An Aboriginal-led consortium approach to chronic disease action for health equity and holistic wellbeing.

ISSUE ADDRESSED: The Wellbeing Economy, which places human and ecological wellbeing at the centre of policy making, aligns with holistic Aboriginal and Torres Strait Islander conceptualisations of health and wellbeing. In order to address chronic diseases in South Australian Aboriginal and Torres Strait Islander populations, the South Australian Aboriginal Chronic Disease Consortium (Consortium) is fostering action in ways that align both with the Wellbeing Economy and with Health in All Policies (HiAP) approaches. METHODS: In June 2017, the Consortium was established as a collaborative partnership between government and non-government organisations, researchers, Aboriginal organisations and communities to lead the effective implementation of three state-wide chronic disease plans. A coordinating centre was funded to support and progress the work of the Consortium. RESULTS: During its first 5 years, the Consortium has developed a foundation for sustained system reform through partnering with stakeholders, leading projects and initiatives, advocating for key priorities, leveraging existing infrastructure and funding, supporting services, and coordinating delivery of priority actions using innovative approaches. CONCLUSIONS: Through the Consortium governance structure, Aboriginal and Torres Strait Islander community members, policy actors, service providers and researchers oversee, drive, influence and support the implementation of priority action initiatives. Sustained funding, competing priorities of partner organisations and project evaluation are constant challenges. SO WHAT?: A consortium approach provides direction and shared priorities, which foster collaboration across and between organisations, service providers and the Aboriginal community. Aligning with HiAP approaches and the Wellbeing Economy, it harnesses knowledge, networks and partnerships that support project implementation and reduce duplication.

High intake of folic acid disrupts embryonic development in mice.

BACKGROUND: Folic acid fortification and supplementation has increased folate intake and blood folate concentrations and successfully reduced the incidence of neural tube defects. However, the developmental consequences of high folate intake are unknown. This study investigated the impact of high folate intake, alone or with methylenetetrahydrofolate reductase (MTHFR) deficiency, on embryonic and placental development in mice. METHODS: Mthfr +/+ or +/- pregnant mice on a control diet (CD; recommended intake of folic acid for rodents) or folic acid-supplemented diet (FASD; 20-fold higher than the recommended intake) were examined for embryonic loss, delay, and defects at 10.5 and 14.5 days post coitum (dpc); 10.5-dpc placenta, and 14.5-dpc embryo hearts were studied histologically. RESULTS: Total plasma folate was 10-fold higher in FASD compared to CD mice; plasma homocysteine levels were not affected by diet. At 10.5 dpc, the FASD was associated with embryonic delay and growth retardation, and may confer susceptibility to embryonic defects. The FASD did not adversely affect 10.5-dpc placental development. At 14.5 dpc, embryos from the FASD Mthfr +/+ group were delayed and the FASD was associated with thinner ventricular walls in embryonic hearts. There was a significant interaction between maternal MTHFR deficiency and a high folate diet for several developmental outcomes. CONCLUSIONS: Our study suggests that high folate intake may have adverse effects on fetal mouse development and that maternal MTHFR deficiency may improve or rescue some of the adverse outcomes. These findings underscore the need for additional studies on the potential negative impact of high folate intake during pregnancy.

Methylenetetrahydrofolate reductase deficiency and low dietary folate increase embryonic delay and placental abnormalities in mice.

BACKGROUND: Despite extensive research on mild methylenetetrahydrofolate reductase (MTHFR) deficiency and low dietary folate in different disorders, the association of these metabolic disturbances with a variety of congenital defects and pregnancy complications remains controversial. In this study we investigated the effects of MTHFR and dietary folate deficiency at 10.5 days post coitum (dpc) in our mouse model of mild MTHFR deficiency. METHODS: Mthfr +/+ and +/- female mice were fed a control or folic acid-deficient diet for 6 weeks, then mated with Mthfr +/- males. At 10.5 dpc, embryos were examined and placentae were collected for histologic evaluation. RESULTS: Maternal MTHFR and folate deficiencies resulted in increased developmental delays and smaller embryos. We also observed a low frequency of a variety of embryonic defects in the experimental groups, such as neural tube, heart looping, and turning defects; these results mimic the low incidence and multifactorial nature of these anomalies in humans. Folate-deficient mice also had increased embryonic losses and severe placental defects, including placental abruption and disturbed patterning of placental layers. Folate-deficient placentae had decreased ApoA-I expression, and there was a trend toward a negative correlation between ApoA-I expression with maternal homocysteine concentrations. CONCLUSIONS: Our study provides biological evidence linking maternal MTHFR and dietary folate deficiencies to adverse pregnancy outcomes in mice. It underscores the importance of folate not only in reducing the incidence of early embryonic defects, but also in the prevention of developmental delays and placental abnormalities that may increase susceptibility to other defects and to reproductive complications.