Tuesday, 11 June 2019

Food and Health – Statistics and Lies

Is highly processed food bad for us?
Can we believe the statistics that are presented to us?

Shopping: a large range of ready-made meals
We live in an era of “dietism”. There are many books and articles on how various aspects of our food are responsible for all sorts of illnesses and threats to our longevity. I have pointed out previously that the past fifty years, since 1970, have seen a major and apparently spontaneous (that is "natural") decline in deaths from coronary heart disease, the end of the greatest epidemic of the 20th century. However this occurred at a time during which we have seen the emergence of “fast food”, that many people regard as “junk food”, and also our supermarkets have become stocked with  food that has been prepared in factories. The food is imaginative and it tastes good. But is it bad for us? Despite such allegations, how is it that the proportion of our population living beyond the 90th birthday continues to increase? Are we not in reality healthier than ever?

Statin trial

Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, Macfarlane PW,
McKillop JH, Packard CJ, for the West of Scotland Coronary Prevention
Study Group. Prevention of coronary heart disease with pravastatin in
men with hypercholesterolemia. N Engl J Med. 1995;333:1301–1307.

We are also in an era of distorted statistics. I have illustrated previously that we are told from the WOSCOPS study (reference above) that pravastatin reduces the risk of death at eight years by 25%, but the reality is that the reduction was just 1%. The absolute reduction in death rates was from 4% to 3%. The 25-fold amplification of the result is manipulative, quoting proportionate reduction in death rate in place of absolute reduction. This means presenting the numerator without reference to the denominator. 

The absolute reduction of 1% tells us clearly that if 100 high-risk men take pravastatin daily for eight years, then the life of one of them will be prolonged. The proportionate reduction of 25% gives no useful information as the denominator is ignored. It is a manipulation to enable sales.

Let me illustrate this manipulation further.

Diet study from Paris

On May 30th 2019 there was a press release in the UK, appearing in many national newspapers and on radio transmissions. It stated that:

The press release indicted an increase of cardiovascular disease by 12% when the proportion of highly processed food in the diet of 105,000 individuals rose from 10% to 20%. Incidentally, is this an increase of 10% or of 100%? 

Read on for further understanding.

It is necessary to look at the original data, some of which was provided in an expansion of the press release in The Guardian, and it is of course found in the original paper in the British Medical Journal.

The study was of 105,000 adults age 18 or greater, and the follow-up was for five years. For the purpose of analysis the population studied was divided into four groups based on the proportion of highly processed food in the diet.


The cardiovascular disease rate in the highest quartile of consumption of highly processed food was 277 per 100,000. This is the usual way of presenting health statistics.

For the lowest quartile of highly processed food consumption the disease rate was 242 per 100,000.

There was thus a higher disease rate in those consuming a diet relatively high in processed food. But how much higher?

Let us note the simple calculation:

277 - 242 = 35

This would appear to be non-controversial. It indicates that if 100,000 people consume a high processed food diet, then 35 more of them will develop cardiovascular disease compared to a similar group with a lower consumption of highly processed food. 

35 out of 100,000  = 0.035 out of 100  =  0.035%

If you are one of the 100,000 would an increased risk of 0.035% make you change your diet? The answer is probably “No”.

If this were the stated result of the study, it would almost certainly be ignored by the media. There would be no press release and the authors would remain in obscurity with no fame and little prospect of future research grants. The cost of the study was not stated but the paper had 13 authors and no doubt many unrecorded assistants and clerical staff employed over 10 years. This would suggest a cost of at least £/€/$ 1.5 million.

The Spin

Turning bad news into good news is a process called “spin”, frequently used by politicians. Enter statistical manipulation.

I have presented absolute proportions, and these enable us to understand the real world, how the results of the study affect "me" as an individual. We now need to look as to how the result is translated into “proportionate” changes.

The increase in disease rate is from 242 to 277, a difference of 35. This number is presented as proportion of 242.

35 / 242 = 0.145

and this represents an increase of 14.5% of cardiovascular disease by consuming a diet high in highly processed food.

0.035% represents a change. But using a proportionate result mean that we can use an increase from the lower number or a decrease from the higher number. 

And so alternatively:  35 / 277 = 0.127

which is a 12.7% decrease by having a diet low in highly processed food realise to a high level diet.

