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OPEN Relationship of cardiovascular

disease risk and hearing loss
in a clinical population
Rachael R. Baiduc 1*, Joshua W. Sun 2, Caitlin M. Berry 2, Melinda Anderson 3 & Eric A. Vance 2

Hearing loss has been associated with individual cardiovascular disease (CVD) risk factors and, to a
lesser extent, CVD risk metrics. However, these relationships are understudied in clinical populations.
We conducted a retrospective study of electronic health records to evaluate the relationship between
hearing loss and CVD risk burden. Hearing loss was defined as puretone average ­(PTA0.5,1,2,4) > 20 dB
hearing level (HL). Optimal CVD risk was defined as nondiabetic, nonsmoking, systolic blood pressure
(SBP) < 120 and diastolic (D)BP < 80 mm Hg, and total cholesterol < 180 mg/dL. Major CVD risk
factors were diabetes, smoking, hypertension, and total cholesterol ≥ 240 mg/dL or statin use. We
identified 6332 patients (mean age = 62.96 years; 45.5% male); 64.0% had hearing loss. Sex-stratified
logistic regression adjusted for age, noise exposure, hearing aid use, and body mass index examined
associations between hearing loss and CVD risk. For males, diabetes, hypertension, smoking, and ≥ 2
major CVD risk factors were associated with hearing loss. For females, diabetes, smoking, and ≥ 2
major CVD risk factors were significant risk factors. Compared to those with no CVD risk factors, there
is a higher likelihood of hearing loss in patients with ≥ 2 major CVD risk factors. Future research to
better understand sex dependence in the hearing loss-hypertension relationship is indicated.

Hearing loss is estimated to affect 27.7 million adults in the ­USA1, and has been associated with d ­ epression2,
reduced quality of ­life , and cognitive ­decline . In older adults, hearing loss is a prevalent health ­condition6
3 4, 5

and often presents comorbidly with other chronic c­ onditions7. Once sensorineural hearing loss related to aging
or systemic disease such as cardiovascular disease (CVD) begins, it cannot be reversed, making identification
and treatment of modifiable risk factors critical for prevention and reduction of morbidity risk. To that end,
numerous epidemiological studies have sought to identify modifiable risk factors for hearing loss with increased
attention being paid to CVD risk factors (e.g. diabetes and smoking).
Various mechanisms might underlie associations between CVD risk factors and auditory dysfunction. Histo-
logical examinations have identified strial atrophy, loss of spiral ganglion neurons and outer hair cells, and basilar
membrane thickening as primary pathologic findings in ­diabetes8–10. In mice, exposure to cigarette smoke leads
to loss of spiral ganglion neurons, likely due to increase in cochlear oxidative ­stress11. Physiological studies in
the spontaneously hypertensive rat demonstrated that the stria vascularis is the primary auditory site of lesion
in ­hypertension12 and further suggest that hypertension accelerates age-related hearing ­loss13. Chinchillas fed a
high-cholesterol diet have increased serum cholesterol levels, cochlear lysosomes, and accumulation of extracel-
lular ­glycogen14. It is thought these morphological changes reflect strial and organ of Corti damage.
In human studies, reports suggest independent associations between hearing loss and tobacco s­ moking15,
­diabetes16–18, ­hypertension19, 20, and h
­ yperlipidemia21. Examination of relationships with overall CVD risk have
also been performed. These reports have explored associations between hearing loss and metabolic s­ yndrome22–26,
the American Heart Association’s Life’s Simple ­727, and Framingham Risk ­Score28. Results of these studies are
inconclusive as some have shown that aggregate CVD risk is associated with hearing ­loss22, 23, 26–28, though
others, including a longitudinal study of metabolic syndrome and incident hearing ­loss24, have ­not25. Further,
most published research on this topic has utilized epidemiological datasets (e.g., National Health and Nutri-
tion Examination Survey [­ NHANES]23, Korean N ­ HANES25, Busselton Healthy Ageing S­ tudy28, Jackson Heart
27
­Study ). Published clinical reports have limited generalizability having been primarily conducted in A ­ sian22
or ­Iranian26 populations. Understanding these relationships in the American clinical population is of interest

1
Department of Speech, Language, and Hearing Sciences, University of Colorado Boulder, 2501 Kittredge Loop
Drive, 409 UCB, Boulder, CO 80309, USA. 2Department of Applied Mathematics, University of Colorado Boulder,
Boulder, CO 80309, USA. 3Department of Otolaryngology, University of Colorado School of Medicine, Aurora, CO,
USA. *email: [email protected]

