Theories of Aging
Aging is a complex set of processes that involve a diverse group of conditions and reactions. This is why the aging process has been challenging to define; it is also why there are multiple theories on it. However, aging processes can be divided into two groups: the amassing various degrees of damage to the cells and the genetically programmed process.
Microaccidents
Microaccidents are random occurrences of various natures that can cause damage to the critical structures in the body on a microscopic level. An example of this would be free radicals, which are very sensitive by-products of normal cellular respiration. These free radicals can cause random damage to crucial molecules such as proteins, DNA, and lipids. For example, the cell membranes that are rich in unsaturated fatty acids are particularly susceptible to free radicals because they are susceptible and reactive to minor intrusions. Mutagens, what are the chemicals that can react with DNA and change its genetic makeup, can destroy or disrupt the function of the genes. In addition, certain chemicals, such as aldehydes, can tie together or cross-link cellular components, lessening their ability to move and function. Although some substances that produce molecular damage originate in the environment (e.g., toxins or ultraviolet rays) can be avoided, many of the dangerous elements are a natural functioning part of the metabolism.
Potentially dangerous molecular occurrences take place in the body's cells all the time. The bulk of them does not cause long-lasting damage because reparation enzymes fix the wound almost immediately. However, the repair systems pass a small number of lesions, and these stay damaged for the long run. Lesions that have not been repaired accumulate; it is then that they begin to affect the vital cellular functions. As we get older, the accumulation of damage that has not been repaired grows, partly because the repair functions themselves have lower levels of efficiency and can even be damaged themselves.
The time span of aging
When age research was in its early years, there was a vigorous debate about the existence of aging clocks. Single-cell organisms and some of the more primitive species do not have aging mechanisms. However, there is now considerable evidence that more complex beings, such as mammals, have multiple types of aging clocks. The majority of normal cells in more developed organisms have a "timer" in the sense that the cells can withstand only a finite number of divisions - as opposed to bacteria, which can grow indefinitely. There also appears to be a "central clock," which is situated in the brain. This timer controls the speed of both development and aging in the organism. There are other clocks, such as menopause, when a woman's reproductive functions shut down. These secondary timers are, to some extent, reliant on the pace of the central and cellular clocks.
There is a big difference between biological and regular clocks. The speed of biological clocks can vary by tremendous amounts between individuals, and it is even more diverse between different species. Various environmental events and factors can make the biological timers slow down or speed up. For example, stress, excessive eating, and insufficient levels of certain nutrients can increase the speed of the aging timer. Conversely, lower stress levels and therapies that renew certain brain structures, specifically the hypothalamus and the pituitary gland, can retard these clocks. In rodents, a low-calorie diet begun before sexual maturity has been shown to cause a massively increased lifespan. This is attributed to the slowing of the biological clock. Sadly, this method of strict diet is not a viable alternative in humans as severely lowered levels of caloric intake when young can cause brain damage. However, it is possible that even a moderate limitation of caloric intake in adults can help to slow aging. Statistical studies of the population show that staying close to ideal body weight effectively maintains longevity in humans.