Autosomal recessive nonsyndromic deafness 42 is a genetic form of hearing loss that mainly affects hearing without other health issues. People with Autosomal recessive nonsyndromic deafness 42 often have hearing loss from birth or early childhood, and it can range from mild to profound. Not everyone will have the same experience, and hearing can be stable or change slowly over time. Lifespan is typically not affected, and many live long and full lives. Care usually focuses on hearing support like hearing aids, cochlear implants, and speech and language therapy, with regular hearing checks for children and adults.
Overview
Autosomal recessive nonsyndromic deafness 42Symptoms
Autosomal recessive nonsyndromic deafness 42 causes permanent hearing loss in both ears without other health issues. Early signs of autosomal recessive nonsyndromic deafness 42 include not startling to loud sounds or delayed speech. Hearing levels range from moderate to profound.
Outlook and prognosis
Many living with autosomal recessive nonsyndromic deafness 42 have stable, early-onset hearing loss that doesn’t affect other body systems. With timely hearing support—hearing aids, cochlear implants, language therapy—children typically develop strong communication. Life expectancy and general health are usually normal.
Causes and risk factors
Autosomal recessive nonsyndromic deafness 42 stems from inheriting two faulty copies of a hearing gene; parents are usually carriers. Risk factors for autosomal recessive nonsyndromic deafness 42 include family history and parental relatedness. Noise and infections may worsen hearing.
Genetic influences
Genetics are central to Autosomal recessive nonsyndromic deafness 42. It’s caused by inheriting two nonworking gene copies, one from each parent, who are usually unaffected carriers. Variants in the implicated gene drive the condition’s onset, severity, and family recurrence risk.
Diagnosis
Diagnosis of Autosomal recessive nonsyndromic deafness 42 starts with newborn or later hearing tests and review of family history and clinical features. Genetic testing confirms the type. Imaging may be used to assess the inner ear.
Treatment and drugs
Treatment for autosomal recessive nonsyndromic deafness 42 focuses on improving hearing and communication. Many benefit from hearing aids; some with greater hearing loss consider cochlear implants. Ongoing hearing checks, speech-language therapy, and school or workplace supports help daily life.
Symptoms
For many families, the earliest clues are how a baby reacts to loud sounds and how speech starts to develop. In daily routines, this might show up as small but noticeable changes. Autosomal recessive nonsyndromic deafness 42 is a genetic type of hearing loss that affects both ears without other medical findings. Common early features of Autosomal recessive nonsyndromic deafness 42 include a reduced response to sounds and delays in speech and language.
Babies may not startle to loud noises or turn toward familiar voices. Older children may seem not to hear their name and may turn the TV or tablet volume up high.
In Autosomal recessive nonsyndromic deafness 42, both ears are affected, often from birth or early infancy. The degree can range from moderate to profound, confirmed by specialized hearing tests.
First words may come later than expected, and pronunciation can be unclear. Early hearing support and speech therapy can help communication grow.
Understanding words is hardest in background noise or group conversations. Classrooms, playgrounds, and busy rooms can make listening especially tiring.
How people usually first notice Autosomal recessive nonsyndromic deafness 42?
Many families first notice something is different when a baby with autosomal recessive nonsyndromic deafness 42 doesn’t startle to sudden sounds, sleeps through loud noises, or doesn’t turn toward a parent’s voice. Newborn hearing screening often flags it within the first days of life, leading to repeat testing like auditory brainstem response to confirm hearing loss without other health or developmental differences. If screening was missed or borderline, the first signs of autosomal recessive nonsyndromic deafness 42 may show up in early infancy as delayed babbling and fewer vocal responses, prompting a hearing check.
Types of Autosomal recessive nonsyndromic deafness 42
People with Autosomal recessive nonsyndromic deafness 42 (often shortened to DFNB42) can share a core feature—hearing loss without other medical findings—but there are recognized variants that differ in when hearing loss starts and how quickly it changes. People may notice different sets of symptoms depending on their situation. Clinicians often describe them in these categories: congenital severe-to-profound loss present from birth, childhood-onset progressive loss, and stable moderate loss. Understanding these types of DFNB42 can help explain why hearing support needs differ over time and across families, and it reflects the known variants of this genetic condition.
