Thursday, April 22, 2010

Review of a Critique, Part 3

(continued) Mr. BS’s fourth test prediction – “Fat overfeeding, without additional carbohydrate, should not result in weight gain since insulin secretion is not increased” - is also invalid.  If one is consuming too much carbohydrate, and is also “fat overfeeding”, the CH would predict additional weight gain.  This is because, as previously discussed, excessive carbohydrate intake results in high levels of insulin secretion, and insulin signals storage of both blood sugar as fat, and of fatty acids in the blood as stored fat.  Insulin also shuts off the body’s ability to liberate stored fat (acts as a master hormone, limiting the effect of the 7 or so hormones that can release stored fat).  In other words, the results Mr. BS reports are consistent with the CH.  Further, synthesis of body fat requires glucose.  With low levels of glucose due to carbohydrate restriction (100g/day maximum), fat synthesis is impeded.  A more accurate test prediction derived from the CH would be as follows:  “Fat overfeeding in the absence of excessive carbohydrate intake will result in a lesser increase in body fat than an isocaloric combination of fat overfeeding and excessive carbohydrate intake.”  Higher levels of fatty acids in the blood from high fat intake, absent high insulin levels, do not require that the fatty acids be converted to stored body fat.  Should there be a need, there’s nothing to prevent fat liberation for oxidation.  GCBC cites studies which indicate that fatty acids are moving in and out of adipose tissue more or less constantly in a normal human.  If, however, carbohydrate intake is excessive, both glucose and fatty acids will be trapped in storage – in other words, in additional adipose tissue.

After his simulated but invalid duel with the CH through his initial four test predictions, Mr. BS posits additional objections he has to the CH.  First, he states that insulin has a hunger reducing effect on the brain, and uses this fact as a refutation that high insulin levels could result in hunger. In other words, he’s suggesting that this one influence – insulin’s appetite suppressive quality – is the main or most significant factor on human hunger.  This is a stunning over-simplification of human hunger, which depends on any number of factors, not all of which are clearly understood.  But as regards insulin, first and foremost, the function of insulin is to protect the brain and nervous system from toxic levels of glucose.  The appetite suppressive effect of insulin may be real, if all other things are equal, but I doubt there’s a one of us that has not noticed being hungry 2-3 hours after a high sugar and/or high carbohydrate meal.  This post-eating hunger cycle is generated after high glucose levels force an insulin response, which results in conversion of glucose to storage, resulting in low glucose levels.  What the insulin levels are at which points in the cycle is not known to me to any level of precision, but I believe that insulin is “consumed” as it does its job of getting glucose out of the blood and into the tissues.  The post eating hunger cycle - “excessive carbohydrate consumption drives high glucose drives insulin response resulting in low glucose and increased hunger” - is characteristic of folks who eat high carbohydrate diets, and most recognize the cycle when they hear it described. 

Mr. BS’s next criticism of the CH is:  “Another thing the carbohydrate hypothesis cannot explain is why there are many lean people who eat moderate to high carbohydrate diets (even people who do not have high daily expenditures).”  First off, the CH as described in GCBC does not assert that all individuals will fatten if they eat a high carbohydrate diet.  Therefore, in no way does it have to explain the phenomenon of the “high carbohydrate skinny dude” to be valid.   That said, even a rudimentary understanding of the topic would lead one to believe that in sensitivity to food intake, or carbohydrate intake, a human population will demonstrate a bell shaped distribution.  That is, some will be able to eat big piles of nearly anything and seemingly never fatten (in shape, these people are often what has been described as ectomorphs – tall, thin, shoulders often smaller than hips, and with ‘stringy’ muscles vice dense or puffy muscles).  Ectomorphs could be said to often be less insulin sensitive than average.  Others, the ones at the other end of the bell shaped curve for insulin sensitivity, are frequently endomorphs; large in the pelvis, soft in appearance as they tend to have more subcutaneous fat, and frequently, they seem to fatten on food that others would starve on.  To invalidate the CH, one would need to show that a test population failed to fatten when on a diet consisting of excess carbohydrate when compared to an isocaloric, low carbohydrate diet.  In other words, there is a very simple explanation for the skinny people we all know who can eat a ton but never get fat – they are relatively insensitive to insulin (not to be confused with pathological insulin resistance). 

Tomorrow we'll hit the last points of Mr. BS's critique.

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