CHAPTER 3
"... so just how poisonous is cyanide?" asked the philosopher. "We shall see", I cried, and called on my chemical friend for a gram of potassium cyanide. He withdrew a phial of the powder from a vest pocket and I mixed it with a freshly drawn pint of ale. I hailed a passing acquaintance and proffered it to him. He felled it and dropped dead at our feet in less than a minute. "See", I exclaimed, "his chance of surviving a dose of 1 gram of potassium cyanide was only 1 in 100,000. He has agreed with the laws of statistics".
My philosophical companion was appalled, "Is nothing safe?" "Of course", I replied. "Chemist, have you any elderberry wine?" He had. The elderberry, unlike most vegetable matter, is a relatively safe ingestant. Its quota of toxic alkaloids is slight. I invited a friend to drink to our health. He dropped dead at our feet in less than a minute. "A pity", I said, "his chance of dying from that was only 1 in 100,000".
Hardly a day passes when the public are not given more advice on how to maintain and improve their health and live for a long time. People should eat more fibre but less salt, fat, alcohol and nearly everything else. They should exercise more -- but not if the sun is shining on them. Smokers must stop consuming tobacco even if giving up causes stress -- which should also be avoided. Et cetera. The avalanche of advice is unending: but what does it mean overall? In principle it should be easy to find out: examine the mountain of evidence that accompanies the avalanche of advice. As might be expected, the practice is more difficult. This chapter is a critical examination of the evidence.
There are basically two kinds of evidence, circumstantial, and controlled trials. Circumstantial evidence can often be quite convincing by itself: The suicide who before your very eyes ingests strychnine and dies at your feet in convulsive agony is quite sufficient evidence to effectively prove the proposition that strychnine is a potent poison even in small quantities. On the other hand, the Prime Minister who assures us that it is the daily drink of his own urine which has preserved his health in his old age, puts up a less convincing case. He may be right, but we are much less inclined to drink urine for our health than we are to shun strychnine for our life.
But suppose we wanted to be very sure that urine did or did not improve health -- it would, after all, be a very cheap tonic -- how would we go about it? Perhaps we should examine the man concerned with careful medical attention. If it turned out that he had the body of a man 20 years older than himself, with terminal cancer of the pancreas and a heart an its last legs, then in spite of his protestations of good health we might be inclined to proceed no further. But if he had indeed the body of a 20 year old stripling instead, would this be sufficient evidence? No. His preternatural health could be due to any or all of a multitude of his other habits of a lifetime; perhaps the orange he ate religiously every night before going to sleep or his Vegemite on toast every Christmas. (Or none of them: If his centenarian father and grandfather came forward to condemn their offspring's dipsouria, we might suspect a good heredity as the cause of his good health.)
No, to find out as nearly as possible the truth about the beneficial effects of urine we would conduct a controlled trial. Take, say, a thousand healthy volunteers and divide them into two groups which are as similar as possible -- age, weight, height, general health, etc. (Healthy individuals are employed even if at risk because of their "unhealthy" life style. The ill constitute a different problem.) The 500 in the first group are then instructed to drink their own urine every morning. (Before volunteering this would have been put to them as a possibility they would have to face.) These people constitute the test group. The other 500 continue their lives as before and constitute a control group.
After, say, 10 years the two groups are compared to determine which contains the healthiest individuals. How is health to be assessed? There are many measures, but perhaps the best is death: the death rates (or the mean ages at death) in the two groups. Other measures are of value and interest but are less convincing. For example, "feeling well" could be such a measure, but if the first group were all dead within a year, protesting to the last that they "felt well", while the control group were all alive and "feeling no different to before", the death rates would probably deserve more weight than the "feel well" rates.
In this chapter the circumstantial evidence concerning just two factors thought to be connected with health -- blood cholesterol and exercise -- is examined in some detail. Then controlled trials which have tested the effects of these and other risk factors are critically examined; this forms the greater part of the chapter.
Overall, these controlled trials have been well conducted so that a clear conclusion can be drawn from them: Improvement in lifestyle and reduction of risk factors does not improve health. Struggle though they might, the proponents of a "healthy" lifestyle must face this ineluctable conclusion. Struggle they have. The authors of these controlled trials have tried hard to support their hypotheses. As will be explained, statistical significance levels have been changed, trial endpoints have been changed, unsound statistical tests have been used, and, ultimately some have simply rejected their own findings. In spite of all, the results remain.
CIRCUMSTANTIAL EVIDENCE: CHOLESTEROL AND EXERCISE
1. Cholesterol
Is an elevated plasma cholesterol concentration in otherwise healthy people associated with excess mortality and morbidity, particularly that associated with coronary heart disease (CHD)? (9) If so, can intervention to reduce plasma cholesterol reduce any such excess? The answer to the first question is by now fairly clear. The answer to the second is the principal subject of this chapter.
Circumstantial evidence has long linked cholesterol and CHD. In 1843, Vogel (cited in Cook, 1958) showed that the atherosclerotic lesion contains cholesterol and this observation was confirmed by later investigations. In 1913, Anitschkow, and Wacker and Hueck (cited in Katz and Stamler, 1953) showed that dietary cholesterol could be important when they induced atherosclerotic lesions in rabbits by feeding them cholesterol in oil.
More recently, epidemiological evidence in the form of prospective studies has appeared. In such studies, a group of people have had their plasma cholesterol measured and they have then been followed for a period of years and correlations between cholesterol levels, mortality and morbidity determined. Most studies have been on men since their substantially higher mortality from CHD produces results more readily (Shurtleff, 1974).
One of the earliest and most influential of these studies was the Framingham Study which showed a clear positive correlation between plasma cholesterol and CHD (Dawber, Moore and Mann, 1957; Shurtleff, 1974). It was followed by other studies, the results of which are summarised in Table 3.1. It should be borne in mind that Table 3.1 summarises a large amount of information within severe constraints. In particular, where it was found that there was "no increased mortality with increasing plasma cholesterol" the relationship between the two was often very complex none the less. The original papers should be referred to for further information.
Table 3.1: Summary of Prospective Studies Examining
Mortality Patterns and Plasma Cholesterol Levels
| Study | No. of Subjects | Duration (years) | Mortality | |
| Total | CHD | |||
| Westlund and Nicolaysen (1966) | 6,886 m | 3.0 | ○ | ↑ |
| Keys (1970) | 12,770 m | 5.0 | ○ | ↑ |
| Shurtleff (1974) | 26,000 m 36,000 m | 18.0 18.0 | ↓ ↓ | ↑ ↑ |
| Peterson et al. (1981) | 10,000 m | 2.5 | ↓ | ↑ |
| Kagan et al. (1981) | 7,961 m | 9.0 | ○ | ↑ |
| Kozarevic et al. (1981) | 11,121 m | 7.0 | ↓ | ○ |
| Dyer et al. (1981) 1 2 3 4 | 1,233 m 1,899 m 6,890 m 5,750 w | 18.0 17.0 5.0 5.0 | ↑ ○ ○ ○ | ↑ ○ ○ ○ |
| Goldbourt et al. (1985) | 10,059 m | 15.0 | ○ | ○ |
| Salmond et al. (1985) | 630 m&w | 17.0 | ○ | ○ |
| Martin et al. (1986) Sherwin et al. (1987) | 361,662 m | 6.0 | ↑ | ↑ |
Notes:
↑ = increased mortality with increasing plasma cholesterol
↓ = decreased mortality with increasing plasma cholesterol
○ = no increased mortality with increasing plasma cholesterol
m = men
w = women
Eight of the studies show a significant and in most cases strong correlation between cholesterol and CHD mortality. None showed a negative correlation. However, the relationship between plasma cholesterol and total mortality is by no means so clear. Because CHD death contributes so much (about one third) to total mortality, a positive correlation between total mortality and cholesterol might have been expected. However, most studies have demonstrated either no correlation or even a negative correlation. Rose and Shipley (1980) have suggested that in some individuals low cholesterol levels are a metabolic consequence of unsuspected cancer. If so, their presence in the study group reduced any tendency to show a positive correlation between cholesterol level and total mortality. There is evidence to oppose this view (Salmond, Beaglehole and Prior, 1985) and the issue is not yet settled.
There are other facts which conflict with the hypothesis that cholesterol and CHD are correlated. At all ages other than 28-42 men have lower plasma cholesterol levels than women (Adlersberg, Schaefer and Steinberg, 1956; Stenhouse, 1979) yet, at all ages, men have substantially higher CHD mortality than women. The Masai of East Africa have plasma cholesterol levels which are about three standard deviations lower than or about half those of comparable European subjects. Yet their hearts are atherosclerotic and "quite like those described in Western Europe and the US." (Mann et al., 1972). The Masai present other problems. Mann et al. found little evidence that the atherosclerotic hearts led to disease and death. Of 600 Masai who were clinically examined, including 350 over the age of 40, only one showed unequivocal electrocardiographic evidence of an infarction. Equally puzzling is the effect of diet on their cholesterol levels. At the age of 12, Masai boys switch from a relatively low-fat diet to a high-fat diet of milk and meat. Their plasma cholesterol levels fall by about 25%. The Masai warrior does not behave like a rabbit. In spite of this discordant evidence the case against cholesterol is sufficiently persuasive to have merited further investigation.
2. Exercise
It is fascinating to observe the way medical fashions come and go. As a teenager, Pitt the younger was prescribed a daily bottle of port wine for his gout (Reilly, 1979). Generations later, port was considered a certain cause of gout (for example, Price, 1942: 430). Even tobacco has been considered a sovereign remedy and prophylactic:
Tobacco was then considered an excellent preservative against the plague, which committed dreadful ravages in the reign of Charles the Second; and the Eton boys were ordered to smoke in school daily. Tom Rogers told Hearne "that he was never whipped so much in his life as he was one morning for not smoking". (Lyte, 1899)
As recently as 1942, a distinguished textbook recommended cigarettes as a preventive for asthma (Price, 1942: 1151).
Exercise, particularly strenuous exercise, is now widely regarded as beneficial to health and life expectancy. Yet during the first half of this century the converse was generally believed. Rook (1954) summarises the condition with a characteristically pithy Cambridge story:
How many regard what they consider to be the folly of undue exertion may be exemplified by the story of the elderly don, himself approaching his hundredth year, who deplored the death of a colleague some three years his junior with the remark that in his youth the dead man had been addicted to climbing mountains, and such exertions must unquestionably have shortened his life.
Rook set out to determine whether exercise did indeed shorten life, an ironic state of affairs given the prevailing views 30 years later. (10) Ideally, to answer that question the average age at death of a group of people who have exercised regularly throughout their lives should be compared with that of a matched, similar group who have not. Such an investigation of 70 or 80 years' duration is not practicable. Instead, Rook and later investigators assumed that a group of people who are voluntarily and vigorously active in their early life will be likely to continue more active than a similar group who enjoyed a more sedentary youth.
Rook (1954) examined the life expectancy of men who represented Cambridge University in sporting events during the years 1860 to 1900. He compared their mortality with that of honours graduates and that of "non-sportsmen" and "non-intellectuals" of the same period. The intellectuals lived longest with an average age at death of 69.41 years, then the sportsmen at 67.97 years and the random group at 67.43 years. Rook concluded "there was no evidence that the sportsmen died at an earlier age than the group chosen at random; the intellectuals lived longer by a period averaging 1.5 years, but this small difference might well be due to chance". The difference might indeed have been due to chance but Rook, though advised by the Cambridge medical school statistician Dr W.L. Smith, did not bother to apply the usual statistical tests to determine if this was the case. From his Table 4-III it seems that the difference in favour of the intellectuals was not in fact significant. It is important to note that Rook excluded deaths due to accident and war but included suicide. For the intellectuals, 4.7% of deaths were due to accident or war injuries compared with 13.6% for athletes; for the intellectuals 4.1% of deaths were due to suicide compared with 0.9% for athletes. Since the intention of the study was to determine the effects of early strenuous activity on the later condition of the body, this selective inclusion of one form of violent death (suicide) and exclusion of others (accidents and war) seems odd. From the data Rook has provided it is not possible to calculate with certainty the mean ages for non-violent death in the different groups. In particular, Rook does not state explicitly the number of suicides or their age at death. At best, however, the sportsmen lived no longer than the intellectuals and at worst their lives were significantly shorter.
