Copper: The Ultimate Mitochondrial Nutrient

There are at least five necessary cofactors for energy production in the mitochondria; two major factors, and three micro factors. The major ones are food and oxygen. The micro cofactors are copper, magnesium, and the B Vitamins. Of the three minor cofactors, copper is the most neglected both in people’s bodies, and in people’s lack of awareness of the necessity of proper copper supplementation. We live in a modern toxin-filled world where most people do not get even 1/10th of the copper in their diets as they did a mere 70 years ago. Furthermore, most people are vastly copper depleted with dysfunctional copper-dependent detoxification abilities, as many toxins are known to build up to very high levels in the average person’s body that deplete copper. Two such toxins are fluoride and bromide. As long as the average person’s body contains 2600 mg fluoride, and 1500 mg bromide, and a mere 70 mg of copper, and consumes less than 0.6 mg of copper per day in the average diet, then the average person is woefully copper depleted.


While magnesium and B Vitamins are relatively well-known factors for energy production, copper is not. Yet copper is clearly the most important of the three, both because people are copper deficient, and because people do not know that energy production is dependent on copper, and because copper is continually slandered as toxic, even in some of the articles listed below that acknowledge copper’s critical role in energy production.

These facts demonstrate why copper supplementation nearly universally gives people more energy, and helps them to feel better.

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Because of this lack of awareness, it is important to cite sources and prove that copper is needed by the mitochondria for energy production.

Increased energy production is perhaps the number one factor to heal the body. Every cell in the body needs enough energy to heal.

There are numerous other ways that copper gives the body energy, such as improved production of neurotransmitters, hormones, and adrenaline, increased red blood cells, increased collagen production, improved wound healing, and detoxification, but those are not the focus of this article. And yet, all of those other “improved functioning and productions” may well be dependent upon increased ATP production from mitochondria.

What is particularly interesting about copper is the many ways it heals the body from so many things that people suffer from. Many sick people have digestive troubles, food intolerances, and allergies to foods. Copper fixes these things, too.

There are 10 excerpts from scientific articles below that talk about the importance of copper in making energy in the mitochondria.

“Copper is essential for life processes like energy metabolism, reactive oxygen species detoxification, iron uptake, and signaling in eukaryotic organisms. Mitochondria gather copper for the assembly of cuproenzymes such as the respiratory complex IV, cytochrome c oxidase, and the antioxidant enzyme superoxide dismutase 1. In this regard, copper plays a role in mitochondrial function and signaling involving bioenergetics, dynamics, and mitophagy, which affect cell fate by means of metabolic reprogramming.”

The proper assembly and functioning of the ETC [electron transport chain] is copper dependent (Kim et al., 2008; Turski and Thiele 2009).

Source: “Role of Copper on Mitochondrial Function and Metabolism” 2021

“All known eukaryotes [cells with a nucleus and mitochondria] require copper for their development and survival. The essentiality of copper reflects its widespread use as a co-factor in conserved enzymes that catalyze biochemical reactions critical to energy production, free radical detoxification, collagen deposition, neurotransmitter biosynthesis and iron homeostasis.” … “While the identification of relevant molecular mechanisms and signaling pathways has proven to be difficult and remains a barrier to our full understanding of the regulation of copper homeostasis, mounting evidence points to the mitochondrion as a pivotal hub in this regard in both healthy and diseased states.”

Source: “The mitochondrion: a central architect of copper homeostasis” 2018

“Mitochondria contain two enzymes, Cu, Zn superoxide dismutase (Sod1) and cytochrome c oxidase (CcO), that require copper as a cofactor for their biological activity.”

Source: ““Pulling the plug” on cellular copper: The role of mitochondria in copper export” 2008

“A host of critical metalloproteins reside in mitochondria, where metallation occurs within the organelle after protein import. Although the pathways by which proteins are imported into the mitochondria are well known, the mechanisms by which their metal partners are imported are more obscure. A new study by Boulet et al. demonstrates that the mammalian SLC25A3 inner membrane transporter, previously known as a phosphate carrier, is also a functional Cu(I) importer, clarifying the source of mitochondrial copper and raising new questions about cellular copper homeostasis.”

“Copper is required within the mitochondrion for the function of two metalloenzymes, COX and SOD1.”
COX is Eukaryotic cytochrome c oxidase.
SOD1 is Superoxide dismutase.

Source: “Filling the mitochondrial copper pool” 2018

That copper is contained in cytochrome C Oxidase, which is contained in mitochrondria, and needed for cellular respiration and energy production, appears to have been discovered simultaneously by two teams in 1995 with the technology of growing crystals and then viewing them through X-ray diffraction.

Source: “The currents of life:The terminal electron-transfer complex of respiration”

“Transition metals are frequently used as co-factors for enzymes and oxygen-carrying proteins that take advantage of their propensity to gain and lose single electrons.”

“Metals are particularly important in mitochondria, where they play essential roles in the production of ATP and detoxification of reactive oxygen species.”

