Developing our understanding of nutrition in depression.

Research to date has convincingly demonstrated that nutrition impacts depression. Population-based studies have shown that diet, food types, dietary supplements, gut bacteria, endocrine systems and obesity all play a role in depression. While nutrition could provide an important therapeutic opportunity in depression, clinical trials have not shown clinically meaningful results, and it appears unlikely that nutrition is a central determinant of depression. Conversely, however, prior research is inconclusive to inferring that nutrition does not have a clinically significant effect. This would require elucidating precisely when nutrition affects depression which necessitates an alternative, more granular, model for the nutrition­depression interaction. The network theory of mental disorders, which studies how mental disorders arise from a causally related network of symptoms and external factors, is proposed as an alternative model for understanding the complexity of the nutrition­depression link. This approach would uncover which relationships, between aspects of nutrition and depression symptoms, warrant further study at a population and laboratory level. Furthermore, from within nutrition science, is a movement dubbed 'New Nutrition Science' (NNS) that aims to integrate biological, social and environmental determinants of nutrition. NNS is important to nutrition­depression research which has yet to reveal how social factors impact the nutrition­depression interaction. Network theory methodology is fully compatible with the network modelling already used in NNS. Embracing both network theory and NNS in future research will develop a full and complex understanding of nutrition in depression.

Hearing loss mediates executive function impairment in sleep-disordered breathing.

BACKGROUND: Sleep-disordered breathing (SDB) is often co-morbid with conductive hearing loss in early childhood due to a shared aetiology of adenotonsillar hypertrophy. Hearing loss is independently associated with impairment of executive function and behavioural difficulties. We hypothesised that these impairments in children with SDB may be mediated through hearing loss. METHODS: Fifty-eight children including 37 snorers awaiting adenotonsillectomy and 21 healthy non-snoring controls, aged 3-5 years, were assessed with pure tone audiometry, Strengths and Difficulties (SDQ), Behaviour Rating of Executive Function (BRIEF-P), and Childhood Middle Ear Disease and Hearing questionnaires. Polysomnography in snoring children generated an obstructive apnoea/hypopnea index (OAHI). Two regression models examined the effect of SDB and the mediating impact of hearing loss on BRIEF and SDQ. RESULTS: Snoring children had significantly poorer hearing, greater past exposure to hearing loss, and higher total SDQ and BRIEF-P scores than non-snoring controls. The first regression model, including all children, demonstrated that the impact of snoring on BRIEF_P, but not SDQ, was entirely mediated by a history of hearing loss exposure but not same-day audiometry. The second model examined snoring children only, categorising the group into 12 with obstructive sleep apnoea (OSA) (OAHI ≥ 5) and 25 without OSA. OSA had a direct effect on SDQ scores, but this was not mediated by a history of hearing loss. CONCLUSION: In early childhood, conductive hearing loss mediates the relationship between SDB, irrespective of severity, and parent report of executive function but not behaviour. Treatment of hearing loss in pre-school SDB might improve executive function.