Author name: adamkuhn

It was only discovered in 2012. It clears the proteins linked to Alzheimer’s disease. And several common habits impair it every night. Until 2012, neuroscientists believed the brain had no system for clearing its own waste. Every other organ in the body uses the lymphatic system to remove cellular debris, toxins, and metabolic byproducts. The brain — separated from the rest of the body by the blood-brain barrier — appeared to have no equivalent. For decades, researchers assumed the brain simply managed waste locally, in ways that weren’t well understood. Then neuroscientist Maiken Nedergaard and her team at the University of Rochester found the brain does have its own dedicated waste clearance pathway. They called it the glymphatic system — and the proteins it clears are the same ones that accumulate in Alzheimer’s disease. How the glymphatic system works The glymphatic system runs along the brain’s blood vessels. Cerebrospinal fluid — the clear fluid that surrounds and cushions the brain — enters the brain tissue through channels that line the outside of arteries. It flows through the spaces between brain cells, flushing out metabolic waste: amyloid-beta proteins, tau proteins, and other cellular debris accumulated during normal waking brain activity. The system depends on specialized water channels called aquaporin-4 (AQP4), which sit on the surface of astrocytes — the support cells of the brain — clustered specifically around blood vessels. These channels act as the plumbing that allows fluid to move efficiently through brain tissue. When AQP4 channels are functioning and properly positioned, the glymphatic system runs efficiently. When they’re disrupted — through aging, certain lifestyle factors, or neurological injury — fluid transport slows, and waste accumulates. Research has confirmed that mice with AQP4 channels deleted show a 55–70% reduction in CSF influx and solute clearance, and develop significantly worse amyloid-beta accumulation and memory deficits compared to normal mice. What the glymphatic system is clearing — and why it matters Amyloid-beta and tau are both normal byproducts of brain metabolism. They’re produced every day as neurons do their work. Under healthy conditions, the glymphatic system clears them overnight at a rate that keeps pace with their production. When clearance falls behind production — for any reason — both proteins begin to accumulate. Amyloid-beta aggregates into plaques between neurons. Tau forms tangles inside neurons. These are the two defining pathological features of Alzheimer’s disease — and both begin accumulating silently, decades before any cognitive symptoms appear. A 2026 randomized crossover trial published in Nature Communications confirmed this directly in humans: during normal sleep, glymphatic processes measurably increased the clearance of both amyloid-beta and tau biomarkers into the bloodstream. During sleep deprivation, that clearance was significantly reduced. Chronic disruption of the glymphatic system may allow the proteins that define Alzheimer’s disease to accumulate faster than they would otherwise. To be precise about what the research does and doesn’t show: this is an association, not a proven causal chain. What it does establish is a plausible, well-supported mechanism connecting glymphatic function to Alzheimer’s pathology — and a clear biological reason to take the factors that impair it seriously. What impairs the glymphatic system Several factors have been identified in the research as direct impairers of glymphatic clearance: Sleep deprivation. Glymphatic clearance is most active during deep slow-wave sleep (NREM stage 3). Insufficient or fragmented sleep directly curtails the system’s operating window. Research has found that even one night of sleep deprivation measurably reduces amyloid-beta clearance. Alcohol. Alcohol has a biphasic effect on the glymphatic system: low doses may modestly enhance function, while higher doses suppress it significantly. Chronic alcohol consumption has been shown to cause irreversible impairment of glymphatic function in animal models. The mechanism involves reduced cerebrovascular pulsatility — the rhythmic movement of blood vessel walls that helps drive CSF flow through brain tissue. Aging. AQP4 channels lose their precise positioning around blood vessels with age — a process called depolarization. As this happens, the efficiency of glymphatic transport declines. This is one reason why the risk of Alzheimer’s disease increases so steeply with age: the system that clears Alzheimer’s-associated proteins becomes less effective precisely when it matters most. Hypertension. High blood pressure impairs the arterial pulsatility that drives CSF flow through the glymphatic pathway. Research has found measurably reduced glymphatic transport in hypertensive animal models compared to normotensive controls. Traumatic brain injury. Even mild TBI disrupts AQP4 channel positioning and impairs glymphatic drainage. This may partly explain the well-documented link between head injuries and increased long-term dementia risk. Chronic stress. Sustained elevation of stress hormones is associated with reduced glymphatic activity, compounding the neuroinflammation that stress already promotes through other pathways. The factors that support it The