Friday, 15 April 2016

The compression and decompression of morbidity

We are living longer but dying more slowly 

It is important to understand terms. Mortality is death: it is inevitable and the term “saving lives” is strictly incorrect; the term should be “prolonging lives”. The maximum human life-span is slightly in excess of 100 years; if free of disease or major injury, people would live to that age. In reality the average life expectancy in the UK during the late 20th century has been about 70 years for men and 75 years for women. During the past forty years the average life expectancy has risen rapidly by about eight years, and a much higher proportion of the population now live beyond their 100th birthday.

Morbidity is the presence of disease, or the after-effects of disease or major injury. Morbidity is illness that if it does not cause death will cause disability. It will reduce our functioning within our society or our families. It will take much of the fun out of life, although many people have a remarkable ability to have a full life despite considerable health disadvantage. There is a difference between life expectancy and active life expectancy. The compression of morbidity brings the active life expectancy closer to the life expectancy.

The Compression of Morbidity

I have read very many medical papers during the past fifty years, and I have saved and collected a few thousand of them, most as photocopies but during the past few years as pdfs. It is very important to obtain information from original research. It is also important not to forget it, or at least not to forget where to find it!

One paper that impressed me at the time was “The Compression of Morbidity”, written by James Fries and colleagues of Stanford University, California. It was published in The Lancet in1989.

It indicated a major change in the health profile of the population during the 20th century. In the first half of the 20th century people experienced several years of morbidity, that is functional deterioration, before death, usually at about 70 years of age.

Morbidity illustrated as blue shaded area

However during the second half of the 20th century things became different. People maintained good function, and death occurred after just a short period of ill-health and functional deterioration, which are recognised as being the inevitable part of “old age”. This compression of morbidity into a much shorter time at the end of life was obviously considered to be a good thing.

Morbidity illustrated as blue shaded area

Fries regarded this important change to be the result of good medicine, and especially of good public health. This was in response to McCormick and Skrabanek from Dublin, who felt that modern medicine, while being very important to individuals, was of little benefit to the population at large. The health of the population is determined by engineers and not by doctors. They give as an example seat-belt legislation; drink-driving legislation would be a similar example, and of course water engineering.

McCormick and Skrabanek worked in the public health department in Dublin. Skrabanek sadly died from prostate cancer at a young age. They challenged much accepted but incorrect wisdom, and they wrote much good sense extremely clearly, in a good Dublin tradition. Some of their work is listed at the end of this post, and it is well worth reading.

The Benefits of Modern Medicine

What is there about modern medicine that could have led to freedom from disability in the later years of life? There are several possibilities.

Perhaps the most commonly-used aid to mobility has been the aluminium walking frame, as invented in 1949 by William Cribbes Robb, of Stretford, a suburb of Manchester, England. This and similar mobility aids can be of great benefit, but they are valuable only to those who have morbidity. They do not prevent morbidity; they just help the disabled retain a small form of mobility.

Reversal of visual failure by cataract extraction and lens implantation clearly reduces morbidity. Blindness is a major cause of disability and its cure is extremely valuable. Cataracts are very common in the elderly and a large number of surgical procedures are carried out at present. 

Cataract operations USA

But this has not always been the case and it is only in the 21st century that we have seen widespread cataract surgery, but very little before the publication of Fries’ paper in 1989. This has not been responsible for a significant reduction in the morbidity of the population.

Hip (and later knee) joint replacement surgery has been perhaps the most important medical innovation to reduce morbidity. It was pioneered by a remarkable surgeon, Sir John Charnley (1911-1982), who was working in Manchester in the 1960s when I was a newly-qualified doctor. His surgical centre became Wrightington Hospital in Lancashire, England.

Sir John Charnley
A large number of hip and knee replacement procedures have been performed in recent years in the UK, 14,424 hip replacements in 2003 increasing to 83,125 in 2014, and a similar number of knee replacements. 

Hip and knee joint replacements, UK

Joint replacement surgery has undoubtedly reduced disability, sometimes in a very major way. However we can see that large-scale joint replacement is a very new development and would not have “compressed morbidity” at the time and on the scale described by Fries and colleagues in 1989.

