Sleep Apnea Risk Factors: Are You at Risk?

Most People With Sleep Apnea Don't Know They Have It

The 2016 AASM "Hidden Health Crisis" report (a joint analysis with the U.S. Centers for Disease Control) estimated that more than 80% of adults with moderate to severe obstructive sleep apnea (OSA) remain undiagnosed. A 2025 prevalence analysis presented at the SLEEP conference put estimated U.S. adult OSA prevalence between 24% and 33%, which works out to roughly 85 million Americans with OSA, of whom an estimated 68 million are unaware of the condition. Many people live with fragmented sleep, chronic fatigue, and mounting cardiovascular risk for years without connecting the dots.

The good news: several well-studied risk factors can help predict whether you are likely to have OSA. The STOP-BANG questionnaire organizes eight of these factors into a quick screening tool used by sleep clinicians worldwide. Beyond STOP-BANG, several additional risk factors covered later in this article (family history, smoking, nasal congestion, endocrine disorders, certain ethnic backgrounds) also matter and deserve a place in any honest self-assessment.

The Eight STOP-BANG Risk Factors

Snoring

Loud, habitual snoring is the most common symptom of OSA. When the airway partially collapses during sleep, air passing through the narrowed space vibrates soft tissue and produces the sound. Not everyone who snores has sleep apnea, but nearly everyone with OSA snores.

"Loud" in clinical terms means louder than talking or audible through a closed door. If a bed partner or family member has commented on your snoring, that counts.

Tiredness

Excessive daytime sleepiness, fatigue that persists despite what should be enough sleep, and difficulty staying awake during passive activities (reading, watching TV, riding as a passenger) are hallmark consequences of OSA. Each time your airway collapses, your brain briefly wakes to restore breathing. These micro-arousals fragment your sleep architecture even if you don't remember waking up.

Observed Apnea

If someone has witnessed you stop breathing, choke, or gasp during sleep, that is one of the strongest indicators of OSA. Many people are unaware this is happening. Bed partners, family members, or roommates are often the first to notice.

Blood Pressure

OSA and hypertension are closely linked. Repeated oxygen drops during apnea events trigger a stress response that raises blood pressure over time. An estimated 30 to 50% of people with hypertension also have OSA. If you are being treated for high blood pressure, especially if it is resistant to medication, OSA may be a contributing factor.

BMI Over 35

Excess body weight, particularly around the neck and upper airway, increases the likelihood of airway collapse during sleep. A BMI above 35 (class II obesity) is a significant risk factor. However, OSA occurs at every BMI. Thin people with certain jaw or airway anatomy can absolutely have sleep apnea.

Not sure about your BMI? The STOP-BANG screener includes a built-in BMI calculator.

Age Over 50

The prevalence of OSA increases with age. Muscle tone throughout the body decreases as we get older, and the muscles that hold the airway open during sleep are no exception. Hormonal changes, particularly after menopause in women, further increase risk.

Neck Circumference Over 16 Inches

A larger neck circumference correlates with more soft tissue around the airway, which increases the chance of collapse. The clinical threshold is 16 inches (40 cm) for men and 15 inches (38 cm) for women. A men's dress shirt collar size 16+ is a rough equivalent.

Male Sex

Men are 2 to 3 times more likely to have OSA than premenopausal women. Differences in fat distribution, airway anatomy, and hormonal protection all play a role. After menopause, the gap narrows significantly. Sleep apnea in women is frequently underdiagnosed because symptoms often present differently.

Other Risk Factors Beyond STOP-BANG

The eight STOP-BANG items are the most efficient single screen, but several additional risk factors are well-documented in the medical literature. If you score borderline on STOP-BANG, these may push you toward getting tested.

Family History

OSA aggregates in families. Having a first-degree relative (parent, sibling, or child) with OSA is associated with elevated risk. Heritability estimates from twin and family studies place roughly 40% of the variance in apnea-hypopnea index across the population on genetic factors, per Mukherjee et al.'s 2018 review in Respirology. The inheritance is not driven by a single gene; it operates through multiple intermediate phenotypes (obesity, craniofacial structure, neurological control of upper-airway muscles, circadian rhythm).

Practical takeaway: if a parent or sibling uses CPAP, mention it at your screening appointment. It is a real signal, not a coincidence.

Smoking

People who currently smoke nicotine products are up to three times more likely to develop OSA than past smokers and people who have never smoked. Smoking inflames the upper airway and increases mucus production, which narrows the breathing passage during sleep. Quitting smoking is among the few modifiable risk factors with both a clear OSA benefit and a long list of unrelated health upsides.

