By David A. Sinclair and Matthew D. LaPlant
Scientists believe we can slow down or even turn back the clock that controls the aging of our cells.
We all age chronologically as time passes, but what about physiological aging, is it also inevitable? As information in the field of epigenetics grows, more and more biologists answer this question in the negative.
But what is epigenetics? This is a field that studies the processes that determine gene expression. If you imagine your inherited genes, your DNA, as a piano keyboard, epigenetics determines how the keys sound. The main actors of this concert are molecules that attach to our genome and leave marks. These markers, in turn, give cells specialized functions and regulate their functioning. If too many markers accumulate—too much "epigenetic noise"—the instructions get mixed up, and cells can no longer perform their intended function.
Over the past decade, scientists have become convinced that these markers can measure biological age with great accuracy (with an error of only a few years). This insight was followed by even more ambitious theories and evidence - that epigenetic markers not only measure but also contribute to 'aging'.
When in 2015 When researchers at Harvard Medical School's Sinclair lab added epigenetic clusters to the genomes of young mice, the mice rapidly lost muscle and bone mass, turned gray, lost vision, and became mildly disturbed. Their ages did not change chronologically, but their epigenomes did.
The results of this experiment and others like it help establish the "information theory" of aging, which states that an increase in epigenetic noise disrupts the genetic data. Chaos causes cells to age, stop reproducing, and cause neighboring cells to do the same. This process is known as aging.
In short, aging can be considered a side effect of our primordial 'program' that helps regulate or repair our cells. In this respect, aging is similar to cancer, which some scientists believe evolved as a survival mechanism that allows cells to abandon essential functions in order to multiply uncontrollably.
Until we knew why cancer happens, we thought it was just a part of life. We now call cancer a disease—a flaw in the body, not a trait—and fight it with all our might. We don't usually look at aging this way, but we should. After all, what is disease if not a condition that prevents the body or mind from functioning normally? That's what aging does.
Indeed, aging can rightly be called the "mother of all diseases." Consider: Although smoking increases the risk of developing cancer several times over, by age 50 alone the risk of cancer increases more than 100 times compared to people a few decades younger. After age 70, this risk increases more than 500 times. Aging is also a major factor in heart disease, dementia, stroke and type 2 diabetes.
If we cured any of these diseases, the average human lifespan would only be increased by a few years. Why? Because the driving force of aging would continue to increase the risk of developing other diseases. But if we tackled the problem starting at the cellular level and targeting aging - we could reduce the risk of all these diseases and significantly extend the productive and healthy lifespan of people.
The theory that we can slow down, stop or "reverse" aging seems very foreign, so skepticism is warranted. But there is no biological law that says we have to age at the rate we are doing now (!) Some other forms of life don't age that much. A bristlecone pine can live for 5,000 years. A jellyfish known as Turritopsis dohrnii is made up of cells that can regenerate themselves, making the jellyfish functionally immortal.
Humans do not have much in common with any of these species, but the Greenland shark, which can be considered closer to humans, can live up to 500 years, and the bowhead whale, an even closer mammal, outlives us by a century.
We now know that epigenetic markers of aging can increase as a result of harmful behaviors: for example, our DNA can be damaged by excessive sun exposure, poor diet, or smoking. Change these habits and cell movement will slow down. Even better: if we could renew the cell, we might have the ability to stop cellular aging (or even reverse it). This would allow the older body to heal and fight age-related diseases just as young people do.
in 2016 Researchers at the Salk Institute in Juan Carlos Belmonte's lab have shown in a study that mice suffering from premature aging could be extended by 30% by temporarily turning on four genes that clear accumulated epigenetic marks and induce "pluripotency," the ability of a cell to develop into any other cell shape. . After partially "restoring" the processes in this way, the mice could taste the life of an immortal jellyfish.
In Sinclair's lab at Harvard, researchers gave blind old mice a combination of three genes and activated them for three weeks. The treatment rejuvenated their optic nerve cells and restored their vision. If something as complex as the retina can be "returned" to a youthful state, perhaps such gene therapy can be applied to our entire body?
This article was originally published in the Wall Street Journal