People with intellectual disability often face barriers accessing mainstream psychological services due to a lack of reasonable adjustments, including the absence of adapted versions of routine outcome measures. Adapted versions of the Patient Health Questionnaire-9 (PHQ-9) and the Generalised Anxiety Disorder-7 (GAD-7) have been created for adults with ID.

This study aims to evaluate the psychometric properties of the adapted PHQ-9 and GAD-7.

The adapted PHQ-9 and GAD-7 and the Glasgow Depression and Anxiety Scales (GDS-ID, GAS-ID) were administered to 47 adults (n=21 clinical group; n=26 community group) with ID. Cross-sectional design and between-group analyses tested for discriminant validity. Concurrent and divergent validity was tested using correlational designs. Reliability was investigated by internal consistency and test–retest analysis.

The clinical group scored significantly higher on the adapted PHQ-9 (t45=–2.28, p=.03, 95% CI [–7.09, –.45]) and GAD-7 (t45=–3.52, p=.001, 95% CI [–7.44, –2.02]) than the community group, evidencing discriminant validity. The adapted PHQ-9 correlated with the GDS-ID (r47=.86, p<.001) and the adapted GAD-7 correlated with the GAS-ID (r46=.77, p<.001). The adapted PHQ-9 (Cronbach’s α=.84, ICC=.91) and GAD-7 (Cronbach’s α=.86, ICC=.77) had good internal consistency and test–retest reliability.

Preliminary research suggests the adapted PHQ-9 and GAD-7 are valid and reliable measures. They could provide a reasonable adjustment for the minimum dataset used in NHS Talking Therapies and can be easily administered in routine clinical practice. Further work to establish additional psychometric properties is now required.

Anxiety disorders are common, and cognitive–behavioural therapy (CBT) is a first-line treatment. Candidate gene studies have suggested a genetic basis to treatment response, but findings have been inconsistent.

To perform the first genome-wide association study (GWAS) of psychological treatment response in children with anxiety disorders (n = 980).

Presence and severity of anxiety was assessed using semi-structured interview at baseline, on completion of treatment (post-treatment), and 3 to 12 months after treatment completion (follow-up). DNA was genotyped using the Illumina Human Core Exome-12v1.0 array. Linear mixed models were used to test associations between genetic variants and response (change in symptom severity) immediately post-treatment and at 6-month follow-up.

No variants passed a genome-wide significance threshold (P=5×10–8) in either analysis. Four variants met criteria for suggestive significance (P<5×10–6) in association with response post-treatment, and three variants in the 6-month follow-up analysis.

This is the first genome-wide therapygenetic study. It suggests no common variants of very high effect underlie response to CBT. Future investigations should maximise power to detect single-variant and polygenic effects by using larger, more homogeneous cohorts.

We previously reported an association between 5HTTLPR genotype and outcome following cognitive–behavioural therapy (CBT) in child anxiety (Cohort 1). Children homozygous for the low-expression short-allele showed more positive outcomes. Other similar studies have produced mixed results, with most reporting no association between genotype and CBT outcome.

To replicate the association between 5HTTLPR and CBT outcome in child anxiety from the Genes for Treatment study (GxT Cohort 2,n = 829).

Logistic and linear mixed effects models were used to examine the relationship between 5HTTLPR and CBT outcomes. Mega-analyses using both cohorts were performed.

There was no significant effect of 5HTTLPR on CBT outcomes in Cohort 2. Mega-analyses identified a significant association between 5HTTLPR and remission from all anxiety disorders at follow-up (odds ratio 0.45,P = 0.014), but not primary anxiety disorder outcomes.

The association between 5HTTLPR genotype and CBT outcome did not replicate. Short-allele homozygotes showed more positive treatment outcomes, but with small, non-significant effects. Future studies would benefit from utilising whole genome approaches and large, homogenous samples.

To examine the use of vitamin D supplements during infancy among the participants in an international infant feeding trial.

Longitudinal study.

Information about vitamin D supplementation was collected through a validated FFQ at the age of 2 weeks and monthly between the ages of 1 month and 6 months.

Infants (n 2159) with a biological family member affected by type 1 diabetes and with increased human leucocyte antigen-conferred susceptibility to type 1 diabetes from twelve European countries, the USA, Canada and Australia.

Daily use of vitamin D supplements was common during the first 6 months of life in Northern and Central Europe (>80 % of the infants), with somewhat lower rates observed in Southern Europe (>60 %). In Canada, vitamin D supplementation was more common among exclusively breast-fed than other infants (e.g. 71 % v. 44 % at 6 months of age). Less than 2 % of infants in the USA and Australia received any vitamin D supplementation. Higher gestational age, older maternal age and longer maternal education were study-wide associated with greater use of vitamin D supplements.

Most of the infants received vitamin D supplements during the first 6 months of life in the European countries, whereas in Canada only half and in the USA and Australia very few were given supplementation.