Chronic Nasal Congestion

Habitual nasal congestion (from allergic rhinitis, deviated septum, chronic sinusitis, or nasal polyps) nearly doubles the risk of moderate-to-severe sleep-disordered breathing, per Young et al.'s 1997 Wisconsin Sleep Cohort analysis (odds ratio approximately 1.8 for adults with chronic allergic congestion). The mechanism is mechanical: when nasal airflow is restricted, you breathe through your mouth, and mouth breathing during sleep promotes airway collapse. If you cannot consistently breathe through your nose, raise the issue with an ENT before assuming the only path forward is CPAP.

Endocrine Disorders

The U.S. National Heart, Lung, and Blood Institute names polycystic ovary syndrome, low thyroid hormone, and high growth hormone as established OSA risk factors. The broader endocrinology literature (Akset et al., Clinical Endocrinology, 2023) extends the list:

• Polycystic ovary syndrome (PCOS): women with PCOS have substantially higher OSA prevalence than age-matched peers, partly through obesity and partly through androgen-driven changes in airway tissue.
• Hypothyroidism: low thyroid hormone slows metabolism and can produce tongue enlargement and pharyngeal myopathy, both of which narrow the airway.
• Acromegaly: growth-hormone excess produces facial bone overgrowth and tongue enlargement, with OSA prevalence reported in the majority of patients.
• Cushing syndrome: the central fat distribution and tissue changes from chronic cortisol excess elevate OSA risk (Akset 2023, not specifically named on the NHLBI causes page).
• Type 1 and type 2 diabetes: the relationship is bidirectional; OSA worsens insulin resistance, and diabetes-associated obesity worsens OSA (Akset 2023; the NHLBI lists diabetes as a consequence of untreated OSA, not specifically as a risk factor).

If you carry one of these diagnoses, your endocrinologist or sleep physician should be aware that it elevates your baseline OSA risk independent of the STOP-BANG checklist.

Pregnancy

Pregnancy can either trigger OSA in women who did not previously have it or worsen pre-existing OSA. The mechanism combines weight gain, hormonal changes affecting upper-airway tone, and (in late pregnancy) the mechanical effect of an enlarged uterus on diaphragm position. Sleep-disordered breathing in pregnancy is associated with higher rates of gestational diabetes and preeclampsia, so it is worth flagging snoring or witnessed apneas to your OB.

Craniofacial Structure and Ethnicity

Skeletal restriction of the upper airway (a small or retropositioned jaw, a short cranial base, a high-arched palate) is a real OSA risk factor independent of weight. People with these anatomic features can have moderate to severe OSA at a normal BMI.

Studies of ethnic differences in craniofacial anatomy (notably Sutherland et al., Respirology, 2012) suggest the contributors to OSA risk are weighted differently across populations:

• Studies of East Asian populations (Chinese, Korean) suggest OSA prevalence comparable to White populations despite markedly lower obesity rates, with skeletal restriction (smaller maxilla, smaller and retropositioned mandible, shorter cranial base) accounting for more of the risk.
• Studies of Black / African American populations suggest OSA risk weighted more heavily toward obesity and enlarged upper-airway soft tissues than skeletal restriction.
• Studies of White populations suggest contributions from both bony and soft-tissue abnormalities.

These are population-level patterns from clinic samples, not individual diagnoses. Practical takeaway: a patient of East Asian descent with a BMI of 26 may warrant evaluation despite a low STOP-BANG score, because skeletal-restriction risk is not captured by BMI alone.

Risk Factors You Can Change

Some risk factors on this list are fixed: you cannot change your age, sex, ethnicity, or skeletal anatomy. But several are modifiable, and addressing them can meaningfully reduce your OSA severity.

Weight loss is the single most impactful lifestyle change. The Wisconsin Sleep Cohort, a long-running prospective study published in JAMA in 2000, found that a 10% reduction in body weight predicts a 26% decrease in apnea-hypopnea index. The Sleep AHEAD randomized trial in adults with type 2 diabetes confirmed the effect: an intensive lifestyle intervention that produced ~10 kg average weight loss reduced AHI by ~10 events per hour at one year compared with usual care. Weight loss does not replace CPAP, but it can reduce the pressure your machine needs and improve overall outcomes.

Smoking cessation removes the chronic upper-airway inflammation that puts current smokers at 3x OSA risk. Effects on AHI take weeks to months to appear, so do not expect overnight improvement.

