Association of Anxiety and Depression in Obstructive Sleep Apnea Patients A Systematic Review and Meta Analysis

Behavioral Sleep Medicine
ISSN: 1540-2002 (Print) 1540-2010 (Online) Journal homepage: https://www.tandfonline.com/loi/hbsm20
Association of Anxiety and Depression in

Obstructive Sleep Apnea Patients: A Systematic
Review and Meta-Analysis
Sergio Garbarino, Wayne A. Bardwell, Ottavia Guglielmi, Carlo Chiorri, Enrica

Bonanni & Nicola Magnavita
To cite this article: Sergio Garbarino, Wayne A. Bardwell, Ottavia Guglielmi, Carlo Chiorri, Enrica
Bonanni & Nicola Magnavita (2020) Association of Anxiety and Depression in Obstructive Sleep
Apnea Patients: A Systematic Review and Meta-Analysis, Behavioral Sleep Medicine, 18:1, 35-57,
DOI: 10.1080/15402002.2018.1545649
To link to this article: https://doi.org/10.1080/15402002.2018.1545649
Published online: 19 Nov 2018.
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BEHAVIORAL SLEEP MEDICINE
2020, VOL. 18, NO. 1, 35–57
https://doi.org/10.1080/15402002.2018.1545649
Association of Anxiety and Depression in Obstructive Sleep Apnea

Patients: A Systematic Review and Meta-Analysis
Sergio Garbarinoa,b, Wayne A. Bardwellc, Ottavia Guglielmia, Carlo Chiorrid, Enrica Bonannie,
and Nicola Magnavitaf
a
Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, and Maternal/Child Sciences (DINOGMI),
University of Genoa, Genoa, Italy; bDepartment of Health Sciences, University of Genoa, Genoa, Italy; cDepartment of
Psychiatry, University of California San Diego, San Diego, California; dDepartment of Educational Sciences, University
of Genoa, Genoa, Italy; eCenter of Sleep Medicine, Neurology Unit, Azienda Ospedaliero-Universitaria Pisana, Pisa,
Italy; fInstitute of Public Health, Università Cattolica del Sacro Cuore, Rome, Italy
ABSTRACT
Background: Obstructive sleep apnea (OSA) has been associated with men-
tal disorders, but the strength of this association is unknown. The aim of our
study was to investigate the association among OSA, depression, and
anxiety in adults and to quantitatively summarize the results. Methods:
A literature search in Medline, PubMed, PsycInfo, Scopus, and Web of
Science was conducted. Seventy-three articles were selected for study.
Results: The pooled prevalence of depressive and anxious symptoms in
OSA patients was 35% (95% CI, 28–41%) and 32% (95% CI, 22–42%),
respectively. Conclusions: The association between OSA, anxiety, and
depression indicates the value of an early diagnosis and personalized
treatment of OSA to improve mental disorders conditioning compliance
to therapy. These conditions share a probably bidirectional relationship.
Obstructive sleep apnea (OSA) is a chronic condition characterized by sleep-related pauses in

respiration, arousals, unrefreshing sleep, and excessive daytime sleepiness (EDS; Young, Peppard,
& Gottlieb, 2002). A recent population-based study conducted in Europe determined that the
prevalence of moderate-to-severe sleep-disordered breathing in older adults (median age of
57 years) is 23.4% in women and 49.7% in men (Heinzer et al., 2015).
The increasing prevalence of OSA across the lifespan has prompted attention to the consequences
of this frequently seen condition. OSA is considered an independent risk factor for the development
of cardiovascular diseases, including hypertension, coronary artery disease, stroke, and cerebrovas-
cular disease (Gottlieb et al., 2010; Peppard, Young, Palta, & Skatrud, 2000) as well as diabetes
(Botros et al., 2009) and metabolic syndrome (Trayhurn, Wang, & Wood, 2008). Repeated sleep
fragmentation, nocturnal hypoxaemia, hypoxia, and hypercapnia, which cause oxidative stress and
sympathetic activation, might be underlying causes of such associations (Gozal & Kheirandish-
Gozal, 2008; Jurado-Gámez et al., 2011; Lavie & Polotsky, 2009).
Current literature also suggests that OSA is associated with depression and anxiety (Bahamman
et al., 2016; Harris, Glozier, Rathnavadivel, & Grunstein, 2009). OSA patients are believed to have
poor mental health (Karkoulias et al., 2013), even if it is well known that report bias may influence
symptom reporting in these patients (Bardwell, Ancoli-Israel, & Dimsdale, 2001a). Field studies also
showed that preclinical suspect OSA cases, identified during medical screening in the workplace,
have poorer mental health than workers without OSA (Garbarino & Magnavita, 2014; Guglielmi,
Magnavita, & Garbarino, 2017).
