Aging

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Time"First we ripen, and then we rot!" (after Alexander Pope, 1733)

 

 

Drawing by Hans Arkeveld, Western Australia

Aging is reviewed from a biological perspective. A distinction is drawn between what seem to be unavoidable biological aging processes and those lifestyle factors that can accelerate aging and pathology.

After considering the effects of aging on the whole body and the major body systems, a closer look is taken at contemporary research into the cellular and genetic aspects of aging.

 

 

 

 

 

 

 

Introduction

The following key concepts will be discussed as we consider the biology of aging:

Think of an elderly person. In what ways is that person different from someone who is younger? Their appearance? The way they move? The way they talk and think? Their susceptibility to infections? Looking from a biological point of view, are these changes inevitable? Or are some of them the result of the way we choose to live?

Stability & Change

Are you the same person now that you were ten years ago? A year ago? Ten minutes ago?

Although we are conscious of changes going on within us (including aging), there are many aspects of ourselves that seem much more consistent over long periods of our lives. For example, allowing for the normal ups and down of living, we each develop a physique, behaviour, and personality that persists over much of our lifetime.

This stability of some characteristics is set against a backdrop of continuous change: in a living human body, the cellular membership and chemical composition of the body are continuously changing: some cells die, and new cells are being formed, while some molecules are entering cells as others are leaving. However, the general form of the body persists, even in the midst of this flow - the body's control mechanisms are usually able to maintain important variables within the narrow limits that are required. This process is called homeostasis.

Candle FlameThe candle flame gives us a good analogy of this contrast between change and stability: the flame is kept ‘alive' by a continuous flow of materials through it, and although the flame flickers and dances in the air currents, it nonetheless has a recognisable form that persists.
Before we delve into this discussion about the biological aspects of aging, let us try a definition of aging before we start - although we shall probably have to modify this later as we take more things into consideration.

 

Definition of Aging

Aging is the term commonly used to describe the continuing changes in bodily structure and function which occur in a person who has already reached adulthood. These changes do not necessarily result from disease or trauma, but they increase the nearness of death. They can be considered as 'lifespan-limiting processes'.

Aging as a Part of Normal Development

Some people have a rather pessimistic view of aging: it is seen as a trend from maturity into irreversible decline. Aging is seen as 'a bad thing'. But it is clear that not everything goes into decline with aging . Some skills and capabilities actually improve, for example: those requiring a good self-awareness and awareness of others, and there are many examples of creativity in old age.

A good way to think about aging is to see It as a part of the normal process of development. As you know, there are age-related changes in body composition and behaviour throughout the entire lifecycle from conception to death. Think of all the milestones we pass through, firstly as a child and then as an adolescent, before reaching the stage we are at now. Taking a close look at this earlier part of our lives, we can begin to see examples of processes that resemble 'aging' even though they occur before we reach maturity. For example, the ovaries of a new-born girl contain many more potential 'eggs' than will be present by the time she reaches puberty - a large proportion of the eggs will die long before there is a possibility of them being released. An even more remarkable example of early 'aging' is shown by the placenta, which shows one or several patches of degeneration by the end of its few months of existence during pregnancy.

Thus, development is more than a trend from simple to complex, from conception to maturity: it includes aging processes too. It seems that aging is a price that must be paid by all complex organisms (not only humans), a consequence of the need to produce highly specialised cells during development.

When we are youngsters, there seems to be a close correlation between our age in years and the things we can do. We learn to walk at a certain age, talk some months later, and so on. However, as we get older and enter adulthood, the connection between age and capabilities becomes looser. Physical and mental health become more important than actual chronological age.

More people are living longer. What are some of the reasons for this?

Primary & Secondary Aging

Some of the changes that we normally think of as aging are probably more to do with our lifestyle than a result of inevitable biological changes. Through poor diet, lack of exercise, and false assumptions about the frailty of old age, many people create problems for their health and produce deteriorations that are not at all due to the biological process of aging.

In the notes that follow, the normal, inevitable, gradual age-related changes that we have no control over will be referred to as primary aging. This includes changes such as greying, thinning hair, pigmented patches of skin (for example on the back of the hands), slowed movements, fading vision, impaired hearing, reduced ability to adapt to stress, and decreased resistance to infections. These changes do seem to be inevitable from a biological point of view and not directly influenced by lifestyle, although future research may change this opinion.

On the other hand, those changes that are neither universal nor inevitable, and more the result of environmental, lifestyle factors such as disease, disuse (eg: lack of exercise), and abuse (eg: smoking, excessive drinking, obesity, malnutrition, and exposure to ultra-violet light) will be referred to as secondary aging.

