Nutrients, Vol. 17, Pages 2109: Are Dietary Habits the Missing Link Between Hashimoto’s Thyroiditis and Osteoporosis?
Nutrients doi: 10.3390/nu17132109
Authors:
Anita Vergatti
Veronica Abate
Francesca Garofano
Antonella Fiore
Gianpaolo De Filippo
Pasquale Strazzullo
Domenico Rendina
Bone metabolism is a dynamic process involving continuous bone formation and resorption, orchestrated by the interplay between osteoblasts and osteoclasts. Osteoporosis (Op), the most prevalent osteo-metabolic disorder globally, results from an imbalance in this remodeling cycle. Hashimoto’s thyroiditis (HT), a chronic autoimmune thyroid disorder, has been increasingly recognized as a contributor to bone loss, even in euthyroid individuals. HT is marked by immune dysregulation, autoantibody production, and chronic inflammation, factors that can alter bone remodeling. Furthermore, both thyroid-stimulating hormone (TSH) and thyroid hormones (THs) independently influence bone health. Low TSH and elevated TH levels, including in subclinical states, have been linked to reduced bone mineral density (BMD) and increased fracture risk. Nutritional factors, particularly selenium and iodine intake, modulate both thyroid and bone function, and can be considered as a link between HT and Op. In particular, antioxidant-rich diets such as the Mediterranean diet may confer protective effects. This review integrates current clinical and experimental evidence linking HT with bone metabolism disorders, emphasizing the multifactorial nature of bone fragility in autoimmune thyroid disease and the potential role of diet in mitigating its impact.
Bone metabolism is a dynamic process involving continuous bone formation and resorption, orchestrated by the interplay between osteoblasts and osteoclasts. Osteoporosis (Op), the most prevalent osteo-metabolic disorder globally, results from an imbalance in this remodeling cycle. Hashimoto’s thyroiditis (HT), a chronic autoimmune thyroid disorder, has been increasingly recognized as a contributor to bone loss, even in euthyroid individuals. HT is marked by immune dysregulation, autoantibody production, and chronic inflammation, factors that can alter bone remodeling. Furthermore, both thyroid-stimulating hormone (TSH) and thyroid hormones (THs) independently influence bone health. Low TSH and elevated TH levels, including in subclinical states, have been linked to reduced bone mineral density (BMD) and increased fracture risk. Nutritional factors, particularly selenium and iodine intake, modulate both thyroid and bone function, and can be considered as a link between HT and Op. In particular, antioxidant-rich diets such as the Mediterranean diet may confer protective effects. This review integrates current clinical and experimental evidence linking HT with bone metabolism disorders, emphasizing the multifactorial nature of bone fragility in autoimmune thyroid disease and the potential role of diet in mitigating its impact. Read More