A previous post introduced some basic functions for copper in human physiology.  Here, let’s take a closer look at an interesting function of this trace metal.  The average adult human body (if there is such a thing!) contains 60-120 mg of copper, with the highest concentrations found in hardworking tissues such as the kidneys, liver, brain, and heart.  Aside from its essential role in the superoxide dismutase enzyme and its function in connective tissue synthesis, copper also appears to play a key role in neurological function.

The nutrient deficiency most commonly associated with myelopathy and/or subacute combined neuronal degeneration is that of vitamin B12.  Some cases, however, may be impacted more by copper deficiency.  The cause for deficiency is not always identifiable, but at least one study indicated that bariatric or other gastrointestinal surgery is a major contributor.  Among forty patients with hematological abnormalities due to hypocupremia unrelated to genetic or constitutional copper deficiency (e.g., Wilson’s disease), ten (25%) had undergone bariatric surgery and another 14 (35%) had undergone other gastrointestinal tract surgeries, most commonly gastric resection.

Among 13 patients with copper deficiency-associated myelopathy and polyneuropathy, a high or high-normal serum zinc level was noted in 7 of the 11 for whom this information was available.  (Copper, iron and zinc influence each other’s absorption and need to be kept in proper balance.)  Oral copper supplementation restored copper levels to normal or near-normal in 7 of the 12 patients for which adequate follow-up data were available, and 3 additional patients had restoration of normal copper levels after parenteral supplementation.  

It is important to note that while repletion of copper prevented further neurological deterioration, it didn’t have much effect on reversing damage that had already occurred.  This is similar to what is seen in the sometimes permanent neurological degeneration resulting from longstanding B12 deficiency:

“Unrecognized copper deficiency appears to be a common cause of idiopathic myelopathy in adults.  The clinical picture bears striking similarities to the syndrome of subacute combined degeneration associated with vitamin B12 deficiency.  Early recognition and copper supplementation may prevent neurologic deterioration.” (Kumar et al., 2004)

Other studies corroborate the finding that copper supplementation can halt continued decline, but it may not turn back the clock on existing damage.  All hope is not lost, though.  One case report of a 53-year-old woman with peripheral neuropathy, anemia and leucopenia without thrombocytopenia, whose B12, methylmalonic acid (MMA), and folate levels were all normal, showed that oral copper supplementation may result in both subjective and objective improvements.  This patient had markedly decreased serum copper and ceruloplasmin levels, along with elevated serum zinc.  She had no history of gastric surgery or prior malabsorption and denied zinc supplementation.  Whatever the reason for the copper/zinc imbalance, oral copper supplementation resolved the anemia within 1 month, and after 4 months, she reported feeling stronger and a neurologic examination showed resolution of proximal weakness.  The neurologic examination was otherwise unchanged, though, and she continued to experience “persistent severe sensory ataxia.”

Another study confirmed elevated zinc and decreased copper levels in a small cohort of patients with neurological symptoms resulting from acquired copper deficiency.  Reasons for the deficiency in 4 out of the 7 patients included decreased intake or absorption (stoma/parenteral nutrition, malabsorption, lack of proper supplementation post-bariatric or gastric surgery), but a perhaps surprising reason for 4 subjects was chronic use of denture adhesive paste containing zinc. (One patient had both of these causes.)  Denture paste! How’s that for a hidden factor?  Six out of the 7 patients showed anemia and lymphopenia.  After copper supplementation, serum copper balance and the hematological abnormalities were the first issues to normalize (within two months), and radiological myelitis disappeared within ten months.  Neurological symptoms improved in 6 out of the 7 patients after a mean follow-up of 2 years.  So it does seem that a certain degree of degeneration is reversible.  Perhaps it depends on the extent and duration of the damage, and possibly also the patient’s general health status.

Bottom line – when assessing patients for non-specific neurological symptoms, particularly when serum B12 and other related markers are normal, don’t forget copper.