Epigenetic test

How old am i really

Discover your real age | The test gives you information about your biological age.

The aging process of every person is individual and depends on various factors such as diet, exercise, habits and stress levels. The patented test procedure uses the methylation markers on your DNA to determine your actual, epigenetic age. Once this base value has been determined, you can put your lifestyle to the test. Because the methylation markers on your DNA are in principle reversible, i.e. reversible.

So your age is in your own hands.

Biological Age @ Age-Science

Scientific background

Aging is an issue that affects everyone. After all, this process is inevitable for many organisms we encounter - including ourselves. Scientists have been researching the mechanisms that cause us to age for decades. Aging is a complex biological process and sometimes people can age faster or slower compared to the actual number of years they have lived. This means that their biological age is different from their chronological age. The calculation of biological age is of great interest to scientists as it can reveal changes that the body will go through in the course of its life. One of the approaches for this “hidden age calculation” is the use of our genetic material, the DNA. This approach was introduced by Professor a few years ago Steve horvath suggested.

One of the most popular theories of aging is the accumulation of significant damage to the macromolecules of cells, especially proteins and nucleic acids. This has many consequences for the cells and for the entire body. Molecular damage to different macromolecules is linked. Damage to the DNA can lead to faulty proteins and the latter can lead to impaired repair of the DNA, which increases the number of defects in the DNA and affects the functioning of the genes. Another symptom of old age is the decrease in the length of chromosomes. Another significant change was recently noted. The proteins that help hold DNA in the chromosome, called histones, also change with age.

The chromosomes in our cells are organized in chromatin. Chromatin is essentially made up of DNA tightly wrapped around blocks of protein that form what is known as a “pearl on a string” structure. The molecular connections between the chromosomal proteins and the DNA are crucial for the normal activity of the cell. When proteins and DNA are very tightly bound, other proteins cannot “read” the information in that particular region of the chromosome. The genes located in these regions fall silent and are not used to make proteins. When the proteins and DNA are loosely bound, the information is much more accessible. Other proteins can land there and transcribe a copy of the gene to another nucleic acid - RNA - which in turn is used to make new proteins.

The strength of the bonds between histones and DNA is regulated by mechanisms that scientists call "epigenetic" - basically, mechanisms that are "above the genes". There are several ways in which these mechanisms can intervene in the chromosome structure. One of the strategies the cell uses to control the accessibility of the DNA in the chromatin is called DNA methylation. This is a process by which a methyl group, CH3, is attached to one of the bases in DNA called cytosine, marking that area of ​​DNA. The addition of a methyl group to a nucleotide is one of the most common epigenetic markings.

Very often epigenetic markings are attached to cytosines that are close to another base - guanine. The areas that have an abundance of cytosine-guanine pairs are called CpG islands. CpG islands are especially abundant in areas of DNA called promoters. Promoters are the landing sites for proteins that initiate the “reading” of genes to produce the proteins encoded by the genes.

It has been found that with certain CpG islands, the number of attached methyl groups increases with the age of the organism, while other areas of the DNA can lose methylation over time. This fact has pointed to the possibility that CpG islet methylation is directly related to age.

Based on this assumption, Steve Horvath, a professor at the University of California, Los Angeles who specializes in human genetics and biostatistics, decided to develop an epigenetic age calculator based on the methylation rate of CpG islets.

In order to develop his computer, Horvath collected a series of data sets containing information about methylation in cells from various tissues in the body. He used both the freely available data in the Internet databases and special data sets made available to him by researchers. In total there were 82 complete sets of information, which comprised a total of 51 cell types. The analysis included the following groups of cells:

Cells of the blood (both red blood cells and white blood cells)
Cells taken from different areas of the brain
Cells of breast tissue
Cells from the inside of the cheek (called buccal cells)
Cells from the intestine

Cartilage cells
Cells from the deeper layers of the skin (dermal cells)
Cells from the upper layer of the skin (epidermis)
Cells from the stomach
Cells from the head and neck area
Cells from the heart
Cells from the kidney
Liver cells
Cells of the lungs
Cells from the bone marrow
Saliva samples
Cells from adipose tissue
Cells from the lining of the uterus
Sperm cells
Cells that make up blood vessels
Muscle tissue

Horvath also analyzed 20 samples from tumors and cancer cell lines to compare the epigenetic age of healthy cells and cells that were cancerous.

The researcher used mathematical and statistical analysis to select the genes that were most affected by aging. His approach allowed him to find 353 CpGs that changed consistently with age. There were 193 CpGs that were more methylated with increasing age, while 160 CpGs in older people had fewer epigenetic markings than in younger people. Horvath also discovered that the genes that acquired more methyl groups with age were near genes controlled by polycomb proteins, which are responsible for regulating gene activity and the state of chromatin.

The newly developed epigenetic clock proved to be reliable. According to the analysis, the clock was set to "zero" at the beginning of the development process of a new embryo. As the new individual grew, so did the clock, and the difference between the chronological age (the number of years the person lived) and the age calculated from the epigenetic clock was no more than 3 years. The predictions of epigenetic or DNAm age were accurate for most tissues except breast tissue, tissues from the uterus, muscle tissue, and skin cells. The results of the DNAm age calculations obtained from different tissues from the same person were also similar.

Further evidence of the accuracy of the DNAm age calculation was provided by analyzing cells obtained from patients with progeria - a syndrome in which patients age rapidly in childhood. The epigenetic age of these cells was significantly higher than the actual age of the patients.

When the researcher examined the cancer cells, he first found that the epigenetic age of cancer was significantly higher than the actual age of the cell. He later discovered that he had made a mistake in his calculations. As mentioned earlier, 20 cancer cell types were tested. Among these, 6 cancer cell types had an older epigenetic age (which means that their age has accelerated). Breast cancer is one of the cancers in which this acceleration occurs. The samples from the other 14 cancers had lower epigenetic ages - they looked younger than expected. This was different from the initial statements that all cancer cells had an older than normal epigenetic age.

Cancer cells are known to harbor several defects in their DNA - called mutations. The epigenetic age was higher in cancer cells that were contaminated with mutations. It was also interesting that cancer cells that had mutations in the gene called p53 had a lower epigenetic age than cells that had no defects in this gene. This gene plays an important role in both normal cell development and cancer, so it is very interesting that it also affects the epigenetic age of a cancer cell.

There were a number of other interesting facts that Horvath's research revealed. For example, he found that epigenetic age can be calculated with similar accuracy in chimpanzees. This fact encourages us to believe that chimpanzees are the most closely related species to humans.

Another interesting finding relates to the so-called stem cells. Stem cells are special cells whose fate is indefinite. They can potentially become any type of cell, depending on their environment. In recent years, researchers have learned to convert "professional" or terminally differentiated cells in the body into undifferentiated stem cells - these cells are called induced pluripotent cells, iPSCs. Horvath found that both stem cells and iPSCs have an epigenetic age of zero. He has also found that the epigenetic age of cells increases when the cell cultures are transferred to another medium, the so-called passage.

The geneticist has also suggested an explanation for why DNA methylation is so closely linked to our age. He concluded that the changing methylation rates reflected the work of what is known as the epigenetic maintenance system (EMS). This system is responsible for keeping the epigenetic markers in place, as there are areas in the chromosomes that should always be methylated. With age, small errors - mutations - can accumulate in the DNA of the cells, which can impair the activity of the EMS.

Steve Horvaths Work is critical to future studies of cell aging and development, as well as cancer biology. Its epigenetic clock is currently used for numerous applications and types of research.

The scientific work of Steve Horvath @ DNA methylation age of human tissues and cell types

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