In the field of psychosomatics, medical and psychiatric problems sometimes merge in acute and disastrous ways. Thiamine deficiency is one such crossroad. Classic presentations of thiamine deficiency include Wernicke’s encephalopathy and beriberi. Beriberi classically has two manifestations. These are a “dry” form, in which a peripheral neuropathy dominates, and a “wet” form, in which congestive heart failure dominates. When wet beriberi develops in an acute and fulminant manner, it is sometimes called “shoshin beriberi.” Shoshin beriberi is rare. Yet its antecedents are not. As many as 80% of patients with alcohol dependence are deficient in thiamine. Surprisingly, up to 30% of U.S. citizens may be deficient in thiamine intake as defined by the U.S. recommended dietary allowances of 1989. Thiamine deficiency is not rare. Despite this, when thiamine deficiency becomes clinically symptomatic, it may not be recognized. As Igata painfully recounted, after taking two years to recognize an outbreak of beriberi in Japan between 1973 and 1975, “in the Meiji and Taisho era (1868–1926) beriberi was a nation-ruining disease,” but was not suspected in 1973 because the malnourished patients were not starving. What follows is a case of shoshin beriberi, in which several well-established risk factors were brought together, recognized late, and dramatically reversed.