Although the underlying mechanism is not fully understood, the best-known long-term complication of thyroidectomy is osteoporosis [3,4].

The most effective treatment for post-thyroidectomy osteoporosis is calcitonin therapy. Cranney et al. [5] conducted a meta-analysis of 30 randomized clinical trials to compare the efficacy of calcitonin with other alternative treatments following prolonged use for over a year. This meta-analysis determined that calcitonin therapy was the most effective method, particularly in reducing the risk of vertebral fractures in postmenopausal women [5].

Several clinical studies have identified weight gain following total thyroidectomy. Jonklaas and Nsouli-Maktabi [6] evaluated 120 cases of total thyroidectomy over a 5-year period. The study revealed that 86% of the patients experienced weight gain and an increase in body mass index [6]. In a meta-analytic study, Singh Ospina et al. [7] assessed 209 total thyroidectomy cases, all of which showed weight gain during a minimum 1-year follow-up. The authors did not clarify the possible causes of the weight increase, which was higher than expected [7].

There is no evidence in the literature to suggest that weight gain following total thyroidectomy is linked to calcitonin deficiency. Traditionally, calcitonin has been associated solely with bone metabolism. However, recent studies indicate that calcitonin also enhances insulin sensitivity, slows gastric emptying, boosts energy expenditure, and promotes satiety and weight loss [8,9]. Chronic treatment with oral salmon calcitonin has significantly lowered both fasting and postprandial glucose and insulin levels. Additionally, both oral and injectable forms of calcitonin have been shown to reduce body weight by 15% [10].

Amylin, a peptide hormone, is secreted alongside insulin by pancreatic β-cells. It interacts with the same family of receptors as calcitonin. In rat studies, dual amylin and calcitonin receptor agonists have demonstrated significant body weight loss [8].

Stein et al. [11] introduced ZP5461, a novel long-acting amylin/calcitonin receptor agonist, which was shown to reduce feeding and body weight in rats. Another amylin/calcitonin receptor agonist, NN1213, was evaluated for its weight loss effects in various rodent models [12]. Additionally, a new longacting amylin analogue, primarily mediated weight loss effects through the calcitonin receptor [13].

In conclusion, the literature suggests that post-thyroidectomy osteoporosis and weight gain may be associated with calcitonin. The beneficial effects of calcitonin on bone metabolism and its effectiveness in treating osteoporosis have been well-documented for many years. However, it is noteworthy that there is no evidence in the literature to suggest that a deficiency in calcitonin resulting from C-cell resection contributes to the etiology of post-thyroidectomy osteoporosis.

Recent research has identified an inverse relationship between serum calcitonin levels and weight gain, prompting numerous studies in this area. However, my literature review revealed no articles addressing the relationship between weight gain and serum calcitonin levels following total thyroidectomy. Furthermore, the literature lacks studies on the anti-obesity effects of calcitonin replacement therapy in patients post-total thyroidectomy. This gap is notable, especially considering the potential challenges and risks associated with such therapy, including the established links between calcitonin-containing drugs and malignancy [13,14].

Total thyroidectomy is commonly performed, particularly in cases of thyroid cancer or other medical indications, because postoperative thyroid hormone deficiency can be easily, inexpensively, and effectively managed with L-thyroxine replacement therapy. These treatment algorithms operate under the assumption that the thyroid capsule contains only the thyroid organ. However, the thyroid capsule actually encompasses two organs: the thyroid and the ultimobranchial organ, which is composed of C-cells.

This article hypothesizes that osteoporosis and weight gain after thyroidectomy may be directly linked to a deficiency in calcitonin. To test this hypothesis, it is recommended that prospective clinical studies be conducted on patients who have undergone a total thyroidectomy. These studies should track and evaluate any correlation between the patients’ serum calcitonin levels, bone densities, and body mass index values from the preoperative period through to the long-term postoperative period.

If the data from these studies support the hypothesis, it may be necessary to reconsider the indications for total thyroidectomy. The surgical treatment algorithms for various thyroid diseases, particularly thyroid cancer, may need to be revised, potentially necessitating thyroid-preserving surgery.

As endocrine surgeons and endocrinologists, we often refer to the thyroid as the “maestro of the body.” These new data could further deepen our understanding of this vital organ’s value.