> The researchers randomly assigned participants to one of two interventions. About half received hearing aids and instruction in how to use them. The other half were assigned to a health education program focused on promoting healthy aging.
I'm advocating that people do studies with randomized interventions—an approach that is capable of proving causation—and not being satisfied with purely observational studies that look at correlations, which are often hopelessly confounded and can't distinguish between "X causes Y" and "Z causes both X and Y". I was pleasantly surprised to find that this study was of the first type rather than the second.
While this take seems popular, this isn't a good way of looking at it because, in my experience, it seems to lead to the dismissal of good evidence or it suggests that we can't build confident causal inferences without a certain study. For example, RCTs are also observational, and it's incorrect to say they can uniquely detect causation.
I think a more helpful way to look at research is to look for a convergence of outcomes across the evidence, like a bunch of needles of various sizes pointing in the same direction (or not) on a gauge. And where there are divergences, and there always will be, which differences in methodology can explain them.
The key phrase is "purely observational". Now, occasionally you end up with a "natural experiment" in which some accident has effectively done the randomization for you—specifically, where the mechanism that puts people in the treatment group vs the control group is something you can be very confident has no other causal interactions. This was a good example: https://twitter.com/PGeldsetzer1/status/1661776663074738176
"Causal evidence that herpes zoster vaccination prevents a proportion of dementia cases [...] To provide causal as opposed to merely correlational evidence on this question, we take advantage of the fact that in Wales eligibility for the herpes zoster vaccine (Zostavax) for shingles prevention was determined based on an individual's exact date of birth. Those born before September 2 1933 were ineligible and remained ineligible for life, while those born on or after September 2 1933 were eligible to receive the vaccine."
But any time you're looking at a scenario where treatment vs non-treatment was the result of individual human choices, that opens up a potentially very wide range of ways for something you didn't know about (and potentially something difficult to accurately control for even if you do know about it) to cause treatment and cause the outcome, instead of the treatment causing the outcome.
> it suggests that we can't build confident causal inferences without a certain study
I do think there's an upper limit to the confidence you can justifiably hold, and that it's often not very high. Consider the studies that observe "A bit of alcohol correlates with better health than zero alcohol". You control for wealth, education, and maybe other things, and the apparent effect remains. How high confidence should you have in the result? Then someone realizes: Some fraction of people who consume zero alcohol do so under doctor's orders because they have health problems, and if you exclude those people then the effect disappears.
No matter how many causal pathways you think you've controlled for, how confident can you really be that there isn't a new one you haven't thought of? (And controlling has its own perils: if your measurements are noisy, or if you end up controlling for the outcome.)
> it's incorrect to say they can uniquely detect causation
Oh, correlational studies can "detect" causation, but the hard part is being certain that the thing detected isn't a false positive.
And it'll also include some number of alcoholics in recovery who are currently consuming no alcohol, but who's bodies have hard years on them, and you'd expect to do worse than overall population average in outcomes.
Yes, and any number of other things you hadn't thought of. The beauty of randomization is that, whatever it is, it will put some of those people in each group.
But even with a random variable, this still only gives you an average result for the group. And the more diverse the group is, the less likely that it's useful in predicting whether it works for you.
I completely agree that randomized intervention studies have enormous value when compared to observational studies.
In this example, it would be particularly hard to establish a causative relationship that said "hearing aids inhibit dementia" or "hearing loss causes dementia" if instead all you had was a population, some of whom used hearing aids, and some of whom had varying levels of hearing abilities, and some of whom developed dementia. In all the noise, you'd be very fortunate to find that a control group of people with undiagnosed (how would you ever measure that!) hearing loss who failed to get hearing aids had cognitive decline in excess of that experienced by those who did get hearing aids. Here, instead, the intervention is "the coin flip said you're in the hearing aid group/you're in the health education group."
Of course, the murky ethical issue here is that this randomized intervention resulted in some people having poorer hearing, perhaps permanently (use it or lose it!) and some people having more rapid cognitive decline. This randomized intervention directly caused real suffering. Nearly 125 people in the heart-health group with increased risk of dementia onset were assigned to a study that just received health education. For at least three years, they had reduced hearing and a reduced ability to communicate, and after three years, they had significantly greater cognitive decline.
