We have had numerous posts which have questioned whether ear/hearing issues are (or can be) associated with hypothyroidism.
This accessible paper, despite having a small number of subjects, is pretty clear that there is much association. Two sentences:
"The most common symptom of hypothyroidism with regard to ear, nose, and throat is hearing insufficiency accompanied with cochlea-vestibular symptoms such as tinnitus and dizziness. "
"It was found that hypothyroidism affects the ear at multiple sites producing various types of hearing impairment − namely, conductive, sensorineural, and mixed."
The effect of L-thyroxine hormone therapy on hearing loss in
hypothyroid patients
Mohammed M. Hussein a, Samir I. Asal b , Tarek M. Salem c, Ahmed M. Mohammed a
a Departments of Otorhinolaryngology,
b Audiology, c Endocrinology Unit, Department of Internal Medicine, Faculty of Medicine, University of Alexandria, Alexandria, Egypt
Correspondence to Samir Ibrahim Asal, Assisstant Professor of Audiology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt. Tel: 012245 49955;
e-mail: samir_asal @yahoocom
Received 11 May 2017
Accepted 11 May 2017
The Egyptian Journal of Otolaryngology
2017, 33:637–644
Objective
The aim of this work was to study whether or not the hearing loss encountered in some hypothyroid patients can be improved with L-thyroxine hormone therapy, as other symptoms of hypothyroidism.
Study design
The study design was a prospective cohort one.
Patients and methods
This study included 30 patients of either sex who were proved to be in a hypothyroid state with an additional symptom of hearing impairment. The study was carried out in Alexandria Main University Hospital and was conducted in a prospective manner.
All selected patients were proved to be in a hypothyroid state in the Endocrinology Department. Moreover, their symptom of hearing impairment was confirmed by thorough audiological examination supplemented by pure-tone audiometry plus tympanometry that was carried out in the ENT Department and the associate Audiology Unit. L-thyroxine treatment for hypothyroidism was initiated in all cases for 6 months to maintain a state of euthyroidism. At the end of 6 months, a repeat audiogram and tympanometry were performed in all patients in order to evaluate the efficacy of the said treatment protocol on the hearing in these patients. Cases proved to have hearing impairment irrelevant to the hypothyroid condition were excluded. Informed consent was compulsory for recruitment in this study.
Results
Post-treatment assessment revealed that variable improvement was achieved in 48% of ears, whereas 52% did not respond to the given treatment, with the impairment remaining nearly the same as it was before. Of the improved ears, in 15% of ears hearing levels were restored to normal hearing levels. Thereby, adherence to replacement therapy may reverse the hearing deficits in a few number of hypothyroid patients.
Conclusion
There is a definitive improvement in hearing with the use of L-thyroxine treatment of hypothyroid patients with hearing impairment.
I'm kicking myself, because a few years ago I found a study which showed that childhood ear problems/ earache are very possibly an early indication of RTH ....cannot find it right now. Grrrr!
I was that child...severe earache then: RTH now.
My hearing has now deteriorated ( as a result?) so I'm wondering if the high dose T3 I take to overcome RTH may stop further decline....given that, with good conversion the LT4 used in the above study would have converted to T3!
I suspect that's my fate too....could be worse!Audiologist said I should wear the hearing aid more....then I discovered she could track how often I wear the b****y thing!
Really?!? I didn't know that! I hate mine, they hurt my ears. And, the audiologist is a very charming man, but pretty useless! I eventually gave up on him, and I'm waiting to win the pools to get myself better hearing aids because these are rubbish! They don't help much at all.
Yes, I was told I should wear them more often, and things would improve, but I didn't find that to be true at all. Nothing improved.
My tinnitus is hugely 'pacified' by wearing a H Aid - wearing at least 16-17 hrs daily, not sure mine is 'trackable' via NHS [can't be bothered with other chronic stuff ].
NHS tracking!? Hey, nothing would surprise me I use CPAP and that now definitely 'tracks' when sleep, wake... Beware 🐍😅 Such a shame the really useful stuff isn't!
