(NaturalNews) It's well established that obesity is characterized by low-level chronic inflammation. Several theories as to how this inflammation occurs have been proposed, but dietary choices seem to be the most important factor involved. It's increasingly recognized that regular consumption of certain foods leads to diet-induced inflammation; which in turn sets the stage for insulin resistance, leptin resistance and other conditions that go hand in hand with overweight and obesity. These conditions make it very hard to lose weight and maintain healthy body weight.
Studies done on non-westernized populations show that hunter-gathereres have virtually no incidence of obesity, even when they have access to an abundance of food. Excellent health is seen regardless of macronutrient ratio and physical activity. Sugar, grains, refined vegetable oils and certain dairy products are not a part of these ancestral diets, while they are eaten in abundance in westernized societies. The available literature shows that humans are poorly adapted to these modern foods and that they promote obesity and inflammation through various mechanisms.
Food and inflammation
Fruits, vegetables and nuts have a cellular storage where they are able to store a maximum density of around 23 percent non-fibrous carbohydrate by mass. These living cells are breached in our digestive system and energy becomes available. Flour and sugar don't have these living cells, and they have a higher carbohydrate density than anything we have consumed on a regular basis during our evolution.
It's already known that obese and lean individuals have different gut flora composition, and Ian Spreadbudy at the Gastrointestinal Diseases Research Unit, suggests that high-carbohydrate dense foods specifically increase the quantity of LPS containing bacteria in the gastrointestinal tract. LPS, Lipopolysaccharide, is an endotoxin which is strongly linked to diet-induced inflammation.
When an inflammatory microbiota is in place, continued consumption of westernized foods increase the absorption of inflammatory molecules into circulation. It's a viscious cycle where a poor diet helps to preserve the inflammatory microbiota, and the microbiota increases our satiety for unhealthy foods.
Some individuals will be more prone to the effects of a poor diet than others. In some regions of the world, cereal grains have been a part of the diet for thousands of years and certain adaptive mechanisms have gotten a chance to evolve.
Low-carbohydrate diets are very effective in promoting weight loss. The reduced carbohydrate consumption in itself and lower insulin levels are often considered the most important factors involved in weight regulation. Based on knowledge about inflammation and obesity, it's likely that the limited consumption of acellular carbohydrates and proinflammatory anti-nutrients and proteins, also are very important in reducing inflammation and promoting weight loss on these diets.
Choosing nuts, fruits and vegetables as carbohydrate sources on a low-carb diet is important when trying to lose weight on a low-carbohydrate diet, even 20-100 grams of carbohydrates from sources like flours and sugar can help maintain an unhealthy gut flora, and the elevated fat intake can then further increase the circulation of LPS and other PAMPS, pathogen-associated molecular patterns. Not paying attention to carbohydrate sources on a low carbohydrate diet is consistent with failure.
Dietary choices are vital
Avoiding processed foods, high-density carbohydrates and other modern food staples will reduce inflammation and promote weight loss.
Reduced carbohydrate consumption is beneficial when trying to improve insulin resistance, leptin resistance etc. Restoring these functions should allow for an increased consumption of fruits, berries, root tubers and other vegetables while still maintaining good health.
Sources for this article include
Spreadbury I., Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Dovepress Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy July 2012, Pages 175 - 189
Lumeng CN, Saltiel AR. Inflammatory links between obesity and metabolic disease. J Clin Invest. 2011;121(6):2111-2117.
Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol. 2011;29:415-45.
Lee YH, Pratley RE. The evolving role of inflammation in obesity and the metabolic syndrome. Curr Diab Rep. 2005 Feb;5(1):70-5.
Herder C, Schneitler S, Rathmann W,. Low-grade inflammation, obesity, and insulin resistance in adolescents. J Clin Endocrinol Metab. 2007 Dec;92(12):4569-74. Epub 2007 Oct 2.
Bastard JP, Maachi M, Lagathu C. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw. 2006 Mar;17(1):4-12.
Cordain L. Cereal Grains: Humanity's Double-Edged Sword World Rev Nutr Diet. 1999;84:19-73.
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