The Coronary Heart Disease Pandemic in the 20th Century

In 2013 I wrote one of my first Blog Posts drawing attention to the epidemic of coronary heart disease (CHD) that occurred in the UK during the 20th century. 

The onset of the epidemic

This has been supplemented by a further Post describing in detail the onset of the epidemic, which occurred after about 1924.  Much of the original work had been published in the British Medical Journal in 1963, by Dr Maurice Campbell, a highly respected and pioneer cardiologist in the UK. As with all epidemics, that of CHD had to become well-established before its presence could be  recognised.

The peak of the epidemic

I also described the peak of the epidemic in about 1970. This was the time that I was heavily involved in emergency medicine, and experience of "heart attacks" was then so very different from what we see today. We would see people, mainly men, admitted via the emergency department (where I worked) every day, in whom the clinical features of severe myocardial infarction (MI, heart attack) were glaringly obvious. They had experienced severe crushing chest pain, and about had 50% died before they got to the hospital: sudden death was a major clinical presentation of CHD. Those who made it to the emergency department were usually very cold and clammy with low blood pressure – they were in cardiogenic shock with high risk of acute left ventricular failure and pulmonary oedema. Recorded hospital mortality was as high as 35%. Cardiac defibrillation had only just been introduced and coronary care units were only in a stage of development. The ECG was used in diagnosis and usually showed the appearance of Q waves, very rarely seen today, MI being a much milder condition than it was then. Cardiac enzyme testing was undertaken but it was not usually necessary for diagnostic purposes.

The decline of the epidemic

I have also described the unexpected decline of CHD deaths after about 1970. The decline was slightly earlier in the USA. The presence of an epidemic had been denied by most people, claiming that the data were unreliable and that the condition had always been present. Most of these people had probably never attempted to investigate the data and had never read the papers of Dr Maurice Campbell. 

However the rapid decline of CHD deaths could not be denied: it occurred at a time of good quality data collection in many countries and standardised by the World Health Organisation (WHO). When it was realised that CHD deaths were in sharp decline, the great surprise  was such that in the USA a Bethesda Conference was called by the National Institutes of Health (NIH) in 1978, the purpose being to explain this unexpected decline.

The result was the establishment of the MONICA  project (Multinational MONItoring of trends and determinants in CArdiovascular disease). After 20 years it concluded that the decline of deaths was mainly the result of a decline of heart events rather than more effective treatment. No conclusion was reached concerning either the specific cause of the epidemic or its decline.

The pandemic

My Posts were concerned with the UK experience, which had been very obvious to me. I have been puzzled as to why so few people had recognised that there was a very serious epidemic of CHD deaths in the UK. I find the lack of curiosity very disappointing, especially a lack of curiosity that deaths from CHD had spontaneously gone into sharp decline.

But it was in reality much more than an epidemic. It was a pandemic, occurring in all continents simultaneously, and in effectively all nations in the temperate zones of the planet.

Dr William G Rothstein

The nature of the pandemic is now described in a new book entitled "The 20th Century Pandemic of Coronary Heart Disease". Its author is Dr William G Rothstein, Professor of Sociology Emeritus at the University of Maryland, Baltimore County.

The book is clear and concise, easy to read but of course the reading of data is slow but essential to full understanding. 

The author explains the problems with classification during the onset of the pandemic. The terms used were "angina pectoris" in the years 1900 to 1930, and the new term "diseases of the coronary arteries" after 1930. The International Classification of Disease (ICD) was introduced in 1948, with later revisions, now revision 11. The new term "ischaemic heart disease" (IHD) ,which is the same as the now more commonly used "coronary heart disease" (CHD), was introduced in 1968.

Rothstein confirms that the emergence of the pandemic of CHD "did not receive the attention that it deserved". This is true as people did not appreciate that there was even a national epidemic. 

I have stated previously that the rapid decline of the pandemic has been effectively denied by the medical profession, probably because a reason for it could not be envisaged. Rothstein's states: "The experts' fatalistic acceptance of of coronary heart disease as the result of lifestyles in modern societies produced amazement and confusion among them when coronary heart disease mortality rates began to decrease steadily and substantially in the 1970s and 1980s in the United States and other advanced countries."

