There are many differences between old and young people. In only some cases are these changes due to true ageing, i.e. due to changes in the characteristic(s) compared with when the person was young.
• 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 (e.g. 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 been exposed to very different physical, social, and cultural environments
• 1° 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
• 2° ageing. Adaptation to changes of 1° ageing. These are commonly behavioural, e.g. reduction or cessation of driving as reaction times ↑
Differences between old and young people are thus heterogeneous, and individual effects may be viewed as:
• Beneficial (e.g. ↑ experiential learning, ↑ peak bone mineral density (reflecting the active youth of older people))
• Neutral (e.g. greying of hair, pastime preferences)
• Disadvantageous (e.g. ↓ 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, from a nadir of around 8 years old, ↑ exponentially with age. In very old age (80–100 years), some tailing off of the rate of ↑ is seen, perhaps due to selective survival, but the ↑ continues nonetheless.
With few exceptions, all animals age, manifesting as ↑ 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.
Reactive oxygen species fail to be mopped up by antioxidative defences and damage key molecules, including deoxyribonucleic acid (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 (e.g. vitamins C and E), clinical trial results have been disappointing.
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.
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.
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.
In many cases, theories are consistent with the view that ageing is a by-product 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 ↑ a mammal’s speed or stamina, while ↑ 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, i.e. people age at different rates and in different ways.
• 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 United Kingdom (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
• Between 1980 and 2013, UK life expectancy at age 65 ↑ by 5.3 years for men and 3.9 years for women (see Table 1.1)
• While projections suggest this trend will continue, it is possible that the modern epidemic of obesity might slow or reverse this
Table 1.1 Predicted UK life expectancy at age 65
Period | Women (years to live) | Men (years to live) |
1980–82 | 16.9 | 13 |
1996–98 | 18.4 | 15 |
2011–13 | 20.8 | 18.3 |
Adapted from data from the Office for National Statistics licensed under the Open Government Licence v.3.0.
UK population statistics (Office for National Statistics) reveal that mean ♂ life expectancy is 78.7 years. However, this is not helpful when counselling an 80-year-old. Table 1.2 demonstrates that as a person gets older, their individual life expectancy actually ↑. This has relevance in deciding on healthcare interventions.
Table 1.2 Predicted life expectancy at various ages for men (UK)
Age at time of estimate | Years left to live | That is, death at age |
Birth | 78.7 | 78.7 |
65 | 18.2 | 83.2 |
85 | 5.8 | 90.8 |
95 | 2.8 | 97.8 |
Adapted from data from the Office for National Statistics licensed under the Open Government Licence v.3.0.
More accurate individualized estimates should take into account sex, previous and current health, longevity of direct relatives, as well as social and ethnic group.
Life expectancy at age 65 is also improving with time, as shown in Table 1.1.
Fertility is defined as the number of live births per adult ♀. It is currently around 1.9 in the UK. If this rate were maintained, then in the long term, the population would fall unless ‘topped up’ by net immigration. In contrast, during the ‘baby boom’ years of the 1950s, fertility rates reached almost 3. This bulge in the population pyramid will reach old age in 2010–2030, ↑ the burden on health and social services.
The driver of mortality decline has changed over the twentieth century, from reductions in infant/child mortality to reductions in old age mortality.
• Infant mortality accounted for 25% of deaths in 1901 but had fallen to 4% of deaths by 1950. Currently, over 96% of deaths occur at >45 years
• Deaths at age 75 and over comprised 12% of all deaths in 1901, 39% in 1951, and 65% in 2001
The most common cause of death in people aged 50–64 is cancer; 39% of ♂ and 53% of ♀ deaths are due to cancer. Over the age of 65, circulatory diseases (heart attacks and stroke) are the most common cause of death. Pneumonia as a cause of death also ↑ with age to account for 1 in 10 among those aged 85 and over.
All these statistics rely on the accuracy of death certification (see Documentation after death, pp. 648–649) which is likely to reduce with ↑ age.
These demonstrate the age/sex structure of different populations. The shape is determined by fertility and death rates. ‘Pyramids’ from developing nations (and the UK in the past) have a wide base (high fertility, but also high death rates, especially in childhood) and triangular tops (very small numbers of older people). In the developed world, the shape has become more squared off, with some countries having an inverted pyramidal shape—people in their middle years outnumber younger people—as fertility declines below replacement values for prolonged periods.
An interactive UK population pyramid can be seen on the Office for National Statistics website ( http://www.ons.gov.uk/ons/interactive/uk-population-pyramid---dvc1/index.html).
Healthy life expectancy is that expected to be spent in good or fairly good health. As total life expectancy rises, it is better for society and the individual to spend as much of this extended life in good health as possible.
It is not known whether ‘compression of morbidity’—where illness and disability are squeezed into shorter periods at the end of life—can be achieved. Trends in data from the United States (USA) suggest that compression of morbidity is occurring, but challenges to public health are different in the UK. Obesity and lack of exercise may negate diminishing morbidity from infectious diseases; as more people survive vascular deaths, they might develop dementia (and other old age-associated diseases). The UK Office for National Statistics compared estimates of healthy life expectancy from 2000 to those from a decade later and showed that we are living longer and that more of this time will be in relative health. A 65-year-old in 2011 should expect to live over half their upcoming life free from disability. However, there are significant variations, depending on the region, socio-economic status, and sex.
