Listen Up! The Connections Between Hearing Loss, Hearing Interventions and Cognitive Decline

Dr. Nathaniel Chin: Welcome back to Dementia  Matters. Today I'm joined by Dr. Frank Lin, director of the Cochlear Center for Hearing and  Public Health and professor of otolaryngology, medicine, mental health, and epidemiology at  Johns Hopkins University. Dr. Lin's research has established the association of hearing  loss with cognitive decline and dementia and has served as the basis for the 2020 Lancet  Commission on Dementia's conclusion that

hearing loss is a leading modifiable risk  factor for dementia. Today he joins us to talk about the NIH-funded Aging and Cognitive  Health Evaluation in Elders study also known as ACHIEVE – very clever – which he serves as  the co-principal investigator on. In July 2023, Dr. Lin published his study in the Lancet,  which investigated whether treating hearing loss through different hearing interventions  could reduce the risk of cognitive decline and

dementia in older adults. So Dr. Lin, welcome  to Dementia Matters. So to begin, what made you interested in studying modifiable risk factors  for dementia, but especially hearing loss? Dr. Frank Lin: You know Nate, this all began like,  I don't wanna go too far back, but you know I did my residency in ENT surgery many, many years ago,  and then at that time I had always had a large

bent toward public health. Both my parents are  public health researchers. I always liked surgery because you get something done and it was a lot  of fun, but as I went through my residency though, I'll tell you one clinical observation which  always jumped down at me more than anything else, was that if I showed you or you saw an audiogram  and it showed basically a mild to moderate loss, which is not uncommon, but that audiogram  belonged to an eight year old – let’s

say an eight year old girl – that would be  critically important. You gotta address it, most insurance companies will cover it. All of a  sudden, you scratch off like Annie and now she's not eight and now she's 88. All of a sudden  it's met with a collective shrug saying like, “Oh yeah, you have a mild to moderate hearing  loss. You know, Annie, you could do something about if you want.” That always jumped out at  me as a huge, well massive, clinical paradox.

How could the same physiologic impact on hearing  be critically important for an eight year old but not for an 88 year old? Part of that was guided,  too, by my grandmother. My grandmother had early adult life hearing loss related to streptomycin .  She got streptomycin many years ago, so she always has lived with essentially a more marked hearing  loss than other people would, but I always grew up with her and I always understood, I saw, witnessed  the impact that it had like on her daily life,

her daily conversations. I couldn't help but think  that that same Annie, eight-year-old audiogram, and my grandmother, how could it not be important  and yet the research was never – well I should say the clinical impression was always that  it meant nothing. As I delved a little deeper into it and developed some collaborators at  the National Institute on Aging and at Hopkins, where I'm based, they’re like, “You know  Frank, you're right. There's actually

just not any research on it,” right?  It's just an empirical clinical guess, probably because it's so common, hearing loss,  but there actually wasn't any research on it.

his next-door neighbor happened to be one  of my mentors. He's an ophthalmologist, epidemiologist and David Freeedman, my colleague,  said, “You know, Frank, you would really benefit from just bouncing some ideas off Luigi”. I  was like, “Okay”. [Laughs] So I met Luigi and

that's where this all began. I mentioned to  him at that point, there was actually – this is crazy to say this – in 1988 or 89, there was a  case-control study published in JAMA so classic, bread-and-butter epidemiology, a case-control  study of hearing and dementia published in JAMAublished in JAMA1989 showing a dose-dependent  relationship between greater hearing loss severity and odds of dementia. From 1989 until when  I came across the paper in 2009, nothing had

been done. No further research. I mean, you  just put in Google Scholar, people cite it, but there's nothing done. Yet, everything would  point toward giving a case-control study at the lowest level of sort of epidemiologic evidence.  What do you do next? You do a longitudinal study, you go from there, blah, blah, blah, blah. It  was never done and I think I had to do a lot with these silos. You know, for me, I'm an ENT  surgeon. I know everything about hearing and now

