Noise-induced hearing loss (NIHL) is a hearing impairment (HI) caused by various clinical factors. Identifying the relationship between NIHL and nutrient consumption could help in reducing the prevalence of hearing loss. The aim of this study was to analyze the relationship between NIHL and dietary factors using data of the Korea National Health and Nutrition Examination survey (KNHANES). The data were collected from The Fifth KNHANES 2010–2012. The survey was taken by a total of 10,850 participants aged 20–65 years. Air conduction audiometry was measured at 500, 1000, 2000, and 4000 Hz in both ears. Metabolic syndrome, noise exposure, alcohol consumption, smoking, income level, marital status, and nutritional intake were evaluated. The differences between non-HI and HI participants in the noise-exposed group showed statistically significant differences in age, sex, marital and smoking status, alcohol consumption, and fasting glucose and triglyceride levels (p<0.05). In a multiple regression analysis of the noise-exposed group, age showed a significant association with HI (OR: 0.604; 95% CI: 0.538–0.678) after adjusting for confounders. In multivariate analysis for dietary factors affecting HI in noise-exposed groups, retinol (OR: 1.356; 95% CI: 1.068–1.722), niacin (OR: 1.5; 95% CI: 1.022–2.201), and carbohydrates (OR: 0.692; 95% CI: 0.486–0.985) showed a significant association with NIHL. Age was identified as the only factor significantly affecting NIHL. When the dietary factors of the noise-exposed group were analyzed, high intake of niacin and retinol and low intake of carbohydrates appeared to reduce the risk of hearing loss.

Transmembrane and tetratricopeptide repeat 4 ( Tmtc4 ) is a deafness gene in mice. Tmtc4 -KO mice have rapidly progressive postnatal hearing loss due to overactivation of the unfolded protein response (UPR); however, the cellular basis and human relevance of Tmtc4 -associated hearing loss in the cochlea was not heretofore appreciated. We created a hair cell–specific conditional KO mouse that phenocopies the constitutive KO with postnatal onset deafness, demonstrating that Tmtc4 is a hair cell–specific deafness gene. Furthermore, we identified a human family in which Tmtc4 variants segregate with adult-onset progressive hearing loss. Lymphoblastoid cells derived from multiple affected and unaffected family members, as well as human embryonic kidney cells engineered to harbor each of the variants, demonstrated that the human Tmtc4 variants confer hypersensitivity of the UPR toward apoptosis. These findings provide evidence that TMTC4 is a deafness gene in humans and further implicate the UPR in progressive hearing loss.

Exposure to loud noise is a common cause of acquired hearing loss. Disruption of subcellular calcium homeostasis and downstream stress pathways in the endoplasmic reticulum and mitochondria, including the unfolded protein response (UPR), have been implicated in the pathophysiology of noise-induced hearing loss. However, studies on the association between calcium homeostasis and stress pathways have been limited due to limited ability to measure calcium dynamics in mature-hearing, noise-exposed mice. We used a genetically encoded calcium indicator mouse model in which GCaMP6f is expressed specifically in hair cells or supporting cells under control of Myo15Cre or Sox2Cre, respectively. We performed live calcium imaging and UPR gene expression analysis in 8-week-old mice exposed to levels of noise that cause cochlear synaptopathy (98 db sound pressure level [SPL]) or permanent hearing loss (106 dB SPL). UPR activation occurred immediately after noise exposure, and the pattern of UPR activation was dependent on noise level, with the proapoptotic pathway upregulated only after 106 dB noise exposure. Spontaneous calcium transients in hair cells and intercellular calcium waves in supporting cells, which are present in neonatal cochleae, were quiescent in mature-hearing cochleae but reactivated upon noise exposure. Noise exposure of 106 dB was associated with more persistent and expansive intercellular Ca ²⁺ signaling wave activity. These findings demonstrate a strong and dose-dependent association between noise exposure, UPR activation, and changes in calcium homeostasis in hair cells and supporting cells, suggesting that targeting these pathways may be effective to develop treatments for noise-induced hearing loss.

Objective: The primary treatment for sudden hearing loss is high-dose steroid therapy. In some countries, hospitalization has been taken for granted. Although most countries appear to treat sudden hearing loss on an outpatient basis, some other countries have considered hospitalization as necessary. Only a few studies have been conducted on the effect of hospitalization on hearing outcomes. Therefore, we compared the hearing outcome of inpatient- and outpatient-based treatments to determine whether hospitalization affects the recovery of sudden hearing loss. Methods: We conducted a retrospective case review of patients diagnosed with sudden sensorineural hearing loss (SSNHL). In total, 439 patients with SSNHL were enrolled and categorized as either inpatients (group I) or outpatients (group O). Pure-tone audiometry was initially performed before the treatment and 3 months post-treatment. “Recovery” was defined as a hearing gain of 15 dB HL and a final hearing of better than 25 dB. “No recovery” was defined as an improvement of hearing gain of <15 dB 3 months after treatment. To exclude the effect of the level of pretreatment hearing loss, we divided the patients into three subgroups based on their hearing level: 70 dB. To assess the effect of the treatment modality, the patients were divided into three treatment subgroups: systemic steroids (SS), intratympanic steroids (ITS), and a combination of both (SS and ITS). Results: The pretreatment hearing level was significantly higher in group I (61.5 ± 25.4 dB) than in group O (50.3 ± 23.0 dB; p < 0.05). The hearing gain was significantly higher in group I (33.3 ± 24.4 dB) than in group O (24.0 ± 21.8 dB; p < 0.05). The “Recovery” ratio was significantly higher in group I (70.2%) than in group O (63.1%) (p < 0.05). A repeated measures ANOVA was performed to assess the statistical differences between hospitalization, treatment modalities, and pretreatment subgroups. The inpatient group showed a significant hearing improvement in all SSNHL patients (p < 0.05). There was a significant hearing improvement in the inpatient group with pretreatment hearing <40 and 40–70 dB (p < 0.05). There was no significant difference between the inpatient and outpatient groups in pretreatment hearing >70 dB (p > 0.05). Conclusions: This retrospective study showed that inpatient treatment for sudden hearing loss is more beneficial for hearing improvement than outpatient treatment. The positive effect of inpatient treatment appears to be significant in patients with a pretreatment hearing level of 70 dB or less.