Causes of Human Aging

Types of aging in the human body are diverse. One such type of aging at the molecular level is telomere shortening. Telomeres are complexes of proteins with RNA that protect the ends of chromosomes. With each cycle of cell division, telomeres are shortened, which leads to “replicative aging” of the cell. Since telomeres shorten during aging in various organs and tissues, their length can be a biomarker of aging. Telomeres are the ends of chromosomes that are thought to have a protective function in chromosomes. Starting from infancy, their sizes are gradually reduced: on average, up to two times by adulthood and up to four by the elderly. According to scientists, this is one of the causes of aging in the body.

Telomeres shorten due to the following factors:

• unhealthy diet (overabundance of sugar and omega-6 in the diet, the use of processed foods);
• overeating and excess weight;
• environmental pollution (chemical, electromagnetic, sound);
• poor emotional and social relationships with other people;
• sedentary lifestyle;
• lack of sleep;
• constant stress;
• chronic pain;
• smoking;
• insulin resistance;
• chronic inflammation;
• vitamin D deficiency.

Another factor that causes the shortening of telomeres, as studies have shown, is infection. In Petteri Ilmonen’s lab, scientists experimentally tested whether Salmonella enterica is the cause of telomere shortening in domesticated wild mice. Mice were challenged several times with five strains of S.enterica over several months. The control group included related mice. A real-time test determined telomere length in white blood cells after infection. The results showed that repeated Salmonella infection causes telomere shortening, especially in males compared to females. Scientists also found that faster telomere shortening increased mortality risk, but these results were not statistically significant.

In people under prolonged stress, telomeres shorten much faster than their peers in a normal situation. The length of telomeres in women experiencing long-term chronic stress is equivalent to that of those who are 10 years older but lead a normal life. Therefore, to prevent cell aging, it is important to keep the body in good shape with the help of physical exercise, learn to manage stress, and lead a healthy lifestyle. Positive emotions and endorphins will also be a good addition to this lifestyle. And even more fun will bring the game to play-fortune.pl/kasyno/wyplacalne-kasyna where bonuses and gameplay will help everyone improve their health and financial condition.

New POI

Now the interests of gerontologists are gradually shifting from telomerase and life extension as such to other biological mechanisms and indicators. If it is impossible to guarantee a person’s lifespan to 100, 120, or 150 years, perhaps there are ways to improve the quality of life in recent years – even if a person lives “only” 80 years. It’s no secret that the last years of life often become a real torment. Many metabolic, autoimmune, malignant, and degenerative diseases develop with age. Of course, many researchers have tried to find a way to prevent this. However, for a long time, the reason for the development of this complex remained unclear.

The main cause of the development of a group of senile pathologies is chronic systemic inflammation that develops with age. Among the many candidates for the role of the causative agent of chronic inflammation, the theory of senescent cells has received the greatest scientific support. In 2011, a breakthrough came in this area when a team led by James Kirkland and Jan van Deursen at the Mayo Clinic showed that deleting cells that carry one of the markers in mice. The so-called p16 protein, involved in cell life cycle control, leads to partial rejuvenation of individuals.

Final Thoughts

Until recently, telomeres were considered the main way to prolong human life. Today, it seems, the “first telomeric winter” is coming: everything that could be done with the help of the “immortality enzyme” has already been done. Telomerase does not point the way to a long life; it only helps us know our limits to understand that the lifespan is between early aging and uncontrolled tumor formation. The attention of scientists is gradually shifting to other ways to combat aging and prolong life. Senescent cells, various diets, and medications – may not fully understand ways to add years to a person. What will happen to the telomere? Perhaps, from hope for humanity, it will turn into a toy for scientists for some time: strange, but in a sense, it is not bad. But for now, recipes for old age should be looked for elsewhere – it could be like climate change, ecology, play-fortune.pl/metody-platnosci/ezeewallet or completely new drugs.Thus, after studying telomeres, scientists can conclude what is necessary for life expectancy: eat right and lead a healthy lifestyle; avoid stressful situations, infections, and obesity; the diet requires a certain amount of vitamins B12, folic acid, B6, E, D and the mineral elements magnesium and zinc. All these factors affect genetics in general and the cell’s lifespan. As mentioned above, a healthy lifestyle is enough to feel young and healthy.

