Perhaps you have heard about telomeres in biology class? They are like the protective caps on shoelaces and help DNA maintain its shape. What is interesting is that these protective caps are constantly being broken down and rebuilt. For the discovery of this mechanism, the Australian researcher Elisabeth Blackburn received the Nobel Prize, and the telomere attrition has been included in the repertoire of the 12 molecular mechanisms that we refer to as Hallmarks of Aging .
As the first hallmark, we have already learned about genomic instability . This accumulation of DNA damage with age seems to almost randomly affect our genetic information. Depending on where damage occurs, different conditions arise.
What do telomeres have to do with aging? A lot, as it turns out, and we will show you the details here. But first, let's take you briefly into biology class and clarify the basics.
What is a telomere?
In almost every cell of our body, the DNA (in German: DNS) is located in the cell nucleus. DeoxyribonucleicNacid, as it is written out, is greatly simplified as a book in which the genetic information is recorded. However, one book is not enough for this analogy – our DNA is more like a whole library. This library contains 23 books in healthy individuals – the so-called chromosomes.
Telomere abrasion – the best comes last
The last chapter of these books is special and is referred to as telomere. Here, no information for proteins is coded or stored anymore, but the telomeres serve as a protective barrier for the DNA. Every time the DNA is duplicated during cell division, the telomeres shorten. The reason for this is very complex and would exceed the scope at this point. What is important is that the shortening of the telomeres is a normal physiological process that occurs in all humans in most cells.
Over time, the following happens: After a certain number of DNA duplications, a threshold is reached and the telomeres are depleted.This circumstance leads to the cessation of cell function, as well as to the inability to divide. Leonard Hayflick discovered this threshold, and since then it has been known as the “Hayflick Limit”.
The exhaustion of telomeres thus explains the limited ability of cells to divide and, consequently, also partially the limited regeneration potential of tissues. In Hayflick's experiment, an average human cell divided approximately 52 times.
Did you know? The magnesium metabolism plays an important role for the telomeres. Magnesium is needed in many places in our body, but is particularly involved in energy production and electron balance. Both are necessary to maintain healthy telomeres. Supplementation of magnesium has been shown to extend telomere length in humans.In return, other publications have shown that low magnesium levels paired with high homocysteine levels lead to shorter telomeres.
Telomerase as the key to immortality?
But what about the remaining cells that are not affected by this telomere shortening? Well, they possess an enzyme called telomerase, which can extend the telomeres again. This enzyme practically grants a cell immortality. Aha! So researchers just need to manage to introduce this telomerase into every cell? As always in science, it is not that simple, after all, nature had a reason for not equipping all cells with it.
Let’s think back to the first hallmark – genomic instability. Uninterruptedly, a drizzle of external and internal influences pelts our genetic information and thereby threatens the integrity of DNA. As a result, mutations and DNA changes occur every second throughout our body, which can mostly, but not completely, be repaired by the very extensive repair system.
If cells with unrepaired genetic mutations possessed the enzyme telomerase, then the altered cell would be able to merrily continue dividing. The result is an increasingly larger pile of completely degenerate cells, better known as cancer – thus, it is indeed a double-edged sword.
Stem cells – the royal class among cells
Include telomerase-privileged cells such as stem cells or bone marrow cells, which are usually located in protected areas of the body. In addition, they are protected as much as possible from harmful influences on their DNA by various properties and mechanisms – much better than the majority of other cells. Accordingly, the risk of degeneration is significantly reduced.
Did you know? The discoverer of telomerase, Elisabeth Blackburn, is still engaged with the topic today. One of her major works examined the relationship between chronic stress and telomere length.Here she could show that chronically stressed people (in her case, mothers caring for chronically ill children), had shorter telomeres and the activity of telomerase was lower than in the comparison groups.
DNA repair – well intended, poorly executed
To include another factor or rather, another protein, our understanding of telomeres must now be expanded. We already know that DNA is not a continuous strand, but is divided into chromosomes, at the end of which are the telomeres. Telomeres are, when viewed this way, DNA strand breaks – places where the DNA ends.
It is well known that our repair system usually recognizes this immediately in its effort to prevent any loose DNA ends and corrects them. Well intended, but poorly executed in the case of telomeres. The mentioned repair must not take place at telomeres under any circumstances, as this could potentially connect two chromosomes.