Montoye et al. (1956) carried out a similar study at Michigan State University for students born during the period 1855 to 1919. They defined an athlete to be "a letter winner in a varsity sport". They compared 629 athletes with 563 non-athletes. The mean age at death of athletes was 73.86 years and of non-athletes was 74.24 years. When accidental deaths were excluded athletes lived 74.43 years and non-athletes 74.59 years. These differences of 0.38 and 0.16 years in favour of non-athletes may or may not have been significant but Montoye et al. neither tested for significance nor published sufficient data to allow the readers of their paper to calculate the significance. They simply stated that "there is little difference existing between the two groups". Since their paper is titled "Study of the longevity and morbidity of college athletes" this omission is rather odd. Still odder is the fact that they did test statistically a number of other characteristics, apart from age at death. Their summary ends:
The results indicated that the longevity of athletes was approximately the same as that of controls and the distribution of causes of death was very similar. A significantly greater percentage of former athletes served in the armed forces and, of those serving a significantly larger proportion served in the Navy and Marine Corps. A significantly greater percentage of former athletes smoked and drank, and their weight in colleges was appreciably greater. There were no significant differences in the number married, weight gain since college days, or strenuousness of activity whilst in the armed Forces.
The commendable zeal with which the authors tested statistically a variety of differences between the two groups is the more striking by comparison with their reluctance to apply the same test to age at death.
Polednak (1972) examined the life expectancy of 6,303 men who attended Harvard College between the years 1880 and 1916. All were sufficiently interested in athletics to have rented a gymnasium locker. He divided them into three groups. "Major"athletes (668 men) had received one or more awards in baseball, football, track, ice hockey, tennis and golf. "Minor" athletes (1501 men) participated in major sports without winning an award or in non-award sports (lacrosse, cricket, basketball, swimming, gymnastics and fencing) or in class sports. Non athletes (4134 men) either had not participated in formal college sports or only as freshmen.
By 1967, 84.5% of the men had died. Polednak summarised his analysis:
Major athletes (lettermen) had the shortest lives, but differences were small. In mean age at death (natural causes) differences were not statistically significant, but major athletes were consistently the shortest-lived group -- by about one to three years in relation to minor athletes and non athletes -- in each of three birth decades. Major athletes died significantly earlier than non-athletes from coronary heart disease; they also died more often and earlier from neoplasms, although differences were not statistically significant for this series.
Prout (1972) compared the life expectancy of 172 oarsmen who had rowed during the years 1882 to 1902 at Harvard and Yale with 172 classmates who had not rowed. The mean lifespan of rowers was 67.85 years and of non-rowers 61.55 years, a statistically significant difference in favour of the rowers.
Pekkanan et al. (1987) followed the history of a group of 636 men who were aged 45-64 in 1964. Of these, 260 were classed as highly active physically and 386 were sedentary. After 20 years, 44.6% of low-activity men were dead compared with 46.0% of high-activity men, a small difference in favour of low-activity men which was not significant. However, there was a significant difference in mean age at death, low-activity men dying on average at 67.4 compared with 69.1 for high-activity men. As the authors stated "there is no evidence that high physical activity has the potential for extending the maximum life-span of this male population. Instead a high level of habitual activity reduced premature mortality".
Like Polednak (1972), Paffenberger et al. (1986) examined mortality in Harvard graduates. They sent questionnaires to 16,936 men who had attended Harvard during the period 1916 to 1950 and determined their physical activity patterns. They found consistently that those who exercised more lived longer so that "By the age of 80, the amount of additional life attributable to adequate exercise, as compared with sedentariness, was one to more than two years". As a measure of physical activity they used the subjects' estimate of weekly miles walked, stairs climbed and sports played. From these figures it is possible to estimate the total time expended on exercise during a lifetime. Paffenberger et al. (1986) in their Table 1 imply that the most active subjects were active for about 7 hours a week. Therefore by the age of 80 those subjects had spent about 2½ years being physically active, a period remarkably similar to the improved life expectancy.
Other studies, for example Schnohr (1971) and Karvonen et al. (1974) have compared athletes with the general population. Such work is open to the serious objection that it ignores the "healthy worker effect", defined by Last (1983) as:
A phenomenon observed initially in studies of occupational diseases. Workers usually exhibit lower overall death rates than the general population, due to the fact that the severely ill and disabled are ordinarily excluded from employment. Death rates in the general population may be inappropriate for comparison if the effect is not taken into account.
To varying degrees the same criticism may be made of those studies which have been described here: those people who are healthiest might be expected to take up sports and athletics. This seems to be reflected in a number of them, where it is found that mortality is higher among non-athletes until middle age after which mortality is lower. For example, Rook (1954) found that at the age of 35, 96.3% of sportsmen were alive compared with 94.8% of intellectuals. Thereafter the reverse was found. At 80, 18.6 % of sportsmen were alive compared with 23.1% of intellectuals.
To summarise, these studies do little to support the hypothesis that exercise increases life expectancy. Perhaps this is not surprising given that the original hypothesis was that exercise decreases life expectancy.
CONTROLLED TRIALS
Overall then, the evidence of studies such as those outlined above must be regarded as inconclusive. While it does not support Hippocrates, who wrote of athletes that "no one is in a more risky state of health than they", nor does it exclude the possibility that exercise may be beneficial in increasing life-expectancy. On its own, evidence of the kind so far considered that a particular factor is harmful is no more than circumstantial and suggestive. How then can it be determined whether a fatty diet and high blood cholesterol is bad -- or good -- for you? Whether exercise is good -- or bad -- for you? Or indeed whether smoking, sunshine, salt or any other factor in everyday life is good or bad? In principle the answer can be obtained very simply by the controlled intervention trial. Take two similar groups of people. Change, so far as possible, the life-style of one group. For example, encourage the group to eat less cholesterol-rich food. Leave the other group to their own devices. After some years compare the two groups. Has the advice worked? Which group has fewer deaths and/or ill subjects?
In practice such experiments are expensive and time-consuming. Thousands of subjects must be followed for many years if sufficient deaths and serious illness are to occur for any difference to become manifest. To make matters worse, the test group may not change their way of life to the extent hoped for -- nor the control group maintain theirs. The difficulties in the conduct and interpretation of such trials are very considerable but within the limits imposed by humanitarian and ethical considerations there seems to be no other approach.
The trials considered here have modified some or all of the following factors in the test group: plasma cholesterol (by diet and/or drugs); smoking; exercise. Tables 3.2a and 3.2b summarise the results of these trials. "Coronary events" is defined by most authors as the sum of both fatal and non-fatal CHD.
Table 3.2a: Effect of Change in Lifestyle on Mortality and
Coronary Events (Intervention Trials -- Various Factors)
| Study | Date | No. of Subjects | Duration (years) | Type of Intervention | Total Mortality | CHD Mortality | Cancer Mortality | Coronary Events | |||
| Diet | Smoking | Exercise | Drugs | ||||||||
| WHO Collaborative Trial | 1971 | 60,881 | 6 | √ | √ | √ | √ | ○ | ○ | • | • |
| Finnish Businessmen | 1972 | 1,212 | 5 | √ | √ | √ | √ | ○ | ○ | ○ | ○ |
| MRFIT | 1972 | 12,886 | 7 | √ | √ | √ | √ | ○ | ○ | ○ | • |
| North Karelia * | 1972 | 12,000 | 5 | √ | √ | √ | • | ○ | ○ | • | • |
| Göteborg | 1970 | 30,022 | 11.8 | √ | √ | • | √ | ○ | ○ | ○ | ○ |
| Oslo | 1972 | 1,232 | 5 | √ | √ | • | • | ○ | ○ | ○ | ↓ |
| AntiCoronary Club | 1957 | 1,277 | 4 | √ | • | • | • | ↑ | ↑ | • | ↓ |
| Finnish Mental Hospitals * | 1959 | 5,000 | 12 | √ | • | • | • | ○ | ↓m○w | ○ | • |
| Veterans Administration | 1959 | 888 | 8 | √ | • | • | • | ○ | ○ | ↑ | ↓ |
| Sydney Diet-Heart Study | 1966 | 458 | 5 | √ | • | • | • | ↑ | ↑ | • | • |
| Whitehall Study | 1978 | 1,445 | 10 | • | √ | • | • | ○ | ○ | ○ | • |
Legend:
√ = method of intervention employed for the test group
○ = no change in mortality (or coronary events) in the last group compared with the control
↑ = increase in mortality (or coronary events) in the last group compared with the control
↓ = decrease in mortality (or coronary events) in the last group compared with the control
• = not applicable or not specified in the paper
m = men
w = women
* = men & women
Table 3.2b: Effect of Change in Lifestyle on Mortality and
Coronary Events (Intervention Trials -- Drugs Only)
| Study | Date | No. of Subjects | Duration (years) | Type of Intervention | Total Mortality | CHD Mortality | Cancer Mortality | Coronary Events | |||
| Diet | Smoking | Exercise | Drugs | ||||||||
| Helsinki Heart Study | 1981 | 4,081 | 5 | • | • | • | √ | ○ | ○ | ○ | ↓ |
| LRC-CPPT | 1973 | 3,806 | 7.4 | • | • | • | √ | ○ | ○ | ○ | ↓ |
| WHO Clofibrate | 1965 | 10,000 | 5.3 | • | • | • | √ | ↑ | ○ | ○ | ↓ |
| CDP: High dose oestrogen | 1965 | 3,907 | 1.5 | • | • | • | √ | ○ | ○ | • | • |
| CDP: Low dose oestrogen | 1965 | 3,880 | 4.7 | • | • | • | √ | ○ | ○ | ↑ | ○ |
| CDP: Dextrothyroxine | 1965 | 3,798 | 3 | • | • | • | √ | ○ | ○ | • | • |
| CDP: Clofibrate | 1965 | 3,892 | 5 | • | • | • | √ | ○ | ○ | ○ | ○ |
| CDP: Niacin | 1965 | 3,908 | 5 | • | • | • | √ | ○ | ○ | ○ | ↓ |
Legend:
√ = method of intervention employed for the test group
○ = no change in mortality (or coronary events) in the last group compared with the control
↑ = increase in mortality (or coronary events) in the last group compared with the control
↓ = decrease in mortality (or coronary events) in the last group compared with the control
• = not applicable or not specified in the paper
The Lipid Research Clinic's Coronary Primary Prevention Trial (LRC-CPPT)
In 1973, one of the most expensive biological experiments ever devised was begun in the U.S.A. (Lipid Research Clinics Program, 1979). It was intended to test the effect of ingestion of the drug cholestyramine. It was hypothesised that cholestyramine would reduce plasma cholesterol levels and thereby reduce the incidence of CHD. A total of 3806 asymptomatic men with primary hypercholesterolaemia were divided into two groups. The treatment group was given the drug and the control group was given a placebo. The trial continued until 1983, the average time of follow-up being 7.4 years.
The trial was designed to include a number of features outlined in a preliminary report which would make its findings water-tight. "Since the time, magnitude and cost of this study make it unlikely that it could ever be repeated, it was essential to be sure that any observed beneficial effect of cholesterol lowering was a real one" (Lipid Research Clinics Program, 1979). In particular, they chose P<0.01 rather than P<0.05 (11) as the level of statistical significance which would determine whether the drug was beneficial or harmful. There were to be two primary end points: (12) CHD death and non-fatal myocardial infarction (MI).
However, when the results of the trial were published these features had vanished. The researchers now accepted as their level of statistical significance 'P<0.05, after adjustment for multiple looks' (Lipid Research Clinics Program, 1984). They also adopted as a new primary end point 'the combination of definite CHD death and/or definite nun-fatal myocardial infarction'. With these new criteria they found a significant (P<0.05) 19% reduction in the new primary end point. There was no significant reduction of total mortality or deaths from any specific cause, even with their flexible significance level.
