Zinc Toxicity (Excess Zinc): Copper Deficiency

Table of Contents

1. What Zinc-Induced Copper Deficiency Feels Like
2. The Mechanism: How Excess Zinc Depletes Copper
3. An Honest Caveat: These Symptoms Have Many Causes
4. Clues That Point to Zinc as the Culprit
5. Where the Excess Zinc Comes From
6. How It Is Diagnosed
7. How It Is Treated and Reversed
8. Red Flags Described in the Research
9. Key Research Papers
10. Connections
11. Featured Videos

What Zinc-Induced Copper Deficiency Feels Like

This is a slow condition. In the 2026 systematic review, the zinc exposure behind the published cases lasted from weeks to years. What people notice is not the zinc itself but the copper deficiency it causes. Its findings fall into two groups, which may appear alone or together. A 2006 Mayo Clinic review notes that the neurological syndrome can be present without the blood changes.

The first group is in the blood:

• Anemia. Anemia was present in nearly all 37 cases in the 2026 review. A 2005 report describes the blood picture of copper deficiency as sideroblastic anemia with neutropenia. A 1997 case report of copper deficiency from long-term tube feeding describes anemia and neutropenia that did not respond to iron and vitamin B12 and improved after copper was given. A 2025 hematology review explains why: copper deficiency impairs ferroxidase activity, which hampers the body’s use of iron to make red cells.
• Low white cells (neutropenia). In the 2026 review, the anemia was most often accompanied by neutropenia and a low total white-cell count. With severe or prolonged exposure, all three blood-cell lines fell (pancytopenia). In a 2005 report of three cases, the diagnosis was first suggested by a bone-marrow examination. How a low neutrophil count affects infection risk is covered on the weakened immunity page.

The second group is neurological. The 2006 Mayo Clinic review describes the most common form as a myelopathy (spinal-cord damage) with a spastic gait and prominent sensory ataxia, a loss of coordination caused by a loss of position sense. Reported findings include:

• Difficulty walking. In a 2004 series of 13 patients with copper-deficiency myelopathy, all presented with prominent gait difficulty. It reflected sensory ataxia from damage to the dorsal columns, the spinal-cord pathways that carry position sense, together with stiffness (spasticity) of the legs.
• Peripheral nerve damage. All 13 patients in that series also had a polyneuropathy. In the 2005 report, two men had a peripheral neuropathy that had been progressing for 8 and 18 months.
• Tingling, sensory loss and falls. A 2009 case report describes a woman with a 2–3 year history of tingling, sensory loss, weakness, ataxia and falls. Over the same period she had received blood transfusions for unexplained anemia and a low white-cell count. The cause was zinc overload from long-term use of a high-zinc denture cream.
• Brain changes in some cases. A 2002 report described two patients with low copper and high zinc who had extensive demyelination in the central nervous system.

The two groups often occur together. In a Mayo Clinic review of 40 patients with copper deficiency and blood abnormalities, most also had neurological findings, most commonly a myeloneuropathy (damage to the spinal cord and peripheral nerves together). Nerve damage recovers less completely than the blood counts, as described in the treatment section below.

Back to Table of Contents

The Mechanism: How Excess Zinc Depletes Copper

Zinc does not destroy copper. It changes how much copper the body absorbs and keeps. The key player is metallothionein, one of a family of small, cysteine-rich proteins that bind metal ions. Brewer and colleagues, who used this effect deliberately to treat Wilson disease (an inherited copper overload), describe the mechanism: zinc induces metallothionein in the cells lining the intestine, and this intestinal metallothionein blocks the absorption of copper from food. It also blocks the reabsorption of the copper the body itself secretes into saliva, gastric juice and intestinal fluids. The result is a negative copper balance: more copper leaves than comes in. In their words, pharmacological doses of zinc taken without food “will usually lead to copper deficiency,” and Brewer notes that long-term overtreatment of Wilson disease with zinc can induce copper deficiency.

An analogy. Picture the gut lining as a border crossing. A steady flood of zinc makes the crossing build extra checkpoints (the metallothionein). Those checkpoints hold back copper arriving in food, and also the copper the body sends out in its own digestive juices and would normally take back. No copper is destroyed; less of it gets through, and over months the body’s supply runs down.

