Tuesday, 31 March 2015

The sun has some benefits - NICE

The advice from the National Institute for Clinical and health Excellence (NICE), included advice on how to avoid skin cancer. This was published in 2010 and indicated that we must avoid all exposure to the sun, that we should apply a high factor sun barrier cream before going outside, to be repeated at regular intervals during the day if outside, and also to wear a hat and clothes that do not allow ultraviolet light penetration.

Observation of our fellow citizens would suggest that only a few people follow this advice, and such people will be relieved to hear that NICE has relaxed its advice.  The full report is not due revision until 2017 but NICE recognises that since 2010 a great deal of information has appeared concerning the importance of the sun to human health.

The NICE report of 2010 was based on advice from dermatologists, and obviously the thrust of the advice was avoidance of damage to the skin by the sun. We all know that the sun is essential for life on Earth. Sunlight is essential for plant growth and therefore directly and indirectly for all our food. It is essential for all our energy sources apart from nuclear and tidal energy (the sun is necessary for tides but by its gravitational effect and not by its radiation). 

The sun is not new and mankind has managed to survive because of it and with it for thousands of years without the advice from NICE. The population of the Earth is booming and there does not appear to be a major problem. But a small proportion of the population has a white skin and this is susceptible to damage from radiation from the sun. It is interesting to note that people with sun damage to the skin, including non-melanoma cancers on the face and head, have on average the best health and survival.

We know that white skin is particularly susceptible to sunburn and it is very important to avoid sunburn as it can be very unpleasant. When your shadow is shorter than your height, there is a danger of sunburn. Keeping in the shade is sensible, and also covering the skin with clothes. Otherwise protection creams should be used if exposure to the sun is prolonged, and especially if at a high altitude.

However NICE now agrees with common experience, that exposure to the skin without producing burn is not dangerous but is beneficial to our health.

There is an acceptable “physiological erythema”. This is transient redness of the skin produced by solar radiation but it different from and does not lead to burn. It will produce skin tan and vitamin D but it will not result in pain. Sunburn is painful but redness need not be. Similarly a hot bath might produce transient redness of the skin but this is not the same as a scald.

So now it is official: the sun is not as dangerous as was stated by NICE in 2010. Exposure to the sun is to be encouraged but sunburn is to be avoided.

Tuesday, 24 February 2015

CFS, ME - now SEID

Chronic fatigue syndrome CFS or Myalgic encephalomyelitis ME

This has always been a controversial illness. It has been recognised medically for only about forty years, but it is still not universally accepted by doctors. There is always the suspicion that it is somehow imaginary, that the sufferers might be frauds.

A new name has recently been suggested in the USA and I think this is a good move. The new name is Systemic Exertion Intolerance Disease - SEID.

I have had a clinical I interest in fatigue syndromes for more than twenty years. I just happened to see sufferers, but see them with an open mind as many doctors had not taken them seriously. I listened carefully to their stories (the basis of clinical medicine, as I had been taught) and a pattern seemed to emerge. I ultimately became the consultant lead within Lancashire and south Cumbria in the north-west of England, with a population of 1.5 million. The condition is rare but I gained great experience and saw more than 400 sufferers from CFS as I called it then. I learned from the patients.

The patients would report that they felt "tired", "exhausted", or "fatigued", hence the development of the term chronic fatigue syndrome. But normal observers would often say: "But I feel tired / exhausted / fatigued as well, implying that the patients / sufferers were frauds or malingerers, that they were effectively normal but just used a medical escape from work or domestic responsibilities.

It is true that normal people can feel tired, exhausted, fatigued. The problem was that the sufferers did not have the language to express what they were experiencing. There was not a suitable non-medical term that could be used - at least in English but I have no information concerning other languages.

