Obesity is now a global epidemic affecting a significant and rapidly increasing number of adults, adolescents, and children. As the incidence of obesity has increased, so has the use of bariatric surgery as a medical solution. A growing number of studies now report that, despite calcium and vitamin D supplementation, the most frequently performed types of bariatric surgery, the Roux-en-Y gastric bypass and the sleeve gastrectomy, cause significant ongoing bone loss. In resources available to the general public and to physicians, this adverse outcome is rarely mentioned or is attributed solely to reduced calcium absorption. Recent studies investigating micronutrient malabsorption and changes in a wide range of hormones induced by bariatric surgery now indicate that calcium malabsorption is the tip of a formidable iceberg. The current article, part 1 of a 2-part series, reviews the latest research findings confirming that obesity prevalence is skyrocketing and that bariatric surgery causes ongoing, accelerated bone loss. Part 1 also discusses the mechanisms through which the bariatric surgery-induced malabsorption of key nutrients adversely affects bone homeostasis. Part 2 discusses the specific changes seen in bone metabolism after bariatric surgery and reviews current data on the underlying mechanisms, in addition to nutrient malabsorption, which are thought to contribute to bariatric surgery-induced ongoing accelerated bone loss. These processes include mechanical unloading and changes in a wide variety of hormones (eg, leptin, adiponectin, testosterone, estradiol, serotonin, ghrelin, glucagon-like peptide 1, and gastric inhibitory peptide). Also, part 2 covers interventions that may help lessen bariatric surgery-induced bone loss, which are now beginning to appear in the medical literature. Bariatric surgery’s adverse effects on bone must be widely recognized and protocols developed to prevent early onset osteoporosis in the recipients of an increasingly utilized and otherwise potentially life-saving surgery.