Chapter 15 Sports Gene

 Chapter 15: The Heartbreak Gene

This chapter starts off talking about a Jamaican immigrant, Kevin Richards, who was an avid runner and was incredibly fast. On race day, he finished second in the race and collapsed, seizing, needing CPR, and ultimately, an AED. His left ventricle started malfunctioning, and caused a circulatory traffic jam, where Kevin ultimately died because of his body water seeping into his lungs drowned him Kevin had HCM. HCM is an enlarged ventricle that causes the most sudden death among young people especially athletes. 

There are18 different genes and 1,452 different mutations of DNA that could cause HCM. This is most commonly due to a missense mutation. There are so many different variations and mutations that HCM can come from. People with HCM are advised to stay away from rigorous exercise. The most tell tale sign of having HCM is having an enlarged heart, which makes it difficult for cardiologists because heart is a muscle, and often trained individuals will have larger hearts just from working out. Should is be required for there be genetic testing for every high school and collegiate athlete to test for HCM? Especially if it is the leading cause of premature death in sports? This is tough because only certain mutations are worse than others.

Another gene looked at in this chapter is the ApoE gene, which contributes to brain function and recovery for certain events. People with ApoE gene variants take more time to recover and are at a greater risk for having dementia later in life. Other genes talked about included the COL1A1 and COL5A1 genes that code for proteins that make up collagen fibrils. These genes can determine someone's risk of an ligament, tendon, or bone injury. Mutation in the SCN9A gene blocks certain pain signals that travel from teh nerve cells to the brain, which leads to insensitivity to pain, and we can see why that can be deadly. The COMT gene, which involves metabolism of neurotransmitters in the brain is also studied for its involvement in pain signaling. 


Overall what I learned from this chapter, is that we could do literally every DNA test in the world to see what type of problems athletes could have in their genetic makeup, but would that deter everyone from participating in their sports. We can't exactly change our DNA, but can we play to our advantages in it, if any?

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