CONTACT Ottavia Guglielmi ottavia.guglielmi@gmail.com Department of Neuroscience, Rehabilitation, Ophthalmology,

Genetics, and Maternal/Child Sciences (DINOGMI), University of Genoa, Largo Paolo Daneo 3, Genoa 16132, Italy.
© 2018 Taylor & Francis Group, LLC
36 S. GARBARINO ET AL.
Nevertheless, some studies failed to show a significant correlation between OSA and psychiatric
disease (Bajpai, Im, Dyken, Sodhi, & Fiedorowicz, 2014; Pillar & Lavie, 1998) and, when the
association was observed, the mechanism underlying such a relationship was not fully elucidated.
Some studies suggest that the high prevalence of mental diseases in OSA could be related to sleep
fragmentation or poor sleep quality (El-Ad & Lavie, 2005; Lee, Paek, & Han, 2016). The disturbance
of sleep quality and continuity predisposes to the development or exacerbation of mental illness
(Sateia, 2009). Likewise, the presence of psychiatric illness may complicate sleep disorders. The idea
has developed that psychopathology may represent both an etiological factor and a complication of
OSA (Haba-Rubio, 2005). Impairment of sleep and of mental health may be different manifestations
of the same underlying neurobiological processes (Sutton, 2014). Hence, both may well be a target
for treatment.
A systematic review recently considered the association of OSA with depressive disorders and
schizophrenia (Stubbs et al., 2016). Other studies systematically reviewed the effects of treatment of
OSA on depressive symptoms (Povitz et al., 2014) and depression (Gupta, Simpson, & Lyons, 2016).
Some rapid reviews on anxiety and depression association with OSA have also been published (Ejaz,
Khawaja, Bhatia, & Hurwitz, 2011; Saunamäki & Jehkonen, 2007). To the best of our knowledge,
however, so far no attempt has been made to determine the strength of the association between OSA
and anxiety or depression.
The aim of this study was to investigate the prevalence of anxious and depressive symptoms in
OSA patients, to compare the prevalence of depression and anxiety symptoms between OSA and
control patients, to analyze which OSA-related risk factors are associated with depressive and
anxious symptoms and to quantify this relationship with a meta-analysis.
Method
This report follows the Preferred Reporting Items for Systematic Reviews and Meta-Analyses
(PRISMA; Moher et al., 2015).
Search strategy
We searched the main electronic databases (PubMed, Scopus, Web of Science, and PsycINFO) to
identify papers published in English, Spanish, French, Italian, and Portuguese up until
February 2017. We combined key words and medical subject indices referring to sleep apnea
syndrome (obstructive sleep apnea, sleep apnea, obstructive sleep apnea syndromes, sleep-
disordered breathing), terms related to anxiety or depression (depression OR anxiety OR mental
disorder OR mood OR psych*), and terms associated with OSA therapy (CPAP OR MAD OR
surgery). We also performed a manual search of reference lists from relevant review articles.
Study selection
Two reviewers (OG and SG) independently screened titles, abstracts, and full texts, and decided on
eligibility of articles. Any disagreement was resolved by discussion and consultation with another
author (NM). The inclusion criteria were: (a) study performed on adults (≥ 18 years), (b) diagnosis
of OSA confirmed with polysomnography or polygraphy, and (c) assessment of anxiety or depressive
symptoms performed using standardized and validated questionnaires.
We considered only cohort studies, case-control studies, cross-sectional studies, pre–post studies
and controlled clinical trials. Case reports, abstract publications, and unpublished studies were
excluded. Studies without instrumental confirmation of OSA diagnosis or without standardized criteria
for psychiatric diagnoses were excluded. The outcomes of interest were anxiety and depression. Studies
that assessed therapy efficacy on symptoms of anxiety or depression were included if baseline rates of
symptoms were reported. Articles discussing the relationship between OSA and other mental disorders
BEHAVIORAL SLEEP MEDICINE 37
were excluded. Only studies performed in the adult population were considered and articles examining
pediatric patients, adolescents, or specific subgroups of the population (e.g., pregnant women or
patients with psychiatric diseases) were excluded. We also excluded studies where the “case” definition
comprised sleep disorders other than OSA, as well as studies that only qualitatively described
psychiatric disorders or those that provided only the median score value of anxiety or depression
questionnaires, without indicating the prevalence of the disorders.
Data extraction, quality assessment, and meta-analysis

The following data were extracted from each eligible article: study design, sample size, study location,
characteristics of the population, outcomes, type, and characteristics (cutoff level, e.g.) of the
questionnaire used to evaluate mental health. Clinical factors that appeared to be associated with
the outcome were also recorded. Finally, the prevalence of anxiety and depression in OSA patients
was recorded.
