"I Say 2016 Is the Year of the Ear."

I guess if this were true, this forum wouldn't be as filled as it is now. There are people having this condition for decades and whom exhausted all possible ways of "treatment" available now... There are also people who take supplements every day for years and still have Tinnitus... It isn't that simple, unfortunately.

The disappearance of your diplacusis might have been for whole other reasons we don't know of. It might be totally unrelated to the supplements.

 

the ringing noise in your ears.

 

This method (along with omega-3's) will prevent tinnitus from getting worse and if it is possible for any healing to occur than it's also worth it. Yes the high pitched ringing seems like it will be here forever, but maybe I can heal 10%? Maybe more so i also continue to take supplements

 

That's it.
If you are sensible about taking supplements and don't take excessive amounts, read about it and don't expect miracle cures it is fine.
After all the body has all these mechanisms to regulate everything.
Homeostasis I think it is called.
Like, if you take vitamin C supplements the body will get rid of all excess vitamin C. As an example that is why I think taking steroids to get extra neurotrophin-3 in the inner ear will not work.
On the other hand, I am absolutely not knowledgeable enough to comment on this.
But not being knowledgeable about something doesn't stop people to have an opinion.
I am one of those people (-;
A reason why I keep coming back to this forum is that there are people here that are knowledgeable and
sometimes take the time to correct and explain how things in the body work.
Feed our brains.

 

What is a fat? What is a protein? What is a carbohydrate?

Really what do those words mean?

Answering these questions for yourself will open the door to the knowledge to cure most health problems and create lasting health

 

Great article on the status of products in development

http://fortune.com/2016/09/26/hearing-loss-cure-biotech-startups/

 

I recovered around 15db after around 9 months by doing nothing other than taking vitamins, minerals and NAC. I'm pretty sure I'd have had the same result without the vitamins as well. In my case it was just the natural recovery process. I had two audiograms done 6 days and 2 weeks after the initial trauma, and then another around 6 months later. The recovery was mainly at 8khz whereby I went from 25db to 10db, but I also had around 5db at some other frequencies. I've got the 9 month one which I'll post here but I've misplaced the other. If I manage to find it I will post the proof here as they both include the dates.

 

Impressive... Mine is not like that

 

Interesting. Out of curiosity; did you notice any change/improvement in your Tinnitus over the last 9 months?

 

None at all unfortunately. The only improvement I've had is in the way I deal with it mentally and emotionally.

 

Err.. someone explain the -5 hearing to me. -5? lol..

 

The human hearing threshold can go up to -10. 0 is not the quietest we can hear; some go above it.

I've always had very acute hearing and could hear mosquito devices when no one else my age could. Now I can't. My hearing up to 8khz is good, but I still have loud tinnitus. Loud enough to be heard all day above pretty much everything except the shower. I also have multiple sounds ranging from hissing, to a lowish drone, and a dentist drill shrill high frequency that cuts through everything. Occasionally I get zaps around my brain and cicadas.

I obviously have hidden hearing damage, or my tinnitus is caused by upper hearing loss.

 

It might be a combination of a few things. Currently I'm thinking three things might be at play.

1. The loss of high-frequency hearing due to damage to hair cells, like you said.
2. Synaptic hearing loss (commonly referred to as "hidden" hearing loss for now).
3. Hyperactivity of tactile neurons.

I don't think hair cell damage (1) as such is a trigger or generator for Tinnitus, but hair cell damage is often found in patients with Tinnitus and therefore linked as a potential cause. Liberman however has shown that synaptic damage happens first, before hair cell damage. The synapses are much more vulnerable than hair cells and Tinnitus patients often show good audiometric results, which mainly tests the response of the hair cells instead of the synapses. Synaptic damage seems to cause trouble hearing sounds with background noise.