Using proportionate figures of 14.5% of 12.7% is much more dramatic than 0.035%, hence widespread newspaper headlines.

Expressing the result of this study as a proportionate rather than an absolute result amplified the diet effect from 0.035% to 12.7%. This is an amplification factor of about 350.

0.035% tells us about the real world, how the health of us as individuals is influenced by our diet. 25% tells us nothing.

This spin is common in medical papers and it ought to stop or be stopped.

Dubious mathematics - changing denominators

Disease incidence per 100,000
We encounter the mathematical effect of manipulating numerators with no reference to the denominator. In this case the numerators were 277 and 242, and the denominator was 100,000. You will see that the manipulation above took no account of the denominator.

Disease incidence per 1000
Let us assume that the denominator was different by a factor of 100:
High consumption group  277 per 1000
Low consumption group   242 per 1000.

The difference of 35 is now per 1000.

35 per 1000 = 3.5 per 100 = 3.5 %.
This is important, a hypothetical effect 100 times greater than the real study result.

But the proportionate calculation would remain just the same:
35 / 242 = 0.145 = 14.5%  or  35 / 277 = 0.127 = 12.7%

Disease incidence per 10,000,000
Let us suppose that the disease incidence is much lower, by a factor of 100. The numerators remain the same but are now found to be per 10,000,000, a much much lower incidence and a therefore a much larger denominator. The results would be:

277 per 10,000,000  and 242 per 10,000,000. 

The difference (numerator) would remain at 35, but now out of 10,000,000.
The absolute difference would be 0.00035%. This is a tiny population effect, but if the sample size is big enough it could achieve statistical significance, even though of no health significance.

However proportionate change manipulation still leaves us with 
35 / 242 = 0.145 = 14.5%  or 35 / 277 = 0.127 = 12.7%

Whatever the disease incidence, the answer is always 12.7% (or 14.5%). 

We can therefore see that proportionate results are meaningless in the real world and give no indication of real risk to the individual who is making a choice of what to eat.

Expressing the proportionate result implies a much higher risk than is really the case. It is intended to frighten the public (and their doctors) into taking tablets or altering their life-styles or to produce an impact much greater than it should be.

Is it acceptable to use numerators without reference to denominators?

This type of manipulation is completely outrageous. It should not be allowed in papers published by reputable journals, or any other form of publication. Numerators should not be separated from their denominators. 

I am no mathematician but I learned about numerators, denominators and percentages when I was in my primary school. I was taught that if the numerator is increased or reduced, then the denominator should be changed by the same proportion:

 3/4 = 6/8, not 6/4.  3/4 = 12/16, not 12/4.

The manipulations that we have seen would result in an examination "fail".

Are my salami sandwiches a form of suicide?

Friday, 8 March 2019

Epidemic and Endemic Coronary Heart Disease

Influenza is always with us and no doubt always has been. It affects a significant number of people each winter and it can cause deaths, especially of the vulnerable very elderly. This is endemic influenza: it is more or less constant within the population (end- means within). But occasionally the population experiences an epidemic of influenza (epi- means without or outside). This affects a large proportion of the population with a much higher death rate than the endemic form. An epidemic of influenza is due to a new, a mutant, strain of the influenza virus to which we have no immunity. However we develop immunity rapidly, and so the epidemic subsides. 

It is the same with coronary heart disease (CHD) and myocardial infarction (MI).

The two major epidemics of the 20th century

Immediately following the end of World War One in 1918 the population of Europe experienced an epidemic of influenza. It became known as “Spanish Flu”, and as it occurred in all continents it can be described as a pandemic. It affected worldwide about 500 million people and it was responsible for the deaths of up to 100 million. 

War cemetery at the beautiful marble Bodelwyddan Church, North Wales.
The graves are of Canadian soldiers who died from influenza
shortly after the end of World War 1

War grave of one of the many Canadian soldiers
The second major epidemic was that of many deaths from CHD. It was a disease the basis of which started at about the same time as the influenza epidemic, but it had a long latent interval before the occurrence of clinical effects and the large number of deaths. 

We have all been aware of the many deaths from CHD that occurred during the 20th century. I have described how this appeared as a new cause of death during the 1920s, rising exponentially to a peak in about 1970. CHD became by far the major cause of death, and it was clearly a well defined epidemic. Indeed, as it occurred in temperate zones in all continents it was an international pandemic. Although CHD deaths were mainly in people over the age of 70 years, there were many deaths in younger people.

