Evidence supporting the use of: Copper
For the body system: Mitochondria

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Synopsis

Source of validity: Scientific
Rating (out of 5): 3

Copper is an essential trace mineral that plays a significant role in mitochondrial function, with scientific evidence supporting its involvement in the mitochondrial body system. Copper is a cofactor for several enzymes critical to cellular respiration, including cytochrome c oxidase (complex IV of the electron transport chain), which is located within the inner mitochondrial membrane. Cytochrome c oxidase is vital for the final step of the mitochondrial electron transport chain, where it facilitates the transfer of electrons to molecular oxygen, enabling the production of ATP, the cell’s primary energy currency.

Deficiencies in copper can impair the activity of cytochrome c oxidase, leading to reduced ATP synthesis and overall mitochondrial dysfunction. Several studies in animals and humans have demonstrated that copper deficiency results in decreased mitochondrial function and associated clinical symptoms, including muscle weakness and neurological deficits. Genetic disorders affecting copper metabolism, such as Menkes disease, also highlight the importance of copper in mitochondrial health.

However, while the biochemical role of copper in mitochondrial enzymes is well established, evidence for copper supplementation specifically enhancing mitochondrial function in individuals with adequate copper status is limited. Most research reinforces the need for adequate dietary copper for normal mitochondrial health, rather than suggesting a benefit from supraphysiological supplementation. In summary, copper’s role in supporting the mitochondrial body system is supported by scientific evidence, primarily through its function as a cofactor in mitochondrial enzymes.

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