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Hearing loss and incident dementia.
ORIGINAL CONTRIBUTION
Hearing Loss and Incident Dementia
Frank R. Lin, MD, PhD; E. Jeffrey Metter, MD; Richard J. O’Brien, MD, PhD;
Susan M. Resnick, PhD; Alan B. Zonderman, PhD; Luigi Ferrucci, MD, PhD
Objective: To determine whether hearing loss is asso-
ciated with incident all-cause dementia and Alzheimer
disease (AD).
Design: Prospective study of 639 individuals who underwent audiometric testing and were dementia free in
1990 to 1994. Hearing loss was defined by a pure-tone
average of hearing thresholds at 0.5, 1, 2, and 4 kHz in
the better-hearing ear (normal, ⬍25 dB [n = 455]; mild
loss, 25-40 dB [n=125]; moderate loss, 41-70 dB [n=53];
and severe loss, ⬎70 dB [n = 6]). Diagnosis of incident
dementia was made by consensus diagnostic conference. Cox proportional hazards models were used to
model time to incident dementia according to severity
of hearing loss and were adjusted for age, sex, race, education, diabetes mellitus, smoking, and hypertension.
Setting: Baltimore Longitudinal Study of Aging.
Main Outcome Measure: Incident caces of all-cause
dementia and AD until May 31, 2008.
Results: During a median follow-up of 11.9 years, 58 cases
of incident all-cause dementia were diagnosed, of which
37 cases were AD. The risk of incident all-cause dementia
increased log linearly with the severity of baseline hearing
loss (1.27 per 10-dB loss; 95% confidence interval, 1.061.50). Compared with normal hearing, the hazard ratio
(95% confidence interval) for incident all-cause dementia
was 1.89 (1.00-3.58) for mild hearing loss, 3.00 (1.436.30) for moderate hearing loss, and 4.94 (1.09-22.40) for
severe hearing loss. The risk of incident AD also increased
with baseline hearing loss (1.20 per 10 dB of hearing loss)
but with a wider confidence interval (0.94-1.53).
Conclusions: Hearing loss is independently associated
with incident all-cause dementia. Whether hearing loss
is a marker for early-stage dementia or is actually a modifiable risk factor for dementia deserves further study.
Participants: Six hundred thirty-nine individuals aged
36 to 90 years.
Arch Neurol. 2011;68(2):214-220
Author Affiliations:
Department of
Otolaryngology–Head and Neck
Surgery, The Johns Hopkins
School of Medicine (Dr Lin),
Center on Aging and Health,
Johns Hopkins Medical
Institutions (Dr Lin),
Longitudinal Studies Section,
Clinical Research Branch,
National Institute on Aging
(Drs Metter and Ferrucci), and
Departments of Neurology and
Medicine, Johns Hopkins
Bayview Medical Center
(Dr O’Brien), Baltimore,
Maryland; and Laboratory of
Behavioral Neuroscience,
Intramural Research Program,
National Institute on Aging,
Bethesda, Maryland
(Drs Resnick and Zonderman).
T
HE PREVALENCE OF DEMEN-
tia is projected to double
every 20 years such that by
2050, more than 100 million people or nearly 1 in 85
persons will be affected worldwide.1,2 The
devastating impact of dementia on affected individuals and the burden imposed on their families and society has
made the prevention and treatment of dementia a public health priority. Interventions that could merely delay the onset of
dementia by 1 year would lead to a more
than 10% decrease in the global prevalence of dementia in 2050. 3 Unfortunately, there are no known interventions
that currently have such effectiveness.
Epidemiologic approaches have focused on the identification of putative risk
factors that could be targeted for prevention based on the assumption that dementia is easier to prevent than to reverse. Candidate factors include low involvement in
leisure activities and social interactions,
sedentary state, diabetes mellitus, and hy-
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214
pertension.4 Some researchers have also
suggested that hearing loss, by reducing
stimulatory input and hampering social interaction, may be associated with dementia,5,6 but, to our knowledge, this hypothesis has never been prospectively studied.
Given the growing number of people with
hearing loss7 and the array of technological interventions currently available for aural rehabilitation, understanding whether
hearing loss is a risk factor for dementia
is important. We performed the present
study to investigate the prospective association of hearing loss with incident dementia within the cohort of the Baltimore Longitudinal Study of Aging (BLSA).
