Rachel Bryant-Waugh

Objective: Increasing numbers of young people (YP) are seeking support for eating disorders, creating a growing unmet need for timely and accessible treatment. While guided self‐help (GSH) interventions have demonstrated effectiveness for other youth mental health difficulties, options for eating disorders remain limited. SPICE (Short Psychological Intervention for Children with Eating Disorders), a transdiagnostic CBT‐based GSH program, was developed to address this gap. This qualitative study explored participant perspectives on the mechanisms through which SPICE may support recovery. Method: SPICE comprises eight weekly modules supported by a 30‐min guided therapy session each week. Six female adolescents with eating disorders and their parents who completed SPICE participated in semi‐structured post‐intervention interviews. Data were analyzed using critical realist thematic analysis. Results: Four key putative mechanisms were identified: (1) Interpersonal support (from the guide and parents) as a catalyst for change and for keeping momentum going. (2) Increased knowledge of eating disorders and associated cognitive and behavioural factors leading to positive changes. (3) In vivo experiential learning as key to implementing specific strategies and taking ownership over change. (4) Context, that is, individual and systemic factors promoting and inhibiting change. Discussion: Interpersonal relationships were perceived to promote engagement and change. Participants reported that psychoeducation empowered them and their families, while experiential learning helped translate strategies into everyday practice. Flexible and tailored approaches were considered important for improving accessibility and effectiveness. Perceived barriers included complex module content, remote delivery, and competing commitments. Findings provide preliminary support for GSH interventions for eating disorders in YP and identify areas for refining future intervention.

Background: Avoidant Restrictive Food Intake Disorder (ARFID) is a relatively newly classified eating disorder which can significantly impact physical health and psychosocial function. This qualitative study aimed to explore the lived experience of ARFID caregivers in order to develop understanding of the condition and how it should be supported. Methods: Semi-structured interviews were conducted with the parents of sixteen children and young people with ARFID, who were recruited from an outpatient eating disorder service in the UK. Interview transcripts were analysed using Reflexive Thematic Analysis. Results: Qualitative analyses revealed four key themes: (1) From fussy eating to something more: The development of ARFID, (2) A fragile process: Factors that worsen and maintain ARFID (3), Developing a toolkit: Learning what helps, and (4) The weight of ARFID: The burden on the whole family. A conceptual model of ARFID development and maintenance is proposed, illustrating the relationships and interactions between the themes captured in the analysis. Conclusions: This study provides insight into the nature and course of ARFID, highlights the widespread impact on the individual and their family, and illustrates the critical role that parents play in managing this eating disorder.

Objective: To assess clinical outcomes and parental experiences following an intensive multidisciplinary intervention (IMI) for children with Avoidant Restrictive Food Intake Disorder (ARFID). Method: A prospective cohort of 28 children (aged 2–8 years) with severe eating difficulties, all meeting ARFID diagnostic criteria at baseline, participated in a 3‐day assessment and an 8‐day IMI involving guided mealtimes, play‐based exposures, nutritional counseling, and caregiver coaching. Clinical outcomes were assessed using the Pica, ARFID, and Rumination Disorder Interview (PARDI) at baseline and at 7–15 months post‐intervention. Parental experience was evaluated using the Experience of Service Questionnaire (ESQ) and the study‐specific Eating Intervention Experience Questionnaire (EIEQ). Results: At follow‐up, 27 of 28 children continued to meet ARFID criteria; however, overall symptom severity decreased significantly ( M = 3.55 → 2.57, d = 0.80, p < 0.001), with reductions in both the sensory ( M = 2.77 → 2.21, d = 0.63, p = 0.002) and low‐interest profiles ( M = 3.48 → 2.50, d = 0.93, p < 0.001), alongside improvements in nutritional status and growth‐related criteria. Parents reported high satisfaction with the intervention, valuing the multidisciplinary approach, tailored support, and practical strategies. Discussion: Findings suggest that intensive, multidisciplinary, nondirective interventions may yield clinically meaningful benefits for young children with severe ARFID, particularly those with combined sensory sensitivity and low interest in eating profiles. Although full remission was uncommon within the follow‐up period, the intervention supported symptom reduction and caregiver competence. Larger controlled studies are needed to establish efficacy and guide development of sustainable models of care.