The pattern is that the muscle and the brain are affected. Heart, liver, kidneys, intestines, blood production and other organs function normally. But the muscle do not. In very severe cases the muscles are not strong enough to support the body sitting in an upright position for more than a a few minutes, with the necessity of lying down, but this would be extremely rare. Usually maintaining a supported sitting posture would be satisfactory, but standing for more than a few minutes would be impossible. Walking for more than a few steps or a short distance would similarly not be possible. If at this point the sufferer would be unable to sit down then collapse would occur. The problem is clearly that of "exertion or exercise intolerance" or "exercise-induced muscle weakness". Once such a term is used, the nature of the illness becomes clear.

There is another illness characterised by exercise-induced muscle weakness, and that is myasthenia gravis. It is different and rather more dramatic. Double vision, drooping of the eyelids and slurring of speech are typical.

In SEID / CFS / ME brain function is also disturbed. This is a failure of concentration and the recording of memory. Conversation becomes very exhausting. Reading a book is impossible: when the bottom of the page has been reached, what was at the top of the page has been forgotten. Storylines of television or films cannot be followed.

We can see the advantage of the new term  Systemic Exertion Intolerance Syndrome. "Systemic" implies a wide-spread illness with perhaps more than one body system involved (muscles and brain. Exertion or exercise intolerance is now self-explanatory. The use of the term "Disease" is interesting, but it does give significant medical acceptance of the condition.

In general I use the term "disease" to describe an illness in which there is an obvious abnormality of anatomy, the structure of the body. This would include cancers, heart attacks (myocardial infarction), pneumonia and many others that we know. A "disorder" can be viewed as an illness in which part of the body does not function in a normal way but the structure appears to be normal. We use the term functional bowel disorder as an alternative to irritable bowel syndrome. But when we understand the biochemical aspect of a condition, such as a high blood sugar in diabetes, we tend to use the term disease. I have usually viewed SEID / CFS as a "disorder" as the muscle biopsies usually show normal appearances and the pathophysiology, the nature of the abnormal function, is not clear.

But with SEID there is some understanding of the nature of the disturbance within the body.

This will be the subject of another post shortly.

Tuesday, 10 February 2015

High cholesterol may not be bad for you - lesson from the liver

Primary biliary cirrhosis

Continuing the theme that the misinformation that we are given that cholesterol is somehow toxic is wrong....

By "toxic" I mean that a chemical substance that causes damage to us in a way that is related to dose and time-span of exposure. We are told that he greater the amount of cholesterol in the blood, and for a longer period of time, the more damaging it is. This assertion is not just over-simplistic but it is in defiance of the evidence. It is clear but generally unstated that it is only in men below the age of 50 that blood cholesterol is an indicator of risk of future manifestations of coronary heart disease (CHD). Above the age of 60, the age after which the vast majority of the deaths from CHD occur, a high blood cholesterol is a positive indicator of better survival.

Therapy is aimed at reducing the cholesterol level in the blood, but can this really be expected to be of any benefit? It does not appear to help.

Nature supplies us with a natural experiment by which we can investigate the effect of a high level of cholesterol in the blood. It is a liver disease called primary biliary cirrhosis (PBC).

PBC is a chronic disease of the liver that affects mainly middle-aged women. It has nothing to do with alcohol. The cause is unknown but it is generally classified as an auto-immune disease. In older women it tends to be a curiosity that is picked up incidentally from "routine" blood tests, but in younger women it is likely to be progressive and serious. There is no cure for this condition but it might lead to liver transplantation.

In PBC there is characteristically a very high level of cholesterol in the blood, and this has been recognised for more than half a century. This has given plenty of time for research.

The large amount of cholesterol in the blood in PBC might be deposited in the skin, creating fat patches that are called  xanthomas, or xanthelasma if there are many of them. They tend to occur on the inner parts of the eyelids, on the knees and in the creases of the palms of the hands.

According to what we are told this would make people with PBC particularly susceptible to early death from CHD. They might be expected to have a large amount of cholesterol deposited in the walls of the arteries causing blockage, but this does not happen.

People with an exceptionally high level of cholesterol can be recognised as having familial hypercholesterolaemia (FH), of which we learn more in a Post to follow shortly. It is however interesting to compare the fortunes of those with PBC and those with FH as both have similarly high levels of blood cholesterol.

