The Obesity Crisis

       In the past few decades alone, we have seen an unprecedented growth in the rate of obesity not only in the United States but worldwide. There are few health issues that pose such severe health consequences and have such wide ranging symptoms. Though there is no singular cause of obesity, there are strong indications that it may be due to a combination of genetic and environmental factors. Two research studies on obesity approach the cause of this problem by looking at the brain specifically and how certain changes in its makeup or underlying genetic differences may make some people more susceptible to obesity.
       One research study done by Dr. Gavini looks at the role of melanocortin-4 receptors and how they regulate homeostasis. In the article, Melanocortin-4 receptor–regulated energy homeostasis, it states that AgRP neurons and POMC neurons seem to be working counteractively to suppress and stimulate hunger which in turn regulates energy expenditure. This means that when more energy is taken in than needed, it leads to an increase in body weight, disrupting the energy balance of the body. Furthermore, the study indicates that certain changes or mutations in these neurons and receptors can have a profound change on homeostasis possibly leading to an increased risk for obesity. Specifically, "MC4R mutations represent the most prevalent form of monogenic obesity" and that a POMC deficiency may also lead to obesity. This shows that changes to a person's cells can materialize in a phenotype that is obesity. These changes can be caused by environmental or genetic factors, and this study shows that people who have these mutations may be much more prone to obesity than people who do not.
       Similarly, a study done by researchers at Montreal Neurological Institute and Hospital explores the effects of how changes in brain structure may also be a cause of obesity. In their article Neurobehavioral correlates of obesity are largely heritable, they state that "increased BMI is associated with decreased cortical thickness in right frontal lobe and increased thickness in the left frontal lobe, notably in lateral prefrontal cortex". This may suggest that, in addition to the role of specific neurons and receptors in the brain, changes to specific regions of the brain may also be a factor in obesity. This idea is feasible in that certain structures located in these brain regions control certain things such as the modulation of food, inhibition, and more. In addition, this article also emphasizes the "genetic vulnerability to BMI" which indicates that one's DNA and genetic makeup can be a risk factor in itself even with no environmental factors. This would mean that obesity may be caused by a combination of both genetics and abnormalities in brain structure. 
        When comparing and contrasting these two studies, we can see that what causes obesity is not always able to be pinpointed to one thing. Most likely, it is a combination of many factors which include both genetic and environmental elements. It should also be considered that not any two people are the same; what causes obesity in one person may be entirely different in another individual. This is why it is important to have a cohesive understanding on the causes of this issue as it will lead to more possible treatments. Another major element that was not fully adressed in these studies is the immense role environment can play in obesity. In this day and age where so much of the available food is high in fat and sugars and low in nutrition, the struggle to eat healthy is ever present.  In conclusion, obesity is a complex issue that is becoming more and more prevalent. Hopefully, there will be a treatment in the future that can help address this issue in all types of people.




Works Cited

Krashes, Michael J, et al. Nature Neuroscience, U.S. National Library of Medicine, Feb. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC5244821/.

Vainik, Uku, et al. “Neurobehavioral Correlates of Obesity Are Largely Heritable.” PNAS, National Academy of Sciences, 11 Sept. 2018, www.pnas.org/content/115/37/9312.