Can you cure tinnitus?

Soundbites cannot be expected to restore hearing. Untreated hearing trauma and hearing loss causes tinnitus.

Soundbites was not designed to treat tinnitus, the beep or ringing that seems to be in the ears. Tinnitus may start with damage to the ear, but persistent tinnitus actually originates in the brain. Tinnitus is a neurological disorder.

Preserving hearing helps prevent tinnitus because the data say hearing loss associated with damage in the inner ear is responsible for about 80% of the cases of tinnitus.


We set out to preserve hearing, not to cure tinnitus. However, anecdotal case report evidence collected since early 2015 suggests a correlation of ongoing use of Soundbites with reduced tinnitus symptoms.


Tinnitus can often start with exposure to high intensity noise, an environmental stress factor that causes damage which can lead to cell death.  


High intensity noise can cause:

  • damage to micro-mechanical properties of sensory transducers (hair cells)1.

  • changes in blood flow in the ear

  • modification in intracellular ion transport properties

  • depletion of sensory cell transmitter substances (e.g. glutamate)2.

  • changes in post synaptic membrane transmitter receptors (e.g. gluR) on afferent nerve fibers (axons)3. of afferent neurons (sensory neurons)4.

  • modification of dispersion and uptake properties of neurotransmitters in extracellular, synaptic spaces

  • changes in postsynaptic membrane biophysical properties that may affect space-and time-constant properties modifying depolarization

  • changes of an excitotoxic nature in postsynaptic membranes causing destruction of afferent neural tissues.

We have two likely theories to explain how Soundbites might be working to treat chronic tinnitus (tinnitus that persists for a long time or constantly recurs.) 

  • Mostly we have focused on the Magnesium (Mg) component in the ACEMg formulation. Mg increases blood flow to the inner ear, removes waste and increases oxygenation of tissues, helping the cells of the inner ear to work at a higher level of efficiency generally.

  • With exposure to loud noise, blood flow to the inner ear decreases, resulting in less efficient cellular function that can lead to tinnitus. One theory is that by blocking the decrease in inner ear blood flow, Mg is preventing the decreased functionality and the resulting tinnitus.

  • Mg is also a calcium blocker. Loud sounds activate a high level of activity of hair cells (inner ear hearing cells), causing the hair cells to release an excess of the neurotransmitter glutamate at their base. The glutamate neurotransmitter activates the post membrane terminals of the neurons that transmit activity to the brain through long, slender axon nerve fiber projections of the nerve cell.

  • The opening of pores in the post membrane terminals allows excess calcium to flow into the terminals and with that water, which causes them to swell and sometimes to burst. The process is referred to as excitotoxicity. The temporary or permanent loss of localized bundles of auditory nerve fibers may cause the tinnitus that is associated with loud noise.

  • In some cases, some auditory nerve fibers may repair with rest (no exposure to loud sounds). In other cases, they cannot.

  • Mg as a calcium blocking agent can prevent excitotoxicity, thus preventing the damage to auditory nerve fibers that causes tinnitus.

  • It is thought that with chronic long term tinnitus the pathology moves to more central locations in the brain and may not be affected by this proposed Mg mechanism.

  • The vitamin component ACE and tinnitus may play a significant supporting role. Excess free radicals can cause release of excess glutamate neurotransmitter. Since ACE eliminates free radicals and the subsequent release of excess glutamate, the vitamins may also be helping prevent excitotoxicity and attenuate tinnitus.

  • In addition, high noise or intense sound levels demand greater activity of the mitochondrial respiratory chain to create ATP5.  . Greater demand for ATP results in excess free radical formation.

  • Typically in the normal ear under normal stress the endogenous antioxidant systems are sufficient to maintain normal homeostatic function of the inner ear, but under high levels of stress the increased free radical formation may contribute to excitotoxicity and will damage DNA and further, through the process of lipid peroxidation6., destroy inner and extracellular membranes.

  • Any one or more of these changes can result in modification of spontaneous activity in individual or small populations of afferent nerve fibers, leading to temporary loss in hearing sensitivity, distortions of sounds, muffling of sounds, perception of tinnitus. and permanent hearing loss associated with cell death.

We are vitally interested using the Soundbites real world studies to assess Soundbites efficacy to reduce or prevent temporary and permanent tinnitus.