METHODS
SUBJECTS
Subjects were participants in the BLSA, an ongoing prospective study of the effects of aging
that was initiated in 1958 by the National Institute on Aging.8 The BLSA cohort consists of
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community-dwelling volunteers who travel to the National Institute on Aging in Baltimore biennially for 21⁄2 days of intensive testing. From 1990 through 1994, 1305 participants completed at least 1 study visit, of whom 976 underwent audiometry
and 749 had both audiometry and cognitive testing. Some participants had missing audiometry or cognitive testing data because of inadequate time for testing or tester unavailability during study visits. After excluding individuals with prevalent
dementia (n=58), those with more than 3 errors on the Blessed
Information Memory Concentration Test (n=39), and those with
suspected dementia (n=13), our baseline cohort consisted of
639 participants who were followed up until May 31, 2008 (median participant follow-up of 11.9 years) (Figure 1). For participants with more than 1 visit during this period, data from
the first assessment were used. All participants provided written informed consent, and the BLSA study protocol was approved by the institutional review board.
1305 BLSA participants with ≥1 study visit,
1990 to 1994
976 BLSA participants with audiometry
testing, 1990 to 1994
749 BLSA participants with audiometry and
cognitive testing, 1990 to 1994
110 Participants excluded
58 With prevalent dementia
39 With >3 errors on the Blessed Test
13 With suspected dementia
639 Participants in baseline study cohort 1990 to 1994
58 Participants diagnosed as having incident all-cause
dementia, including 37 with AD, 1991 to 2008
COGNITIVE TESTING AND
DIAGNOSIS OF DEMENTIA
The protocol for adjudication of dementia in the BLSA has been
used continuously since 1986 and has been described previously.9 Participants 65 years or older underwent a complete neurological and neuropsychological examination using a standard battery of tests. Participants younger than 65 years first
underwent screening with the Blessed Information Memory Concentration Test and underwent further examination if they made
3 or more errors. Dementia diagnosis was established during a
multidisciplinary consensus diagnostic conference using the Diagnostic and Statistical Manual of Mental Disorders (Third Edition Revised) for diagnosis of dementia10 and the National Institute of Neurological and Communicative Disorders and
Stroke–Alzheimer Disease and Related Disorders Association
criteria for diagnosis of Alzheimer disease (AD).11 If participants were determined to have clinically significant cognitive
decline (typically memory) but did not meet criteria for dementia, they were classified as having suspected dementia, which
corresponds to the current diagnosis of mild cognitive impairment.12 Participants initially underwent evaluation for dementia every 2 years during their routine BLSA follow-up visits. In
1997, follow-up was shifted to a sliding-scale schedule to reduce participant burden and improve data collection. Participants older than 80 years were examined annually; those aged
60 to 80 years, biennially; and those younger than 60 years,
every 4 years.
AUDIOMETRY
Audiometry was performed in the BLSA from 1958 to 1994.
During the entire period from 1990 through 1994, when the
baseline evaluation for this analysis was performed, hearing
thresholds were measured using an automated testing device
(Audiometer Model 320; Virtual Equipment Co, Portland, Oregon) in a soundproof chamber under unaided conditions. A
pure-tone average (PTA) of air conduction thresholds at 0.5,
1, 2, and 4 kHz was calculated for each ear, and the PTA in the
better-hearing ear was used for subsequent analyses because
that ear would be the principal determinant of hearing and
speech perception ability on an everyday basis. We used the
PTA in decibels as both a continuous variable and a categorical variable defined by the following commonly used levels of
hearing loss: normal (⬍25 dB), mild loss (25-40 dB), moderate loss (41-70 dB), and severe loss (⬎70 dB). Before 1990, audiometric testing was performed using a Bekesy audiometer (GSI
1701; Grason Stadler, Littleton, Massachusetts), and these data
were used in analyses of prebaseline hearing trajectories.
Figure 1. Selection of participants for study inclusion. AD indicates
Alzheimer disease; Blessed Test, Blessed Information Memory Concentration
Test; and BLSA, Baltimore Longitudinal Study of Aging.
