Global cancer prevention: an important pathway to global health and development.

Cancer is a leading global cause of death and disability, responsible for approximately 7.6 million deaths each year. Around one-third of cancers are attributable to a small number of preventable risk factors - including smoking and the harmful consumption of alcohol - for which effective interventions exist at the population level. Despite this, progress in global cancer control has been slow and patchy, largely due to the weak and fragmented nature of both the global and national responses. This has been exacerbated by the economic crisis and the tendency for other challenges involving food, energy security and climate change to overshadow cancer on the global policy agenda. This paper reviews the global burden of cancer, and summarizes knowledge about effective interventions. Responding to the global challenge of cancer requires a comprehensive and integrated approach that includes legislation and regulation. A re-invigorated approach to global cancer prevention, within the broader context of non-communicable disease prevention, is an important pathway to global health and development.

Explanation for the decline in coronary heart disease mortality rates in Auckland, New Zealand, between 1982 and 1993.

BACKGROUND: We sought to determine how much of the recent, substantial fall in coronary heart disease (CHD) mortality rates in New Zealand can be attributed to "evidence-based" medical and surgical treatments and how much can be attributed to cardiovascular risk factor reductions. METHODS AND RESULTS: A cell-based mortality model was developed and refined. This model combined (1) the published effectiveness of cardiological treatments and risk factor reductions with (2) data on all medical and surgical treatments administered to all CHD patients and (3) trends in population cardiovascular risk factors (principally smoking, cholesterol, and hypertension) from 1982 to 1993 in Auckland, New Zealand (population 996 000). Between 1982 and 1993, CHD mortality rates fell by 23.6%, with 671 fewer CHD deaths than expected from baseline mortality rates in 1982. Forty-six percent of this fall was attributed to treatments (acute myocardial infarction 12%, secondary prevention 12%, hypertension 7%, heart failure 6%, and angina 9%), and 54% was attributed to risk factor reductions (smoking 30%, cholesterol 12%, population blood pressure 8%, and other, unidentified factors 4%). These proportions remained relatively consistent after a robust sensitivity analysis. CONCLUSIONS: Approximately half the CHD mortality rate fall in Auckland, New Zealand, was attributed to medical therapies, and approximately half was attributed to reductions in major risk factors. These findings emphasize the importance of a comprehensive strategy that maximizes the population coverage of effective treatments and actively promotes a prevention program, particularly for smoking, diet, and blood pressure reduction.

Globalisation and the prevention and control of non-communicable disease: the neglected chronic diseases of adults.

The growing global burden of non-communicable diseases in poor countries and poor populations has been neglected by policy makers, major multilateral and bilateral aid donors, and academics. Despite strong evidence for the magnitude of this burden, the preventability of its causes, and the threat it poses to already strained health care systems, national and global actions have been inadequate. Globalisation is an important determinant of non-communicable disease epidemics since it has direct effects on risks to populations and indirect effects on national economies and health systems. The globalisation of the production and marketing campaigns of the tobacco and alcohol industries exemplify the challenges to policy makers and public health practitioners. A full range of policy responses is required from government and non-governmental agencies; unfortunately the capacity and resources for this response are insufficient, and governments need to respond appropriately. The progress made in controlling the tobacco industry is a modest cause for optimism.

Increased treatment of hypertension does not explain the decline in stroke mortality in the United States, 1970-1980.

The steady decline in mortality from stroke in the United States accelerated markedly in the 1970s. It has been widely assumed that an increase in the rate of treatment of hypertension is the most likely explanation for this major public health achievement. An analysis of available information, however, suggests that improvements in the community control of hypertension in the United States in the period 1970-1980 have contributed in only a minor way. There were 45,357 fewer deaths from stroke in 1980 among those aged 35-74 years than might have been expected if the death rates had stayed the same as in 1970. Data from the National Health and Nutrition Surveys indicate that six million more people received antihypertensive medication in 1980 than in 1970. Results from a pooled analysis of randomized controlled trials of the treatment of hypertension suggest that between 6% and 16% of the reduction in stroke mortality was due to the increased treatment of hypertension. Epidemiological observations indicate that between 16% and 25% of the overall decline in stroke mortality can be attributed to the treatment of hypertension, suggesting that clinical trials probably underestimate the community-wide benefits of treatment. These results also suggest that at least three quarters of the decline in stroke mortality in the United States in the period 1970-1980 is due to factors other than antihypertensive treatment.

