Solsaem Clinic (Dr. Minbo Shim) Experience
- Thread starter JohnAdams
- Start date
- Status
Member
Would you get that service in the US from a shitty ENT? no. Would the BTA and ATA lobby for that novel treatment? no.
You'd have to beg for a predisone steroid which a GP would laugh and say no.
Yeah there's a nasty paradigm in western civilization right now. They restored hearing in gerbils 7 years ago and haven't followed through with humans yet. They haven't even tried. why? I showed you that study about IGF-1, why isn't that happening? I'm so confused.
I would. I would donate so much.
- May 29, 2015
- 664
- 30
- Tinnitus Since
- 2012
- Cause of Tinnitus
- I had tinnitus for as long as I can remember. Got bad later.
"The application of IGF1 maintains hair cell number of postnatal mammalian cochleae after various kinds of ototoxicity including aminoglycoside treatment, noise exposure, and ischemia. The positive effects of IGF1 on hair cell damage have been confirmed with in vivo animal experiments; hearing recovery in patients with sudden sensorineural hearing loss refractory to systemic glucocorticoid treatment has also been shown to occur following IGF1 treatment."
"Patients (n = 120) were recruited from nine tertiary referral hospitals in Japan and were randomly selected to receive either gelatin hydrogel impregnated with IGF1 on the round window membrane (62 patients) or intra-tympanic injections with Dex (58 patients)."
"In the IGF1 group, 66.7% (95% CI, 52.9–78.6%) of the patients showed hearing improvement compared to 53.6% (95% CI, 39.7–67.0%) of the patients in the Dex group."
"A trend, however, was observed: a higher proportion of patients with ≥30 dB HL improvements in pure-tone average hearing thresholds was measured for the IGF1 group than in that the intra-tympanic steroids group."
" In this trial, no adverse events were observed."
Source:
Insulin-like growth factor 1: A novel treatment for the protection or regeneration of cochlear hair cells
IGF-1 by itself is not approved for eardrum injections in clinical applications. However, there are sources for it in the human body.
One is bone marrow:
"MSCs isolated from different tissues, such as bone marrow, adipose tissue, placental chorionic villi, and fetal membranes, express and secrete IGF-1 and/or IGF-2 in vitro. It was shown that ectopic IGF-1 expression in MSCs enhances their proliferation with lower apoptosis."
Source:
The Roles of Insulin-Like Growth Factors in Mesenchymal Stem Cell Niche
Another source is Platelet Rich Plasma:
"The growth factors and other cytokines present in PRP include:
- platelet-derived growth factor
- transforming growth factor beta
- fibroblast growth factor
- insulin-like growth factor 1
- insulin-like growth factor 2
- vascular endothelial growth factor
- epidermal growth factor
- Interleukin 8
- keratinocyte growth factor
- connective tissue growth factor"
Now if we just knew of someone that had bone marrow and PRP injected into their ears to see if they have reported any reduction in tinnitus or improvements in hearing loss.
It would be really nice if @David from the BTA would take note of this.
Maybe @Steve can tell him since they know each other. This could help so many people. I'm not trying to be a prick or anything. It's just obvious that IGF-1 is a scientifically validated intervention for acute stage noise damage, and potentially even for chronic stage.
"The application of IGF1 maintains hair cell number of postnatal mammalian cochleae after various kinds of ototoxicity including aminoglycoside treatment, noise exposure, and ischemia. The positive effects of IGF1 on hair cell damage have been confirmed with in vivo animal experiments; hearing recovery in patients with sudden sensorineural hearing loss refractory to systemic glucocorticoid treatment has also been shown to occur following IGF1 treatment."
"Patients (n = 120) were recruited from nine tertiary referral hospitals in Japan and were randomly selected to receive either gelatin hydrogel impregnated with IGF1 on the round window membrane (62 patients) or intra-tympanic injections with Dex (58 patients)."
"In the IGF1 group, 66.7% (95% CI, 52.9–78.6%) of the patients showed hearing improvement compared to 53.6% (95% CI, 39.7–67.0%) of the patients in the Dex group."
