Mechanism of Action
Copper acts as a cofactor for several essential enzymes. In the antioxidant defence chain, it enables the function of superoxide dismutase (an enzyme that neutralises the most reactive free radicals in the body). Structurally, copper activates lysyl oxidase, responsible for the cross-linking (the chemical bridging that provides strength) of collagen and elastin. Without this cross-linking, support fibres lose their mechanical resistance.
Copper also participates in iron metabolism via ceruloplasmin (a transport protein that converts iron into a usable circulating form). It is involved in melanin synthesis (the pigment that protects skin and hair). It also contributes to energy production within mitochondria (the energy powerhouses of cells). This multiplicity of roles explains why insufficient intake manifests across several fronts simultaneously.
Key Benefits
- Strong
Copper contributes to the protection of cells from oxidative stress. Metabolic studies show that copper status directly correlates with erythrocyte superoxide dismutase activity.
- Strong
Copper contributes to the maintenance of normal connective tissues. The cross-linking of collagen and elastin, carried out by copper-dependent lysyl oxidase, determines the mechanical strength of skin, vessels and joints.
- Strong
Copper contributes to the normal function of the immune system. Controlled trials indicate that adequate intake supports lymphocyte proliferation and neutrophil activity.
- Moderate
Copper contributes to normal iron transport in the body via ceruloplasmin. Metabolic studies in humans confirm impaired iron metabolism when copper intake is insufficient.
- Moderate
Copper contributes to normal energy-yielding metabolism. It is involved in cytochrome c oxidase, the final step of the mitochondrial respiratory chain, essential for ATP production.
- Moderate
Copper contributes to the normal functioning of the nervous system. Neurotransmitter synthesis and nerve fibre myelination depend on copper-dependent enzymes.
- Moderate
Copper contributes to normal skin and hair pigmentation. Tyrosinase, the enzyme responsible for melanin synthesis, requires copper as an essential cofactor.
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. | ||||