Jason's expertice on the topic is immediately apparent, and I trust this man completely to tell it like it is
Elevated cortisol directly inhibits GH receptor signaling in target tissues and increases hepatic GH resistance, meaning even if you achieve a GH pulse, downstream IGF-1 production and metabolic signaling are impaired
The activated form of folic acid is increased, which helps with cardiovascular and cancer risks
The complexities of a childs physiology and biological processing of drugs come into play, demanding a more tailored approach to pediatric medication dosing
So, why does this question even exist
As an example, one case study involving someone with a history of alcoholic pancreatitis tied an acute pancreatitis episode to starting semaglutide three months before