If this happens and the cell wants to divide later, it leads to harmful "chromosome breaks" – the genetic material is unevenly distributed to the daughter cells. Both too much and too little genetic information then hinders cell function.
Shelterin – does the name deceive?
As so often, nature comes to the rescue, as we humans and also some other organisms possess shelterin. Shelterin is a complex of six proteins that binds to telomeres and protects them from the repair system (Eng. "shelter"). This initially solves the major problem of chromosome breaks and the impending degeneration of cells – assuming functioning Shelterin.
However, telomeres are not immune to DNA damage, as we have learned in the context of genomic instability. Since telomeres are invisible to DNA mechanics due to Shelterin, actual DNA damage cannot be repaired. This does not sound good at first, as the mentioned circumstance leads to more and more damage that over time can contribute to senescence (intermediate state, a kind of "zombie cell") or cell death.
DNA damage in the area of telomeres is not extraordinarily severe, as it is a non-coding region, meaning that no information for the construction of proteins is read.
Short telomeres and diseases
Shelterin thus protects us from the greater evil. The loss of a few cells is a smaller problem than that of degenerated cells and chromosome breaks. If shelterin or parts of it are missing, a rapid decline in regenerative capacity and accelerated aging has been observed – a phenomenon that also occurs when telomeres actually have a normal length.
In addition to shelterin deficiency, telomerase deficiency also leads to the premature development of diseases.Specifically, lung hardening (technical term: pulmonary fibrosis), anemia with a reduction of all blood cells (technical term: aplastic anemia), and a rare skin disease called dyskeratosis congenita are meant.
All three diseases result in the loss of the regenerative capacity of various tissues. Furthermore, summarized studies have shown a correlation between short telomeres and mortality risk, especially at a young age.
Can we stop telomere shortening?
In mouse experiments, initial successes regarding telomere therapies have already been achieved. For example, telomerase was successfully genetically reactivated in prematurely aged mice with a telomerase deficiency. Another experiment showed a delay in normal aging, without an increase in cancer occurrence, through pharmacological activation.
The next years and decades will show whether our future regarding telomere research looks as rosy as that of mice. In the meantime, we can take a look at what is already proven to work in humans. How can we extend our telomeres?
Did you know? Omega-3 fatty acids are an important part of a healthy diet. They occur in nature mainly in three forms, abbreviated ALA, DHA, and EPA. Scientists have studied for 6 years whether there is a connection between the Omega-3 index and telomeres. And indeed. Patients who consumed little DHA and EPA (and consequently had a low Omega-3 index), showed a much faster telomere attrition rate.
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Plant-based nutrition extends telomeres
The publications on telomere research are sometimes confusing and contradictory. This is also due to how the studies are structured and which telomeres are measured. The simplest way is to measure the telomere length of leukocytes (white blood cells). But this may not always be the best measurement method.
To understand the impact of nutrition, we need to look at the big picture.In the context of genomic instability, we have already seen that our DNA is constantly exposed to oxidative stress. A little of it is beneficial, too much seems to accelerate aging. A plant-rich diet, rich in secondary plant compounds seems to promote this balance and thus indirectly contributes to longer telomeres.
Sirtuins and Telomeres – two partners for longevity
If you take a closer look at the molecular connections between telomeres and secondary plant compounds, you will encounter the sirtuins. Sirtuins are often described as longevity genes, as Sirt-1 and Sirt-6 are particularly associated with better health.
The Sirtuins can be particularly effectively activated by fasting , but some secondary plant compounds like resveratrol are also potent Sirt activators. High Sirtuin levels help us preserve DNA from damage, support telomeres, and affect epigenetics.
Conclusion on telomere attrition
Telomeres play an important role in the aging process. For a certain period, telomeres were even the "stars" in aging research. It was believed that one simply needed to extend them to live forever.It's not quite that simple, and despite some setbacks, we know much more about this important structure in our cells today, thanks in part to Elisabeth Blackburn. As part of the Hallmarks of Aging, they are a building block on our path to slowing down aging.
The next article in this series will focus on the third hallmark of aging: Epigenetic changes.
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