I understand a lot about dementia. Back then I  understood a little bit, I entered into public health, I had done my PhD at the School of Public  Health, but people weren't thinking about that, and people in the dementia, neurology  space understood nothing about hearing, right? So it's a classic effect of silos, and  it just happened that I was able to bridge that silo with Luigi, who was interested  in collaborating, and I was interested in

collaborating. Then the rest is sort of  the last 15 years of my life actually.

hearing loss and the odds of dementia, but it’s  a case-control study. What the track of research that I began around 2010 in collaboration with  Luigi Ferrucci and colleagues at the NIA was beginning to look at that in deeper depth using  longitudinal studies, right? So next step,

longitudinal study, observational studies of older  adults beingfollowed for many many years. In the BLSA, the Baltimore Longitudinal Study of Aging,  one of the longest ongoing studies of aging in the United States funded internally by the NIA,  coincidentally they had measured hearing on their participants in the early 90s. They did it for  a few years until – I'm not joking – the booth broke, the audiometer broke, and they said,  “Ah no, one's using the hearing data anyway,

let's just stop doing it,” right? But for four  years they had very good hearing data. And then, coincidentally – not coincidentally – a big  feature of the BLSA study is to focus on aging, especially neurological outcomes, so they  had adjudicated dementia diagnoses as well, tracked longitudinally with people followed every  two or three years. So the analysis – I got to

tell you – is just simple. We did an analysis of  looking at baseline hearing, looking at the risk, basically the hazard of incident dementia over  time, adjusting for and controlling for age and

sex and diet– pretty much any other confounder  you could think of we adjusted for. And we saw in that study, which was published in 2011  – back when it was Archives of Neurology, now it's called JAMANeurology – no surprise  compared to the case-control study, a dose-dependent effect between greater hearing  loss and the risk of being diagnosed with dementia

over time. And I say dose-dependent because it was  market. It was basically, compared to people with normal hearing, people with a mild, a moderate,  or severe hearing loss basically had a twofold, a threefold, and a fivefold increased hazard or  risk of dementia. Those are huge risk estimates, as we all know. I'll be honest, when Luigi and I  first saw this, it was sort of like an exciting, but “oh no” sort of moment as we’re saying, “Do  we really believe this?” right? But you know we

did all the sensitivity analyses and it all held  up no matter what we did with analyses. It was published in JAMA Neurology, Archives of Neurology  back then, in 2011. We were a little guarded about it actually, like “What's gonna happen?”. As you  know the hallmark of good science though, Nate, is just replication, replication from people who  you don't know at all. So then a year later in Neurology, John Gallacher's group in Oxford,  they realized their longitudinal study also

had had hearing measured at some point too and  and never looked at risk for dementia. They did the exact same analysis basically as us. Lo  and behold, same set of results. Since then, it’s been replicated multiple times, so that is a  relationship. I guess the next question – I hope you're gonna ask Nate but maybe I’ll ask for you –  is why, right? I mean, so what gives here? This is what I spent a lot of my time in 2010 literally  going through Psychology and Neurology and

books going back all the way back to the sixties.  Really thinking about, there were some hypotheses proposed in the original Uhlmann paper from 1989,  but they weren't really – it wasn't really thought of that well yet. I basically took a deep dive  into it. From my perspective coming at it from, I understand everything about the ear and how the  brain processes sound, I did a crash course and really getting a deeper dive with Luigi's help  and Susan Resnick’s help looking into dementia

and dementia disorders and things like that. And  ultimately we – and also with Marilyn Albert, working with her at the time – we hypothesized an  initial paper and subsequently sort of codified, a little later in a broader theory-based  paper, sort of the three major mechanisms now, which I think probably are well established now –  well accepted, I should say – of being the three major mechanisms to which hearing loss increases  dementia risk and cognitive decline. The first