Congenital profound
Hearing loss is present at birth and is typically severe to profound. Parents may notice no startle to loud sounds or missed newborn hearing screens. Early hearing aids or cochlear implants are often considered.
Childhood progressive
Hearing starts near normal and then worsens over childhood into adolescence. School hearing checks or trouble following speech in noise may be the first clues. Regular hearing tests help time stronger support as loss progresses.
Stable moderate
Hearing loss is present early but tends to remain moderate and relatively steady. People may do well with consistent amplification and classroom or workplace accommodations. Not everyone will experience every type.
Family-specific variant
Some families show a pattern that sits between these types, reflecting different gene changes within DFNB42. Researchers describe these categories to better understand patterns of the condition. Genetic testing can clarify the underlying variant and guide counseling about types of DFNB42.
What genetics can tell you about symptoms
Variants in the ILDR1 gene can disrupt how inner ear hair cells connect, leading to early, usually severe sensorineural hearing loss in both ears. People with two changed copies often notice little or no benefit from hearing aids, with stable or slowly progressive loss.
Causes and risk factors
Autosomal recessive nonsyndromic deafness 42 is caused by inheriting two changes in the ILDR1 gene. When both parents carry the same ILDR1 change, each pregnancy has a 25% (1 in 4) chance of an affected child. Risk is higher in families with shared ancestry or when parents are related by blood. Everyday factors do not cause autosomal recessive nonsyndromic deafness 42 but loud noise, ear infections, and some medicines can worsen hearing. Some risks are modifiable (things you can change), others are non-modifiable (things you can’t).
Environmental and biological risk factors
Autosomal recessive nonsyndromic deafness 42 is typically present from birth and largely reflects internal biology rather than outside exposures. Doctors often group risks into internal (biological) and external (environmental). For this condition, known risks are mostly internal, and common environmental triggers that cause acquired hearing loss are not known to raise its likelihood. Here are the environmental and biological elements to know about risk for this specific form.
The hearing system forms early in pregnancy, and built-in differences present from conception drive this condition. These are internal biological influences rather than effects from infections, medications, or noise during pregnancy.
Conception with an older father slightly increases the chance of new biological changes in sperm. For this specific form, this pathway is considered a minor contributor to overall risk.
Older maternal age is mostly associated with chromosome conditions, not this pattern of hearing loss. It is not a major driver of risk for this condition.
Infections during pregnancy such as cytomegalovirus or rubella can cause acquired hearing loss. They are not known to increase the chance of this specific form that arises from internal biology.
Genetic risk factors
Many families learn that Autosomal recessive nonsyndromic deafness 42 traces back to changes in a single gene called ILDR1. The genetic causes of Autosomal recessive nonsyndromic deafness 42 involve receiving two nonworking copies of ILDR1—one from each parent—so parents usually have normal hearing and are carriers. Some risk factors are inherited through our genes. In some communities with shared ancestry, the same ILDR1 change can appear in multiple relatives.
ILDR1 gene changes: Changes in the ILDR1 gene disrupt inner-ear function and lead to this nonsyndromic form of hearing loss. Most affected people have harmful changes in both copies of ILDR1. Genetic testing can confirm which changes are present.
Autosomal recessive pattern: A child must inherit one nonworking ILDR1 copy from each parent to be affected. If only one copy is changed, the person typically has normal hearing.
Carrier parents: When both parents carry an ILDR1 change, each pregnancy has a 25% (1 in 4) chance of a child with this condition. There is also a 50% (1 in 2) chance the child will be an unaffected carrier.
Silent carriers: Carriers usually have normal hearing and may not realize they carry an ILDR1 change. This is why Autosomal recessive nonsyndromic deafness 42 can appear suddenly in families with no known history.
Compound heterozygosity: The two ILDR1 changes do not have to be the same. Many affected people inherit two different changes—one from each parent—that both reduce how the gene works.
Consanguinity: When parents are related by blood, they are more likely to carry the same ILDR1 change. This increases the chance their child inherits two nonworking copies.
Founder variants: In some families with shared geographic or cultural ancestry, the same ILDR1 change appears across many relatives and generations. This founder pattern can make the condition more frequent within that community.
Family history: Having a sibling or close relative with similar early-onset nonsyndromic hearing loss suggests ILDR1 changes may run in the family. If both parents are carriers, future children have the same 25% (1 in 4) chance in each pregnancy.