Drawing by Hans Arkeveld, Western Australia

Biological Perspectives

Several hypotheses have been proposed to explain biological aging. These include the idea that aging is 'programmed', in the sense that there is a genetic predisposition to aging built into the developmental program. Another idea is that aging is the result of wear and tear - the accumulation of errors, waste products, damage, and degradation of function. We shall consider these ideas more carefully. (For a good recent review of aging, see the collection of articles in the journal Nature, 408, 231-269, 9th November 2000.)

Aging at the Whole Person Level

With age, there are general changes in the appearance of the face, skin, hair, body contours and posture. The skin becomes more wrinkled, drier, less elastic, and hangs loosely in regions where the underlying tissues such as fat and muscle begin to shrink. These changes are especially noticeable in regions that have been most exposed to sunlight - they have been damaged by ultra-violet radiation. Hairs become grey and fewer in number, resulting in baldness in some men, and the growth of fingernails and toenails slows down.

Aging brings a gradual decline in the functions of some senses: smell, taste, sight, and hearing. There may be unsteadiness on the feet. Although these changes give an outward indication of the aging process, it is possible by careful grooming, 'acting young', and even cosmetic surgery, to disguise them to some extent.

Changes at the System Level

At the level of the body systems, aging tends to be gradual and cumulative. The systems, including the immune system, become slower and less adaptive. As a consequence, the person becomes more susceptible to disease. with aging, homeostatic mechanisms are less easily maintained within normal limits when faced by challenges from the environment For example, an elderly person is more likely to have difficulties in maintaining normal levels for body temperature, blood pressure, blood sugar, acid-base balance, cerebral blood flow, numbers of blood cells, and gases such as oxygen and carbon dioxide in the blood.

Skeletal Muscle

Muscle mass tends to increase during the first 40 years of life, and then declines. The muscle cells decrease in number and diameter. Some of this muscle shrinkage can be attributed to disuse, so to that extent it can be considered as secondary aging. As the muscle diminishes, there is often an increase in the proportion of fat, so that body weight may not diminish at the same rate as the muscle. When we reach our 60's and 70's, fat is increasingly deposited between individual muscles and internal organs.

Skeletal System

With aging, there is some shrinkage in height - ranging from 2 to 5 cms. This is partly because we become more stooped or bent when we stand, and partly due to thinning of the intervertebral discs. The calcium content of bones is gradually reduced - especially in women who might lose up to 25% of bone calcium in a condition called osteoporosis. The bones become more brittle and fragile with age, and take longer to heal after fracturing because of a less vigorous blood supply and healing process.

Cardiovascular System (Heart and Blood Vessels)

The health of the cardiovascular system has a great influence on the general health of the aging person. Cardiovascular disease is a leading cause of death in this country in men over 45 and women over 65.

The heart does not rest from the time it first begins to beat in the embryo, 3 weeks after conception, to the time the person dies. On average, it pumps 75 gallons of blood per hour in a resting adult, and up to 10 times as much during strenuous activity. In a lifetime, the heart may beat 3,000,000,000 times.

In an aging person, the collagen content of the heart increases, and a layer of fat may be deposited on the outer surface. There is often a gradual increase in size of the heart with age. However, cardiac output decreases about 1% per year from the age of 20. The maximum heart rate that can be achieved also declines with age.

The walls of arteries gradually become less elastic with age, and may show signs of calcification. The collagen content increases. Fatty materials may be deposited in the walls of the arteries, resulting in narrowing of the vessels and increased resistance to blood flow. This causes blood pressure to rise. The general resistance to blood flow increases with age, although vital organs such as the heart and brain are partially protected from a reduced blood flow, at least initially. The reduced blood flow may explain several of the degenerative processes associated with aging. A proportion of these changes can be related more to lifestyle than to primary aging processes.

Common Cardiovascular Problems

Age-related and lifestyle-related changes in the cardiovascular system can give rise to several clinical problems:

Respiratory System

There is a gradual reduction in efficiency of the respiratory system with age, and the lungs accumulate damage caused by air pollution, smoking, and respiratory infections. Some of the gradual changes are as follows:

Some of these changes are probably a result of the reduced level of exercise of older people - they are examples of secondary aging.