same research that identifies what impairs the glymphatic system also points to what supports it — and the interventions map directly onto what VitalLife is built around. Sleep position. Multiple studies have found that glymphatic clearance is most efficient in the right lateral (side-sleeping) position, with measurably more CSF clearance compared to sleeping on the back or stomach. Gravity affects CSF movement, and the lateral position appears to optimize it. Neurodegenerative patients spend a disproportionate amount of time sleeping on their back — a pattern the research associates with reduced clearance efficiency. Aerobic exercise. A 2026 review published in Brain, Behavior and Immunity Integrative found that structured aerobic exercise increases glymphatic and meningeal lymphatic activity, improves vascular dynamics, reduces systemic inflammation, and improves sleep quality — each of which directly supports glymphatic clearance. The mechanism runs partly through AQP4 polarization: exercise appears to help maintain the proper positioning of the water channels that drive the system. Omega-3 fatty acids. Omega-3 polyunsaturated fatty acids have been found to support glymphatic activity, likely through their effect on AQP4 expression and their broader anti-inflammatory properties. The research is preliminary but consistent in direction. Time-restricted eating. Intermittent fasting has been associated with enhanced waste clearance through multiple pathways, including glymphatic activity. Avoiding food in the hours before sleep — which VitalLife teaches as a foundational practice — may support glymphatic function by reducing the

Vascular health and cognitive decline are more connected than most people realize — and it’s more reversible than you’d expect. Most people think of vascular health as a heart issue. Blood pressure, cholesterol, arteries — that’s cardiology territory. But your brain runs on blood flow just like every other organ in your body — and when that blood flow is compromised, the damage shows up in your brain before it shows up anywhere else you’d notice. Why your brain is so dependent on blood flow Your brain makes up roughly 2% of your body weight, but it consumes 15 to 20% of your body’s total blood flow. No other organ demands that much relative to its size. Brain tissue has essentially no capacity to store energy — it depends on a constant, uninterrupted supply of oxygen and glucose delivered through the bloodstream. When blood vessels become narrowed, stiffened, or damaged — through high blood pressure, high cholesterol, insulin resistance, or atherosclerosis — that supply gets interrupted. Researchers call this chronic cerebral hypoperfusion: a sustained reduction in blood flow to the brain. And it doesn’t need to cause a stroke to cause damage. The brain can be quietly starved of oxygen and nutrients for years before any symptom appears. This is now understood to be one of the central mechanisms behind vascular dementia — and a significant contributing factor in Alzheimer’s disease as well, even in cases where vascular issues weren’t the primary diagnosis. What this looks like on an MRI This isn’t theoretical. The damage from poor cerebral blood flow is visible on brain imaging, often in people who have no cognitive symptoms at all. Two findings show up repeatedly in the research: White matter hyperintensities These are bright spots that appear on MRI scans, representing areas of damage in the brain’s white matter caused by chronically reduced blood flow. Research consistently shows the majority of people over 65 have some degree of white matter hyperintensities on MRI — in many studies, the figure exceeds 90%. The volume and location matter: larger volumes are consistently associated with cognitive impairment, dementia, and slower processing speed. Silent lacunar infarcts These are small areas of brain tissue damaged by tiny blockages in deep blood vessels — essentially miniature strokes that produce no obvious symptoms. They’re called “silent” because the person experiencing them often has no idea anything happened. Population studies have found silent lacunar infarcts in roughly 20% of adults over 65 — a figure that climbs above 35% in those over 80. And research shows these silent infarcts more than double the risk of stroke and dementia. Neither of these findings requires a major cardiovascular event. They accumulate quietly, the result of years of blood vessels working harder than they should — and the brain paying the price. A test most people have never heard of If vascular damage is accumulating silently, the obvious question is: how would you know before it shows up as cognitive decline? One of the more useful tools for this is a coronary artery calcium (CAC) score — a low-dose CT scan that measures calcified plaque in the arteries of your heart. It was developed as a cardiovascular risk tool, but research has since found it tells you something about your brain too. Multiple studies have found that higher CAC scores are associated with worse cognitive performance, smaller brain volume, more white matter hyperintensities, and reduced blood flow to specific brain regions — independent of standard Alzheimer’s biomarkers. One large cohort study found that CAC progression in midlife was associated with measurably worse performance