Showing posts from June, 2010

So I'm reading some GCBC again ...

... and on p. 408 of my Sony ebook version (this will not coincide with the hard copy, but it is after the glycerol 3P section), Taubes writes: By the mid-1960's, 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. (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 ... Note the wording "facts".  Kinda hard to use the weasely "it's a hypothesis" defense for all the misinformation when one words things this way.  But let's consider these in order: (1) We know this isn't true, protein elicits an insulin response.  Furthermore fats have been shown to at least amplify insulin responses by, for example, stimu

Speaking of Taubes and the Pima ...

I feel honored that James Krieger stopped by my little corner of the LC blogosphere recently!  He is a fellow critic of Gary Taubes and posted links to blog posts in comments here.  As he updates this series I'll link to them.  Here was James' first installment:  Good Calories, Bad Calories: The Mythology of Obesity, or The Mythology of Gary Taubes? In reading this I was reminded of a call-out I wanted to make on Mr. Taubes regarding the Pima Indians.  If one goes to ~7.5 minutes into this presentation , you will see a picture of the Pimas.  EDIT 1/12/11:  The presentation appears to be broken.  I'm not sure if this is the same presentation, but it is available on You Tube (7 parts).   The slide in question appears around the 7 min mark.  I've posted the slide in question below. Now the picture quality is poor, but the abundant food atop those heads seems to resemble that of carbohyd

Triglycerides and Leptin Resistance

Been reading a lot about leptin and leptin resistance lately and the recent theory that triglycerides cause leptin resistance.  Leptin is secreted by fat cells essentially in correlation to fat mass and it is supposed to tell us to stop eating when we have accumulated too much fat.  The leptin resistance theory of obesity is that our brains don't receive the leptin signal so we keep eating and get fatter. Triglycerides Induce Leptin Resistance at the Blood-Brain Barrier Abstract Obesity is associated with leptin resistance as evidenced by hyperleptinemia. Resistance arises from impaired leptin transport across the blood-brain barrier (BBB), defects in leptin receptor signaling, and blockades in downstream neuronal circuitries. The mediator of this resistance is unknown. Here, we show that milk, for which fats are 98% triglycerides, immediately inhibited leptin transport as assessed with in vivo, in vitro, and in situ models of the BBB. Fat-free milk and intralipid, a source of

Excess carbs coverted to fat?

Thanks to reader LynMarie for prompting me to exhume this post that has been in the "draft" hopper for months!  I'll probably update with some comments at a later time, but wanted to get this article/link out there. This is a repeated mantra in the LC community ... if only it were true to any significant extent. We've heard it from Taubes, and Sisson, and -- the worst offender -- Nora Gedgaudas who goes so far as to claim that all fat in the body comes from glucose!  I even emailed her once about this and she stuck by this claim -- "I didn't make it up" No common energy currency: de novo lipogenesis as the road less traveled The model of the human macronutrient energy economy that emerges   from the study of McDevitt et al is consistent with previous   work ( 2, 3, 8, 9 ). In the hierarchy of fuels, dietary carbohydrate   appears to have a higher priority for oxidation than does dietary   fat; when both are present, carbohydrate is chosen. The 2 maj

Wheat & Sugar & Overeating

Wheat and sugar are oft-cited culprits in the obesity epidemic.  This isn't going to be a science-backed post -- although I've read a good deal about this.  This is more an observational post.  I'm was a child in the sixties and early 70's.  Raised in a "healthy household" we didn't eat Wonder bread and Sugar Frosted Flakes (back when you could use the word for what the frosting is made of!), but most of my classmates did.  I look back at class pics from elementary school and there's one or two "fat kids" --  by today's standards these kids aren't even all that large.  And yet, I think back on what most of my classmates had for snacks -- fruit rollups (yeah, not much fruit in those) and saltines were big items.  For lunch it was usually a sandwich of some sort on white bread (PB&jelly were as popular as cold cuts), milk or juice, and a Twinkie or cookies.  Does anyone remember Pixie stix and Lick'm'ade?  These were nothi

Fun with Statistics ~ Mean vs. Median using Fructose as an example

A bit of a ramble {grin} Lately, all the buzz is on fructose as being the root of all evil.  All of a sudden, all fructose from all sources is suspect for ills ranging from obesity to hang nails!  Many studies involve doses of 50g isolated at one time or up to 200g as part of the diet during the day.  Fructose consumption is often reported to average ~50g/day in Western diets.  And yet when I think what a "moderate" fructose consumption would involve, I just don't see lots of people around me eating like that. I believe that using the mean (average) as a measure of center for consumption is misleading and a better measure of center would be the median consumption. For those not fluent in statistics, the mean (average) and the median (physical midpoint separating the bottom 50% of a population from the top 50%) are different ways to represent the "center" of a data set.   In most applications, the mean is the number reported (usually along with the standard

