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Tuesday, August 30, 2011

Why Insulin Levels & Lipolysis Do NOT Dictate Weight Loss ~ Part I

I'm really rather amazed that at this point we're still having to discuss this topic.  As a good friend of mine once said to me in an email (paraphrasing):  One would expect these sorts of myths to persist back in the 80's and 90's.  But in this day and age of information availability on the internet, it seems impossible that enough people continue to be influenced by such easily debunked notions.  Low carb Wiener anyone? {grin}

In any case, it seems that no amount of demonstrating the lack of any correlation between fasting insulin levels and weight loss will convince some people.  I really would think that the scatterplot (weight loss v. fasting insulin), discussed in this post,  would be impossible to explain away, and yet many just dismissed it from their minds.  It's that proverbial black swan all the Eades Popperites (or is that all you can eat (Eade)sous vide popper-bites?) constantly seek.  

I was yet again reminded of that paper that got me thinking and started all the fuss.  Yes, I'm talking about the infamous (around these parts anyway) 2003 Reshef paper Glyceroneogenesis and the Triglyceride/Fatty Acid Cycle that is cited as a reference in GCBC.  This is telling.  Some seven months after I first reported on this fact to my readers (to a whopping roughly 200-300 "page hits" at the time), Gary Taubes finally addressed Reshef by dismissing it as mostly rat studies.  But my interview with Jimmy apparently also got Gary to obtain a copy of Frayn's Metabolic Regulation (a later edition than the one referenced in GCBC) and get around to reading it.  In there he found a nice little picture about fat storage and the fatty acid cycle.

In any case, as Taubes now says, he knew all along that you could store fat w/o carb, you had to, because of the mere existence of the TAG/FFA cycle.  Below is the full "cycle" -- actually two cycles:

Now, I would be remiss if I didn't stress yet again how his G3P theory has always been a load of bunk.  Look at that picture.  See those bold solid arrows from pyruvate to G3P, and the rather more faint dashed arrows from glucose to G3P?  But right below that diagram in the article is a entitled "Measurement of the triglyceride/fatty acid cycle in vivo".  This is literally *right under* the diagram above, and is the Table I indicated in the caption.  I'm only including the first few lines relevant to this post (human adults!) 

In the fasted state, when according to theory we should be losing our weight because that's when lipolysis is high, almost half of fatty acids released by lipolysis are burnt and the rest are recycled back to triglycerides.  Interestingly systemic (liver) recycling is roughly 5X that of adipose.  The line below that labeled "burn" is for severe burn patients.  This is a rapid event due to acute injury.  Of note, the delivery rate of fatty acids from the fat tissue is increased a little over 3-fold.  Systemic recycling is reduced to roughly half as a percent (which would still increase the absolute amount of systemic recycling by over 50% -- or >1.5X fasting) while adipose uptake/recycling is increased almost 5-fold by percent -- this would correspond to absolute uptake and recycling back to triglyceride of roughly 15X more in absolute amounts of fatty acids.    In all, 64% of the excessive NEFA release is recycled in this scenario.  

We can add to this information from the table on p.4 of this study PDF.  I'll be blogging on this one at some future point, but looking at the "C" - normal controls - we see that NEFA (measured as oleic acid) concentrations and turnover rates are increased by exercise, but accompanied by an increase in proportion taken up.  

What does this tell us? 
  • More fatty acids are continually released from fat cells than are actually used by the cells.  The supply of NEFA is thus in perpetual excess of needs.
  • The amount of NEFA released is proportional to need thus more are released in response to activity (not included in table) or stress as in the burn scenario.
  • Increased demand seems to elicit an "over-reaction" to mobilize NEFA accompanied by a corresponding "call to action" for adipose to quickly take up excesses.
  • I think we can all agree that the "burn" cannot simultaneously cause increased and decreased insulin levels that would be required to produce the "burn" effect if insulin is sole regulator of fatty acid trafficking.  In the burn scenario, if insulin was dropped to release NEFA dramatically, then how to explain the roughly 15-fold concurrent increase in uptake/recycling?  
  • Ditto for the exercise scenario.  Exercise is known to lower insulin and increase lipolysis, which is demonstrated in the linked study.  So NEFA are delivered in greater excess.  Even with greater utilization, proportionally more are taken back up.  
  • Taken together these last two bullet points demonstrate clearly that something other than *just* insulin is controlling the TAG/FA cycle in adipose tissue.  
  • A case can be made that uptake percents are dictated by how much is utilized by the cells for energy needs and how much remains in circulation.  In exercise ("fight or flight") or injury, the excess NEFA delivery is even more excessive to assure meeting needs.  And the fat tissue takes up the excesses just as rapidly to avoid spiraling lipid content in the blood.
So ... what dictates weight (fat mass) loss?  Mass balance.   The only way for fatty acid mass to get out of the body is through beta-oxidation to CO2 (or very minor losses of ketones).  If you oxidize more fatty acids than you take in, you lose fat mass.  If you take in more fatty acids than you oxidize, you gain fat mass.  