Less speculation would allow it to be again “just” an important element for biological, biochemical, and genetic research. Of course, it is a pity if this road to immortality ends as a dead end. But what can you do: many useful lessons can be learned from the experience with telomerase. In a year or ten, a discovery in the field of chromosomal genetics will explode the scientific world and raise a new wave of interest in telomeres and their features.

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At the same time, there is new data on the pathogenesis of atherosclerosis, the analysis of which may be reflected in the approach to the treatment of this group of patients. Atherosclerosis appears to be an age-associated disease. Premature biological aging (which usually differs from that chronological aging) contributes to the pathogenesis of atherosclerosis. This is confirmed by the results of clinical studies, indicating that in stable atherosclerotic plaques, there is a small number of old cells. In contrast, in complicated atherosclerotic plaques, there is a deposition of old cells. Telomere shortening serves as a biological trigger mechanism that explains cellular aging.

Oxidative Stress – Atherosclerosis and Telomere Length

Oxidative stress is a common pathophysiological mechanism responsible for the development of age-related diseases and aging. At a high local level of reactive oxygen species (ROS), their biological effects consist of a direct oxidative effect on all cell components (including proteins, lipids, and DNA), which leads to the initiation of chain chemical reactions. Such as lipid peroxidation, which occurs mainly within the bilayer of membranes, nuclei, and mitochondria. Telomeres and risk factors for atherosclerosis:

• Smoking. There is a direct correlation between smoking and oxidative stress. This may explain the results of numerous studies that indicate a shorter telomere length in tobacco users.
• Arterial hypertension. The results of numerous studies indicate that there is a relationship between telomere length and blood pressure. In contrast, the shortening of telomeres, causing changes in phenotypic expression in vascular cells, can contribute to hypertension.
• Obesity. There is no doubt that obesity is closely associated with the risk of developing diseases associated with the cardiovascular system. An overweight patient usually has risk factors such as hypertension, metabolic syndrome, and dyslipidemia. Adipose tissue is a source of ROS, pro-inflammatory cytokines, and various bioactive molecules that affect function and structural integrity.
• Diabetes. Obesity is only the beginning of a cascade of physiological events that lead to various age-associated diseases, including diabetes mellitus (DM). It is now known that hyperglycemia, even at the stage of pre-diabetes (impaired glucose tolerance), increases oxidative stress and, ultimately, leads to cellular aging.
• Insulin Resistance. The presence of insulin resistance harms endothelial function. This relationship is explained by the effect of insulin on mitogenesis. Under hypoxia conditions, excess insulin promotes the secretion of various growth factors and cytokines, leading to pathological vascular remodeling of blood vessels (hypertrophy of smooth muscle cells, endothelial dysfunction, thickening of the intima-media).

Ways to Protect Against Cellular Aging

Drug and non-drug therapy of clinical manifestations of atherosclerosis can indirectly affect the processes of cellular aging. Among non-drug methods, an active lifestyle, a high level of physical activity, a healthy diet, and a reduction in the salt intake should be noted.

The Cherkas LF study showed that a sedentary lifestyle (in addition to smoking, a high body mass index, and a low socioeconomic status) impacts telomere length and can accelerate the aging process. The study included 2401 twins from England.

(2152 women and 249 men aged 18 to 81). It turned out that the length of telomeres in more active participants was 200 nucleotides more than less active (7.1 and 6.9 kilobases, respectively).

Similar results were obtained in a study by J. Krauss, who analyzed the length of telomeres in 944 patients with a stable course of coronary heart disease. Telomere length in individuals with a low level of physical activity was less than in individuals with a high-level physical activity (53493781 b.p. and 5566±3829 p.o., respectively).

The issue of rational nutrition is also important, in particular, a sufficient diet of omega-3 polyunsaturated acids. A sufficient dietary intake of omega-3s is associated with low levels of F2-isoprostane (a standard indicator of systemic oxidative stress) and higher levels of antioxidant enzymes (catalase and superoxide dismutase), which reduce oxidative stress.