I find it difficult to understand how medical interventions could have reduced  morbidity in the last years of life on the large scale identified by Fries and colleagues. But there is an intervention by Nature that clearly did.

The epidemic of death - coronary heart disease

Reduction of morbidity and disability in later life can be prevented by sudden and premature death at an early age. War with a large number of casualties would do this, and this happened during the first half of the 20th century. The prolonged morbidity of the population during this time, as identified by Fries and colleagues, would have been much greater without the two world wars.

However the 20th century was characterised by one of the greatest epidemics – coronary heart disease (CHD), in the UK and also described in the USA. This undoubted epidemic started in the mid-1920s, reached its peak in about 1970, and is currently very close to its end. 

Epidemic of coronary heart disease

The epidemic of CHD caused about 10 million deaths in the UK alone. It was responsible for 25% of all deaths at the height of the epidemic. Deaths from CHD occur now almost exclusively in the very elderly.

Now that the epidemic of CHD has almost come to an end, the compression of morbidity has also come to an end. This has been happening since its peak, and since 1970 about 10 million people in the UK have not died from CHD, assuming they would have done had the 1970 incidence of deaths from CHD (550 per 100,000 per annum, age standardised) been maintained. They have thus lived longer than they would have done without CHD, and many of them very much longer.

I repeat the illustration of the number of non-CHD deaths:
Numbers not dying from CHD in the UK since the 1970 peak

And also the great and exponential increase in the number who live to reach their 100th birthday:

Centenarians in the UK, projected beyond 2015

The Decompression of Morbidity

So in the pre-1980 years, men would work until the age of 65 years, live a further five or ten years, and then die, usually suddenly. Living to the age or 90–100 is different. People find that it is not possible to work after the age or 70 or 75 years, as physical deterioration then takes place. We therefore find perhaps 20 years of morbidity, from age 80 to age 100. 

We are now experiencing the “Decompression of Morbidity”. On average we are now returning to an increasing level of chronic illness and disability during several years before death after the age of 90 or 100. This is illustrated in Figure.

Morbidity illustrated as blue shaded area

This is already putting tremendous strains on the economy, and the problem is going to be much bigger. Pension funds must support not just 10 years of retirement but perhaps 30 years. This puts a burden on the working population who pay into the pension funds. 

Many of the retired will be unable to survive an independent life, but will require support at home or residential care. For both there is a cost, but more importantly there is a need for labour. Where will it come from? Importing the labour from overseas creates a “Ponzi Scheme” – it just makes the problem far worse in the future when the immigrant care-workers themselves become old.

The crisis has already happened in the UK, and no doubt in other countries. The demand for emergency admission to hospital has increased to beyond the number that can be accommodated. The elderly and frail have a longer recovery time for a given illness, the reason being a lower level of physiological reserve. Discharge from hospital might be delayed because of social factors at home. Length of stay is thus longer, with a requirement for more hospital beds. The hospital expenses exceed income and debt results. 

But again and more importantly, if there is a need for more hospital beds, from where do we obtain a greater number of doctors and nurses? Early warning of the huge increase in the number of the very elderly has effectively been ignored during the past 40 years, but to plan for this future appears to be beyond human ability.

What are the ethical considerations if we import doctors and nurses from other countries whose need for health professionals are greater than our own?

BBC February 29th 2016

The future

The present problem is very serious, and the future can only be regarded as a nightmare. It is unlikely to be possible to provide ideal social and health care when after 2030 the number of centenarians exceeds 100,000, and the number of those between 90 and 100 about three times that. This group of the population will have a level of disability and cannot be expected to be part of the workforce, a significant proportion of which will need to care for them. It is inevitable that people who are viewed as elderly but without serious disability will need to join the caring workforce, perhaps as volunteers rather than as paid staff.

Population control requires war, famine and pestilence. We have none of these at present. It is too late for simply a reduction of the number of births, and this will be necessary now only for the benefit of the 22nd century. 

Further pestilence is very likely and new epidemics will occur. But now we are able to spot epidemics very early, as international epidemiological systems are in place, mainly the World Health Organisation. Modern medicine also has a great ability to intervene very rapidly. 