Those with PBC have a fundamental disadvantage in that they have a serious liver disease. It is only in recent years that liver transplantation has become available as otherwise the younger ones would die early because of liver failure. Transplantation has proved to be every effective in this condition although it can sometimes recur in the new liver.

During the 20th century people with FH have been at a considerable disadvantage in respect of CHD with premature death. However it is now clear that in contrast people with PBC are not at any disadvantage. They do not develop premature CHD and this has been demonstrated in a number of studies. The conclusion of one study is that "(in people with primary biliary cirrhosis) marked hypercholesterolaemia ....is not associated with an excess risk of cardiovascular disease."

If CHD were due to a high blood cholesterol with simple deposition of cholesterol from the blood then we would expect people with PBC to be very much at risk. But we can see that this is not so. This natural experiment casts serious doubt on the widely-accepted model of CHD. It indicates that CHD is not simply due to large amounts of cholesterol in the blood being deposited in the tissues.

We have seen in a recent Post that cholesterol in the wall of the arteries is not the result of simple deposition from the blood. It is an integral part of body defence mechanism and an important part of the inflammatory reaction.

Longo M et al.
Hyperlipidaemic state and cardiovascular risk in primary biliary cirrhosis.
GUT 2001 51 265-269.

Wednesday, 14 January 2015

What is the purpose of cholesterol?

We all know about cholesterol and we are all told that it is very bad for us. We are given the information that "the less of it the better", but we have seen in a previous post that this is not true in respect of women and in men above the age of 50. Above the age of 70, it is good for us, "the more the better".

Ancel Keys (1904–2014)
This means the blood level. It is assumed that this is derived from the diet and we have been told for more than half a century to avoid foods that contain cholesterol.  This message originated from Ancel Keys, the leader of the Seven Countries Study. We have seen this in a previous Post. It was not good quality research and it is said that the conclusion was decided before the study took place. Keys became a very successful evalangelist of fat and cholesterol avoidance, and he and his wife wrote books on the subject. His influence was remarkable but unfortunately wrong.

To avoid fat and cholesterol in the diet is of no health benefit. The reality is that cholesterol is synthesised within the body, something that was not considered by Keys.

This raises a problem: why should the body produce a substance that we are told is very dangerous? It would appear to be a great error of evolution, but this makes no sense. Cholesterol must have a benefit and perhaps the idea that cholesterol is bad for us is not correct.

Uffe Ravnskov b 1934

There is one person who has been almost a lone voice in trying to bring about an understanding of cholesterol. He is Uffe Ravnskov (b 1934).

Uffe was born in Copenhagan in 1934 and practised medicine in Sweden. In recent years he has been an independent researcher and most certainly independently minded. He has given the function of cholesterol a great deal of thought and has added a great deal to our understanding. I have been very impressed by his work and his ability to think differently from the main-stream.

It has been identified elsewhere that people with a high blood cholesterol have a health advantage. Firstly in the age group above 70 years on average the higher the cholesterol the greater the survival. It has also been identified that people with a high cholesterol have relative protection against AIDS, and also a reduced incidence of respiratory infections and post-operative infection complications.

LDL lipoprotein particle

LDL-cholesterol is alleged to be the "bad" cholesterol. LDL stands for Low Density Lipoprotein. This is not too important in itself but it is a combination of a fat (lipid) in the form of cholesterol and protein that enables its transportation throughout the body. It has been noted in the laboratory that LDL will neutralise bacterial toxins in serum.

These observations give more than a hint that the body is not in error in synthesising cholesterol because cholesterol is of considerable benefit. But what seems to be going wrong in coronary heart disease (CHD) and why is there a build-up of LDL-cholesterol in the walls of the coronary arteries?

