A Review of The Carbohydrate Hypothesis of Obesity: a Critical Examination (Stephan Guyenet, PhD)
This is a layman’s point of view of an article written by Stephan Guyenet, PhD, in his blog, Whole Health Choice, in August, 2011. The article is titled, The Carbohydrate Hypothesis of Obesity: a Critical Examination. It is a critique of the Carbohydrate Hypothesis of Obesity, proposed by Gary Taubes in his book, Good Calories, Bad Calories. The critique respectfully concluded that the Carbohydrate Hypothesis of Obesity was false. After examining the critique and its arguments, I’ve found that I can’t agree with it, at least based on the information and arguments provided. The following videos will serve to introduce Stephan Guyenet and Gary Taubes. They both made presentations at the Ancestral Health Symposium in August, 2011.
Dr. Guyenet’s critique may be correct. Perhaps I’ve missed something or misunderstood. It will nevertheless help me, and perhaps others, to know more about the arguments posed in the critique. This critique plays a part in the kind of activity we need in the field of nutrition and obesity to hopefully reach some kind of consensus on what causes obesity. I appreciate both Stephan Guyenet and Gary Taubes for their accomplishments and leadership in this area. They stand behind conflicting hypotheses so a public discourse to compare them is important. As described by Gary Taubes in a recent article on this topic, each piece of evidence being used to support each hypothesis needs to be “rubbed back and forth a few times” to consider all the variables and study constraints in light of whether it is consistent or inconsistent with either hypothesis.
For the following analysis, the evidence presented in the critique was assumed to be true at face value.
The original wording from Good Calories, Bad Calories for the Carbohydrate Hypothesis of Obesity is as follows (from page 359), in 3 parts:
1) Obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of energy intake and expenditure.
2) Insulin plays a primary role in this fattening process, and the compensatory behaviors of hunger and lethargy.
3) Carbohydrates, and particularly refined carbohydrates– and perhaps the fructose content as well, and thus perhaps the amount of sugars consumed– are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity.
The critique examined the hypothesis part by part:
|Hypothesis Part 1: Obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of energy intake and expenditure.
- The critique included a discussion of the value of Leptin as a key agent in fat metabolism but didn’t refute the hypothesis on that basis. The remainder of the discussion of Hypothesis Part 1 was actually found in Part II of the critique (as follows).
- 13 studies were referenced to establish that higher insulin levels increase satiety, reduce food intake, and increase energy expenditure. The rationale for why these results preclude the existence of a “regulatory defect in fat metabolism” was not presented.
- One study was provided that directly addressed fat metabolism. In that study, disabling insulin receptors in rodent brains resulted in increased fat mass. According to the critique this was “suggesting that its (insulin’s) normal function involves constraining fat mass”. This “suggestion”, however, was directly contradicted by a statement made earlier in Part II of the critique that “Insulin suppresses the release of fat from fat cells (via hormone-sensitive lipase), and increases the transport of fat into fat cells (via lipoprotein lipase)”.
- The critique claimed that Hypothesis Part 1 was false from the paragraph below. Although evidence was cited relative to the effects of insulin (from paragraph 1. above), the more complex topic of fat metabolism and distribution of energy was not addressed or supported with evidence.
Therefore, if insulin doesn’t increase energy intake (if anything, the combination of insulin and amylin that the pancreas releases in response to carbohydrate decreases it), and doesn’t decrease energy expenditure (if anything, it increases it), then how exactly is it supposed to cause energy accumulation in the body as fat? There is no energy fairy. Obese people are obese despite having higher fasting insulin, not because of it. The fact is, insulin spikes after meals temporarily decrease fat release from fat cells, but if you look at total 24 hour energy balance, insulin spikes do not cause fat accumulation. This is exactly how you would expect the system to work if it were designed to constructively handle a wide variety of macronutrient ratios, which it is. Just as cholesterol did not evolve to give us heart attacks, insulin did not evolve to make us fat. Hypothesis falsified (#1).
|Hypothesis Part 2: Insulin plays a primary role in this fattening process, and the compensatory behaviors of hunger and lethargy.
- The critique related the results of an unsuccessful search for a link between genetic problems with insulin (the pancreas) and resultant symptoms of obesity. Instead, genetic links were found between brain function and obesity. This can be considered an indication, but not a proof, that Insulin doesn’t play a primary role in the fattening process.
- The critique claimed, with insufficient evidence, that Hypothesis Part 2 was false from the sentence below. The underlined portion of the sentence was supported by clinical evidence, but the remainder was unsubstantiated.
“There is no defect in the ability of fat cells to release fat in obesity, the problem is that the fat that is released is not being oxidized (burned) at a rate that exceeds what is coming in from the diet, therefore it all ends up back in the fat tissue. Hypothesis falsified (#2).”
|Hypothesis Part 3: Carbohydrates, and particularly refined carbohydrates– and perhaps the fructose content as well, and thus perhaps the amount of sugars consumed– are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity.
- A study was referenced that contrasted the insulin response to different types of food using the Insulinogenic Index (II). II measures the area under the insulin response curve relative to the number of calories consumed. It is different than the Glycemic Index (GI) or Glycemic Load (GL) measurements we typically use to characterize diet foods. The GI and GL measurements calculate the area under the blood glucose response curve relative to the number of grams (GI) or portions (GL) consumed. Questions were raised about why some foods created a more significant II response than others. The critique concluded that, based on these questions, “post-meal insulin is not a compelling explanation for the potentially different effects of protein, unrefined carbohydrate, refined carbohydrate and sugar on body fatness”. While interesting, this conclusion didn’t preclude that carbohydrates, and particularly refined carbohydrates, fructose and sugar can be the prime suspects in the chronic elevation of insulin.
- The last two arguments (one on primitive cultures, and one on the historical growth of carbohydrate consumption over the last century) were limited by the author to a subset of the original hypothesis: “the hypothesis that carbohydrate consumption per se causes body fat accumulation”. These arguments, in other words, ignored the impact of refined carbohydrates, fructose, and sugar.
- The critique concluded that Hypothesis Part 3 was false without additional evidence.
This is strictly my opinion. I hope it will be helpful.
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