedes this with what he seems think is information either unbeknownst to or forgotten by researchers in the field -- that fatty acids are continually cycling in and out of fat tissue, and that caloric excess is not required for deposition, nor is caloric deficit required for mobilization.

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Glyceroneogenesis & The Triglyceride/Fatty Acid Cycle Revisited

Glyceroneogenesis and the Triglyceride/Fatty Acid Cycle   (TAG/FA)

JBC Papers in Press, June 4, 2003, DOI 10.1074/jbc.R300017200

Lea Reshef, Yael Olswang, Hanoch Cassuto, Barak Blum, Colleen M. Croniger, Satish C. Kalhan, Shirley M. Tilghman , and Richard W. Hanson

The above paper is referenced in Good Calories, Bad Calories, and is a paper I believe one cannot read thoroughly and still believe that dietary carbohydrate is required in order to "fix" fat and become obese.  It has been quite a while since I read it in its entirety.  Doing so in recent days I've noticed even more information in this paper that counters the whole notion that more dietary carb leads to more glycerol-3-phosphate leads to more esterification of fatty acids to the storage triglyceride form.   More specifically, these four paragraphs/excerpts were somewhat drowned out for me in my first reading:

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Why We Get Fat ... Lessons from Obese Humans & Cafeteria Rats

Vacation bump!  Original Post Date:  3/9/11

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One of the more interesting things (to me) to come out of the "cafeteria rat study" is what the composition of the diet eventually chosen by the rats came out to be.  I'm just going to focus on the SC (standard chow) and CAF (SC + human snack foods) diets in this post.

To recap, the SC had a composition F/C/P of 10/64/26.  When offered this chow along with a rotating selection of three human snack foods from the following list, the rats only ate 15% of their diet as chow (the wording of this is unclear, but their total consumption is ultimately what's important).  The composition of the diet they ended up eating?  CAF was F/C/P of 44/46/10  (note: I've detected slight discrepancies in the numbers here that involve a 1-2% swing in either direction) .  One might think the rodies were only offered fatty snacks, but this is not the case as can be seen in the table below:

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UPDATE: Label Change for GCBC Fact Check

Since he has the new book out, I've decided to use a new label to categorize posts that refute various Taubesianisms:  Gary Taubes Fact Check.  Taubes hasn't disappointed from the get go with Why We Get Fat (WWGF) - that thanks to a benevolent reader, I now have a copy of!

I hope any who find this place from links to my old label will see this post and check out the new label link below for more updated information.  Cheers!

Gary Taubes Fact Check

GCBC Reference Check ~ Part IV of ? ~ Kipnis

In a recent post, following up on discussion of Grey & Kipnis as  in the Fasting Insulin & Weight Loss post,  I noted that G&K was  but one study (of many) where calories were controlled that demonstrated definitively that it was calories, and only calories, and not carbohydrates or any hormonal effect thereof, that determined weight loss/stability.

Taubes made the slanderous claim on his blog:

... the value of controlling variables in a scientific experiment is something that a reasonably well-educated child supposedly understands. And what I want to know is why don’t nutritionists understand it and those researchers out there doing diet trials and studying obesity and weight regulation. Because their failure to do so — and I would argue that it may be a willful failure — has led to what may be another of the great misconceptions in modern nutrition research.

I ended my post with the following:

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Fasting Insulin & Weight Loss II

I finally found a study that demonstrates a correlation between fasting insulin levels and weight loss.  In this study, they manipulated fasting insulin levels through macronutrient composition an diets administered at various caloric levels.   Below is the scatter plot of the data for all subjects:  

Horizontal axis = change in fasting insulin level between time points

Vertical axis = change in weight 

See the correlation?

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Calories, fat or carbohydrates? Why diets work (when they do).

It was inadvertently (I think) brought to my attention that, while constructing my Fasting Insulin & Weight Loss post, I had "in my hand" the perfect study to discuss the title of this post.

