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TABLE 7-2 Effects of Copper (Cu) Intake on Copper Status



Duration of Study

Dietary Cu Intake (mg/d)


Turnlund et al., 1990

11 healthy men

90 d

1.68 × 24 d

Plasma Cu, ceruloplasmin, superoxide dismutase (SOD), urinary and salivary Cu: no change due to Cu intake

Cu sweat losses very low

0.79 × 42 d

7.53 × 24 d

Milne and Nielsen, 1996

10 post-menopausal women, aged 49–75 y (mean 63 y)

≈ 6 mo

0.57 × 105 d

Urinary Cu: no change throughout study

Plasma Cu and ceruloplasmin: no significant change

SOD and platelet cytochrome c oxidase: significantly lower after depletion, but no increase during repletion

Platelet Cu declined during depletion and increased with repletion

2.57 × 35 d (2 mg as supplement)

Turnlund et al., 1997

11 healthy men, mean age 26 y

90 d

0.66 × 24 d

Plasma Cu, SOD, ceruloplasmin, and urinary Cu declined with depletion and increased with repletion

0.38 × 42 d

2.49 × 24 d

obligatory losses. This approach provides supporting evidence for the EAR based on copper status estimated above. Endogenous losses, estimated from total parenteral nutrition (TPN) data, were estimated to be 300 μg/day by Shike and coworkers (1981). This estimate was based on gastrointestinal losses from patients without excessive gastrointestinal secretions (less than 0.3 L/day) of 191 μg/day and urinary losses of 90 μg/day, which are higher than urinary losses in normal, healthy adults, and would provide an increment for miscellaneous losses. The TPN patients received no copper orally, but copper from TPN ranged from 250 to 1,850 μg/day.

There are no data on obligatory copper losses in healthy people; therefore the study with the lowest copper intake and data on

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