Eating Onset Research Articles

Relation between ARFID symptomatology and picky eating onset and duration

BackgroundPicky eating (PE) is common in early childhood, peaking between ages 1 and 5 years. However, PE may persist beyond this normative period and pose threats to health and psychosocial functioning. Avoidant/restrictive food intake disorder (ARFID) involves restrictive eating driven by appetite, preference/selectivity, and/or fear of eating, leading to significant medical and/or psychosocial impairment. This retrospective study examined the relation between early childhood PE onset/duration and ARFID eating restrictions and symptoms. MethodParents of children ages 6–17 (N = 437) completed a survey about their child's eating behavior, including the Nine-item ARFID Screen (NIAS) and questions about PE onset and impacts. Children were then categorized into groups based on PE onset (before or after age 5) and duration: never picky, normative picky, persistent picky, and late-onset picky. ResultsThe groups differed (all p < .05) in mean NIAS subscales (picky eating, NIAS-PE; appetite, NIAS-A; fear, NIAS-F) and total scores (NIAS-T). Tukey post-hoc tests found that persistent PEs had significantly higher NIAS-PE, NIAS-A, and NIAS-T scores than never or normative PEs (all p < .05). Chi-Square tests found that persistent PEs were significantly more likely than all other groups to endorse ARFID criteria. ConclusionFindings from this study suggest that PE that persists beyond or is identified after the normative period is associated with elevated ARFID symptoms compared to normative and never PEs. Persistent PE increases risk of impairment from PE and other ARFID eating restrictions. Given the health and psychosocial risks associated with ARFID, early identification and intervention for this group is warranted.

Neuronal activity and reward processing in relation to binge eating.

Studies increasingly show the importance of reward processing in binge eating and provide evidence of associated changes in the neurobiological reward system. This review gives an up-to-date overview of the neurobiological substrates of reward processing subconstructs in binge eating. Neural findings are linked to different behavioral theories and the clinical relevance is discussed. Increased neural responses in the orbitofrontal cortex, anterior cingulate cortex as well as striatum during anticipation and receipt of food rewards are found in association to binge eating. Increased model-free learning is also found and associated with altered brain reward reactivity. Data in rest report reduced striatal dopamine release and lower frontostriatal connectivity. Mechanisms of onset of binge eating are less clear, but specific personality traits, related to frontostriatal dysconnectivity, probably increase the risk of binge eating onset. Both structural and task-based imaging studies show differences in the neurobiological reward system in binge eating. These changes are linked to specific reward processing, such as altered reward responsiveness to food cues, reinforcement learning, and habitual behavior. Findings are lined with different behavioral theories of binge eating, and a staging model is described, from onset to full illness development. Understanding the specific underlying aberrant reward mechanism in binge eating, associated with different stages of the illness, enables caregivers to focus their treatment more precisely.

Examination of onset trajectories and persistence of binge-like eating behavior in mice after intermittent palatable food exposure.

Binge eating is a persistent behavior associated with a chronic course of illness and poor treatment outcomes. While clinical research is unable to capture the full course of binge eating, preclinical approaches offer the opportunity to examine binge-like eating from onset through chronic durations, allowing identification of factors contributing to binge eating persistence. The present study quantified the trajectories of binge-like eating onset and modeled cycles of abstinence/relapse to develop a translational model for binge eating persistence. Adult male and female C57Bl6/J mice were randomized to a binge-like palatable food access schedule (daily 2-hr, 3×/week) or continuous, nonbinge like palatable food access for 12 days (Experiment 1). Persistence of palatable food consumption in both binge-like palatable food access groups was then examined across three cycles of forced abstinence and reexposure to palatable food (incubation) to model the persistence of binge eating in clinical populations. Mice with daily 2-hr palatable food access escalated their intake more than mice in the 3×/week or continuous groups (Experiment 1). This pattern was more pronounced in females. In addition, this pattern of palatable food intake reemerged across multiple cycles of behavioral incubation (Experiment 2). These findings provide a model of binge-like eating in mice that can be used in future studies examining both environmental factors and neural mechanisms contributing to binge eating persistence. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Temporal associations between nightly sleep with daytime eating and activity levels in free-living young adults.

