[Causes and prevention of chronic diseases in the elderly; the Erasmus Rotterdam health and the elderly study].
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Biomedical subjects
Publications and source records attributed to D E Grobbee.
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In this paper the Rotterdam Elderly Study is presented. The aim of the study is to investigate determinants of disease occurrence and progression in the elderly. In addition to contributing to our understanding of the etiology of geriatric illnesses, the study is expected to lead to specific recommendations for intervention. The study focuses on causally related determinants of major diseases in the elderly. Fields of interest for the Rotterdam Elderly Study are conditions which interfere the most with the quality of life for the elderly. The aims of the Rotterdam Elderly Study are: (1) To investigate, by means of epidemiologic, clinical and basic research, the determinants of diseases in order to assess their etiologic significance. (2) To investigate potentially modifiable determinants in order to be able to develop preventive strategies by providing specific recommendations for intervention studies. The Rotterdam Elderly Study focuses on four primary areas of research: neurogeriatric diseases, cardiovascular diseases, locomotor diseases and ophthalmologic diseases. It is a prospective follow-up study, in which determinants of disease and determinants of progression of disease will be investigated in the total population of 55 years or over of the district of Ommoord in Rotterdam. It is anticipated that about 10,000 people will participate in the study and they will be examined in the period of 1991 to 1995.
In a sample of 1190 children (574 boys and 616 girls), aged 6.8-10.7 years, bone mineral content was studied using quantitative röntgen microdensitometry (QMD) at the diaphyseal and the metaphyseal site of the left second digit. Percentile curves of bone mineral density was determined by skeletal age for boys and girls separately. Bone mineral content at the diaphyseal site was significantly associated with skeletal age, height and body weight in boys and girls and with chronological age at the metaphyseal site in boys. In girls higher levels of bone mineral content were observed in those with a skeletal age greater than 7.3 years, compared to those with a skeletal age equal to or less than 7.3 years, adjusted for height and body weight. In boys a higher level of bone mineral content was found in those with a height greater than 138 cm, adjusted for skeletal age, compared to those with a height equal or less than 130 cm, at the diaphyseal and metaphyseal site. Girls with a relatively higher body weight had lower levels of bone mineral content at the metaphyseal site.
To study the effects of caffeine on serum lipids and blood pressure, we conducted a double-blind, randomized trial with two parallel groups in 69 young, healthy subjects. After a 3-wk run-in period, subjects were randomly assigned to one of two groups receiving either 4-6 140-mL cups filtered decaffeinated coffee per day and an equal number of pills containing 75 mg caffeine or 4-6 140-mL cups filtered decaffeinated coffee per day and an equal number of placebo pills, for 9 wk. In both groups caffeine intake from other sources was not allowed. The main finding of this study is that abstinence from caffeine for a period of 9 wk has no effect on either serum lipids or blood pressure.
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In an attempt to study and prevent the development of hypertension, there is a growing interest in measuring blood pressure in children. The aim of this is to detect and monitor those with a relatively high level of blood pressure. Until now, reference values on blood pressure in children are based on data from North-American youngsters. The present study provides percentile charts based on pooled data from studies on blood pressure conducted in six North-West European countries among 28,043 children. These blood pressure centiles are presented as age-, height- and gender-specific. Brief guidelines for blood pressure measurements in childhood and for detection of children with a relatively high blood pressure are included.
This article addresses the methodology of sodium sensitivity assessment. There have been reports to suggest that a high sodium intake is a cause of elevated blood pressure and trials to indicate that a reduction in sodium intake may reduce blood pressure that is already high; the implications of these findings are discussed. Many studies on sodium sensitivity suffer from what could be called the "normal probability fallacy"; without appropriate control conditions, an intervention such as sodium restriction may incorrectly be assigned to a more pronounced response in a subgroup of the study population. As an example, findings are reviewed of age and sex as determinants of a response of blood pressure to variations in sodium intake. The limited data available suggest that subjects that are older and have higher blood pressure levels seem to benefit more from a reduction in sodium intake. In addition, elderly subjects at a high dietary sodium intake may have a higher risk of developing hypertension. Findings in both nonexperimental and experimental studies tend to support this view. Findings on sex differences are less consistent. A systematic approach to the assessment of factors and mechanisms responsible for sodium sensitivity in some subjects is needed to determine who might benefit most. Until more data are available, there is little basis to discriminate sodium-sensitive from sodium-resistant hypertensive subjects.