Caution is good, but in general I have no problem personally with the 'shut up and multiply' application of ethics in this case. There are 8 billion people all getting old, and more being born every day who will eventually get older. It's very important as a species to know that hearing aids slow cognitive decline, and if that meant that 119 people were placed at a slightly increased medical risk, 119 divided by 8 billion is a pretty small number, and 7.999999881 billion who are now more likely to get hearing aids and have slower cognitive decline is a lot of positive utility. But it wasn't me or my mom who can no longer hear and who is suffering from dementia, and some will draw a hard line and say that you can't perform studies that will put even a small number of people at increased risk.
We should be careful to evaluate merit and limit harm, but we should perform more randomized intervention studies.
I largely agree, except that choosing a denominator of 8 billion is really dubious. The number of people for whom this study will result in them getting a hearing aid when they otherwise wouldn't is unknown, but unlikely to be nearly that high.
You can't actually do that math. Or rather, you can but the inputs to your spreadsheet are whatever you made up.
Attempting to do the math is better than the alternative of going with your gut. The numerator is also an overestimate, not everyone suffered excessive cognitive decline.
If this was a critical decision (like it was for the authors of the study, unlike it is for the authors of Internet comments) you can work for better inputs.
Most importantly, though, we're trying to understand if that fraction is greater than one or less than one. There's a number that might be 8 billion or might be a tenth or a hundredth of that in the denominator, and a number that's on the order of 100 - or maybe 10x that, or maybe 1/10th that. But it doesn't matter, because it's not close, the ratio is still a million to one.
The retracted paper discusses an association since it was observational:
> We used Cox proportional hazards models to estimate hazard ratios... between self-reported hearing aid use status (hearing loss with or without hearing aids) at baseline and risk of dementia
The top-level article discusses a randomized controlled study and therefore can make a much stronger claim of causality:
> The researchers randomly assigned participants to one of two interventions. About half received hearing aids and instruction in how to use them. The other half were assigned to a health education program focused on promoting healthy aging. Both groups received follow-up visits every six months to reinforce the training.
“When the paper first appeared, it seemed to confirm a widely held belief – that hearing loss is associated with developing dementia, and using hearing aids can help to reduce risk – about which the scientific evidence has been mixed, Blustein, the hearing loss researcher, told Retraction Watch. In her view, public health messaging and media coverage of the question has been “misleading.”
The findings were picked up quickly and disseminated among the community of people following the question of hearing loss and dementia, she said. “I don’t think people are necessarily aware of retractions.”
Another pull quote:
“Most notably, he found that hearing aid use did not correspond to a lower rate of dementia for people with hearing loss, as the authors reported. He found the opposite: among people with hearing loss, the dementia rate was higher for those using hearing aids.”
In context, I would be careful taking this conclusion at face value quite yet, though it does seem intuitive, just as the other one was.
“About 250 healthy older adults came from a long-term study of heart health … 739 people were newly recruited. . . . Participants recruited from the heart-health study had more risk factors for developing dementia, including being older and having faster rates of cognitive decline than those from the general community.
In the main analysis of all study participants, the researchers saw no difference in the rate of change in cognitive functioning between people who received the hearing aids and those who didn’t.
However, when the analysis focused on people from the heart-health study, who had a higher risk of dementia, the benefit of the hearing aids was substantial. Those who received hearing aids had an almost 50% reduction in the rate of cognitive decline.”
Would you be willing to clarify that? Is she talking about losing cognitive abilities when someone fails to get hearing aids when they should? I'm starting to deal with some hearing issues and would like to make sure to stay on top of this issue.
Deaf-infant cochlear implants can make a significant difference in IQ (less language audio input affects IQ if not mitigated ASAP: a principle that extends from deaf to normal hearing children). With this principle in mind, it isn't surprising that hearing aids slow cognitive decline later in life. Though, I'm not implying that it may be a 1:1 mechanism.
I'm sure it would help, but in my experience, I don't find them a replacement for hearing aids.