Lifestyle risk factors
Autosomal recessive nonsyndromic deafness 42 is a genetic hearing loss; lifestyle habits do not cause it. However, daily choices can protect any residual hearing, support communication, and lower the risk of added ear problems or listening fatigue. Understanding how lifestyle affects Autosomal recessive nonsyndromic deafness 42 can help you preserve function and wellbeing over time. The points below focus on practical, behavior-based factors you can modify.
Repeated exposure to loud music, machinery, or events can further damage cochlear hair cells in people with this condition. Limiting time in loud settings helps preserve any residual hearing.
Consistent use of earplugs or earmuffs in noisy environments reduces additional inner-ear strain. This can slow further hearing decline and make sound through devices clearer.
High-volume earbuds concentrate sound directly into the ear and can worsen hearing thresholds. Keeping volume below 60% and taking listening breaks supports long-term hearing comfort.
Nicotine and smoke reduce inner-ear blood flow and may worsen tinnitus and sound distortion. Avoiding tobacco supports cochlear health and can improve device benefit.
Risk prevention
Because autosomal recessive nonsyndromic deafness 42 is inherited, you can’t fully prevent the condition itself, but you can lower risks around delayed diagnosis, language setbacks, and avoidable hearing damage. Planning steps before or during pregnancy and early checks after birth make the biggest difference. Knowing your risks can guide which preventive steps matter most. Protecting any remaining hearing and staying ahead of ear health issues also helps long term.
A genetics professional can explain inheritance, carrier chances, and options before pregnancy. They can also map out next steps for you and relatives.
A simple blood or saliva test can check if you and a partner carry the gene change. If both carry it, you can discuss risks and options for future pregnancies.
In vitro fertilization with embryo testing can help select embryos without the condition. Some may consider donor eggs or sperm, or prenatal testing to prepare for care.
Ensure your baby completes state or national newborn hearing checks soon after birth. Early symptoms of autosomal recessive nonsyndromic deafness 42 can be subtle, so screening catches issues quickly.
Transmission
Autosomal recessive nonsyndromic deafness 42 is not infectious and does not spread from person to person. It is inherited in an autosomal recessive way: a child is affected only when they receive two nonworking copies of the same gene, one from each parent who usually have normal hearing and are carriers.
With each pregnancy between two carriers, there is a 25% (1 in 4) chance the child will have the condition, a 50% chance the child will be a carrier like the parents, and a 25% chance the child will inherit neither changed copy. The chance of two carriers pairing up is higher in families where both parents share ancestry or are related by blood (for example, cousins). New gene changes can happen, but genetic transmission of Autosomal recessive nonsyndromic deafness 42 most often involves two carrier parents and follows these same odds.
When to test your genes
Autosomal recessive nonsyndromic deafness 42 is a genetic/congenital condition, so consider testing if there’s early-onset hearing loss in you or close relatives, especially with consanguinity or a known family variant. Test before pregnancy for reproductive planning, or in infancy/childhood to guide hearing care. Retest if gene panels update or results were previously inconclusive.
Diagnosis
For many families, the first clue is a newborn hearing screen that doesn’t pass, or later, a child who doesn’t turn to their name or needs the TV louder than expected. Because this condition affects hearing without other body systems, testing focuses on confirming sensorineural hearing loss and then looking for a genetic cause. Genetic testing may be offered to clarify risk or guide treatment. Autosomal recessive nonsyndromic deafness 42 is confirmed when hearing tests point to inner-ear or nerve-related hearing loss and genetic results match known patterns.
Hospitals use quick tests to check a baby’s response to sound shortly after birth. A “refer” result twice usually leads to a full hearing evaluation.
Tests such as auditory brainstem response and otoacoustic emissions help confirm sensorineural hearing loss and its severity. Older children and adults may also have pure-tone audiometry to chart hearing across pitches.
A medical exam looks for signs that hearing loss is part of a broader syndrome, which are typically absent here. Doctors also review pregnancy history, infections, medicines, and noise exposure to understand possible causes.
A detailed family and health history can help show whether hearing loss runs in the family or if relatives had early hearing changes. This information supports decisions about which tests to order.