Relatively few observational (i.e., nonexperimental) studies have been conducted to examine the role of antihypertensive drug therapy in the primary prevention of coronary heart disease. To draw valid conclusions from experimental or observational studies, internal validity should be ensured. In particular, similarity of "extraneous" effects, of information, and of prognosis between the treatment groups compared in a particular study is needed. Because allocation of participants to antihypertensive drug therapy in observational studies is nonrandomized by definition, special efforts should be made to achieve comparability of prognosis, that is, to avoid "confounding by indication." Follow-up and case-control studies, the two main types of observational studies, also offer certain advantages over randomized clinical trials, particularly when different classes of drugs are compared. Although few valid observational studies on the efficacy of drug therapy for hypertension in the primary prevention of first coronary events have been published, the available data suggest that beta-blockers might confer greater protection than other drug regimens. However, more evidence is needed to confirm these findings. It is concluded that observational studies could play an increasing role in the assessment of the role of antihypertensive therapy in the primary prevention of coronary heart disease when the inherent potentials and pitfalls of these studies are appreciated.
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The relation between the presence of calcified plaques in the thoracic aorta, as detected on chest x-rays, and the development of cardiovascular disease is examined during 12 years of follow-up of the Framingham cohort (n = 5,209). The prevalence of aortic calcified plaques approximately doubled with each decade of age, with only a trivial male predominance. Its presence was associated with a twofold increase in risk of cardiovascular death in men and women younger than age 65, even after other risk factors were taken into account. Similar increases in risk were found for coronary artery disease, stroke and intermittent claudication among middle-aged women. In middle-aged men these risks were less marked. The predictive value of aortic calcified plaques generally diminished with age. Risk of sudden coronary death in men with calcified plaques in the thoracic aorta ranged from a sevenfold increase at age 35 to no excess risk at age 70 years. These results support the view that atherosclerosis is a generalized process. The finding of aortic calcified plaques in a relatively young subject on a routine chest x-ray should be regarded as a sign for potential development of clinically manifest atherosclerotic disease in the cardiac, cerebral and peripheral arterial circulation.
BACKGROUND: For many years, an association between coffee consumption and the risk of coronary heart disease has been suspected. Although based on small numbers of end points, a prospective study has suggested a particularly strong association between recent coffee drinking and the incidence of cardiovascular disease. METHODS: We examined prospectively the relation of coffee consumption with the risk of myocardial infarction, need for coronary-artery bypass grafting or angioplasty, and risk of stroke in a cohort of 45,589 U.S. men who were 40 to 75 years old in 1986 and who had no history of cardiovascular disease. RESULTS: During two years of follow-up observation, 221 participants had a nonfatal myocardial infarction or died of coronary heart disease, 136 underwent coronary-artery surgery or angioplasty, and 54 had a stroke. Total coffee consumption was not associated with an increased risk of coronary heart disease or stroke. The age-adjusted relative risk for all cardiovascular disease among participants who drank four or more cups of coffee per day was 1.04 (95 percent confidence intervals, 0.74 to 1.46). Increasing levels of consumption of caffeinated coffee were not associated with higher risks of cardiovascular disease. Higher consumption of decaffeinated coffee, however, was associated with a marginally significant increase in the risk of coronary heart disease (relative risk, 1.63; 95 percent confidence interval, 1.02 to 2.60). Finally, we observed no pattern of increased risk across the subgroups of participants with increasing intakes of caffeine from all sources. Adjustment for major cardiovascular-risk indicators, dietary intake of fats, and cholesterol intake did not materially alter these associations. CONCLUSIONS: These findings do not support the hypothesis that coffee or caffeine consumption increases the risk of coronary heart disease or stroke.
OBJECTIVE: To assess the association between sodium and potassium intake and the rise in blood pressure in childhood. DESIGN: Longitudinal study of a cohort of children with annual measurements during an average follow up period of seven years. SETTING: Epidemiological survey of the population of a suburban town in western Netherlands. SUBJECTS: Cohort of 233 children aged 5-17 drawn at random from participants in the population survey. MAIN OUTCOME MEASURES: At least six annual timed overnight urine samples were obtained. The mean 24 hour sodium and potassium excretion during the follow up period was estimated for each participant and the sodium to potassium ratio calculated. Individual slopes of blood pressure over time were calculated by linear regression analysis. RESULTS: No significant association was observed between sodium excretion and the change in blood pressure over time. The mean systolic blood pressure slopes, however, were lower when potassium intake was higher (coefficient of linear regression -0.045 mm Hg/year/mmol; 95% confidence interval -0.069 to -0.020), and the change in systolic pressure was greater when the urinary sodium to potassium ratio was higher (0.356 mm Hg/year/unit; 95% confidence interval 0.069 to 0.642). In relation to potassium this was interpreted as a rise in blood pressure that was on average 1.0 mm Hg (95% confidence interval -1.65 to -0.35) lower in children in the upper part of the distribution of intake compared with those in the lower part. The mean yearly rise in systolic blood pressure for the group as a whole was 1.95 mm Hg. Urinary electrolyte excretion was not associated with diastolic blood pressure. CONCLUSION: Dietary potassium and the dietary sodium to potassium ratio are related to the rise in blood pressure in childhood and may be important in the early pathogenesis of primary hypertension.
