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Old 02-01-2005, 11:06 PM   #1
Rene Renteria
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In the thread on Grains for Life, Brad mentioned reading an article that talked about the laws of thermodynamics as related to how we process and burn food for fuel. He made the important point that all dietary calories are not equal, meaning that diets of the same number of calories can lead to either weight loss, maintenance, or gain depending on the macronutrient balance. A couple of reviews I’ve seen are available on the Web. They examine the argument that low carb diets have a “metabolic advantage”. Basically, a calorie of carbohydrate consumed is not the same as a calorie of protein or fat consumed because the different metabolic pathways that these substances travel have different efficiencies. Also, intake of macronutrients (such as protein) can stimulate processes that themselves cost energy.

Here are links to the two reviews, which are from the same authors and have similar information, and a couple of snippets from each. The first is shorter and reviews some of the literature while the second takes a deeper look at metabolic processes for different macronutrients to examine why a calorie does not have to equal a calorie:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1528202 8
"A calorie is a calorie" violates the second law of thermodynamics
Richard D Feinman1 and Eugene J Fine
…We review here some aspects of thermodynamics that bear on weight loss and the effect of macronutrient composition. The focus is the so-called metabolic advantage in low-carbohydrate diets….

…If we assume a diet composition of CHO:fat: protein of 55:30:15, within the range of commonly recommended diets, the calculated effective yield is 1848 kcal. We now consider the effect of reducing carbohydrate progressively and substituting the calories removed equally between fat and protein. Figure 2 shows that the wasted calories due to thermogenesis increase as carbohydrate is reduced and reach 100 kcal at 21 % carbohydrate.


http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1558828 3
Thermodynamics of weight loss diets
Eugene J Fine1,2 and Richard D Feinman
…In this review, for pedagogic clarity, we reframe the theoretical discussion to directly link thermodynamic inefficiency to weight change. The problem in outline: Is metabolic advantage theoretically possible? If so, what biochemical mechanisms might plausibly explain it? Finally, what experimental evidence exists to determine whether it does or does not occur?


Someone also asked about what the brain uses for fuel (glucose vs. ketones) and in what proportion. The second paper above states this about the issue (here, “metabolic advantage” means to the diet, not necessarily to the body, which has to expend more energy to generate the glucose not coming in as carbohydrates!) This fits in with what I know about brain metabolism, that glucose predominates and is critical:

Gluconeogenesis-stimulated protein turnover in carbohydrate restriction
The following hypothesis is suggested from classic studies of starvation done in chronically fasted obese individuals [27,28]. The brain's metabolism requires 100 grams of glucose per day. In the early phase of starvation, glycogen stores are rapidly reduced, so the requirement for glucose, is met by gluconeogenesis. Approximately 15–20 grams are available from glycerol production due to lipolysis, but fatty acid oxidation generally cannot be used to produce glucose. Therefore, protein breakdown must supply the rest of substrate for conversion to glucose in the early phases of starvation. By 6 weeks of starvation, ketone bodies plus glycerol can replace 85% of the brain's metabolic needs, the remainder still arising from gluconeogenesis due to protein. It should be mentioned that, since the fundamental role of ketones is to spare protein, it might be expected that the reliance on protein would actually decrease with time, perhaps relating to the anecdotal observation of "hitting the wall" on weight loss diets.

Very low carbohydrate diets, in their early phases, also must supply substantial glucose to the brain from gluconeogenesis. For example, the early phase of the popular Atkins or Protein Power diet restricts dieters to about 20–30 grams of carbohydrate per day, leaving 60–65 grams to be made up from protein-originated gluconeogenesis. One hundred grams of an "average" protein can supply about 57 grams of glucose so 110 grams protein would be needed to provide 60–65 grams glucose. Increased gluconeogenesis has been directly confirmed using tracer studies on day 11 of a very low carbohydrate diet (approx 8 grams/day) [29]. If indeed, 110 grams of endogenous protein is broken down for gluconeogenesis and re-synthesized, the energy cost, at 4–5 kcal/gram could amount to as much as 400–600 kcal/day. This is a sizable metabolic advantage. Of course, the source of protein for gluconeogenesis may be dietary rather than endogenous. Whereas endogenous protein breakdown is likely to evoke energetically costly re-synthesis in an organism in homeostasis, dietary protein may conserve energy. The source of protein for the observed gluconeogenesis [29] remains an open question, but there is no a priori reason to exclude endogenous rather than dietary sources. This is therefore a hypothesis that would need to be tested. The extent to which the protein for gluconeogenesis is supplied by endogenous protein would explain very high-energy costs. It should be noted, however, that even if limited to breakdown of dietary protein sources, there would be some energy cost associated with gluconeogenesis.


Note that this last bit about “endogenous [i.e., muscle] rather than dietary [i.e., food] sources” is critical to most of us here at CrossFit. We don’t want to stimulate catabolism and lose any of that hard-earned muscle tissue!

I saw another article that may be of interest here, with all the talk about glycogen stores and using chocolate milk to refill them. Brain tissues, particularly glia, have glycogen. These are seen in electron micrographs of brain tissue and show up as dark granules that identify glial cells. People have typically thought that the brain doesn’t use glycogen as an energy source because the concentration is relatively low compared to, say, muscle and because the brain generally cannot function without glucose circulating in the blood. This paper describes some recent evidence that the brain may use this glycogen as an energy source, after all. It also at least has a summary figure of how glycogen is made in different tissues:

http://www.blackwell-synergy.com/links/doi/10.1111/j.1471-4159.2004.02421.x/full /
REVIEW
Brain glycogen re-awakened
Angus M. Brown *,+
Abstract

The mammalian brain contains glycogen, which is located predominantly in astrocytes, but its function is unclear. A principal role for brain glycogen as an energy reserve, analogous to its role in the periphery, had been universally dismissed based on its relatively low concentration, an assumption apparently reinforced by the limited duration that the brain can function in the absence of glucose. However, during insulin-induced hypoglycaemia, where brain glucose availability is limited, glycogen content falls first in areas with the highest metabolic rate, suggesting that glycogen provides fuel to support brain function during pathological hypoglycaemia. General anaesthesia results in elevated brain glycogen suggesting quiescent neurones allow glycogen accumulation, and as long ago as the 1950s it was shown that brain glycogen accumulates during sleep, is mobilized upon waking, and that sleep deprivation results in region-specific decreases in brain glycogen, implying a supportive functional role for brain glycogen in the conscious, awake brain. Interest in brain glycogen has recently been re-awakened by the first continuous in vivo measurements using NMR spectroscopy, by the general acceptance of metabolic coupling between glia and neurones involving intercellular transfer of energy substrate, and by studies supporting a prominent physiological role for brain glycogen as a provider of supplemental energy substrate during periods of increased tissue energy demand, when ambient normoglycaemic glucose is unable to meet immediate energy requirements.


Have fun,
Rene’
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Old 02-02-2005, 09:30 AM   #2
Ryan Atkins
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Great stuff, Rene. Keep it coming.

Ryan
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