IB-BWBS ~ It can kill you!

No ...

This is not some new version of irritable bowel syndrome.

IB-BWBS stands for:

Intellectual Bullying - aka - Baffling With Bull Shit

It can kill you.  How?  Because you'll follow down a path that someone "smarter" than you leads you ... ignoring your common sense.

Don't do it!!!

Elevated Free Fatty Acids Further Impair Glucose Tolerance in IGT but not NGT

Elevated plasma nonesterified fatty acids are associated with deterioration of acute insulin response in IGT but not NGT

High concentrations of nonesterified fatty acids (NEFA) are a risk factor for developing type 2 diabetes in Pima Indians. In vitro and in vivo, chronic elevation of NEFA decreases glucose-stimulated insulin secretion. We hypothesized that high fasting plasma NEFA would increase the risk of type 2 diabetes by inducing a worsening of glucose-stimulated insulin secretion in Pima Indians.

The subjects were 151 Pima - 107 with normal glucose tolerance (NGT) and 44 with impaired glucose tolerance (IGT) at the outset of the study.  At the outset none of the subjects had been diagnosed with frank diabetes.  These subjects were part of a study on pathogenesis of diabetes in the Pima and returned for annual visits to have various tests performed.  Of note, offspring of diabetic mothers were excluded from the analysis, thus the NGT group did not include this "at risk" group. 

Is LC Morphing to HAES? Part I: Define Healthy

After returning from the LC Cruise, Jimmy Moore - arguably the most prominent Atkins-inspired low carber out there these days - scrubbed the weekly weigh-in scroll from his blog and wrote this:

After the Low-Carb Cruise and hearing all the stories of the people in Sweden eating a low-carb, high-fat (LCHF) diet not for weight loss but their health, I've decided to refocus this menus blog by taking the spotlight off of my weight and back on the quality of the food I'm consuming. That's not to say I no longer care about my weight, but it's not the single obsession of why I eat the way I do. Sure, your weight can be an incredible marker for tracking your progress, but your blood sugars, cholesterol, and other such cardio-metabolic markers are much MORE important. 

As I'm tracking my low-carb meal plans, I will likely track my blood sugar levels more than I have been doing because I think that will be more revealing about what my diet is doing for my health.

If you've listened to any of Jimmy's new podcasts (Low Carb Conversations) the whole "health" angle is woven throughout.  I'm going to address some of these in future part(s) of this series.

Food Reward and Low Carb Substitutes

Over on his blog, Stephan Guyenet has been unveiling his theories on food reward, setpoint and weight regulation.   I'm not sure I'm really getting how the food reward itself - or lack thereof - re-sets one's adipostat, but that's neither here nor there.  

This is going to be a rather short post from me.  GRIN ;-)

Observations on long term low carb aficionados.  Many:

• Lose a little or no weight at all - remaining obese or overweight
• Lose significant weight but plateau out at a weight that is still obese or overweight 
• Struggle to maintain weight loss and regain despite adherence to the low carb WOE

Why Stephan Got Fat

Of course that's a play on the title of Gary Taubes' definitive treatise on obesity in America.

And, of course, the Stephan I'm referring to, Stephan Guyenet, is not only not fat, but rather lean near as I can tell.

But in his recent interview with Chris Kresser, Stephan discussed what he eats.  Stargazey summarized it in the comments:

Why We Get Fat ~ Fast Food?

I'm on the record with my belief that a goodly portion of those struggling with excess weight got that way by "passive overeating".  It's certainly how I got my fattest in my post-ED years.  

So I came across this study:  

Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis

Triglycerides: Atherosclerotic or SAD-context Biomarker?

Something that's been on my mind a lot over the past couple of years is the meaning of fasting triglycerides in the context of a low carbohydrate diet.  Many, myself included, tend to look at fasting triglycerides and HDL as more important biomarkers and these two both tend to improve rather greatly on a low carbohydrate diet.  But I've always wondered if the reduced triglycerides of LC really indicate a "reduced risk" compared to the generally higher fasting triglycerides of healthy people eating a higher carbohydrate diet.

I blogged recently about triglycerides increasing on a high carb/low fat diet.  Basically, the elevated VLDL in the high carbers was attributed to reduced clearance and not overproduction in the liver.  So I got to asking if it's the triglycerides themselves that are atherogenic or if they are merely indicative of an underlying pathology.

Paleo v. Neo ~ Some Thoughts

Some thoughts on the best human diet ...

 vs. 

Flashback! High Fat Paleo??

There's a little sea change going on out there folks.

More prominent bloggers than I raising a question that's been on my mind for a very long time.

Was our ancestral diet REALLY VLC and high fat? 

So I tip my hat today to Don Matesz of Primal Wisdom for asking a similar question:

Who Said Paleo Diet Had High Fat Percentages? Part 1

It is interesting to me that the LC triad of Westman, Volek and Phinney cite Eaton in The New Atkins.  It's how I found this paper if memory serves.  