Furthermore, as Pinckney and Smith (1987) have pointed out, the LRC-CPPT committed the statistical solecism of using one-tailed statistical tests which halved their P values. In effect, they assumed that cholestyramine could not possibly increase mortality. This is ironic since in their discussion of deaths from specific causes they say "The only noteworthy difference (P=0.08) was 11 deaths from accidents and violence in the cholestyramine group, compared with 4 in the placebo group". And in their discussion of side effects they considered the frequency of hospitalisation in the two groups: "The only significant difference was a greater number in the cholestyramine group (40 versus 23) of operations or procedures involving the nervous system". The possible connection between these two statements seems to have eluded the investigators because they state: "Since no plausible connection could be established between cholestyramine treatment and violent or accidental death, it is difficult to conclude that this could be anything but a chance occurrence". The possibility that cholestyramine might reduce life expectancy must be considered in determining the statistical test to be used. This would still be true even if there were not these indications that the drug appeared to have harmful side-effects.
Such rejection of statistically significant results and acceptance of non-significant results is disturbingly common in epidemiological studies. For example, the only randomised, controlled trial of the effects of giving up smoking (Rose et al., 1982) produced only one statistically significant change in mortality. Non-lung cancer deaths increased by 140% (P=0.01) in subjects who gave up smoking. Here also, the authors concluded that this was due to chance, as was their failure to find any reduction in deaths due to lung cancer, or to any other cause, or to all causes. They concluded: "the policy of encouraging smokers to give up the habit should not be changed". This is curious science.
The change in end point, change in significance level, adoption of one-tailed statistical tests and rejection of their own findings do not conceal the fact that the LRC-CPPT project found no beneficial effects on mortality or morbidity as a consequence of cholestyramine-induced reduction of plasma cholesterol. This is an important result in itself and should have been reported. A ten-year study by 214 authors and costing $US150,000,000 deserved better.
The Multiple Risk Factor Intervention Trial (MRFIT)
Over a period of several years, 12,866 men at increased risk of death from CHD were recruited across the USA (Multiple Risk Factor Intervention Trial Research Group, 1982). They had no clinical evidence of CHD but were designated as being at increased risk because their levels of 3 risk factors -- cigarette smoking, serum cholesterol and diastolic blood pressure -- were sufficiently high to place them in the upper 10% of a risk score distribution based on data from the Framingham study. Half were assigned to a special intervention group (SI) and were treated conventionally with drugs for their hypertension, encouraged to stop smoking and consume less cholesterol and saturated fats. The other men were a "usual care" (UC) group and received no special treatment other than that provided by their personal physicians.
The men were examined annually and followed for an average of 7 years each. The three risk factors declined in both groups but the reductions were larger throughout the trial in the SI group, being significant at P<0.01 at each annual visit. For example, after 6 years, 50% of SI men who were smokers had quit compared with 29% of the UC. Diastolic blood pressure fell in the two groups by 10.5 and 7.3 respectively. Plasma cholesterol fell in the two groups by 12.1 and 7.5 mg/dl respectively, which primarily represented changes in low-density lipoprotein cholesterol and not high-density lipoprotein cholesterol. The unexpected decline in cholesterol in the UC group and a smaller than predicted decline in the SI group meant that the SI-UC difference was about half of that expected. At the end of the follow-up period, the mortality rates were SI 41.2 and UC 40.4/1000. The CHD death rates were 17.9 and 19.3/ 1000. Neither death rates from CHD nor any other cause were reported as significantly different in the two groups.
The investigators were reluctant to accept their own results and examined sub-groups within their study. They found that SI men with hypertension as an important risk factor and with resting ECG abnormalities had a substantially raised mortality. This, they consider, would have been due to an unexpected deleterious effect of the SI program, particularly toxic effects of the diuretics used. They reported this at a news conference which presented their findings (Kolata, 1982).
After removal of the men with resting ECG abnormalities from their results, total mortality rates for SI and UC men were 37.2 and 39.5/1000 and for CHD 14.8 and 18.8/1000. Again, none of these differences were significant.
The original goal of the MRFIT was to determine whether reduction of the risk factors smoking, cholesterol and elevated blood pressure in high-risk but otherwise healthy men would reduce CHD mortality, non-fatal MI or CHD, cardiovascular mortality and mortality from all causes (Zukel, Paul and Schnaper, 1981). Their paper answers these questions thus:
In conclusion we have shown that it is possible to apply an intensive long-term intervention program against three coronary risk factors with considerable success in terms of risk factor changes. The overall results do not show a beneficial effect on CHD or total mortality from this multifactor intervention. (Multiple Risk Factor Intervention Trial Research Group, 1982)
In other words, they found that changing the "risk factors" does not apparently change the risks. This necessarily means that the "risk factors" are not as important as was thought. Indeed, it should be concluded that the "risk factors" were no such thing, at least as far as this trial is concerned.
The Oslo Study
From May 1972 to December 1973, all men in Oslo, aged 40-49 years, were invited to take part in a study of health (Leren, Askenvold, Foss et al., 1975). Of 17,965 men examined initially, 1,232 healthy, normotensive (normal blood pressure) men who were considered to be at "high risk" were selected to take part in a controlled intervention trial of the effects of reducing risk factors. 'High risk" meant they had serum cholesterol levels of 290-380 mg/dl and "coronary risk scores (based on cholesterol levels, smoking habits and blood pressure) in the upper quartile of the distribution, and systolic blood pressures (mean of two measurements) below 150 mm Hg" (Hjermann et al., 1981).
Half the men (the intervention group) were encouraged to lower their plasma lipid concentrations by change of diet and to stop smoking. The other half (control) were uncounselled. The results of the trial were reported after 5 years (Hjermann et al., 1981) and after 7.5, 8.5 and 10 years (Holme et al., 1985). After 5 years, risk factors had declined in both groups but significantly more in the intervention group (P<0.01). "In the intervention group there was a reduction of 17% of mean serum cholesterol from screening to first follow up. The mean difference in serum cholesterol between the two groups during the 5 years was 13%." And "the mean of the average values of fasting serum triglyceride levels was 20% lower and the mean of non-fasting swum triglyceride levels was 25% in the intervention group than in the control group. Tobacco consumption (expressed as number of cigarettes per man per day; pipe smoking is included taking one pack of pipe tobacco weekly to equal 7 cigarettes daily) fell about 45% more in the intervention group than in the controls". The presumed effects of these changes were reported. Although their original protocol (Leren et al., 1975) had specified P<0.01 as the acceptable level of significance using a t-test, the 5-year report changes the level to P<0.05. With this new level of significance, total mortality was not significantly different in the two groups (intervention group 26/1000, control group 38/1000, P=0.246) but there was a significant difference in sudden coronary death in favour of the intervention group (5/1000 versus 18/1000, P=0.024). Two and a half years after the trial had ended and interviewing with the intervention group had stopped subjects were recalled. The investigators reported (Holme et al., 1985) that risk factors were still different in the two groups, but less so. For cigarette smoking this occurred as a result of the control group continuing to smoke almost as much as before, with the intervention group tending to return to their previous smoking habits. For cholesterol, the control group's values dropped while the intervention group's remained unchanged.
A new endpoint was selected for this extended follow-up period: "major CHD events (non-fatal + fatal MI + sudden death)" and a one-sided test rather than a two-sided test was used. Major CHD events for the 8.5-10 year period were "25 and 45 in intervention and control groups, respectively (P ≈ 0.02)". Total deaths were 19 and 31 (P ≈ 0.05). There was no more detailed presentation of their endpoints.
Given the authors' shifting statistical criteria it is difficult to produce a conclusion as to the benefit of intervention in this trial, but if one must be drawn it is surely that there was no statistically significant benefit. The statements "P ≈ 0.02" and "P ≈ 0.05" (that is, "the probability is about 0.02" and "the probability is about 0.05") are unusual to say the least.
The WHO Clofibrate Trial
During the years 1964 to 1972, 15,745 men, aged 30-59, were recruited from approximately 30,000 volunteers in Edinburgh, Budapest and Prague to take part in a controlled trial of the effects of lowering serum cholesterol as a result of ingestion of the drug clofibrate. All subjects were healthy and, in particular, free from ischaemic heart disease (IHD). The methods and the initial results were reported by Heady (1973) and by the Committee of Principal Investigators (1978, 1980, 1984).
Subjects were divided into 3 equal groups, according to serum cholesterol level. Group I comprised half those in the high third of the cholesterol distribution of 30,000. Group II comprised the other half of the upper third. Group III comprised half of those in the bottom third. Group I was treated with clofibrate and groups II and III given a placebo, the treatment phase of the project lasting, on average, 5.3 years.
When the first results were reported in 1978, serum cholesterol in Group I had fallen by 9% but Group III continued to have the lowest levels. There was no significant difference between IHD mortality rates in Groups I and II (1.6 and 1.4/1000) but there were significant increases in mortality in the intervention group for all causes (4.9 and 3.8/1000), as well as for a variety of other causes.
By 1980, subjects had been followed for an average of 4.3 years from the end of the intervention period. Total mortality in the intervention Group I continued to be higher (8.1/1000) than in the control Group II (6.6/1000) (P<0.01). Mortality from IHD was not significantly higher in the intervention group (3.2/1000) compared with the control (2.9/1000). By 1984, with a mean follow-up time of 7.9 years, there was no significant difference in total mortality between the two groups (8.6 and 7.9/1000) or IHD mortality (3.6 and 3.5/1000).
The authors did find a consistent and significant reduction in non-fatal MI in the intervention group. Even this positive result was obtained only after the abandonment of their original protocol (Heady, 1973): "The 1% level of significance will be used to assess differences. ..." But, as they concluded in their 1984 paper, "The excess of deaths in the 'treated' group has, not unnaturally, diverted attention from this result".
The Coronary Drug Project (CDP)
From 1965 to 1969, over 8,000 men, aged 30-64, with evidence of one or more myocardial infarctions in the past but who were otherwise healthy, were recruited into an investigation of the efficacy of a number of drugs which reduce plasma lipid levels and are used for the treatment of CHD (Coronary Drug Project Research Group, 1970). They were randomly allocated to six groups who received, respectively, low dose oestrogen, high dose oestrogen, clofibrate, dextrothyoxine, niacin and placebo. The primary endpoint was to be the 5 year total death rate. The results were reported over the next 10 years.
High Dose Oestrogen
After an average of 1.5 years follow-up, the investigators reported their preliminary results for the group who received high doses of oestrogen (Coronary Drug Project Research Group, 1970). The effect on plasma lipids was not reported. It was found that "certain non-fatal adverse affects were occurring substantially more often" in the intervention group than in the placebo group. Breast enlargement, breast tenderness, impotence and testicular atrophy had been expected but, in addition, non-fatal MI was significantly (P<0.05) more frequent (6.2% versus 3.2%) as were pulmonary embolism and thrombophlebitis. Coronary death, sudden death and total mortality were also higher but not significantly so, according to their "two approaches for evaluation of statistical significance" which were specially developed by CHD statisticians. The authors concluded; "These findings lessen the potential long-term value of this 5.0 mg dosage level of oestrogen in men with previous MI". The trial was abandoned in 1970.
Low-dosage oestrogen
The results of the low-dosage oestrogen trial (Coronary Drug Project Research Group, 1973) are confusing. Unlike the earlier paper on the effects of high-dosage oestrogen (Coronary Drug Project Research Group, 1970), "classical" statistical tests as well as their specially developed modified sequential testing and a "Bayesian approach yielding a numerical value designated RBO (relative betting odds)" were used. It is not immediately obvious why such a sophisticated analysis was required or even felt desirable.
With their own tests, after an average follow-up of 56 months, there was no significant difference in mortality or morbidity between the treatment and placebo groups. With the more conventional tests, total mortality was not significantly higher in the treatment group, but pulmonary embolism (1.5% versus 0.8%), all-sites cancer (1.27% versus 0.47%) and lung cancer (0.54% versus 0.14%) were all significantly higher. Changes in plasma lipids were described cursorily as a slight reduction in serum triglyceride. As a result of these findings, the trial was abandoned in 1973.
Dextrothyroxine
After an average follow-up of 3 years, the results of treatment with dextrothyroxine were presented (Coronary Drug Project Research Group, 1972). There was a "fall of about 12% in serum cholesterol level and 15% to 20% in fasting triglyceride level" which are presumably significant changes.
