The Carb-Sane Asylum

From nutritiondata.com  (using 100g) for avocado oil: Summary: ~71% MUFA, Predominantly oleic acid (>95%) ~12% Saturated Fat, Predominantly palmitic acid (almost 95%) ~14% PUFA  Omega 6:Omega 3 ratio = 13:1 Yes, as sometimes happens with the data from this website, the numbers don't add up exactly.

This is an open "question post" to my readers, many of whom I'm aware are followers of Paleo-derived WOE's.   I'm particularly addressing those that advocate limiting protein and eating a very high fat  (60-80%) very low carb (close to zero) diet. What research am I missing that counters the work of Eaton?  Links to his works that I've blogged on HERE and HERE .  The first work was even referenced in The New Atkins to indicate that a high fat diet is what we evolved to eat.   Seems Eaton mostly points to a diet a little higher in carbs (~40%) and protein (~35%) and much lower in fat (~25% is the highest estimate) than most of the paleo/primal plans I've seen.  I don't see much reason to question this work.   Where does the very high fat come from?  What am I missing?  

Note:  This version slightly differs (only at the end beginning with italics) from my original post so I "bumped" the publish date and noted where I made a few changes. So Jimmy Moore recently posted an interview with Gary Taube$:  Podcast HERE I have much more to say about this interview, Taubes' most recent lecture and his upcoming book, but that will have to wait for another day. What I am bothered by is Taubes continued trashing of the scientific community while basically admitting the same for himself (though not realizing it). I would agree with Taubes that one of the problems with scientific research in general these days is the funding process/stream.  Been there, done that.  If you're a nobody with big ideas, good luck.  If you're a big name trying to get another MS or PhD thesis on some minor topic, it shouldn't be a problem.  There's ALWAYS a lag between funding, research and publication -- several years is more the norm than the excepti...

I just can't lose weight no matter what I try.  I went on WW and ate 1000 cal/day and didn't lose weight.  Or even, I've cut out all carbs, dairy, gluten, omega 6's, etc. from my diet and I still can't lose weight.   How many times have we heard statements like these?   Can they be true?  Are we destined to be fat?  It seems to me that any number of overweight and obese folks have uttered something like this at one point or another and/or flirted with the notion that they are just destined to be so for the rest of their lives.  These people seem to be convinced that they have "messed up" or "broken" metabolisms that cannot be fixed.   Is that true?  As regards obesity and metabolism, the only thing that can't be reversed is a certain point in the progression of T2 diabetes -- that being beta-cell damage.  (The popular belief that this occurs because we exhaust or wear out our beta cells with excessive insulin requirements is probably no...

Influence of human obesity on the metabolic fate of dietary long- and medium-chain triacylglycerols ABSTRACT The metabolic fate of an oral long-chain-triacylglycerol (LCT) load and of a mixed oral LCT and mediumchain-triacylglycerol (MCT) load was followed for 6 h in eight control and eight obese subjects with normal postabsorptive triacylglycerol concentrations. Labeled triacylglycerol and indirect calorimetry were used. Results showed that LCTs were less oxidized in obese than in control subjects (3.2 ± 0.5 compared with 6.0 ± 0.4 g, P < 0.01). Moreover, the amount of LCT oxidized was negatively correlated with fat mass (r = 20.77, P < 0.01).   Appearance in plasma of dietary triacyglycerol-derived long-chain fatty acids was blunted in obese subjects and it was negatively related to fat mass (r = 20.84, P < 0.01) and positively to LCT oxidation (r = 0.70, P < 0.01). On the contrary, MCT oxidation was ...

Another one of those mostly bookmark posts with no commentary Metabolic Fate of Chylomicron Phospholipids and Apoproteins in the Rat The researchers injected radiolabeled chylomicrons into rats to determine the fate of the components.  The results: Catabolism of chylomicrons is associated with a rapid transfer of phospholipid, apoA-I, and possibly apoA-IV into HDL. Chylomicron phospholipid appears to give rise to vesicles which are probably incorporated into preexisting HDL. Chylomicron surface components may be an important source of plasma HDL.

So let me start by saying that I've gleaned a lot of useful information over at Dr. Davis' Heart Scan Blog .  But one thing I've noticed is that he rarely responds to comments left at his site.  Now, obviously, he's under no obligation to do so, but when the comments are corrective in nature, not doing so leaves the impression that he didn't even bother to read the comments and/or take them under advisement. The first time I noticed this was in this post .   Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins ( chylomicrons, chylomicron remnants , VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.  I'll leave the rest of that alone and deal with just the ...

This post will seem out of context, but I wanted to post some definitions to be able to link to in the future for when some of these terms are used incorrectly.  (Note, let's ignore for simplicity diacylglycerides etc.) Lipolysis:  This is the breakdown of a TAG/triglyceride, three fatty acids attached to a glycerol backbone -- into the component parts, e.g. glycerol + free fatty acids.  Lipolysis is often referred to in the context of mobilizing stored fats, but is also involved in the digestion of dietary fats. Free Fatty Acids / Non-Esterified Fatty Acids (FFA/NEFA) :  Usually used to refer to the long chain fatty acids (LCFA) consisting of a carbon-hydrogen "chain" with a carboxyl (COOH) terminal end (sometimes referred to as the "head") .   FFA's can pass through cell membranes by facilitated diffusion (often get some "help" and move from areas of high concentration to low concentration).  FFA's are also the form of lipids that are fed...

I would like to give a shout out to Colby Vorland over at Nutritional Blogma for posting about this here: The Complex Lipidome Quantified Lipidome = a play on words presumably derived from genome to describe the spectrum of lipids in human circulation. Please do go visit Colby and share with him your comments.  I will, however, share two direct links with you here: The full text article:   Lipidomics reveals a remarkable diversity of lipids in human plasma The research consortium that generated the article:   Lipid MAPS No doubt I'll be spending some time at the Lipidomics Gateway in the near future!

I thought I would post the following graphic from the Shai Study  that compared Low Fat, Low Carb and Mediterranean diets over 2 years.  Just to refresh regarding weight loss, when one compares LC to MDTN, at around 1 year the average weight loss was comparable and essentially the same at the 2 year mark.  Therefore the changes in diabetic markers are (at least on average) independent of weight loss.  As a limitation, although there were roughly 100 participants in each group, only 11-13 of them were T2 diabetics, so the sample size here is quite small.  Also, to refresh, the LC group reduced carb intake by around 125g and caloric intake by ~550 cal on average while the MDTN group's intakes were reduced by around 45-50g and 350 cal respectively. The legend doesn't give stats for the non-diabetics, but there was no difference between the three diets for FBG, there does not appear to be much difference for HOMA-IR (measure of insulin resistance), but a fasting...

Reader Ryan emailed me this link a while back and I've been remiss in getting around to it.  Better late than never!  Thanks for the link Ryan! Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans Mitochondrial dysfunction and oxidative stress have been implicated in the disease process, but the underlying mechanisms are still unknown. Here we show that in skeletal muscle of both rodents and humans, a diet high in fat increases the H 2 O 2 -emitting potential of mitochondria, shifts the cellular redox environment to a more oxidized state, and decreases the redox-buffering capacity in the absence of any change in mitochondrial respiratory function. Furthermore, we show that attenuating mitochondrial H 2 O 2  emission, either by treating rats with a mitochondrial-targeted antioxidant or by genetically engineering the overexpression of catalase in mitochondria of muscle in mice, completely preserves i...