If the obese did not mobilize sufficiently excess NEFA to meet needs, you're cells would not be "starving" making you hungry ... You would probably be dead.

Fat Burning:  Lipolysis/release of NEFA = NEFA uptake/oxidation + NEFA recycling
Lipolysis is not the rate limiting step, it delivers NEFA in excess by design.  Uptake and oxidation is the rate limiting step.  That, and not lipolysis, determines weight (fat) loss or gain in conjunction with intake.


Lerner said...

Once upon a time, I came across a post on some site which said that Taubes believes that you can't store fat without eating carbs... the implication being that he didn't know that proteins can be insulinogenic. So I went to amazon and used the 'search this book' feature to search GCBC. Going now from memory, I didn't find 'insulin index' or 'insulinotropic' at all. The word 'insulinogenic' appeared once, only in the title of a reference. Those words seem necessary to me when discussing the insulin provoking property of proteins.

Also, his very theory is mis-named as the carb-hypothesis, because it's really an insulin hypothesis. Can it be that he associated insulin solely with carbs because he truly never knew about proteins? :)

I did make one post last week on Ned's site (and I also saw him posting here). I described how when I'd first heard of Taubes several years ago, I immediately knew from experience that he had no valid conception of how Glycemic Index works* - and how that could be medically harmful. Way back then, I had posted my criticism about how such a supposed genius could get something fundamental so wrong, so that it seemed apparent he had never even bothered to look at a GI table. The answer I got back then was "don't worry about that, just look at how brilliant he and his book are". Well, maybe now the house of cards is finally coming down, but still Taubes is largely immune from criticism over his gaffes. Except maybe for here :)

*E.g., Taubes claims that 'processed' grains are necessarily high GI and whole grains are not.

Evelyn aka CarbSane said...

Hi Lerner, When I re-read sections of GCBC I can't help but think he was unaware of the insulinogenic properties of protein. <a href=">Because he says specifically in GCBC </a>:

By the mid-1960's, four facts had been established beyond reasonable doubt:
(1) Carbohydrates are <b>singularly</b> responsible for prompting insulin secretion.
(2) Insulin is singularly responsible for inducing fat accumulation. ...

I think you'll get a kick out of the comments on that blog post where David Isaak tried to convince me that I don't know the meaning of the word "singularly" in the context it is used. Even by his definition, that is incorrect.

The funny thing these days is that in a recent lecture Taubes claimed that w/o sugar it may even be impossible to become obese. That fructose doesn't elicit insulin is totally inconsistent with his carb or insulin or carb via insulin drives obesity nonsense.

Lerner said...

Haha! Yep, you're right: even by any definition, Taubes apparently doesn't mention beef and dairy anywhere in his book so Taubes' claims are singularly misleading in any light.

Back when I was still reading Eades' blog, there was an "ask Taubes a question" event. More than one reader asked about Japan. What occurred to me was: why hadn't Taubes addressed that in his book? He hadn't ever heard of Japan?

I see Taubes as being the poster boy for The Emperor's New Clothes. People refuse to see his gaffes.

If Taubes were weaving baskets instead of errant theories, here's how I'd envision things going: he'd first lay out each reed precisely, then measure, label, categorize and catalog each one. He'd come up with detailed figures and designs and even graphs. His notes would take up 300 pages. Then he'd put together something terribly misshapen, with gigantic holes so that the basket can't hold anything. If I were to point out the holes (Japan, the New Guinea highland natives existing almost solely on yams, Twinkie diet), his true-believers would say, "don't worry about that, just look at how brilliant and methodical and detailed his work is! And he's got hundreds of references!!"

Ah well, it's to laugh :)

So once upon a time, not long ago, there was a guy who wanted to counter the movement to brand potatoes as being bad for you. As we know, he ate nothing but potatoes (and probably peeled them, making them 'processed'!) and didn't get fat. So he's like the little boy in The Emperor's New Clothes - except some still don't listen. It's irrational. Nutrition science has become like politics.

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