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Author: admin, 30.08.2015. Category: Cure Ringing Ears

New research from Yale University reveals that genetically reducing AMPK activity delays hereditary hearing loss in mice.
While more research is needed, the study results point to possible strategies for preventing or treating deafness associated with mitochondrial dysfunction and aging in people. An enhanced diet is likely to help curb hearing loss due to genetic abnormality that is most commonly responsible for childhood deafness, new research suggests. A study found that an antioxidant regimen of beta carotene (precursor to vitamin A), vitamins C and E and magnesium helped slow progression of hereditary deafness in mice, with a deletion in Connexin 26 gene —a protein found on the gene and the most common cause of innate hearing loss. Connexin 26 alterations are responsible for at least 20 per cent of all genetic hearing loss and 10 percent of all childhood hearing loss. But, the enhanced diet had the opposite effect on another altered mouse modelling with auditory neuropathy — a rare type of hearing loss. The negative outcome in this mouse model suggested that different mutations might respond to the special diet in different ways, the researchers noted. Mice in the study, published in the journal Scientific Reports, received the antioxidant regimen post-natally and in the womb in separate experiments. In the Connexin 26 mouse model, the enhanced diet was associated with a slower progression of hearing loss and small but significant improvement in hearing thresholds. However, the mice with auditory neuropathy experienced the opposite outcome, showing accelerated progression of deafness following the diet. The research follows a case study University of Michigan published in 2015 in which the same nutritional supplements were associated with slowing the progression of deafness for a boy with a Connexin 26 mutation. Antioxidants have been shown to reduce the impact of oxidative stress in neuronal disorders, cancer, heart diseases and inflammatory diseases. As we age, our ears are exposed to a lifetime of noises such as lawnmowers, telephones, industrial machinery, leaf blowers, chain saws, industrial noise, hair dryers, weapons, and recorded and live music. Have you been exposed regularly to loud noise at work, during recreation or in military service? Sensorineural hearing loss occurs when tiny hair cells within the inner ear (the cochlea) are damaged. The most common sensorineural hearing loss is a high-frequency hearing loss, typically associated with aging or noise exposure, and often both.
Conductive hearing loss most often results from a blockage of the normal air conduction sound pathways.
People with untreated hearing loss (people with hearing loss who do not wear hearing aids) experience a decreased quality of life.


In a new study, a Yale-led research team successfully applied genetic modification to delay inherited hearing loss in mice. Shadel, the collaborative research team genetically altered mice to develop a model of hearing loss caused by a defect in mitochondria (specialized compartments within cells). The absence of this molecule appears to be responsible for noise-induced hearing loss, one of the most common causes of deafness. Please see your physician or an audiologist if you suspect that you or a family member may have a hearing loss. Sensorineural hearing loss is permanent and in most cases there are no medical or surgical treatment options.
High-frequency hearing loss may be difficult for patients to “self-diagnose” because it occurs slowly over decades.
Conductive hearing loss may be due to ear wax (cerumen) blocking the ear canal or perhaps a foreign object may be lodged in the ear canal.
As its name implies, it involves both sensorineural and conductive hearing loss components.
Untreated hearing loss has been shown to cause sadness, depression, anxiety, paranoia, and poor social relationships. Hearing loss in these mice was found to involve dysfunction in specialized tissues in the inner ear. Although hearing loss is often associated with aging, hearing loss is clearly present in newborns, children, teenagers, young adults and adults.
Persons with high-frequency sensorineural hearing loss often note they can hear, but they cannot hear clearly. Another example of a conductive hearing loss is when fluid occupies the middle ear space, as might occur with common ear infections (otitis media). People with untreated hearing loss may have a difficult time in their careers—often earning thousands of dollars less than their hearing peers. The research team determined that activation of a stress-response enzyme called AMPK triggered this dysfunction. Healthy human ears can perceive an enormous range of sounds in terms of pitch and loudness and it is a vital link for communicating with others.
Causes for acquired hearing loss include a genetic predisposition, ear disease, noise exposure (including music, industrial, military and more), ototoxic medicines, head trauma, and others.
In some situations, such as when hearing aids have not been beneficial for particular patients with severe and profound sensorineural hearing loss, these people may benefit from cochlear implantation.


They may say “people don’t speak as clearly as they used to…” These are common observations from people with high-frequency sensorineural hearing loss. However, the difference in wages between people with untreated and treated hearing loss is reduced by half, when people wear hearing aids. Genetically reducing AMPK activity (by knocking out one of its genes) had no impact on mice with normal hearing, but delayed or prevented hereditary hearing loss in the deafness-model mice. Audiometric tests performed on individuals with mutations in this gene subsequently revealed an unusually high level of diversity in hearing impairments, in terms of both severity and characteristics.
Their observations revealed an astonishing variation in hearing impairments from one mouse to the next, ranging from mild to profound hearing loss.
Young mice are highly vocal for the first three weeks after they are born, particularly when feeding. The scientists observed that as the number of mice in the cage increased, so did their hearing threshold - the minimum sound level at which they are able to hear sounds.
Using direct, controlled acoustic stimulation, the scientists were able to prove that the auditory system of mice lacking in pejvakin is affected by their acoustic environment.The scientists then set about investigating the physiological causes of this phenomenon. They observed that in mice without pejvakin, the auditory sensory cells are damaged as soon as they are exposed to even seemingly harmless sounds - the equivalent of a minute spent in a nightclub for humans. The scientists also identified the noise-sensitive element in the cell as being the peroxisome, a small organelle involved in detoxification.
When a standard hearing test was performed on these hearing-impaired individuals, the responses of their auditory sensory cells and neurons, although normal to begin with, gradually worsened as the test went on as a result of the sounds used.Noise-induced hearing loss is becoming increasingly prevalent. Urban crowding means that large cities are getting noisier, particularly in developing countries.
WHO predicts that by 2030, one billion people will be at risk of noise-induced hearing loss. However, we don't yet know what percentage of the population is either lacking in pejvakin or has a less effective form of the protein.



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