Cornell scientists researching the effects of environmental toxins to the onset of obesity and Type II Diabetes, discovered that—unlike other factors such as eating too many unhealthy foods—the extent of damage caused by pollutants depends not on what a person puts into her mouth, but on what is already living within her gut.
Prof. Suzanne Snedeker, food science, and Prof. Anthony Hay, microbiology, researched the contribution that microorganisms in the gut and environmental toxins known as “obesogens” have on ever rising obesity levels. Their work, which was published last October in the journal Environmental Health Perspectives, reported a link between composition of gut microbiota, exposure to environmental chemicals and the development of obesity and diabetes. The review, “Do Interactions Between Gut Ecology and Environmental Chemicals Contribute to Obesity and Diabetes?” combined three main ideas: predisposed gut microbe composition can increase an individual’s risk of obesity and Type II Diabetes, gut microbe activity can determine an individual’s metabolic reaction to persistent pollutants such as DDT and PCB and certain pharmaceuticals can also be metabolized differently depending on the community of microbes in the gut.
The microbe community influences many metabolic pathways within the gut, Snedeker said. Our bodies metabolize chemicals, but how they are metabolized, and how much fat is stored, depends on gut ecology. Microbes are responsible not only for collecting usable energy from digested food, but also for monitoring insulin levels, storage of fat and appetite. Gut microbes also play an integral role in dealing with any chemicals that enter the body. According to Snedeker, differences in gut microbiota can cause drugs like acetaminophen to act as a toxin in some people while providing no problems for others. While pharmaceutical and microbe interactions are well understood, there is little information in the area of microbe response to environmental toxins.
She said, there are more than three dozen chemicals called obesogenic compounds, that can cause weight gain by altering the body’s normal metabolic responses and lipid production.
“It seems probable that gut microbes are affecting how our bodies handle these environmental chemicals,” Snedeker said. According to Snedeker, enzymes that are influenced by interactions of gut microbes break down approximately two-thirds of the known environmental toxins. Therefore, differences in the gut microbe community strongly affect our bodies’ ability to get rid of environmental pollutants. Obesogens can alter normal metabolic behavior by changing the levels of fat that our bodies store. Snedeker and Hay suggested that the microbes in the gut of humans determine the way in which these chemicals are metabolized and thus could contribute to obesity.
Snedeker and Hay concluded that although high levels of obesogenic chemicals are bound to cause some kind of disruption in the gut microbe community responsible for breaking these chemicals down, the degree of the disturbance is dependent upon gut microbial composition. In other words, the amount of weight an individual is likely to gain when exposed to environmental toxins, or her risk of acquiring Type II Diabetes, could depend on the microorganism community in their gut.
“We’re proposing that we have to look much more closely at how inter individual variation is affecting how we metabolize this class of chemicals because it might affect what’s retained in the body after exposure, which might in turn affect obesity and diabetes risk,” Snedeker said. Scientists are now working on “humanizing the rodent gut” by adding microbes found in the gut of humans to those of rodents, thus making it easier to see the effects of obesogenic compounds on specific individuals and discover how environmental chemicals are metabolized, Snedeker said. This may allow scientists to one day single out particular combinations of microbes that can more effectively break down obesogenic or diabetogenic toxins and insert them into the gut of people lacking the microbe. Hay said that, in the future, he hopes to see the research trending toward finding “diagnostic biomarkers that will help assess risk for individual people,” based on their gut ecology.