Antioxidants May Slow Progression of Genetic Hearing Loss in Children
15 Mar 2016
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15 Mar 2016 --- An enhanced diet containing Vitamins A, C, E and magnesium is likely to help curb hearing loss due to genetic abnormality that is most commonly responsible for childhood deafness, new US research suggests.
A diet with added nutritional supplements 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 percent of all genetic hearing loss and 10 percent of all childhood hearing loss.
"Many babies born with a genetic mutation that causes deafness pass their newborn screening test but then lose their hearing later in life," says author Glenn Green, M.D., associate professor of pediatric otolaryngology at C.S. Mott Children's Hospital.
"These patterns suggest that for some children, there may be an opportunity to potentially save cells present at birth. For these childhood cases it's crucial that we identify therapies that prevent progression and reverse loss of hearing.”
"These patterns suggest that for some children, there may be an opportunity to potentially save cells present at birth. For these childhood cases it's crucial that we identify therapies that prevent progression and reverse loss of hearing.”
“Our findings suggest that a particular high dose of mineral and vitamin supplements may be beneficial to one genetic mutation,” said one of the authors Yehoash Raphael, professor at the Michigan University.
However, 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 postnatally 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.
This 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.
"These findings are encouraging for those of us who treat children with progressive connexin 26 hearing loss, and possibly for other mutations not yet tested," says 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."
Antioxidants have been shown to reduce the impact of oxidative stress in neuronal disorders, cancer, heart diseases and inflammatory diseases.
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