CHD, like atherosclerosis in general, is the result of an inflammatory process within the walls of the arteries. This in turn is result of invasion of the walls of the arteries by micro-organisms. The 20th century epidemic appearance of CHD suggests that the cause has been a single micro-organism, possibly but not definitely Chlamydia pneumoniae,  but perhaps several micro-organisms are involved. Because of the obsession with diet and cholesterol, research into the role of micro-organisms in the development of CHD has been seriously neglected.

Treponema pallidum
There is however another micro-organism that gives rise to heart disease and arterial disease. It is a spirochaete, Treponema pallidum, the cause of syphilis, which a hundred years ago was a very major cause of disability and death. So do not take notice of people who tell you that CHD could not possibly be due to a micro-organism: it can be and it is.

Micro-organisms cause other forms of heart disease, disease of the valves of the heart. Streptococcus pyogenes causes rheumatic fever and as a result chronic disease of the mitral valve in particular. Rheumatic heart disease used to be very common, but not now.

Viruses can cause acute disease of the heart muscle, viral myocarditis.

Another infection of the heart is endocarditis, infection settling on the heart valves. A variety of micro-organisms are involved, in the past mainly Streptococcus viridans , which passes from the mouth into the blood-stream.

So there is no reason why a microbial cause of CHD should not be considered seriously.

The coronary arteries on the surface of the heart

When a micro-organism invades the wall of the arteries, then as in other parts the body, a defensive inflammatory process takes place. The first line of defence in the tissues is LDL-cholesterol and it accumulates very rapidly in response to the infection. The second line takes the form of large white cells called macrophages, the "big eaters". They clean up the inflamed tissues and ingest the cholesterol. This development in the walls of the arteries is called "atherosclerosis". Antibody reactions also occur and are very powerful.

As in other parts the body, such as skin and joints, an inflammatory process is associated with swelling and that is the case with CHD.  This is usually an advantage in terminating the disease, but sometimes there is just a controlling action, not curative. This is typical of chronic inflammatory and auto-immune diseases.

Atheromatous plaque in an coronary artery
The inflammatory process can be such that the activity of macrophages cannot keep up with LDL cholesterol deposition, itself a defensive process. Swollen patches called plaques then develop in the wall of the artery, and they obstruct the flow of blood. In a similar way inflammation in the throat of a small child can cause swelling and obstruction and the illness of “croup”. Also inflammation in the intestine of people with Crohn’s disease will produce swelling, which can cause intestinal obstruction.

In the coronary arteries it is "rupture" of the surface of the plaque with the formation of a blood clot that brings about a total obstruction to the artery. The result of this is a heart attack, myocardial infarction, often with sudden death. Statins can stabilise plaques, thus inhibiting disruption, acting through an anti-inflammaory process and not inhibition of cholesterol synthesis.

So we can understand that CHD is likely to be due to a micro-organism, this explaining why it has been an epidemic otherwise not explained, and that it clusters in families. It has been much more common in locations with poor sun exposure and low vitamin D levels, and also in other circumstances in which immunity is low (after chemotherapy or organ transplantation). The cholesterol deposited in the arteries is a result of the infection, the inflammatory process unfortunately obstructing the flow of blood.

As inherited immunity has developed within the population, so the epidemic of CHD has subsided and is almost at an end. It is however possible that similar epidemics will emerge in the future. If a microbial cause is accepted and the putative micro-organism identified, then protection through immunisation can be anticipated.

Thursday, 18 December 2014

Peace to all

Christmas Peace

We are at the time of the mid-winter festival dating back to times before the Christian era. The celebration is illustrated by holly, ivy, mistletoe, snow, ice, robins etc. The western Christian church decided that this was a good time to celebrate the birth of Jesus, adding shepherds, wise men, sheep, camels, and donkeys to the winter scene. The fact that Jesus was born on Sunday March 1st 7BC is not of immense importance in itself. For many centuries we have enjoyed Christmas at this time of the year.

Jesus was born at a time of major civil strife and an insurrection of the Jewish people against their Roman overlords was imminent. It did not happen until 53 years later, culminating in the destruction of Jerusalem in 71AD (or CE) and the dispersion of the Jewish people. 