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because providers routinely treat patients with CVD risk factors. Using NHANES 1999–2010 data, Saydah
et al.29 found that ~ 70% of U.S. adults ≥ 18 years have at least one CVD risk factor with multiple comorbidities
being common.
Sex differences factor into both hearing and cardiovascular health. For example, evidence suggests that women
­ en30. Male sex
with certain CVD risk factors (e.g., diabetes) are at higher risk of CVD events (e.g. stroke) than m
has been associated with hearing loss in h ­ umans31 and reduced cochlear integrity in rhesus ­monkeys32. There
is a higher risk of incident hearing loss among men, even for low-risk men (e.g. thin, educated, non-smoker)33.
Some studies relating hearing loss to CVD risk factors suggest sex-specific associations. A significant relation-
ship between self-reported myocardial infarction and cochlear impairment was observed in the Epidemiology
of Hearing Loss Study, but only in w ­ omen34. A study of Medicare beneficiaries in the Health, Aging, and Body
Composition study found that high blood pressure (BP) was associated with hearing loss, but only in white ­men35.
An investigation of persons > 80 years old found the association between CVD risk factors and hearing loss to
be stronger in men, a finding partly explained by cardioprotective effects of e­ strogen36. Together this evidence
suggests that there may be sex-based differences in hearing status related to CVD-risk factors although significant
gaps in our understanding remain.
The aim of the present retrospective chart review was to investigate the relationship between hearing loss and
CVD risk factor burden in a clinical sample. Our assessment of CVD risk was based on risk factors commonly
managed in the primary care setting; namely, hypertension, hyperlipidemia, tobacco smoking, and diabetes.
Adjusting for potential confounders, we compared hearing in patients with major CVD risk factors to hearing
in patients with optimal CVD risk status (i.e. no major risk factors). A secondary aim was to evaluate sex differ-
ences in these relationships. We hypothesized that increasing CVD risk load would be associated with greater
odds of hearing loss. In doing so, we sought to advance understanding of the relationship between CVD risk and
hearing loss, which may illuminate pathways for improved prevention and intervention.

Materials and methods
Study design and setting.  We conducted a retrospective review of clinical data from patients seen at UCHe-
alth, a large Colorado academic medical center, between 1-Jan 2011 and 31-Jul 2019. Patients aged ≥ 18 years
who underwent audiological and general health evaluations (including BP measurement and glucose and lipid
panels) were identified via query of Health Data Compass Data Warehouse electronic health records (EHRs).

Chart review.  We manually extracted audiological data from the records of 7069 patients, which were
entered into a deidentified database. We directly exported all other data including patient demographics and
CVD risk factor status from EHRs. Identifiable personal health information was not included in the database.
Ethical approval and informed consent statements were exempted (#19-1400) by the Colorado Multiple Insti-
tutional Review Board. All methods were carried out in accordance with relevant guidelines and regulations.
From the core group of patients, we excluded individuals with bilateral abnormal tympanograms (i.e. static
acoustic admittance < 0.3 or > 1.8 mmohs or peak pressure < − 150 daPa), suspected or diagnosed conductive
pathology (primarily identified by measurement of an air–bone gap > 10 dB at one or more frequencies between
250 and 4000 Hz), sudden sensorineural hearing loss, history of otologic surgery, acoustic neuroma, cochlear
implants, ototoxic medication use, and missing CVD risk factor or audiometric data resulting in a final sample
of 6332 patients (Fig. 1).

Determination of cardiovascular disease risk status.  Diabetes, tobacco smoking, hyperlipemia,

