Rodney Jackson

Differences between respondents and nonrespondents in a multicenter community-based study vary by gender and ethnicity☆

Abstract This study provides data on differences between respondents and nonrespondents by gender and ethnicity in a multicenter community-based study that is rarely collected and that may be useful for estimating bias in prevalence estimates in other studies. Demographic, general health, and cardiovascular risk factors were examined in black and white respondents and nonrespondents to the Atherosclerosis Risk in Communities (ARIC) Study, a prospective study investigating cardiovascular risk factors in approximately 16,000 adults that was initiated in 1986 in four U.S. communities. In one of the communities (Jackson, MS) black participants were recruited exclusively; in another (Forsyth County, NC) 12% of the eligible sample were black, whereas the samples in Washington County, MD and the northwestern suburbs of Minneapolis, MN were almost all white. Demographic and health characteristics were collected during a home interview. Subjects who subsequently agreed to complete a clinical examination were defined as respondents, while eligible participants who only took part in the home interview were considered to be nonrespondents. Approxmately 75% of age-eligible individals (45–64 years) in each community completed the home interview. In three of the communities 86–88% of those who took part in the home interview also completed the clinic examination, whereas only 63% did so in Jackson. Among white participants, response rates were similar in men and women and between communities. Among black participants, the response rates were considerably lower, particularly in men. White male respondents reported a higher socioeconomic status, better general health and a lower prevalence of cardiovascular disease and associated risk factors than white male nonrespondents. The difference between white respondents and nonrespondents were greater for men than women despite similar response rates. Among black participants, respondent/nonrespondent differences were usually of smaller magnitude or absent, particularly in women. General health status and recent hospitalization rates were almost identical in black respondents and nonrespondents. Low response rates can bias estimates of prevalence in community-based studies although differences between respondents and nonrespondents tend to exaggerate real differences beween respondents and the eligible population sampled. For example, among white males 25% of respondents and 44% of nonrespondents were current smokers, yet the estimated community prevalence of smoking was 31%. In conclusion, differences observed between respondents and nonrespondents were in the expected direction, but were greater for men than women and for whites than blacks.

Association of angiotensinogen gene T235 variant with increased risk of coronary heart disease

Several genes, including some encoding components of the renin angiotensin system, are associated with the risk of cardiovascular diseases. There have been reports linking a homozygous deletion allele of the angiotensin converting enzyme (ACE) gene (DD) with an increased risk of myocardial infarction, and some variants of the angiotensinogen gene with an increased risk of hypertension. In a case-control study of a caucasian population from New Zealand, we examined the associations with coronary heart disease (CHD) of ACE DD and of a mis-sense mutation with methionine to threonine aminoacid substitution at codon 235 in the angiotensinogen gene (T235). We studied 422 patients (mean age 62 years, 81% male) with documented CHD (50% with myocardial infarction) and 406 controls without known CHD (frequency-matched to cases by age and sex). Risk factors for CHD were assessed by standard questionnaire, physical examination, and blood tests. Genomic DNA from leucocytes was analysed for various ACE and angiotensinogen alleles. Angiotensinogen T235 homozygotes were at significantly increased risk of CHD generally (odds ratio 1.7, 2 p = 0.008) and of myocardial infarction specifically (1.8, 2 p = 0.009). Adjustment for several risk factors increased the estimate of CHD risk associated with this allele to 2.6 (2 p < 0.001) and the estimate for myocardial infarction risk to 3.4 (2 p < 0.001). By contrast, there was no evidence of a significant increase in the risk of CHD or myocardial infarction among individuals with ACE DD. We conclude that the T235 polymorphism of the angiotensinogen gene is an independent risk factor, which carries an approximately two-fold increased risk of CHD. In this study, however, ACE DD was not associated with any detectable increase in CHD risk.