I mentioned above that the surprise was such that the NIH Bethesda Conference was assembled in 1978. Rothstein draws attention to the comment from a participant in the conference: "The announcement for this reversal in the long-term trend [of CHD deaths] was received with great astonishment, both in the United States and other countries." This "astonishment" was kept very quiet in the UK, if not in other countries.

The epidemic in North America

The author has assembled data mainly from the USA. These have come from national and state statistics, but also from Life Insurance organisations, which in the early 20th century have been more concerned with accurate cause of death data than national and state registries. 

A simplified presentation of these data are shown in Figures 4 and 5 below.

Rothstein describes the epidemic of CHD in the USA as having the same time characteristics in all states, but the highest death rates in the north-east states. 

He describes the epidemic in Canada as having the same characteristics as in the USA.

The pandemic in other continents

He continues to identify that there was a true pandemic. The sudden appearance and decline of CHD deaths occurred in three continents continents simultaneously, North America, Europe, Australia and New Zealand.

He describes the pandemic in Western Europe, the UK having by far the best data collection. He identifies that mortality rates from CHD were highest in countries north of the 51st parallel (north of 51 degrees latitude), that is Ireland, UK, Belgium, Netherlands, Denmark, Norway, Sweden and Finland. They were lowest in the southerly European nations, Portugal, Spain, France, Switzerland and Italy. Importantly Rothstein notes that the data indicate that the peak and decline of the pandemic was simultaneous in all European countries, for all age-groups and for both men and women. Reliable data are not available for eastern European countries.

The book also describes the pandemic in Australia and New Zealand, with good quality data indicating a peak and decline of CHD death rates simultaneous with Europe and North America.

The pandemic appears not to have occurred in Central and South America. The exception is Argentina, which experienced the pandemic but in a milder form compared other continents. Central and much of South America are effectively tropical, such zones having not experienced the pandemic of CHD. Argentina is clearly in the southern hemisphere temperate zone. 

Age differences

Rothstein indicates that there appears to be a background form of CHD that was present before the pandemic, and is now appearing in the present post-pandemic era. The background CHD was and now is a disease of the elderly. The characteristic feature of the pandemic is that it caused the deaths of millions of people (mainly men) in middle age. It is this that is coming to an end.

The "non-causes" of the epidemic

The purpose of the book is to describe the pandemic, not to explain its cause. However Rothstein looks briefly at suggested causes of the pandemic of CHD and finds them all inadequate to explain it. He emphasises that the simultaneous rise and fall of the epidemic in all continents indicates a single and world-wide cause.

Diet - No dietary factor has been show consistently to be a a causative factor of CHD, and there was no significant change in the American diet between 1920 and 1950. Rothstein states that it is inconceivable that a single dietary factor could explain the rise and fall of the pandemic in all continents simultaneously. The appearance of "fast food" (which many consider to be bad for us) was in the 1970s, at the time of rapid decline of CHD death rates.
Cigarette smoking Although an accelerating factor of CHD, cigarette smoking cannot be regarded as the cause as toward the height of the epidemic, similar proportions of smoking and non-smoking proportions of the population died from CHD. Rothstein indicates that the rapid decline of the CHD pandemic occurred at a time when there was no reduction in lung cancer deaths, a reliable measure of cigarette smoking death.  
Male sex  
In all nations experiencing the pandemic of CHD the incidence has been about three times higher in men than in women.
Diabetes
At the time of the decline of the CHD pandemic the prevalence of diabetes was unchanged. Diabetes could not have been a significant causative factor of the CHD pandemic.   
Obesity
The decline of the CHD pandemic has occurred at a time of concerns about the increasing prevalence of obesity.

Changes in lifestyle risk factors were not responsible for the emergence or decline of the CHD pandemic.

Statin drugs were introduced after the major part of the decline of the CHD epidemic and had no obvious impact.


Explanations

In a previous book that identified the epidemic of CHD in the USA, Rothstein similarly eliminated a reduction of known risk factors as responsible for the epidemic and its rapid decline. In a review he was criticised "for not providing an alternative explanation". This is a false criticism. It was and still is not Rothstein's responsibility to identify the cause that has eluded all of medical science internationally.  Just because he cannot identify an alternative explanation does not mean that one of eliminated "explanations" must be correct.