As with the oestrogen trials, the statistical treatment is confusing. Total mortality in the test group was 14.8% and in the placebo group 12.5%, a difference which is not significant by either conventional tests or their specially devised tests, nor were mortalities for specific causes different. There was no reduction in major coronary events or cardiovascular death. However, they go on to say "Further analysis by the life-table method revealed that the absolute difference in mortality between these two groups tended to increase progressively with duration of medication (Figure 1). At the 28th month of follow-up and thereafter these differences exceeded two standard errors of the difference". The investigators concluded that, at best, treatment with dextrothyroxine, although it reduced plasma lipids, did not reduce total mortality or mortality for any cause and was possibly harmful. The trial was abandoned in 1971.
Clofibrate
The statistical tests used in this part of the study were conventional (Coronary Drug Project Research Group, 1975). Over the five years follow-up period, the mean reduction in plasma lipids in the treatment group relative to the placebo group was a 65% fall in cholesterol and a 22.3% fall in triglyceride. Total death rates were not significantly different in the two groups (20.0% clofibrate, 20.9% placebo). The only significant difference was an increase in definite or suspected fatal or non-fatal pulmonary embolism or thrombophlebitis in the clofibrate group (5.2% versus 3.3%, P<0.01). Several side effects were more common in the treated group. The investigators concluded that they had provided "no evidence on which to recommend the use of clofibrate in the treatment of persons with coronary heart disease."
Niacin
Statistical tests used in this final part of the study were also conventional (Coronary Drug Project Research Group, 1975). The niacin-treated group experienced a mean decrease in plasma cholesterol of 9.9% and in triglyceride of 26.1%. The 5-year mortality rates were not significantly different in the treated group (21.2%) and placebo group (20.9%), nor were there differences for any specific cause of death. However, the incidence of definite, non-fatal MI was 27% lower in the treated group (P<0.005). As with the clofibrate group, a variety of side effects were more common in the treated group. The authors concluded that niacin did not influence mortality but it might be slightly beneficial in protecting persons to some degree against recurrent non-fatal MI. "However, because of the excess incidence of arrhythmias, gastro-intestinal problems and abnormal chemistry findings in the niacin group, great care and caution must be exercised if this drug is to be used for treatment of persons with coronary heart disease."
The results of the Coronary Drug Project can be summed up briefly: At best, the drugs employed did no harm. Again it must be emphasised that the subjects were essentially in good health in spite of their earlier heart troubles. For the ill, the drugs' worth could well outweigh any harmful side-effects.
The North Karelia Project
Coronary heart disease is exceptionally common in Finland and particularly so in the county of North Karelia. This study (Puska, Tuomilehto, Salonen et al., 1979; Salonen, Puska and Mustaniemi, 1979) aimed at reducing risk factors and, as a consequence, at reducing mortality and morbidity. Five thousand people were recruited in North Karelia as subjects. Seven thousand were recruited as subjects in the control county of Kuopio, selected because of its similarity to North Karelia. The Karelian test subjects were encouraged to reduce their cardiovascular disease risk factors over the period of 1972-7 and their progress was compared with the control subjects.
Men
Initially, high mean values for most risk factors were common in North Karelia. Significantly more cigarettes were consumed per smoker, serum cholesterol was higher and systolic blood pressure was higher. The prevalence of smoking (proportion of the population smoking) was the same. Only diastolic blood pressure was lower. By 1977, all risk factors were the same or, in the case of systolic and diastolic blood pressures, lower in North Karelia than in Kuopio.
In spite of the initial differences in risk factors, the initial total mortalities were the same in test and control areas (test 13.8 versus control 13.6/1000 men) as were cardiovascular mortalities (7.7 versus 7.7/1000 men). Even before the trial started, therefore, a disinterested observer would have had reason to doubt the connection between "risk factors" and actual risks. At the end of the trial, despite the lowered risk factors in North Karelia, total mortalities (11.6 versus 11.4/1000 men) and cardio-vascular mortalities (6.3 versus 5.8/1000 men) were still the same. "All" acute MI is described as significantly lower in North Karelia (11.1 versus 12.8/1000 men) but since "definite" acute MI was if anything, higher, such a result in a non-blind trial is very suspect.
Women
The results for women were similar. Initially, risk factors were worse for North Karelian women. Serum cholesterol and systolic blood pressures were higher. By 1977, risk factors were the same (amount of tobacco consumed per day, serum cholesterol) or lower (prevalence of smoking, systolic and distolic blood pressures.)
Again, in spite of the difference in risk factors, initial total mortalities in North Karelia and Kuopio were the same (4.8 versus 5.0/1000), as were cardiovascular mortalities, nor was there any difference at the end of the trial (total mortality 3.9 versus 3.8/1000 women). There was, however a significant reduction in "all" acute MI (2.3 versus 3.8/1000 women). As with the men, this result must necessarily be treated with caution since the North Karelian study was not a blind trial. "Definite" acute MI was not reduced (1.1 versus 0.8/1000 women).
With no change in total mortality or CHD mortality it must be concluded that this trial of the effects of intervention to reduce CHD found no benefit.
The Finnish Businessmen's Study
This was a randomised five-year multifactorial prevention trial of vascular disease (Miettinen, Huttunen, Naukkarinen et al., 1985). An intervention group of 612 forty-eight year old businessmen, considered to be at high risk of cardiovascular disease, were encouraged to change their diet (particularly with regard to fat intake) to reduce smoking and to take more exercise. Where blood pressure and serum lipid levels did not fall sufficiently, the subjects were treated with a variety of drugs, mainly diuretics and beta-blockers and probucol and clofibrate. A similar group of 610 men was uncounselled and untreated except that 15% of them received anti-hypertensive drugs. After 5 years, most risk factors, including weight, blood pressure, serum cholesterol and triglycerides and tobacco consumption had improved significantly (P<0.01) in the intervention group compared with the control group.
At the end of 5 years, total mortality in the intervention group was 10/612 and in the control group 5/610, a non-significant difference. There were no significant differences in mortality from specific causes nor in morbidity except for non-fatal stroke which was more common in the control group (8 versus 0, P<0.01). In brief, improvement in lifestyle did not reduce CHD deaths or total deaths.
The Finnish Mental Hospital Study
This was a controlled study of the effects of a cholesterol lowering diet on 10,000 people in two Finnish mental hospitals (Mettinen, Turpeinen, Karvonen et al., 1972; Turpeinen, Karvonen, Pekkarinen et al., 1979). In Hospital 1, from 1959 to 1965, patients were placed on a cholesterol-lowering diet while Hospital 2 served as a control. Milk was replaced by soybean oil in skim milk and butter and margarine were replaced by a "soft" margarine with a high content of polyunsaturated fatty acids. The overall fat content of the diet was unchanged. In 1965, Hospital 2 patients became the test group and Hospital 1 the control. During the 12 years of the study death rates during hospitalisation were examined.
Males
Biopsy revealed that the fatty acid composition of adipose tissue changed to reflect the change in diet, and serum cholesterol levels fell by 18% and 13% during the trial periods in the 2 hospitals. Pooled results from the 2 hospitals showed that the CHD mortality fell from 14.08 in the control period to 6.61/1000 person years (P<0.002) during the test period. Total mortalities for control and test periods were not significantly different (control 39.50 and test 34.84/1000), nor were any other cause-specific mortalities.
Females
The reductions in serum cholesterol in the two hospitals during the test periods were 12% and 13%. In both test and control periods, serum cholesterol was higher in women than in men. Comparing control and test periods, there was no significant change in total mortality (control 29.01 versus test 30.87/1000), CHD mortality (control 7.90 versus 5.21/1000) or any other cause-specific mortality.
These results are consistent with and support the idea that a cholesterol-lowering diet can reduce the incidence of CHD. This is in fact the only trial to produce a significant reduction in CHD, if only in men.
The WHO Collaborative Trial
In this trial, (WHO European Collaborative Group, 1974, 1982, 1983, 1986) 60,881 working men, aged 40-59 were recruited from 80 factories in Belgium, Italy, Poland and the U.K. Half received an appropriate treatment of advice for a cholesterol lowering diet, cessation of cigarette smoking, daily physical exercise, weight reduction and hypotensive therapy.
Over 6 years, all risk factors fell more in the intervention than in the control group, although serum cholesterol fell only by 1.2%. The estimated change in all risk factors (multiple logistic function, MLF) was -11.1% with a range "from a reduction of 28% in Italy down to 4% in UK and Cracow". (The MLF is a mathematical measure of all the risk factors investigated here.) At the end of the 6 years, the intervention group had 6.9% fewer fatal CHD, 14.8% fewer non-fatal MI and 5.3% fewer total deaths but none of these changes were statistically significant. The authors in their final report (WHO European Collaborative Group, 1986) claimed that "the pooled result was non-significant because the large UK Centre had little success in sustained risk factor control (Δ mlf -4%), so that its failure to reduce CHD was not surprising". This cannot be the explanation. Not only was there an increase in mortality in the UK, but the same risk factor reduction was observed in Poland with a quite different result: "a large overall benefit to the intervention group". (WHO European Collaborative Group, 1986; cf. tables 2 and 4 in WHO European Collaborative Group, 1983). One cannot have it both ways. If the 22% reduction in Polish CHD is to be credited to the drop in risk factors, then the 14% increase in the UK should also be credited to the same drop in risk factors.
The Anti-Coronary Club Program
In 1957, 814 New York men were recruited to take part in the anti-coronary club program (Christakis, Rinzler, Archer et al., 1966; Rinzler, 1968). They were placed on a diet rich in polyunsaturated fats. A similar group of 463 men formed a control group. After 4 years, the risk factors for CHD -- obesity, hypertension and hypercholesterolaemia -- all diminished significantly in the treated group as compared with the control. Serum cholesterol in the test group fell from 260 to 230 mg/100 ml after 1 year and remained low, that in the control group was unchanged at 250 mg/100 ml.
After 4 years, there were 27 deaths (3.3%) in the test group and 6 (1.3%) in the control group. These results are not stated explicitly and have been extracted from the text (Christakis et al., 1966). There were 9 CHD deaths (1.1%) in the test group and none in the control group (0%). The authors made nothing of these alarming findings and concluded that "a statistically significant difference was observed between the two groups in morbidity from new CHD". Two years later, further results were presented (Rinzler, 1968) but the authors refrained from presenting any mortality figures.
The Veterans Administration Study
Middle-aged and elderly male veterans living in the "Los Angeles domicile" were asked, in 1959, to take part in this study (Dayton, Pearce, Hashimoto et al., 1969; Dayton and Pearce, 1969). After randomisation, 424 men formed a test group and 424 a control group. The geometric mean age was 65.5. Over 8 years, the test group was given a diet which was low in cholesterol and high in unsaturated fats but otherwise similar to the conventional food received by the control group. Serum cholesterol in the test group, relative to the control, fell by a mean value of 2.7% and serum total lipids fell by 6.6%. Biopsy of adipose tissue revealed a 3-fold increase in linoleic acid concentration in test men considered to be "good adherers" to the diet.
After 8 years, there were 177 deaths in the control group and 174 deaths in the experimental group. This result is presented in Dayton et al., (1969, Table 27) and although Dayton and Pearce (1969) give the figures reversed, i.e. 177 test deaths and 174 control deaths, it appears to be correct. The difference in either case was not significant. There were significantly (P<0.05) fewer deaths from acute atherosclerotic events in the test group (48) compared with the control group (70). However, Mann (1977) has analysed their results further and concluded that there were also significantly more deaths from cancer (P<0.05) in the test group (32) compared with the control group (17) so that one difference cancelled out the other. (This is also relevant to the earlier discussion of cholesterol and cancer. See "Cholesterol" section, this chapter.)
In brief, the improved diet produced no change in total mortality or CHD mortality.
