Calcium: Understanding Your Blood Test Series

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

Calcium is the most abundant mineral in the human body, with 99% stored in bones and teeth as hydroxyapatite, providing structural integrity. The remaining 1% in blood and soft tissues is tightly regulated because it is essential for:

· Neuromuscular function: Nerve impulse transmission, muscle contraction (including cardiac muscle)

· Blood coagulation: Cofactor for multiple clotting factors

· Enzyme regulation: Cofactor for many enzymes

· Hormone secretion: Triggers insulin, parathyroid hormone, and others

· Cell signalling: Intracellular second messenger

· Bone metabolism: Dynamic exchange with skeletal stores

Blood calcium exists in three forms:

· Ionised (free) calcium: 50% – the biologically active form, regulated by parathyroid hormone (PTH) and vitamin D

· Protein‑bound calcium: 40% – primarily bound to albumin

· Complexed calcium: 10% – bound to anions (citrate, phosphate, bicarbonate)

Most laboratories measure total serum calcium, which includes all three fractions. However, because a large proportion is albumin‑bound, total calcium must be interpreted with the patient's albumin level. Ionised calcium is measured directly when free calcium status is critical (severe illness, massive transfusion, parathyroid surgery, critical care settings).

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2. What does it measure

a. Units of measurement

· Total serum calcium: Milligrams per decilitre (mg/dL) or millimoles per litre (mmol/L)

· Ionised calcium: mmol/L (or mg/dL)

· Conversion: 1 mg/dL = 0.25 mmol/L; 1 mmol/L = 4 mg/dL

b. Normal range

Reference intervals vary slightly by laboratory. The following are representative:

Total serum calcium (adults): 8.5 – 10.2 mg/dL (2.1 – 2.55 mmol/L)

· Mild hypercalcaemia: 10.3 – 12.0 mg/dL

· Moderate hypercalcaemia: 12.1 – 14.0 mg/dL

· Severe hypercalcaemia (hypercalcaemic crisis): >14 mg/dL

Total serum calcium (children): Slightly higher during growth; ranges vary by age.

Ionised calcium: 1.15 – 1.32 mmol/L (4.6 – 5.3 mg/dL)

Adjusted (corrected) calcium:

Because calcium binds to albumin, a commonly used correction formula is:

Corrected calcium (mg/dL) = Measured total calcium (mg/dL) + 0.8 × [4.0 – Serum albumin (g/dL)]

This adjusts for the average binding; individual variation exists. Direct ionised calcium measurement is preferred in critical situations.

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3. Other factors connected to this

a. Direct correlation (factors that affect calcium levels)

Hormonal regulators:

· Parathyroid hormone (PTH): Increases serum calcium by stimulating bone resorption, renal tubular reabsorption, and activating vitamin D.

· Vitamin D (calcitriol): Increases intestinal calcium absorption and renal reabsorption.

· Calcitonin: Lowers calcium by inhibiting bone resorption (minor role in humans).

· Thyroid hormone: Excess can increase bone resorption and calcium.

· Growth hormone: Increases intestinal calcium absorption.

· Glucocorticoids: Decrease intestinal absorption; long‑term use can lower calcium.

Physiological factors:

· Age: Children have slightly higher levels; elderly may have lower due to decreased absorption.

· Pregnancy: Total calcium falls due to hypoalbuminaemia; ionised calcium remains normal.

· Immobility: Prolonged bed rest increases bone resorption, raising calcium.

· Dietary intake: Acute large intake (calcium supplements) can transiently raise calcium.