Resistance to thyroid hormone (RTH) caused by mutations of the TRB gene can cause hearing problems because the TRB1 receptors are expressed in the liver, pituitary, some bits of the brain and in the developing inner ear and retina. This is different to hearing loss caused by loss of the fine hairs in the ear that transmit sound.
Here are two relevant papers, I haven't read either.
A study that suggests the TRB1 receptor is cruical to development of hearing doi.org/10.1172/JCI6397 .
A study of hearing loss in RTH patients doi.org/10.1210/jcem.81.8.8... . Without reading the paper I get the impression that RTH hearing loss is permanent because the ear fails to develop properly.
Dippydame, I don't think TRB RTH applies to you as patients present with elevated fT3 / fT4 and a non-suppressed TSH.
This paper, though, does identify multiple loci of impairment - not just hairs:
Once it was accepted that there is a relationship between hypothyroidism and hearing loss, the location of the affected part in ear has been subject to many new studies, which showed that one or multiple parts such as endocochlear, retrocochlear, or central hearing ways might be affected.
Dippydame, I don't think TRB RTH applies to you as patients present with elevated fT3 / fT4 and a non-suppressed TSH.
Agree, I think that was ruled out some time ago but something else is causing my RTH....otherwise I'd be dead now given the amount of T3 it takes to keep me functioning!!
Geneticist suggested an as yet unknown variant.
My point really, was that severe earache in children has been shown to indicate RTH in later life (that source exists somewhere, I rely too much on my raddled old brain!!) and could that also suggest later hearing impairment.
You mention "retina" ....but breath easy, I won't start on my inherited bad eyesight...now known 4 generations back!
My sons used to say, many years ago, " Mum you have wonky genes"!!
Which is an issue that makes me very wary of current genetic tests such as DIO1 and DIO1 - even if they look at all known variants of both.
It seems improbable that there aren't many genetic variants which, individually or in multiple combinations, result in RTH (or other thyroid issues).
Where we are right now means that not having the known DIO1/DIO2 variants can all too easily be taken as evidence of not having any genetic basis. (Not that you or I would do so. ) Thus, not having RTH or whatever is being considered.
I am glad your geneticist actually said that - and I'd hope those trained in the discipline would be very careful. Others might not be so thoughtful.
The studies into deiodinase genes look at common polymorphisms and how they affect levothyroxine therapy. There are no doubt rarer mutations that have different effects.
RTH (or 'genetic RTH' as I prefer to call it) is a consequence of mutations to the thyroid hormone receptor genes (TRα and TRβ) that affect the ability of T3 to bind to receptors. I coined the term 'acquired resistance to thyroid hormone' (ARTH) to refer to forms of RTH caused by endocrine disrupting chemicals (EDCs). I believe ARTH is common, at least in minor forms, but this is not recognised because although endocrinologists are aware of EDCs they are reluctant to look for their effects in patients - presumably because it is more challenging than just looking at a blood test.
There are no doubt rarer mutations that have different effects.
Not sure we can claim they are, individually, rarer? There is an awful lot yet to be understood about combinations. It is so much easier to identify a single SNP, go through a bit of statistical analysis, and shout "Eureka!", than to discern that certain complex combinations exist, let alone their effects.
Listened to a radio program the other day which discussed how the pervasiveness of atmospheric lead pollution was identified, reported, and ignored. Taking until 2018 for Yemen to ban it - despite many other countries getting rid of it many years ago.
(The UK was somewhat behind many other countries. Even after many vehicles could use unleaded, such fuel wasn't widely available for a considerable period.)
Lead was an awful lot simpler to identify and even to remove from its primary source than many of the other endocrine disrupting compounds which exist.
I can't guarantee there are as yet unfound polymorphisms butstudies refer to 'common' ones implying they are aware of others. I feel pretty sure there are other less common polymorphisms as genes have a habit of mutating. Whether they are clinically relevant is another matter.
In any event my view is that the deiodinase polymorphisms are a bit of a red herring, if someone was previously well then they should be well if their fT3, fT4 are restored to normal levels. Frequently this does not happen, they need higher doses of T3 than a healthy thyroid secretes. Therefore, the problem must be something more than a deiodinase polymorphism.
