The Carb-Sane Asylum

Laugh if you get it! In comments on my last Thermodenyics post , I made the following statement: The β-oxidation + Krebs part is the "metabolism" of fatty acids resulting in production of some heat, some ATP, and a large number of so-called "reducing equivalents" that will produce much more ATP (cellular energy currency) in the Electron Transport Chain. You don't see mass escaping your body, but the carbons that were originally contained in the larger fatty acid molecules are exhaled as carbon dioxide. Atkins' original claim was that enough molecules escaped the Krebs cycle and were excreted before being fully metabolized for their caloric content. The vast majority of β-oxidation to burn fat for energy occurs in organs like the heart and skeletal muscle. Once a fatty acid is committed to the β-oxidation pathway they are oxidized completely down to carbon dioxide. In comments , Kindke quoted that last bolded line and inquired: I'm interes...

I don't follow Jack Kruse's antics much any more.  Every now and then, however, he comes up in a social media or email note.  He's still at it -- though there is no longer an answer at his practice phone number, so hopefully that means he's no longer actively performing neurosurgery.  From a Krusite on FB :   Humans are designed to eat an electron dense diet because they have a shortened gut and expanded brain that steepens their energy needs and restricts their sleep needs to 7.5- 8.5 hours. This implies that humans must have evolved around a diet high in electron density from food and their environment. It is hard to believe Jack has been talking this electron nonsense for going on two years now.  I suppose this is what happens in a community that fails to police itself when it comes to science ... but I digress. In any case, I have apparently missed the first however many incoherences Jack has created in his EMF series but since he's still on the ...

This notion of being a "sugar burner" vs. a "fat burner" -- with the latter being touted as preferable based on nothing I've seen in the scientific literature -- is getting really out of hand.  This is not a new idea, but it certainly seems to be being pushed more lately, particularly in the area of athletic performance.  There were a smattering of posts about the diets of Olympians about the net and I just have to shake my head at the one that goes something like "just imagine how much better fill in the blank  would do if (s)he didn't eat grains" or "ate LCHF" or "went paleo".  C'mon already ... Michael Phelps is a prime offender of all laws and gods nutritional, but will someone please remind me how many medals he's earned and records he's held/broken in his career?  Gawd forbid any of these elite athletes set a bad example by having their face put on a box of Wheaties!  I dunno ... it all seems so silly when Phel...

NEFA = Non-Esterified Fatty Acids aka Free Fatty Acids (FFA) (By the way, I've just always preferred the NEFA acronym because in my head it sounds out more nicely than "ef ef ay" -- and for whatever reason, I sound it out "knee fah", though a reader once wondered about "neh fay".  I don't know there's a correct pronunciation for acronyms like this!) On a hypothetical Metabolic SAT test NEFA are to lipids what glucose is to carbohydrates and amino acids are to proteins.  These are the forms of the three macronutrient classes that are absorbed/transported into and out of cells and circulation and the forms that enter into the energy-producing pathways.  By contrast, lipids are stored as triglycerides (aka triacyl glycerols, TAG), while carbs are stored in rather more limited quantities as glycogen, and there exists essentially no true storage depot for protein in excess of "tissue maintenance" needs.

The confusion with this whole mitochondria-based theory of obesity continues.  I'm not sure what's driving this other than a desperate clinging to the notion that one's obesity can not be the result of one's overeating and/or sedentary lifestyle, however they came about.  The more I read on this the more bizarre it all seems, but it comes down, once again, this notion that "fat burning" is related to fat accumulation or loss.  This is nonsense.  If your body requires 2000 cal/day to meet energy needs, it's pretty much all the same to your body where it gets that energy from.  And it will always be getting its energy from some mix of substrates:  glucose, fatty acids, and yes, amino acids and ketones.  Nobody disputes that energy is partitioned and substrates are oxidized in different manners largely at the direction of hormones ... insulin and leptin having well characterized roles in this regard.

A trial balloon, for those who do not claim English as their primary language, is a term relating to "floating an idea", usually in hypothetical context, to gauge reaction.  The notion being one of plausible deniability (I never really meant to say/do that).  This is the only explanation I can come up with for why Peter/Hyperlipid is going down this whole mitochondrial dysfunction path of his.  In his most recent post , he floats the following (I've numbered the steps): Mitochondrial dysfunction leads to cytosolic fatty acid derivative accumulation. This leads to chronic hyperinsulinaemia via insulin resistance. This leads to adipocyte distension. This leads to adipocyte insulin resistance. This leads to increased plasma FFA delivery at a given level of insulin. This leads to increased cytosolic FFA derivatives. This leads to mitochondrial ATP production being normalised. He concludes:  " The cost is increased insulin resistance. Oh, and the MECHANISM for impr...

I've been looking at respiratory quotient a bit after my post series on the Ranneries paper on metabolisms of the formerly obese ( Part I ,  Part II , Part III ) and found some interesting things.  One is this paper: Resting Metabolic Rate and Respiratory Quotient in Human Longevity In this study they compared three groups of women, I've included the table of various parameters below:

Below is a wonderfully simple depiction of the mitochondria that depicts one of the points I've been trying to raise above the current internet noise about mitochondrial dysfunction.  That being that when it comes to carb burning (glycolysis) the initial steps occur outside the mitos while fat burning (ß-oxidation) occurs within the mitos.  However both create Acetyl-CoA, and from that point on, metabolism and energy production is the same.  

Continuing the discussion from Part I Fat metabolism in formerly obese women Ranneries, et.al.  AJP-Endo, 1998. In this part I wish to address the respiratory quotient, RQ.  The RQ is a measure of the relative amounts of energy derived from glucose oxidation vs. fatty acid oxidation.   To recap the subjects of this study, when obese, the FO (formerly obese) subjects had body weights in excess of 120% normal weight.  They followed a conventional CRD to lose the weight and were weight stable for at least 2 months at 110% normal weight.  So weight losses were in excess of 10% bw and ranged from 15-20kg (33-44 lbs).    The FO & C groups were well matched as seen in  Table 1 .

I hadn't paid much attention to this whole mitochondria thing, mostly because it would require some sort of en masse genetic switcharooni for dysfunctional mitochondria to have spurned the epidemic in diobesetes* in this country (and around the world).   I had just happened across the paper briefly discussed in my last post looking for something else.  It is interesting what a simple PubMed search on the apparent head of the research group:  Dr. John Holloszy turns up.  Lots and lots about mitochondrial biogenesis.   One such paper is this fairly recent, 2008, review paper by Holloszy.   Skeletal muscle ‘‘mitochondrial deficiency’’ does not mediate insulin resistance

Lots of buzz over mitochondria of late.  So I thought I'd share this find: High-fat diets cause insulin resistance despite an increase in muscle mitochondria It has been hypothesized that insulin resistance is mediated by a deficiency of mitochondria in skeletal muscle. In keeping with this hypothesis, high-fat diets that cause insulin resistance have been reported to result in a decrease in muscle mitochondria.    In contrast, we found that feeding rats high-fat diets that cause muscle insulin resistance results in a concomitant gradual increase in muscle mitochondria.