Clinical Disorders of the Respiratory System

Several respiratory disorders are more common in the elderly:

Digestive System

There is a gradual decline in digestive function that affects mainly the movement and digestion of ingested food, but with less effect on absorption:

Urinary System

Endocrine System

Clearly there are changing patterns of hormone production and actions throughout life, commencing from before birth. However, although the activities of individual glands will change with time, these may not be indicators of primary aging since many of the changes are potentially reversible The pituitary gland and parathyroids show no obvious changes in size or activity with increasing age. The thyroid gland becomes infiltrated with an increasing amount of connective tissue, but this does not appear to restrict its normal functioning.

Glucose metabolism can become a problem in aging people, but it appears this is not necessarily a consequence of a decline in pancreatic function. The pancreas may produce sufficient insulin for the body's needs, but for some other reason the cells of the body become less able to take up glucose from the blood stream. This can result in mature onset diabetes.

In the cells of the adrenal glands, a pigment called lipofuscin accumulates (this will be described more fully in a later section) and there is an increase in the proportion of fibrous connective tissue. The output of androgens (male hormones) by the glands declines in old age.

The thymus gland reaches its maximum size by puberty, and after that decreases in size and is gradually replaced by fatty tissue.

Reproductive System

In the aging female, changes in the reproductive system are closely linked with changes in hormone production. When the ‘change of life' comes in middle age, the ovaries cease functioning and eventually the menstrual cycle stops - menopause. Oestrogen and progesterone production by the ovaries drop away. The production of follicle stimulating hormone (FSH) and luteinising hormone (LH) by the pituitary rises, but the aging ovaries are unable to respond. As a result of these changes, the vagina becomes thinner walled, less readily lubricated during sexual activity, and perhaps reduced in size. The secondary effects of the hormonal changes can be at least partially reversed by hormone replacement therapy (HRT).

In the male, there does not appear to be a change equivalent to the menopause in women. Sperm production continues throughout later life, although at a gradually diminishing level. The prostate has a tendency to enlarge in many men, and may obstruct the release of urine from the bladder.

It has been observed in some species that that reproductive function carries a price in the sense that longevity is reduced. If reproductive maturity is encouraged to appear earlier, this results in reduction of lifespan, while delayed onset of reproductive maturity prolongs the lifespan. From an evolutionary viewpoint, it could be argued that when the reproductive role is complete, there is not much point in the individual remaining alive. Whether this applies also to human longevity remains to be determined.

Nervous System

The nervous system regulates the activities of many systems in the body, so that age-related changes can be expected to have significant and widespread effects. However, relatively few elderly people develop the confusion and disorientation often assumed to be associated with aging. In the past it was difficult to distinguish between primary and secondary aging of this system, but modern scanning techniques that can reveal the functioning of the brain are helping to make that distinction.

The brain gradually becomes lighter with age, losing about 5% of its mass by age 70. Some of that loss is due to the death of neurons (nerve cells) that are not replaced - this process begins early in life and continues into old age. Some surviving neurons have a reduced number of dendrites; many begin to accumulate waste products and fibrils within their cytoplasm. There is also a gradual increase in the volume of the fluid-filled ventricles within the brain. The electrical activity of the brain shows gradual changes with age, with an increased proportion of slow-wave activity.

Patterns of sleeping change with age: periods of sleep become more broken, disturbed by brief periods when breathing stops (sleep apnoea) or when leg muscles twitch (nocturnal myoclonus).

There is a gradual diminution with age in the power of some spinal reflexes, for example the knee-jerk reflex. Similarly, the responses of the autonomic nervous system become slower and somewhat diminished.

Immune System

The immune system seems to decline in efficiency with age. For example, in the elderly there is an increased incidence of infections such as tuberculosis, urinary tract infection, shingles, and endocarditis, and the consequences are often severe. These clinical observations suggest a decrease in the efficiency of the immune response to infection in old age.

The thymus gland, which plays a central role in setting up the immune system during development, reaches its maximum size at puberty and then begins to shrink. In the elderly only small nodules of active thymic tissue can be found. Lymphocytes formed in the bone marrow from stem cells are transported by the bloodstream to the thymus, where they undergo further differentiation. The number of stem cells and their ability to produce lymphocytes appear to remain constant, even into old age. As the thymus ages, fewer mature T cells are produced. The involution of the thymus is paralleled by a similar decline in the activity of the lymphocytes maturing within it. Although the actual number of circulating lymphocytes changes little with age, there is evidence that the responsiveness of the cells to non-self antigens diminishes considerably in the elderly. Their cell surfaces are different from those in younger people. In addition, they are less able to divide readily when stimulated. (Similar findings have been obtained in other mammalian species. It is not clear yet whether the increased incidence of cancer in the elderly can also be linked with the reduced effectiveness of cell-mediated immunity.)