However it is probably true that once all known risk factors have been eliminated as the cause of the epidemic of CHD, people somehow seem to "switch off" and stop thinking, as though they do not want to know the truth.

The cause

And so it is in Rothstein's book The 20th Century Pandemic of Coronary Heart Disease. The identification of the cause is not offered. Rothstein's purpose is to identify what the vast majority of people (including medical professionals) are unaware of: that during the 20th century the world witnessed one of the most serious pandemics of all times.

Rothstein states that it is "....inconceivable that the many advanced countries on three continents that experienced the pandemic underwent identical changes in their diets and lifestyles at the same times before the emergence of the pandemic and identical reverse changes in their diets and lifestyles at the same times before the decline of the pandemic."

I have suggested in a previous Blog Post that the only plausible explanation of the pandemic of CHD death must be an environmental biological agent, in other words a micro-organism. Only this would affect all continents simultaneously, with a rapid appearance of the disease and then a rapid decline as inherited herd immunity developed. A specific organism has not yet been identified, but a search unlikely to have even started. It is always after the acceptance of an epidemic (or pandemic) being due to a micro-organism that this line of investigation occurs (for example, AIDS and HIV).

CHD in the 21st century

Rothstein indicates that in the 21st century, in the post-pandemic era,  CHD became primarily a disease of the very old, as it had been a century earlier.

He suggests that the need for restraints in health care expenditure in many countries necessitate the re-evaluation of methods of prevention of the condition in healthy persons, including accepted risk factors. 

He wonders if statin drugs currently used widely in healthy people are necessary in the post-pandemic era.

Data presented

William Rothstein presented a great deal of supportive data in his book. His descriptive data from the USA was divided into the groups White Men, White Women, Non-white Men, Non-white Women. 

During the CHD pandemic deaths rates were lower in women than in men. The development of the CHD pandemic was slightly later in non-whites compared to whites.

I would like to display some of Rothstein's data in a simplified graphical format, and in the interests of simplicity I will display only the data for white men in the USA, but for all men in the UK.

Figure 1 All cause mortality in white men in the USA

In Figure 1 we can see data from the USA illustrating all cause mortality. In all four age-groups the death rates were lower in the years 1931-35 than in the years 1911-15. Obviously there are more deaths in the older age-groups.

Figure 2 Deaths from angina pectoris in white men in the USA

In Figure 2 we see in contrast that in all age-groups, deaths from the heart disease angina pectoris (a manifestation of CHD today) increased very significantly during the same time periods. Death rates more than doubled in the younger age-groups.

Figure 3 Deaths from disease of the coronary arteries in white men in the USA

Figure 3 show the other classification category of what we now call coronary (or ischaemic) heart disease. Once again there was a major increase, more than doubling during the first half of the 20th century. This clearly the onset of the pandemic.

Figure 4 Deaths from CHD in white men in the USA

In the 1940s the introduction of a new international classification of disease (ICD) led to the term ischaemic (later coronary) heart disease. In Figure 4 the US data assembled by Rothstein shows clearly the pattern of the pandemic in the USA, similar in all age-groups but more deaths in the older age-groups. In this figure we see the percentage of deaths from CHD in each age-group and not absolute death rates.

Figure 5 Deaths from CHD in white men in the USA

Figure 5 shows the same data but presented by age-group. The same epidemic pattern can be see in each age-group. Once again we see the percentage of deaths from CHD in each age-group and not absolute death rates.
In Figure 6 we can see more recent data, again for simplicity just white men in the USA. Between 1970 and 2010 there was a reduction of all cause death rates in all age-groups, especially in those aged 65–74. It is this that has led to a great increase in the elderly and very elderly in the countries that experienced the pandemic of CHD.

Figure 6 Death rates from all causes in white men in the USA

Figure 7 Deaths from CHD in white men in the USA

We can see in Figure 7 that the reason for the reduction of all cause death rate was an even more dramatic reduction of deaths from CHD. This is the clear decline of the US epidemic. Please remember that statin drugs only came use in about 1990, and into widespread use after 2000. The decline of the pandemic was "spontaneous", meaning that it was not explained by a decline of known risk factors.

