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In epidemiologic analytical studies, the primary goal is to obtain a valid and precise estimate of the effect of the exposure of interest on a given outcome in the population under study. A crucial source of violation of the internal validity of a study involves bias arising from confounding, which is always a challenge in observational research, including life course epidemiology. The increasingly popular approach of meta-analyzing individual participant data from several observational studies also brings up to discussion the problem of confounding when combining data from different populations. In this study, we review and discuss the most common sources of confounding in life course epidemiology: (i) confounding by indication, (ii) impact of baseline selection on confounding, (iii) time-varying confounding and (iv) mediator–outcome confounding. We also discuss the issue of addressing confounding in the context of an individual participant data meta-analysis.
Maternal mental disorders have been associated with the risk of attention-deficit/hyperactivity disorder (ADHD) in children. Within the context of a mother–child cohort, we examined whether maternal anxiety, depression and sleep disorders are associated with pre-school ADHD symptoms.
The study included 3634 singletons from the Italian NINFEA (Nascita e INFanzia: gli Effetti dell'Ambiente’) cohort. Maternal doctor-diagnosed anxiety, depression and sleep disorders before and during pregnancy were assessed from the questionnaires completed during pregnancy and 6 months after delivery. Mothers rated child ADHD symptoms at 4 years of age, according to the Diagnostic and Statistical Manual of Mental Disorders. Hyperactive–impulsive (ADHD-H), inattentive (ADHD-I) and total ADHD scores were analysed in the models adjusted for child's gender, first-born status, maternal age, education, alcohol consumption and smoking during pregnancy.
The total ADHD score at age 4 was associated with maternal lifetime anxiety (17.1% percentage difference in score compared with never; 95% CI 7.3–27.9%), sleep disorders (35.7%; 95% CI 10.7–66.5%) and depression (17.5%; 95% CI 3.2–33.8%). Similar positive associations were observed also for ADHD-H and ADHD-I traits, with slightly attenuated associations between maternal sleep disorders and child ADHD-I score, and maternal depression and both ADHD scores. All the estimates were enhanced when the disorders were active during pregnancy and attenuated for disorders active only during the pre-pregnancy period.
Maternal anxiety, depression and sleep disorders are associated with a relative increase in the number of ADHD-H, ADHD-I and total ADHD symptoms in preschoolers.
Coeliac disease (CD) is a malabsorptive disorder of the small intestine resulting from ingestion of
gluten. The HLA risk factors involved in CD are well known but do not explain the whole genetic
susceptibility. Several regions of potential linkage on chromosomes 3q, 5q, 10q, 11q, 15q and 19q
have already been reported in the literature. These six regions were analyzed with the Maximum Lod
Score method on a dense set of markers. A new sample of 89 Italian sibpairs was available for study.
There was no evidence for linkage for any of the regions tested, except for chromosome 5q. For this
region, our data, as well as a sample of 93 sibpairs from our first genome screen (Greco et al. 1998),
are compatible with the presence of a risk factor for CD with a moderate effect.
Coeliac disease (CD) is a multigenic and multifactorial enteropathy triggered by gluten-composing
proteins. A possible involvement of the intestinal Aminopeptidase N (APN) was investigated by an
association analysis. SSCP analysis detected four variants at position 281, 378, 956 and 2957
(referred to no. g178535, GenBank) that were studied in 193 Italian CD families. The haplotypic
combinations were determined from family segregation and pairwise linkage disequilibria
(D′ = D/Dmax) between the polymorphic sites were calculated. Significant D′ values ranged between 0.78
and 0.31. Association with CD was tested by TDT (Transmission Disequilibrium Test) utilizing as
markers the nucleotide substitutions and their haplotypic combinations. No statistically significant
transmission distortion to the probands or to their clinically silent sibs was observed. Our data
exclude an involvement in CD of the tested markers and of further undetected variation in strong
linkage disequilibrium (D′ ≅ 1) with them. The power of the test was not adequate to detect an
association with an unknown polymorphism which is not in complete linkage disequilibrium with
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