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Whole Health Source: The Carbohydrate Hypothesis of Obesity: a Critical Examination — 3 Comments

  1. I am finding myself moving toward a rather different position: tune the “machine” as best you can by whatever means works, and let those that want to approach it scientifically go do their thing and have their differences.

    I have experienced some very significant health improvements recently simply by starting to apply basic principles that I have known about for a year but had never gotten around to trying. I introduced fermented vegetables into my diet, along with fresh herbs. Couldn’t be easier.

    Why does it work? I don’t know. This is an area that is not all that well understood scientifically, but it has been understood culturally for millennia. I am all for the science, but I may not live long enough to see it sorted out.

  2. There are other limitations –
    in GCBC, gary taubes cites numerous examples of people on bland high carbohydrate semi starvation diets. Invariably the people on these diets remained ‘ravenously hungry’ throughout the experiment and developed severe physical/psychological symptoms (including self-mutilation and suicide threats).
    For example, in 1944 Ancel keys and his colleagues replicated benedict’s experiment on semi starvation diets. The subjects ate 1570 calories a day consisting mostly of whole wheat bread, potatoes, cereals, turnips and cabbage. This diet would hardly evoke the food-reward feedback loop that Stephan claims is the cause of overeating…so why were they still so ‘ravenously hungry’?

    By contrast Gary refers to various experiments were subjects are placed on comparably low calorie low carbohydrate diets and the results are contra positive – the subjects are satiated on the sparse caloric diet and exhibit no symptoms of malnutrition or hunger.
    For example, Ohlsen tested Pennington’s low carb low calorie diet a number of times and even though the subjects were restricted to eating 1400-1500 calories a day they reported feeling satisfied. Arguably eating meat and fatty foods are going to be more rewarding than eating potatoes and turnips, so again this contradicts Dr.Guyenet’s assertion that food-reward dominates hunger and calorie intake.

    This critique does not explain why some researchers have been able to produce weight loss in subjects on high calorie low carbohydrate diets, again gary taubes cites copious examples in his book.
    One such case was the DuPont experience published in the journal ‘industrial medicine’ authored by pennington in june 1949. Subjects ate a minimum of 2400 calories a day and averaged 3000 calories a day yet still lost between 9 and 54 pounds averaging 2 pounds a week.

    Dr.Guyenet does not explain why some groups and subcultures have become obese on low calorie semi-starvation diets in which the predominant food was simple sugars. For example, in Trinidad a team of nutritionists from the United States reported in 1966 that one third of the women were obese and that they achieved this condition eating fewer than 2000 calories a day.
    By 1973 in Jamaica 10% of adult men were obese and nearly two thirds of the women were obese in a society in which “malnutrition in infancy and early childhood remains one of the most important disorders contributing to childhood mortality”. Presumably, if the kids are starving, the adults are probably not eating many calories either.

    Since Dr.Guyenet maintains that weight gain and loss is determined solely by calories consumed vs. calories burnt one would expect that force feeding high calorie diets would produce marked and significant increases in adipose if combined with a sedentary lifestyle.
    IN GCBC, there are a number of studies that contradict this assumption, for example a study conducted in the late 1960s by endocrinologist Ethan Sims at the University of Vermont.
    In this study he used convicts at the Vermont state prison, who raised their food consumption to 4000 calories a day. They gained a few pounds but then their weight stabilized. So they ate 5000 calories a day, then 7000, then 10,000, while remaining sedentary.
    Of his 8 subjects that went 200 days on this regimen, two gained weight easily and six did not. One convict managed to gain less than 10 pounds after 30 weeks of this forced gluttony. One would expect that should all be obese if calories and not a metabolic defect was the critical element in obesity.

    Dr.Guyenet admits that chronic inflammation contributes to leptin resistance, which in turn contributes to obesity; but neglects to mention that carbohydrates and particularly refined sugars create reactive oxygen species and raise HBA1C, a measure of glycation – all of which contributes to chronic inflammation.

  3. This was an interesting critique that raised some difficult questions. Overall I did not find it very convincing because Dr.Guyenet failed to address some key points:
    Raising insulin only improves insulin sensitivity short term in the same way that opium improves opioid sensitivity short term by increasing the size and number of protein receptors for that chemical on the cell membrane. Long term use of opium will eventually cause the protein receptors to shrink and die off, leading to opioid resistance. That is why drug addicts continually need a higher dose to get the same ‘high’ that they used to get at a lower dose.
    The same thing happens with insulin – in the short term raising insulin improves insulin sensitivity. However long term exposure to chronically raised insulin levels eventually leads to insulin resistance. Here is the proof –

    Raising glucose, raises insulin, increases insulin resistance…
    Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study.
    Diabetologia (2004) 47:31–39
    “Conclusion/interpretation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in “normal” glucose tolerant individuals.”

    Barbara B. Kahn and Jeffrey S. Flier, Harvard Medical School
    The Journal of Clinical Investigation, August 2000 | Volume 106
    “Hyperinsulinemia per se can cause insulin resistance by downregulating insulin receptors and desensitizing postreceptor pathways, as was confirmed by overexpression of insulin in livers of otherwise normal transgenic mice. This transgene resulted in an age-related reduction in insulin receptor expression, glucose intolerance, and hyperlipidemia without any primary genetic defect in insulin action or secretion.”
    And again…
    Alternative Approach to Treating Diabetes Tested
    ScienceDaily (June 10, 2011)
    From; Deletion of Insulin-Degrading Enzyme Elicits Antipodal, Age-Dependent Effects on Glucose and Insulin Tolerance.
    Plos One June 2011 | Volume 6 | Issue 6
    “It’s an example of too much of a good thing [insulin] becoming bad for you…chronic hyperinsulinemia seemed to actually cause diabetes. As they aged, the mice appeared to adapt to the chronically high insulin levels, for example, by reducing the number of receptors for insulin in their tissues. These adaptations make the mice less sensitive to insulin, which is the exact cause of type 2 diabetes.”
    And again…
    Insulin: In need of some restraint? Salk Institute
    Proceedings of the National Academy of Sciences,March 07, 2007
    “the study reveals the “dark side” of high insulin production, the kind that results from over eating and obesity. “Insulin is very effective at lowering blood sugar, and promotes fat storage, preparing the animal for times when food may not be available,” he says. “But when the hormone [insulin] is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organ.”

    And of course insulin resistance goes hand in hand with leptin resistance. Gary taubes’ preoccupation with insulin was a tad myopic, and apparently he did not know how it interrelated with leptin resistance.
    But his conclusions were still probably sound; I see nothing in this critique to refute that.

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