Source: “Iron and Copper in Mitochondrial Diseases” 2014

My commentary: This refutes the need to supplement with expensive copper 1. The point here is that copper moves back and forth between copper 1 and copper 2 in the body, as copper gains and loses electrons.

“It has been documented that dietary copper (Cu) deficiency impairs mitochondrial respiratory function…”

“Impaired mitochondrial function and energy production in copper (Cu)-deficient hearts are implied by a number of reports showing swelling and ultrastructural changes in cardiac mitochondria (1–4) and depression of cytochrome c oxidase (CCO)2 activity (5–7).”

Source: “Copper Deficiency Decreases Complex IV but Not Complex I, II, III, or V in the Mitochondrial Respiratory Chain in Rat Heart” 2007

The lack of copper has been associated with anemia, myelodysplastic syndromes and leukemia as well as with a loss in complex IV activity and an enlarged mitochondrial morphology. Mitochondria play a key role during the differentiation of hematopoietic stem cells by regulating the passage from a glycolytic to oxidative metabolism. The former is associated with cell proliferation and the latter with cell differentiation. Oxidative metabolism, which occurs inside mitochondria, is sustained by the respiratory chain, where complex IV is copper-dependent. We have hypothesized that a copper deficiency induces a mitochondrial metabolic reprogramming, favoring cell expansion over cell differentiation in erythropoiesis. Erythroid progression analysis of the bone marrow of mice fed with a copper deficient diet and of the in vitro erythropoiesis of human CD34+ cells treated with a bathocuproine – a copper chelator – showed a major expansion of progenitor cells and a decreased differentiation. Under copper deficiency, mitochondria switched to a higher membrane potential, lower oxygen consumption rate and lower ROS levels as compared with control cells. In addition, mitochondrial biomass was increased and an up-regulation of the mitochondrial fusion protein mitofusin 2 was observed. Most copper-deficient phenotypes were mimicked by the pharmacological inhibition of complex IV with azide. We concluded that copper deficiency induced a mitochondrial metabolic reprogramming, making hematopoietic stem cells favor progenitor cell expansion over cell differentiation.”

Source: “Copper deficiency-induced anemia is caused by a mitochondrial metabolic reprograming in erythropoietic cells”

Heme synthesis by copper-deficient cells was investigated to elucidate the nature of the defect in intracellular iron metabolism. Iron uptake from transferrin by copper-deficient reticulocytes was 52% of normal, and the rate of heme synthesis was 33% of normal. Hepatic mitochondria isolated from copper-deficient animals were deficient in cytochrome oxidase activity and failed to synthesize heme from ferric iron (Fe III) and protoporphyrin at the normal rate. The rate of heme synthesis correlated with the cytochrome oxidase activity. Heme synthesis from Fe(III) and protoporphyrin by normal mitochondria was enhanced by succinate and inhibited by malonate, antimycin A, azide, and cyanide. It is proposed that an intact electron transport system is required for the reduction of Fe(III), thereby providing a pool of ferrous iron (Fe II) for protoheme and heme a synthesis.”

In other words, your body does not make red blood cells from iron very well, 66% decreased, in copper deficiency! “and failed to synthesize heme from ferric iron… at the normal rate”

Source: “Role of copper in mitochondrial iron metabolism” 1976

“Here we will focus on describing the pathways involved in the delivery of copper to cytochrome c oxidase (COX), a mitochondrial metalloenzyme acting as the terminal enzyme of the mitochondrial respiratory chain. The catalytic core of COX is formed by three mitochondrially-encoded subunits and contains three copper atoms.”

“Aerobic life depends on cellular copper homeostasis and distribution since this element is a critical component of enzymes involved in primary metabolism (1). Copper ions can undergo unique chemistry due to their ability to adopt distinct redox states, either oxidized [Cu(II)] or reduced [Cu(I)], and they serve as important catalytic cofactors in redox chemistry for proteins that carry out fundamental biological functions. A copper-containing metalloenzyme, mitochondrial cytochrome c oxidase (COX), is the final electron acceptor in the mitochondrial electron transport chain and is required for aerobic ATP production.”

“Over the last 15 years COX biogenesis has received significant attention because of its medical relevance. Defective COX biogenesis results in mitochondrial diseases frequently involving brain, skeletal muscle and heart…”

IN OTHER WORDS, COPPER IS IMPORTANT! And of course, why would COX be defectively made? Copper deficiency, of course. And again, copper moves back and forth in the body between copper 1 and copper 2. This is how copper functions, this going back and forth. Thus, there is no need to spend vastly more money for one form over another. Copper 2 is just fine.

“The enzyme catalyzes electron transfer from cytochrome c to molecular oxygen. This reaction occurs concurrently with vectorial proton pumping from the matrix to the intermembrane space, thus contributing to the generation of a transmembrane proton gradient which is subsequently used by the mitochondrial ATP synthase to drive the synthesis of ATP.”

In other words, we need copper in cytochrome c in the mitochrondria to turn oxygen into ATP for energy

Source: “Mitochondrial Copper Metabolism and Delivery to Cytochrome c Oxidase” 2010