OTHER COVARIATES
A diagnosis of diabetes mellitus was based on a fasting glucose
level of more than 125 mg/dL (to convert to millimoles per liter,
multiply by 0.0555), a pathologic oral glucose tolerance test result, or history of a physician diagnosis plus treatment with oral
antidiabetic drugs or insulin. The diagnosis of hypertension was
based on a systolic blood pressure of greater than 140 mm Hg
and/or diastolic blood pressure of at least 90 mm Hg or treatment with antihypertensive medications. Race (white/black/
other), education (in years), smoking status (current/former/
never), and hearing aid use were based on self-report.
STATISTICAL ANALYSES
Baseline characteristics of cohort members were compared using
1-way analysis of variance for continuous variables and ␹2 or
Fisher exact test for categorical variables. Cox proportional hazards models were used to study time to incident all-cause dementia or AD. Participants not diagnosed as having dementia
were censored at the time of their last negative cognitive evaluation finding. Time-on-study (ie, time of entry into the baseline study cohort) was used as the time scale with the exception of 1 model that used age as the time scale.
All Cox models included covariates of sex, age, race, education, diabetes, smoking, and hypertension. Diabetes and hypertension were included as covariates in the analysis because
they have been found to be risk factors for dementia.4 Additional models included baseline Blessed scores (residual variability in cognition after definition of the baseline cohort) and
hearing aid use. All covariates were treated as time-constant
variables. Cox model proportionality assumptions and the linear association between hearing loss and dementia were tested
using the Schoenfeld residuals method.13 To examine the graphical association between hearing threshold and dementia, we used
a smoothing spline for the hearing threshold and age in the Cox
proportional hazards model.14 A locally weighted scatterplot
smoother (loess smoother) was then applied to the exponential of the partial residuals derived from the hazards model against
the hearing threshold. A bootstrap procedure was used to generate 10 000 data sets that were then used to estimate the 95%
confidence interval (CI) for the loess smoother. Analysis of hearing loss trajectories before baseline was performed using a ran-
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Table 1. Demographic and Clinical Characteristics of Baseline Study Cohort by Hearing Loss Status
Hearing Loss Status a
Male sex
Age, mean (SD), y
Race
White
Black
Other
Education, mean (SD), y
Diabetes mellitus
Smoking
Current
Former
Never
Hypertension
Hearing aid use b
Blessed Information Memory
Concentration Test score
0
1
2
3
Development of all-cause dementia
during follow-up
Normal
(n=455)
Mild
(n = 125)
Moderate
(n = 53)
Severe
(n = 6)
225 (49.5)
59.9 (12.2)
94 (75.2)
71.1 (8.6)
36 (67.9)
77.0 (8.4)
5 (83.3)
77.7 (4.8)
404 (88.8)
44 (9.7)
7 (1.5)
16.6 (2.8)
62 (13.6)
121 (96.8)
4 (3.2)
0
16.2 (3.0)
20 (16.0)
49 (92.5)
4 (7.5)
0
16.7 (3.6)
12 (22.6)
6 (100.0)
0
0
16.2 (4.0)
1 (16.7)
19 (4.2)
244 (53.6)
192 (42.2)
204 (44.8)
6 (1.5)
1 (0.8)
85 (68.0)
39 (31.2)
79 (63.2)
14 (11.9)
1 (1.9)
35 (66.0)
17 (32.1)
38 (71.7)
39 (78.0)
0
3 (50.0)
3 (50.0)
6 (100.0)
4 (66.7)
265 (58.2)
112 (24.6)
49 (10.8)
29 (6.4)
20 (4.4)
65 (52.0)
32 (25.6)
19 (15.2)
9 (7.2)
21 (16.8)
31 (58.5)
13 (24.5)
6 (11.3)
3 (5.7)
15 (28.3)
0
2 (33.3)
3 (50.0)
1 (16.7)
2 (33.3)
P Value
⬍.001
⬍.001
.17
.74
.27
.05
⬍.001
⬍.001
.08
⬍.001
a Hearing loss is defined by the pure-tone average (PTA) of 0.5, 1, 2, and 4 kHz, with tones presented by air conduction in the better-hearing ear. A PTA of less
than 25 dB indicates normal hearing; 25 to 40 dB, mild loss; 41 to 70 dB, moderate loss; and greater than 70 dB, severe loss. Unless otherwise indicated, data are
expressed as number (percentage) of participants. Percentages have been rounded and might not total 100.
b Data on hearing aid use were missing for 72 individuals. Participants with hearing aid use data per hearing loss category included 393 with normal hearing,
118 with mild loss, 50 with moderate loss, and 6 with severe loss.
