Telomeres act as "protective caps" at the ends of our chromosomes. There, they allow our cells to divide without losing valuable genetic material. Instead, our telomeres shorten with each division process. When they reach a critical shortening, cell death is initiated and our aging process begins. So in theory, telomeres determine how old our cell can become without external influences. But what exactly does this mean for our aging process?
All our genetic information is stored in our chromosomes. There it is present in a long strand on the DNA, which "codes" our genes in specific structures. This coding ultimately determines the building instructions for every protein - and thus every structure - in our body. In the human cell nucleus there are a total of 46 chromosomes, which always act in pairs. Thus, humans have 23 pairs of chromosomes in each cell. The exception is sperm cells or egg cells, which have only half of the chromosomes (these combine with the respective other gametes during reproduction and thus form 46 chromosomes again in the cells of a new human being). Within each pair, the same genes are fixed and are responsible for guiding different parts of our bodies.
So much for the chromosomes, but what does this have to do with the aging process?
At the end of these DNA strands is a structure that has no function in the coding of new proteins: The telomeres. On the one hand, they ensure there that our chromosomes are not mistakenly perceived by our own body as damaged or diseased. On the other hand, they are crucial for the aging of our cells.
Telomeres have a predetermined length at birth. However, our cells divide regularly, which is accompanied by a complex sequence of microbiological processes. In short, it is not possible for our cells to divide and produce identical cells without losing a minimal piece of the chromosomes. And this is where evolution has taken advantage of telomeres. Because instead of our valuable genetic information, our cells shorten the genetically "irrelevant" telomeres every time they divide.
This means that every time our cells have to divide, we lose a piece of our telomeres. If these exceed a certain shortening, the affected cell can no longer divide and cell death, also called apoptosis, is initiated. This becomes noticeable in our body through different signs. They can include everything from "classic" signs of aging, such as gray hair or wrinkles, to diseases. In these areas of our body, the death of our cells becomes noticeable more quickly because the cells in our hair, skin, and also in our immune system divide more frequently than in other parts of our body. This also causes the telomeres to shorten more quickly.
Does this mean that there is nothing we can do about this process?
Yep. Of course, there is nothing that will keep our cells young forever or keep us from the natural progression of life. That is part of it! However, researchers have discovered that not only does our lifestyle influence the shortening of our telomeres, but they can even become longer again through a special enzyme called telomerase! In 2009, Elisabeth H. Blackburn of the University of California in San Francisco, Jack W. Szostak of Massachusetts General Hospital in Boston and Carol W. Greider of the John Hopkins School of Medicine in Baltimore were awarded the Nobel Prize for Medicine for their research on telomeres and the discovery of the enzyme that could lengthen them again.
But telomerase is not equally active in all cells. It is found mainly in rapidly dividing cells such as parts of the immune system, bone marrow cells, and with particularly high activity in cancer cells (which keeps them from dying naturally).
So what does this mean for our aging?
First, it means for us that if we want to protect our telomeres, we need to know what accelerates their shortening!
Many studies have already looked at telomeres and found that shortening is accelerated by obesity, among other things. In one study, women who gained weight after the age of 30 were found to have shortened telomeres. The reason for this could be that obesity causes a kind of chronic inflammation in the cells that produces oxidative damage. These attack our telomeres in particular. However, there are also studies that suggest a more complex relationship between telomere length and physique. In some cases, longer telomeres are associated with a higher BMI, while other studies say the opposite. Age, in particular, appears to have a major impact on the effect of weight on telomere shortening.
Where there is no doubt, however, is that high alcohol consumption can be associated with short telomeres. The constant stress placed on our cells by regular, excessive alcohol consumption accelerates cell division and damages telomeres.
This effect, which probably won't surprise you, has also been proven for other influences that oxidatively damage our cells such as too much sun, air pollution, radiation, nicotine or even junk food.
Researchers also agree that chronic stress leads to shortened telomeres and an accelerated aging process. What can be learned from this? Prolonged stress is not only bad for our moods, but also for our cells!
So much for how we can slow down the shortening. But can we also increase the lengthening?
Yes! One study found that a plant-based, low-fat diet with lots of vegetables, legumes, and fruits was instrumental in increased telomerase activity!
The other big support for our telomerase is primarily (it won't surprise you): exercise! Regular exercise stimulates our telomerase and provides amplified lengthening of our telomeres. Scientists have found that especially out-of-distance sports have great effects here!
Telomeres are true marvels of our cells and chromosomes. Without them, our cells would not be able to divide without taking massive damage. But this is not possible indefinitely - at a certain point the telomeres are too short, the cells that can no longer divide as a result die and our aging process progresses faster. Through a healthy lifestyle, we can try to protect our telomeres or even lengthen them again!