Hearing Loss: Does Gender Play a Role?

, University of Washington Medical Center; , University of Washington Medical Center, Virginia Merrill Bloedel Hearing Research Center


Medscape General Medicine. 1997;1(2) 

In This Article

Metabolic Presbycusis

The better pure-tone audiometry thresholds of women at all ages at frequencies above the 1000- to 2000-Hz range are paradoxically accompanied by a "gender reversal" in which women have a poorer capacity to hear at frequencies below 1000 to 2000Hz[12,14,15,18] than do men (Fig. 2). The effect is true prior to advanced stages, and it increases with both age and degree of hearing loss. The increased rate of low-frequency hearing loss in women may be due to metabolic presbycusis (ie, biologic factors). Strial atrophy, for example, is known to be related to low-frequency hearing loss. Metabolic presbycusis is characterized by patchy atrophy of the stria vascularis, which is most prominent in the middle and apical turns of the cochlea. The blood supply to the cochlea is most distal at the apex, where low-frequency sounds are transduced; therefore, one would expect factors that decrease blood flow in the inner ear to produce strial atrophy and a subsequent low-frequency hearing loss. A greater incidence[31] and prevalence[12] of low-frequency hearing loss have been demonstrated in women compared with men. Several biologic factors have been studied to determine a gender basis for differences in hearing and hearing loss.

Figure 2. The gender reversal phenomenon. Average audiograms of 341 males and 346 females in age range 50 to 89 years. Adapted with permission from J Am Acad Audiol (1993;4:42-49), Copyright © 1993, American Academy of Audiology. [18]

Ovarian steroid hormones and hearing loss in women. The better hearing at high frequencies observed in women may be due, at least in part, to the effect of ovarian steroid hormones. Ovarian steroid hormones may improve hearing by direct effect and/or by indirect effects such as fluid volume changes in the inner ear. Studies of auditory brainstem responses (ABRs) and otoacoustic emissions (OAEs) have demonstrated interesting relationships between ovarian steroid hormones and hearing in women.[32,33,34,35]

During ABR studies, a series of waves representing activity in the auditory pathway are recorded: wave I represents activity in the cochlear nerve; wave II, activity in the cochlear nerve nucleus; wave III, activity in the neurons of the superior olivary complex; wave IV, activity in the lateral lemniscus; and wave V, activity in the inferior colliculus. Wave V is usually the largest and most consistent component observed at threshold intensities, and it is used in the assessment of peripheral hearing. Latencies of the various waveform components are measured and used to assess the function of the auditory pathway.

Sound impulses travel the auditory pathway faster in women. Numerous studies have established that latencies of the various ABR waves, particularly wave V, are consistently shorter in women.[32,36,37,38,39,40] While the cause of this gender difference is not known, ovarian steroid hormones are thought to be contributory, since ABR latencies have been shown, in some studies, to change during the course of the menstrual cycle.

Initially, studies of the impact of the menstrual cycle on the ABR were contradictory. Fagan and Church[41] did not observe any changes in waveform latency as a function of menstrual cycle phase. In contrast, Dehan and Jerger[42] found a shortening of wave V latency during the luteal phase of the menstrual cycle.

Elkind-Hirsch and colleagues[33,34] described the effect of estradiol and progesterone on the ABR in a series of experiments. In the first study, Elkind-Hirsch and coworkers[34] observed an increase in wave III and V peak latencies during the high estradiol state at midcycle, suggesting that brainstem auditory pathways are sensitive to estradiol during the menstrual cycle. Their study showed that the latency increase for the wave III to V interpeak interval was greater than that for the wave I to III interpeak interval, suggesting that the effect of estradiol is stronger at higher sites in the central auditory pathway. The individual effects of estradiol and progesterone on the ABR could not be determined in the first study.

Elkind-Hirsch and associates[34] then evaluated the individual effects of estradiol and progesterone on the ABR by studying patients with premature ovarian failure who were receiving hormone replacement. A significant lengthening of wave V peak latency and the wave I to V interpeak interval was noted in the estradiol-only treatment group. Despite equivalent circulating estradiol levels, both wave V peak latencies and wave I to V interpeak intervals were significantly decreased during the estradiol + progesterone replacement phase compared with the estradiol-only replacement phase. The findings of these studies suggest that estrogen and progesterone have opposite effects on the speed with which sensory information travels in the auditory brainstem nuclei; estrogen decreases, whereas progesterone increases, the speed of transmission. How, specifically, do estrogen and progesterone exert their effects?

Elkind-Hirsch and others[34] hypothesized that steroid hormones act at the level of synaptic transmission through auditory pathways in the brainstem. They proposed that estradiol and progesterone modulate secretion of the inhibitory neurotransmitter gamma-amino-butyric acid (GABA) in a counter-regulatory fashion. Estradiol may enhance the inhibitory effects of GABA on the auditory system by affecting the level and turnover of GABA, as demonstrated in a study by Frankfurt and colleagues,[43] as well as upregulating GABA cell receptors.[44] Conversely, progesterone may reduce the inhibitory effects of GABA on the auditory system by lowering brain GABA concentrations and inhibiting estrogen-stimulated GABA secretion.[34]

OAEs are faint sounds that originate within the cochlea and are recorded in the ear canal.[45] OAEs are a by-product of the active processes in the cochlea, which are necessary for hearing. Measurement of OAEs has added a new dimension to clinical audiometry. OAEs may be spontaneous (SOAEs) or evoked (EOAEs). SOAEs can be measured in the ear canal in the absence of an external acoustic stimulus.[45] EOAEs, in contrast, occur during or after the presentation of an external acoustic stimulus.

