Periodic Reporting for period 1 - PAREAT (Pediatric Avoidant and Restrictive Eating: A biopsychosocial investigation)
Reporting period: 2020-04-01 to 2022-03-31
Avoidant Restrictive Food Intake Disorder (ARFID) is a psychological disorder that was first introduced in 2013 in the Diagnostic and Statistical manual of Mental Disorders- 5th edition. ARFID is characterized by the consumption of a limited quantity or range of foods not due to weight or shape concerns, that results in failure to meet nutritional needs, poor growth, and/or significant psychosocial impairment. While ARFID may affect up to 3% of children, between 13-34% of young children engage in avoidant/restrictive eating that does not meet full criteria for ARFID, making it a significant public health problem.
Patients with ARFID most commonly engage in restrictive eating due to a combination of presumed sensory sensitivity to food qualities (e.g. taste, smell, texture), low interest in food/appetite, and/or fear of adverse consequences of eating (e.g. choking, vomiting, pain). A recent attempt to inform the pathophysiology of ARFID has been made through the Three-Dimensional Neurobiological Model of ARFID (Thomas et al., 2017) which posits that these symptom dimension can co-occur and are rooted in dimension-specific biological vulnerabilities. As ARFID symptoms are first identified in early childhood, it is essential to gain a deeper understanding of biological vulnerabilities for ARFID in early childhood and how they interact with social factors in ARFID etiology to develop effective and efficient interventions for affected children and their families.
The aims of this project are to 1) identify biological vulnerabilities for the sensory sensitivity and fear dimensions of avoidant/restrictive eating in early childhood and 2) test how a child’s biological vulnerabilities are exacerbated or remediated by parent feeding behavior in relation to the child’s ARFID symptoms.
Patients with ARFID most commonly engage in restrictive eating due to a combination of presumed sensory sensitivity to food qualities (e.g. taste, smell, texture), low interest in food/appetite, and/or fear of adverse consequences of eating (e.g. choking, vomiting, pain). A recent attempt to inform the pathophysiology of ARFID has been made through the Three-Dimensional Neurobiological Model of ARFID (Thomas et al., 2017) which posits that these symptom dimension can co-occur and are rooted in dimension-specific biological vulnerabilities. As ARFID symptoms are first identified in early childhood, it is essential to gain a deeper understanding of biological vulnerabilities for ARFID in early childhood and how they interact with social factors in ARFID etiology to develop effective and efficient interventions for affected children and their families.
The aims of this project are to 1) identify biological vulnerabilities for the sensory sensitivity and fear dimensions of avoidant/restrictive eating in early childhood and 2) test how a child’s biological vulnerabilities are exacerbated or remediated by parent feeding behavior in relation to the child’s ARFID symptoms.
To achieve these aims, a sample of 66 children ages 4-7 years (36 with avoidant/restrictive eating and 30 typically developing age/sex matched healthy controls) participated in the study. Participating children and their parent completed a parent interview of child avoidant/restrictive (AR) eating symptoms, parent questionnaires (assessing eating and feeding behavior, child emotional-behavioral functioning, sensory perception, and parent mental health), and a child behavioral and physiological assessment of sensory perception and eating behaviors at the laboratory. At the laboratory assessment, each child complete three tests of sensory perception; U’Sniff test (odor identification), mystery box (tactile perception), and PROP test (bitter flavor detection); followed by small meal with their parent that was later coded for parental feeding and child eating behavior.
The findings from this study showed that sensory sensitivity symptoms of AR eating were associated with parental report of tactile and taste/odor sensory problems but were not related to behavioral tests of odor identification and bitter taste perception, the child’s self-rated enjoyment of sensory stimuli, or activation of facial action units associated with disgust expressions and negative affect more broadly. Hyperactivation of the defensive motive system, assessed via heart rate and electrodermal activity response to sensory stimuli and eating, was not found to be associated with fear or sensory sensitivity symptoms of ARFID. However, heart rate dynamics in response to odor stimuli were consistent with delayed odor inhalation among children with elevated sensory sensitivity symptoms (Figure 1). This suggests that these children may have been behaviorally avoiding odor stimuli. However, it should be noted that odor stimuli were always presented first during the experiment, so this effect could be unique to odor stimuli or driven by the novelty of the sensory stimuli presentation. Further, child trait anxiety was found to be associated with both fear of aversive consequences symptoms of ARFID, as well as sensory symptoms, suggesting it is not a uniquely linked to fear symptoms.
