This is a contribution from a member of THINCS, 
The International Network of Cholesterol Skeptics

Sept 26, 2002

Emigration  and deadly heart disease risk

1 - Keeping The Social Network Intact Offers Protection

Of all the risk factors for heart disease, there is one that barely gets a mention, yet it is probably the most deadly risk factor of all — emigration.

When the Japanese move from Japan to America, their rate of Heart Disease quadruples, and this is independent of any dietary change.

Asian Indians, moving from the Indian subcontinent to the USA, increase their rate of heart disease by up to fifteen times! Again, this is completely independent of dietary change, or a change in any of the other ‘classical’ risk factors.

A study of Asian Indians in the USA came to the following conclusions:

Asian Indians have the highest rates of coronary artery disease (CAD) of any ethnic group studied, despite the fact that nearly half of this group are life-long vegetarians. CAD occurs early in age and generally follows a malignant course, although the incidence of classic risk factors is low.’ (Enas A Clin Cardiol Mar 1995)

In more detail, the figures from Asian Indians in the USA were as follows:

Risk factor

Asian Indians





Obesity (rate)









Raised LDL




So, here we see three times the rate of heart disease of the surrounding population, with a very, very low rate of classical risk factors. Interestingly, wherever Asian Indians move, they suffer an explosion in the rate of heart disease. And they and the Japanese are not alone; almost all emigrant populations suffer the same fate.

Well almost, but not quite all.

For instance, if we look at the Rosetan community of Pennsylvania, a population of Italian immigrants living in the USA, we can see that they historically had a very low rate of heart disease.

According to a report in Newsweek (March 16,1998, by Geoffrey Cowley and Anne Underwood):

Call it the Pennsylvania paradox. Until about 1965, the people of Roseto, a small town in the eastern part of the state, seemed all but immune to heart diseases. They smoked as much as the folks in nearby Bangor. They ate similar food, and they relied on the same doctors and hospitals. Yet their death rate from heart attacks was significantly lower. Why? Roseto’s most striking distinction was its tightknit social life. Founded in 1882 by immigrants from southern Italy, it was full of three-generation households with strong commitments to church and family. But when those traditions eroded in the 1960s, so did Roseto’s health. By the mid ‘70s, the residents were as mobile and anonymous as other Americans — and just as prone to heart disease. The "Roseto effect" had vanished.


So, maybe emigration doesn’t cause heart disease after all? Well, it depends on what you mean by emigrating.

From the perspective of heart disease, it doesn’t mean geographical dislocation; it means social or community dislocation. By this, I mean, disrupting the social ties. A Christian, Caucasian, American can move over three thousand miles — from Boston to Atlanta. But culturally, they haven’t really moved much at all.

On the other hand, a peasant farmer from Pakistan can move to London, and the culture shock is almost incalculable: a different language, a different religion, a completely different culture altogether.

However, the Rosetans, by establishing a ‘little corner of Italy’ within the USA, moved four thousand miles, but kept the social network intact, and by keeping the social network intact, they protected themselves against heart disease.


2 - How Emigration Causes Heart Disease

In the previous section, I pointed out the impact of emigration, or ‘social dislocation’ on heart disease. This can range from a potential fifteen-fold increase in risk (with emigrant Asian Indians) to zero risk (with the Italian Rosetan community in Pennsylvania).

The reason for this discrepancy and the better health of the Rosetans, is almost certainly that they maintained their culture and social structures, even though they moved over four thousand miles to live in a new country. For what is certain is that, when the Rosetan community started to ‘break-up’ and assimilate into American culture, their protection against heart disease disappeared.

‘We found a sharp increase in myocardial infarction among Rosetans when long established cohesive social patterns began to weaken and be replaced by more egocentric attitudes.’ (Wolf S Acta Physio Scand Suppl 1997)

The idea that retaining lifestyle, or social networks, may protect against heart disease is further supported by some elegant work by Marmot during the 1970s on Japanese who moved from Japan to the USA. Why his work is not more widely known is, quite frankly, amazing. To me, his are the most fascinating studies ever done on heart disease, and when you start thinking about what they mean, they illuminate a whole new area of thought.