Stages of Autosomal recessive nonsyndromic deafness 42
Autosomal recessive nonsyndromic deafness 42 does not have defined progression stages. This type of hearing loss is usually present from birth or early childhood and tends to be identified by hearing tests rather than changing in clear step-by-step phases. In practice, early symptoms of autosomal recessive nonsyndromic deafness 42 are often picked up through newborn hearing screening or when a child doesn’t respond to sounds as expected. Different tests may be suggested to help confirm the diagnosis, including detailed hearing checks, an ear exam to rule out other causes, and sometimes genetic testing to look for the underlying cause.
Outlook and prognosis
Hearing tends to be stable in many people with Autosomal recessive nonsyndromic deafness 42, though some notice slow changes over time. Daily life often centers on communication choices—hearing aids, cochlear implants, captioning, sign language, or a mix—so the long-term outlook often improves as technology and support services are put in place. Early care can make a real difference, especially for children, because timely hearing support helps with language, learning, and social development. This type of hearing loss does not typically affect other organs, so life expectancy is normal, and DNFB42 itself is not linked to higher mortality.
The outlook is not the same for everyone, but most people with Autosomal recessive nonsyndromic deafness 42 can expect good overall health and active, independent lives. Some people experience stable hearing thresholds for years, while others notice gradual shifts that call for updated devices or mapping. Looking at the long-term picture can be helpful, since regular hearing checks can spot changes early and keep communication tools working well. If you’re wondering about early symptoms of Autosomal recessive nonsyndromic deafness 42 in children, newborn screening or early childhood hearing tests often pick it up, allowing families to plan sooner.
In medical terms, the long-term outlook is often shaped by both genetics and lifestyle. Access to audiology care, speech and language support, education services, and community resources often guides day-to-day outcomes more than the diagnosis name itself. Talk with your doctor about what your personal outlook might look like, including how often to test hearing and when to consider new devices or settings. Support from friends and family can help maintain strong communication at home, school, and work, which often matters as much as the medical plan.
Long-term effects
People with this condition tend to have a lifelong hearing difference that starts in infancy or early childhood, which shapes how they communicate and learn. Long-term effects vary widely, depending on the degree of hearing loss and access to language. Families often first notice early symptoms of Autosomal recessive nonsyndromic deafness 42 in the first year, like limited responses to sound or delayed babbling. Over time, the condition usually remains focused on hearing, without other organs being affected.
The hearing loss is usually bilateral and present from early childhood. The hearing loss in Autosomal recessive nonsyndromic deafness 42 is commonly severe to profound and sensorineural in type. In many, the profile stays relatively stable over time.
Differences in access to sound can shape spoken-language development. Many children show early language delays tied to audibility rather than learning ability. These differences often become noticeable in the toddler and preschool years.
Communication in classrooms and workplaces often centers on visual information rather than sound. Reading and learning outcomes typically reflect the clarity of language access over time. Adults may continue to prefer visual or text-based communication.
Most people do not have chronic balance problems. Everyday physical activities are usually unaffected. Persistent vertigo is uncommon.
How is it to live with Autosomal recessive nonsyndromic deafness 42?
Life with autosomal recessive nonsyndromic deafness 42 often centers on communication choices and access, not on illness or pain. Many people thrive with early identification, hearing technology such as hearing aids or cochlear implants when appropriate, and strong language development—spoken, signed, or both—supported by family, schools, and community. Day to day, this can mean planning for visual alerts, captioning, quiet spaces, and clinicians who understand hearing diversity, while loved ones learn clear communication habits and sometimes basic signing to stay connected. With the right tools and inclusive environments, most build full, independent lives, with relationships and careers shaped more by opportunity and support than by the diagnosis itself.
Treatment and drugs
Autosomal recessive nonsyndromic deafness 42 is managed by improving hearing and communication rather than changing the underlying gene. Treatment plans often combine several approaches, including hearing aids to amplify sound, cochlear implants if hearing loss is severe and hearing aids don’t help enough, and early speech and language therapy to build communication skills. Some may also use assistive listening devices, subtitles, and classroom supports, and many benefit from learning sign language for clear, reliable communication in all settings. Genetic counseling can help families understand inheritance and testing options for relatives or future pregnancies. Ask your doctor about the best starting point for you, and revisit your plan over time as needs change.
Non-drug treatment
Living with Autosomal recessive nonsyndromic deafness 42 most often centers on communication, learning, and daily connection with others. Non-drug treatments often lay the foundation for building language, supporting school or work, and staying engaged with family life. Recognizing early symptoms of autosomal recessive nonsyndromic deafness 42 in infancy can speed access to hearing support and early intervention. Options are tailored to age, hearing level, and family preferences, and they can be combined over time.