dom effects analysis and adjusted for age. Populationattributable risk (PAR) was calculated using the following
equation15:
PAR=(Pexposed([R–1])/(1⫹Pexposed[RR–1]),
where Pexposed was the prevalence of baseline hearing loss of at
least 25 dB and RR was the rate ratio (hazard ratio [HR]) of
dementia risk associated with hearing loss. Participants with
missing data were excluded from analyses; this represented
less than 0.2% of the study sample (1 participant) for all
analyses except for analyses incorporating hearing aid use,
in which there were more extensive missing data (typically
among normal-hearing participants who did not respond).
Significance testing for all analyses was 2 sided with a type I
error of .05. The statistical software used was a free available
software environment (R, version 2.9.1; http://www.r-project
.org).
RESULTS
Baseline demographic characteristics of participants by
hearing loss category are presented in Table 1. In general, participants with greater hearing loss were more likely
to be older, male, and hypertensive. Blessed scores did
not differ by hearing loss category (P=.08), although the
range of errors was narrow (0-3) because participants with
more than 3 errors were excluded from the study cohort
at baseline.
Baseline covariates associated with an increased risk
of incident all-cause dementia are hearing loss, age, hypertension, hearing aid use, and Blessed score (Table 2).
Independent of age, in the 15 years before baseline
assessment (520 participants with 2678 observations),
participants who later developed incident dementia experienced an average PTA loss of 0.52 dB/y (95% CI, 0.340.70 dB/y) compared with 0.27 dB/y (0.21-0.33 dB/y) in
those who did not develop dementia.
In Cox proportional hazards models adjusted for sex,
age, race, education, diabetes, smoking, and hypertension (base model), the excess risk of incident dementia per
10 dB of hearing loss was 1.27 (95% CI, 1.06-1.50)
(Table 3). The risk of incident dementia became evident for hearing loss of greater than 25 dB and thereafter increased log linearly with more severe loss
(Figure 2). This association remained significant after
censoring participants who developed dementia within
a 2-, 4-, or 6-year washout period from baseline (P=.008,
P =.003, and P=.04, respectively).
Confirmatory analyses from models including baseline Blessed error score (to account for baseline cognitive function) or models using age as the time scale rather
than time-on-study (to account for residual confounding between age and hearing loss) produced virtually unchanged findings (cf Table 3). Restricting the analytical
cohort to participants 65 years or older at baseline
(n=315) or excluding participants at baseline with a history of stroke or transient ischemic attack (n=19) also
did not substantially change the main findings (Table 3).
There was no evidence to suggest that self-reported hearing aid use was associated with a reduction in dementia
risk (HR, 0.97; P =.92).
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Table 3. Cox Proportional Hazards Models for Incident
All-Cause Dementia per 10 dB of Hearing Loss
Table 2. Demographic and Clinical Characteristics
of Baseline Study Cohort by Incident Dementia a
Dementia
(n=58)
Univariate
HR (95% CI)
18.8 (13.9)
32.6 (17.0)
1.1 (1.0-1.1) c
435 (74.9)
104 (17.9)
38 (6.5)
4 (0.7)
327 (56.3)
62.2 (12.3)
20 (34.5)
21 (36.2)
15 (25.9)
2 (3.4)
33 (56.9)
78.3 (6.4)
1 [Reference]
4.9 (2.6-8.8)
12.1 (6.2-23.9)
21.9 (5.1-94.2)
1.1 (0.6-1.8)
1.2 (1.2-1.2)
523 (90.0)
51 (8.8)
7 (1.2)
16.5 (3.0)
84 (14.5)
57 (98.3)
1 (1.7)
0
16.6 (3.0)
11 (19.0)
1 [Reference]
0.2 (0.02-1.2)
20 (3.4)
333 (57.3)
228 (39.2)
286 (49.2)
47 (9.2)
1 (1.7)
34 (58.6)
23 (39.7)
41 (70.7)
16 (30.2)
1 [Reference]
2.3 (0.3-17.0)
2.1 (0.3-15.3)
2.9 (1.7-5.2)
5.3 (2.9-9.6)
338 (58.2)
140 (24.1)
64 (11.0)
39 (6.7)
23 (39.7)
19 (32.8)
13 (22.4)
3 (5.2)
1 [Reference]
2.1 (1.2-3.9)
2.8 (1.4-5.6)
1.2 (0.4-4.1)
Model
In subsequent analyses, we categorized hearing loss
according to commonly accepted levels of hearing loss
severity. Compared with those with normal hearing, participants with mild hearing loss had an HR for incident
dementia of 1.89 (95% CI, 1.00-3.58; P=.049), those with
moderate hearing loss had an HR of 3.00 (1.43-6.30;
P=.004), and those with severe hearing loss (n=6) had
an HR of 4.94 (1.09-22.40; P = .04).
