What Causes Tinnitus? The 6 Main Causes Explained by a Dietitian
What causes tinnitus is a question with a complex but well-mapped answer: the phantom ringing, buzzing, or hissing sound is not a disease itself but a symptom arising from one or more of six primary biological pathways — noise-induced cochlear damage, age-related hair cell degeneration, ototoxic medications, vascular abnormalities, central neurological changes, and nutritional deficiencies. Approximately 15% of U.S. adults experience tinnitus, according to the National Institute on Deafness and Other Communication Disorders, making it one of the most prevalent chronic health complaints in the country.
This guide breaks down each cause with clinical evidence, explains the biology behind why it generates phantom sound, identifies the subgroups most at risk, and connects these upstream causes to the evidence base for nutritional and supplemental interventions.
TL;DR
- Tinnitus is not a disease but a symptom with six primary cause categories: noise, aging, medications, vascular abnormalities, neurological changes, and nutritional deficiencies.
- Noise-induced cochlear hair cell damage is the single most common identifiable cause, accounting for most cases with a documented peripheral trigger.
- Over 200 medications can trigger or worsen tinnitus — including aspirin at high doses, aminoglycoside antibiotics, and cisplatin chemotherapy.
- Pulsatile tinnitus that beats with the heartbeat is a distinct subtype with vascular causes that often have treatable structural explanations.
- Deficiencies in magnesium, zinc, and vitamin B12 each impair cochlear function through distinct mechanisms and are more addressable than structural hearing loss.
The Biology of Phantom Sound: Why Tinnitus Exists
Before exploring specific causes, it helps to understand why cochlear or auditory nerve damage generates phantom sound rather than silence.
The auditory cortex in the brain’s temporal lobe is calibrated to expect a continuous stream of sensory input from cochlear hair cells. When that input is partially or wholly interrupted — by damaged hair cells, severed synaptic connections, or degraded nerve signaling — the auditory cortex does not simply go quiet. Instead, it undergoes compensatory neuroplasticity: it upregulates its own spontaneous firing rates, increases its internal gain, and begins generating electrical activity in the absence of corresponding sensory input. This central auditory compensation is experienced consciously as sound — tinnitus.
This mechanism — peripheral damage triggering central gain elevation — is now well-supported by neuroimaging evidence. Eggermont JJ, Roberts LE. “The neuroscience of tinnitus.” Trends Neurosci. 2004 Nov;27(11):676-82. PMID: 15474168 provides an influential review of how deafferentation-driven changes in auditory cortex excitability produce the phantom percept. Critically, this central mechanism explains why tinnitus can persist even when no ongoing peripheral damage is occurring — once the central auditory system has reorganized around a pattern of heightened spontaneous activity, it can maintain the phantom signal independently.
Understanding this neuroplasticity model is essential for interpreting both the causes and the potential responses to nutritional and supplemental interventions, which we cover in our companion guide how tinnitus supplements work.
Cause 1: Noise-Induced Cochlear Hair Cell Damage
Noise-induced hearing loss (NIHL) and its associated tinnitus are the most common consequence of excessive sound exposure. The cochlea contains approximately 15,000–16,000 outer hair cells and 3,500 inner hair cells arranged along the basilar membrane. These cells — organized tonotopically, with high-frequency-sensitive cells at the cochlear base and low-frequency-sensitive cells at the apex — cannot regenerate in mammals once destroyed. Their permanent loss reduces sensory input to the auditory cortex, triggering the central gain elevation described above.
The mechanism of noise-induced hair cell damage:
Intense sound exposure forces cochlear hair cells to sustain enormous mechanical deflections. This metabolic overload generates reactive oxygen species (free radicals) that attack cell membranes, mitochondria, and DNA. Glutamate excitotoxicity at hair cell-to-auditory nerve synapses compounds the damage: excessive glutamate release during acoustic trauma destroys the ribbon synapses, causing cochlear synaptopathy even when the hair cells themselves survive. Kujawa SG, Liberman MC. “Adding insult to injury: cochlear nerve degeneration after ‘temporary’ noise-induced hearing loss.” J Neurosci. 2009 Nov 11;29(45):14077-85. PMID: 19906956 demonstrated in landmark research that a single moderate noise exposure causing only temporary threshold shift destroyed up to 50% of cochlear synapses permanently — what researchers now call “hidden hearing loss” or cochlear synaptopathy.