But despite all this, Christmas has in recent years become a time of peace and this must be a good thing. The unofficial Christmas truce at the trenches of the First World Ward was quite remarkable but unfortunately the truce was allowed to continue for only a few hours. The killing then resumed.

2014 has been a time of major civil, ethnic, sectarian, and religious conflict in many countries of the world, especially those of the middle east. Peace seems to be ever more distant.

This brings to my mind a poem that I learnt at my primary school, in 1953 when I was ten. I have always remembered it but only now have I realised its immense importance as a message of peace and “Good-will to all men”.

Abou ben Adhem was written by the English poet James Henry Leigh Hunt, who died in 1859. He based the poem on the story of the mystic Ibrahmin ibn Adam, who was born in 712 and who lived his life in Syria, This country more than any needs him now.


Abou Ben Adhem (may his tribe increase!)
Awoke one night from a deep dream of peace,
And saw, within the moonlight in his room,
Making it rich, and like a lily in bloom,
An angel writing in a book of gold:— 
Exceeding peace had made Ben Adhem bold,
And to the Presence in the room he said
"What writest thou?"—The vision raised its head,
And with a look made of all sweet accord,
Answered "The names of those who love the Lord."
"And is mine one?" said Abou. "Nay, not so,"
Replied the angel. Abou spoke more low,
But cheerily still, and said "I pray thee, then,
Write me as one that loves his fellow men."

The angel wrote, and vanished. The next night
It came again with a great wakening light,
And showed the names whom love of God had blessed,
And lo! Ben Adhem's name led all the rest.

Greetings of peace to all.

Wednesday, 10 December 2014

Dietary fat and heart deaths - the Seven Countries Study

Dietary fat and heart deaths - the Seven Countries Study

For many years I have been concerned about the serious misunderstanding that is generally called the Diet-Cholesterol-Heart Hypothesis. This indicates that coronary heart disease (CHD) is due to cholesterol in the blood, which in turn is due to cholesterol in the diet.

We now know that this is not correct. Initial research was not of good quality and has been misinterpreted but it has become engrained in “popular wisdom”. It remains the paradigm at the present time, wrong as it is. The observation that CHD took the form of an epidemic during the latter part of the 20th century indicates that diet could not realistically have been its cause. There was no major change of diet between 1924 and 1970 that was suddenly reversed after 1970. A low fat and cholesterol diet is not of demonstrated benefit. 

What led to this misconception?

The first observation was made by pathologists at autopsy examination. It was noted that cholesterol was present in large amounts in the walls of the arteries, obstructing blood flow. The cholesterol was mainly in large white cells called macrophages (= big eaters). But where did the cholesterol come from and what was it doing there? The assumption was that it came from the blood and from the diet. Diet had to be investigated in detail as cholesterol in food appeared to be very poisonous, responsible for many thousands of premature deaths.

The arteries that supply the heart muscle are the coronary arteries. They form the “coronet” of arteries on the surface of the heart and they supply blood to the heart muscle. When they block completely the person can become very ill or die suddenly, the result of myocardial infarction (MI, heart attack).

It has been incorrectly assumed that cholesterol is simply deposited from the blood, and that it turn it originates in the diet. It was as though the arteries “furred up” with cholesterol in a physical process. However rather than being deposited on the lining of the arteries, the cholesterol is within the wall. But the “furring-up” idea of the “diet-cholesterol-heart hypothesis” has dominated thinking during more than half a century. Even though it is clearly wrong it seems to be impossible to shake it off. The reason for this is that there is no strong competing hypothesis: if CHD is not due to diet then there is only a big question mark. No-one likes too much uncertainty and a false hypothesis continues in the absence of an alternative.

