Selenium: Understanding Your Blood Test Series

1. Overview: What this test reveals and why it is important

Selenium is an essential trace mineral that plays a critical role in human health as a component of selenoproteins, including glutathione peroxidases, thioredoxin reductases, and iodothyronine deiodinases. These enzymes are fundamental to antioxidant defence, redox signalling, thyroid hormone metabolism, immune function, and reproduction.

Measuring blood selenium levels provides insight into nutritional status and helps identify both deficiency and toxicity. Selenium status varies dramatically by geography due to soil content, which directly affects the selenium concentration in plant-based foods grown in that region. Populations in parts of Europe, China, Africa, and New Zealand may have lower selenium intake, while those in North America, Japan, and Venezuela typically have higher intake.

Clinical assessment of selenium status is indicated in:

· Malabsorption syndromes – Crohn's disease, ulcerative colitis, short bowel syndrome, cystic fibrosis

· Prolonged parenteral nutrition – risk of deficiency if not adequately supplemented

· Thyroid disorders – particularly in Hashimoto's thyroiditis and Graves' orbitopathy

· Critical illness – selenium levels often low and associated with worse outcomes

· Geographic origin – patients from low‑selenium regions with unexplained symptoms

· Suspected toxicity – occupational exposure, excessive supplementation

Unlike many other trace elements, selenium has a narrow therapeutic window – both deficiency and excess cause disease. Interpretation requires integration with clinical context and other laboratory parameters.

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2. What does it measure

a. Units of measurement

· Serum or plasma selenium: Micrograms per litre (mcg/L) or micromoles per litre (µmol/L)

· Whole blood selenium: Reflects longer‑term status (incorporation into red blood cells)

· Urinary selenium: Used for toxicity assessment or population studies

· Conversion: 1 µmol/L = 78.96 mcg/L (divide mcg/L by 78.96 to obtain µmol/L)

b. Normal range

Reference intervals vary by laboratory, population, and geographical region. The following are representative:

· Serum selenium (adequate): 70 – 150 mcg/L (0.9 – 1.9 µmol/L)

· Optimal for selenoprotein synthesis: >80 mcg/L

· Suboptimal / marginal deficiency: 50 – 70 mcg/L

· Deficient: <50 mcg/L (associated with clinical manifestations)

· Toxicity (selenosis): >150–160 mcg/L (symptoms may appear >300 mcg/L)

Critical interpretive principle: Selenium exists in multiple chemical forms with different bioavailability. Dietary selenium (selenomethionine, selenocysteine) is more bioavailable than inorganic forms. Functional status may be better assessed by measuring selenoprotein activity (e.g., glutathione peroxidase) rather than selenium concentration alone.

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3. Other factors connected to this

a. Direct correlation (factors affecting selenium levels)

· Geographical location and soil selenium content:

· High‑selenium regions: parts of USA (Dakotas), Canada, Venezuela, Japan, China (Enshi)

· Low‑selenium regions: parts of Europe, New Zealand, Australia, China (Keshan region), Africa, India (some regions)

· Dietary intake:

· Brazil nuts (Bertholletia excelsa) – exceptionally high; one nut can provide >100 mcg

· Fish, shellfish, organ meats – rich sources

· Grains and seeds – content depends entirely on soil

· Vegetarian/vegan diets in low‑selenium areas may be at risk

· Protein status: Selenium is incorporated into proteins; malnutrition lowers levels

· Renal function: Chronic kidney disease may alter selenium distribution; interpretation complex

· Inflammation: Acute phase response can lower serum selenium (redistribution)

· Pregnancy: Levels decline physiologically due to haemodilution and placental transfer

b. Indirect correlation (factors influencing selenium requirements or function)

· Thyroid status: Selenium is essential for deiodinase enzymes that convert T4 to active T3; deficiency exacerbates thyroid dysfunction

· Iodine status: Selenium and iodine interact; combined deficiency worsens thyroid pathology

· Heavy metal exposure: Mercury, cadmium, and arsenic may sequester selenium, increasing requirements

· Oxidative stress: Increased demand for glutathione peroxidases may deplete selenium in critical illness

· Genetic polymorphisms: Variations in selenoprotein genes (SELENOP, GPX) affect individual requirements

· Medications:

· Oral contraceptives – may lower selenium

· Valproic acid, carbamazepine – possible effects

· Cisplatin – increases urinary selenium loss

· Alcohol use disorder: Associated with lower selenium due to poor intake and increased oxidative stress

c. Methodological considerations

· Sample type: Serum, plasma, and whole blood give different information; whole blood reflects longer‑term status

· Contamination: Avoid trace element‑free collection tubes; use royal blue top tubes

· Haemolysis: May affect results; discard haemolysed samples

· Assay method: ICP‑MS (gold standard), atomic absorption spectroscopy, or fluorometry

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4. Disorders related to abnormal values

a. When low (selenium deficiency)

Clinical syndromes associated with severe deficiency:

· Keshan disease: Endemic cardiomyopathy named after a region in China with extremely low soil selenium. Presents as acute or chronic heart failure, cardiogenic shock, cardiac enlargement, and arrhythmias. More severe in children and women of childbearing age. Preventable by selenium supplementation.

