It may be that something else is going on here:
http://www.digitalnaturopath.com/cond/C269841.html
http://www.merck.com/mmpe/sec01/ch005/ch005c.html
Quote:
Acquired Copper Deficiency
If the genetic mechanisms controlling copper metabolism are normal, dietary deficiency rarely causes clinically significant copper deficiency. The only reported causes are kwashiorkor, persistent infantile diarrhea (usually associated with a diet limited to milk), severe malabsorption (as in sprue), and excessive zinc intake. Deficiency may cause neutropenia, impaired bone calcification, and hypochromic anemia not responsive to iron supplements. Diagnosis is based on low serum levels of copper and ceruloplasmin. Treatment is directed at the deficiency's cause, and copper 1.5 to 3 mg/day po (usually as copper sulfate) is given. nherited Copper Deficiency
Inherited copper deficiency (Menkes' syndrome) occurs in male infants who inherit a mutant X-linked gene. Incidence is about 1 in 50,000 live births. Copper is deficient in the liver, serum, and essential copper proteins, including cytochrome-c oxidase, ceruloplasmin, and lysyl oxidase. Symptoms are severe mental retardation; vomiting; diarrhea; protein-losing enteropathy; hypopigmentation; bone changes; arterial rupture; and sparse, steely, or kinky hair. Diagnosis is based on low copper and ceruloplasmin levels, usually in infants < 2 wk old. Parenteral copper (given as cupric sulfate) 20 to 30 mg/kg IV once/day is the usual treatment. However, parenteral copper does not enter the copper-containing enzymes. Copper histidine 100 to 600 mg sc once/day may be more effective; monitoring is essential during treatment.
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This paper has some treatment options listed as well:
http://www.emedicine.com/ped/topic1417.htm
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Weezie looking at petunias 8.25.2017
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