A new study looked at how long animals live and how quickly their genetic code mutates.
©GENIA SAVILOV – AFP
It is this hypothesis that British researchers from the Wellcome Sanger Institute are working on, who compared the differences in the speed of these genetic evolutions depending on the species.
Atlantico: According to a study published in the journal Nature and conducted on 16 species by researchers at the Wellcome Sanger Institute, the lifespan of animals is related to how quickly their genetic code mutates. They analyzed how quickly mutations occur in species with different lifespans. The researchers found that mammals – from tigers to humans – have about the same number of mutations by the time they die of old age. What are the main lessons from this study and this work, especially on senile diseases in mammals?
Lawrence Alexander: Initially, it was believed that there was a relationship between the size of the animals and the incidence of cancer. We realized that this is not the case. This is consistent with Peto’s well-known paradox, according to which, at the species level, the incidence of cancer does not seem to correlate with the number of cells in the body. Another issue has arisen besides cancer, which is only a fraction of the causes of death. The question was whether there is a link between mutation rate and aging. This study offers the first answer. This shows that there is indeed a fairly small difference between the number of mutations we have between two species in relation to lifespan, meaning that the most important point in determining lifespan between two species is the number of mutations that occur during a lifetime. life, as well as mechanisms that promote mutations, and mechanisms that protect against mutations.
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The origin of cancer has been demonstrated in the elephant. Because of its size, an elephant should have a lot of crayfish. In fact, elephants don’t have very high rates of cancer compared to their size. This is because it has multiple copies of a cancer-protective gene (the TP53 gene).
These expansions of research began several years ago to try to understand the connection between our DNA, its mutations, and our diseases.
The new fact is that this correlation has been proven here in this study, in a certain number of animals, in sixteen species. This is already significant. Thus, it contributes to demonstrating the fact that there is a direct relationship between mutation rate and lifespan. In humans, fifty mutations occur in each cell in a year of life. The intuition we had for a long time was that these mutations favor cancer and the mechanism of aging, and therefore affect lifespan. This has been proven for cancer, but has not yet been proven for life expectancy. This study expands on earlier studies showing that age-related mutations increase the risk of developing cancer and proves that there is a correlation of the same nature between mutation rates and mechanisms of aging.
Why do some animals have a short lifespan? Can this be explained by analyzing their DNA? What is the relationship between mutations and lifespan?
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We are talking about mutations that do not occur in the testicles and ovaries. We are not talking about mutations that will be passed on to children. We are talking about mutations for cells that are not transmitted. Our cells age and accumulate mutations over time. Cellular mechanisms correct a very important part of the mutations, but not all. The cellular mechanism for correcting DNA abnormalities is remarkably effective, but not 100%. But there are many mutations that occur due to DNA breaks. Every second, two trillion DNA breaks occur in every person, if we take all of our one hundred trillion cells.
These breaks promote mutations. Fortunately, the vast majority of these breaks are repaired and there is no mutation behind them. But recovery is not perfect, which explains why mutations accumulate in each of our cells. On average, in terms of life expectancy, we have just under 50 mutations per year of life. Among these mutations, some have no consequences, while others affect the cellular machinery, slowing it down, disrupting the metabolism of our cells and contributing to the deterioration of cellular quality, which contributes to aging.
There are a lot of DNA breaks and spontaneous mutations in our cells. The vast majority are repaired by a completely extraordinary DNA repair mechanism. But some are not repaired. This contributes to the development of cancer and cell aging.
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Thus, it is necessary to remember a fundamental figure: every second in our chromosomes, in our DNA, there are two trillion breaks. Even if the vast majority are repaired, a certain number of times this repair is not carried out.
Given this work on animals, can we learn anything about a person’s own aging cycle, or about certain diseases such as cancer (with mutations in our DNA)? Can we “slow down” this cycle of aging, mutation, or disease by learning from this study and these 16 species studied? Will this work help solve a conundrum known as “Peto’s Paradox” (which concerns large animals that live long lives and don’t have extremely high rates of cancer)?
We knew that there was a link between mutation rates and cancer. This is why when we are too exposed to the sun, skin cancer appears. When you smoke, it causes lung cancer. This is why when you drink alcohol, cancers of the digestive tract and liver occur. Alcohol and tobacco damage cells and increase the rate of mutation.
The relationship between the number of mutations and cancer is known. Therefore, to avoid cancer, it is best to avoid smoking, excessive drinking or excessive sun exposure, factors that promote DNA mutations such as certain drugs or rays.
Cancer prevention tips are all tips to reduce the number of mutations. Avoiding cancer means reducing the number of mutations.
The new fact, on the other hand, concerns the reduction in the number of mutations, which has an effect on cancer. Obviously, it slows down aging. Until now, this has been known in the particular case of skin aging. The sun increases skin mutations. This leads to the destruction of stem cells, fibroblasts, which contribute to the elasticity of the skin. People who are exposed to the sun age their skin more than people who do not expose themselves to the sun for a long time and those who wear sunscreen. Ski instructors at thirty would have the skin of a seventy-year-old man if they didn’t protect their skin.
This study shows that what we knew about skin cancer and aging is actually more general and applies to all aging while also having an impact on our lifespan. Thus, limiting mutations reduce wrinkles, reduce cancer, and also increase lifespan. So these results are a stimulus for further work on preventing mutations and then on drugs that could reduce the rate of mutations and improve the way our DNA is repaired to reduce this aging-influencing mechanism.