hypertension served as independent variables. We classified tobacco smoking status (Never/Current/Former)
based on self-report. We defined diabetes as use of antihyperglycemics, fasting plasma glucose ≥ 126  mg/dL,
random serum/plasma glucose ≥ 200 mg/dL [or 11.1 mmol/L]), and/or physician diagnosis indicated by Inter-
national Classification of Disease codes (versions 9 and 10). We categorized BP into four strata based on sys-
tolic (S) and diastolic (D) BP levels: [a] SBP ≥ 160  mmHg or DBP ≥ 100  mmHg, or use of antihypertensives,
[b] SBP 140–159 or DBP 90–99 mmHg (elevated), [c] SBP 120–139 or DBP 80–89 mmHg (not optimal), and
[d] SBP < 120 and DBP < 80 mmHg (optimal; reference group)37. We defined four strata for total cholesterol:
[a] ≥ 240 mg/dL or statin use, [b] 200–239 mg/dL (elevated), [c] 180–199 mg/dL (not optimal), and [d] < 180 mg/
dL (optimal; reference group). Diabetes, current smoking, cholesterol group (a), and BP group (a) were classified
as major risk factors.
Based on the four CVD risk factors, we defined CVD risk burden categorically and continuously. First, per
Bogle et al.37 we created five mutually exclusive risk categories: [a] optimal levels of all four CVD risk factors,
[b] ≥ 1 CVD risk factors non-optimal, [c] ≥ 1 CVD risk factors elevated, [d] exactly 1 major CVD risk factor, and
[e] ≥ 2 major CVD risk factors. Second, we computed Framingham Risk Scores per D’Agostino et al.’s ­algorithm38.
This score represents 10-year absolute CVD risk and risk of individual events (e.g. heart failure, peripheral arte-
rial disease, etc.).

Audiological assessment and outcome variables.  Audiological data consisted of information

obtained during audiological examination (i.e. otoscopy, tympanometry, and air and bone conduction audi-
ometry). Audiologic evaluations were completed by a licensed audiologist based on our institution’s standard
of care. We captured portions of the assessment, including case history, and air- and bone-conduction puretone
audiometry (Air: 0.5, 1, 2, 3, 4, 6, 8  kHz; Bone: 0.5, 1, 2, 4  kHz). If necessary, masking was performed, and
masked thresholds were used in place of unmasked thresholds in statistical models. For all frequencies, in the
case of nonresponse, thresholds were defined as 130 dB HL. Finally, noise exposure history (recreational, non-

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Figure 1.  Flowchart of patient exclusions.

military occupational, and military) was determined via case history. For statistical analysis, noise history was
collapsed into one binary variable (Yes/No).
Our primary outcome variable was hearing loss, which we defined as average threshold at 0.5, 1, 2, and 4 kHz
(hereafter, puretone average ­[PTA0.5,1,2,4]) > 20 dB HL in the poorer ear. We also evaluated hearing thresholds
continuously at discrete audiometric frequencies.

Statistical analysis.  We report continuous measures as mean (SEM) and categorical measures as number
(percent). We compared categorical variables using the Chi-square test and continuous variables with two-tailed
t-tests. We used logistic regression to determine associations between hearing loss and CVD risk (four indi-
vidual risk factors and overall risk). We used linear regression to compare thresholds at individual audiometric
frequencies between the five CVD risk strata using the optimal group as reference. We also used linear regression
to examine the relationship between P ­ TA0.5,1,2,4 and Framingham Risk Score. Fully adjusted models included
age, sex (unless stratified), noise exposure, hearing aid use (yes/no), and body mass index (BMI) as covari-
ates. Models for individual risk factors (e.g. diabetes) were adjusted for the other three CVD risk factors. We fit
models separately for men and women. Additional models were constructed for prediabetes and former tobacco
smoking although these factors were not considered for aggregate CVD risk classification. P-values < 0.05 were
considered statistically significant. Analysis was done using the glm function in R (R Core Team (2019) v. 3.6.1).

Conference presentation.  Portions of this work were presented at the Association of Diabetes Care and
Education Specialists conference in August of 2020 and at the American Academy of Audiology conference in
April of 2021.

Results
We present patient characteristics in Table 1. We identified 4052 patients with hearing loss. Individuals with hear-
ing loss were older than those without hearing loss (68.75 [SEM = 0.19] vs. 52.67 [SEM = 0.28] years; p < 0.001).
The hearing loss group contained more males than the normal hearing group (49.85% vs. 37.68%, respectively;
p < 0.001). For both groups, most individuals were non-Hispanic white. High cholesterol, hypertension, and dia-
betes were more common in patients with hearing loss; the prevalence of current smoking was similar between
groups.
Table 2 shows noise exposure history and average hearing sensitivity ­(PTA0.5,1,2,4) by hearing loss status. Noise
exposure, particularly military-related, was more common in persons with hearing loss than those without.
For those with hearing loss, most (84.35%) had bilateral loss and on average, hearing loss was mild (worse ear
­PTA0.5,1,2,4 of 39.83 dB HL [SEM = 0.26]). Supplementary Table S1 reports the distribution of hearing loss by CVD
risk status and sex. For both sexes, the prevalence of hearing loss generally increased as CVD risk load increased.
For each risk strata, there were more males with hearing loss than females. This difference was greatest in the
lowest risk stratum wherein 54.86% (95% CI 47.18–62.32) of males, but only 25.44% (95% CI 20.56–31.01) of
females, had hearing loss.
Supplementary Table S2 reports unadjusted hearing thresholds which tended to increase (worsen) with
increasing CVD risk load. On average, hearing sensitivity was 7.27 dB worse in men than women. Sex-stratified