Anyway, what Marmot found was that, unsurprisingly, when Japanese move to the USA, their rate of heart disease increased by a factor of about four. The first variable risk ‘factors’ that Marmot looked at to explain this difference were the usual suspects: diet, cholesterol levels, hypertension, smoking, etc. However, he couldn’t find any significant correlation with any of the ‘classical risk factors’.

This may not be terribly surprising because as he later found out, during the 1980s, as the diet of the Japanese changed to a more "Western" diet, their cholesterol levels did rise, slightly, but the rate of heart disease actually went down!

‘Considerable increases in total serum cholesterol levels do not offer an explanation of the recent decline in mortality from coronary heart disease in Japan.’ (Okayama A, Marmot MG Int J Epidemiol Dec 1993)

So much for an elevated cholesterol level being a risk factor for Coronary Heart Disease (CHD).

Marmot then looked at other possible reasons for the increase in heart disease in emigrant Japanese, and found something very unexpected. Not all Japanese emigrants suffered from a high rate of CHD. Some were protected. And what exactly protected them? Exactly the same thing that protected the Rosetan community.

‘Japanese culture is characterised by a high degree of social support. There is evidence that this may contribute to the low rate of heart disease in Japan, and among Japanese-Americans who retain their traditional culture. (Marmot MG J Psychosom Res 1983)

In short, the Japanese who retained their lifestyle were not at increased risk of heart disease, and this protection was completely independent of any other risk factor. According to Marmot:

To test the hypothesis that social and cultural differences may account for the CHD differences between Japan and the United States, 3809 Japanese-Americans in California were classified according to the degree to which they retained a traditional Japanese culture. The most traditional group of Japanese-Americans had a CHD prevalence as low as that observed in Japan. The group that was most acculturated to Western culture had a three- to five-fold excess in CHD prevalence. This difference in CHD rate between most and least acculturated groups could not be accounted for by differences in the major coronary risk factors. (Marmot MG Am J Epidemiol Sep 1976)

And it wasn’t just Marmot who found this to be true. Other researchers shortly thereafter confirmed his finding:

Statistically significant inverse relationships were found between CHD incidence and all of these variables that reflect the degree of exposure to Japanese culture during childhood. In multivariate analyses where the major CHD risk factors were taken into account, years spent in Japan and ability to read and write Japanese remained significant. Hence, exposure to Japanese culture during childhood appears to protect against CHD in adulthood. This may explain, in part, the gradient of CHD frequency among Japanese in Japan, Japanese-Americans, and Caucasians that could not be entirely attributed to the established risk factors.’ (Yano K Am J Epidemiol Apr 1979)

What we are seeing here is a very consistent correlation between retention of social structures and protection against heart disease.

But why?

At this point, it is time to reveal the hypothesis that explains how a breakdown of social structures, support, and culture leads to heart disease, and it goes like this:

1.      Breakdown of social structures leads to chronic stress

2.      Chronic stress leads to a disruption of the Hypothalamic-Pituitary-Adrenal axis (HPA-axis)

3.      Disruption of the HPA-axis leads to an increase in circulating stress hormones

4.      Increased stress hormones cause insulin resistance

5.      Insulin resistance causes "Syndrome X" or metabolic syndrome (and type II diabetes)

6.      Syndrome X causes CHD

In the next segment I will reveal the enormous pile of research that fully supports this hypothesis.


