Researchers have linked a hormone known to adjust levels of key brain chemicals to the quality of our hearing as we age. The more of the hormone that older people have in their bloodstream, the better their hearing is, and the less of the hormone, the worse their hearing is.
The hormone, aldosterone, is known to regulate kidney function and also plays a role in controlling levels of two crucial signaling chemicals in the nervous system, potassium and sodium. For nerves to send signals crisply and work properly, potassium and sodium must be in precise proportion, without any disruption in the molecular channels or gates through which they move. Levels of potassium are particularly crucial in the sensitive inner ear, where fluid rich in potassium plays a central role in converting sounds into signals that the nervous system recognizes.
The team of scientists in Rochester, N.Y., put 47 healthy men and women between the ages of 58 and 84 through a battery of sophisticated hearing tests. Scientists also measured their blood levels of aldosterone, which is known to drop as people age. They found that people with severe hearing loss had on average about half as much aldosterone in their bloodstream as their counterparts with normal hearing. The researchers noted, however, that the levels of aldosterone found in all the participants is considered normal, and that no patients or physicians should consider altering aldosterone levels without more research.
The findings come from researchers at the International Center for Hearing and Speech Research (ICHSR), a group funded by the National Institute on Aging that is recognized as a leader in research on age-related hearing loss. The center includes scientists from the National Technical Institute for the Deaf at Rochester Institute of Technology and neuroscientists from the University of Rochester.
"The inner ear is especially sensitive to any disruption in potassium levels," said Robert D. Frisina, Ph.D., professor of Otolaryngology at the University of Rochester Medical Center and an adjunct professor at Rochester Institute of Technology. "We know that potassium levels in the inner ear seem to decrease as we age and that these falling levels play a role in age-related hearing loss, and we also know that blood levels of aldosterone generally decrease with age.
"We found a direct link between blood levels of aldosterone and the ability of people to hear normally as they age. Depressed hormone levels may hurt hearing both in the inner ear and the part of the brain used for hearing. More research is needed, however, to understand the precise role that aldosterone plays -- for instance, whether it's a cause of failed hearing, or whether it's symptomatic. Before we understand the issue more fully, people should not worry about their aldosterone levels or look to boost the amount in their bloodstream."
The team led by Frisina published its results in the November issue of the journal Hearing Research. This week at the annual international meeting of the Association for Research in Otolaryngology in Baltimore, the team presented its latest results showing just how important potassium regulation is to age-related hearing loss.
In Baltimore, Otolaryngology medical resident Jared Spencer, M.D., presented results from "knockout" mice whose genes controlling the potassium channels in the inner ear don't function properly, and confirmed that malfunctioning potassium channels are central to age-related hearing loss, or presbycusis. The channels are highly concentrated in a part of the brain that plays an important role providing feedback from the brain to the ears. Frisina's team previously discovered that the feedback system is one of the first things to go wrong in age-related hearing loss, often declining in people who are in their 40s and 50s, usually before they even realize their hearing is declining.
"We are now working out some of the underlying biology about how the decline occurs," said Frisina. "We have evidence that these potassium channels may play an important role in the failure of the feedback system, which is a big part of age-related hearing loss."
Nearly everyone wrestles with failing hearing at some point. While some people suffer from hearing damage as a result of exposure to loud noise, or from other causes such as the side effects of some medications, for many people hearing problems occur with no known cause. Some people notice problems in their 40s and 50s, but the process becomes very noticeable for most people in their 60s and older.
Frisina said that until the biology of the problem is better understood, the best advice for people concerned about hearing loss is to limit exposure to loud, damaging noise and to medications that are toxic to the ears. He also counsels people to eat healthy and to exercise -- "all those things you know you should be doing to stay healthy with age," he said.
Meanwhile, his team is looking at the possibility of using gene therapy to try to correct the problem. It may be possible some day to modify a person's inner ear to correct the potassium imbalance that is central to hearing loss. Such an approach might also address the biggest cause of congenital deafness, which involves a genetic mutation that mucks up the potassium balance in the inner ear.
The new findings come from a research group founded by Robert Frisina's father, D. Robert Frisina, Ph.D., founding director of NTID, who heads one of the largest research groups in the world studying age-related hearing loss. The group has attracted top researchers from around the world to come together to study the problem. Members of the group, which numbers more than two dozen, hail from Egypt, Brazil, Russia, China, Korea, India, and the United States.
In addition to Frisina, Frisina and Spencer, the team includes post-doctoral research associate Sherif Tadros, M.D., of both the University and NTID, who is first author of the Hearing Research paper; research nurse Susan Frisina of both NTID and the University; audiologist Frances Mapes of NTID; and otolaryngologist Xiaozia Zhu, M.D., of the University.
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