High Protein LoBAG Diet for Type II Diabetes

When doing some protein research in the whole high protein v. high fat LC debate, I came across the following article: Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 These researchers call their diet LoBAG which stands for Low BioAvailable Glucose.   This particular study was on moderately overweight men (average weight in the high 2-teens) with untreated T2 diabetes.  For five weeks, the men followed one of two diets:   LoBAG = 30% Protein / 50% Fat / 20% Carb Control = 15% Protein / 30% Fat / 55% Carb The LoBAG diet was designed to provide enough carbs to prevent ketosis which was checked with ketostix to confirm the absence of this.  The study was intended to be consuming a weight stable diet, but both groups lost around 4 lbs during the course of the study.  Unfortunately the actual diets are not stated, but for men of this weight I would presume around 2500 to 3000 cal/day to maintain.  This would equate to 188 - 225g protein a

Protein for Energy

I've held off on posting this for a while because it's a screen shot and I have no idea whom to credit. But, since the metabolic pathways are common knowledge, I've decided there's no real harm done "publishing" any depiction of them on my li'l old blog. (If anyone recognizes the graphic, please notify me so I can extend credit) An enduring point of controversy exists in the LC community over higher protein intake vs. higher fat. My personal experience is that the former works for me, but there are plenty of folks doing well on high fat controlled protein approaches. One of the advocates of lower protein intake is Dr. Bernstein the diabetes specialist. Most that advocate his approach agree with his central premise that excess protein is converted to sugar or metabolized as such. While theoretically possible, I've been doing some "re-educating" of myself where protein metabolism, specifically what becomes of any excess is concerned.

Credibility of Authorities

A rant, if you will :) One need not delve very deeply into the LC blogosphere, websites and discussion forums to find an enormous contempt for "mainstream" nutritional advice, etc.  Several darlings championing LC alternatives have emerged and their writings are taken as indisputed "truth" spurring almost cult-like followings.  Anyone who dares to challenge these *authorities* risk the wrath of these followers. I didn't discover this LC world until almost 2 years into my most recent lifestyle change to low carb.  This was my third major try at this after discovering Atkins more than a decade ago.  I mostly just did the key components of Atkins from memory. My rhetorical question here is this.  How many times does an authority of the LC "Movement" need to be wrong for their credibility to be questioned?   I agree that FAR too often mainstream thought has been flat out wrong about one thing or another in terms of dietary advice, blood lipids and dis

Deleterious Effects of Elevated NEFA - I: Monocytes and Vascular Adhesion

Elevated Concentrations of Nonesterified Fatty Acids Increase Monocyte Expression of CD11b and Adhesion to Endothelial Cells First, a layperson friendly description of Monocytes : Monocytes are a type of leukocyte or white blood cell which play a role in immune system function. Depending on a patient's level of health, monocytes make up between one and three percent of the total white blood cells in the body. They can be counted as part of a blood test, and changes in their levels can indicate changes in a patient's health. As a general rule, a low monocyte count is a good sign, and a high count indicates that a problem is present... ... Levels of monocytes in the blood tend to rise when someone has an infection, because more of these cells are needed to fight it. Monocytes can also increase in response to stress and other factors. A high monocyte count may be referred to as monocytosis, and it is typically addressed by determining why the count is so high, and addressing th

Deleterious Effects of Elevated NEFA - Background

I though I would summarize the events/research leading up to my decision to group certain posts under a summary title. Without a doubt, the most disturbing aspect of my research into the effects of LC (VLC) diets has been the discovery of further elevated NEFA/FFA.  Most in the low carb community -- particularly diabetics -- focus almost singularly on blood glucose levels and insulin action for the maintenance of BG's.   To the extent that lipids are considered, there is a big focus on lower fasting triglyceride levels and increased HDL.  While not all LC'ers see an increase in LDL, many will see an increase -- sometimes dramatic -- in LDL.  Usually these are dismissed because VLC will result in more of the "fluffy" large particles that are considered less atherosclerotic.  One of my worries is that we don't have a huge (or even much of any) pool of data for modern day low carb eaters.  So while these trends seem promising, I think it is premature to get too exc