3 - Social Dislocation - How It Causes Heart Disease

"Twenty-five hundred years ago, Hippocrates, recognizing the impact of life experience on health wrote: "Those things which one has been accustomed to for a long time, although worse than things to which one is not accustomed, usually give less disturbance" (Bruhn & Wolf 1978). Since Hippocrates, much evidence has emerged to suggest that social stability is conducive to health, while social change, especially rapid change, may predispose to illness. The idea that sensory information from ordinary life experiences contributes in a major way to shaping the activities of the brain, took root in the 18th century with Pierre Gassendi and John Locke." Wolf S Acta Physio Scand Suppl 1997


This passage goes on into impenetrable medical jargon. However, I shall paraphrase:

If you are exposed to social change, or social dislocation, this has measurable effects on the structure of the brain, and on the function of the brain. And a critical part of the brain involved (the part deals with stress) is the Hypothalamic Pituitary Adrenal - axis. (HPA-axis).

The HPA-axis is a very complex beast, and I don’t think anyone fully understands how it works. I certainly claim no vast expertise. However, at a very basic level, the HPA-axis operates, as follows:

A large, venomous, spider drops onto your hand. Your eyes fire a message to your hypothalamus, which recognises that this situation means danger. The hypothalamus sends a message to your pituitary gland which then starts to produce all sorts of stress, or ‘fight and flight’ hormones. These then travel through the bloodstream to the adrenal glands, which start to generate adrenaline and cortisol - amongst other stress hormones.

At the same time, your hypothalamus sends messages to your autonomic (subconscious) nervous system, this system then lights up and sends messages throughout your body to get ready for action. Blood supply diverts from your stomach to your muscles, digestion ceases (you may suddenly be sick as the system tries to void foodstuff). You may do even more unsavoury voiding things as well. Your heart rate speeds up, your pupils dilate. You’ve seen the movies; you know the kind of thing.

In about one second, you are ready for action. Alert, all senses operating at max. And something else just happened to you at the same time. Not that you would notice, or care. You just became almost totally resistant to the effects of insulin.

What the body needs when faced with emergency situations, is emergency energy supplies, mainly sugar in the blood. So the last thing you need is insulin trying to lower the blood sugar level. Therefore, in stress situations, the body over-rides the actions of insulin.

When dealing with deadly spider attack, this doesn’t matter one jot. However, if the stress is chronic, and the levels of stress hormones are chronically raised, then the insulin resistance also becomes chronic. Although work in this area receives almost zero publicity, the connection between chronically raised stress hormones and insulin resistance has actually been studied, many, many times, and the results published in peer-reviewed medical journals. Here are just two such studies:

"Psychosocial stress may affect the pituitary-adrenocortical system (HPA-axis) in complex ways, contributing thereby to insulin resistance, (and) hyperinsulinemia.’"Keltikangas-Jarvinen L Metabolism Dec 1998

"The statistical associations between stress and cardiovascular and other prevalent diseases have not been explained. Perceived stress, resulting in an uncontrollable defeat reaction, has been shown by James Henry to be followed by specific endocrine abnormalities, including sensitization of the hypothalamo-pituitary-adrenal (HPA) axis, and inhibited sex steroid and growth hormone secretions." Bjorntorp P Acta Physiol Scand Suppl 1997

From these studies, and others, it is clear that chronic stress, the type of stress caused by social dislocation, leads (in many people), to a dysfunctional HPA-axis. And this impacts on a whole series of pituitary hormones - leading to insulin resistance - as the stress hormones, particularly cortisol, are direct insulin antagonists.

Perhaps the most stark example of the connections between social dislocation, chronic stress, abnormalities of the HPA-axis/cortisol secretion and CHD comes, not from emigrants, but from a study done in Sweden and Lithuania.

A further little publicised fact about heart disease (CHD), is that, since the collapse of communism in Eastern Europe, the rate of CHD has exploded. Eastern European countries now have the highest rate of heart disease in the world. That is, all of them. At present Lithuania has the unwelcome distinction of world leader in Heart Disease. Why?

Those things which one has been accustomed to for a long time, although worse than things to which one is not accustomed, usually give less disturbance.

