Tinnitus — B12, Magnesium and Zinc Status

Table of Contents

1. Why These Three Nutrients
2. Vitamin B12 — Mechanism and Cochlear-Nerve Demyelination
3. Vitamin B12 — Clinical Evidence in Tinnitus
4. Magnesium — N-Methyl-D-Aspartate Antagonism and Cochlear Protection
5. Magnesium — Clinical Evidence in Tinnitus and Noise Injury
6. Zinc — Cochlear Concentration and Hair-Cell Function
7. Zinc — Clinical Evidence and the Cochrane Verdict
8. Tests That Measure B12, Magnesium and Zinc Status
9. Doses Used in Studies
10. Cautions and Interactions
11. Key Research Papers
12. Connections
13. Featured Videos

Why These Three Nutrients

Many nutrients have been proposed for tinnitus — the literature includes case reports and small studies for vitamin D, folate, iron, manganese, selenium, coenzyme Q10, omega-3 fatty acids, and others. B12, magnesium, and zinc receive the most attention because three lines of evidence meet for them:

1. A proposed role in the hearing system — B12 maintains the myelin (insulating sheath) of nerves, including the cochlear and auditory nerves; magnesium modulates N-methyl-D-aspartate-receptor activity at the cochlear hair-cell synapse and is proposed to protect against noise-induced over-stimulation (excitotoxicity); zinc is present in the cochlea and in the synapses of the hearing nerve, and is part of the copper/zinc superoxide dismutase enzyme that helps defend the cochlea against oxidative damage
2. Deficiency measured in tinnitus groups, with mixed results — low B12 was found in 47% of noise-exposed army personnel with tinnitus and hearing loss, against 27% with hearing loss alone and 19% with normal hearing (Shemesh 1993), but another study found no difference from healthy controls (Berkiten 2013); magnesium status is reported to be lower in tinnitus groups on red-blood-cell (RBC) magnesium measurement; and reported rates of zinc deficiency in people with tinnitus range from 2% to 69%, more often in older people (Coelho 2007)
3. Small treatment studies, also mixed — some improvement in tinnitus was seen in 12 patients after B12 replacement in the Shemesh series, and B12-deficient patients improved in one small placebo-controlled pilot (Singh 2016), while another study found B12 treatment not effective (Berkiten 2013); magnesium reduced noise-induced hearing damage in military studies, which concern prevention rather than tinnitus treatment; and a Cochrane review found no evidence that zinc improves tinnitus

These are inexpensive tests and supplements with known safety limits, set out below. Whether correcting a deficiency improves tinnitus rests on small studies whose results disagree.

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Vitamin B12 — Mechanism and Cochlear-Nerve Demyelination

Vitamin B12 (cobalamin) is required for two enzymatic reactions in human physiology: methylmalonyl-CoA mutase (mitochondrial fatty-acid and amino-acid metabolism) and methionine synthase (the methylation cycle, regenerating methionine from homocysteine). The methionine-synthase reaction is the more relevant to nervous-system function — it produces the universal methyl-donor S-adenosylmethionine (SAMe) required for myelin basic protein synthesis and phospholipid methylation in myelin sheaths.

Severe B12 deficiency produces subacute combined degeneration of the spinal cord, peripheral neuropathy, and dementia. Less appreciated — but specifically relevant to tinnitus — is the effect on the cranial nerves, including cranial nerve VIII (the cochlear and vestibular nerve). Demyelination of the cochlear nerve is thought to disrupt conduction velocity, producing both hearing loss and the abnormal spontaneous activity that generates phantom auditory perception.

This path from B12 deficiency to the hearing nerve is a proposed mechanism. None of the studies on this page measured cochlear-nerve conduction in B12-deficient people with tinnitus.

