Obesity: The Rising Epidemic


According to the Center for Disease Control and Prevention website, “…. There has been an increase in obesity in the United States and rates remain high. More than one-third of U.S. adults (35.7%) and approximately 17% (or 12.5 million) of children and adolescents aged 2-19 years are obese”. Furthermore, apart from the health consequences of obesity, which includes, but is not limited to, coronary heart disease (CHD), type 2 diabetes (T2DM), and various cancers, obesity has direct and indirect effects on the nation’s economy. Direct medical costs incorporate the diagnostic and treatment services that are related to obesity, while indirect costs comprise of morbidity costs and mortality costs. To expand further, morbidity costs are defined as “the value of income lost from decreased productivity, restricted activity, absenteeism, and bed days.” Finally, mortality costs are the costs tagged on the future losses of income as a result of premature death.


These facts are unsettling. Clearly, intervention is needed, but at what point is government able to intervene? Does government intervention obstruct a person’s free will? Can the government dictate what items are sold in grocery stores, or how much a person can buy, or what ingredients can be used in products. The list of questions goes on and unfortunately, they are not easy questions to answer. However, what might help in answering these questions is the increasing amount of scientific evidence pointing to dysregulations in brain chemicals that contribute to obesity and obesity-related diseases. Due to the ongoing and increasing epidemic of obesity and diabetes in the US (and worldwide), scientists feel a sense of urgency to study insulin and leptin resistance. Growing evidence suggests that neuronal signals generated by insulin may overlap with signals activated by leptin, which would explain similarities seen in their effects.


Briefly speaking, both insulin and leptin work on neurons in the hypothalamus (as well as other locations in the brain). More specifically, insulin and leptin act on receptors found on neurons in the arcuate nucleus of the hypothalamus. One type of neuron found in this location is called a POMC neuron. They are activated by insulin and leptin to secrete a-MSH. When stimulated, the POMC neuron reduces food intake and increases energy expenditure. The other main type of neuron found in the arcuate nucleus is called an AgRP/NPY neuron. As opposed to POMC neurons, AgRP/NPY neurons are stimulated by decreases in insulin and leptin levels and stimulate food intake. AgRP/NPY neurons would be activated during periods of weight loss and prolonged absence of food in order to increase a person’s intake of food. After significant research, scientists have concluded that both insulin and leptin function as fat signals and have multiple similar physiological effects. Furthermore, insulin and leptin share their key sites of action in the hypothalamus suggesting that they have similar intracellular properties by which disruption in these pathways lead to resistance of their actions. Understanding the mechanisms by which these hormones affect energy homeostasis shows promise in promoting insight into practical and effective targets for therapy of obesity.


I think such therapies show more promise in treating the rising epidemic of obesity in the country. I am afraid that preventative courses of action obstruct a person’s free will more than therapeutic treatments in response to developed obesity do. Ideally, people would take responsibility for their own health in eating the right things and exercising daily, but evidence shows that this does not always happen. It remains clear that people need a more serious and invasive way to treat obesity. Without putting limits on what a person can or cannot buy, we need a way to counteract the negative effects that obesity has on a person’s lifestyle and the negative effects obesity has on society. I am hopeful that scientists are on the right track and will soon be successful in finding ways to counteract these effects. However, I also feel that such therapies will only be successful if paired with healthy dieting and exercise. Success does not come in simply administering a drug that works to decrease the nation’s high rates of obesity. Success comes when we reduce the nation’s obesity and promote education to prevent the further rise of obesity in the nation and stimulate the nation’s productivity.

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