What is causing 'Young and Healthy' people to suddenly die lately? - My theory: Inner Ear Damage!

Neurostudent

Neurostudent

Registered Member
https://pubmed.ncbi.nlm.nih.gov/24021919/

Inner ear insult suppresses the respiratory response to carbon dioxide

Compensated respiratory acidosis has been observed in a significant number of patients with active vestibular disease. We therefore hypothesized that the inner ear may play an unrecognized integral role in respiratory control. To test this premise, we investigated whether mice with induced inner ear injury demonstrated any alteration in their respiratory response to inhaled carbon dioxide (CO(2)). Experimental mice and control mice were included in two separate experiments. Intra-tympanic gentamycin injections were administered to induce inner ear damage in experimental animals. Hearing loss and vestibular dysfunction were tested 1-week after injections to confirm presence of inner ear insult, following which the animal's respiratory response to inhalation of 8% CO(2) was examined. Mice with inner ear injury (n=60) displayed a significantly diminished hypercapnic ventilatory response (HCVR). This contrasted with the normal HCVR seen in control mice that had not undergone tympanic injections (n=30), controls that received tympanic injections with saline (n=5), and controls that had gentamicin administered systemically (n=5). In response to inspired CO(2), the mean respiratory frequency of control mice increased by an average of 50% over their baseline values for both parts of the experiment. In contrast, the ear-damaged experimental group mean values increased by only three breaths per minute (bpm) (2%) in the first experiment and by 28 bpm (11%) in the second experiment. Inner ear damage significantly reduces the respiratory response to CO(2) inhalation. In addition to the established role of the inner ear organ in hearing and balance, this alludes to an unidentified function of the inner ear and its interconnecting neuronal pathways in respiratory regulation. This finding may offer valuable new clues for disease states with abnormal respiratory control where inner ear dysfunction may be present.

5.2. The vestibular nucleus and its potential link to SIDS Allen et al. developed an experimental mouse model that uses gentamicin-induced loss of hair cells in the inner ear to examine the potential relationship between auditory/vestibular and respiratory physiology (Allen et al., 2011). These gentamicin-exposed mice exhibited an attenuated ventilatory response to a hypercapnic stimulus. Post-mortem histological analysis revealed a decrease in hair cell number accompanied with a decrease in the number of large neurons within the lateral vestibular nucleus and no discernible changes in the cochlear nucleus (Allen et al., 2011). These findings not only support the potential interaction between hair cell loss and attenuated responses to respiratory stimuli, but also suggest that the mechanism leading to this deficit may involve the central nervous system at the level of the vestibular nucleus (VN).
 
Neurostudent said:
The hair cells of the inner ear contribute to most of the hypercapnic ventilatory response (HCVR) which is a good measure of chemosensitivity. The hair cells of the inner ear are also chemoreceptors, and they detect the level of carbon dioxide in the blood and send this information to the brain.

Audiology Online even says that loss of these vital hair cells can trigger death;

https://www.audiologyonline.com/releases/ears-may-hold-answers-to-4038

https://pubmed.ncbi.nlm.nih.gov/21130842/
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SIDS
Why not just start with that?
 
The stereocillia of the inner ear don't just detect sound and movement they also detect levels of carbon dioxide and oxygen in the blood, and tell the brain to make the lungs breathe. A group of scientists found this out over a decade ago, and experiments in mice proved these cells are vital for automatic breathing. These researchers said that damage to these cells can cause sudden respiratory failure and death during sleep. The inner ear's vital role in the regulation of breathing is grossly underlooked. If the inner ear hair cells are the chemoreceptors responsible for the regulation of autonomic breathing, it makes sense that a virus which is known to damage these cells may not cause death directly, but those that have incurred inner ear damage could be free of the virus for a long time before they succumb to the effects of a loss of chemoreceptor (inner ear hair cell) function. The researchers noticed that in thirty people who suddenly died of respiratory failure in their sleep, they all had hearing loss in their right ear.

In short, Covid doesn't kill these people directly, but Covid causes inner ear damage. It is then this inner ear damage which results in sudden respiratory failure during sleep, as the inner ear hair cells are the chemoreceptors involved in breathing, and researchers have said that damage to these cells alone can cause sudden death from respiratory failure during sleep, since the ears are critical for the regulation of autonomic breathing.
 
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Neurostudent said:
The stereocillia of the inner ear don't just detect sound and movement they also detect levels of carbon dioxide and oxygen in the blood, and tell the brain to make the lungs breathe.
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Your primary respiratory drive comes from chemoreceptors in your carotid body and your brainstem. They cause most of your respiratory drive.
Your backup respiratory drive also comes from chemoreceptors in your carotid body. They are backup only, and are one of the reasons that breathing patterns get so messed up at high altitude. Your breathing slows when you sleep and your CO2 receptors are fine with that, but you are no longer getting enough oxygen. Once the backups kick in you take three or four very deep breaths, which often wakes people up - leading to interrupted sleep.

The fluid in your inner ear is not blood, it is made of two types of lymph - perilymph and endolymph. Since it is not blood it cannot be used to sense oxygen or CO2 levels.