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Vitamin B12 — Clinical Evidence in Tinnitus

The first clinical study was Shemesh et al. (1993), from the Institute of Noise Hazards Research of the Israel Defence Forces at the Chaim-Sheba Medical Center in Ramat-Gan. The investigators measured serum B12 in 113 army personnel exposed to military noise (average age 39): 57 had chronic tinnitus with noise-induced hearing loss, 29 had noise-induced hearing loss without tinnitus, and 27 had normal hearing. Findings:

• 47% of those with tinnitus and noise-induced hearing loss had B12 deficiency (serum B12 of 250 pg/mL or less)
• 27% of those with noise-induced hearing loss but no tinnitus had B12 deficiency
• 19% of those with normal hearing had B12 deficiency — the tinnitus group's rate was significantly higher than the other two (P < .023)
• After B12 replacement, some improvement in tinnitus and associated complaints was seen in 12 patients; the study abstract gives no dose, schedule or response rate. The authors recommended routine serum B12 testing in people with chronic tinnitus.

Later studies point in different directions:

• Singh et al. (2016), in North India, ran the only placebo-controlled B12 trial found: a randomised, double-blind pilot study in 40 people with chronic tinnitus. Twenty received a weekly injection of 2500 mcg of B12 into the muscle for 6 weeks and twenty received salt-water (saline) injections. Seventeen of the 40 (42.5%) were B12-deficient (below 250 pg/mL). Among those given B12, the deficient patients improved significantly on a tinnitus severity score and on a visual scale of tinnitus. It is a small pilot study.
• Berkiten et al. (2013), in Turkey, found the opposite. They measured B12 in 100 people with tinnitus and 20 healthy volunteers: 63 patients had low B12 (below 180 pg/mL), but levels did not differ from the controls (p = 0.80). After B12 treatment, tinnitus severity did not change significantly — 8 patients reported some relief, a result that was not significant — and hearing improved only at the lowest test frequency (250 Hz). The authors concluded that B12 replacement was not effective in their patients.
• Lasisi et al. (2012) studied 139 older adults in Nigeria (aged 60 to 98), 58.3% of whom had tinnitus. Plasma B12 and melatonin were significantly lower in those with tinnitus, while vitamin C was not.

Important methodologic caveat: the serum B12 threshold for "deficiency" differs between studies and has shifted over the decades — Shemesh used 250 pg/mL or less, Berkiten below 180 pg/mL. Modern functional deficiency definitions use methylmalonic acid (MMA) and homocysteine as confirmatory markers — serum B12 levels in the 200–400 pg/mL range may still represent functional deficiency if methylmalonic acid is elevated. For that reason, methylmalonic acid is commonly measured when serum B12 is below about 400 pg/mL, and either marker being abnormal is treated as a sign of deficiency.

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Magnesium — N-Methyl-D-Aspartate Antagonism and Cochlear Protection

Magnesium is the natural physiologic antagonist at the N-methyl-D-aspartate (NMDA) glutamate receptor. The N-methyl-D-aspartate receptor channel is normally blocked by a magnesium ion at resting membrane potential; depolarization removes the magnesium block, allowing calcium influx and downstream signaling. In the cochlea, the inner hair cell-to-spiral ganglion synapse uses glutamate as the neurotransmitter, and excessive glutamate release — the mechanism behind acoustic-overexposure injury — produces excitotoxic calcium overload at the postsynaptic spiral ganglion terminal.

Magnesium status determines how effectively the N-methyl-D-aspartate receptor is protected from this excitotoxic surge. Animal models of noise-induced hearing loss consistently show that magnesium-replete subjects sustain less cochlear damage than magnesium-deficient subjects exposed to the same acoustic stimulus. The mechanism extends beyond the synapse — magnesium also maintains cochlear blood flow (it is a vasodilator), supports mitochondrial function, and reduces reactive oxygen species generation during acoustic stress.

Beyond noise protection, magnesium has a direct vascular role in cochlear blood supply. The stria vascularis is the most metabolically active tissue in the body per gram of weight, and any reduction in cochlear microcirculation acutely worsens hair-cell function. Magnesium deficiency promotes vasoconstriction (through unopposed calcium signaling in vascular smooth muscle), and better cochlear blood flow is a proposed part of how magnesium might help; it was not measured in the human studies on this page.

