We thank Dr. Fuller-Thomson for her letter, which addresses the public health implications of our study, Hearing Impairment and Incident Dementia and Cognitive Decline in Older Adults (1). In our observational study, we documented that moderate (vs no) hearing impairment was associated with a 55% increase in risk of all-cause dementia over 9 years in a biracial cohort with a mean age of 76 years. This finding is consistent with a growing body of observational epidemiologic research showing strong and consistent associations between audiometric hearing impairment and cognitive decline and incident dementia (2,3).
As Dr. Fuller-Thomson correctly points out, the interpretation of our finding in the context of dementia prevention hinges on whether hearing impairment is a causal risk factor or simply a marker of residual or unmeasured confounding factors. The association must be causal if we are to decrease dementia risk through hearing impairment treatment. In our article, we presented three possible biological mechanisms through which hearing impairment could be causally related to dementia and cognitive decline. Alternatively, we speculated that our findings could be driven by a shared underlying pathology such as vascular disease. It is possible that other factors, such as lead exposure, inflammation, or other processes related to aging, could also give rise to both hearing impairment and dementia and thus confound the relationship we reported.
Lead exposure is consistently weakly associated with faster rates of cognitive decline in older adults (4–6), and it has been suggested that some decline considered “normal” cognitive aging, may in fact be due to lifetime exposure to neurotoxicants including lead (6). Studies of the relationship between lead exposure and hearing loss have been primarily conducted in children and in occupationally-exposed groups. As highlighted by Dr. Fuller-Thomson, two studies in the general population have suggested increasing levels of hearing impairment with increasing lead levels in blood (7) and bone (8).
We agree with Dr. Fuller-Thomson that future studies are needed to unpack the relationship between hearing impairment and dementia and cognitive decline. Ideally, observational studies would adjust for all possible confounders of the association. Unfortunately, often possible confounders may be un- or mis-measured, leading to possible bias in the results. Given the strong relationship between hearing and cognitive decline and dementia, it is unlikely that any one confounding factor is responsible for observed results.
An important study that will help us to understand if hearing impairment is causally related to cognitive decline is the Aging and Cognitive Health Evaluation in Elders (ACHIEVE) study (9). Currently recruiting participants, ACHIEVE is an National Institute on Aging (NIA)-funded randomized clinical trial designed to definitively test whether a best-practices hearing intervention (vs successful aging education control) can reduce cognitive decline in older adults with mild-to-moderate hearing impairment.
As highlighted in the Lancet report referenced by Dr. Fuller-Thomson, dementia is “the greatest global challenge for health and social care in the 21st century” (2). Observational epidemiologic research meaningfully contributes to a larger body of scientific evidence related to dementia prevention, but causal interpretations of risk factor-outcome associations in these studies can be challenging. Randomized studies, including ACHIEVE, will help determine whether hearing impairment treatment delays cognitive decline and dementia in older adults.
Funding
This research was supported by National Institute on Aging (NIA) Contracts N01-AG-6-2101; N01-AG-6-2103; N01-AG-6-2106; NIA grant R01-AG028050, and NINR grant R01-NR012459. This research was funded in part by the Intramural Research Program of the NIH, National Institute on Aging. Dr. Deal is supported by NIH/NIA grant K01AG054693.
Conflict of Interest
None reported.
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