Figure 8 All cause death rates in white men in the USA

Figure 8 shows the decline of all cause death rates in the four age-groups in the USA. Once again this is numerically mainly in the older age group (65–74) creating a rapid increase in the number of elderly.

Figure 9 CHD death rates in white men n the USA

Figure 9 shows specifically the decline in the US epidemic of CHD in the four age-groups, responsible for the decline of all cause death rates shown in Figure 8.

Figure 10 CHD death rates in elderly white men in the USA

In Figure 10 we see Rothstein's data on the  elderly in the USA. There is a major decline in CHD death rates between 1970 and 2010. It is interesting to note death rates being greater in the 75–84 age group compared to those more than 85 years old.

Figure 11 All cause death rate in men in the the UK

In Figure 11 we see Rothstein's data illustrating the decline of death rates from all causes  following the peak of the CHD epidemic in men the UK.

Figure 12 CHD deaths in men in the UK

In Figure 12 we see the decline of CHD deaths in the UK following the peak of the epidemic in 1970.

Figure 13 CHD deaths in white men in the USA

Figure 13 displays the USA epidemic of CHD in white men in the USA.

Figure 14 CHD deaths in white women in the USA

Figure 14 shows the same, but for white women in the USA. The epidemic is clear but not as dramatic as in men in Figure 13. The effective the epidemic in the USA in younger women was minimal.

Figure 15 CHD deaths in white men and women aged 65-74 in the USA

In Figure 15 we can see the USA epidemic in white men and white women aged between 65 and 74 years of age. It shows the much greater impact of the epidemic in men compared to women.

Acknowledgement:

I would like to thank Professor Rothstein for permission to present this review of his excellent and informative book, and also for his permission to present his data in a simplified graphical format.

Multiple Sclerosis, micro-organism and the Sun - the link becomes more plausible

West of Scotland: John Lowrie Morrison – Jolomo

Multiple sclerosis (MS) is a well-recognised disabling and often ultimately fatal neurological disease that affects young adults. Its cause is not known. 



The "Cause"

The cause of MS is said to be "auto-immune", which means that inflammatory processes are involved with immune reactions. However "auto-immune" can only be a mechanism of disease and not a true cause.

Figure 1. MRI scan of brain showing multiple deep seated sclerotic lesions as light grey patches

The cause of a disease is its prime mover, the initiator of the disease process. It is invariably identified from the epidemiology of the disease, its distribution within society and the world. Examples are cigarette smoking and lung cancer, aniline dyes and bladder cancer, contaminated water and cholera, family patterns and genetic conditions. In particular, clues arise from changes in the incidence of the disease and its spread in time or geography.

It has been known for many years that the geographical incidence of MS (new cases per year) varies considerably. It is very rare south of the European Alps, and its incidence is much higher in Northern Europe. The world's highest incidence appears to be in the West of Scotland.

Figure 2. Geography of MS, higher incidences in darker colours

We have seen this pattern previously. The epidemiology of MS is remarkably similar to that of coronary heart disease (CHD). The link is likely to be a common susceptibility rather than specific cause.

I have previously stated my contention that CHD is due to one or more micro-organisms, the identity of which we cannot yet be certain, or of which we are completely ignorant. Although a number of micro-organisms are likely to be responsible for background sporadic CHD, a specific single micro-organism must have been responsible for the 20th century epidemic. So it is for influenza: a number of strains can cause the illness over many years, but a specific strain is responsible for an epidemic.

Epidemics

Epidemics give important clues as to causation, whether a micro-organism or a chemical poison. Epidemics are never due to genetic factors.

Figure 3. Location of the Faroe Islands in the North Atlantic

Epidemics of MS have been described in the Faroe Islands in the Northern Atlantic during World War 2. Previously MS was thought to be unknown in the isolated Faroe Islands, but in 1943 there were 23 new cases, in a population of only 25,000. There were subsequently smaller epidemics of 10, 10 and 12 cases.