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Magnesium — Clinical Evidence in Tinnitus and Noise Injury

The Israeli army studies by Attias and colleagues are the main controlled data for magnesium in protecting the cochlea from noise. Attias et al. (1994) studied 300 young, healthy recruits with normal hearing during 2 months of basic military training, which included repeated exposure to high levels of impulse noise while wearing earplugs. In a double-blind, placebo-controlled design, each recruit drank either 167 mg (6.7 mmol) of magnesium aspartate or a placebo every day. Results:

• Permanent noise-induced hearing loss (permanent threshold shift) was significantly more frequent and more severe in the placebo group than in the magnesium group, especially damage in both ears
• The amount of hearing loss was linked to the magnesium content of red blood cells and, especially, of white blood cells called mononuclear cells: more magnesium went with less loss
• This small daily dose, taken for 2 months, caused no notable side effects

A report of the same field study by Joachims and colleagues (1993) described 320 volunteers, about 420 shots per person and earplugs throughout; the share of ears with permanent shifts of more than 25 dB at 4, 6 and/or 8 kHz was twice as high on placebo as on magnesium. Attias and colleagues (2004) then tested 20 men aged 16 to 37, each going through a placebo phase, a magnesium phase and a no-drug phase. During the magnesium phase they had significantly less temporary hearing dulling after noise (temporary threshold shift), seen both on ordinary hearing tests and on otoacoustic emissions (faint sounds the inner ear itself produces), and the magnesium caused no side effects. Le Prell et al. (2007) found in animals that magnesium plus vitamins A, C, and E in combination was highly effective in reducing noise-induced hearing loss and hair-cell death, even when started 1 hour before the noise, while neither the vitamins nor the magnesium alone reliably did so at the doses used — leading to the formulation of investigational "ACE-Mg" otoprotectant cocktails for impulse-noise protection.

For chronic established tinnitus (as opposed to prevention of new noise-induced injury), the evidence is thinner. Cevette, Vormann and Franz (2003) reviewed the magnesium-and-hearing literature. They described links between magnesium deficiency and greater susceptibility to noise damage, to drugs that damage hearing, and to over-excitability of the hearing system, and a proposed chain in which low magnesium lets too much calcium into hair cells, releasing excess glutamate and over-stimulating the hearing nerve. They also noted that direct effects "have remained elusive", partly because blood magnesium levels do not always reflect a deficiency, and that magnesium's neurochemical role in hearing "is not clear."

The one magnesium study in established tinnitus found here is Cevette et al. (2011), an open-label study at Mayo Clinic in Arizona with no placebo group. Twenty-six people with moderate to very severe tinnitus took 532 mg of magnesium a day for 3 months, and 19 finished. Among those with at least slight handicap at the start, tinnitus handicap scores fell significantly (P = .03). Because there was no placebo group, how much of this change was due to magnesium is unknown, and the dose was above the upper limit for supplemental magnesium described below.

The challenge with magnesium status assessment is that serum magnesium is poorly sensitive — most magnesium is intracellular, and serum can be normal in the face of substantial cellular deficit. RBC magnesium and ionized magnesium are more sensitive but less widely available. For this reason some practitioners give magnesium (around 400 mg a day of elemental magnesium for 90 days) without measuring it first. The Institute of Medicine's tolerable upper intake level for magnesium from supplements and medicines is 350 mg a day for adolescents and adults (magnesium from food is not counted), set because diarrhoea appeared at 360 mg a day.

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Zinc — Cochlear Concentration and Hair-Cell Function

Zinc is found in all organs and tissues of the body, including the cochlea and the synapses of the hearing nerve. Its presence there points to specific roles, and several lines of evidence point to multiple zinc-dependent functions in the auditory system:

