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. 2012;5:175-89.
doi: 10.2147/DMSO.S33473. Epub 2012 Jul 6.

Comparison With Ancestral Diets Suggests Dense Acellular Carbohydrates Promote an Inflammatory Microbiota, and May Be the Primary Dietary Cause of Leptin Resistance and Obesity

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Comparison With Ancestral Diets Suggests Dense Acellular Carbohydrates Promote an Inflammatory Microbiota, and May Be the Primary Dietary Cause of Leptin Resistance and Obesity

Ian Spreadbury. Diabetes Metab Syndr Obes. .
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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.

Keywords: Paleolithic diet; carbohydrate density; metabolic syndrome; nutrition transition.

Figures

Figure 1
Figure 1
The carbohydrate densities of ancestral foods are distinctly lower than those of the Westernized diet. (A) The carbohydrate density (excluding fiber) of a broad selection of foods, in descending order of carbohydrate density (data from USDA). Modern foods (gray bars) are those that have undergone refinement or desiccation, or are derived from grains. “Ancestral” foods (white bars) are unprocessed whole-foods from the categories of meats, eggs, fish, nuts, fruits, tubers, and leafy vegetables. (B) Carbohydrate density and caloric density of modern and ancestral foods. Some ancestral foods have caloric densities as high as modern foods, notably meats and nuts. (C) Carbohydrate density and glycemic index of modern and ancestral foods. Once again, there is no distinction between the two categories of food, and no correlation between the density of a carbohydrate and the nature of the blood glucose response it will elicit.
Figure 2
Figure 2
Schematic of the hypothesis. Notes: The acellular dense carbohydrates of modern foods are proposed to produce an inflammatory microbiota from the mouth onwards, initially producing periodontal disease. The small bowel is exposed to lipopolysaccharide (LPS) and other pathogen-associated molecular patterns (PAMPs) from the oral microbiota, and proinflammatory modulation of its own small populations of bacteria by concentrated acellular carbohydrates. With systemic absorption enhanced by dietary fat, the inflammatory bacterial compounds induce leptin resistance and hyperphagia. The contents of the gray box represent the existing understanding of the effects of diet-induced obesity on energy homeostasis. Abbreviations: CCK, cholecystokinin; PPY, peptide YY; CART, cocaine and amphetamine related transcript; CB1, cannabinoid receptor type 1; MCH, melanin concentrating hormone.

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References

    1. Zimmet PZ, McCarty DJ, de Courten MP. The global epidemiology of non-insulin-dependent diabetes mellitus and the metabolic syndrome. J Diabetes Complications. 1997;11(2):60–68. - PubMed
    1. Chakravarthy MV, Booth FW. Eating, exercise, and “thrifty” genotypes: connecting the dots toward an evolutionary understanding of modern chronic diseases. J Appl Physiol. 2004;96(1):3–10. - PubMed
    1. Lindeberg S, Lundh B. Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava. J Intern Med. 1993;233(3):269–275. - PubMed
    1. Lindeberg S, Nilsson-Ehle P, Terent A, Vessby B, Schersten B. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study. J Intern Med. 1994;236(3):331–340. - PubMed
    1. Foster-Powell K, Holt SHA, Brand-Miller JC. International table of glycemic index and glycemic load values. Am J Clin Nutr. 2002;76(1):5–56. - PubMed

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