Aims: To examine the effect that within-person variation has on the estimated risk associations between cigarette smoking, physical inactivity, and increased body mass index(BMI) and the development of cardiovascular ...Aims: To examine the effect that within-person variation has on the estimated risk associations between cigarette smoking, physical inactivity, and increased body mass index(BMI) and the development of cardiovascular disease(CVD) in middle aged Britishmen. Methods and results: In total, 6452 men aged 40-59 with no prior evidence of CVD were followed for major CVD events(fatal/non-fatal myocardial infarction or stroke)and all-cause mortality over 20 years; lifestyle characteristics were ascertained at regular points throughout the study. A major CVD event within the first 20 years was observed in 1194 men(18.5%). Use of baseline assessments of cigarette smoking and physical activity in analyses resulted in underestimation of the associations between average cumulative exposure to these factors and major CVD risk. After correction for within-person variation, major CVD rates were over four times higher for heavy smokers(≥40 cigarettes/day) compared with never smokers and three times higher for physically inactive men compared with moderately active men. Major CVD risk increased by 6%for each 1 kg/m2 increase in usual BMI. If all men had experienced the risk levels of the men who had never regularly smoked cigarettes, were moderately active, and had a BMI of ≤25 kg/m2(6%of the population), 66%of the observed major CVD events would have been prevented or postponed(63%before adjustment for within-person variation). Adjustment for a range of other risk factors had little effect on the results. Similar results were obtained for all-cause mortality. Conclusion: Failure to take account of within-person variation can lead to underestimation of the importance of lifestyle characteristics in determining CVD risk. Primary prevention through lifestyle modification has a great preventive potential.展开更多
Context: Inverse associations between birth weight and subsequent blood cholesterol levels have been used to support the “fetal origins”hypothesis of the relevance of fetal nutrition to adult disease. Objectives: To...Context: Inverse associations between birth weight and subsequent blood cholesterol levels have been used to support the “fetal origins”hypothesis of the relevance of fetal nutrition to adult disease. Objectives: To perform a systematic review of the association between birth weight and total blood cholesterol levels, and to explore the impact of including unpublished results, adjusting for potential confounders. Data Sources and Study Selection: Relevant studies published by September 30, 2004, were identified through literature searches using EMBASE and MEDLINE and MeSH heading search strategy(using terms such as birth weight, intrauterine growth retardation, fetal growth retardation and cholesterol, lipoprotein, lipid). Studies that reported qualitative or quantitative estimates of the association between birth weight and total blood cholesterol, or had recorded both measures but not reported on their associations, were included. Data Extraction: A total of 79 relevant studies involving a total of 74122 individuals were identified; 65 had reported on the direction of the association between birth weight and total blood cholesterol. Although regression coefficients were published for only 11 studies and other quantitative estimates for 3 other studies, regression coefficients(published or unpublished)were obtained for 58 studies among 68974 individuals. Data Synthesis: Inverse associations were observed in 11 of 14 studies that had previously published quantitative estimates but in only 18 of the remaining 51 that had reported on the direction of this association(heterogeneity P=.004). Similarly, the weighted estimate for the 11 studies was -1.89 mg/dL(-0.049 mmol/L)total cholesterol per kilogram birth weight compared with -0.69 mg/dL(-0.018 mmol/L)per kilogram for 47 studies that provided unpublished regression coefficients(heterogeneity P=.009). Overall, the weighted estimate from the 58 contributing studies was-1.39 mg/dL(-0.036 mmol/L)per kilogram(95%confidence interval, -1.81 to -0.97 mg/dL [-0.047 to -0.025 mmol/L]), but there was significant heterogeneity between their separate results(P< .001). Part of this heterogeneity appears to reflect stronger associations reported from smaller studies and studies of cholesterol levels in infants. Conclusion: These findings suggest that impaired fetal growth does not have effects on blood cholesterol levels that would have a material impact on vascular disease risk.展开更多
文摘Aims: To examine the effect that within-person variation has on the estimated risk associations between cigarette smoking, physical inactivity, and increased body mass index(BMI) and the development of cardiovascular disease(CVD) in middle aged Britishmen. Methods and results: In total, 6452 men aged 40-59 with no prior evidence of CVD were followed for major CVD events(fatal/non-fatal myocardial infarction or stroke)and all-cause mortality over 20 years; lifestyle characteristics were ascertained at regular points throughout the study. A major CVD event within the first 20 years was observed in 1194 men(18.5%). Use of baseline assessments of cigarette smoking and physical activity in analyses resulted in underestimation of the associations between average cumulative exposure to these factors and major CVD risk. After correction for within-person variation, major CVD rates were over four times higher for heavy smokers(≥40 cigarettes/day) compared with never smokers and three times higher for physically inactive men compared with moderately active men. Major CVD risk increased by 6%for each 1 kg/m2 increase in usual BMI. If all men had experienced the risk levels of the men who had never regularly smoked cigarettes, were moderately active, and had a BMI of ≤25 kg/m2(6%of the population), 66%of the observed major CVD events would have been prevented or postponed(63%before adjustment for within-person variation). Adjustment for a range of other risk factors had little effect on the results. Similar results were obtained for all-cause mortality. Conclusion: Failure to take account of within-person variation can lead to underestimation of the importance of lifestyle characteristics in determining CVD risk. Primary prevention through lifestyle modification has a great preventive potential.
文摘Context: Inverse associations between birth weight and subsequent blood cholesterol levels have been used to support the “fetal origins”hypothesis of the relevance of fetal nutrition to adult disease. Objectives: To perform a systematic review of the association between birth weight and total blood cholesterol levels, and to explore the impact of including unpublished results, adjusting for potential confounders. Data Sources and Study Selection: Relevant studies published by September 30, 2004, were identified through literature searches using EMBASE and MEDLINE and MeSH heading search strategy(using terms such as birth weight, intrauterine growth retardation, fetal growth retardation and cholesterol, lipoprotein, lipid). Studies that reported qualitative or quantitative estimates of the association between birth weight and total blood cholesterol, or had recorded both measures but not reported on their associations, were included. Data Extraction: A total of 79 relevant studies involving a total of 74122 individuals were identified; 65 had reported on the direction of the association between birth weight and total blood cholesterol. Although regression coefficients were published for only 11 studies and other quantitative estimates for 3 other studies, regression coefficients(published or unpublished)were obtained for 58 studies among 68974 individuals. Data Synthesis: Inverse associations were observed in 11 of 14 studies that had previously published quantitative estimates but in only 18 of the remaining 51 that had reported on the direction of this association(heterogeneity P=.004). Similarly, the weighted estimate for the 11 studies was -1.89 mg/dL(-0.049 mmol/L)total cholesterol per kilogram birth weight compared with -0.69 mg/dL(-0.018 mmol/L)per kilogram for 47 studies that provided unpublished regression coefficients(heterogeneity P=.009). Overall, the weighted estimate from the 58 contributing studies was-1.39 mg/dL(-0.036 mmol/L)per kilogram(95%confidence interval, -1.81 to -0.97 mg/dL [-0.047 to -0.025 mmol/L]), but there was significant heterogeneity between their separate results(P< .001). Part of this heterogeneity appears to reflect stronger associations reported from smaller studies and studies of cholesterol levels in infants. Conclusion: These findings suggest that impaired fetal growth does not have effects on blood cholesterol levels that would have a material impact on vascular disease risk.