Medications increasing calcium:

· Thiazide diuretics (reduce urinary excretion)

· Lithium (alters PTH set point)

· Vitamin D analogues

· Calcium supplements (especially with renal impairment)

· Tamoxifen, oestrogens (rare)

· Theophylline (mild effect)

Medications decreasing calcium:

· Loop diuretics (furosemide – increase excretion)

· Bisphosphonates (inhibit bone resorption)

· Calcitonin

· Glucocorticoids

· Anticonvulsants (phenytoin, phenobarbital – alter vitamin D metabolism)

· Proton pump inhibitors (long‑term use reduces calcium absorption)

· Cinacalcet (calcimimetic – lowers PTH)

b. Indirect correlation (factors affecting interpretation)

· Albumin: The most important confounder. Hypoalbuminaemia (liver disease, malnutrition, nephrotic syndrome) causes falsely low total calcium. Always correct or measure ionised calcium.

· pH: Acidosis increases ionised calcium (decreased protein binding); alkalosis decreases ionised calcium. Critical in ventilated patients.

· Paraproteins: Multiple myeloma can cause falsely high total calcium due to protein binding (but ionised calcium normal).

· Haemoconcentration: Prolonged tourniquet use during venepuncture can falsely elevate total calcium.

· Sample handling: Delayed separation from red cells can cause falsely low calcium (uptake by cells).

· Renal function: Determines phosphate excretion and vitamin D activation.

· Phosphate: Inversely related to calcium through PTH regulation and precipitation.

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4. Disorders related to abnormal values

a. When elevated (hypercalcaemia)

Primary hyperparathyroidism (most common outpatient cause):

· Due to parathyroid adenoma (85%), hyperplasia (15%), or carcinoma (<1%)

· Chronic, often mild hypercalcaemia (10.5 – 11.5 mg/dL)

· Associated with low or inappropriately normal PTH (should be suppressed by hypercalcaemia; in primary hyperparathyroidism, PTH is elevated or inappropriately normal)

· May be asymptomatic or cause "bones, stones, abdominal groans, and psychic moans"

Malignancy (most common inpatient cause):

· Humoral hypercalcaemia of malignancy: Solid tumours (squamous cell lung, renal, breast, ovarian) secrete PTH‑related protein (PTHrP)

· Local osteolytic hypercalcaemia: Bone metastases (breast, myeloma, lymphoma) release cytokines activating osteoclasts

· Multiple myeloma: Lytic lesions, often with normal or low PTH, elevated paraproteins

· Usually more severe and rapid onset than hyperparathyroidism

Other causes:

· Vitamin D intoxication: Excessive supplementation; also granulomatous diseases (sarcoidosis, tuberculosis) produce calcitriol

· Thyrotoxicosis: Increased bone turnover

· Thiazide diuretics: Reduced urinary excretion

· Milk‑alkali syndrome: Excessive calcium carbonate intake (antacids, supplements) with dehydration

· Immobilisation: Especially in young, growing individuals with high bone turnover

· Familial hypocalciuric hypercalcaemia (FHH): Genetic disorder; benign, asymptomatic; low urinary calcium excretion; PTH normal or mildly elevated

· Addison's disease: Rare; due to volume depletion and haemoconcentration

Clinical features of hypercalcaemia:

· Neurological: Fatigue, weakness, confusion, depression, coma (severe)

· Gastrointestinal: Nausea, vomiting, constipation, anorexia, pancreatitis

· Renal: Polyuria, polydipsia (nephrogenic diabetes insipidus), nephrolithiasis, nephrocalcinosis

· Cardiovascular: Hypertension, shortened QT interval, bradycardia, arrhythmias

b. When low (hypocalcaemia)

Hypoparathyroidism:

· Post‑surgical: Most common cause (thyroidectomy, parathyroidectomy, neck dissection)

· Autoimmune: Isolated or part of polyglandular autoimmune syndrome

· Genetic: DiGeorge syndrome, familial isolated hypoparathyroidism

· Infiltrative: Haemochromatosis, Wilson's disease, metastases

· Radiation‑induced

Vitamin D deficiency or resistance:

· Nutritional deficiency (inadequate intake, malabsorption)

· Chronic kidney disease (impaired 1‑hydroxylation)

· Liver disease (impaired 25‑hydroxylation)