As no clear biological vulnerabilities for the sensory sensitivity and fear of aversive consequences symptoms were identified in this study, the relationship between parental feeding behavior and child eating was evaluated in the whole sample, exploring child sensory perception and anxiety as moderators. These analyses suggest that when children are presented with standardized foods, the relationship between increased child food refusal and greater parental pressure to eat is observed only among children with altered sensory perception (those who could taste the PROP bitter flavor and those with low odor identification accuracy). However, as PROP taster status and odor identification accuracy were not linked to ARFID symptoms, these do not represent unique vulnerabilities for children with ARFID, but instead young children more broadly. Further, as parental pressure to eat was unrelated to the number of bites eaten by the child, these data suggest that parental pressure to eat may be more associated with mealtime conflict rather than enhanced nutritional intake by the child during the meal.
These findings have been disseminated to the academic medical community via four international research conferences as well as to the public at a local science night in Geneva, Switzerland. Further, the findings of the study will be communicated to children and their parents affected by avoidant/restrictive eating in Geneva, Switzerland through a psycho-educational group and a parent newsletter.
The findings from this study showed that sensory sensitivity symptoms of AR eating were associated with parental report of tactile and taste/odor sensory problems but were not related to behavioral tests of odor identification and bitter taste perception, the child’s self-rated enjoyment of sensory stimuli, or activation of facial action units associated with disgust expressions and negative affect more broadly. Hyperactivation of the defensive motive system, assessed via heart rate and electrodermal activity response to sensory stimuli and eating, was not found to be associated with fear or sensory sensitivity symptoms of ARFID. However, heart rate dynamics in response to odor stimuli were consistent with delayed odor inhalation among children with elevated sensory sensitivity symptoms (Figure 1). This suggests that these children may have been behaviorally avoiding odor stimuli. However, it should be noted that odor stimuli were always presented first during the experiment, so this effect could be unique to odor stimuli or driven by the novelty of the sensory stimuli presentation. Further, child trait anxiety was found to be associated with both fear of aversive consequences symptoms of ARFID, as well as sensory symptoms, suggesting it is not a uniquely linked to fear symptoms.
As no clear biological vulnerabilities for the sensory sensitivity and fear of aversive consequences symptoms were identified in this study, the relationship between parental feeding behavior and child eating was evaluated in the whole sample, exploring child sensory perception and anxiety as moderators. These analyses suggest that when children are presented with standardized foods, the relationship between increased child food refusal and greater parental pressure to eat is observed only among children with altered sensory perception (those who could taste the PROP bitter flavor and those with low odor identification accuracy). However, as PROP taster status and odor identification accuracy were not linked to ARFID symptoms, these do not represent unique vulnerabilities for children with ARFID, but instead young children more broadly. Further, as parental pressure to eat was unrelated to the number of bites eaten by the child, these data suggest that parental pressure to eat may be more associated with mealtime conflict rather than enhanced nutritional intake by the child during the meal.
These findings have been disseminated to the academic medical community via four international research conferences as well as to the public at a local science night in Geneva, Switzerland. Further, the findings of the study will be communicated to children and their parents affected by avoidant/restrictive eating in Geneva, Switzerland through a psycho-educational group and a parent newsletter.
These findings help to advance our understanding of ARFID etiology in early childhood in several ways. While this study did not identify differences in sensory perception (odor identification or bitter taste perception) when assessed behaviorally, a pattern of behavioral avoidance of novel sensory stimuli was found to be associated with the sensory sensitivity symptoms of ARFID. Such a pattern of avoidance of sensory stimuli may contribute to the parent-reported sensory sensitivities also found to be associated with sensory sensitivity symptoms of ARFID. It remains unclear what are the most salient drivers of food avoidance among young patient with ARFID. It is possible this avoidance could be driven by unassessed aspects of sensory perception, such as oral texture perception, retronasal olfaction and taste perception. Additionally, negative appraisals of food experiences associated with the novelty of the experience could be a contributing factor. Further research is warranted to clarify the role of these factors in ARFID etiology.
These findings, in combination with behavioral data from the meal task suggest that for young children who do experience altered taste of odor perception, parental pressure to eat during meals is not associated with the increased food intake, but instead greater food refusal. This finding speaks to the importance of understanding young children’s sensory profiles, to balance the introduction of new and nonpreferred foods without enhancing mealtime conflict. However, to fully understand these relationships, it is necessary that future studies assess these factors across multiple timepoints to understand how parent and child behavior drive one and other, to better inform parent feeding interventions.
These findings, in combination with behavioral data from the meal task suggest that for young children who do experience altered taste of odor perception, parental pressure to eat during meals is not associated with the increased food intake, but instead greater food refusal. This finding speaks to the importance of understanding young children’s sensory profiles, to balance the introduction of new and nonpreferred foods without enhancing mealtime conflict. However, to fully understand these relationships, it is necessary that future studies assess these factors across multiple timepoints to understand how parent and child behavior drive one and other, to better inform parent feeding interventions.