Hypokalaemic thyrotoxic periodic paralysis is an enigmatic and uncommon condition which occurs exclusively in males of Asian descent. The underlying causes of thyrotoxicosis may be any of the well-recognized etiologies including a toxic multinodular goiter, Graves' disease or iodine excess. Beside thyrotoxicosis, a number of other hormonal factors have been hypothesized to contribute to hypokalaemic thyrotoxic periodic paralysis, particularly postprandial hyperinsulinaemia and testosterone. We hereby present a case of a 48-year-old hepatitis C positive gender-assigned man in whom all of these factors are proposed to interact, lending further support to these hypotheses. The patient presented with interferon-induced thyroiditis causing acute generalized weakness whilst undergoing combination interferon-alpha-2beta and ribavirin therapy. As part of his hepatitis C infection, marked insulin resistance with hyperinsulinaemia was also present, exacerbating the paresis. Initial treatment with beta-blocker failed to normalize his serum potassium concentration, requiring the novel use of spironolactone, despite euthyroidism. This continued to be required until his testosterone supplement dissipated.