Behavioral outcomes of picky eating in childhood: a prospective study in the general population.

BACKGROUND: Picky eaters in the general population form a heterogeneous group. It is important to differentiate between children with transient picky eating (PE) and persistent PE behavior when adverse outcomes are studied. We analyzed four PE trajectories to determine the associations with child mental health prospectively. METHODS: From a population-based cohort, 3,748 participants were assessed for PE at 1.5, 3, and 6 years of age using maternal reports. Four trajectories were defined: persistent (PE at all ages); remitting (PE before 6 years only); late-onset (PE at 6 years only); and never (no PE at any assessment). Child's problem behaviors were assessed with the Teacher's Report Form at 7 years of age. We examined associations between picky eating trajectories and emotional problems, behavioral problems and pervasive developmental problems using logistic regressions. Analyses were adjusted for child, parental, and socioeconomic confounders. We also adjusted for maternal-reported baseline problem behavior at age 1.5 years; the never picky eating group was used as reference. RESULTS: Persisting PE predicted pervasive developmental problems at age 7 years (OR = 2.00, 95% CI: 1.10-3.63). The association remained when adjusted for baseline pervasive developmental problems at 1.5 years (OR = 1.96, 95% CI: 1.10-3.51). Persistent PE was not associated with behavioral (OR = 0.92, 95% CI: 0.53-1.60) or emotional problems (OR = 1.24, 95% CI: 0.74-2.07). Other PE trajectories were not related to child behavioral or emotional problems. CONCLUSIONS: Persistent PE may be a symptom or sign of pervasive developmental problems, but is not predictive of other behavioral problems. Remitting PE was not associated with adverse mental health outcomes, which further indicates that it may be part of normal development.

Trajectories of picky eating during childhood: A general population study.

OBJECTIVE: This cohort study describes the prevalence of picky eating and examines prognostic factors for picky eating trajectories during childhood. METHODS: 4,018 participants of a population-based cohort with measurements from pregnancy onwards were included. Picky eating was assessed by maternal report when children were 1.5, 3, and 6 years old. The associations of child and family characteristics with trajectories of picky eating were examined using logistic regression. Never picky eaters were used as the reference group. RESULTS: Prevalence of picky eating was 26.5% at 1.5 years of age, 27.6% at the age of 3 and declined to 13.2% at 6 years. Four main picky eating trajectories were defined: (1) never picky eating at all three assessments (55% of children), (2) remitting (0-4 years, 32%), (3) late-onset (6 years only, 4%), and (4) persistent (all ages, 4%). This implies that almost two thirds of the early picky eaters remitted within 3 years. Male sex, lower birth weight, non-Western maternal ethnicity, and low parental income predicted persistent picky eating. More often late-onset picky eaters were children of parents with low income and non-Western ethnicity. DISCUSSION: We found that nearly half (46%) of children were picky eaters at some point during early childhood. Remittance was very high. This suggests that picky eating is usually a transient behavior and part of normal development in preschool children. However, a substantial group of persistent picky eaters, often from a socially disadvantaged background, continues to have problems beyond the preschool age.

Loss of Hoxb8 alters spinal dorsal laminae and sensory responses in mice.

Although Hox gene expression has been linked to motoneuron identity, a role of these genes in development of the spinal sensory system remained undocumented. Hoxb genes are expressed at high levels in the dorsal horn of the spinal cord. Hoxb8 null mutants manifest a striking phenotype of excessive grooming and hairless lesions on the lower back. Applying local anesthesia underneath the hairless skin suppressed excessive grooming, indicating that this behavior depends on peripheral nerve activity. Functional ablation of mouse Hoxb8 also leads to attenuated response to nociceptive and thermal stimuli. Although spinal ganglia were normal, a lower postmitotic neural count was found in the dorsalmost laminae at lumbar levels around birth, leading to a smaller dorsal horn and a correspondingly narrowed projection field of nociceptive and thermoceptive afferents. The distribution of the dorsal neuronal cell types that we assayed, including neurons expressing the itch-specific gastrin-releasing peptide receptor, was disorganized in the lumbar region of the mutant. BrdU labeling experiments and gene-expression studies at stages around the birth of these neurons suggest that loss of Hoxb8 starts impairing development of the upper laminae of the lumbar spinal cord at approximately embryonic day (E)15.5. Because none of the neuronal markers used was unexpressed in the adult dorsal horn, absence of Hoxb8 does not impair neuronal differentiation. The data therefore suggest that a lower number of neurons in the upper spinal laminae and neuronal disorganization in the dorsal horn underlie the sensory defects including the excessive grooming of the Hoxb8 mutant.

