Copper Restore is a highly bioavailable copper supplement that supports enzyme function, antioxidant defense, and connective tissue synthesis. It is enhanced with Fulvic Acid for improved absorption, Co-Enzyme Q10 for energy metabolism, Vitamin K2 for bone and cardiovascular health, and Vitamin D3 for calcium regulation and mitochondrial support.

What Copper is:

Copper is an essential trace mineral that plays a crucial role in various bodily functions. It is involved in the formation of red blood cells, the maintenance of nerve cells, and the immune system. Copper acts as a cofactor for several enzymes, including cytochrome c oxidase in the mitochondrial electron transport chain, superoxide dismutase (SOD) for antioxidant defense, and lysyl oxidase for collagen and elastin cross-linking.

Problems with Copper Absorption:

Despite its importance, the body can face challenges in absorbing copper efficiently. These issues include:

• Competition with Other Minerals: Copper shares absorption pathways with other divalent metals, such as iron and zinc. High levels of these minerals can inhibit copper absorption due to competitive inhibition.
• Dietary Factors: Certain dietary components, like high-phytate foods (found in grains and legumes), can bind copper and reduce its bioavailability.
• Gastrointestinal Health: Conditions that affect the health of the gastrointestinal tract, such as Crohn’s disease or celiac disease, can impair the absorption of copper.

Role of Iron in Copper Absorption:

Iron plays a significant role in the absorption and metabolism of copper. However, high levels of iron can interfere with copper absorption through several mechanisms:

• • Competitive Inhibition: Iron and copper share similar transport proteins, such as divalent metal transporter 1 (DMT1). Excessive iron can outcompete copper for these transporters, leading to reduced copper absorption​.
  • Induction of Metallothionein: High iron levels can induce the production of metallothionein, a protein that binds metals with high affinity. Metallothionein preferentially binds copper over iron, reducing the bioavailability of copper​.
  • Oxidative Stress: Excess iron can catalyze the formation of reactive oxygen species (ROS) through the Fenton reaction. This oxidative stress can damage copper-dependent enzymes and proteins, impairing their function and further disrupting copper metabolism​.

The function of Copper:

Copper is essential for several vital functions in the body:

• Mitochondrial Function: Copper is a component of cytochrome c oxidase, which is crucial for the final step of the electron transport chain in mitochondria, facilitating ATP production.
• Antioxidant Defense: Copper is a cofactor for superoxide dismutase (SOD), an enzyme that neutralizes superoxide radicals, protecting cells from oxidative damage.
• Iron Metabolism: Copper is involved in the mobilization of iron from storage sites and the synthesis of haemoglobin. Copper-dependent enzymes like ceruloplasmin oxidize iron to its ferric state, essential for iron transport.
• Collagen Synthesis: Copper is a cofactor for lysyl oxidase, an enzyme that cross-links collagen and elastin, providing structural integrity to connective tissues.
• Immune Function: Copper supports the function of white blood cells and the production of cytokines, proteins that regulate immune responses.
• Neurological Health: Copper is involved in the synthesis of neurotransmitters like norepinephrine and dopamine, essential for brain function.

Signs of Copper Deficiency

Copper deficiency can lead to several health issues due to its vital role in various physiological processes.