ASP action in vivo in humans

Coordinated release of acylation stimulating protein (ASP) and triacylglycerol clearance by human adipose tissue in vivo in the postprandial period This paper demonstrated ASP actions in vivo for humans in the postprandial (post-meal) period.  ASP levels were measured locally to the adipocytes  (venous output side) and systemically in the arterially "supply" side.  This was important because many who would dismiss the action of ASP look at systemic ASP levels and claim no connection.  However, this paper demonstrated otherwise: Abstract  The objective of this study was to determine whether Acylation Stimulating Protein (ASP) is generated in vivo by human adipose tissue during the postprandial period.  After a fat meal, samples from 12 subjects were obtained (up to 6 h) from an arterialized hand vein and an anterior abdominal wall vein that drains adipose tissue. Veno-arterial (V-A) gradients across the subcutaneous adipose tissue bed were calculated.  The data demonstrate

Fatty Acid Re-esterification rates

Alterations in adipocyte free fatty acid re-esterification associated with obese and weight reduced man This is a bit of a tough read, but the main conclusions are interesting. ABSTRACT Using a newly developed in vitro technique, the rate of re-esterification of lipolyzed free fatty acids (FFA) in small fragments of human subcutaneous adipose tissue was measured. When related to simultaneous glycerol release, this measure permits the calculation of the molar ratios of glycerol and FFA leaving the adipocyte. In weight-stable, never-obese control subjects the molar ratio of FFA:glycerol leaving the adipocytes is 1.4:1. During fasting, this ratio climbs to 2.7:1, close to the theoretical maximum of 3.0:1. Adipocytes from weight-stable obese subjects do not differ significantly from adipocytes of control in regard to this ratio. However, the adipocytes of weight-stable reduced-obese (RO) subjects display a significantly higher FFA:glycerol ratio than the adipocytes of either control or

ASP activates Glucose transport in Human Adipocytes

ASP stimulates glucose transport in cultured human adipocytes   (Full Text PDF) Introduction Acylation Stimulating Protein (ASP) is the most potent stimulant of triglyceride synthesis in human adipocytes yet described.1 The rate at which triglycerides are cleared from the plasma appears to be related not only to the functional activity of LPL but also to the capacity of peripheral tissues to store fatty acid as intracellular triglycerides. The ability of ASP to regulate this process may, therefore, be of physiological importance.2,3 As human adipocytes differentiate, they become competent to synthesize and secrete the three proteins necessary to generate ASP. These are the third component of complement (C3), factor B, and adipsin.4 The capacity to produce ASP appears relatively late in differentiation but before the sharp increase in the capacity of adipocytes to synthesize triglyceride.5 Subsequently, the mass of triglycerides within adipocytes, the rate at which they synthesize t

Dietary Fat v. Endogenous Fat for energy

It has become increasingly clear to me that regardless of the macronutrient composition of one's diet, dietary fat is only marginally "burnt" for energy on a given day.  The exception to this would be medium and shorter chain fatty acids that are not included in this discussion. There's a lot of misinformation out there spread by various LC gurus regarding fat burning and storage.  Without carbs, we can still store fat and we do!  The energy substrate for "fat burning" ( is the free fatty acid (NEFA/FFA).  Where do most of these come from? 1.  Lipolysis of "lipid droplets" of stored triglycerides within the cells, often called intramyocellular triglycerides (IMTG)  2.  Lipolysis of adipose tissue.   3.  Lipolysis of other circulating triglyceride-carrying lipoproteins   4.  NEFA/FFA's that "escape" the re-esterification process. Sources 2-4 are all circulating FFA's and my research all points to the conclusion that circulating N

Chylomicron-specific enhancement of ASP

Chylomicron-specific Enhancement of Acylation Stimulating Protein and Precursor Protein C3 Production in Differentiated Human Adipocytes ABSTRACT: Acylation stimulating protein (ASP) is a potent stimulator of adipocyte triacylglycerol storage. In vivo studies have shown that ASP production by adipocytes increases locally after a fat meal. Initial in vitro studies demonstrated increased production of ASP in the presence of chylomicrons (CHYLO). ... We hypothesize that TTR mediates the transfer of the active components from CHYLO to adipocytes, which then stimulates increased C3 and ASP production. Thus the CHYLO provides the physiologic trigger of the ASP pathway. I'm going to C&P copious parts of the abstract and discussion here because they provide a fairly readable and comprehensive discussion of ASP and it's role in fat storage.  To maintain focus on ASP, I'll merely paraphrase the part about Protein C3 as it being a precursor to ASP. ASP can actively stimulate t