Lack of effects of copper gluconate supplementation

Pratt, William B.; Omdahl, John L.; Sorenson, John R. J.

doi:10.1093/ajcn/42.4.681

Cited by 75 publications

(62 citation statements)

References 2 publications

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“…The signi®cant increase in serum Cu levels of the young adult females in the present study, when supplemented with 3 and 6 mg Cuaday compared to placebo, could indicate that their habitual intake of Cu was inadequate and that the females had depleted Cu stores. Several studies of apparently healthy adults have reported a lack of response of circulating Cu to daily supplementation of the usual diets with additional Cu (in the range 2 ± 10 mgaday; Pratt et al, 1985;Medeiros et al, 1991;Eaton-Evans et al, 1996;Milne & Nielsen, 1996;Kehoe et al, 2000). However, serum Cu is generally considered an unreliable index of Cu status (Strain, 1998).…”

Section: Discussionmentioning

confidence: 99%

No effect of copper supplementation on biochemical markers of bone metabolism in healthy young adult females despite apparently improved copper status

et al. 2001

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Objective: To investigate the effects of increasing Cu intakes, above the usual dietary intake, on biomarkers of bone metabolism in healthy young adult females (aged 21 ± 28 y) over a 4 week period. Design: A double-blind, placebo-controlled randomised repeat crossover Cu supplementation trial. Setting: The study was conducted at the Royal Veterinary and Agricultural University (RVAU), Copenhagen, Denmark. Subjects: Sixteen healthy young adult females aged 20 ± 28 y were recruited from among students at the RVAU. Intervention: During the 4 week intervention periods in this randomised, crossover trial (3Â4 weeks with a minimum 3 week wash-out period), each subject received, in addition to their usual diet, either 3 or 6 mg elemental Cuaday as CuSO 4 or a matching placebo. On the last 3 days of each dietary period 24 h urines were collected. In addition, blood was collected on the last day of each dietary period. Results: Serum Cu and erythrocyte superoxide dismutase (but not caeruloplasmin protein concentration or activity (putative indices of Cu status)) were signi®cantly increased (P`0.05) after daily Cu supplementation with 3 and 6 mgaday for 4 weeks. Serum osteocalcin (biomarker of bone formation), urinary creatinine (Cr) concentration, urinary pyridinoline (Pyr)aCr or deoxypyridinoline (Dpyr)aCr excretion, or daily urinary Pyr or Dpyr excretion (biomarkers of bone resorption) were unaffected by Cu supplementation. Conclusion: Copper supplementation of the usual diet in healthy young adult females, while apparently improving Cu status, had no effect on biochemical markers of bone formation or bone resorption over 4 week periods. Sponsorship: Funding from the European Commission.

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Section: Discussionmentioning

confidence: 99%

No effect of copper supplementation on biochemical markers of bone metabolism in healthy young adult females despite apparently improved copper status

et al. 2001

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“…The SCF (2003) set a No Observed Adverse Effect Level (NOAEL) of 10 mg/day on the basis of a supplementation study lasting 12 weeks, which showed the absence of adverse effects on liver function at this dose (Pratt et al, 1985). Using an uncertainty factor of two, a Tolerable Upper Intake Level (UL) of 5 mg/day was established for adults, but not for pregnant and lactating women, owing to the absence of adequate data.…”

Section: Biochemical Functionsmentioning

confidence: 99%

Scientific Opinion on Dietary Reference Values for copper

Products¹

2015

EFSA Journal

137

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Following a request from the European Commission, the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) derived Dietary Reference Values (DRVs) for copper. Owing to the absence of appropriate biomarkers of copper status and the limitations of available balance studies, the Panel was unable to derive Average Requirements (ARs) and Population Reference Intakes (PRIs). Hence, Adequate Intakes (AIs) were defined based on mean observed intakes in several European Union (EU) countries, given that there is no evidence of overt copper deficiency in the European population. Data from balance studies were used as supportive evidence. For adults, AIs of 1.6 mg/day for men and 1.3 mg/day for women are proposed. For children, AIs are 0.7 mg/day for children aged 1 to < 3 years, 1 mg/day for children aged 3 to < 10 years, and 1.3 and 1.1 mg/day for boys and girls aged 10 to < 18 years, respectively. For infants aged 7-11 months, based on mean observed intakes in four EU countries, an AI of 0.4 mg/day is proposed, which is supported by upwards extrapolation of estimated copper intake in exclusively breast-fed infants. For pregnant women, an increment of 0.2 mg/day is estimated to cover the amount of copper deposited in the fetus and the placenta over the course of pregnancy and in anticipation of the needs for lactation, and for lactating women the same increment is estimated to cover the amount of copper secreted with breast milk. Thus, for pregnant and lactating women, the Panel derived an AI of 1.5 mg/day. Copper is an essential micronutrient required for electron transfer processes. It is a central component of many enzymes, including those involved in neurotransmitter synthesis, in energy metabolism and in collagen and elastin cross-linking.The main food group contributing to the copper intake of all population groups except infants is grains and grain-based products. Another important contributor to copper intake is the food group meat and meat products.Based on balance studies and other studies, the Panel considered that copper absorption from the diet is around 50 % for all age and life-stage groups.The primary site of copper absorption is the upper small intestine. Uptake is through a carrier protein, Ctr1, and once in the cell, the copper is directed towards its target via one of a series of chaperone proteins that ensure the metal is present in a non-toxic form. In the gut, the major pathway of transport into the portal circulation is via a Cu-ATPase, ATP7A. In the portal circulation, copper is bound to histidine, albumin or possibly transcuprein and transported to the liver, where it is incorporated into ceruloplasmin, which is then secreted into the systemic circulation. It is taken up into the liver through Ctr1 and, if it is not incorporated into ceruloplasmin, it is stored as metallothionein. Excess copper is excreted in bile after transport across the apical membrane of the hepatocytes via another ATPase, ATP7B. This copper is not reabsorbed. In humans, between 80 and 95 % of the copper in...

