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I make two key points here: 1) the incidence of transient CHI in premature neonates is (I believe) unknown 2) although the pancreas secretes insulin and C-peptide in equal amounts, they are metabolised and excreted very differently. Insulin is primarily metabolised by the liver, whereas C-peptide is excreted by the kidneys. Levels therefore reflect both hepatic and renal function. Differential metabolism/excretion is therefore responsible for what is known as the ‘molar ratio’. The molar ratio, and not the absolute levels, is the important value. Premature (as do all) neonates have relatively impaired hepatic function along with a tendency towards losing protein in the urine. Healthy hepatic and renal function in the fasting state will give you a positive molar ratio, whereas poor hepatic and renal function (reduced rate of insulin metabolism plus increased C-peptide loss in the urine) while on a glucose infusion will give you a negative one. 3) because of this, you can’t apply reference ranges derived in other populations to premature babies. In the absence of population reference ranges for premature neonates of different birth weights and gestational ages, and in the presence of a lack of understanding of these dynamics, this test should not be being used to diagnose CHI in premature babies, or should only be used with caution. I think point 2 particularly is VERY important for everyone to understand, because if you want to make an argument for Lucy’s innocence, you MUST be able to explain HOW those insulin results may have physiologically occurred. It isn’t enough simply to say the results were wrong (they probably weren’t), but the understanding of insulin handling in premature neonates applied in this case to date is flawed, and more research is needed. Please note that all opinions expressed here are my own and do not represent those of any organisations I may be associated with. Respectful comments and questions are welcome 🙏 Read the full article on my blog here: https://www.drellenstorm.com/post/luc...