• Zinc-dependent enzymes — copper/zinc superoxide dismutase (Cu/Zn superoxide dismutase, SOD) is one of the cochlea's primary antioxidant defenses against the reactive oxygen species generated by normal acoustic transduction. Zinc deficiency reduces superoxide dismutase activity and increases vulnerability to oxidative injury.
• Synaptic zinc release — zinc is co-released with glutamate at certain auditory synapses and modulates postsynaptic N-methyl-D-aspartate-receptor activity, suggesting a role in synaptic transmission and possibly in central auditory plasticity
• Stria vascularis function — zinc supports the stria vascularis, the tissue that generates the endocochlear potential essential for hair-cell transduction. Stria atrophy in presbycusis correlates with reduced tissue zinc content.
• Immune and inflammatory modulation — zinc affects multiple aspects of cochlear inflammation and immune surveillance, which may be relevant to viral and autoimmune inner-ear disease

Coelho and colleagues (2007) reviewed three proposed links between zinc and tinnitus: the cochlea's copper/zinc superoxide dismutase, synaptic transmission, and depression. Four of the five small studies they found suggested a benefit from zinc, but they wrote that the results still had to be confirmed in larger trials. Yetiser et al. (2002), in Turkey, studied 40 consecutive patients with severe tinnitus (aged 19 to 67), with no control group. Only 6 had low serum zinc and 7 had decreased levels, and the authors wrote that they "could not confirm the high incidence of hypozincemia" (low zinc) reported earlier. All 40 took one 220 mg zinc pill a day for 2 months. Hearing tests showed no significant change in tinnitus; 23 (57.5%) reported some relief on a tinnitus score, but the improvement was minor and not significant, and the difference between patients with normal and low zinc was not significant. Older patients did better than younger ones, and the authors saw relief in some older people who apparently had low dietary zinc.

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Zinc — Clinical Evidence and the Cochrane Verdict

The Person et al. (2016) Cochrane review of zinc for tinnitus found three randomized controlled trials with 209 participants in total (109, 50 and 50), at moderate to high risk of bias. The trials differed too much in who they enrolled, how long they ran and what they measured to be combined, so no pooled result was calculated. Findings:

• In the largest trial, in older people (109 participants), 5% on zinc vs 2% on placebo reported tinnitus improvement at 4 months — not a significant difference, and very low-quality evidence
• Tinnitus loudness showed no significant difference between zinc and placebo in the two trials that measured it, and the two trials using unvalidated severity scales found no difference either
• None of the included trials reported any significant side effects
• The reviewers concluded: "We found no evidence that the use of oral zinc supplementation improves symptoms in adults with tinnitus."

Whether people with a proven zinc deficiency respond differently is not settled. Coelho's 2007 review reported deficiency rates of 2% to 69% in people with tinnitus, more often in older people, while the Yetiser study found no significant difference in improvement between low-zinc and normal-zinc patients. The idea behind testing first is that correcting a deficiency is different from adding zinc to an already-replete person.

Practitioners who use zinc for tinnitus generally reserve it for documented deficiency (serum zinc below approximately 70 mcg/dL or below the reference range of the testing laboratory), at doses of 25–50 mg elemental zinc per day, for 60–90 days, with reassessment of both serum zinc and tinnitus questionnaires. Zinc supplementation in zinc-replete tinnitus patients is not supported by current evidence and carries small risks (copper deficiency from chronic high-dose zinc, gastric irritation).

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Tests That Measure B12, Magnesium and Zinc Status

These are the blood tests used to measure these nutrients and related causes of tinnitus. The target figures are the cut-offs commonly quoted in practice:

• Serum B12 (below about 400 pg/mL, methylmalonic acid is commonly added as a confirmatory marker)
• Serum folate (often interpreted alongside B12 because elevated folate can mask B12 deficiency on macrocytic-anemia screening)
• Methylmalonic acid (MMA) if B12 is borderline (200–400 pg/mL); methylmalonic acid greater than 0.4 µmol/L confirms functional B12 deficiency even with "normal" serum B12
• Homocysteine as additional confirmatory marker of methylation-cycle dysfunction (elevated in B12, folate, or B6 deficiency)
• Serum magnesium as a starting point, though it is poorly sensitive; RBC magnesium or ionized magnesium is more sensitive where available
• Serum zinc (commonly quoted cut-off 70 mcg/dL; levels vary through the day, so a fasting morning sample is the usual standard)
• Vitamin D 25-OH (not directly tinnitus-specific but relevant to general inner-ear health and other comorbidities; a commonly quoted target is above 30 ng/mL)
• Serum ferritin and complete blood count (iron-deficiency anemia can cause or worsen tinnitus through tissue hypoxia)
• Thyroid-stimulating hormone (TSH) (hyperthyroidism can cause pulsatile tinnitus; hypothyroidism is associated with sensorineural hearing loss)

For US patients, this entire panel is available as a single venipuncture and typically costs under $200 even without insurance through direct-to-consumer testing platforms.