on cognitive testing decades later. Another found that a CAC score above 300 was linked to a steeper rate of cognitive decline over time. Calcification in your coronary arteries reflects the same disease process — atherosclerosis — that can be happening in the vessels supplying your brain. A CAC score is a window into vascular health you can’t see or feel. It’s a simple test, widely available, and one Dr. Pardue considers a valuable piece of the full picture for patients concerned about cognitive risk. The part most people don’t know: your brain makes its own cholesterol The cholesterol in your bloodstream and the cholesterol in your brain are almost entirely separate systems. Cholesterol from your blood is too large to cross the blood-brain barrier in meaningful amounts. So your brain manufactures nearly all of the cholesterol it needs on-site — and it needs a lot. The brain holds the highest concentration of cholesterol of any organ in the body, most of it embedded in the membranes that insulate nerve fibers and allow electrical signals to move quickly between brain cells. This means brain cholesterol metabolism runs largely independent of what shows up on your standard blood panel. It has its own production, its own recycling system, and its own transport proteins — most notably apolipoprotein E, the same APOE gene we covered in a previous email. The brain’s cholesterol system isn’t broken by what you eat in the way your blood cholesterol can be. It’s a closed loop, built for stability. Why does this matter for vascular health? Because it reframes the conversation. Protecting your brain isn’t really about lowering cholesterol numbers on a lab report. It’s about protecting the blood vessels that deliver oxygen and nutrients to the system that builds and maintains that cholesterol in the first place. Vascular health and brain health are connected — but not in the way most people assume. Why this is one of the most actionable risk factors there is Unlike some risk factors for cognitive decline, vascular health responds dramatically to intervention. High blood pressure, insulin resistance, and metabolic syndrome are among the most modifiable contributors to dementia risk identified in the research. “The patients with vascular risk factors — high blood pressure, pre diabetes, metabolic syndrome — are some of the most responsive patients I see. Blood vessels are remarkably capable of healing when you remove the underlying stress. Nutrition, movement,

One gene variant is the strongest known genetic risk factor for Alzheimer’s. Here’s what it means — and what you can do about it. There’s a gene that researchers now consider the single strongest genetic risk factor for late-onset Alzheimer’s disease. It’s called APOE — apolipoprotein E. Most people have never heard of it. But for anyone paying attention to brain health, it may be the most actionable piece of genetic information available. Here’s what it is, what it means, and why the people who carry the highest-risk variant are often the ones who respond most to what we do in VitalLife. What the APOE gene does Every gene in your body works the same basic way: it carries instructions. Your APOE gene instructs your body on how to produce apolipoprotein E, a protein that does two critical jobs. First, it manages how your body transports cholesterol and fats through the bloodstream. Second — and this is the part that matters for your brain — it plays a central role in how your brain clears amyloid-beta, the protein fragment whose accumulation is the hallmark of Alzheimer’s disease. When the APOE gene gives clear, effective instructions, your brain’s cleanup system runs well. When the instructions are compromised, amyloid builds up, inflammation increases, and the metabolic environment of the brain begins to shift in ways that increase Alzheimer’s risk. The version of the gene you inherited determines how well those instructions work. The three versions — and what each one means APOE comes in three forms, called alleles: ε2, ε3, and ε4. Everyone inherits two copies — one from each parent. The combination you carry is your APOE genotype, and it’s one of the strongest genetic predictors of Alzheimer’s risk identified in modern research. APOE ε2 — The protective variant The rarest of the three, carried by roughly 5–10% of the population. Carrying even one copy of ε2 appears to reduce Alzheimer’s risk by up to 40% compared to the most common variant. When Alzheimer’s does occur in ε2 carriers, it tends to develop later in life. APOE ε3 — The neutral variant The most common form, present in approximately 78% of alleles worldwide. ε3 is used as the research baseline — neither increasing nor decreasing Alzheimer’s risk. Most people carry at least one copy. APOE ε4 — The risk variant Present in approximately 14–15% of the general population, but found in an estimated 40% of late-onset Alzheimer’s patients. This is the variant Dr. Pardue wants every patient to know about. One copy of ε4 (ε3/ε4): 2–3x increased risk of Alzheimer’s Two copies of ε4 (ε4/ε4): 8–12x increased risk — the highest genetic risk profile To put that in perspective: approximately 2–5% of the population carries two copies of ε4. That group faces a significantly earlier average age of onset and the steepest risk curve of any common genetic variant