Wed, Jul-04-18, 13:46
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Senior Member
Posts: 6,498
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Plan: VLC, mostly meat
Stats: 202/200/165
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
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Quote:
Thus, the carbohydrate-insulin model of obesity (CIM) proposes that a high-carbohydrate diet — including large amounts of refined starchy foods and sugar, as commonly consumed in the low-fat diet era — produces postprandial hyperinsulinemia, promotes deposition of calories in fat cells instead of oxidation in lean tissues, and thereby predisposes to weight gain through increased hunger, slowing metabolic rate, or both.
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So, carbs and insulin used to confirm CICO.
Quote:
Like the conventional model, the CIM obeys the First Law of Thermodynamics specifying conservation of energy. However, the CIM considers overeating a consequence of increasing adiposity, not the primary cause. That is, the causal pathway relating energy balance to fat storage flows opposite to the conventional direction (Figure, B). From this perspective, calorie restriction can be viewed as symptomatic treatment, destined to fail for most people in the modern food environment. Low-calorie, low-fat diets may actually exacerbate the underlying metabolic problem by further restricting energy available in the blood — triggering the starvation response comprised of rising hunger, falling metabolic rate, and elevated stress hormone levels.
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Euh, that's not what the first part of the paragraph said. If causality is indeed reversed, it should say instead: " predisposes to weight gain through fat deposition in fat cells, and in turn this promotes increased hunger and slower metabolic rate, or both".
That's all fine and dandy, but it's still incomplete. Fat gain and loss occurs not during a meal, but in-between meals. It may be caused by the meal content, but that's not when the subsequent gain and loss occurs. Here, we're dealing with fasting insulin. We're no longer dealing with insulin stimulus from the meal. Instead, we're dealing with insulin degradation at the liver. I can't use Ludwig's explanation for that, just doesn't cut it. To explain that, we need my paradigm ( link).
In short, ketones activate insulin receptors. Insulin inhibits ketogenesis. Too much insulin (from a high-carb meal) results in little or no ketones that would otherwise activate insulin receptors in the liver, where a sequence of steps occurs, ending with degradation of insulin. Failure to perform this last step allows insulin in the blood to remain higher than otherwise.
I skimmed the rest. Good start, but Ludwig is out of his element on some mechanistic and logic stuff.
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