Early hearing checks help find hearing loss in the first weeks of life. Quick referral to specialists allows timely fitting of devices and early therapy. This early start supports speech, language, and social development.
These devices amplify sound to match your hearing profile. They can improve access to speech and environmental sounds in one or both ears. Regular adjustments keep them working well as needs change.
For severe to profound hearing loss, implants can bypass damaged inner-ear cells and directly stimulate hearing nerves. Surgery is followed by careful programming and listening therapy. Many people notice clearer access to speech over time.
These systems send sound through bone to the inner ear, which can help when regular hearing aids are not effective or comfortable. They may be worn on a soft band in children or implanted later. A hearing team can advise which setup fits best.
Your genes may have an impact on how drugs work for you
Some medicines used for hearing-related care can work differently depending on your genes, affecting how quickly you clear a drug or how strongly you respond. While the deafness itself is genetic, pharmacogenetic testing can guide safer dosing and avoid side effects.
Pharmacological treatments
There are currently no approved medicines that reverse or correct hearing loss caused by autosomal recessive nonsyndromic deafness 42 (DFNB42). Medicines may still play a role for related issues, like treating ear infections or protecting hearing in certain medical situations. Alongside drug therapy, hearing aids and cochlear implants remain important. Medicines do not change early symptoms of autosomal recessive nonsyndromic deafness 42, but they can help reduce preventable setbacks to hearing health.
Used for sudden sensorineural hearing loss that appears over hours to days. It has not been shown to improve the baseline, lifelong hearing pattern seen in DFNB42. Doctors may consider it only if a sudden, new drop in hearing occurs.
Treats acute middle-ear infections that can temporarily worsen hearing thresholds. Clearing infection and fluid can help people with DFNB42 make the most of their hearing aids. Ask your doctor why a specific drug was recommended for you.
An antioxidant studied to help protect hearing from loud noise or certain medicines. It does not restore genetic hearing loss in DFNB42 but may be discussed for specific risks. Evidence is mixed, so your clinician will weigh potential benefits and side effects.
In some chemotherapy plans, this drug can help protect against cisplatin-related hearing damage, especially in children. It does not treat DFNB42 itself but may prevent additional loss when cisplatin is necessary.
Genetic influences
In most families, Autosomal recessive nonsyndromic deafness 42 is linked to changes in a gene called ILDR1 that helps the inner ear’s sound‑sensing cells communicate. A “carrier” means you hold the gene change but may not show symptoms. The condition is inherited in an autosomal recessive way: when both parents are carriers, each pregnancy has a 25% (1 in 4) chance of a child with hearing loss, a 50% (1 in 2) chance of a child who is a carrier, and a 25% (1 in 4) chance of a child without the gene change. Because it’s nonsyndromic, the gene change affects hearing without involving other organs. For some families, the early symptoms of Autosomal recessive nonsyndromic deafness 42 are noticed when a newborn does not pass routine hearing screening, and severity can range from moderate to profound. Genetic testing can confirm changes in ILDR1 and help clarify carrier status for parents and relatives, which can guide healthcare planning and support.
Is Autosomal recessive nonsyndromic deafness 42 genetic?
Genetics are central to Autosomal recessive nonsyndromic deafness 42. It’s caused by inheriting two nonworking gene copies, one from each parent, who are usually unaffected carriers. Variants in the implicated gene drive the condition’s onset, severity, and family recurrence risk.
Pharmacogenetics—how genetics influence drug effects
Treatment for Autosomal recessive nonsyndromic deafness 42 mostly centers on hearing technology and communication support, but medicines still matter during ear infections, surgeries, or other health needs. The ILDR1 gene changes that cause this condition don’t typically change how most drugs are broken down or cleared. A separate genetic factor can be important, though: certain changes in the mitochondrial MT-RNR1 gene can cause severe, permanent hearing damage after standard doses of specific hospital antibiotics called aminoglycosides (such as gentamicin or tobramycin). Genetic testing can sometimes identify how your body responds to these antibiotics so doctors can choose safer options when possible.
