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In 1989, I commenced a research project to investigate the processes of metabolic adaptation after birth. One aspect was to investigate the endocrine and metabolic responses to neonatal hypoglycaemia.1 ,2 When notified out of hours of admission of a ‘hypoglycaemic’ baby to a neonatal unit I would rush from meals and family commitments, access stores of dry ice in a remote outhouse of the hospital, and conduct fiddly centrifuging, pipetting and snap freezing of tiny blood samples. The study sample size was perhaps larger than it should have been as the diagnostic cut-off of 2.6 mmol/l had found its way into use (more of that below). Many babies on my arrival seemed surprisingly well and were physically resisting all efforts to site nasogastric tubes and intravenous cannulae, and were returning to the sender the volumes of formula milk that were given to them with the best of intentions. Imagine my dismay, especially on the part of the babies and their mothers, when laboratory measurements demonstrated that for many babies, the admission glucose was not confirmed as being in the hypoglycaemic range and that the initial near-patient testing strip had proved to be an inaccurate measurement (again more of that below). Or a baby admitted to the neonatal unit for another reason had a blood glucose measurement very shortly after birth, at the time of the universal nadir described below and on the basis of this single measurement the baby was labelled as hypoglycaemic, while if left to his own devices or with normal neonatal unit care, his blood glucose would have subsequently risen.
Further, as the study elapsed and following discussion with experts such as the late Marvin Cornblath, it became evident that many babies did not have a pathological condition, rather they were simply doing what babies do …
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