The Institute of Medicine’s 2001 review found that every study measuring the zinc–copper interaction showed a decrease in the activity of erythrocyte copper-zinc superoxide dismutase, a red-cell enzyme that indicates copper status. One study reported this effect at a total zinc intake of about 60 mg/day (a 50 mg supplement plus about 10 mg from food) for up to 10 weeks. The report notes that the clinical significance of the lower enzyme activity is unknown.

The harm comes from what copper does in the body:

• Blood formation. The 2025 hematology review describes two effects of copper deficiency. Impaired ferroxidase activity hampers the use of iron, and impairment of the copper enzymes cytochrome c oxidase and superoxide dismutase reduces neutrophil survival. The result is anemia and neutropenia. A 2012 review lists bone-marrow features of copper deficiency, including vacuoles in red- and white-cell precursors, excess iron stores and ringed sideroblasts.
• The nervous system. The clinical and imaging features of copper-deficiency myelopathy resemble the subacute combined degeneration of the spinal cord seen in vitamin B12 deficiency, according to the 2006 Mayo Clinic review. A 1998 review of copper’s role in humans describes copper as necessary for the structure and catalytic activity of copper-containing enzymes.

In these cases the symptoms come from a shortage of one mineral caused by an excess of another: excess zinc is the cause, and copper depletion produces the illness.

Back to Table of Contents

An Honest Caveat: These Symptoms Have Many Causes

None of these findings is unique to copper deficiency, and zinc is only one cause of copper deficiency. The 2026 systematic review describes zinc-induced blood toxicity as uncommon but under-recognized. In the Mayo Clinic review of 40 patients with copper deficiency and blood abnormalities, the most common backgrounds were bariatric (weight-loss) surgery, in 10 patients (25%), and other gastrointestinal surgery, in 14 more (35%). In 12 patients no cause was found. The same review calls copper deficiency an uncommon but very treatable cause of blood abnormalities that is frequently misdiagnosed.

The anemia and low blood counts overlap with other conditions:

• Vitamin B12 deficiency. The 2025 hematology review notes that copper deficiency often mimics vitamin B12 deficiency.
• Bone-marrow disorders. Copper deficiency can masquerade as myelodysplastic syndrome, according to the Mayo Clinic review. In the 2026 review, vacuolated blood-forming cells and ring sideroblasts in the bone marrow often led to an initial misdiagnosis of myelodysplastic syndrome. A 2012 review describes copper deficiency as an under-recognized cause of reversible anemia and low white-cell counts that is often misdiagnosed this way, and lists the marrow features that tell the two apart.

The numbness and unsteady gait also have many causes:

• Vitamin B12 deficiency. A 2004 series found that copper-deficiency myelopathy bears striking similarities to the subacute combined degeneration of vitamin B12 deficiency. The two deficiencies can also occur together.
• Other spinal-cord diseases. In a 2023 case series, the conditions excluded before copper deficiency was diagnosed included vitamin E and folic acid deficiency, tabes dorsalis, HIV myelopathy, HTLV infection and multiple sclerosis. The woman in the 2009 case report had been referred to a multiple sclerosis clinic before the zinc-related copper deficiency was found.
• Other causes of numb feet. Numbness in the feet has many other causes, covered on the pages on diabetic neuropathy and peripheral neuropathy.

Numb feet or an anemia do not by themselves point to copper deficiency. What the research adds is narrower. A 2012 review states that copper and ceruloplasmin levels should be measured in patients with refractory anemia and low white-cell counts, with or without neurological deficits. A 2004 Mayo Clinic report states the same for the serum ceruloplasmin level in patients with otherwise unexplained myelopathies. The next section lists the findings that point to zinc as the cause.

Back to Table of Contents

Clues That Point to Zinc as the Culprit

In the published cases, excess zinc was identified when several findings lined up:

