Showing posts from May, 2013

The Paleolithic Diet According to S.Boyd Eaton and Melvin Konner - Version 2010

S. Boyd Eaton, who along with Melvin Konner is generally considered one of the "Founding Fathers of Paleo", published   Paleolithic Nutrition:  A Consideration of its Nature and Current Implications   ( request doc share  if link is broken)    in the New England Journal of Medicine in 1985.  In 1997, this duo (with SB Eaton III) published  Paleolithic nutrition revisited: A twelve-year retrospective on its nature and implications   ( request doc share  if link is broken) in the European Journal of Clinical Nutrition.   As time progressed, these authors would collaborate with various others, including two with which most in the paleo community are well familiar:  Loren Cordain and Staffan Lindeberg.  These four were among the authors of the 2002 article in Preventative Medicine entitled Evolutionary Health Promotion , and a followup in the same journal authored by Eaton, Cordain and Lindeberg entitled Evolutionary Health Promotion: A Consideration of Common Counterarguments

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

Why We Get (Sick) Fat (and Sick Livers) - Lessons from a Cafeteria Rat

Since we're talking about fructose and the liver of late, I thought I'd bump this post.  In this study groups of rats were fed one of four diets.  The "low fat" diet is better described as a high sucrose diet as 35% of the diet was sucrose.  This replaced 35% of the fat in the 45% "high fat" diet.  While the LF and HF rats gained a little more weight than the standard (also LF at 12%) chow rats, it is clear that the high fat has rather more negative metabolic effects.  I don't think the 35% sucrose diet was beneficial, rather the contrary, but that level of sucrose consumption, every single day for 10-15 weeks (which is quite a long time for a rat) is also hardly indicative of even SAD consumption. Original Posting:  3/8/11 It seems fairly generally accepted that whatever the cause or progression, the so-called Metabolic Syndrome, Syndrome X and Type 2 Diabetes are associated with a dysregulation of adipose tissue metabolism, and fat tissue that

Biomarkers: Context and Are They Causative Agents?

I received a comment recently on the Blood Sugar 140 series that prompted this post.  Actually, it prompted a post on the best predictor for T2 which will be forthcoming, but in fleshing out some background for that, I realized it was worth a post on its own. Below are links to previous post series I'm referring to: Blood Sugar 140: Where did the 140 mg/dL threshold come from? Blood Sugar 140: Context is Everything I - Diabetic vs. Non Blood Sugar 140: Context is Everything II: The OGTT Blood Sugar 140: Diabetic Neuropathy, Is it All About Hyperglycemia? "Cliff Notes" Blood Sugar 140:   There is a commonly repeated "fact" out there that blood glucose levels over 140 mg/dL lead to nerve damage (and organ damage) generally attributed to the process of glycation.  Also implied in this is that such damage is cumulative such that any excursion over 140 is inflicting a little damage along the way.  This traces back to the following page on Jenny Ruhl's

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 argum

Do Carbohydrates Turn into Fat?

From Discovering Nutrition Insel, Turner & Ross,  copyright 2010 20

Scientific Review of Lustig's Fat Chance

Scientific Review of Lustig's Fat Chance I don't often put blog posts up on someone else's works of this nature, but I'm going to make an exception because Mark Kern has done a thorough job of looking at some of the "science" Lustig puts forth in his book.  {I await the predictable dismissal ;-) }

Stick a Toothpick in It? Taubes' 4-pronged Carb/Insulin "Fork" Loses its Tines

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


There hasn't been much buzz about this year's LC Cruise, but a couple of days ago, a tweet from the presentation of one Dr. Dwight Lundell made a little splash on Twitter and FB.   The most toxic chemical in the human diet is GLUCOSE. -Dr. @ dwightlundell #sugarkills #LCCruise13 — Dietitian Cassie, RD (@dietitiancassie) May 7, 2013

Let's play What's Wrong with This Graphic


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

An American Justice System for Food ~ Part I Intro and Carbs in General

The cornerstone of the American justice system:  Innocent until proven guilty.  According to Wikipedia : sometimes referred to by the Latin expression Ei incumbit probatio qui dicit, non qui negat (the burden of proof lies with who declares, not who denies).  I like the first part of that Latin expression and suggest that what is truly needed in nutritional circles is to put the burden of proof on those making claims.  My point here is not a political one, it is not to argue the merits of my country's justice system or its implementation, or anything of the sort.  It is to put forth a suggestion -- that ALL who demonize foods be tasked with proving their charges.   I suggest this because it is darned near impossible to do the opposite especially in the face of baseless charges.   It is a bit of a stretch, but keep in mind that many of the compounds, such as water, can be toxic at some level of ingestion.  Furthermore, some of the chemical and/or physical properties of many

Surrogate Biomarkers for NEFA?

For reasons related largely to the difficulty (thus presumably expense) in measuring them, one fasting lipid that is not routinely assessed in lipid panels are the free fatty acids (FFA) aka the non-esterified fatty acids (NEFA -- Wholly irrelevant but I prefer the latter acronym as I like to sound them out in my head and knee-fah "sounds" better than eff eff ay to me ).  And yet, like glucose, it is NEFA that is elevated in diabetes.  Unlike glucose, however, NEFA is elevated in non-diabetic obese as well as elevated NEFA preceding frank hyperglycemia in the progression of Type 2.   One of insulin's primary roles vis a vis adipose tissue is to regulate the "basal" triglyceride/fatty acid cycle, acting on both adipocytes and the liver, to keep NEFA in a relatively small range of levels (amounting to roughly half to three-quarters of a gram in circulation under normal fasted circumstances).  

Revisiting Taubes' Four Facts from the Sixties

In Good Calories Bad Calories , Gary Taubes wrote the somewhat shockingly definitive summary paragraph below (I've separated out the numbered statements for clarity):   By the mid-1960s, four facts had been established beyond reasonable doubt: (1) carbohydrates are singularly responsible for prompting insulin secretion; (2) insulin is singularly responsible for inducing fat accumulation; (3) dietary carbohydrates are required for excess fat accumulation; and (4) both Type 2 diabetics and the obese have abnormally elevated levels of  circulating insulin and a “greatly exaggerated” insulin response to carbohydrates in the diet, ...  (Kindle Locations 8010-8014)