Nutrient Fates after Absorption

Random Bump

This held the top spot in terms of readership here at the Asylum for quite some time.  Always worthy of a bump.

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Original post:  7/15/10

Nutrient effects: post-absorptive interactions BY ERIC JEQUIER   (1995)

After a meal, the metabolic fuel selection at the whole-body level depends on the plasma concentrations of nutrients such as glucose, non-esterified fatty acids (NEFA) , amino acids, and on hormonal responses. Over the last 10 years, there has been great interest in studying the metabolic effects following the ingestion or the intravenous (i.v.) infusion of the three macronutrients, carbohydrate (CHO), fat, and protein (or amino acids for i.v. infusion). The aim of the present brief review  {I'm thinking it's not so brief!}  is to summarize the main mechanisms which determine the post-absorptive interactions between the nutrients.

This is an older paper, but still recent enough to provide some good info on the basics.  I'm going to do something a bit different with this one and I otherwise would be quoting huge chunks.  So I'll do bullet point summaries with select summary quotes from the paper in italics.

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The NEAT part about Moving More

Random Bump!

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Original publish date:  4/21/12

In writing up a post on metabolic rate and weight loss, I couldn't help but come across a ton of stuff I had in my draft bin and hard drive vis a vis exercise, lean body mass and metabolic rate.  This got me thinking about the usefulness of ELMM = Eat Less Move More as a strategy to flip the CICO balance along with other things we can do.  

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The LoBAG Diets for treatment of Type II Diabetes and IGF-I: Updated & Expanded

Bump ...

Does dietary protein raise blood glucose?  Not in normal or Type 2 diabetics it doesn't.  This will be the topic of a post today or tomorrow.  There is a disturbing, in my opinion, trend in the low carb community to now demonize protein.  Your usual Atkins style diet is no longer "good enough" or "well formulated" enough for most.  This keto kraze has gotten really krazy!

As far as I'm concerned, the danger of people like Jimmy Moore is no better epitomized than by this trend.  You have lots of people regurgitating his claims that his liver makes too much glucose out of protein and this is implicated in his weight issues.  Nevermind all of the evidence to the contrary.  Leaving weight loss aside, yes, this is anecdotal, but we have no other "evidence" to go by!  Long term low carbers seem to have worsening glucose tolerance over time.  Almost to a one, and these are people who were not diabetic or in some cases even IR (by HOMA) at baseline.  

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Where do triglycerides come from? Part I (Updated)

This post contains sufficient updates from the original (dated 5/11/11) that I consider it more of a fully updated version vs. a bump.   This began with my intent to link to this post in an upcoming discussion of triglycerides, when I noticed that Dr. Ronald Krauss was amongst the authors.   This study originally caught my eye because of   Marc Hellerstein's name, he of DNL not a major pathway in humans fame, that I've blogged on previously.

Now I have excerpted copiously from the discussion because the authors make several points relevant to the discussion of what comprises a healthy lipid profile.  As part of updating, I am breaking those excerpts up a bit more and adding some/more emphasis and additional commentary.

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Protein Metabolism

This one I'm bumping for myself, but perhaps some folks might find it interesting.  The red bolding is new.

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Original Publication:  4/17/10

Looking for some info on protein, I came across this link:

http://www.nutrition-partner.com/index.cfm?C27B8FF7FABF494CAA480EF21E0D228D

The page focuses on changes in dietary requirements and/or the impact on the body of malnutrition, disease and stress, but I found this site through the following graphic on protein metabolism:

Something in the numbers doesn't add up here, but I was surprised to see how much protein is "recycled" in our guts.  Perhaps the total protein synthesis is balanced by catabolism/turnover and that is the missing number?  Not sure.  Here is the quoted text referring to this diagram (my apologies for the messed up formatting).  