· Anticonvulsant therapy

· Vitamin D‑dependent rickets types I and II

Chronic kidney disease:

· Hyperphosphataemia, reduced calcitriol production, skeletal resistance to PTH

· Often with high PTH (secondary hyperparathyroidism)

Magnesium disorders:

· Hypomagnesaemia: Impairs PTH secretion and action; common cause of refractory hypocalcaemia

· Hypermagnesaemia: Suppresses PTH secretion

Other causes:

· Acute pancreatitis: Calcium sequestration in saponified fat

· Massive transfusion: Citrate in blood products chelates calcium

· Drugs: Bisphosphonates, cinacalcet, foscarnet, ketoconazole

· Hungry bone syndrome: After parathyroidectomy for severe hyperparathyroidism; rapid bone uptake

· Pseudohypoparathyroidism: End‑organ resistance to PTH; high PTH, low calcium, high phosphate

· Sepsis / critical illness: Multiple mechanisms

Clinical features of hypocalcaemia:

· Neuromuscular irritability: Paraesthesias (perioral, fingertips), muscle cramps, tetany, carpopedal spasm

· Chvostek sign: Facial muscle contraction on tapping facial nerve

· Trousseau sign: Carpal spasm induced by blood pressure cuff inflation

· Central nervous system: Seizures, basal ganglia calcification, parkinsonism, dementia (chronic)

· Cardiovascular: Prolonged QT interval, arrhythmias, heart failure

· Psychiatric: Anxiety, depression, irritability

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5. Best way to address aberrant levels

Critical principle: Calcium is tightly regulated; deviation from normal always signifies an underlying disorder. Treatment is directed at the cause, not simply the number. Acute, severe abnormalities require immediate medical attention. All management must be supervised by a physician.

a. Quick ways or using Medications (Medical Management)

Hypercalcaemia:

Acute, severe hypercalcaemia (>14 mg/dL or symptomatic) is a medical emergency requiring hospitalisation and aggressive management.

· Intravenous normal saline:

· First and most urgent intervention.

· Corrects volume depletion (almost always present due to polyuria/vomiting).

· Enhances renal calcium excretion.

· Initial rate: 200–500 mL/hour, guided by cardiac and renal status.

· Intravenous bisphosphonates:

· Pamidronate: 60–90 mg IV over 2–4 hours

· Zoledronic acid: 4 mg IV over 15 minutes (more potent)

· Inhibit osteoclast‑mediated bone resorption. Onset 2–4 days; duration weeks.

· Monitor renal function; adjust dose in CKD.

· Calcitonin:

· 4–8 IU/kg IM/SC every 6–12 hours

· Rapid onset (hours) but short duration (tachyphylaxis within days)

· Useful for rapid initial lowering while waiting for bisphosphonates

· Glucocorticoids:

· Effective in vitamin D intoxication, granulomatous diseases, myeloma, lymphoma

· Prednisolone 20–40 mg daily; reduces calcitriol production

· Denosumab:

· Monoclonal antibody against RANKL; inhibits osteoclast formation

· Used in bisphosphonate‑refractory cases or malignancy‑associated hypercalcaemia

· 60–120 mg SC; monitor calcium closely

· Haemodialysis:

· For extreme, life‑threatening hypercalcaemia with renal failure

· Low‑calcium dialysate

· Treatment of underlying cause:

· Primary hyperparathyroidism: Parathyroidectomy for symptomatic, young, or calcium >1 mg/dL above upper limit

· Malignancy: Chemotherapy, radiotherapy, surgery as appropriate

· Granulomatous disease: Treat underlying condition; glucocorticoids

· Thiazide‑induced: Discontinue drug

Hypocalcaemia:

Symptomatic hypocalcaemia (tetany, seizures, prolonged QT) requires urgent intravenous calcium. Asymptomatic or chronic hypocalcaemia is managed orally.