The methodological quality of all included studies was assessed by two authors (OG and SG) using
the Newcastle-Ottawa Scale (NOS; Wells et al., 2017). This inventory, which is used to check the
quality of nonrandomized studies, is based on three broad perspectives: the study and control group
selection criteria, the comparability of the groups and the ascertainment of the exposure or outcome of
interest. Disagreement on quality assessment was resolved by discussion and consensus finding.
Statistical analysis
The pooled prevalence of depressive and anxious symptoms was computed by the meta-analytic
weighting of the original frequencies of people exceeding the cutoff scoring that had been adopted in
each study. From all of the articles selected for systematic review, quantitative syntheses for
depression and anxiety were carried out using 34 and 10 studies, respectively. From the articles
that evaluated depression, a large number of publications were not included in the meta-analysis
because they did not show the data of interest (Akmal, Ezat, Raafat, Hamed, & Bediwy, 2013;
Ashgary, Mohammadi, Kamrava, Tavakoli, & Farhadi, 2012; Bardwell et al., 2001b; Bardwell, Ancoli-
Israel, & Dimsdale, 2007a; Beutler, Ware, Karacan, & Thornby, 1981; Bliwise, Yesavage, Sink,
Widrow, & Dement, 1986; Dominici & Gomes, 2009; Gall, Isaac, & Kryger, 1993; Guglielmi,
Sánchez, Jurado-Gámez, Buela-Casal, & Bardwell, 2011; Gylen, Anttalainen, & Saaresranta, 2014;
Husaine et al., 1997; Kawahara, Akashiba, Akahoshi, & Horie, 2005; Klonoff, Fleetham, Taylor, &
Clark, 1987; LaGrotte et al., 2016; Lee, Bardwell, Ancoli-Israel, Loredo, & Dimsdale, 2012; Luik et al.,
2015; Macey, Woo, Kumar, Cross, & Harper, 2010; Mysliwiec et al., 2015; Pillar & Lavie, 1998; Quan
et al., 2014; Reynolds et al., 1984; Ruberto & Liotti, 2011; Sampaio, Pereira, & Winck, 2012; Sanchez,
Buela-Casal, Bermudez, & Casas-Maldonado, 2001; Sforza, de Saint Hilaire, Pelissolo, Rochat, &
Ibanez, 2002; Wells, Day, Carney, Freedland, & Duntley, 2004; Wells, Freedland, Carney, Duntley, &
Stepanski, 2007; Yue et al., 2003) or the questionnaire’s cutoff employed was not specified (Borak,
Cieslicki, Koziej, Matuszewski, & Zielinski, 1996; Cheshire, Engleman, Deary, Shapiro, & Douglas,
1992; Pierobon et al., 2008), or the cutoff’s value was different from that used in the others researches
included in the meta-analysis (Jackson et al., 2011; Pochat, Ferber, & Lemoine, 1993; Yamamoto,
Akashiba, Kosaka, Ito, & Horie, 2000; Yusunkaya, Kutlu, & Cihan, 2016). We also excluded from the
meta-analysis two articles from the same authors and same years (Aikens & Mendelson, 1999b;
Aikens, Vanable, Tadimeti, Caruana-Montaldo, & Mendelson, 1999d) to avoid the use of the same
data more than one time. From the 23 articles that evaluated anxiety symptoms, some publications
were not included in the meta-analysis because they did not show the data of interest (Akmal et al.,
2013; Ashgary et al., 2012; Bardwell et al., 2007b; Guglielmi et al., 2011; Macey et al., 2010; Sanchez
et al., 2001; Sforza et al., 2002; Yue et al., 2003) or the questionnaire’s cutoff employed was not
specified (Borak et al., 1996; Cheshire et al., 1992; Lehto et al., 2013; Pierobon et al., 2008). The
pooled prevalence of anxiety and depression in patients with OSA was obtained from studies that
employed different questionnaires with homogeneous cutoffs, which determine a mild disorder. We
reported results according to a random-effect model. The I2 statistic was used to evaluate the
between-study heterogeneity, with a value greater than 50% interpreted as substantial heterogeneity
(Borenstein, Hedges, Higgins, & Rothstein, 2009). Source of heterogeneity was assessed with
moderator analysis including the following a priori variables: country of origin, age, sex, obesity,
EDS, OSA severity (measured by the Apnea Hypopnea Index [AHI]), and type of questionnaire used
to assess mental disorders. Each study was classified according to the characteristics of the variables
analyzed.
In the anxiety symptoms subgroup, only the influence of country and questionnaire type was
analyzed, because variables that could influence the anxiety prevalence in OSA patients, like BMI,
EDS, and sex, were not reported in the papers.
Publication bias was evaluated using the funnel plot (Thornton & Lee, 2000) and was quantified
by Egger’s test (Egger, Davey Smith, Schneider, & Minder, 1997). Analyses were performed with
Comprehensive Meta-Analysis, version 2.2.064 (Biostat, Inc. Englewood, NJ 07631 USA) software.
Results
Description of search and study characteristics
In the literature search, 4,248 articles were found.
After application of exclusion criteria and elimination of duplicate records, 126 full-text articles
were retrieved and assessed for eligibility. Finally, 73 publications were included in the qualitative
synthesis. Table 1 reports the characteristics of the studies included.
A total of 17,844 participants had been recruited in the selected studies. Sample size varied from
20 to 2,271 patients (meansamplesize ¼ 244patients). The mean age ranged from 36.2 to 68.8 years,
and the prevalence of females ranged from 0 to 59.1% (see Table 1).
Thirty-two studies were carried out in the United States, 3 each in France, Japan, Korea, Spain,
and Egypt, 2 each in Iran, UK, China, Canada, Israel, Italy, and the Netherlands, and 12 in other
countries. Of these, 27 articles (37.0%) were descriptive or case-series, without controls, and 24
(32.9%) were cross-sectional studies with a control group or case-control studies. Only 2 studies had
adopted a longitudinal design and 1 was a controlled clinical trial. Overall, only 3 studies were
population-based (Hrubos-Strøm et al., 2012; LaGrotte et al., 2016; Ruberto & Liotti, 2011) and 70
(95.9%) were based upon clinical sequential sampling.
With respect to outcomes, most of the studies focused on depression (50, 68.5%), or on both
anxiety and depression (22, 30.1%). Only one study analyzed anxiety, without considering depres-
sion (Lehto et al., 2013). We included these studies in the subsequent meta-analysis.
Most of the articles had a low quality of evidence according to the Newcastle-Ottawa Scale. Two
studies (Björnsdóttir et al., 2016; Hrubos-Strøm et al., 2012) had a medium quality and 3 studies
(LaGrotte et al., 2016; Lee et al., 2012; Peppard, Szklo-Coxe, Hla, & Young, 2006) had a high quality
of evidence. Table 2 reports the characteristics of the studies that analyzed the association between
OSA, depression, and anxiety.
The most common questionnaire used to assess depressive symptoms was the Beck Depression
Inventory (BDI; BDI-II), which was used in 23 studies (31.5%). The Center for Epidemiologic
Studies Depression scale (CES-D) and the Zung Self-Rating Depression Scale (SDS) were used in
7 studies each (9.6%). The Minnesota Multiphasic Personality Inventory–2 (MMPI-2) and the
Hospital Anxiety and Depression Scale (HADS) were used in 6 studies each (8.2%). In a few studies,
depression was evaluated by diagnostic interview. Specifically, Bjornsdottir et al. (2016) used the
Mini International Neuropsychiatric Interview (MINI) and Balan et al. (1998), El-Sherbini et al.
(2011), and Hrubos-Strøm et al. (2012) used the Structured Clinical Interview for DSM-IV (SCID-I).
The most-used tools to evaluate anxiety symptoms were the HADS (21.7%), the State-Trait
Anxiety Inventory (STAI; 13%) and the Beck Anxiety Inventory (BAI; 13%).
Table 1. Characteristics of the studies included in the systematic review.

Study Method of OSA
Sample size design Mean age (SD); % diagnosis (AHI or Psychiatric outcomes
Study ID (location) (Quality) Population female RDI cutoff) (tool for evaluation)
Aikens, Caruano-Montaldo, 178 (USA) CS* Clinical 48.3 (11); 13% PSG (IAH ≥ 5) Depression (MMPI)
Vanable, Tadimeti, population
&Mendelson, 1999a
Aikens &Mendelson, 1999b 98 (USA) CCS* Clinical 48 (13); 23% PSG (no data) Depression (MMPI)
population
Aikens, Mendelson & Baehr, 33 (USA) CCS* Clinical 55 (12.1); 45.4% PSG (no data) Depression, anxiety
1999c population (SCL-90)
Aikens, Vanable, Tadimeti, 108 (USA) CCS* Clinical No data PSG (no data) Depression (MMPI)
Caruana-Montaldo, & population
Mendelson, 1999d
Akashiba et al., 2002 94 (Japan) CCS * Clinical 46.4 (11.1); 4.2% PSG (AHI no data) Depression (SDS)
population
Akmal, Ezat, Raaf, Hamed, & 20 (Egypt) PPT* Clinical 43.6 (4.1); 30% PSG (no data) Depression (HRSD),
Bediwy, 2013 population anxiety (HAS)
Aloia et al., 2005 93 (USA) CS * Clinical 52.2 (11.1); 34.4% PSG (RDI no data) Depression (BDI-II)
population
Ashgary et al., 2012 685 (Iran) CCS * Clinical 47.6 (11.7); 27.4% PSG (AHI ≥ 5) Depression/Anxiety (BDI/
population BAI)
Balan et al., 1998 100 (Israel) CCS* Clinical No data; no data PSG (no data) Depression and anxiety
population (SCID)
Bardwell, Ancoli-Israel, & 64 (USA) CS * Clinical 49.3 (7.9); 15.6% PSG (RDI > 15) Depression (CES-D)
Dimsdale, 2001b population
Bardwell, Ancoli-Israel, & 56 (USA) CS * Clinical 46.6 (9.8); no data PSG (RDI > 15) Depression (CES-D)
Dimsdale, 2007a population
Bardwell et al., 2000 106 (USA) CCS * Clinical 47.2 (no data); 20.7% PSG (RDI > 15) Depression (CES-D)
population
Bardwell, Moore, Ancoli-Israel, & 60 (USA) CS * Clinical 49.1 (7.5); 15% PSG (RDI > 15) Depression (CES-D)
Dimsdale, 2003 population
Bardwell, Norman, Ancoli-Israel, 38 (USA) PPT* Clinical (no data) 13,1% PSG (RDI ≥ 15) Depression and anxiety
Loredo, Lowery, Lim, & population (BSI)
Dimsdale, 2007b
Beutler et al., 1981 50 (USA) CCS* Clinical No data PSG (no data) Depression (MMPI)
population
Bjoirnsdottir et al., 2016 284 (Iceland) CS ** Clinical 53.9 (9.1); 21.5% Polygraphy (no Depression (MINI)
population data)
Bliwise et al., 1986 336 (USA) CCS* Clinical No data PSG (RDI ≥ 5) Depression (GDS)
population
Borak, Cieslicki, Koziej, 20 (Poland) PPT* Clinical 46 (6); 0% PSG (no data) Depression (BDI) Anxiety
Matuszewski, &Zielinski, 1996 population (MAS)
Cheshire, Engleman, Deary, 29 (UK) CS* Clinical 50 (no data); 13,8% PSG (IAH ≥ 15) Depression and anxiety
Shapiro, & Douglas, 1992 population (HADS)
Daabis & Gharraf, 2012 102 (Egypt) CCS * Clinical No data; 19.6% PSG (AHI ≥ 5) Depression or anxiety
population (HADS)
Dai, Li, Zhang, Wang, Sang, Tian, 1.327 (China) CS * Clinical 47 (no data); 19.3% PSG (AHI ≥ 5) Depression (SDS)
Cao & 2016 population
Diamanti et al., 2013 41 (Greece) PPT* Clinical 51,9 (10,5); 14,6% PSG (no data) Depression (CES-D)
population
Dominici & Gomes, 2009 123 (Brasil) CCS * Clinical 18–65; 25.2% PSG (AHI ≥ 5) Depression (BDI)
population
Edwards, Mukherjee, Simpson, 293 PPT* Clinical No data; 38,3% PSG (IAH ≥ 5) Depression (PHQ-9)
Palmer, Almeida & Hillman, (Australia) population
2015
El-Sharbini, Bediwy, & El- 37 (Egypt) PPT* Clinical 44.9 (8,8); 35,1% PSG (no data) Depression (SCID)
Mitwalli, 2011 population
Gall et al., 1993 27 (Canada) CCS* Clinical No data PSG (no data) Depression (SCL-90)
population
Guglielmi, Sánchez, Jurado- 100 (Spain) CCS * Clinical 52.9 (8.4); 30% PSG (AHI ≥ 5) Depression; anxiety
Gámez, & Buela-Casal, 2011 population (IDER, STAI)
Guillelminault, Eldridge, Tilkian, 25 (USA) CS* Clinical 44.3 (no data); 0% PSG (IAH ≥ 5) Depression (MMPI)
Simmons, & Dement, 1977 population
Gylen et al., 2014 223 (Finland) CCS * Clinical 51.5(11.7); 47.1% PSG (AHI ≥ 5) Depression (DEPS)
population
Hashmi et al., 2006 98 (USA) CS * Clinical 53.2 (10.1); 0% PSG (AHI > 15) Depression (BDI)
population
(Continued )
Table 1. (Continued).
Study Method of OSA
Hrubos-Strøm et al., 2012 290 (Norway) CCS ** Community 48.2 (11.2); 44.1% PSG (AHI ≥ 5) Depression and anxiety
sample (SCID-I; BDI)
Husain et al., 1997 42 (UK) CCS* Clinical No data; 11.9% PSG (RDI ≥ 15) Depression (BDI)
population
Ishman et al., 2014 44 (USA) PPT* Clinical 44 (10); 27.3% PSG (IAH ≥ 5) Depression (BDI-II)
population
Ishman et al., 2010 104 (USA) CCS * Clinical 47.5 (no data); no PSG (AHI≥ 5) Depression (BDI-II)
population data
Jackson et al., 2011 53 (USA) CCS * Clinical No data; 26.4% PSG (RDI > 5) Depression (BDI-II)
population
Kawahara, Akashiba, Akahoshi, 170 (Japan) PPT * Clinical No data PSG (IAH ≥ 20) Depression (SDS)
&Horie, 2005 population + EDS
Klonoff, Fleetham, Taylor, &Clark, 22 (Canada) PPT* Clinical 48.9 (no data); 0% PSG (IAH ≥ 15) Depression (MMPI)
1987 population
LaGrotte et al., 2016 1.137 (USA) Long *** Community 49.3 (13.3); 48% PSG (AHI ≥ 5) Depression (MMPI)
sample
Lee et al., 2012 56 (USA) CCT*** Clinical No data PSG (IAH ≥ 10) Depression (CES-D)
population
Lee et al., 2015a 655 (Korea) CS * Clinical 49.8 (11.7); 13.1% PSG (AHI ≥ 5) Depression; anxiety (BDI,
population STAI)
Lee, Lee, Chung, Kim, 2015b 302 (Korea) CS * Clinical 48.4 (11.3); 0% PSG (AHI > 30) Depression (BDI)
population
Lee et al., 2016 1.281 (Korea) CS * Clinical 51.3 (11.6); 21.1% PSG (AHI ≥ 5) Depression (BDI)
population
Lehto et al., 2013 61 (Finland) PPT* Clinical No data Polygraphy Anxiety (15D)
population (IAH ≥ 5)
Luik et al., 2015 491 CCS * Community 61.87 (5.4); 52.3% PSG (AHI ≥ 5) Depression (CES-D)
(Netherlands) sample
Macey et al., 2010 49 (USA) CS * Clinical 46.8 (9.1); 24.5% PSG (AHI ≥ 5) Depression; anxiety (BDI,
population BAI)
McCall, Harding, O’Donovan, 121 (USA) CS * Clinical 54.7 (14.1); 24% RDI (no data) Depression (BDI)
2006 population
Mean et al., 2003 39 (USA) PPT* Clinical 57.8 (11.2); 10% PSG (no data) Depression (BDI)
population
Millman et al., 1989 55 (USA) PPT* Clinical 50.4 (1.6); 17,6% PSG (IAH ≥ 5) Depression (SDS)
population
Mysliwiec et al., 2015 58 (USA) PPT* Clinical 36. (7.7); 0% PSG (no data) Depression (QIDS)
population
Peppard, Szklo-Coxe, Hla, & 1.408 (USA) Long *** Clinical 50.5 (no); 44% PSG (AHI ≥ 5) Depression (Zung SDS)
Young, 2006 population
Pierobon et al., 2008 157 (Italy) CS * Clinical 47.8 (11.9); 32% PSG (AHI > 10) Anxiety; depression
population (STAI; CBA 2.0)
Pillar & Lavie, 1998 2271 (Israel) CS* Clinical 48.1(11.1); 12,9% PSG (RDI > 10) Depression, anxiety
population (SCL-90)
Pochat et al., 1993 24 (France) CS* Clinical 54.5 (11.39); 25% PSG (IAH ≥ 5) Depression (MADRS),
population anxiety (HARS)
Quam et al., 2014 239 (USA) CCS * Clinical 44.6 (14.1); 49.8% PSG (AHI > 15) Depression (HAM-D)
population
Ramos-Platón & Espinar-Sierra, 40 (Spain) PPT* Clinical No data PSG (IAH ≥ 20) Depression (MMPI)
1992 population
Razaeitalab et al., 2014 178 (Iran) CS * Clinical 50.3 (no data); 14.4% PSG (AHI ≥ 5) Depression; anxiety (BDI,
population BAI)
Rey de Castro & Rosales- Mayor, 312 (Peru) CCS * Clinical 46.1 (11.7); 11.5% PSG (AHI ≥ 5) Depression (BDI-II)
2013 population
Reyes Zuñiga et al., 2012 382 (Mexico) CS * Clinical 50.8 (13.6); 38.2% Polygraphy or Depression; Anxiety
population PSG (AHI ≥ 5) (HADS)
Reynolds et al., 1984 25 (USA) CS* Clinical 50 (11.8); 0% PSG (no data) Depression (KIDS)
population
Ruberto & Liotti, 2011 335 (Italy) CCS * Community 48 (3); 47% PSG (AHI ≥ 15/ Depression (Zung SDS)
sample ODI ≥ 5)
Sampaio, Pereira, & Winck, 2012 111 CS * Clinical 53.5 (8.6); 29.7% Polygraphy Depression (HADS)
