The effects of age on a human being are immediately obvious to the outside observer. Skin wrinkles, hair loses its color, the body becomes fragile, and eventually the body's internal systems begin to fail. Why must this be? Is it necessary that biological organisms cease functioning after an allotted time?
At this time, there is no definitive answer to these questions. There are, however, several prominent theories that partially explain senescence, the process of aging.
The prospect of deciphering the aging process brings up yet more questions: Can the process be slowed down? ... Stopped? ...How? ... In these web pages, we begin to answer these questions.
Theories on the Causes of Aging
Some possible answers to the questions above.
Playing with Fate
Musings on the possibility and wisdom of slowing down or stopping the aging process.
As always, the answers do not end here. Here you will find a list of links to the sources we used, as well as others that may be of interest to the curious traveler.
While thinking about these theories, one must remember the differences between cause and effect. Some are based on observations of aging cells. While the following theories may be valid causes of aging, they may also simply note an effect of the aging process. For example, gray hair is found primarily in the elderly, but does not play an active part in the aging process. Also keep in mind that individually, these explanations do not account for the complex process of biological aging. Thus, aging may be most accurately described by the synthesis of several of the following theories.
Current theories can, in general, be separated into two groups:
DNA Damage Theories
Aging is caused by accumulated damage to DNA, which in turn inhibits cells' ability to function and express the appropriate genes. This leads to cell death and overall aging of the organism.
Built-In Breakdown Theories
Aging is a direct consequence of genetic programming. The causes for aging are directly built into the genome and cellular structure, as a sort of molecular clock.
DNA damages occur continuously in cells of living organisms. While most of these damages are repaired, some accumulate, as the DNA Polymerases and other repair mechanisms cannot correct defects as fast as they are apparently produced. In particular, there is evidence for DNA damage accumulation in non-dividing cells of mammals. These accumulated DNA damages probably interfere with RNA transcription. It has been suggested that the decline in the ability of DNA to serve as a template for gene expression is the primary cause of aging. Most damage comes in the form of oxidative damage, and hence is likely to be a prominent cause of aging.
In general, a free radical is any molecule with one or more unpaired electrons in its valence shell. In the discussion of aging, the free radicals of importance are oxygen-based molecules such as superoxide (O2-), hydroxy radical (OH), singlet oxygen (O), hydrogen peroxide (H2O2), and hypochlorous acid (HOCl). Free radicals, though attractive and charming, are damaging to the body because they are extremely reactive; they tend to rip electrons off of other molecules in order to pair off their lone electrons. In other words, free radicals are strong oxidizing agents.
Unfortunately, free radicals cannot be avoided since they are byproducts of essential reactions in the body, such as the process of metabolizing oxygen. Free radicals can also be found in abundance in the environment: air pollution, tobacco smoke, radiation, toxic waste, and certain chemicals.
Free radicals wreak havoc at a cellular level since they are able to:
These effects are known as oxidative stress, and may lead to DNA mutations, cell death, and disease, all of which contribute to the overall effects of aging. To prevent oxidative stress, one should reduce environmental burdens in the body (chemicals/heavy metals), reduce stress, improve the quality of one's food supply, and (if possible) increase one's antioxidant mechanisms.
Antioxidants are the body's solution to oxidative stress. These molecules neutralize free radicals by supplying them with extra electrons. This exchange results in lowering the reactivity of the free radical and leaving the antioxidant itself with an unpaired electron. The structure of an antioxidant, however, is not damaging to the body since it is stabilized through chain reactions with other antioxidants.
Known antioxidants include:
This, perhaps one of the most respected and well-studied theories, rests on the fact that oxidants induce a variety of distinct biochemical changes in target cells. Hydrogen peroxide is considered one of the more troublesome oxidants, as it diffuses into target cells where site-directed hydroxyl radical formation injures specific targets. DNA is particularly sensitive to hydroxyl radical-induced damage: both DNA strand breakage and base hydroxylations can be detected. The breakage of the DNA strand activates a DNA binding protein (poly(ADP-ribose)polymerase), which forms polymers of ADP-ribose bound to various nuclear proteins using NAD as its substrate. NAD turnover under these circumstances increases so dramatically that it affects ATP synthesis, to the point where high enough concentrations inactivates mitochondrial ATP synthesis.
If the concentration of hydrogen peroxide is high enough, these pathways will lead to cell death, and, therefore, hydrogen peroxide-induced alterations will not be passed on to future generations. If, however, cells are exposed to sub-lethal concentrations of hydrogen peroxide, the ensuing injury could cause permanent and transmissible cellular alterations which could be biologically detrimental. For instance, if hydroxyl anion-induced DNA damage fails to be repaired or is improperly repaired, this DNA damage could lead to genetic alterations such as mutations, deletions, and rearrangements. Moreover, if these genetic alterations occur in critical genes that are involved in cell growth and differentiation, they could lead to deregulated cell growth and differentiation and ultimately contribute to the malignant transformation of cells. Hence, the growing number of free radical diseases includes the two major causes of death, cancer and arteriosclerosis.
Since hydrogen peroxide easily defuses through cell membranes, hydroxyl anion formation may occur extra- or intracellularly, depending on the availability of transition metals. Because of its high reactivity, the hydroxyl radical will always cause site- directed damage at the site of its formation. However, the body does possess some natural antioxidants in the form of enzymes which help to curb the dangerous build-up of these free radicals, without which cellular death rates would be greatly increased, and subsequent life expectancies would decrease.