Those >80 are the fastest growing age group in the UK. Currently, around a quarter of the population is >60 years old, but by 2030, this will rise to a third. Governments can encourage migration (economic migrants are mostly young) and extend working lives (e.g. ↑ pensionable age for women), but these will have little effect on the overall shift. The impact of this demographic shift on society’s attitudes and economies is huge. Examples include:
• Financing pensions and health services—in most countries, these are financed on a ‘pay-as-you-go’ system, so they will have to be paid for by a smaller workforce. This will inevitably mean greater levels of taxation for those in work or a reduction in the state pension. Unless private pension investment (which works on an ‘insurance’ system of personal savings) improves, there is a risk that many pensioners will continue to live in relative poverty
• Healthcare and disability services—the prevalence and degree of disability ↑ with age. American Medicare calculations show that more than a quarter of healthcare expenditure is on the last year of a person’s life, with half of that during the last 60 days
• Families are more likely to be supporting older members
• Retired people comprise a growing market and companies/industries that accommodate the needs/wishes of older people will flourish
• Transport, housing, and infrastructure must be built or adapted
• Political power of older people (the ‘grey lobby’ in America) will grow
How can success be defined, i.e. towards what aim should public health and clinical medicine be striving? The following definitions are, to some extent, stereotypical and culture-sensitive. More flexible definitions would acknowledge individual preferences.
• Successful ageing. Without overt disease, with good physical and cognitive function, a high level of independence, and active engagement with the broader society. Usually ended by a peaceful death without a prolonged dying phase
• Unsuccessful ageing. Accelerated by overt disease, leading to frailty, poor functional status, a high level of dependence, social and societal withdrawal, and a more prolonged dying phase where life quality may be judged unacceptable
Office for National Statistics. http://www.ons.gov.uk.
One of the paradoxes of medical care of the older person is that the frequency of some presentations (‘off legs’, delirium . . . ) and of some diagnoses (infection, dehydration . . . ) encourages the belief that medical management is straightforward and that investigation and treatment may satisfactorily be inexpensive and low-skilled (and thus intellectually unrewarding for the staff involved).
However, the objective reality is the reverse. Diagnosis is frequently more challenging, and the therapeutic pathway less clear and more littered with obstacles. However, choose the right path, and the results (both patient-centred and societal (costs of care, etc.)) are substantial.
• Present atypically and non-specifically
• Cause greater morbidity and mortality
• May progress much more rapidly—a few hours’ delay in diagnosis of a septic syndrome is much more likely to be fatal
• Health, social, and financial sequelae. Failures of treatment may have long-term wide-ranging effects (e.g. nursing home fees >£900/week)
• Co-pathology is common. For example, in the older patient with pneumonia and recent atypical chest pain, make sure myocardial infarction (MI) is excluded (sepsis precipitates a hyperdynamic, hypercoagulable state, ↑ the risk of acute coronary syndromes; and a proportion of atypical pain is cardiac in origin)
• Lack of physiological reserve. If physiological function is ‘borderline’ (in terms of impacting lifestyle or precipitating symptoms), minor deterioration may lead to significant disability. Therefore, apparently minor improvements may disproportionately improve function. Identification and correction of several minor disorders may yield dramatic benefits
• Investigative procedures may be less well tolerated by older people. Thus, the investigative pathway is more complex, with decision-making dependent on clinical presentation, sensitivity and specificity of the test, side effects and discomfort of the test, hazards of ‘blind’ treatment or ‘watchful waiting’, and of course the wishes of the patient
• Consider the significance of positive results. Fever of unknown cause is a common presentation, and urinalysis a mandatory investigation. But what proportion of healthy community-dwelling older women have asymptomatic bacteriuria and a positive dipstick? (A: around 30%, depending on sample characteristics). Therefore, in what proportion of older people presenting with fever and a positive dipstick is urinary tract infection (UTI) the significant pathology? (A: much less than 100%)
The practical consequence of this is the under-diagnosis of non-urinary sepsis.
When treating disease in older people, they:
• May benefit more than younger people from ‘invasive’ treatments, e.g. percutaneous coronary intervention (PCI). On a superficial level, think ‘which is more important—saving 10% of the left ventricle (LV) of a patient with an ejection fraction (EF) of 60% (perhaps a healthy 50-year-old) or of a patient with an EF of 30% (perhaps an 80-year-old with heart failure)?’. Note that the significant criterion here is more the left ventricular ejection fraction (LVEF) than the age, the principle being that infarcting a poor LV may cause long-term distress, morbidity, and mortality, whereas infarcting a part of a healthy myocardium may be without sequelae
• May benefit less than younger people. Life expectancy and the balance of risks and benefits must be considered in decision-making. For example, the priority is unlikely to be control of hypertension in a frail 95-year-old who is prone to falls
• May have more side effects to therapies. In coronary care, β-blockade, aspirin, angiotensin-converting enzyme (ACE) inhibitors, PCI, and heparin may all have a greater life (and quality-of-life)-saving effect in older patients. Studies show these agents are underused in MI patients of all ages, but much more so in the elderly population. The frequency of side effects (bradycardia and heart block, profound hypotension, renal impairment, and bleeding) is greater in older people, although a significant net benefit remains
• May respond to treatment less immediately. Convalescence is slower, and the doctor may not see the eventual outcome of his/her work (the patient having been transferred to rehabilitation, for example)
• The natural history of many acute illnesses is recovery independent of medical intervention, particularly in the young. Beware false attributions and denials of benefit:
• The older person frequently benefits from therapy, unwitnessed by medical staff
• The younger person recovers independent of medical efforts, though his/her recovery is falsely attributed to those interventions (by staff and patient)