Large population increases will inevitably come to an end but in rather unpleasant ways. It is difficult to know which to choose. Who wants massive casualties from another world war? Who wants famine on a large scale? Who wants pestilence? 

But coronary heart disease (CHD) was an epidemic, almost certainly the result of a pestilence. 

CHD caused very large numbers of deaths without significant suffering, mainly sudden and unpredicted death. The deaths occurred in middle age, and usually a very short time after productive work had come to an end. It certainly constrained the number of very elderly and compressed very significantly the morbidity of the population. 

In the future we might look back on CHD and view it as an advantage to the population sent by nature. 


Fries JF. Aging, natural death, and the compression of morbidity. N Engl J Med 1980; 303: 130-136.

Fries JF, Green LW, Levine S. Health promotion and the compression of morbidity. Lancet 1989; 333: 481- 483.

McCormick J, Skrabanek P. Coronary heart disease is not preventable by population interventions. Lancet 1988; 332: 839-841.

Wednesday, 23 March 2016

The population without pestilence - life after the end of the epidemic of CHD

Life after the end of the epidemic of  coronary heart disease.

Pestilence - William Blake, 1805. Museum of Fine Arts, Boston.

I have described in previous Posts that during the second half of the 20th century we experienced a very serious epidemic, that of coronary heart disease (CHD). It occurred in the UK, in the USA, and in all "western" countries. It became the major cause of death, responsible for the deaths of 25% of the population. It was clearly very serious, but not at the time acknowledged as an epidemic. People, especially men, died prematurely in large numbers before the age of 70 years. The epidemic has now effectively come to an end.

The populations of what we call the western world are now free of major diseases. Not only has the epidemic of CHD come to an end, but the risk of an individual developing a stroke has diminished profoundly, and cancer risk has also declined (the larger population means that there are more people with cancer).

There have been no major wars during the past half-century, and consequently there has been a remarkably low number of deaths from warfare. There is no famine: we are all well-fed, arguably too well-fed. We are healthier and many more of us live longer than at any time in history.

The large number of premature deaths from CHD at the height of the epidemic can be seen in Figure 1, data from 1968.

Figure 1: Profile of age of death, 1968
Men in particular show a bulge of deaths in middle age, and very few lived beyond the age of 85. The death profile for women was much better, with a wider spread of deaths throughout the latter decades of life.

These life expectancy tables were taken for granted at the time. They were natural, and a great improvement on the first half of the 20th century, when there were many deaths from what were  diseases obviously caused by micro-organisms. The fact that life expectancy for men was shorter than that for women was presumed to be the effect of smoking and alcohol, industrial and wartime injuries, and generally a more careless male approach to life.

In 1968–1970 the major cause of death in the population was myocardial infarction (MI), the most important and at that time the usually fatal clinical manifestation of CHD. This was again part of nature, the assumption being that it had always been present, an assumption that we now know was seriously wrong.

I have indicated in previous posts that the rapid decline in deaths from CHD was sudden and completely unforeseen. It was also unexplained, but of course many people assume that it was the result of medical interventions. This was not the case as most of the decline occurred twenty years before effective treatments became available.

Between 1970 and 1990 the CHD death rate in England & Wales dropped from its peak of 550 to about 100 per 100,000 per year (an 85% reduction). This was not appreciated or acknowledged at the time and it would appear that has not incorporated into health service planning.The assumption would have been that an annual; mortality rate from CHD would have continued at 550 per 100,000.

Figure 2 shows the decline.

Figure 2: Decline of deaths from CHD

What it meant was that in 1980 300 per 100,000 people in the UK did not die from CHD, that is who would have done had the 1970 mortality rate been sustained. By 1990 this was 450 per 100,000. These people would thereafter live into an older age and experience the infirmity that is inevitably part of it.

During the years 1970 to 2010 a very large number of people each year did not die, as shown in Figure 3.

Figure 3: Numbers not dying from CHD
The number of people not dying because of the end of the epidemic of CHD was cumulative year on year. In total it was about 16,000 per 100,000 of the population. With the UK population of 60 million, this represents just under ten million, during the 40 years 1970 to 2010. 