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“…Patients with copper deficiency have been successfully treated with oral copper in the past 5 but not in the form of copper gluconate because of its poor bioavailability. 18 Given that the cause of our patient's deficiency was her abnormal gastrointestinal anatomy, we opted to treat her with parenteral copper chloride.…”

Section: Discussionmentioning

confidence: 99%

Copper Deficiency as Cause of Unexplained Hematologic and Neurologic Deficits in Patient with Prior Gastrointestinal Surgery

Ricker

Muench

2006

The Journal of the American Board of Family Medicine

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Copper is a trace mineral essential to hematopoiesis and to the structure and function of the nervous system. Copper deficiency is a rare cause of anemia, leukopenia, and myeloneuropathy, but should be considered in the differential diagnosis in a patient with prior gastrointestinal surgery. We report the case of a 51-year-old woman admitted for nonspecific neurologic symptoms ultimately found to be due to copper malabsorption. Case ReportsA 51-year-old female presented to the emergency department complaining of numbness and tingling in her distal lower extremities that had progressively worsened over the previous 4 weeks and had begun to affect her fingers 2 days before presentation. In addition, the patient stated that over the past 2 weeks she had experienced a progressively worsening shortness of breath, generalized weakness, fast heartbeat, and light-headedness.She had undergone a gastrectomy 16 years ago with Roux-en-Y and partial small bowel resection for treatment of Zollinger-Ellison syndrome as well as a Whipple procedure for chronic pancreatitis. Since her surgeries, she received vitamin B12 supplementation intramuscularly and was converted to oral supplementation several months before her presentation in the emergency department.On presentation, the patient's vital signs included a temperature of 36.7°C, blood pressure of 121/84, pulse of 80, respiratory rate of 18, oxygen saturation of 100% on room air, and weight of 43.2 kg. Initial neurological evaluation revealed diminished sensitivity to light touch and vibration and decreased proprioception in her toes and ankles. Her Babinski's reflex was positive bilaterally, and her Romberg was strongly positive. Her patellar and brachioradialis deep tendon reflexes were hyperreflexic bilaterally, but Achilles tendon reflexes were normal. Her cranial nerves were intact, and her sensation of pain and temperature were normal. Her motor strength was normal, but she had significant difficulty walking because of her sensory deficits. The physical examination was otherwise unremarkable.Laboratory tests in the emergency department included a hematocrit of 17% (normal range, 33% to 44.6%) with a mean corpuscular volume (MCV) of 105.9 fL (normal range, 80 to 96 fL). At this point, the patient was admitted for management of anemia and further evaluation of neurologic symptoms. She received a transfusion of 2 units of packed red blood cells, which brought her hematocrit up to 27%. She was also started on 100 mcg of vitamin B12 intramuscularly daily and 1 mg of folate orally daily.The patient's neurological and laboratory findings were initially attributed to vitamin B12 or folate deficiency, given her history of gastrointestinal surgery and recent conversion to oral vitamin B12 supplementation. However, her vitamin B12 and folate levels were available by the third day of hospitalization, with a vitamin B12 level of 738 pg/mL (normal range, 200 to 950 pg/mL) and folate level greater than 24 ng/mL (normal level, Ͼ0.9 ng/mL). Methylmalonic acid was 0.77 mol/L (normal lev...

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Lack of effects of copper gluconate supplementation

Cited by 75 publications

References 2 publications

No effect of copper supplementation on biochemical markers of bone metabolism in healthy young adult females despite apparently improved copper status

No effect of copper supplementation on biochemical markers of bone metabolism in healthy young adult females despite apparently improved copper status

Scientific Opinion on Dietary Reference Values for copper

Copper Deficiency as Cause of Unexplained Hematologic and Neurologic Deficits in Patient with Prior Gastrointestinal Surgery

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