Evaluating the impact of a child sponsorship programme on paediatric health and development in Calauan, Philippines: A retrospective audit.

AIM: International child sponsorship programmes comprise a considerable proportion of global aid accessible to the general population. Team Philippines (TP), a health care and welfare initiative run in association with the University of Notre Dame Sydney since 2013, leads a holistic sponsorship programme for 30 children from Calauan, Philippines. To date, empirical research has not been performed into the overall success and impact of the TP child sponsorship programme. As such, this study aims to evaluate its effectiveness in improving paediatric outcomes. METHODS: Study cohorts comprised 30 sponsored and 29 age- and gender-matched non-sponsored children. Data were extracted from the TP Medical Director database and life-style questionnaires for July-November 2019. Outcome measures included anthropometry, markers of medical health, dental health, exercise, and diet. Statistical analyses were performed in SPSS. RESULTS: Sponsorship resulted in fewer medical diagnoses and prescription medications, superior dental health, and improved diet. Further, sponsored children may show a clinically significant trend towards improved physical health. Sponsorship did not affect growth and development metrics, or levels of physical activity. CONCLUSIONS: The TP child sponsorship programme significantly impacts positive paediatric health outcomes in the Calauan community. The strength of the programme lies in its holistic, sustainable, and community-based model, which is enabled by effective international child sponsorship. This study further supports the relationship between supporting early livelihood and improved health in the paediatric population.

Assessing the role of nocturnal core body temperature dysregulation as a biomarker of neurodegeneration.

The vast majority of patients with idiopathic rapid eye movement sleep behaviour disorder will develop a neurodegenerative α-synuclein-related condition, such as Parkinson's disease or dementia with Lewy bodies. The pathology underlying dream enactment overlaps anatomically with the brainstem regions that regulate circadian core body temperature. Previously, nocturnal core body temperature regulation has been shown to be impaired in Parkinson's disease. However, no study to date has investigated nocturnal core body temperature changes in patients with idiopathic rapid eye movement sleep behaviour disorder, which may prove to be an early objective biomarker for α-synucleinopathies. Ten healthy controls, 15 patients with idiopathic rapid eye movement sleep behaviour disorder, 31 patients with Parkinson's disease and six patients with dementia with Lewy bodies underwent clinical assessment and nocturnal polysomnography with core body temperature monitoring. A validated cosinor method was utilised for core body temperature analysis. No differences in mesor, nadir or time of nadir were observed between groups. However, when compared with healthy controls, the amplitude of the nocturnal core body temperature (mesor minus nadir) was significantly reduced in patients with idiopathic rapid eye movement sleep behaviour disorder, Parkinson's disease with concurrent rapid eye movement sleep behaviour disorder and dementia with Lewy bodies (p < 0.001, p = 0.043 and p = 0.017, respectively). Importantly, this relationship was not seen in those patients with Parkinson's disease without rapid eye movement sleep behaviour disorder. In addition, there was a significant negative correlation between amplitude of the core body temperature and self-reported rapid eye movement sleep behaviour disorder symptoms. Changes in thermoregulatory circadian rhythm may be specifically associated with the pathology underlying rapid eye movement sleep behaviour disorder rather than simply that of α-synucleinopathy. These findings implicate thermoregulatory dysfunction as a potential early biomarker for development of rapid eye movement sleep behaviour disorder-associated neurodegeneration, and suggest that subpopulations with differing pathological underpinnings might exist in Parkinson's disease.