Goteborg Trial
In 1970 middle aged men of Goteborg were assigned to either an intervention group or one of two control groups (Wilhelmsen et al., 1986). The participants were 47-55 years of age with a mean of about 51. There were approximately 10,000 men in each group. Men in the intervention group who were found to be at risk because they had elevated serum cholesterol (>300 mg per 100 ml), elevated blood pressure (systolic >175 mm Hg or distolic >115 mm Hg) or smoked more than 15 cigarettes per day were treated and counselled appropriately: cholesterol was lowered by change of diet and where this failed after 6 months "clofibrate and/or nicotinic acid (according to lipoprotein type) was given, but clofibrate was stopped when the adverse effects of this treatment were reported".
Men with high blood pressure were treated with conventional antihypertensive drugs including beta-blockers and diuretics. Smokers were invited to join anti-smoking groups and in some cases were given nicotine chewing gum.
When examined after 4 and 10 years, each of the 3 risk factors was on average lower in the intervention group than in the 2 control groups although the difference was more pronounced at 4 years than 10: risk factors were reduced in the control groups as well as in the intervention group, though less so.
After a mean follow up period of 11.8 years there was "no effect on coronary heart disease, a slight non-significant decrease in fatal stroke, and a slight (far from significant) effect on total mortality". In all there were 1293 deaths in the intervention group and 1304 and 1332 deaths in the two control groups. The authors concluded: "Strategies other than intervention on high risk individuals must be chosen if a major impact on disease incidence is to be achieved in the general population". An unusually frank statement.
Sydney Diet-Heart Study
In 1966, 458 men aged 30-59 with clinical coronary disease took part in a controlled trial of the effects of change in dietary fat intake (Woodhill et al., 1977). A control group of 237 men was given no specific dietary instruction "apart from restriction of calories if thought to be overweight". In addition they were "allowed to use polyunsaturated margarine instead of butter if they wished".
The intervention group comprised 221 men who were "advised and tutored individually to reduce saturated fat intake to approximately 10% of calories and dietary cholesterol to 300 mg or less per day. They were encouraged to use food containing polyunsaturated fatty acids to 15% or more of their daily calories". At follow up, serum cholesterol was significantly lower in the intervention group (250.2 mg/100 ml), than in the control group (262.3 mg/100 ml), a difference of 5%. After 5 years "Survival was significantly better in the P [control] group, although the difference was not marked". In fact, 17.6% of the intervention group died compared with 11.8% in the control group. 94% of the deaths were from cardiovascular disease, 3% from cancer and 3% from motor accidents. The authors concluded that their subjects were "not a good choice for testing the lipid hypothesis" and that weight loss and other changes "may well have more important beneficial effects than changes in dietary lipids". Bearing in mind their mortality results one cannot but admire the author's mastery of the understatement.
The authors further complained that, because the control group had of their own volition also "improved" their life-style "that the difference in diet between P [control] and F [test] groups was smaller than we had hoped". Given the result of the trial one might reasonably regret, for the sake of all subjects, that there was any change in diet at all.
Helsinki Heart Study
This study was intended to determine the effectiveness of the drug gemfibrozil in preventing coronary heart disease in middle-aged men who had raised non-high-density lipoprotein cholesterol levels (Frick et al., 1987). In a controlled trial, 2051 men were given the drug and a similar group of 2030 were given a placebo over a period of 5 years. This resulted in a sustained change in plasma fats in the treated group: "The total cholesterol level was initially reduced by 11%, the level of LDL cholesterol by 10%, that of non-HDL cholesterol by 14% and that of triglycerides by 43%." There was also an increase in the HDL cholesterol, which is thought to be beneficial.
During the course of the trial the mortality rate in the treated group was 21.9/1000 and in the placebo group 20.7/1000. This was not a statistically significant difference. Nor were there significant differences for any of the specific causes of death. There were significantly fewer (27.3/1000) "cardiac end points" (non-fatal MI, fatal MI, sudden cardiac death and unwitnessed death) in the treated group compared with the control (41.4/1000). Against this must be set the significantly greater number of gastrointestinal operations in the test group 81 versus 53).
Overall then this study found no reduction in either total mortality or CHD mortality after treatment with the cholesterol-lowering drug gemfibrozil.
The Whitehall Study
Smoking is a possible factor which has been tested but once. In 1968, 1445 British civil servants who smoked were recruited to take part in a trial of the effects of giving up smoking (Rose and Hamilton, 1978; Rose et al., 1982). Half were advised and counselled to give up smoking, the other half were not.
After one year reported cigarette consumption in the intervention group was one-quarter of that in the normal-care group. Over 10 years the difference in cigarette consumption between the two groups continued although it diminished.
Cigarette consumption is widely believed to be injurious to health. Just as widely believed is the notion that people who give up smoking become healthier and live longer. No such result was found in this study. After 10 years, 17.2% of the test group had died, as had 17.5% of the control group. There was no statistically significant change in mortality from CHD, lung cancer or any other cause except for cancer at sites other than the lung where 28 deaths (3.9% occurred) in the group who gave up smoking compared with 12 (1.7%) in those who did not. The authors believed this significant result was due to chance and give their reasons for so believing in one page of their seven page paper. Equally, they believed that their failure to find any reduction in total mortality or mortality from lung cancer or any other specific cause was also due to chance, so they could conclude the summary to their paper with the sentence: "The policy of encouraging smokers to give up the habit should not be changed". I am aware of no other controlled trial of the effects of giving up smoking. Curiously, even this lone study has been omitted from the Surgeon-General's report on passive smoking (Koop, 1986), although he had earlier (Koop, 1982) praised it for "pointing up the positive consequences of cessation in an authoritative manner".
DISCUSSION
Tables 3.2a and 3.2b (at the end of this chapter) summarise a vast amount of information regarding subjects in intervention studies. The studies constitute aver a million subject-years of experience conducted at a cost of billions of dollars. Has intervention to "improve" life-style increased life expectancy? The answer is clear: In not one of the 19 studies is there any beneficial effect. On the contrary, in 3 of them there was a significant reduction in life expectancy. Since the thrust of recent campaigns aimed at changing our life-style is the elimination of premature and unnecessary death, it is evident that such campaigns are founded upon a false premise, or at least fail to take into account the inescapable conclusion of these studies so that the exhortations are quite misleading and pointless. If anything, so-called improvements in our life-style are deleterious, certainly with respect to life expectancy. Could it be however that these subjects felt better even if they lived no longer? Were they "healthier" in a way not directly connected with mortality? Such a question is much harder to answer and is not the prime consideration in these trials, but the likely answer is no. I have two reasons for saying this. First, subjects in studies which involved drugs often experience unpleasant and unwelcome side effects of the drugs, as described earlier. Second, subjects in studies which required changes in diet, smoking and exercise habits may be assumed to have responded like most of us: we may change our diet, smoke less and exercise more if we believe it will improve our overall life expectancy or reduce our mortality from other causes but the change per se is rarely welcome. Dieters and ex-smokers are notorious recidivists. Exercisers may be an exception. Many people claim they require regular exercise for their well-being. This may be the case and indeed it is difficult to see how such a belief could be refuted. The sight of exhausted joggers cluttering lunch-time streets is common enough today in cities around the world. It would be interesting to know how many would persist if the orthodox medical view of the nineteenth century were to revive and they found themselves faced with public health campaigns warning that exercise was shortening their lives.
Even though none of these trials has found increased life expectancy with "improved life-style", it is worth summarising the resorts to which some of the researchers have been driven to make a case where none really exists:
- Change of statistical significance level (i.e., P-value)
- The Lipid Research Clinic's Coronary Primary Prevention Trial
- The Oslo Study
- The WHO Clofibrate Trial
- Change of trial endpoint
- The Lipid Research Clinic's Coronary Primary Prevention Trial
- Unsound use of a one-tailed statistical test
- The Lipid Research Clinic's Coronary Primary Prevention Trial
- Rejection of significant results
- The Lipid Research Clinic's Coronary Primary Prevention Trial
- The Whitehall Study
- The Anti-Coronary Club Program
- Sydney Diet-Heart Study
These exercises in scholarly gymnastics attempt to defend what cannot be proven from their material. This is an odd approach to science.
It needs to be emphasised, once again, that the subjects in the trials discussed here were essentially in good health and the results therefore apply to the healthy. The acutely ill must be considered separately. For example, someone with congenital hypercholesterolaemia may have a plasma cholesterol level many times greater than the population average and be threatened by terminal heart disease while still a teenager. Such a person may well require draconian treatment. That does not mean that the rest of us should also be subject to such treatment or any at all. For the healthy, intervention to "improve" life-style does not reduce the overall death rate nor deaths from particular causes and the only likely consequence is an increase in anxiety and the unnecessary elimination of some of life's pleasure.
CONCLUDING REMARKS
The noblest work of man is the rational interrogation of nature and the dispassionate analysis of nature's responses. That, or something less pompous, is how the average non-scientist might well define science. By implication the scientist is a cool observer of the universe, experimenting and ready to change his views to accommodate new data, his main goal being the pursuit of knowledge. Although there is some truth in such a definition, the practising scientist knows there is much more to his craft. Practical science is more like a competition in which the scientist attempts to outwit both nature and his fellow scientists and emerge as the winner of a great game. And to win the laurel scientists, whether great or slight, have throughout history been prepared to take the measures thought necessary. An extreme example is Sir Isaac Newton's use of grossly unethical tactics to show that he, and not Gottlieb Leibnitz, was the discoverer of the calculus. Newton's life is stained by his appalling treatment of his fellow scientists which surely reached its nadir with Leibnitz. Westfall (1976) sums up the wretched events:
As president of the Royal Society, he appointed an "impartial" committee to investigate the issue, secretly wrote the report officially published by the Society, and reviewed it anonymously in the Philosophical Transactions. Even Leibnitz's death could not allay Newton's wrath, and he continued to pursue the enemy beyond the grave. The battle with Leibnitz, the irrepressible need to efface the charge of dishonesty, dominated the final 25 years of Newton's life. It obtruded itself continually upon his consciousness. Almost any paper on any subject from these years is apt to be interrupted by a furious paragraph against the German philosopher, as he honed the instruments of his fury ever more keenly. In the end, only Newton's death ended his wrath.
Few may behave with such extremity as Newton but his behaviour was more like that of an average scientist than our postulated cool observer of the universe. It is not surprising that scientists should be so. Like others, they require sustenance and seek recognition, yet the only means of achieving these objects are their ideas and results, their intellectual property. Such property is only of worth if it is original and that is why so much of research is nagged by the question of priority. When scientists collaborate, as has been usual for many years, the question becomes one of relative contribution and for the same reason. These under-currents rarely come to the lay attention but when they do -- as with the publication of J.D. Watson's The Double Helix -- the public appear both surprised and amused by the discovery that scientists are hum.
A consequence of the need to win is the temptation to cheat. Just as an athlete might take drugs to win a race, so a scientist might change his observations (or invent them) to obtain a predicted conclusion. The founder of genetics, Mendel, is thought to have falsified his observations because they are almost too good to be true -- or likely. There have been several notorious examples of fraud during the last ten years and this has caused some alarm in the scientific community. By its very nature, fraud is difficult to prove but there is a natural concern about its incidence. Unfortunately, practical science necessarily involves what amounts to fraud. There can be few if any scientists who have not discarded a result because the experiment "went wrong". This is deliberate suppression of an observation but without such filtering, progress would stop. (Here I think may be found the distinction between the great scientist and the rest. All strive to order the universe so that the world becomes a place of regular patterns with predictable future events. Discordant, ugly results will naturally tend to be discarded or overlooked. The great observer can distinguish between an ugly false result and an ugly true result and bear substantially on the distinction. In T.H. Huxley's words, "God give me strength to face an ugly fact though it slay me".) The extent to which such filtering is permissible or even desirable very much depends on the particular instance and there can be no general answer.
