Reconsidering Mineral Formulations in Human Health and Disease: Molecular Mechanisms, Bioavailability and Metabolic Fates

Minerals are essential nutrients involved in enzymatic catalysis, signal transduction, cellular bioenergetics, and the maintenance of structural integrity. However, much of the existing research in mineral nutrition has evaluated physiological effects primarily at the elemental level, without adequately distinguishing whether a mineral is ingested as part of an organic matrix in natural foods or enters the biological system as an ionized species from inorganic salts or aqueous solutions. This review examines the criteria by which the conceptual definitions of organic and inorganic minerals have been established and explores the historical, analytical, and methodological factors underlying the lack of clear distinctions between these categories. In addition, it analyzes how the chemical form of minerals governs intestinal transport pathways, systemic bioavailability, tissue-specific accumulation, and intracellular metabolic handling. Using vanadium, silicon, zinc, and selenium as representative paradigms, this review contrasts the distinct molecular and toxicological fates of organic complexes versus inorganic salts-highlighting critical pathways such as protein tyrosine phosphatase (PTPase)-mediated insulin signaling, collagen cross-linking, mitochondrial mitochondrial aconitase (m-aconitase) regulation, and selenoprotein-dependent redox homeostasis. Furthermore, this review addresses the pharmacological and toxicological windows associated with high-dose inorganic salt exposure versus sustained food-bound assimilation. The purpose of this review is not to assert the absolute superiority of one mineral form over another, but rather to clarify poorly defined conceptual boundaries, reassess the interpretative scope of existing findings, and emphasize the necessity for future nutritional and biomedical research to adopt precise, form-specific molecular frameworks.