This study aimed to quantify the temporal associations between nightly sleep quantity and timing with daytime eating behavior and activity levels in free-living (i.e. non-experimental) settings. Generally healthy young adults (N = 63; 28.9 ± 7.1 years) completed concurrent sleep (wrist actigraphy), eating (photo-assisted diet records), and activity (waist actigraphy) assessments over 14 days. Multilevel models quantified the associations between nightly sleep (total sleep time, timing of sleep and wake onset) with next-day eating behavior (diet quality, caloric intake, timing of eating onset/offset, eating window duration) and activity levels (total physical activity, sedentary time). Associations in the reverse direction (i.e. eating and activity predicting sleep) were explored. Models adjusted for demographic and behavioral confounders and accounted for multiple testing. At within- and between-subject levels, nights with greater-than-average total sleep time predicted a shorter eating window the next day (all p ≤ 0.002). Later-than-average sleep and wake timing predicted within- and between-subject delays in next-day eating onset and offset, and between-subject reductions in diet quality and caloric intake (all p ≤ 0.008). At within- and between-subject levels, total sleep time was bidirectionally, inversely associated with sedentary time (all p < 0.001), while later-than-average sleep and wake timing predicted lower next-day physical activity (all p ≤ 0.008). These data underscore the complex interrelatedness between sleep, eating behavior, and activity levels in free-living settings. Findings also suggest that sleep exerts a greater influence on next-day behavior, rather than vice versa. While testing in more diverse samples is needed, these data have potential to enhance health behavior interventions and maximize health outcomes.

0003 On the Same Wavelength? Quantifying the Associations between Eating Timing and Rest-Activity Rhythms in Free-Living Adults

Abstract Introduction Misalignment between the central circadian clock and daily behaviors increases cardiometabolic morbidity and mortality risk, likely due to internal misalignment between central and peripheral circadian rhythms. Experimental studies suggest food intake may act as a time cue (‘zeitgeber’) for resetting circadian rhythms, representing a potential behavioral target to ameliorate circadian misalignment and associated health consequences. However, the extent to which eating timing relates to circadian rhythms in free-living adults is unclear. Therefore, we tested the associations between eating timing with 24-h rest-activity-rhythms (RAR), a free-living proxy for endogenous circadian rhythms, in non-shift-working adults. Methods Adults without chronic health conditions or sleep disorders completed 14 days of 24/7 wrist accelerometry to evaluate RAR variables of interdaily stability (IS; day-to-day stability in RAR), intradaily variability (IV; within-day fragmentation of RAR), relative amplitude (RA; difference between peak vs. trough activity), L5 onset time (5-h period with lowest activity), and M10 onset time (10-h period with highest activity). Concurrently, time-stamped image-assisted diet records were obtained to generate average eating timing variables, including daily eating onset (time of first caloric intake after awakening), offset (last caloric intake time), duration (time elapsed between eating onset and offset), and caloric midpoint (time at which 50% of daily kcals were consumed), and variables illustrating irregularity in eating timing (standard deviation of eating timing variables). Pearson’s correlations quantified the associations between RAR and eating timing variables. Results Participants (N=30) were 28.0±6.6 years, 57% female, with a BMI of 23.8±2.5 kg/m2. Higher IS was correlated with lower irregularity in both eating onset (r=-0.55, p&amp;lt;0.01) and duration (r=-0.51, p&amp;lt;0.01). Higher RA correlated with earlier eating onset (r=-0.47, p&amp;lt;0.01), longer eating duration (r=0.53, p&amp;lt;0.01), and lower eating onset irregularity (r=-0.37, p&amp;lt;0.05). Later L5 correlated with later eating onset (r=0.67, p&amp;lt;0.001), offset (r=0.58, p&amp;lt;0.001), caloric midpoint (r=0.56, p&amp;lt;0.01), and greater eating offset irregularity (r=0.53, p&amp;lt;0.01). Later M10 correlated with later eating offset (r=0.40, p&amp;lt;0.05). Conclusion Preliminary findings indicate that eating timing and RAR are moderately correlated in free-living adults. Earlier eating timing, increased eating regularity, and longer daily eating duration may represent behavioral targets for improving circadian rhythms and subsequent cardiometabolic outcomes. Support (If Any): Support provided by the American Heart Association (#831488) and a University of Delaware Research Fund-Strategic Initiative Award.

