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POPULATION INTERVENTION
718
Letters
to
the Editor
POPULATION INTERVENTION
S!R,—The idea advanced by Dr Fries and colleagues (March 4, 481) of compression of morbidity--of adding life to years rather than years to life-is both attractive as an aim for health promotion p
and cogent
response to McCormick and Skrabanek.l The accompanying paper by Dr Gunning-Schepers and her co-workers as a
(p 479) is neither. They assume that intervention involving life-style changes is harmless. Where is the evidence? There is some basis for believing that such intervention is not harmless, as outlined by McCormick and Skrabanek; however, the burden of proof must lie with the proponents of the intervention. To suggest that there is as yet insufficient evidence to stop advice (which may or may not be harmless) is a very strange sort of justification. The example of vaccination is inappropriate since immunisation differs from interventions intended to reduce coronary disease in being a one-off measure and in conferring a population benefit of transmissible disease control to those not vaccinated. Furthermore, individual risks and benefits are assessed, and only in the face of positive evidence of benefit are vaccination programmes justifiable. Gunning-Schepers et al argue that the effects of smoking cessation should not be evaluated merely in terms of cardiovascular disease prevented (an argument which in no way challenges McCormick and Skrabanek). They suggest that we consider the combined effects of intervention on all causes of death: in the MRFIT study2 there were more deaths in the intervention group. MRC Epidemiology Unit (South Wales),
4 Richmond Road,
JAMES GILBERT
Cardiff CF2 3AS
1. McCormick J, Skrabanek P. Coronary heart disease is not preventable by population interventions. Lancet 1988; ii: 839-41. 2. Multiple Risk Factor Intervention Trial Research Group. Coronary heart disease death, non-fatal acute myocardial infarction, and other clinical outcomes in the multiple risk factor intervention trial. Am J Cardiol 1986; 58: 1-13.
Life table 1981-84.
graphs for male residents of three Sheffield wards,
Differences between the health of residents of the wards of Sheffield have been highlighted before,and differences between social groups in both mortality3 and morbidity4 are well known on a national scale. Unlike Japanese people, Mormons, and American doctors, the people of Sheffield share many things in common; the main differences between these wards lie in their lifestyles, their environment, and their occupations. Do Fries et al believe that someone from Sharrow who moved to Ecclesall and adopted the lifestyle, pastimes, and occupation of a typical Ecclesall resident would gain no mortal benefit? Medical Care Research Unit, University of Sheffield, Department of Community Medicine, Sheffield S10 2RX
J. P. NICHOLL
1. Office of
Population Censuses and Surveys Mortality statistics 1983: England and (DH1 no 14). London: HM Stationery Office, 1984. 2. Johnson IS, Coyne AM, Milner PC, et al. Health care and disease—a profile of Sheffield. Sheffield: Sheffield Health Authority, 1987. 3. Whitehead H. The health divide: inequalities in health in the 1980s. London: Health Education Council, 1987. 4. Blaxter M. Evidence on inequality in health from a national survey. Lancet 1987; ii. Wales.
SIR,-Dr Fries and his colleagues add their voices to those of McCormick and Skrabanek in suggesting that there is no evidence that health promotion and any consequent reduction in risk factor prevalence leads to a reduction in age-specific mortality and an increase in life expectancy. They also suggest that there is no reason to expect health promotion to extend life expectancy. Fries and colleagues compare the life expectancies of Japanese, Mormons, and doctors, who have very different risk factor profiles, stating that despite the differences the life expectancies are similar. However, they are wrong to claim that there is no difference in the life expectancy of groups with different life styles. Here in Sheffield the life expectancy at birth of residents of electoral wards which are not much more than a mile apart differ by up to eight years (table). By the age of 65 only 63% of the male residents of Sharrow are still living compared with 83% in Ecclesall (and 75% nationally1), and even for those who survive to 65 there are still differences of three years or more in life expectancy. These differences become manifest after the age of 45 (figure)-that is, at about the time that cardiovascular diseases become the major cause of death in males. LIFE EXPECTANCY IN THREE ELECTORAL WARDS OF SHEFFIELD IN
1981-84 AND IN ENGLAND AND WALES
IN
1981--83
30-33.
