Amplification of the Obesity Crisis Through COVID-19

   Amplification of the Obesity Crisis Through COVID-19

             Over the last few decades, the obesity crisis has grown drastically throughout the world. According to The Centers for Disease Control and Prevention, 42.4% of the U.S. population fell under the obese category in 2018. This figure is an increase from 30.5% in 2000 (CDC, 2020). Due to socioeconomic inequalities and disparities in access to healthy food options, obesity disproportionately impacts the Black and Hispanic populations, with obesity rates of 49.6% and 44.8% respectively (CDC, 2020). Considering the fact that obesity directly leads to potentially deadly conditions like type II diabetes, stroke, heart disease, etc., the above data represent a grim prognosis (CDC, 2020). For this reason, researchers like Dr. Jennifer Beshel and her colleagues aim to gain greater insight into the genetic and behavioral components of obesity. As their findings demonstrate, obesity is still not fully understood, and there is a great need to increase research in this field as figures continue to rise at quicker rates each passing year. The recent onset of COVD-19 serves to underscore the urgent nature of the obesity crisis. As seen in newly published studies, obese individuals face a significantly greater threat from this pandemic.

In the article “A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila,” Dr. Jennifer Beshel and colleagues investigated leptin, a significant weight regulating hormone in mammals, by studying the leptin homolog unpaired 1 (upd1) in Drosophila. First, the researchers found that upd1 affects obesity phenotypes by acting in brain tissue. When upd1 was knocked out in the fat body (FB), the researchers noticed no change in weight or feeding behavior. Next, by utilizing qRT-PCR, it was found that flies showed greater upd1 expression in the fed state. Subsequently, after knockout of upd1 in brain tissue, fed flies demonstrated the same level of attraction to food as starved flies. After these upd1 neural tissue knockout flies were exposed to high fat and high sugar diets, similar to many diets individuals eat today, they stored fat and gained weight at disproportionately higher levels as compared to flies with upd1 intact. This demonstrates that environmental conditions, such as diets consisting mainly of fat, contribute greatly to obesity. To demonstrate the powerful effect of upd1 in modulating obesity, the researchers demonstrated that when upd1 was reinstated in adult Drosophila neural tissue after knockout, flies’ obesity phenotypes returned to normal levels. Conversely, when upd1 was knocked out in the adult fly brain tissue, obesity phenotypes emerged. The researchers then further investigated how upd1 functions in the brain. Data indicated that when the domeless receptors for upd1, homologs of leptin receptors, were knocked out specifically on neurons containing neuropeptide f (npf), the homolog of mammalian neuropeptide Y (NPY), flies acted as if they were starved when presented with food, and presented many other obesity phenotypes. From here, the researchers concluded that the elimination of either upd1 or domeless receptors on neural tissue, resulted in the loss of inhibition on npf neurons, causing these neurons to function indistinguishably in starved and fed flies. When extrapolated to humans, these findings provide significant insight on the role of leptin in obesity.

In order to find an urgent motivation to conduct more studies looking into obesity, similar to Dr. Beshel’s research, one can look at the currently ongoing COVID-19 pandemic. According to the recently published article “Obesity is a potential risk factor contributing to clinical manifestations of COVID-19,” Zhenyu Kang and colleagues demonstrate, through a retrospective study on COVID-19 patients at Wuhan Union Hospital, that obesity exacerbates the effect of COVID-19 in patients. The researchers first split 95 COVID-19 patients into two groups, those with a BMI equivalent or greater than 25 were termed obese, while those with a BMI below 25 were considered normal weight. No significant difference in gender or age existed between the two groups. After analyzing data, the researchers found that the obese group faced significanlty more COVID-19 related complications. The obese group had a high moratlity rate of 5.5%, compared to 0% for the other group. When first admitted into the hospital, the obese group showed a larger number of underlying diseases, including endocrine issues, heart disease, respiratory disease, etc.. These obesity linked diseases made it harder for these patients to fight off COVID-19. Furthermore, chest CT images indicated that the obese patients showed a greater distribution and overall level of lung injuries, resulting in a higher CT score. Considering how COVID-19 is a respiratory disease, this finding indicates how the obese face a greater impact of COVID-19 symptoms. Obese patients also exhibited significanlty higher level of triglycerides, monocytes, lymphocytes, and inflammation markers like hsCRP, ESR, and IL-4. This is indicative of abnormal metabolism in obese patients, and therefore resulting in an ineffective immune response against COVID-19. Taken altogether, obesity is one of the largest risk factors for COVID-19.

In her talk, Dr. Jennifer Beshel brought up the interesting point about a much greater response to the COVID-19 pandemic compared to the obesity crisis, although the latter arguably presents an equally important public health concern. Looking at how the obesity figures continue to rise uncontrollably, it appears that one of the greatest factors hindering a greater reaction to obesity is that the general population is still not entirely cognizant of its dangers. Considering how people are becoming aware of how significant of a risk factor obesity is for COVID-19, hopefully this may serve as an important catalyst for a greater united response against the obesity crisis. 

Works Cited

“Adult Obesity Facts.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 29 June 2020, www.cdc.gov/obesity/data/adult.html. 

Beshel, Jennifer, et al. “A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila.” Cell Metabolism, vol. 25, no. 1, 2017, pp. 208–217., doi:10.1016/j.cmet.2016.12.013. 

Kang, Z., Luo, S., Gui, Y. et al. Obesity is a potential risk factor contributing to clinical manifestations of COVID-19. Int J Obes (2020). https://doi.org/10.1038/s41366-020-00677-2