Abstract EP61: Short Sleep Duration, Late Sleep Timing, And Late Eating Timing: A Trilogy Of Behavioral Risk Factors For High Blood Pressure?

Introduction: Short sleep duration (&lt;7 h/night) is a risk factor for hypertension and other cardiovascular diseases (CVD). Not clear is if delayed timing of sleep or eating behaviors adds to this risk. We tested the hypothesis that later sleep and eating timing would be associated with higher blood pressure (BP), and that adults with short sleep + late behavior timing would have the highest BP vs those with one (short sleep OR late timing) or no risk behaviors (adequate sleep + early timing). Methods: Over a 14-day period, 30 healthy, non-shift working adults wore wrist actigraphs to evaluate sleep duration and onset timing, and completed image-assisted diet records to estimate eating onset (time of first caloric intake after awakening) and offset (time of last caloric intake before sleep). Fasted morning systolic (SBP) and diastolic BP (DBP) were obtained. Regression models of SBP and DBP tested associations with sleep onset, eating onset, and eating offset. Sleep duration (&lt;7 vs ≥7h) and behavior timing metrics (median split) were dichotomized, and ANOVAs compared BP between sleep duration + behavior timing groups. Results: Participants were 28±7y, 43% male, BMI 23.9±2.6 kg/m 2 , and BP 114±10/70±7 mmHg. Sleep duration was 6.8±0.8 h, sleep onset 23:45±1.3 h, eating onset 08:49±1.5 h, and eating offset 20:40±1.2 h. Independent of age and sex, later sleep onset was associated with higher SBP (B= 3.0±1.3 mmHg/h, p =0.03) and DBP (B= 2.5±0.9 mmHg/h, p =0.01). Later eating onset was associated with higher DBP (B= 2.1±0.9 mmHg/h, p =0.03), and later offset with higher SBP (B= 4.1±1.4 mmHg/h, p &lt;0.01) and DBP (B= 3.3±1.0 mmHg/h, p &lt;0.01). When grouped according to sleep duration and eating offset, short sleep + late timing participants exhibited higher DBP vs adequate sleep + early timing (75±7 vs 67±7, p =0.03) and tended to exhibit higher SBP and DBP vs short sleep OR late timing (both p =0.07). Conclusion: These data indicate later sleep and eating timing, especially in the setting of short sleep, exemplifies a chrono-behavioral phenotype of CVD risk.

A longitudinal test of impulsivity and depression pathways to early binge eating onset

The very early engagement in bulimic behaviors, such as binge eating, may be influenced by factors that dispose individuals to impulsive action as well as by factors that dispose individuals to depressive symptomatology. Using a longitudinal design, we conducted the first test of the simultaneous operation of both risk factors as children transition from elementary to middle school. In a sample of 1,906 children, we assessed risk for impulsive action (negative urgency, which is the tendency to act rashly when distressed, and eating expectancies, which are learned anticipations that eating will alleviate negative mood) and risk for depression (negative affect and depressive symptomatology) and binge eating behavior at three time points using a longitudinal design: the end of fifth grade (last year of elementary school: T0), the beginning of sixth grade (first year of middle school: T1), and the end of sixth grade (T2). Both the impulsive action and depression pathways predicted very early engagement in binge eating: each accounted for variance beyond the other. Mediation tests found that T1 eating expectancies mediated the predictive influence of T0 negative urgency on T2 binge eating (z = 2.45, p < .01) and that T1 depressive symptoms mediated the influence of T0 negative affect on T2 binge eating (z = 2.04, p < .05). In children, elevated levels of both negative urgency and negative affect predict early binge eating. This finding has important clinical implications because there are different interventions for the two different risk processes.

