Ousting the Obesity Outbreak

            Obesity rates have been rising rapidly in the United States, doubling for children and tripling for teens over the past 30 years, according to the Centers for Disease Control and Prevention. Obesity has become a nationwide epidemic, affecting the health of Americans and causing medical bills to rise. Still, medical researchers struggle to find a sole reason to explain obesity’s prevalence. Some blame obesity on poor eating habits, while others target a lack of physical exercise. Now, researchers have validated the popular claim that obesity can be caused by a “slow metabolism.” In a study conducted at the Institute of Metabolic Science in Cambridge, researchers found that a mutated form of the gene KSR2 facilitates obesity by increasing appetite, while slowing metabolism. Metabolism is made up of all the chemical reactions that occur within an organism. All organisms need energy to live. The combination of anabolic pathways (reactions that store energy) and catabolic pathways (reactions that release energy) within the human body make up metabolism. People with obesity and a slow metabolism cannot burn enough calories to release excess energy that has been stored in fat in the body. Now, scientists are hopeful that knowledge of the causes of obesity will enable them to end this epidemic.

            To conduct the research, scientists studied the DNA of 2,101 patients with obesity. It was concluded that less than 1% of people have a mutated form of the KSR2 gene, while 2% of children with obesity under the age of 5 have the mutated gene. Additionally, it was observed that mice without the KSR2 gene gained weight more easily. The mutated version of KSR2 causes people to feel hungrier because it alters the way the brain receives signals from hormones, therefore slowing the rate of metabolism. The researchers hope to gain insight on how to cure obesity from their findings.

            I was immediately interested upon reading this article because I have observed how common obesity is in my community and school. I am interested in children’s health and medicine, and I was intrigued that obesity might be solved with drugs that can correct a single gene. This article ties into the mystery of obesity and the widespread hope that it can be corrected.

            While reading this article, I felt agreeable and receptive to the ideas that were put forth. I felt that the experiment and results were realistic, helping me to accept the idea that obesity can actually be caused by genetic components that lead to a slow metabolism. Before reading this article, I had the bias that obesity is usually a lifestyle choice, the result of unhealthy eating and a lack of exercise. I had adopted these opinions after reading a series of articles and books on food this summer for my AP Language assignment. Those particular authors blamed obesity on fast food, overeating, and public policy. These views are not necessarily scientific, but based on social prejudices and assumptions. For some people, as this study shows, this may not be true. They may need more than diet plans to affect their health conditions. As I began to accept this new metabolism theory, I could draw connections between my own observations. I have relatives and family friends who have attempted various diets and exercise routines to lose weight, but even the most rigorous plans do not have an effect. For most of these people, obesity also runs in their families. These observations are consistent with this research study. The mutated KSR2 gene could be passed within the family, resulting in a slow metabolism that makes it difficult to maintain a healthy weight. This study helped to give me a better understanding of the causes of obesity and the struggles that people go through to attempt to lose weight.

            The science accompanying this research study seems to be mostly accurate and reliable. By testing the genes of both humans and mice, the scientists were able to create reasonable conclusions about the role of the KSR2 gene. The only part of the study that I question is the relatively small test group. Just over 2,000 obese patients were tested, and nobody with a healthy weight was tested for comparison. Of the 2,000 people tested, only about 1% have the mutated gene, which shows that it is not very common. Additionally, other causes and genes should be tested to determine that the KSR2 gene is the sole gene that affects metabolism. Furthermore, healthy eating and exercise should not be discounted as ways to affect obesity. The science surrounding this research is reliable but limited by the small test group.

            The knowledge gained from this study opens up many possibilities in medical research and healthcare. Drugs could be developed to correct the mutated KSR2 gene along with appropriate health plans that counteract the gene’s effect. Additionally, tests could be introduced to test children and adults with a genetic risk for the mutated KSR2, just like patients with a family history of allergies, genetic disorders, or certain types of cancer can be tested. Treatment of obesity would then take on a preventative measure, possibly even opening new jobs in the medical field for specialists in the area.

            The results of this research show promising progress in finding a cure for obesity. In the future, maybe health risks and medical costs related to obesity will be eliminated, ending the war against obesity in America.

References

Adult obesity facts. (2013, August 16). Centers for Disease Control and Prevention. Retrieved December 8, 2013, from http://www.cdc.gov/obesity/data/adult.html

Campbell, N. A., & Reece, J. B. (2005). Biology (7th ed.). San Francisco: Pearson, Benjamin Cummings.

Childhood obesity facts. (2013, July 10). Centers for Disease Control and Prevention. Retrieved December 9, 2013, from http://www.cdc.gov/healthyyouth/obesity/facts.htm

Gallagher, J. (2013, October 24). Slow metabolism 'obesity excuse' true. BBC News. Retrieved December 5, 2013, from http://www.bbc.co.uk/news/health-24610296

Bad News for Baby?

