Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity
Gastrointestinal Diseases Research Unit, Queen’s University, Kingston, Ontario, Canada
Diabetes Metab Syndr Obes. 2012; 5: 175–189.
Published online Jul 6, 2012. doi: 10.2147/DMSO.S33473
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.
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 dietary pattern with carbohydrates exclusively from cellular low-density sources may remove the root cause of a range of our most prevalent diseases. The potential savings in health-care costs should be borne in mind, and the hypothesis tested.
The increased storage life and convenience of some of our oldest agricultural products may come with a hitherto unrecognized metabolic cost. The foods eaten by hunter-gatherers, non-cereal horticulturalists, and those following a modern Paleolithic or “primal” diet are sharply delineated from modern foods by their lower carbohydrate densities.
Consumption of exclusively low-density carbohydrates is suggested to produce a less inflammatory GI microbiota, and may explain the apparent absence of overweight and metabolic disease in two of these groups, and the promising early data from the third.
This hypothesis may also explain:
(1) Why obesity incidence scales with refined food intake, but has such confusing correlatory patterns with macronutrients.
(2) Why calorie-controlled diets of Westernized foods require a perpetual fight with homeostatic correction mechanisms.
(3) The link between periodontal disease and systemic atherosclerotic disease and obesity.
(4) Why the benefits of a diet of fruit and vegetables have not been replicated by supplements of the constituent antioxidants, vitamins, minerals, and fiber alongside a Western diet.
(5) Why low-carbohydrate diets produce ad libitum weight loss, but low-fat diets do not.
(6) The relative resistance of European people to obesity and diabetes from Westernized diets.
We should not settle for the meager improvements attainable from the consensus dietary advice when it is already clear that so much more might be achieved. Our sights should be set high, to see how close we can move levels of industrialized metabolic health toward those enjoyed by non-Westernized populations. While many will resist making dietary changes of such magnitude, official advice must nonetheless point in the correct direction, allowing individuals to make informed decisions.
The social and financial burden of the epidemic of obesity and metabolic syndrome threatens the long-term viability of our health-care systems and perniciously undermines the other benefits of modern civilization, including redirection of scarce financial resources. If this dietary pattern is confirmed to work, practical policy solutions must be sought. Some grain cultivars may be found to produce less inflammation, sprouting techniques may be found to be of benefit, or grain production may be replaced with root-vegetable cultivation where practical.
Over time, the interplay between market forces, attainable agricultural yields, and the practicalities of food-distribution networks may allow shifting demand from a newly informed populace to reshape global agribusiness.A dietary pattern with carbohydrates exclusively from cellular low-density sources may remove the root cause of a range of our most prevalent diseases. The potential savings in health-care costs should be borne in mind, and the hypothesis tested.
Link to the original paper: Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity