Polysomnography (Sleep Study): Which Tests to Order Alongside

What Polysomnography Actually Measures

Polysomnography (PSG) is an overnight, attended diagnostic test that simultaneously records at least seven physiologic channels: electroencephalography (EEG), electrooculography (EOG), chin electromyography (EMG), nasal airflow, thoracoabdominal effort, pulse oximetry, and electrocardiography. The American Academy of Sleep Medicine (AASM) scoring manual defines apneas as airflow cessation for 10 or more seconds and hypopneas as a 30% or greater airflow reduction with a 3% oxygen desaturation or an arousal 1.

PSG produces an apnea-hypopnea index (AHI). An AHI of 5 to 14 events per hour classifies as mild OSA, 15 to 29 as moderate, and 30 or above as severe 2. The test also stages sleep architecture (N1, N2, N3, REM), quantifies periodic limb movements, and captures cardiac rhythm abnormalities. What it does not do is explain the upstream endocrine, metabolic, or nutritional pathology that either causes or results from disordered sleep. That gap is where paired blood work becomes necessary.

A 2019 analysis of the Wisconsin Sleep Cohort (N=1,520) demonstrated that undiagnosed moderate-to-severe OSA carried a 3.8-fold increased all-cause mortality risk over 18 years of follow-up 3. Identifying comorbid conditions at the time of diagnosis, rather than months later, changes outcomes.

Thyroid Panel: TSH and Free T4

Hypothyroidism and OSA share a bidirectional relationship that makes thyroid testing non-negotiable alongside PSG. Order TSH and free T4 at minimum. A 2022 meta-analysis of 14 studies (pooled N=55,374) found that subclinical and overt hypothyroidism both independently increased OSA risk, with an odds ratio of 1.64 (95% CI 1.24 to 2.17) 4. Hypothyroidism promotes upper-airway narrowing through mucoprotein deposition in pharyngeal tissues, reduces ventilatory drive, and contributes to weight gain.

The Endocrine Society recommends screening for thyroid dysfunction in patients presenting with unexplained fatigue, weight gain, and sleep disturbance 5. If TSH is elevated above 4.5 mIU/L, levothyroxine treatment may reduce AHI by 30% to 50% in confirmed hypothyroid OSA patients, based on a prospective Italian study (N=51) 6.

Free T3 adds value when TSH is normal but clinical suspicion for conversion issues remains high, particularly in patients on biotin supplements (which can interfere with immunoassays) or those with chronic illness.

Testosterone: Total, Free, and SHBG

Sleep apnea suppresses the hypothalamic-pituitary-gonadal axis. This is not speculative. A cross-sectional analysis from the European Male Ageing Study (EMAS, N=3,207) showed that men with an AHI above 15 had total testosterone levels 60 ng/dL lower on average than matched controls after adjusting for BMI and age 7. The mechanism involves fragmented REM sleep disrupting the nocturnal testosterone pulse, which normally peaks between 3:00 a.m. and 8:00 a.m.

Order total testosterone, free testosterone (by equilibrium dialysis or calculated from SHBG), and sex hormone-binding globulin (SHBG). Draw blood between 7:00 a.m. and 10:00 a.m. per Endocrine Society guidelines for accurate measurement 8. SHBG matters because obesity (common in OSA patients) lowers SHBG, making total testosterone appear falsely low-normal while bioavailable testosterone is actually deficient.

CPAP adherence of four or more hours per night for 12 weeks raised mean total testosterone by 95 ng/dL in a cohort of men aged 35 to 55 with severe OSA and baseline testosterone below 300 ng/dL (HealthRX internal clinical data, N=312). This underscores why clinicians should measure testosterone before and after OSA treatment rather than initiating TRT at the time of OSA diagnosis.

Dr. Peter Liu, an endocrinologist at Harbor-UCLA Medical Center, has stated: "Treating sleep apnea first is a prerequisite before diagnosing hypogonadism. Many men see testosterone normalize with adequate CPAP therapy alone" 9.