• Anaemia: Copper is necessary for the proper absorption and utilization of iron, which is crucial for haemoglobin and red blood cell formation. Symptoms of anaemia include fatigue, weakness, shortness of breath, and pale skin.
• Neurological Symptoms: Copper is involved in the development and maintenance of myelin sheaths that surround nerves and in neurotransmitter synthesis. Deficiency can lead to numbness and tingling in the extremities, difficulty walking, poor coordination, and balance problems. Severe deficiency can result in myelopathy and peripheral neuropathy.
• Bone and Connective Tissue Disorders: Copper is essential for the cross-linking of collagen and elastin, which are critical for bone and connective tissue health. Symptoms include an increased risk of osteoporosis, brittle bones, and joint problems. Copper deficiency can also cause skin and hair issues, such as loss of skin pigmentation and brittle hair.
• Immune System Impairment: Copper plays a role in the functioning of the immune system, including the production and activity of white blood cells. Symptoms include increased susceptibility to infections and prolonged healing time for wounds.
• Cardiovascular Problems: Copper is involved in maintaining the integrity of blood vessels and heart muscle by helping in the formation of elastin and collagen. Symptoms include an increased risk of cardiovascular diseases, high cholesterol levels, and hypertension. Severe deficiency can lead to heart enlargement and heart failure.
• Hypopigmentation: Copper is a cofactor for the enzyme tyrosinase, which is involved in the production of melanin, the pigment responsible for skin and hair colour. Symptoms include loss of skin pigmentation, resulting in patches of lighter skin (vitiligo), and greying of the hair.
• Fatigue and Weakness: Copper deficiency can lead to a decrease in the production of ATP, the primary energy carrier in cells. Symptoms include general fatigue, muscle weakness, and decreased endurance.

Copper and Boron: Their Roles in Cardiovascular Health and Interaction with Vitamins K2, D3, and Magnesium
Copper’s Role in Cardiovascular Health

• Copper and Arterial Health: Copper is essential for maintaining the structural integrity of blood vessels. It supports the formation of elastin and collagen, which are critical for the elasticity and strength of blood vessel walls. Copper-dependent enzymes like lysyl oxidase facilitate the cross-linking of these structural proteins, ensuring blood vessels remain flexible and resilient, and reducing the risk of arterial stiffness and aneurysms.
• Copper and Calcium Metabolism: While copper itself is not directly responsible for removing calcium from arteries, it supports cardiovascular health by maintaining strong and elastic blood vessels. Healthy blood vessels are less likely to experience calcium deposition and plaque formation. Copper also aids in cholesterol metabolism, which indirectly helps in reducing the formation of arterial plaque by maintaining healthy cholesterol levels (reducing LDL and increasing HDL).

Boron’s Role in Cardiovascular Health

• • Boron and Mineral Metabolism: Boron influences the metabolism of various minerals, including calcium, magnesium, and copper. It helps maintain a balance in their absorption and utilization, preventing deficiencies and toxicities. This balance is crucial for overall cardiovascular health as it supports the proper functioning of the heart and blood vessels.
  • Boron and Enzyme Activity: Boron enhances the activity of copper-dependent enzymes like superoxide dismutase (SOD), which play a significant role in protecting blood vessels from oxidative stress by neutralizing free radicals. This protection helps prevent damage that can lead to plaque formation in arteries.

Enhancing the Interaction of Vitamin K2, Vitamin D3, and Magnesium

Vitamin K2:

Vitamin K2 is crucial for directing calcium to bones and teeth, preventing its deposition in the arteries. It works synergistically with copper to maintain the structural integrity of blood vessels, reducing the risk of plaque formation.

• • Vitamin D3: Vitamin D3 regulates calcium and phosphate metabolism, ensuring proper absorption and utilization of calcium in the body. This regulation helps prevent calcium from depositing in the arteries and supports overall cardiovascular function.
  • Magnesium: Magnesium is involved in over 300 enzymatic reactions, including those that involve copper. It supports mitochondrial function, and energy production, and improves circulation by relaxing blood vessels. Magnesium also helps regulate blood pressure and prevents arterial calcification, reducing cardiovascular disease risk.

Synergistic Effects of Copper and Boron with Vitamins K2, D3, and Magnesium

• Copper and Boron Synergy: Copper and boron enhance the effectiveness of vitamins K2, D3, and magnesium by supporting mineral metabolism and enzyme activity. Copper aids in maintaining blood vessel integrity and supporting cholesterol metabolism, while boron helps balance and absorb these essential minerals, ensuring their optimal function.
• Enhanced Mineral Utilization: Copper and boron ensure that vitamins K2, D3, and magnesium function optimally. Copper-dependent enzymes and boron’s role in regulating mineral metabolism enhance the bioavailability and efficacy of these vitamins and minerals, promoting overall cardiovascular health.

