The relationship between Diabetes and sensorineural hearing loss has been observed for over 150 years and was first noted in a patient with the early onset of a diabetic coma. Despite constant observation until recently, knowledge surrounding the correspondence between the two has been relatively abstract. However, recent advances in biomedical research have helped to gather data on how the impact of diabetes contributes to the development of Sensorineural hearing loss.
Auditory abnormalities in diabetes have been largely conflicting in several studies involving large sample sizes. Although the data has been conflicting, what has been deciphered from a review of the literature is that sensorineural hearing loss seems to be more prevalent in diabetic subjects with poor glycemic control. Therefore studies involving HBA1C measurement can be used as a prognostic factor to determine auditory acuity in diabetic subjects.
A significant proportion of studies determines reduced auditory acuity in diabetic subjects in comparison to non-diabetic. Inclusion criteria were largely based on the presence of diabetes, hyperlipidemia and hypertension, in contrast to healthy controls. Exclusion criteria included the presence of congenital auditory defects and ototoxic medication. The common assessment of auditory acuity in both the subjects and control groups included Pure tone Audiometry and Auditory Brainstem response (largely used in rodent studies) all showing a significantly increased mean difference in auditory thresholds in diabetic groups.
Figure 1. comparative in auditory thresholds in type 1 diabetic subjects in comparison to control using pure-tone audiometry (PTA). The audiogram also highlights increasing significant difference at higher frequencies (mean ± SD) (Dabrowski, 2014)
Figure 2 identifies delayed latencies in waves 3 and 5 during a comparative auditory brainstem response comparative between diabetic (red) and non-diabetic (blue) subjects which may be explained by the presence of myelinopathy, affecting signal transduction (Dabrowski, 2014)
Reduced auditory function in diabetic subjected with poor glycemic control has been attributed to the formation of Advanced glycation end products. Advanced glycation end products are formed by non-enzymatic interactions between the amino group in proteins and reducing sugars. Over time, glycation end products become advanced and form crosslinks with anatomical structures compromising the integrity of vessels resulting in vasculopathy. Advanced glycation end products are thought to also stimulate the production of reactive oxygen species which further damage vessels leading to vasculopathy and neuropathy in diabetic subjects.
Rodent studies using diabetes-induced mice have shown consistency in findings following histopathological examination of the cochlea. There was a significant loss of outer hair cells in the organ of Corti of diabetic mice compared to controls and damage to the stria vascularis. Similar findings were also noted in the study of human diabetic subjects in post-mortem examination of the cochlea.
On the whole, in light of the evidence provided, it seems unfair to state that diabetes is the sole cause of hearing loss due to insufficient evidence showing that diabetic people with well-controlled HBA1c suffer the same damage to the cochlea, therefore it could be considered that poor glycemic control is the leading cause of sensorineural hearing loss in diabetic subjects, rather than diabetes itself.
Figure 3. schematic representation of the various pathways resulting in the formation of AGE (Wu, et al, 2011)
Understanding this knowledge opens up many avenues in the exploration of antioxidant use to attenuate the effects of sensorineural hearing loss as shown in some rodent studies.
In a broad context, the implications of these finding could mean that a large percentage of individuals with advanced diabetes could require audiological screening as part of their diabetes care and will at some point require hearing aids. At the moment, the current UK guidance only screens for retinopathy and vasculopathy.
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