Endogenous v. Exongenous Hormones

I'm going to be using insulin as my example in this post.  Endogenous insulin is the insulin produced in your body by your pancreas.  Exogenous insulin would be that derived from outside the body - e.g. insulin injections.  For the most part exogenous hormones are obtained through some "pharmaceutical" route.  In the case of insulin, subcutaneous injections.

Now I’m sure most of my readers are familiar with the picture below:

Science for Smart People

I think I may just blow a few minds here when I say, I highly recommend Tom Naughton's recent lecture from the Low Carb Cruise entitled "Science for Dummies Smart People".

I don't normally encourage getting one's science from non-scientists, but I can appreciate the value of learning this kind of thing from a layperson - and in humorous fashion I might add.  For a change, Tom gets this mostly if not entirely right.  Where I have some things to add, it's that Tom does not seem to take or understand his own advice at times.

Where did the fat in this blood come from? ~ An Ead-iotic Analysis

It was perhaps serendipity to have come upon the subject of recent post on the fatty acid sources of VLDL triglycerides while Dr. Eades was still fresh on my mind from his latest foray of peddling pseudoscience, and  having someone mention Diane Kress' Metabolism Miracle on Jimmy Moore's forum just a short while back.  This all reminded of a discussion on Jimmy's forum over his interview with Kress.  Those discussions with links to the podcasts are:   Part 1 , Part 2.

In that second part, member Vesna linked to "a fascinating post in which he [Eades] deconstructs recent ABC anti-fat news segment."  

That fascinating post was:  ABC’s big meal propaganda, the subject of which is the video I've embedded below:

The Scientific Method in the Low Carb Echo-Chamber

I don't know how many of my readers share this impression I have of the low carb online community on the whole, but here it is.  To me it seems this community has fallen victim to the same kind of group-think many have long decried, hanging out at sites where non-believers are turned away.  No differing opinions allowed in such echo chambers.  

The result of which is that we see the sort of repetition of catch phrases that would make a political party proud.  You know what I'm talking about ... when the various mouthpieces making the rounds of the Sunday shows, morning shows and various cable and talk radio shows all seem to have the same speech patterns.

And so it is now that low carb cookbook authors and comedians give speeches on how to critically evaluate scientific studies.  The former individual I'm speaking of is Dana Carpender.  Her speech on the recently concluded Low Carb Cruise (Jimmy Moore) was posted online:  Part 1, Part 2.  (Direct links:  Part 1, Part 2.)

Lost Content

Blogger was down for quite some time since sometime last night.  To get things back up they had to "temporarily" remove new posts from some time on 5/11 forward.  Well, as of this post, they have not reinstated said posts.  I'm going to wait a bit to decide if it's worthwhile to reconstruct my missing post - maybe it will show up - but there are also missing comments.  Where I can I'll C&P them when I get a chance.  Just wanted to let you all know this wasn't my doing.  

Where do triglycerides come from? Part I

Anyone who has spent any time perusing low carb sites is probably aware of the hallmark of carbohydrate restriction:  Lower fasting triglyceride levels, aka VLDL.   LC diets almost invariably outperform the alternatives in reducing fasting triglyceride levels.  Therefore the obvious conclusion is that carbohydrates cause triglyceride formation in the liver - and these are from de novo lipogenesis - aka converting excess carbs into fat.  With no attribution, Taubes postulates in GCBC that as much as 30% of carbohydrate in a meal is destined down this path.  

I've discussed this here before, and won't rehash it.  But lo and behold I was meandering about the net looking at at something triglyceride related and this study pops up:

Effects of a low-fat, high-carbohydrate diet on VLDL triglyceride assembly, production, and clearance 

A name amongst the authors caught my eye ... Marc Hellerstein.  He of DNL not a major pathway in humans fame, that I've blogged on previously.

The Myth of Starving Cells

On the heels of my last post discussing Tom Naughton's novel theory on obesity and blood glucose regulation, I'm reminded again of the whole "fatty acids are locked away in the fat cells" - what I'll call the Starving Cells  Myth - of obesity.  Dr. Eades is weighing in on his blog on Taubes' Why We Get Fat and reiterates once again the fallacy that is the locked away fat.  Here's how he puts it:

... A non-obese person eats, uses the energy from the food and stores the rest. During the time between meals and during sleep, the non-obese person draws on the stored fat to provide energy. When the fat cell mass decreases to a certain critical point, the body signals the brain that the fat cells need a refill, so the brain initiates the hunger response. The non-obese person eats, uses some energy for immediate needs, fills the fat cells with the rest, uses the stored energy as needed, and then the cycle repeats.