Who is most at risk:
- Workers in manufacturing, construction, mining, agriculture, and military service
- Musicians, concert attendees, and individuals using personal audio devices at high volumes
- Those with prior ear infections, genetic susceptibility variants affecting cochlear antioxidant enzymes, or magnesium deficiency (which amplifies noise-induced cochlear vulnerability)
The NIDCD estimates that approximately 17% of teens and 16% of adults in the United States have some degree of noise-induced hearing loss. This is the primary preventable cause of tinnitus, and hearing protection during exposure to sounds above 85 dB(A) is the evidence-supported prevention strategy.
Cause 2: Age-Related Hearing Loss (Presbycusis)
Presbycusis — age-related sensorineural hearing loss — involves the progressive degeneration of cochlear hair cells, auditory nerve fibers, and stria vascularis (the cochlea’s internal blood supply structure) over decades. This degenerative process begins in the high-frequency hair cells at the cochlear base and progresses apically with age.
Gates GA, Mills JH. “Presbycusis.” Lancet. 2005 Sep 24;366(9491):1111-20. PMID: 16182900 provides a comprehensive review of presbycusis epidemiology, estimating that over 25% of adults aged 65–74 and more than 50% of those over 75 have disabling hearing loss. Tinnitus prevalence tracks closely with presbycusis prevalence: as more hair cells are lost, more auditory cortex territory is deafferented, and the probability of central gain elevation producing detectable phantom sound increases.
Several biological mechanisms drive presbycusis:
Oxidative stress accumulation: Decades of metabolic activity generate cumulative free radical damage to cochlear mitochondria. Hair cells’ high metabolic rate and limited antioxidant reserves make them particularly vulnerable. Mitochondrial DNA mutations accumulate in cochlear cells with age, reducing their capacity to sustain the ion cycling that underlies sound transduction.
Stria vascularis atrophy: The stria vascularis maintains the endocochlear potential — the electrochemical gradient that powers hair cell transduction — by actively pumping potassium ions. Age-related degeneration of stria vascularis cells (marginal cells, basal cells, intermediate cells) reduces endocochlear potential, directly impairing hair cell function independently of hair cell loss.
Auditory nerve fiber loss: Primary neuronal degeneration — loss of spiral ganglion neurons — can occur independently of hair cell loss in aging, further degrading auditory signal transmission. This “hidden” neural presbycusis explains why some older adults with relatively intact audiograms still have significantly reduced word recognition ability and tinnitus.
Aging interacts with prior noise exposure multiplicatively: an ear carrying 30 years of cumulative noise-induced hair cell loss ages faster than a protected ear. This explains why disentangling “noise” from “age” as distinct tinnitus causes is practically impossible in many older adults.
Cause 3: Medication-Induced Tinnitus (Ototoxicity)
Over 200 pharmaceutical agents are documented as ototoxic, meaning they can damage the cochlea, auditory nerve, or both — triggering tinnitus as a direct side effect. The clinical significance ranges from mild, transient, and fully reversible to severe and permanent.
Major categories of ototoxic medications:
Salicylates (aspirin): High-dose aspirin — typically above 6–8 grams per day — is a classic cause of reversible tinnitus. The mechanism involves aspirin’s effects on cochlear prestin (the outer hair cell motor protein), arachidonic acid signaling in the stria vascularis, and ion channel function. Aspirin-induced tinnitus typically resolves within 24–72 hours of dose reduction. McFadden D. “Aspirin can potentiate the temporary hearing loss induced by noise.” Hear Res. 1984 Sep;16(2):251-60. PMID: 6510427 demonstrated that aspirin substantially amplifies noise-induced temporary threshold shifts, a clinically relevant interaction for people combining NSAID use with noise exposure.
Aminoglycoside antibiotics: Gentamicin, tobramycin, amikacin, streptomycin, and neomycin accumulate in cochlear hair cells and destroy them through iron-catalyzed free radical generation. Unlike aspirin-induced ototoxicity, aminoglycoside cochleotoxicity is typically permanent and dose-dependent. The risk is substantially increased by concurrent loop diuretic use, renal impairment (reducing aminoglycoside clearance), and genetic variants in the mitochondrial 12S rRNA gene.