Passive smoking as well as active smoking increases the risk of acute stroke

OBJECTIVE To estimate the relative risk of stroke associated with exposure to environmental tobacco smoke (ETS, passive smoking) and to estimate the risk of stroke associated with current smoking (active smoking) using the traditional baseline group (never-smokers) and a baseline group that includes lifelong non-smokers and long-term (>10 years) ex-smokers who have not been exposed to ETS. DESIGN AND SETTING Population-based case-control study in residents of Auckland, New Zealand. SUBJECTS Cases were obtained from the Auckland stroke study, a population-based register of acute stroke. Controls were obtained from a cross-sectional survey of major cardiovascular risk factors measured in the same population. A standard questionaire was administered to patients and controls by trained nurse interviewers. RESULTS Information was available for 521 patients with first-ever acute stroke and 1851 community controls aged 35–74 years. After adjusting for potential confounders (age, sex, history of hypertension, heart disease, and diabetes) using logistic regression, exposure to ETS among non-smokers and long-term ex-smokers was associated with a significantly increased risk of stroke (odds ratio (OR) = 1.82; 95% confidence interval (95% CI) = 1.34 to 2.49). The risk was significant in men (OR = 2.10; 95% CI = 1.33 to 3.32) and women (OR = 1.66; 95% CI = 1.07 to 2.57). Active smokers had a fourfold risk of stroke compared with people who reported they had never smoked cigarettes (OR = 4.14; 95% CI = 3.04 to 5.63); the risk increased when active smokers were compared with people who had never smoked or had quit smoking more than 10 years earlier and who were not exposed to ETS (OR = 6.33; 95% CI = 4.50 to 8.91). CONCLUSIONS This study is one of the few to investigate the association between passive smoking and the risk of acute stroke. We found a significantly increased risk of stroke in men and in women. This study also confirms the higher risk of stroke in men and women who smoke cigarettes compared with non-smokers. The stroke risk increases further when those who have been exposed to ETS are excluded from the non-smoking reference group. These findings also suggest that studies investigating the adverse effects of smoking will underestimate the risk if exposure to ETS is not taken into account.

Alcohol consumption and risk of coronary heart disease.

OBJECTIVE--To investigate the hypothesis that the apparent protective effect of habitual alcohol consumption on coronary heart disease is due to drinkers at high risk of coronary heart disease becoming non-drinkers. DESIGN--Case-control population based study. Data were obtained from interviews with patients with non-fatal myocardial infarction and their controls and with the next of kin of those who had died of coronary heart disease and their controls. SETTING--Auckland, New Zealand. SUBJECTS--Two groups of cases were studied. The first comprised 227 men and 72 women with non-fatal myocardial infarction identified from a population based surveillance programme for coronary heart disease; controls were 525 men and 341 women randomly selected from the same population group and matched for age and sex. The second group comprised 128 men and 30 women who had died of coronary heart disease and had been identified from the surveillance programme; controls were a sample of the previous control group and comprised 330 men and 214 women matched for age and sex. All participants were aged 25-64 years and without diagnosed coronary heart disease. MAIN OUTCOME MEASURES--Regular alcohol consumption; high density lipoprotein cholesterol and low density lipoprotein concentrations. RESULTS--Men with myocardial infarction and men who had died of coronary heart disease were more likely to have been never drinkers (had never drunk more than once a month) than controls (18% v 12% and 23% v 13% respectively). After possible confounding factors had been controlled for, people in all categories of drinking (up to more than 56 drinks per week) had at least a 40% reduction in risk of fatal and non-fatal coronary heart disease compared with never drinkers. Former drinkers also had a lower risk of non-fatal myocardial infarction than never drinkers (relative risks 0.41 and 0.10 in men and women respectively) but a similar risk of death from coronary heart disease. The reduction in risk was consistently greater in women than in men in all drinking categories but there was no clear dose-response effect in either sex. CONCLUSIONS--The results support the hypothesis that light and moderate alcohol consumption reduces the risk of coronary heart disease. This protective effect in this population was not due to the misclassification of former drinkers with a high risk of coronary heart disease as non-drinkers.