Which Dieters Are at Risk for the Onset of Binge Eating? A Prospective Study of Adolescents and Young Adults

Dieting is a well-established risk factor for binge eating, yet the majority of dieters do not develop binge eating problems. The purpose of the current study was to examine psychosocial factors involved in the relation between dieting and binge eating over a 10-year follow-up period. A population-based sample (n = 1,827) completed surveys assessing eating habits, psychological functioning, and weight status at 5-year intervals spanning early/middle adolescence (time 1), late adolescence/early young adulthood (time 2), and early/middle young adulthood (time 3). Dieting, along with depression symptoms, self-esteem, and teasing experiences at time 1 and time 2, was used to predict new onset binge eating at time 2 and time 3, respectively. Interactions between dieting status and varying degrees of these psychosocial factors in relation to binge eating onset were also tested. Dieters were two to three times more likely than nondieters to develop binge eating problems over 5-year follow-ups. At most time points, depression symptoms and self-esteem predicted binge eating onset beyond the effects of dieting alone. Detrimental levels of these factors among dieters (relative to nondieters) increased the likelihood of binge eating onset only during the later follow-up period. Depression and self-esteem appear to be particularly salient factors involved in the relation between dieting and binge eating onset among adolescents and young adults. Early identification of these factors should be a priority to prevent the development of binge eating problems among already at-risk individuals.

Parental substance use history of overweight men and women with binge eating disorder is associated with distinct developmental trajectories and comorbid mood disorder

Objective To examine the significance of parental histories of substance use disorders (SUDs) in the expression of binge eating disorder (BED) and associated functioning. Method Participants were 127 overweight patients with BED assessed using diagnostic interviews. Participants were administered a structured psychiatric history interview about their parents ( N = 250) and completed a battery of questionnaires assessing current and historical eating and weight variables and associated psychological functioning (depression and self-esteem). Results Patients with BED with a parental history of SUD were significantly more likely to start binge eating before dieting, had a significantly earlier age at BED onset, and reported less time between binge eating onset and meeting diagnostic criteria for BED than did patients without a parental history of SUD. For psychiatric comorbidity, patients with BED with a parental history of SUD were significantly more likely to meet the criteria for a mood disorder. A parental history of SUD was not significantly associated with variability in current levels of binge eating, eating disorder psychopathology, or psychological functioning. Discussion Our findings suggest that a parental history of SUD is associated with certain distinct trajectories in the development of binge eating (earlier binge onset predating dieting onset) and with elevated rates of comorbidity with mood disorders in patients with BED.

The onset and course of binge eating in 8- to 13-year-old healthy weight, overweight and obese children

Objectives This study aimed to (1) determine the prevalence of binge eating and overeating in 8- to 13-year-old children; (2) identify factors that cross-sectionally predict binge eating and overeating; and (3) identify factors that prospectively predict onset of binge eating and overeating. Methods Participants were 259 boys and girls who were assessed at baseline and one-year follow-up, using a range of semi-structured interviews that included the Child Eating Disorder Examination. Results At baseline, 9% of children reported binge eating and 6% reported overeating. Obese children were most at risk for these behaviours. Dietary restraint and the tendency to use food to regulate emotions were significant in predicting binge eating onset prospectively, and eating concern was significant in predicting binge eating cross-sectionally. Conclusion Results provide support for current cognitive-behavioural models of binge eating, and have implications for guiding binge eating prevention and intervention efforts with children.

