By Raj Trikha
Due to the increase in high-fat, high-sugar, calorically-dense foods, coupled with a sedentary lifestyle, obesity has become a worldwide health crisis. As a result, the obesity rate within the U.S. is expected to be greater than 50% of the population in the next 10 years. The health consequences associated with obesity are broad, and they can affect nearly every organ system in the body. As such, obese individuals are at an increased risk for developing chronic diseases, such as cardiovascular disease, diabetes, Alzheimer’s, depression, and cancer. Underlying causes describing this relationship are still unclear; however, many people are exploring the contribution of the microbiota and how alterations here might be an important link between diet and chronic disease.
The human intestinal tract contains trillions of different bacterial species, known collectively as the gut microbiota. The presence of these bacteria in our intestinal tract has been known for over 100 years. However, the discovery of their vast contributions to human health and disease has been far more recent and is growing exponentially. Current evidence suggests that the microbiota first appear during birth and become established around two years of age. The gut microbiota can be manipulated by diet, environment, and prescription drugs (i.e. antibiotics). These bacteria engage in a mutualistic relationship with us; playing a role in protection against pathogens and drug detoxification, while we consume foods that allow a variety of species to survive. Greater diversity in our microbiota is highly correlated with improved health and disease. We can aid in the growth of a variety of bacterial species by eating different fiber-rich foods; promoting a healthy gut microbiota. Or restrict beneficial bacterial growth by consuming a high-fat, high-sugar, calorically-dense diet.
Dysbiosis is broadly defined as changes to the diversity and richness of the gut microbiota and has been associated with many obesity-driven diseases. The gut microbiota is primarily populated by two groups, Bacteroidetes and Firmicutes, that each contain various subgroups that play unique roles. But with the development of obesity, the ratio between these two groups becomes altered; resulting in the loss of many important functions of the gut microbiota. The presence of the bacterial species found in our intestines is similar to a scale, where balance between different groups promotes health. However, with the development of disease, the scale is tipped to one side. Currently, we are still unsure what ratio of groups promotes optimal health. Additionally, due to the diversity of the human diet and our individual microbiota, the exact mechanisms by which dysbiosis contributes to disease remain largely unidentified.
One hypothesis that connects diet and disease is metabolic endotoxemia– an inflammatory condition that arises from changes in intestinal barrier function, leaky gut, resulting in unwanted movement of chemicals from the intestines into the blood. Endotoxins are a group of compounds that are found in some microbial species in the intestines. When these bacteria die, the endotoxins can be released into the intestines and ultimately, into the bloodstream. Altogether, this results in an inflammatory response that has been indicated in the development of many chronic diseases.
We’ve known for quite some time that obesity increases the risk of developing chronic diseases, however the exact mechanisms remain hidden. More recently, the role of gut microbiota in promoting disease via dysbiosis and metabolic endotoxemia has become more convincing. As we continue to better understand how the foods we eat play a role in the development of diseases, the recommendations of what to eat to fend off chronic disease will begin to unfold. In the meantime, when you sit down to eat, remember that you’re eating for two, your microbiota and you.
Peer-edited by Rhea Jayaswal