How is hearing loss related to cognitive decline and dementia?
Cognitive load. One mechanism which has been hypothesized to link hearing loss and cognitive decline is the idea of cognitive load. In other words, when you can't hear well, the ear is constantly sending a garbled auditory signal to the brain. Does the brain constantly have to work harder to process that poor signal? Is the brain reallocating resources, per se, to constantly dealing with that garbled auditory signal and does it come at the expense of other systems?
In 1973, Danny Kahneman put forth his model of cognitive resource capacity (Kahnerman, 1973). Cognitive resource capacity is the idea that we have a pool of cognitive resources for thinking, planning, memory. We now know that over time with aging, we can lose some of these resources from things such as synaptic loss of the brain. Increasingly, we are beginning to understand that a hearing loss likely taxes the system as well. The brain is constantly having to re-allocate resources to help with deciphering and decoding that much more garbled auditory signal.
The sensory system, particularly the hearing system, is fundamentally unique. It's a system that is always on. Even in the middle of the night, we are still processing sound. We are constantly processing auditory stimuli to learn about the auditory environment. It comes from an evolutionary perspective. We can't turn this system off.
Jonathan Peale and his team at Washington University in St. Louis conducted some studies using functional MRI images. They looked at patterns of brain activation in people with poor hearing (mild to moderate hearing loss) versus same-aged peers with good hearing. Consistently, MRI images reveal that people with poor hearing have reduced activation of the primary auditory cortex (the part of the brain critical for sound processing). That makes sense. If you have an impoverished auditory signal from the ears because of hearing loss, you get reduced language-driven activity in primary auditory pathways. Interestingly, in these same people with hearing loss, we also observe what we believe to be increased compensatory language-driven activity in the prefrontal cortical areas of the brain. The prefrontal cortex part of the brain is typically not needed for sound processing, and yet we are seeing an activation of this part of the brain in people with even a mild to moderate hearing loss (as compared to normal hearing individuals). In other words, different regions of the brain are being recruited for auditory and language stimuli in order to compensate for a reduced auditory signal, and the brain needs to expend more effort to decode the signal. This is one pathway through which hearing loss could directly impact cognitive decline and dementia.
Brain structure/function. A second, related pathway connecting hearing loss with cognitive decline is the idea that hearing loss in and of itself may lead to changes in terms of brain structure and, as a result, brain function. This finding is based on studies conducted on large groups of older adults with hearing loss over many years using brain MRI scans. In several different studies, they found that people with hearing loss have faster rates of brain atrophy. Again, we think that's because of the impoverished auditory signal which leads to cascading effects on brain structure and hence, brain function (Lin & Albert, 2014). The structural integrity of the brain dictates its function. The two most important conditions that can damage the brain over time are microvascular disease (i.e., small vessel disease from high blood pressure, diabetes, etc.) as well as the more classic Alzheimer's neuropathology. Not coincidentally, these are the two major causes of dementia in late life.
Social isolation. The third mechanism which has been hypothesized is the idea that for some people, hearing loss can lead to social isolation problems. In the field of gerontology, studies have repeatedly shown that social isolation is arguably one of the biggest predictors of morbidity and mortality in older adults. We see consistently that social isolation relates to poor outcomes through several different pathways. Health and behavioral pathways are affected by things such as adherence to medical treatments, as well as smoking, diet, and exercise. In addition, psychological pathways are impacted by a person's self-esteem, self-efficacy, sense of well-being and the ability to cope. Recently, however, one of the more compelling theories is the idea that social isolation or loneliness is directly linked to physiologic changes in the body, which precipitates adverse events.
John Cacioppo and colleagues conducted research in 2007 and 2011 comparing people who were socially isolated with those who were socially integrated. Consistently, the research suggested that socially isolated people had an increased upregulation of pro-inflammatory genes and increased inflammation, which causes a lot of adverse events and aging processes in the body. This research directly provided the link showing how loneliness leads to adverse events in older adults in later life. This finding allows us to understand how hearing loss over and above any type of common pathology is linked to adverse events like cognitive impairment and dementia, at least from a theoretical construct (Cole et al., 2007; Cole, Hawkley, Arevalo, & Cacioppo 2011).
This Ask the Expert is an excerpt from the CE Course, Hearing Loss & Aging: A Public Health Perspective. For more information please visit the CaptionCall Partner Page on AudiologyOnline.
Kahneman, D. (1973). Attention and effort (Vol. 1063). Englewood Cliffs, NJ: Prentice-Hall.
Cole, S. W., Hawkley, L. C., Arevalo, J. M., Sung, C. Y., Rose, R. M., & Cacioppo, J. T. (2007). Social regulation of gene expression in human leukocytes. Genome biology, 8(9), R189.
Cole, S. W., Hawkley, L. C., Arevalo, J. M., & Cacioppo, J. T. (2011). Transcript origin analysis identifies antigen-presenting cells as primary targets of socially regulated gene expression in leukocytes. Proceedings of the National Academy of Sciences, 108(7), 3080-3085.