• A clear source of extra zinc. In the 2026 systematic review, the exposures were mostly oral supplements, denture adhesive creams and swallowed coins, at reported daily doses from about 50 mg to more than 1,500 mg of elemental zinc. Zinc given as a medical treatment also appears in the case reports: one patient in the 2005 report was receiving zinc for acrodermatitis enteropathica, an inherited zinc-absorption disorder. In the denture-cream series, the patients used very large amounts of cream chronically, and all 11 patients in a 2009 series had ill-fitting dentures that required large amounts of cream.
• An anemia that has not responded to iron. A 2012 review describes copper deficiency as a cause of reversible refractory anemia and neutropenia. In one case report, anemia and neutropenia did not respond to iron and vitamin B12, and the blood counts improved after copper was given.
• The blood-and-nerve combination. Low blood counts together with a myeloneuropathy is the pattern described in the Mayo Clinic review of 40 patients. The 2006 Mayo Clinic review notes that the nerve syndrome can also occur without the blood changes.
• A B12-like picture with a very low ceruloplasmin. In the 2004 series of 13 patients, the picture resembled B12-deficiency spinal-cord disease, and the first clue to the diagnosis was a very low ceruloplasmin, the main copper-carrying protein in the blood.
• Stomach or bariatric surgery. Previous gastrointestinal surgery was the most common background in the Mayo Clinic review of 40 patients. A 2004 report describes copper deficiency as a possible delayed complication of gastric surgery, appearing many years later.

High zinc intake has other effects too. At very high intakes, the overt toxicity symptoms listed in a 1990 review are nausea, vomiting, epigastric pain, lethargy and fatigue (see nausea and stomach upset). The low neutrophil count of copper deficiency is covered on the weakened immunity page.

Back to Table of Contents

Where the Excess Zinc Comes From

The Institute of Medicine’s 2001 report sets the Recommended Dietary Allowance for adults at 8 mg per day for women and 11 mg per day for men. It sets the Tolerable Upper Intake Level (UL) at 40 mg per day for total zinc intake from food, water and supplements, fortified foods included. The UL comes from a lowest-observed-adverse-effect level of 60 mg/day (the 50 mg supplement plus about 10 mg of dietary zinc that lowered the copper-dependent red-cell enzyme), divided by an uncertainty factor of 1.5. The report notes that the UL is not meant to apply to people receiving zinc under medical supervision, and it found no evidence of adverse effects from zinc that occurs naturally in food. A 1990 review reported induced copper deficiency, with anemia and neutropenia, at 100–300 mg of zinc a day. The sources described in the research are:

• Zinc supplements. Oral supplements were the most common source in the 2026 systematic review, at daily doses from about 50 mg upward. Zinc from multivitamins, standalone tablets, lozenges and combination products all counts toward the total intake the UL covers. Some formulas deliver large amounts: the Age-Related Eye Disease Study (AREDS) tested a daily 80 mg of zinc as zinc oxide, given with 2 mg of copper as cupric oxide.
• Medical zinc therapy. A 1978 report described low copper in an adult with sickle cell anemia who had received zinc for two years, with small red cells and a relatively low neutrophil count. Copper raised the red-cell size and white-cell count. The authors also saw low ceruloplasmin in several other patients on oral zinc therapy, which copper easily corrected.
• Zinc-containing denture adhesive cream. A 2008 report described four patients with low copper, high zinc and neurological disease. All wore dentures and used very large amounts of denture cream chronically, and the two creams tested contained about 17,000–34,000 µg of zinc per gram. In a 2009 series of 11 patients with progressive nerve damage, low copper and high zinc, denture cream was the source in every case, and copper and zinc levels returned to normal after the patients stopped using it. A 2025 laboratory study of denture adhesives notes that the trend in these products is shifting toward zinc-free formulations because of the health concerns associated with zinc.
• Swallowed coins. Coin ingestion was among the main sources in the 2026 systematic review.

Because the UL covers total intake, zinc from every source counts, not only the product labeled “zinc.” The authors of the 2026 review conclude that routine assessment of zinc exposure and copper status can prevent misdiagnosis.

Back to Table of Contents

How It Is Diagnosed

In the published cases, the diagnosis came from linking a history of high zinc intake to the blood and neurological findings and a small set of blood tests. A 2016 laboratory study notes that diagnosis is often delayed, which allows severe and usually irreversible neurological symptoms to develop.

The core blood tests are serum copper, serum zinc and ceruloplasmin. Serum copper was low in every case in the 2026 review. In the 2004 series of 13 patients, a very low ceruloplasmin was the first clue, and serum zinc was high or high-normal in 7 of the 11 patients in whom it was measured. In the 2016 study, 15 of 20 patients (75%) with a low plasma copper and a high plasma zinc turned out to have zinc-induced copper deficiency; the authors call the combination strongly predictive. A high zinc does not always mean a zinc source, though: the 2006 Mayo Clinic review notes that a high zinc level can occur even when no outside source of zinc is taken. How copper status relates to blood formation is covered on the companion page about hemoglobin and ceruloplasmin.

