Mechanism of Action
Copper acts as a cofactor for several essential enzymes. In antioxidant defence, it drives superoxide dismutase, the enzyme that neutralises the most reactive free radicals in the body. Structurally, it activates lysyl oxidase, which chemically welds collagen and elastin fibres together. Without this bonding, support fibres lose their mechanical strength.
Copper also takes part in iron metabolism 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. This range of roles explains why insufficient intake shows up on several fronts at once.
Key Benefits
- Strong
Better protection against oxidative wear: copper status correlates directly with the activity of superoxide dismutase in red blood cells. On this basis, copper contributes to the protection of cells from oxidative stress.
- Strong
Support tissues that keep their strength: copper activates lysyl oxidase, the enzyme that welds collagen and elastin fibres together. This bonding underpins the resilience of skin, vessels and joints. Copper contributes to the maintenance of normal connective tissues.
- Strong
Immune defences that stay operational: controlled trials note that adequate intake supports the multiplication of lymphocytes and the activity of neutrophils. Copper contributes to the normal function of the immune system.
- Moderate
Iron that circulates properly: metabolic studies in humans show iron metabolism disrupted when copper intake is insufficient. This link runs through ceruloplasmin, which converts iron into its transportable form. Copper contributes to normal iron transport in the body.
- Moderate
Energy produced all the way down the chain: copper keeps cytochrome c oxidase running, the final step by which mitochondria make ATP. Copper contributes to normal energy-yielding metabolism.
- Moderate
A nervous system that carries its signals well: neurotransmitter production and myelin formation depend on copper-activated enzymes. Myelin is the sheath that insulates nerve fibres and speeds transmission. Copper contributes to the normal functioning of the nervous system.
- Moderate
Skin and hair colour maintained: tyrosinase, the enzyme that makes melanin (the natural pigment), needs copper to work. Copper contributes to normal skin and hair pigmentation.
Dosage & Forms
Several copper forms exist in supplementation. Copper sulphate and oxide, historical inorganic forms, show modest bioavailability. Free ions interact with phytates and intestinal fibres, limiting their absorption. Gluconate offers an intermediate profile.
Chelated forms (bisglycinate, citrate) use amino acid transporters. This mechanism bypasses competition with zinc and iron at intestinal ion channels.
The European recommended daily intake is 1 mg per day for adults. The safe upper limit is set at 5 mg per day by the European scientific committee. The dose selected by Singular is calibrated within this nutritional range, in bisglycinate form.
In the Singular Formula
Inclusion rationale
Essential trace element present in minute amounts in the body, yet indispensable to numerous biological functions. Copper contributes to the maintenance of normal connective tissues, to the normal transport of iron in the body, to the normal functioning of the nervous system, to normal energy metabolism and to the protection of cells against oxidative stress. Copper is a cofactor of copper-zinc superoxide dismutase (Cu/Zn-SOD), one of the first lines of enzymatic defense against free radicals. This enzyme works in tandem with zinc (also present in the formula in bisglycinate form), each occupying a distinct catalytic site on the same protein. Copper is also essential to the activity of lysyl oxidase, the enzyme responsible for cross-linking collagen and elastin, the two proteins that give connective tissues their strength and elasticity. It also participates in iron transport via ceruloplasmin (iron is available in the formula for profiles that require it). In the bisglycinate form, where copper is chelated to two glycine molecules, it is absorbed via the amino acid transporters of the intestine. This absorption pathway limits interactions with other minerals and reduces the digestive irritation sometimes associated with inorganic copper salts.
Selected form
Copper bisglycinate: each copper atom is chelated to two glycine molecules, the smallest amino acid naturally present in the body. This chelated bond protects copper from interaction with dietary fibres and phytates, which block the absorption of conventional inorganic forms (sulphate, oxide). Copper contributes to the normal function of the immune system and to the maintenance of normal connective tissues. Pure raw material. Quality: vegan, non-GMO, no excipient, Halal and Kosher certified.
Formula dosage
0 to 1 mg.
Synergies in the formula
Linked Biomarkers
Safety & Precautions
Copper is well tolerated at nutritional doses (1 to 2 mg per day). Adverse effects (nausea, digestive discomfort) generally appear above 5 mg per day. The bisglycinate form is associated with better digestive tolerance than inorganic salts.
Individuals with a hereditary copper metabolism disorder should avoid any copper supplementation. Concurrent high-dose zinc intake (above 40 mg per day) can reduce copper absorption by stimulating intestinal metallothionein.
Taking copper alongside antacids or high-dose zinc is not recommended. During pregnancy, breastfeeding, or when taking medication, consulting a healthcare professional before supplementation is advised.
Scientific Studies
| Authors | Year | Type | Journal | |
|---|---|---|---|---|
| Turnlund JR et al. | 1998 | Randomised Controlled 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 Controlled metabolic study using a stable isotope to measure copper absorption, excretion and retention in young men at different intake levels. | ||||
| Uauy R et al. | 1998 | Systematic 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 | Systematic 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 | Systematic Review | Journal of Trace Elements in Medicine and Biology | View on PubMed |
Dietary copper and human health: Current evidence and unresolved issues Synthesis of current evidence on copper intake and human health, identifying unresolved questions about optimal copper status. | ||||
| Klevay LM | 2011 | Systematic 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 | Systematic 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. | ||||