This leads me to think Tinnitus might be a combination of 2 and 3, where 2 is the trigger potentially leading to 3. Liberman is researching if 2 in itself might be a generator for Tinnitus and/or Hyperacusis (which might very well be) and Shore is researching the hyperactivity of tactile neurons as a result of auditory input loss (possibly by 2). This hyperactivity is difficult to correct if auditory input for certain frequencies isn't possible anymore, possibly leading to it's persistence.

This would explain your case for example, where recovery of auditory tresholds doesn't result in reduction of Tinnitus like one would expect if Tinnitus has something to do with haircells.

Just my personal thoughts however.

 

I agree @Vinnitus, I've done a lot of research on this - as I believe many of us do - and believe the most likely scenario for me is nerve damage.

This is only a small study of 15 people, but it's very relevant to my situation. You've most likely already seen this but I'll post an excerpt below:

'However, around 10% of tinnitus patients do have a normal audiogram, i.e. their hearing thresholds are in the normal range and they are thus not considered to have cochlear damage. Does this mean that their tinnitus is generated by a different mechanism, or could it be that audiometry actually failed to detect more subtle damage to structures of the inner ear?

We decided to investigate the latter scenario and recruited a study group of 15 women (average age 35 years) with tinnitus and normal hearing thresholds, and an age-matched control group of 18 women without tinnitus, also with normal hearing. Apart from classical hearing tests and tinnitus characterisation, we subjected them to auditory brainstem response (ABR) measurements.

The ABR is electrical activity generated by the first processing stages of the auditory system, and it can be measured by placing electrodes behind the ears and on the forehead. In the human ABR, five waves can be distinguished, each corresponding to responses of a different structure of the auditory system. In our analysis, we concentrated on wave I, which is generated by the auditory nerve, and wave V which arises at the level of the midbrain. We found that at high sound intensities, our tinnitus group showed a significant reduction of the amplitude of wave I, whereas the amplitude of wave V was normal.

A recently published study on mice (Kujawa and Liberman, 2009) helped us deduce which kind of damage to the cochlea could reduce the amplitude of wave I while not affecting the hearing thresholds: After noise exposure at night club sound levels (2 hours at 100 dB SPL), the mice showed a temporary shift of the hearing thresholds that recovered to normal levels within days, but there was a permanent reduction of the amplitude of wave I, similar to our tinnitus group. A closer inspection of the inner ears of the mice showed that a large fraction of their auditory nerve fibres had lost the contact to the hair cells in the cochlea, which is a bit like unplugging half the cables between an array of microphones and the sound recorder. The mice had retained just enough auditory nerve fibres to still be able to hear soft sounds, but the loss of contact between many auditory nerve fibres and the hair cells meant that for loud sounds, much fewer fibres were responding, thus reducing the total output of the auditory nerve.

How such ‘hidden hearing loss’ can lead to tinnitus can be directly understood with the help of our computer model. As a large fraction of the auditory nerve fibres no longer respond to sound, the overall signal from the auditory nerve is decreased, and therefore the nerve cells in the auditory brain receive less input and become less active overall. When these nerve cells then try to get their mean activity back up to the healthy target level, they increase their response gain and respond more vigorously to incoming signals.

This increased gain could also be seen in our human ABR data, as the amplitude of wave V was normal in the tinnitus group even though wave I (the input signal) was smaller than normal. However, a side-effect of the gain increase is an amplification of neuronal noise, which gives rise to increased spontaneous activity of the nerve cells – the model develops tinnitus.

Our results have helped me to understand my own tinnitus, which was caused by exposure to loud music in 1997. Two weeks after the festival, my hearing was tested, and my hearing thresholds were fine. In fact, they still are in the normal range today, 14 years later. However, just like the noise-exposed mice, I might have ‘hidden hearing loss’ despite normal hearing thresholds, which gives rise to my tinnitus.'

http://www.tinnitus.org.uk/tinnitus-and-hidden-hearing-loss

 

@Ed209 - how severe are your symptoms. I also fall into the "normal" hearing range to 8k. My hearing improved in the 2 weeks following my incident and I have a feeling it'd be even better now (at almost 6 months). My tinnitus has improved greatly, but it still makes me nuts.

