Revelations from Gedankenexperiments vs. Wirklichenlebenexperiment

Traffic Bump!

Occasionally I see traffic to old posts whilst perusing stats.  I saw this was getting a few hits and decided to bump it.  Especially since the fervor for finding the single bogeyman dietary agent of all doom seems to be hitting a fever pitch lately.  Even Dr Oz is getting on board, and as the Judith Mazel of the low carb world tells us:

Dr Oz is one of the most well respected conventional doctors—and he has major influence because he is educating millions of people every single day on his show.

{you can stop laughing now ...}

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Disgusted with Diet Doctor

The Swedish Diet Doc (does he have any patients?) has been on a roll of late, and it's reached a point where I just have to comment.

For starters, although it would be impossible for every bariatric doc or even a small minority of them to be real-life examples (in the been there, done that department) to be able to promote what has worked for them, at least one might expect that such a doctor wouldn't hold such disdain for them.  When you think about it, medicine is one of those professions where the experts rarely have first-hand knowledge of the fields in which they are often doling out the most personal of advices.  But if you don't like "fat people" then why are you making a living off of "treating" them and dissing them behind their backs (and to their faces)?  

Diet Doc even has a label:  Why Americans are Obese.  Sounds OK though.  Yeah, obese is the technical term.  But here is one of the posts on that label: http://www.dietdoctor.com/why-americans-are-fat-part-2.  Note that I didn't change the bare URL which belies the original title of the post, and many others, before someone informed the doc that calling people fat might be insulting and not appropriate for a person of his stature to be doing.

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The Vascular Functions of Insulin

Random Replay

Was having a discussion on FB about insulin this morning and while going through some blog posts this one popped up.  I find reading some old stuff interesting at times ... this is over 3 years old.  

If someone goes on a low carb diet and this manages their hyperglycemia, this is a classic example of treating symptoms while not addressing the cause of the problem which is pancreatic beta cell dysfunction, and in the case of the T2, coupled with hepatic insulin resistance.  

What low carb doesn't do is restore normal insulin secretion and signaling, and insulin plays many roles in the body beyond glucose transport.  For one, it also assists amino acid transport (and protein synthesis) which is why the IR often have elevated circulating levels of the most insulinogenic (e.g. insulin requiring) amino acids, the BCAAs.  

This post is a flashback of some of the other things insulin does.  Further it discusses the role of NEFA in all of this ... the forgotten biomarker I think most low carbers with whacky lipids should have measured as they are likely elevated.  

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Bump: The Diabetes "Crash" Cure & Pancreatic Fat

Today's 8/15/13 bump was inspired by a comment by Tsimblist (thanks!) alerting me to this paper:  Type 2 Diabetes Etiology and reversibility

Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content.

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Aug. 1 Over the Hump Bump: Baby your Pancreas? Part I: The Tired Pancreas

Another two-fer for the Thursday post bumps again this week.  More explanation for why this set in the next bump.

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Original Publish Date:  7/26/11

In the comments on a recent post on beta cell lipotoxicity, Ned Kock (of Health Correlator blog) posted a link to a post he made a while back entitled:  Lipotoxicity or tired pancreas? Abnormal fat metabolism as a possible precondition for type 2 diabetes.  This article deals with the concept of the "tired pancreas" in the development of diabetes.  It seems that (and hopefully he corrects me if I'm wrong here) Ned and I agree that this is not a likely explanation for diabetes.   Ned summarizes the progression of obesity induced T2 diabetes from Unger & Zhou, 2001.  It is worth mentioning that Unger is often summarily dismissed from the "scientific discussion roundtable" by low carbers because of the unfortunately titled "Gluttony and Sloth" paper, that, even more unfortunately also included a biblical verse.   Unger's hypothesis is very leptin-centric, but not at all incompatible with other lipotoxicity based theories.  Basically, lipotoxicity is the result of dysfunctional adipocytes leading to excessive "spill-over" of fatty acids into circulation and accumulation in ectopic tissues.   Unger & Zhou identify dysfunction in leptin secretion and/or signaling as the initiating factor in this process.  One thing that doesn't quite add up for me here is that I keep finding citations indicating leptin action increases free fatty acids which would seem counterintuitive.  In any case ...

