Pediatric chronic pain is common and predicts risk for psychological and pain problems into adulthood. Biopsychosocial risk factors for the development of chronic pediatric pain have been examined, but the key health behavior of caloric consumption has not been explored. Adult and animal data suggest that caloric intake is positively related to chronic pain, and that adiposity and stress-related biological factors may serve as potential mediators. This study predicted that among children: 1) adiposity, flattened diurnal cortisol slopes, and caloric consumption are related to chronic pain, and 2) the caloric consumption—pain relation is mediated by elevated adiposity and/or flattened diurnal cortisol slopes. Methods: Twin children (N = 733) were drawn from the Arizona Twin Project sample. Measures included caregiver-reported caloric intake via five daily food diaries (Age-8); adiposity (composite of waist circumference, body mass index, body fat percentage) and diurnal cortisol slopes via three days of salivary cortisol sampling (Age-9); and caregiver-reported monthly chronic pain (Age-10). Results: Multilevel models (accounting for clustering within families) with sex, age, socioeconomic status, puberty, race/ethnicity as covariates, showed that caloric intake predicted greater waist circumference, which in turn predicted elevated chronic pain. However, adiposity, waist circumference, and diurnal cortisol slopes did not mediate the caloric intake-chronic pain relation. Discussion: Consistent with the literature, caloric intake predicted adiposity, and adiposity predicted pain in a diverse sample of children. More comprehensive assessment of behavioral (sleep, diet quality) and biopsychosocial factors (e.g. inflammation, cortisol; injury; catastrophizing) may aid efforts to prevent pediatric chronic pain.

Sensory over-responsivity, a subtype of sensory modulation disorder, is characterized by extreme negative reactions to normative sensory experiences. These over-reactions can interfere with daily activities and cause stress to children and their families. The etiology and developmental course of sensory over-responsivity is still largely unknown. We measured tactile and auditory over-responsivity in a population-based, typically developing sample of twins (N=978) at age two years via a caregiver report temperament questionnaire and again at age seven years via a sensory over-responsivity symptom inventory. Participating twins were treated as singletons although all analyses controlled for clustering within families. Children were divided into four trajectory groups based on risk status at both ages: low symptom (N=768), remitted (N=75), late-onset (N=112), and chronic (N=24). A subset of children who screened positive for SOR in toddlerhood (N = 102) took part in a pilot study focused on sensory over-responsivity at four years of age. Children in the chronic group had more severe symptoms of sensory sensitivity at age four years, including more motion sensitivity, than the other trajectory groups. Children in the chronic group had a younger gestational age and were more likely to be low birth-weight than the low symptom group. Differences between remitted and late-onset groups and the low-symptoms group were inconsistent across measures. Sensory over-responsivity was modestly correlated across ages (r = .22 for tactile over-responsivity and r = .11 for auditory over-responsivity), but symptoms were more stable among children born prematurely or who had more fearful and less soothable temperaments. A clear implication is that assessment over development may be necessary for a valid sensory processing disorder diagnosis, and a speculative implication is that sensory over-responsivity symptoms may be etiologically heterogeneous, with different causes of transient and stable symptoms.