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Normal hearing
Hearing loss (N = 4052)* (N = 2280)
Mean or % SEM or N Mean or % SEM or N P value
Demographic variables
 Sex, male 49.85% 2020 37.68% 859  < 0.001
 Age, years 68.75 0.19 52.67 0.28  < 0.001
 Race
  American Indian and Alaska Native 0.32% 13 0.18% 4
  Asian 3.58% 145 2.72% 62
  Black or African American 6.24% 253 7.24% 165
  Multiple race 0.81% 33 1.14% 26
 < 0.001
  Native Hawaiian and other Pacific Islander 0.10% 4 0.00% 0
  Other 6.71% 272 6.40% 146
  Unknown 0.74% 30 2.28% 52
  White or Caucasian 81.49% 3302 80.04% 1825
 Ethnicity
  Hispanic 6.42% 260 7.06% 161
  Non-Hispanic 92.30% 3740 90.70% 2068
0.016
  Patient refused 0.59% 24 0.83% 19
  Unknown 0.69% 28 1.40% 32
Cardiovascular variables
 BMI (kg/m2) 27.86 0.09 27.36 0.13 0.001
 Total cholesterol (mg/dL) 177.31 0.66 185.33 0.82  < 0.001
 Use of cholesterol lowering medication 43.02% 1743 18.29% 417  < 0.001
 Cholesterol strata (mg/dL)
   < 180 22.88% 927 35.09% 800
  180–199 11.77% 477 17.24% 393
 < 0.001
  200–239 17.47% 708 22.11% 504
   ≥ 240 or statin use 47.88% 1940 25.57% 583
 Systolic blood pressure (mm Hg) 130.90 0.30 124.98 0.37  < 0.001
 Diastolic blood pressure (mm Hg) 74.20 0.16 75.15 0.22  < 0.001
 Use of antihypertensives 29.15% 1181 13.25% 302  < 0.001
 Blood pressure strata (mm Hg)†
  SBP < 120 and DBP < 80 19.97% 809 34.43% 785
  SBP 120–139 or DBP 80–89 31.24% 1266 35.70% 814
 < 0.001
  SBP 140–159 or DBP 90–99 15.28% 619 13.42% 306
  BP ≥ 160 or DBP ≥ 100, or use of antihypertensives 33.51% 1358 16.40% 374
 Estimated average glucose (mg/dL)‡ 128.53 0.60 117.91 0.60  < 0.001
 Glucose tolerance fasting (mg/dL)‡ 102.43 6.19 108.80 3.32 0.387
 Glucose serum/plasma (mg/dL)‡ 109.72 0.68 98.90 0.65  < 0.001
 Glucose random serum/plasma (mg/dL)‡ 106.08 0.67 97.44 0.84  < 0.001
 Use of antihyperglycemics 15.70% 636 6.23% 142  < 0.001
 Diabetes
  No 20.06% 813 31.45% 717
  Yes 36.85% 1493 19.52% 445  < 0.001
  Prediabetes 43.09% 1746 49.04% 1118
 Smoking
  Never 53.33% 2161 68.29% 1557
  Current 5.70% 231 4.78% 109  < 0.001
  Former 40.97% 1660 26.93% 614
 CVD risk burden
Continued

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Normal hearing
Hearing loss (N = 4052)* (N = 2280)
Mean or % SEM or N Mean or % SEM or N P value
  All risk factors ­optimal§ 4.15% 168 12.72% 290
   ≥ 1 risk factors not ­optimal‖ 10.61% 430 20.26% 462
   ≥ 1 risk factors ­elevated¶ 14.19% 575 21.84% 498  < 0.001
  1 major risk ­factor# 32.97% 1336 28.46% 649
   ≥ 2 major risk factors** 38.08% 1543 16.71% 381
  Framingham risk ­score‡,†† 0.21 0.00 0.09 0.00  < 0.001

