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Background Increasingly, patients are asking their physicians about the benefits of dietary and alternative approaches to manage their diseases, including thyroid disease. We seek to review the evidence behind several of the vitamins, minerals, complementary medicines, and elimination diets which patients are most commonly using for the treatment of thyroid disorders. Summary Several trace elements are essential to normal thyroid function, and their supplementation has been studied in various capacities. Iodine supplementation has been implemented on national scales through universal salt iodization with great success in preventing severe thyroid disease, but can conversely cause thyroid disorders when given in excess. Selenium and zinc supplementation has been found to be beneficial in specific populations with otherwise limited generalizability. Other minerals, vitamin B12, low-dose naltrexone, and ashwagandha root extract have little to no evidence of any impact on thyroid disorders. Avoidance of gluten and dairy have positive impacts only in patients with concomitant sensitivities to those substances, likely by improving absorption of levothyroxine. Avoidance of cruciferous vegetables and soy has little proven benefit in patients with thyroid disorders. Conclusion While many patients are seeking to avoid conventional therapy and instead turn to alternative and dietary approaches to thyroid disease management, many of the most popular approaches have no proven benefit or have not been well-studied. It is our responsibility to educate our patients about the evidence for or against benefit, potential harms, or dearth of knowledge behind these strategies.

The hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-gonadal (HPG) axis are very sensitive and can be affected by external factors like stress, starvation, and medication. Medication-induced suppression of these axes can cause adrenal insufficiency (AI) and hypogonadism. Exogenous glucocorticoid use is the most common cause of iatrogenic AI. Our aim is to bring attention to another broadly prescribed medication, megestrol acetate (MA), as the cause of suppression of both these axes. We report a case of symptomatic hypogonadism and asymptomatic AI in a male patient secondary to MA. The patient presented with decrease in testicular size and erectile dysfunction. His total testosterone and morning cortisol levels were low, but FH, LH, and TSH were normal. His pituitary MRI was unremarkable. Upon discontinuation of MA, the patient's testosterone and cortisol levels normalized and his symptoms resolved. Hypogonadism and AI are known adverse effects of MA, but symptomatic hypogonadism as the primary manifestation has only been reported once in previous literature. Prolonged hypogonadism can lead to sarcopenia, depression, and osteoporosis, while asymptomatic AI carries the risk of becoming overt AI. Thus, heightened awareness of the impact of MA on both these axes is necessary.

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