The expectation of CHD being due to cholesterol in the diet led to The Seven Countries Study. This was a monumental observational study undertaken by Ancel Keys of the University of Minnesota, initiated in 1958, conducted for about fifteen years and published in 1980. Although ambitious it was not as carefully controlled as would be expected today. It was very much opportunistic depending on an international network of interested physicians. The underlying hypothesis (the null hypothesis) was that animal fat was the main cause of CHD. The clear objective of the study was to “prove” this, whereas the scientific method should have attempted to “disprove” it. It was designed to look at population characteristics in various countries, comparing dietary patterns with death rates from CHD. Such an epidemiological studies, observing who gets the disease, is the main way of identifying possible causes. 

A list of the “Seven Countries” can be seen in Table 1. The study was undertaken at a time when Serbia and Croatia were all part of the nation of Yugoslavia, before its traumatic fragmentation. Five of the seven original countries studied are in Europe, with recruitment of subjects from defined locations allowing geographical comparisons. Two city locations were in Japan, but again defined locations. 

The other country was the USA, where railway workers were the subjects. Without a defined location this group did not add anything and can be ignored. The independent US Railway Workers Study was originally designed to make comparisons of various rail occupations having different levels of physical activity but was later incorporated into the Seven Countries Study.

The subjects were people of different occupational and social groups and they could not be standardised. For example in Belgrade they were university staff, and in other countries manual workers, not strictly comparable between nations. 

The main results showed that total deaths and CHD deaths in particular tended to be highest in northern European countries, shown in Table 2. The subjects in East Finland had the highest death rate.

Dietary factors were recorded, concentrating on dietary fat. Table 3 shows the proportion of dietary calories that were fat. We can see that, like deaths, the highest tend to be the northern European countries. 

We can record this graphically on a scattergraph, Figure 1. Each point represents a single geographical location, the position of the point being defined by the death rate from CHD and the proportion of diet that comes from fat. We can see that the points lie close to a trend-line that slopes from bottom left to top right, meaning that the association of the two variable factors looks good. The statistic R2 = 0.7421 gives an indication of the strength of association, close to 1.0 indicating strong association and close to 0.0 indicating no association. 0.7421 indicates quite strong association.

Figure 2 is another scattergraph, this time showing the relationship between total deaths and fat intake. The scatter points are now not as close to the trend-line, indicating a weaker association. This is also shown by a much lower R2 at 0.2654. In other words fat intake seems to specifically associated with CHD deaths rather than overall death rate.

It is important to remember that association does not necessarily indicate a cause–effect relationship, but this result of the study was interpreted as evidence that a high fat diet was responsible for the high age-adjusted death rates in northern Europe. We can hardly expect the reverse, that death causes a high fat diet, but it could be that there is something about northern Europe that leads to both a high fat diet and also to a high death rate, especially from CHD.

This was not considered at the time, but there is a geographical factor. Death rates from CHD might be greater with greater distance from the equator, and latitude also determines agricultural practice. The type of food produced is very different in the southern European Mediterranean countries than in those in northern Europe. 

It is now clear that adjusting diet with reduction of fat intake has no demonstrated effect of CHD death rate.  Could it be that high fat intake is just a risk indicator for the climate-related geographical variation of CHD death rates? 

This will be discussed further in a future Post, to appear shortly.


Some interesting reflections on the conduct of the Seven Countries Study can be found in the publication (available as pdf):


By Henry Blackburn, MD, University of Minnesota School of Public Health

Sunday, 23 November 2014

Cigarette smoking - lessons from doctors (1950s)

During the 20th century there was a major decline in deaths from tuberculosis. This decline has never been satisfactorily explained but it must have been the result of an improvement of the general health and immunity of the population. In the years following the Second World War the decline continued, and antibiotic therapy in the form of streptomycin was introduced in 1952.

The major clinical features of tuberculosis (TB) were cough productive of sputum, often with blood (haemoptysis), together with weight loss. This could go on for many years but it was often fatal. The course of the illness could be quite rapid. It was usually called “consumption”, meaning that the body was effectively “consumed” by the disease, what we would now call a malignant process. 

But with the decline of TB there remained a similar illness with a more rapid decline. This illness was characterised by cough, haemoptysis (coughing blood), weight loss, and deterioration. It was lung cancer, also known medically as carcinoma lung or carcinoma bronchus.

