Although case studies in avoidant/restrictive food intake disorder (ARFID) indicate severe nutritional deficiencies in those with a highly limited amount or variety of food intake, systematic analyses on food intake in treatment-seeking children and adolescents with ARFID are lacking. Within this study, n = 20 patients with an interview-based diagnosis of ARFID (0–17 years) were included and compared to n = 20 healthy controls individually matched for age and sex. Children or parents completed three-day food diaries and a food list. Macronutrient, vitamin, and mineral supply was determined based on the percentage of their recommended intake. The results showed a significantly lower total energy and protein intake in ARFID versus controls, with trends for lower fat and carbohydrate intake. ARFID subtypes of limited amount versus variety of food intake significantly differed in macro-, but not micronutrient intake. Those with ARFID met only 20–30% of the recommended intake for most vitamins and minerals, with significantly lower intake relative to controls for vitamin B1, B2, C, K, zinc, iron, and potassium. Variety of food intake was significantly reduced in ARFID versus controls in all food groups except carbohydrates. This study demonstrated that ARFID goes along with reduced everyday life macro- and micronutrient intake, which may increase the risk for developmental and health problems. Future studies additionally assessing serum nutrient levels in a larger sample may further explore differences in food intake across diverse ARFID presentations.

Different forms of maltreatment are thought to incur a cumulative and non-specific toll on mental health. However, few large-scale studies draw on psychiatric diagnoses manifesting in early childhood and adolescence to identify sequelae of differential maltreatment exposures, and emotional maltreatment, in particular. Fine-grained multi-source dimensional maltreatment assessments and validated age-appropriate clinical interviews were conducted in a sample of N = 778 3 to 16-year-olds. We aimed to (a) substantiate known patterns of clinical outcomes following maltreatment and (b) analyse relative effects of emotional maltreatment, abuse (physical and sexual), and neglect (physical, supervisory, and moral-legal/educational) using structural equation modeling. Besides confirming known relationships between maltreatment exposures and psychiatric disorders, emotional maltreatment exerted particularly strong effects on internalizing disorders in older youth and externalizing disorders in younger children, accounting for variance over and above abuse and neglect exposures. Our data highlight the toxicity of pathogenic relational experiences from early childhood onwards, urging researchers and practitioners alike to prioritize future work on emotional maltreatment.

Objective: The IGF/IGF1R axis is involved in the regulation of human growth. Both IGF1 and IGF2 can bind to the IGF1R in order to promote growth via the downstream PI3K/AKT pathway. Pathogenic mutations in IGF1 and IGF1R determine intrauterine growth restriction and affect postnatal body growth. However, to date, there are only few reports of pathogenic IGF2 mutations causing severe prenatal, as well as postnatal growth retardation. Results: Here we describe a de novo c.195delC IGF2 variant (NM_000612, p.(Ile66Serfs*93)) in a 4-year-old patient with severe pre-and postnatal growth retardation in combination with dystrophy, facial dimorphism, finger deformities, as well as a patent ductus. Cloning and sequencing of a long-range PCR product harboring the deletion and a SNP informative site chr11:2153634 (rs680, NC_000011.9:g.2153634T>C) demonstrated that the variant resided on the paternal allele. This finding is consistent with the known maternal imprinting of IGF2. 3D protein structure prediction and overexpression studies demonstrated that the p.(Ile66Serfs*93) IGF2 gene variation resulted in an altered protein structure that impaired ligand/receptor binding and thus prevents IGF1R activation. Conclusion: The severity of the phenotype in combination with the dominant mode of transmission provides further evidence for the involvement of IGF2 in growth disorders. Figure 3Illustration of potential conformational changes in p.I66S protein structure. (A) Schematic diagram of IGF2 maturation. IGF2 encodes an inactive 180-aa precursor protein which is post-translationally cleaved into a 67-aa bioactive protein. First, the terminal signal peptide is proteolytically removed creating a 156-aa sequence. In the next step, the trailer sequence is proteolytically cleaved at two separated sites (TQRLRR 104 and PAKSER 68 ) generating the bioactive protein. (B) Illustration of p.I66S protein structure. Sequence analyses of the cleavage sites indicated a changed aa sequence at basic residues in the mutant: TQRLRR→PSACAG and PAKSER→PPSPRG. (C) Comparison of the WT (IGF2-WT, blue) and mutant (IGF2-I66S, red) protein structure.3D protein structure was predicted based on the crystal structure of IGF2-WT (pdb: 1IGL) using the iTASSER server and superpositioned with the WT structure. The mostly unstructured C-terminal extension due to the lack of posttranslational processing is illustrated. (D) Upper panel: Schematic presentation of IGF2 plasmids. The position of the c.195delC mutation is marked in red. Lower panel: Cell lysates and supernatants from transfected cells after immunoblotting with the indicated antibodies. (E) Whole-cell lysates from IGF1 stimulated (30 min) cells transfected with an IGF1R plasmid were subjected to immunoblotting using antibodies as indicated. (F) Whole-cell lysates were prepared from IGF1R transfected cells after stimulation (30 min) with IGF2-WT supernatants and immunoblotted for pIGF1R, total IGF1R and β-actin as loading control. Representative blot out of three independent experiments is shown.Figure 4...

