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Articles by G. Davey Smith
Total Records ( 2 ) for G. Davey Smith
  B St. Pourcain , K Wang , J. T Glessner , J Golding , C Steer , S. M Ring , D. H Skuse , S. F. A Grant , H Hakonarson and G. Davey Smith
  Objective:

Recent genome-wide analysis identified a genetic variant on 5p14.1 (rs4307059), which is associated with risk for autism spectrum disorder. This study investigated whether rs4307059 also operates as a quantitative trait locus underlying a broader autism phenotype in the general population, focusing specifically on the social communication aspect of the spectrum.

Method:

Study participants were 7,313 children from the Avon Longitudinal Study of Parents and Children. Single-trait and joint-trait genotype associations were investigated for 29 measures related to language and communication, verbal intelligence, social interaction, and behavioral adjustment, assessed between ages 3 and 12 years. Analyses were performed in one-sided or directed mode and adjusted for multiple testing, trait interrelatedness, and random genotype dropout.

Results:

Single phenotype analyses showed that an increased load of rs4307059 risk allele is associated with stereotyped conversation and lower pragmatic communication skills, as measured by the Children's Communication Checklist (at a mean age of 9.7 years). In addition a trend toward a higher frequency of identification of special educational needs (at a mean age of 11.8 years) was observed. Variation at rs4307059 was also associated with the phenotypic profile of studied traits. This joint signal was fully explained neither by single-trait associations nor by overall behavioral adjustment problems but suggested a combined effect, which manifested through multiple sub-threshold social, communicative, and cognitive impairments.

Conclusions:

Our results suggest that common variation at 5p14.1 is associated with social communication spectrum phenotypes in the general population and support the role of rs4307059 as a quantitative trait locus for autism spectrum disorder.

  D. Kuh , G. D. Mishra , S. Black , D. A. Lawlor , G. Davey Smith , L. Okell , M. Wadsworth and R. Hardy
 

Aims We investigated pathways linking offspring birth weight to maternal diabetes risk in later life by taking into account a range of prospective early-life and adult maternal factors.

Methods In a national birth cohort study, we examined the relationship between offspring birth weight and maternal glycated haemoglobin (HbA1c) at age 53 years in 581 mothers who had a first birth between age 19 and 25 years, and had data on potential confounders or mediators.

Results Mean age at first birth was 21.5 years. After adjustment for maternal body mass index (BMI), mean percentage change in maternal HbA1c per kilogram increase in offspring birth weight was −1.8%[95% confidence interval (CI) −3.5, −0.1; P=0.03]. This relationship was mostly accounted for by gestational age that was inversely related to maternal HbA1c (−0.9%; 95% CI −1.5, −0.4; P=0.001). Other risk factors for high HbA1c were smoking and high BMI at 53 years. There was a significant interaction between offspring birth weight and maternal childhood social class (P=0.01). Mothers from a manual background with higher birth weight offspring had lower HbA1c (BMI adjusted: −3.1%; 95% CI −5.0, −1.1); this was not observed for mothers from a non-manual background (BMI adjusted: 1.9%; 95% CI −1.3, 5.0).

Conclusions Short gestational age and low offspring birth weight may be part of a pathway linking impaired early maternal growth to diabetes risk in later life. A second possible pathway linking higher offspring birth weight to later maternal glucose status was also identified. These potential pathways require further investigation in cohorts with a wider maternal age range so that the early targeting of public health initiatives can be assessed.

 
 
 
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