mechanism gets at the idea of cognitive load. What  I mean by that is when you have impaired hearing, what it basically means is that it's not that you  can't hear, it's just that your ear is constantly sending a much more garbled signal to your brain  because the ear has been damaged progressively. The ear is post mitotic, so it doesn't matter who  you are, everyone's hearing gets worse gradually

over your lifetime. If the brain is constantly  receiving a much more garbled signal from the ear, what essentially has to happen – we know this  from the auditory literature – the brain actually reallocates resources to help with hearing.  It's like you're constantly shuttling more brain resources to dealing with a much more  garbled sound and, in turn, the understanding

is that, colloquially, it comes with expense for  thinking and memory. But why? The thought there is not so much that hearing loss causes dementia,  but hearing loss taps into the cognitive reserve that otherwise could have been used to buffer  against amyloid neuropathology, that could have been buffered against microvascular pathology. But  that buffer that we all know exists at cognitive reserve, which we know exists many ways, it  constantly taxes and taps that buffer. And then,

I'll tell you, that goes beyond just theory  now. You actually see this on FMRI Studies. You see resource allocation, people even with  a mild hearing loss basically using parts of the frontal lobe for auditory processing, which  you normally do not need to use, and yet you're seeing that with hearing loss. It's not so much  that hearing loss causes dementia, but hearing loss leads to much earlier phenotypic exposure to  dementia because you're tapping into that reserve

that otherwise could have buffered against known  demential pathologies. So, that's one mechanism. The second mechanism – it's interesting because  it sounds similar but it's actually completely different and there's actually a line of  evidence for this too. It's the idea that auditory deprivation, an impoverished auditory  signal sending to the brain, actually does lead to trophic effects on structural atrophy of the  brain. And we see this. Actually it's interesting,

you can do animal studies. You can section a  guinea pig's hearing or give it hearing loss and you actually see the section pathologically,  months later, the effects it has on the brain, actually structural loss. You see this in human  studies in terms of longitudinal MRI scans, so we've done this in the BLSA and other studies  now. You follow a cohort of older adults,

people 50, 60 and plus. You see who has hearing  loss, who doesn't in the beginning. You'll get their brains in the beginning, not much difference  in size cross-sectionally, but if you follow them longitudinally what you see is accelerated rates  of atrophy, particularly over the lateral temporal lobe among those with greater hearing loss  versus those with normal hearing. Now, again, it gets to the idea maybe very much – I shouldn't say  colloquially use or lose it, but in a way auditory

deprivation leads to structural atrophies. So  that's a second mechanism. Sounds similar but it's actually different, because that second  mechanism really implies actually that hearing loss is quote, unquote, possibly directly damaging  the brain in terms of its structural integrity, right? The third mechanism is going to be the most  intuitive for almost anyone. It's the idea that if you can’t hear well, you may not go out as much.  You may not participate as much in conversations.

You may not participate as much in cognitively  stimulating activities. I mean sounds like common sense, but if you really believe that, I mean, I  think many people would agree and the literature is still little all over – I shouldn’t say all  over the place, but the logic is inconsistent. No one knows the exact mechanism, but participation  in cognitively stimulating activities, social activities, let's just say it's good for  the brain. So in the end, it's three mechanisms,

none of which are mutually exclusive. It's likely  a combination of all three now. What we never knew with these hypotheses in place though is does it  actually reflect distally and actually rates of cognitive decline and dementia. And if you believe  epidemiological literature, it sure does. I mean to the two now – you mentioned in your really kind  introduction the Lancet Commission on Dementia.

Out of all known existing potentially modifiable  risk factors – I mean theoretically they classify both in their 2017 and their 2020 meta-analyses  that hearing loss is singlehandedly the single largest, potentially modifiable risk factor for  dementia, purely because of many ways of the risk ratio between hearing loss and dementia in the  literature, but also because hearing loss is so common, right? I mean the prevalence of hearing  loss doubles with every age decade. By the time

you look at seniors 65+, two thirds of everyone  over 65 has a hearing loss. It's all of us, right? It's not only a risk factor that is really  common, but the risk ratios are large as well.

cognitive decline and/or dementia, depending on  what the studies measure. A natural corollary to that then as well, does that mean is this  just a theoretical like academic tidbit, or does it actually mean, at the population  level or the individual level, if someone quote, unquote treated their hearing loss, does  that reduce risk of cognitive decline or dementia?