Let’s assume that, since the collapse of communism, there has been massive social change in Eastern Europe. The old social structures blown apart to be replaced, in many cases, by virtual anarchy. So, if we study the Lithuanians, we should find a number of things:

1.      Raised levels of stress

2.      Disturbance of the HPA-axis

3.      Raised levels of stress hormones (specifically cortisol)

A study looking at this was done comparing Sweden and Lithuania. The first thing they found was that rate of CHD was four times higher in Lithuania than Sweden, despite the fact that:

"Small differences were found for traditional risk factors for CHD; systolic blood pressure was higher in Vilnius men, smoking was similar and plasma LDL cholesterol levels higher in Linköping men." (Vilnius is in Lithuania, Linkoping in Sweden)

Thus, no difference in ‘traditional risk factors. But what they did find was extremely interesting:

"Compared to compared to Linköping men, Vilnius men had unfavorable psychosocial coronary risk factors. They reported more job strain, more social isolation, less effective coping strategies, lower self-esteem, more depression and vital exhaustion. This pattern could indicate a state of chronic stress. In a standardized laboratory stress test, no differences were found between the groups in cardiovascular reactivity. In contrast, there was a large difference in cortisol reactivity: Vilnius men showed an attenuated response to stress and also, in the groups tested at eight o'clock in the morning, higher baseline cortisol. In multivariate analyses, high baseline cortisol and high vital exhaustion both related to low cortisol response. Vilnius men also had an attenuated prolactine response to stress. This attenuated stress response has earlier been shown in states of chronic stress."

So there you have it. Absolutely clear cut evidence to support part one of the hypothesis. Social dislocation leads to chronic stress. Chronic stress upsets the HPA-axis, leading to abnormal cortisol secretion. And cortisol is a direct antagonist to insulin.

In this way, chronic stress leads to insulin resistance. And insulin resistance causes syndrome X. Therefore, what we should see, in most emigrant populations, is a very high level of syndrome X. Is this what we find?



4 - Social Dislocation, Stress And Heart Disease

So far, in the argument that social dislocation/emigration causes heart disease, I have shown that social dislocation creates a great deal of long-term, chronic stress. This is turn disrupts the hypothalamic pituitary adrenal axis (HPA-axis), creating a high circulating level of cortisol. The high circulating level of cortisol, in turn, leads to insulin resistance. Chronic insulin resistance then leads to Syndrome X, the metabolic syndrome.

This pathway from stress to syndrome X is summarized in work done by Bjorntorp and his team in Sweden.

‘The conspicuous similarities between Cushing's syndrome (excess cortisol secretion) and the Metabolic Syndrome X open up the possibility that hypercortisolemia is involved also in the latter. Salivary cortisol is possible to measure during undisturbed conditions including perceived stressful events during everyday life. Such measurements clearly show that normally regulated cortisol secretion is associated with excellent health in anthropometric, metabolic, and hemodynamic variables. Upon perceived stress cortisol secretion is increased and followed by the Metabolic Syndrome X.’ Bjorntorp P Ann NY Acad Sci Nov 1999

Which means that when we study populations that have suffered social dislocation/emigration - at least the ones that suffer a high rate of CHD - we should see a very high rate of syndrome X. Unfortunately, there is a problem with doing this, which is, as follows. When syndrome X becomes severe, the blood sugar level rises very high. High enough, in fact, that syndrome X becomes ‘diagnosed’ as type II diabetes.

For in the strange world of type II diabetes, it doesn’t matter what the underlying cause may be, when your blood sugar reaches a fasting level of 8.1mmol/l (European figures), you have type II diabetes. And all of the other causes of a raised blood sugar (See list) become lost.


Cushing’s disease
Long term steroid use
HIV lipodystrophy
Acute stress (trauma, pain etc.)
Spinal cord injury
Type I diabetes
Type II diabetes?

