Читать книгу Aging - Harry R. Moody - Страница 32

The organic process of life is a delicate balance between forces that wear down structures—forces that lead to cell death, for instance—and those that repair damage at the molecular and cellular levels. The structure and metabolism of each living thing maintain this balance over time. But over time, the balance begins to shift: Damage occurs faster than it can be repaired. Moreover, repair capacity is not unlimited; mechanisms for maintenance and repair can be maintained only at a certain cost. In other words, there are trade-offs involved in longevity. As a result, damage tends to accumulate with age, and the body gradually loses its capacity to repair that damage.

Like other components of the body, DNA in the nucleus of cells is always being damaged and repaired, although not always perfectly. Among mammals, the longer-lived species are the ones that have greater capacity to repair damaged DNA. But as DNA replicates over and over, those small errors, or mutations, progressively alter the organism’s genetic code.

Can we conclude that we could possibly control aging by reprogramming our genes? Perhaps, but manipulating genes to slow down aging might not increase the human lifespan. Imagine that an older person starts to exhibit signs of arteriosclerosis, and so we “fix” the individual’s DNA. We might prolong one person’s life, but we haven’t really done anything to prolong the lives of that person’s children or successive generations; they will also need DNA fixes when they become older. The problem is that a harmful mutation expressed at an advanced age, only after reproduction, will not be removed from the gene pool. In fact, we may want to leave a mutation that contributes to aging in place for the next generation because the mutated gene could have positive effects at an earlier age. In other words, the same biological processes promoting health and vigor among young organisms can have a negative impact in later life.