That is by no means guaranteed, right? Because  when you quote, unquote treat hearing loss with a hearing aid and associated audiological support  services, you're not reversing the hearing loss. That hearing loss is still there. I mean, it is  a rehabilitative intervention. There is still damage to the cochlea. The cochlea is still  sending an impaired signal to the brain. It's just that with a hearing aid and using it well  and learning how to use it, you're providing a

clear auditory input which can lessen that burden  on the brain. Does that actually transfer across, and does that reduce risk? I mean, it’s such a  basic question. Okay, hearing loss is related to cognitive decline and dementia, but if you  treat it with our existing interventions does it actually reduce risk? Before the ACHIEVE  trial – which I’ll get to in a second – we can

never answer that because observational studies  – you could actually look at these studies. About 20 percent of people on average use hearing  aids who have hearing loss and you can look at that data. Do they do better than people who  don't use hearing aids? I never talk about this, and I never show it in the papers. They  actually do for the most part, right,

but you can't believe it though, right? Because  you can imagine people who have hearing loss who use hearing aids versus those with hearing loss  who don't use hearing aids, they're completely different people, right? People who get hearing  aids, they are healthier, they are wealthier, they're more health-conscious, right? All of  which would bias toward a positive effect,

so certainly you can't contribute causation  with intervention from observational study. So, the ACHIEVE trial was a definitive – essentially  you can call it technically more of a phase three,

this is not a pharmacologic study. It was  designed to be a definitive study looking at whether hearing intervention – basically  hearing aids and associated audiological support services – does that, versus an  education control intervention – basically a general health education control intervention  – does that reduce rates of cognitive decline, global cognitive decline, over a three-year period  in older adults. These are specifically older

adults in the study. The inclusion criteria was 70  to 84-year-old older adults; cognitively intact, basically they have a certain threshold Mini  Mental score non-indicative of dementia; and they had to have a mild to moderate level of  hearing loss. For t perspective, that is about 50 percent of people – five zero people – 70 to  84 would have that level of hearing loss. This is not extreme. The majority of people have that  level of hearing loss. The trial is fundamentally

– they got randomized, half got hearing  intervention, half got educational control. They were then followed semi-annually with an annual  battery of a 45-minute neurocognitive battery, and we looked at rates of cognitive decline.  The trial itself was pretty unique. We partnered actually with an existing study called the ARIC  study, or the Atherosclerosis Risk In Community studies. This is a study that's been funded by the  NHLBI, the Heart, Lung and Blood Institute. It's a

very long-standing, observational epidemiologic  study. It started thirty-five years ago looking at midlife older adults back then followed to the  present day, just looking at how midlife vascular risk factors contribute to late-life vascular  disease, basically cardiovascular events. These 16,000 people initially have been followed for  almost thirty-five years at four different sites across the country. David Knopman is part of that  study. For the last ten years it’s transitioned

more to a cognition study. This ARIC study was  based off of just a random sample of older adults 30 years ago, been followed to the present day,  represent just a general population now at this point with attrition. Fortunately in ARIC though,  they have all these protocols. They had the cognitive testing protocols, dementia adjudication  overseen by Marilyn Albert and David Knopman, so nesting the trial within there was great. The  ACHIEVE trial was based within the ARIC field

sites, and then for the ACHIEVE trial we shared a  lot of the same existing testing protocols. About a quarter of the nearly thousand people who were  recruited to the trial were recruited directly from ARIC. Basically people who were already  being followed by ARIC for over 30 years, we saw their hearing, because they were being tested  already as part of ARIC's study, and we said, “Hey you could be in the study. Do you want  to join?” And they said, “Yeah sure why not,