The epidemic of CHD in the USA, 1940 to 2000. Data from W Rothstein.

The peak of the epidemic in 1970

1970 was time of medical drama, the peak of the epidemic of severe high-mortality CHD. At this time I was busy as a young doctor working in emergency hospital medicine and I remember it vividly. There were many patients admitted severely ill with obvious myocardial infarction (MI). They had a high death rate: almost half died before they reached the hospital, and 35% of those admitted died in hospital. 

They were found to be very likely to suffer from the new experience of “cardiac arrest”, later identified as the immediate result of ventricular fibrillation (VF). ECG monitoring, cardio-pulmonary resuscitation (CPR) and defibrillation came into existence; coronary care units had to be invented. But this was in 1970, very different from the present time, or even in 1990.

Case fatality rate after admission to hospital due to MI,
peak of the epidemic and during its decline

This was the greatest epidemic of the 20th century, and also a worldwide pandemic. Over a much longer time-span (fifty years rather than weeks), it was responsible for more deaths than Spanish Flu. Short memories and a long time-scale mean that few people appreciate it as an epidemic, but it was.

CHD before the epidemic

It is likely that CHD existed before the emergence of the epidemic in the mid-1920s. Historical evidence is far from complete as soft tissues such as arteries decompose after death – except when the body is embalmed. Examples of this are found in Egyptian mummies, and evidence of atherosclerotic disease has been identified. Atherosclerosis, hardening of the arteries, is the background of CHD, with plaque disruption and rupture being the precipitating event of MI (“heart attack”). In the ancient Egyptian experience, CHD, although present, could not be identified as the cause of death. 

Cross-section of a critically narrowed coronary artery,
obviously having caused death.
CHD as a disease can be present for many years without it ever causing symptoms or illness, or even death.

During the Korean war (1950–53), autopsies performed on young soldiers killed in action established the presence of arteriosclerotic CHD in almost 80%, and severe disease in almost 20%. This was twenty years before the peak of the epidemic. It demonstrates a long lead time, and had they not been killed in military action they would probably have died at the peak of the epidemic twenty years later, some earlier, some later. The disease process of the epidemic was well established before 1950. In fact by the time of the Vietnam war (1968–78) the prevalence of atherosclerotic disease in soldiers killed in action had fallen by half, and by the time of the Iraq and Afghanistan wars it had almost disappeared.

Evidence of asymptomatic CHD in young US soldiers killed in action in successive wars.
The decline of the disease is obvious.

Chest pain ?cause

In the years following 1970 there were many people who presented to emergency services with chest pain suggestive of MI. The great majority were not ill and they survived. The ECG was normal and blood enzyme tests were also normal. There was thus no objective evidence of MI/CHD, or any other active disease process. This was in the era before the extensive use of coronary artery imaging. 

A large sample of this group of patients with what was called “chest pain ?cause” was identified in Nottingham, UK, and reviewed after the lapse of a few years. After one year none of those whose diagnosis was chest pain ?cause had died, compared to 30% of patients with a diagnosis of MI. This excellent outcome of chest pain ?cause was obviously very reassuring.

CHD since the end of the epidemic

The main feature during the epidemic of CHD was the very high death rate, but the clinical scene is very different now. A patient who presents to the hospital emergency department today with chest pain is likely to have a normal ECG

Normal ECG

The “Q wave MI”, common in 1970, is now extremely rare. During the latter years of the epidemic we would see an abnormal ECG with ST segment elevation even if no Q wave, but at present we find an ECG with neither Q wave nor ST elevation . This is the “non-STEMI” (non-ST elevation myocardial infarction). This means a normal ECG, indicating minimal heart damage, a condition that would have been diagnosed as “chest pain ?cause” in 1970, with an excellent prognosis.

Q wave MI, common in 1970, rare today

Changes in the diagnosis of MI

When the heart muscle is damaged, enzymes are released from the cells into the blood, where they can be detected and used as confirmatory evidence of MI. The enzyme tests used in the 1970s are no longer in use because they lack “sensitivity”. This means that it was possible that some people in the “chest pain ?cause” group had actually experienced a very “mild” MI without it being recognised, ECG and enzyme tests of the day being normal. 

