Copper

Copper acts as a cofactor for enzymes such as: 

Cytochrome c Synthase (CCS) and Cytochrome c Oxidase (Complex IV): Inserts copper into cytochrome c for its oxidase role in the electron transport chain. Vital for ATP production, the molecule in the human body responsible for the manifestation that is ENERGY.

NAD+ Synthetase:  Catalyzes the final step in the biosynthesis of NAD+, and while it doesn't directly involve copper, copper deficiency can indirectly impact its activity by affecting Copper-transporting ATPase 1" (ATP7A), which transports copper into the trans-Golgi network for incorporation into ceruloplasmin, an enzyme that plays a role in iron metabolism, which indirectly impacts NAD+ synthesis due to the involvement of iron-sulfur cluster-containing enzymes in NAD+ biosynthesis.

Lysyl Oxidase (LOX) and Lysyl Oxidase-like (LOXL) enzymes: Catalyzes the cross-linking of collagen and elastin. Essential for robust connective tissue, uniform skin free of stretch marks/cellulite, blood vessels, angiogenesis, and the foundational matrix of bones. Copper and manganese synergistically support hair growth by facilitating melanin production and keratin synthesis, contributing to hair color and follicle strength.

Ceruloplasmin: Facilitates the oxidation of ferrous iron to its ferric form, essential for iron binding to transferrin and subsequent transport in the bloodstream. Ceruloplasmin also acts as a ferroxidase, converting ferrous iron (Fe^2+) to ferric iron (Fe^3+) for incorporation into ferritin, the main intracellular iron storage protein. Ensuring ideal iron transport and metabolism in a safe state. Preventing anemia, iron overload and oxidative damage from unbound iron. Copper is essential for the synthesis and function of proteins involved in iron metabolism, including transferrin and ceruloplasmin. Transferrin transports iron throughout the body, and copper is necessary for its synthesis and stability. 

Hephaestin: Similar to ceruloplasmin, involved in iron transport at the level of the intestinal barrier very important for the safe metabolism of fresh dietary iron.

Mono and Di Amine Oxidases (MAO) (MAO-B) (DAO): Catalyzes the oxidation of amines. Degrades neurotransmitters such as dopamine, norepinephrine, and serotonin. Degrades histamine and other polyamines. Without proper function of these enzymes histamine intolerance and neurotransmitter dysregulation may occur. This can seriously affect digestion, mood and energy levels.

Superoxide Dismutase (CCS), (SOD1) and (SOD3): Protects cells from oxidative damage by converting highly reactive superoxide into hydrogen peroxide and oxygen. In the catalytic cycle, copper alternates between its Cu²⁺ (oxidized) and Cu⁺ (reduced) states. This redox cycling is essential for the enzyme to convert superoxide radicals into less harmful molecules. The copper ion directly participates in the electron transfer that converts superoxide radicals into oxygen and hydrogen peroxide.

Tyrosinase: Catalyzes the conversion of tyrosine to melanin, the pigmentation required to protect skin from increasing sun exposure.

Dopamine β-Hydroxylase (DBH): Converts dopamine to norepinephrine. A vital step in neurotransmitter balance and function. Required proper brain function and mood regulation. Those with variations in this gene may develop hypotension in a copper deficient state.

Heme Oxygenase (HO): Copper facilitates heme degradation indirectly by supporting the activity of enzymes that maintain the necessary oxidative environment and redox balance, protecting against oxidative stress, ensuring efficient electron transfer and NADPH production.

Amino Acid Oxidase: Involved in the oxidative deamination of amino acids to their corresponding keto acids that serve as precursors for the synthesis of other important molecules, including non-essential amino acids, nucleotides, and certain neurotransmitters.

Peptidylglycine α-Amidating and α-Hydroxylating Monooxygenases (PAM) and (PHM): Involved in the biosynthesis of peptide hormones. Catalyzes the conversion of glycine-extended peptides to amidated products, essential for bioactive peptide function. Copper deficiency impairs peptide hormone function, maturation and signaling.

Aconitase: Iron-sulfur cluster-containing enzyme involved in the tricarboxylic acid (TCA) cycle, and while it does not directly require copper, copper deficiency can impair its function indirectly by disrupting iron metabolism, affecting its iron-sulfur cluster cofactor.

Copper also has modulating effect on Matrix Metalloproteinases (MMPs) and ADAMTS enzymes for extracellular matric remodeling 

An imbalance of copper relative to other nutrients can disrupt the activity of these important enzyme functions. In regards to copper status within the body, it should be noted that excess copper is just as serious as copper deficiency. To recap copper plays a crucial role in these enzymes involved in antioxidant defense, electron transport, melanin synthesis, the citric acid cycle, NAD+ biosynthesis, extracellular matrix degradation, cell cycle regulation, heme availability, neurotransmitter function and overall energy metabolism.

Understanding the relationship between copper, molybdenum, and manganese, along with their roles in enzymatic functions and iron metabolism, demonstrates the complexity of biochemical processes essential for maintaining cellular functions and overall health. By managing their introduction sequence and recognizing their synergistic effects, we can optimize their roles in physiological processes and enhance biological function.

What is driving the controversy around copper?

Environmental exposures that inhibit COPPER METABOLISM and more importantly they inhibit whole body metabolism. Therefore introducing copper into a system suffering from too many of these environmental toxicities will result in potentially uncomfortable and damaging reactions. 

- Halogen toxicity (fluoride, bromide, chlorine)

- Heavy metal toxicity (including but not limited to iron)

- Glyphosate

- Vitamin A overload (copper forces detox of A giving very uncomfortable feelings)

- Mycotoxins from Mold

- Aluminum

- Micro plastics

- Excess omega 6

Its ULTRA rare that someone is clean of all 8 of these.. most have at least 3 of them in a problematic state without at least 6 months depletion of these copper supplementation is ill advised without professional titration of cofactors.

Its introduction into the body must be carefully managed, with molybdenum serving to mitigate potential reactivity with hydrogen sulfide, ensuring copper's effectiveness.