Friday, November 30, 2007

Natural Strategies for Preventing Hearing Loss

I wonder if this would apply at all to people with DS who have hearing loss? I know much of hearing loss in DS is due to fluid in the ears, etc. But, still, this is interesting.

Natural Strategies for Preventing Hearing Loss

Alarmingly, nearly half of all baby boomers today suffer from some degree of hearing loss. While its onset can be almost imperceptible, the end result is an impaired ability to interact with the world that significantly detracts from quality of life.

For more than 20 years, leading otolaryngologist Dr. Michael Seidman has been searching for the underlying causes of age-related hearing loss and for natural strategies to prevent and even reverse this debilitating condition. His remarkable research and clinical experience shows that it is now possible to slow the progression—and sometimes even reverse hearing loss—using an integrative approach that includes optimal nutritional and lifestyle choices.

In the following excerpt from Save Your Hearing Now (Warner Wellness, 2006), Dr. Seidman reveals the intimate link between aging andhearing loss, and how you can implement a program today to protect your hearing against the ravages of aging.

After treating hundreds of patients suffering from hearing loss— and seeing the devastating effects it had on their lives—I decided to look for a natural solution. Knowing that antioxidants counteract the damage caused by free radicals, I thought there might be a way to use those same safe, natural substances to protect and/or restore hearing.

But first, the fact that there was a link between free-radical damage and hearing loss had to be established.

So the first study my colleagues and I conducted was designed to find out if there was a connection between damaged hearing in humans and the common hearing loss seen with aging. To measure free-radical damage, scientists can look for certain “markers,” chemical or cellular signposts that indicate change within a cell. In humans, one of these markers is known as the common aging deletion.

It is a sign of both advancing years and free-radical damage to the DNA of tiny organelles within each cell known as mitochondria.

From previous research in our lab and by others, we knew four things:

  1. Common aging deletions accumulate as we grow older.

  2. Blood flow to the cochlea, home to the nerve endings that make hearing possible, decreases as we age.1

  3. At the same time, our hearing apparatus becomes less sensitive.2,3

  4. As we age, our bodies produce more free radicals and fewer of the antioxidants that protect our hearing from free-radical damage.4

To test the theory that aging damages hearing and common aging deletions are a sign of that damage, we examined the temporal bones (those found at the sides and base of the skull) of thirty-four individuals, seventeen with normal hearing and seventeen who had age-related hearing loss. Temporal bones house the cochlea, the snail-shell-shaped organ responsible for hearing, and this is why we focused on that particular area. We found the common aging deletion in fourteen of the seventeen individuals with hearing loss and in eight of those with normal hearing.

Why didn’t the deletion appear in all seventeen of those with hearing loss? And why did it appear in bones of people whose hearing was fine? At least two reasons: The common aging deletion is only one type of hearing loss. It could be that other deletions contribute to hearing loss, too. In addition, there are four different types of age-related hearing loss.

The common aging deletion may not be responsible for all four. At any rate, this study provided us with enough evidence to conclude that the common aging deletion is associated with aging and hearing loss.5

Supporting the First Findings

The link between aging and hearing loss was underscored by our next study. It involved a number of rats, which were divided into four age groups: young, mid-young, mid-old, and old. We tested the sensitivity of rats’ hearing and examined their DNA for the common aging deletion, to determine if there was an association between the two.

We found that, like humans, rats tend to have higher levels of the common aging deletion as they grow older, and they have an increased tendency to develop hearing loss as well.6

Now we had established that the aging process resulted in an increase in common aging deletions, which weakened the mitochondria and damaged hearing. But could the damage be slowed, prevented, or possibly even repaired with supplements of naturally occurring antioxidants?

That’s the question we set out to answer with two additional studies. In one clinical trial, we followed animals from approximately several months old to the day they died. One group received a calorie-restricted diet, shown to reduce free-radical production, reduce mitochondrial damage, and to increase life span.

For purposes of comparison, a placebo-controlled group was allowed to eat freely. Other groups were treated with antioxidants, including vitamins E and C, and the hormone melatonin. With this study, we demonstrated that free radicals and damage to the mitochondria that occurs with aging leads to presbycusis, the medical term given to agerelated hearing loss.

Furthermore, we were able to demonstrate that dietary moderation and specific nutrients reduce the progression of age-related hearing loss, and we concluded that it is likely that a combination therapy would provide a synergistic protective effect on presbycusis and possibly on aging as well.7

But even more dramatic results occurred in our next clinical trial. In this study, we used twenty-one two-year-old rats, senior citizens in the rodent world, and divided them into three groups of seven each.

For six weeks, one group was given ALC (acetyl-L-carnitine), the second was given ALA (alpha-lipoic acid), and the third group, used as a control, received a placebo (sugar pill).

When we tallied the results, it was clear that hearing in the control (placebo) group had deteriorated at a rate typical for animals of that age. But that didn’t happen with either group of supplemented animals. Instead, we discovered the ALA and ALC did something pretty amazing. The supplemented rats not only avoided hearing loss, but their hearing actually improved. In other words, supplements didn’t just stop age-related hearing loss—they reversed it!8

During the study, the control group lost anywhere from 3 to 7 dB of hearing, while the ones treated with ALC or ALA had a 7 to 10 dB improvement in their hearing, with the greatest improvements occurring after six months of treatment. While the ALA was more effective for protecting hearing at low frequencies, ALC did better at higher frequencies. We demonstrated that taking both supplements is the best way to protect against hearing damage in general.

Of all the research I’ve done, I consider this study the most important. It clearly demonstrates that hearing loss can be prevented—and even reversed—by simply taking a combination of antioxidants that includes ALA and ALC. Both these substances have been popular in Europe for some time, and are widely considered nontoxic, very effective in treating hearing loss, and also capable of providing overall antiaging and wellness benefits.

