From David Grimes, Royal Infirmary
Blackburn, Lancashire
On 6 April (Forum, p 47) you printed an article entitled “They burn heretics,
don’t they?” This put forward the very powerful idea that science (including
medicine) is based on paradigms and not on evidence. Evidence comes later and
generally speaking will refute a paradigm.
We have within medicine a very powerful paradigm that coronary heart disease
is due to “misbehaviour”—due to the way in which we live our lives, what
we eat and whether we smoke, and so on. But the evidence indicates that dietary
manipulation is of no benefit and therefore diet cannot be causative, despite
the paradigm.
A high cholesterol level is associated with coronary heart disease and it is
assumed that “cholesterol is toxic”. But the benefits in lowering cholesterol by
drugs are very small. The idea that a high blood cholesterol is due to diet is a
paradigm that is hard to shake.
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My colleagues and I have taken a different look at the relationship between
cholesterol and coronary heart disease by trying to answer the question: “Why do
the northwestern parts of the British Isles and northern Finland have the
world’s highest incident rate of coronary heart disease?” We have explored how
climate might be involved, not as the cause but as a factor influencing
susceptibility. We have looked at sunlight and demonstrated that it might well
be involved in the metabolism of cholesterol and protection against coronary
heart disease.
I also noted your recent article “Can you catch a heart attack?” (8 June, p
38). This looks at Chlamydia pneumoniae as a possible cause of coronary
heart disease. About eight years ago, I was unable to find anyone to publish an
article that I had written entitled “Is coronary heart disease due to a
microbe?”. Once again, we are faced with a paradigm and the idea that the
disease was due to a microbe was, at the time, too far-fetched even to be
considered.
Things are now changing and your article demonstrates this. The
article mentions that C. pneumoniae is only likely to be important if
the coronary arteries are damaged by cholesterol. I believe that it is the other
way round and that the prime mover is the cause (the infection), with
cholesterol producing a secondary effect.
A high cholesterol level is only important in people who have coronary heart
disease. The problem is how do we identify the disease until a clinical event
happens?