Table 1.  Patient demographic and cardiovascular characteristics by hearing status. P-values from Chi-square
tests (categorical variables) or t tests (continuous variables). BMI body mass index, DBP diastolic blood
pressure, PTA pure-tone average SBP systolic blood pressure, SEM standard error of the mean. *Defined as
­PTA0.5,1,2,4 > 20 dB HL in the worse ear. † One patient was excluded from logistic regression models due to
missing BP group status. ‡ N for hearing loss and normal hearing groups, respectively. Estimated average
glucose: N = 2944, 1465; Glucose tolerance fasting: N = 7, 54; Glucose serum/plasma: N = 3824, 2113; Glucose
random serum/plasma: N = 3251, 1576; Framingham Risk Score: N = 5452 overall. § All CVD RFs optimal:
BP < 120 and < 80 mmHg, total cholesterol < 180 mg/dL, not currently smoking, and no diabetes. ‖  ≥ 1 CVD RF
not optimal: BP 120–139 or 80–89 mmHg or total cholesterol 180–199 mg/dL, not currently smoking, and no
diabetes. ¶  ≥ 1 CVD RFs elevated: 140–159 or 90–99 mmHg, or total cholesterol 200–239 mg/dL, not currently
smoking, and no diabetes. # Exactly 1 major CVD RF: SBP ≥ 160 or DBP ≥ 100 mmHg or on treatment, or
cholesterol ≥ 240 mg/dL or on treatment, or diabetes, or current tobacco smoking. ** ≥ 2 major CVD RFs:
having at least 2 RFs from footnote #. †† Defined per D’Agostino et al. (2008).

No hearing loss
Hearing loss (N = 4052)* (N = 2280)
Characteristic Mean or % SEM or N Mean or % SEM or N
Audiological data
 Noise exposure, yes 39.17% 1587 28.64% 653
  Recreational 9.97% 404 11.32% 258
  Non-military occupational 12.22% 495 8.95% 204
  Military 10.98% 445 4.43% 101
  Unknown/type not reported 10.37% 420 6.40% 146
 Puretone average,† dB HL
  Better ear 33.83 0.22 11.18 0.09
  Worse ear 39.83 0.26 13.50 0.09
  Hearing loss better ear, yes 84.35% 3418 0.00% 0.00
  Hearing loss poorer ear, yes 100.00% 4116 0.00% 0.00

Table 2.  Audiological characteristics by hearing status. dB HL decibels hearing level, SEM standard error of
the mean. *Defined as ­PTA0.5,1,2,4 > 20 dB HL in the worse ear. † Defined as average threshold at 0.5, 1, 2, 4 kHz.

ear-specific audiograms adjusted for age, BMI, hearing aid use, and noise exposure are shown in Fig. 2. Males
had more severe and more steeply sloping hearing loss than females. In males, those with ≥ 1 non-optimal CVD
risk factor had significantly better hearing at 4.0 kHz (right ear) and those with ≥ 2 major CVD risk factors had
poorer hearing at 0.5 kHz (right ear) and 8.0 kHz (left ear) vs. the optimal risk group. In females, compared to
the optimal risk group, those with ≥ 2 major CVD risk factors had significantly poorer hearing at all frequencies
between 1.0 and 8.0 kHz (right ear) and at 2.0, 3.0 and 4.0 kHz (left ear).
Associations between hearing loss and CVD risk factors are shown in Table 3, which includes age-sex and
multivariable-adjusted models. The age-sex adjusted model shows that diabetes, hypertension (specifically, BP
group [d]), current and former smoking, and having 1 or ≥ 2 major CVD risk factors were associated with hear-
ing loss. Except former tobacco smoking and hypertension, the significance of these associations was retained
in the fully adjusted model. The strongest relationships were those with current smoking (OR = 2.02 [95% CI
1.52–2.71]) and ≥ 2 major CVD risk factors (OR = 2.23 [95% CI 1.67–3.00]). The odds of hearing loss increased
with increasing BP and total cholesterol levels, and with increasing CVD risk.
Next, because sex-specific relationships were identified upon audiometric analysis (Fig. 2), we report sex-
stratified multivariable adjusted ORs (MVOR) for hearing loss in Fig. 3. Amongst females, diabetes, current
smoking, and having ≥ 2 major CVD risk factors were significantly associated with increased odds of hearing
loss (MVOR = 1.48; [95% CI 1.13–1.94]; MVOR = 2.10 [95% CI 1.40–3.17]; MVOR = 2.52 [95% CI 1.66–3.86],