And no, people with damaged inner ears do not stop breathing and die.

Where do you get this nonsense?
 
billvon said:
Your primary respiratory drive comes from chemoreceptors in your carotid body and your brainstem. They cause most of your respiratory drive.
Your backup respiratory drive also comes from chemoreceptors in your carotid body. They are backup only, and are one of the reasons that breathing patterns get so messed up at high altitude. Your breathing slows when you sleep and your CO2 receptors are fine with that, but you are no longer getting enough oxygen. Once the backups kick in you take three or four very deep breaths, which often wakes people up - leading to interrupted sleep.

The fluid in your inner ear is not blood, it is made of two types of lymph - perilymph and endolymph. Since it is not blood it cannot be used to sense oxygen or CO2 levels.

And no, people with damaged inner ears do not stop breathing and die.

Where do you get this nonsense?
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That is out dated information. The chemoreceptors that drive breathing are not located in the medulla or carotid bodies. New (within the past 15 years) research has shown that the inner ear hair cells are what drive the respiratory response to high CO2 or low O2 levels. The inner ear hair cells detect levels of O2 and CO2 in the blood, and send this information to the respiratory centre of the brain. If these hair cells are damaged or destroyed - for example, with gentamicin, noise induced hearing loss, congenital defects, disease, etc - there can be a total loss of chemoreceptor function, even if there is no damage to surrounding neuronal structures (the researchers intentionally made sure to rule this possibility out to ensure that it is the loss of hair cells themselves that results in a loss of chemosensing.)

Perilymph and endolymph are very similar in composition to CSF. Perhaps these hair cells sense CO2 and O2 levels in the perilymph and endolymph, as a rise in bodily CO2 levels or drop in O2 levels also causes a drop or rise in the CO2 and O2 levels of the perilymph and endolymph.

I have tried several times to edit the Wikipedia articles relating to chemoreceptors and the inner ear to provide up-to-date information about the inner ear chemoreceptors, but my edits kept getting reverted, despite me providing sources from NIH and Audiology Online.
 
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Neurostudent said:
Perilymph and endolymph are very similar in composition to CSF.
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Yep. And none of them are a good proxy for gas concentrations in your blood, since they lag significantly. If you relied on sensing CO2 and/or O2 levels in either of the three you'd be quickly dead even though the ppO2/ppCO2 concentrations in those sorts of lymph were close to normal.
I have tried several times to edit the Wikipedia articles relating to chemoreceptors and the inner ear to provide up-to-date information about the inner ear chemoreceptors, but my edits kept getting reverted, despite me providing sources from NIH and Audiology Online.
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Perhaps there are some actual scientists who have wisely prevented you from posting woo?

I'd try Facebook. Their standards are far lower.
 
billvon said:
Yep. And none of them are a good proxy for gas concentrations in your blood, since they lag significantly. If you relied on sensing CO2 and/or O2 levels in either of the three you'd be quickly dead even though the ppO2/ppCO2 concentrations in those sorts of lymph were close to normal.

Perhaps there are some actual scientists who have wisely prevented you from posting woo?

I'd try Facebook. Their standards are far lower.
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This is not true since mice whose ears were damaged using gentamicin only increased their breathing rate by 2% in response to 10% CO2.

The mice with undamaged ears increased their breathing rate by up to 60%.

The authors of that study, T Allen, Reubens, et al, later went to the media concluding that these hair cells not only detect sound and movement, but that they are respiratory chemoreceptors which detect levels of carbon dioxide and O2.

Audiology Online had a related article on this, stating that damage to these inner ear hair cells can trigger death, as these cells are 'pivotal' for regulating breathing.
 
Neurostudent said:
This is not true since mice whose ears were damaged using gentamicin only increased their breathing rate by 2% in response to 10% CO2.
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From the Mayo Clinic, gentamicin side effects include:
  • difficult or troubled breathing
  • irregular, fast or slow, or shallow breathing
So you don't need to make up a secondary reason to explain changes in breathing after exposure to heavy doses of that antibiotic.
 
billvon said:
From the Mayo Clinic, gentamicin side effects include:
  • difficult or troubled breathing
  • irregular, fast or slow, or shallow breathing
So you don't need to make up a secondary reason to explain changes in breathing after exposure to heavy doses of that antibiotic.
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To rule out side effects being the cause, they did the CO2 challenge 8 days after they injected gentamicin into the mouse's ears.

When just one ear was injected, the mice lost almost 50% of their chemosensitivity. When both ears were injected, they lost virtually all of it.
 
billvon said:
Yep. And none of them are a good proxy for gas concentrations in your blood, since they lag significantly. If you relied on sensing CO2 and/or O2 levels in either of the three you'd be quickly dead even though the ppO2/ppCO2 concentrations in those sorts of lymph were close to normal.

Perhaps there are some actual scientists who have wisely prevented you from posting woo?

I'd try Facebook. Their standards are far lower.
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Makes a change from people being choked by their own thymus glands, or spontaneous combusting though, eh? :D

This is Gaiagirl/Frank Baker/Faceurchin etc etc etc, i.e. the bizarre death scenarios obsessive, back again.
 
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