Figure 4. Faroe Islands

These small but significant epidemics followed the establishment of RAF (Royal Air Force) bases on the Faroe Islands. The purpose of these was to provide air support for war-time shipping convoys crossing the North Atlantic.

In the absence of alternatives, it was thought that the epidemics must have resulted from transmission of a micro-organism from the staff of the RAF who were stationed on the islands. The identity of the micro-organism could not be established at that time, and it has not been stablished subsequently.

Figure 5. RAF Bristol Blenheim bomber as was stationed on the Faroe Islands

The transmission of micro-organisms around the world is well-known. The sea voyage of Christopher Columbus to the West Indies in 1492 made land-fall in what is now known as the Dominican Republic. 90% of the population were shortly to die from smallpox, contracted from the crew. Smallpox was unknown in the Americas and the populations had no immunity (that is inherited or "herd" immunity). 

In return the crew brought syphilis from the Americas to Spain, and thus to Europe. It ravaged the population, which had no immunity, and it was four hundred years before the microbial cause was identified.

MS in the Armed Forces of the UK

New evidence has just become available, supporting the transmissible nature of MS and the likelihood that it is due to a micro-organism. 

It has been identified that the incidence of MS is much higher in former members of the armed forces (military) than in the general population. 

The incidence of MS in this study has been based on deaths, rather than true incidence (new cases per year) or prevalence (number of cases at a moment in time) of the condition. However MS tends to be ultimately fatal and so death rate is a useful measure.


The study was based on 3,688,916 deaths in the UK among men aged 20–74 years. Occupations of the deceased had been recorded and there were 26,507 whose last recorded occupation was "military". There were 7485 deaths from MS, and 129 of these were in the military group.

Therefore in the general population dying during a period of 30 years, 7485 out of 3,688,916 deaths were the result of MS, and in those who had been in the armed forces 129 out of 26,507 their death  was the result of MS. 

These findings can be expressed the Proportional Mortality Ratio (PMR). The PMR standardises the frequency of deaths in the overall population at 100. This is compared to the subgroup under investigation. A PMR in the subgroup greater than 100 indicates that the cause of death is more common, and a PMR less than 100 indicates that it is more rare.

Table. Proportional (Standardised) Mortality Rate of MS in former military workforce

[The mathematical process of standardisation is quite simple. To standardise the population PMR at 100, the mathematical formula is 100 x  0.002029 / 0.002029 = 100. To find the relative PMR of military personnel the formula will be 100 x   0.004867 /   0.002029 = 240.]

We can see in the table that the PMR for MS in former armed forces workers is 240, which is of course two and a half times that of the general population.

This is a major difference in incidence, much higher in people who had been in the armed forces. Why should this be?

Transmission of a biological agent

There appears to be no explanation in terms of chemical exposure, as the difference remained unchanged during each of the three decades included in the study.

The authors felt that the only plausible explanation concerned the fact that members of the armed forces live and work closely together during many years. This implies a transmissible agent as the cause. Person to person transmission is usually a biological agent, a micro-organism.

Is there a reason why MS could not be due to a micro-organism? The answer is "no". There is no competing putative cause, and the experience of the Faroe Islands and the UK military is strong. Direct transmission studies in humans would hardly be ethical and animal inoculations are unlikely to work. Whereas tuberculosis could be transmitted to a variety on animals, this experience does not extend to many other disease–animal experiments.

One of the problems of research into MS is the lack of available pre-mortem biopsy material, the disease being located deep within the brain. The cerebro-spinal fluid (CSF) is readily available for sampling, but it is not as useful as affected brain tissue.

There have been previous suggestions of a micro-organism causing MS, spirochetes and cytomegalovirus, but without transmission studies the identification of a causative organism is unlikely to be conclusive. 

There is the precedent of neuro-syphilis, which leads to the clinical syndromes of the dementing condition general paralysis of the insane (GPI) and also the disabling condition tabes dorsalis (TD). Both manifestations of neuro-syphilis are chronic and ultimately fatal, rarely seen today but a very major health problem a century ago. It was about 350 years before the neurological condition was linked to the primary sexually transmitted infection, and a further 50 years before the causative spirochaetal organism Treponema pallidum was identified. Unethical and effectively criminal human transmission studies were undertaken in the mid-20th century, before medical ethics was established. Such  conclusive studies cannot be undertaken today.