Platinum chemotherapy agents: Cisplatin is the most cochleotoxic agent in clinical oncology. It causes permanent outer hair cell loss — primarily at the cochlear base, producing high-frequency hearing loss followed by progression to lower frequencies with cumulative dosing. The incidence of cisplatin-induced ototoxicity ranges from 40–80% in adults receiving standard oncologic doses. Rybak LP, Whitworth CA, Mukherjea D, Ramkumar V. “Mechanisms of cisplatin-induced ototoxicity and prevention.” Hear Res. 2007 Apr;226(1-2):157-67. PMID: 17113254 reviews the mechanisms and potential protective strategies, including antioxidant approaches being studied for hearing preservation during cancer treatment.
Loop diuretics: Furosemide, ethacrynic acid, and bumetanide — at high intravenous doses — can cause temporary and occasionally permanent ototoxicity by disrupting potassium secretion in the stria vascularis. The risk is highest with rapid IV infusion, concurrent aminoglycoside use, and renal failure.
Quinine and antimalarials: Quinine at therapeutic antimalarial doses frequently causes reversible tinnitus and hearing changes that resolve after treatment ends. Chloroquine and hydroxychloroquine can cause ototoxicity at high cumulative doses, though this is less common than retinal toxicity with these agents.
If you are experiencing new tinnitus onset after starting a new medication or increasing a medication dose, report this to your prescribing physician immediately. Dose reduction or drug substitution — when medically feasible — can halt or partially reverse drug-induced ototoxicity if caught early.
Cause 4: Vascular Causes and Pulsatile Tinnitus
Vascular tinnitus — also called pulsatile tinnitus — is a clinically distinct entity from the more common non-pulsatile continuous tinnitus caused by cochlear damage. In pulsatile tinnitus, the phantom sound has a rhythmic quality synchronized to the heartbeat, typically described as whooshing, throbbing, or pulsing rather than ringing or hissing. This rhythmic character is the diagnostic key: it indicates that a real physical sound source — turbulent blood flow in a nearby vessel — is being conducted to the inner ear and perceived as tinnitus.
Major vascular causes of pulsatile tinnitus:
Arteriovenous malformations (AVMs) and fistulas: Abnormal direct connections between arteries and veins near the temporal bone create turbulent, high-velocity blood flow audible to the cochlea. Dural arteriovenous fistulas — between dural arteries and venous sinuses — are a particularly important cause of objective pulsatile tinnitus (sound detectable by a clinician with a stethoscope placed over the patient’s skull or mastoid region).
Carotid artery stenosis and atherosclerosis: Narrowing of the carotid artery produces turbulent flow (a Venturi effect) that generates a bruit — a vascular sound audible to the patient and often to the clinician. Patients with unilateral pulsatile tinnitus and cardiovascular risk factors (hypertension, diabetes, hyperlipidemia, smoking) should have carotid Doppler ultrasound.
Benign intracranial hypertension (idiopathic intracranial hypertension / pseudotumor cerebri): Elevated cerebrospinal fluid pressure compresses the transverse venous sinuses, creating turbulent venous flow that patients perceive as rhythmic tinnitus. This condition disproportionately affects overweight women of reproductive age. The tinnitus is often accompanied by headache and transient visual obscurations.
Glomus tumors: Glomus jugulare and glomus tympanicum tumors are vascular paragangliomas arising in or near the jugular bulb and middle ear. They are highly vascular lesions that transmit their pulsatile flow directly to cochlear structures. Glomus tympanicum can occasionally be visualized as a red pulsatile mass behind the tympanic membrane on otoscopy.
High-output cardiac states: Conditions producing elevated cardiac output — severe anemia, pregnancy, hyperthyroidism — increase the volume and velocity of blood flow through the labyrinthine artery, producing pulsatile tinnitus through a purely hemodynamic mechanism without structural vascular pathology.
Pulsatile tinnitus with any headache, visual changes, or neurological symptoms warrants urgent medical evaluation. For detailed differentiation between tinnitus types and the warning signs requiring medical workup, see our tinnitus vs hearing loss guide.
Cause 5: Neurological and Central Auditory Causes
While most tinnitus originates from peripheral cochlear dysfunction, a meaningful proportion arises from or is substantially driven by changes in the central auditory nervous system — the auditory brainstem, inferior colliculus, medial geniculate body, and auditory cortex.
