Comparison With Ancestral Diets Suggests Dense Acellular Carbohydrates

Wagner83

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This looks interesting, but quite possibly not much in line with Peat's thoughts, at least not on some points. At least it should be a good gathering of references.

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity

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.

Trailer:

A nice table with ancestral diets in it, along with a brief discussion on this topic.

Grain-free whole-food diet: early results in Westerners
Whole grains are mooted to be healthier than refined grains,39 yet comparisons between grain consumption habits in industrialized societies indicate the effects of replacing refined grains with

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The source of the LPS is thought to be the GI tract, with ingestion of high-fat and high-carbohydrate Western-style meals found to produce postprandial “metabolic endotoxemia”: an increase in circulating LPS levels and other inflammatory changes.53

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Dietary fat also appears able to facilitate translocation of PAMPs from the gut lumen into the circulation by promoting a microbiota that reduces the expression of tight-junction proteins.55

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In the same study, germ-free mice were monocolonized with either a wild-type Escherichia coli or a mutant form with less immunogenic penta-acylated LPS. The less immunogenic bacterium produced lower LPS levels in the portal vein, and was associated with lower macrophage infiltration and inflammation of white adipose tissue, indicating a role for LPS in this effect. However, leptin and insulin levels were even higher in mice monocolonized with the mutant E. coli, suggesting non-LPS PAMPs play a considerable role in leptin and insulin resistance.

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Children from rural Burkina Faso have a considerably different microbiota to those from Europe, a difference thought to be primarily dietarily mediated. With a lifestyle comparable to early Neolithic subsistence farmers, these children carry a large representation of Bacteroidetes, with an unusual prevalence of species suggested to bear genes for hydrolysis of dietary fiber.76

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The rodent diet-induced obesity models discussed above predominantly make use of high-fat chows to produce their effects, which for a proportion of dietary fat of 72% (lard and corn oil) produced around a 2.7-fold increase in circulating LPS, while 40% fat chows produced 1.4-fold changes in LPS.79 It has also been shown that diets of differing fatty acids are able to differentially produce endotoxemia and complex patterns of inflammatory processes.80 Saturated fatty acids themselves are also able to activate the LPS receptor TLR4; this appears to require concentrations in the high micromolar range.8183
Etc..
 
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Wagner83

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benaoao

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It’s actually quite in line with RP. Grain free, lots of fruits, leaves could be juiced, and tubers - RP is fine with sweet potatoes.

I think it’s nothing new that refined sugar and fats cause a lot of potentially troublesome mechanisms and combining them is quite absurd from an evolutionary perspective. Some love their Mexican coke and butter and ice cream; my opinion is it should always be a minor component of anyone’s diet. Just because RP found a rationale for them doesn’t mean they can be freely consumed. Especially in a context of widely spread inflammation and insulin resistance
 

Dr. B

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It’s actually quite in line with RP. Grain free, lots of fruits, leaves could be juiced, and tubers - RP is fine with sweet potatoes.

I think it’s nothing new that refined sugar and fats cause a lot of potentially troublesome mechanisms and combining them is quite absurd from an evolutionary perspective. Some love their Mexican coke and butter and ice cream; my opinion is it should always be a minor component of anyone’s diet. Just because RP found a rationale for them doesn’t mean they can be freely consumed. Especially in a context of widely spread inflammation and insulin resistance
doesnt Peat prefer regular potatoes due to less beta carotene? are they otherwise similar in nutrients?
 

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