I have tried this a bit with first-generation Airpod Pros. Wearing them for a long time is annoying, in part due to battery life. But they are much better than hearing aids for recorded music, so I swap between my hearing aids and airpods depending on what I'm doing.
Download the app “Mimi Hearing Test”. It allows you to do a quick test using your AirPods. And the results you can upload in your iPhone’s accessibility settings. So the phone will increase frequencies you don’t hear well. You can also set a general amplification.
So, yes, I’d very much think AirPods can be of benefit here.
I suspect most people think that both are caused by old age, rather than that deafness causes (or accelerates) dementia. It's not like there's a well known group of congenitally deaf people who get dementia young to inspire a causal connection.
My mum started noticeably losing her hearing after her dementia symptoms got quite bad. She may well have lost her hearing sooner and we just didn't notice, just as in retrospect there were huge warning signs of dementia well before the diagnosis and we just didn't realise what we were observing.
Thinking I was born 3 years earlier than I was. Forgetting how to read maps. Higher anxiety causing her to ask me to drive dangerously slowly, and in so doing revealing she didn't know the speed limit on that category of road. Forgetting to renew her road tax (I have no idea how she wasn't fined for that, given the rest of the family noticed this six months after it was due).
Which to me shouldn't be that surprising given that we know neurons seek to connect with other neurons based on activation patterns, and that the brain stays plastic into old age.
I've seen similar with movement. Once they break a hip or something which severely reduces their physical activity level, cognitive abilities usually go downhill fast. Part of that is probably cardio-related, but I've long thought it was related to lack of stimulus.
Just doing the dishes or feeling the wind creates a ton of sensations, and may trigger memories, that sitting in a chair watching daytime TV just won't.
I wonder if some of that could be solved via VR or even just video games. Not as good as the real thing but should be more mentally stimulating than passively watching.
There's a ton of research into this idea, have a search on PubMed.
Unfortunately it suffers from at least two problems.
First, generalisable effects from specific interventions often fail to replicate, so for example subjects tend to get better at a specific task but it doesn't necessarily carry over to real-world contexts. There are a few promising potential directions, although even those results are modest and uncertain.
Second, people with even mild/early signs of dementia are extremely unlikely to continue with an intervention. Even if they do they often modify it, e.g. unplugging a smart device to save energy, or taping over buttons to prevent accidentally pressing them.
I would hunt out references but I'm on mobile, they shouldn't be hard to find.
> why can't people that loose hearing later, learn sign language, and thus stay active, just like the deaf.
Did their friends and family learn sign language as well? People who are deaf young tend to get a social circle who can communicate with deaf people, while old people are unlikely to rebuild all of that.
Very few adults learn a new language to a high level. It can be done, but most get to the level of ordering a beer and call it good if they get alcohol.
If you don't need to use the language except for a one week tour (where you are still mostly with people who speak your language) this is good enough. However if you are suddenly without ability to communicate you probably can't suddenly learn fast enough to combat decline.
Fun fact: auditory signals are the fastest path to human reflexes, way faster than vision. I forget the exact numbers, but visual reactions are on the order of 300ms whereas auditory reactions are sub 100 IIRC. Feel free to correct me if anyone can find numbers.
So all those blind fights in the matrix cartoons or daredevil are sill, but not quite as silly as you might have expected. There is actually a significant reaction time advantage. But good look hearing a sword swing at your face vs your leg lol
There's a lot more between the actions there image to display, mouse to computer that have nothing to do with internal meatbag reactions. Especially when we're already measuring in milliseconds.
I'm referring to the paper cited in the linked site, which quotes about 50ms of difference in reaction time between auditory and visual, not 200ms like stated in the comment above.
Seems rather unsurprising, given what we already know of the brain. Though I guess specific studies like this is more actionable.
Good thing hearing aids have become more affordable lately, from over-the-counter models to DIY style using cheap microcontrollers for developing countries.
Different mechanisms, you’re born with ~100x the amount of neurons you’ll have as an adult, those normally used for hearing get adapted and trained on other stimuli.
> The researchers randomly assigned participants to one of two interventions. About half received hearing aids and instruction in how to use them. The other half were assigned to a health education program focused on promoting healthy aging.