The next development was a new blood test of “troponin”, again detecting chemicals released from damaged heart muscle cells. This was a more sensitive test: it was positive in cases when the ECG was normal and when the older enzyme tests would be normal. This means that more people with “chest pain” would be diagnosed with MI.

And then in the early 21st century, there was the development of the high-sensitivity troponin test, so that even more people with chest pain would be diagnosed with MI. In previous years this diagnosis was not possible: the patient would have discharged with a label of “Chest pain ?cause”, knowing that there was a good outlook and no cause for concern.

Evaluation has shown that there is no need for concern in people diagnosed as “MI” the basis of only elevated high-sensitivity troponin. It creates more “patients” (patient mongering), with no benefit to themselves, but probably much more anxiety, and of course more activity and income for doctors and other health professionals. 

Coronary angiography

In the 1970s coronary angiography was something very new and not available on a wide scale. Today it is a readily available investigation and the number of angiograms has increased dramatically. The purpose is to identify the condition of the coronary arteries (the arteries that supply blood to the heart muscle). 

Diagrammatic representation of the coronary arteries,
showing the presence of disease and narrowing.

At present about 250,000 coronary angiograms are performed each year in the UK. The purpose of the investigation is not to diagnose MI but to assess the degree of coronary artery disease, and a measure of narrowing of coronary arteries. Following angiography, stent insertion is performed if necessary, about 100,000 per year in the UK.

In respect of patients with MI diagnosed in the traditional way, we expect to see critical coronary artery narrowing, perhaps an 80% or greater narrowing. Under this circumstance the insertion of coronary artery stents would be important, the purpose being to prevent further episodes of MI and possible sudden death. 

It is unfortunate that widespread coronary artery stent insertion was not readily available during the epidemic of CHD. Now that it is readily available we find that the epidemic of severe and high-mortality CHD has come to an end. We are in an era of endemic CHD, a disease that might have been with us since antiquity, and which is in a mild form with a low mortality rate. Most MIs would not have been identified in the past, but now they are. 

A diagnosis of MI is followed as soon as possible by coronary angiography, but today coronary artery disease is much milder and severe stenosis is much less common. Nevertheless coronary artery stents are used more than ever, and this has led to criticism concerning overuse of stents when risk of death is low.

The cause of endemic  CHD

Few people seem to be aware that CHD has undergone a major change since the peak of deaths in 1970, mainly because those, like me, who were at the front end in 1970 are no longer in clinical practice. Personal experience forms opinions. But what has happened: what is the reason for this change?

I have expressed previously thoughts on the causation of CHD . First, an epidemic cannot be genetic, and its development is the result of external factors. These could be chemical or biological. Chemicals from cigarette smoke appear to be accelerating rather than the prime mover of CHD. Chemicals in the diet (mainly cholesterol) have been assumed to be the cause, but confirmatory evidence is far from clear: it must be concluded that CHD is not a dietary disease. It has only recently that CHD has been accepted as being an inflammatory disease, and it is most likely that inflammation is driven by infection.

The infection is the result of micro-organisms circulating within the blood stream, a common or even “normal” event, a low-grade bacteraemia. Bacteria can enter the walls of the arteries through the vasa vasorum (the blood vessels of the blood vessels). 

Diagram of the wall of an artery.
The vasa vasorum provide a blood supply to the wall of the artery, in particular to the media, the muscular part of the artery. It is here that the disease process of atherosclerosis begins, NOT from deposition of cholesterol from the blood on to the internal surface of the artery (the intima)

Body defence mechanisms then come into play, so as to control and neutralise the bacterial invasion. The first line of defence is LDL-cholesterol. Although this leads to the accumulation of cholesterol in the artery wall, its purpose is defensive. If the micro-organism is recognised by immune memory, elimination of a bacterium is aided by the mobilisation of immune mechanisms,.

Bacteraemia is common, the result of a wide variety of micro-organisms, some known and some (probably most) not yet identified. It is inevitable that during life we will encounter a large number of bacterial invasions of our arteries, more if our immunity is impaired. As a result we will accumulate the low-grade inflammatory process that becomes atherosclerosis. This might ultimately lead to low-grade endemic CHD.

The cause of the epidemic of CHD

But a high virulence organism might appear, a novel micro-organism to which there is no innate immunity, and this would cause an epidemic. An epidemic arises with the appearance of a new micro-organism, and it later subsides because of the development of immunity, which will be inherited to protect future generations.