(Portugal) population (AHI ≥ 5)
(Continued )
Study Method of OSA
Sanchez et al., 2001 51 (Spain) PPT* Clinical 48.0 (8.6); 7,8% Polygraphy Depression (BDI);
population (IAH≥ 10) Anxiety (STAI)
Schwartz & Karatinos, 2007 50 (USA) PPT* Clinical 53 (11.3); 22% PSG (RDI ≥ 15) Depression (BDI-SF)
population
Schwartz et al., 2005 50 (USA) PPT* Clinical 48.4 (9.3); 44% PSG (RDI ≥ 15) Depression (BDI-SF)
population
Sforza et al., 2002 44 (France) CCS * Clinical 53.3 (1.7); no data PSG (AHI ≥ 10) Depression, anxiety
population (HADS)
Sforza et al., 2016 825 (France) CS * Clinical 68.8 (1); 59.1% Polygrafy Depression; anxiety
population (AHI ≥ 15) (Pichot quest, Goldberg)
Surani, Rao, Surani, Guntupalli, & 51 (USA) CS * Clinical No data PSG (AHI ≥ 5) Depression; anxiety
Subramanina, 2013 population (HADS)
Vandeputte & de Weerd, 2003 917 CS* Clinical No data PSG (no data) Depression (BDI)
(Netherlands) population
Wells, Day, Carney, Freedland, & 135 (USA) CS * Clinical 45 (no data); 55% PSG (AHI ≥ 10) Depression (BDI)
Duntley, 2004 population
Wells et al., 2007 54 (USA) PPT* Clinical 47.6 (10.7); 45% PSG (no data) Depression (BDI)
population
Yamamoto, Akashiba, Kosaka, & 47 (Japan) PPT* Clinical 49.5 (10.8); 0% PSG (no data) Depression (SDS)
Horie, 2000 population
Yue, Hao, Liu, Liu, Ni, & Guo, 60 (China) CCS * Clinical No data; 16.7% PSG (AHI no data) Depression and anxiety
2003 population (SCL-90)
Yusunkaya, Kutlu, & Cihan, 2016 200 (Turkey) CS* Clinical 46.5 (9.9); 12.5% PSG (AHI ≥ 5) Depression (BDI)
population
OSA: Obstructive Sleep Apnea; CS: cross-sectional study; CCS: control-case study; PPT: pre–post study; Long: longitudinal study;
CCT: controlled clinical trial. MMPI: Minnesota Multiphasic Personality Inventory; SCL-90: Symptoms Check List-90; BDI: Beck
Depression Scale; SCID: Structured clinical Interview for DSM-IV; SDS: Zung Self-Rating Depression Scale; PS: Primary Snorers; IPD:
Insomnia with psychiatric disorders; HADS: Hospital Anxiety and Depression Scale; CES-D: Center for Epidemiological Studies
Depression Scale; PLMD: Periodic Limb Movement Disorder; IPD: Insomnia with psychiatric disorders; PHQ-9: Patients Health
Questionnaire; MAS: Taylor’s Manifest Anxiety Scale; HARS: Hamilton Anxiety Rating Scale; MADRS: Montgomery-Asberg
Depression Rating Scale; QoL: Quality of Life; EDS: Excessive daytime sleepiness; STAI: State-Trait Anxiety Inventory; MINI: The
Mini-International Neuropsychiatric Interview; BMI: Body Mass Index; AHI: Apnea Hypopnea Index; SaO2:oxygen saturation; RDI:
Respiratory Disturbance Index; SDB: Sleep Disordered Breathing; BAI: Beck Anxiety Inventory; QD2A: Self-Report Inventory on
Depressive Symptomatology; %S1: % of stage 1 of sleep; NREM: non-REM sleep. * = low quality of evidence; ** = medium
quality of evidence; *** = high quality of evidence. No data: data not available in the article. RDI: Respiratory Disturbance Index.
AHI: Apnea Hypopnea Index.
The different tools were used to define the “caseness,” namely, the probability that the patient
examined was suffering from anxiety or depression. Thirty-four studies indicated the prevalence of
depression and 10 studies indicated the prevalence of anxiety. In the case of researchers who used the
same questionnaire, the cutoff score was often chosen with different criteria. Given the impossibility
of making these criteria homogeneous, we were limited to recording the percentage of anxiety and
depressive symptoms as reported by the various studies.
