A new study shows that diet can activate an inflammatory response that influences the development of obesity related disorders.
This relationship could be the key link between high saturated fat intake — a recognized risk factor for obesity-related disorders — and the development of diseases like type II diabetes and atherosclerosis.
Researchers also discovered that ingesting fats similar to those in a Mediterranean-type diet, featuring low saturated fat and high monounsaturated fat, appears to decrease the inflammatory response, both in comparison to a high saturated fat diet, as well as in relation to a low-fat diet.
Study finding appear in the Journal of Nutritional Biochemistry.
“It has been recognized that obesity — a disorder characterized by abnormally high accumulation of fats in the body — and an unhealthy diet can increase the risk of chronic metabolic diseases such as atherosclerosis, type II diabetes, and Alzheimer’s disease, but not in everyone,” says lead author C. Lawrence Kien, M.D., Ph.D.
Inflammation, which involves the release of chemicals called cytokines from cells, is a normal part of the immune system’s defense against infection.
“However,” says Kien, “some environmental, internal, and even dietary compounds can masquerade as inflammatory stimuli, causing side effects that also occur during infections, and this can lead to long-term health consequences.”
Since prior research has shown that saturated fat generally has metabolic effects via indirect mechanisms, Kien and his team developed a hypothesis: that the pro-inflammatory effect of saturated fat might facilitate how saturated fat impacts the risk of metabolic disease. This theory is consistent with the acknowledged fact that metabolic diseases have an inflammatory component.
“Scientists have strived to understand the effects of dietary fats on inflammation by studying isolated cells and animal model systems,” Kien says. A 2011 study reported that palmitic acid, the most prevalent saturated fat in the diet, increased the production of the inflammatory cytokine, interleukin-1beta (IL-1beta) via a process involving activation of an innate immune system response called the NLRP3 inflammasome.
“However,” says Kien, “the question remained whether these findings were relevant to human diets.”
In their latest study, Kien and colleagues demonstrate for the first time that varying the normal range of palmitic acid found in common human diets influences the production of IL-1beta.
They studied healthy, lean, and obese adults, enrolled in a randomized, cross-over trial comparing three-week diets, separated by one-week periods of a low fat diet. One experimental diet was similar to the subjects’ habitual diet and was high in palmitic acid; the other experimental diet was very low in palmitic acid and high in oleic acid, the most prevalent monounsaturated fat in the diet.
After each diet, a number of outcomes were measured, including those related to inflammation. Relative to the low palmitic acid diet, the high palmitic acid diet stimulated the production of cytokines modulated by the NLRP3 inflammasome, thus creating more inflammation and associated risk for metabolic disease.
“Ultimately, we would like to understand how these dietary fats behave — both shortly after ingestion, as well as when stored in adipose tissue as a consequence of many months of ingestion — and thus contribute to inflammation and the risk of metabolic disease,” Kien says.
“In other words, habitual diet and especially the type of fat ingested may determine, in part, the risks associated with obesity.”
However, adds Kien, “it is important to acknowledge that other factors — for example, physical activity — and other features of complex diets will determine how persistent, high intake of saturated fat will impact health.”