This begs the question what is type II diabetes? A raised blood sugar level. And what causes a raised blood sugar level? Why, type II diabetes, of course.

Yes, I know this is actually a little loop of semantic madness. Logically, something has to cause the blood sugar level to rise, and that’s the disease, not the high blood sugar level.

My apologies for taking you on this little detour. But I think it is important to explain why it is impossible to provide figures showing that emigrant populations have a high rate of Syndrome X. They are all, usually, misdiagnosed as having type II diabetes instead. Ah, the joys of epidemiology.

Anyway, assuming that a high rate of type II diabetes in a population really means a high rate of Syndrome X, what are the figures? If we look at the Japanese, first, we can see that in Japan, they have a rate of Syndrome X of 1.6% (luckily someone measured this in Japan).

The prevalence of Syndrome X as characterized by an association of glucose intolerance, hypertension and hypertriglyceridaemia was 1.6% (n = 39) in all subjects examined. Imamura M Clin Exp Pharmacol Physiol Suppl 1995

However, in second generation Japanese emigrants, this rate increases to 16.2%. Which is a nice round one thousand per cent rise.

The prevalence of diabetes in Japanese Brazilians (12.8 and 16.2% for first and second generations) are higher than the rates reported for Japan at comparable age groups. Franco LJ Diabetes Res Clin Pract Oct 1996

And what of Asian Indians? In the UK, immigrant Asian Indians are no more obese than the surrounding population, yet, as a study in Lancet by McKeigue demonstrated:

‘In comparison with the European group, the South Asian group had a higher prevalence of diabetes (19% vs 4%), higher blood pressures, higher fasting and post-glucose serum insulin concentrations, higher plasma triglyceride, and lower HDL cholesterol concentrations.’ Lancet 1991 Apr 20

In some studies on Asian emigrants, the level type II diabetes has been found at more than 60%. And other studies in the UK have found rates approaching 30% (Bhopal R et al BMJ Jul 24 1999).

So, before getting too tangled up. What does this mean? What it means is that we can see a clear pathway emerge between emigration/social disruption and Syndrome X through a series of well established physiological mechanisms.


5 - What Is Heart Disease Anyway?

For those who have followed the argument in the last few issues, I hope that it is clear that emigration, or social dislocation, can cause heart disease. Actually, I think I’ve made it clear how emigration can cause syndrome X (a cluster of metabolic disorders that represent a major risk of coronary heart disease or CHD). But how does syndrome X cause heart disease?

To answer this, it is best to turn the discussion around through one hundred and eighty degrees, and look at the actual disease process in heart disease. Only when you know this can you understand how syndrome X leads to heart disease.

But before going down this route, clear your mind of everything that you have heard about heart disease and what may cause it. Enter the state of complete open-mindedness. What you are about to hear now, you have (probably) never heard before, and you may find some of it more than slightly surprising.

For today, at the cutting edge of research into heart disease, or atherosclerosis, all sorts of things are starting to emerge that are turning everything that everyone previously thought upside down.

What is heart disease? Heart disease is narrowing of the arteries. Narrowing of the arteries can happen anywhere in the body, but is most common, and severe, in the arteries in the heart. The narrowings in the arteries are called plaques, or atherosclerotic plaques. When these become large they block blood flow and give rise to coronary artery disease, or CHD.

How does a plaque start? Good question. You probably think that a plaque starts when cholesterol leaks through the artery wall, because that is the message that everyone has been bombarded with for the last fifty years. But the lining of the artery wall, the endothelium, when it is healthy, cannot be penetrated by cholesterol.

I will let that statement sink in for a moment.

You may think that this cannot be true. But it is.

So, how does cholesterol get into the plaque, if it can’t get past the endothelium? At the risk of introducing too many concepts too quickly, the first thing to bear in mind here is that cholesterol is not floating around free in the blood, because it is insoluble in water. Instead, it sits within a small spherical container known as lipoprotein. Lipoproteins are manufactured by the gut, or liver.

