The research team, led by Esra Hoşoğlu of Necmettin Erbakan University’s Meram Faculty of Medicine, recruited children aged 2 to 6 years from a child and adolescent psychiatry outpatient clinic and from family health centers in Konya. Every ASD diagnosis was confirmed by experienced child and adolescent psychiatrists using DSM-5 criteria. To keep the comparison clean, the researchers excluded children taking appetite-altering medications and those with chronic conditions such as diabetes, cerebral palsy, epilepsy, or gastrointestinal disease, since these factors can independently disrupt eating. Parents whose children had a sibling or parent with autism were also barred from the control group, and families in which a parent was currently receiving psychiatric treatment were excluded from both arms of the study.

The measurement toolkit was comprehensive. Parents completed the Children’s Eating Behavior Questionnaire, a validated 35-item instrument that captures both food-approach tendencies, such as food responsiveness and emotional overeating, and food-avoidant tendencies, such as satiety responsiveness, slowness in eating, emotional undereating, and food fussiness. Child autism severity was rated with the Childhood Autism Rating Scale, while developmental level was gauged using the Ankara Developmental Screening Inventory, which covers language-cognitive, fine motor, gross motor, and social domains. Behavioral problems were assessed with the Aberrant Behavior Checklist, and parental mental health was screened with the Brief Symptom Inventory, a 53-item measure spanning anxiety, depression, somatization, hostility, and negative self-concept.

The statistical strategy was deliberately conservative. Because the mothers and fathers of autistic children were significantly older than the control parents, the researchers used multivariate analysis of covariance to adjust for these baseline imbalances. The group effect on eating behaviors remained stubbornly non-significant: Pillai’s Trace was 0.064 with a p-value of 0.688 in the fully adjusted model, and adding overall developmental level as a further covariate did not change the picture. The team then applied the Benjamini–Hochberg false discovery rate procedure to all within-group analyses, a mathematical safeguard against the false positives that inevitably accumulate when dozens of correlations are tested simultaneously. The study was powered to detect only medium-to-large between-group effects, meaning subtle differences could have slipped through undetected.

Within the autistic group itself, however, the data hinted at meaningful patterns, even if most of them dissolved under strict correction. The most robust finding was a positive correlation between hyperactivity and noncompliance, measured on the Aberrant Behavior Checklist, and satiety responsiveness, with a Spearman coefficient of 0.449 that survived false discovery rate correction in the primary analysis with an adjusted p-value of 0.022. In plain terms, children whose parents described them as more restless and defiant were also reported to feel full more quickly and disengage from meals sooner. The researchers speculate that highly distractible children may be pulled away from their plates by environmental stimuli, leading caregivers to interpret this disengagement as early fullness, a mechanism consistent with prior work on attention-deficit hyperactivity symptoms and mealtime behavior.

Nominally significant, but statistically fragile, associations also emerged involving developmental milestones. Fine motor skills showed positive nominal links to food responsiveness, enjoyment of food, and desire to drink, and a negative nominal link to slowness in eating, with standardized coefficients ranging from negative 0.289 to 0.404. Cognitive-language development nominally predicted lower emotional overeating and higher satiety responsiveness. These relationships make biological sense: self-feeding is a fine motor milestone, and children with better language may communicate hunger and fullness cues more effectively. But after false discovery rate correction across the eight regression models, not a single one of these associations retained statistical significance, with all corrected q-values landing at or above 0.292. The authors are careful to frame these results as exploratory and hypothesis-generating rather than established findings.

Parental mental health, a factor the study was specifically designed to probe, told a similar story of tantalizing signals that failed to solidify. Maternal and paternal depressive symptoms both correlated nominally with children’s emotional overeating, and paternal depression and somatization showed nominal associations with slower eating, yet none withstood correction. The researchers caution that this should not be read as evidence that parental psychology is irrelevant. Prior studies have linked maternal anxiety to restrictive feeding and maternal depression to pressure to eat, and in autism families specifically, higher parental anxiety and depression have been tied to more problematic feeding behaviors and controlling strategies. The present study measured only general psychiatric symptoms, not mealtime-specific emotions or feeding practices, which may be the more proximal levers through which parental distress shapes a child’s relationship with food.

Why did the autistic preschoolers look so much like their typically developing peers? The authors offer several converging explanations. First, early childhood is precisely the developmental window when picky eating peaks in nearly all children, regardless of diagnosis. In typically developing youngsters these behaviors typically fade, whereas in autism, sensory sensitivities and insistence on sameness can cause them to persist and harden. The trajectories of the two groups may simply not have diverged yet, a hypothesis supported by an earlier Italian study that found no eating differences between autistic and non-autistic children aged 2 to 5.9 years but clear differences by ages 6 to 9.5. Second, by excluding children with chronic illness and medication use, the team may have inadvertently filtered out the autistic children with the most severe and complex feeding problems. Third, cultural context matters: research in Türkiye suggests that parents there often continue feeding children well beyond the age typical in Western samples, perceive higher body weight as a sign of health, and favor overprotective feeding styles, all of which could compress group differences on a parent-report instrument.

The study’s limitations deserve honest weight. The sample of 93 children is modest, the post hoc power analysis indicated that only effects of Cohen’s d of 0.59 or larger could be reliably detected, and every measure, from eating behavior to parental symptoms, relied on parent report rather than direct mealtime observation. Notably, previous research comparing questionnaire scores with observed mealtime behavior in autistic children found almost no correspondence, raising the possibility that parental perception, stress, and cultural expectations color the data. The Ankara Developmental Screening Inventory also lacks validated norms for autistic populations, and the cross-sectional design makes it impossible to determine whether behavioral difficulties drive eating problems or vice versa. The researchers themselves emphasize that their findings require replication in larger, longitudinal studies using standardized developmental assessments and multi-method measurement.

Still, the work carries real clinical significance precisely because of when it was conducted. The preschool period is a critical window for establishing eating behaviors that persist from childhood through adolescence into adulthood, and eating problems that emerge at this stage can seed long-term nutritional and weight-related difficulties, whether through the obesity risk associated with food-approach behaviors or the underweight and inadequate intake linked to food avoidance. If the divergence between autistic and typically developing children’s eating patterns genuinely emerges later, then early intervention may have a wide window of opportunity before feeding difficulties consolidate into something more resistant to change. Conversely, if subtle differences were missed for want of statistical power, the study serves as a call for adequately powered longitudinal cohorts that track autistic children from toddlerhood through school age, pairing parent questionnaires with observational mealtime data, sensory processing assessments, and measures of behavioral rigidity. Either way, the message for clinicians is nuanced: a preschool diagnosis of autism does not automatically forecast the severe eating problems so often described in older children, but the hyperactivity-eating connection, however tentative, hints that managing early behavioral dysregulation might protect mealtimes before problems take root.

Subject of Research: Eating behaviors in preschool children with autism spectrum disorder and their developmental, behavioral, and parental correlates

Article Title: Eating behaviors in preschoolers with autism spectrum disorders: associations with developmental and behavioral features and parental mental health

Article References: Eating behaviors in preschoolers with autism spectrum disorders: associations with developmental and behavioral features and parental mental health. (n.d.). https://doi.org/10.3389/fpsyt.2026.1902816

Image Credits: AI Generated

DOI: 10.3389/fpsyt.2026.1902816

Keywords: autism spectrum disorder, preschool children, eating behaviors, food selectivity, satiety responsiveness, parental mental health, hyperactivity, developmental assessment, case-control study, picky eating, Frontiers in Psychiatry, Eating