Particularly noteworthy are drugs that are prescribed for the treatment of diseases of the cardiovascular system. Acetylsalicylic acid is known to have antithrombotic and anti-inflammatory effects. In addition, ASA reduces the synthesis of dimethylarginine, an endogenous inhibitor of NO synthase, thereby reducing oxidative stress and the rate of aging of endothelial cells. Some scientists hypothesize that the effect of drugs of this group on telomeres can explain the increased survival rates of cardiac patients on long-term statin therapy. Spyridopoulos proved that statins could increase the migratory ability of endothelial progenitor cells through the effect of the TRF2 protein, which is part of the telomere T-loop shelterin complex.

Conclusion

Treatments aimed at delaying cellular aging by influencing telomeres and telomerase. The development and progression of atherosclerosis, in most cases, occurs over decades and does not always have clinical manifestations in the early stages. Analysis of individual risk factors for atherosclerosis is not always highly effective. Numerous studies indicate that telomere length reflects the total degree of DNA damage throughout a person’s life by factors responsible for the development of atherosclerosis and its complications. The rate of telomere shortening increases even before the onset of a clinical disease, which may be of diagnostic and prognostic value – measuring the length of telomeres in the first years of life may indicate a genetic predisposition to CVD.

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Telomeres are regions of DNA at the ends of chromosomes that do not code for any trait. Telomeres are needed to protect the bulk of the DNA from damage during cell division. Before the cell divides, a special DNA enzyme, polymerase, moves along the DNA strand and synthesizes a copy. But the polymerase is not able to start working from the very tip of the chromosome, so it starts doubling it by moving slightly away from the edge. As a result, the chromosome shrinks slightly after each division. To ensure that the coding regions are not affected by this reduction, telomeres are located at the ends of the chromosomes. But gradually, after new and new cycles of division, telomeres will shrink more and more – this is the aging of the cell.

Telomere shortening is associated with aging and age-related diseases, but when studying these processes, telomeres are usually measured in cells that are easy to obtain from the patient, most commonly blood cells. Until now it has remained unclear to what extent telomeres in blood cells can reflect the pattern in other body tissues.

To investigate this question, the authors of the work used the Genotype-Tissue Expression (GTEx) project, which collects tissue samples from a large number of people. In total, they analyzed more than 6,000 samples of 23 different tissues from about a thousand people. They found that of these 23 tissues, 15 showed a clear positive correlation with telomere length in whole blood cells, confirming the use of blood cells as an indicator of telomere length in hard-to-reach tissues such as brain and kidney tissue.

Along the way, the scientists tested several previous theories about telomere length in various individual cases. Some have been confirmed, such as longer telomeres in people of African descent. Others were not, such as the assumption of longer telomeres in women. The report of shorter telomeres in smokers was only partially confirmed; this is indeed observed, but only in certain tissue types. These results will help to understand the extent to which telomere length is genetically determined, and how it can be affected by lifestyle, environmental exposure, or epigenetic changes over the course of a person’s life.

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A study conducted by U.S. scientists shows new ways to treat congenital dyskeratosis and other diseases associated with telomere defects and premature aging of cells. An article about this work was published in the journal Stem Cell.

Telomeres are the end sites of chromosomes that serve protective and regulatory functions. In each cycle of cell division telomere sequences shorten due to the peculiarities of the DNA polymerase enzyme. This fact became the basis for the so-called marginotomy, a theory that views telomeres as similar to a chromosomal timer that counts down the cell divisions remaining until cell death.

Some cells in the body (e.g., stem cells) synthesize the telomerase enzyme, which completes the chromosomes after divisions and allows cells to remain “forever young. If telomerase expression is disrupted, body tissues begin to age prematurely. This can lead to the development of a whole range of diseases – in addition to the aforementioned dyskeratosis, pulmonary fibrosis and non-alcoholic cirrhosis of the liver.

Dyskeratosis itself can be caused by one of many mutations. Most of these mutations disrupt telomerase formation or function, particularly by destroying two molecules called TERT and TERC, the main subunits of the enzyme. TERT is a telomeric reverse transcriptase, a molecule capable of catalyzing DNA synthesis on the RNA matrix. TERC is the very matrix required for telomere completion.