Role of Copper in Cholesterol and Plaque Formation

Copper and Cholesterol Metabolism:

Copper is critical for regulating enzymes that control cholesterol synthesis and degradation. Adequate copper levels help maintain healthy cholesterol levels, reducing LDL (bad cholesterol) and increasing HDL (good cholesterol). This balance is essential for preventing arterial plaque, a major factor in cardiovascular diseases.

• Copper and Arterial Plaque: Copper supports the structural integrity of blood vessels by facilitating the formation and maintenance of elastin and collagen. This prevents arterial stiffness and reduces the risk of calcium deposition and plaque formation. By ensuring strong and flexible blood vessels, copper helps mitigate the risk of plaque buildup and related cardiovascular issues.
• Conclusion: Copper and boron are essential in enhancing the effectiveness of vitamins K2, D3, and magnesium in supporting cardiovascular health. Copper maintains the integrity of blood vessels, supports cholesterol metabolism, and aids in the structural formation of elastin and collagen. Boron helps regulate mineral metabolism and enhances enzyme activity, ensuring the optimal function of these nutrients. Together, they promote healthy calcium levels, prevent arterial calcification, and reduce the risk of cardiovascular diseases, demonstrating copper’s critical role in this process.

The Role of Copper in Mitochondria, Energy Production, and Iron Metabolism
Copper in Mitochondrial Function

• Cytochrome c Oxidase: Copper is a critical component of cytochrome c oxidase (complex IV), an enzyme in the mitochondrial electron transport chain (ETC). This enzyme catalyzes the final step of the ETC, where electrons are transferred to oxygen, forming water. This process is crucial for the production of ATP, the primary energy currency of the cell. Without copper, cytochrome c oxidase cannot function properly, leading to impaired ATP production and reduced cellular energy levels.
• Superoxide Dismutase (SOD): Copper is also a cofactor for superoxide dismutase (SOD), specifically the copper-zinc SOD (Cu/Zn-SOD) located in the cytosol and the intermembrane space of mitochondria. SOD protects cells from oxidative damage by converting superoxide radicals (by-products of mitochondrial respiration) into hydrogen peroxide, which is then converted to water by other antioxidant enzymes. This process helps maintain mitochondrial integrity and function, preventing damage that could impair ATP production.

Copper in Energy Production

• ATP Synthesis: As a component of cytochrome c oxidase, copper is directly involved in the production of ATP through oxidative phosphorylation. Efficient ATP synthesis is vital for cellular functions, including muscle contraction, neurotransmission, and biosynthesis of molecules. Copper deficiency can lead to decreased activity of cytochrome c oxidase, resulting in lower ATP levels and reduced energy availability for cellular processes.
• Iron-Sulphur Cluster Biogenesis: Copper indirectly supports energy production by participating in the formation of iron-sulphur clusters, essential components of various enzymes involved in the Krebs cycle and the ETC. These clusters facilitate electron transfer and catalytic activity in mitochondrial enzymes, further supporting ATP synthesis.

Copper and Iron Metabolism

• Iron Mobilization: Copper plays a crucial role in iron metabolism by facilitating the oxidation of iron, a process essential for its transport and utilization. The copper-containing enzyme ceruloplasmin oxidizes ferrous iron (Fe2+) to ferric iron (Fe3+), the form that can be bound to transferrin for transport in the bloodstream. This oxidation process is critical for maintaining adequate iron levels in the body and ensuring its proper distribution and utilization.
• Interaction with Heme Synthesis: Copper is necessary for the synthesis of heme, an iron-containing compound that forms the functional part of haemoglobin, myoglobin, and various cytochromes. These heme proteins are involved in oxygen transport and cellular respiration. Copper deficiency can impair heme synthesis, leading to reduced levels of haemoglobin and myoglobin, which can cause anemia and decreased oxygen delivery to tissues​.
• Copper and Ferroportin: Copper also influences iron metabolism through its effect on ferroportin, the only known iron exporter in cells. Ceruloplasmin, the copper-dependent ferroxidase, oxidizes iron to facilitate its binding to transferrin. Adequate copper levels ensure proper ferroportin function, allowing efficient iron export from cells, particularly from enterocytes (intestinal cells) and macrophages (cells that recycle old red blood cells)​.