Normal human hearing is dependent on proper function of the outer hair cells in the organ of Corti. Outer hair cells are responsible for the good sensitivity, sharp frequency selectivity, and wide dynamic range associated with normal hearing.[46] When outer hair cells are absent or nonfunctional, a 40- to 50-dB SNHL occurs, frequency selectivity is reduced, response growth as a function of stimulus intensity is altered, and evoked OAEs cannot be measured.[47] Thus, OAEs are a noninvasive tool for studying hearing impairment resulting from outer hair-cell dysfunction.

If the improved sensitivity of the female auditory system is due, at least in part, to the effect of ovarian steroid hormones, one would expect a difference in the number of SOAEs between men and women. In fact, females generally exhibit more SOAEs than males, and this gender difference exists from birth.[35] Furthermore, in individual women, the number of SOAEs varies with ovarian steroid hormone levels. Recent studies have documented variations in the frequency of SOAEs with the menstrual cycle.[47,48,49] Ovarian steroid hormones do play a role in SOAE generation; however, it is not clear whether the effect of ovarian steroid hormones is direct or mediated through secondary metabolic changes such as fluid volume in the cochlea.

A hormonal mechanism for hearing loss in women is suggested by the temporal association between the onset of hearing loss and the decline in reproductive hormone production. However, this association does not exist in isolation; it is confounded by the effect of aging itself, comorbid disease, and its associated medications. In 1964, Weston[50] found that combination estrogen and testosterone improved hearing by 40% in elderly subjects; however, the study did not report the magnitude of improvement nor did it include a control group. The role of estrogen in hearing loss is an active area of investigation. We have examined the effect of estrogen replacement therapy in a small number of healthy postmenopausal women (167) and did not find an effect on hearing (Gates and colleagues, in press). Differences in hearing between women and men are multifactorial, and reflect, in part, differing levels of noise exposure. A primary effect of ovarian hormones cannot be excluded. Further research is needed before specific targets of therapeutic intervention are identified.

The role of CVD in hearing loss. The cochlea is not immune to the effects of vascular disease. The stria vascularis, the "battery" that powers hearing, is likely susceptible to the same pathophysiologic changes associated with vascular disease throughout the rest of the body. Hypertension, atherosclerosis, hypercholesterolemia and hypertriglyceridemia, and diabetes mellitus all likely exert deleterious effects on the end-vasculature of the cochlea.

Hearing loss in adults has been linked to CVD.[20,21,22,23,24] Gates and associates[51] compared the hearing status of a cohort of 1662 elderly male and female members in the Framingham cohort with their 30-year prevalence of CVD. They were able to show that low-frequency hearing loss (250-1000Hz) was related to CVD events in both genders, but more in women. In women, decreases in both low- and high-frequency average thresholds were associated with coronary heart disease, intermittent claudication, stroke, and total CVD events. The association with CVD events was strongest with decreases in low-frequency average thresholds.

In the only study to date examining the relationship between hypertension and hearing in women, Gates and coworkers[51] found that age-adjusted low-frequency hearing in hypertensive women was significantly worse than in nonhypertensive women. This finding provides evidence of a significant modifiable risk factor other than noise exposure for hearing loss in women. The results of studies examining the effect of hypertension on hearing in men are less conclusive. Gates and others[51] found no relationship between age-adjusted systolic blood pressure level and any of the hearing measures in men in the Framingham cohort. In 1000 50-year-old Scandinavian men, no relationship was found between hearing and hypertension or CVD.[52] In contrast, Brant and associates[53] found a statistically significant relationship in men between systolic blood pressure levels and hearing loss in the speech frequencies.

Studies examining the effects of serum triglycerides and cholesterol on hearing have produced mixed findings. In a crossover study with a 5-year follow-up, Rosen and colleagues[54] documented a relationship between dietary fat and hearing status; subjects placed on a low-fat diet had better hearing, whereas subjects receiving a diet high in saturated fat experienced a worsening of hearing. In contrast, Lowry and Issacson[55] found no difference in cholesterol level between elderly men with and without presbycusis. Gates and others[51] found no relationship between any of the hearing variables and serum cholesterol or triglyceride levels in either gender. Interestingly, however, an inverse relationship between age-adjusted high-density lipoprotein (HDL) level and low-frequency pure-tone thresholds was noted in women. This may suggest a protective effect of HDL on hearing thresholds. Given the observational nature of the study, no causal relationship between serum HDL levels and superior hearing can be presumed.[51]

Smoking has not been shown to be a strong risk factor for hearing loss in the speech frequencies.[51,53,56,57]

Two of the components of presbycusis, socioacusis, and nosocusis are important because they represent the sites at which we can intervene to prevent hearing loss in women. The above-mentioned relationships of hearing loss in women with noise-induced hearing loss, ovarian steroid hormones, and CVD are encouraging because they suggest means of preventing hearing loss in women. However, as is clearly evident, we are just beginning to understand the relationship between hearing loss in women and potentially modifiable risk factors.