The association between short stature and sensorineural hearing loss

Barrenäs, Marie-Louise; Bratthall, Åsa; Dahlgren, Jovanna

doi:10.1016/j.heares.2005.03.019

Cited by 32 publications

(36 citation statements)

References 59 publications

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“…It would be of interest to analyze the British 1958 Birth Cohort to determine whether a subgroup of infants who were light for gestational age at birth, but subsequently overweight or obese in adulthood (as suggested by thrifty phenotype hypothesis (Barrenas et al 2003)), showed increased risk of hearing impairment. Hearing threshold in the Swedish conscripts was also associated with short stature (Barrenas et al 2005a), a finding consistent with other reports (e.g. Burr et al 2008).…”

Section: Comparison With Other Studiessupporting

confidence: 91%

“…High body weight was associated with hearing threshold levels at low frequencies only. Fransen also found that taller people had, on average, better hearing, replicating a previous finding by Barrenas (Barrenas et al 2003(Barrenas et al , 2005a. In a separate study, Barrenas found an association between being born short or light for gestational age and higher hearing threshold levels at age 17-24yrs among Swedish male conscripts (Barrenas et al 2005b).…”

Section: Introductionsupporting

confidence: 74%

“…gender, family history of hearing impairment, mother's weight at birth, social class at birth, childhood hearing impairment, middle ear dysfunction in childhood, as well as noise at time of adult test (binary). Additional adjustment was made for birthweight in order to allow for possible 'thrifty phenotype' effects (Barrenas et al 2003(Barrenas et al , 2005a). …”

Section: Statistical Analysesmentioning

confidence: 99%

See 2 more Smart Citations

BMI over the lifecourse and hearing ability at age 45 years: a population based study

Ecob¹,

Russ

Davis

2011

LLCS

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Section: Comparison With Other Studiessupporting

confidence: 91%

Section: Introductionsupporting

confidence: 74%

Section: Statistical Analysesmentioning

confidence: 99%

See 1 more Smart Citation

BMI over the lifecourse and hearing ability at age 45 years: a population based study

Ecob¹,

Russ

Davis

2011

LLCS

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show abstract

“…It has been suggested that Mondini dysplasia should be regarded as arising as a result of fetal growth retardation (Barrenäs et al, 2005), which is consistent with some of the known effects of IGF1R deficiency, but the fact that similar phenotypes have been reported in mice with mutations in FoxG1, Six1, or Eya1 (Zheng et al, 2003;Pauley et al, 2006) suggests that the Mondini dysplasia reflects a specific pathological phenotype and that IGF signaling could interact in a common pathway with FoxG1, Six1, and Eya1.…”

Section: Regulation Of Atoh1 Expression In the Developing Cochleamentioning

confidence: 58%

Insulin-Like Growth Factor Signaling Regulates the Timing of Sensory Cell Differentiation in the Mouse Cochlea

Okano¹,

Xuan²,

Kelley³

2011

J. Neurosci.

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The mammalian auditory sensory epithelium, the organ of Corti, is a highly ordered cellular structure that comprises two types of auditory hair cells and several types of nonsensory supporting cells. During embryogenesis, a stereotyped sequence of cellular and molecular events is required for its development. These processes are assumed to be regulated by multiple growth and transcription factors. However, the majority of these factors have not been identified. One potential regulator of cochlear development is the insulinlike growth factor (IGF) signaling family. To examine the roles of the IGF pathway in inner ear formation, cochleae from Igf1r mutant mice were analyzed. Deletion of Igf1r leads to several changes in inner ear development including a shortened cochlear duct, a decrease in the total number of cochlear hair cells, and defects in the formation of the semicircular canals. In addition, maturation of the cochlear sensory epithelium was delayed at the transition point between cellular proliferation and differentiation. To determine the molecular basis for these defects, inhibition of IGF signaling was replicated pharmacologically in vitro. Results indicated that IGF signaling regulates cochlear length and hair cell number as well as Atoh1 expression through the phosphatidylinositol 3-kinase/Akt signaling pathway. These results demonstrate novel roles for IGF signaling in inner ear development including regulation of vestibular formation, length of the cochlear duct, and the number of cochlear hair cells. The results also provide new insights regarding the pathological processes that underlie auditory defects in the absence of IGF signaling in both humans and mice.

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“…Although prematurity and low birthweight are known to be associated with congenital hearing loss, the causal pathway has not been clearly delineated. One study in Atlanta showed elevated relative risks of bilateral sensorineural hearing impairment among children with lower birthweights: prevalence was 0.4/1000 in children weighing ≥4000 g, compared with 1.27/1000 for 1500-1499 g and 5.1/1000 for those <1500 g (Barrenas et al 2005b) and in males of short stature (Barrenas et al 2005a). This interesting finding has led to the hypothesis that fetal programming arising from intrauterine growth retardation might result in delayed cell cycles during development of the cochlea which eventually leads to development of SNHL in adulthood (Niskar et al 2001).…”

Section: Environmental Causes Of Hearing Lossmentioning

confidence: 99%

A Life Course Approach to Hearing Health

Russ¹,

Tremblay

Halfon

et al. 2017

Handbook of Life Course Health Development

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Challenges to hearing health are a significant public health problem. At least ten million Americans have a hearing loss that interferes with the understanding of normal speech. If lesser degrees of loss are included, the number rises to 28 million. Although there have been considerable advances in understanding the etiology of hearing loss, with genetic causes now thought to account for up to 50% of congenital losses, in many individual cases, the cause of hearing loss remains unknown. This lack of knowledge of the basic pathophysiology of hearing difficulties hampers prevention and treatment efforts. Growing interest in life course theory has led to suggestions that it could prove useful to apply a life course lens to the study of hearing loss, and of hearing health, throughout the life span. In this paper we consider the implications of the Life Course Health Development model for understanding the mechanisms, pathways, and determinants of hearing ability. We consider the implications of early hearing loss for health development over the life course and the factors through the life course that contribute to hearing ability in adult life. We consider the concept not just of hearing loss but of “hearing health” and how to achieve it, the research priorities that are suggested by this review, and the implications for policy and practice.

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The association between short stature and sensorineural hearing loss

Cited by 32 publications

References 59 publications

BMI over the lifecourse and hearing ability at age 45 years: a population based study

BMI over the lifecourse and hearing ability at age 45 years: a population based study

Insulin-Like Growth Factor Signaling Regulates the Timing of Sensory Cell Differentiation in the Mouse Cochlea

A Life Course Approach to Hearing Health

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