Objective This study presents a psychometric evaluation of the avoidant/restrictive food intake disorder (ARFID) module 2.0 for the Eating Disorder Examination (EDE), its child (ChEDE), and parent version. Within a pediatric sample seeking treatment for restrictive feeding or eating disorders and non‐treatment‐seeking controls, the module's interrater reliability, parent–child agreement, and its convergent, divergent, and discriminant validity were examined. Method The child, adult, and/or parent version of the German ARFID module was administered to N = 176 children and adolescents (0–17 years) and their parents, as were the (Ch)EDE, well‐established measures on food‐avoidance behaviors, food variety, and body esteem, and objective anthropometric measures. Results Across all versions of the ARFID module, substantial to almost perfect interrater reliability was shown. Parent–child agreement for ARFID diagnosis was substantial. Based on medium‐to‐large associations between interview‐assessed avoidant/restrictive food intake and questionnaire‐assessed food‐avoidance behaviors, food variety, and objective weight status, the module showed high convergent validity, especially for the child and parent version. Low associations of avoidant/restrictive food intake with weight and shape concern demonstrated divergent validity. Individuals with ARFID differed significantly from those with anorexia nervosa and individually matched controls in a range of clinical characteristics, indicating discriminant validity. Discussion This comprehensive validation supports the EDE ARFID module to be a valuable measure for the assessment and diagnosis of ARFID in 0–17‐year‐olds based on self‐ and parent‐report. Validation of the ARFID module against other interview‐based measures on ARFID and its evaluation in an adult sample are pending. Public Significance Based on good reliability and validity of the avoidant/restrictive food intake disorder (ARFID) module for the Eating Disorder Examination (EDE) in its child, adult, and parent version, the present study paves the way for the clinical and research use of the interview‐based EDE ARFID module for assessing ARFID across childhood and adolescence.

Background The first years of life are a significant period for child development, when children are particularly sensitive and prone to crises. This early phase lays the foundation for healthy growth. Clinical assessment of psychological symptoms in early infancy and adequate treatment are both important in improving the diagnostic outcome and preventing later long-term developmental consequences. The most common psychological problems in the first 3 years of life are regulatory disorders. The aim of this trial is to investigate the efficacy of Parent-Infant Psychotherapy (PIP) for infants and young children (aged 0–36 months, diagnosed with at least one regulatory disorder) and their mothers, compared to care as usual (CAU). Methods In this open multicentre randomised controlled trial, 160 mother-infant dyads are randomised to receive PIP or CAU for 6 weeks of intervention in clinical or outpatient (including home treatment) settings. The primary outcome is the maternal sensitivity (sensitivity scale of the Emotional Availability Scales (EAS)) after 6 weeks. Secondary outcomes include assessment of interaction, mental health problems, attachment, development, psychological factors, treatment adherence, health care system utilisation, and costs, after 6 weeks and 12 months. Discussion This study will evaluate whether a manualised focus-based short-term psychodynamic psychotherapeutic intervention in mother-child dyads improves the care situation for families of children diagnosed with regulatory disorders, and helps prevent long-term psychopathologies. Assessment of the intervention in different settings will support the development of more tailored interventions for affected infants and their mothers. Trial registration German Clinical Trial Register, ID: DRKS00017008. Registered 03/20/2019.