Using Hair Tissue Mineral Analysis (HTMA) to Guide Nutritional Support During and After Cancer Treatment

Using Hair Tissue Mineral Analysis (HTMA) to Guide Nutritional Support During and After Cancer Treatment

1. Introduction: Why Assessing Mineral Balances Matters in Cancer Care

Hair Tissue Mineral Analysis (HTMA) provides a clinically relevant, non-invasive method for monitoring mineral status and toxic metal burden in individuals undergoing or recovering from cancer treatment. Given the growing body of evidence linking both deficiencies in essential elements and toxic metal overload with cancer progression and treatment-related complications, HTMA is emerging as a valuable adjunct for clinicians to personalise supportive care.

Cancer and its therapies—chemotherapy, radiotherapy, surgery—can disrupt nutrient balance through multiple mechanisms:

• Reduced intake due to anorexia, nausea, or mucositis
• Malabsorption from mucosal damage
• Increased excretion from renal/hepatic strain
• Oxidative stress and inflammation driven by tumour metabolism

Studies confirm frequent deficiencies in zinc, selenium, magnesium, and copper, all critical for antioxidant defence, immune regulation, and DNA repair (Mousavi et al., 2023; Pal et al., 2024)

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2. Role of HTMA in Monitoring Cancer-Related Mineral Disruption

Hair Mineral Analysis in Cancer Patients A 2023 study by Mousavi et al. used HTMA to assess mineral and toxic element status in cancer patients. Hair levels were significantly associated with nutritional status and treatment response. The authors concluded that HTMA may be a practical tool for monitoring metabolic disruption and guiding nutritional care in oncology.

(Mousavi et al., 2023;) https://doi.org/10.1007/s12011-023-03818-6

HTMA offers a unique retrospective view into mineral status and toxic metal burden over the preceding 3–4 months, allowing practitioners to identify persistent imbalances that may not be visible in serum or plasma testing. This includes:

• Early detection of depletion: e.g., magnesium loss from cisplatin or radiation treatment.
• Monitoring recovery: e.g., repletion of selenium or zinc status after mucosal recovery.
• Evaluating toxic burden: e.g., identifying high levels of cadmium, lead, or arsenic—metals known to promote oxidative DNA damage, impair repair enzymes, and contribute to carcinogenesis (Khoshakhlagh et al., 2024; Pal et al., 2024).

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3. Evidence-Based Insights: Mineral Status and Cancer Outcomes

Drawing from the comprehensive review by Tobalina et al. (2022) in Cancers (doi:10.3390/cancers14051256), each mineral contributes uniquely to genomic stability, redox homeostasis, transcription, and tumour progression:

• Zinc (Zn): Integral to DNA replication, transcription, and repair. Zinc deficiency impairs p53 function and transcription factor activity, promoting genomic instability.
• Iron (Fe): Crucial for mitochondrial respiration and DNA synthesis, but excess iron fosters ROS production via the Fenton reaction, leading to mutagenesis.
• Copper (Cu): Cofactor for enzymes like SOD1 and LOX. While essential for redox balance and angiogenesis, high copper levels can drive tumour progression.
• Selenium (Se): Regulates oxidative stress through GPx and TR1. Low selenium reduces antioxidant defence, while optimal levels may support apoptosis in cancer cells.
• Magnesium (Mg): Required for DNA polymerase, ATP synthesis, and cellular signalling. Depletion during chemotherapy compromises cell recovery and immune resilience.
• Calcium (Ca): Involved in signal transduction and apoptosis regulation. Dysregulated calcium homeostasis contributes to tumour invasion and drug resistance.
• Phosphorus (P): Vital for nucleotide synthesis and cellular energy. Altered phosphate metabolism impacts cell proliferation and transcription control.

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4. Clinical Applications: Personalised Nutritional Strategies with HTMA

HTMA data allows practitioners to:

• Tailor antioxidant and mineral supplementation to support immune and detoxification pathways.
• Avoid unnecessary supplementation of minerals that may feed tumour progression (e.g., copper).
• Track detoxification response post-treatment using sequential HTMAs.
• Address systemic effects of cancer treatment—such as fatigue, poor wound healing, neuropathy—via targeted nutrient support.

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5. Conclusion

The integration of HTMA into oncology-supportive care provides practitioners with an evidence-based tool to personalise nutritional therapy, mitigate toxic exposures, and monitor recovery. Given the complex interplay between minerals and cancer biology, HTMA offers a unique lens to optimise resilience during treatment and reduce the risk of recurrence through ongoing monitoring.

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Select References:

• Khoshakhlagh A, et al. The preventive and carcinogenic effect of metals on cancer: a systematic review. BMC Public Health. 2024;24:2079. https://doi.org/10.1186/s12889-024-19585-5
• Pal S, Firdous SM. Unraveling the role of heavy metals xenobiotics in cancer: a critical review. Discover Oncology. 2024;15:615. https://doi.org/10.1007/s12672-024-01417-y
• Mousavi S, et al. Hair elemental analysis in cancer patients: associations with nutritional status and outcomes. Biol Trace Elem Res. 2023. https://doi.org/10.1007/s12011-023-03818-6
• Tobalina L, et al. Metals and trace elements in cancer development: Molecular mechanisms and cellular pathways. Cancers. 2022;14(5):1256. https://doi.org/10.3390/cancers14051256