Protein in the body is not static; protein synthesis and breakdown is constantly taking place. However, the total body protein pool in a healthy adult is constant. Synthesis of protein from endogenous and exogenous amino acids is equal to degradation and external losses. Some proteins have a long lifetime, such as muscle protein and plasma albumin, while others have a high turnover rate. Muscle protein constitutes up to approximately 50% of total body protein, but contributes only approximately 30% of the protein turnover in the body, because in visceral and other organs, protein turnover rates are several times higher than in muscle tissue.  Protein metabolism is dependent on a vast number of endogenous mediators. These mediators define the balance between anabolic and catabolic processes. Insulin is the major anabolic hormone and also has an important role in amino acid and protein homeostasis. During injury and stress two major alterations in insulin are noted: a catecholamine-mediated suppression of insulin release and an insulin resistance, leading to a release of skeletal muscle amino acid for gluconeogenesis and, at the same time, a decreased utilisation of glucose by insulin-dependent tissues. This mechanism provides glucose to the insulin-dependent tissues that are important for survival and the healing of injury, such as the central nervous system (CNS), immune system and red blood cells. Other hormones, like glucagon and the catecholamines, control or counteract the effects of insulin and are more or less proteolytic; the exact role of catecholamines is still under discussion, however. In order to define protein requirements, an overview of protein metabolism is necessary. By determining the renewal of proteins susceptible to measurement, such as plasma, muscle and digestive secretion proteins, it has been possible to estimate the daily turnover in proteins. Considerable recycling of endogenous amino acids seems to occur, the quantity amounting to twice the daily intake.   Hence, normal protein metabolism incorporates about 100 g of dietary amino acids and over 200 g of endogenous amino acids daily. Allowance must therefore be made for increased losses of endogenous proteins when assessing patients´ protein intake.

So fully 2/3rds of our daily protein metabolism comes from proteins in our body -- the amino acid pool in our cells and/or breakdown of tissues.  Another factoid:  Structural proteins have about a 6 month half life, while hormones/peptides/etc. can have half-lives of a matter of minutes.  However hormones etc. constitute a very small amount of protein weight wise.

That 5000 Calorie Jokesperiment

Note:  I started this article with the intent of it being a single stand-alone before Smash the Fat's Sam Feltham had done his final summary of his overeating stunt.  Since then, however, he has written said summary and I've written two posts discussing this disconnect between the you-can-eat-all-the-calories claims and the current uber-restrictive low carb plans many long time low carbers are actually following themselves.  See:  Fast or Feltham and Fast or Feltham II

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Apologies in Advance:  I wrote this with updates/edits over several days and with "new information" coming in the interim.  It could probably use a good bit of editing and crunching down, but as this is just a blog, I'm going to publish it up w/o wasting time on that.  Please forgive the length, repetitiveness, etc.  Thanks!

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The Heritage of Corpulence

OBESITY is a disorder which, like venereal disease, is blamed upon the patient. The finding that treatment doesn’t work is ascribed to lack of fortitude. Corpulence in America is regarded along with narcotic addiction as something wicked, and I shall not be surprised if soon we have a prohibition against it in the name of national security. The condition is referred to in disparaging terms, including the most impolite references to the appetite. Appetite is held to be the cause, but I say it is hunger. I wish to propose that obesity is an inherited disorder and due to a genetically determined defect in an enzyme; in other words, that people who are fat are born fat, and nothing much can be done about it. I would like further to propose that the more serious of the consequences of being fat are not due to the corpulence but to the inherited defects; if this be so and we like food, we might as well eat up and be happy.

Astwood, 1962  

Adding:  A free double Cherry Pickin' Martini for anyone who can get me the full text of this.  Carbsane at gmail dot com.  Thanks in advance!

Why Fructose is NOT Like Alcohol

Where did this come from?

Beginning with his viral YouTube video (I won't link to it, every additional view is one view too many!), and continuing on, Dr. Robert Lustig has been making the claim that fructose is metabolized like alcohol by the liver.  You cannot make your misinformation more clear than to title a section in your book as Lustig did in Fat Chance --  Fructose versus Ethanol:  Pick Your Poison.

Before Lustig, I don't think I'd ever heard anyone equate sugar to alcohol on a metabolic level.  A few may have made an addiction analogy, but it was Lustig who "taught" us the "science" that the liver processes sugar just like alcohol.