Background: Avoidant Restrictive Food Intake Disorder (ARFID) is a feeding/eating disorder characterised by intake of an insufficient quantity or variety of food. ARFID symptoms often emerge early, yet there is limited research on possible early life feeding and growth factors associated with the disorder. Methods: We used data from Gemini, a British prospective birth cohort study with parent-reported ARFID symptoms measured at 12-13 years (n=968). Exposures of interest (measured in the first year of life) included appetite, infant milk-feeding, parental concern about their child’s weight, parental feeding practices (pressure and restriction) and infant growth (e.g., weight-for age z scores, weight gain trajectories). Logistic regressions (adjusted for clustering of twins in families) examined associations with later ARFID symptoms and linear mixed models compared weight gain trajectories between the suspected ARFID and non-ARFID participants. Results: Appetite, specifically early slower feeding (OR=1.47, 95%CI= 1.13, 1.90) and sensitivity to satiety (OR = 1.35, 95%CI= 1.03, 1.77) were associated with increased odds of later ARFID symptoms. Infants whose parents were concerned about their child’s weight had higher odds of ARFID symptoms (OR= 1.76, 95%CI = 1.15, 2.70). Having a higher weight at birth, three, six, nine and twelve months was associated with 12-20% lower odds of ARFID symptoms and trajectory analyses suggest that children with ARFID symptoms may have a slower weight gain trajectory compared to children without ARFID symptoms. Conclusion: Findings indicate that poor appetite (especially slower feeding and getting full more quickly) and weight stagnancy in infancy may be potential risk factors for later ARFID symptoms, some of which (e.g. poor appetite) may play a role in the disorder’s development.

Background: Despite its common early onset, little is known about the prevalence and clinical presentation of avoidant restrictive food intake disorder (ARFID) in very young children, hindering early identification and intervention. Differentiating ARFID from normative selective eating is particularly challenging, yet validated parent-reported screening tools are lacking. This study aimed to estimate the point prevalence and describe the clinical characteristics of ARFID in preschoolers. It also evaluated the psychometric properties of the parent-reported ARFID-Brief Screener by assessing its agreement with a diagnostic interview for ARFID. Methods: Parents of 645 children (50.5% male, mean age 3.2 years) completed the ARFID-Brief Screener and a neurodevelopmental screener during 2.5- and 4-year routine check-ups at 21 child health centers in West Sweden. Parents of all screen-positive and of randomly selected screen-negative children were invited to a follow-up diagnostic interview via phone. Additional clinical data were extracted from health records. Results: Of the 42 children (6.5%) who screened positive for ARFID, 29 were followed up via diagnostic interview, and 21 received an ARFID diagnosis, yielding a positive predictive value of 72%. Negative predictive value, sensitivity, specificity, and overall accuracy of the ARFID-Brief Screener were 94%, 91%, 79%, and 84%, respectively. The estimated point prevalence of ARFID was 5.9%. All diagnosed children exhibited both sensory-based avoidance and low interest in eating. Only 13.5% met ARFID criteria based on weight- or nutrition-related impairment (DSM-5 Criteria A1-A3). Two fifths (39.1%) of children with ARFID exhibited early language delays compared to 13.5% of children without ARFID. More extensive neurodevelopmental problems were associated with greater ARFID severity and with higher scores on the sensory and concern profiles. Conclusions: ARFID is not uncommon among preschoolers, though prevalence may be slightly overestimated in this study. It is primarily characterized by sensory-based avoidance and low interest in eating, and by psychosocial impairment instead of physical health consequences, underscoring the need to assess impact beyond weight, growth, and nutrition. Early neurodevelopmental difficulties are overrepresented, highlighting their relevance for early detection and intervention. The ARFID–Brief Screener demonstrated promising psychometric properties and may be a valuable tool for routine screening, though follow-up assessments remain necessary to confirm a diagnoses.

Objective: Fear of Aversive Consequences (FOAC), such as choking or vomiting, is an important associated feature of Avoidant/Restrictive Food Intake Disorder (ARFID). However, the manifestation of FOAC in young children is poorly understood. This study aimed to describe the fears of children with ARFID symptoms and examine the concordance between parent and child ratings of fear.Method: Child‐reported FOAC was assessed using an interview designed for children between 6 and 10 years old, the Gustatory Avoidance and Gastrointestinal Stress Symptoms (GAGSS). Parents were administered a semi‐structured diagnostic interview regarding their child's symptoms, the Pica, ARFID, and Rumination Interview.Results: Among 68 children with ARFID diagnoses or symptoms (41.2% female, 85.3% White, mean age = 8.2 years, SD = 1.1 years; range 5.2–9.9 years), 91.2% of children endorsed at least one fear relative to 26.5% of parents. Among parent–child dyads, 36.8% disagreed about the child's fear of stomach pain (κ = 0.12) and 48.5% disagreed about the child's fear of vomiting, (κ = 0.08), both indicating low inter‐rater reliability. On average, children endorsed 4.3 (SD = 2.3) fears out of 9 options. The most frequently endorsed fears were that food will “taste bad,” (n = 43, 63.2%), “make you gag” (n = 37, 54.4%), and “look disgusting” (n = 36, 52.9%).Discussion: Findings highlight ways in which fear may manifest in children with ARFID that are not easily discernable by adults. Greater precision in depicting childhood fears may facilitate the earlier detection of problematic eating behaviors.