So scientists' dispassionate judgement may fail them in ambitious defence of their intellectual property and most are so if only to a trivial degree. However, ambition does not appear adequate to account for the curious distortions of scientific data which have been described in earlier chapters. There is, for example, little to be gained by the successive re-drawings of Borkenstein's graph which relates blood alcohol and road accidents. Another explanation must be found. The solution may lie in a common thread which joins all the examples I have given and many more that could be given. In every example, scientific method and results have been used as a weapon to deter people from enjoying themselves. Science has been recruited to the cause of puritanism, the "haunting fear that someone, somewhere, may be happy" (H.L. Mencken). Medicine has throughout history been conscripted in the cause of puritanism: certain acts and activities have been proscribed as both immoral and unhealthy. Indeed, it was because of their immorality that such acts were harmful. Masturbation, for example, was contrary to natural law and so produced "masturbation insanity", a favourite illness of the Victorians (Buchan, 1818; Szasz, 1980). Food was always of particular interest. George Cheyne was an enormously popular 18th century physician whose reputation continued undiminished into the 19th century. In the many editions of his An Essay of Health and Long Life he expounded his view that the secret to a healthy, long life was an abstemious diet. This rested on his religious beliefs. God had shortened man's life after the deluge by the expedient of permitting him to eat meat, a food for which the human frame had not been designed (Cheyne, 1745: 93). God was:
obliged (that the Globe of the Earth might not, from the long lives of its inhabitants, become a Hell and a Habitation for incarnate Devils) to shorten their lives from 900 or 1,000 years, to 70. He wisely foresaw that animal food and artificial Liquors would naturally contribute towards this End; and indulged, or permitted, the Generation that was to start the Earth again after the Flood, the Use of these for Food; knowing that though it would shorten the Lives and plait a Scourge of Thorns for the Backs, of the Lazy and Voluptuous, it would be cautiously avoided by those who knew it was their Duty and Happiness to keep their Passions low, and their Appetites in subject.
With God beside him, Cheyne was able to preach his medical ideas to the public with great success. Vegetables constituted the prudent diet, although even vegetables were a little suspect since they might contain insects and other small animals. Luckily, Cheyne was able to avoid a completely nutrition-free diet:
But, besides what I have said, of Nature being quite altered and changed from what was originally intended, there is a great Difference between destroying and extinguishing an animal Life (which otherwise might subsist many Years) by Choice and Election to gratify our Appetites, and indulge Concupiscence; and the casual and unavoidable crushing of those who, perhaps otherwise, would die within the Day, or at most, the Year, and obtain but an inferior kind of Existence and Life at best.
Quite apart from his theological views, the absurdity of his argument today seems transparent. If animal food is harmful to the body it should be so whether it is eaten accidentally or deliberately. In spite of this and many other inanities, he achieved enormous success and was widely regarded as one of the greatest physicians of his day, both in his lifetime (1671-1744) and for a century later. Curiously, Cheyne was prone to obesity, at one time weighing 32 stone (204 kg) and scarcely able to walk.
These are not aberrant examples in the history of medicine: moralising by medicalising permeates the fabric of the discipline from Hippocrates to the present (although Hippocrates is a detached observer with little to say about morality compared with many of his successors) a view which has been eloquently developed by Szasz (1977). As recently as 1942, Price's textbook of medicine, still esteemed in its more recent editions, pronounced nasal catarrh to be due to "sexual excess and masturbation" (Price, 1942: 1085). It is not my purpose to here defend this thesis, except to suggest that doubters should simply browse through any pre-war textbook of medicine and see for themselves.
The reference to "pre-war textbooks" implies that there has been a change during the past 40 years. That is indeed the case. God is out of fashion and old-fashioned morality is no longer considered sufficient medical reason to interfere with diet, sexuality or any other aspect of human behaviour. The wowsers (13) have been obliged to look elsewhere for justification. They have found it in a new morality which was expressed in a work of fiction (Ligeia) by Edgar Allan Poe: "Man doth not yield himself to the angels nor unto death utterly, save only through the weakness of his feeble will".
Our ill-health and death are our own fault. If we lived properly, that is, if we lived as the wowsers and puritans think we should, then we would live forever, or at least a very long time. That is the tacit morality which underpins much of modem medicine. It is a scandal that so many people should die of cardio-vascular disease and cancer. (What should people die of?) It is not good enough that in Australia male life expectancy should be 72 years and female 78. The foundations of this secular morality are both shaky and changeable. The financial cost to the nation because of alleged premature death is sometimes mentioned. Sometimes it is the threat to others posed by the smokers or drinkers. In fact there is scarcely any substance to this new morality. Wowserism is self-sufficient and self-justified.
We live in an age of superstition, the worse for being promoted as an age of enlightenment. Medical and scientific vandals have hijacked the tools and results of science and prostituted them to their own ends. Secure in the knowledge that the great majority of a deceived populace believe them, they have untrammelled freedom to persecute oppressed minorities. It is time for change. Let those with an interest in public health and a sense of fair play examine the facts for themselves and draw their own conclusions.
MAKING THE NANNY STATE HONEST
One of the more notable features of the democratic state during the last twenty years has been the proliferation of campaigns designed to improve the "lifestyles" of its citizens. There have always been people keen to tell us about the alleged dangers of alcohol, tobacco, and of certain foods, but it is only in more recent times that the state, usually through the auspices of its public health departments, has seen fit to run sustained campaigns warning us about the dangers inherent in our lifestyles and how modification of those lifestyles can lead to longer and healthier lives. (14)
This relatively new development of the welfare state has been dubbed, both here and in Britain, the "Nanny state". (15) "Nanny" is admittedly a slighting tern designed to draw attention to certain features of the state's behaviour which many adults thought had been left behind in childhood. For example, it is explicitly paternalistic in its concern for individual well-being. For the sake of that well-being, Nanny utters blunt but sweeping claims that impress the message upon the mind. The various campaigns and messages emanating from public health departments around the country take it for granted that it is properly the state's concern to tell its citizens what is wrong with their "lifestyles" and that they ought to change the way they live. That the state does so with taxpayers' money goes without saying. No doubt many citizens simply accept the intrusion; perhaps they even heed some of the messages. Detractors find Nanny's proscriptions little more than a killjoy campaign; a species of old-fashioned, intrusive wowserism. Nanny's defenders naturally declare their interest to be no more than a concerted educational mission to enhance awareness and promote healthy living.
Narrowly conceived, the "Nanny state" refers only to those organs of the state proper which carry out the programmes of lifestyle enlightenment. Viewed more broadly, however, the "Nanny state" also includes those "private" individuals and organisations which aid and abet the state's works: (16) either by proffering advice (expert or otherwise) which can be incorporated into state policy or by acting as agents for spreading the word in their own campaigns. (17) The presence of these individuals, agencies, lobby groups and publicists in the field of health, together with their roles as advisers and supporters of state policy blur what otherwise might be a neat distinction between the "Nanny state" and "private" busybodies. Between them, however, we have been told, among other things, (18) to get more exercise, give up smoking, avoid certain sorts of foods (notably those said to contain cholesterol) and limit our alcoholic intake to a certain number of standard drinks per day.
The messages are reinforced by the medical profession and the popular press. Most GPs, surgeons and their professional organisations lend their weight to many of the claims made by the life-style campaigners, particularly those relating to tobacco. Journalists find easy copy repeating the claims about the latest danger to our well-being. The "lifestyle" supplements of the press often contain articles about the dangers of alcohol, smoking, and more recently, "passive smoking". Dietary "dangers", too, are an ever-popular topic -- perhaps because there is an almost limitless supply of potential threats to be discovered. Salt, sugar, butter, red meat, shellfish, cream, avocados, caffeine: each, in turn, is linked (via the latest scientific research) to some form of cancer or vascular disease and a new regime of healthy eating is recommended.
The ordinary citizen is thus bombarded on TV and radio and in papers and magazines with messages, some more authoritative than others, about his or her lifestyle, what is currently wrong with it, how he or she should change it. No doubt many of the more popular, dietary recommendations are taken with a grain of salt, if for no other reasons than the periodic recantations that take place and the sheer strain that would be imposed upon life (let alone its style) if every possible recommendation were to be heeded. The more authoritative messages -- those delivered under the reproving eye of the family physician, those which stem from various groups and lobbies with impressive names and credentials, and those presented by health ministers and public health departments, often by means of campaigns replete with media launches, glossy brochures, toolkits, workshops and bumper stickers -- might be presumed to have a more penetrating and lasting effect.
Two relatively unquestioned assumptions underpin Nanny's actions. First, it is assumed that the messages that Nanny delivers are soundly based on the best available scientific evidence. Second, it is seldom questioned whether it is proper for Nanny to obtrude into the lives of citizens in the way she does.
Most of my account challenges the first assumption. It questions the conclusions that Nanny and her scientific advisers have drawn from the available scientific literature as it bears upon certain matters of health. In particular, Dr Johnstone challenges the oft made claims that link "passive" smoking to lung cancer and the assertion that various modifications to lifestyle (involving diet, smoking, and exercise, for example) have beneficial results in terms of preventing premature death. It is these claims, among others, (19) repeated by health authorities around the world, upon which the state makes its pronouncements and upon which it campaigns. Given my findings, however, one is forced to conclude that the evidential base for many of Nanny's pronouncements is so weak that the campaigns Nanny has conducted -- in particular those which advocate lifestyle modification -- have constituted little more than a waste of time and taxpayers' money.
At first sight this conclusion seems barely credible. So accustomed are we to hearing the mutually supporting claims of experts around the world that, for example, unhealthy lifestyles are the big killers and that lifestyle modification would prevent many premature deaths, that to question them seems heresy if not treason. But the charge goes further than the simple claim that Nanny is wrong (for even she can make mistakes). Somewhere in the web that links research with advice and policy making there has been more made than a simple mistake. Rather, the conclusions presented in this paper challenge the integrity of Nanny's advice. (20)
The failures that have occurred have taken place at a number of levels. Sometimes, it seems, individual scientists have been careless with their results, or have not properly acknowledged their own errors, or worse, have failed to maintain the protocols that ought to underpin scientific research. All too frequently, it appears, they draw conclusions which are not supported by their own evidence.
Shocking as it may seem to many on the outside, there has long been evidence that, despite an array of institutional and prudential checks within the scientific enterprise for exposing error, improprieties do occur in the scientific world. These range from the relatively rare cases of fraud to the more common instances of simple carelessness, to flawed experimental design or even idiosyncratic interpretation that is not really supported by the weight of the evidence. Just how frequently different forms of impropriety do occur and how in fact the institutional checks have been by-passed are fiercely contested points, not yet clearly resolved. But the trend is worrying. (21) Of course, none of this implies that all, or even most, scientists are dishonest -- only some and probably not many. But it is as well to be aware that there is an increasing concern within the scientific community that the mechanisms for exposing error (whether deliberate or not) are not doing their job as well as they might. Nor is there any harm in reminding ourselves that, white lab coats aside, scientists are in many ways very much like other people: often moved by the same mixture of base and pure considerations and subject to the same human frailties.
Concerns about the detection and exposure of error and impropriety apply to biomedical research as well. As the recent literature shows, medical and biological research is susceptible to fudging. (22) This might not happen very often, but the temptation remains strong because success, or apparent success, leads to funding and fame. The temptation to give governments and state bodies what they wish to hear, though it might not involve dishonesty, is quite likely to warp judgement and scientific objectivity. This means that studies such as those cited in the main work ought to be subjected to very careful examination and consideration before their findings are regarded as established.
On other occasions and at a different level, it is the "experts" -- be they individuals or authoritative advisory bodies -- who have failed to make a balanced and comprehensive assessment of the available evidence (purged of its erroneous or dubious findings). One of the functions of such authoritative bodies is to supply advice to others who lack either the time or the competence to assess the scientific evidence for themselves, Yet in light of the evidence presented in this paper, I am forced to conclude that they either have not read the available scientific literature; have read it, but consistently misunderstood it; or have simply ignored those findings which do not chime in with orthodox belief. None of these alternatives sits well with the trust placed in experts.
Wedded to these is another abuse of trust: that between state and citizen. Again, we appear to be faced with alternatives which impugn either Nanny's competence or her honesty. If we are to be burdened with Nanny's constant reminders about what is good for our health and if we, as citizens, are expected to fund them under the guise of "education" campaigns, then it is surely incumbent upon her to take care that what she says is accurate, or at least accurate within reasonable limits. Approve of her badgering or not, one thing that ordinary citizens might trust her to do is get the story right. In the light of my findings, it seems clear that on several occasions she has not. If there is something like a "duty of care" which attaches to those who would offer professional advice to their clients that they make reasonable efforts to ensure that their advice is sound, then Nanny has failed to meet it. (23) Given that, for example, none of the intervention trials which I cited showed any connection between intervention and increased life expectancy, one wonders how it is possible that the state could persist with campaigns involving some of the same forms of intervention. Why doesn't Nanny make sure that the results justify her chiding before she spends our money on telling us to be good? At its worst it is quite possible for Nanny, if she is careless with the facts, to promulgate biased and misleading information and the nursery will not trust her.
