In high school, we have all been taught that genes—which influence who we are, what we look like, and what we do—are passed down by our parents through things called chromosomes. However, many recent studies suggest that there is far more to genetics than just chromosomes. This opens up a new field called “epigenetics,” which studies how things other than our genetic code, passed down from our parents, affect us. One of the many things epigeneticists study are telomeres, which protect the ends of chromosomes when cells divide. Many disorders and diseases, ranging from post-traumatic stress disorder to cancer, can be linked to telomeres.
As a kid, I still remember being suffocated in Banana Boat Sunscreen before being allowed to play in the sand on beach trips. This wasn’t some sick joke my mom was playing on me 15 to 30 minutes before letting me enjoy the warm, sunny beach— it was meant to protect the DNA in my cells from damage.
Over time, our DNA is damaged due to natural chemical reactions as well as other factors, such as UV rays from the sun. These break down the proteins that, according to Dr. Jan Hoeijimakers at Erasmus University Rotterdam, give DNA the double-helix shape we’re all familiar with.
DNA damage is a known cause of cancer, and we can only prevent damage from the “other factors.”
Telomeres are caps at the end of chromosomes meant to prevent them from getting damaged. Just like we wear gloves in the winter to prevent ourselves from getting frostbite, our chromosomes have telomeres to prevent damage from natural chemical reactions and other factors.
According to Dr. Leonard Hayflick, normal body cells divide around 60 times before dying. Each time they divide, the telomeres on each chromosome get shorter. Shorter telomeres are associated with an increased risk of cell death. This means that when telomeres are too short, cells can no longer divide normally and will die.
A recent study by Dr. John A. Batsis, an Associate Professor of Medicine at Dartmouth, tested 8,000 subjects for a correlation between obesity and telomere length. The study found that among those studied, participants with obesity, especially younger participants, had shorter telomeres compared to their relatively healthier counterparts. The study concludes that early health decisions influence telomere length, which can have a significant influence in later stages of life.
A second study on older Korean veterans of the Vietnam War by Dr. Tae Yong Kim had a similar conclusion. The study explored the link between post-traumatic stress disorder (PTSD) caused by the Vietnam War, telomere length, and cell aging. Although the study could not suggest that PTSD directly resulted in shorter telomeres, it did conclude that PTSD caused by trauma increased the rate of cell aging. Essentially, this increased rate of cell aging means that PTSD caused by trauma leads to cells dying faster.
Similar to Dr. Batsis’ study, this study found that actions in earlier stages of life can have long-term effects on telomere length. The same study also examined telomere length in PTSD patients who were and patients who were not taking antidepressants called selective serotonin reuptake inhibitors (SSRIs). Patients being treated with SSRIs had longer telomeres than those who were not taking SSRIs. The study found that SSRIs can help prevent the increased rate of cell aging caused by trauma described earlier.
A similar study by Dr. Timothy Powell at King’s College in London tested telomere length in patients with bipolar disorder as well their relatives. Although this study found that antidepressants, like SSRIs, had no effect on telomere length, it did find that lithium, a common treatment for patients with bipolar disorder, was associated with longer telomeres compared to patients not being treated. Surprisingly, this study suggests a genetic component to telomeres. Compared to a control group who were not related to a patient with bipolar disorder, children of parents with bipolar disorder were found to have shorter telomeres. This suggests that there is a possibility for telomere length to be inherited from our parents as well.
Telomeres are like a double-edged sword: shorter ones are associated with earlier cell deaths and longer ones are known to be a central characteristic of cancer cells.
Normal cells stop growing and die as their telomeres shorten over time. However, cancer cells are known for their resilience. They manage to avoid dying by one of two ways: by allowing cells to increase their response to an enzyme called telomerase, which extends telomeres; or by a mechanism aptly named “alternative lengthening of telomeres.” Alternative lengthening of telomeres is similar to the process that DNA uses to repair some breaks and natural damage. This process involves taking an identical part of the DNA made during cell division (before it was damaged), called the sister chromatid, and repairing it by using an enzyme called DNA polymerase. Alternative lengthening of telomeres involves the same process, but repairs telomeres instead of actual DNA.
Together, these processes are what allow cancer cells to avoid natural cell death and continue to divide, creating tumors.
Understanding these processes is critical in cancer treatments. By stopping the mechanisms cancer cells use to grow uncontrollably, we can help stop the spread of cancer in an individual, increasing the success rate of treatment.
However, telomeres are not a fountain of youth. Although shorter telomeres are associated with shorter cell life cycles, longer telomeres don’t necessarily translate to longer lifespans. It is well known that longevity of life is dependent on many factors, such as environment and genetics. The only real secret to a long life is a balance of health, genetics, diet, exercise, and positive environmental factors.
This research is very new, so many contradicting studies are constantly being published. We can apply the current research to many applications, allowing us to further understand previously unknown mechanisms such as what allows cancers to metastasize and what effect psychiatric disorders have on our cells. As research furthers, perhaps high schools should begin shifting their focus away from traditional genetics and begin incorporating epigenetics into a more modern curriculum.
by: T. Lodhi
References:
Batsis, J., S. Bartels, et al., “Association of adiposity, telomere length, and mortality: Data from NHANES 1999-2002.” Nature. (2017): E-publication ahead of print. DOI: 10.1038/ijo.2017.202
Hayflick, Leonard. “The serial cultivation of human diploid cell strains.” Experimental Cell Research. 25:3 (1961) 585-621. DOI: 10.1016/0014-4827(61)90192-6
Hoeijmakers, Jan. “DNA Damage, Aging, and Cancer.” New England Journal of Medicine. 361.15 (2009): 1475-85. DOI: 10.1056/NEJMra0804615
Powell, Timothy, Gerome Breen, et al. “Telomere length and Bipolar Disorder.” Neuropsychopharmacology. (2017) DOI: 10.1038/npp.2017.125
Roake, Caitlin and Steven Artandi. “DNA repair: Telomere-lengthening mechanism revealed.” Nature 539.7627 (2016): 35-36. DOI: 10.1038/nature19483
Tae Yong Kim, Jee In Kang, et al. “The effect of trauma and PTSD on telomere length: An exploratory study in people exposed to combat trauma.” Nature. 7.4375 (2017): DOI: 10.1038/s41598-017-04682-w