Mortality from asthma: a new epidemic in New Zealand

Trends in mortality attributed to asthma in the 5-34-year age group were examined in New Zealand, Australia, England and Wales, the United States, Canada, and West Germany for the years 1959-79. An epidemic of deaths from asthma occurred in the mid-1960s in New Zealand, Australia, and England and Wales but not in the other countries. In Australia and England and Wales the death rate quickly returned to pre-epidemic levels, but in New Zealand the decline in mortality was slow, and by 1974 the death rate was still almost double the pre-epidemic level. Of great concern was an abrupt increase in reported deaths from asthma in New Zealand after 1976 with the mortality rate during 1977-9 being greater than during the previous epidemic. In contrast, asthma mortality had remained relatively stable in the other populations. The new epidemic in New Zealand was investigated and appeared to be real. It could not be explained by changes in the classification of deaths from asthma, inaccuracies in death certification, or changes in diagnostic fashions. The most likely explanation appeared to be related to the management of asthma in New Zealand, and this is being investigated.

Prostate cancer risk and consumption of fish oils: a dietary biomarker-based case–control study

SummaryExperimental studies suggest that the risk of prostate cancer is reduced with the intake of long-chain n-3 polyunsaturated fatty acids derived from marine foods, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). However, few human studies have been conducted due to difficulties in assessing the dietary intake of these fatty acids. The authors examined the relationship between prostate cancer risk and EPA and DHA in erythrocyte biomarkers in a population-based case–control study in Auckland, New Zealand during 1996–1997 involving 317 prostate cancer cases and 480 age-matched community controls. Reduced prostate cancer risk was associated with high erythrocyte phosphatidylcholine levels of EPA (multivariate relative risk = 0.59; 95% confidence interval 0.37–0.95, upper vs lowest quartile) and DHA (multivariate relative risk = 0.62; 95% confidence interval 0.39–0.98, upper vs lowest quartile). These analyses support evidence from in vitro experiments for a reduced risk of prostate cancer associated with dietary fish oils, possibly acting via inhibition of arachidonic acid-derived eicosanoid biosynthesis.

Non-steroidal anti-inflammatory drugs and prostate cancer progression.

Experimental studies have suggested that the biosynthesis of arachidonic acid‐derived eicosanoids such as prostaglandin E2 via the cyclo‐oxygenase pathway may play a significant role in supporting cell proliferation in human prostate cancer cell lines. However, the aetiological significance of this for clinical prostate cancer has remained unclear. In particular, the potential for prostate cancer chemoprevention using non‐steroidal anti‐inflammatory drugs (cyclo‐oxygenase inhibitors; NSAIDs) has received little attention. The purpose of our study was to investigate associations between prostate cancer risk and use of NSAIDs. A population‐based case‐control study was carried out over 13 months from 1996 in metropolitan Auckland, New Zealand. A total of 317 newly diagnosed prostate cancer cases (including 192 “advanced” cases) representative of all cancer cases in the study population were identified from urology clinic referrals and histology reports. A total of 480 age‐matched controls were recruited following random selection from the study population using electoral rolls as the sampling frame. After adjusting for potential confounding by socio‐economic status and dietary fat consumption, there was a trend toward reduced risks of advanced prostate cancer associated with regular use of total NSAIDs (RR = 0.73; 95% CI 0.50–1.07) and total aspirin (RR = 0.71; 95% CI 0.47–1.08). However, these associations failed to reach statistical significance at the usually accepted levels. Weaker inverse associations were found for total prostate cancers, which included a number of small, low‐grade tumours of less clinical significance. These findings lend support to proposed underlying aetiological hypotheses which imply a role for cyclo‐oxygenase activity in prostate cancer progression. Int. J. Cancer 77:511–515, 1998.