As for the explanation for these failures -- perhaps we will only find out when we see the responses elicited by the evidence and arguments in the preceding essay. I place the onus on those responsible for advising and implementing health policy to explain their failure to note the weaknesses in some of the evidence they have hitherto depended upon, their willingness to ignore large bodies of accessible evidence which conflict with the health images of the age, and their endorsement of campaigns for which there is little or no supporting evidence. Justification should be an interesting exercise.
* * *
Just as interesting, but from a quite different point of view, are the broader political considerations that surround the whole Nanny enterprise. Though they are only peripheral to my aims in this paper, this seems as useful a place as any to raise and discuss them.
Capturing that which is questionable about Nanny's activities is not as easy as it might at first seem. Part of the reason for this is that even those who might take offence at the state's paternalistic zeal will sometimes admit that, on occasions, it can sometimes get the story right and that under some circumstances it can therefore do some justifiable good. The other reason is that, questions of content aside, a good deal that is questionable lies in the tone and the style of Nanny's behaviour -- particularly with the lifestyle campaigns.
Recognising this, let us make a number of assumptions which will help us to determine how a liberal state might reasonably behave towards its citizens, given that it is, after all, going to enter into the realm of lifestyle education. Thus, let us assume, for the moment, (24) that Nanny sometimes does get the scientific story right and gets it right sufficiently often to be trustworthy. Let us further assume that some pieces of information are public goods of the sort that are liable to be undersupplied in a free market (because it is impractical to exclude people, who if they could be excluded would pay for the information, from obtaining the pieces of information once they become known) and that the information gleaned from research about lifestyle and health is just such a good. Finally, let us assume that the state considers its citizens sufficiently rational and responsible to make lifestyle decisions for themselves once they have obtained the relevant information.
The assumptions are neither unreasonable, nor in the light of practical considerations, unrealistic. The first, as we have already seen, is crucial to the whole Nanny enterprise. If the information supplied is not accurate or not accurate often enough to inspire confidence, then the campaigns lose their raison d'etre.
The second, of course, might be challenged by those of a libertarian persuasion who perceive the actions of the Nanny state as little more than theft of my money in order to give you information about the damage you might be doing to your health. Unlike public sanitation or information about communicable diseases, so the argument might continue, the interests or rights of third parties are not at stake. The state, therefore, has no reason to intervene. Further, the libertarian might well counter that the markets for such information could be improved (probably by means of improved intellectual property rights) and that the quota of misinformation supplied by the state is so great that even an imperfect market might be a better alternative. Both claims may be true -- although it is still arguable whether the market for information gained from research could ever overcome the difficulty posed by the need for speedy public exposure of research findings, a need which, hitherto, has formed an integral part of scientific activity. Whatever the possibilities for improved markets, the point of the assumption is again heuristic: that is, it is posited in order to ascertain what might be expected of a state that in all likelihood is going to intervene anyway.
The third assumption is, in part (but only in part) tacitly acknowledged by the lifestyle messages themselves. Although the democratic state has other means at its disposal for limiting the incidence of certain practices its officers believe pernicious -- for example, by applying taxes of various sorts, or restricting and regulating advertising for certain products -- it has not yet declared the consumption of say, tobacco or alcohol to be illegal. (25) Rather, the implicit logic of the Nanny state's messages seems to be: "listen to the facts; once you are acquainted with them you can make an informed decision about whether to modify your lifestyle". For all the advertising slickness and the exhortation to reform that surrounds the "educational" content, it is obvious from the campaigns themselves that final decisions in such matters rest with the individual citizen and not with the state. Although it is probably this third assumption that Nanny is least likely to concede, not to accept it implies a strange position which is both illiberal and anti-democratic. For if adults are to be trusted to participate in the political life of the state -- which includes voting for the officers of the state -- then surely they an be trusted to manage their private affairs once they have been informed.
Armed with these assumptions let us see what follows from them and how the results compare with typical Nanny activities.
First, a reasonable attempt to provide information about lifestyle would restrict itself to just that. If there is a market deficiency, it is in the realm of information generated by medical, biological and epidemiological research. Advice and exhortation against doing X or for taking up Y are, on my assumptions, quite out of place. The state has a limited paternalistic role to ensure that its citizens are informed about X and Y -- nothing more. It should, therefore, eschew any inclination to "take sides" in the argument about lifestyle modification.
Second, the state must present a balanced and impartial account of the facts about say, longevity and X, based upon the available scientific literature. Thus, if the evidence is inconclusive, if for example, only 60 per cent of the studies about X and health point to one conclusion and the other 40 per cent point elsewhere, it should acknowledge those differences. Likewise, it should further acknowledge disputes within the scientific community about say, the reliability of a particular finding or the appropriateness of a certain methodology. To gloss over such differences for the sake of some other end (believed more valuable by the officers of the state) would do injustice to both the first assumption (truth) and the third (individual responsibility).
Third, it follows that if the state is to provide accurate information, it would need to ensure that it was well-informed and that it had active mechanisms to expose scientific error or outdated information contained in its own messages. Only by doing so could it hope to deal effectively with excusable mistakes, such scientific impropriety as exists and with the dangers posed by relying upon a small number of advisers. More, it would need to demonstrate a willingness to admit error in public -- to recall defective campaigns, as it were. Without such willingness it is unlikely the state could build the long-term trust necessary for its success.
Finally, the state would need to carefully consider what means it would employ to promote its informational messages. Although the question of method is not as important as that of content, the two are related. The salient method of delivery used hitherto has been the mass advertising campaign on television and in the print media. Most, if not all, advertising makes some use of emotive, non-rational techniques in order to "get the message across". For the sake of "effectiveness" it also tends to simplify the message that is being delivered. If the modem advert is to be the medium for the message, then the state will need to exercise caution to ensure that "puffery" and simplification do not threaten the informational point of its enterprise -- by, for example, allowing the puffery to obscure or distort the message, or by allowing simplification to slide into oversimplification. (26) In other words, the requirements for a balanced account of the truth together with the educational point of the state's activities both serve as limits to the use of emotive techniques in conveying the message. Matters are complicated, however, when judgements about the seriousness of the message or the urgency of its dissemination arise. It is possible to imagine cases where clearcut evidence about some hitherto unsuspected relationship between say, X and premature death, might warrant not only a simple, blunt message, but an eye-catching or "shocking" mode of delivery as well. But even in these cases the requirements of truth still hold. Moreover, failure to reserve the use of "emotive" campaigns for the most urgent or serious cases (backed by the evidence of course) runs the risk of being counterproductive.
In summary, then: to ensure the point of the state's activities and the integrity of the informational content of its messages, the state should avoid the use of those techniques of dissemination that are likely to obscure, distort or oversimplify the message. If it must use emotive, non-rational means, they should be reserved for cases where the scientific evidence is very strong and the need to inform serious and urgent.
All in all, then, there are five requirements that flow from the adoption of my original assumptions. A state bound by those assumptions, I have argued, would be required to:
- limit its activities to the provision of information;
- present balanced information that encompasses divergent findings and acknowledges the existence of scientific differences;
- institute its own means for ensuring that the information it supplies is up-to-date and accurate;
- be prepared to acknowledge error publicly;
- avoid the use of emotive techniques in the provision of information.
From what we have already considered it seems clear that Nanny does not shape up well when compared with the foregoing ideals. First, it is clear that most of Nanny's campaigns attempt more than the provision of information. Although there are putative facts provided in most of the campaigns (e.g. every year so many thousands of Australians will die from X, evidence indicates that if you stop X, then you'll live longer, etc), there is nearly always some sort of appeal to quit X, or limit X, or take up Y, prominently attached to that information. It is precisely these exhortations, which constitute the unwarranted paternalistic element in the Nanny enterprise, that need to be excised from the campaigns. Any attempt to justify such exhortation on the grounds that, "we know best", or "people can't be trusted to make the right decisions" is, therefore, unacceptable. Such overt paternalism runs counter to the assumption about the role of the individual citizen as a responsible agent and leads to that curious anti-democratic position noted earlier. If such claims are to be made at all plausible then they require an independent argument. Knowing more about X, of itself, says nothing about the desirability of giving up X or, indeed, for taking it up. If Nanny is to justify her moralising she will have to do so on other grounds. The most obvious candidate is an argument that points to the effects of X on parties other than the agent who is the target of the lifestyle campaign.
Second, if my conclusions are sound, then Nanny has not prodded balanced and comprehensive information to her citizens. But even if he should, in turn, be shown to be wrong, we should at least expect more of Nanny in the way she conducts herself: more caution, more in the way of explanations, more open acknowledgement, with Oscar Wilde, that "the truth is rarely pure, and never simple". No doubt some of Nanny's agents will be dismayed at such a suggestion: blunt generalisations backed by unpleasant images and catchy jingles are more fun to produce than less ambitious, more informative and patient exercises in education. Yet to do otherwise invites either a disrespect for a balanced account of the truth or an unwillingness to allow adults to make up their m minds. (27)
It is sometimes claimed that slick advertising by, say, junk-food and tobacco companies justifies Nanny's calling the Bunyip at the bottom of the garden to her aid. This is saying that half-truth must be matched with half-truth: that the state not only may but should match the lower standards of openness and truth which are legally (although perhaps not morally) acceptable among its citizens. That argument will not do: the state is not only not disciplined by competition but has special responsibilities for, and poses special dangers to, the citizen which mean that exceptional standards of truth and openness should be required of it.
Whether Nanny has the means to ensure that she is well-informed and, in turn, possesses the mechanisms and the willingness to publicly acknowledge error (should it be revealed) will probably best be determined by the way she responds to those who challenge accepted biomedical belief -- of whom there is a growing number. In the United States, for example, there has been a recent controversy about the alleged dangers of cholesterol prompted by Thomas J. Moore's book, Heart Failure, which, among other things, questions the conclusions drawn from the massive and expensive intervention trials that have been conducted there. Writing about the National Cholesterol Education Program and the coalition of interests that supported it (which included cholesterol researchers, the heart institute, the American Medical Association and drug companies) Moore comments:
There is no reason to doubt the honesty, sincerity, and expertise of any of these men, or a dozen others with multiple roles in the cholesterol establishment. The terrible danger of such a closed loop is that important and basic questions are neither asked nor answered. And that is exactly the problem that occurred when a panel of lipid researchers and heart institute officials designed the National Cholesterol Education program. (28)
Whether we can afford to be as sanguine as Moore about the honesty and competence of Nanny and her agents is a moot point. What is important to note here is the possibility of the "closed loop" of advice and policy making which prevents the examination of important questions. Such loops make it extremely difficult for external critics to gain a hearing -- especially when those inside the circle have the sanction of the state (and the authority that goes with it). (29)
Peter D. Finch makes similar points about the lack of balance and comprehensiveness in some health promotion campaigns and the difficulties faced by those who dissent from them. (30) Taking the recent campaigns against passive smoking as an example, Finch points to the possible dangers arising from the application of the so-called "Lalonde Doctrine" (after Marc Lalonde, a former Canadian Minister of National Health and Welfare). Lalonde proclaimed that public health messages must be presented even if the scientific evidence was incomplete or divided, that these messages must be "loud, clear and unequivocal", and that this therefore justified the suppression of the "ifs", "buts", and "maybes" that abound in science. The doctrine, Finch argues, not only involves distortions of the truth and a general politicisation of health promotion, but presents formidable barriers to dissent as well. Like Moore, Finch has few doubts that the motivation for shearing the qualifications from the evidence and its interpretations is a straightforward desire on the part of health promoters to improve our health. One unfortunate and worrying consequence of this desire to "do something", however, is that it generates a dogmatic body of belief, the content of which is more concerned with successful behavioural modification than with the strengths of the supporting scientific evidence and argument. In such a context, anyone wishing to take issue with biomedical orthodoxy -- that is, to assert the "ifs" and "buts", or to question whether the evidence sufficiently supports the conclusions drawn -- is considered at best unreasonable and at worst malicious. "Dissent", argues Finch, "is no longer seen as part of the normal process of assessing evidence, but as an attempt to thwart the public policy of behaviour modification that has been based upon it". (31) The recent campaigns waged by anti-smoking lobbies against "passive smoking", Finch suggests, provide examples of the way in which "ifs" and "buts" have been suppressed and the way "health promoters edit the facts to match their convictions". (32) He concludes, in part:
... scientific dissent has sometimes been dismissed as eccentric opposition to desirable health policy, and the public has been denied knowledge of the normal caveats of scientific enquiry.