associated with Alzheimer’s. And carrying ε4 does not mean Alzheimer’s is inevitable. That distinction matters, and we’ll come back to it. Why ε4 changes how the brain works The ε4 variant doesn’t just increase risk on paper. It changes the brain’s operating environment in measurable ways — some of which begin decades before any symptoms appear. APOE4 impairs the brain’s ability to clear amyloid-beta effectively, allowing it to accumulate earlier and faster than in ε3 carriers. It also disrupts glucose metabolism in the brain — meaning ε4 carriers’ neurons are less efficient at using their primary fuel source. Research has found that these glucose metabolism differences can appear in cognitively normal APOE4 carriers decades before any cognitive symptoms emerge. APOE4 also promotes neuroinflammation and impairs lipid transport in the brain — two factors directly linked to the synaptic damage that underlies memory loss. This is why Dr. Pardue calls it an operating environment problem, not just a risk statistic. The brain of an ε4 carrier functions differently. And that means the interventions that matter most are the ones that address that underlying metabolic environment. The patients at highest risk respond best to metabolic intervention Here is what Dr. Pardue has observed consistently in his patients — and what the emerging research supports: “People who carry two copies of APOE4 are the ones I feel most urgency about. Their risk is real and it’s elevated. But they are also, in my clinical experience, the patients who respond most favorably to the kind of metabolic work we do in VitalLife. When the brain has been running in a compromised state for years, and you give it what it actually needs — the right nutrition, sleep, exercise and peace – the response can be dramatic. Genetics loads the gun. Lifestyle pulls the trigger. It works the other way too: the right lifestyle can keep that trigger from ever being pulled.” — Dr. Randy Pardue The underlying research points the same way. Studies have found that because APOE4 impairs glucose metabolism in the brain, ε4 carriers appear to shift metabolic dependency toward ketones — an alternative fuel source. Interventions that support metabolic flexibility, reduce insulin resistance, and optimize the brain’s fuel supply show particular promise for this population. The VitalLife protocols are built around exactly that substrate. Should you get tested? This is a question worth thinking through carefully — not because the answer is complicated, but because knowing your APOE status carries real weight, and you should go in prepared. The case for knowing: If you carry ε4 — one copy or two — that information gives you a concrete reason to act now rather than later. The interventions that protect cognitive health work best when they start early, before any symptoms appear. Knowing your status gives you something real to work with — and a clear reason to start now rather than wait. One important note before you test: Federal law (GINA) protects you from genetic discrimination by health insurers and most employers — but that protection does not extend to life insurance, long-term care insurance, or disability insurance. If you don’t currently have those policies and plan to get them, it may be worth

A major JAMA study compared structured coaching to self-guided lifestyle change for cognitive protection. The results weren’t close. In July 2025, the U.S. POINTER study published its results in JAMA — the Journal of the American Medical Association. POINTER was a two-year, multi-site clinical trial testing lifestyle interventions in older adults at risk for cognitive decline. It compared two approaches: a structured, coached multidomain lifestyle intervention covering diet, exercise, cardiovascular health, and cognitive engagement — and a self-guided version encouraging the same lifestyle goals but with far less structure, coaching, and accountability. Both groups improved. But the structured, coached group showed significantly greater improvement in global cognition compared to the self-guided group — protecting participants from normal age-related cognitive decline over the nearly two-year study period. Same information. Different outcomes. Why brain health is not a self-directed project Improving cognitive health through lifestyle change is not like following a recipe. A recipe has fixed ingredients, fixed quantities, and a predictable result. Protecting your brain requires ongoing calibration — dozens of variables, each one affecting the others, each one needing to be adjusted differently depending on the person. Think of it as a soundboard with dozens of knobs. Nutrition. Sleep architecture. Exercise intensity and type. Stress physiology. Metabolic markers. Blood flow. Methylation. Hormonal balance. Toxin burden. Chronic infections. Each one affects cognitive health. Each one needs to be adjusted — but in a different order, at a different level, for each individual person. Turn the wrong knob first, or too far, and the others don’t respond the way you’d expect. No single intervention drives the outcome — it’s the combination, the sequencing, and the personalization that determines whether someone improves, plateaus, or declines. A 2023 study published in the Journal of Alzheimer’s Disease followed 34 participants through