It doesn’t work that way in the obese. Obese people eat, use the energy required for immediate needs and store the rest. But–and this is the extremely important ‘but’– during the time between meals and during sleep, obese people can’t access their fat stores because their baseline insulin is too high. When they can’t get to their stored fat, the lack of access to energy sets in motion all the same biochemical signals in the obese person that get sent in the non-obese, who have depleted the energy storage in their fat cells. And these signals are converted by their brains into the drive to feed, i.e., intense hunger. They have to eat to provide for their immediate energy needs because, thanks to chronically elevated insulin levels, they can’t get into to their own stored fat, even though it’s there waiting in massive quantities.

Now this all sounds perfectly reasonable, which is probably why so many just accept this as truth coming from an expert and all.   

Q: What's worse than an education in Human Metabolism from a journalist?

A:  An education in Human Metabolism from a comedian.

Blogger stats are interesting things at times.  It's curious to see where people find this place from.  Following my Insulin Wars series, I was rather shocked to see the Tom Naughton, aka Fat Head, installment shoot up my most read posts list, where it remained for a very long time.  As that series went, that particular post was no big deal.   I had quite a lot of traffic coming from Tom's blog.  What this tells me is that a LOT of people are getting their information from a comedian!  This guy actually has a lecture DVD out now.

This isn't good folks!!

Starvation Diets?

You know what happens when someone discusses a study like Grey & Kipnis in low carb circles?  Almost invariably someone will refer to the 1500 cal/day diet given to three of the subjects as a "starvation diet".   This designation seems to trace to the Minnesota Starvation Experiment.  

The MSE was done in the mid-40's on men.  Men who, at that time, maintained on 3200 calorie mixed diet.  They took these men and cut their intake roughly in half to 1560 calories.  (Can you say Biggest Loser?).  But they did something else.  Their 1560 calories were composed of potatoes, rutabagas, turnips, bread and macaroni.  A very high carb and likely very low fat and protein diet.  And unless most of this was potatoes, not complete protein at that.  I'd imagine almost 6 months eating such a nutrient deficient diet would indeed be starvation for anyone.

Chris Masterjohn on Cherry Picking (and the Metabolic Advantage of Fructose)

... at least in rodents ;-)

Let Us Honor Ancel Keys, Our Patron, As We Cherry Pick Studies to Bash Fructose (Revised and Extended)

Hats off to you Chris!

The Metabolic Advantage of Fructose

Is fructose making us fat?  Apparently the answer is no if you get your fructose in the form of candy!

Thanks to MM for sending me this paper.

Candy consumption was not associated with body weight measures, risk factors for cardiovascular disease, or metabolic syndrome in US adults: NHANES 1999-2004 

For the purposes of this study, candies were defined as follows:

Sugar candy consists of sugar in crystalline form or semisolid (amorphous) forms with other ingredients including flavors and colors; examples include peppermint, lollipops, licorice, and gum drops. Chocolate candy is a mixture of processed cacao, cocoa butter, and sugar and often contains other ingredients, including milk, fruit, nuts, and caramels.

 This group analyzed 3 sets of NHANES data to look at candy consumption defined as:

Candy consumers were defined as those participants consuming any amounts of candy/confection except gum and were placed in 1of 3 overlapping consumption groups: (a) any candy (including chocolate candy and sugar candy), (b) chocolate candy only, and (c) sugar candy only

Aspirin for Insulin Resistance ~ Revisited

I've previously blogged on the effects of high doses of salicylates, aka aspirin, and insulin resistance.  In summary from that paper/post:

... high doses of salicylates reverse hyperglycemia, hyperinsulinemia, and dyslipidemia in obese rodents by sensitizing insulin signaling.

So I was poking around in my Downloads folder the other day and happened across this paper:


Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes  (I've cleaned up the excerpts from the citation #'s as I find them distracting)

Therapeutic diets for normal people?

Just some thinking out loud here ....

When one picks up a copy of The New Atkins they will probably be influenced by the forward written by Dr. Eric Kossoff of  Ketogenic Diet Center fame at Johns Hopkins.  Now my ebook software is not working with my copy of TNA at the moment (you can see some of this book in Google books), but I blogged previously on my observation that discussions on ketosis or the ketogenic diet are curiously absent from this updated version of Atkins.  

More recently, the low carb internet is abuzz with news that a ketogenic diet reversed nephropathy in mice.

Whole Foods

No ... I'm not going to weigh in on Whole Foods (the store) pushing a vegan agenda or anything like that.  I want to talk about the eating paradigm advocating "whole foods" - aka "real foods".  

I will absolutely not argue against any whole/real food diet.  I'll even go a step further and state that IMO, most such diets truly comprised of whole/real foods, no matter the type/source, are likely infinitely more healthy than the alternative.

No, CarbSane hasn't gone over to the dark side or lost her feeble mind (don't you just love it when former bunny-eared anonymous bloggers refer to themselves in the third person?) .  No.  I want to talk specifics and definitions here.

Old Hat

This Weeks' Citation Classic

Curious if anyone in my audience notices what I did when I found this.