Normally with steady state population the number deaths per year equals total population divided by the average age at death. With the UK population of 60 million and with average age at death of 75, we would expect a total of 800,000 deaths per year, which amounts to 32 million deaths in 40 years. This equates to the 1970 level of 25% of deaths being due to CHD.

The increasing number people not dying from CHD represents a fairly rapid population growth, but of people mainly beyond working age and at an age of increasing health and social care requirements.

Of course not all the ten million who have not died from CHD during the past 40 years will still be alive. The population growth will not be so much, but whereas CHD usually resulted in sudden death from MI, the ten million people will experience or will have experienced a much slower process of dying, with much greater health need. 

The profile of ages of deaths in the UK can be seen in Figure 4. 

Figure 4: Profile of ages at death, 2010

The contrast with Figure 1 is remarkable. The late middle age bulge for male deaths has disappeared completely. For women there are many fewer deaths in late middle age and more in the very elderly. Note also many fewer deaths in the first year of life.

A further recent change in the age structure of the population is an increase in centenarians. The number of those living beyond the age of 100 years rose from 1080 in 1970 to 12,640 in 2010. We can see from Figure 5 that the rise is exponential.

Figure 5: Number of centenarians in the UK

Unless another epidemic occurs to control the population of the very elderly, it is estimated that the number of centenarians will be 22,000 in 2020, 90,000 by 2034, and 250,000 by 2050.

The socio-economic effects of this are already noticeable and will be increasingly so in the future.

It would appear that throughout human existence famine, war, and pestilence are necessary to control the size of the population. At the present time we have none of them.

The Four Horsemen of the Apocalypse, Pestilence, War, Famine, Death.

Wednesday, 2 March 2016

A simple view of the ECG

A simple view of the electrocardiogram (ECG)

This Post should be taken together with the Post entitled:
"The epidemic of coronary heart disease – the peak in 1967–70”.

We have all heard of the ECG, and today everyone will have seen
the ECG in use in health centres, in hospitals, or on television programmes. We are accustomed to seeing paper traces, and on the television programmes flashing lights and electrical traces.

There is no necessity to go into details and I will indicate only the basic features. The reason for doing this is that many of my Posts have been on the subject of coronary heart disease (CHD), the major clinical consequence of which is myocardial infarction (MI), loosely called a heart attack. The ECG is a major defining feature of the MI. A Post on this subject will appear shortly and so I have written this Post on the ECG in anticipation. To include clinical MI details and details of the ECG in a single Post would be cumbersome.

The normal ECG

The standard ECG has 12 simultaneous recordings taken from nine leads, each looking at the heart from a different direction and therefore able to detect abnormalities in different parts of the heart. I will not go into any detail, about these 12 recordings.

The normal ECG shows three components:

  • the “P” wave results from contraction (electrical depolarisation) of the atriums (atria);
  • the “QRS” complex results from contraction (electrical depolarisation) of the ventricles;
  • the “T wave” results from recovery (electrical repolarisation) of the ventricles.

The QRS complex has three components, Q,R and S. 

  • Q is an initial downward (negative) deflection of the recording. This does not occur in the normal ECG, except certain leads that need not concern us. It appearance usually indicates serious damage.
  • R is an upward (positive) deflection. it is usually the initial part of what is effectively an RS complex. It can however follow an initial Q wave.
  • S is a downward (negative) deflection that follows an R wave. It is not always present.

It might be asked as to why the nomenclature of the waves is in the form of the letters “P….T”. The answer lies in the history of the electrical recording of the heart. 

The Heart

There is no necessity to go into the structure of the heart in detail, just a reminder of the circulation sequence of right atrium, right ventricle, pulmonary artery and circulation through the lungs, then left atrium, left ventricle and aorta leading into systemic circulation.

The relaxation phase of the ventricles (diastole) sucks blood into the right and left sides of the heart, and then the early contraction of the atriums (the P wave) completes the filling of the ventricles with a final “push”. The contraction of the ventricles follows (systole) with ejection of blood into the pulmonary and systemic circulations.

