Biotin (Vitamin B7) Test
The biotin test measures circulating vitamin B7, a cofactor for five carboxylases essential to energy metabolism. It is ordered to confirm deficiency in patients with alopecia, dermatitis, or neurological signs, to screen for biotinidase deficiency, and to establish baseline before high-dose biotin therapy; pharmacological supplementation interferes with many immunoassays.
1
Biomarkers
Blood (serum)
Sample
5–7 business days
Turnaround
No
Fasting
What is the Biotin test?
The Biotin (Vitamin B7) Test measures circulating biotin concentration and is ordered to confirm or exclude deficiency when clinical features — unexplained alopecia, seborrhoeic dermatitis, neurological signs, or lactic acidosis — suggest impaired carboxylase function. It is also used to screen newborns and infants with suspected biotinidase deficiency, a treatable inherited disorder, and to establish baseline status before initiating high-dose biotin therapy in multiple sclerosis or other neurological conditions. Because biotin is integral to energy metabolism and gene regulation, deficiency affects rapidly dividing tissues — skin, hair, and the nervous system — first. The test is not part of routine wellness panels; practitioners order it when the history (raw-egg consumption, total parenteral nutrition, long-term anticonvulsant use) or the clinical picture points to B-vitamin insufficiency that is not explained by deficiencies of thiamine, riboflavin, or niacin.
What does the Biotin test measure?
Biotin is a water-soluble B-vitamin that functions as a covalently bound cofactor for five mammalian carboxylases — enzymes critical to gluconeogenesis, fatty-acid synthesis, branched-chain amino-acid catabolism, and odd-chain fatty-acid oxidation. It is synthesised by intestinal bacteria and absorbed predominantly in the small intestine via the sodium-dependent multivitamin transporter. Circulating biotin is largely protein-bound; the vitamin is recycled by biotinidase, an enzyme whose deficiency leads to profound biotin depletion despite normal intake.
Clinical biotin deficiency is rare in individuals consuming a varied diet, because the vitamin is widely distributed in foods and produced by gut flora. When deficiency does occur — through prolonged raw-egg-white consumption (which contains the binding protein avidin), biotinidase deficiency, parenteral nutrition without biotin supplementation, or certain anticonvulsants — it manifests as alopecia, scaly dermatitis, conjunctivitis, ataxia, and developmental regression in infants. Conversely, high-dose biotin supplementation (often marketed for hair and nail health or used at pharmacological doses in multiple sclerosis) can interfere with a wide range of immunoassays, producing spurious laboratory results.
Why is the Biotin test ordered?
- Infants and children with unexplained developmental regression, hypotonia, seizures, or metabolic acidosis, particularly when newborn screening suggests biotinidase deficiency
- Adults or children presenting with the classic triad of alopecia, seborrhoeic (scaly, eczematous) dermatitis, and conjunctivitis without another identified cause
- Patients receiving long-term total parenteral nutrition without multivitamin supplementation, especially if skin or neurological changes emerge
- Individuals on chronic high-dose anticonvulsant therapy (valproate, carbamazepine, phenytoin) who develop signs compatible with biotin depletion
- Baseline measurement before starting pharmacological-dose biotin (≥100 mg daily) for progressive multiple sclerosis, to document pre-treatment status
- Investigation of unexplained organic aciduria or lactic acidosis when defects in biotin-dependent carboxylases are considered
- Confirmation of dietary deficiency in patients with documented prolonged raw-egg-white ingestion or highly restrictive diets
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No
Collection method
Venipuncture at patient service centre
Turnaround
5–7 business days
Collection notes
Phlebotomy via Quest patient service centre. Patients should discontinue biotin supplements for at least 72 hours before the draw to avoid assay interference and to obtain a baseline reflective of endogenous status; longer washout (up to 1 week) may be needed after very high pharmacological doses. No fasting required.
Specimen requirements
Minimum 1 mL serum. Separate from cells and freeze if not assayed promptly. Protect from light during storage.
What can affect Biotin results?
Pharmacological biotin (typically ≥5 mg daily, often 100–300 mg in neurological protocols) raises circulating concentrations far above physiological ranges and interferes with streptavidin–biotin immunoassays, producing false elevations or suppression of many hormone and cardiac markers.
Egg whites contain avidin, which binds biotin with extremely high affinity and prevents absorption; chronic consumption without cooking can induce frank deficiency.
Valproate, carbamazepine, phenytoin, and primidone accelerate biotin catabolism or inhibit intestinal and renal reabsorption, lowering circulating concentrations over months to years of therapy.
Loss of the enzyme that recycles biotin from biocytin causes progressive depletion despite normal intake; newborn screening detects most cases, but partial deficiency may present later.
Intestinal bacteria contribute to biotin supply; prolonged broad-spectrum antibiotics or severe dysbiosis may modestly lower endogenous production, though dietary sources usually suffice.
What do Biotin results mean?
Elevated
Elevated biotin almost always reflects recent supplementation, particularly high-dose regimens (≥5 mg daily). Pharmacological concentrations do not indicate toxicity — biotin has no established upper intake limit — but they do interfere with many immunoassays (thyroid function, troponin, NT-proBNP, vitamin D, and others). Practitioners must document supplementation and consider a washout period (typically 48–72 hours minimum, longer for very high doses) before ordering immunoassay-based tests.
Normal
A result within the reference interval, in the absence of high-dose supplementation, indicates adequate biotin status and functional carboxylase activity. It effectively excludes biotin deficiency as the cause of dermatological or neurological symptoms.
Reduced
Low biotin suggests inadequate intake (restrictive diet, prolonged raw-egg consumption, unsupplemented parenteral nutrition), increased catabolism (anticonvulsants, pregnancy), or impaired recycling (biotinidase deficiency). Clinical features — dermatitis, alopecia, neurological signs, or organic aciduria — guide the urgency of replacement. Isolated low values without symptoms may reflect assay variability and warrant repeat testing and assessment of carboxylase activity (via urine organic acids or plasma acylcarnitines) if deficiency is suspected.
Note: Circulating biotin correlates poorly with tissue stores; functional assessment (urinary 3-hydroxyisovalerate, plasma propionylcarnitine) is often more informative when carboxylase deficiency is suspected. Reference intervals are assay-dependent and influenced by recent supplementation. Document all biotin-containing supplements — including multivitamins and hair/nail formulations — because even moderate doses can confound laboratory tests for days.
Frequently asked questions
The classic triad is alopecia, seborrhoeic (scaly) dermatitis around the eyes and mouth, and conjunctivitis. Neurological features — ataxia, hypotonia, developmental delay, and seizures — occur in infants with biotinidase deficiency or severe dietary lack, and organic aciduria or lactic acidosis may be present.
How to access the Biotin test
The Biotin reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: October 7, 2026
Last reviewed: October 7, 2026
- Mock DM. Biotin: from nutrition to therapeutics. J Nutr. (2017)
- Sedel F, et al. High doses of biotin in chronic progressive multiple sclerosis: a pilot study. Mult Scler Relat Disord. (2015)
- Trüeb RM. Serum biotin levels in women complaining of hair loss. Int J Trichology. (2016)
- Li D, et al. Biotin interference in immunoassays: a problem that needs attention. Clin Chem Lab Med. (2020)
- Wolf B. Biotinidase deficiency: 'if you have to have an inherited metabolic disease, this is the one to have'. Genet Med. (2012)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.
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