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Year : 2017  |  Volume : 146  |  Issue : 3  |  Page : 430-431

Ocular lesions from copper deficiency

Professor Emeritus of Internal Medicine, University of North Dakota, School of Medicine & Health Sciences, Grand Forks, USA

Date of Submission09-Feb-2017
Date of Web Publication18-Jan-2018

Correspondence Address:
Leslie M Klevay
Professor Emeritus of Internal Medicine, University of North Dakota, School of Medicine & Health Sciences, Grand Forks
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijmr.IJMR_246_17

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How to cite this article:
Klevay LM. Ocular lesions from copper deficiency. Indian J Med Res 2017;146:430-1

How to cite this URL:
Klevay LM. Ocular lesions from copper deficiency. Indian J Med Res [serial online] 2017 [cited 2021 Jun 16];146:430-1. Available from:


Bharathselvi et al[1] found negative correlations between plasma copper and homocysteine or homocysteine-thiolactone in patients with age-related macular degeneration (ARMD). They suggest that copper deficiency may play an important role in pathogenesis, partly because the thiolactone inhibits a copper enzyme. Specifically, Cu-Zn superoxide dismutase in human retina may be decreased in ARMD[1].

Some interrelationships among the homocysteine compounds and copper metabolism have been summarized[2],[3]. In brief, copper deficiency in rats increases homocysteine and feeding homocysteine to rats disrupts copper utilization. The thiolactone is an irreversible inhibitor of lysyl oxidase, an enzyme dependent on copper for activity has also been noted by the authors. Men supplemented with copper have decreased homocysteine in plasma [2],[3],[4].

The epidemic of neuropathy responsive to copper supplementation may be worldwide. It has been called 'human swayback' because of similarity to deficient lambs[5]. Poor balance is the most common complaint. It resembles the neuropathy of pernicious anaemia and may be as prevalent[6]. The neuropathy seems rare enough to be published, but common enough that 10-15 cases can be reported from single clinic[7],[8].

Most authors reported myelopathy or peripheral neuropathy with sensory/motor involvement from copper deficiency. Visual complaints were less frequent, perhaps because these were more subtle and thus were less likely to be noticed. Gregg et al[9] mentioned optic neuritis briefly. Spinazzi et al[10] noticed optic nerve involvement. Naismith et al[11] described a woman with an acute onset of blindness. Khaleeli et al[12] described a man with reduced visual acuity. Pineles et al[13] found progressive optic neuropathy. Decreased myelination of optic nerves has been found in deficient animals[14],[15]. These latter experiments and a clinical case[12] revealed that ocular pathology was not peculiar to copper deficiency resulting from gastrointestinal surgery.

None of the studies have addressed the most appropriate dose, duration, route and form of copper supplementation, although Kumar[5] provided some guidelines. Anaemia if present, can be cured rapidly. It has been suggested that supplementation leads to (neurological) stabilization rather than improvement[7]; therapy for 12 months may be necessary for improvement[8]. Plasma copper may be an insensitive test of deficiency; numerous experiments with animals reveal that plasma copper may be normal or increased even though copper in liver or other organs is low[16]. Supplementation with at least 4 mg elemental copper daily (such as gluconate) may be effective[16].

The Age-related Eye Disease Study Research Group[17] observed 3640 people over the age of 55 for more than six years. Three treatment groups and a placebo group were evaluated to determine the effect of dietary supplements on ARMD. Both zinc and antioxidants plus zinc significantly reduced the odds of developing advanced ARMD[17]. Zinc received a major emphasis in the various reports of this study, but no one received zinc without receiving copper as well. Perhaps, copper supplementation rather than zinc was beneficial.

It is not clear whether low cure rates result from insufficient supplementation or severe deficiency. Nerves grow slowly and re-myelination also may be slow. It is clear that copper deficiency leads to neuropathy; eyes should be examined carefully when it is present. Copper deficiency and homocysteine metabolism should receive more attention in studies of ARMD.

Conflicts of Interest: None.

   References Top

Bharathselvi M, Biswas S, Raman R, Selvi R, Coral K, Narayanansamy A, et al. Homocysteine & its metabolite homocysteine-thiolactone & deficiency of copper in patients with age related macular degeneration – A pilot study. Indian J Med Res 2016; 143 : 756-62.  Back to cited text no. 1
Klevay LM. How dietary deficiency, genes and a toxin can cooperate to produce arteriosclerosis and ischemic heart disease. Cell Mol Biol (Noisy-le-grand) 2006; 52 : 11-5.  Back to cited text no. 2
Klevay LM. IHD from copper deficiency: A unified theory. Nutr Res Rev 2016; 29 : 172-9.  Back to cited text no. 3
Tamura T, Turnlund JR. Effect of long-term, high-copper intake on the concentrations of plasma homocysteine and B vitamins in young men. Nutrition 2004; 20 : 757-9.  Back to cited text no. 4
Kumar N. Copper deficiency myelopathy (human swayback). Mayo Clin Proc 2006; 81 : 1371-84.  Back to cited text no. 5
Ropper AH, Samuels MA. Adams and Victor's principles of neurology. 9th ed. New York: McGraw-Hill Medical; 2009.  Back to cited text no. 6
Kelkar P, Chang S, Muley SA. Response to oral supplementation in copper deficiency myeloneuropathy. J Clin Neuromuscul Dis 2008; 10 : 1-3.  Back to cited text no. 7
Prodan CI, Rabadi M, Vincent AS, Cowan LD. Copper supplementation improves functional activities of daily living in adults with copper deficiency. J Clin Neuromuscul Dis 2011; 12 : 122-8.  Back to cited text no. 8
Gregg XT, Reddy V, Prchal JT. Copper deficiency masquerading as myelodysplastic syndrome. Blood 2002; 100 : 1493-5.  Back to cited text no. 9
Spinazzi M, De Lazzari F, Tavolato B, Angelini C, Manara R, Armani M, et al. Myelo-optico-neuropathy in copper deficiency occurring after partial gastrectomy. Do small bowel bacterial overgrowth syndrome and occult zinc ingestion tip the balance? J Neurol 2007; 254 : 1012-7.  Back to cited text no. 10
Naismith RT, Shepherd JB, Weihl CC, Tutlam NT, Cross AH. Acute and bilateral blindness due to optic neuropathy associated with copper deficiency. Arch Neurol 2009; 66 : 1025-7.  Back to cited text no. 11
Khaleeli Z, Healy DG, Briddon A, Lunn MP, Reilly MM, Land J, et al. Copper deficiency as a treatable cause of poor balance. BMJ 2010; 340 : c508.  Back to cited text no. 12
Pineles SL, Wilson CA, Balcer LJ, Slater R, Galetta SL. Combined optic neuropathy and myelopathy secondary to copper deficiency. Surv Ophthalmol 2010; 55 : 386-92.  Back to cited text no. 13
Dake Y, Amemiya T. Electron microscopic study of the optic nerve in copper deficient rats. Exp Eye Res 1991; 52 : 277-81.  Back to cited text no. 14
Mishima K, Dake Y, Amemiya T, Nishimura M. Electron microscopic study of optic nerves of macular mice. Exp Eye Res 1996; 63 : 85-90.  Back to cited text no. 15
Klevay LM. Is the western diet adequate in copper? J Trace Elem Med Biol 2011; 25 : 204-12.  Back to cited text no. 16
Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with Vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no 8. Arch Ophthalmol 2001; 119 : 1417-36.  Back to cited text no. 17


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