The Carb-Sane Asylum

Some folks have been having a bit of a go at me over at Peter/Hyperlipid's blog.  I guess it all started by Peter taking some sort of offense to my post on his Potatoes and weight loss  post entitled Insulin Caused Cerebral Stress .  My intent with my post was not to mock Peter.  It was to point out how so inconsistent with observations the carb/insulin hypothesis is, so as to elicit elaborate explanations such as the scenario Peter described to explain a simple phenomenon:  Voight lost weight eating potatoes by estimating his energy needs and eating a controlled amount of predominantly potato-derived calories.   Peter, himself, started that post discussing the time/pages he had spent developing his theory.  I don't question/contest that what he says regarding insulin, sensitivity, etc. may actually be true.  I do believe, however, it is irrelevant.  I say that because I just do not see consistent evidence to support his assertion that: The ultimate determinant of weight

Dietary Animal and Plant Protein and Human Bone Health: A Whole Foods Approach According to a reliable source, I should be very concerned about the following table: Because: Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus.

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.

I received the following email a couple of days ago: I have spent about half an hour on your blog trying to find some kind of specific entries that explain why you, per your headline, don't buy what most of the low-carb community says about why it works, but you live it anyway. Do you have a post or two that sort of sums it up?  Because I just got lost and it seemed that in order to understand what you were talking about I would have to commit to starting at the beginning and read everything, including all the links - AND I'd have to have the ability to understand it all, which I do not. So... could you give me a hand in getting a grounding in how you seem to be pretty hostile to a whole lot of low-carb stuff while living low carb. Much obliged for your help. I've come to realize that I don't have such a post or two to point to, so I thank this reader (I'll let him/her ID themselves if they so desire) for bringing this to my attention.

"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.

I just have to comment on this because this stupid Chunky soup commercial was just on the tube.  "What can you do with plain white rice?  When you pour Chunky Sirloin Burger soup over it, you can do dinner".  Complete with slender woman enjoying a dish that doesn't even look appetizing to me!

I've decided to start yet another blog just for the purposes those "bookmarking" posts I do from time to time.  Links to various journal articles I come across in my travels about the web that I haven't yet gotten around to blog on.  I doubt I'll get to blogging about even 1/10th of the links I'll probably put there, and some of the stuff is not necessarily "up my alley" but may be of interest to some of you.  I don't have comments on in that blog.  If you see something that peaks your interest and would like me to blog on, drop me a line through my profile.  I can't guarantee that I will be able to honor the request, but I'm always open to discussing what interests YOU. The blog has been "live" for a while, and if Blogger would cooperate (export/import is not working properly), I plan to migrate all such posts from here to there.   CarbSane's Library

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:  DO = diet only DA = diet + aerobic exercise DR = diet + resistance exercise

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.

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):

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?)

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

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:

Relationship Between Body Fat Mass and Free Fatty Acid Kinetics in Men and Women    {Hat tip MM, thanks!} Alterations in free fatty acid (FFA) metabolism are involved in the pathogenesis of insulin resistance, diabetes, dyslipidemia, and cardiovascular disease ( 1 , 2 ). Excessive plasma FFA availability impairs the ability of insulin to suppress hepatic glucose production and to increase skeletal muscle glucose disposal ( 1 , 3 ). Plasma FFAs are also the primary source of fatty acids for hepatic very low-density lipoprotein–triglyceride (TG) production ( 4 , 5 , 6 , 7 ), and plasma very low-density lipoprotein–TG concentration is an important risk factor for cardiovascular disease ( 8 , 9 ). In addition, the accumulation of intracellular fatty acid metabolites stimulates the production of inflammatory proteins ( 10 ), which can also contribute to insulin resistance and atherosclerosis ( 1 ). Therefore, understanding the factors that affect FFA metabolism has important physiological

A Sustained Increase in Plasma Free Fatty Acids Impairs Insulin Secretion in Nondiabetic Subjects Genetically Predisposed to Develop Type 2 Diabetes Type 2 diabetes is characterized by defects in both insulin secretion and insulin action (1). Subtle defects in β-cell function and insulin resistance precede the development of hyperglycemia in individuals at high risk of developing type 2 diabetes

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

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