Motherhood negatively impacts a woman based on an examination of her telomeres. These are essential parts of human cells that affect how the cells age.
When researchers at George Mason University in Virginia examined the caps at the end of each strand of DNA that protects the chromosomes, they found that the telomeres of women who had children are the same length as 11-year-old girls who are childless, Stars at 60 reported.
Greater than shortening caused by smoking
The telomeres shorten and get worn over time when people age, the study – published in the Human Reproduction journal – said. After the researchers studied data from around 2,000 women aged 20 to 44, they observed that in mothers, the shortening of telomeres was greater than the shortening caused by smoking or being overweight.
It was seen in women who had five or more children. When compared to women who had no children, their telomeres were shorter. When they were compared with women who had four or fewer kids, it was relatively shorter for the women with five or more children, Anna Pollack, a researcher, said.
For each year, women lost about 10 base pairs of DNA. But in the case of women with five or more children, she had 116 fewer pairs of DNA. Pollack noted that some studies likened the length of the telomeres to mortality risk and risk of other major ailments.
However, Pollack stressed that the findings do not mean early death by 11 years for women who had many children. She stressed that the study should not be interpreted as a sign for women to stop bearing children.
Charging the telomeres
Meanwhile, researchers at Arizona State University found a new way to potentially supercharge the telomeres. The little caps that sit at the end of each arm of the X-shape are made up of repeating sequences of DNA. It takes the hit with each cell division so that no important genetic information is lost, New Atlas reported.
In turn, cell division is dictated by the genetic blueprints contained in the chromosomes, the X-shaped threads of DNA. With every division, a small piece of information is lost until the chromosome degrades eventually to the point that the cell can no longer divide. The reduced cell growth is seen in disease associated with aging.
Even if the telomeres are the body's natural defenses against the process, it could not keep up with taking the hit forever. Over time, the telomeres wear down which correlates with the length of the telomeres with human lifespan and healthspan.
After the researchers realized the relationship, for years they tried to find ways to slow down the degradation of telomeres, repair it, or increase its length. Most of the research target the telomerase, the enzyme that replenishes the telomeres when it degrades. Although it could hold off aging for a while, in the end, the telomeres die.
How the telomeres work
To find a way to help the telomeres, the scientists studied how it works. The researchers explained that the telomerase encodes a repeating string of six nucleotides – GGTTAG – onto the tips of chromosomes. After each sequence, the researchers noticed a pause signal while the cycle restarts. The signal, though, stays active during the next sequence which could reduce the telomerase's efficiency.
Julian Chen, the lead researcher of the study, explained that to ensure the precise synthesis of correct telomeric DNA repeats, the telomerase has a built-in braking system. But the brake also limits the overall activity of the telomerase enzyme.
If scientists could find a way to properly release the brakes on the telomerase enzyme, it could potentially restore the lost telomere length of adult stem cells and even reverse cellular aging, Chen said. If they could target the pause signal, the researchers said that it could supercharge the function of telomerase and keep adult stem cells healthier for a longer time.
But the brake cannot be removed. The scientists pointed out that it is an important safety feature of the telomerase. Like a vehicle without a brake, it can crash or in human body terms, cause cancer. Since tumors are basically cells that grow out of control, cancer cells hijack the telomerase to keep growing. To avoid that situation, the researchers said that any potential anti-aging treatment that eases the brakes in telomerase must target adult stem cells only.
They emphasized that the activity of telomerase in adult stem cells only slows down the countdown of the molecular clock. It does not completely immortalize the cells, News-Medical.net pointed out. In old people, adult stem cells become exhausted because of the shortening of the telomeres. The result is longer healing times and eventual degradation of organ tissues from inadequate cell populations.
Some of the human diseases that have been genetically linked to mutations that negatively affect telomerase activity and speed up the loss of telomere length are dyskeratosis congenital, aplastic anemia, and idiopathic pulmonary fibrosis.
[researchpaper 리서치페이퍼=Vittorio Hernandez 기자]