Declining 1-year case-fatality of stroke and increasing coverage of vascular risk management: population-based cohort study

Background The authors estimated trends in 1-year case-fatality of stroke in relation to changes in vascular risk management from 1997 to 2005.Methods A cohort study was implemented using data for 407 family practices in the UK General Practice Research Database, including subjects with first acute strokes between 1997 and 2005. One-year case-fatality was estimated by year and sex. Rate ratios were estimated using Poisson regression.Results There were 19 143 women and 16 552 men who had first acute strokes between 1997 and 2005. In women, the 1-year case-fatality declined from 41.2% in 1997 to 29.2% in 2005. In men, the decline was from 29.2% in 1997 to 22.2% in 2005. The proportion of general practices that prescribed antihypertensive drugs to two-thirds or more of new patients with stroke increased from 6% in 1997 to 48% in 2005, for statins from 1% to 39% and for antiplatelet drugs from 11% to 39%. The rate ratio for 1-year mortality in 2005, compared with 1997--1998, adjusted for age group, sex, prevalent coronary heart disease, prevalent hypertension and deprivation quintile was 0.79 (0.74 to 0.86, p<0.001). After adjustment for antihypertensive, statin and antiplatelet prescribing, the rate ratio was 1.29 (1.17 to 1.42).Conclusions Reducing 1-year case-fatality after acute stroke may be partly explained by increased prescribing of antihypertensive, statin and antiplatelet drugs to patients with recent strokes. However, these analyses did not include measures of possible changes over time in stroke severity or acute stroke management

Three-year tracking of fatty acid composition of plasma phospholipids in healthy children

Objectives: The fatty acid composition of plasma phospholipids reflects the dietary fatty acid intake as well as endogenous turnover. We aimed at investigating the potential tracking of plasma phospholipid fatty acid composition in children that participated in a prospective cohort study. Methods: 26 healthy children participated in a longitudinal study on health risks and had been enrolled after birth. All children were born at term with birth weights appropriate for gestational age. Follow-up took place at ages 24, 36 and 60 months. At each time point a 24-hour dietary recall was obtained, anthropometric parameters were measured and a blood sample for phospholipid fatty acid analysis was taken. Results: Dietary intake of saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids at the three time points were not correlated. We found lower values for plasma MUFA and the MUFA/SFA ratio at 60 months compared to 24 months. In contrast, total PUFA, total n-6 and n-6 long-chain polyunsaturated fatty acids (LC-PUFA) were higher at 60 months. Significant averaged correlation coefficients (average of Pearson's R for 24 versus 36 months and 36 versus 60 months) were found for n-6 LC-PUFA (r = 0.67), n-6/n-3 LC-PUFA ratio (r = 0.59) and arachidonic acid/linoleic acid ratio (r = 0.64). Partial tracking was found for the docosahexaenoic acid/alpha-linolenic acid ratio (r = 0.33). Body mass index and sum of skinfolds Z-scores were similar in the three evaluations. Conclusions: A significant tracking of n-6 LC-PUFA, n-6 LC-PUFA/n-3 LC-PUFA ratio, arachidonic acid/ linoleic acid ratio and docosahexaenoic acid/alpha-linolenic acid ratio may reflect an influence of individual endogenous fatty acid metabolism on plasma concentrations of some, but not all, fatty acids. Copyright (c) 2007 S. Karger AG, Basel

Is low birth weight in the causal pathway of the association between maternal smoking in pregnancy and higher BMI in the offspring?

A number of cross-sectional and prospective studies suggested a priming effect of maternal smoking in pregnancy on offspring’s obesity. It has been hypothesized that this association might be explained by low birth weight and subsequent catch-up growth in the causal pathway. We therefore examined the role of birth weight in children exposed versus not exposed to cigarette smoking in utero on later body mass index (BMI). Using data of 12,383 children and adolescents (3–17 years of age) recorded in a German population-based survey (KiGGS), we assessed mean body mass index standard deviation scores (BMI-SDS) in different birth weight SDS categories, stratified for children with smoking and non-smoking mothers. We calculated spline regression models with BMI-SDS as outcome variable, cubic splines of birth weight SDS, and potential confounding factors. Children whose mothers had been smoking during pregnancy had lower birth weight SDS and higher BMI-SDS at interview compared to children of non-smoking mothers. However, we observed a linear association between birth weight SDS and BMI-SDS in crude analyses for both groups. Similarly, almost linear effects were observed in adjusted spline regression analyses, except for children with very low birth weight. The respective 95% confidence bands did not preclude a linear effect for the whole birth weight SDS distribution. Our findings suggest that low birth weight is unlikely to be the main cause for the association between intrauterine nicotine exposure and higher BMI in later life. Alternative mechanisms, such as alterations in the noradrenergic system or increased food efficiency, have to be considered