· Kashin‑Beck disease: Endemic osteoarthritis affecting children and adolescents in selenium‑deficient and mycotoxin‑contaminated regions of China, Tibet, and Siberia. Characterised by joint degeneration, cartilage necrosis, and growth retardation.

· Myxoedematous cretinism: In combined selenium and iodine deficiency, impaired deiodinase activity leads to hypothyroidism and neurological damage.

Other associations (causality not always established):

· Autoimmune thyroid disease: Low selenium associated with higher risk of Hashimoto's thyroiditis and Graves' disease. Supplementation reduces anti‑TPO antibodies in some studies.

· Miscarriage and infertility: Selenium essential for sperm motility and oocyte health.

· Immune dysfunction: Impaired neutrophil and lymphocyte function.

· Increased cancer risk: Epidemiological associations with prostate, lung, colorectal cancer – but supplementation trials disappointing (SELECT trial).

· Cognitive decline: Some observational data, inconsistent.

· Critical illness: Low selenium predicts worse outcomes; supplementation trials mixed.

Causes of deficiency:

· Inadequate dietary intake (low‑soil regions)

· Malabsorption (Crohn's, coeliac, short bowel, cystic fibrosis)

· Parenteral nutrition without adequate selenium

· Liver cirrhosis (impaired selenoprotein synthesis)

· Bariatric surgery

· Eating disorders

· HIV infection

· Chronic diarrhoea

b. When high (selenium toxicity / selenosis)

Clinical features of chronic selenosis:

· Gastrointestinal: Garlicky breath odour (dimethyl selenide), metallic taste, nausea, diarrhoea

· Dermatological: Brittle hair and nails, hair loss, nail discolouration and loss, skin rashes

· Neurological: Peripheral neuropathy, paraesthesias, hyperreflexia, fatigue, irritability

· Other: Hepatotoxicity, myocardial injury, increased risk of type 2 diabetes (observed in SELECT trial with 200 mcg/day selenomethionine)

Acute selenium toxicity (rare, usually industrial accident or massive overdose):

· Nausea, vomiting, diarrhoea

· Pulmonary oedema

· Myocardial infarction

· Death at very high doses

Causes of toxicity:

· Excessive supplementation (most common cause in clinical practice)

· Occupational exposure (selenium refining, electronics, paint manufacturing)

· High‑selenium soil regions consuming locally grown foods

· Industrial accidents

· Selenium‑rich plants (certain Astragalus species accumulate selenium – "locoweed")

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5. Best way to address aberrant levels

Critical principle: Selenium has a narrow therapeutic window. Both deficiency and excess cause harm. Intervention must be guided by measured blood levels, clinical context, and careful dosing. Never self‑prescribe selenium supplements without knowing your baseline status.

a. Quick ways or using Medications (Medical Management)

Selenium deficiency:

· Oral supplementation (first‑line for mild‑moderate deficiency):

· Form: Selenomethionine is the preferred form – naturally occurring, better absorbed and retained than inorganic forms (sodium selenite, sodium selenate). It incorporates non‑specifically into body proteins, providing a reservoir.

· Dose:

· Mild deficiency (50–70 mcg/L): 50–100 mcg daily

· Moderate deficiency (30–50 mcg/L): 100–200 mcg daily

· Severe deficiency (<30 mcg/L): 200 mcg daily initially, then reduce once replete

· Monitoring: Recheck serum selenium after 3–6 months.

· Caution: Do not exceed 400 mcg daily without specialist supervision; risk of toxicity.

· Intravenous supplementation (for malabsorption, parenteral nutrition, critical illness):

· Sodium selenite is typically used intravenously.

· Dose: 60–100 mcg daily in parenteral nutrition; higher doses (500–1000 mcg) used in some critical illness trials but not routine.

· Must be prescribed by clinical nutrition team.

· Treat underlying cause:

· Manage malabsorption syndromes

· Optimise protein intake

· Address alcohol use disorder

· Discontinue medications causing selenium loss if possible

Selenium toxicity (selenosis):

· Discontinue all selenium supplements immediately.

· Avoid high‑selenium foods: Brazil nuts, selenium‑rich fish, organ meats.

