Nutrition from the Inside Out

Abstract

Nearly 50 years ago, I set out to investigate the clinical problem of hypoglycemia in children with illnesses that limited their food intake. My goal was to gather accurate and precise measurable data. At the time, I wasn't interested in nutrition as a discipline defined in its more general or popular sense. To address the specific problem that interested me required development of entirely new methods based on stable, nonradioactive tracers that satisfied the conditions of accuracy and precision. At the time, I had no inclination of the various theoretical and practical problems that would have to be solved to achieve this goal. Some are briefly described here. Nor did I have the slightest idea that developing the field would result in a fundamental change in how human clinical investigation was conducted, with the eventual replacement of radiotracers with stable isotopically labeled ones, even for adult clinical investigation. Additionally, I had no inclination that the original questions would open avenues to much broader questions of practical nutritional relevance. Moreover, only much later as the editor of The American Journal of Clinical Nutrition did I appreciate the policy implications of how nutritional data are presented in the scientific literature. At least in part, less accurate and precise measurements and less than full transparency in reporting nutritional data have resulted in widespread debate about the public policy recommendations and guidelines that are the intended result of collecting the data in the first place. This article provides a personal recollection (with all the known faults of self-reporting and retrospective memory) of the journey that starts with measurement certainty and ends with policy uncertainty.

Loss of Function of von Hippel‐Lindau Trigger Lipocalin 2‐Dependent Inflammatory Responses in Cultured and Primary Renal Tubular Cells

“…LCN2 mediates several cellular processes, including apoptosis, proliferation, epithelial-to-mesenchymal differentiation, and matrix metalloproteinase 9 stabilization [12]. High levels of LCN2 expression have been observed in renal, breast, ovary, colon, and brain cancer cells [13][14][15]. In addition, LCN2 is a member of the lipocalin superfamily of proteins that transport hydrophobic molecules, such as retinoids, fatty acids, and organic iron chelators [16].…”