Acoustic neuroma (vestibular schwannoma): This benign slow-growing tumor arises from the Schwann cells of the vestibulocochlear nerve (cranial nerve VIII) — typically from the vestibular division. As the tumor grows, it compresses the auditory division of the nerve, producing unilateral tinnitus, progressive unilateral hearing loss, and often mild imbalance. Acoustic neuromas account for approximately 6–8% of all intracranial tumors. The clinical pattern of unilateral tinnitus combined with unilateral hearing loss and any vestibular symptoms requires MRI with gadolinium contrast to exclude this diagnosis.
Menière’s disease: Menière’s disease is caused by endolymphatic hydrops — excess endolymph fluid pressure within the membranous labyrinth — that episodically distorts and ruptures cochlear membranes. Classic Menière’s produces the triad of episodic vertigo (lasting 20 minutes to several hours), fluctuating low-frequency sensorineural hearing loss, and tinnitus that may vary in character and intensity between episodes. Over time, the hearing loss becomes permanent and the tinnitus typically stabilizes as a constant low-frequency roar or hissing. The cause of endolymphatic hydrops is not fully understood, but autoimmune factors, viral triggers, and anatomic variants in the endolymphatic duct are implicated.
Multiple sclerosis: Demyelinating plaques in the auditory brainstem pathways — cochlear nuclei, superior olive, lateral lemniscus, inferior colliculus — can disrupt auditory signal processing and generate tinnitus, typically in younger patients with other neurological symptoms. Tinnitus in MS is often intermittent, coinciding with disease relapse episodes.
Temporomandibular joint (TMJ) dysfunction: The TMJ is anatomically adjacent to the external auditory meatus and shares musculature and innervation with middle ear structures through the tensor tympani and tensor veli palatini muscles. TMJ disorder can alter middle ear pressure, affect tympanic membrane tension, and trigger tinnitus through somatosensory pathways that project to cochlear nucleus neurons — a phenomenon called somatic tinnitus, where jaw clenching or neck movements can modulate tinnitus loudness and pitch.
Central sensitization and tinnitus chronification: Even when the initial trigger was peripheral (noise exposure, ototoxic drug), tinnitus can become “centralized” — maintained by the brain’s own compensatory hyperactivity rather than by ongoing peripheral damage. This is why tinnitus often persists long after noise exposure ends or ototoxic drugs are stopped. The limbic system — particularly the amygdala — plays a key role: when tinnitus is perceived as threatening or distressing, amygdala-driven attention amplifies auditory cortex responsiveness to the phantom signal, making it louder and more intrusive. This emotional amplification loop explains why psychological factors, sleep disturbance, and stress strongly influence tinnitus severity independently of its physical cause.
Cause 6: Nutritional Deficiencies
Three nutritional deficiencies are specifically associated with elevated tinnitus risk and worse tinnitus outcomes through distinct cochlear mechanisms. These deficiencies are particularly prevalent in older adults — the same population with the highest tinnitus rates — and represent potentially modifiable contributors to tinnitus burden.
Magnesium deficiency:
Magnesium is essential for cochlear health through two distinct mechanisms. First, as a physiological calcium channel antagonist, magnesium promotes vasodilation of cochlear capillaries, supporting the stria vascularis blood supply that maintains the endocochlear potential. Second, magnesium ions physically block NMDA glutamate receptor channels at rest — reducing the probability of excitotoxic activation when glutamate is released in excess during acoustic stress or ischemia. When magnesium is deficient, NMDA receptors become pathologically overactive: cochlear hair cells and auditory nerve synapses are far more vulnerable to noise-induced and ischemic damage.
Attias J, Weisz G, Almog S, et al. “Oral magnesium intake reduces permanent hearing loss induced by noise exposure.” Am J Otolaryngol. 1994;15(1):26-32. PMID: 8190452 remains a landmark RCT demonstrating that oral magnesium supplementation during high-noise occupational exposure significantly reduced permanent hearing threshold shifts compared to placebo. The NIH Office of Dietary Supplements reports that a substantial proportion of Americans — particularly older adults, those with type 2 diabetes, and chronic alcohol users — have habitually low magnesium intake below the recommended dietary allowance. Our magnesium and tinnitus evidence guide provides a complete breakdown of the trial evidence.