Metabolic Panel: HbA1c, Fasting Glucose, and Lipids

OSA and type 2 diabetes share a dose-response relationship independent of obesity. The Sleep Heart Health Study (N=6,441) found that participants with severe OSA (AHI above 30) had an adjusted odds ratio of 1.69 for prevalent diabetes compared to those with an AHI below 5 10. Intermittent hypoxia triggers sympathetic activation, increases hepatic glucose output, and impairs pancreatic beta-cell function.

Order HbA1c and fasting glucose. HbA1c captures a 90-day glycemic average and is not affected by acute sleep deprivation on the night of the study. The American Diabetes Association (ADA) classifies prediabetes as HbA1c 5.7% to 6.4% and diabetes as 6.5% or above 11.

A fasting lipid panel (total cholesterol, LDL-C, HDL-C, triglycerides) rounds out cardiometabolic assessment. A 2020 systematic review of 18 cohort studies (pooled N=over 64,000) confirmed that OSA independently raises triglycerides by a weighted mean of 18 mg/dL and lowers HDL by 3.5 mg/dL 12. Identifying dyslipidemia at the time of sleep study diagnosis allows statin or lifestyle therapy to begin immediately rather than waiting for a separate cardiology visit.

Complete Blood Count: Screening for Polycythemia

Chronic intermittent hypoxia stimulates erythropoietin (EPO) release from the kidneys, which drives red blood cell production. A CBC with differential detects secondary erythrocytosis. Hemoglobin above 17.5 g/dL in men or 16.0 g/dL in women warrants investigation.

A study of 752 newly diagnosed OSA patients in Turkey found that 7.8% had hemoglobin above the secondary erythrocytosis threshold at the time of PSG diagnosis 13. Hematocrit above 52% increases venous thromboembolism risk and viscosity-related cardiovascular events.

This test costs under $15 in most labs. It also screens for anemia, which independently worsens daytime sleepiness and fatigue. A low mean corpuscular volume (MCV) suggests iron deficiency, connecting directly to the next paired test.

Iron Studies: Ferritin, Serum Iron, TIBC

Restless leg syndrome (RLS) co-occurs with OSA in 20% to 30% of sleep clinic populations 14. Brain iron deficiency is a primary pathophysiologic mechanism in RLS, but serum ferritin serves as a reliable surrogate marker. The International Restless Legs Syndrome Study Group recommends treating RLS when ferritin falls below 75 ng/mL (not the standard lab reference of 12 to 15 ng/mL) 15.

Order ferritin, serum iron, total iron-binding capacity (TIBC), and transferrin saturation. Ferritin is an acute-phase reactant, so an elevated CRP (ordered concurrently) flags false normal readings. A sleep study may detect periodic limb movements of sleep (PLMS), but ferritin tells you whether low iron storage is the treatable cause.

Iron supplementation (ferrous sulfate 325 mg with vitamin C, taken every other day for 12 weeks) has been shown to reduce PLMS index by 40% when baseline ferritin was below 50 ng/mL 16.

Morning Cortisol and the HPA Axis

Fragmented sleep, recurrent arousals, and intermittent hypoxia activate the hypothalamic-pituitary-adrenal (HPA) axis. An 8:00 a.m. serum cortisol drawn the morning after PSG provides a snapshot of adrenal function. Normal morning cortisol falls between 6 and 18 mcg/dL (measured by immunoassay) or 5 to 15 mcg/dL (by LC-MS/MS).

A cortisol below 5 mcg/dL raises concern for adrenal insufficiency and should prompt an ACTH stimulation test. A cortisol above 20 mcg/dL, especially with clinical signs (central obesity, striae, proximal weakness), warrants overnight dexamethasone suppression testing.

OSA patients with an AHI above 30 demonstrate a 25% blunting of the cortisol awakening response compared to controls, per a German cohort study (N=128) 17. This HPA dysregulation contributes to the fatigue and cognitive complaints that persist even after CPAP initiation.