The thymus appears to be the ‘clock' that controls aging in the T cells. The functioning of the thymus is influenced by activities of the hypothalamus, pituitary gland, and by stress and dietary factors, so research is under way to see whether thymic involution can be delayed or slowed in some way.

There are small but significant changes in the levels of circulating immunoglobulins as a person ages. The concentrations of IgA and IgG rises with age, while IgM tends to decrease. However, there seems to be little change in the number of stem cells or in the number of circulating B cells. It seems to be the T cell dependent humoural responses that deteriorate with age, suggesting once again a link with the shrinking thymus - the functioning of the T helper cells diminishes in the elderly. On the other hand, the secondary response to re-infection and the antibody response to vaccination remain unimpaired in old age.

Autoantibodies against gastric cells and thyroid cells, and autoantibodies such as rheumatoid factor and anti-nuclear antibodies increase in some but not all elderly people. Thus, while the humoural response to extrinsic antigens diminishes with age, there seems to be in some people an increasing sensitivity to intrinsic antigens. It has been suggested that this is the result of deterioration in the function of some suppressor T cells, although the scientific evidence at this stage is not clearcut. It is not clear yet whether the autoantibodies produced in the elderly contribute to disease.

Phagocytic cells are generally the first line of defence against extrinsic antigens. In both humoral and cell-mediated immunity the macrophage processes antigens and then passes on information to T or B lymphocytes. It appears that the number and activity of macrophages remains intact during the aging process.

Common Infections in the Elderly

Fever is caused by a protein in the blood called endogenous pyrogen. This substance is produced by phagocytes when they ingest bacteria, dead tissue, or antigen-antibody complexes. Infections are the major cause of fevers, but other causes such as cancer and connective tissue disorders are possible.

Tuberculosis is a problem for the elderly. One explanation suggested is that a previously latent infection becomes reactivated in old age as a consequence of decreased cell-mediated immunity. Shingles in the elderly, produced by the virus Varicella zoster, does seem to be linked with impaired immunity.

The Lifespan

The potential length of the lifespan differs from one species to another:

Single-celled species such as the amoeba and some bacteria seem to be ageless, and continue dividing generation after generation. However, even single-celled organisms sometimes resort to special forms of reproduction in order to retain their vitality: they exchange and modify genetic information in ways that are similar to sexual reproduction

Multi-cellular organisms have a clearly prescribed lifespan, beyond which they can rarely survive. In general, small very active creatures tend to be shorter-lived, while large, metabolically slower animals tend to be longer-lived. Many species show similar patterns of aging with respect to changes in the skin, hair, posture, muscle strength, and vigour, and a diminishing ability to adapt effectively to environmental challenges.

The longest authenticated lifespan (so far!) for a human being is 122 years - Madame Jeanne Calment died in 1997. On average, though, women live to about 78 years and men live to about 70. (What do you think the reasons are for this sex-related difference in life expectancy?)

Extending the Lifespan

Many people have been motivated to search for the ‘fountain of youth', or an ‘elixir of life'. (Some have become rich through claiming to have found one and selling it to those who want it.)

Research in other animals has shown that average lifespan can be increased by several strategies, although for each there may be a price to pay. For example, chronic undernutrition can prolong life expectancy, but only at the expense of stunting of growth, increased susceptibility to infection, impairment of behavioural development, and increased infant mortality. For a recent discussion of this strategy of calorie control in the human context see: Weindruch, R. (1996) Caloric restriction and aging, Scientific American, 32-38 (July).

There is evidence that reproductive activity carries a cost in the sense that it tends to reduce the lifespan. If reproduction can be delayed, limited, or avoided altogether, there seems to be an increase in lifespan. It appears that reproduction diverts resources away from general repairs and maintenance of the organism in order to establish the next generation (Promislow, 1998; Westendorp and Kirkwood, 1998).

Also, being reared at lower than normal temperatures can prolong the lifespan, as can the chemical removal of damaging free radicals from the tissues. In the human context, it would seem that, given our present understanding of aging, we can best prolong our lives by sensible diet, regular exercise, and maintenance of a strong sense of purpose!

It is interesting that if single cells such as fibroblasts are removed from a multicellular organism and then grown artificially in nutrient media, they might thrive for a while and divide, but only for a particular number of generations (about 40 to 60) before dying. This has become known as the ‘Hayflick limit', after the researcher who first described this feature. It is as if cells contain a ‘clock' that determines when they must die.