          Everyone knows that babies can get sick easily. One infection or virus could be life-threatening. Many babies are strong and healthy at birth, but their bodies seem to lack the ability to protect them from disease. Until recently, it was assumed that babies have weaker immune systems than children and adults. It could be that the immune cells of babies are less developed than those of adults. I thought that seemed like a logical explanation until coming across a new study. Now, scientists at Cincinnati Children’s Hospital Medical Center believe that infant immune cells are not underdeveloped. Rather, they are prevented from functioning by immune-suppressing cells. It seems nearly impossible that the infant immune system evolved to favor cells that prevent immune cells from doing their job of preventing infectious disease. Despite this, researchers have completed a study that supports the theory that infants’ immune systems are being inhibited by a special kind of cell. As scary as it seems that infants may be intentionally vulnerable to any illness, this might not be bad news for baby.

            According to the study, babies do not have immature immune cells, but extra immune-suppressive cells, called CD71+ cells. These special cells eventually develop into red blood cells. CD71+ cells contain the enzyme arginase-2, which helps to repress immune cells. Enzymes are biological proteins within cells that lower the activation energy needed for certain reactions to occur. If arginase-2 is inhibited by other molecules, which means it can no longer function due to a change in structure, its ability to reduce the effectiveness of immune cells is prevented. This also occurs in the presence of the molecule L-arginase. To test this, the researchers used newborn mice and blood cells from umbilical cord blood. In both test subjects, CD71+ cells were found in increased concentrations. They concluded that the presence of these cells allows infants to adapt to the increased stimuli and microbial presence after birth. For example, beneficial bacteria have to colonize in the intestines to aid with digestion, and many other types of bacteria will be present on the skin. If the immune system is not suppressed, the infant experiences increased inflammation in the intestines, and necessary bacteria would not be able to colonize. As the infant grows, the presence of CD71+ declines and the immune system becomes more effective. The researchers concluded that it is most important for the infant’s body to adapt to its environment and to allow bacteria to colonize before it can prevent infection.

            These new findings are intriguing, and can possibly explain trends in infant mortality. In history class, we learned about infant mortality rates throughout time. In the 19^th century, as Americans moved into cities, the likelihood of survival for infants and children greatly decreased. In these urbanized areas, disease was prevalent, due to primitive waste disposal systems and open sewage areas. Maybe the inability of the infant immune system to prevent infection at a young age was a weakness rather than an adaptation in that historical environment. I believe research should be conducted to explain and prevent trends like this.

            In the future, these findings could be used to lower infant mortality, especially in countries where disease control is poor. The researchers intend to explore the possibility of strengthening the infant immune system while still allowing the CD71+ cells to assist in the colonization of bacteria in the intestines. The CD71+ cells could be manipulated or drugs could be used to increase immunity to harmful bacteria. This would change the future of medicine and could improve the outlook for infants who are exposed to disease. I hope to become a pediatrician in the future, so this is especially interesting to me. If doctors could protect newborns from harmful diseases, their job would consist of more active measures of prevention. Instead of telling families to limit their infants’ exposure to people who might carry diseases, doctors could prescribe medicines to protect their bodies. This would allow infants to be around family members and in places such as daycares. Further research could have an interesting impact on medicine and children’s health.

           Though this study is compelling, I question the scientific and ethical issues accompanying the research. The impact of the CD71+ cells was only observed in mice and in umbilical cord blood, not in human infants. Of course, for safety reasons, human newborns cannot be tested, but it might be difficult to compare humans and mice. Humans have a more complex immune system compared to mice, and are exposed to a wide range of disease-carrying microbes. Even with complex trials, it will be difficult to tell how potential medicines or prevention techniques will affect humans. Additionally, the ethical concern over testing on live animals is raised. Before reading this article, I strongly believed that researchers should not use animals – even mice – as test subjects. After reading the study, I have a greater understanding of why it is important to test on the mice. Before administering drugs or new techniques to human babies, it is crucial to know that the method is safe and effective. As long as the testing methods are humane and necessary, I now feel more comfortable supporting testing on animals to ensure the safety of human infants.

            At a time when so much important medical research is being conducted, it is exciting to learn that scientists might be able to combat infectious disease in newborns. The possibilities for this research seem promising, and could impact both patients and professionals in the medical field. It is amazing to think that the most basic unit of life, the cell, can be manipulated to save lives.

Works Cited

Elahi, Shokrollah. "Immunosuppressive CD71+ erythroid cells compromise neonatal host defence against infection." Nature. N.p., n.d. Web. 22 Nov. 2013. <http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12675.html>.

"Immune-suppressing cells explain newborn infection vulnerability." Medical News Today. MediLexicon International, n.d. Web. 20 Nov. 2013. <http://www.medicalnewstoday.com/articles/268394.php>.