BackgroundChildren of parents with mental disorder face multiple challenges.AimsTo summarise evidence about parental mental disorder and child physical health.MethodWe searched seven databases for cohort or case–control studies quantifying associations between parental mental disorders (substance use, psychotic, mood, anxiety, obsessive–compulsive, post-traumatic stress and eating) and offspring physical health. Studies were excluded if: they reported perinatal outcomes only (<28 days) or outcomes after age 18; they measured outcome prior to exposure; or the sample was drawn from diseased children. A meta-analysis was conducted. The protocol was registered on the PROSPERO database (CRD42017072620).ResultsSearches revealed 15 945 non-duplicated studies. Forty-one studies met our inclusion criteria: ten investigated accidents/injuries; eight asthma; three other atopic diseases; ten overweight/obesity; ten studied other illnesses (eight from low-and middle-income countries (LMICs)). Half of the studies investigated maternal perinatal mental health, 17% investigated paternal mental disorder and 87% examined maternal depression. Meta-analysis revealed significantly higher rates of injuries (OR = 1.15, 95% CI 1.04–1.26), asthma (OR = 1.26, 95% CI 1.12–1.41) and outcomes recorded in LMICs (malnutrition: OR = 2.55, 95% CI 1.74–3.73; diarrhoea: OR = 2.16, 95% CI 1.65–2.84). Evidence was inconclusive for obesity and other atopic disorders.ConclusionsChildren of parents with mental disorder have health disadvantages; however, the evidence base is limited to risks for offspring following postnatal depression in mothers and there is little focus on fathers in the literature. Understanding the physical health risks of these vulnerable children is vital to improving lives. Future work should focus on discovering mechanisms linking physical and mental health across generations.Declaration of interestNone.
BackgroundHigher 25(OH)D3 levels are associated with lower HbA1c, but there are limited UK interventional trials assessing the effect of cholecalciferol on HbA1c.Aims(1) To assess the baseline 25(OH)D3 status in a Manchester cohort of children with type 1 diabetes (T1D). (2) To determine the effect of cholecalciferol administration on HbA1c.MethodsChildren with T1D attending routine clinic appointments over three months in late winter/early spring had blood samples taken with consent. Participants with a 25(OH)D3 level <50 nmol/L were treated with a one-off cholecalciferol dose of 100,000 (2–10 years) or 160,000 (>10 years) units. HbA1c levels before and after treatment were recorded.ResultsVitamin D levels were obtained from 51 children. 35 were Caucasian, 11 South Asian and 5 from other ethnic groups. 42 were vitamin D deficient, but 2 were excluded from the analysis. All South Asian children were vitamin D deficient, with mean 25(OH)D3 of 28 nmol/L. In Caucasians, there was a negative relationship between baseline 25(OH)D3 level and HbA1c (r = −0.484, P < 0.01). In treated participants, there was no significant difference in mean HbA1c at 3 months (t = 1.010, P = 0.328) or at 1 year (t = −1.173, P = 0.248) before and after treatment. One-way ANCOVA, controlling for age, gender, ethnicity, BMI and diabetes duration showed no difference in Δ HbA1c level.ConclusionWe report important findings at baseline, but in children treated with a stat dose of cholecalciferol, there was no effect on HbA1c. Further studies with larger sample sizes and using maintenance therapy are required.
Ghrelin is a pleiotropic hormone, whose effect on growth hormone secretion, through the growth hormone secretagogue (GHS) receptor, is one of its many actions. Relationships between GHS receptor gene variants and human height, both in healthy individuals and in patients with growth disorders have been identified. These include constitutional delay in growth and puberty, idiopathic short stature, and isolated growth hormone deficiency. In this review, we provide an overview of the role of ghrelin in growth.
Background Children with short stature of undefined aetiology (SS-UA) may have undiagnosed genetic conditions. Purpose To identify mutations causing short stature (SS) and genes related to SS, using candidate gene sequence data from the European EPIGROW study. Methods First, we selected exonic single nucleotide polymorphisms (SNPs), in cases and not controls, with minor allele frequency (MAF) < 2%, whose carriage fitted the mode of inheritance. Known mutations were identified using Ensembl and gene-specific databases. Variants were classified as pathogenic, likely pathogenic, or variant of uncertain significance using criteria from the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. If predicted by ≥ 5/10 algorithms (eg, Polyphen2) to be deleterious, this was considered supporting evidence of pathogenicity. Second, gene-based burden testing determined the difference in SNP frequencies between cases and controls across all and then rare SNPs. For genotype/phenotype relationships, we used PLINK, based on haplotype, MAF > 2%, genotype present in > 75%, and Hardy Weinberg equilibrium P > 10–4. Results First, a diagnostic yield of 10% (27/263) was generated by 2 pathogenic (nonsense in ACAN) and a further 25 likely pathogenic mutations, including previously known missense mutations in FANCB, IGFIR, MMP13, NPR2, OBSL1, and PTPN11. Second, genes related to SS: all methods identified PEX2. Another 7 genes (BUB1B, FANCM, CUL7, FANCA, PTCH1, TEAD3, BCAS3) were identified by both gene-based approaches and 6 (A2M, EFEMP1, PRKCH, SOS2, RNF135, ZBTB38) were identified by gene-based testing for all SNPs and PLINK. Conclusions Such panels improve diagnosis in SS-UA, extending known disease phenotypes. Fourteen genes related to SS included some known to cause growth disorders as well as novel targets.
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