Geography and the Sun

The geography of MS fits in with a microbiological cause. An increasing incidence of disease with increasing distance from the equator (in both hemispheres) indicates a simple latitude factor, the incident sunlight energy at ground level. There is further evidence of the importance of vitamin D in the development of MS. There is a seasonal effect: the highest incidence is in people born in the spring. This means that the later stages of gestation would have been during the winter when sun intensity is at its lowest.

Figure 6. Month of Birth and risk of MS in the UK

It is known that vitamin D enhances immunity. A failure of full immunity results in greater susceptibility to infection. We can therefore appreciate that whereas MS is extremely rare in countries such as Italy and Greece, the world's highest incidence is in the West of Scotland (tuberculosis and CHD are similar). Even further north in the Faroe Islands immunological defence would be low but MS only occurred when the causative micro-organism arrived in 1943.

Links:

MS in the Faroe Islands
https://www.ncbi.nlm.nih.gov/pubmed/371519

MS deaths in UK armed forces
https://academic.oup.com/occmed/article/67/6/448/3872312/Mortality-from-multiple-sclerosis-in-British

Risk of MS and month of birth http://www.bmj.com/content/330/7483/120

High blood cholesterol gives a survival advantage

High cholesterol is good

Previous Posts have shown that the existing dogma that "a high level of cholesterol in the blood is bad" is only true in men below the age of 50 years. In women of this age, the blood level of cholesterol is of no value in determining coronary risk or life expectancy.

The most important source of information is the 30 year follow-up of the observational US Framingham study, published in 1987. The conclusion (effectively ignored) is as follows:

The study did not extend beyond the age of 70 years and so the conclusion is limited. However other studies have shown that beyond this age a high cholesterol level is associated with the best survival. There are three important studies showing this that I have reviewed previously: the Paris study, the Honolulu study, and the Stamford (USA) study. There are several other studies showing the same thing. 

New evidence

Now there is a further study, this from the Aging Research Centre at the Karolinska Institute – Stockholm University.

Serum total cholesterol and risk of cardiovascular and non-cardiovascular mortality in old age: a population-based study 

Liang et al. BMC Geriatrics (2017) 17:294 DOI 10.1186/s12877-017-0685-z 

The study involves the observation of 3090 adults aged 60 years or above, from a population cohort. The average length of follow-up was 7.2 years, that is 23,196 person-years of observation. During this time 1059 participants died, 34.3%.

Compared with those who were still alive at the end of follow-up, and after controlling for age, those who died during follow-up were:

• older, 
• less likely to have a university education, 
• less likely to be former smokers or current smokers (surprising), 
• more likely to be physically inactive, 
• more likely to have a lower level of total cholesterol, 
• more likely to have diabetes, 
• more likely to have cognitive impairment, 
• more likely to have mobility limitation. 

Whether or not the participants died or did not die did not differ significantly: 

• in the male/female proportion,
• in the prevalence of heavy alcohol drinking, 
• in the prevalence of obesity, 
• in the prevalence of hypertension,
• in use of cholesterol-lowering  medications. 

For the purpose of survival analysis all the participants were divided into three groups based on the blood level of cholesterol at the onset of the study: 

• less than 5.18mmol/L, 
• 5.18 to 6.21, 
• greater than 6.21.

The results are displayed in Figure 1.

Figure 1. All cause mortality based on blood cholesterol level

It is clear in Figure 1 that the highest mortality rate (71.8 per 1000 person-years) is in those with the lowest blood levels of cholesterol, less than 5.18 mmol/L. The lowest mortality rate (35.6 per 1000 person-years) is in those with the highest blood levels of cholesterol, half the death rate than in those with the lowest cholesterol. Why is this not publicised?.

Statin effect

During the past 20 years an increasing number of the population have been commenced on long-term cholesterol-lowering therapy, and especially statins. This has added a complication to cholesterol-related observation studies, but it is good to see that such studies continue, demonstrating an academic scepticism of the often-stated dogma that “The lower cholesterol the better”. My recent Post of evolocumab shows that this simply is not true, but it is as well that other people think the same as I do.

