SummaryAn elegant design stratagem for an organ intended to carry loads for life without fracturing, rupturing or wearing out would make those loads determine the organ's strength. It seems load-bearing mammalian bones, joints, fascia, ligaments and tendons do exactly that. Physiologists begin to understand how they do it, and that led to the Utah paradigm of skeletal physiology. Those adaptations occur in two major steps. The first step creates the genetically predetermined newborn skeleton with its anatomical relationships and biologic machinery. The second step adds to the first one all postnatal adaptations to mechanical and other challenges that would affect an organ's strength, size, architecture and composition. During postnatal growth, increasing loads make tissue-level biologic mechanisms correspondingly increase the strength of such organs. Mechanical strain-dependent signals help to control that process, which muscle strength, muscle anatomy and neuromuscular physiology strongly influence. Its problems seem to cause or help to cause numerous skeletal and some extraskeletal disorders. A Table in the article lists examples of them.This article summarizes salient features of the Utah paradigm, which includes both facts and some meanings inferred from them. Other times and people must resolve any questions about those meanings and about the devils that can lie in the details. Parenthetically, instead of the accuracy of the facts on which that paradigm stands, the above questions usually concern the different meanings people can infer from facts, and whether particular facts and ideas would be relevant to a particular issue.