Are parents' anxiety and depression related to child fussy eating?

OBJECTIVE: To examine the association between parental anxiety and depression with child fussy eating-that is, consistent rejection of particular food items. DESIGN: This study was embedded in Generation R, a prospective cohort from fetal life onwards in the Netherlands. SETTING: Population-based. PARTICIPANTS: 4746 4-year-old children and their parents. EXPOSURE: Parental internalising problems (ie, symptoms of anxiety and depression) were assessed with the Brief Symptoms Inventory during pregnancy and the preschool period (child age 3 years). MAIN OUTCOME MEASURE: The food fussiness scale of the Children's Eating Behaviour Questionnaire. RESULTS: Maternal anxiety during pregnancy and during the child's preschool period was related to higher food fussiness sum-scores in children. For instance, per point on the anxiety scale in pregnancy, children had on average a 1.02 higher sum-score (95% CI 0.59 to 1.46) on the food fussiness scale, after adjustment for confounders. Likewise, mothers' depressive symptoms at both time points were associated with fussy eating behaviour in their children (eg, in the antenatal period: per point on the depression scale, children had a 0.91 point higher sum-score on the food fussiness scale, 95% CI 0.49 to 1.33). We found largely similar associations between fathers' internalising problems and children's fussy eating. However, fathers' anxiety during the antenatal period was not related to child fussy eating. CONCLUSIONS: Maternal and paternal internalising problems were prospectively associated with fussy eating in preschoolers. Healthcare practitioners should be aware that non-clinical symptoms of anxiety and depression in parents are risk factors for child fussy eating.

Role of ghrelin in the pathophysiology of eating disorders: implications for pharmacotherapy.

Ghrelin is the only known circulating orexigenic hormone. It increases food intake by interacting with hypothalamic and brainstem circuits involved in energy balance, as well as reward-related brain areas. A heightened gut-brain ghrelin axis is an emerging feature of certain eating disorders such as anorexia nervosa and Prader-Willi syndrome. In common obesity, ghrelin levels are lowered, whereas post-meal ghrelin levels remain higher than in lean individuals. Agents that interfere with ghrelin signalling have therapeutic potential for eating disorders, including obesity. However, most of these drugs are only in the preclinical phase of development. Data obtained so far suggest that ghrelin agonists may have potential in the treatment of anorexia nervosa, while ghrelin antagonists seem promising for other eating disorders such as obesity and Prader-Willi syndrome. However, large clinical trials are needed to evaluate the efficacy and safety of these drugs.

Spinal inhibitory interneuron pathology follows motor neuron degeneration independent of glial mutant superoxide dismutase 1 expression in SOD1-ALS mice.

Motor neuron degeneration and skeletal muscle denervation are hallmarks of amyotrophic lateral sclerosis (ALS), but other neuron populations and glial cells are also involved in ALS pathogenesis. We examined changes in inhibitory interneurons in spinal cords of the ALS model low-copy Gurney G93A-SOD1 (G1del) mice and found reduced expression of markers of glycinergic and GABAergic neurons, that is, glycine transporter 2 (GlyT2) and glutamic acid decarboxylase (GAD65/67), specifically in the ventral horns of clinically affected mice. There was also loss of GlyT2 and GAD67 messenger RNA-labeled neurons in the intermediate zone. Ubiquitinated inclusions appeared in interneurons before 20 weeks of age, that is, after their development in motor neurons but before the onset of clinical signs and major motor neuron degeneration, which starts from 25 weeks of age. Because mutant superoxide dismutase 1 (SOD1) in glia might contribute to the pathogenesis, we also examined neuron-specific G93A-SOD1 mice; they also had loss of inhibitory interneuron markers in ventral horns and ubiquitinated interneuron inclusions. These data suggest that, in mutant SOD1-associated ALS, pathological changes may spread from motor neurons to interneuronsin a relatively early phase of the disease, independent of the presence of mutant SOD1 in glia. The degeneration of spinal inhibitory interneurons may in turn facilitate degeneration of motor neurons and contribute to disease progression.