The heart has a natural pacemaker to control its rate to to stimulate an orderly contraction. It is called the sino-atrial (SA) node and it is situated in the right atrium, at the point of entry of the major veins, the superior and inferior vena cava.

Electrical conducting tissue of the heart

Spread of electrical impulse within the heart

The electrical impulse that stimulates contraction of the heart muscle starts in the upper part of the right atrium and spreads across both atriums. It is picked by a secondary pacemaker, the atrioventricular (AV) node, which is situated it the junction of the atriums and the ventricles. This passes the signal though two bundles of conductive tissue, one in the wall of each ventricle. These stimulate an orderly contraction of the ventricles.

How the heart works

During the 1780s Luigi Galvani (1737–1798) at the University of Bologna, followed by Alessandro Volta (1745–1827) discovered that muscles contract (twitch) in response to electrical stimulation, the “frog legs experiments”. The interaction between electricity and muscles was far from clear, but during the following century it gradually became more clear.

Luigi Galvani

Alessandro Volta

In the 1880s it was realised that the heart muscle, like skeletal muscle, worked by electro-chemical processes. Chemical reactions created an electric potential (like in a battery) and sudden release of that electric potential (depolarisation) enabled immediate muscle activity, that is contraction as that is what muscle do. Following this muscle action the chemical process would re-charge the electric potential within the cells of the heart muscle, the process of repolarisation).

We can see this in the ECG: the first thing that happens is the P wave. This is a recording of the electrical depolarisation of the atriums (preferred international English, otherwise atria). The muscle bulk of the atriums is low and so the P wave is of very small amplitude. There is no visible wave produced by the repolaristion of the atriums  as  it coincides with the QRS complex that represents the depolarisation of the ventricles.

The QRS complex is followed after a brief delay (technically the Q-T interval) by the T wave, representing the repolarisation of the ventricles. There is then a rest until the next heart beat, the next P wave.

The depolarisation of the ventricles leads their immediate contraction and thus the blood within the ventricles is ejected into circulation, from the right ventricle into the pulmonary artery and thus through the lungs, and from the left ventricle into the aorta. The muscle of the left ventricle is of much greater thickness than the right (the blood must be propelled a much greater distance and against a much greater pressure) and its depolarisation makes the dominant contribution to the QRS complex.

The history of the ECG

The slow advances during the 19th century of the understanding of the physiology, the functioning, of the heart led to some practical albeit rudimentary developments. The British physiologist Augustus Waller (1856–1922) was a lecturer at St Mary’s Hospital, London. In 1870 he invented a device for recording the electric activity of the heart. He used “A,B,C….” to identify the recorded phases of the heart beat. He used a capillary tube filled with mercury to identify the electrical impulse of the heart, a change in height of the mercury column allowing a pattern to be observed.

Augustus Waller
Willem Einthoven

In 1902, the Dutch physiologist Willem Einthoven constructed a different type of machine, a string galvanometer, which was very cumbersome and required five men to operate it. When it came to a side-by-side assessment of the two machines, the wave-forms on Einthoven’s ECG were given the symbols “P,Q,R,S,T”. Despite being of no practical value in respect of patient care (remember that Einthoven was a physiologist and not a clinical cardiologist) it proved to be a superior method of recording heart  activity and its nomenclature has persisted. It was about 15 years later that the ECG came into clinical use, and the machines have become much smaller over years.

Einthoven's ECG machine, 1902

The use of the ECG

Early concerns were of the functioning of the heart, and they were purely academic studies. Coronary heart disease (CHD) and myocardial infarction (MI) were almost completely unknown at the time of Waller and Einthoven. 

Earlier, before his fame and knighthood, Sir James Mackenzie (1853–1925), the father of English cardiology, was working in Burnley, Lancashire, and at its hospital (where I worked). He invented a mechanical “polygraph”, a device that recorded the rhythm of the heart. 

Sir James Mackenzie

The subsequent electrical recordings were superior but it was only the rhythm of the heart that was of clinical importance. 