An important point is that a low level of cholesterol in an individual can be a “natural” level, a person-characteristic, or it can be the result of statin or other cholesterol-lowering medication in someone with a naturally higher level.

In the Stockholm study the participants are divided into whether or not they take statins (and other cholesterol-lowering medications), but statin intervention was not part of the study: it was purely observational.

In the results we see mortality displays for all the participants (as in Figure 1), those not taking cholesterol-lowering medications, and those who during the study were taking cholesterol-lowering medications (mainly statins).

We also see analysis of all-cause mortality, cardio-vascular disease (CVD) mortality, and non cardio-vascular disease mortality.

All cause mortality

Figure 2 shows all-cause mortality, the most important outcome measure.

Figure 2. Mortality from all causes related to blood cholesterol level

We can see a similar pattern to Figure 1, but it is a little more complicated.  The blue columns, all participants, are as in Figure 1. But we see in addition the division between those not taking statins (green) and those were taking statins (yellow).

The first group of three columns concerns those with low cholesterol (<5.18). We can see that those not taking statins (green column) have the highest mortality. This is a natural low cholesterol and it is clear that it gives a distinct survival disadvantage – it is a bad thing.

But the yellow column, those taking statins, does not really tell us very much. These participants would have a natural cholesterol significantly higher, but we do not have the information, we do not know the pre-statin cholesterol level. 

We can see in the second group (5.18–6.21) and the third group (>6.21) that having a higher cholesterol is associated with a lower mortality rate, a survival advantage, compared to the first group. The participants in the yellow column of first group (those taking statins) would have a similar natural cholesterol level to the second and third groups.

Cardiovascular mortality

In Figure 3 we can see the same analysis but looking at death from cardio-vascular disease (CVD) – strokes and heart attacks.

Figure 3. Cardiovascular mortality related to blood cholesterol level

The pattern is the same. Those with the lowest blood level of cholesterol have the highest mortality, the opposite of what we have been told. Those taking statins (yellow) in the first group would have a natural cholesterol as in the higher cholesterol groups, and therefore have a similar lower mortality rate. 

Non-cardiovascular mortality

Finally we see in Figure 4 mortality due to to causes other than cardio-vascular disease. Such conditions would be cancers or  pneumonia. 

Figure 4. Non-cardiovascular mortality related to blood cholesterol level

The pattern is the same, but course the number of deaths is lower in the subgroups than in the total numbers shown in Figure 2.

Low cholesterol is not a good thing, but if the low cholesterol is because of taking statins, then the mortality rate is similar to those with higher levels of cholesterol.

Conclusion

This is another good quality study that demonstrates clearly, and contrary to what we are generally told, that a high cholesterol level in the blood is a good indicator for a longer than average life expectancy.

Why are we not told this? The information has been available for many years but it has been suppressed. 

There are so many vested interests in perpetuating the myth that cholesterol is effectively poisonous, killing us in proportion to its level in the blood. This is the basis of many academic careers and the rationale of cholesterol-lowering medications, especially statins. 

The self-appointed and powerful Cholesterol Treatment Trialists’ (CTT) Collaboration controls public and government policy, and falsely perpetuates the identity of cholesterol as the "cause" of heart disease and premature death. 

We can see that this is wrong.

In a person over the age of 60 years, a high blood cholesterol is clearly a good thing. Correspondingly a low blood cholesterol level gives a serious survival disadvantage. However this is only true if the low cholesterol level is "natural". 

If low blood cholesterol is the result of statin or other cholesterol-lowering medication, then there is no survival disadvantage and there is no need for concern.

We can conclude that it is not really the cholesterol level of the blood that determines future health and survival, but what we might regard as "the constitution" of the individual that is responsible that natural cholesterol level.

PURE study - vegetables are good

PURE - Fruit, Vegetables, and Legumes 

We have already looked at the large multinational Prospective Urban Rural Epidemiology (PURE) study. The objective of the study was investigate the dietary advice to which we have been subjected during the past half-century. 

