I have been thinking about writing this article for many years. You may ask, why haven’t you? Because it flies in the face of the current NHS medical model of heart disease and its causes and how much did I want to stick my head above the parapet?!
Why am I fascinated by heart disease?
As an osteopath, it’s not really my remit, or is it? As osteopaths’, health is our remit and although in this century we are pigeon holed into musculoskeletal work, helping patients’ whole health is really where we sit.
I became interested in heart disease because of the French paradox – how do they smoke like chimneys, drink like fish, eat foie gras, think vegetarians should be shot and slather everything in cream and butter and still have a fifth of the heart disease rate that we do in the UK?
Heart disease – atherosclerosis (blocking of the large arteries by plaques) is mostly what we are talking about here, as there are many facets to “heart disease”. The standard thinking since the 1950’s is the diet heart hypothesis or the cholesterol hypothesis. In basic terms, eating saturated fat raises your cholesterol levels and the excess cholesterol was deposited in your arteries in the form of plaques which would eventually block them causing a heart attack, stroke or similar depending on which artery was blocked.
If this isn’t the cause of heart disease – what is, I hear you ask? And why has it been the prevailing opinion for so many years.
After the second world war men in the US were dying at an alarming rate from heart attacks (I say men, 10:1 men: women), something needed to be done and a now famous researcher, Ancel Keys with his ready prepared heart disease hypothesis stepped into the breach. 30 years later despite the lack of supporting evidence in the form of gold standard trials the diets of some 220 million US and 56 million UK citizens by 1983 had been altered to reduce the level of saturated fat.
I have talked about cholesterol but in fact we really need to be talking about lipoproteins as that is how cholesterol is carried in the blood – the current lipoprotein blamed for cardiovascular disease is low density lipoprotein or bad cholesterol. Today cholesterol and lipoproteins have been heavily studied and it is now beyond doubt that saturated fat consumption CANNOT raise cholesterol or low density lipoprotein levels.
But surely even if that is the case – there must be no doubt that high bad cholesterol causes the blocking of the arteries – after all plaques are full of cholesterol, statins lower cholesterol and reduce heart disease and so does polyunsaturated fats in the diet?
Is that really what happens?
There have been excellent, gold standard, large studies that dispute the final conclusion – so in the case of polyunsaturated fats and statins – they do decrease cholesterol levels but critically they do not reduce the overall risk of death. In fact, in women there was a 40% risk reduction in mortality in those with the highest levels of cholesterol (for those who like the numbers, up to 7 mmol/l) This work is not new – it was done in the 70’s but not published until much more recently (2016).
Cholesterol plays a massive role in human health – our livers manufacture about 5 grams a day, every day. Cholesterol stabilises cell membranes throughout the body allowing cells to carry out their functions. It’s critical for the health and support of neurons, as well as making new synapses in the brain. It acts as a backbone for essential hormones and vitamin D etc.
So, if lowering cholesterol (Low density lipoprotein) does not increase life expectancy then what could be causing heart disease and what can we do to reduce our risk?
This is much trickier to pin down and this isn’t surprising as if we haven’t done so yet, it must be complicated and it may well be that there is no single, simple cause but a bunch of risk factors leading to a multifactorial cause. That isn’t good enough – how do those risk factors come together to make atherosclerotic plaques in the large arteries?
The way to look at this may be to consider a process rather than a single cause and that same process happens in response to the vast number of risk factors.
That process is the thrombogenic hypothesis (blood clot hypothesis) – the theory is that there is damage to the lining of the artery wall in some way. This damage is covered by a clot, a bit like a scab if you cut your skin. In most cases a new layer of arterial wall grows over the clot and the clot is resorbed. However, if there is increased rate or bigger damage or poor repair processes, then repeated clotting at the same place will lead to a plaque getting bigger and eventually narrowing or blocking of the artery or parts break off (thrombus) and can block other arteries elsewhere. Most of this process is not disputed; it is only the start of the process, damage to the artery wall and clot formation that is considered controversial.
I realise that this article is a whistle stop tour and probably poses more questions than it answers but if you are at risk, or know someone who is then before you consider a treatment perhaps look at the process involved and look at reducing your risk. Information is out there and although I have read many books and papers over the years an easy place to start if you are new to this is reading the works of Dr Malcolm Kendrick, his latest book, The Clot Thickens is written for the lay public and explains the theory with appropriate referencing very well.