It is in the public interest to monitor these consequences of the Lalonde doctrine and to make it known that the dicta of health promoters are sometimes designed to influence both public and governments by the deliberate suppression of anything that might suggest that the bases of their proposals are less than certain. (33)
In short, both Moore and Finch remind us that if we want the truth, then there must be some place for dissent. Rather than placing formidable barriers to dissent and disagreement, we should instead treat them seriously. This does not mean that the "dissenters" will always, or even often, be correct. But it does mean that the sorts of questions that are likely to tease out the truth will stand a better chance of being asked, with consequent gains for public health policy.
A "reformed" state would therefore behave quite differently from the one we witness now. It would be less paternalistic, more open, more critically directed to its own efforts and more trusting of those it is supposed to serve. Stripped of its exhortative capacities, it would have no need to side with pro- or anti-cases or the groups which support them. Private protagonists and antagonists could safely be left to argue about the "good life for man" by themselves.
There would be other benefits as well. For a start, a state dedicated to providing reliable information would be less likely than the current Nanny state to run the risk of not being believed. As mentioned before, the state not only has to get the story right, but get it right often enough to be trustworthy. If it succeeds in getting the story right, even if that means that its messages are less blunt and sweeping than is currently the case, if it can demonstrate a creditable track record in such matters, and if, even in the light of acknowledged error, it can claim that it did its level best, then it is more likely to be believed when something serious arises. In short, people are quick to distrust those who cry "wolf" or who otherwise show themselves to be careless with the truth. Moreover, a reputation for being untrustworthy in one field can quickly call into question reliability in more important areas of the state's relations with its citizens.
A further benefit, at least to those of libertarian views, would be the acknowledgement, by the state, that there were limits to its intrusiveness in the lives of its citizens. As mentioned before, there are ways in which the state may intervene other than providing information -- among them prohibition, taxation, and regulation of advertising -- the use of any of which involves some loss of liberty for those who are subject to them. There is, of course, no telling what future research may reveal about some currently accepted "innocuous" practice and say, longevity, or about the health of second parties. There is, therefore, no apparent limit to the range of practices about which the state may choose to inform its citizens or about which it might contemplate even "sterner" forms of intervention. But it would be limited in the manner in which it could justify its intervention. What it cannot do, if it were limited by the principles mentioned above, is build up a constituency for say, prohibition of X, by means of constant exhortation to give up X. In other words, if there were to be a case for any form of intervention stronger than providing information, then it would have to be argued on the evidence about damage done to the rights of other parties -- subject to the same strictures about "getting the story right" that hold for lifestyle education. Dispossessed of any paternalistic arguments stronger than information provision, and robbed thereby of any propaganda advantage that stems from them, the state would have to argue its case for intervention on the evidence and upon the rights of all parties affected.
One further and allied point might be mentioned. One of the achievements of the modern liberal state is its promotion and defence of the principle of toleration -- that is, for living with (though not necessarily approving of) the expression of quite diverse views about all manner of things (including, notably, quite diverse religious beliefs) and of ways of life founded upon them. Without wishing to draw too long a bow, the Nanny state, as she currently conducts herself, poses some threat to that principle. For example, smokers, (34) in particular, have increasingly been subject to social pressure, isolation and sometimes, abuse -- and this long before the so-called "passive smoking" debate began. Although the concern here may seem minor, it is in the nature of toleration that it cuts many ways and short of very strong evidence that someone else's private vice poses significant harm to oneself, intolerance of this nature prompts its reciprocation in other forms. Even if we assume that this sort of consequence was not intended or foreseen, Nanny's "authoritative" exhortations cannot but help promote such divisiveness, and so long as she continues to exhort, rather than inform, she will continue to promote it.
* * *
Whether the Nanny state can or will be reformed remains to be seen. Some of her critics, in Australia and Britain, have already raised some of the same issues discussed here -- for example, the unwarranted paternalism, the threats to liberty and toleration, and the dubious tactics employed to deliver the messages. Those critics have gone further than this paper is prepared to go and have claimed to detect the motives that underlie Nanny's zeal: for example, a New Class puritanical morality in one case; a totalitarian prompting in another. (35) It is true that the prospects for reform will depend to a great extent upon what it is that does motivate Nanny's key agents and whether they have, for example, a concern for truth and for the rights and responsibilities of individual citizens. But rather than speculate about such matters, we have been content to document the misuse of science that has occurred and demonstrate the questionable nature of the premises upon which the Nanny state is built.
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ENDNOTES
9. There is considerable variation in terminology. Coronary heart disease (CHD) atherosclerotic heart disease (ASHB) and ischaemic heart disease (IHD) as well as other terms have been used according to investigator preference. See Dawber (1980) and National Heart Foundation (1967) for a discussion of this point. Serum cholesterol, plasma cholesterol and unspecified or "blood" cholesterol are terms which have all been used in the literature but the difference between serum and plasma levels is small and the terms are here used interchangeably according to author preference. Plasma levels are about 3% higher than serum (Myant, 1981).
10. Rook's 1954 paper and some of those discussed below are reprinted in Polednak, (1979).
11. P < 0.01 means that the probability of being wrong is less than 1 in 100; P < 0.05 means it is less than 1 in 20.
12. An endpoint is an awaited event. For example, in a trial to determine whether a treated group will live longer than an untreated group, the end point is death.
13. "A wowser is one who wants to compel everybody else ... to do whatever he thinks right, and abstain from everything he thinks wrong": OEDictionary, citing Nation.
14. There was, however, a time when state intervention to save us from eternal damnation was neatly universal.
15. It is reputed that the term "Nanny State" was first coined by Bernard Levin.
16. For example, in Australia, the various bodies devoted to educating the public and offering policy advice about cardiovascular disease and cancer, some professional associations of physicians and surgeons, and increasing, the government-sponsored "peak councils" which claim to represent the interests of consumers, environmentalists, those with a concern for public health, etc. For an account of these last-mentioned groups, their nature, membership, activities and funding, together with an assessment of the dangers they pose to the democratic process and business activity, see Bob Browning, The Network, especially pages 3 to 55 and 145 to 186.
17. This is not confined to the realms of health. Modem democratic governments are quite happy to consult specialist interests and lobby group in all manner of policy formation and implementation. Lobbies and special interests are often more than happy to oblige. Modern public choice theory explains a good deal of the phenomenon.
18. Australian campaigns which have some connection with the subject matter of this paper that have been conducted at bath State and Federal levels include "Life. Be In It" (exercise); "Quit" (smoking); "DrinkSafe" (drinking) and a number of "healthy food" crusades. (The names of the campaigns sometimes vary from State to State.) Other "lifestyle"-improving exercises have dealt with safe sex and drug abuse. It remains to be seen whether currently fashionable "green" concerns will generate "EnviroHealth" campaigns.
19. The connection between "direct" (as distinct from "passive") smoking and disease is not examined here. Those interested in the matter are referred to H.J. Eysenck's article, "Smoking and Health" in Robert Tollison (ed.), Smoking and Society, pages 17-38, in which Eysenck carefully examines the evidence connecting smoking and disease, and points to some methodological weaknesses of the orthodox position. For some interesting arguments about how the commonly-quoted statistics concerning smoking and health have been selectively presented or interpreted, see Peter D. Finch, "The Health Effects of Smoking Misreading the Evidence".
20. Again, the connections between the original researchers, the expert bodies, the high-profile lobby groups and the officers of the state make it difficult to ascribe responsibility to the Nanny state narrowly conceived -- hence the note of caution.
21. For an entertaining introduction to all sorts of scientific quackery see Martin Gardner, Fads and Fallacies in the Name of Science. For a spectacular and tragic example of scientific fraud, see A. Koestler, The Case of the Midwife Toad. For a wider sweep which includes both historical and more recent episodes, together with a critical discussion of the extent of scientific impropriety and the problems of its detection, there are two excellent works: William Broad and Nicholas Wade, Betrayers of the Truth; and Alexander Kohn, False Prophets.
22. For more recent examples, see Broad and Wade, op. cit. and Kohn, op. cit. For a startling revelation of the extent of scientific impropriety in the USA (notably in the realm of biomedical research) and the difficulties in detecting and publicising it, see the four US House of Representatives Committee Reports on fraud in science: Fraud in Biomedical Research, Scientific Fraud and Misconduct and the Federal Response, Fraud in NIH Grant Programs, and Federal Response to Misconduct in Science: Are Conflicts of Interest Hazardous to Our Health? listed in the bibliography (under "U.S. Congress").
23. All the more important if, as I assert, (Chapter 3) some of the intervention trials (upon which lifestyle modifications are recommended) reveal a significant reduction in life expectancy.
24. But only for the moment. Nothing said in this section is intended to question my findings. The assumption is made on heuristic grounds only.
25. The United States' experiment with Prohibition being the notable exception.
26. For a critical account of the different mass advertising methods used in some recent British government campaigns, the problems of balance and fairness involved, and the effectiveness of such campaigns in achieving government aims, see Digby Anderson, The Megaphone Solution: Government attempts to cure social problems with mass media campaigns.
27. That is, treat them like children. But why? Overly simple presentations are appropriate for children (young ones at least), but surely not for adults. Given sufficient incentive (and personal health is a fairly strong incentive for most of us) people will make the effort to understand the unfamiliar or consult someone else whose judgement they trust to advise them.
28. Thomas J. Moore, Heart Failure, page 70. (Emphasis added.)
29. A minor example from my experience with a senior government health educator: I challenged him, in writing, to make good his public claim that the evidence linking passive smoking with lung cancer was "very strong". I suggested that of the (then) 15 studies in the scientific literature, 13 failed to find any statistically significant correlation, and that the other 2 had been roundly criticised by the scientific community. His substantive response: "I am content to rely on the conclusions of the National Health and Medical Research Council, World Health Organisation, and the US Surgeon General". Busy public servants are, of course, as much entitled to appeal to authority as the rest of us, but one wonders about the intellectual curiosity of those responsible for health education when they respond in this way.
30. Peter D. Finch, "The Lalonde Declaration in Action: The Campaign Against Passive Smoking", Policy, Winter 1990, 6 (2), pages 22-25.
31. Ibid., page 23.
32. Ibid., page 24 and page 25.
33. Ibid., page 25. In a subsequent article, "The Health Effects of Smoking: Misreading the Evidence", in Policy, Spring 1990, pages 22-25, Finch argues that some members of the anti-smoking lobby have distorted the evidence about "active smoking" as well -- either by ignoring studies that do not support their position or by interpreting the available evidence in one-sided ways.
34. And not just smokers. There is good, if anecdotal evidence, that some obese people have suffered public taunts and humiliation simply because they are overweight -- and not just in the school playground. See "Having a thin time of it?", The Times, 18 December 1989, in which a New York Times commentator is reported to have proposed "that we should 'get tough with fat people' as a means of saving their lives. She proposed a fat tax, and roping off areas in restaurants for fat diners in the same way as for smokers".
35. See, for example, Gerard Henderson, "In loathing of the Nanny State", The Weekend Australian, April 9-10, 1988, Bernard Levin, "The wowsers are charging our glasses", The Australian, February 8, 1988 [reprinted from The Times] and Bernard Levin, "Time for a heartfelt toast to this scourge of the wowsers", The Times, 11 August 1990. For less journalistic treatments of narrower topics, see Digby Anderson (ed.), A Diet of Reason: Sense and Nonsense in the Healthy Eating Debate, and Digby Anderson, The Megaphone Solution.
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