Why do we age: The most accurate hypotheses explain the aging process of the body

Why do we all have to grow old? It is a question that has caused scientists to scratch their heads for decades. But in the end, they found some answers. And these are the closest we have to date.

One of the oldest theories on aging is called the damage accumulation hypothesis . German biologist August Weisman proposed it for the first time in 1882. According to him, cells and organisms are complex systems with many components, all of which are extremely interconnected. delicate.

But the complex systems of the body are actually very fragile. Of the trillions of cells that make up your body, there are always a number of cells that are damaged over time. The body can repair a part of them, but as the remaining damage accumulates more and more, it will cause the body to wear out and lose the ability to repair itself.

The result leads to aging and diseases of old age.

German biologist August Weisman.

The hypothesis of free radicals

The free radical aging hypothesis is another version of the damage accumulation theory, introduced by American biologist Rebeca Gerschman and American Daniel Daniel in 1954. By 1956, it continued to be Denham Harman. , an American chemist, developed further.

According to this hypothesis, free radicals are natural byproducts generated by the body's breathing and metabolism processes. They constantly accumulate over time. Harman realized that both cell damage and free radicals increased with age, so he hypothesized that it was the free radicals that were responsible for the damage.

The free radicals that Harman focused his research on are what he called "reactive oxygene species -ROS species". They are produced by mitochondrial cells in the process of converting nutrients into energy for the cell to function.

Scientists have found that ROS can attack and react with DNA, proteins and lipids (fats), altering their properties and functions. In experiments, increasing ROS production in yeast, worms, and fruit flies shortened their lifespan.

Harman's hypothesis dominated geriatric research from the 1990s until the early 2000s. But then, some studies began to find conflicting results with the hypothesis.

Tests on animals, such as salamanders and rats, show that when scientists turn off the antioxidants and decompose free radicals in these animals, their lifespans do not change.

To reconcile these contradictory findings, scientists propose that ROS is only a factor that acts as a signal for other aging activation processes to occur. It seems that, until now, the theory of free radicals is gradually being rejected and overshadowed by other hypotheses that explain aging.

Scientists have discovered that ROS can attack and react with DNA.

The hypothesis of evolution nourishes disease

Before continuing the journey to discover the hypotheses that explain aging, we need to turn into a small corridor in the theory of evolutionary biology.

We know that genes are critical to and control many processes that occur in the body, including protein production as well as our appearance.

Genes can be altered through mutations. We are all carrying mutations on many genes. Most of these mutations are hidden only, meaning they do not affect your life or appearance. But there are a number of mutations that cause negative and positive effects also.

The theory of evolution by natural selection suggests that if a gene (or mutation) provides an advantage for the survival of an organism, it has a greater chance of being passed on to the next generation. But if a gene mutation is considered bad, it will be removed during evolution.

Among the diseases that humans are suffering from, there are many genetic diseases that are caused by mutations. If that is true, why do these mutations still exist without being removed by natural selection?

People today possess genes that support development and reproduction at a young age, but as they age, the genes return to attack us and cause disease.

In 1957, an American evolutionary biologist named George Williams proposed an answer. According to his " antagonistic pleiotropy " hypothesis (opposite effect), a gene mutation can lead to both good and bad traits. But if a good trait is outperforming a trait, the mutation will not be eliminated.

For example, the mutations that cause Huntington's disease can improve fertility and reduce the risk of cancer; sickle cell mutation protects patients from malaria; and mutations associated with cystic fibrosis also help the teeth fertility. These are just a few of many other examples for this hypothesis.

We are carrying many beneficial mutations in our youth - they help you survive, develop and maintain your offspring by reproduction. But in return, mutations will create disadvantage in later part of life.

That may be the explanation for the diseases that weaken us as we age.

But can Williams Williams's theory explain the aging itself? Can we find specific genes that cause harm in the later part of our lives and turn them off? Does that bring immortal life?

Can we find specific genes that cause harm in the later part of our lives and turn them off?Does that bring immortal life?

Hypotheses enhance geneee function

The questions above were answered by Mikhail Blagosklonny, a professor of oncology in New York, in a hypothesis he proposed in 2006. He thinks the cause of aging is proteins (and genes). responsible for creating them).

These proteins initially function as a signaling cell to the presence of nutrients. Some of these proteins are enzymes that are supporting the chemical reactions that occur in our bodies. And a special enzyme is called TOR by Professor Blagosklonny.

When the TOR enzyme works, it guides the cells to grow. We need TOR in the early stages of life, to develop and mature sexually. But for the rest of life, TOR is no longer so necessary.

In fact, if the function of TOR is overactive after adulthood, it may be associated with many diseases including cancer.

Now, if TOR and other nutrient-sensing genes are at the root of aging, are they related to the accumulated damage in the body or ROS?

Experiments have now demonstrated that the enhanced function at TOR can increase cell growth but at the same time reduce its defense mechanisms, including antioxidants. That means the accumulated damage in the body is not the root cause of aging, but it is the result of an increase in the activity of some genes.

Scientists are now looking for experimental evidence for the hypothesis that gene function enhancement could be used to explain aging. And so far, the results are still supportive of its correctness. These advances promise to give us a better understanding of the aging process, until its roots.

If we can do this, we can target to treat and prevent many aging-related diseases. And does not exclude the ability to turn off some specific genes to create immortal creatures.

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