Ageing

The ageing person

There are many differences between old and young people. In only some cases are these changes due to true ageing, ie due to changes in the characteristic(s) compared with when the person was young.

Changes not due to ageing

Selective survival. Genetic, psychological, lifestyle, and environmental factors influence survival, and certain characteristics will therefore be over-represented in older people
Differential challenge. Systems and services (health, finance, transport, retail) are often designed and managed in ways that make them more accessible to young people. The greater challenge presented to older people has manifold effects (eg impaired access to health services)
Cohort effects. Societies change, and during the twentieth century, change has been rapid in most cases. Young and old have therefore been exposed to very different physical, social, and cultural environments

Changes due to ageing

Primary ageing. Usually due to interactions between genetic (intrinsic, ‘nature’) and environmental (extrinsic, ‘nurture’) factors. Examples include lung cancer in susceptible individuals who smoke, hypertension in susceptible individuals with high salt intake, and diabetes in those with a ‘thrifty genotype’ who adopt a more profligate lifestyle
- Additionally there are genes which influence more general, cellular ageing processes. Only now are specific genetic disease susceptibilities being identified, offering the potential to intervene early and to modify risk
Secondary ageing. Adaptation to changes of primary ageing. These are commonly behavioural, eg reduction or cessation of driving as reaction times increase

Ageing and senescence

Differences between old and young people are thus heterogeneous, and individual effects may be viewed as:

Beneficial (eg increased experiential learning, increased peak bone mineral density (reflecting the active youth of older people))
Neutral (eg greying of hair, pastime preferences)
Disadvantageous (eg decreased reaction time, development of hypertension)

However, the bulk of changes, especially in late middle and older age, are detrimental, especially in meeting pathological and environmental challenges. This loss of adaptability results from homeostatic mechanisms that are less prompt, less precise, and less potent than they once were. The result is death rates that increase exponentially with age, from a nadir around age 12. In very old age (80-100 years), some tailing off of the rate of increase is seen, perhaps due to selective survival, but the increase continues nonetheless.

Further reading

Evans JG, Williams TF, Beattie BL, et al. (eds) (2003). Oxford Textbook of Geriatric Medicine, 2nd edition, Section 2. Oxford: Oxford University Press.

Theories of ageing

With few exceptions, all animals age, manifesting as increased mortality and a finite lifespan. Theories of ageing abound, and over 300 diverse theories exist. Few stand up to careful scrutiny, and none has been confirmed as definitely playing a major role. Four examples follow.

Oxidative damage

Reactive oxygen species fail to be mopped up by antioxidative defences and damage key molecules, including DNA. Damage builds up until key ‘ metabolic processes are impaired and cells die.

Despite evidence from in vitro and epidemiological studies supporting beneficial effects of antioxidants (eg vitamins C and E), clinical trial results have been disappointing.

Abnormal control of cell mitosis

For most cell lines, the number of times that cell division can occur is limited (the ‘Hayflick limit’). Senescent cells may predominate in tissues without significant replicative potential such as cornea and skin. The number of past divisions may be ‘memorized’ by a functional ‘clock’— DNA repeat sequences (telomeres) shorten until further division ceases. In other cells, division may continue uncontrolled, resulting in hyperplasia and pathologies as diverse as atherosclerosis and prostatic hyperplasia.

Protein modification

Changes include oxidation, phosphorylation, and glycation (non-enzymatic addition of sugars). Complex glycosylated molecules are the final result of multiple sugar-protein interactions, resulting in a structurally and functionally abnormal protein molecule.

Wear and tear

There is no doubt that physical damage plays a part in ageing of some structures, especially skin, bone, and teeth, but this is far from a universal explanation of ageing.

Ageing and evolution

In many cases, theories are consistent with the view that ageing is a byproduct of genetic selection: favoured genes are those that enhance reproductive fitness in earlier life but which may have later detrimental effects. For example, a gene that enhances oxidative phosphorylation may increase a mammal’s speed or stamina, while increasing the cumulative burden of oxidative damage that usually manifests much later.

Many genes appear to influence ageing; in concert with differential environmental exposures, these result in extreme phenotypic heterogeneity, ie people age at different rates and in different ways.

Demographics: life expectancy

Life expectancy (average age at death) in the developed world has been rising since accurate records began and continues to rise linearly
Lifespan (maximum possible attainable age) is thought to be around 120 years. It is determined by human biology and has not changed
Population ageing is not just a minor statistical observation but a dramatic change that is easily observed in only a few generations
- In 2002, life expectancy at birth for women born in the UK was 81 years, and 76 years for men
- This contrasts with 49 and 45 years, respectively, at the end of the nineteenth century
Although worldwide rises in life expectancy at birth are mainly explained by reductions in perinatal mortality, there is also a clear prolongation of later life in the UK as shown by calculations of life expectancy at 50 or 65 (see Fig. 1.1)
- Between 1981 and 2002, life expectancy at age 50 increased by 4.5 years for men and 3 years for women
- While projections suggest this trend will continue, it is possible that the modern epidemic of obesity might slow or reverse this

Individualized life expectancy estimates

Simple analysis of population statistics reveals that mean male life expectancy is 76 years. However, this is not helpful when counselling an 80 year old. Table 1.1 demonstrates that as a person gets older their individual life expectancy actually increases. This has relevance in deciding on healthcare interventions.

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