Can Nutritional Supplements Cut Genetic Hearing Loss in Children?

Can Nutritional Supplements Cut Genetic Hearing Loss in Children?

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A recent study has revealed that an enhanced diet can help reduce hearing impairment in mice when a genetic transmutation is the cause of deafness in children.

The research discovered that an antioxidant regimen of beta-carotene (precursor to vitamin A), Vitamin C and E as well as magnesium aided in the slow progression of genetic deafness in mice with a deletion of connexin 26 gene. Transmutations in this gene are chiefly responsible for hereditary hearing impairment in many people.

In the meantime, it was also discovered that improved diet had the reverse effect on another mutant mouse modeled onAUNA1 – not a typical type of hearing impairment – researchers from the University of Michigan’s Kresge Hearing Research Institute andU-M’s C.S. Mott Children’s Hospital said.

Glenn Green, the study author, M.D., as well as associate professor of pediatric otolaryngology at C.S. Mott Children’s Hospital, said that many babies born with a genetic transmutation responsible for deafness pass their newborn screening test, but then in their later stages of life experience hearing loss. Such patterns hint towards the fact that for some children there could be an opportunity to potentially save cells active during the time of birth. For these childhood cases, it is extremely vital that therapies are discovered which prevent progression and undo hearing impairment.

Yehoash Raphael, the senior author, Ph.D., and professor in the Department of Otolaryngology-Head and Neck Surgery at the Michigan Medical School University further added by saying that their findings indicate that a high dosage of a particular vitamin and mineral supplements may prove helpful for one genetic mutation.

However, the unwarranted results in the AUNA1 mouse model indicate that different mutations may respond to the special diet in multiple ways.

During the research, the mice received the antioxidant regimen in the postnatal phase and in utero in other experiments. In the connexin 26 mouse model, the improved diet was linked to a slower progression of hearing impairment and small but significant development in hearing thresholds. But mice having the AUNA1 gene mutation faced the opposite outcome, i.e. exhibiting accelerated development of deafness after the diet.

In the inner ear, lowering oxidative stress connected with overstimulation has proven to protect sensory hair cells and hearing, points Josef Miller, the author and U-M professor emeritus, Ph.D., who developed the formulation based on micronutrients.

It is a proven fact that antioxidants reduce the impact of oxidative stress in neuronal disorders, heart diseases, cancer and inflammatory diseases – according to Miller. The treatment based on antioxidant has also been shown to protect gap junctions, which are the cellular components bearing direct relationship with the loss of connexin 26.

These study results have brought a ray of hope for those of us who treat kids suffering from connexin 26 hearing loss and probably for other mutations not yet put to the test, mentioned Green. “Further studies are needed to confirm these findings in children and to explore whether oral administration of antioxidants could someday be considered as an effective treatment.”

The new research is based on a case study the University of Michigan released in the preceding year in which the similar nutritional supplements were linked with slowing the development of deafness for a boy having a connexin 26 mutation.