· Supportive care:

· Gastrointestinal decontamination if acute ingestion within hours (activated charcoal).

· Intravenous fluids for hydration.

· Monitor liver function, electrolytes.

· No specific antidote. Selenium is slowly excreted in urine. Withdrawal of source leads to gradual normalisation over weeks to months.

· Vitamin C: High‑dose vitamin C has been proposed to enhance selenium excretion, but evidence is weak; not standard care.

· Chelation therapy: Not indicated; may worsen toxicity.

Do not self‑manage selenosis. Seek immediate medical attention if toxicity is suspected.

b. Using Supplements or Holistic medicine

The supplement guidance above (selenomethionine) is the evidence‑based approach. The following are additional considerations and cautions.

· Selenium forms compared:

· Selenomethionine (organic): Preferred for oral supplementation. Incorporates into proteins; provides sustained release. Higher bioavailability and lower toxicity risk than inorganic forms.

· Sodium selenite / selenate (inorganic): Used in some supplements and parenteral nutrition. Absorbed but not retained as well; may have pro‑oxidant effects at high doses.

· Selenium‑enriched yeast: Contains selenomethionine; acceptable but content variability.

· Avoid: Inorganic selenium for long‑term supplementation if organic available.

· Synergistic nutrients:

· Iodine: Selenium and iodine are interdependent for thyroid health. Ensure adequate iodine status before selenium supplementation in hypothyroidism (to avoid precipitating hypothyroidism in iodine deficiency).

· Vitamin E: Works synergistically with selenium in antioxidant systems; deficiency may increase selenium requirements.

· Zinc and copper: Balance important; long‑term high‑dose selenium may affect copper status.

· Herbs and Phytochemicals from Indian subcontinent:

· Ashwagandha (Withania somnifera): Not a source of selenium, but adaptogenic properties may support overall health in deficiency. Use standardised root extract.

· Amla (Emblica officinalis): Rich in vitamin C, which may support antioxidant systems alongside selenium. Fresh fruit, juice, or extract.

· Tulsi (Ocimum sanctum): Adaptogenic and antioxidant; may complement selenium's role in oxidative stress reduction.

· Guduchi (Tinospora cordifolia): Immunomodulatory; may support immune function in deficiency.

Note: These herbs do not provide significant selenium. They are adjunctive, not corrective.

· Important cautions:

· Do not combine multiple selenium‑containing supplements – total intake can easily exceed safe limits.

· Avoid "proprietary thyroid support" blends that often contain selenium, iodine, tyrosine, and herbs in unknown amounts and ratios.

· Brazil nuts: While natural, they are highly variable in selenium content (10–400 mcg per nut). Do not rely on them for therapeutic dosing; risk of toxicity with regular consumption.

· Disclose all supplements to your physician. Selenium interacts with anticoagulants (theoretical) and may potentiate antiplatelet effects.

c. Using Diet and Foods (Following a plant‑forward, ecologically sustainable approach)

Dietary selenium intake is entirely dependent on soil selenium content. In low‑selenium regions, even a well‑planned plant‑based diet may be insufficient without careful food choices or supplementation. The ecological hierarchy guides choices, but adequacy must be ensured.

Plant‑based selenium sources (soil‑dependent):

· Brazil nuts (Bertholletia excelsa): The richest known food source. One nut (5–7 g) can provide 50–400 mcg selenium, depending on origin.

· Ecological note: Brazil nuts are harvested from wild trees in the Amazon rainforest; sustainable harvesting supports forest conservation. However, they are not a cultivated crop and supply is limited. Imported nuts have carbon footprint.

· Practical guidance: One Brazil nut every 2–3 days is sufficient to maintain adequate status in most individuals. Do not consume daily in large quantities; toxicity risk.

· Caution: Brazil nuts also contain radium and barium, though levels are not clinically significant at moderate intake.

· Sunflower seeds: Grown in varying soil conditions; selenium content variable. Can contribute to intake.

· Chia seeds, flaxseeds, hemp seeds: Variable; generally low unless grown in selenium‑rich soil.

· Mushrooms: Especially shiitake, white button, and oyster mushrooms – accumulate selenium if present in growth medium. Some commercial mushrooms are grown in selenium‑enriched substrates.

· Grains (wheat, rice, oats, barley): Content reflects soil. In low‑selenium regions, grains are poor sources.

· Legumes (lentils, chickpeas, beans): Similarly soil‑dependent.

· Garlic, onion, leek: Can accumulate selenium if grown in selenium‑enriched conditions (selenised vegetables).

Fungi and algae:

· Selenium‑enriched mushrooms: Some producers cultivate mushrooms in selenium‑enriched substrates; these can be reliable sources. Look for labelled products.

