Insulin-like growth factor (IGF), particularly IGF-1, has been investigated for its role in bone metabolism and potential in supporting or treating osteoporosis. Scientific interest centers on IGF-1’s anabolic effects on bone: it stimulates osteoblast proliferation and differentiation, enhances collagen formation, and supports bone matrix mineralization. Observational studies have consistently found that low serum IGF-1 levels correlate with decreased bone mineral density (BMD) and increased fracture risk in aging populations, suggesting a physiological relevance to osteoporosis risk.

However, clinical trials directly testing IGF-1 administration for osteoporosis have been limited in both number and scope. Some small-scale trials have shown that recombinant human IGF-1, alone or combined with growth hormone, can increase markers of bone formation and sometimes BMD in specific populations (such as GH-deficient adults or elderly women). Nevertheless, these increases are generally modest, and the safety profile (risk of hypoglycemia, edema, etc.) limits routine clinical use. Major osteoporosis guidelines do not recommend IGF-1 as a standard therapy.

In summary, while the biological rationale and some preliminary human data exist, the overall evidence base is limited and does not approach the robustness of first-line osteoporosis treatments (bisphosphonates, denosumab, etc.). Thus, IGF-1 is not widely used clinically for osteoporosis, and evidence supporting its use rates as low to moderate.