Other tests described in the case reports:

• A complete blood count to document the anemia and low white-cell count, alongside routine labs such as a Comprehensive Metabolic Panel.
• A vitamin B12 level, because B12 deficiency produces a similar spinal-cord syndrome and, according to the 2006 Mayo Clinic review, the two deficiencies can coexist.
• Nerve and spinal-cord studies. In the 2004 series, somatosensory evoked potentials (tests of the nerve pathways that carry sensation) showed impaired conduction in the central position-sense pathways in all 8 patients tested. A spine MRI showed signal change in the dorsal columns in 3 of the 13 patients. The 2009 case report used nerve conduction studies, electromyography, brain and spine MRI and spinal-fluid analysis.
• Bone-marrow examination. In the 2005 report, the diagnosis was first suggested by the bone-marrow findings in all three cases. The Mayo Clinic review of 40 patients lists marrow clues to the diagnosis: vacuoles in myeloid precursors, iron-containing plasma cells, fewer granulocyte precursors and ring sideroblasts.

Because these marrow findings often led to an initial misdiagnosis of myelodysplastic syndrome, the authors of the 2026 review conclude that assessing zinc exposure and copper status can prevent misdiagnosis and support timely treatment.

Back to Table of Contents

How It Is Treated and Reversed

The case reports describe two steps taken together: ending the zinc excess and replacing copper. The 2026 systematic review found that stopping zinc exposure, together with copper supplementation, led to blood-count recovery in most cases, typically within weeks to months.

• Ending the excess zinc. In the 2009 denture-cream series, copper and zinc levels returned to normal after the patients stopped using the cream. In the 2008 series, serum zinc improved in three patients after they stopped. In the 2009 case report, management was a change to a low-zinc denture cream and oral copper.
• Replacing copper. In the 2004 series, oral copper restored normal or near-normal copper levels in 7 of the 12 patients with adequate follow-up, and copper given by injection or infusion restored normal levels in 3 more. In the 2008 denture-cream series, copper and zinc levels were rechecked at varying intervals after treatment.

The two parts of the illness recover differently:

• The blood usually recovers. The 2006 Mayo Clinic review states that copper supplementation resolves the anemia and neutropenia “promptly and completely.” In the 2002 report, the blood counts recovered after copper, both at first and again after a relapse when copper was stopped.
• The nerves recover only partly. In the 2004 series, copper prevented further neurological deterioration, but the degree of actual improvement varied. The 2006 Mayo Clinic review describes improvement, when it occurs, as often subjective and mainly in sensory symptoms. In the 2002 report the neurological problems only stabilized, and in the 2008 denture-cream series copper led to mild neurological improvement in two patients. In the 2026 review, neurological problems improved more slowly than the blood counts and sometimes incompletely.

Because the nerve damage may be lasting, the 2004 series concludes that early recognition and copper supplementation may prevent neurological deterioration. The Institute of Medicine’s UL of 40 mg/day applies to total zinc intake from all sources. Copper itself can be harmful: a 1998 review describes it as an essential nutrient with potential toxicity if the load exceeds tolerance. Decisions about zinc or copper supplements and their doses belong with a clinician.

Back to Table of Contents

Red Flags Described in the Research

The sources on this page single out a few situations, either because a serious cause has to be excluded or because copper deficiency does the most lasting harm when it is found late:

• Progressive numbness, tingling, an increasingly unsteady walk or falls. This is the picture of copper-deficiency myelopathy in the 2004 series and the 2009 case report. Nerve damage in these reports recovered slowly and sometimes incompletely, and the 2016 study links delayed diagnosis to severe, usually irreversible neurological symptoms.
• An anemia or low white-cell count that has not responded to iron. A 2012 review states that copper and ceruloplasmin should be measured in patients with refractory anemia and low white-cell counts.
• Frequent or severe infections with a known high zinc intake, which may reflect a low neutrophil count.
• Any of these with a history of high zinc intake — long-term high-dose supplements, medical zinc therapy or heavy denture-cream use. The 2008 denture-cream report notes that when a high zinc level is found, its source “often remains elusive,” and both denture-cream series found the source only by examining denture-cream use.
• Unexplained low blood counts being investigated for a marrow disorder. The 2026 review found that the marrow findings of zinc-induced copper deficiency often led to an initial misdiagnosis of myelodysplastic syndrome.