The effect of nonresponse on prevalence estimates for a referent population: Insights from a population-based cohort study

Characterization of nonrespondents, with the aim of detecting nonresponse bias, is a crucial component of prospective studies. This study was undertaken to investigate the demographic and health characteristics of nonrespondents to a population-based cohort study of cardiovascular disease, to determine whether early-stage nonrespondents differ from late-stage nonrespondents, and to estimate the bias in prevalence estimates for the source population. Sixty-seven percent of eligible subjects completed all phases of the cohort recruitment. Compared to respondents, nonrespondents were less likely to be married, less likely to be employed, and less likely to be well educated. Nonrespondents tended to describe their general health in less favorable terms and were more likely to be smokers. Their reported disease profile, however, was not dissimilar to that of respondents. For several demographic and health characteristics, including marital status, education, and smoking, early-stage nonrespondents differed from respondents more than did late-stage nonrespondents. For example, 42% of early nonrespondents were smokers compared to 37% of late nonrespondents and 22% of respondents. Overall, the bias in prevalence estimates related to nonresponse was small (< 5%) for most of the measured characteristics. Although nonresponse to health surveys is associated with typical attributes, early nonrespondents differ from respondents more than do late-stage nonrespondents. With few exceptions, however, a 33% nonresponse rate did not appear to introduce substantial bias into prevalence estimates for the source community.

Guidelines on preventing cardiovascular disease in clinical practice.

Papers pp 671, 676, 677 General practice pp 680, 686, 690 Education and debate pp 702, 705, 709 Ten years ago clinical recommendations on preventing cardiovascular disease focused primarily on managing individual risk factors, particularly raised blood pressure and cholesterol concentrations. Typically, separate guidelines were developed for each risk factor and treatment was recommended when that factor was above a specified level1 The recommendations were informed mainly by evidence from cohort studies showing increased relative risks of cardiovascular disease in people with raised levels of the risk factor2 and by evidence from randomised controlled trials showing relative benefits from lowering the factor.3 4 Over the past decade we have witnessed a remarkable change from these recommendations based on relative risk to ones based on absolute risk—that is, incidence. If Geoffrey Rose, arguably the most influential cardiovascular disease epidemiologist ever, was living today, he would support this revolution, which echoes his 1991 advice that “All policy decisions should be based on absolute measures of risk; relative risk is strictly for researchers only.”5 This weeks BMJ brings together a range of papers relevant to this paradigm shift in cardiovascular risk management. One of the most recent examples of guidelines based on absolute risk is the Joint British Recommendations on the Prevention of Coronary Heart Disease in Clinical Practice, published late last year6 and summarised in this issue (p 705).7 Taking the lead from the European societies of cardiology, atherosclerosis, and hypertension, which jointly published coronary heart disease prevention guidelines in 1998, 8 the British Cardiac Society, British Hyperlipidaemia Association, and British Hypertension Society joined forces to develop the current British recommendations. These new clinical guidelines recommend that priority for treatment should be given to patients at high absolute risk …

Plasma 25-hydroxyvitamin D3 and its relation to physical activity and other heart disease risk factors in the general population

The relation between plasma levels of 25-hydroxyvitamin D3, the main metabolite of sun-induced vitamin D, and major coronary heart disease risk factors was examined in 295 men, aged 35 to 64 years, who were randomly sampled from the general population. Men who did regular vigorous leisure-time activity had a mean plasma 25-hydroxyvitamin D3 level that was 4.8 nmol/L (95% confidence limits: 0.1, 9.5) higher than that in inactive men, with the increase greatest in the winter months. Plasma 25-hydroxyvitamin D3 was positively associated with weekly hours of sun exposure (r = 0.27, P < 0.01), and showed a weak inverse association with age (r = -0.12, P < 0.05) and diastolic blood pressure (r = -0.15, P < 0.05), although this latter finding was no longer significant when allowance was made for the effects of age and season on vitamin D levels. In contrast, plasma 25-hydroxyvitamin D3 had no relation with either serum total or high-density-lipoprotein cholesterol levels, body mass index, or cigarette smoking. We hypothesize that vigorous leisure-time activity may protect against coronary heart disease, in part, by increasing body levels of vitamin D.