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Did low fat diets cause the obesity epidemic in the US?

click to enlarge

The title of this post is a common theme repeated by the likes of Swedish diet doctor Andreas Eenfeldt - That somehow going low fat (thus high carb) has caused the obesity epidemic.  At best, by percentage only, the USofA has decreased fat consumption from 37% to 33% (or 36% to 33% for women) ... this 3-4% reduction in fat percentage has been accompanied by a 7% increase in carbs (42-to-49% men, 45-to-52% women).  As you can see in the graphs, absolute fat content is basically flatlined -- we didn't cut fat, women (who tended to "comply" on the fat recs moreso than men)  even added a small amount.  Any way you cut it, this relatively insignificant change would be insufficient to cause some sort of carb triggered, insulin-induced fat cell mutiny!  Confronted with such facts the insulin hypothesis, or what I call TWICHOO, is changed ever so slightly to focus on how carbs cause you to eat more -- to the tune of some 300-500 calories/day and gain weight.   (I would note that NuSI discounts any ineffectiveness of various LC diets that are not really LC and use 40% carbs -- If you don't see an effect there, you will do nothing to pin the obesity epidemic on the lowly carbohydrate.)

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Ectopic Fat

A nice overview I just thought I'd share here.  Ectopic Fat Depots and Cardiovascular Disease

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Laura Dolson on the recent meeting of the American Society of Bariatric Physicians

*** Can you help a girl out?  Where is the traffic coming from?? Thanks! ***

In the past week, I've noticed a sustained trickle of traffic to this post of mine from over a year ago (original publish date 4/28/12) .  Therefore, rather than write another post on a somewhat older topic, I decided to bump this one and add some comments.   For most of this year I have been under attack for posts of this nature and all I can do to counter those is to point out that this post is not a personal attack.  What I've written is as respectful as can be when the subject is someone who, were she promoting veganism or McDougall's diet would be vilified and likely destroyed in the LC community.   Yet I haven't done so even though I believe Laura Dolson is deserved of some criticism for not telling the full story here.

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Battle of the Obesity Experts!

Sam Feltham and Zoe Harcombe "battle it out" over 5-a-Day!

UPDATE:  

@CarbSane @zoeharcombe Thank you for the critique Evelyn but that Sky interview was last year and my opinions have evolved from then...
— Sam Feltham (@samfeltham) June 22, 2013

I've now asked him how he was eating in 2010.  He's already, in another tweet, said he was lifting 2X/day back then for a competition in Men's Health.  Due to time constraints he only lifts 12 min/week now.  

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!

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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Chronic Exposure to Free Fatty Acid Reduces Pancreatic β-Cell Insulin Content by Increasing Basal Insulin Secretion That Is Not Compensated For by a Corresponding Increase in Proinsulin Biosynthesis Translation

Coming next in the discussion of diabetes I am going to discuss insulin secretion in greater detail.  I was reminded of this post in the writing process.  So ... Bump!

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Original Publish Date:  4/4/11

Chronic Exposure to Free Fatty Acid Reduces Pancreatic β-Cell Insulin Content by Increasing Basal Insulin Secretion That Is Not Compensated For by a Corresponding Increase in Proinsulin Biosynthesis Translation

JD McGarry contributing author.

{Please note:  Excerpts from the text will be edited somewhat to avoid "cluttering" references, statistical values, and some rounding of numbers.  Text will sometimes be presented in bullet form or with paragraph breaks to ease reading.  It is not my intent to plagiarize nor to alter the content.  If anyone feels I've altered the content in any meaningful way, do please let me know!}  Direct quotes will be indented.

FFA are an important physiological fuel for islets, and act as a supplemental nutrient secretagogue to potentiate insulin release acutely in the presence of glucose.

Translation:   β-cells run on fatty acids but this fuel also serves to stimulate insulin secretion.

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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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Thoughts on Childhood Obesity - The Half Man Angus T. Jones

True confession time:  I love watching reruns of the early years of the TV show Two and a Half Men.   It's been many years since I followed any TV series "live" and not in reruns, and as I'm not into Ashton Kutcher (not seeing it gals, you?) I never had any urge to watch the new shows.  As such, I was rather surprised by pictures of the son, played by Angus T. Jones, at age 19.  He's all grown up ... and decidedly not obese or even overweight.  One might call him svelte even.  Then I saw an old episode and he was a very chubby child.  

This post is about children and weight.  I think we've gotten ridiculous as a society about this in some ways.  Robert Lustig laments over some obesity epidemic in 6 month olds.  Really?  My husband was born prematurely at 4 lbs and change.  I was born full term at a robust (especially for these days) 8 lbs.  I was a "chubby" baby, he was not.  I have a picture of me at age 1 where I'm still quite chubby.  By age 4 or so, I was, if anything, too thin and I remained that way naturally until puberty (when I chubbed out a bit but was never more than 20 lbs overweight).  My husband was not a fat kid, but he was pudgy, especially in those middle school years.  But by high school he leaned out a bit.

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Some Suggested Reading ...

In light of other recent events, I present some suggested posts from this blog on the questionable accuracy of the blogging of one Peter Dobromylskyj aka Hyperlipid.

