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Health Protocols

Hearing Loss and Tinnitus

How Hearing Loss Occurs

Over the years, scientists have gained a better understanding of how noise can damage the auditory system, particularly a part of the inner ear known as the cochlea. The cochlea contains specialized nerve cells, known as hair cells, which help translate sound waves into interpretable signals for the brain. Loud sounds damage hair cells through direct mechanical trauma and secondary metabolic damage. Direct mechanical trauma typically causes immediate structural damage to cochlear hair cells and can potentially cause immediately detectable hearing loss. The metabolic effects of loud noise, however, can accumulate for days or even weeks after initial sound exposure (Oishi 2011).

Loud noise affects metabolism in hair cells by decreasing oxygen supply and increasing energy demands. Loud noise can disrupt the flow in blood vessels that supply oxygen to hair cells, depriving these cells of nutrients needed to function and leading to cell damage through a process known as ischemia. At the same time, the increased stimulation due to noise forces the hair cells to be metabolically more active. The end result is that, during this period of intense stimulation, these hair cells burn through their energy reserves, resulting in the formation of reactive oxygen species (ROS). These ROS have the ability to damage proteins and lipids and can ultimately lead to death of the hair cells (Henderson 2006).

Hair cells may also be damaged by inflammatory mediators known as cytokines. Animal studies have found an increase in certain pro-inflammatory cytokines in response to loud noise. These cytokines include interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), two compounds that can be toxic to nerve cells at high levels (Fujioka 2006). In addition, overstimulation of hair cells can cause them to release large amounts of the neurotransmitter glutamate. Although glutamate release is needed to help translate sounds into neurological signals, too much glutamate can result in significant “excitotoxicity”, in which excessive stimulation damages nerve cells (Pujol 1999).