A recurring point in the case reports is that the diagnosis depended on someone connecting the zinc exposure to the blood counts and the copper studies.

Back to Table of Contents

Key Research Papers

1. Willis MS, Monaghan SA, Miller ML, McKenna RW, et al. (2005). Zinc-Induced Copper Deficiency: A Report of Three Cases Initially Recognized on Bone Marrow Examination. American Journal of Clinical Pathology;123(1):125-131. — DOI: 10.1309/v6gvyw2qtyd5c5pj. — doi:10.1309/v6gvyw2qtyd5c5pj
2. Kumar N (2006). Copper Deficiency Myelopathy (Human Swayback). Mayo Clinic Proceedings;81(10):1371-1384. — DOI: 10.4065/81.10.1371. — doi:10.4065/81.10.1371
3. Kumar N, Gross JB, Ahlskog JE (2003). Myelopathy due to copper deficiency. Neurology;61(2):273-274. — DOI: 10.1212/01.wnl.0000073542.02761.5f. — doi:10.1212/01.wnl.0000073542.02761.5f
4. Halfdanarson TR, Kumar N, Li CY, Phyliky RL (2008). Hematological manifestations of copper deficiency: a retrospective review. European Journal of Haematology;80(6):523-531. — DOI: 10.1111/j.1600-0609.2008.01050.x. — doi:10.1111/j.1600-0609.2008.01050.x
5. Patterson WP, Winkelmann M, Perry MC (1985). Zinc-Induced Copper Deficiency: Megamineral Sideroblastic Anemia. Annals of Internal Medicine;103(3):385-386. — DOI: 10.7326/0003-4819-103-3-385. — doi:10.7326/0003-4819-103-3-385
6. Kumar N (2010). Neurologic Presentations of Nutritional Deficiencies. Neurologic Clinics;28(1):107-170. — DOI: 10.1016/j.ncl.2009.09.006. — doi:10.1016/j.ncl.2009.09.006
7. Spinazzi M, Armani M (2009). Denture Cream: An Unusual Source of Excess Zinc, Leading to Hypocupremia and Neurologic Disease. Neurology;73(1):76. — DOI: 10.1212/01.wnl.0000349696.89948.b7. — doi:10.1212/01.wnl.0000349696.89948.b7 — (Letter: a comment on Nations et al. 2008, listed below.)
8. Hedera P, Peltier A, Fink JK, Wilcock S, et al. (2009). Myelopolyneuropathy and pancytopenia due to copper deficiency and high zinc levels of unknown origin II: The denture cream is a primary source of excessive zinc. NeuroToxicology;30(6):996-999. — DOI: 10.1016/j.neuro.2009.08.008. — doi:10.1016/j.neuro.2009.08.008
9. Prodan CI, Holland NR, Wisdom PJ, Burstein SA, et al. (2002). CNS demyelination associated with copper deficiency and hyperzincemia. Neurology;59(9):1453-1456. — DOI: 10.1212/01.wnl.0000032497.30439.f6. — doi:10.1212/01.wnl.0000032497.30439.f6
10. Carpenè E, Andreani G, Isani G (2007). Metallothionein functions and structural characteristics. Journal of Trace Elements in Medicine and Biology;21(Suppl 1):35-39. — DOI: 10.1016/j.jtemb.2007.09.011. — doi:10.1016/j.jtemb.2007.09.011
11. Uauy R, Olivares M, Gonzalez M (1998). Essentiality of copper in humans. American Journal of Clinical Nutrition;67(5 Suppl):952S-959S. — DOI: 10.1093/ajcn/67.5.952S. — doi:10.1093/ajcn/67.5.952S
12. Nations SP, Boyer PJ, Love LA, et al. (2008). Denture cream: an unusual source of excess zinc, leading to hypocupremia and neurologic disease. Neurology;71(9):639-643. — PubMed PMID: 18525032
13. Kumar N, Gross JB Jr, Ahlskog JE (2004). Copper deficiency myelopathy produces a clinical picture like subacute combined degeneration. Neurology;63(1):33-39. — PubMed PMID: 15249607
14. Kumar N, Crum B, Petersen RC, et al. (2004). Copper deficiency myelopathy. Archives of Neurology;61(5):762-766. — PubMed PMID: 15148156
15. Kumar N, Ahlskog JE, Gross JB Jr (2004). Acquired hypocupremia after gastric surgery. Clinical Gastroenterology and Hepatology;2(12):1074-1079. — PubMed PMID: 15625652