I’ll join the study”. So about a quarter of  people came from ARIC participants. The other three quarters of people we basically recruited  from a healthy de novo cohort – people who respond to Facebook ads about a study on cognition,  aging, and health; eople respond in registries; people interested in cognition studies, and things  like that. So two different study populations. One population from ARIC, probably represents  much more of a general population. The healthy

volunteers, de novo group, representing really… I  would say the worried well, in a good way. These are healthy community volunteers interested in an  aging study. When we did the trial they are all – nearly thousand people – were recruited from 2018  to 2019. Fortunately, everyone got recruited and randomized before the pandemic hit. They were  randomized through hearing intervention versus the education control and then they were then  followed for three years with annual measures.

This is a global neurocognitive battery that  we've been using in ARIC for the last ten years, developed actually originally by David Knopman,  Tom Mosley, Marilyn Albert and a bunch of other people involved with ARIC study. We had the last  three-year visit at the end of 2022, about three to four months for database lock. We finished  database lock in April of 2023. We had the initial trial readout in April 2023. We submit our  results to The Lancet mid-June 2023, and it

was accepted and published a month later. It's a  crazy timeline, it was a hectic few months. Yeah, so it's fundamentally a pivotal – technically I  guess you could call it Phase 3 in a way – Phase 3 clinical trial looking at, does treating  hearing loss reduce cognitive decline?

“Oh eff” moment. [Laughs] It was like, “Oh god  what do we do?”. But – and this is the big, big, big but – one of our pre-specified other  analyses that always was pre-planned was that we would replicate the primary cohorts, the primary  analysis of global cognitive decline, in the ARIC cohort and the de novo cohort differently because  we realize that these two cohorts may be very,

very different. That's where the fun stuff  is. In the ARIC cohort, you see over three years – statistically significant by far – nearly  a 50% reduction in global cognitive decline over three years. In the de novo cohort, over three  years hearing intervention was no different. So like, why? Well this, in 20/20 hindsight,  makes complete sense. The de novo cohort over three years, the control group, basically had no  cognitive decline, right? Because – and it makes

sense – these were the healthy volunteers. If you  have a healthy volunteer who joins a cognition study, they don't have cognitive decline because  they’re too healthy. In three years they really had literally, when I say no cognitive decline,  they declined by about 0.15 standard deviation units, so not much. Lo and behold, if the hearing  intervention is predicated on reducing cognitive

decline, you can't reduce something that's not  really declining. In contrast, in the ARIC cohort, the control subjects had about nearly a threefold  faster rate of cognitive decline over three years than de novos. They basically had about a 0.4  standard deviation effect size change over three years, which is a lot. 0.5 standard deviations is  a lot and they change 0.4 standard deviations over three years in the control group. Lo and behold,  in that ARIC cohort with the hearing intervention

you see about 50 percent reduction in cognitive  decline. I mean, it's really, really stunning, right? So yeah, in the combined cohort, nothing.  It was basically the de novos masked everything, right? Actually it's interesting, there  are two thoughts. Why do the de novos not decline over three years? One clear  thing is that they're likely, honestly, the worried well. These are like high-level people  who respond to Facebook ads about cognition and,

no surprise, three years they don't decline  very much, right? So that's one. And if you look at baseline demographic factors between ARIC  versus de novos, de novos had higher education, higher income, lower rates of hypertension and  lower rates of diabetes, right? Their baseline cognitive scores were higher than the ARIC’s  right? So this all glides in that direction,

that all makes sense. Another reason which  is really interesting, Nate, that came up a lot when we presented these results of the  Alzheimer's Association meeting in Amsterdam was the fact that the de novo cohort was essentially a  cognitively-testing naive cohort. As we all know, it has been shown in many, many studies there  are true practice effects of cognitive testing