Microphotograph of chromosomes with labeled telomeres / © Stat
Microphotograph of chromosomes with tagged telomeres / © Stat
The authors of a new paper led by Sunit Agarwal showed several years ago that the PARN gene is involved in the development of telomere diseases. Its proper functioning is important for normal TERC formation and stabilization. In the current study, scientists focused on PAPD5, a protein that suppresses PARN and destabilizes the TERC molecule.

The scientists conducted extensive screening studies to identify PAPD5 inhibitors, testing more than 100,000 known chemicals. Having obtained an initial list of 480 candidates, the scientists further narrowed their choice down to a small number of potential inhibitors. These molecules were tested on cell cultures obtained from patients with dyskeratosis.

All of the tested substances increased TERC levels in the cells and promoted telomere regeneration to their normal length. However, the more difficult task was to find out whether the treatment would be safe and specific, affecting only stem cells containing the desired molecules.

To do this, the selected compounds were tested on laboratory mice, which had previously been transplanted human stem cells with mutations in the PARN gene, leading to the development of dyskeratosis. The action of PAPD5 inhibitors led to restoration of telomere length in the transplanted cells without affecting the animals’ ability to form different types of blood cells.

In the future, Agarwal and his colleagues hope to confirm the benefits of inhibiting PAPD5 for other diseases associated with telomere and telomerase malfunction – and possibly affect the aging process in general. The two substances, codenamed BCH001 and RG7834, are considered the most promising of all potential drug candidates by the scientists.

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The international T2T consortium announced the successful completion of the work. Twenty years after sequencing the human genome, scientists have figured out the remaining portions – about eight percent – that were the most difficult to sequence. This is reported in a press release from the U.S. National Institutes of Health (NIH); an article about the work was published in the journal Science.

The human genome was almost completely defined back in 2003, as part of a global study of the Human Genome Project. For that time, the task was enormous, and hundreds of researchers from different universities and countries participated in its solution. They had successfully sequenced about 92 percent of DNA – the genes and sections between them that make up euchromatin. In cells, euchromatin is active, so it remains “unraveled” and twists into a more compact form only to divide.

In contrast, heterochromatin permanently maintains its compact form and does not encode proteins. It performs primarily auxiliary functions, maintaining the structure and integrity of chromosomes, ensuring their interaction with proteins, and the like. Heterochromatin is located, for example, in centromeres – the sites where a pair of sister chromosomes join together to form a recognizable “X” – and in telomeres, the end sites of chromosomes. This DNA is characterized by the presence of long repetitive sequences, the identification of which is a great challenge.

Recall that to sequence a strand of DNA, you have to cut it into many fragments, then determine the nucleotide sequence of each fragment and, finally, combine the resulting codes in the correct original order. But if the code is hundreds of short repeats that are indistinguishable from one another, such work becomes virtually impossible. That is why the Human Genome Project participants had to skip this small part of the genome, for the benefit of science and medicine it plays far from the main role.

However, a complete understanding of the structure of the genome requires at least a complete sequence, and over time, sequencing technologies have made great strides forward. Therefore, a new consortium Telomere to Telomere (T2T) began its work a few years ago with the goal of understanding heterochromatin regions. In 2021, its participants presented a “rough” result, and now – the final, covering the missing eight percent of the genome.

To do this, the biologists had to go for a little trickery, using DNA from a cell line with a hereditary disorder for sequencing, as a result of which they carry two identical copies of each chromosome (instead of one maternal and one paternal). Therefore, the T2T consortium has not completed its work: at least its members have yet to sequence the heterochromatin on the unpaired Y chromosome.

The importance of this work should not be underestimated. In the past, many sections of heterochromatin were indeed considered “junk” DNA, accumulated over billions of years of evolution and playing no role in the life of the human body. Today, scientists understand that these fragments have important functions, not only structural, but also, for example, regulatory, controlling the activity of euchromatin genes. Many severe diseases are associated with heterochromatin malfunction.

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Telomeres are the end sections of chromosomes. The telomeric portions of chromosomes are characterized by their lack of ability to attach to other chromosomes or their fragments and serve a protective function. The genes in question are TERT and TERC, which are present in 51% and 72% of the world’s population, respectively, but their variations are very rare.