Does that title sound familiar?  It should!  Because this was the title of Gary Taubes' second blog post:
Calories, fat or carbohydrates? Why diets work (when they do)

As I've stated many times, unless someone provides me with a complimentary copy of Why We Get Fat, I'll not be reading the dumbed down version of GCBC, even for the groundbreaking new information it is purported to contain.   Reportedly, one of those groundbreaking items is a chapter on the very topic of that blog post.  A blog post that was a sort of preview teaser in advance of his book release.  But that post wasn't the first time he discussed this novel idea that he claims supports his alternate carbohydrate/insulin hypothesis.  

Most of my readers are probably aware of when ol' CarbSane here really hit Gary below the belt by playing on words,  "called Gary a sheister", and - GASP! - put a $ in his name, when I addressed his discussion of Shai in a lecture.  I guess the plays on words there using Shai-ster and Shai-t were just too much for his devoted followers to handle.  Who knew a $ could draw such ire!  I suggest if any of these things are going to throw you into ketogenic paranoid seizure, you click on that X in the upper right corner of your browser now.

Really ... I mean it!  DON'T click the "Read More" below if you can't handle it!!!  I'm gonna get nasty here!

Really really.

OK ... last warning (VVVBEG)

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Insulin Resistance ~ Taubes v. McGarry ~ Speaking of Banting ...

J. Denis McGarry's Banting Lecture ~ 2001 Dysregulation of Fatty Acid Metabolism in the Etiology of Type 2 Diabetes

This post is fast fowarding to the final contribution to the field by JD McGarry.  I'll back track and be posting works in between in coming weeks.  According to this tribute to McGarry, he was quite ill by this point, and indeed he was unable to deliver the lecture, but was present at its delivery.  It is unfortunate that Taubes has misrepresented McGarry's work, because as I read more and more about this man and from this man, he really was a scientist in the vein of bucking conventional wisdom ... something that should have perked Taubes' interest.

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GCBC Reference Check ~ Part V of ? ~ Insulin Resistance: Taubes v. McGarry

"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.    

~Gary Taubes (p. 409 Sony ebook version of GCBC)

Now, before you click below and go on to read what I interpret this excerpt from GCBC to mean, and  some works of McGarry, write down what that statement means to you.

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Diet, Cardio, Resistance Training & Insulin

Thanks to Mirrorball for "putting a bug in my ear" regarding the impact of exercise on insulin levels.  The basic thought being that if Taubes' theory that lowering insulin makes you lose weight, then exercise should be very effective, especially if you couple it with carbohydrate restriction.  Because, if you "overeat" protein and fat calories those don't impact body weight right?

So I found this study:

Effects of Aerobic or Resistance Exercise and/or Diet on Glucose Tolerance and Plasma Insulin Levels in Obese Men 

Basically they took three groups of men averaging 40-47 years of age, ~100kg weight, ~32 BMI and did 3 interventions: 

1. DO = diet only
2. DA = diet + aerobic exercise
3. DR = diet + resistance exercise

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Does exercise make you hungry?

Thanks to MM, I now have the full text of the following study.  I'm going to do a test for sharing this with y'all through Google Docs.  Please let me know if it doesn't work:


Acute compensatory eating following exercise is associated with implicit hedonic wanting for food  (I'm going to intersperse quotations from all over this paper)

The efficacy of exercise to promote weight loss could potentially be undermined by its influence on explicit or implicit processes of liking and wanting for food which in turn alter food preference. The present study was designed to examine hedonic and homeostatic mechanisms involved in the acute effects of exercise on food intake.

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Exercise & Weight Management

I've been having a little discussion of this over at Taubes' forum based on his comments on the Dr. Oz show.  He basically regurgitated two points that he's never really offered up much scientific proof of:

1.  Exercise just makes you hungry, and

2.  You'll compensate for the increased activity during exercise by lazing around the rest of the day.

On point 1, Taubes loves to use the "have you ever heard the phrase working up an appetite" line.  At least he sounded a little less condescending asking that this time as compared to when he asked Jillian Michaels in his 2007 Larry King appearance.  

