Obesity: How Might Plants (Indirectly) Make Us Fatter?
The number one epidemic affecting America is now not cancer, in any shape or form. Obesity has taken over as king, killing up towards half a million people annually in the form of heart disease, according to the Center of Disease Control and Prevention. America has always had a troubled past with obesity with rates skyrocketing in recent years. However, this epidemic has grown to such proportions where a hamburger now is a more fitting symbolism of death in America than a cigarette.
With this in mind, one naturally asks, how can this be? What might be a cause for this sweeping blight known by the name of obesity? There have been many factors discovered, ranging from a sedentary lifestyle to genetics. But now, growing interest in the effects of pesticides on the human body may help the image of obesity‘s causes grow clearer.
Pesticide use has become an increasingly ubiquitous aspect of modernized farming; according to a 2012 study conducted by the Environmental Protection Agency, agriculture accounted for about 80% of the more than 1 billion pounds of pesticides used by the United States annually.
While there is no doubt that pesticides do their job well, numerous complaints have been historically cited against the usage of artificially synthesized pesticides. There have been charges anywhere from environmental destruction to a possible link with Alzheimer’s. But the link between pesticides and obesity is one that grows all the more pressing as more and more people in America are affected by obesity with each passing day.
Certain chemicals such as tributyltin have been found to promote adipose tissue (fat cell) growth in the abdominal area. Tributyltins refer to a class of organic compounds, and tributyltin oxide is its most widely used form. This class of chemicals is currently most widely used an agricultural and aquatic fungicide. Tributyltins have been one of the many classes of pesticides to come under closer scrutiny in recent times.
In the case of tributyltin, scientists found that exposure of tributyltin towards smalls mammals like mice resulted in a propensity to a greater production rate and size of produced adipose cells. Animals with more adipose tissue have a greater tendency to become and remain obese due to adipose cells‘ hormonal secretions that call for more consumption of food when starved.
Tributyltin was also found to disrupt body weight hormonal regulations within the mice’s brains, resulting in the mice remaining morbidly obese even with an introduced diet of limited caloric intake. This chemical was found to disrupt, among other pathways, the insulin glucose regulatory pathway, preventing the cascade reaction from occurring and thus causing cells in the body to grow more resistant to insulin. Insulin is a hormone that is needed for cells to be able to allow glucose in through the GLUT-2 channel, and with the pathway disturbed by tributyltin, the mice cells were unable to transport glucose into the cell for energy. Without adequate amounts of sugar, the starved adipose cells called for more food, leading to further ingestion of food that could not be absorbed into the cells with a disrupted insulin pathway. This viciously self-sustaining cycle led to mice more obese than they ever should have been.
Although the results of pesticide usage on obesity has revealed some alarming facts, keep in the mind that the usage of pesticides has been regulated by the EPA, and that the levels of pesticides currently used on crops are all within prescribed levels. Of course, more research must be done, especially on multigenerational effects of pesticides on such epidemics like obesity.
<Edward Kim, Oxford Academy 10th Grade