16. Spain RI, Leist TP, De Sousa EA (2009). When metals compete: a case of copper-deficiency myeloneuropathy and anemia. Nature Clinical Practice Neurology;5(2):106-111. — PubMed PMID: 19194390
17. Brewer GJ, Hill GM, Dick RD, et al. (1985). Interactions of trace elements: clinical significance. Journal of the American College of Nutrition;4(1):33-38. — PubMed PMID: 3886759
18. Brewer GJ (2001). Zinc acetate for the treatment of Wilson's disease. Expert Opinion on Pharmacotherapy;2(9):1473-1477. — PubMed PMID: 11585025
19. Prasad AS, Brewer GJ, Schoomaker EB, et al. (1978). Hypocupremia induced by zinc therapy in adults. JAMA;240(20):2166-2168. — PubMed PMID: 359844
20. Institute of Medicine, Panel on Micronutrients (2001). Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Chapter 12: Zinc. Washington, DC: National Academies Press. — National Academies Press, chapter 12 (Zinc)
21. Fosmire GJ (1990). Zinc toxicity. The American Journal of Clinical Nutrition;51(2):225-227. — PubMed PMID: 2407097
22. Dutta A, Chaudhary V, Kumari S, et al. (2026). Zinc-Induced Hematologic Toxicities: A Systematic Review of Descriptive Studies. Biological Trace Element Research;204(9):6628-6642. — PubMed PMID: 42087025
23. Duncan A, Talwar D, Morrison I (2016). The predictive value of low plasma copper and high plasma zinc in detecting zinc-induced copper deficiency. Annals of Clinical Biochemistry;53(Pt 5):575-579. — PubMed PMID: 26586851
24. Takami A, Uchino K (2025). Discovering the hidden link: hematological disorders caused by copper deficiency. International Journal of Hematology;122(3):358-367. — PubMed PMID: 40653562
25. Lazarchick J (2012). Update on anemia and neutropenia in copper deficiency. Current Opinion in Hematology;19(1):58-60. — PubMed PMID: 22080848
26. Camblor M, De la Cuerda C, Bretón I, et al. (1997). Copper deficiency with pancytopenia due to enteral nutrition through jejunostomy. Clinical Nutrition;16(3):129-131. — PubMed PMID: 16844585
27. Peña I, Sarmiento J, Porras C, et al. (2023). Myelopathy due to copper deficiency: a case series and review of the literature. Biomédica;43(2):171-180. — PubMed PMID: 37433165
28. Age-Related Eye Disease Study Research Group (2001). A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Archives of Ophthalmology;119(10):1417-1436. — PubMed PMID: 11594942
29. Reymann J, Narayanan Ramakrishnan A, Ludtka C, et al. (2025). Impact of the Physiological Parameters of the Oral Cavity on the Mechanical Properties of Zinc-stabilized and Zinc-free Adhesive Creams: A Comparative In Vitro Study. Journal of Adhesive Dentistry;27:21-29. — PubMed PMID: 40063077

PubMed Topic Searches

1. PubMed: Zinc-induced copper deficiency
2. PubMed: Copper deficiency myeloneuropathy
3. PubMed: Denture cream, zinc, and neurologic copper deficiency
4. PubMed: Copper deficiency anemia, neutropenia, and MDS mimicry
5. PubMed: Metallothionein and zinc–copper intestinal absorption

Back to Table of Contents

Connections

• All Minerals
• Zinc Toxicity Symptom Hub
• Zinc Toxicity and Nausea & Stomach Upset
• Zinc Toxicity and Weakened Immunity
• Zinc Overview
• Zinc Deficiency Hub
• Copper Overview
• Copper and Neurological Health
• Hemoglobin and Ceruloplasmin
• Iron
• Vitamin B12
• Anemia
• Peripheral Neuropathy
• Diabetic Neuropathy
• Comprehensive Metabolic Panel

Back to Table of Contents

×

Featured Videos