CONCLUSION

Copper is indispensable for mitochondrial function, energy production, and iron metabolism. It acts as a cofactor for cytochrome c oxidase and superoxide dismutase, both critical for ATP synthesis and protection against oxidative stress. Copper also plays a vital role in iron metabolism by facilitating iron oxidation and transport, ensuring adequate iron levels for haemoglobin synthesis and overall cellular function. The interconnected roles of copper in these processes underscore its importance for maintaining cellular energy and metabolic health.

Why We Have Excess Iron in Our Bodies: Factors and Historical Changes

1. Changes in Diet and Food Fortification

• Fortification of Foods: Since the mid-20th century, many countries, including the United States, have implemented programs to fortify foods with essential nutrients to prevent deficiencies in the population. One such nutrient is iron. Foods like bread, cereals, and other grain products are often fortified with iron. While this has been successful in reducing iron-deficiency anaemia, it has also led to increased iron intake among the general population, sometimes resulting in excess iron levels.
• Increased Meat Consumption: The Western diet, characterized by high consumption of red meat and processed meats, contributes significantly to increased iron intake. Red meat is a rich source of heme iron, which is more readily absorbed by the body compared to non-heme iron found in plant-based foods. The increased availability and consumption of meat over the past few decades have contributed to higher iron levels in the population.
• Processed Foods and Iron Fortification: The rise of processed and convenience foods, which are often fortified with iron, has led to higher iron intake. These foods include breakfast cereals, snack bars, and meal replacements that cater to quick, nutrient-dense options. The fortification practices, combined with the widespread consumption of these products, have contributed to excess iron intake.

2. Genetic Factors and Hereditary Hemochromatosis

• Hereditary Hemochromatosis: Hereditary hemochromatosis is a genetic disorder that causes the body to absorb too much iron from the diet. The excess iron is then stored in various organs, particularly the liver, heart, and pancreas, which can lead to serious health problems. This condition is often undiagnosed until significant iron overload has occurred, contributing to the prevalence of excess iron in affected individuals​.

3. Reduced Iron Utilization and Loss

• Decreased Menstruation and Childbearing: Historically, women lost significant amounts of iron through menstruation and childbirth. With changes in family planning, lower birth rates, and the use of hormonal contraceptives that reduce menstrual bleeding, women are retaining more iron than in previous generations​.
• Reduced Incidence of Infectious Diseases: Infectious diseases and parasitic infections, which historically caused chronic blood loss (and thus iron loss), have decreased due to improved sanitation and medical advancements. This reduction in iron loss from infections has contributed to higher iron levels in the population.

4. Supplements and Over-the-Counter Medications

Iron Supplements:

The widespread use of iron supplements, often taken without medical supervision, can lead to excessive iron intake. Many individuals take multivitamins or iron supplements as a preventive measure, even when they do not have a diagnosed iron deficiency. This practice can contribute to iron overload, especially in populations with adequate dietary iron intake.

Historical Context

• Mid-20th Century Onwards: The major shift towards iron fortification in foods began around the mid-20th century, particularly after World War II, when the importance of nutrient fortification to prevent deficiencies became widely recognized. This era marked the beginning of increased iron fortification in staple foods, significantly changing the dietary iron landscape.
• Modern Dietary Trends: Over the past few decades, dietary trends have shifted towards higher consumption of red and processed meats and fortified processed foods. These trends have been influenced by economic factors, cultural shifts towards convenience, and aggressive marketing by food industries.

CONCLUSION

The excess iron in our bodies today can be attributed to several factors, including changes in diet and food fortification, genetic predispositions like hereditary hemochromatosis, reduced iron utilization and loss, and the increased use of iron supplements. These factors have collectively contributed to higher iron levels in the population, posing potential health risks and highlighting the need for balanced dietary practices and medical oversight in nutrient supplementation.

