The gut microbiota plays a multifaceted role in calcium homeostasis and bone metabolism —acting through metabolic, immunological, and hormonal pathways that collectively constitute the gut–bone axis. The microbiota influences calcium bioavailability through several overlapping mechanisms that act in the intestine. Moreover, microbial fermentation products may directly impact the osteoblast–osteoclast interplay and, by modulating immune and endocrine functions, are crucial for bone metabolism. A healthy microbiota supports bone formation; however, intestinal dysbiosis may impair bone structure and function. This narrative review aims to present pathways linking the gut microbiota to bone metabolism, both in health and disease. First, we will discuss the influence of gut microbiota on calcium absorption. We will then outline the role that microbial metabolites, such as bile acids and short-chain fatty acids (SCFAs), play in regulating bone structure and function. In the following section, we will discuss the role of the microbiota in the immunological and hormonal modulation of bone metabolism. Finally, we will discuss how dysbiosis affects bone and how therapeutic interventions, such as probiotics, prebiotics, and postbiotics, may influence bone tissue quality.

Obesity is a chronic, recurrent, and heterogeneous disease whose effective treatment requires an approach that goes beyond assessment of body mass index and short-term weight loss. Contemporary management should integrate assessment of adipose tissue distribution and function, obesity phenotype, complications, and cardiometabolic risk with individualized nutritional, behavioral, pharmacological, and—if appropriate—surgical interventions. This paper presents the ADIPO–CARE Plan, a practical, structured model for the comprehensive assessment and long-term treatment of people living with obesity. The model comprises two interconnected stages. The ADIPO defines a comprehensive clinical assessment process: A—Assess adiposity, which includes assessing the degree and distribution of excess adipose tissue; D—Define obesity phenotype, which aims to identify the clinical phenotype of obesity; I—Identify complications, which includes detecting obesity-related diseases and complications; P—Profile cardiometabolic risk, which serves to determine global cardiometabolic risk and disease severity; and O—Overall treatment goals, defining individual, realistic therapeutic goals that go beyond weight loss. The second phase, CARE, organizes the treatment and long-term follow-up strategy: C—Comprehensive lifestyle intervention, with particular emphasis on nutritional therapy, physical activity, behavioral interventions, and lifestyle modifications; A—Anti-obesity pharmacotherapy, encompassing the rational use of pharmacotherapy as a complement to lifestyle interventions; R—Response-guided treatment optimization, involving systematic assessment of response and intensification or modification of therapy; and E—Evaluate long-term effectiveness, focusing on maintenance of effects, safety, adherence, relapse prevention, and long-term disease control. The ADIPO–CARE Plan proposes a shift from an approach focused primarily on body weight to a model focused on phenotype, risks, complications, and long-term health benefits. This framework can facilitate the systematization of clinical decisions and the integration of nutritional therapy with other elements of modern, personalized obesity therapy.