A study with almost 500,000 people has shown that the chromosome end fragments in the white blood cells of the immune system are shortened by cigarette smoking. These final fragments are known as telomeres, and the telomer length is an indicator of how quickly we age and the ability of the cells to regenerate and repair themselves.
The study shows that the smoking status and the number of smoked cigarettes can shorten the length of the leukocyte elomers, an indicator of aging, tissue regeneration and self-tolerance. This means that smoking cigarettes can accelerate the aging process when quitting in order to significantly reduce the associated risk.
Telomers are like metal or plastic shits that stop the fringing of laces. They are repeated DNA sequence lengths that the chromosome ends. The telomeres become a little shorter every time a cell shares and gradually becomes so short that the cell is no longer able to share and die.
This process is part of aging. The length of the telomeres in white blood cells, which are known as leukocytes, was associated with smoking, but there were not many studies as to whether the amount smoked and smoking status actually led to the telomer length shortened.
The data was analyzed from the British Bio Chancer, which contains health and genetic information from 500,000 people. They examined whether a person was currently smoking, a former smoker or a nie smoker addiction level, the number of smoking cigarettes (smoking years) and the information on leukocyten telomer length obtained from blood tests.
They used a method known as Mendelian randomization, in which gene variations, which are referred to as individual nucleotide polymorphisms, are used, which we inherit to lead to how the exposure to a variable environmental factor that contains smoking Condition or a health problem such as shorter leukocytes -elomeren is associated.
Mendel’s randomization avoids the challenge of other, often unknown factors that influence the results, which enables researchers to examine whether a specific factor causes a disease instead of just being connected to it.
Data from 472,174 British BioKank participants were used, and 113 individual nucleotide polymorphisms associated with smoking status, 15 individual nucleotide polymorphisms for participants who are currently smoking, 78 single nucleotide polymorphisms for participants who have never smoked, and 20 individual nucleotid policies for Participants who had to smoke for participants before smoking were for participants.
The researchers found that there was a statistically significant connection between the current smoke status and a shorter leukocyte telomer length, while former smokers and never smokers did not show a shorter length of the Leukocyten -Telomer length.
People who previously smoked tends to have a shorter telomer length, but this was not statistically significant. A shorter length of Leukocyten -Telomer length was observed for people who smoked most cigarettes.
In summary, smoking can shorten the length of the Leukocytes telomer, and the shortening effect is stronger if more cigarettes are smoked.
Observation studies have associated a length of Leukocyten -Telomer length with numerous diseases, including muscle loss, diabetes and cardiovascular diseases.