I like the route you are taking there - but isn't it possible at least some people can manage to make lots of T3, equivalent to what they take as T3, until they can't? And that could be how they always were. After all, many never have a thyroid test of any sort until things go downhill.
That’s what I did with my children, especially the three daughters. I had them all take a baseline test to find their “healthy normal” levels so if/when anything should go wrong, they’ll know what’s “normal” for them.
Surprisingly close, but not identical and certainly nothing like mine as I'd already developed Hashimotos. My eldest was 26 when I developed Hashi's and their ages (for the girls at least) were 5 years apart from each other, so I guess the eldest had her first test at around 29, the middle one was 24 and the youngest was 19. My son was 27. The eldest two daughters have since had further tests (early morning) which did show a marked increase in TSH in them both, but the FT3 and FT4 readings were still pretty well in range so I've just told them to keep an eye on them. The middle daughter is a qualified midwife which comes in very handy for private venous blood draws!
Hmmmm yes!When the endo I saw briefly was sniffy about my having any form of RTH ( despite at that point coping well with high dose T3) I mentioned acquired resistance....he just looked at me, shook his head and said nothing.
They are reluctant to look further than their crib sheet for diagnosing...
I had diffiiculty hearing people in crowded environments which resolved when my hypothyroidism was treated. We lose the fine hairs in the ear causing hearing impairment, they may regrow when the hypothyroidism is treated.
I definitely had very bad hearing impairment and it greatly improved on Levothyroxine and ND, the tinitus persists. My colour vision was also affected and has recovered with thyroid hormone treatment.
That's interesting re colour vision. When under an intense period of stress at age 11 my daughter lost the ability to see certain shades of green. It all resolved itself within 10 days of the stressful situation being resolved.
How strange, I wonder if high stress chemicals affect colour vision. Mine was as if allThe colour was drained out of everything a sort of brownish dingy world. It was amazing as the colours came back as if someone turned the lights back on.
I have been complaining of hearing issues for years. Then in 2011 I developed tinnitus after having flu for 3 weeks. I am now under an absolutely brilliant NHS audiologist. She has identified that I have a different type of hearing loss. I can hear the sound when someone talks, but I have difficulty working out what they are saying. Its particularly bad trying to work out what people are saying in groups. It definitely seems to be thyroid related. Cognitive impairment springs to mind.
You do not surprise me. I can see analogies to the impact of hypothyroidism on sight/vision.
I have long found it extremely difficult to use a phone held to my right ear - but my left is OK. Despite the fact that if I try to compare/contrast the sound, I cannot identify any actual difference. (The left/right difference seemed minor when tested.)
(I've had tinnitus for many years - seemed to start when I was about 8 years old and, while it has varied, it has never gone away.)
My tinnitus varies through the day. As I'm dosing T3 5x a day, it seems reasonable is connected. For example, tinnitus is screaming at me at the moment. But I took my 10am dose 90 minutes late. My tinnitus will calm down in a bit. Also seems to be related to hunger??? Not as illogical as it sounds, as the body needs food for processing of thyroid hormones. I'll go and have breakfast and it'll go away. OK, I know, breakfast at 12:35 😆 but then I didn't wake until 11:15 and I've been reading your very interesting posts since then! I really must get up.
We see so many foreign papers, etc., that CBC seems to be working its way into UK use.
Although I am loath to see NHS charging for anything, it is extremely disappointing that we don't usually have an option to get lab tests done by our local NHS labs even if we pay.
I know a few people have been offered phlebotomy for a fee (and others have had it done without any fee - most often alongside NHS blood draws). Also that Exeter and Black Country Pathology services make their services available on a commercial basis. But it doesn't seem a big ask for phlebotomy and/or tests to be done for a fee based on cost plus a small profit. Especially if they can manage their workload so as not to impact on existing services. (Maybe even reduce costs by increasing volume - thus getting a better per test rate from suppliers.)
If done like this, the results should optionally be put onto our NHS records. Thus potentially reducing NHS costs by avoiding repeats of tests that have already been done.
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