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Figure 2.  Sex-stratified ­audiograms* (mean [95% CI] by ear and CVD risk group. Filled symbols indicate
P < 0.05 in comparison to optimal CVD (reference group). Data points jittered on x-axis to provide greater visual
clarity of error bars. *adjusted for age, hearing aid use, BMI, noise exposure.

respectively). Similarly, in males, estimated associations of hearing loss with diabetes, smoking, and ≥ 2 major
CVD risk factors were as follows: MVOR = 1.73 (95% CI 1.28–2.34), MVOR = 2.03 (95% CI 1.35–3.10), and
MVOR = 1.88 (95% CI 1.23–2.86), respectively. High BP was also associated with hearing loss with MVOR = 1.67
(95% CI 1.20–2.32) and MVOR = 1.68 (95% CI 1.23–2.29) for BP groups (b) and (a), respectively.
Finally, the strength of the relationship between Framingham Risk Score and P ­ TA0.5,1,2,4 is reflected by the R
value of 0.419 shown in Supplementary Fig. S1, suggesting that as risk increased, hearing sensitivity worsened.

Discussion
This study evaluated the relationship between CVD risk factors and hearing loss in 6332 patients. We used CVD
risk metrics commonly employed in primary care and hypothesized that there would be a positive relationship
between increasing CVD risk factor load and likelihood of hearing loss. First, our results demonstrated that dia-
betics and current smokers had increased odds of hearing loss. Having ≥ 2 major CVD risk factors was associated
with 92% increased odds of hearing loss compared to the optimal CVD risk stratum. Second, hypertension was
associated with hearing loss, but only in males. Other relationships were similar between the sexes.
Of the CVD risk factors, the strongest relationship we observed was that with current smoking, which was
associated with hearing loss in both sexes (MVOR = 1.85 [95% CI: 1.40–2.46]). Our findings are consistent with
cross-sectional reports from the Epidemiology of Hearing Loss ­Study15, Korean ­NHANES39, and the UK Biobank
­Resource40, which utilized a speech-in-noise test. Prospective research has also linked smoking to hearing ­loss41.
In our study, former smoking was not associated with hearing loss, which has been shown p ­ reviously40. Former
smokers may adopt other positive lifestyle changes (e.g. improved diet, physical activity, BP control), which could
be protective for auditory health. Smoking cessation may mitigate the excess risk of hearing loss associated with
smoking, although further research is needed to corroborate this possibility.
Diabetics were at 43% higher odds of hearing loss than non-diabetics. The strength of this association was
similar between the sexes. The link we observed with diabetes is consistent with past r­ eports8, 16, 17, 42. In a meta-
analysis, Akinpelu et al.16 reported a slightly more robust association with diabetes than we found. Based on six
studies, they calculated an average OR for hearing loss of 1.91 (95% CI 1.47–2.49). The studies they evaluated
defined hearing loss using a cut point of 25 dB HL whereas we used 20 dB HL. Other factors such as diabetic
control, disease duration, and participant demographics could also account for variable strength of the reported
associations.
Previous studies on the relationship between hearing loss and hyperlipemia are inconclusive and report
contradictory ­results21, 25, 43–45. We did not find evidence to support an association between high cholesterol
and hearing loss. There was widespread use of statins in our sample. In patients with hearing loss, 43% were on
statins. Moreover, 18% of individuals with normal hearing were on treatment. A cross-sectional analysis of Blue
Mountain Hearing Study participants aged ≥ 50 years found cholesterol-lowering medication to be negatively

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Age-sex* adjusted Multivariable† adjusted

