Abstract
Twin and adoption studies point towards a genetic contribution to tinnitus; however, how the genetic risk applies to different forms of tinnitus is poorly understood. Here, we perform a familial aggregation study and determine the relative recurrence risk for tinnitus in siblings (λs). Four different Swedish studies (N = 186,598) were used to estimate the prevalence of self-reported bilateral, unilateral, constant, and severe tinnitus in the general population and we defined whether these 4 different forms of tinnitus segregate in families from the Swedish Tinnitus Outreach Project (STOP, N = 2305). We implemented a percentile bootstrap approach to provide accurate estimates and confidence intervals for λs. We reveal a significant λs for all types of tinnitus, the highest found being 7.27 (95% CI (5.56–9.07)) for severe tinnitus, with a higher susceptibility in women (10.25; 95% CI (7.14–13.61)) than in men (5.03; 95% CI (3.22–7.01)), suggesting that severity may be the most genetically influenced trait in tinnitus in a sex-dependent manner. Our findings strongly support the notion that genetic factors impact on the development of tinnitus, more so for severe tinnitus. These findings highlight the importance of considering tinnitus severity and sex in the design of large genetic studies to optimize diagnostic approaches and ultimately improve therapeutic interventions.
Highlights
Subjective tinnitus is the phantom perception of sound in the absence of a corresponding external acoustic stimulus
We aimed to quantify the familial aggregation of tinnitus by estimating λs for different forms of tinnitus, namely, bilateral or unilateral, constant, and severe, using data from 2446 participants from the Swedish Tinnitus Outreach Project (STOP)
We identified four large national studies, the combination of which allowed us to determine the prevalence for bilateral, unilateral, constant, and severe tinnitus (Table 1)
Summary
Subjective tinnitus is the phantom perception of sound in the absence of a corresponding external acoustic stimulus. Recent studies converge towards the notion that subjective tinnitus results from a maladaptive plasticity in response to sensory deprivation, such as hearing loss [4]. Damage in the hearing system (the cochlea) leads to central neural compensatory responses (central gain) along the auditory pathway, something which is observed in both animals and humans [5]. Limbic structures (e.g., amygdala) have been found to interact with the auditory pathway in animals and humans with tinnitus and is thought to exacerbate tinnitus-related hyperactivity [6]. It has been suggested that the lack of effective treatment may be due to the heterogeneity of tinnitus [7], whose subtypes remain to be established [8]
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