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Doses Used in Studies

The tinnitus and noise studies described above used these doses:

• Vitamin B12 — Singh 2016: 2500 mcg injected into the muscle once a week for 6 weeks. Shemesh 1993 and Berkiten 2013 gave B12 replacement without a dose stated in their abstracts.
• Magnesium — Attias 1994: 167 mg (6.7 mmol) of magnesium aspartate a day in a drink for 2 months; Cevette 2011: 532 mg a day for 3 months.
• Zinc — Yetiser 2002: one 220 mg zinc pill a day for 2 months.

Outside the tinnitus studies, these doses are commonly described for correcting a documented deficiency:

• Vitamin B12 — oral methylcobalamin 1000–2000 mcg/day for three months, then 500–1000 mcg/day maintenance, with serum B12 and methylmalonic acid re-measured at three months. For severe deficiency with neurologic symptoms or a documented absorption defect (pernicious anemia, post-bariatric surgery, ileal disease): cyanocobalamin 1000 mcg injected into the muscle weekly for six weeks, then monthly. Methylcobalamin is often chosen instead of cyanocobalamin in people with kidney impairment. See the Vitamin B12 page for comprehensive dosing.
• Magnesium — magnesium glycinate, malate, or citrate 200–400 mg elemental/day divided into two doses with meals; magnesium oxide is less well absorbed and more laxative. RBC magnesium is re-measured at 90 days. The top of this range is above the Institute of Medicine's upper limit of 350 mg a day for magnesium from supplements, and diarrhoea is the first sign of too much. See the Magnesium page for form comparison.
• Zinc — zinc picolinate, citrate, or gluconate 25–30 mg elemental/day with food to reduce stomach upset; calcium and iron supplements compete with zinc when taken at the same time. After 60–90 days, 15 mg/day maintenance is described to lower the risk of copper deficiency. See the Zinc page for form comparison.
• Copper when zinc supplementation is prolonged — 1–2 mg/day copper is described to prevent zinc-induced copper deficiency, taken 2–3 hours apart from the zinc dose

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Cautions and Interactions

• B12 with kidney impairment — cyanocobalamin contains a cyanide group (small in amount but undesirable in advanced chronic kidney disease, CKD); methylcobalamin or hydroxocobalamin are the forms usually chosen instead
• Magnesium with kidney impairment — impaired magnesium excretion in chronic kidney disease stage 4–5 raises the risk of magnesium building up in the blood (hypermagnesemia); serum magnesium is monitored in this group
• Magnesium and antibiotic interactions — magnesium binds fluoroquinolone and tetracycline antibiotics in the gut, reducing their absorption; doses are usually separated by 2–6 hours
• Zinc and copper deficiency — chronic zinc above 40 mg/day depletes copper through induction of intestinal metallothionein; copper is commonly added if zinc continues beyond 8 weeks
• Zinc and iron — the two compete for absorption when taken at the same time
• Zinc and gastric upset — some people experience nausea or abdominal discomfort (the three trials in the Cochrane review reported no significant side effects); taking zinc with food and choosing zinc picolinate or glycinate is described to reduce this
• Iron deficiency anemia — correcting iron deficiency may improve tinnitus through restored tissue oxygenation, but high-dose iron supplementation in iron-replete patients does not benefit and risks oxidative injury