 

My tinnitus changes daily but there is a constant baseline which is permanent. It may have been worse in the first few weeks or so, but this is hard to clarify. The reason is because our memories become distorted after months of comparing, and I have no real objective way of comparing. Although, I do distinctly remember in the early days that my symptoms would change in real time. I used to get this sound that would stop and start randomly. This is archived on this very site in my own words. I no longer have this so maybe that can be considered an improvement.

I still strongly believe that stress (cortisol) has something to do with the whole process on some level. I'll repost below something I posted a while back which I found quite interesting:

There are certain signs that stress can play an important role in tinnitus, and more studies in this area may begin to show some solid conclusive proof. There is some evidence however - scientific and anecdotal - that shows stress is a very important contributor.

A common feature of burnout syndrome, for example, is tinnitus. Why is this? You could find a relationship between excessive cortisol levels in the bloodstream - over an extended period of time - and problems with tinnitus arising or getting worse. There is certainly a lot of evidence to support this from the frequent reports of tinnitus arising after intense periods of emotional stress. Excessive cortisol is not good for us and can cause all kinds of problems if left unchecked. Another issue is that many people are simply unaware that their cortisol levels are high, as they adapt or get used to it. Stress in this instance is a hidden danger.

Here is a link explaining more on the subject; I will copy and paste the content below:
http://www.deutsche-tinnitus-stiftung-charite.de/en/projects/tinnitus_and_stress/

"Many people who suffer from tinnitus believe that stress is the cause. And first studies indicate that there is indeed a connection. What is lacking is scientific proof.
The project “Influence of emotional stress on auditory functions” (for short: “Tinnitus and Stress”) is contributing to remedying this lack. It draws on research done by the molecular biology research laboratory of the ENT Clinic and the Tinnitus Center Charité.

It is established that chronic stress can in general induce and exacerbate changes to the auditory system. They include above all the hypersensitization of auditory perception (hyperacusis), tinnitus, and Menière's disease, a disorder of the inner ear that leads to attacks of rotatory vertigo, one-sided hearing loss, and ringing in the ears.

But how does stress arise? As a rule it develops when people cannot cope with the growing and/or unexpected demands of their environment. They live under constant emotional pressure. The most frequent reaction is to deny any physical risk in an effort to enhance one's own achievement potential and staying power.

The physical effects of stress include increased production of the stress hormone cortisol. This raises the blood sugar level (gluconeogenesis) and intensifies the breakdown of stored fat (lipolysis), as well as protein breakdown (proteolysis), making more energy available. Higher blood pressure, a high pulse rate, and constipation are the result. But the immune system also suffers. Many patients complain of sleeplessness and a lack of appetite, psychomotor disturbances, and growing feelings of anxiety.

According to Professor Birgit Mazurek, “All these stress-induced mental changes can also influence auditory phenomena, leading, for example to the development of tinnitus or the exacerbation of an existing tinnitus. In the ear, cortisol causes a massive release of glutamate into the neurons. This ultimately leads to a greater accumulation of calcium, which damages auditory sensory cells and nerve cells in the ear.”

With the “Stress and Tinnitus” project, the Foundation seeks to promote research in this field to develop better individual therapeutic approaches for patients with tinnitus and hyperacusis.

The HEINZ AND HEIDE DÜRR FOUNDATION is contributing € 150,000 over a period of three years to fund the research project."