SECONDARY PREVENTION OF CORONARY HEART DISEASE
SiR,—Your March 4 editorial asserts that serum total cholesterol "is not a major risk factor in survivors of a myocardial infarction". Recent results from the British Regional Heart Study and a review of other studies, taken as a whole, suggest that serum total cholesterol is associated with the risk of new major ischaemic heart disease (IHD) events in men who had previously had a myocardial infarction.1 Whether serum total cholesterol can be called a major risk factor amongst these men depends on how one measures the importance of a risk factor. In our study 428 of the 7735 men screened had previously had a myocardial infarction. 102 had a further major IHD event in 7-5 years of follow-up. Those with a high serum total cholesterol (top third of the overall distribution) experienced a higher rate of new major IHD events than those in the bottom third-namely, 35-3 per 1000 per year above 6-7 mmol/1 vs 16-9 per 1000 per year below 5-8 mmol/1 (p =0-01). The relative risk was 35-3/16-9 (=2-1). This is smaller than the relative risk in men with no pre-existing IHD (8-8 per 1000 per year above 67 mmol/1 vs 3-1per 1000 per year below 5-8 mmol/1, relative risk=29). By use of relative risk, serum total cholesterol appears to be a somewhat less important risk factor for new IHD events in survivors of a myocardial infarction than it is in
healthy men. However, the difference in risk rate between those with high and low serum total cholesterol levels was much greater amongst men with a previous myocardial infarction (35’3-16’9= 184 per 1000 per year) than amongst men with no evidence of pre-existing IHD
Letters
to
the Editor
POPULATION INTERVENTION
S!R,—The idea advanced by Dr Fries and colleagues (March 4, 481) of compression of morbidity--of adding life to years rather than years to life-is both attractive as an aim for health promotion p
and cogent
response to McCormick and Skrabanek.l The accompanying paper by Dr Gunning-Schepers and her co-workers as a
(p 479) is neither. They assume that intervention involving life-style changes is harmless. Where is the evidence? There is some basis for believing that such intervention is not harmless, as outlined by McCormick and Skrabanek; however, the burden of proof must lie with the proponents of the intervention. To suggest that there is as yet insufficient evidence to stop advice (which may or may not be harmless) is a very strange sort of justification. The example of vaccination is inappropriate since immunisation differs from interventions intended to reduce coronary disease in being a one-off measure and in conferring a population benefit of transmissible disease control to those not vaccinated. Furthermore, individual risks and benefits are assessed, and only in the face of positive evidence of benefit are vaccination programmes justifiable. Gunning-Schepers et al argue that the effects of smoking cessation should not be evaluated merely in terms of cardiovascular disease prevented (an argument which in no way challenges McCormick and Skrabanek). They suggest that we consider the combined effects of intervention on all causes of death: in the MRFIT study2 there were more deaths in the intervention group. MRC Epidemiology Unit (South Wales),
4 Richmond Road,
JAMES GILBERT
Cardiff CF2 3AS
1. McCormick J, Skrabanek P. Coronary heart disease is not preventable by population interventions. Lancet 1988; ii: 839-41. 2. Multiple Risk Factor Intervention Trial Research Group. Coronary heart disease death, non-fatal acute myocardial infarction, and other clinical outcomes in the multiple risk factor intervention trial. Am J Cardiol 1986; 58: 1-13.
Life table 1981-84.
graphs for male residents of three Sheffield wards,
Differences between the health of residents of the wards of Sheffield have been highlighted before,and differences between social groups in both mortality3 and morbidity4 are well known on a national scale. Unlike Japanese people, Mormons, and American doctors, the people of Sheffield share many things in common; the main differences between these wards lie in their lifestyles, their environment, and their occupations. Do Fries et al believe that someone from Sharrow who moved to Ecclesall and adopted the lifestyle, pastimes, and occupation of a typical Ecclesall resident would gain no mortal benefit? Medical Care Research Unit, University of Sheffield, Department of Community Medicine, Sheffield S10 2RX
J. P. NICHOLL
1. Office of
Population Censuses and Surveys Mortality statistics 1983: England and (DH1 no 14). London: HM Stationery Office, 1984. 2. Johnson IS, Coyne AM, Milner PC, et al. Health care and disease—a profile of Sheffield. Sheffield: Sheffield Health Authority, 1987. 3. Whitehead H. The health divide: inequalities in health in the 1980s. London: Health Education Council, 1987. 4. Blaxter M. Evidence on inequality in health from a national survey. Lancet 1987; ii. Wales.
SIR,-Dr Fries and his colleagues add their voices to those of McCormick and Skrabanek in suggesting that there is no evidence that health promotion and any consequent reduction in risk factor prevalence leads to a reduction in age-specific mortality and an increase in life expectancy. They also suggest that there is no reason to expect health promotion to extend life expectancy. Fries and colleagues compare the life expectancies of Japanese, Mormons, and doctors, who have very different risk factor profiles, stating that despite the differences the life expectancies are similar. However, they are wrong to claim that there is no difference in the life expectancy of groups with different life styles. Here in Sheffield the life expectancy at birth of residents of electoral wards which are not much more than a mile apart differ by up to eight years (table). By the age of 65 only 63% of the male residents of Sharrow are still living compared with 83% in Ecclesall (and 75% nationally1), and even for those who survive to 65 there are still differences of three years or more in life expectancy. These differences become manifest after the age of 45 (figure)-that is, at about the time that cardiovascular diseases become the major cause of death in males. LIFE EXPECTANCY IN THREE ELECTORAL WARDS OF SHEFFIELD IN
1981-84 AND IN ENGLAND AND WALES
IN
1981--83
30-33.
SECONDARY PREVENTION OF CORONARY HEART DISEASE
SiR,—Your March 4 editorial asserts that serum total cholesterol "is not a major risk factor in survivors of a myocardial infarction". Recent results from the British Regional Heart Study and a review of other studies, taken as a whole, suggest that serum total cholesterol is associated with the risk of new major ischaemic heart disease (IHD) events in men who had previously had a myocardial infarction.1 Whether serum total cholesterol can be called a major risk factor amongst these men depends on how one measures the importance of a risk factor. In our study 428 of the 7735 men screened had previously had a myocardial infarction. 102 had a further major IHD event in 7-5 years of follow-up. Those with a high serum total cholesterol (top third of the overall distribution) experienced a higher rate of new major IHD events than those in the bottom third-namely, 35-3 per 1000 per year above 6-7 mmol/1 vs 16-9 per 1000 per year below 5-8 mmol/1 (p =0-01). The relative risk was 35-3/16-9 (=2-1). This is smaller than the relative risk in men with no pre-existing IHD (8-8 per 1000 per year above 67 mmol/1 vs 3-1per 1000 per year below 5-8 mmol/1, relative risk=29). By use of relative risk, serum total cholesterol appears to be a somewhat less important risk factor for new IHD events in survivors of a myocardial infarction than it is in
healthy men. However, the difference in risk rate between those with high and low serum total cholesterol levels was much greater amongst men with a previous myocardial infarction (35’3-16’9= 184 per 1000 per year) than amongst men with no evidence of pre-existing IHD