Zinc deficiency:
Zinc is concentrated in cochlear tissue at higher levels than almost any other body organ. It serves as an essential cofactor for superoxide dismutase (SOD), the cochlea’s primary antioxidant enzyme, and plays roles in auditory nerve signal transduction and outer hair cell stereocilia function. Arda HN, Tuncel U, Akdogan O, Ozluoglu LN. “The role of zinc in the treatment of tinnitus.” Otol Neurotol. 2003 Jan;24(1):86-9. PMID: 12544032 randomized 41 tinnitus patients with verified zinc deficiency and found that zinc supplementation significantly reduced tinnitus severity scores compared to placebo — with the strongest effects in older patients. The NIH Office of Dietary Supplements zinc factsheet reports zinc inadequacy affects approximately 12% of the U.S. population, with higher rates in older adults, vegetarians, and those with malabsorption conditions.
Vitamin B12 and folate deficiency:
Vitamin B12 is required for myelin synthesis throughout the peripheral nervous system, including the auditory nerve. Deficiency causes progressive demyelination that degrades the fidelity and timing of auditory signal transmission from cochlea to brainstem — altering auditory cortex input in ways that can trigger compensatory central gain elevation and tinnitus. Lasisi AO, Fehintola FA, Yusuf OB. “Age-related hearing loss, vitamin B12, and folate in the elderly.” Otolaryngol Head Neck Surg. 2010 Jun;142(6):826-30. PMID: 20493347 found significantly lower B12 and folate levels in older adults with age-related hearing loss compared to age-matched controls with normal hearing. Folate and B6 additionally regulate homocysteine — elevated homocysteine is directly toxic to vascular endothelium, damaging cochlear microcirculation through a mechanism complementary to magnesium deficiency. For the full clinical trial breakdown by individual B vitamin, see our B vitamins and hearing guide.
Overlapping Causes: Why Most Tinnitus Is Multi-Factorial
In clinical practice, identifying a single pure cause of tinnitus is the exception. Most tinnitus in middle-aged and older adults reflects multiple overlapping contributors: a construction worker with three decades of occupational noise exposure also carries age-related stria vascularis atrophy, magnesium insufficiency that amplified his NMDA receptor vulnerability, and metabolic syndrome that impairs cochlear microcirculation. Attributing his tinnitus to one factor misrepresents the biology.
This multi-factorial reality is why comprehensive tinnitus assessment — audiological evaluation, medication audit, and nutritional status review — yields more than seeking a single cause.
What Worsens Tinnitus Even After the Initial Cause
Even when the original trigger is no longer active, several factors can substantially amplify tinnitus perception:
Sleep deprivation: Chronic sleep debt reduces GABAergic inhibitory tone in auditory circuits, increasing spontaneous auditory firing rates and making tinnitus more prominent.
Stress and anxiety: Stress-driven catecholamine release promotes auditory cortex sensitization. Elevated cortisol increases auditory cortex excitability, and amygdala activation amplifies tinnitus perception when the sound is emotionally tagged as threatening.
Loud sound re-exposure: Without hearing protection, re-exposure to loud environments continues destroying cochlear hair cells, progressively worsening both hearing loss and tinnitus.
The Role of Nutritional Supplements in Addressing Tinnitus Causes
Understanding what causes tinnitus illuminates where nutritional intervention has plausible mechanistic support. Supplements cannot reverse destroyed hair cells or undo structural cochlear damage. However, several evidence-based nutritional strategies target the modifiable elements of the causal picture:
- Correcting magnesium deficiency reduces NMDA receptor excitotoxicity and supports cochlear blood flow — addressable causes that precede hair cell death
- Correcting zinc deficiency restores cochlear SOD antioxidant activity and may improve tinnitus severity in demonstrably deficient individuals
- Correcting B12 and folate deficiency supports auditory nerve myelin integrity and reduces homocysteine-driven cochlear vascular damage
- Antioxidant support (NAC, alpha-lipoic acid, vitamin E) during active noise exposure provides cochlear protection at the window when oxidative damage is occurring
Several multi-ingredient tinnitus supplement formulas aim to address these modifiable pathways simultaneously. Our Wave-1 product reviews assess each formula’s ingredient panel against clinical evidence:
- Audifort review — mechanism coverage and dose analysis for this multi-component tinnitus formula
- Quietum Plus review — plant extract and B-vitamin combination targeting vascular and neuroprotective pathways
- Zeneara review — GABA-precursor and B-vitamin formula with central auditory support rationale
- ZenCortex review — antioxidant and circulation-focused plant extract formula
- RhythmONE review — multi-ingredient tinnitus support formula review
- Sonic Solace review — herbal and nutrient combination formula assessment
- Echoxen review — ingredient panel and mechanism analysis
For an explanation of how these mechanisms actually function at the molecular level, see our companion guide how tinnitus supplements work. Our editorial standards and review methodology are detailed on our about page; our financial relationships are disclosed on our affiliate-disclosure page.