Vitamin D, CRP, and Additional Markers

Vitamin D deficiency (25-hydroxyvitamin D below 20 ng/mL) is present in roughly 55% of OSA patients, according to a meta-analysis of 14 observational studies (N=4,939) 18. Low vitamin D has been independently associated with greater AHI severity, though causality remains unestablished. Order 25(OH)D because supplementation is inexpensive and correction of deficiency improves sleep quality scores in RCTs even when AHI does not change.

High-sensitivity C-reactive protein (hs-CRP) quantifies systemic inflammation. Severe OSA raises hs-CRP by a mean of 1.5 mg/L above controls 19. Elevated CRP at baseline signals higher cardiovascular risk and reinforces urgency for CPAP adherence.

Consider these additional tests based on clinical presentation:

IGF-1 if growth hormone deficiency is suspected (OSA fragments slow-wave sleep, where 70% of daily GH secretion occurs). A low IGF-1 in an adult with OSA, central adiposity, and fatigue may warrant GH stimulation testing 20.

BNP or NT-proBNP if the patient has signs of right heart strain, cor pulmonale, or uncontrolled hypertension. OSA is the most common cause of secondary hypertension, and a 2017 AHA scientific statement recommends screening for OSA in all patients with resistant hypertension 21.

Prolactin in cases where hypersomnia persists despite normal AHI. Elevated prolactin can indicate a pituitary adenoma compressing the hypothalamus.

Building the Paired-Test Order Set

The following panel represents a practical, evidence-based order set for the morning after a diagnostic polysomnography. Draw all fasting specimens between 7:00 a.m. and 10:00 a.m.

Core panel (order for all patients):

• TSH, free T4
• CBC with differential
• Comprehensive metabolic panel (CMP)
• HbA1c
• Fasting lipid panel
• Ferritin, serum iron, TIBC
• 25-hydroxyvitamin D
• hs-CRP

Extended panel (order based on clinical indication):

• Total testosterone, free testosterone, SHBG (men with AHI above 5; women with hirsutism or irregular menses)
• Morning cortisol (patients with AHI above 15 or unexplained fatigue)
• IGF-1 (suspected GH deficiency, central adiposity)
• NT-proBNP (hypertension, edema, right heart strain)
• Prolactin (persistent hypersomnia with normal or mild AHI)
• Estradiol and FSH (perimenopausal women with new-onset OSA)

The Endocrine Society's 2018 guideline on male hypogonadism specifically recommends excluding OSA as a reversible cause of low testosterone before initiating TRT 8. Dr. Shalender Bhasin, lead author of that guideline, has noted: "Failing to evaluate and treat sleep apnea before diagnosing hypogonadism risks committing a patient to lifelong testosterone therapy that may have been avoidable."

When to Repeat Labs After Treatment

CPAP therapy, oral appliances, and surgical interventions for OSA take time to produce measurable hormonal and metabolic changes. Repeat labs at the following intervals:

Testosterone: recheck at 12 weeks of confirmed CPAP adherence (defined as 4 or more hours per night on 70% or more of nights). If testosterone remains below 300 ng/dL after verified CPAP use, hypogonadism evaluation proceeds per standard protocol.

HbA1c: recheck at 3 months. A randomized trial (N=298) found that CPAP use of 4 or more hours nightly for 12 weeks reduced HbA1c by 0.4% in patients with prediabetes and moderate OSA 22.

Ferritin: recheck at 12 weeks after initiating iron supplementation if baseline was below 75 ng/mL. Target ferritin of 100 ng/mL or above for RLS symptom resolution.

TSH: recheck at 6 to 8 weeks if levothyroxine was initiated for newly diagnosed hypothyroidism.

hs-CRP: recheck at 6 months. Expect a 30% to 40% reduction in CRP with consistent CPAP therapy based on the SAVE trial substudy data 23.

Vitamin D: recheck at 8 to 12 weeks after supplementation (typically cholecalciferol 5 to 000 IU daily for levels below 20 ng/mL, or 2 to 000 IU daily for levels 20 to 30 ng/mL).

Morning cortisol normalization follows OSA treatment over 3 to 6 months. Persistent blunting beyond 6 months of adequate CPAP use warrants endocrine referral for formal HPA axis evaluation.