When the outcome of the analysis was restricted to incident AD (37 of the 58 cases of dementia), hearing loss
was associated with an excess risk of 1.20 per 10 dB of hearing loss (95% CI, 0.94-1.53). This result is comparable to
the risk seen for all-cause dementia (Table 3) but with a
wider CI, possibly owing to the smaller sample size.
We estimated the proportion of incident all-cause dementia risk that was attributable to hearing loss for participants older than 60 years in our cohort, assuming that
hearing loss could be causally associated with dementia. Hearing loss of at least 25 dB in the better-hearing
ear was present in 43% of this subcohort, and the rela-
HR (95% CI) a
P
Value
638
638
1.27 (1.06-1.50)
1.24 (1.04-1.48)
.008
.01
638
566
1.29 (1.08-1.53)
1.33 (1.07-1.64)
.005
.008
Abbreviations: CI, confidence interval; HR, hazard ratio.
a Hearing loss is defined by the pure-tone average of hearing thresholds at
0.5, 1, 2, and 4 kHz, with tones presented by air conduction in the
better-hearing ear.
b Base model covariates include sex, age, race, education, diabetes
mellitus, smoking, and hypertension.
1.0 (0.9-1.1)
1.6 (0.9-3.0)
Abbreviations: CI, confidence interval; HR, hazard ratio; PTA, pure-tone
average.
a Unless otherwise indicated, data are expressed as number (percentage)
of participants. Percentages have been rounded and might not total 100.
b Hearing loss is defined by the PTA of hearing thresholds at 0.5, 1, 2, and
4 kHz, with tones presented by air conduction to the better-hearing ear.
c Indicates hazard per 1 dB of PTA.
d A PTA of less than 25 dB indicates normal hearing; 25 to 40 dB, mild
loss; 41 to 70 dB, moderate loss; and greater than 70 dB, severe loss.
e Data on hearing aid use were missing for 72 individuals. Participants with
hearing aid use data include 514 with no dementia and 53 with dementia.
No. of
Participants
Base b
Base and Blessed
Information Memory
Concentration Test score
Base with age as time scale
Base and hearing aid use
12
10
8
Hazard
Hearing loss, mean (SD),
PTA b
Hearing loss d
Normal
Mild
Moderate
Severe
Male sex
Age, mean (SD), y
Race
White
Black
Other
Education, mean (SD), y
Diabetes mellitus
Smoking
Current
Former
Never
Hypertension
Hearing aid use e
Blessed Information
Memory Concentration
Test score
0
1
2
3
No
Dementia
(n=581)
6
4
2
0
0
20
40
60
80
100
Hearing Loss, dB
Figure 2. Risk of incident all-cause dementia by baseline hearing loss after
adjustment for age, sex, race, education, diabetes mellitus, smoking, and
hypertension. Hearing loss is defined by the pure-tone average of thresholds
at 0.5, 1, 2, and 4 kHz in the better-hearing ear. Upper and lower dashed
lines correspond to the 95% confidence interval.
tive risk (HR) of dementia associated with hearing loss
was 2.32 (95% CI, 1.32- 4.07). Thus, the attributable risk
of dementia associated with hearing loss in this subcohort was 36.4% (95% CI, 12.8%-58.6%).
COMMENT
In this study, hearing loss was independently associated
with incident all-cause dementia after adjustment for sex,
age, race, education, diabetes, smoking, and hypertension, and our findings were robust to multiple sensitivity analyses. The risk of all-cause dementia increased log
linearly with hearing loss severity, and for individuals older
than 60 years in our cohort, more than one-third of the
risk of incident all-cause dementia was associated with
hearing loss.