"A trend, however, was observed: a higher proportion of patients with ≥30 dB HL improvements in pure-tone average hearing thresholds was measured for the IGF1 group than in that the intra-tympanic steroids group."
" In this trial, no adverse events were observed."
Source:
Insulin-like growth factor 1: A novel treatment for the protection or regeneration of cochlear hair cells
IGF-1 by itself is not approved for eardrum injections in clinical applications. However, there are sources for it in the human body.
One is bone marrow:
"MSCs isolated from different tissues, such as bone marrow, adipose tissue, placental chorionic villi, and fetal membranes, express and secrete IGF-1 and/or IGF-2 in vitro. It was shown that ectopic IGF-1 expression in MSCs enhances their proliferation with lower apoptosis."
Source:
The Roles of Insulin-Like Growth Factors in Mesenchymal Stem Cell Niche
Another source is Platelet Rich Plasma:
"The growth factors and other cytokines present in PRP include:
https://en.wikipedia.org/wiki/Platelet-rich_plasma
- platelet-derived growth factor
- transforming growth factor beta
- fibroblast growth factor
- insulin-like growth factor 1
- insulin-like growth factor 2
- vascular endothelial growth factor
- epidermal growth factor
- Interleukin 8
- keratinocyte growth factor
- connective tissue growth factor"
Now if we just knew of someone that had bone marrow and PRP injected into their ears to see if they have reported any reduction in tinnitus or improvements in hearing loss.
It would be really nice if @David from the BTA would take note of this.
Maybe @Steve can tell him since they know each other. This could help so many people. I'm not trying to be a prick or anything. It's just obvious that IGF-1 is a scientifically validated intervention for acute stage noise damage, and potentially even for chronic stage.
It seems like the research was done for people with very recent onset of hearing loss. How long after your hearing problems did you go to do this procedure?
8.5 months.
But just because the subjects may have been in acute stage doesn't mean it would be ineffective for chronic stage. And even if so, if this was accepted as a treatment, we could easily have gone to the doctor as soon as we had our acoustic trauma and got something like this to recover. So if anything, acute patients need something like this, which they cannot legally get, and further studies need to be conducted for chronic patients.
@JohnAdams congratulations for your bravery, life is the take action , and you did it, that is a very respectful act of you. Thanks also for sharing your thoughts and improvements, the easy would be stay away from all this and you are here posting your experience, this is of inmense help to give us the information to evaluate any potential treatment.
Thanks a lot coleague!
Thanks a lot coleague!
@JohnAdams I think the IGF-1, which should regrow hair cells, and neurotrophin, which regrows synapses or nerve cells (study here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842978/), would be an even better combination. Do you think he would be able to obtain neurotrophin and inject it as well?
Excerpt:
The primary degeneration of cochlear nerve synapses will eventually lead to death of the spiral ganglion cells in the absence of intervention1, however, the death of the cell body and central axon takes months to years1, during which time the neurons likely remain electrically excitable, given that cochlear implants continue to function for years after hair cell loss. Thus, there may be a long therapeutic window within which to regenerate the peripheral axons and/or synaptic connections in cases where the hair cells remain intact.
It has been argued that the permanent loss of spontaneous and sound-driven activity in a subgroup of cochlear nerve fibers leads to a central gain readjustment that drives hyperactivity in central auditory pathways and thereby causes tinnitus5.
Thus, there is likely a significant clinical population with some degree of hearing impairment (or tinnitus) that could be addressed by a treatment analogous that used here in noise-exposed mice56. The present experiments show that round window delivery can be effective local access route to the inner ear, even for a protein as large as NT-3 (13.6 kD molecular weight). Here, we used a poloxamer, a thermoreversible hydrogel that is liquid at 4 °C but gels at body temperature, to extend the drug delivery time57, which is important for a molecule like NT-3 with a short half-life once it enters body fluids58. Prior studies have seen biological effects of neurotrophins delivered to the round window using a variety of slow-release strategies59.
Although the success of local NT-3 delivery in regenerating cochlear synapses when administered 24 hrs post exposure is an important proof of concept, many key questions remain, most importantly how long after the insult can neurite extension and synaptogenesis still be elicited.
