Prevalence of toddler, child and adolescent overweight and obesity derived from primary care electronic medical records: an observational study.

BACKGROUND: Population monitoring and surveillance of objectively measured child weight data in Canada is limited to national surveys with poor regional applicability, and no healthy weight data are available for children less than 2 years of age. We aimed to determine the prevalence of childhood overweight and obesity using objective measures derived from primary care electronic medical records. METHODS: Observational data included all height and weight records for children less than 20 years of age, between 2004 and 2013, from 3 Ontario primary care research networks. We calculated body mass index (BMI)-for-age and weight-for-length using the World Health Organization Growth Standards and Reference to assign growth status indicator categories by age group. Descriptive data and prevalence estimates were generated for 2013. We also compared weight-for-length for children less than 2 years of age with a corresponding billing code for known well-child visits. RESULTS: Our study included 8261 children with a corresponding growth status indicator, a sample close to 4 times larger than the national survey sample. In 2013, 28.4% of children aged 5-19 years, and 6% of children aged 0-5 years, were categorized as overweight or obese. Between 2008 and 2013, the total number of 18-month well baby visit billing codes was 1152; 6.9% of this group were categorized as overweight or obese; 19.2% were categorized as having risk of overweight. INTERPRETATION: Primary care electronic medical records show good potential for ongoing population monitoring of overweight and obesity, particularly for very young children for whom early intervention is likely to show the greatest positive health impact.

Chronic antidepressant medication attenuates dexamethasone-induced neuronal death and sublethal neuronal damage in the hippocampus and striatum.

Dexamethasone, a synthetic corticosteroid, which can induce a range of mood disorders including depression and affective psychosis, is toxic to specific hippocampal and striatal neuronal populations. Chronic administration of antidepressants can induce neuroprotective effects, potentially by raising cellular levels of brain-derived neurotrophic factor (BDNF). We accordingly tested the hypothesis that chronic pretreatment of rats (Sprague-Dawley, male) with antidepressants would attenuate dexamethasone-induced neuronal damage as revealed by reductions in the level of neuronal death and in sublethal neuronal damage shown by the increase in the number of MAP-2 immunoreactive neurons. In support of this hypothesis, we demonstrate that chronic treatment with a range of antidepressants prior to dexamethasone administration (0.7 mg/kg, i.p.) attenuated the levels of neuronal death and loss of MAP-2 immunoreactivity in both the hippocampus and striatum. The antidepressants used were: desipramine (8 mg/kg, i.p., tricyclic), fluoxetine (8 mg/kg, i.p., selective serotonin reuptake inhibitor) and tranylcypromine (10 mg/kg, i.p., monoamine oxidase inhibitor) with each drug being injected once per day for 10 days. In contrast, acute injection of none of the antidepressants exerted a protective effect from dexamethasone-associated neuronal damage. Similarly, injection of neither cocaine nor chlordiazepoxide (benzodiazepine) exerted protective effects when injected either chronically or acutely. The observed protection from dexamethasone-induced neuronal damage is in keeping with the potential of chronic antidepressant medication to increase BDNF levels. The potential for dexamethasone to induce disorders of mood by damaging specific neuronal populations in the hippocampus and dorsomedial striatum is discussed.