Background: Despite its common early onset, little is known about the prevalence and clinical presentation of avoidant restrictive food intake disorder (ARFID) in very young children, hindering early identification and intervention. Differentiating ARFID from normative selective eating is particularly challenging, yet validated parent-reported screening tools are lacking. This study aimed to estimate the point prevalence and describe the clinical characteristics of ARFID in preschoolers. It also evaluated the psychometric properties of the parent-reported ARFID-Brief Screener by assessing its agreement with a diagnostic interview for ARFID. Methods: Parents of 645 children (50.5% male, mean age 3.2 years) completed the ARFID-Brief Screener and a neurodevelopmental screener during 2.5- and 4-year routine check-ups at 21 child health centers in West Sweden. Parents of all screen-positive and of randomly selected screen-negative children were invited to a follow-up diagnostic interview via phone. Additional clinical data were extracted from health records. Results: Of the 42 children (6.5%) who screened positive for ARFID, 29 were followed up via diagnostic interview, and 21 received an ARFID diagnosis, yielding a positive predictive value of 72%. Negative predictive value, sensitivity, specificity, and overall accuracy of the ARFID-Brief Screener were 94%, 91%, 79%, and 84%, respectively. The estimated point prevalence of ARFID was 5.9%. All diagnosed children exhibited both sensory-based avoidance and low interest in eating. Only 13.5% met ARFID criteria based on weight- or nutrition-related impairment (DSM-5 Criteria A1-A3). Two fifths (39.1%) of children with ARFID exhibited early language delays compared to 13.5% of children without ARFID. More extensive neurodevelopmental problems were associated with greater ARFID severity and with higher scores on the sensory and concern profiles. Conclusions: ARFID is not uncommon among preschoolers, though prevalence may be slightly overestimated in this study. It is primarily characterized by sensory-based avoidance and low interest in eating, and by psychosocial impairment instead of physical health consequences, underscoring the need to assess impact beyond weight, growth, and nutrition. Early neurodevelopmental difficulties are overrepresented, highlighting their relevance for early detection and intervention. The ARFID–Brief Screener demonstrated promising psychometric properties and may be a valuable tool for routine screening, though follow-up assessments remain necessary to confirm a diagnoses. Plain English summary: Avoidant restrictive food intake disorder (ARFID) often starts early in life, but little is known about how common it is in very young children. This study looked at how many preschool-aged children have ARFID and what their eating difficulties look like. We also tested how well a short parent questionnaire, the ARFID-Brief Screener, can help identify children at risk. Parents of 645 Swedish children filled out the screener during routine health check-ups at age 2.5 or 5. Children who screened positive and a randomly selected group of screen-negative children were invited to a follow-up interview. Based on these interviews, we estimated that about 5.9% of preschoolers may have ARFID. All children with ARFID avoided food due to sensory sensitivities or had little interest in eating. Few had weight or nutrition problems, but many experienced difficulties in daily life, such as stressful mealtimes. Children with ARFID were more likely to have early neurodevelopmental challenges such as delayed language development, suggesting that these symptoms may aid in identifying children at risk for ARFID. The ARFID-Brief Screener performed well in detecting at-risk children, but follow-up assessments are still needed to confirm a diagnosis.