Our findings contribute significantly to the discussion
in the literature on whether hearing loss is a risk factor for
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dementia. Previous studies suggested that individuals with
hearing loss are more likely to have a diagnosis of dementia5,6 and poorer cognitive function.16 Supporting this hypothesis, smaller prospective studies have observed that
hearing loss is associated with accelerated cognitive decline in individuals with prevalent dementia.17,18 Although a prospective study19 of cognitively normal elderly volunteers failed to find any meaningful association
between hearing loss at study entry and later cognitive function, the results of that study are questionable because of
the short (5-year) follow-up and a 50% dropout rate. In our
study, hearing loss, a condition that is highly prevalent in
older adults and that often remains untreated,20 was strongly
and prospectively associated with incident dementia.
A number of mechanisms may be theoretically implicated in the observed association between hearing loss
and incident dementia. There may be an overdiagnosis
of dementia in individuals affected by hearing loss or, vice
versa, an overdiagnosis of hearing loss in individuals with
cognitive impairment at baseline. An overdiagnosis of dementia in our study is unlikely because the diagnostic
protocol for incident dementia relied on a consensus conference that examined information from multiple sources.
We also conducted sensitivity analyses censoring individuals diagnosed as having dementia during a 6-year
washout period from baseline that did not affect our results. In such an analysis, individuals would already have
had normal findings on several cognitive examinations
with hearing loss before being diagnosed as having dementia, likely indicating that the dementia diagnosis was
not confounded by poor communication. Hearing loss
(short of profound deafness) also minimally impairs faceto-face communication in quiet environments (ie, during cognitive testing), particularly in the setting of testing by experienced examiners who are accustomed to
working with older adults.21
An overdiagnosis of hearing loss is also unlikely because no evidence suggests that mild cognitive impairment would affect the reliability of audiometric testing.
Pure-tone audiometry has been performed in children as
young as 5 years. We also excluded any individuals with
recognized cognitive impairment at baseline (mild cognitive impairment or Blessed score ⬎3), and our results were
robust to models controlling for baseline Blessed scores.
Another possibility is that hearing loss and progressive cognitive impairment are caused by a common neuropathologic process, possibly the same that leads to AD.
However, pure-tone audiometry is typically considered
a measure of the auditory periphery because detection
of pure tones relies solely on cochlear transduction and
neuronal afferents to brainstem nuclei and the primary
auditory cortex. Perception of pure tones does not require higher levels of auditory cortical processing,22 and
results of auditory brainstem response testing of these
pathways are usually normal in patients with AD.23 In contrast, central auditory nuclei required for higher-order
auditory processing can be affected by AD neuropathology,24-26 and tests of central auditory function have been
found to be associated with AD.27
The likelihood of another neurobiological process such
as vascular disease or factors related to family history (eg,
apolipoprotein E [ApoE] status) causing hearing loss and
dementia also cannot be fully excluded. However, risk
factors for vascular disease such as diabetes, smoking, and
hypertension were adjusted for in our models, and a preliminary study has not found a positive association between ApoE status and hearing loss.28 Other variables,
such as mental and leisure activities, were not included
as covariates in our models because these variables would
not be expected to cause hearing loss and act as meaningful confounders in our models. Our results were also
robust to excluding individuals at baseline who had a history of stroke or transient ischemic attack.
Finally, hearing loss may be causally related to dementia, possibly through exhaustion of cognitive reserve, social isolation, environmental deafferentation, or
a combination of these pathways. Cognitive reserve reflects interindividual differences in neurocognitive processing that allow some individuals to cope better with
neuropathology than others.29 Functional magnetic resonance imaging studies showing interindividual variation in efficiency of task-related neural processing provide some evidence of this concept.30,31 Cognitive reserve
has also been used to explain discrepancies between the
extent of neuropathology seen at autopsy and clinical expression of dementia.32 The potential effect of hearing loss
on cognitive reserve is suggested by studies demonstrating that, under conditions in which auditory perception
is difficult (ie, hearing loss), greater cognitive resources
are dedicated to auditory perceptual processing to the detriment of other cognitive processes such as working
memory.33,34 This reallocation of neural resources to auditory processing could deplete the cognitive reserve available to other cognitive processes and possibly lead to the
earlier clinical expression of dementia.35
Communication impairments caused by hearing loss
can also lead to social isolation in older adults,36,37 and epidemiologic38,39 and neuroanatomic studies40 have demonstrated associations between poor social networks and dementia. Our results also seem to support this possible
pathway because the risk of dementia associated with hearing loss appeared to only increase at hearing thresholds
of greater than 25 dB, which is considered the threshold
at which hearing loss begins to impair verbal communication.41 Finally, a hypothetical mechanism by which hearing loss could directly affect AD neuropathology is suggested by animal studies demonstrating that environmental
enrichment (possibly analogous in humans to having access to auditory and environmental stimuli) can reduce
␤-amyloid levels in transgenic mouse models.42 This hypothesis is also supported by studies showing that individuals who remain engaged in leisure activities have a
lower risk of dementia.43
In the present study, self-reported hearing aid use was
not associated with a significant reduction in dementia risk,
but data on other key variables (eg, type of hearing aid used,
hours worn per day, number of years used, characteristics of participants choosing to use hearing aids, use of other
communicative strategies, and adequacy of rehabilitation) that would affect the success of aural rehabilitation
and affect any observed association were not gathered. Consequently, whether hearing devices and aural rehabilitative strategies could affect cognitive decline and dementia remains unknown and will require further study.