It is shocking to me that his video was produced and distributed by an institution of higher learning as a "Mini Medical School for the Public" presentation.  This implies to me that the content has been somewhat vetted.  Apparently it has not been, and also, nobody within that establishment has ever seen fit to correct the record?  Again, apparently not, as there is that Skinny on Obesity series out there repeating many of the previous errors.

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A Quote for Thought

... After shedding pounds of cognitive dissonance, I adopted the idea that health problems were likely the result defective energy metabolism.

While this may sound abstract, the idea shifts the conversation to the health of the living cell, rather than speculative theories about evolution or reductionist physiology obsessed with blood sugar, cholesterol and insulin.

Danny Roddy

De Novo Lipogenesis Again (and Science and Science Reporting)

In my last post, I just posted a graphic taken from an "FYI" inset by a scientist, Marc Hellerstein, whose work I've blogged on quite a bit here. (Anyone wanting to refresh can click on the image and enlarge.)  One good post to begin with if you are not familiar with that name is Where do Triglycerides Come From? I would say that between Marc Hellerstein's No common energy currency: de novo lipogenesis as the road less traveled and the works of Eric Jequier such as Nutrient effects: post-absorptive interactions, the case that hepatic DNL is quantitatively insignificant in human energy balance/fat accumulation is strong and has not been refuted by some newer scientific findings.    

I do hope to expand on the role of adipose DNL at some future point -- teaser: I have a paper showing that reducing WAT lipolysis upregulates adipose DNL and improves glucose homeostasis in the IGT irrespective of body weight  -- but adipose DNL had not been central to the arguments of folks from Taubes to Lustig to Eades to Naughton to a list far too long to go through here.  The claim has been that excess carbs are converted in the liver to fat and sent to the fat tissue for storage.  

Does this occur?  Yes.  Is it significant?   Only if you consider a couple grams fat synthesis per day significant at the metabolic cost "wasting" one gram carb for every four grams converted to fat ... and only if you consider a few grams of fat significant in the context of consuming 100, 200 or more grams of fat that is already fat.

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Do Carbohydrates Turn into Fat?

From Discovering Nutrition

Insel, Turner & Ross,  copyright 2010

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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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Carbohydrates as a source of energy ~ Eric Jequier, 1994

Carbohydrates as a source of energy
Eric Jéquier  Am J Clin Nutr 1994; 59(suppl):682S-5S.

Carbohydrates are the main energy source of the human diet. The metabolic disposal of dietary carbohydrates is direct oxidation in various tissues, glycogen synthesis (in liver and muscles), and hepatic de novo lipogenesis. This latter pathway is quantitatively not important in man because under most conditions the rate of de novo lipogenesis does not exceed the concomitant rate of lipid oxidation in the whole body.  Thus, dietary carbohydrates do not appear to increase an individual’s fat content by de novo lipogenesis. The intake of dietary carbohydrates mainly has the effect of inhibiting fat oxidation while glucose oxidation is increased. Dietary carbohydrates are involved in the control of energy balance because the regulation of food intake depends, in part, on the carbohydrate need of the individual.  Because there is an obligatory requirement for glucose in several organs such as the brain, a spontaneous increase in food intake is seen when the diet has a low-carbohydrate, high-fat content.  Therefore, the present nutritional advice of increasing the proportion of carbohydrate energy while decreasing that of fat in the everyday diet has strong scientific support in terms of the regulation of the energy balance.

Quite an interesting read.  More later.

Further reading:  Nutrient Fates after Absorption , Metabolic Advantage, Obesity and Eric Jequier

Ancestral Rabbit Starvation Medical Vacations! The next craze?

I came across this study a bit ago and it caught my eye as I was transfering some stuff between computers:  Marked Improvement in Carbohydrate and Lipid Metabolism in Diabetic Australian Aborigines After Temporary Reversion to Traditional Lifestyle

The rationale for the present study was that temporarily reversing the urbanization process in diabetic Aborigines should improve all aspects of their carbohydrate and lipid metabolism that are linked to insulin resistance. Ten full-blood, diabetic Aborigines from the Mowanjum Community (Derby, Western Australia) agreed to be tested before and after living for 7 wk as hunter-gatherers in their traditional country in northwestern Australia. They were middle aged (53.9 ±1.8 yr) and overweight (81.9 ± 3.4 kg), and all lost weight steadily over the 7-wk period (average, 8 kg). A detailed analysis of food intake over 2 wk revealed a low energy intake (1200 kcal/person/day). Despite the high contribution of animal food to the total energy intake (64%), the diet was low in total fat (13%) due to the very low fat content of wild animals.