Background: Food fussiness (FF) describes the tendency to eat a small range of foods, due to pickiness and/or reluctance to try new foods. A common behaviour during childhood, and a considerable cause of caregiver concern; its causes are poorly understood. This is the first twin study of genetic and environmental contributions to the developmental trajectory of FF from toddlerhood to early adolescence, and stability and change over time. Methods: Participants were from Gemini, a population‐based British cohort of n = 4,804 twins born in 2007. Parents reported on FF using the Child Eating Behaviour Questionnaire ‘FF’ scale when children were 16 months ( n = 3,854), 3 ( n = 2,666), 5 ( n = 2,098), 7 ( n = 703), and 13 years old ( n = 970). A mixed linear model examined the trajectory of FF, and a correlated factors twin model quantified genetic and environmental contributions to variation in and covariation between trajectory parameters. A longitudinal Cholesky twin model examined genetic and environmental influences on FF at each discrete age. Results: We modelled a single FF trajectory for all children, which was characterised by increases from 16 months to 7 years, followed by a slight decline from 7 to 13 years. All trajectory parameters were under strong genetic influence (>70%) that was largely shared, indicated by high genetic correlations. Discrete age analyses showed that genetic influence on FF increased significantly after toddlerhood (16 months: 60%, 95% CI: 53%–67%; 3 years: 83%; 81%–86%), with continuing genetic influence as indicated by significant genetic overlap across every age. Shared environmental influences were only significant during toddlerhood. Unique environmental influences explained 15%–26% of the variance over time, with some enduring influence from 5 years onwards. Conclusions: Individual differences in FF were largely explained by genetic factors at all ages. Fussy eating also shows a significant proportion of environmental influence, especially in toddlerhood, and may, therefore, benefit from early interventions throughout childhood. Future work needs to refine the FF trajectory and explore specific trajectory classes.

The high co‐occurrence of autism and eating disorders is well established, including for those with Avoidant Restrictive Food Intake Disorder (ARFID). It is therefore important to consider autism and identify possible autism when people present to eating disorder services to ascertain whether further assessment is indicated, to support clinical formulation and to make appropriate adaptations during interventions. This paper explores the utility of a validated autism screening measure, the AQ‐10, in a population of children and adolescents who presented to an outpatient eating disorders clinic for an assessment of possible ARFID. Over 19 months, 335 young people were assessed and 246 families with children aged between 4 and 17 years completed one of three versions of the AQ‐10 (Child, Adolescent, and Adult), as part of a battery of routinely administered pre‐assessment questionnaires. Results indicated that 80.2% (n = 69) of those with an existing autism diagnosis scored above clinical threshold of ≥6 (M = 7.2, SD = 1.9), 43.9% (n = 43) of those queried to be autistic scored above clinical threshold (M = 5.2, SD = 2.5), and 6.5% (n = 4) of non‐autistic individuals scored above clinical threshold (M = 2.8, SD = 1.8). Additionally, the AQ‐10 satisfactorily discriminated between those with a known autism diagnosis and those who are not autistic across all age groups and sex. We conclude that the AQ‐10, alongside a comprehensive clinical assessment and clinical judgment, is a useful screening tool that can support clinicians to identify appropriate onward referrals for autism assessments, aid clinical formulation, and consider appropriate adaptations and reasonable adjustments during ARFID interventions.

BackgroundFood fussiness (FF) describes the tendency to eat a small range of foods, due to pickiness and/or reluctance to try new foods. A common behaviour during childhood, and a considerable cause of caregiver concern; its causes are poorly understood. This is the first twin study of genetic and environmental contributions to the developmental trajectory of FF from toddlerhood to early adolescence, and stability and change over time.MethodsParticipants were from Gemini, a population-based British cohort of n=4804 twins born in 2007. Parents reported on FF using the Child Eating Behaviour Questionnaire ‘food fussiness’ scale when children were 16 months (n=3854), and 3 (n=2666), 5 (n=2098), 7 (n=703) and 13 years old (n=970). A mixed linear model examined the trajectory of FF, and a correlated factors twin model quantified genetic and environmental contributions to variation in and covariation between trajectory parameters. A longitudinal Cholesky twin model examined genetic and environmental influences on FF at each discrete age.ResultsA single FF trajectory was identified for all children, characterised by increases from 16 months to 7 years, followed by a slight decline from 7-13 years. All trajectory parameters were under strong genetic influence (>70%) that was largely shared, indicated by high genetic correlations. Discrete age analyses showed that genetic influence on FF increased significantly after toddlerhood (16 months: 60%, 95%Cl:53%-67%; 3 years: 83%; 81%-86%), with continuing genetic influence as indicated by significant genetic overlap across every age. Shared environmental influences were only significant during toddlerhood. Unique environmental influences explained 15-26% of the variance over time, with some enduring influence from 5 years onwards. ConclusionsIndividual differences in FF were largely explained by genetic factors at all ages. Early life interventions for fussy eating may be most effective during toddlerhood when malleable environmental factors play a sizeable role.