· Intravenous calcium (acute, symptomatic):

· Calcium gluconate 10%: 10–20 mL (1–2 g) diluted in 50–100 mL D5W, infused slowly over 10–20 minutes (central line preferred; extravasation causes severe tissue necrosis)

· Calcium chloride 10%: 5–10 mL (contains 3× more elemental calcium than gluconate; more irritating – central line essential)

· Followed by continuous infusion (1–2 mg/kg/hour) titrated to symptoms and calcium levels

· Continuous ECG monitoring mandatory

· Oral calcium (chronic, stable):

· Elemental calcium: 1–3 g daily in divided doses

· Calcium carbonate: 40% elemental calcium; requires gastric acid for absorption; best with meals

· Calcium citrate: 21% elemental calcium; better absorption in achlorhydria, elderly, or PPIs; does not require meals

· Form preference: Calcium citrate is generally preferred for long‑term supplementation due to consistent absorption and lower risk of kidney stones

· Vitamin D supplementation (essential in most hypocalcaemia):

· Calcitriol (1,25‑dihydroxyvitamin D3): Active form; used in hypoparathyroidism, CKD, vitamin D‑dependent rickets. Dose 0.25–2 mcg daily. Rapid onset/offset.

· Cholecalciferol (vitamin D3): For nutritional deficiency, malabsorption. Requires intact renal function. Source: Lichen‑derived (plant‑based).

· Ergocalciferol (vitamin D2): Less effective; not preferred.

· Magnesium repletion:

· Check magnesium in ALL hypocalcaemic patients.

· If low, replace first (or concurrently). Hypomagnesaemia impairs PTH secretion/action and makes hypocalcaemia refractory.

· Oral: Magnesium citrate, glycinate, or chloride. Intravenous: Magnesium sulphate (for severe deficiency, cardiac arrhythmias).

· Phosphate management:

· In CKD, hyperphosphataemia worsens hypocalcaemia; use phosphate binders (calcium acetate, sevelamer)

· Treatment of underlying cause:

· Hypoparathyroidism: Long‑term calcium and calcitriol; consider PTH analogue (teriparatide) in refractory cases

· Vitamin D deficiency: Replete vitamin D

· Post‑thyroidectomy: Monitor calcium closely; transient hypoparathyroidism common

· Hungry bone syndrome: Aggressive calcium and vitamin D supplementation post‑parathyroidectomy

Do not self‑prescribe calcium or vitamin D without knowing your levels and the cause. Hypercalcaemia from excess supplementation can cause kidney stones, vascular calcification, and arrhythmias.

b. Using Supplements or Holistic medicine

For documented deficiency, the supplements above are medical therapy, not "alternative." The following considerations apply to calcium and its cofactors.

· Calcium forms:

· Calcium citrate: Preferred for long‑term use, especially in older adults, those on acid‑reducing medications, or with history of kidney stones (less likely to promote stones than carbonate? – citrate actually inhibits stones).

· Calcium carbonate: Acceptable if taken with meals; cheaper. Risk of constipation, gas.

· Avoid: Calcium from unrefined sources (bone meal, dolomite, oyster shell) – may contain lead or other heavy metals.

· Do not exceed 500–600 mg elemental calcium per dose – absorption saturates.

· Cofactors for calcium utilisation:

· Vitamin D3: Essential for absorption. Use lichen‑derived cholecalciferol.

· Vitamin K2 (menaquinone): Directs calcium into bone rather than arteries. MK‑7 form (from natto) or MK‑4. Plant sources: natto (fermented soy), sauerkraut; otherwise supplement.

· Magnesium: Required for PTH secretion and vitamin D activation. Many are deficient.

· Boron: Trace mineral; may affect calcium metabolism. Found in plant foods (prunes, raisins, nuts).

· Herbs and Phytochemicals from Indian subcontinent:

· Horse gram (Macrotyloma uniflorum): Traditionally used for kidney stones; thought to inhibit calcium oxalate crystallisation. Not a calcium source.

· Punarnava (Boerhavia diffusa): Ayurvedic herb for kidney health; used in urinary disorders including stones.