There is a high barrier to the development of gliomas, and perhaps because the brain has special protection.

The TERT and TERC genes are responsible for lengthening telomeres. However, as Wrench notes, this has both positive and negative qualities. Long telomeres are not only responsible for longevity, but also lead to the development of glioma.

Glioma is a tumor that is part of a heterogeneous group and is of neuroectodermal origin. It is the most common primary brain tumor.

Although longer telomeres may be a good thing for humans, reducing some health risks and slowing down aging, they can also cause some cells to live longer than they should, and this, it is suggested, may be a sign of cancer development.

In the study, scientists analyzed the genomic base of nearly 40,000 people. They found that short telomeres were associated with cardiovascular disease.

Wrench and her colleagues examined data from 1,644 glioma patients and 7,736 healthy individuals. She found that most glioma patients had variations in TERT and TERC genes as well as enlarged telomeres.

Scientists are to continue the study and study the influence of the TERT gene in the development of lung, prostate, breast, leukemia and colorectal cancers.

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How does the “freezing” process work? Through perfusion – the process of replacing blood in the body with a non-freezing solution – a cryoprotectant that prevents cellular damage when frozen. The substance is injected into the person immediately after death is fixed, after which the body is frozen to liquid nitrogen temperature – minus 196˚C – and stored in Dewar vessels.

In the strict sense, cryonics is not a science, but a field of practice. It arose out of the ideas of cryobiology, which studies the effect of low temperatures on living organisms. Experiments with freezing and thawing certain types of tissues, cells, organs and embryos led to the idea and later to the cryopreservation of the human brain and human beings.

According to the law of accelerated returns (referring to the exponential acceleration of technological progress), medical technologies that can improve biological systems, prevent disease and even reverse aging may appear in the next 30-40 years.

Optimists are confident that these predictions will come true and those who have been frozen in our time will be able to meet people they know, such as their adult grandchildren, and enjoy a healthy life in the distant future.

Biohacking
Biohacking originated in Silicon Valley; literally, the term means hacking the body and implies reaching new levels of physiological and psychological processes in the body.
Adherents of biohacking plan to live as long as possible, refining the mind and body while maintaining and multiplying physical and mental health, youthfulness, awareness and productivity.

In their attempts to break the body, biohackers practice different kinds of fasting, different dietary trends, spiritual practices, regularly submit to all kinds of tests and research, take handfuls of biological supplements and serious medications, undergo experimental and questionable procedures, implant electronic chips and implants, wear especially sensitive hearing aids. And what else is being done… The most desperate do it all at once.

Biohacking is usually not cheap. One of the most famous biohackers, Sergei Fage published an article in which he painted his way to become superhuman. In order to become a perfect version of himself and live longer, he had already spent 200 thousand dollars.
Biohackers practice self-improvement at the genetic level as well. A former NASA employee and head of the startup Odin, Jos Zeiner, injected himself with an injection that should insert the superpower genes into his DNA. The biohacker claimed that in six months or a little more he would gain incredible muscle mass.

At the end of March 2017, the public was excited by the news about the new brainchild of inventor and businessman Ilon Musk: he announced the creation of the company Neuralink, which will deal with the technology of direct connection of the human brain with the computer.
The “electronic lace” technology (neural lace), according to the founder of Tesla and SpaceX, will allow a person to receive any information from the Internet and transmit messages to a computer without any physical interaction with it. Work on such an interface began in 2016.

Avatar
Can a person become immortal? In 2013 in New York at the Global Future conference, this question was stated in the international Avatar project.

The authors of the project of unlimited extension of human life offered not a new remedy Macropoulos, not the secrets of immortality worms-planarium and not even a super diet, but very real achievements of neurotechnology and computer technology.

Tens of millions of people already live among us with artificial artificial hips and knees, implanted pacemakers, and brain-implanted electrodes for epilepsy and Parkinson’s disease treatment. The gradual replacement of failing human organs with their artificial counterparts is quite realistic in the coming decades.