that sometimes pan out three to four years later.  How much of actually very little cognitive decline over three years – I think 0.16 standard deviation  unit change over three years – is somewhat because these people are still getting better at cognitive  testing? In contrast, don't forget ARIC with not only their slightly higher risk factors – these  people have been followed over 30 years who get routine cognitive testing every one to three  years. I mean, you're not – I assume – you're

not seeing practice effects anymore after 30  years. What you're observing ARIC may be just much more a true rate of cognitive decline. These  are not benefiting from practice effects anymore, whereas de novos could be a combination.  They honestly were healthier and had a better cognitive baseline but how much are they  still benefiting from practice effects too?

not huge. Even if you had 10,000 people, you  look at the treatment effect and it's like, “Oh that's great, but is it really that meaningful?”  That's honestly the only reason it’s statistically significant because the 240 is big – it's not  that big – but the effect size was large. I mean 48 percent reduction is nothing to sneeze at,  right? Another thing I’ll add too which is really interesting too, Nate, that this is brought up  by Tom Mosley, who's one the coinvestigatstors.

He works at the University of Mississippi and  leads the MIND Center there. He found it really personally scientifically compelling too, that the  ARIC participants are the ones at greatest risk, right, and yet you're still seeing a benefit  because how often do we see interventions where it’s too little, too late for a group, right? The  other interesting thing too is that one measure we did at baseline is something called – it's a  terrible name – it's called the Hearing Handicap

Inventory. It's basically a self-reported scale of  communication impairment, right? So Likert scale, “Do you struggle when you go to restaurants?”, “Do  you feel embarrassed when you go out in a large group?”, so it's a self-reported communication  scale. If you look at those scores at baseline, what's really interesting is that among the ARIC  and the de novos at baseline they basically had similar levels of objective hearing. There’s  this thing called the Pure Tone Average,

about 40, which is the mild to moderate  range. They're basically identical; both groups are I think 39.8 and 39.6, but  the same levels of objective hearing. But the de novos actually had a much higher level  of communication impairment at baseline, and that makes sense. If you're joining a  hearing and aging study, you're probably joining it because you wanted free hearing aids  so it made sense. Whereas the ARIC participants,

their hearing handicapped scores are actually  much lower. They're at the level where typically those people you wouldn't think would even want  to come in for a hearing aid. Honestly I think they wouldn't, only because they joined the study  because they’re already in this other study. The reason I'm saying this is the fact that people who  wouldn't even want to come in for hearing aids, who weren't even really noticing that they were  having communication issues, were the ones who

benefited from this intervention. It sort of blows  my mind because it actually guides public health strategies. If you're saying, “Okay just nowadays  if people come in and need a hearing aid, we'll pay for it for them,” right? You actually can't  go by that strategy in a way. It's almost like you have to reach out to people and say, “Listen, even  though you don't feel like you have any problems,

your hearing level objectively is at a level  where you could possibly really benefit”. So there are a lot of little nuggets here  that we’re even just still teasing out.

would carry residual effects to reduce dementia  onset many years down the road. That's going to be hard to ever figure out though. What I  mean by that is actually the ACHIEVE trial, now that we're finished with the three-year  follow-up we've actually – very generously courtesy of the NIH – it's being funded for  another three years of follow-up. So we’ll

have long term six year results as well too. Maybe  we'll be able to answer that in six years because there'll be more cases accruing over the timeline,  but I don't know if we ever have the numbers to sort of look at dementia. I mean, fortunately  dementia is relatively a rare event in a good way, right? That the definitive evidence of whether  treating hearing loss can reduce dementia risk, that I think would be – I mean most  dementia trials – don’t forget, for not

in a rich cohort for amyloid or anything  like that or MCI. Those are two, three, four thousand person studies that really get  those numbers and we do not have that in ACHIEVE, so I don't think we'll have a hard outcome of  dementia because the numbers will never be there to – going from primary prevention all the way  to dementia is really, really hard, right? This is not in a rich population for any people at  risk of cognitive decline or dementia at all.