In a "I think I gotcha moment", one commenter posted this study as evidence of eating more:  (I only have the abstract for this one):

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The Dr. Oz Show: Cholesterol and Gary Taubes

It may surprise many but I actually agree with GT in large part on what he says about cholesterol.  Problem with that part of GCBC was that he wasn't really saying anything new.    My first cholesterol test was back in the days when just total cholesterol was your basic test.  Mine was slightly high - only moderately overweight at 20 or so years of age.  A few years later the LDL/HDL breakdown became more the norm and my HDL was high.  Now we all know the progression with particle numbers, sizes, etc that has developed over the years and with it less concern over some types, more over others.

So there's lots of moaning going on over at GT's blog and around the LC web over Taubes' appearance on the Dr. Oz TV show 3/7/12.   I'm no fan of Dr. Oz.  I don't watch any of that sort of TV on anything other than a passing basis in doc/dental waiting rooms and such   I did watch the YouTube videos of Dr. Oz with GT on Larry King back in 2007 (is there a part III?) and I'm well aware of Oz's relationship with Oprah.   I'm especially not fond of Dr. Oz after reading this post over at Yoni Freedhoff's Weighty Matters blog.

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Insulin, Weight & Fat Accumulation

Yes folks, if you go to any Biochemistry or Endocrinology text, you will find that insulin's action is to put fat into fat cells and suppress its release.  Therefore insulin makes us fat.  Lower insulin, lose weight.  Raise insulin, get fat.  Right?

I've recently posted on two rat studies (here and here) that demonstrate unequivocally that it is not so simple.  I've also previously addressed the study that is the focus of this post in my Insulin Wars series with Todd Becker.  But wanted to further highlight that study here in a separate post.  

The Effect of Diet Composition on the Hyperinsulinemia of Obesity

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Ketogenic Diet increases Fat Mass and Fat:Total Body Mass Ratio

Ketogenic diet-fed rats have increased fat mass and phosphoenolpyruvate carboxykinase activity

This study looked at body weight, fat mass, blood lipid and glucose levels and PEPCK (rate limiting enzyme in glyceroneogenesis pathway for G3P production for esterification of fatty acids - fat deposition) activity in the liver and fat cells.  Two ad libitum diets were compared, a control standard chow and a ketogenic zero carb chow.  This study was in normal, young (30 days old at start) Wistar rats and lasted 6 weeks.

The diet compositions are shown below:

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Another Hormone Involved in Lipid Mobilization? Atrial Natriuretic Peptide

This article is a bit heady, and I won't go into a detailed analysis but will try instead to present some relevant excerpts to the gist of this post.   That being, adipocyte metabolism, the continual cycling of fats in and out of adipose tissue, the continual cycle of esterification and hydrolysis, is mediated by more than just insulin.

Atrial natriuretic peptide contributes to the physiological control of lipid mobilization in humans

According to the save date on my computer, I found this one a year ago.  Ever heard of atrial natriuretic peptide?  Me neither.  

According to Wikipedia, ANP is:

.... a powerful vasodilator, and a protein (polypeptide) hormone secreted by heart muscle cells.^[1][2] It is involved in the homeostatic control of body water, sodium, potassium and fat (adipose tissue). It is released by muscle cells in the upper chambers (atria) of the heart (atrial myocytes), in response to high blood pressure. ANP acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressure.^[1]

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Insulin Wars IV.2a: The Discussion with Todd Becker/Getting Stronger continues

If you haven't read the discussion thus far, or just to recap, here are the links:

Insulin Wars IV: Todd Becker of Getting Stronger blog
Insulin Wars IV.1: Todd Becker of Getting Stronger blog responds
More Todd Becker (Getting Stronger blog) on Insulin (this last one links to his piece on his blog)
{Todd quoted the relevant prior exchanges in his email, so most can probably follow along just with this post}

I've been putting off posting this for too long, mostly because in its entirety it is very lengthy (15 pages!) and I haven't had the length of uninterrupted time to devote to a thorough point by point response to the entire email.  So I decided to break this installment (IV.2) up into parts (a,b..., however many) so we can keep this discussion alive and continuing.  I'm also likely to address some topics out of order from Todd's email response.   Eventually it will all get up here :-)  I very much appreciate all the hard work Todd put into his response and our continuing discussion.  Please do bear with us, as we'll no doubt get a bit repetitive at times.   I do hope you'll enjoy the complete exchange.  I appreciate any heads-up on dropped links etc. that may have occurred with my C&P.    Thanks again to Todd Becker!