Factors related to tracking of blood pressure in children. U.S. National Center for Health Statistics Health Examination Surveys Cycles II and III.

In this paper we examine the relationship of growth, obesity, and the degree of sexual and bone maturation to blood pressure in a U.S. national probability sample of 2165 children examined by the U.S. National Center for Health Statistics on two occasions, approximately 4 years apart. Subjects who maintained, increased, or decreased their peer rank order of blood pressure are described. Children who maintained their blood pressure in the upper quintile were taller, heavier, more obese, had greater bone age, greater numbers of permanent teeth, and were more sexually mature than their peers, while those maintaining their blood pressure in the lowest quintile of blood pressure were shorter, lighter, less obese, had lesser bone age, fewer permanent teeth, and were less sexually mature. Subjects whose blood pressures were initially in the lowest four quintiles and then rose to the top quintile were also taller, heavier, more obese, and had greater bone age, while those with blood pressures falling to the lowest quintile from the upper four quintiles were shorter, lighter, less obese, and had lesser bone age. Thus, the level at which blood pressure tracks during childhood is related to growth, obesity, and to the degree of maturation acquired. In addition, children whose blood pressures are rising or falling in relation to their peers have body growth and maturation characteristics similar to those who maintain their rank order high or low respectively.

The effect of exercise episode duration on blood pressure.

OBJECTIVE: To investigate the effect on blood pressure for 10-min compared with 40-min episodes of physical activity for 4 days. DESIGN AND METHODS: The design used a randomized crossover trial of two exercise episode durations, involving 17 subjects, which were performed in a university setting. The intervention was exercise on a stationary bicycle for four consecutive days, at 50% of maximal oxygen uptake (determined by heart rate), for episode durations of 10 or 40 min. A rest period of 10 days followed before exercise for the alternative duration was performed. The main outcome measure was blinded assessment of blood pressure 24 h after the last exercise episode. RESULTS: Significant reductions were found in systolic and diastolic blood pressure after 4 days of 40 min but not after 4 days of 10 min stationary cycling. The reduction in blood pressure was significant for both systolic and diastolic blood pressure for 4 days of 40 min of exercise episodes. CONCLUSION: Exercise of moderate intensity on a stationary bicycle for 10 min for 4 days is not effective in lowering blood pressure in comparison with the same exercise for 40 min for 4 days. The experimental design employed in the present study has potential for monitoring the effects of exercise on blood pressure.

Does physical activity lower blood pressure: a critical review of the clinical trials.

This review critically appraises 22 recent articles of trials of physical activity, as a means of reducing blood pressure. The quality of the literature remains poor and of the 13 controlled trials of habitual activity only one did not have a major design fault. Overall, blood pressure was reduced by physical activity in both hypertensive and normotensive persons. This effect was independent of weight loss and in some studies blood pressure reduction occurred in the presence of weight gain. The average reduction in the better designed studies was approximately 6-7 mmHg for both systolic and diastolic blood pressure which compares favourably with studies of pharmacological treatment. The better designed studies reported smaller reductions than studies with poorer design. All activities, including circuit weight training, lowered blood pressure and daily activity produced greater blood pressure reduction than when performed three times per week. It is concluded that physical activity has an independent capacity to lower blood pressure.

International trends in asthma mortality: 1970 to 1985.

