Aging and Life Expectancy
Aging is defined as the general physical deterioration of an organism ending eventually in death. In 1513, Spanish explorer Ponce de Leon landed in Florida, searching for the fountain of youth, a miraculous life-restoring pool. Today, scientists continue the pursuit of extended life span by seeking to understand the role genetics play in aging.
Frenchman Jeanne Calment (1875-1997) holds the record for human longevity-122 years and 164 days. Calment's relatives also lived to an exceptionally old age. People living in some mountainous regions of the Earth have reported lives of extraordinary duration. The Vilcabamba tribe of Equador, natives of Azerbaijan, a former Soviet province, and Hanzukuts of Pakistan claim many of their people live beyond 100, and some up to 160 years. While these cases are not officially documented, the facts still point to a genetic connection to longevity.
Scientists distinguish between life expectancy and life span. Life expectancy is a term used by actuaries, people who calculate statistics and probability for insurance use. Average life expectancy means that of 100 people born in a specific year, the age at which half are still alive. For example, in the year 2000 a person born in 1923 has an average life expectancy of 77. Half the people born that year are alive. The cause of death could be disease, accidents, or anything. At the beginning of the 1900s, the average life expectancy was 40 years. This figure reflects the many children who died from childhood diseases that have now been conquered.
Life span is different. This age represent the maximum number of years an organism would live if untouched by disease or other outside force. The maximum lifespan for humans is about 120 years. For dogs, it is about 20 and for tortoises, 150 years. Each species seems to have lifespan programmed into the genes. With medical breakthroughs and healthy life-style awareness, average life expectancy is going up. Life span remains the same.
Genetics may soon change this long held paradigm that life span cannot be increased. Dramatic laboratory studies have expanded life span in animals through selective breeding and genetic engineering. Scientists are studying the genetic contribution to aging in the following ways: twin studies, populations like the people of the mountainous regions, experimental manipulation with species, such as fruit flies and mice, and molecular biology.
Scientists agree that no single theory can account for life changes. Aging is many processes with interactive and independent factors related to life span and health. These lead to great variations among individuals and even among processes with a single individual. For example, aging of the liver is much less rapid than aging of the skin. Teenagers are usually surprised to find that a group of seventy-year-olds is more diverse in health and looks than a group of sixteen-year-olds. Scientists estimate that longevity due to genetic inheritance is between 25-30 percent; individual interaction with the environment accounts for the rest.
Chronic disease and mental decline are not part of normal aging. As treatments are developed to prevent, treat, or control diseases, the rush is on to determine which are influenced by genetics, environment, and lifestyle. Major advances for understanding the genetics of aging have come from experiments with lower animals like Drosophila, Caeorhabditis elegans, a species of round worm, and yeast. Yeast cells have revealed 14 genes related to aging. Researchers have found that mutations in C. elegans allow the worm to live three times longer than normal. The mutant gene slows the organism's metabolism, switching the worm from fast burning of energy to storage of fat. Studies have connected reduced calorie diet to longer life for 75 years, but genetics is now explaining it.
Researchers have shown that normal cells are genetically programmed to die. Depending on the cell type, the cell loses its ability to divide after about 50 divisions. Leonard Hayflick found this occurrence, which bears his name, the Hayflick limit. Recent studies have shown that each time a cell divides, chromosomes are shortened at the ends. This end cap is called a telomere. Each division causes the telomere to get shorter until the cap is worn away and can no longer protect the genes. Cell division slows, and the cells die. The term apoptosis is used to describe programmed cellular death or PCD. Recent studies have shown cells may die in other forms, such as paraptosis, which occurs during brain development and neurodegeneration.
Telomeres are the cell's molecular clocks. Research continues to investigate the role of the telomeres. An enzyme telomerase helps add DNA segments to create two kinds of immortal cells: germ line cells that produce egg and sperm (not the sperm itself) and cancer cells. Scientists are researching the mechanism that regulated telomerase, which may lead to restoring telomeres to their normal length and "immortalize" cells. Cells have been immortalized in the laboratory, but no one knows if the process can be translated to animals.
Another line of research into the genetics of aging involves free-moving molecules of oxygen or free radicals. The superoxide molecules, by-products of cellular metabolism of oxygen, are known to attack proteins, cell membranes, and DNA. The enzymes superoxide dismutase (SOD) and catalase defend against these molecules. Genes that encode for the production of SOD may serve as longevity assurance genes or LAGs. Researchers have found long-lived mutant genes in yeast cells and fruit flies that overproduce SOD and catalase. Scientists propose these may be hundred of these longevity genes. Whether these genes have human homologs, or counterparts, in the human genome is not known.
A new perspective of aging is describing the crucial role of mitochondria, bean or sausage-shaped organelles in the cytoplasm of cells, which store energy. Mitochondria have their own DNA, which is separate from the DNA in the nucleus. DNA is transmitted 99.99 percent through the mother and almost none from the father. Scientists are studying the connection between mitochondria and aging and believe mitochondrial decay is central to the aging process. Oxidants are the main source of damage to mitochondria. If the damage is not repaired, it can result in mutations. No treatments for these disorders now exist although gene therapy may be a future possibility.
If a woman is 35 years or older at the time she conceives a child, she may be at risk for a baby born with chromosomal aberrations. The female egg precursor, or oocytes, are determined early in embryonic development, so women are born with all the eggs they will have. Aging may cause errors in meiosis, resulting in damage to chromosomes or in extra chromosomes as in Down syndrome. Men produce sperm continually, and risk is less associated with the age of the father.
Abnormal gene products, telomere shortening, or other factors may explain cell aging or senescence. Another focus is the role of proteins in aging and longevity. Since genes code for proteins, the search is on for what substances turn these genes off and on. Some scientists assert that science might be asking the wrong questions in seeking how humans age, arguing that research should focus on genes that code for protecting life process. A new branch of medicine called regenerative medicine is using the newfound research not only to protect life process, but also reverse aspects of the aging process.
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