Characterization of hearing loss in aged type II diabetics

Abstract

Presbycusis - age-related hearing loss - is the number one communicative disorder and a significant chronic medical condition of the aged. Little is known about how type II diabetes, another prevalent age-related medical condition, and presbycusis interact. The present investigation aimed to comprehensively characterize the nature of hearing impairment in aged type II diabetics. Hearing tests measuring both peripheral (cochlea) and central (brainstem and cortex) auditory processing were utilized. The majority of differences between the hearing abilities of the aged diabetics and their age-matched controls were found in measures of inner ear function. For example, large differences were found in pure-tone audiograms, wideband noise and speech reception thresholds, and otoacoustic emissions. The greatest deficits tended to be at low frequencies. In addition, there was a strong tendency for diabetes to affect the right ear more than the left. One possible interpretation is that as one develops presbycusis, the right ear advantage is lost, and this decline is accelerated by diabetes. In contrast, auditory processing tests that measure both peripheral and central processing showed fewer declines between the elderly diabetics and the control group. Consequences of elevated blood sugar levels as possible underlying physiological mechanisms for the hearing loss are discussed.

Fig. 1

For all frequencies tested, diabetics had higher tone thresholds than non-diabetic controls. Note that differences were greater at low frequencies, and were greater for the right ear compared to the left. See Table 1 for PTA frequency ranges. Right ear main effect: p < 0.0001, F = 30.8, df = 1; right ear post-hoc for PTA1: p < 0.05, t = 2.88; PTA2: p < 0.01, t = 3.44; PTA3: p < 0.05, t = 2.57, df = 1. Left ear main effect: p < 0.001, F = 13.8, df = 1; left ear post-hoc for PTA2: p < 0.05, t = 3.03, df = 1. Error bars are SEM.

Fig. 2

Diabetics showed a dramatic increase in white noise (WN) thresholds for both ears. Like pure tones, a greater difference was found for the right ear. ANOVA showed significant main effect for subject groups (p < 0.0001, F = 76.7, df = 1). Pairwise comparisons for each ear were also highly significant (right: p < 0.001, t = 6.42, df = 1; left: p < 0.001, t = 5.97, df = 1). Interactions were not significant. Error bars are SEM.

Fig. 3

At all frequencies, DPOAEs were smaller for diabetics relative to non-diabetics. Like the threshold measures presented in the previous figures, the right ear was more affected than the left. ANOVA showed significant main effects of subject group (right: p < 0.0001, F = 31.1, df = 1; left: p < 0.0001, F = 15.2, df = 1). Interactions and subject group Bonferroni post-hocs were not significant, except for the right ear at 2 kHz: p < 0.05, t = 2.82, df = 1. GM = geometric mean of f1 and f2. Error bars are SEM.

Fig. 4

Similar to the DPOAEs, diabetics showed smaller TEOAEs amplitudes than non-diabetics. The differences were not statistically significant. Error bars are SEM.

Fig. 5

Although not as dramatic as the white noise threshold differences, speech reception thresholds were significantly lower for non-diabetic controls relative to diabetics. ANOVA showed significant main effect for subject groups (p < 0.0001, F = 16.5, df = 1). The pairwise comparison for the right ear was also significant (p < 0.05, t = 3.56, df = 1). Interactions and left ear differences were not significant. SRT: speech reception threshold. Error bars are SEM.

Fig. 6

HINT speech thresholds were lower for non-diabetics than diabetics for all background noise speaker locations. HINT speech recognition in quiet was better for non-diabetics (not shown). ANOVA showed significant main effects of subject group (p < 0.0001, F = 20.5, df = 1) and background noise location (p < 0.0001, F = 14.3, df = 2). Bonferroni post-hoc tests for subject groups were significant for 90 (p < 0.05, t = 2.49, df = 1) and 270 (p < 0.01, t = 3.27, df = 1) degree background noise locations. Error bars are SEM.

Fig. 7

Diabetics had longer gap thresholds than controls (p < 0.02, F = 6.32, df = 1) and 4 kHz thresholds were shorter than 1 kHz thresholds (p < 0.02, F = 5.94, df = 1). Error bars are SEM.

Fig. 8

Flow diagram of possible biochemical pathways involved in the detrimental effects of type II diabetes on sensory end-organs such as the cochlea. See Section 4 for detailed explanations of these pathways and their likely effects on the auditory system.