Mechanism of Action
In the laboratory, copper acts at the centre of several essential enzymes. In antioxidant defence, it is the cofactor of superoxide dismutase, the enzyme that neutralises the superoxide radicals cellular respiration releases continuously. Structurally, it activates lysyl oxidase, which chemically welds collagen and elastin fibres together. Without this bonding, support fibres lose their mechanical strength.
Still in the laboratory, copper takes part in iron transport through ceruloplasmin (a protein that makes iron transportable in the blood). It enters the synthesis of melanin, the pigment of skin and hair. Finally, it contributes to energy production within the mitochondria, the cell's energy factories. None of these enzymes works without the copper it carries.
Key Benefits
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Better protection against oxidative wear: in the laboratory, copper is the cofactor of superoxide dismutase, the enzyme that neutralises superoxide radicals. On this basis, copper contributes to the protection of cells from oxidative stress.
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Support tissues that keep their strength: in the laboratory, copper activates lysyl oxidase, the enzyme that welds collagen and elastin fibres together. This bonding is what gives connective tissues their firmness. Copper contributes to maintenance of normal connective tissues.
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Immune defences that stay operational: in the laboratory, several enzymes of the defence cells work only in the presence of copper, which is what earned this mineral its status as an essential trace element. Copper contributes to the normal function of the immune system.
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Iron that circulates properly: in the laboratory, iron only leaves cells once oxidised by ceruloplasmin, an enzyme that works only with copper. Copper contributes to normal iron transport in the body.
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Energy produced all the way down the chain: in the laboratory, copper is the cofactor of cytochrome c oxidase, the enzyme that closes the mitochondrial respiratory chain. Copper contributes to normal energy-yielding metabolism.
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A nervous system that carries its signals well: in the laboratory, neurotransmitter production and myelin formation depend on copper-activated enzymes. Myelin is the sheath that insulates nerve fibres and speeds transmission. Copper contributes to normal functioning of the nervous system.
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Skin and hair colour maintained: in the laboratory, tyrosinase, the enzyme that makes melanin (the natural pigment), needs copper to work. Copper contributes to normal skin pigmentation and to normal hair pigmentation.
Dosage & Forms
Several forms of copper coexist in supplementation: sulphate, gluconate, citrate and bisglycinate, copper chelated to two glycine molecules. The question of form arises differently here than for other minerals. Human copper absorption is high, and it adjusts by itself to intake. There is therefore no absorption shortfall for a form to correct, and no direct human comparison separates bisglycinate from sulphate on this point.
The European nutrient reference value, the one used for labelling, is 1 mg per day: a benchmark for comparing products, not an individual requirement. Metabolic balance studies place copper equilibrium at around 0.8 mg per day in young men.
The safe upper limit, set at 5 mg per day by the European scientific committee, was re-examined in 2023 and maintained. It applies to total intake from all sources combined, and it does not cover pregnancy or breastfeeding.
In the Singular Formula
Inclusion rationale
An essential trace element present in minute amounts in the body, yet indispensable to functions nothing else performs. Copper contributes to the protection of cells from oxidative stress: it is the catalytic cofactor of copper-zinc superoxide dismutase, one of the first lines of enzymatic defence against free radicals, where zinc (also present in the formula) occupies the structural site that holds the assembly together. It also contributes to maintenance of normal connective tissues through lysyl oxidase, the enzyme that cross-links collagen and elastin, the two proteins that give support tissues their strength and elasticity. Finally, it contributes to normal iron transport in the body via ceruloplasmin, which matters for profiles receiving iron in their formula. The body regulates its copper closely and absorbs proportionally more when dietary intake is low: the formula therefore delivers it only when a blood panel shows low status, never by default.
Selected form
Copper bisglycinate: each copper atom is chelated to two glycine molecules, the smallest amino acid naturally present in the body, and itself part of the formula as a bioactive in its own right. Chelation binds the mineral to an amino acid rather than to a mineral salt such as sulphate or oxide. Copper contributes to the normal function of the immune system and to maintenance of normal connective tissues. Pure raw material. No excipient.
Formula dosage
0 to 1 mg.
Dose expressed as active substance, excluding excipients and carriers of the raw material.
Synergies in the formula
Linked Biomarkers
Safety & Precautions
Copper is well tolerated at the intakes covered by an ordinary diet. The thresholds at which digestive discomfort has been measured in adults were obtained with copper sulphate dissolved in water and drunk on an empty stomach, a presentation far removed from an intake taken with a meal.
Individuals with a hereditary copper metabolism disorder should avoid any supplementation. The health profile collects this information, and copper is then excluded from the formula.
Taking zinc at high doses alongside copper reduces copper absorption. Zinc stimulates intestinal metallothionein, a protein that holds metals within the intestinal wall. The lowest intake that has produced this effect in humans is 50 mg of zinc per day for ten weeks.
During pregnancy, breastfeeding, or when taking medication, consulting a healthcare professional before any supplementation is advised.
Scientific Studies
| Authors | Year | Type | Journal | |
|---|---|---|---|---|
| Turnlund JR et al. | 1998 | Clinical Trial | American Journal of Clinical Nutrition | View on PubMed |
Copper absorption, excretion, and retention by young men consuming low dietary copper determined by using the stable isotope 65Cu Eleven young men followed for 90 days in a metabolic unit, over three sequential periods in which each man is his own control, without randomisation or a control group. Fractional absorption rises markedly during the low-intake period, but this regulation is no longer sufficient at 0.38 mg per day. | ||||
| Turnlund JR et al. | 1989 | Clinical Trial | American Journal of Clinical Nutrition | View on PubMed |
Copper absorption and retention in young men at three levels of dietary copper by use of the stable isotope 65Cu Eleven young men followed for 90 days in a metabolic unit, at three levels of intake. The absorbed share of copper moves from 12.4% at high intake (7.53 mg per day) to 55.6% at low intake (0.785 mg per day), and balance is reached from 0.8 mg per day. | ||||
| Uauy R et al. | 1998 | Review | American Journal of Clinical Nutrition | View on PubMed |
Essentiality of copper in humans Review of essential copper functions in humans, including enzymatic roles, consequences of insufficient intake and nutritional requirements. | ||||
| Collins JF et al. | 2010 | Review | Nutrition Reviews | View on PubMed |
Metabolic crossroads of iron and copper Analysis of metabolic interactions between iron and copper, particularly the role of ceruloplasmin and hephaestin in iron transport. | ||||
| Bost M et al. | 2016 | Review | Journal of Trace Elements in Medicine and Biology | View on PubMed |
Dietary copper and human health: Current evidence and unresolved issues Synthesis of human studies published since 1990. For intakes of 0.6 to 3 mg per day, the authors find no link between copper and the major health risks examined. They rate as limited the evidence for impaired immune function in healthy adults at a very low intake, 0.38 mg per day. | ||||
| Klevay LM | 2011 | Review | Journal of Trace Elements in Medicine and Biology | View on PubMed |
Is the Western diet adequate in copper? Analysis of copper intake adequacy in Western diets, suggesting a significant fraction of the population has suboptimal intakes. | ||||
| Harvey LJ, McArdle HJ | 2008 | Review | British Journal of Nutrition | View on PubMed |
Biomarkers of copper status: a brief update Update on copper status biomarkers, evaluating the relevance of ceruloplasmin, serum copper and superoxide dismutase activity. The authors conclude that no marker that is both sensitive and specific has yet been identified. | ||||