Effect of dietary and antismoking advice on the incidence of myocardial infarction: a 16-year follow-up of the Oslo Diet and Antismoking Study after its close.
ABSTRACT The Oslo Diet and Antismoking Study was a 5-year randomised controlled trial initiated in 1972-1973 and ended in 1977-1978, which showed that dietary change and smoking cessation reduced the incidence of coronary heart disease among high risk middle-aged men. In an extended follow-up we studied the incidence of myocardial infarction (MI) 16 years after the end of the trial in the intervention and control groups.
The primary endpoint was the first occurrence of non-fatal and fatal MI including sudden death up to December 31 1993. Cases of fatal MI were identified by linkage to Statistics Norway using each subject's individual personal number. Cases of non-fatal MI were extracted from the hospital records. Cox proportional hazards regression models estimated relationships between changes in total cholesterol and triglyceride concentrations and smoking status and the primary endpoints up to 16 years following the end of the trial.
At 5 and 10 years following the end of the trial the incidence of MI among the 604 men in the intervention (I) and 628 in the control (C) group differed significantly (5-year event rate (I/C) =0.059/0.090; P=0.038 and 10-year event rate (I/C) =0.111/0.155; P=0.023), but the difference faded slowly and subsequently (P=0.069 at 16 years). The reduction in MI in the intervention group was primarily explained by the differences in total cholesterol and triglyceride concentrations between the groups.
This extended follow-up of the Oslo Diet and Antismoking Study found a prolonged benefit of the intervention lasting for at least a decade after the close of the trial. This finding is in accordance with statin and other studies showing that the effect of cholesterol lowering may be prolonged after the end of the intervention.
- [Show abstract] [Hide abstract]
ABSTRACT: Reduction and modification of dietary fats have differing effects on cardiovascular risk factors (such as serum cholesterol), but their effects on important health outcomes are less clear. To assess the effect of reduction and/or modification of dietary fats on mortality, cardiovascular mortality, cardiovascular morbidity and individual outcomes including myocardial infarction, stroke and cancer diagnoses in randomised clinical trials of at least 6 months duration. For this review update, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and EMBASE, were searched through to June 2010. References of Included studies and reviews were also checked. Trials fulfilled the following criteria: 1) randomised with appropriate control group, 2) intention to reduce or modify fat or cholesterol intake (excluding exclusively omega-3 fat interventions), 3) not multi factorial, 4) adult humans with or without cardiovascular disease, 5) intervention at least six months, 6) mortality or cardiovascular morbidity data available. Participant numbers experiencing health outcomes in each arm were extracted independently in duplicate and random effects meta-analyses, meta-regression, sub-grouping, sensitivity analyses and funnel plots were performed. This updated review suggested that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of cardiovascular events by 14% (RR 0.86, 95% CI 0.77 to 0.96, 24 comparisons, 65,508 participants of whom 7% had a cardiovascular event, I(2) 50%). Subgrouping suggested that this reduction in cardiovascular events was seen in studies of fat modification (not reduction - which related directly to the degree of effect on serum total and LDL cholesterol and triglycerides), of at least two years duration and in studies of men (not of women). There were no clear effects of dietary fat changes on total mortality (RR 0.98, 95% CI 0.93 to 1.04, 71,790 participants) or cardiovascular mortality (RR 0.94, 95% CI 0.85 to 1.04, 65,978 participants). This did not alter with sub-grouping or sensitivity analysis.Few studies compared reduced with modified fat diets, so direct comparison was not possible. The findings are suggestive of a small but potentially important reduction in cardiovascular risk on modification of dietary fat, but not reduction of total fat, in longer trials. Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups, should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturates. The ideal type of unsaturated fat is unclear.Cochrane database of systematic reviews (Online) 01/2011; · 5.70 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Cardiovascular disease (CVD) today is responsible for approximately one-third of deaths worldwide, and that figure will surely increase in both developing and developed countries as risk factors for the disease--primarily dyslipidemia, hypertension, obesity, diabetes, physical inactivity, poor diet, and smoking--continue to increase. Although these risk factors are modifiable, to date there is a relative paucity of measures to prevent or control them, particularly in developing countries. A population strategy combined with a high-risk strategy for CVD prevention could greatly reduce the burden of disease in the coming decades. Many initiatives are working, but many more are needed. This chapter provides background on the global burden of CVD and provides the context for the subsequent chapters addressing nurses' roles in reversing the bleak predictions for the ravages of CVD if risk factors are left unchecked in the coming decades.European Journal of Cardiovascular Nursing 07/2011; 10 Suppl 2:S5-13. · 2.04 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: A family history, reflecting genetic susceptibility as well as shared environmental and behavioral factors, is an important risk factor for common chronic multifactorial diseases such as cardiovascular diseases, type 2 diabetes and many cancers. The purpose of the present paper is to discuss the evidence for the use of family history as a tool for primary prevention of common chronic diseases, in particular for tailored interventions aimed at promoting healthy lifestyles. The following questions are addressed: (1) What is the value of family history information as a determinant of personal disease risk?; (2)How can family history information be used to motivate at-risk individuals to adopt and maintain healthy lifestyles in order to prevent disease?; and (3) What additional studies are needed to assess the potential value of family history information as a tool to promote a healthy lifestyle? In addition to risk assessment, family history information can be used to personalize health messages, which are potentially more effective in promoting healthy lifestyles than standardized health messages. More research is needed on the evidence for the effectiveness of such a tool.BMC Public Health 01/2010; 10:248. · 2.08 Impact Factor