Zinc- Copper Imbalance

    An elevated level of copper, particularly in its unbound, “free radical” form, generally reflects the body’s ability to deal with other toxic metals. Free copper is determined by an equation that compares total copper and total ceruloplasmin in the blood. Copper overload is defined as an elevated total copper level, an increased ratio of copper to ceruloplasmin, and an elevated ratio of copper to zinc.

    Copper in the brain is involved in the conversion of dopamine to norepinephrine. An overload of “free copper” leads to an increase in the anxiety-producing “fight or flight” neurotransmitter and a decrease in the pleasure and reward center neurotransmitter dopamine.

    Elevated copper levels are associated with anxiety conditions, postpartum depression, bipolar disorder, insomnia, and depression. Chronic low zinc levels and high free copper levels are a risk factor for cognitive decline and dementia.

    Copper imbalance can also impair methylation, particularly when high copper is associated with low zinc. Zinc is an important cofactor in the removal of SAH (S-Adenosyl Homocysteine), a methylation inhibitor. A functional approach emphasizes nutritional balance to address neurotransmitter function, as dopamine, norepinephrine, and serotonin are impacted by high copper and/or low zinc.

 Three primary markers for copper metabolism:

-Total copper – High levels may suggest accumulation of copper in tissues, representing potential oxidative damage to cells.

-Ceruloplasmin – Low levels relative to copper generally indicate an imbalance, leading to increased free copper and risk of tissue damage.

-Plasma zinc – Zinc acts as a natural counterbalance to copper, with low zinc levels often seen alongside high copper, impacting antioxidant defenses and immune health.