telomeres – BioQuakes

Have you ever wondered why humans age? Why we can’t stay alive forever? Or is it even possible to? According to a recent article from Scientific American, scientists are actively researching what lifestyle choices and diets can lead to a longer life.

Firstly, before we dive into that, let me explain why the article says we age and what causes cells to lose their ability to regenerate. The article says that cells are constantly being damaged in our body, from UV rays to poor nutrition, which causes them to regenerate to become healthy again. Regenerating cells divide into new healthy ones by making copies of their chromosomes, which contain DNA. But this is where the aging process begins. Each time a cell divides, the end or caps of the chromosome, called telomeres, shrink, and when they become too short, the cells cannot divide further. This cell state is called senescence. This state of the cell is dangerous, so we secrete chemicals to activate our immune system and eliminate them, but when our body does not destroy them, they cause neighboring cells to go into this state as well. If the senescence cells keep spreading to their neighbors, the body and brain work slower, causing our body to deteriorate, become susceptible to disease, and die.

This is where the scientists come in! According to the article, experts often believe in the popular disposable soma theory. This theory indicates that our bodies have limited lifetime energy and that humans use a good amount of it to do reproductive functions. So, if you choose not to reproduce, you could live a longer life. Is that not a hard choice? Children or a longer life? I know I wish there could be a happy medium! But, according to experts, if people try to reach a compromise, they risk mutations and major issues in decedents. Therefore, it is hard to combat the aging of humans from this perspective, not only for ethical reasons but also on the subject of time. In an article by Antonello Lorenzini, he states that time and environmental pressures cause constraints for us to repair damaged cells and reproduce in the limited window we have. Therefore, we as humans must maximize the time and energy we have as it is imperative for our aging process not to slow down at an earlier stage of our lives.

Since this approach did not work, researchers in the article looked at the perspective of targeting short telomeres and preventing cells from entering senescence. Yet, there is a problem in both of these ideas as well. People with long telomeres have more telomerase, which is the enzyme that keeps telomeres long; the problem with this is that cancer cells can use this telomerase to multiply unchecked. As well as this, people with longer telomeres tend to have a more likely chance of getting cancer and brain tumors as well. Is a longer life worth a higher chance of getting cancer? Personally, I do not think so. So researchers also tried to prevent cells from going into a senescent state, but they had a similar problem. The cells researchers need to target are the ones that induce aging, but they must avoid the cells benefitting the body, or else it will cause more catastrophe for human cells.

Next, researchers looked at ideas for extending our lifespan through caloric restriction. A study from Nature displayed that people who ate 15% fewer calories had less body aging. This is also shown in the research from AARP, which said researchers at the National Institutes of Health found that adults who had 12% less caloric intake over two years opened biological pathways associated with healthy aging. But, back to the original article from Scientific American, it says this must be done carefully. Caloric restriction may extend life span but also may cause side effects, such as decreasing gray matter in the brain. So, as researchers try to find a solution that does not cause any harm to us as a species beyond a balanced diet and exercise, aging will not stop anytime soon. (Very sad, I know.)

Lastly, I want to connect this to something we learned in AP Biology this year. In this unit, we discuss cell division and the cell cycle. This relates to the topic of anti-aging/aging because of the cell reproduction rate and the ability of the cell to replicate. As said above, as the cells are damaged, they must replicate. This process starts with interphase, where the cell will go through the G1, S, and G2 phases or the growing and replicating phases. The cell has normal functions, copies DNA, and doubles its organelles in preparation for mitosis. Next, it will move into mitosis, where it will divide the nucleus through kinetochore and nonkinetochore, and finally go into the stage of cytokinesis, where the cytoplasm is split. This can further relate to the topic through the telomeres and the telomerase. As said above, people with more telomerase can have a higher chance of getting cancer because the cancer can multiply unchecked. They can multiply unchecked because most cancer cells use telomerase to divide indefinitely, as it will continue to replicate and not die, which causes tumors to form. So, suppose our normal cells start to use telomerase. In that case, our cells will act similarly in replication to cancer, and our bodies will not be able to tell the difference.

Most cells only divide when given a chemical signal, but cancer cells do not obey this. They will divide even though they did not receive a chemical signal. In AP Bio, we learned that cancer cells also do not have the signal to stop replicating, which is where the telomerase comes in. Since cancer cells do not receive the signal to stop copying and they have long and reconstructing telomerase that allows them to do this, they will never die.