let's say, very proximal stuff. Think of  that and then yes, distally that has cut care of effects. I mean and fortunately hearing  intervention is about as no risk, or low risk. I mean I really can't think of a risk of using  hearing aids [laughs] or anything like that, right? I mean maybe – I don't know –  I mean theoretically I guess you can give you some ear irritation but it's a no risk  intervention, right,hat only has positive upsides,

right? It's funny and a lot of people brought  this up at the AAIC meeting and I didn't want to answer it because a lot of AAIC now –  there's a lot around amyloid-lowering agents, right? Amyloid therapies and there's new results  presented there and it really is exciting. I mean, it's really an example of just really good  understanding from basic biology, drug development

and trials, right? As we all know those therapies  are not without risk. So people kept on asking, “Well Frank what do you think about that?”  andI'm not touching that with a ten-foot pole. [laughs] But it is – in terms of a no risk  intervention that only has carryover benefits on just socialization and communication and, oh  yeah, it could confer 50 percent reduction in cognitive decline – it does seem to be a  no brainer if you ask me, right? Because,

I mean, what is the downside? I don't know. Okay  actually, I'll tell one downside and we can go in this way but we don't have to. This is outside the  purview of this podcast but it's how I spend a lot of my time now. There's cost. They're bloody  expensive, right? That's something years ago, I began working with Congress and the White House  National Academies. We got a law passed actually six years ago now, went into effect last year  now as some people may realize. Hearing aids are

officially over-the-counter in the United States,  but it's just the tip of the iceberg. The big companies that are likely planning to enter this  space, the big consumer tech companies who could really innovate – these companies like Samsung or  companies like Apple – they have not entered yet, but if you look at news reports it's only a matter  of time. So that changed the dynamics very quickly of pricing, accessibility, appeal, innovation of  hearing technologies that we’re just beginning to

see now. Over the next few years, I think you're  gonna see a ton of really exciting innovation, accessibility around hearing devices. I  mean, tongue and cheek, but are those Airpod Pros you’re wearing or are those hearing  aids? Well they could be one and the same, right? I think that makes it very exciting because  I think one real risk actually is well “Frank, costs,” right? But I think that is going to be  changing very dynamically in the next few years.

deaf with their Walkmans!” and blah, blah, blah,  blah, right? It hasn't happened, and what I mean by that is the Walkmans of forty years ago are  far worse than this current generation because back it was an analog device. You could turn that  sucker as loud as you want to, right? Every pair of wireless earbuds now function on a digital  platform. Yes, you could theoretically turn it way up, but the control settings are much much  better now. More importantly, from that whole

era of the – actually let's look at the data.  The actual data really hasn't borne out. If you look at population prevalence risk estimates of  hearing loss in, let's say 40-year-olds nowadays, 30 years after – or maybe 50-year-olds now  is, you know, 30 years after Walkmans came out – versus a generation ago. They're really no  different. I mean, maybe very, very, very subtly, at best. The reason why it is though, right,  is because it doesn't matter who you are,

right? Everybody's hearing begins monotonically  declining, right? Steady state decline over your entire lifetime beginning roughly you’re age  twenty because your inner ear is postmitotic. It does not regenerate. So over a lifetime of noise  exposure, aging, genetic susceptibility, everyone loses some hearing. So, yes noise – especially  workplace industrial noise, gunfire noise, those big things – that make a difference. Airpods,  walkmans, subtly, probably to some degree too,

but maybe not actually, right? It's a different  order of magnitude than like a generation ago with artillery noise and gunfire noise and factories,  right? I don't think it's really being borne full out by the literature. Subtly maybe, but how  much does that compare with everything else that affects your hearing of your lifetime? Aging,  cardiovascular risk factors which can affect your hearing too. It's probably a relatively small drop  in the bucket. It's definitely not good for you,