Recent international trends in asthma mortality among people aged five to 34 years were examined as a follow-up to an epidemic of asthma deaths in the late 1970s which appeared to be confined to New Zealand. Mortality rates were compared in 14 countries with suitable statistics; Australia, Canada, England and Wales, Finland, France, Japan, Israel, the Netherlands, New Zealand, Singapore, Sweden, Switzerland, the United States, and West Germany, for the period 1970 to 1984/5. In New Zealand, asthma mortality in this age group more than trebled from 1.3 per 100,000 in 1974 to 4.2 per 100,000 in 1979 and since then has declined substantially to 1.85 per 100,000 in 1985. Asthma death rates vary more than six-fold among the other countries examined, and although the New Zealand experience has not been seen to the same degree elsewhere, a gradual increase in reported asthma mortality has occurred since the mid to late 1970s in the majority of countries studied. The increase and subsequent decline in asthma mortality in New Zealand could not be explained by changes in diagnostic fashions or in the International Classification of Disease coding rules. Similarly, the US data do not suggest there is diagnostic transfer among diseases of airway obstruction. However, part of the differences in asthma mortality among the countries examined and the recent increases in asthma death rates, could be due to changing diagnostic fashions rather than true differences in mortality. International studies on the validity of asthma death statistics and on asthma prevalence are required to clarify these issues.

Trends in dietary fat and cigarette smoking and the decline in coronary heart disease in New Zealand.

Coronary heart disease (CHD) mortality declined by approximately 23.5% in New Zealand men aged 35-64 years between 1968 and 1980. The contributions of secular trends in dietary fat and tobacco consumption to this decline were examined using data from national consumption statistics and population based studies of risk factor levels. Per capita saturated fat and dietary cholesterol consumption fell by approximately 12% and 10% respectively during this period while polyunsaturated fat consumption increased by 73%. Per capita tobacco consumption fell by approximately 15%. Using equations developed by Keys and Hegsted it was calculated that the mean serum cholesterol level declined by between 6.6 and 10.3 mg/dl (2.9%-4.4%) during this period. The potential impact of these risk factor changes on CHD mortality was estimated using a Framingham multivariate logistic risk function. Between 38% and 51% of the observed decline in CHD mortality in men aged 35-64 years in New Zealand between 1968 and 1980 could be accounted for by the calculated changes in serum cholesterol and tobacco consumption. If serum cholesterol and cigarette smoking were reduced further to meet current recommendations, it is estimated that CHD mortality would decline by a further 26%-30% from the 1980 level.

Trends in coronary heart disease mortality and morbidity in Auckland, New Zealand, 1974-1986.

Routine mortality statistics show that coronary heart disease (CHD) death rates have declined consistently in Auckland men since 1968; in women, death rates declined between 1968 and 1986 but since 1981 there may have been a reduction in the rate of decline. Data from CHD registers conducted in Auckland, New Zealand in 1974, 1981, and since 1983 as part of the WHO MONICA Project, have been used to investigate the validity and reasons for the decline in the age group 35-64 years. In Auckland age-standardized sudden coronary death rates in men declined by approximately 2% per year between 1974 and 1986; there was no apparent decline in women. There was also an indication of a decline in age-standardized definite myocardial infarction rates but again only in men; 28 day case fatality in patients with a definite myocardial infarction has not changed significantly in the period 1981-1986. These results validate the mortality trends based on death certificates and in particular the differing recent trends in men and women. The decline in CHD mortality in men without a concomitant change in case fatality and the lack of recent decline in women, suggest that changes in the natural history of the disease rather than treatment are responsible for the mortality trends. Since disease events are rare in absolute numbers, long-term monitoring of coronary heart disease in large population groups will be necessary to usefully study disease trends, particularly in women.

Blood pressure and migration in children.

The effect of migration on childhood blood pressure levels has been studied by comparing children before and after migration to New Zealand with children who stayed at home on the Pacific atolls of Tokelau. Data were collected in 1971 on 502 children (97% response rate) aged 5--14 years resident in Tokelau and follow-up data were collected in New Zealand and in Tokelau in 1975--1977 (respknse rate 91%). No selection factors were detected before migration. After migration, the younger migrants had significantly higher blood pressures and were heavier, but not taller, than the non-migrants. Weight differences explained some but not all of the blood pressure differences. There were no differences in body size between the 2 groups of older children although the older non migrant girls had higher blood pressure than the migrant girls.

