Why Do We Age



          As we learned as to who ages and how we age, now we will find out why we age. We will examine how individual molecules in our tissues work together to bring us the aging process. This means we are going to examine not the world of the organ, but the world of the cell. We will find that survival of some cells depends on their ability to stop the activation of a pre-programmed self-destruct mechanism. We will start by describing two theories of aging that incorporate the selective activation and deactivation of genes in the cells. Then we will review some basic molecular biology, talking about how genes and proteins normally work in a healthy cell. A description of how genes know when to turn on or off.
              The two dominant theories about aging are error accumulation and genetic program activation. The idea that ageing results from chance events that escape proof reading mechanisms, which gradually damages the genetic code is known as error accumulation. This theory hypothesizes that the aging of aging of organisms occurs because of a genetic conspiracy, that a much deliberate breakdown occurs, with banks of suicide genes, turning on at specific times, making cells debilitate and tissues deteriorate. These two hypotheses are mutually exclusive.
                    The world of molecular biology is a complex, fascinating interaction between many tiny players. The Lilliputians genes, permanently chained to their nuclear dungeon, must somehow communicate their protein-making information to cytoplasm. They do this by employing a molecular Xerox machine, the now familiar RNA polymerase, to copy the instructions. This copy, this mRNA, can leave the nucleus and communicate with the rest of the world. Growing old ultimately comes down to asking why cells decide to quit working. This chapter has given to us the background necessary to discuss these ideas in terms of genes turning on and off.