Teleintervention's effects on breastfeeding in low-income women in high income countries: a systematic review and meta-analysis.

BACKGROUND: Many mothers in high-income countries (HIC) do not breastfeed to the World Health Organisation's recommendation of two years. This is particularly true for low-income women (LIW). They often face additional socio-structural barriers that encourage early discontinuation and are inadequately supported by current healthcare interventions. Teleinterventions are flexible and widely used following the global pandemic and increase maternal autonomy over intervention delivery. They show promise in improving other maternal conditions in LIW, including postpartum depression. Teleinterventions can increase breastfeeding rates in the wider maternal population, however their efficacy for this underserved population has not yet been systematically assessed. This meta-analysis aimed to identify if teleinterventions increase 'exclusive' or 'any' breastfeeding by LIW in HIC at 1-, 3-4, and 6-months postpartum. METHODS: We searched five online databases for randomised controlled trials assessing breastfeeding teleinterventions for LIW in HIC. Risk ratios (RR) were used to calculate the average effect of teleinterventions on 'any' and 'exclusive' breastfeeding at at 1-, 3-4, and 6-months postpartum using random effects meta-analysis. Study bias was assessed using the Revised Cochrane risk-of-bias tool for randomised trials (RoB2), and outcome quality was evaluated against GRADE criteria. RESULTS: Nine studies met inclusion criteria: six providing telephone calls, two text messages and one an online support group. All the studies were conducted in the United States, with small sample sizes and a high risk of bias. Pooled results indicate teleinterventions modestly increase 'any' and 'exclusive' breastfeeding at all time points, with a statistically significant increase in 'exclusive' breastfeeding after 3-4 months (RR 1.12, 95% CI [1.00,1.25]). At 3-4 months teleinterventions providing peer support were more effective than educational teleinterventions at promoting any and exclusive breastfeeding. Evidence for all outcomes were rated 'low' or 'very low' quality using the GRADE tool, mainly due to high attrition and low power. CONCLUSIONS: Despite insufficient high-quality research into breastfeeding teleinterventions for LIW, our results suggest teleinterventions may improve exclusive and any breastfeeding. Given breastfeeding is particularly low in LIW population from HIC, our findings are promising and require further exploration by larger, methodologically sound trials in other HIC.

Adrenal Dysfunction in Mitochondrial Diseases.

Cortisol is central to several homeostatic mechanisms including the stress and immune response. Adrenal insufficiency and impaired cortisol production leads to severe, potentially fatal disorders. Several fundamental stages of steroidogenesis occur within the mitochondria. These dynamic organelles not only contribute ATP for steroidogenesis, but also detoxify harmful by-products generated during cortisol synthesis (reactive oxygen species). Mutations in nuclear or mitochondrial DNA that impair mitochondrial function lead to debilitating multi-system diseases. Recently, genetic variants that impair mitochondrial function have been identified in people with isolated cortisol insufficiency. This review aimed to clarify the association between mitochondrial diseases and adrenal insufficiency to produce cortisol. Mitochondrial diseases are rare and mitochondrial diseases that feature adrenal insufficiency are even rarer. We identified only 14 cases of adrenal insufficiency in people with confirmed mitochondrial diseases globally. In line with previous reviews, adrenal dysfunction was most prevalent in mitochondrial deletion syndromes (particularly Pearson syndrome and Kearns-Sayre syndrome) and with point mutations that compromised oxidative phosphorylation. Although adrenal insufficiency has been reported with mitochondrial diseases, the incidence reflects that expected in the general population. Thus, it is unlikely that mitochondrial mutations alone are responsible for an insufficiency to produce cortisol. More research is needed into the pathogenesis of adrenal disease in these individuals.