
Chronic aging of the skin
Chrono-aging of the skin is a physiological process of aging of the skin, due to age-related changes in the body, associated with hormonal changes.
Table of Contents
The skin is the largest organ of our body, therefore all the processes that take place in our body are displayed externally on the condition of the skin. Age processes in the body are no exception.
Causes of skin aging
Skin aging is conventionally divided into aging under the influence of external factors and internal aging (chrono-aging).
External Aging Factors
The leading external factors of aging include photoaging, exposure to air pollution toxins, chemical factors and nicotine. Of the listed external factors of skin aging, the leading role is assigned to skin photoaging.

Photoaging is considered the main cause of skin aging. It is believed that 70-80% of skin aging is due to photoaging. Photoaging is a cumulative process of damage and aging of the skin under the influence of ultraviolet rays in the composition of solar radiation. Read more - Photoaging of the skin. Methods for correcting photoaging are described in the Photorejuvenation section.
Smoking also plays an important role in skin aging. In dermatology, the concept of "smoker's skin" has been introduced, which describes changes in the skin. Read more - Smoking and skin.
Internal causes of aging
There is no single theory of the aging of the body. The opinions of scientists are divided. Each theory has strong arguments.
Genetic aging
Adherents of the theory of genetic aging argue that changes in the body are programmed in our genetic code, which "turns on" various programs at different periods of life. Numerous studies are trying to find the root cause, the so-called key gene of aging.
Telomeres and cell aging
Telomeres have boomed in the genetic theory of aging. Interest continues to this day.

According to research, a cell loses part of its telomere with each division. This determines the age of the cell. When the critical number of telomeres is reached, the cell loses its ability to divide and dies. This hypothesis was put forward by the Russian scientist A. M. Olovnikov in 1971, and in 2009 the Nobel Prize was awarded to the Australian scientist Elizabeth Blackburn.

Telomere research has given rise to special research methods for measuring length, as well as products for telomere lengthening. The body's enzyme telomerase is responsible for lengthening telomeres. In some cells of the body, telomerase is active and provides "eternal" cell life. Normally, telomerase provides unlimited division of germ cells, so they are not subject to aging. Drugs that activate telomerase have not received the status of pharmaceuticals due to the lack of convince flax clinical evidence base. Therefore, they are dietary supplements and are mostly plant extracts.
Magic number 52 - Hayflick limit
This is how many times most of the cells of the human body can divide. After which the cell ceases to exist. In science, this is called the Hayflick limit (Hayflick limit) after the name of the scientist who discovered this phenomenon in 1961. This discovery gave rise to a deeper study of the role of telomeres.

Hormonal Aging
This theory connects changes in the body with a decrease in the synthesis of hormones. As a result, cells lose their ability to reproduce themselves. Much attention is paid to sex hormones. Studies have shown that sex hormone replacement therapy does not prolong life, but can significantly improve quality of life.
With a decrease in the level of sex hormones, the skin loses its turgor and becomes dry. Hormone replacement therapy improves these indicators, but unfortunately does not slow down aging.
Literature
- HAYFLICK L, MOORHEAD PS. The serial cultivation of human diploid cell strains. Exp Cell Res. 1961 Dec; 25: 585-621. doi: 10.1016/0014-4827 (61) 90192-6. PMID: 13905658.
- Capper R, Britt-Compton B, Tankimanova M, Rowson J, Letsolo B, Man S, Haughton M, Baird DM. The nature of telomere fusion and a definition of the critical telomere length in human cells. Genes Dev. 2007 Oct 1; 21 (19): 2495-508. doi: 10.1101/gad.439107. PMID: 17908935; PMCID: PMC1993879.