INFECTOBESITY: THE IMMUNE-MICROBE-METABOLIC CONNECTION
Bacterial endotoxin from the gut are not the only microbial link to obesity and diabetes. Elevated levels of circulating inflammation-stimulating immune cells have been observed in overweight and obese adults and children and in those with metabolic syndrome. For example, one study involving more than 6,500 people found a strong correlation between total leukocyte counts and metabolic syndrome. The researchers report that the increased neutrophil, monocyte, and eosinophil levels were strong and independent risk markers for obesity. (All these components are routinely measured on commercial blood tests.)
Consequences of obesity-associated skewing of the immune system include functional impairments in metabolism, namely blood sugar and fat, or lipid imbalance, which lead to insulin resistance, type 2 diabetes, metabolic syndrome, and heart disease.
The term infectobesity has emerged among scientists to describe the link between being overweight and the presence of low-grade, nonpathogenic microbial manifestation. With ample scientific reports confirming the presence of bacterial imbalances in the mouth, small intestine, colon, and bloodstream, and even an increase in antibodies to viruses, microbes deserve proper recognition as possible agents promoting obesity. Clearly, this new understanding means a change in treatment of weight loss and metabolic disorders, with a focus on immune modulation.
The hypervigilant, proinflammatory immune state accompanying increased levels of body fat can be described as generalized immune exhaustion. Hence, overweight persons are more susceptible to infections and related complications, periodontal disease, and autoimmunity.
For the first time, in the late 1990s, scientists proved the association between viral infection and obesity in humans, confirming the findings of extensive previous animal studies. A few years later, the banal human adenovirus-36 that causes the common cold and upper respiratory tract illness was also shown to increase fat mass, blood triglycerides, cholesterol, and insulin resistance in adults. Studies also link other nonlethal viruses such as herpes simplex virus (HSV)-1, HSV-2, and enterovirus to an increase in body fat.
While studies of viruses have been unable to confirm that infection causes obesity or that obesity-related changes in the immune system makes one more susceptible to viral infection, studies clearly point to an association. For example, researchers in San Diego found that 78 percent of a large group of children testing positive for adenovirus were obese. Korean researchers also found a high correlation among obesity and adenovirus infection in children, and suggested that the adenovirus may increase fat-synthesizing enzymes in the fat cells.
One scientific report found that obese children and adults were at increased risk of hospitalization from the 2009 H1N1 influenza pandemic. Another study found that 50 percent of Californian adults hospitalized with the 2009 H1N1 infection were obese and had an increased risk of death, and a report published in the prestigious English medical journal, The Lancet, concluded that obesity is a risk factor for infectious disease.
Recent immune system analyses suggest that while increased fat mass is linked to inflammation, or a generalized amplification of immune defenses, there appears to be a decline in the functioning of key antiviral immune cells, such as dendritic cells (DCs) and natural killer (NK) cells, which would predispose one to infection.
This research supports the notion that metabolic and hormonal response from poor dietary choices of overweight and obese persons is inflammatory, which over time leads to a state of immune exhaustion and poor defenses. Furthermore, when overweight people start exercising, studies show they experience a significant reduction in symptoms during upper respiratory tract infections and take fewer sick days.