The abstract of an interesting paper follows. The authors are trying to explain something I think needs no explanation - why do low carb diets "spontaneously" reduce weight in ways other macronutrient combinations do not?
Answer: we shouldn't be eating so many carbohydrates, because they raise glucose levels to toxic thresholds and therefore demand an insulin bolus as metabolic self defense. IOW - high carb intake creates repeated metabolic emergency of excess glucose. The chronically excess glucose makes a metabolic mess ("metabolic derrangement").
They would answer by saying that some populations eat high percentages of carbohydrates and do not get fat. That is true, but there also practices that those populations maintained which reduced the intensity of the carbohydrate bolus - fermentation being one. Further, the referenced populations also tended to live in isolated locations for many generations, and did not have access to fructose or other sugars in large quantities.
The author's answer:
The present hypothesis suggests that in parallel with the bacterial effects of sugars on dental and periodontal health, acellular flours, sugars, and processed foods produce an inflammatory microbiota via the upper gastrointestinal tract, with fat able to effect a "double hit" by increasing systemic absorption of lipopolysaccharide. This model is consistent with a broad spectrum of reported dietary phenomena.
Which is to say, they think the excessively dense carbs create bacteria which dis-regulate the leptin based homeostasis system, causing over-consumption.
The point of science is to identify possible cause effect relationships, and then attempt to disprove them. The most interesting question is - how could one design an experiment to isolate causality between this hypothesis and the insulin hypothesis?
Abstract: A novel hypothesis of obesity is suggested by consideration of diet-related inflammation and evolutionary medicine. The obese homeostatically guard their elevated weight. In rodent models of high-fat diet-induced obesity, leptin resistance is seen initially at vagal afferents, blunting the actions of satiety mediators, then centrally, with gastrointestinal bacterial-triggered SOCS3 signaling implicated. In humans, dietary fat and fructose elevate systemic lipopolysaccharide, while dietary glucose also strongly activates SOCS3 signaling. Crucially however, in humans, low-carbohydrate diets spontaneously decrease weight in a way that low-fat diets do not. Furthermore, nutrition transition patterns and the health of those still eating diverse ancestral diets with abundant food suggest that neither glycemic index, altered fat, nor carbohydrate intake can be intrinsic causes of obesity, and that human energy homeostasis functions well without Westernized foods containing flours, sugar, and refined fats. Due to being made up of cells, virtually all "ancestral foods" have markedly lower carbohydrate densities than flour- and sugar-containing foods, a property quite independent of glycemic index. Thus the "forgotten organ" of the gastrointestinal microbiota is a prime candidate to be influenced by evolutionarily unprecedented postprandial luminal carbohydrate concentrations. The present hypothesis suggests that in parallel with the bacterial effects of sugars on dental and periodontal health, acellular flours, sugars, and processed foods produce an inflammatory microbiota via the upper gastrointestinal tract, with fat able to effect a "double hit" by increasing systemic absorption of lipopolysaccharide. This model is consistent with a broad spectrum of reported dietary phenomena. A diet of grain-free whole foods with carbohydrate from cellular tubers, leaves, and fruits may produce a gastrointestinal microbiota consistent with our evolutionary condition, potentially explaining the exceptional macronutrient-independent metabolic health of non-Westernized populations, and the apparent efficacy of the modern "Paleolithic" diet on satiety and metabolism.http://www.dovepress.com/comparison-with-ancestral-diets-suggests-dense-acellular-carbohydrates-peer-reviewed-article-DMSO
Answer: we shouldn't be eating so many carbohydrates, because they raise glucose levels to toxic thresholds and therefore demand an insulin bolus as metabolic self defense. IOW - high carb intake creates repeated metabolic emergency of excess glucose. The chronically excess glucose makes a metabolic mess ("metabolic derrangement").
They would answer by saying that some populations eat high percentages of carbohydrates and do not get fat. That is true, but there also practices that those populations maintained which reduced the intensity of the carbohydrate bolus - fermentation being one. Further, the referenced populations also tended to live in isolated locations for many generations, and did not have access to fructose or other sugars in large quantities.
The author's answer:
The present hypothesis suggests that in parallel with the bacterial effects of sugars on dental and periodontal health, acellular flours, sugars, and processed foods produce an inflammatory microbiota via the upper gastrointestinal tract, with fat able to effect a "double hit" by increasing systemic absorption of lipopolysaccharide. This model is consistent with a broad spectrum of reported dietary phenomena.
Which is to say, they think the excessively dense carbs create bacteria which dis-regulate the leptin based homeostasis system, causing over-consumption.
The point of science is to identify possible cause effect relationships, and then attempt to disprove them. The most interesting question is - how could one design an experiment to isolate causality between this hypothesis and the insulin hypothesis?
Abstract: A novel hypothesis of obesity is suggested by consideration of diet-related inflammation and evolutionary medicine. The obese homeostatically guard their elevated weight. In rodent models of high-fat diet-induced obesity, leptin resistance is seen initially at vagal afferents, blunting the actions of satiety mediators, then centrally, with gastrointestinal bacterial-triggered SOCS3 signaling implicated. In humans, dietary fat and fructose elevate systemic lipopolysaccharide, while dietary glucose also strongly activates SOCS3 signaling. Crucially however, in humans, low-carbohydrate diets spontaneously decrease weight in a way that low-fat diets do not. Furthermore, nutrition transition patterns and the health of those still eating diverse ancestral diets with abundant food suggest that neither glycemic index, altered fat, nor carbohydrate intake can be intrinsic causes of obesity, and that human energy homeostasis functions well without Westernized foods containing flours, sugar, and refined fats. Due to being made up of cells, virtually all "ancestral foods" have markedly lower carbohydrate densities than flour- and sugar-containing foods, a property quite independent of glycemic index. Thus the "forgotten organ" of the gastrointestinal microbiota is a prime candidate to be influenced by evolutionarily unprecedented postprandial luminal carbohydrate concentrations. The present hypothesis suggests that in parallel with the bacterial effects of sugars on dental and periodontal health, acellular flours, sugars, and processed foods produce an inflammatory microbiota via the upper gastrointestinal tract, with fat able to effect a "double hit" by increasing systemic absorption of lipopolysaccharide. This model is consistent with a broad spectrum of reported dietary phenomena. A diet of grain-free whole foods with carbohydrate from cellular tubers, leaves, and fruits may produce a gastrointestinal microbiota consistent with our evolutionary condition, potentially explaining the exceptional macronutrient-independent metabolic health of non-Westernized populations, and the apparent efficacy of the modern "Paleolithic" diet on satiety and metabolism.http://www.dovepress.com/comparison-with-ancestral-diets-suggests-dense-acellular-carbohydrates-peer-reviewed-article-DMSO
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