Alcohol and sedatives relax airway muscles and worsen OSA. Avoiding alcohol within 3 to 4 hours of bedtime can reduce the number of events per night.

Sleep position matters. Sleeping on your back (supine) increases airway collapse due to gravity. Side sleeping often reduces event frequency. Positional therapy is not a standalone treatment, but it can supplement CPAP therapy.

Nasal-congestion treatment is a quiet win. If allergies, a deviated septum, or chronic sinusitis are keeping you from breathing comfortably through your nose, addressing the underlying problem can both reduce OSA severity and make CPAP therapy more comfortable.

These changes work alongside treatment, not instead of it. Discuss any modifications with your provider.

When to Get Tested

If three or more of the STOP-BANG risk factors apply to you, the clinical recommendation is to discuss a sleep evaluation with your healthcare provider. Add to that count if you have a strong family history of OSA, current smoking, chronic nasal congestion, an endocrine disorder on the list above, or you are pregnant with new-onset snoring. Testing typically involves either a home sleep test or in-lab polysomnography. Both are straightforward, and insurance commonly covers them.

You do not need to check every box. Two STOP-BANG factors plus a bed partner who reports snoring and breathing pauses is worth a conversation with your doctor.

Do not put off testing because you think you would "know" if you had sleep apnea. Most people with moderate to severe OSA are unaware of their nighttime breathing pauses. The symptoms (daytime fatigue, poor concentration, morning headaches) are common enough that many people attribute them to stress, aging, or poor sleep habits rather than a treatable medical condition.

Already Diagnosed?

If you are already using CPAP therapy, you can analyze your SD card data, track your therapy score, and understand your nightly events in detail with CPAP Clarity's free analyzer.

Take the Screener

Ready to check your risk? The STOP-BANG Sleep Apnea Screener takes about two minutes and gives you an instant result with guidance on next steps.

Sources

• Aurora RN, Quan SF. Quality Measure for Screening for Adult Obstructive Sleep Apnea by Primary Care Physicians. Journal of Clinical Sleep Medicine. 2016;12(8):1185-1187.
• American Academy of Sleep Medicine. Hidden Health Crisis Costing America Billions: Underdiagnosing and Undertreating Obstructive Sleep Apnea Draining Healthcare System. 2016 (with CDC). Source for the >80% undiagnosed estimate. aasm.org announcement (opens in new tab)
• Benjafield AV et al. Prevalence and Unmet Need of Obstructive Sleep Apnea in the United States. SLEEP 2025;48(Supplement_1):A278 (abstract #0637). Source for the 24-33% prevalence and 85.6M / 68.5M unaware figures.
• National Heart, Lung, and Blood Institute. Sleep Apnea: Causes and Risk Factors. (opens in new tab) Source for PCOS, hypothyroidism, and acromegaly as named OSA risk factors.
• Akset M, Poppe KG, Kleynen P, Bold I, Bruyneel M. Endocrine disorders in obstructive sleep apnoea syndrome: a bidirectional relationship. Clinical Endocrinology. 2023;98(1):3-13. Source for the broader endocrine list including Cushing syndrome and type 1/2 diabetes.
• Wetter DW, Young TB, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Archives of Internal Medicine. 1994;154(19):2219-2224. Source for the smoking 3x risk figure.
• Young T, Finn L, Kim H. Nasal obstruction as a risk factor for sleep-disordered breathing. Journal of Allergy and Clinical Immunology. 1997;99(2):S757-S762. Source for the ~80% increased risk with chronic nasal obstruction.
• Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA. 2000;284(23):3015-3021. Source for the 10% weight loss → 26% AHI decrease finding (and the asymmetric 10% gain → 32% AHI increase finding).
• Foster GD, Borradaile KE, Sanders MH, et al. A randomized study on the effect of weight loss on obstructive sleep apnea among obese patients with type 2 diabetes (Sleep AHEAD). Archives of Internal Medicine. 2009;169(17):1619-1626.
• Sutherland K, Lee RWW, Cistulli PA. Obesity and craniofacial structure as risk factors for obstructive sleep apnoea: impact of ethnicity. Respirology. 2012;17(2):213-222.
• Mukherjee S, Saxena R, Palmer LJ. The genetics of obstructive sleep apnoea. Respirology. 2018;23(1):18-27. Source for ~40% AHI variance heritability. PubMed Central PMC7308164 (opens in new tab)

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