PURPOSE: The objective of this study was to examine the effect of low-dose aspirin (325 mg on alternate days) on the primary prevention of angina pectoris in the United States Physicians' Health Study. Despite a postulated role of platelets in atherogenesis and myocardial ischemia, the effect of chronic platelet inhibition on the development of clinical angina pectoris is unknown. SUBJECTS AND METHODS: The Physicians' Health Study is a randomized, double-blind, placebo-controlled trial among 22,071 male physicians aged 40 to 84 years, free from previous myocardial infarction, stroke, and transient cerebral ischemia at entry, and followed for an average of 60.2 months. The 21,738 physicians who were also free from angina pectoris at baseline constituted the study population for the present analyses. RESULTS: During 106,652 person-years of follow-up, 331 patients with confirmed angina pectoris were diagnosed, 194 of whom underwent a coronary revascularization procedure (coronary artery bypass graft surgery or coronary angioplasty). As compared to participants assigned placebo, the relative risk of confirmed angina pectoris in the aspirin group was 1.10 (95% confidence interval [CI], 0.88 to 1.38). For coronary revascularization, the relative risk was 1.19 (95% CI, 0.88 to 1.59). After simultaneous control for other coronary risk factors in a proportional-hazards model, these relative risks remained near unity at 1.07 (95% CI, 0.84 to 1.36) and 1.11 (95% CI, 0.81 to 1.52), respectively. When the risks of angina pectoris were examined according to year of randomization in the trial, there was no pattern of increasing benefit with longer duration of treatment. CONCLUSION: These randomized trial data indicate that chronic platelet inhibition with low-dose aspirin for an average duration of 60.2 months does not reduce the incidence of angina pectoris.
The influence of coffee and caffeine consumption on hemostatic factors was studied in 2 randomized trials. Both studies were conducted in young, healthy adults. In the first study, 107 participants were randomly allocated to one or 3 intervention groups, drinking filtered coffee, boiled coffee or no coffee at all, respectively, for a period of 9 weeks. In the second study, 69 subjects received either 4-6 tablets containing 75 mg caffeine or the same amount of placebo tablets, while using decaffeinated coffee. In this double-blind study caffeine intake from any other source was not allowed. Blood samples for hemostatic factors were obtained at baseline and after 9 weeks of intervention. The findings indicate no effect of coffee consumption on fibrinogen, clotting factor VII activity, factor VIII antigen, protein C and protein S and also no effect of caffeine consumption on fibrinogen and factor VII activity.
The effects of the use of oral contraceptives on serum lipids and blood pressure were studied among young women who participated in a longitudinal survey of risk factors for coronary heart disease (CHD) in the Netherlands. Fifty-three participants, ages 14 to 24 years, initiated oral contraceptive use during follow-up to the primary study on CHD. They continued oral contraceptive use for at least 2 subsequent years. From 53 age-matched control subjects, who did not use oral contraceptives, data were obtained for the same follow-up period. Women using oral contraceptives showed a significantly greater rise in serum total cholesterol levels than did the reference subjects (14 mg/100 ml/2 year vs 4 mg/100 ml/2 year; 95% confidence interval of the difference was 0.1 to 19.6). The increase in systolic blood pressure (4.7 mm Hg/2 year vs 2.1 mm Hg/2 year; 95% confidence interval of the difference was -1.8 to 6.9) did not differ between the groups. These findings suggest that oral contraceptive use may be associated with an enhanced rise in total cholesterol during adolescence.
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The blood pressure (BP) in children has been studied since the beginning of this century, and in the past decade the potential association between childhood BP levels and adult hypertension has gained increasing interest. From several longitudinal studies, many of them comprising large numbers of children and youngsters, it appears that the BP of children is significantly associated with BP on follow-up measurements and that childhood BP is related to adult levels. Whether the objective is to predict future BP, or the aim is to shed light on the early pathogenesis of primary hypertension, it is of major importance to find out why BP rises in some and stays the same in others. To achieve this, characteristics need to be detected that are related to changes in BP in the first decades of life. Although not many reports on these dynamic relations are presently available, age, height, body weight, initial BP level, and a family history of hypertension have been put forward as determinants of children's BP change over time. Moreover, there are data to support the effect of dietary factors, most notably certain electrolytes, on BP regulation early in life. Also, certain hemodynamic and neural characteristics, such as changes in cardiac output and left ventricular mass, renal blood flow, and sympathetic nervous system activity, may be related to a subsequent rise in BP and future hypertension. Findings from nonexperimental and experimental studies on determinants of BP in children and youngsters will be reviewed.