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Our study has limitations. First, only the severity of hearing loss at baseline was considered in the analysis, and information was not available on the trajectory of hearing loss
after baseline assessment or on the possible etiology of the
hearing loss. However, it is unlikely that this limitation substantially biased our findings given that reversible hearing
loss is rare, and hearing loss tends to only worsen with time.
Residual confounding by other environmental, genetic, or
neuropathologic processes is also plausible but speculative based on our current knowledge of established risk factors for hearing loss and dementia. Given the very close
association between age and both hearing loss and dementia, there is a possibility of unaccounted residual confounding. However, this is unlikely because we also confirmed
our findings in a statistical model using age rather than timeon-study as the time scale to account for nonlinear effects
of age on hearing and cognition.44 Our findings were also
unchanged after restricting our cohort to participants 65
years or older at baseline.
Finally, caution must be applied when generalizing
the results of our current study because the BLSA is a volunteer cohort of individuals of high socioceconomic status. Further confirmation of our results will need to be
performed in larger studies using more representative,
community-based samples. However, this potential limitation to broad generalizability could strengthen the internal validity of our findings given the relative homogeneity of the study cohort in observed and likely
unobservable characteristics.
If confirmed in other independent cohorts, the findings of our study could have substantial implications for
individuals and public health. Hearing loss in older adults
may be preventable45 and can be practically addressed with
current technology (eg, digital hearing aids and cochlear implants) and with other rehabilitative interventions focused on optimizing social and environmental conditions for hearing. With the increasing number of people
with hearing loss, research into the mechanistic pathways linking hearing loss with dementia and the potential of rehabilitative strategies to moderate this association are critically needed.
Accepted for Publication: April 29, 2010.
Correspondence: Frank R. Lin, MD, PhD, Department
of Otolaryngology–Head and Neck Surgery, The Johns
Hopkins School of Medicine, JHOC 6120, 601 N Caroline St, Baltimore, MD 21287 ([email protected]).
Author Contributions: Drs Metter and Ferrucci had full
access to all the data in the study and take responsibility
for the integrity of the data and the accuracy of the data
analysis. Study concept and design: Lin, Metter, and Ferrucci. Acquisition of data: Metter, O’Brien, Resnick, Zonderman, and Ferrucci. Analysis and interpretation of data:
Lin, Metter, O’Brien, Resnick, Zonderman, and Ferrucci.
Drafting of the manuscript: Lin and Metter. Critical revision of the manuscript for important intellectual content: Lin,
O’Brien, Resnick, Zonderman, and Ferrucci. Statistical
analysis: Lin, Metter, Zonderman, and Ferrucci. Obtained
funding: O’Brien and Resnick. Administrative, technical, or
material support: O’Brien and Zonderman. Study supervision: Resnick and Ferrucci.
Financial Disclosure: None reported.
Funding/Support: This work was supported by the Intramural Research Program of the National Institute on
Aging and grant 1K23DC011279-01 from the National
Institute on Deafness and Other Communication Disorders (Dr Lin).
Role of the Sponsor: The National Institute on Aging
funded the design and conduct of the study; collection,
management, analysis, and interpretation of the data; and
preparation and review of the manuscript. The sponsor
was not involved in manuscript approval.
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