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What is Diabetes?

"the proinsulin disorder in diabetes is not 

only ubiquitous but it is also precocious"

As a second post setting up for future discussions on insulin resistance and it's role in diabetes (especially type 2)  I wanted to share the following paper with you here:

PROINSULIN, PROAMYLIN AND THE BETA CELL ENDOPLASMIC RETICULUM: THE KEY FOR THE PATHOGENESIS OF DIFFERENT DIABETES PHENOTYPES

It is a long paper, almost 18 full pages of text, and more than 9 to list the 298 (yikes!) references. I will by no means attempt to address it in its entirety here, rather I shall focus on the section entitled "INCREASED PROINSULIN AS THE MAIN BETA CELL SECRETORY DEFECT".  But first, the abstract of this 2007 paper:

Based on our clinical and epidemiological data, we have sustained for a long time the unitary character of the various phenotypes of the diabetic syndrome. In this paper, we add several arguments sustaining that the unitary character of diabetes is related to a common primary defect in the function of the beta cell endoplasmic reticulum, leading to an inadequate processing of the two main secretory molecules: pre-proinsulin and pre-proamylin. The post-translational changes of these molecules might explain the main proapoptotic and anti-regenerative pathogenic mechanisms leading to a progressive decrease in the β cell mass/function. In our view, the increased proinsulin levels encountered in various diabetes phenotypes could be not only a marker of beta cell dysfunction but also could indicate the main β cell defect, suggesting also its location.

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Fat Burning Beast?

I gotta say, whenever I hear about these low carb athletes, blog posts and such flickering through the feed reader and such ... I tune out.   Why?  Because almost invariably when it comes to touting the superiority of the low carb diet, the tent gets very large indeed.  Anyone eating fewer carbs than the mythical "average" American consuming 500g/day is a low carber.  Which is ridiculous on its face, but makes for great hyperbole to blame the carbs for obesity and all manner of evil in the world.  In any case, when one looks a little deeper into the diets of these low carb athletes, they aren't really low carb at all.   

I'm quite tired of this double standard applied by purveyors of low carb wisdom and light.  You see if a study shows even the slightest benefit to LC over the rival diet, it is touted as further evidence of LC greatness, even if after more careful consideration, it was hardly a low carb diet after all.  Yet that same diet fails to elicit the famed LC magic, and all of a sudden low carbers notice and point out that it wasn't really a low carb diet after all.  Sorry.  Can't have it both ways.  

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NuSI ... or Just Do It!

Imagine if you will, that a decade or more ago someone told you that if you really wanted to build your journalism career tearing down scientists, you needed to look at diet and nutrition research.  You picked up a copy of Atkins and lost a couple of pounds.  You began cultivating your schtick that simple obesity (the kind of the epidemic) was not about overeating or sedentary behavior, it was something else.  And you received three-quarters of a million dollars to research and write a book.  The book was a best seller and garnered you a cult following in certain circles and you were off to the races giving talks around the globe.  

There were doctors and others who bought into your hypothesis, spreading the word as fact and growing the movement.  But a following from one segment of the population remained elusive:  scientists.   Rather than address the reasons why (serious holes in your hypothesis), you double down and trash scientists more openly and frequently.  You also publish a second book with a dumbed down, even less scientific, hypothesis.  By all indications, this book falls far short of expectations ... and still the scientists are not coming around.  Worse still, many who had believed your hypothesis was plausible, at least worthy of investigation, were abandoning it.

