Zinc-Induced Copper Deficiency: Supplement Risk and Certification Original paper

Researched by:

  • Dr. Umar Aitsaam ID
    Dr. Umar Aitsaam

    User avatarClinical Pharmacist and Master’s student in Clinical Pharmacy with research interests in pharmacovigilance, behavioral interventions in mental health, and AI applications in clinical decision support. Experience includes digital health research with Bloomsbury Health (London) and pharmacovigilance practice in patient support programs. Published work covers drug awareness among healthcare providers, postpartum depression management, and patient safety reporting.

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October 22, 2025

Researched by:

  • Dr. Umar Aitsaam ID
    Dr. Umar Aitsaam

    User avatarClinical Pharmacist and Master’s student in Clinical Pharmacy with research interests in pharmacovigilance, behavioral interventions in mental health, and AI applications in clinical decision support. Experience includes digital health research with Bloomsbury Health (London) and pharmacovigilance practice in patient support programs. Published work covers drug awareness among healthcare providers, postpartum depression management, and patient safety reporting.

    Read More

Last Updated: 2025-10-22

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Dr. Umar Aitsaam

Clinical Pharmacist and Master’s student in Clinical Pharmacy with research interests in pharmacovigilance, behavioral interventions in mental health, and AI applications in clinical decision support. Experience includes digital health research with Bloomsbury Health (London) and pharmacovigilance practice in patient support programs. Published work covers drug awareness among healthcare providers, postpartum depression management, and patient safety reporting.

What was studied?

This original research article presents a detailed case study of zinc-induced copper deficiency resulting in sideroblastic anemia and neutropenia in a patient who consumed an over-the-counter zinc-containing supplement. The focus keyphrase, “zinc-induced copper deficiency,” is central to the investigation, as the report meticulously documents how excessive zinc intake can disrupt copper metabolism, leading to significant hematological disturbances. The study explores clinical presentation, diagnostic process, laboratory findings, treatment, and patient recovery, emphasizing the pathophysiology of zinc-induced copper deficiency and its impact on hematopoiesis. This case is used to highlight the importance of comprehensive medication reviews, especially regarding over-the-counter supplements, within the context of heavy metal certification and regulatory frameworks.

Who was studied?

The subject of this study was a 74-year-old Caucasian female with a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, chronic kidney disease, and treated breast cancer. She developed progressive fatigue and anemia after taking a vision supplement (PreserVision) containing zinc and copper. There was no prior history of anemia, blood transfusions, or excessive dietary zinc intake. The patient’s clinical course, laboratory parameters, bone marrow findings, and response to the cessation of the supplement and addition of copper therapy were thoroughly documented. This individual case provides an in-depth clinical narrative on the effects of zinc-induced copper deficiency in a real-world context, which is particularly relevant for establishing safe thresholds and monitoring protocols in heavy metal certification programs.

Most important findings

Critical PointsDetails
Clinical PresentationThe patient experienced severe anemia, neutropenia, and fatigue. Laboratory tests revealed low hemoglobin, low neutrophil count, macrocytic anemia, and low reticulocyte count.
Laboratory and Diagnostic FindingsMarkedly elevated zinc levels (188 µg/dL; normal: 44–115 µg/dL), severely decreased copper (6 µg/dL; normal: 80–158 µg/dL), and very low ceruloplasmin (<3 mg dl; normal: 19–39 dl). bone marrow biopsy showed ringed sideroblasts (15%) and cytoplasmic vacuolization in myeloid precursors, confirming sideroblastic anemia due to copper deficiency.< td>
Supplement Source and DosageThe zinc-induced copper deficiency was traced to an over-the-counter supplement, PreserVision, taken at a dosage of 80 mg zinc and 2 mg copper daily (2 tablets/day). This exceeds the recommended daily zinc intake and approaches levels associated with impaired copper absorption. No other sources of zinc excess were identified.
Treatment and RecoveryDiscontinuing the supplement and initiating oral copper supplementation (2 mg daily) resulted in normalization of copper, ceruloplasmin, and zinc levels. Hemoglobin and neutrophil counts improved markedly within four weeks, and the patient remained stable without further supplementation at six-month follow-up.
Mechanistic InsightsExcess zinc induces overproduction of metallothionein in enterocytes, which binds copper preferentially and prevents systemic absorption, leading to copper deficiency and subsequent hematological disorders. This mechanism is critical for heavy metal certification to understand risk thresholds and interaction effects in multi-mineral products.
Regulatory and Certification RelevanceThe case underscores the need for rigorous heavy metal certification, including setting upper intake limits for zinc in supplements, comprehensive labeling, and regular review of over-the-counter products. It also highlights the risk of supplement-induced trace metal imbalances and the importance of including supplement use in clinical and regulatory histories.

Key implications

This study demonstrates that zinc-induced copper deficiency, resulting in severe hematologic abnormalities, can stem from over-the-counter supplement use. For heavy metal certification programs, it highlights the necessity of regulatory oversight, maximum allowable zinc limits, and mandatory copper-to-zinc ratio disclosures to prevent adverse health outcomes associated with trace metal imbalances.

Citation

Stagg MP, Miatech J, Majid B, Polala R. Zinc-Containing Over-The-Counter Product Causing Sideroblastic Anemia and Neutropenia. Cureus. 2024 May 7;16(5):e59796. doi:10.7759/cureus.59796