The cause of TB had been identified by the great German pathologist Robert Koch as due to a micro-organism, Mycobacterium tuberculosis. Lung cancer was not obviously transmissible and its cause was not clear. Although cigarette-smoking was very common in the post-war years, there was a suspicion that it might be the cause of lung cancer.

Further study was necessary but this was before the present era of medical statistics. The era was introduced by Sir Richard Doll and Sir Austin Bradford Hill. 

They understood the social variation of disease, that the poor had worse health and earlier death. It was necessary to “stratify” and study, that is to look at just one stratum or level of society. Doctors were chosen as the researchers had easy access to them. The “Doctors Study” became famous for identifying that lung cancer, in the vast majority of cases, is the result of smoking cigarettes.

“Proof” is generally not understood but it will be defined in a future Post. In brief it means the fulfilment of predetermined criteria. At the present time we rely on the randomised controlled clinical trial. However this is not always possible and it would certainly not be possible to randomise a group of doctors so that half would have to smoke cigarettes and the other half not. 

The alternative was to use observational studies to demonstrate causation. Although these are not as powerful as the randomised control trial, of which the study of streptomycin was the first modern example, observational studies are usually the closest we can get to the truth. The application of observational studies was the specific role of the statistician Austin Bradford Hill and it was a great achievement of his (see future Post).

Lung Cancer deaths

Richard Doll dealt with the doctors and determined their pattern of cigarette smoking, the number of cigarettes smoked each day, if any. He then observed their ages of death and the causes of death. He was able to identify those who had died from lung cancer and the results are shown in Figure 1.

It can be seen that people die with the passage of time. But the greater the number of cigarettes smoked each day, the higher was the mortality from lung cancer. In those over the age of 75 years almost 18% of heavy smokers died from lung cancer. It was just under 4.5% before the age of retirement.

We can also see that a very small number of non-smokers over the age of 75 died from lung cancer, indicating that there must be other causes that are not of great numerical significance.

There was a “dose-response” effect - the greater the number of cigarettes smoked each day the greater the likelihood of death from lung cancer. This is a very powerful indicator of causation as determined by Bradford Hill. The conclusion of the study was that cigarette smoking causes lung cancer.

Coronary Heart Disease deaths

The study included deaths from coronary heart disease (CHD). At the time CHD had become a serious cause of death but its cause was far from clear, and that is still the case. Deaths of the doctors from CHD were also recorded year on year. 

By the 1950s death from coronary heart disease (CHD) had become a major problem but the epidemic had not yet reached its 1970 peak. There was concern that cigarette smoking might be the cause of CHD and the study of doctors gave a good opportunity for further research.

As with lung cancer, the ages and causes of death of the doctors were recorded and deaths from CHD were identified. In both groups the causes of death were not robust as specific investigations were still in their infancy. The data was however the best available.

The pattern of deaths from CHD, as shown in Figure 2, was very different from the lung cancer graphs. We can see that the graph lines run close together and there was not the separation seen in the lung cancer graphs. Above the age of 75 cigarette smoking had no influence on the likelihood of dying from CHD. In all smoking groups about 20% died from CHD.

If we look at the age-group 55-64, we can see that heavy smokers had almost twice the deaths than non-smokers, 8.8% versus 4.9%. Again there was a “dose-response” relationship and it was concluded that cigarette smoking increases the risk of death from CHD in middle age.

If we now look horizontal variation choosing a death risk of about 10%, we can see that this will occur at the age-group 55–64 in heavy smokers, but about ten years later in the age-group 65–74 in non-smokers. In other words if an individual is going to die from CHD, smoking cigarettes will bring death forward by up to ten years depending on the number of cigarettes smoked.

We can conclude that cigarette smoking is bad and has an important and detrimental accelerating influence on CHD. However in view of the high death rate of non-smokers from CHD, we cannot conclude that  cigarette smoking is “the cause”.

Advice not to smoke is good advice.