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Ketone and Fat "Burning" are Not the Same Thing to Your Mitochondria

This notion of being a "sugar burner" vs. a "fat burner" -- with the latter being touted as preferable based on nothing I've seen in the scientific literature -- is getting really out of hand.  This is not a new idea, but it certainly seems to be being pushed more lately, particularly in the area of athletic performance.  There were a smattering of posts about the diets of Olympians about the net and I just have to shake my head at the one that goes something like "just imagine how much better fill in the blank would do if (s)he didn't eat grains" or "ate LCHF" or "went paleo".  C'mon already ... Michael Phelps is a prime offender of all laws and gods nutritional, but will someone please remind me how many medals he's earned and records he's held/broken in his career?  Gawd forbid any of these elite athletes set a bad example by having their face put on a box of Wheaties!  I dunno ... it all seems so silly when Phelps sports one of the leanest torsos on the planet burning sugar.  But I digress ...

But with ketomania in full-blown fad form, there's a new twist on the fat burning meme which is to confuse fat burning with ketone burning.  It is not.  Yes, ketones are produced mostly from the breakdown of fatty acids (they are also produced from some amino acids), so you "burn fat" in your liver to produce them.  If you are in caloric deficit, the source of the fatty acids will be body fat.  However, if you're fueling the other cells of your body with ketones, this is not the same as the mitochondria in those cells "burning fat".  

Below is a schematic of a brain cell mitochondria and the metabolic pathways showing where ketones feed into Krebs (aka the TCA), from:  D-β-Hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease (thus it shows the points of issue for these two diseases) 

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AHS(?) Bumpity Bump Bump: When is Fat a Fat?

Soooo ... I've been following the #AHS12 hashtag on Twitter, and I'm not sure this came directly from there or from me clicking on an ID on one of the tweets and then checking out other tweets ... but anyway, I stumbled across this exchange between Aaron Blaisdell and Robb Wolf:

9 AugRobb Wolf ‏@robbwolf

Ruminant fermentation converts cellulose to fats. Cows actually run on a 60-70% FAT diet.

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16hAaron Blaisdell ‏@AaronBlaisdell

@robbwolf Paul Jaminet wrote the same thing in his book Perfect Health Diet

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7hEvelyn ‏@CarbSane

@AaronBlaisdell @robbwolf SCFA are not metabolized as "fats" . Ruminants convert the bulk of these via DNL to LCFA.http://carbsanity.blogspot.com/2011/02/when-is-fat-fat.html

FWIW, Robb retweeted this.  Now I'm pretty sure since he's at AHS12, this tweet came from a statement someone made in their presentation.  This is a claim I hear made from time to time -- that pretty much every animal being on the planet somehow consumes a high fat diet because when one eats the "right" carbs, gut bacteria convert them into short chain fatty acids.  This is a highly misleading concept as I attempted to outline in this post.   I hope that in revamping and adding to the book, the Jaminets will clarify the section on chain length to distinguish long, short and medium chain FA's (and leave out the part about SCFA qualifying as "fat burning" entirely ... it is generally the other way around in ruminants).

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Is it Possible? "Smarter Science" worse than "Good" Science Journalism?

I'm really disgusted folks.  I'm sorry, but I get a whole heckuhlot of criticism for checking the references of one Gary Taubes.  I must be some obsessed, hermit crab stalker type to spend my time and a few dollars to actually look into what he says his references say, vs. what they actually say.  Nah, rather that I just accept what he says at face value.  Taubes' misuse of the Pima as an example of his carbs-make-you-fat-and-diabetic garbage is one where you don't even need to try to understand the science.  He flat out misrepresents this "poster population" for his hypothesis to have people believe their's was a lower carbohydrate diet back when.  But, in fact, it was far higher in carbohydrate than the SAD, to the tune of 80+%.  Still ... no program has approved GCBC for their curricula to the best of my knowledge.

Well, Jonathan Bailor is giving The Master a run for his money when it comes to misinterpreting/misrepresenting studies in his Smarter Science of Slim book.  Only since Taubes explicitly avoided modern peer review research, while Bailor likens his "research" to meta-analysis of same, Bailor is far more insidious.  Even as a "review" of the research it is turning out to be horribly misleading and inaccurate time and again.  How then did this happen?

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