If an aminoglycoside is urgently needed, your team will balance the benefits and risks, consider alternatives, and monitor hearing when feasible. Other medicines—like the chemotherapy drug cisplatin or high-dose loop diuretics—can also harm hearing; tests to predict who is most at risk are still being studied and aren’t used routinely. Share any prior genetic results and any history of medication-related ear symptoms so your clinicians can tailor antibiotics, anesthesia, and pain control with hearing safety in mind.
Interactions with other conditions
People living with Autosomal recessive nonsyndromic deafness 42 may also have other health issues that change how well they communicate day to day. Ear problems like repeated middle ear infections or fluid behind the eardrum can add a temporary “conductive” layer on top of the permanent hearing loss, making hearing aids or speech-reading less effective until the infection clears. Medicines that can harm hearing—such as certain antibiotics (aminoglycosides), chemotherapy drugs, or very high-dose loop diuretics—may further reduce any remaining hearing, so it’s important to review treatments before starting them. Infections that inflame the inner ear (for example, meningitis) can speed up inner ear damage and may also affect cochlear implant planning, which is why timely vaccines and urgent care for severe infections matter. Other long-term conditions, including diabetes and cardiovascular disease, have been linked to additional hearing changes over time, and vision problems can amplify communication challenges even though this form of deafness is not part of a broader syndrome. Talk with your doctor about how your conditions may influence each other.
How genes can cause diseases
Humans have more than 20,000 genes, each carrying out one or a few specific functions in the body. One gene instructs the body to digest lactose from milk, another tells the body how to build strong bones and another prevents the body's cells from beginning to multiply uncontrollably and developing into cancer. As all of these genes combined are the building instructions for our body, a defect in one of these genes can have severe health consequences.
Through decades of genetic research, we know the genetic code of any healthy/functional human gene. We have also identified that in certain positions on a gene, some individuals may have a different genetic letter from the one you have. We call these hotspots "Genetic Variations" or "Variants" in short. In many cases, studies have been able to show that having the genetic letter "G" in the position makes you healthy, but having the letter "A" in the same position disrupts the gene function and causes a disease. Genopedia allows you to view these variants in genes and summarizes all that we know from scientific research, which genetic letters (Genotype) have good or bad consequences on your health or on your traits.
History
Families and communities once noticed patterns of children born with normal appearance who did not respond to voices or everyday sounds. In some villages, grandparents recalled cousins who learned to communicate through signs at home. School records and family stories captured these details long before hearing tests were widely available.
First described in the medical literature as clusters of hearing loss without other health issues, early reports grouped many situations together. Over time, descriptions became more precise. Doctors separated hearing loss that travels with other features—like vision or balance problems—from cases where hearing is the only concern. This is where autosomal recessive nonsyndromic deafness 42 fits: hearing loss alone, typically beginning at birth or early in life, and running in families in a recessive pattern.
From early theories to modern research, the story of autosomal recessive nonsyndromic deafness 42 reflects how naming and tools advance hand in hand. Before modern genetics, clinicians relied on careful family trees, noting when parents with typical hearing had more than one child with significant hearing loss. These observations hinted at a hidden, paired inheritance pattern. As newborn hearing screening spread in the late 20th and early 21st centuries, more infants were identified early, allowing researchers to compare features and map patterns more accurately.
Advances in genetics changed the pace. Once labs could scan many genes at once, researchers matched specific gene changes to particular family patterns of nonsyndromic hearing loss. Multiple numbered forms emerged as scientists distinguished different gene-related types that look similar on the surface but have distinct genetic causes. Autosomal recessive nonsyndromic deafness 42 became one of these numbered categories, reflecting its place in a growing catalog rather than its severity or prognosis.
In recent decades, awareness has grown that autosomal recessive nonsyndromic deafness 42, like related forms, can vary in how severe the hearing loss is and how it progresses. Not every early description was complete, yet together they built the foundation of today’s knowledge. Careful pairing of detailed hearing evaluations with genetic testing helped confirm which families shared the same underlying cause, and which did not.
Today, the history of autosomal recessive nonsyndromic deafness 42 shows a clear arc: from community observations, to clinical grouping as “nonsyndromic,” to pinpointing the genetic cause in affected families. Looking back helps explain why the name is specific and technical—it marks a distinct genetic subtype within a larger, diverse landscape of hereditary hearing loss—while the lived experience remains centered on hearing and communication.