Lipoproteins come in a variety of different sizes, ranging from the huge chylomicron to the relatively tiny high density lipoprotein. Whatever their size, the main role of lipoproteins is to transport fats, and cholesterol, through the system, as no fat is soluble in water.

Forgetting about the other lipoproteins for a moment, the lipoprotein of greatest interest, in CHD, is the Low Density Lipoprotein (LDL). It contains about half fat and half cholesterol. (Cholesterol is not a fat). LDL is though to be the lipoprotein that causes CHD.

Therefore, if we are going to be accurate, the artery wall is not actually impenetrable to cholesterol, it is impenetrable to LDL. And the reasons why it is impenetrable to LDL is that there are no receptors for LDL on an artery wall, and without a receptor no molecule can penetrate a (healthy) cell wall. (And you can’t squeeze between the cracks either).

A little bit of a conundrum? Cholesterol is a major component of many atherosclerotic plaques, yet it cannot penetrate the healthy endothelium. Despite this, most CHD researchers are still trying to propound increasingly complex mechanisms of action whereby cholesterol can get through the undamaged arterial wall. Why? Because the orthodoxy is that cholesterol is the cause of CHD. It is the villain, and so some mechanism must be discovered to explain how cholesterol actually starts the plaque in the first place.

However, it is actually very simple to see how cholesterol gets into plaques, if you discard the idea that a LDL, raised or not, is the cause of CHD. All you need to do is to look at plaque formation from a different viewpoint. And when you do this, it is simple to see that the presence of cholesterol in a plaque is a result of the disease process, not the cause.

The story goes like this.

To start a plaque, you must first damage the endothelium (single cell layer, lining the artery). There are many different possible ways to damage the endothelium. And here are a select few ‘factors’:

1.      Smoking

2.      Turbulant blood flow (high blood pressure)

3.      High blood sugar level

4.      High cortisol level

5.      High insulin level

6.        High triglyceride level

All of these factors can stress, or ‘damage’ the endothelium. When you damage the endothelium a very strong message is sent out that the damage must be covered over, or plugged. And the way that the body does this is to form a small blood clot over the area of damage. Thus endothelial ‘injury’ stimulates the formation of a blood clot or thrombus over the damaged area.

One of the key components of a thrombus is a substance called lipoprotein (a). And what is Lipoprotein (a)? Confusingly, lipoprotein (a) is actually a low density lipoprotein (LDL) molecule, with a protein stuck to it called apolipoprotein (a). On the other hand, LDL is a low density lipoprotein with apolipoprotein B-100 stuck to it. (Listen, I never made up this mad form of nomenclature).

Lipoprotein (a) is used by mammals, that cannot manufacture vitamin C, to protect against vitamin C deficiency. For, one of the first things that happens when the level of vitamin C drops, is a breakdown of the artery wall, allowing blood to leak through. (An important sign of scurvy is bleeding gums). And the primary function of Lipoprotein (a) is to stick to areas of damaged artery and ‘plug’ them shut.

Thus damaged artery walls attract lipoprotein (a), amongst other clotting factors, and this form of LDL then sticks onto the area of damage. Because of the special structure of the apolipoprotein molecule, clots formed in this way are very tough, and cannot be destroyed by the normal clot-busting enzymes. So they cling to the artery wall very tightly.

Over time, the endothelium grows back over the blood clot - a bit like wound healing - effectively drawing the clot into the arterial wall. And, as the clot is drawn in, so is apolipoprotein (a), and apolipoprotein (a) (as it is a form of LDL) is full of cholesterol. And this is how cholesterol gets past the endothelial barrier into a plaque.

Of course, an inevitable consequence of this new concept of atherosclerosis formation is to utterly destroy the hypothesis that cholesterol causes CHD. As you can see, cholesterol is, in reality, an innocent passenger in a lipoprotein, not the cause of CHD. Which is why you will have probably heard very little about this area of research. However, this new way of looking at plaque development does make sense, and fits all of the known facts about CHD.

