Smoking in preeclamptic women is associated with higher birthweight for gestational age and lower soluble fms-like tyrosine kinase-1 levels: a nested case control study

<p>Abstract</p> <p>Background</p> <p>Smoking paradoxically increases the risk of small-for-gestational-age (SGA) birth but protects against preeclampsia. Some studies have reported a "U-shaped" distribution of fetal growth in preeclamptic pregnancies, but reasons for this are unknown. We investigated whether cigarette smoking interacts with preeclampsia to affect fetal growth, and compared levels of soluble fms-like tyrosine kinase-1 (sFlt-1), a circulating anti-angiogenic protein, in preeclamptic smokers and non-smokers.</p> <p>Methods</p> <p>From a multicenter cohort of 5337 pregnant women, we prospectively identified 113 women who developed preeclampsia (cases) and 443 controls. Smoking exposure was assessed by self-report and maternal hair nicotine levels. Fetal growth was assessed as z-score of birthweight for gestational age (BWGA). sFlt-1 was measured in plasma samples collected at the 24-26-week visit.</p> <p>Results</p> <p>In linear regression, smoking and preeclampsia were each associated with lower BWGA z-scores (β = -0.29; p = 0.008, and β = -0.67; p < 0.0001), but positive interaction was observed between smoking and preeclampsia (β = +0.86; p = 0.0008) such that smoking decreased z-score by -0.29 in controls but increased it by +0.57 in preeclampsia cases. Results were robust to substituting log hair nicotine for self-reported smoking and after adjustment for confounding variables. Mean sFlt-1 levels were lower in cases with hair nicotine levels above vs. below the median (660.4 pg/ml vs. 903.5 pg/ml; p = 0.0054).</p> <p>Conclusions</p> <p>Maternal smoking seems to protect against preeclampsia-associated fetal growth restriction and may account, at least partly, for the U-shaped pattern of fetal growth described in preeclamptic pregnancies. Smoking may exert this effect by reducing levels of the anti-angiogenic protein sFlt-1.</p

Associations of free sugars from solid and liquid sources with cardiovascular disease: a retrospective cohort analysis

Abstract Background The World Health Organization recommends a 10% total energy (TE%) limit for free sugars (i.e., added sugars and naturally occurring sugars in fruit juice, honey, and syrups) based on evidence linking higher intakes with overweight and dental caries. Evidence for cardiovascular disease (CVD) is limited. Impacts may differ by sex, age group, and solid vs. liquid sources; liquids may stimulate more adverse CVD profiles (due to their rapid absorption in the body along along with triggering less satiety). We examined associations of consuming total free sugars ≥ 10 TE% with CVD within four sex and age-defined groups. Given roughly equal free sugar intakes from solid and liquid sources, we also evaluated source-specific associations of free sugars ≥ 5 TE% thresholds. Methods In this retrospective cohort study, we estimated free sugars from 24-h dietary recall (Canadian Community Health Survey, 2004–2005) in relationship to nonfatal and fatal CVD (Discharge Abstract and Canadian Mortality Databases, 2004–2017; International Disease Classification-10 codes for ischemic heart disease and stroke) through multivariable Cox proportional hazards models adjusted for overweight/obesity, health behaviours, dietary factors, and food insecurity. We conducted analyses in separate models for men 55 to 75 years, women 55 to 75 years, men 35 to 55 years, and women 35 to 55 years. We dichotomized total free sugars at 10 TE% and source-specific free sugars at 5 TE%. Results Men 55 to 75 years of age had 34% higher CVD hazards with intakes of free sugars from solid sources ≥ 5 TE% vs. below (adjusted HR 1.34, 95% CI 1.05- 1.70). The other three age and sex-specific groups did not demonstrate conclusive associations with CVD. Conclusions Our findings suggest that from a CVD prevention standpoint in men 55 to 75 years of age, there may be benefits from consuming less than 5 TE% as free sugars from solid sources

The double jeopardy of clustered measurement and cluster randomisation

Michael S Kramer and colleagues suggest that double clustering might explain the negative results of some cluster randomised trials and describe some strategies for avoiding the proble

Novembre-décembre 1993 en France : Chronologie

Cheyron Christiane. Novembre-décembre 1993 en France : Chronologie. In: Hommes et Migrations, n°1172-1173, Janvier-février 1994. Minorités au Proche-Orient. pp. 111-113