But there is another reason this study stands out. Medical research is full of surprises. Sometimes what makes perfect sense on paper just doesn’t work in the lab. Other times we are literally astonished by the unanticipated benefits. That’s what happened in this particular study. Along with improved hearing in the supplemented animals, we found a much lower level of common aging deletions in the mitochondria all throughout the body.

The supplements actually reduced the amount of free-radical damage everywhere, creating an antiaging effect that improved hearing and carried over to other cells throughout the body. In other words, we had proven that age-related hearing loss can be reversed in mammals, with allnatural, side-effect-free substances.

Although this research was groundbreaking at the time, other scientists have since shown that ALA, ALC, and various other substances, including the antioxidant coenzyme Q10 (CoQ10) and glutathione, provide substantial protection for the mitochondria and thereby support healthy hearing.

How Aging Affects Hearing

Age-related hearing loss affects approximately one-third of all people aged sixty-five and older. Technically known as presbyacusia or presbycusis, age-related hearing loss is due to the changes that occur in the body as we grow older. Circulatory disorders, for example, which limit the flow of blood throughout the body, as well as to the brain and auditory system, are common in later years.

There are any number of reasons why circulation slows down as we grow older, among them heart disease, hardening of the arteries, diabetes, and sedentary lifestyles.

My research and that of many colleagues clearly show that the same things that protect us from the damage done by passing years also prevent damage to our hearing. In order to understand how hearing can be saved by slowing the clock, let’s take a look at the aging process and what happens in the body, especially the auditory system, as time passes.

Aging Begins in the Cells

During a normal lifetime, our cells divide anywhere from twenty to thirty times. This ongoing process of cellular expansion turns a child into an adult, and then cell division slows. Ultimately, because of inherent limits, our cells are no longer able to divide.

So although we continue to need new cells, later in life our bodies are not as efficient as they once were at producing them. The result: Disease or malfunctions occur because faulty cells are not replaced with fully functional versions.

In addition to the inherent limitations on new cell production, other factors are thought to play a role in aging. There are several different theories about the process, including the free-radical or mitochondrial clock theory, dysdifferentiation theory, and the telomerase theory. Thus far, the free-radical theory hasthe widest acceptance.

The Enemy: Free Radicals

In simplest terms, a free radical is an unstable molecule or cluster of molecules that is missing an electron. Like mini-atomic bombs, free radicals damage or destroy cells they come in contact with.

Free radicals are by-products of everything from eating to living in a world filled with toxic chemicals and pollution. In other words, they are unavoidable.

Although some free radicals are actually beneficial, others damage healthy cells. Free radicals can cause errors in genetic “messages” by altering DNA (deoxyribonucleic acid, the “blueprint” that governs cell growth).

This can, among other things, lead to a reduced blood supply to organs such as the inner ear and brain, thereby damaging hearing. When one of these loose cannon free-radical molecules binds with a healthy cell, it wreaks havoc on the cell’s ability to function. Mother Nature did not leave us completely defenseless, though.

Our bodies produce enzymes known as antioxidants—such as superoxide dismutase (SOD), catalase, and glutathione peroxidase—to counteract the damage. We can also obtain antioxidants from certain foods and supplements.

But if inadequate production or a poor diet results in a shortage of antioxidants, cellular damage may not be repaired, and sooner or later, we become ill. There have been many studies documenting that free radicals are responsible for more than a hundred human diseases, including Alzheimer’s, cancer, heart attacks, strokes, and arthritis, as well as aging.

Even though free radicals are microscopic and exist for far less time than it takes to blink an eye, they are capable of doing considerable damage simply because of their sheer numbers.

According to research at Emory University, each human cell receives approximately ten thousand free-radical hits each day. Further calculations have shown that this equals 7 trillion (7,000,000,000,000!) insults per second throughout our bodies.9

Certainly, 7 trillion is a staggering number, but the body counteracts this assault with its own arsenal of antioxidant enzymes. Unfortunately, there is a significant decline in these enzymes as we grow older. In fact, we now know that by the time the average person reaches the late twenties, production of these detoxifying enzymes has declined dramatically.

Based on the findings of scientists studying free radicals and human health, the best approach to slowing aging is one that provides the body with plenty of antioxidant ammunition against free radicals.

That means increasing intake of antioxidants, something that can be done in part with the proper diet or, more effectively, by taking supplements.

The Mighty Mitochondria

To measure free-radical damage, scientists can look for certain “markers,” chemical or cellular signposts that indicate change within a cell. In humans, one of these markers is known as the common aging deletion.

It is a sign of both advancing years and free-radical damage to the DNA of tiny organelles within each cell known as mitochondria. About 98 percent of our body’s energy is produced in mitochondria, so they are often described as the cells’ powerhouses. A number of studies have shown that the functions of the mitochondria decrease with age, leading some experts to speculate that this may be why many people feel less energetic as they grow older.

The hardworking mitochondria also serve as the cells’ “gatekeepers,” with the power to determine whether a cell lives or dies, so it’s doubly important to keep the mitochondria healthy.10

The mitochondria have their own DNA, which is completely separate from the DNA found in the cells. When free radicals ravage the cellular DNA, it can be repaired, but the mitochondria’s cannot. The mitochondria can be weakened or may even die, creating a slowdown in many essential processes. Even an incredibly small mutation in the mitochondrial DNA can dramatically slow energy production.

In fact, the drop in mitochondrial activity is the basis of the free radical or mitochondrial clock theory of aging. According to this theory, the aging body increases its production of free radicals, which damage the body’s tissues and subcellular elements, such as the mitochondria.

When we see the common aging deletion in mitochondria, we know the cells’ little energy factories aren’t fully functioning.

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