If AD Th2 inflammation, on the one hand, is protective against fracture risk because it inhibits bone resorption by inhibiting osteoclastogenesis, promoting the anabolic effects of PTH, and decreasing the activated nuclear factor receptor-kβ ligand/OPG ratio, dietary restrictions, on the other hand, negatively affect peak bone mass (PBM), an important determinant of fracture recovery in the future, because they cause suboptimal levels of calcium and vitamin D during periods crucial for bone mineralization and physical inactivity characterizing AD patients [76]. The gene discussed is PTH; the disease is Alzheimer disease.