1. Causal role of Insulin in fat accumulation.

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Free Fatty Acids (FFA), A Link between Obesity and Insulin Resistance

FREE FATTY ACIDS (FFA), A LINK BETWEEN OBESITY AND INSULIN RESISTANCE

Evidence, gained from human studies, is reviewed showing that elevation of plasma FFA levels produce peripheral and probably also hepatic insulin resistance in obese healthy and diabetic subjects. First, plasma FFA levels are elevated in most obese subjects. Second, physiological elevations of plasma FFA inhibit acutely as well as chronically insulin stimulated glucose uptake in a dose dependent fashion. Responsible for this inhibition is a FFA induced defect in insulin stimulated glucose transport and/or phosphorylation which develops after 3-4 hours of raising plasma FFA and a second defect, consisting of inhibition of glycogen synthase, the rate limiting enzyme of glycogen synthesis, which develops after 4-6 hours. FFA induced inhibition of fatty acid oxidation (Randle effect) does not affect insulin stimulated glucose uptake or glycogen synthesis and thus does not cause insulin resistance.

Elevated plasma FFA levels also modestly increase insulin suppressed endogenous glucose production (EGP) although this effect has not been found by all investigators. The reasons why it has been difficult to demonstrate unequivocal effects of FFA on EGP include 1) the fact that FFA promote insulin secretion which counteracts its effect on EGP (FFA increase, while insulin decreases EGP); 2) the recognition that FFA induced increase in gluconeogenesis may be compensated by intrahepatic downregulation of EGP (i.e., by a decrease in glycogenolysis).

The FFA induced insulin resistance is physiologically important during starvation by preserving carbohydrate for oxidation in the central nervous system and during pregnancy, where the well recognized accelerated starvation pattern provides carbohydrate for the growing fetus. In obesity, however, there is no need to spare carbohydrate and the FFA induced insulin resistance may result in type 2 diabetes and other cardiovascular risk factors.

Mostly a bookmarking post for the time being.  An excellent review by Dr. Guenther Boden of Temple.  That name might ring a bell to my readers as he was one of the researchers Gary Taubes contacted around a year ago to discuss glyceroneogenesis/G3P and such.  Boden, like Frayn, is author to a large body of research in the area of fat metabolism.  

Non-esterified fatty acid metabolism and postprandial lipaemia

Non-esterified fatty acid metabolism and postprandial lipaemia

Yet another gem from ... who else? ... Keith Frayn!

Non-esterified fatty acids (NEFA, or free fatty acids) are an important metabolic fuel. Both the concentration of NEFA and their flux through the circulation vary widely from hour to hour, reflecting nutritional state and physical activity. Inappropriately elevated plasma NEFA concentrations may have a number of adverse effects on both carbohydrate and lipid metabolism.

As my regular readers know well, this is a focus of my research.

These adverse effects are likely to be most marked in the postprandial period, when NEFA release from adipose tissue is usually suppressed. Although the regulation of NEFA release in the postabsorptive state is well understood in molecular terms, the predominant pathway for release of NEFA in the postprandial state is the action of lipoprotein lipase (LPL) in adipose tissue capillaries on chylomicron-triacylglycerol (TG). Fatty acids released by LPL may either be sequestered in the adipocytes by esterification, or released as NEFA into the plasma. The regulation of this branch-point, which may be of crucial significance for postprandial metabolism, is not well understood. Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein.

1998 Keith Frayn

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