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Copper is one of many metals that humans require. But there is a narrow range, sometimes a bit ironically referred to as the Goldilocks limits, where too little copper is harmful and too much copper is also harmful.  In the tangled web of human biochemistry there is more in play than simply consuming foods like beef liver, sunflower seeds, lentils, almonds, dried apricots, dark chocolate, blackstrap molasses, asparagus, mushrooms and turnip greens that have trace elements of copper. There is considerable disagreement about how much copper is required:  as one might expect there are variations for age (infancy, young child, senior), and condition (pregnancy, lactating, recovering from malnutrition), but from 1 to 2 milligrams per day seems to be adequate to avoid anemias due to hemoglobin defects, leaky gut, liver damage and developmental difficulties.

Time for readers to cringe: so far eight genes have been designated as involved in copper metabolism – either allowing processing of ingested copper, transportation of copper to where it is needed or excretion of excess copper. If anyone knows of additional genes, I’d appreciate hearing about it. Here’s the list so far (gene name comma chromosome space location on the chromosome comma associated disease or syndrome

STEAP3,2 q14.2,hypochromic microcytic anemia with iron overload 2 (AHMIO2)

AFP,4 q13.3,Alpha-fetoprotein hereditary persistence (HPAFP)

WASHC5,8 q24.13,Spastic paraplegia type 8

ATP7B,13 q14.3,Wilson Disease – copper

PRNP,20 p13,Wilson Disease – copper – this acts as a modifier of ATP7B

SOD1,21 q22.1,amyotrophic lateral sclerosis (ALS)

note: we use 23 to designate the X(Y) chromosomes
CCDC22,23 p11.23,Ritscher-Schinzel syndrome 2 (RTSC2)

ATP7A,23 q21.1,Menkes syndrome
occipital horn syndrome and X-linked cutis laxa are considered mild forms of Menkes syndrome

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