Relation of binge eating age of onset to functional aspects of binge eating in binge eating disorder.

This study examined whether age of binge eating onset in binge eating disorder (BED) is related to affective binge eating antecedents and consequences. Participants included women (N = 44) with BED who participated in a group cognitive-behavioral therapy (CBT) study. Measures included the Eating Hedonics Questionnaire, Beck Depression Inventory, Multidimensional Personality Questionnaire Negative Emotionality factor, Restraint Scale, Three-Factor Eating Questionnaire Restraint factor, and Eating Behaviors-IV. Participants were classified according to reported age of binge eating onset, with early onset defined as </=13 years (EOB; n = 25) and later onset >13 years (LOB; n = 19). Compared with LOB, EOB was associated with reductions in postbinge subjective anxiety, but not depression. This study suggested that EOB in BED may be associated with binge eating as an affective means of coping, particularly with anxiety, and further supported age of binge eating onset as a clinically meaningful way to delineate BED subclassifications.

Risk factors for binge eating onset in adolescent girls: A 2-year prospective investigation.

Risk factors for binge eating onset in adolescent girls: A 2-year prospective investigation.

Risk factors for binge eating onset in adolescent girls: A 2-year prospective investigation.

Because little is known about the predictors of binge eating (a risk factor for obesity), a set of putative risk factors for binge eating was investigated in a longitudinal study of adolescent girls. Results verified that binge eating predicted obesity onset. Elevated dieting, pressure to be thin, modeling of eating disturbances, appearance overvaluation, body dissatisfaction, depressive symptoms, emotional eating, body mass, and low self-esteem and social support predicted binge eating onset with 92% accuracy. Classification tree analysis revealed an interaction between appearance overvaluation, body mass, dieting, and depressive symptoms, suggesting qualitatively different pathways to binge eating and identifying subgroups at extreme risk for this outcome. Results support the assertion that these psychosocial and biological factors increase risk for binge eating.

Sleep-Related Eating Disorders: Polysomnographic Correlates of a Heterogeneous Syndrome Distinct from Daytime Eating Disorders

Over a 5-yr period, 19 adults presented to our sleep disorders center with histories of involuntary, nocturnal, sleep-related eating that usually occurred with other problematic nocturnal behaviors. Mean age (+/- SD) at presentation was 37.4 (+/- 9.1) yr (range 18-54); 73.7% of the patients (n = 14) were female. Mean age of sleep-related eating onset was 24.7 (+/- 12.9) yr (range 5-44). Eating occurred from sleep nightly in 57.9% (n = 11) of patients. Chief complaints included excessive weight gain, concerns about choking while eating or about starting fires from cooking and sleep disruption. Extensive polysomnographic studies, clinical evaluations and treatment outcome data identified three etiologic categories for the sleep-related eating: (a) sleepwalking (SW), 84.2% (n = 16); (b) periodic movements of sleep (PMS), 10.5% (n = 2) and (c) triazolam abuse (0.75 mg hs), 5.3% (n = 1). DSM-III Axis 1 psychiatric disorders (affective, anxiety) were present in 47.4% (n = 9) of the patients, and only two patients had a daytime eating disorder (anorexia nervosa), each in remission for 3-7 yr. Nearly half of all patients fulfilled established criteria for being overweight, based on the body mass index. Onset of sleep-related eating was linked directly to the onset of SW, PMS, triazolam abuse, nicotine abstinence, chronic autoimmune hepatitis, narcolepsy, encephalitis or acute stress. In the SW group, 72.7% (8/11) of patients had nocturnal eating and other SW behavior suppressed by clonazepam (n = 7) and/or bromocriptine (n = 2) treatment. Both patients with PMS likewise responded to treatment with combinations of carbidopa/L-dopa, codeine and clonazepam. Thus, sleep-related eating disorders can generally be controlled with treatment of the underlying sleep disorder.