OR (95% CI) P value MVOR (95% CI) P value
Diabetes
 No diabetes 1.0 [Ref] 1.0 [Ref]
 Diabetes 1.55 (1.29, 1.86)  < 0.001 1.58 (1.30, 1.93)  < 0.001
 Prediabetes 0.95 (0.81, 1.11) 0.518 0.96 (0.81, 1.13) 0.624
Blood pressure (mm Hg)
 Optimal, SBP/DBP, < 120/ < 80 1.0 [Ref] 1.0 [Ref]
 SBP, 120–139 or DBP 80–89 1.05 (0.90, 1.23) 0.525 1.01 (0.85, 1.21) 0.881
 SBP 140–159 or DBP 90–99 1.13 (0.92, 1.38) 0.236 1.11 (0.89, 1.38) 0.365
 SBP/DBP, ≥ 160/ ≥ 100 or medication use 1.24 (1.03, 1.5) 0.020 1.20 (0.98, 1.47) 0.078
Total cholesterol (mg/dL)
 Optimal, < 180 1.0 [Ref] 1.0 [Ref]
 180–199 1.00 (0.82, 1.23) 0.962 0.98 (0.79, 1.21) 0.829
 200–239 1.11 (0.93, 1.33) 0.258 1.11 (0.91, 1.34) 0.305
  ≥ 240 mg/dL (or statin use) 1.14 (0.96, 1.34) 0.128 1.13 (0.95, 1.35) 0.175
Tobacco smoking
 Never 1.0 [Ref] 1.0 [Ref]
 Current 1.93 (1.47, 2.56)  < 0.001 2.02 (1.52, 2.71)  < 0.001
 Former 1.18 (1.03, 1.35) 0.016 1.11 (0.96, 1.28) 0.165
 CVD risk factor ­burden§
 All RF optimal 1.0 [Ref] 1.0 [Ref]
  ≥ 1 risk factor not optimal 1.18 (0.89, 1.56) 0.250 1.20 (0.89, 1.63) 0.241
  ≥ 1 risk factor elevated 1.26 (0.96, 1.65) 0.097 1.31 (0.98, 1.76) 0.069
 1 major risk factor 1.48 (1.14, 1.91) 0.003 1.44 (1.09, 1.91) 0.011
  ≥ 2 major RF 2.19 (1.68, 2.86)  < 0.001 2.23 (1.67, 3.00)  < 0.001

Table 3.  Age-sex* and multivariable adjusted† odds ratios (95% CI) for hearing ­loss‡. Significant values are
in italics. DBP diastolic blood pressure, MVOR multivariable adjusted odds ratio, SBP systolic blood pressure.
*All CVD risk factors are covariates in individual risk factor models. † Adjusted for age, sex, noise exposure,
hearing aid use, and BMI. Individual risk factors are covariates in individual risk factor models. ‡ Defined as
­PTA0.5,1,2,4 > 20 dB HL in the worse ear. § Defined as per Table 1.

associated with hearing l­oss21. One contested possibility is that treatment positively influences auditory status,
which may obscure any negative influence of hyperlipidemia itself. However, a randomized trial of the effect of
atorvastatin on hearing loss progression did not find evidence to support this h ­ ypothesis46.
The one sex-specific relationship we observed was that between hearing loss and hypertension, which was
limited to males. The prevalence of hypertension was 42% overall (45% in males and 39% in females; data not
shown). Cross-sectional reports including those from the N ­ HANES31, Busselton Healthy Ageing S­ tudy28, and
47
Hispanic Community Health Study/Study of ­Latinos have identified significant relationships between hyperten-
sion and hearing loss. Sex differences have also been reported. For example, a study of 3315 participants (aged
52–99 years) from the Rotterdam Study reported a significant relationship between low-frequency hearing loss
and systolic BP in men, but not w­ omen48. An association between hypertension and high-frequency hearing loss
was reported in men, but not women, from the Framingham c­ ohort49. Wattamwar et al.36 observed a stronger
relationship between CVD risk factors and hearing loss in elderly males than females. The underpinning(s) of
these sex differences is unknown but may relate to the otoprotective effects of estrogen, which has been proposed
for age-related and noise-induced hearing l­ oss50.
Results of this study extend the current literature on CVD comorbidities and hearing loss. Our multivariate
model showed that having ≥ 1 major CVD risk factors significantly increases odds of hearing loss. This is impor-
tant because most individuals had ≥ 1 major CVD risk factors, with hyperlipidemia being the most common. Of
the patients with hearing loss, the majority (71%) had ≥ 1 major risk factors while only 45% of individuals with
normal hearing had ≥ 1 major risk factors (Table 1). In the overall sample, we observed a graded association
between CVD risk and likelihood of hearing loss with MVORs for exactly 1 and ≥ 2 major risk factors being 1.44
(95% CI 1.09–1.91) and 2.23 (95% CI 1.67–3.00), respectively. We also observed a correlation between PTA and
Framingham Risk Score (Supplementary Fig. S1).
We observed dose-dependent relationships between odds of hearing loss and BP and total cholesterol levels,
but these associations were not significant in the overall sample. Our findings indicate that increasing risk fac-
tor load is associated with greater likelihood of hearing loss. However, this seems to be the case only for major
CVD risk factors as non-optimal risk factor status (e.g. prediabetes) was not significantly related to hearing loss.
Our approach to defining CVD risk differs somewhat from prior reports. Nonetheless, comparisons to past
research can be made. With an average participant age similar to ours, Tan et al.28 identified a graded association
between Framingham Risk Score and hearing loss in the Busselton Healthy Ageing Study. Sun et al.23 found a

