Longitudinal, dual-energy X-ray absorptiometry (DXA) hip data from 4187 mostly white, elderly women from the Study of Osteoporotic Fractures were studied with a structural analysis program. Cross-sectional geometry and bone mineral density (BMD) were measured in narrow regions across the femoral neck and proximal shaft. We hypothesized that altered skeletal load should stimulate adaptive increases or decreases in the section modulus (bending strength index) and that dimensional details would provide insight into hip fragility. Weight change in the ∼3.5 years between scan time points was used as the primary indicator of altered skeletal load. “Static” weight was defined as within 5% of baseline weight, whereas “gain” and “loss” were those who gained or lost >5%, respectively. In addition, we used a frailty index to better identify those subjects undergoing changing in skeletal loading. Subjects were classified as frail if unable to rise from a chair five times without using arm support. Subjects who were both frail and lost weight (reduced loading) were compared with those who were not frail and either maintained weight (unchanged loading) or gained weight (increased loading). Sixty percent of subjects (n = 2559) with unchanged loads lost BMD at the neck but not at the shaft, while section moduli increased slightly at both regions. Subjects with increasing load (n = 580) lost neck BMD but gained shaft BMD;​ section moduli increased markedly at both locations. Those with declining skeletal loads (n = 105) showed the greatest loss of BMD at both neck and shaft;​ loss at the neck was caused by both increased loss of bone mass and greater subperiosteal expansion;​ loss in shaft BMD decline was only caused by greater loss of bone mass. This group also showed significant declines in section modulus at both sites. These results support the contention that mechanical homeostasis in the hip is evident in section moduli but not in bone mass or density. The adaptive response to declining skeletal loads, with greater rates of subperiosteal expansion and cortical thinning, may increase fragility beyond that expected from the reduction in section modulus or bone mass alone.