Over a 25-year period, more than half of adults in a long-running community cohort developed hearing loss. Among 436 participants at risk at baseline, 56 percent developed loss, according to a recent analysis of Framingham Offspring Study participants. Incidence was 61 percent in men (99 of 163) and 54 percent in women (146 of 273). About two thirds of incident cases were mild, while roughly one third were moderate to moderately severe or worse. Average thresholds rose by about 15 decibels across key speech frequencies, with the steepest deterioration at high frequencies—about 36 decibels—compared with roughly 8 decibels at low frequencies.
Age remained the strongest predictor of incident loss. Adults older than 50 years with hypertension or a higher Framingham Stroke Risk Profile had greater odds of developing hearing loss. Long-term high noise exposure—occupational or recreational—was associated with nearly twice the odds of incident loss versus little or no exposure. Educational attainment also appeared protective: participants with at least some colleges were less likely to develop hearing loss and showed slower worsening over time.
For progression, women experienced greater worsening than men. Among adults older than 50 years, hypertension and higher diastolic blood pressure were linked to faster progression, whereas a higher Framingham Stroke Risk Profile in this age group was related to incident loss but not to progression.
Investigators analyzed Framingham Offspring Study participants who completed one audiometric assessment in 1995–1998 and a second in 2019–2022. Baseline thresholds were obtained in a sound-treated booth by certified audiologists; follow-up thresholds were measured with a supervised tablet-based audiometer using a noise-attenuating headset in a quiet, monitored room. Hearing loss was defined as a worse-ear pure-tone average greater than 25 decibels at 0.5, 1, 2, and 4 kHz. Progression was defined as the annualized increase in that average. Statistical models adjusted for age, sex, and education, with stratification by sex or baseline age (≤50 vs >50 years) when interactions were present. The incident analysis included 436 adults without baseline loss; the progression analysis included 511 adults with paired audiometry (mean age about 52 years; about 42 percent male).
Different audiometric modalities were used at baseline and follow-up, which could introduce measurement variability, although prior work indicated comparable thresholds within test–retest reliability. The cohort was predominantly White and middle-aged at baseline, which may have also limited generalizability to more diverse or younger populations. Risk factors were measured at baseline and may not reflect changes during follow-up, and unmeasured influences—such as ototoxic medication use or other environmental exposures—could have affected hearing.
The study documented long-term incidence and progression of hearing loss in a community cohort, distinguishing factors related to onset from those related to worsening and showing that supervised tablet-based audiometry can support large-scale follow-up. The work outlines priorities for future research, including replication in more diverse populations and closer examination of cardiovascular and noise-related pathways across the life course. To contextualize potential mechanisms, lead author Lauren K. Dillard, PhD, of theMedical University of South Carolina wrote: “It has been hypothesized that cardiovascular conditions may lead to a reduced blood supply to the stria vascularis of the cochlear lateral wall, which maintains the endocochlear potential that powers sensory cells in the inner ear.”
Full disclosures can be found in the published study.
Source: JAMA Network Open