Hypocupremia secondary to excessive zinc supplementation and gastric surgery

In humans, copper deficiency is a rare cause of myeloneuropathy. The neurologic syndrome was first recognized in ruminants afflicted with an ataxic myelopathy colloquially referred to as “swayback disease,” which describes the characteristic swaying hindquarters in animals. The incidence and recognition of acquired copper deficiency in humans is increasing alongside the frequency of bariatric surgery and other gastrointestinal surgeries1 and excessive zinc ingestion.2 Copper is primarily absorbed through the stomach and duodenum and is important in the normal function of both the central and peripheral nervous systems.3 Excessive zinc consumption causes increased expression of metallothionein in enterocytes, which preferentially binds copper. As a result, most of the copper ingested is not absorbed but rather sloughed off with the enterocytes into the lumen.2