a personalized multimodal intervention covering nutrition, movement, stress, nutraceuticals, and infection burden. After six months, MoCA scores improved significantly — from 19.6 to 21.7 — and every domain of cognitive function assessed improved. POINTER confirmed it at scale in a randomized trial. The four pillars — and what comes after them VitalLife is built around four foundational pillars that the research consistently identifies as the primary drivers of cognitive health: nutrition, exercise, sleep, and pursuit of peace. These are addressed first, because they move the needle for most people — and because you can’t accurately assess what else is going on until the foundations are in place. For some participants, the four pillars are sufficient. Metabolic markers improve, inflammatory load decreases, sleep architecture recovers, and cognitive function responds. For others, progress stalls despite consistent adherence to the pillars. When that happens, the conversation turns toxic burden — heavy metals, environmental exposures, mold — and chronic infections that the immune system is managing at the cost of neurological resources. Both are documented contributors to cognitive decline in a subset of patients, and addressing them requires a different level of investigation. The point is not that every participant has a toxin or infection problem. Most don’t. The point is that the knobs often include them. And knowing which ones to turn — and when — requires someone who has the clinical training to read the picture as it evolves. What the coaching research shows The FINGER trial, one of the most rigorous long-term lifestyle intervention studies in the dementia prevention literature, followed 1,259 adults at elevated dementia risk over 11 years. Participants who engaged consistently with their coached intervention had better cognitive trajectories than both the control group at the seven-year mark — five years after the active intervention ended — and continued to outperform low-engagement participants at eleven years. The benefit didn’t come from information. It came from sustained, supported implementation. “The patients I see who make the most progress are not the ones who know the most. They’re the ones who have someone walking alongside them — adjusting the protocol as their labs change, holding them accountable when motivation slips, and knowing when to push harder and when to pull back. Brain health is a long game. You don’t win it alone.” — Dr. Randy Pardue The VitalLife coaching team In VitalLife, you work with our three coaches: Kyra Fowler – Family Nurse Practitioner & Health Coach Kyra brings 15+ years of specialized experience in medical nutrition management and reversing chronic disease through lifestyle change. Her approach is rooted in science, relationship, and the conviction that lasting change is possible when someone shows you not just what to change, but how. Carly Slagle – Registered Dietitian & Health Coach Carly’s background as a Registered Dietitian grounds her coaching in the science of how food affects the body at a root level. She helps participants understand why their nutrition matters — not just what to eat — and has a gift for meeting people where they are in the middle of full, busy lives. Arielle DeVito – Personal Trainer & Health Coach Arielle brings 18 years of experience in behavior change and sustainable lifestyle modification, holding multiple certifications through the American Council on Exercise including Behavior Change Specialist and Lifestyle & Weight Management Consultant. She specializes in helping people build the habits that make everything else work. The VitalLife Brain Health Cohort starts September 8. The cohort is a structured, coached, multidomain program — the same model the research consistently shows outperforms self-directed approaches. Every participant works directly with a VitalLife coach, reviewing labs and adjusting protocols as your biology changes. The July cohort sold out at 30 participants. The September cohort is open now and spots are filling. There’s a free Preview Night on August 25 — no commitment, no obligation. Come meet the team, see what the program involves, and decide whether it’s right for you. Free Preview Night — next Tuesday, August 25 Meet Dr. Pardue and the team. See the program. Ask your questions. REGISTER FOR THE FREE PREVIEW NIGHT VitalLife Brain Health Cohort Begins — Tuesday, September 8th → Learn more about the VitalLife program: LEARN MORE For your health,

The world’s leading dementia research commission ranks hearing loss among the largest modifiable risk factors. In 2024, the Lancet Commission on Dementia Prevention, Intervention, and Care — the most authoritative ongoing review of dementia science in the world — published its latest report identifying 14 modifiable risk factors that together account for approximately 45% of global dementia cases. Hearing loss ranked among the largest of all 14, accounting for an estimated 7% of global dementia cases — more than physical inactivity, obesity, smoking, diabetes, or depression individually. Why hearing loss damages the brain The connection between hearing loss and cognitive decline runs through four distinct mechanisms. Increased cognitive load. When hearing is impaired, the brain must work significantly harder to