Is There a Genetic Component to Tinnitus?
Tinnitus, the perception of sound in the absence of an external sound, emerges from a complex interaction between otologic health, general health/disease, and environmental stressors. Most people experience transient tinnitus at some point, but do genes play a role in susceptibility to chronic tinnitus? As expected this is not an easy question to answer given the heterogeneity of tinnitus.
Recently, Gilles et al (2017) performed the first genome-wide association study (GWAS) to examine the association between reported tinnitus and 4,000,000 single-nucleotide polymorphisms (i.e. variation in a single nucleotide that occurs in a specific position in the genome) using specialized statistical procedures. To perform the study blood samples were acquired from subjects in Antwerp (Belgium). Unhealthy subjects were excluded. Of the genotyped individuals, tinnitus information was available for 916 persons, of which 167 reported tinnitus; noise exposure history was also considered.
None of the SNPs reached the threshold for genome-wide significance. However, with consideration of noise three genes VDAC1, NKTR, and COG3 approached significance. Further, several genes involved in metabolic pathways were implicated (RAS pathway, vascular smooth muscle contraction, NDK Dynamin, and coenzyme A biosynthesis). However, all genotyped SNPs had a cumulative effect accounting for only 3.2 percent of variance for reported tinnitus.
Gilles et al. (2017) A Pilot Genome-Wide Association Study Identifies Potential Metabolic Pathways Involved in Tinnitus, Front Neurosci 11: 71.