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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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.

The post What technologies, other than telomeres, can lead to the abolition of human aging, the real rejuvenation of the body? appeared first on Telomere Science.

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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А. Weismann considered aging to be the result of evolution: “…non-aging organisms are not only not useful, but also harmful, since they take the place of young ones”, which is why, in his opinion, evolution leads living organisms to aging.

The idea of aging as a result of evolution was debunked by English biologist Sir Peter Brian Medawar in 1951 in a report to the Royal Society of London entitled An Unresolved Problem in Biology. He noted that animals in nature rarely live to old age, so the course of evolution has no effect on the aging process.

In 1960, Medawar, together with the Australian virologist Sir Frank Macfarlane Burnet, received the Nobel Prize in Physiology or Medicine “for the discovery of artificial immune tolerance”, but they could not explain anything specific about the causes of aging. The deciphering of DNA structure in 1953 did little to clarify either, only posing even more questions to scientists with many unknowns.

British biologist Francis Crick, American biologist James Dewey Watson and British-New Zealand scientist Maurice Hugh Frederick Wilkins were credited with deciphering the structure of DNA in 1962.

In those years, scientists were inclined to believe that the human cell was capable of proliferation in the body and could reproduce indefinitely in culture. If this were true, it would mean that people age and die not according to the program of cellular degradation, but due to extracellular processes occurring at a higher physiological level (Kvitko A.V., Koneva I.I. et al., 2000).

Only forty years later scientists began to approach more or less general views on the theory of aging. In 1961, the American scientist Leonard Hayflick, professor of anatomy at the University of California in San Francisco, discovered that even in ideal conditions the cell is capable of dividing only a limited number of times, and that as this limit is reached, the signs of aging appear. Hayflick L., Moorhead PS, 1961).

The division limit is established for cells of almost all multicellular organisms. The greatest number of divisions depends on the type of cell and on the organism. It was found that for most human cells this limit is 52 divisions. It was also found that as the age of the donor increases, the number of divisions decreases significantly.

That is, in the body of any living being there is something like a “biological clock”, a division counter that sets a limit on the total number of cells (Hayflick L., 1998). This limit is called the Hayflick limit.

How does this “counter” work? In 1971, the Soviet scientist Alexey Olovnikov, based on data on the principles of DNA synthesis in cells, proposed the theory of marginotomy (the theory of marginotomy), explaining the mechanism of such a “counter”. According to Olovnikov, during matrix synthesis of polynucleotides DNA polymerase is unable to fully reproduce the linear matrix; the replica comes out always shorter than its initial part. Thus, with each cell division the DNA is shortened, which limits the proliferative potential of the cells and seems to be the “counter” of the number of cell divisions (Olovnikov AM, 1971).

In the late 1980s, a series of discoveries by scientists Elizabeth H. Blackburn, Jack W. Szostak, and Carol W. Greider confirmed Olovnikov’s hypothesis. It was these three scientists who were awarded the Nobel Prize in Physiology or Medicine in 2009. They managed to figure out the mechanism by which chromosomes are copied completely during cell division, that is, somehow the chromosomes are protected from degradation.

The solution was found at the ends of the chromosomes: the telomere (from the Greek Telos – end and meros – part, a name suggested by Herman Joseph Meller in 1932) and the enzyme that forms the telomere, telomerase. The long spirals of DNA molecules carrying gene information are packed into chromosomes that have telomeres, protective caps, at their ends.

It has been found that the shorter the telomere, the older the cell, and vice versa, if telomerase activity is high, the same telomere length is constantly maintained – the cell does not age, but there is a danger of cancer cells developing, also striving for immortality. Certain hereditary diseases are characterized by the presence of defective telomerase, which leads to rapid aging of the cell. The mysterious telomere of a chromosome contains a genome, the carrier of which is a DNA molecule.

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