but is it – I think it's probably relatively a  drop in the bucket's contribution. I don't put much in store by that necessarily of risk per  se. And besides even if it was like what are you going to do about it? Tell my daughter not to  use her Airpods? I mean, like let's just get on with it and say we can say all we want but society  moves on and lets just like deal with it, right? Your other point about just personal prevention,  no that is real. And I shouldn't pooh-pooh it too

much because I always say hearing loss is honestly  inevitable to some degree, right? Everyone's hearing changes, but you can change that slope  to some degree. Listen, the big obvious ones epidemiologically, the big, big risk factors for  hearing loss epidemiologically: age, sex, race. Can't do anything about that. Interesting that I  mentioned those too. Race is a really interesting one. This is people who – I shouldn’t say race,  it's really skin color – people of darker skin

have a much, much, much lower risk of hearing loss  with aging. That has to do with the corresponding amount of melanin in the cochlea, as in your skin,  and that melanin in their ear actually protects in their ear. It's crazy but the risk reduction  with skin color – race being a proxy, I guess, for skin color – is huge actually. Anyway, but  age, sex, race, can’t do anything about. Sex, you can imagine, women have less hearing loss  than men, probably has to do with an environmental

indicator. You know men do more stupid stuff,  right? But also estrogen might have a protective effect in the inner ear too. But so age, sex,  race, let's say you can't do anything about it. The other big ones are noise. We talked about  that and that is something you can do about. The general rule of thumb I use in my daily life is  that if you are in an environment where at arm's length you have to really raise your voice to be  heard, that is a situation where, given enough

time, it can be damaging to your hearing.  Obviously if you're in the subway platform, it is really loud for the few seconds as the  train passes, not as big a deal. But if you're in that subway working as a worker nine hours a  day, that can add up, right? Likewise, if you're mowing the lawn that is loud enough that you  can't talk someone arm's length, you need to use

ear protection. I think that’s just a good rule  of thumb anytime you’re in an environment where arm’s length you have to raise your voice to be  heard, that environment is theoretically enough to damage your hearing given enough time. If you're  gonna be there for a long time, absolutely throw some headphones or earbuds or ear muffs or foam  ear plugs in without a doubt. Then the other risk

factor to hearing loss, really the only one you  can really control I gotta be honest is noise. All the other ones which are shown epidemiologically  are basically the cardiovascular risk factors, likely because the same things that lead to  microvascular disease of the brain and other parts of the body can lead to microvascularin  the inner ear. Again, yes, follow a healthy diet, exercise for your hearing, I guess, but you're  doing that anyway. So I don't bother mentioning

it because it's almost moot. You're gonna do it  for your heart, not for your ear right? The only way unique to the ear is obviously noise, and that  is real and that is something that is, honestly, I think easy to deal with. Just if you're going to a  concert, just bring some earplugs. If you're using power equipment, throw on a pair of earmuffs. If  you're firing guns, wear earmuffs too. Besides that I mean, again, assume you're not in an  industry where you really do have to be careful

about it. Fortunately there I think there's fifty  years now of OSHA protections – Occupational Safety Health Administration protections – around  hearing. Obviously not always followed, but I think it's clearly going the right direction.  We'll continue to go in the right direction.

outreach and production. Donate at the link in  the description. Dementia Matters is brought to you by the Wisconsin Alzheimer's Disease Research  Center at the University of Wisconsin--Madison. It receives funding from private, university,  state, and national sources, including a grant from the National Institutes on Aging for  Alzheimer's Disease Research. This episode of Dementia Matters was produced by Amy Lambright  Murphy and Caoilfhinn Rauwerdink and edited by

Alexia Spevacek. Our musical jingle is "Cases  to Rest" by Blue Dot Sessions. To learn more about the Wisconsin Alzheimer's Disease Research  Center, check out our website at adrc.wisc.edu, and follow us on Facebook and Twitter. If you  have any questions or comments, email us at dementiamatters@medicine.wisc.edu.  Thanks for listening.