· Gokshura (Tribulus terrestris): Traditionally for urinary and reproductive health; some use for stones.

· Amla (Emblica officinalis): Rich in vitamin C; may reduce urinary calcium loss? Evidence limited.

· Turmeric (Curcuma longa): Anti‑inflammatory; may benefit bone health.

These herbs are not calcium sources or primary treatments for calcium disorders. They may support kidney and bone health but should not replace medical therapy.

· Important cautions:

· Calcium supplements may increase cardiovascular risk in some studies, especially when taken without vitamin K2 or when exceeding 1000–1200 mg/day from supplements (dietary calcium appears safe).

· Do not take calcium with iron or thyroid hormone – they interfere with absorption. Separate by at least 2 hours.

· Avoid calcium supplementation in sarcoidosis or other granulomatous disorders unless documented deficiency and under specialist care (risk of hypercalcaemia).

· Disclose all supplements to your physician.

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

Dietary calcium is preferred over supplements whenever possible. A well‑planned plant‑based diet can provide adequate calcium, but requires knowledge of high‑calcium plant sources and factors affecting absorption.

Plant‑based calcium sources (excellent options):

· Leafy greens (cooked): Kale, collard greens, mustard greens, turnip greens, bok choy. Calcium in these is well absorbed despite oxalate content (cooking reduces oxalates).

· Note: Spinach, Swiss chard, beet greens are high in calcium but also high in oxalates, which bind calcium and reduce absorption. They are still healthy but should not be relied upon as primary calcium sources.

· Fortified plant milks: Soy milk, almond milk, oat milk – check labels for calcium carbonate or tricalcium phosphate fortification. Typically 300–450 mg per cup.

· Tofu: Calcium‑set tofu (made with calcium sulphate) is an excellent source. Check label; varies by brand. 100–300 mg per 100 g.

· Tempeh: Fermented soy; contains some calcium, less than calcium‑set tofu.

· Legumes: Chickpeas, black beans, kidney beans, lentils – contribute moderate calcium.

· Nuts and seeds:

· Almonds: 75 mg per 30 g

· Sesame seeds (til): 90 mg per tablespoon; tahini (sesame paste) is concentrated

· Chia seeds: 90 mg per tablespoon

· Flaxseeds: 25 mg per tablespoon

· Amaranth: Cooked amaranth grain and leaves – good source.

· Ragi (finger millet): Staple in parts of India; exceptionally high in calcium (350 mg per 100 g). Gluten‑free.

· Dried fruits: Figs (dried), apricots, prunes – moderate sources.

· Oranges and orange juice (fortified).

· Blackstrap molasses: 200 mg per tablespoon.

Fungi and algae:

· Mushrooms: Minimal calcium; not a source.

· Seaweed (kelp, wakame, hijiki): Contain calcium, but also high iodine and potential heavy metals (hijiki high in arsenic – avoid). Use seaweed in moderation.

· Spirulina, chlorella: Contain some calcium; not primary sources.

Biotechnology / fermentation‑derived:

· Fortified plant products: Many are available; rely on fortification with well‑absorbed calcium salts.

· Mycoprotein (Quorn): Contains some calcium; not a major source.

Dairy and eggs:

· Milk, yoghurt, cheese: Traditional calcium sources; permitted but not emphasised. Fermented dairy (yoghurt, kefir) preferable.

· Eggs: Minimal calcium (in shell, not egg).

Meat, fish, poultry (lowest priority):

· Small fish with bones (sardines, canned salmon): High calcium; ecological cost significant.

· Meat and poultry: Very low calcium.

Factors affecting calcium absorption:

· Enhancers: Vitamin D, adequate stomach acid, lactose (in dairy, not relevant for plant sources), certain amino acids.

· Inhibitors:

· Oxalates: In spinach, rhubarb, beet greens, Swiss chard. Cooking reduces but does not eliminate.

