Obesity-Inflammation Related; Common Thread with Diseases Part 3

For the past couple of weeks we have published articles on obesity and Michael Glade’s belief that inflammation, as the result of poor diet, environmental factors, and others is the primary cause of obesity.  People who are high is visceral fat have a high risk of developing metabolic syndrome, prediabetes, and diabetes. 

University of California, San Diego School of Medicine researchers “discovered that inflammation provoked by immune cells called macrophages leads to insulin resistance and Type 2 diabetes. Macrophages, found in white blood cells in the bone marrow, are key players in the immune response. When these immune cells get into tissues, such as adipose (fat) or liver tissue, they release cytokines, which are chemical messenger molecules used by immune and nerve cells to communicate. These cytokines cause the neighboring liver, muscle or fat cells to become insulin resistant, which in turn can lead to Type 2 diabetes. The hope is to block or disarm the macrophage inflammatory pathway to interrupt the cascade that leads to insulin resistance and diabetes. A small molecule compound to block JNK1 could prove a potent insulin-sensitizing, anti-diabetic agent. The research also proved that obesity without inflammation does not result in insulin resistance. Olefsky, researcher, explained that when an animal or a human being becomes obese, they develop steatosis, or increased fat in the liver. The steatosis leads to liver inflammation and hepatic insulin resistance.” ScienceDaily (Nov. 7, 2007)”  See this article in it’s entirety at http://www.sciencedaily.com/releases/2007/11/071106133106.htm

Of interest, the National Center for Complementary & Alternative Medicine (NCCAM)  has the following clinical trial posted on its website.  I was disappointed to see the study fell short of criteria which might further substantiate Dr. Glade’s position or lead to a broader study.  Six weeks is hardly enough time for a fair assessment of any meaningful conclusion regarding long term effects of inflammation.  I also found it interesting that fish oils were not included nor excluded since they are recognized to influence inflammation and immune system markers. The low number of participants does not represent the population adequately, either. Hopefully, this is just an initial step in a broader study that will change the way we approach the subject of inflammation and metabolic syndrome and diabetes II. 

Estimated Enrollment was 36 .  Details include being on the ADA diet for 5 weeks, then randomized to either ADA or AI for 6 weeks.  Other restrictions apply related to the diet as well as looking at blood markers that show how the immune system responds to the different diets. The expectation is the AI will result in less inflammation and a better response by the immune system than the ADA diet as well as looking at the effects of lipids and glucose. Levels of blood lipids and glucose will be considered to evaluate any effects.  Of course, appropriate inclusion criteria related to diabetes is listed and the following exclusion criteria.