Esssentially, it has become increasingly clear that atherosclerotic plaques grow through a process of repeated endothelial damage and repeated thrombotic episodes over the same ‘damaged’ area. Which is why the term atherothrombosis is increasing in popularity. By the way, this concept was first proposed by Karl von Rokitansky in 1852.

So, now that you can understand how atherosclerotic plaques are formed. It is possible to link back to syndrome X, to see how the metabolic abnormalities of syndrome X lead, inevitably to CHD. At which point you will have enough information to understand everything you need to know about heart disease.


6 - Linking It All Together

For those who have come this far, it is time to link everything together. I have demonstrated that emigration/social dislocation leads to a damaged hypothalamic pituitary adrenal axis (HPA-axis). This, is turn, causes increased cortisol secretion, leading to insulin resistance/syndrome X and then CHD.

I then outlined the mechanisms that cause atherosclerotic plaques (the underlying pathology in CHD) to develop. Essentially, in order to start a plaque, you need to damage the endothelium, and then a clot forms over the area of damage. The clot is drawn into the artery wall, forming the start of a plaque. Over time, repeated episodes cause the plaque to grow, until, in the end, plaque rupture, followed by a major clot, can block a coronary artery completely, causing an MI (heart attack) and death.

Therefore, factors that damage the endothelium, and factors that make the blood more likely to clot, will to lead to CHD. In syndrome X you have a number of these factors in place: high blood sugar, high blood pressure, high insulin, high cortisol, high clotting factors, etc.

And so, knowing all of this, we can see a very clear pathway linking emigration/social dislocation to premature death from CHD. See diagram:


At this point, you can play a little game; one that I play every day, and have done so for the last ten years. Think of a risk factor for CHD and see where, and how, it fits into that diagram.

Take smoking, for example. How does this fit?

Smoking impacts in a number of ways. It alters the HPA-axis, and increases cortisol secretion. It also, independently, damages the endothelium and raises blood clotting factors. So it is easy to see how, and where, smoking fits into this scheme.

What about depression?

Again this is simple. Depression leads to HPA-axis abnormalities, increased cortisol secretion, and syndrome X.

What about AIDS?

Unknown to most of you, I suspect, is the fact that many AIDS patients suffer from a condition usually referred to as HIV-lipodystrophy. This is, actually, another name for syndrome X. So, how does AIDS cause syndrome X?

Well, it took me a while to find this out. But when AIDS patients take protease inhibitors - the main form of medication used against HIV, this causes a reduction in DHEA (a cortisol antagonist), and a rebound increase in cortisol secretion, leading to syndrome X. It turned out to be remarkably straightforward.

What about a raised LDL/cholesterol level? Well, this doesn’t fit at all. Which suggests that a raised cholesterol level cannot be a cause of CHD, and it isn’t.

But there are two questions that the diagram I have presented do not answer. They are complex questions, but unless they can be answered, then for all the clever argumentation I have put forward, I haven’t actually presented the cause of CHD. I spent five years working out the answer to these questions. So, either I am thick, or they were quite tough.

Question one:

Obesity leads to insulin resistance and then type II diabetes. Yet how do the Pima Indians, a population with the highest rate of type II diabetes in the world and also, therefore, the highest rate of insulin resistance, have a low rate of CHD? Answer that.

Question two:

The French have identical risk factors to the British, and I mean identical. Their rate of insulin resistance/type II diabetes is also identical. There is no evidence for a lower prevalence of stress/social dislocation in France; in fact their use of anxiolytics (anxiety medication) is much higher than in the UK. Yet the French rate of CHD is almost exactly one quarter that of the British. How so?

When you can answer these two questions, you’ve got it.  


More essays by Malcolm Kendrick