Comparability of old and new World Health Organization criteria for definite myocardial infarction.

New epidemiological criteria for definite myocardial infarction are now in use as part of the international study of trends and determinants of cardiovascular disease coordinated by the World Health Organization (MONICA Project). In this paper we use data from a myocardial infarction register to assess the comparability of the old and new World Health Organization criteria for definite myocardial infarction. The new criteria were applied to 905 cases who had been categorized as definite myocardial infarction on the old criteria. 739 (82%) of these cases met the new criteria for definite myocardial infarction; a further 157 cases (17%) met the new criteria for possible myocardial infarction. This study indicates that the two sets of criteria produce results that are too dissimilar for reliable comparisons to be made between studies using different criteria for definite myocardial infarction.

A family study of blood pressure in Polynesians.

The family aggregation of blood pressure was studied in Tokelau Island children aged 5-14 years and their parents resident on their home islands in 1971. Five hundred and two (97 per cent) of the children had a recorded blood pressure and they formed 210 sibling groups. The sibship similarity of blood pressure z scores adjusted for year of age and sex was examined by analysis of variance between and within sibships in the 133 sibships with more than one member. For both systolic and diastolic pressure a statistically significant sibship similarity exists which is independent of family size, level of pressure, and the sibship similarity of Quetelet Index. The correlation coefficient of the z score of one index child chosen at random and the remaining siblings is 0-14 (n = 282, p = 0-017). Of the parental variables studied the mother's systolic pressure is the best, and only, predictor of the child's systolic z score. These results suggest that in the Tokelau islanders a family similarity of blood pressure is established relatively early in life.

Approaches to the problems of measuring the incidence of stroke: the Auckland Stroke Study, 1991-1992.

BACKGROUND: Stroke registers are the preferred choice for determining incidence, case-fatality and severity of acute stroke in defined populations. This paper highlights some of the problems likely to be encountered in this endeavour by describing the experience of measuring acute stroke prospectively. METHODS: The Auckland Stroke Study is a community-based study among 945,000 residents of the Auckland region, New Zealand. Standard definitions and overlapping case-finding methods were used to identify all new acute stroke events occurring during the 12-month period ending 1 March 1992. Particular attention was directed at including non-fatal strokes managed outside hospital. The latter were identified by use of a cluster sample, a technique suitable for populations where residents have a personal primary health care physician. RESULTS: The comprehensive sources of referral to the study involved the review of 5736 records, less than one-third of which met the criteria for inclusion. The majority of included acute stroke events (n = 1803) were found through routinely available sources such as hospital admission records (63%) and death registrations (10%). The remainder (27%) were identified through intensive efforts at case-finding of stroke events managed outside hospital. The 1803 events were registered in 1761 people, 817 men and 944 women; for 587 (72%) men and 718 (76%) women, the stroke was the first ever experienced. CONCLUSIONS: While time-consuming, costly and demanding, there appears to be no easier alternative to a register to estimate incidence. This study demonstrates the importance of the use of comprehensive case-finding sources and suggests approaches to overcoming the difficulties in monitoring stroke incidence in large populations.

Decreased blood selenium and risk of myocardial infarction.

The relationship between whole blood selenium levels and risk of acute myocardial infarction was investigated in a community-based control study in Auckland, New Zealand. A pilot study in 14 patients admitted to hospital within 4 hours of onset of symptoms demonstrated that selenium levels were stable in the first 16 hours after admission for an acute myocardial infarction. Some 252 cases (199 men, 53 women) presenting to hospital within 20 hours of onset of acute myocardial infarction were compared with 838 controls (500 men, 338 women), group-matched for age and sex. Myocardial infarction patients had significantly lower mean selenium levels: 82.8 and 87.9 micrograms/l in male cases and controls (p = 0.003) and 82.1 and 88.5 micrograms/l in female cases and controls (p = 0.02) respectively. The relative risks of myocardial infarction in participants with selenium levels below the median level (85 micrograms/l) in comparison with participants above the median were 1.6 (95% CL 1.1-2.2) and 1.7 (95% CL 0.9-3.5) in men and women respectively. The effects of a low selenium level on risk of myocardial infarction were confined to cigarette smokers. These results suggest the hypothesis that a decreased blood selenium in the presence of cigarette smoking is a risk factor for coronary heart disease.