· Phytates: In whole grains, legumes, nuts, seeds. Soaking, sprouting, fermenting reduce phytates.

· Excessive sodium: Increases urinary calcium excretion.

· Excessive caffeine: Mild calciuric effect.

· Excessive protein (especially animal protein): Increases urinary calcium.

· Phosphate (soft drinks): May affect calcium balance.

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

1. Base your intake on fortified plant milks and calcium‑set tofu. One cup fortified milk (300 mg) + 100 g calcium‑set tofu (150 mg) provides nearly half daily needs.

2. Include cooked leafy greens daily: Kale, collards, mustard greens.

3. Use ragi (finger millet) regularly: Roti, porridge, or cooked grain.

4. Add sesame seeds (tahini) to meals.

5. Include almonds, chia seeds, and dried figs.

6. Ensure adequate vitamin D (sunlight or supplement) and vitamin K2 (fermented foods or supplement) to direct calcium to bone.

7. Soak and sprout legumes and grains to reduce phytates.

8. Limit sodium, caffeine, and phosphate‑rich soft drinks.

9. If dietary intake consistently <800 mg/day, consider a low‑dose calcium citrate supplement (500 mg or less) rather than increasing animal product consumption.

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

Acute hypercalcaemia:

· Intravenous saline and calcitonin: Improvement within hours.

· Bisphosphonates: Peak effect 2–4 days; calcium normalises over days.

· Retest: Daily during acute management; after stabilisation, weekly then as outpatient.

Chronic hypercalcaemia (primary hyperparathyroidism):

· After parathyroidectomy: Calcium normalises within hours to days. May transiently dip (hungry bone syndrome). Monitor daily post‑op, then weekly.

· Medical management (if not surgical): Monitor calcium every 3–6 months.

Acute symptomatic hypocalcaemia:

· Intravenous calcium: Immediate symptom relief (within minutes).

· Continuous infusion titrated to symptoms and levels; daily monitoring.

· Once stable, transition to oral.

Chronic hypocalcaemia (hypoparathyroidism, vitamin D deficiency):

· Oral calcium and calcitriol: Gradual improvement over days to weeks.

· Retest: Weekly initially until stable, then every 3–6 months. Annual monitoring thereafter.

· Vitamin D deficiency: Recheck 25(OH)D at 3 months.

Indications for retesting:

· Monitoring therapy: As above.

· New symptoms: Suggesting recurrence or overcorrection.

· Change in medications: Affecting calcium (thiazides, loop diuretics, glucocorticoids, bisphosphonates).

· Pregnancy planning: In women with calcium disorders.

· Not indicated for routine population screening in asymptomatic low‑risk individuals.

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Conclusion

Calcium is the structural pillar of the skeleton and the signalling currency of the cell. Its concentration in blood is guarded by a hormonal triumvirate – PTH, vitamin D, and calcitonin – with a vigilance that reveals disease only when regulation fails. Hypercalcaemia whispers of parathyroid adenoma, shouts of malignancy, and murmurs of granuloma. Hypocalcaemia speaks of absent parathyroids, deficient vitamin D, or magnesium's hidden hand. The blood test, interpreted with albumin and context, unveils these secrets. Treatment is cause‑specific, precise, and potentially urgent. The ecological path to calcium sufficiency is paved with fortified plant milks, calcium‑set tofu, ragi, sesame seeds, and cooked greens – foods that nourish without depleting the planet. Calcium citrate supplements, when needed, are chosen over oyster shell or bone meal. Vitamin D from lichen, vitamin K2 from natto, and magnesium from greens complete the picture. Calcium is not just a bone mineral; it is a messenger, a mediator, and a mirror reflecting the health of multiple systems. Measure it with respect, interpret it with care, and treat the person, not the number.

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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. A well‑planned plant‑based diet can meet all calcium requirements through fortified foods, calcium‑set tofu, leafy greens, sesame seeds, ragi, and other plant sources, without recourse to dairy or fish.

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