1.  Bloggo Science ~ A Hypothetical Post ~ III: Fasting Insulin & Weight Loss

Summary:  The third post in a series (links to I & II within) outlining how Peter deliberately fudged the data from the "infamous" Grey & Kipnis study.  He even told his readership he was doing it and tips his hat to Ancel Keys.  I feel to this day that if anyone can read this series and take Peter seriously after that.  It was done in all seriousness on his part.  

2.  Bloggo Science ~ LIRKO Wars Edition

Summary:  Peter blogged on the LIRKO mouse with a "cute" quiz about making jam from the urine of this mouse.  One problem, LIRKO doesn't get glucosuria.  Other claims made are also easily dispelled including that this mouse's liver (and other cells) can't process glucose so they burn through fatty acids like mad and that's why they don't get fat,  and that this mouse's muscle cells "internalise their insulin receptors".

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Hyperinsulinemia, Insulin-Suppressive Drugs & Obesity (and Lustig)

The recent buzz about hyperinsulinemia being at the root of obesity (whatever the mechanism) has had me thinking again about the insulin lowering drugs.   Studies in this regard were referenced in the recent article in Cell from Dr. James Johnson's research group at UBC.   If this is really all there is to it, why not just treat obesity with such drugs?  Or at least give them to the reduced-obese so they won't regain the weight, and/or the so-called pre-obese who start gaining at some point in life before they become obese.  This is really the bottom line of studies like the recent one from UBC.  Because if all we need to do is suppress the hyperinsulinemia (however it is caused) to prevent obesity it would be done.  There is a relatively rare condition, called by many names, but most descriptively neo-natal or infant hyperinsulinism.  These children must be treated ASAP to avoid the consequences of hypoglycemic episodes.  I surmise the drugs octreotide and diazoxide were developed at least in part for treating this condition, though often partial removal of the pancreas is required.

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Gary Debunks Taubes II ~ It's the Frucose Stupid, revisited

Gary Taubes had a problem on his hands for his "Alternate Hypothesis" on the cause of obesity. While Why We Get Fat was in the writing stage, a couple of NIH biophysicists remained pesky thorns in Gary's side having challenged him on a lynch-pin of TWICHOO (Taubes Wrong Insulin-Carbohydrate Hypothesis Of Obesity).   Not to mention an equally pesky then-anonymous bunny-eared blogger who posted some pretty damning stuff on the subject, especially when she looked at his seminal reference on the subject from GCBC.  Downplay as he might, try to move on and have everyone forget, as he eventually relented and did, Taubes' original WWGF remains enshrined in the first journalistic effort on the topic: Good Calories Bad Calories.

It wasn't all that long ago that people were shouted down in forums and comment sections of the low carb persuasion for daring to suggest that people could gain weight on low carb.  Remember the meme?  At least you won't gain weight being a fat glutton?  Can't gain weight so long as there's no carb around?  It was all there in black and white in GCBC-- you need glucose to make alpha glycerol phosphate (aka glycerol-3-phosphate) to store fat.  

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Exaggerations?

direct image link

The following comes from a slide presented by (?) at the Low Carb Down Under tour.  You can click to enlarge, but here's what the slide says under the title "What changed in the 1900s?"

• Sat fat down 83%
• Veggie oil/margarine up 535%
• Sugar up 1150%

Now, no doubt there are changes in eating habits, and perhaps "down under" people changed their eating habits even more dramatically than we Americans have, or are purported to have.  I've blogged many times that something's "off" with any stats indicating that Americans actually consume a low fat diet, but I'm not going to address the fat claims above.  It's the sugar claim that just screams -- that can't be so?!

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Does a high animal protein/fat diet forestall obesity?

Don Matesz had an interesting blog post the other day that I tweeted:  Grass-Fed Animal Products Prevent Obesity and Cardiovascular Disease?  He writes:

Not for Mongolians.

Mongols eat a diet largely composed of milk products, meat, and fat from free-ranging, organic, grass-fed animals. They consume few plant foods because few edible plants grow in the cold continental climate of Mongolia. The climate forced them into a natural experiment in low-carb nutrition based on grass-fed animal products.

I have an interest in Mongolians because there's definitely some influence of these people in my husband's ancestral line.   I went looking for any peer review literature that might address the Mongolians and found an interesting article.  But before that, I also found some other info.  Don points out in a note to WAPF (presumably aimed at their promotion of raw milk) that the Mongols boiled their milk and made cheese from it.  But one of the accountings of the diets comes from the WAPF site:  Diet of Mongolia.  

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Weight Loss Celebs & Credibility

I’ve read that [he] has regained quite a bit of the weight. When I’ve seen him [in pictures] lately, it’s only from the shoulders up.

Questions:

1. Who is "he"?
2. Who said this?
3. What is he/she implying about the subject?

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