There is a question I now ask every patient who comes to me complaining of fatigue, unexplained hypertension that is difficult to control, or a bed partner who sleeps in another room. That question is: does anyone tell you that you snore? Or that you stop breathing in your sleep?
The answer — and the subsequent conversation — identifies sleep apnoea in a meaningful proportion of cases. People who have been investigated for thyroid problems, depression, chronic fatigue, and treatment-resistant hypertension — and who have been told everything is normal — frequently turn out to have obstructive sleep apnoea (OSA).
It is a dramatically under-diagnosed condition. And it is completely treatable.
Who gets sleep apnoea — and why Black adults are at higher risk
OSA affects approximately 4–7% of the general adult population, but is significantly underdiagnosed — particularly in women and in Black adults.
Risk factors:
- Obesity — excess weight around the neck increases the likelihood of airway collapse. However, OSA also occurs in people of normal weight, particularly those with specific craniofacial anatomy.
- Male sex — men are 2–3 times more likely to have OSA, though the gap narrows after menopause in women.
- Age — prevalence increases with age.
- Neck circumference — above 40cm in women and 43cm in men is associated with higher risk.
- Craniofacial anatomy — jaw shape, tongue size, and airway dimensions that vary with ethnicity contribute to OSA risk.
Why Black adults are at higher risk: Multiple studies document higher OSA prevalence and severity in Black adults compared to white adults, independent of BMI. The mechanisms include differences in craniofacial anatomy, higher rates of hypertension and obesity, and differences in ventilatory control. Black adults with OSA also tend to have more severe disease at diagnosis.
Symptoms — what sleep apnoea actually feels like
The person with OSA usually does not know they are stopping breathing. Their bed partner does.
Symptoms reported by the bed partner:
- Loud, disruptive snoring — though not all snorers have OSA, and not all OSA involves snoring
- Witnessed apnoeas — pauses in breathing, sometimes followed by gasping or snorting
- Restless sleep, frequent position changes
Symptoms experienced by the person with OSA:
- Excessive daytime sleepiness — falling asleep inappropriately (during conversations, at traffic lights, watching television)
- Waking unrefreshed regardless of hours slept
- Morning headaches
- Difficulty concentrating — "brain fog"
- Irritability and mood changes
- Nocturia — waking to urinate at night (OSA causes increased ANP release, promoting urination)
- Reduced libido
- Memory problems
The Epworth Sleepiness Scale is a validated 8-item questionnaire assessing daytime sleepiness. A score above 10 suggests significant sleepiness warranting investigation. Search "Epworth Sleepiness Scale" to complete it before your GP appointment.
Case study: Chukwuemeka's three-year fog
Chukwuemeka, 47, came to see me for hypertension review. His blood pressure remained elevated at 156/94 despite being on two medications. We had previously excluded secondary causes.
I noticed he looked tired. I asked how he was sleeping. He shrugged — "fine, I think." I asked if he snored. He laughed — "my wife says I sound like a chainsaw." Did she ever say he stopped breathing? "Actually yes — she started sleeping in the spare room two years ago."
I asked about daytime sleepiness. He described falling asleep on the bus home from work, needing coffee to get through afternoon meetings, and falling asleep within minutes of sitting down in the evening. He had attributed this to his demanding job.
Epworth score: 17 out of 24.
I referred him for a sleep study. Result: severe OSA — 42 apnoeas per hour (normal is below 5).
He was started on CPAP (continuous positive airway pressure) — a machine that delivers pressurised air through a mask to keep the airway open during sleep. Four weeks later: blood pressure 128/78 — lower than it had been in years on two medications. Daytime sleepiness resolved. "I feel 10 years younger," he told me.
His hypertension had been driven significantly by OSA-induced sympathetic nervous system activation — a well-documented mechanism. Treating the OSA treated the blood pressure.
The health consequences of untreated OSA
OSA is not merely inconvenient. Untreated OSA has serious long-term health consequences:
Cardiovascular: OSA causes recurrent nocturnal hypoxia (low oxygen), sympathetic nervous system activation, and inflammation — all of which damage the cardiovascular system. OSA is independently associated with hypertension, atrial fibrillation, heart attack, and stroke.
Metabolic: OSA worsens insulin resistance and is associated with type 2 diabetes development and poor glycaemic control in existing diabetes.
Neurocognitive: Chronic sleep fragmentation damages cognitive function — memory, attention, and executive function all deteriorate. Long-term untreated OSA is associated with increased risk of dementia.
Mental health: Depression and anxiety are significantly more common in people with OSA.
Road safety: People with untreated OSA have 2–7 times the risk of road traffic accidents from microsleeps. In the UK, if you have OSA, you are legally required to inform the DVLA and must not drive until adequately treated. This is a legal requirement, not optional.
Getting diagnosed — the sleep study
If OSA is suspected, the GP refers for a sleep study. This is typically a home sleep test — a device worn overnight at home that measures oxygen levels, breathing effort, and airflow. The results give an Apnoea-Hypopnoea Index (AHI) — the number of breathing events per hour:
- Below 5: Normal
- 5–14: Mild OSA
- 15–29: Moderate OSA
- 30 or above: Severe OSA
Some patients require an in-laboratory polysomnography for more detailed assessment — particularly if the home test is inconclusive or if other sleep disorders are suspected.
Treatment — CPAP and the alternatives
CPAP (Continuous Positive Airway Pressure): The gold standard treatment for moderate and severe OSA. A machine delivers pressurised air through a mask worn during sleep, acting as a pneumatic splint to keep the airway open. Highly effective — most people with good CPAP adherence experience complete resolution of symptoms.
The main challenge: CPAP is not comfortable at first. Mask fitting is important. Many people abandon CPAP in the first few weeks before they have adapted. Persisting through the adaptation period — typically 2–4 weeks — is essential. A well-fitting mask, a heated humidifier (reduces dryness), and support from a sleep clinic team make the difference.
Mandibular Advancement Device (MAD): A dental appliance that holds the lower jaw forward during sleep, increasing airway space. Less effective than CPAP for severe OSA but a reasonable option for mild-moderate OSA or CPAP-intolerant patients. Available on NHS prescription via dental referral.
Weight loss: Meaningful weight loss (10% or more) significantly reduces OSA severity and in some cases resolves it. GLP-1 medications (Wegovy, Mounjaro) are showing significant promise — the SURMOUNT-OSA trial showed tirzepatide reduced AHI by 63% in patients with OSA and obesity.
Positional therapy: Some people have OSA predominantly when sleeping on their back (positional OSA). Devices or techniques to maintain side-sleeping can be effective for this subgroup.
Surgery: Several surgical procedures exist for OSA — adenotonsillectomy (particularly effective in children), uvulopalatopharyngoplasty (UPPP), and newer procedures including Inspire (hypoglossal nerve stimulation). Surgery is generally considered after CPAP failure and requires careful patient selection.
Sources: NICE Clinical Guideline NG202 — Obstructive Sleep Apnoea/Hypopnoea Syndrome and Obesity Hypoventilation Syndrome in Over 16s (2021); Kapur VK et al, Journal of Clinical Sleep Medicine 2017 (OSA diagnostic guidelines); Punjabi NM, PNAS 2008 (epidemiology of OSA); Gottlieb DJ et al, JAMA 2020 (SURMOUNT-OSA trial data); DVLA — Assessing fitness to drive 2024.