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Figure 3.  Sex-stratified forest plots of multivariable adjusted odds ­ratios* (95% CI) for hearing l­oss†. DBP
diastolic blood pressure, RF risk factor, SBP systolic blood pressure. * Adjusted for age, noise exposure,
hearing aid use, and BMI. Individual risk factors are covariates in individual risk factor models. † Defined as
­PTA0.5,1,2,4 > 20 dB HL in the worse ear.

higher number of metabolic syndrome components to be related to hearing loss in the NHANES and a separate
NHANES study determined diabetes and smoking to be a particularly harmful c­ ombination51.
The clinical implications of this work are relevant to medical practitioners across specialties. Early identifica-
tion of auditory dysfunction in persons with modifiable risk factors such as smoking is critical to reducing the
disease burden of hearing loss. Knowledge that certain risk factors and high-risk factor load are associated with
hearing loss may guide recommendations for hearing evaluations and intervention for at-risk patients. With
increased attention to personalized medicine and patient-centered care, these findings support holistic medi-
cal care. In the future, clinical implications will be better understood once prospective studies can address how
baseline CVD risk status influences long term auditory function.
This retrospective study has important limitations. The cross-sectional design hampers determinations regard-
ing causality and progression of hearing loss. In some instances, we were unable to capture CVD comorbidity
status on the day of audiological evaluation as visits for hearing and other health concerns did not always coin-
cide. We used CVD risk factor and BMI data from the date of the closest clinical encounter and cannot account
for potential day-to-day variability in these measures. We did not adjust for medication use as the definition
of CVD risk stratification included treatment. Our audiometric analysis did not adjust for multiple hypothesis
tests. Data from primarily white cohorts were used to develop the Framingham Risk Score algorithm. It may
not provide precise CVD risk estimates for all racial/ethnic groups. Data used to develop the original algorithm
were from subjects aged 30–74 years whereas patients in our dataset ranged from 18–97 years. Last, we were
only able to calculate risk scores for 5452 patients as calculation requires information that was not available for
all individuals (namely, high-density lipoprotein levels).
In conclusion, this study provides data on hearing status as it relates to adverse cardiovascular health. Dia-
betes, smoking, and the presence of ≥ 2 major CVD risk factors significantly increased the odds of hearing loss.

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In males, hypertension was also a significant predictor. Improved glucose control, smoking cessation, and early
BP management (for males) may promote healthy hearing although such strategies would need to be borne out
by longitudinal studies.

Data availability
All relevant data are within the paper and tables/figures. Raw data that support the findings of this study are
available from the corresponding author upon reasonable request.

Received: 22 June 2022; Accepted: 20 January 2023

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Acknowledgements
We thank Brynne Stevens for her contributions to data management. This work was supported by the Health
Data Compass Data Warehouse project (healthdatacompass.org). Publication of this article was funded by the
University of Colorado Boulder Libraries Open Access Fund.

Author contributions
R.R.B. and M.A. conceptualized and designed the study and obtained funding. M.A. guided development of the
audiologic and health records database. E.A.V. designed the statistical analysis plan and oversaw analysis. J.S.
and C.B. carried out the analysis and created tables and figures. R.R.B. drafted the manuscript and all authors
provided critical edits.

Funding
This work was funded by a grant from the American Hearing Research Foundation (University of Colorado
Boulder and University of Colorado School of Medicine).

Competing interests 
The authors declare no competing interests.

Additional information
Supplementary Information The online version contains supplementary material available at https://​doi.​org/​
10.​1038/​s41598-​023-​28599-9.
Correspondence and requests for materials should be addressed to R.R.B.
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