Frequently Asked Questions
What causes tinnitus?
Tinnitus is caused by six primary categories: noise-induced cochlear hair cell damage, age-related presbycusis, ototoxic medications, vascular abnormalities causing pulsatile tinnitus, neurological changes in the central auditory system, and nutritional deficiencies in magnesium, zinc, and B vitamins. Most cases in middle-aged and older adults reflect multiple overlapping causes rather than a single isolated trigger.
What is the most common cause of tinnitus?
Noise-induced hearing loss is the most common identifiable peripheral cause, affecting approximately 15% of U.S. adults in some form according to the NIDCD. However, age-related cochlear degeneration frequently overlaps with prior noise exposure, making these two causes difficult to separate in clinical practice.
Can medications cause tinnitus?
Yes — over 200 medications can trigger or worsen tinnitus, including high-dose aspirin, aminoglycoside antibiotics, platinum-based chemotherapy agents (especially cisplatin), loop diuretics at high IV doses, and quinine derivatives. Aspirin-induced tinnitus is typically reversible with dose reduction; aminoglycoside and cisplatin cochleotoxicity is often permanent.
What does pulsatile tinnitus mean?
Pulsatile tinnitus — rhythmic sound beating in time with the heartbeat — usually indicates vascular pathology rather than cochlear hair cell damage. Causes include arteriovenous malformations, carotid artery stenosis, benign intracranial hypertension, and glomus tumors. Pulsatile tinnitus requires medical evaluation because it often has a treatable structural cause.
Can nutritional deficiencies cause tinnitus?
Yes — magnesium, zinc, and vitamin B12 deficiencies each impair cochlear function through distinct mechanisms. Magnesium deficiency increases NMDA excitotoxicity; zinc deficiency impairs cochlear antioxidant defense; B12 deficiency demyelinates the auditory nerve. These deficiencies are particularly prevalent in older adults with high tinnitus rates.
Is tinnitus caused by stress?
Stress does not directly damage the cochlea but strongly amplifies tinnitus perception through catecholamine-driven auditory cortex sensitization, vasoconstriction impairing cochlear blood flow, and amygdala-mediated emotional amplification of the auditory signal. Stress makes existing tinnitus significantly louder and more intrusive for most patients.
When is tinnitus a warning sign requiring urgent evaluation?
Tinnitus warrants prompt medical evaluation when it is: (1) unilateral — affecting only one ear, which raises concern for acoustic neuroma or other structural lesion; (2) pulsatile — rhythmic with the heartbeat, suggesting vascular pathology; (3) associated with sudden hearing loss, which is an audiological emergency; (4) accompanied by vertigo, facial weakness, or other neurological symptoms; or (5) of sudden onset after starting a new medication. See our tinnitus vs hearing loss guide for the complete red-flag checklist.
The Bottom Line
What causes tinnitus is not a simple answer — it is a matrix of six biological pathways producing the phantom sound that an estimated 50 million Americans experience. Noise-induced hair cell destruction and age-related cochlear degeneration account for most cases. Ototoxic medications, vascular abnormalities, central neurological changes, and nutritional deficiencies complete the causal picture with increasingly well-characterized mechanisms and specific implications for prevention.
The most actionable insight: nutritional deficiencies in magnesium, zinc, and B12 are common, measurable, and potentially correctable. They represent the portion of tinnitus’s causal matrix most accessible to dietary and supplemental intervention — not a remedy for existing cochlear damage, but genuine modulators of cochlear vulnerability that can be addressed without waiting for pharmaceutical innovation.
For a deep dive into how supplements target these mechanisms at the molecular level, see how tinnitus supplements work. For specific evidence on the most-studied individual nutrients, see magnesium and tinnitus evidence and B vitamins and hearing. For understanding whether what you are experiencing is tinnitus or hearing loss — and which symptoms require medical evaluation — see tinnitus vs hearing loss.
These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease. The information in this article is for educational purposes only and does not constitute medical advice. Consult a qualified healthcare professional before starting any supplement program, particularly if you have a diagnosed medical condition, take prescription medications, or are experiencing any of the warning symptoms described in this article.