Abnormalities of heart rhythm

The most well-recognised abnormality of rhythm is atrial fibrillation AF). The characteristic of this is a complete irregularity of the pulse, which might become very fast. If this is the case then the pulse will also be low in volume. The output from the heart (cardiac output) is low because the filling phase of the heart (diastole) is too short to allow the ventricles to fill adequately with blood. Also the final push of filling, atrial contraction, is absent.

Atrial fibrillation is a failure of the atriums to contract properly because they are “fibrillating”, that is very rapid unco-ordinated contraction of individual muscle fibres (cells). There are no P waves. The spread of the electrical impulse from the SA node into the atriums is impaired. The response of the ventricles via the AV node is haphazard, and so the ECG shows an irregularity of the QRS complexes.

ECG: atrial fibrillation

It was for the treatment of atrial fibrillation that Digitalis was introduced by the Birmingham-based botanist and physician William Withering (1741–1799). This treatment was an extract of the plant Digitalis purpurea (common foxglove) and was based on a folk medicine for the treatment of “dropsy”, this being oedema or swelling of the legs due to heart failure, atrial fibrillation often being associated.

William Withering

Also common are ventricular ectopic beats, that all people might experience as a “missed beat”. They are only very rarely of importance. A ventricular ectopic beat occurs spontaneously, not triggered by or following an atrial beat. The ECG will show a QRS complex, out of sequence with the others and not preceded by a P wave. The QRS complex is likely to be a different appearance depending on the part of the ventricle from which it originated.

ECG: 2 ventricular ectopic beats

The atrial beats and ventricular beats can become disconnected, and this is called “heart block”. The P waves will be present and also the QRS complexes, but the sequence of them is random. The AV node is not picking up or transmitting the stimulus from the atriums. The ventricles will develop their own rhythm, but the rate becomes very slow. This causes problems such as blackouts, and an implanted artificial pacemaker is necessary to speed up the heart.

ECG: complete heart block, dissociation of P waves and QRS complexes

Finally for our purposes there is ventricular fibrillation (VF). The ventricles just fibrillate like jelly wobbling. There is no actual contraction of the heart and this is what happens in a “cardiac arrest”.

ECG: ventricular fibrillation

The ECG in CHD and MI

It was only in the 1920s that the ECG was used in the diagnosis of MI as it was only in that decade that the disease appeared. 

The ECG recorded from an individual tells us of events that have happened in the past - ten seconds ago or ten years ago. There is no prediction of the future.

Similarly there is no feature of CHD as such. CHD is a disease (atherosclerosis) that takes place in the arteries on the surface of the heart. The ECG tells us about damage to the heart muscle and the conducting tissue within the muscle.

Only when something is happening either now or in the past does the ECG become abnormal. Someone can have a normal ECG today but develop an MI tomorrow. We cannot predict future health from an ECG. There is no reassurance value from a “routine” ECG performed at a time of good health.

The detection of MI is the main use of the ECG, after identification of rhythm disturbances. It is quite simple and there are two specific changes.

A Q wave might appear, and this indicates major damage to the heart muscle. It is a permanent abnormality and remains as a historical marker of an MI in the past. When a Q wave is seen it cannot be concluded that an MI has just occurred. This would only be the case if it was not present on a previous ECG, or after other tests have been performed. A Q wave resulting from MI is often followed in the long term by an inverted T wave.

ECG: Q wave followed by inverted T wave

ST segment elevation after an MI is a temporary abnormality at the time of the event. If the ECG is delayed after the development of chest pain, the ST elevation might be missed, having resolved rapidly.

ECG: ST segment elevation, also small Q waves

When the Q wave is associated with ST segment elevation the diagnosis of an acute MI is clear. This is a "STEMI", ST Elevation MI.

ECG: small Q wave with high ST segment elevation

The ECG in angina

Angina used to be a disabling but not fatal result of CHD. It is recurrent chest pain occurring on exercise, due to a narrowing of a coronary artery. The ECG at rest is normal, but on exercise ST segment elevation might occur (the exercise ECG). There can rarely be transient elevation of the ST segment at the time of a severe attack of angina.


I hope that this brief review of the ECG is informative but not incomprehensible.