Article series: The relationship between telomeres and cancer 1. What is a telomere? Do smoking and obesity trigger telomere shortening?

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Telomeres are structures found at both ends of chromosomes. They protect our genome, all our genetic information, against degradation. As we know, cells are the basic building blocks of our bodies. Our body cells multiply using a system called mitosis . During each division, DNA is copied so that an equal amount of genetic information passes to the cells and two cells of the same type are formed. During this copying, telomeres at both ends of chromosomes shorten. This is a natural process, and telomere shortening has been associated with aging.
When telomere length reaches a critical point, our cells stop dividing by mitosis and undergo apoptosis , called programmed cell death , and are eliminated. In light of all this information, telomeres act like a biological clock determining a cell's lifespan.
Although telomere shortening is both a natural process and a protective mechanism preventing excessive, uncontrolled cell division, poor nutrition or exposure to harmful chemicals accelerates telomere shortening.
Examining telomere structure reveals long sequences of bases. We can think of these as letters in a book. If we imagine these letters beginning to disappear with every division, we can better understand the importance of telomeres.
Can telomere length be increased?
The answer to this question is the activity of enzymes called telomerase . These enzymes add new letters to the ends of the book, repairing the erased sections. The cell thereby escapes aging. Telomerase activity is very high during embryonic development, then is suppressed and becomes inactive. One reason cancer cells are called cells that never die is that they reactivate their telomerase enzymes.
Recent studies have found that obesity and smoking trigger telomere shortening. Particularly in tobacco users, greater telomere shortening has been observed in blood cells. It was found that 25.7-27.7 base sequences are deleted from telomeres in women's white blood cells each year. Another interesting aspect of the research is that smoking a pack a day causes the deletion of an additional 5 base sequences. Thus, a person smoking a pack every day for 40 years loses a further 7.4 years of life because of telomere shortening. According to the scientists who conducted the research, telomere length can be used as a useful biomarker to examine the effects of smoking on the body and may help measure each individual's rate of aging.
Obesity has an effect on telomere shortening associated with increased levels of certain substances inside cells that damage DNA. Called free oxygen radicals, these substances create stress inside cells, causing DNA damage and telomere shortening. Numerous studies demonstrate this mechanism. Telomeres in obese women have been found to be shorter than those in other women of the same age. Telomere shortening has been determined to cause a loss of 8.8 years from average life expectancy in obese people.
How does telomere shortening trigger cancer development?
Numerous studies have demonstrated that telomere shortening triggers cancer development. Shortened telomeres create genomic irregularities. Returning to the book example, neglect begins to erase the book's letters over time. Erasing the letters makes the book meaningless. Similarly, cells whose genetic information has been erased become unable to perform their normal functions and begin to multiply uncontrollably and become cancerous. This is why telomeres in cancer cells have been found to be very short. People with short telomeres have been reported to have a high risk of lung, liver, gastrointestinal, head and neck cancers. However, cells that become cancerous have changed to protect their telomeres; therefore, attempting to lengthen telomeres artificially (through external intervention) carries a serious cancer risk. A cell becoming cancerous cannot be explained by telomere length alone (see, the 10 hallmarks of cancer)
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