Myocardial infarction is inversely associated with plasma 25-hydroxyvitamin D3 levels: a community-based study.

The relation between the plasma level of 25-hydroxyvitamin D3, the main metabolite of sun-induced vitamin D, and myocardial infarction (MI) was investigated in a community-based case-control study. Some 179 MI patients presenting to hospital within 12 hours of the onset of symptoms were individually matched with controls by age, sex and date of blood collection. MI patients had significantly lower mean 25-hydroxyvitamin D3 levels than controls (32.0 versus 35.5 nmol/L; p = 0.017), with the case-control differences being greatest in winter and spring. The relative risk of MI for subjects with 25-hydroxyvitamin D3 levels equal to or above the median was 0.43 (95% confidence limits = 0.27, 0.69) compared to subjects below the median. The decrease in MI risk associated with raised vitamin D3 levels was observed in all seasons. These results provide support for the hypothesis that increased exposure to sunlight is protective against coronary heart disease.

Varicose veins in the South Pacific.

The prevalence of varicose veins has been studied in several population-based samples in the South Pacific. There is a striking gradient in the age-standardized prevalence rates (0 x 8 per cent to 43 x 7 per cent) with atoll dwellers having the lowest rates, Rarotongans intermediate rates, and New Zealand Maoris and Pakehas the highest rates. The relationship between varicose veins and age, sex, height, weight, body mass and parity is examined and it is concluded that none of these factors are responsible for the observed gradient. The consumption of refined carbohydrates follows the same gradient and the possible aetiological role of this factor is discussed.

CHD in Australia and New Zealand.

Death rates from coronary heart disease (CHD) have been declining in Australia and New Zealand for 20 years. Data from the three MONICA Project Centres in Newcastle (Australia), Perth (Australia), and Auckland (New Zealand) show similar trends for fatal CHD but differing trends for non-fatal myocardial infarction (MI). In Auckland, there has been a consistent decline in out-of-hospital death rates but no decline in non-fatal MI rates. In Perth, the greater contribution to the overall decline has been from out-of-hospital deaths, but in-hospital death rates and non-fatal MI rates have also declined. There is also some evidence of an increase in survival following MI in Perth. In Newcastle, both death rates and non-fatal MI rates have declined. The limited data available suggest that at least one-half of the decline in mortality can be attributed to improvements in population risk-factor levels. Improvements in medical management of both risk factors and established disease are also making contributions to the decline.

Potential misclassification in studies of physical activity.

Regular physical activity is associated with a reduced risk of coronary heart disease, although debate still occurs over the level of intensity required for cardioprotection. The use in epidemiological studies of the arbitrarily defined categories of light, moderate, and hard, as proxy measures of relative intensity has administrative merit but risks potential misclassification, particularly in women and the elderly. This potential misclassification is the result of the inappropriate categorizing of activity based upon absolute intensity values regardless of age or gender. Coronary heart disease is more common in the elderly and recent activity more important than remote for cardiac benefit. It is thus essential to resolve the issue of the level(s) of exercise intensity needed to provide health benefits. Only when this information is available will it be possible to give rational and safe public health advice.

Science, advocacy and health policy: lessons from the New Zealand tobacco wars.

The New Zealand Smoke-Free Environments Act was passed in August 1990 and is a central component of a comprehensive tobacco control policy. The passage of the Act was preceded by a long campaign. The essential components of this campaign were: international scientific evidence and the estimates of tobacco-caused mortality in New Zealand; activists groups supported by established health charities and the health professions; a sympathetic Health Department bureaucracy; a committed and powerful Minister of Health; and a relatively weak industry. The legislation passed despite adverse timing, the absence of bipartisan political support, and the pressure of industry-supported sports lobby groups. The campaign provides a model for other health issues in New Zealand and lessons for the tobacco wars elsewhere.