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obviously, combinations of such factors bring proportional
increases in risks. Indeed, it has been estimated that up to ⅓rd of
men aged 30/39 years with high cholesterol and blood pressure
will develop clinical signs of the disease within 10 years. Furthermore,
a Medical Research Council survey covering civil servants
in 12 large towns revealed that those living in soft water areas
registered higher blood pressures, more blood cholesterol and
faster heart rates than those from the hard water regions. Fatty
changes in the coronary artery linings induced by these agencies
tend, eventually, to give rise to the formation of thrombi or
clots which occlude the artery and damage the heart. Mortality
arising from an initial coronary attack varies between 35% and
40% of which total 16% of deaths occur instantaneously and up
to approximately 63% within one hour. A number of cases
from the latter group could probably be saved if an electrical
defibrillator was close at hand for immediate use. It is encouraging
to learn that some 70% of patients who survive an initial attack
are alive after 10 years.
It must be pointed out that every week some 1,000 Londoners
have an attack of coronary thrombosis of whom over 300 die and
one half of these deaths occur within one hour of the attack. It
has been estimated that special care units in hospital could
reduce this mortality by up to 30% but much depends upon the
speed with which the cases reach hospital.
The fact that the first stages in a process giving rise to coronary
thrombosis can begin in childhood and remain symptomless
until adulthood is evidence of the need for early preventive measures
on general lines without awaiting the development of clinical
signs or a full aetiological exposition. In this respect our views
on what constitutes ideal nutritional standards need modification.
In the early years of life the young are deliberately encouraged
to raise their intake of "protective" foods such as butter, cream,
cheese, eggs and meat etc., the very foods which are considered
causal agents in the increase in ischaemic heart conditions. When
does a rich or "protective" diet become harmful?
Given that the genetic aspects of causation are not, at present,
capable of solution, then manipulation of environmental circumstances
remains the sole method open to preventive services
in their efforts to contain this scourge of modern, wealthy
societies. However, it is undeniable that many of the predisposing
factors have their origins in the self-indulgence engendered by
a growing affluence which so often leads to dietary indiscretions,
excessive use of the motor car and addiction to smoking and
alcohol and which demand a "positive" health education