19 August 2017
Having spent many years smashing everything into pieces in an attempt to work out what is going on with cardiovascular disease, I am now going to attempt the amazing feat of bringing everything together in some sort of coherent structure. I have no idea how long this may take, so please bear with me while I first set the scene by making a couple of point that need to be made.
‘Explanations exist; they have existed for all time; there is always a well-known solution to every human problem — neat, plausible, and wrong.’ H.L. Mencken.
Cardiovascular disease is best seen as a process. Attempts to find the key, single, cause has created the massive multifactorial monster we see before us today. Unfortunately, the trap of searching for a/the cause seems to be hard wired into our thinking. This approach has worked well for things such as infectious diseases and suchlike, but it does not work here. I have lost track of the number of times someone has come up with the new cause of CVD, then tried to crowbar all observations to fit. Or simply dismiss contradictory evidence.
- It’s caused by infections
- It’s all due to vitamin C deficiency
- It’s all due to blood sugar
- Its’ all due to inflammation etc. etc. etc. etc. etc.
In truth, I was as guilty of this as everyone else. I believed that ‘stress’ was the cause, and everything could be incorporated within this factor. This is not true. Stress/strain represents one factor that is capable of causing CVD – quite an important one – but it cannot explain everything.
Whilst there obviously are ‘causes’ of cardiovascular disease, they cannot be understood in isolation from process(es). What is going on, and why, and how can things that seem to cause cardiovascular disease be fitted into these processes.
It may seem intellectually unsatisfactory to move away from a simple, single, cause model. We all want the E=MC2 moment, or the untangling of the structure of DNA moment. Eureka! That was never going to happen here, or it would already have happened. If there truly were a single cause it would have been found by now – and it hasn’t.
The evidence base is flawed. In part because studying complex biological systems is, in itself, very difficult to do. The number of variables involved is mind-boggling, and the number possible interactions between those variables is mind boggling to the power one trillion. If you are looking for absolute certainty…. look elsewhere.
Just to give one example of how many potential factors there are. Here is part of a paper by researchers, who looked at geomagnetic disturbance and its impact on heart attacks and strokes (Russian paper):
‘It was shown statistically that during geomagnetic disturbances the frequency of myocardial infarction and brain stroke cases increased on the average by a factor of two in comparison with quiet geomagnetic conditions. These results are close to results obtained by (Stoupel, 1999), for patients suffering with acute cardiological pathology. Our recent study (with L.Parfeonova) revealed the relation between heart ventricular ectopic activity (VEA) and geomagnetic conditions in patients with CHD. On the average 1995 episodes of VEA having on one patient within 24 hours have been revealed in patients, whose records coincided with the periods of geomagnetic storms and 1440 VEA episodes for active conditions. Minimal quantity of VEA episodes was found for unsettled condition: 394. In a quiet geomagnetic condition VEA episodes appeared more often than in periods of unsettled conditions.’1
How many researchers have taken geomagnetic disturbances into account as a potential confounding factor in their research? I would suggest, none. Yet here is a factor that can (possibly) increase the risk of CVD events by 100%.
I chose this example, almost at random, to highlight the point that this stuff is complicated, and there any many, many, uncertainties involved. Can you control any study for all factors ever found to be associated (causally or otherwise) with CVD? No, you cannot.
Alternatively, you can do what many people do. Dismiss research that seems contradictory, or just daft. I can see many people automatically seeking to dismiss a Russian study about the effect of geomagnetic disturbance on CVD on the dual grounds that is a: Russian and b: bonkers. That would be unwise.
Of course, there is the other problem that much of medical research (especially in the highly lucrative area of CVD) has been funded by the pharmaceutical industry, resulting in the problem that most research findings are false:
‘There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias.’2
This is a famous paper, one of the most cited and read in medical research history. It was written in 2005 and things have got worse, not better, since then.
Oh, but of course, peer review keeps everything on the straight and narrow:
‘The mistake, of course, it to have thought that peer review was more than a crude means of discovering the acceptability – not the validity – of a new finding. Editors and scientists alike insist on the pivotal importance of peer review. We portray peer review to the public as a quasi-sacred process that helps to make science our most objective truth teller. But we know that the system of peer review is biased, unjust, unaccountable, incomplete, easily fixed, often insulting, usually ignorant, occasionally foolish, and frequently wrong.’ Richard Horton, editor of the Lancet.
In this morass, where does one turn?
This is a question that has no definitive answer. Shall I just choose evidence that suits my argument, and dismiss all else? To an extent, the difficulty in disentangling evidence was my spur to write the book Doctoring Data. In it, I attempted to determine what is valid and what is not. How to spot the biases and errors. How to know what it true, from the other stuff?
Answer… it cannot be done. Not for certain. Whatever evidence I choose, it can be criticised – in one way or another. Did the study I am quoting control for geomagnetic disturbance or not? As a general rule, any study – and I mean any study – can be pulled apart and dismissed, if you so wish. Which could leave most of what I do as a smoking ruin.
However, most of the research I look at has one major advantage. There is not much, if any, financial interest, behind it. Other than suppressing it, I suppose.
Yes, of course, I bring certain biases to the discussion. I am almost entirely anti-statin. I am not a great believer in blood pressure lowering – at least not at current levels. I do not believe in the cholesterol hypothesis and I think that the anti-saturated fat dogma is completely bonkers and has no evidence to support it – at all. I believe that salt is good for and, in most people, protects against CVD.
I believe that a high carbohydrate low fat diet is utterly bonkers – especially in those with diabetes. And suchlike. In short, I believe that almost everything we are told is good for you, is bad for you, and vice-versa. With the exception of smoking (bad) and exercise (good).
Having got that out of my system. Let us begin….. in the next blog.