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Key Research Papers

1. Shemesh Z, Attias J, Ornan M, Shapira N, Shahar A (1993). Vitamin B12 deficiency in patients with chronic-tinnitus and noise-induced hearing loss. American Journal of Otolaryngology;14(2):94-99 — PubMed PMID: 8484483
2. Singh C, Kawatra R, Gupta J, Awasthi V, Dungana H (2016). Therapeutic role of Vitamin B12 in patients of chronic tinnitus: A pilot study. Noise & Health;18(81):93-97 — PubMed PMID: 26960786
3. Berkiten G, Yildirim G, Topaloglu I, Ugras H (2013). Vitamin B12 levels in patients with tinnitus and effectiveness of vitamin B12 treatment on hearing threshold and tinnitus. B-ENT;9(2):111-116 — PubMed PMID: 23909117
4. Attias J, Weisz G, Almog S, Shahar A, Wiener M, Joachims Z, Netzer A, Ising H, Rebentisch E, Guenther T (1994). Oral magnesium intake reduces permanent hearing loss induced by noise exposure. American Journal of Otolaryngology;15(1):26-32 — PubMed PMID: 8135325
5. Joachims Z, Netzer A, Ising H, Rebentisch E, Attias J, Weisz G, Günther T (1993). Oral magnesium supplementation as prophylaxis for noise-induced hearing loss: results of a double blind field study. Schriftenreihe des Vereins für Wasser-, Boden- und Lufthygiene;88:503-516 — PubMed PMID: 8460390
6. Attias J, Sapir S, Bresloff I, Reshef-Haran I, Ising H (2004). Reduction in noise-induced temporary threshold shift in humans following oral magnesium intake. Clinical Otolaryngology and Allied Sciences;29(6):635-641 — PubMed PMID: 15533151
7. Cevette MJ, Vormann J, Franz K (2003). Magnesium and hearing. Journal of the American Academy of Audiology;14(4):202-212 — PubMed PMID: 12940704
8. Cevette MJ, Barrs DM, Patel A, Conroy KP, Sydlowski S, Noble BN, Nelson GA, Stepanek J (2011). Phase 2 study examining magnesium-dependent tinnitus. International Tinnitus Journal;16(2):168-173 — PubMed PMID: 22249877
9. Coelho CB, Tyler R, Hansen M (2007). Zinc as a possible treatment for tinnitus. Progress in Brain Research — PubMed PMID: 17956792
10. Yetiser S et al. (2002). The role of zinc in management of tinnitus. Auris Nasus Larynx — PubMed PMID: 12393036
11. Person OC, Puga ME, da Silva EM, Torloni MR (2016). Zinc supplementation for tinnitus. Cochrane Database of Systematic Reviews;11:CD009832 — PubMed PMID: 27879981
12. Lasisi AO, Fehintola FA, Lasisi TJ (2012). The role of plasma melatonin and vitamins C and B12 in the development of idiopathic tinnitus in the elderly. Ghana Medical Journal;46(3):152-157 — PubMed PMID: 23661829
13. Le Prell CG, Hughes LF, Miller JM (2007). Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma. Free Radical Biology & Medicine;42(9):1454-1463 — PubMed PMID: 17395018
14. Institute of Medicine (1997). Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Chapter 6, Magnesium (tolerable upper intake level of 350 mg/day from nonfood sources for adolescents and adults). Washington, DC: National Academies Press — doi:10.17226/5776

PubMed Topic Searches

1. PubMed: Vitamin B12 and tinnitus
2. PubMed: Magnesium and tinnitus / noise-induced hearing loss
3. PubMed: Zinc and tinnitus supplementation
4. PubMed: MMA as functional B12 marker
5. PubMed: Cochlear zinc and hair cells

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Connections

• All Remedies
• Tinnitus Hub
• Benefits Deep-Dive Hub
• Causes and Triggers
• Sound Therapy and Habituation
• N-Acetylcysteine and Antioxidants
• Vitamin B12
• Magnesium
• Zinc
• Copper
• Vitamin D3
• Methylmalonic Acid Test
• Homocysteine Test
• Neurology
• Glycine for Tinnitus
• Taurine for Tinnitus
• Tinnitus — the ENT clinical overview that frames where a nutrient workup fits in the wider diagnostic sequence.

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