It has been suggested that the lifespan of an individual can be selected for (in an evolutionary sense) in just the same way as other biological traits. Thus, the same kinds of environmental pressures that have resulted in, say, giraffes with long necks, have also produced species-specific lifespans.

Events at the cellular level

In elderly people, it is possible to detect changes in cells when compared with the cells of younger people. The rate at which new cells are being formed by cell division has slowed down. There is a slowing in RNA and protein synthesis. Some abnormal proteins are found in cells. Oddly enough, while the ‘normal' cells of the body are showing signs of aging and running down, it is the abnormal cells that have transformed into cancer cells that show more vitality, dividing actively and migrating through the body, although generally in a disorganised and destructive way. Genes that are active during prenatal development and then become inactive in the adult become activated again in old age.

Two explanations have been put forward for the biological changes in cells seen during aging: programmed aging, and aging through wear and tear. There is still discussion about the relative merits of these proposals, and there may well be alternative mechanisms that we have not yet considered, but for now it will be interesting to compare the evidence for these two views.

Programmed Aging

Essentially this is a genetic explanation. Since the earlier stages in development are under genetic control to a significant degree, it is possible that later developmental changes such as puberty and menopause - including the changes associated with primary aging - are also the consequence of a genetic influence. However, opinions differ about where such a genetically controlled ‘clock' might be located: some suggest that every cell contains one, but others place a controlling clock in a single centre (usually in the hypothalamus of the brain).

Wear & Tear Aging

This is based on the idea that a living organism - like a machine - will accumulate damage and simply ‘wear out'. There are several ways of interpreting this possibility.

One centres on the repair of DNA, the molecule found in chromosomes. Remember that DNA carries the genetic information required by each cell and the organism as a whole, and is vulnerable to damage either when it is doing normal things such as replicating before cell division or transcribing information onto RNA, or damaged by certain chemicals and radiations. Regardless of how the damage is caused, the effect might be to produce randomly-placed ‘aging hits' on the chromosomes. (There is now evidence that particular sequences of genetic information are especially vulnerable to damage in this way, predisposing to a non-random pattern of damage.) In consequence, DNA molecules can become cross-linked (that means that chemical bridges join parts of the molecule together in a way that precludes normal functioning), broken, or the information they carry altered (mutations).

Under normal conditions, DNA has a great capacity to repair itself. Three main mechanisms have been found so far:

As cells age, damage can accumulate faster than the repairs can be made. Therefore, we might expect that as errors accumulate in the DNA, abnormal enzymes and proteins derived from the damaged sequences of DNA would appear in the cells. Although there is some evidence of abnormal substances being produced in ‘aging' cells, it remains unclear whether this is therefore the most important factor in biological aging.

Not only DNA molecules are vulnerable to damage: other large molecules may also become modified by cross-linkages between them. These chemical changes alter the physical properties of the tissues. Thus, elastin and collagen fibres in aging connective tissue become cross-linked and this reduces the elasticity and adaptability of the tissue. (Think of the thinning and fragility of skin and bone, the loss of elasticity of the lungs and rib cage, and the stiffening of blood vessels, joints, and muscles.)

Associated with this idea of age-related chemical change is the oxygen free-radical hypothesis. Free-radicals are unstable chemicals formed in tissues during metabolic processes, especially those involving oxygen. The radicals combine with other molecules and alter their activity, for example DNA, the lipid (fat) molecules in membranes, and mitochondrial enzymes. The mitochondria are believed to be especially vulnerable to damage by free radicals, given that many of the radicals form as a consequence of aerobic metabolism. Long-lasting tissues such as nerve and muscle are probably more at risk of accumulating free-radical damage.

Two cellular enzymes have been found which scavenge and neutralise free radicals, and experiments are in progress to see whether cells containing a greater abundance of scavengers will have a greater lifespan.

In addition to the accumulation of chemical damage and modification, there is also the accumulation over time of a substance called lipofuscin in many cells of the body, especially those long-lived cells such as neurons which cannot be replaced. Although lipofuscin is a relatively inert substance, it is thought that the steady accumulation in cells might in some way interfere with their normal activities.

Cellular Indicators of Aging

When the cells of elderly people are examined under the microscope, some characteristic differences can be seen compared with cells from younger people. There is evidence of chemical cross-linkage of larger molecules such as DNA and connective tissue fibres, and accumulation of some unusual substances:

Genes & Aging

The genetic store we receive from our parents at conception will strongly influence our subsequent development and health, as will the environmental influences we are exposed to before and after birth. It is quite a common observation that long-lived parents tend to have long-lived children. As the Bible suggests "choose well your ancestors"! Also, genetically identical twins tend to have similar life spans. This would imply a genetic influence, although we would have to be careful to take into account the possible contribution of similar environmental backgrounds when making this interpretation.

