Does the Aging of the Gut Microbiome Contribute Meaningfully to Hearing Loss?
In today's open access paper, researchers discuss the link between the gut microbiome, chronic inflammation in aging, and the onset of age-related hearing loss due to hair cell death and destruction of axons connecting hair cells to the brain. It is definitively the case that changes in the balance of microbial populations in the intestine contributes to rising inflammation in older individuals. But how significant is this effect in comparison to other sources of chronic inflammation, such as excess visceral fat tissue, senescent cells, molecular waste and debris resulting from cell death and dysfunction due to other processes of aging, and so forth? It is very hard to answer that sort of question without fixing just the one contributing cause of inflammation in isolation, without affecting any of the others, and then see what happens. Identifying the mechanism is one thing, assessing its relative importance quite another.
That said, a study to determine whether or not the gut microbiome contributes significantly to age-related hearing loss could be started tomorrow, were there someone willing to put up the funds and manage the regulatory burden that attends even simple tests in humans. Gather a hundred aged volunteers in the early stages of age-related hearing loss, perform fecal microbiota transplants from young donors, and then assess the progression of their condition over the next five years or so. It is well established in animal models that fecal microbiota transplantation resets the gut microbiome to a youthful configuration for an extended period of time, reduces inflammation, improves health, and even extends life expectancy in short-lived species such as killifish. So why not try?
Age-Related Hearing Loss: The Link between Inflammaging, Immunosenescence, and Gut Dysbiosis
Age-related hearing loss (ARHL), or presbyacusis, is a type of sensorineural hearing loss that primarily affects the elderly. However, the age of onset, rate of decline, and severity of hearing loss vary widely. ARHL is the most common sensory disorder, with a high economic impact. The World Health Organization (WHO) estimates that by 2050, 2.5 billion people, predominantly over 60, will be living with some degree of hearing loss . Despite the high prevalence of this sensory disorder, there is a paucity of both preventative and treatment strategies other than prosthetic devices (hearing aids and cochlear implants).
Presbyacusis typically presents as bilateral, progressive, and irreversible. The increasing prevalence of presbyacusis may be attributable to environmental factors, notably noise exposure and the rise in metabolic diseases. This sensory disorder can be characterised by reduced hearing sensitivity and speech understanding in background noise, slowed central processing of acoustic information, and impaired localisation of sound sources. Hearing loss affects high frequencies initially and eventually spreads to lower frequencies involved in speech understanding. Untreated hearing impairment contributes to social isolation, loss of self-esteem, depression, and cognitive decline. Even mild levels of hearing loss increase the long-term risk of cognitive decline and dementia.
ARHL has a complex pathophysiology linked to genetic risk factors that determine the rate and extent of cochlear degeneration. However, the severity of the hearing loss is also influenced by previous otological diseases, chronic illnesses, cumulative noise exposure, use of ototoxic drugs, and lifestyle. Moreover, this condition has been associated with numerous comorbidities, including dementia, frailty, Alzheimer's disease, and type II diabetes. A common trait of these disorders is chronic inflammation in target organs.
Various stimuli can sustain inflammaging, including pathogens, cell debris, nutrients, and gut microbiota. As a result of ageing, the immune system can become defective, leading to the accumulation of unresolved inflammatory processes in the body. Gut microbiota plays a central role in inflammaging because it can release inflammatory mediators and crosstalk with other organ systems. A proinflammatory gut environment associated with ageing could result in a leaky gut and the translocation of bacterial metabolites and inflammatory mediators to distant organs via the systemic circulation. Here, we postulate that inflammaging, as a result of immunosenescence and gut dysbiosis, accelerates age-related cochlear degeneration, contributing to the development of ARHL. Age-dependent gut dysbiosis was included as a hypothetical link that should receive more attention in future studies.