As well as this, we can link the idea from the senescent state – the cells researchers need to target are the ones that induce aging, but they must avoid the cells benefitting the body, or else it will cause more catastrophe for human cells – to this as well. If genes are damaged when they are targeting aging cells, this can cause oncogenes to form. Oncogenes will cause the cells to divide when no signal is sent. This would lead to tumors because of the rapid cell replication. Similarly, suppose a mutation damages the tumor suppressor in the cell. In that case, there will be nothing stopping the oncogenes from replicating, allowing them to do what cancer does and replicate non-stop. Therefore, the process of anti-aging and cancer remarkably coincide as the very thing that we want to use for anti-aging is something that causes cancer to be able to divide indefinitely. That is pretty amazing and crazy to me! How can something in our bodies allow that to happen? What do you think?

Do YOU want to learn the secret to having BIG, LONG telomeres?

OF COURSE YOU DO!

Do you know what Telomeres are?

Umm….

you might not know what they are, but I’m pretty sure you’re gonna want long ones,

and a few scientists lead by Eli Puterman, an assistant professor of kinesiology at the University of British Columbia in Vancouver, just made a huge breakthrough regarding telomeres.

let me explain.

New research done on Data collected in University of Michigan’s Health and Retirement study and reported on by TheScientist, has found that A.) accumulation of stressful events over the course of a lifetime are associated strongly with shorter telomeres later in life and B.) stressful experiences during childhood have a far greater effect on the shortening of Telomeres in adults than those that occur later in life.

First of all back up. What are Telomeres? And when it comes to Telomeres, does length really matter?

I’ll tell you.

(spoiler alert: length always matters)

Telomeres are caps that go on the end of our DNA. You can think of them like aglets on the end of shoelaces. Telomeres work to protect DNA from becoming damaged, and with that preventing the functionality of DNA from becoming compromised. They’re exactly like that little plastic bit on your shoelaces prevents your lace from becoming frayed, and ruining your shoelace, and your day, and your life.

(the pinks parts are the telomeres)

And a moment of thanks, to the great man who invented aglets.

Harvey Kennnedy,

Thank you.

Back to your telomeres. As we know cells are constantly copying themselves, creating new cells, and every time this happens the telomeres on the end of our DNA become shorter and shorter, before eventually they fail to adequately protect the DNA, causing our cells to lose functionality, and on a larger scale, causing you to age faster. Essentially throughout our lives our telomeres get shorter and shorter, like a candle thats burning lower and lower, it’s a marker for our aging process. A constant reminder of our mortality as humans. A literal ticking clock. We’re all gonna die. Life is meaningless.

You know what’s not meaningless though… BIOLOGY! So while we can never escape the grim reality that our lives are nothing more than the blink of an eye on a fleck of dust that’s drifting through an empty abyss of nothingness, why not try to extend that blink of an eye for as long as we can, so that we can read about research findings in the world of biology! speaking of which…

In the study, a group of 4,598 Americans that had an average age of 69 were asked to identify stressful incidents that occurred in both their youth and later adulthood. They then had their telomere lengths measured from cells from saliva samples. In the study, Part of the study’s findings were that “Each additional adverse event during childhood was associated with an 11 percent-increased odd of shorter telomeres”. These results are staggering to be sure, but are not totally out of the blue. One Judith Carroll who researches the links between behavior and health at UCLA said after the study had been completed “The findings are consistent with other reports suggesting that early life is a particularly vulnerable time when the body is rapidly growing and adapting to its surroundings”.

These results were very strong, however some have taken issue with extrapolating stressful incidents to higher mortality. While it is acknowledged that the shortening of telomeres is associated with aging, some wished the study had gone a step further, and examined whether these shorter telomeres really do result in earlier death. As it is said by Iris Hovatta, a scientist at the University of Helsinki (in Finland)(a country I have never been to, so I can’t confirm whether or not it actually exists)(which is neither here nor there)(whether or not ‘there’ really does exist) “this study did not address the effect of stress on health or lifespan and whether individuals with shorter telomeres have an increased mortality” It’s a fair criticism, but as far as we know now, shortening of telomeres causes aging, and this study puts forth strong evidence of an association between stressful events over the course of a lifetime, especially during youth, and shortening of telomeres.

So what does this mean?

if you don’t want to age, avoid stressful events during your youth.

avoid stuff like forgetting when your blog post was due, then staying up until 3 in the morning to finish it.

Then again biology its pretty much all I have to live for.

give and take I guess, we all have to find a balance that works.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: telomeres

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