Genes which have a harmful influence later in life will tend to accumulate over evolutionary time because natural selection will not be effective in eliminating them - the genes will be passed on already to the next generation before being expressed in the parents. It is also possible that genes that are deleterious in later life can be beneficial at earlier stages. In the same way that development before birth is an interaction between genetic and environmental factors, so will aging be influenced by genetic and environmental factors.

Telomeres

It is interesting to look for the possibility of a genetic involvement in the patterns of aging seen at the cellular level. In an influential experiment it was found that human cells kept alive in culture dishes are not immortal - there is a limit to the number of times they can divide. Usually they stop dividing after 40-60 generations, as if there is a pre-determined lifespan at the cellular level. This limit may be associated with the telomeres - the special ends of the chromosomes. Because of a peculiarity in the way that DNA is replicated, the telomeres fray progressively with each cell division. It is suggested that they act like a counter or a clock, and when they become shorted beyond a certain extent the cell can no longer divide. During gametogenesis, the telomeres are rebuilt by a special enzyme, so that the gametes (eggs & sperm) have chromosomes with full-length telomeres. A similar mechanism is thought to occur in cancer cells, allowing them to escape from the normal constraints on cell division. However, telomere shortening cannot be the only mechanism involved in aging at the cellular level. Some cells become senescent even before their telomeres have shortened substantially, as for example when oncogenes are activated.

Programmed Cell Death - Apoptosis

Even during prenatal development, some cells appear to die at specific times as part of the normal developmental process - for example, the fingers become separated from each other when the cells between them die. This has been interpreted as evidence for the existence of a genetic ‘clock' in each cell line, and the possibility of programmed cell death. More recently, the term apoptosis has been introduced in relation to cells which ‘close down' when they receive an appropriate signal from other cells or respond to an internal signal.

Genes Linked with Aging

We should remember that in one sense the body contains cells of different ‘ages' - some cells are regularly replaced after a short period of existence (eg: some blood cells, epidermal cells of the skin, the cells lining the intestinal lumen), while others last for most of the person's lifespan without the possibility of replacement (eg: nerve cells and skeletal muscle cells). However, groups of proliferating cells, such as those producing new blood cells, often show declines in productivity with age, rather like the cells (described above) that are kept in culture dishes.

There is an increasing number of reports linking specific genes with aging. For example, a gene has been identified that is involved with Werner's syndrome, which is characterised by premature aging. Also, gene mutations have been found in a nematode worm that have a profound effect on lifespan. It is anticipated that these genes act as controllers of sets of other genes. A single mutation has been described in a mouse gene that accelerates pathologies linked with later life (Kuro-o et al, 1997). The gene has been named klotho, after one of the Greek Fates who spun the thread of life.

The maturation and functioning of the immune system has a significant genetic component. In aging people, this system loses some of its effectiveness, so that change too might have a genetic causation. There is a decline in the numbers of immunocompetent cells produced, and less ability to recognise and eliminate those body cells that are beginning to transform into cancer cells. The immune system loses some of its specificity with age, and may even set about the destruction of the body's own vital organs. The thyroid gland, adrenal glands, and lining of the stomach are common targets for this form of auto-immune disease.

The genes that control immune reactivity are located within the major histocompatability complex (MHC). Genes linked to this complex not only regulate immune responses but may also influence maximal life spans. This association lends support to the suggested link between immune function and aging.

Summary

Drawing by Hans Arkeveld, Western AustraliaIt does seem that aging is an inevitable biological process - it should be viewed as a part of the whole sequence of development from conception to death. The differentiation of cells is accompanied by the potential for aging. However, some of the negative changes we tend to associate with old age are more the consequence of lifestyle than biological process. We can readily identify aging at the whole person level, and there is now a wealth of scientific information about aging at the cellular level.

Mechanisms of aging - an analogy...

Imagine a new Blu-Ray or HD-DVD recorder/player. What are the different ways in which it might ‘age' over a period of time to the point where it can no longer work? Here are some suggestions:

 

 

 

Questions on Aging

Here are some questions for you to think about and discuss with your friends:

Here are some statements that relate to attitudes about aging - what do you think?

References

Learning Outcomes

When you have studied these materials, you should be able to:

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