This theory suggests that the loss of effectiveness of one of the cell's key organelles paves the way for age-related degenerative diseases. The mitochondria, which are the energy-producing bodies within a cell, have their own genome (mtDNA). This mtDNA is synthesized at the inner mitochondrial membrane near the sites of formation of highly reactive oxygen species. Mitochondrial DNA seems unable to counteract the damage inflicted by these by-products of respiration because, unlike the nuclear genome, it lacks advanced repair mechanisms. Thus, the cell loses its ability to produce energy, and gradually dies. This theory is supported by observations confirming the genomic instability of mitochondria, as well as widespread mtDNA deletions and other types of injury to the mitochondrial genome.
This theory is focused primarily on the aging of skin cells, as they are most directly affected by external sources of radiation. Radiation can create free radicals in cells, as the radiation strikes surrounding water molecules and other proximal targets. Thus the aging process goes back to the free radical theory on aging mentioned above, with radiation serving to increase its rate. Experimental studies have recently shown that the shorter, more energetic spectrum of the ultraviolet range (UVB) is responsible for the dermal connective tissue destruction observed in photoaged skin. Also, it has been shown that UVA and infrared radiation contribute significantly to photoaging, producing, among other changes, severe elastosis. Thus, even small amounts of radiation is enough to accelerate the aging process, although this theory is, as they say, only skin-deep.
Soma, or somatic cells, are all the cells in the body except gametes and cells involved in gamete formation. This theory suggests that because of the requirement for reproduction, natural selection favors a strategy that invests fewer resources in maintenance of somatic cells than are necessary for indefinite survival. Therefore, energy will be spent to ensure minimum damage to molecular structures such as DNA, and to ensure that the animal remains in sound condition through its natural life expectancy in the wild, where accidents are the predominant cause of death. Since longevity is costly energy- wise, and since with age there is no longer any ability to reproduce and hence pass genetic material onto subsequent generations, there is simply no reason to keep an organism alive past its time of procreation.
Experiments have shown that human cells will divide less than 100 times outside the body. Also, there is an inverse correlation between the number of cell divisions and the age of the person from which the cells were taken. This theory suggests that cell senescence is an active process, as even though they are unable to divide, senescent cells are actively metabolizing. It has been suggested that senescence is genetically programmed, and that its phenotype is dominant, illustrated by the fact that when normal and immortal human cells were fused, they showed limited division potential. Senescent cells express highly abundant DNA synthesis inhibitory mRNA's and produce a surface membrane associated protein inhibitor of DNA synthesis not expressed in young cells. Thus, this theory suggests that aging is predetermined in the genome, and that it is a dominant condition, although the onset of the phenomenon is still unknown.
It is well documented that the effectiveness of the immune system peaks at puberty and gradually declines thereafter with advance in age. This seems to be based primarily on T-cells, and it is generally associated with an increase in susceptibility to infections as well as in incidence of autoimmune phenomena in the elderly. T-cells lose effectiveness in early life due to the decay of the thymus gland. In other words, the quality and quantity of T-cells begins to decline after puberty. Therefore, as one grows older, certain antibodies lose their effectiveness, and fewer new diseases can be combated effectively by the body, which causes cellular stress and eventual death.
This theory suggests that cell death is caused by the shortening of telomeres, which are "caps" on the ends of chromosomes. It has been observed that with each cell division the telomeres are shortened by approximately 65 base-pairs. Telomeres function by permitting complete replication of eukaryotic chromosomes, and by protecting chromosome ends from recombination. It has been shown experimentally that cell strains with shorter telomeres undergo significantly fewer doublings than those with longer telomeres. These observations suggest that telomere length is a biomarker of somatic cell aging in humans and is consistent with a causal role for telomere loss in this process. When the telomeres get too short, the cell stops replicating at an appreciable rate, and so it dies off, which eventually leads to the death of the entire organism.
Diseases Involving Accelerated Aging
Several diseases have the effect of rapidly increasing the rate at which the carrier ages. For example, patients afflicted by progeria suffer from arteriosclerosis, coronary artery disease, congestive heart failure and non-healing fractures by the age of seven. Degeneration of hair follicles leads to balding. Most progeria sufferers die by the age of 30. Several other diseases are known to have similar effects, including Cockayne syndrome and Werner's syndrome.
As things stand, the maximum human lifespan is about 120 years. As a whole, human knowledge is increasing at an exponential rate. By this logic, some scientists believe the human lifespan could be increased to between 400 and 1,000 years within the next 20 years. (Of course, we wouldn't really know for 400 more years...)
The following are some theories on increasing the human lifespan:
By increasing the amount of antioxidants in one's system, one will have less damaging free radicals in the body. The necessary antioxidants can be found in several sources:
Telomerase has been discovered in some germs and cancer cells, but not in most normal organisms. This enzyme replaces/repairs shortened telomeres such that the cells are able to replicate (theoretically) forever. If the telomerase gene could be activated or spliced into regular human cells (assuming telomere theory is correct), human longevity would be greatly increased.
A mutant form of the gene age-1 in the worm C. elegans caused the worm's lifespan to double. The gene apparently codes for an enzyme important in the mediation of cellular communication and signal transmission. Increased lifespan was observed when the age-1 gene was nonfunctional.
Injection of growth hormone into men seemed to reverse some signs of aging. Experiments with other hormones, such as estrogen and testosterone, are ongoing.
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National Institute on Aging
Institute of Longevity Research
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