· Spirulina and chlorella: Contain some selenium but levels variable; not reliable as primary source.

· Yeast: Selenium‑enriched yeast is a supplement, not a whole food.

Biotechnology / fermentation‑derived:

· Selenium‑enriched yeast: Produced by fermenting Saccharomyces cerevisiae in selenium‑rich medium; contains selenomethionine. Used in supplements.

· Mycoprotein (Quorn): Not a significant selenium source.

Dairy and eggs:

· Eggs: Selenium content depends on hen feed. Eggs from hens fed selenium‑enriched feed can be good sources. Pasture‑raised hens may have higher levels if soil adequate.

· Milk, yoghurt, cheese: Moderate sources in regions with adequate soil selenium. Organic dairy may have higher selenium in some studies.

Meat, fish, poultry (lowest priority):

· Fish and seafood: Generally good sources (tuna, sardines, oysters). Ecological cost: overfishing, bycatch, ocean pollution, high carbon footprint.

· Organ meats (liver, kidney): Rich sources. Not plant‑based; ecological concerns.

· Meat and poultry: Selenium content reflects animal feed; animals in low‑selenium regions are often supplemented.

Practical dietary approach to optimise selenium intake (with ecological hierarchy):

1. Know your regional soil status. If you live in a low‑selenium area (much of Europe, New Zealand, parts of India), you cannot rely on locally grown plant foods alone.

2. Incorporate one Brazil nut every 2–3 days. This is the most effective plant‑based strategy. Store in cool, dark place to prevent rancidity.

3. Choose selenium‑enriched mushrooms if available.

4. Include sunflower seeds, chia seeds, and flaxseeds as part of a diverse diet, but do not rely on them.

5. If plant sources are insufficient, consider a low‑dose selenomethionine supplement (50–100 mcg daily) rather than increasing animal product consumption.

6. Avoid regular consumption of high‑selenium fish (tuna, swordfish) due to mercury content and ecological concerns.

7. Test, don't guess. If you have a condition affecting selenium status, measure blood levels before changing diet or supplementing.

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6. How soon can one expect improvement and the ideal time frame to retest

Selenium repletion:

· Oral supplementation with selenomethionine: Serum levels begin to rise within days; steady state reached in 2–3 months.

· Sodium selenite: Shorter half‑life; levels normalise faster but decline rapidly after cessation.

· Glutathione peroxidase activity: Normalises within weeks to months of adequate intake.

· Clinical improvement:

· Cardiomyopathy (Keshan disease): Improvement in cardiac function over weeks to months with supplementation.

· Thyroid autoantibodies: Reduction in anti‑TPO observed after 3–6 months of selenium supplementation (200 mcg/day) in some studies.

· Hair and nail changes in deficiency: May take months to resolve.

Selenium toxicity:

· After discontinuing supplements: Serum levels decline over weeks to months. Selenomethionine is retained longer than inorganic forms.

· Symptom improvement: Garlicky breath resolves within days; hair and nail changes take months to grow out.

· Monitoring: Repeat serum selenium at 1 month, then 3 months until normal.

Retesting indications:

· Deficiency: Recheck serum selenium 3 months after initiating supplementation to confirm repletion. Then annually if risk persists.

· Toxicity: Recheck at 1 month, 3 months, then as clinically indicated.

· Chronic conditions affecting selenium status: Annual monitoring if stable; more frequent if clinically changing.

· Not indicated for routine population screening in asymptomatic individuals without risk factors.

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Conclusion

Selenium is the trace element of thresholds – a little is life‑giving, a little more is life‑taking. It is the guardian of the thyroid, the shield against oxidative stress, and the silent partner in hundreds of enzymatic reactions. Yet its story is written in soil; where selenium is scarce, hearts falter in Keshan, joints crumble in Kashin‑Beck, and thyroids struggle in silence. Where it is abundant, garlic breath and brittle nails warn of excess. The blood test cuts through this geographic and dietary uncertainty, revealing the truth of selenium status. Treatment is precise and narrow: selenomethionine for the deficient, removal for the toxic. The ecological path to adequacy honours the rainforest by revering the Brazil nut, chooses selenium‑enriched mushrooms over overfished tuna, and supplements judiciously when soil fails us. Selenium teaches us that more is not better, that natural is not always safe, and that the line between cure and poison is drawn in micrograms. Measure it, respect it, and never guess.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

This approach reflects ecological responsibility, antibiotic stewardship, and the urgent need to reduce the environmental footprint of dietary recommendations. In the case of selenium, a single Brazil nut every few days provides an effective, plant‑based solution in most cases, avoiding the need for animal sources or excessive supplementation.

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