Although the exact causes of aging remain unknown, scientists are learning a great deal about the aging process and the mechanisms that drive it. Some of the most promising research on the aging process focuses on the microscopic changes that occur in all living cells as organisms age. In 1965 American microbiologist Leonard Hayflick observed that under laboratory conditions, human cells can duplicate up to 50 times before they stop. Hayflick also noted that when cells stop normal cell division (see Mitosis), they start to age, or senesce. Since Hayflick’s groundbreaking observations, scientists have been searching for the underlying cause, known as the senescent factor (SF), of why cells stop dividing and thus age.
Different theories have been proposed to explain how SF works. One theory is based on the assumption that aging, and diseases that occur more frequently with advancing age, are caused by structural damage to cells. This damage accumulates in tiny amounts each time the cell divides, eventually preventing the cell from carrying out normal functions.
One cause of this damage may be free radicals, which are chemical compounds found in the environment and also generated by normal chemical reactions in the body. Free radicals contain unpaired electrons and so carry an electric charge that makes them highly reactive. In an effort to neutralize their electric charge, free radicals constantly bombard cells in order to steal electrons in a process called oxidation. Free radicals are thought to greatly increase the severity of—or perhaps even cause—such life-shortening diseases as diabetes mellitus, strokes, and heart attacks. Researchers have observed that free radicals exist in smaller amounts in those species with relatively long life spans. Increasing human life span may depend on our ability to prevent free radical damage, and scientists are currently examining the role of chemical compounds, called antioxidants, that prevent or reverse oxidative damage in the aging process.
Another theory suggests that SF is genetically regulated—that is, cells are genetically programmed to carry out about 50 cell divisions and then die. Researchers have identified at least three genes that are involved with human cellular senescence. They have also discovered a protein on the surface membranes of senescent cells that inhibits production of deoxyribonucleic acid (DNA), the essential molecule that carries all genetic information.
Another theory proposes that extra, useless bits of DNA accumulate over time within a cell’s nucleus. Eventually this so-called junk DNA builds up to levels that clog normal cell action. If this idea is correct, scientists may be able to find ways to prevent accumulation of junk DNA, thereby slowing down the process of senescence in cells.
Other studies focus on cell division limits. Each time a cell divides, it duplicates its DNA, and in each division the sections at the ends of DNA, called the telomeres, are gradually depleted, or shortened. Eventually the telomeres become so depleted that normal cell division halts, typically within 50 cell divisions. Scientists have found that an enzyme produced by the human body, called telomerase, can prolong the life of the telomeres, thus extending the number of cell divisions. In laboratory studies, cells injected with telomerase continue to divide well beyond the normal limit of 50 cell divisions. These promising results have triggered worldwide attention on telomerase and its relationship to aging.
A number of other studies are underway to investigate the effects of aging. Scientists have found, for example, a possible explanation for why women have longer average life spans than men. The difference seems to be biologically determined, and male and female sex hormones are probably responsible. The blood levels of female sex hormones drop sharply during menopause. At that time, the incidence of heart disease and high blood pressure in women increases to match the incidence in men, suggesting that the presence of female sex hormones offers some protection against heart disease.