Excerpt:
The primary degeneration of cochlear nerve synapses will eventually lead to death of the spiral ganglion cells in the absence of intervention1, however, the death of the cell body and central axon takes months to years1, during which time the neurons likely remain electrically excitable, given that cochlear implants continue to function for years after hair cell loss. Thus, there may be a long therapeutic window within which to regenerate the peripheral axons and/or synaptic connections in cases where the hair cells remain intact.
It has been argued that the permanent loss of spontaneous and sound-driven activity in a subgroup of cochlear nerve fibers leads to a central gain readjustment that drives hyperactivity in central auditory pathways and thereby causes tinnitus5.
Thus, there is likely a significant clinical population with some degree of hearing impairment (or tinnitus) that could be addressed by a treatment analogous that used here in noise-exposed mice56. The present experiments show that round window delivery can be effective local access route to the inner ear, even for a protein as large as NT-3 (13.6 kD molecular weight). Here, we used a poloxamer, a thermoreversible hydrogel that is liquid at 4 °C but gels at body temperature, to extend the drug delivery time57, which is important for a molecule like NT-3 with a short half-life once it enters body fluids58. Prior studies have seen biological effects of neurotrophins delivered to the round window using a variety of slow-release strategies59.
Although the success of local NT-3 delivery in regenerating cochlear synapses when administered 24 hrs post exposure is an important proof of concept, many key questions remain, most importantly how long after the insult can neurite extension and synaptogenesis still be elicited.
Last edited:
Liberman et al. wrote that. If it is that simple to regenerate just to inject, why is the drug still in "Drug Discovery" phase of Decibel Therapeutics?
https://www.decibeltx.com/pipeline/
There is a reason those bright minds at Decibel Therapeutics have decided to not yet initiate Phase 1 trials with Neurotrophins...
https://www.decibeltx.com/pipeline/
There is a reason those bright minds at Decibel Therapeutics have decided to not yet initiate Phase 1 trials with Neurotrophins...
It very well may work for one better than the other because of the circulation in the cochlea in my opinion.If Dr. Shim's treatment works for high and low frequency hearing loss we can rest assured that many of us will be booking our flights there this upcoming summer
The chart on his website seems to show better results with lower frequency regeneration.
A rule of thumb since my tinnitus onset was that if I didn't sleep at least 8 hours my tinnitus would be horrible all day the next day without fail. I had to be at work at 6 AM today so I only slept for about 6 hours. I sat in a very quiet room that had sound proofing panels on the wall for 11 hours. My tinnitus was seriously 1% of what it normally is and I could plug both of my ears and not hear any tinnitus. My right ear has been that way for about a month and my left ear has been humming along, at a lower volume, until today. It has kinda came back a little in my left ear but not significantly at all. I do still have slight hyperacusis though.
- May 7, 2015
- 1,050
- Tinnitus Since
- 29.09/2014
- Cause of Tinnitus
- Acoustic trauma using headphones
I feel like I can distinguish between sounds such as like on talk radio and there's some music or other sounds in the background. Yes music sounds better and clearer.
I'm still not 100%. I wish this never had happened to me in the first place. I still had to avoid my son running around and playing last night. He has this toy dump truck and when he shuts the dump part it makes a loud sound and I felt bad having to tell him to stop and getting away from him. I still feel like my quality of life is being impacted by hearing damage in a way that makes me feel like I'm living a nightmare.Fucking super happy to hear it, man. Thoroughly deserved too
- Nov 25, 2015
- 1,705
- Tinnitus Since
- 11/2015
- Cause of Tinnitus
- Large caliber rifles&machine guns, +30 years of loud clubs
Avoiding further damage is the worst part of this curse.
Good to read that you are having improvements - this clinic is not too far from where I live so it's on my radar for sure
Good to read that you are having improvements - this clinic is not too far from where I live so it's on my radar for sure
John Adams, thank you for your reports. I admire your tenacity. I have a couple of questions if you might be kind enough to reply. Are you suggesting your tinnitus is 1% of what it was previously? Also, I see you say you have slight hyperacusis. Was your hyperacusis slight before the treatment or has the treatment improved your hyperacusis?
Thanks.
Thanks.