When syphilis first came to Europe in the early 16th century, it caused a sexually transmitted disease that appears to have been much more severe than it was 400 years later. It became a long-term epidemic that was often disabling and fatal, as the result of its later neurological and cardiovascular disease processes. Syphilis is due to the bacterium Treponema pallidum, and it was the cause of an epidemic of heart disease which came to an end at about the same time as the emergence of the epidemic of CHD.

Treponema pallidum, a spirochaete,
the cause of syphilis, that can cause serious and fatal heart and arterial disease

Rheumatic fever in Europe became almost extinct during the 20th century. Its origin is far from clear, but its decline was probably spontaneous, helped (as with syphilis) by susceptibility of the causative micro-organism to penicillin. It was another microbial cause of serious and fatal heart disease, due to the bacterium Streptococcus pyogenes.

Streptococcus pyogenes, strings of spherical bacteria (cocci).
The cause of rheumatic heart disease.
The long-term endemic form of CHD is due to a variety of low-pathogenicity bacteria, but the epidemic must have been due to just one micro-organism, almost certainly Chlamydia pneumoniae, or a specific mutant of it.

Chlamydia pneumonia, a tiny and ancient bacterium
that can only survive within the cells of a host.

Chlamydia pneumoniae is usually but not always detected in CHD. Although it is likely to have been the cause of the epidemic of high-mortality CHD, the endemic disease due to a variety of other micro-organisms continued during and after the epidemic. 

Review of the Chlamydia pneumoniae story will follow in a future Blog post.

Sunday, 13 January 2019

Atmospheric pollution, illness and the sun

The atmosphere, pollution, health, and the sun

There is currently a great deal of concern about atmospheric pollution, which is said to be killing thousands, if not millions. But of course atmospheric pollution is not a recognised cause of death, and a specific disease must be the true cause of death, with atmospheric pollution being an initiating or an accelerating factor.

Industrial townscape, LS Lowry

Urban and rural deaths

The industrial revolution in the UK and several other countries of Europe commenced in a major way during the 18th century. It was based on the energy released by the burning of coal, and it created a huge amount of atmospheric pollution. The population of the new industrial towns experienced a serious health and survival disadvantage compared to people who remained living in surrounding rural villages.This was shown in a study of Manchester and Liverpool, undertaken by a Manchester physician Thomas Percival (1740–1804). His monograph, “Observations on the population of Manchester and other adjacent places” was published in 1773.
Thomas Percival 1740–1804
Whereas today we would report the number of deaths per 100,000 of the population, in 1773 Percival reported that 1 in 28 of the population of Manchester died each year, and this was similar to the experience of Liverpool, just 50km distant. The population of Manchester was 27,246 at the time. A death rate of 1 in 28 is equivalent to 3571 per 100,000, extremely high compared to present times.

In contrast, the death rate in the surrounding villages was half this, at 1 in 56 of the population. This is equivalent to 1786 per 100,000, again very high compared to  present years (about 900 per 100,000 per year).

The obvious difference between industrial cities and rural villages is atmospheric pollution. The observation of 1773 remained the same two centuries later.


What became obvious in the new industrial cities was the emergence of rickets in children, a result of serious atmospheric pollution blocking the vital benefit of sunlight. The experience in Glasgow was that if the sick children were moved to the coastal fishing villages (from which the families originated), then the rickets would heal and the children’s health would improve.  In Austria, there was also an emergence of rickets in the new industrial cities, with improvement following movement to the mountain villages.

+ tuberculosis

There was an obvious link between rickets (the direct result of lack of vitamin D from sunlight) and tuberculosis. Glasgow, a major industrial city, became the rickets, and then the tuberculosis, capital of the world. The link was also obvious in Austria: it gave rise to the Heidi story in which the sick girl (presumably with tuberculosis) was taken from the city to the clean air of the mountains  and there was restored to good health.

Although atmospheric pollution was a serious health problem for children and adults, a compounding factor was long hours of indoor work. A Manchester surgeon Thomas Bellot stated that it was not uncommon for factory children "to be checked in their growth, to become lame and deformed in their legs...and eventually to die of consumption" as a result of "their long confinement in heated and unventilated rooms, and of their being constantly on their legs during their long hours of labour. [quoted from Peterloo: the Story of the Manchester Massacre, by Jacqueline Riding]


The atmospheric pollution of the early industrial cities caused serious problems up to the mid-20th century, especially in the UK. The winter smogs of London reached a peak in 1952 that lead to the UK Government Clean Air Act in 1956. Following this there was a remarkable improvement in air quality. 

