Abstract
Evidence suggests that age-associated differences in body composition-bone/muscle/adipose tissue-are nonlinear, but their timing, sex-specific features, and relation to osteosarcopenic adiposity (OSA) phenotype remain poorly defined. OSA is characterized by the coexistence of osteopenia/osteoporosis, sarcopenia, and excess or redistributed adiposity. We examined sex- and age-specific patterns and inflection points for bone, muscle, fat, and intramuscular adipose tissue (IMAT) in cross-sectional data from 9717 Caucasian adults aged 20-90 years. Body composition was assessed using BIA-ACC, a nonionizing bioelectrical impedance analysis that estimates total body bone, skeletal muscle, fat mass, and IMAT. Prespecified operational thresholds for the BIA-ACC-derived bone and muscle mass scores and sex-specific fat mass percentages were used to define reduced bone and muscle mass, adiposity, and the BIA-ACC-based OSA phenotype. LOESS nonparametric regression was used to model age-related body composition patterns without assuming a predefined functional relationship between age and each outcome and to identify inflection points. For sensitivity analyses, all LOESS curves were fitted with stiffness/span parameter (f) and confidence intervals were calculated. Men showed earlier peaks and relative midlife stability in bone and muscle, followed by lower later life values than women. Women showed lower baseline values, multiple early-life inflection points, and sharper midlife downturns, particularly around menopause. Fat mass increased steadily in men but followed multiphasic patterns in women, whereas IMAT increased progressively with age in both sexes. Adults meeting the operational BIA-ACC criteria for OSA (identified even in the youngest participants) demonstrated less stable trajectories, earlier downturns in bone and muscle components, and more complex fat and IMAT patterns. Distinct sex-specific patterns and adverse association between BIA-ACC-defined OSA and body composition patterns were identified. Early identification of this phenotype may support preventive assessment of accelerated musculoskeletal decline and increasing adiposity.