Recently, time-series correlations of aggregated data have been used to demonstrate the length of latency periods for environmental factors, such as economic conditions and alcohol consumption, in influencing heart disease mortality. Latency periods were specified by lagging mortality rates relative to the economic indicators or rates of alcohol consumption until the highest correlations were achieved. The tendency has been to interpret these correlations without regard to whether the latency periods described are biologically plausible. The authors have identified four models which represent all the possible outcomes of correlational studies of time-series data. Using United States and Canadian mortality rates in relationship to alcohol consumption, they have demonstrated the application of each of these models. For three of the four models, the time-series (lag) correlations are uniform regardless of the number of years mortality is lagged relative to alcohol consumption, and this uniformity does not permit a latency period to be identified. Only the lag correlations between two nonlinear variables show variations over time, depending on the degree of correspondence between the increasing and decreasing line segments of the two curves. Correlations ranging from high positive to high negative are possible, and several peak correlations (positive and negative) can occur. However, the biologic interpretation of multiple peaks with the same or different signs is problematic. The authors conclude that time-series correlations of aggregated data are not useful for the study of latency periods, and that analysis of time-series correlations for this purpose can be at best ambiguous, and at worst, completely misleading.
The association between consumption of alcoholic beverages (spirits, beer and wine) and coronary heart disease (CHD) mortality, especially the incidence of sudden coronary death (SCD), was investigated in a 5-year prospective population study comprising 4,532 men aged 40-64 years. The amount of alcohol used was estimated on the basis of answers to a self-filled structured questionnaire. The incidence of SCD was statistically significantly lower among abstainers than among alcohol consumers. The relative risk of SCD of alcohol consumers in comparison with abstainers was largest in the oldest age group and it became more apparent after a follow-up of a couple of years. Only the consumption of spirits was positively associated with the incidence of SCD. Among non-smokers the incidence of SCD was statistically significantly higher in consumers than in abstainers, a similar but not significant trend was observed among current smokers. The positive association between alcohol consumption and incidence of SCD was detected both in CHD-free men and in men with prior CHD. Consumption of alcoholic beverages, and in particular of spirits, is associated with an increased risk of SCD in Finnish men.
High alcohol consumption is one of the major risk indicators for premature death in middle-aged men. An indicator of alcohol abuse--registration with the social authorities for alcoholic problems--was used to evaluate the role of alcohol in relation to general and cause-specific mortality in a general population sample. Altogether 1,116 men (11%) out of a total population of 10,004 men were registered for alcoholic problems. Total mortality during 11.8 years' follow-up was 10.4% among the non-registered men, compared to 20.5% among men with occasional convictions for drunkenness and 29.6% among heavy abusers. Fatal cancer as a whole was not independently associated with alcohol abuse, but oropharyngeal and oesophageal cancers together were seven times more common in the alcohol-registered groups. Total coronary heart disease (CHD) was significantly and independently associated with alcohol abuse, but nearly all the excess CHD mortality among the alcohol-registered men could be attributed to sudden coronary death. Cases with definite recent myocardial infarction were not more common in the alcoholic population. A combined effect of coronary arteriosclerosis and heart muscle damage secondary to alcohol abuse is suggested. Other causes of death strongly associated with registration for alcohol abuse include pulmonary embolism, pneumonia and peptic ulcer, as well as death from liver cirrhosis and alcoholism. Of the excess mortality among alcohol-registered subjects, 20.1% could be attributed to CHD, 18.1% to violent death, 13.6% to alcoholism without another diagnosis and 11.1% to liver cirrhosis.
Ten years after a health screening examination was offered to 50 year old men 32 of the 2322 participants and 12 of the 454 nonparticipants had died of ischaemic heart disease. Of these, 26 and 11 respectively had suffered sudden death, for which necropsy was performed. Half of the men who had died suddenly had been registered for alcohol intemperance up to 1973, which was four times the prevalence of such registrations in the general population. Registration at both the Swedish Temperance Board and the Bureau of Social Services was associated with an odds ratio of 3.74 for sudden death as compared with not being registered at either. Logistic analysis including the classical risk factors for ischaemic heart disease together with registration for alcohol intemperance and at the Bureau of Social Services showed only the two types of registration and systolic blood pressure to be independent risk factors. On the other hand, there was no overrepresentation of subjects entered in the registers among those surviving a myocardial infarction. For non-fatal myocardial infarction blood pressure and serum triglyceride concentration were significant risk factors and serum cholesterol concentration, smoking, and body mass index probable risk factors; the two types of registration were not independent risk factors. Alcohol intemperance is strongly associated with an increased risk of sudden death after myocardial infarction.
The association between oral analgesics and the risk of death from ischaemic heart disease (IHD), cardiovascular disease, disease other than IHD, and any disease was studied in a cohort of 3551 men aged 30-59 years, based on a random sample from the population of eastern Finland. A number of potential coronary risk factors were allowed for in multiple logistic models. On the basis of these data, a regular use of oral analgesics is associated with a decreased risk of death from IHD. The relative risk was 0.6 with 95% confidence interval (CI) of 0.2-0.9 for IHD death and 0.6 (95% CI = 0.4-0.9) for cardiovascular death. No significant association was found between oral analgesics and the risk of death from diseases other than IHD.
INTRODUCTION: The aim of the present study was to quantify the impact of different dietary factors on the mortality from ischaemic heart disease in Denmark. METHODS: Relative risks and knowledge on the distribution of different dietary factors were used to estimate etiological fractions. RESULTS: It is estimated that an intake of fruit and vegetables and saturated fat as recommended would prevent 12 and 22%, respectively, of deaths from ischaemic heart disease in Denmark. An intake of fish among those at high risk for ischaemic heart disease, would lead to a 26% lower mortality, while alcohol intake among abstainers would have no significant quantitative effect. DISCUSSION: These results suggest that changes in dietary habits according to current recommendations would have an impact on public health in Denmark.
In metropolitan areas, road traffic is a major contributor to ambient air pollution and the dominant source of community noise. The authors investigated the independent and joint influences of community noise and traffic-related air pollution on risk of coronary heart disease (CHD) mortality in a population-based cohort study with a 5-year exposure period (January 1994-December 1998) and a 4-year follow-up period (January 1999-December 2002). Individuals who were 45-85 years of age and resided in metropolitan Vancouver, Canada, during the exposure period and did not have known CHD at baseline were included (n = 445,868). Individual exposures to community noise and traffic-related air pollutants, including black carbon, particulate matter less than or equal to 2.5 µm in aerodynamic diameter, nitrogen dioxide, and nitric oxide, were estimated at each person's residence using a noise prediction model and land-use regression models, respectively. CHD deaths were identified from the provincial death registration database. After adjustment for potential confounders, including traffic-related air pollutants or noise, elevations in noise and black carbon equal to the interquartile ranges were associated with 6% (95% confidence interval: 1, 11) and 4% (95% confidence interval: 1, 8) increases, respectively, in CHD mortality. Subjects in the highest noise decile had a 22% (95% confidence interval: 4, 43) increase in CHD mortality compared with persons in the lowest decile. These findings suggest that there are independent effects of traffic-related noise and air pollution on CHD mortality.