Here is another study that finds evidence of stress having a direct effect on tinnitus. Again, I will quote some excerpts below, but I highly recommend reading the whole study:

http://www.biomedcentral.com/1472-6815/12/4

"We report three novel findings that establish differences between tinnitus participants and controls in terms of cortisol hypersuppression, longer-lasting effects of the DEX test on basal cortisol levels, and hearing discomfort threshold. The first novel finding is that tinnitus participants had more strongly suppressed cortisol levels than controls after pharmacological challenge, despite similar basal cortisol levels. This is consistent with the normal diurnal and blunted response to psychosocial stress in tinnitus participants described in a previous study [23], and supports the hypothesis that tinnitus participants have greater sensitivity to HPA axis negative feedback. Hypersuppression in the presence of normal or near-normal basal cortisol levels has also been found in other clinical populations, such as patients with chronic fatigue syndrome [45–47] and burnout [48]. All these findings are consistent with the notion that basal cortisol and post-DEX cortisol suppression are mediated by two separate receptor feedback systems. More importantly, the suppression effect was independent of hearing loss. This is a key finding, because these factors are difficult to disentangle in tinnitus studies [19, 23], and it argues for a true effect of tinnitus in addition to, but unrelated to, hearing loss. Our findings therefore directly link tinnitus to a stress-related disorder, and not just to a hearing-related disorder, as some recent population studies suggest [12, 49].

The second important finding is that tinnitus participants showed a long-lasting carryover effect of cortisol manipulation. They had lower basal cortisol the day after the post-DEX day assessment compared to the two other basal cortisol assessment days, indicating not only cortisol hypersuppression, but also a longer-lasting effect of DEX administration. Although it cannot be excluded that these findings could be related to slower DEX clearance in these patients, this possibility is unlikely, because there is no rationale for altered liver function in this particular group, which moreover did not differ from controls in terms of age, BMI, or physical or mental health. Furthermore, the carryover effect was observed in the tinnitus participants approximately 36 hours after DEX administration, whereas cortisol and DEX levels should return to baseline 24 hours after oral administration of 0.5 mg DEX [50]. A likely interpretation is that the carryover effect might have been due to HPA axis homeostatic vulnerability, and that hypersuppression might have been caused by increased glucocorticoid sensitivity."

"Subjective tinnitus ("tinnitus") is the perception of sound in the ears or head in the absence of an external sound and difficult to treat. Individuals with tinnitus can experience severe emotional distress, depression, anxiety, and insomnia [1–5]. A recent study in 14,278 adults reported an overall prevalence of 25.3% for any experience of tinnitus in the previous year and 7.9% for frequent or constant (at least once a day) tinnitus [6]. Prevalence increases with age, peaking at 31.4% and 14.3% from age 60 to 69 years for these two tinnitus frequencies, respectively [6]. The increasing prevalence with age is not surprising, because hearing loss is known to be an associated risk factor for tinnitus [7]. With increasing life expectancy, and because hearing loss and noise exposure are increasingly affecting military personnel [8, 9] and youth [10], tinnitus has become a significant public health issue.

Hearing loss predicts tinnitus presence, but not severity [11, 12]. Conversely, individuals with hearing loss do not necessarily experience tinnitus. There is therefore a need to determine other factors for this debilitating hearing disorder and its consequences for health in order to better prevent and treat it. One likely candidate is stress. Because stress has long been identified as a trigger or co-morbidity of tinnitus, based mainly on anecdotal and retrospective reports, this idea has been taken for granted in classical teachings on tinnitus [13]. In addition, recent large population studies have established that emotional exhaustion and long-term stress are predictors of hearing disorders, including tinnitus [14, 15]. Functional and electroencephalographic brain imaging studies have also shown aberrant links between limbic (involved in emotions) and auditory system structures [16–18]. Structural brain differences (i.e., grey matter decrease) in tinnitus involving parts of the limbic system have also been reported. More specifically, less grey matter in the nucleus accumbens [18, 19] and the left hippocampus [20] suggests a depletion that could be related to long-term exposure to stress, among other factors."

"Our findings suggest heightened glucocorticoid sensitivity in tinnitus in terms of an abnormally strong GR-mediated HPA-axis feedback (despite a normal MR-mediated tone) and lower tolerance for sound loudness with suppressed cortisol levels. Long-term stress exposure and its deleterious effects therefore constitute an important predisposing factor for, or a significant pathological consequence of, this debilitating hearing disorder."

 

I didn't know there was 1 to 10 scale.

 

There isn't, that's -10db rather than 0db