@JRC1
"Are you suggesting your tinnitus is 1% of what it was previously?"
Yesterday during the day it was. Around 9Pm the highest frequency aspect of the sound that's around 13-14khz or so, started kinda creeping back. This morning it was like it was as it was last night, but now, ~1:30 PM, it's back to that 1% mark, with some tiny fluctuations in the HF sound. Like it's coming and going. Before I went to Korea it never did that. It used to be the same from the time I woke up pretty much until the next day. My theory on that is that my brain, despite having the ability to hear these frequencies better is still stuck on generating the tinnitus sound in the absence of me hearing them and that's why I can residually inhibit so well, like for hours.
I welcome any thoughts about this.
"Also, I see you say you have slight hyperacusis. Was your hyperacusis slight before the treatment or has the treatment improved your hyperacusis?"
Hyperacusis didn't set in for me until about 3 months in, about the same time as my eye floaters. From about fall of last year until my trip, my hyperacusis started getting horrendous and fluctuating from not too bad to bad. I didn't really have any hyperacusis before, and during my trip to Korea. About a week after I got back it started to return. I have had a handful of bad hyperacusis days since I've been back. Right now as I type this, I have none. It is still too early to tell what if any effect it has had on my hyperacusis.
I welcome any thoughts about that as well.
"Are you suggesting your tinnitus is 1% of what it was previously?"
Yesterday during the day it was. Around 9Pm the highest frequency aspect of the sound that's around 13-14khz or so, started kinda creeping back. This morning it was like it was as it was last night, but now, ~1:30 PM, it's back to that 1% mark, with some tiny fluctuations in the HF sound. Like it's coming and going. Before I went to Korea it never did that. It used to be the same from the time I woke up pretty much until the next day. My theory on that is that my brain, despite having the ability to hear these frequencies better is still stuck on generating the tinnitus sound in the absence of me hearing them and that's why I can residually inhibit so well, like for hours.
I welcome any thoughts about this.
"Also, I see you say you have slight hyperacusis. Was your hyperacusis slight before the treatment or has the treatment improved your hyperacusis?"
Hyperacusis didn't set in for me until about 3 months in, about the same time as my eye floaters. From about fall of last year until my trip, my hyperacusis started getting horrendous and fluctuating from not too bad to bad. I didn't really have any hyperacusis before, and during my trip to Korea. About a week after I got back it started to return. I have had a handful of bad hyperacusis days since I've been back. Right now as I type this, I have none. It is still too early to tell what if any effect it has had on my hyperacusis.
I welcome any thoughts about that as well.
@JohnAdams i feel happy for you! The fact that your tinnitus is fluctuating, and is 1% of what it was, it is a big success in my personal opinion and personally (I think that there is regeneration going on in your auditory system.
Let us know how everything keeps going but I thanks a lot for keep with sharing with us your news, it is very brave from your part and please feel happy for your progress!
Let us know how everything keeps going but I thanks a lot for keep with sharing with us your news, it is very brave from your part and please feel happy for your progress!
Somethings happening. I don't know if I lost hair cells, or just synapses, or just wore out certain nerves or what. Those growth factors I received heal many different tissues, and at this point, relating to the inner ear, nobody is sure about anything. Maybe I had any combination of these conditions: Dead haircells, dead supporting cells, destroyed ribbon synapses, damaged auditory nerves, dead nerves. I have my own ideas, and I know something is definitely happening, but I am not exactly sure what. There are those conditions above mixed with the various things I received from my PRP and marrow injections. I also had some dex shots. Did the growth factors in my PRP and marrow initiate healing in my damaged or dead haircells? Did they heal my synapses? Did the stem cells in my bone marrow do those things by some action alone or in conjunction with the growth factors? Did my tinnitus start changing around within the window of my recovery period by coincidence?
My opinion right now is that my acoustic trauma resulted in hair cell damage and subsequent damage resulting in changes to my nerves' connections to the sensory cells and that higher than normal exposure to certain growth factors involved in healing have stimulated some kind of healing response and my brain is just slowly readjusting. There's also a process called paracrine that may have been involved. If you want to know more about paracrine just google it.
- Status
Log in or register to get the full forum benefits!
Similar threads
