- Telomeres are the short caps at the ends of our DNA strands that prevent the DNA from unraveling.
- You can compare telomeres with the caps at the ends of shoelaces which prevent them from unraveling.
- With each cell division telomeres become shorter.
- After many cell divisions, the telomeres have become so short that they cannot protect the DNA anymore, which starts to get damaged.
- Telomeres not only shorten, but also get more and more damaged during aging, which also leads to cellular stress and DNA instability.
- Telomere length is not strongly correlated with lifespan. However, the speed at which telomeres shorten is strongly correlated with lifespan.
- Cancer cells have the ability to continuously lengthen their telomeres, making them “immortal” in the sense they can keep dividing without their telomeres becoming too short, which would lead to cell death.
- This led many scientists to believe that lengthening telomeres increases the risk of cancer.
- However, studies have shown that lengthening telomeres does not contribute to a higher cancer risk. In fact, longer telomeres can protect against cancer, especially given short telomeres are associated with genetic instability, which increases the risk of cancer.
THE THREADS OF LIFE
Telomeres are short pieces as the end of our DNA strands.
You can compare telomeres to the caps on our shoelaces that prevent the laces from raveling out.
With every cell division, telomeres become shorter. When they are too short, cells stop dividing. These cells cannot continue supporting and forming our tissues properly.
When after many cell divisions the telomeres have become too short, the DNA strand starts to unravel: it becomes unstable, leading to damage to the cell.
Too short telomeres also send out several “damage signals” to the cell, which then starts to function less properly.
You can look at telomeres as a clock that ticks down with every cell division until the time is up.
The Aging Process
Given that during aging telomeres become shorter after each cell division, it was assumed that telomere length could tell you something about your remaining lifespan. The shorter your telomeres, the less long you would live.
However, various studies showed that there is no clear correlation between telomere length and lifespan (R).
Which is not surprising. Mice for example have telomeres that are ten times longer than humans. But mice don’t live ten times longer than humans.
These insights led a lot of people to believe that telomere length is not important in aging.
However, studies show that the speed at which telomeres shorten is significantly correlated with the rate of aging (R). Telomere length is not correlated with lifespan, but the rate at which telomeres shorten is.
To give a concrete example: mice have telomeres that are much longer than telomeres in human cells. But given that mice telomeres shorten much faster than human telomeres, these little critters age much faster.
Another misconception is the idea that there are cells in the body that hardly divide (like muscle cells or brain cells), so their telomeres do not really become shorter, but still these cells age. That is true, but during aging, the telomeres still become damaged (without really becoming shorter), which also contributes to cellular dysfunction.
Secondly, there are many dividing cells surrounding and supporting the non-dividing brain cells or muscle cells, such as blood vessel cells, fibrous tissue cells, macrophages, and glial cells (these cells support and nurture the brain cells). If these supporting cells become older because of telomere shortening due to their divisions, they will start to malfunction, leading to damage to the non-dividing brain cells or muscle cells.
Another misconception is that lengthening telomeres will automatically result in an increased risk of cancer. After all, cancer cells are immortal cells that can keep dividing thanks to their ability to lengthen their telomeres with the aid of an enzyme called telomerase. Studies have indeed shown that in mice with upregulated telomerase there is an increased risk of cancer.
However, in these studies the telomerase was continuously activated since birth. This results in continuous, uncontrolled telomere activity. On the other hand, other studies show that if the telomerase is upregulated in adult mice only occasionally, the mice live longer and do not have an increased risk of cancer (R,R). In other words, upregulating telomerase in a factulative (now and then) manner instead of in a constitutional (continuous) way does not lead to an increased risk of cancer. It could even lead to a decreased risk of cancer given that too short telomeres lead to genetic instability which can in fact increase the risk of cancer.
Other studies showed that mice with very long telomeres live longer and don’t have an increased risk of cancer (R). In these mice, the telomere activity was not increased, they had extra long telomeres since birth.
Some people are born with genetic mutations leading to short telomeres. These are diseases like pulmonary fibrosis, aplastic anemia, and dyskeratosis congenita. These people suffer from problems with the immune system (white blood cells are fast dividing cells of which the telomeres grow short quickly), hair and nails (also fast dividing tissues) and the blood cell formations (the stem cells that create blood cells divide very fast; every second two million red blood cells are created).
These and other observations suggest that telomere shortening is especially important for fast dividing cells, like the stem cells that generate white blood cells, red blood cells, hair, and skin cells.
NOVOS’ Approach to Telomere Shortening
NOVOS Core contains ingredients that can maintain telomere length for longer.
For example, pterostilbene can induce telomerase, an enzyme that lengthens telomeres.
Magnesium is also necessary for proper functioning of telomerase.
Lithium intake has been correlated with longer telomeres.