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In each division cycle of a somatic cell, telomeres are shortened by 50-200 bp due to incomplete synthesis of the lagging strand during DNA replication ( Srinivas et al., 2020 ). This is due to the inability of DNA polymerase to completely replicate the 3′-end of the DNA chain (a phenomenon commonly referred to as the “end replication problem”) ( Watson, 1972 ; Olovnikov, 1973 ). Moreover, since the G-rich telomere repeat sequence is known to be very susceptible to oxidative damage ( Oikawa and Kawanishi, 1999 ), telomeres can be directly damaged by oxidative stress, leading to cell aging ( Barnes et al., 2019.). Given this, it has recently been suggested that telomere-induced aging of postmitotic cells may be a key factor in aging ( von Zglinicki et al., 2020 ).

In culture, somatic cells have a limited replication potential, reaching a point in time when cell division ceases. This point in time is characterized by the shortening (“depletion”) of certain telomeres to a critical size incompatible with their function, leading to cell cycle arrest and cell aging. Therefore, TL is thought to limit the number of cell divisions and act as a “mitotic clock” in the cell ( Olovnikov, 1996 ), and telomere shortening may cause a decrease in proliferative potential and be a marker of cellular aging ( Liu et al., 2019a). In multicellular organisms, TLs are very heterogeneous in different tissues and cell types, depending at least in part on the rate of tissue-specific proliferation, but they generally tend to decrease with age in all proliferating tissues ( Demanelis et al., 2020 ).

The size of critically short (“unclosed”) telomeres can be stabilized by telomerase, a reverse transcriptase enzyme that can lengthen the ends of chromosomes de novo . The two major components of human telomerase are telomerase reverse transcriptase (TERT) and telomerase RNA-component (TERC), which serve as the matrix for telomere elongation (Rubtsova and Dontsova, 2020). In humans, this enzyme is known to be expressed early in intrauterine development, is inactivated in most adult cells except germline cells, embryonic stem cells, and immune cells, and is reactivated in most cancers ( Shay and Wright, 2019 ) .) Telomerase has been shown to be insufficient to maintain normal TL even in proliferating stem cells that can express it; consequently, these cells also experience gradual telomere shortening ( Lai et al., 2018 ; Celtikci et al., 2020 ) ( Figure 1 ) . Since most human somatic cells have low or no telomerase activity, this leads to age-related telomere erosion and related pathological processes. Thus, telomerase activation is considered by some authors as a promising therapeutic method for the treatment of degenerative aging disorders (Bernardes de Jesus and Blasco, 2011 ; Prieto-Oliveira, 2020). However, although telomerase does have potential in anti-aging medicine, the fact that it is overexpressed in approximately 90% of human cancers raises doubts about the applicability of telomerase activators in clinical practice (Smith-Sonneborn, 2020).

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What is the essence of the Nobel results of Blackburn, Shostak and Greider, and how do they correlate with Olovnikov’s hypothesis? Telomeres are the ends of linear chromosomes. The role of telomeres in ensuring the “correctness” and stability of chromosome inheritance became apparent as early as the 1930s (by correctness and stability we mean that each of the daughter cells receives the entire set of maternal chromosomes and this process can occur an infinite number of times). It was also understood that telomeres of different chromosomes were interchangeable. At the beginning of the 1980s, the mechanism of the stabilizing function of chromosomes was unknown. The main focus of Liz Blackburn’s scientific work before her Nobel results was to study the linear DNA of the infusoria Tetrahymena. This single-celled organism has a gigantic size compared to normal cells, and therefore the genes in the genome itself are not sufficient to meet the needs of the huge volume of cytoplasm. The problem is solved by amplification (increasing the number of copies) of some important genes. In this case, each amplified gene is located on a separate linear DNA molecule. These linear molecules are “properly” distributed into daughter cells, i.e. they behave as mini-chromosomes. The ends of such mini-chromosomes can be considered as telomeres.