Stalybridge, Manchester 1950
The burning of coal was the major problem, and much of this was for domestic heating. Also, electricity was generated by many small coal-fired power stations that operated very inefficiently. Gas was produced by heating coal. Factories were powered by coal-fired steam engines, and railway steam locomotives were powered by coal. Coal was King, and it underpinned the industrial revolution.


During the 19th century whales were the main source of oil, to be used mainly for lighting. Fossil oil was discovered and came into production at the turn of the century, just in time to prevent the total extinction of whales. It was after the second world war that oil came to be used in place of coal, for domestic heating, electricity production, and diesel locomotives. Natural gas came to replace coal gas and we developed an oil-based economy. This happened at just the right time to enable the effectiveness of the Clean Air Act.

River Thames, London. 1950
The cleaning of the atmosphere of the UK during the second half of the 20th century was remarkable. The diminishing use of coal led to a reduction of  particles of unburned carbon and also a reduction of oxides of the sulphur contaminants of coal. This was helped by the improved and more complete combustion of coal in fewer and larger power stations with much taller chimneys. 

But invisible pollutants continue, mainly carbon dioxide, and as this is heavier than nitrogen and oxygen, much of it it stays in the lower atmosphere. To this is added pollutants from the engines of road traffic vehicles. Diesel engines give more particulate pollutants than petrol engines as the diesel fuel is mush less refined. The growth of road transport has led to a resurgence of atmospheric pollution in our cities. It is the particles of unburned carbon that are responsible for the blockage of sunlight penetration. 


The imperative is to progress from an oil-based economy to electricity, which to be used by transport and domestic heating in particular. Coal, oil and gas must not be used for electricity production, and must be replaced by renewable natural energy sources (gravity, wind, sun) together with nuclear power.

Health effects of atmospheric pollution

Although it is generally considered that atmospheric pollution does not kill directly and it is not a recordable cause of death, this has been subject to a legal challenge in the Uk in January 2019. A girl living close to major road in south London died from "asthma". Her mother is seeking a legal change to record the cause of death as "Atmospheric pollution". 

However there will always be an intermediary disease, in which pollution is a driving factor or an accelerating factor. It is necessary to recognise ways in which atmospheric pollution might damage human health.

There are two major possibilities: pollutants that when inhaled might be toxic, and atmospheric pollution blocking sunlight. Another less important possibility is road traffic accidents due to poor visibility.

China – no visible sun on a "clear" day in Beijing

The nature of atmospheric pollutants

The atmosphere provides the oxygen that is necessary for essential metabolic activities of animal life. Oxygen is put into the atmosphere by the photosynthesis of plants. Oxygen is highly reactive and it readily combines with other atoms to produce oxides, for example carbon dioxide, sulphates, iron oxides. It was only after the evolution of plant life (containing chloroplasts, initially free-living entities)  that oxygen was released into the atmosphere, allowing the evolution of animal life. This was the era of the great oxygenation event, nearly three billion years ago.

Burning carbon fuels inevitably results in the release of carbon dioxide (CO2) into the atmosphere. If carbon is partially oxidised, carbon monoxide (CO) will be released. 

If the combustion of carbon is inefficient, then non-combusted particles of carbon will be released into the atmosphere. Particulate matter is divided into PM-10 (10 micrometers or less) and PM-2.5 (2.5 micrometers or less).

Nitrogen-containing contaminants will be oxidised to nitric oxide (NO), nitrous oxide (N2O) or nitrogen dioxide (NO2). Sulphur-containing contaminants will be oxidised to sulphur dioxide (SO2). These oxides form acids when they dissolve in water.

All these oxides are heavier than oxygen and nitrogen, and they will remain within about 100 metres of ground level. They can be dispersed by strong winds and rain.

Chronic respiratory disease

Our European neighbours referred to Chronic Bronchitis as the “English Disease” (the English referred to syphilis as the “French Disease”). Chronic bronchitis was a common disease in the UK during most of the 20th century, and was characterised by a productive winter cough usually with but sometimes without wheezing. It was often fatal after years or decades of ill-health and respiratory disability. Cigarette smoking obviously added to inhaled smoke pollutants. 