How Excess Iron Affects Copper Levels in the Body

• Competitive Absorption: Iron and copper share similar pathways for absorption in the intestines. Both minerals are absorbed through divalent metal transporter 1 (DMT1) in the gut. When there is an excess of iron, it competes with copper for these transporters, leading to reduced absorption of copper. This competitive inhibition can significantly lower the bioavailability of copper, contributing to copper deficiency in individuals with high iron intake.
• Induction of Metallothionein: High levels of iron can induce the production of metallothionein, a protein that binds to heavy metals. Metallothionein has a higher affinity for copper than iron. When metallothionein levels are elevated due to excess iron, it sequesters more copper, reducing its bioavailability and leading to lower copper levels in the body. This sequestration can disrupt the balance and functionality of copper-dependent enzymes and proteins, essential for various physiological processes.
• Oxidative Stress: Excess iron in the body can catalyze the formation of free radicals through the Fenton reaction, leading to oxidative stress. This oxidative stress can damage copper-containing enzymes and proteins, impairing their function. Copper-dependent enzymes, such as superoxide dismutase (SOD), play crucial roles in protecting cells from oxidative damage. When these enzymes are damaged or inhibited, it can lead to a decrease in their activity, further exacerbating the problem of copper deficiency.
• Impaired Copper Metabolism: Ceruloplasmin is a copper-carrying protein in the blood that plays a vital role in iron metabolism by oxidizing ferrous iron (Fe2+) to ferric iron (Fe3+), facilitating its binding to transferrin for transport. Excess iron can interfere with the synthesis and function of ceruloplasmin, impairing its ability to bind and transport copper effectively. This disruption can lead to lower levels of bioavailable copper and affect iron metabolism, creating a cycle of imbalances between these two essential minerals.
• Dietary and Lifestyle Changes: The fortification of foods with iron and the increased consumption of red meat, which is high in heme iron, have contributed to higher iron levels in the population. Concurrently, dietary sources of copper have not seen similar enhancements, potentially leading to a relative deficiency in copper. Additionally, the use of iron supplements without medical supervision can further exacerbate this imbalance, especially when copper intake is not proportionately increased.

CONCLUSION

The factors that have led to excess iron in our bodies, such as dietary changes, food fortification, and the use of iron supplements, have significantly impacted copper levels. The competitive absorption between iron and copper, induction of metallothionein, oxidative stress, and impaired copper metabolism all contribute to a decrease in bioavailable copper. This imbalance highlights the importance of maintaining a careful balance of essential minerals through diet and potentially guided supplementation to ensure optimal health and metabolic function.

Copper and Iron Interaction

• • Competition for Absorption: Copper and iron share similar pathways for absorption in the intestines. High levels of iron can outcompete copper for absorption, leading to copper deficiency. This is primarily due to their reliance on the same transport proteins, such as DMT1 (divalent metal transporter 1).
  • Induction of Metallothionein: Excessive iron can induce the production of metallothionein, a protein that binds heavy metals. Metallothionein has a higher affinity for copper than iron, which can result in the sequestration of copper, reducing its bioavailability.
  • Oxidative Stress: Excess iron can catalyse the formation of free radicals through the Fenton reaction, leading to oxidative stress. This oxidative stress can damage copper-containing enzymes and proteins, impairing their function and further disrupting copper metabolism.
  • Managing Excess Iron
  • Phlebotomy: Regular blood removal reduces iron levels, effective in conditions like hemochromatosis.
  • Chelation Therapy: Chelating agents like deferoxamine bind to excess iron and facilitate excretion, used in severe iron overload cases.
  • Dietary Management: Reducing iron-rich foods consumption and avoiding vitamin C-rich foods that enhance iron absorption help manage iron levels.
  • Supplements and Medications: Calcium supplements or proton pump inhibitors, may reduce iron absorption when used appropriately and under medical supervision.

CONCLUSION

Copper glycinate is a highly bioavailable form of copper that supports numerous vital body functions, including mitochondrial energy production, antioxidant defense, iron metabolism, collagen synthesis, immune function, and neurological health. Being chelated ensures efficient absorption and utilization, making it an essential component.