decode speech and environmental sound. Cognitive resources that would otherwise be available for memory encoding, executive function, and attention are diverted toward basic auditory processing. Over years and decades, this chronic overallocation of cognitive resources accelerates decline. Sensory deprivation and brain atrophy. Reduced auditory input from the environment directly affects brain structure. People with untreated hearing loss show measurably reduced temporal lobe volume on MRI — including in regions directly involved in memory and language. Auditory deprivation causes the neural networks that process sound to reorganize and atrophy, and the damage extends into adjacent cognitive regions. The brain shrinks where it stops receiving input. Social isolation and withdrawal. Hearing loss makes conversation effortful and often embarrassing. People pull back from dinner tables, from social events, and from phone calls. Social isolation is itself one of the 14 Lancet Commission risk factors for dementia, independently of hearing. Untreated hearing loss can trigger both simultaneously, compounding the cognitive cost of each. Depression and reduced cognitive reserve. Chronic communication difficulty is associated with depression in older adults, and depression is another of the 14 Lancet Commission risk factors. Hearing loss leads to social withdrawal, social withdrawal leads to depression, depression depletes cognitive reserve, and reduced cognitive reserve accelerates the clinical expression of underlying neurological changes. What happens when hearing loss is treated The ACHIEVE trial — the largest randomized controlled trial of hearing intervention for cognitive protection ever conducted — was published in The Lancet in July 2023. The trial enrolled 977 adults aged 70 to 84 with untreated mild-to-moderate hearing loss and followed them for three years. In the overall trial population, the hearing intervention did not significantly outperform the control group. But when researchers focused on the pre-specified subgroup of participants who were at higher risk for cognitive decline — older adults with more cardiovascular risk factors and faster baseline rates of cognitive change — hearing intervention slowed cognitive decline by 48% over three years. A separate 2023 meta-analysis combining data from more than 137,000 participants found that hearing aid use was associated with a 19% lower risk of long-term cognitive decline across studies with follow-up periods ranging from two to twenty-five years. The research doesn’t prove that treating hearing loss prevents dementia. What it does establish is a consistent, biologically plausible association — confirmed across multiple study designs — between untreated hearing loss and accelerated cognitive decline, and between hearing intervention and slower decline in higher-risk populations. A risk factor most people haven’t checked since grade school Age-related hearing loss develops gradually — often over years — and most people adapt to it without realizing how significant the change has become. Unlike blood pressure or blood sugar, hearing loss doesn’t trigger a warning signal. It gets rationalized away — gradually, invisibly, over years. The Lancet Commission’s recommendation is direct: make hearing aids accessible for people with hearing loss and decrease harmful noise exposure to prevent it. Getting a hearing assessment is the starting point — and it’s something adults over 50 are routinely encouraged to do — but rarely prioritize. A standard audiological assessment is straightforward. Many primary care physicians can perform basic screening. A formal evaluation by an audiologist gives a complete picture of the type and degree of any loss and whether intervention is warranted. “Hearing loss is the kind of risk factor that accumulates slowly for years before anyone notices. By the time it’s obvious, the cognitive cost has already been taking its toll. Hearing loss belongs in every brain health conversation. It is not an afterthought, but one of the more actionable things on the list.” — Dr. Randy Pardue The next VitalLife Brain Health Cohort starts soon. The VitalLife Brain Health Cohort addresses the lifestyle-modifiable factors identified by the Lancet Commission — across nutrition, movement, sleep, and pursuit of peace — with Dr. Pardue’s clinical oversight and the VitalLife coaching team alongside you throughout. If this email has raised questions, the Preview Night on August 25 is where you get them answered. No commitment, no obligation. Meet Dr. Pardue and the team, see the program, and decide whether it’s right for you. The July cohort sold out at 30 participants. → Sign Up for the VitalLife program: SIGN UP Free Preview Night Meet Dr. Pardue and the team. See the program. Ask your questions. 6:30pm at Vital Wellness, 9965 Kingston Pike. → REGISTER FOR THE FREE PREVIEW NIGHT For your health, Adam (on behalf of Dr. Pardue) P.S.  If you’re over 50 and haven’t had a hearing assessment in the last few years, it’s worth scheduling one. Ask your primary care physician for a referral to an audiologist — it’s a step most people skip. P.P.S If you are tech savvy, you can also take a validated clinical-grade hearing test using your iPhone and AirPod Pro headphones. I did it this morning. Takes about 5 minutes.