Chronic bronchitis is a clinical term that is used little 
today: it has been replaced by the term Chronic Obstructive Pulmonary Disease (COPD) which puts more emphasis on the obstruction of small airways rather than the production of sputum.

Chronic bronchitis was linked to and caused by inhalation of atmospheric pollutants and cigarette smoke, and its incidence has fallen during the second half of the 20th century. During this time we have experienced a major reduction of atmospheric pollution and also a major reduction of cigarette smoking.

Tuberculosis and the sun

Tuberculosis, with its old name of “consumption” is primarily a lung disease, although it can affect any part of the body from the skin to the brain, heart, and bones. Its close relationship to atmospheric pollution and rickets indicates that reduction of sunlight penetration to ground level is the important common factor. Reduction of vitamin D synthesis damages not just bone development but also immunity. In more recent years AIDS has resulted in an increased risk of tuberculosis in the sufferers.

In the 1950s India also experienced a strong association between rickets and tuberculosis, and once again the common factor was deficiency of sunlight. However, whereas in the UK it was mainly the poor who were affected, in India it was the wealthy. In India poor people worked the fields, while the wealthy people stayed indoors – out of the sun.

Other diseases linked to pollution.

Glasgow became the rickets capital of the world, and then the tuberculosis capital. It was also renowned for the dreadful state of dentition of its inhabitants. It became the lung cancer capital, and during the latter half of the 20th century it became the coronary heart disease capital.

A particular high incidence of deaths from coronary heart disease (CHD) during the 20th century epidemic was in places and people with high levels of atmospheric pollution, cloud cover, and geographical reasons for low sunlight penetration. The populations of places with reduced levels of sunlight penetration have had more CHD deaths as well as an average shorter life expectancy. Also a number of cancers are more common where there is low sunlight penetration.

The mechanism behind this is that vitamin D has an important role in developing important immunological defence mechanisms. These are very important in controlling and preventing the development of CHD and many cancers. 

The UK today

Although there is understandable concern about atmospheric pollution in our cities, mainly the result of diesel vehicles, the pollution levels are nowhere near what they were in the 1950s and before. There is also concern about carbon dioxide production and resultant global warming, but that is something different.

River Thames, London.  2018

Despite present-day pollution the health of the UK population is better than ever and we are living longer than ever. More and more people pass their 90th birthday. There are dire warnings about the future, and in particular that atmospheric pollution will cause thousands of deaths, but deaths from what? A recent statement from the Royal College of Paediatricians indicated that atmospheric pollution in damp winter weather will cause respiratory problems in children, but these are acute infections and nothing that will shorten lives.

The state of the atmosphere depends not just on the production of pollutants but also on their removal by wind and rain, and there is generally no shortage of these in the weather of the UK. On recent visits to London I have been impressed by the brightness of the late afternoon winter sun, but nevertheless when seen from just a modest elevation there is a dark layer of polluted air at ground level. 

London, looking north from Greenwich. Dark polluted air close to the ground is visible

Linz, Austria, looking south across the city from Pöstlingberg, with dark polluted air visible

The far East today

What we experience in London UK, or Linz in Austria, fades into insignificance when we see the amount of atmospheric pollution in, for example, Beijing or Delhi. The pollution levels result in the sun being almost invisible, and penetration through particulates is very much less than through all but the thickest water-containing clouds. 

Of course there is little cloud in these arid cities; there is little rain and very little wind. Face-masks to prevent inhalation of polluted air might be of some benefit, but the major problem must be serious obstruction to sunlight penetration and therefore the impairment of  vitamin D synthesis in the skin.

The effects of blockage of the sun with consequent vitamin D synthesis will not be immediately obvious. As in Glasgow and other European industrial cities more than a century ago, we can anticipate serious health problems in the children who are not yet born. When they are born they are likely to be deficient in vitamin D and likely to develop rickets. Poor immunocompetence is likely to result in more tuberculosis or other infections and illnesses prevalent at the time.

Despite the history of atmospheric pollution in European cities, the importance of blockage of sunlight does not appear to be appreciated by those with responsibilities for public health at present.

Xian, China, 2000. A "bright sunny day". The mountains are no longer visible.