The study of the mechanisms of inheritance of mini-chromosomes in infusoria (a fundamental problem extremely far removed from the needs of the economy, medicine, etc.) was complicated by methodological difficulties of working with infusoria, in particular by the impossibility of using powerful genetic approaches. Jack Szostak studied plasmids – small self-replicating DNA molecules – in yeast, one of the favorite objects of molecular biology and genetics. He showed that while ring plasmids are stably inherited during yeast cell division, linear plasmids, in contrast, are rapidly lost. Although yeast chromosomes are linear, they are not lost and are inherited stably. What is the reason for the different behavior of linear plasmids and chromosomes? In a paper published in 1982, Shostak and Blackburn showed that if the end sites (telomeres) of linear amplified infusoria DNA molecules are placed on the ends of linear yeast plasmids, such hybrid plasmids are stably inherited. After the publication of this work, Shostak did not actually deal with the telomere problem. However, the experimental system he created made it possible to easily detect the function of telomeres (in terms of their ability to ensure stable inheritance of linear plasmids) in yeast. Since molecular biologists have at their disposal a huge arsenal of effective methods for studying yeast, further progress was a matter of technique. Very soon it became clear that the presence of a terminal short DNA sequence was necessary and sufficient to stabilize the inheritance of linear plasmids. This sequence must be repeated several times and is called a telomere repeat. It is very important that it would have been impossible to obtain such data in Tetrahymena, the organism that started it all, neither then nor now.

The fact that the same section of DNA functions both in infusoria and in yeast, organisms that are evolutionarily very far apart, meant that researchers were dealing with a fundamental mechanism that ensures stable inheritance of linear DNA molecules in many or even all living organisms. There could be a great number of such mechanisms (e.g. “looping” of linear DNA molecules at the moment of cell division, when the probability of loss of linear DNA is the highest). The task was to determine which mechanism is actually implemented.

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Researchers from the University of Leicester and Leicester General Hospital (UK) examined data from 405,981 people stored at the British Biobank and confirmed that a faster walking pace, regardless of overall physical activity level, is associated with telomere length, the end sections of chromosomes considered a marker of biological age. The findings are published in the journal Communications Biology.

Walking is a simple and accessible form of exercise for people of all ages. Scientists have long claimed that walking is not only generally beneficial, but also reduces the risk of cardiovascular disease and all-cause mortality, and if one walks at a faster pace daily, one can even increase life expectancy. However, it has not been fully understood how walking speed is related to biological age, which reflects the degree of development and maturity of the body.

Telomeres are a complex of telomere DNA and associated proteins, they protect the ends of chromosomes from degradation, fusion and abnormal recombination of DNA strands. Telomeric regions gradually shorten with each cell division, contributing to replicative, or cellular aging (caused by the loss of the cell’s ability to divide). In addition, telomere shortening is regulated by factors such as oxidative stress and inflammation.

As suggested by previous studies, there is a link between high levels of physical activity and endurance and longer chromosome endings: therefore, physical activity via telomere lengthening helps to slow biological aging. But according to the Leicester scientists, most of the work on this topic that involved humans was small and did not fully address the causal relationship between simple types of exercise like walking and telomere length.

The average age of the British Biobank participants, whose genetic information formed the basis of the new study, was 56.5 years old, had a body mass index of 27.2, 54% were female and 95% were white. About half of the participants (212,303, 52.3%) reported walking “at a medium pace,” 6.6% (26,835) walked slowly, and 41.1% (166,843) walked at a fast pace. Compared with those who were not in a hurry, people in groups one and three were slightly younger, more likely to have never smoked and less likely to have taken cholesterol or blood pressure lowering medications, less likely to have chronic illnesses or to be restricted in movement. Those who were “slow” were more likely to be obese and prone to drinking alcohol.

“Those who walked at a medium or fast pace had significantly longer telomeres than those who walked slowly,” the researchers wrote. A secondary analysis, in which data from an accelerometer were taken into account, showed that if one did most of the daily physical activity at a higher intensity, the end sections of the chromosomes would be longer. The relationship persisted after other factors were taken into account.

“We found evidence that walking pace has a causal relationship with telomere length. Depending on the simulated difference in walking pace (from slow to medium pace or from medium to fast), there was an increase in the standard deviation of telomere length of 0.192 and 0.226 before and after accounting for body mass index, respectively,” the researchers add. They calculate that there is a 16-year difference in biological age between fast- and slow-moving individuals, although the adjusted analysis gives a difference of two years.

In the future, the researchers plan to confirm whether behavioral interventions aimed at increasing walking speed or increasing the intensity of physical activity can slow telomere degradation.

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