The first paper concentrated on fats and carbohydrate. The conclusion was that dietary fat advice has been wrong: a higher proportion of the fat intake of the diet is associated with a lower rate of total deaths, cardiovascular disease (CVD) events, and CVD death. A higher proportion of  carbohydrate intake is associated with worse health outcomes.

Reducing total food intake might be necessary weight control, but reduction of the proportion on calories from fat, although encouraged officially, is not correct.

The second PURE publication in The Lancet is devoted to the relationship between health outcomes and intakes of fruit, vegetables and legumes. 135,335 individuals from 18 countries were included in this analysis. The countries included 3 high-income (Canada, Sweden, and United Arab Emirates), 11 middle-income (Argentina, Brazil, Chile, China, Colombia, Iran, Malaysia, occupied Palestinian territory, Poland, South Africa, and Turkey) and 4 low-income countries (Bangladesh, India, Pakistan, and Zimbabwe). 

The investigation of fats and carbohydrate in the first paper looked at the relative proportions of each in the diet. Inevitably therefore, if the proportion of fat was reduced (on advice), then the proportion of carbohydrate must increase, and vice versa.

The second paper is different in this respect. It looks at the consumption of fruit, vegetables and legumes in absolute measures, the actual amount consumed. 

Because of the large number of participants in the study from many countries, it was not possible to measure the amounts in mass units (eg grams). The measurement used was simply the number of portions per day, recognising that the size of a protion would vary from one person to another. 

Results

During a median follow­-up of 7·4 years, there were 4784 major cardiovascular disease events. Greater fruit, vegetable, and legume intake was associated with a lower risk of major cardiovascular disease events.

Overall, higher total fruit, vegetable, and legume intake was inversely associated with major cardiovascular disease, myocardial infarction, cardio­-vascular mortality, non-­cardiovascular mortality, and total mortality when adjusted for age.

Figure 1

The overall results can be seen in Figure 1 above, a rainbow graph that can be broken down into its constituent parts.

For example, in Figure 2 we see just total deaths. 

Figure 2

The group with the lowest intake of fruit, vegetables and legumes (<1 portions per day), we see a relatively high death rate from total deaths (all causes) of 8% during the study period, compared to 3% in those who consume more than 3 portions per day.

If we look again at Figure 1, we see the pale blue bars which represent cardiovascular events. We can see that there are 4% cardiovascular events in the consuming up to 5 portions of fruit, vegetables and legumes per day, compared to 3% in those in the groups consuming more than  5 portions per day.

All morbidity and mortality events are higher in this with the lowest consumption of fruit, vegetables and legumes.

It is interesting to look at the geographical variations of consumption of fruit, vegetables and legumes. The total amounts can be seen in Figure 3.

Figure 3 Geographical variation of consumption of fruit, vegetables and legumes

The highest consumption is in the Middle East, and this is due to a particularly high consumption of fruit.

It is also found that people who consumed more fruits, vegetables and legumes had higher education, higher levels of physical activity, lower rates of smoking, and higher energy, red meat and white meat intake, and were more likely to live in urban areas. 

Summary

A greater fruit, vegetable and legume intake is associated with a lower risk of major cardiovascular disease, myocardial infarction, cardiovascular mortality, non­-cardiovascular mortality, and total mortality in the analyses adjusted for age 

In this study,  3·2 servings is equivalent to 400 g of fruit, vegetables and legumes per day. Many dietary guidelines in North America and Europe recommended intake ranging from 400 to 800 g/day, but for most individuals in poorer countries in other continents these targets are unaffordable .

The study indicates that even three servings per day (375 g/day) show benefit against non­-cardiovascular and total mortality, and indicate that optimal health benefits can be achieved with a more modest level of consumption, an approach that is likely to be much more affordable. 

Mechanism

The PURE study is observational and it does not try to investigate the possible ways in which diet might influence human health.  It is a public health investigation, to look for empirical ways in which diet can be recommended to improve health and survival. A high fruit, vegetable, and legume diet can be encouraged without understanding the mechanism of benefit.

Several mechanisms have been proposed to explain the lower risk of cardiovascular disease with higher consumption of fruits, vegetables, and legumes. This would include cereals as a diet high in fibre has been related to lower CHD risk, but there is no conclusion as to mechanism.