The thrifty phenotype hypothesis and hearing problems

摘要

While looking for solutions to sensorineural hearing loss (SNHL) induced by age or noise, a serious incurable health problem, we became interested in the thrifty phenotype hypothesis because diseases related to this hypothesis are sometimes those linked to SNHL. According to the hypothesis, events during fetal life, such as malnutrition, may cause disease in adulthood. The malnourished fetus makes metabolic adaptations, which may become permanently programmed, persisting throughout life and causing disease later in life. For example, cardiovascular disease, hypertension, obesity, and hypercholesterolaemia are related to reduced fetal growth as reflected by a reduced birth size and to SNHL. The mechanisms behind the thrifty phenotype hypothesis are unclear, but links to insulin-like growth factor Ⅰ (IGF-Ⅰ) have been suggested. During development, IGF-Ⅰ is crucial for several organs. This includes the size of the cochlea and auditory neurones; the innervation of the auditory sensory cells; and the postnatal survival, differentiation, and maturation of auditory ganglion cells. Intrauterine growth retarded newborn babies and malnourished pregnancies have lower concentrations of IGF-Ⅰ. Also, in Turner syndrome SNHL is associated with short stature and lower concentrations of IGF-Ⅰ. To test the thrifty phenotype hypothesis on SNHL, we reanalysed data from two previous samples, assuming that people who are short in stature are over-represented among non-syndromic individuals with SNHL.