Consensus on complementary feeding from the Latin American Society for Pediatric Gastroenterology, Hepatology and Nutrition: COCO 2023

Abstract Complementary feeding (CF) is defined as infant feeding that complements breastfeeding or, alternatively, breastfeeding with a breast milk substitute, and is a process that goes beyond simply providing guidance on what and how to introduce foods. The information provided by health professionals should be up-to-date and evidence-based. There are different guidelines or position papers at the international level, which, although most of the recommendations may be applicable, there are some others that require regionalization or adaptation to the conditions and reality of each area. The Nutrition working group of the Latin American Society of Pediatric Gastroenterology, Hepatology and Nutrition convened a group of experts, representatives from each of the countries that make up the society, with the objective of developing a consensus on CA, incorporating, when possible, local information that adapts to the reality of the region. The purpose of this document is to show the results of this work. Through Delphi methodology, a total of 34 statements or statements regarding relevant aspects of CA were evaluated, discussed and voted upon.Resumen La alimentación complementaria (AC) se define como la alimentación de los lactantes que complementa a la lactancia materna o en su defecto, a la lactancia con un sucedáneo de la leche materna, y es un proceso que va más allá de simplemente una guía sobre qué y cómo introducir los alimentos. La información brindada por parte de los profesionales de la salud debe ser actualizada y basada en evidencia. Existen diferentes guías o documentos de posición a nivel internacional, que, aunque la mayoría de las recomendaciones pueden ser aplicables, hay algunas otras que requieren una regionalización o adecuación a las condiciones y realidad de cada zona. El grupo de trabajo de Nutrición de la Sociedad Latinoamericana de Gastroenterología, Hepatología y Nutrición Pediátrica convocó a un grupo de expertos, representantes de cada uno de los países que conforman la sociedad, con el objetivo de desarrollar un consenso sobre la AC, que incorporó cuando así fue posible, información local que se adapte a la realidad de la región. El objetivo de este documento es mostrar los resultados de dicho trabajo. A través de metodología Delphi, se evaluaron, discutieron y votaron un total de 34 declaraciones o enunciados con respecto a aspectos relevantes de la AC

Modulating mitophagy in mitochondrial disease

Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage. While the core autophagic machinery is highly conserved and common to most pathways, the signaling pathways leading to the selective degradation of damaged mitochondria are still not completely understood. Type 1 mitophagy due to nutrient starvation is dependent on PI3K (phosphoinositide 3-kinase) for autophagosome formation but independent of mitophagy proteins, PINK1 (PTEN-induced putative kinase 1) and Parkin. Whereas type 2 mitophagy that occurs due to damage is dependent on PINK1 and Parkin but does not require PI3K. Autophagy and mitophagy play an important role in human disease and hence could serve as therapeutic targets for the treatment of mitochondrial as well as neurodegenerative disorders. Therefore, we reviewed drugs that are known modulators of autophagy (AICAR and metformin) and may effect this by activating the AMP-activated protein kinase signaling pathways. Furthermore, we reviewed data available on supplements, such as Coenzyme Q and the quinone idebenone, that we assert rescue increased mitophagy in mitochondrial disease by benefiting mitochondrial function