How prevalent are symptoms of depression and anxiety in OSA patients?

The prevalence of depressive symptoms across all included studies ranged from 2.9% (Balan et al.,
1998) to 78% (Ramos-Platón & Espinar-Sierra, 1992). The prevalence of anxiety ranged from 2.9%
(Balan et al., 1998) to 70% (Borak et al., 1996).
Although 73 papers were included in the systematic review, quantitative analysis was carried out
using the articles that followed the inclusion criteria and showed the prevalence of the mood disorder
and the tool’s cutoff employed. Thirty-four papers about depression and 10 about anxiety were included
in the meta-analysis (see Figure 1). The pooled prevalence of depressive symptoms in OSA patients was
35% (95% CI, 28–41%). The prevalence of anxiety symptoms was 32% (95% CI, 22–42%).The pooled
42
Table 2. Main results, prevalence of anxious and depressive symptoms, and factors related.
Study ID Main results Prevalence of mental disorder (cutoff) Factors related
Aikens et al. 1999a Depressive symptoms and others psychological 32% of OSA patients showed significant elevation in Depression were not correlated with BMI or any
problems are presents in OSA patients. depression scale (MMPI T score ≥ 70) polysomnographic parameters.
Aikens et al., 1999b Compared to primary snoring patients, those with 49% of OSA patients presented depressive symptoms General psychopathology is associated with SaO2 only
OSA have more depressive symptoms (vs. 24.5% primary snoring patients; MMPI in OSA patient.
T score ≥ 70).
Aikens et al. 1999c Patients with PLMD showed higher general 36% of OSA patients showed depressive symptoms (vs. Association not evaluated.
psychiatric distress that OSA or primary snoring 91% of PLMD and 46% of PS patients); 27% of patients
S. GARBARINO ET AL.
patients with OSA showed anxious symptoms (SCL-90 T score

> 63).
Aikens et al. 1999d Patients with untreated PLM or IPD are more likely 25% of OSA patients showed depressive symptoms (vs. Association not evaluated.
to experience clinically significant psychological 58.3% of PLM, 55.2% of IPD and 15.8% insomnia
difficulties than those with either OSA or patients) (MMPI T score > 70)
psychophysiological insomnia
Akashiba et al., 2002 Patients with OSA significantly more depressive 48% of patients with OSA presented SDS > 50 Depression related with QoL and not associated with
than control (p < 0.01). (prevalence of depression in control group not polysomnography parameters, nor with ESS or BMI.
showed).
Akmal et al., 2013 Patients with OSA have depressive and anxious No prevalence reported. Association not evaluated.
symptoms that can be reversed with CPAP.
Aloia et al., 2005 One third of the participants scored in the mild to 33.3% of patients with OSA presented depressive Depression related with RDI, BMI, T90, EDS.
severe range of depression. symptoms (BDI II > 14).
Ashgary et al., 2012 OSA severity was not associated with depression No prevalence reported. Anxiety and depression related with sex and EDS and
and anxiety not either related with AHI or obesity.
symptoms.
Balan et al., 1998 Subjects with sleep disturbance presented high 2.9% of OSA patients showed depressive symptoms; Association not evaluated
level of depressive symptoms 2.9% showed anxious symptoms (SCID)
Bardwell et al., 2000 Patients with OSA showed lower depressive 32.8% of patients with OSA presented depressive Depression in OSA is related to sleep architecture.
symptoms than control group. symptoms (CES-D ≥ 16; vs. 59% of control group;
p > 0.05; CES-D ≥ 16).
Bardwell et al. 2007a Therapeutic CPAP and oxygen supplementation No prevalence reported. Hypoxemia may play a stronger role than sleep
treatment decrease psychological symptoms disruption in causing psychological distress.
Bardwell et al., 2001b Personality characteristic could be related to No prevalence reported. Depression is related to sex, BMI and coping style.
depressive symptoms in OSA patients.
Bardwell et al., 2003 Depression is the strongest predictor of fatigue 33.3% of patients with OSA presented depressive Depression is associated with fatigue in OSA patients.
symptoms (CES-D ≥ 16)
Bardwell et al., 2007b Depression is the strongest predictor of fatigue. 27.8% of patients with OSA presented depressive Depression is associated with fatigue in OSA patients.
symptoms (CES-D ≥ 16).
Beutler et al., 1981 Narcoleptic and OSA patients presented No prevalence reported. Association not evaluated
depressive symptoms higher than control
(Continued )
Björnsdóttir et al., 2016 Depression is a symptom seldom showed in OSA 15.5% of patients with OSA presented dysthymia, 6% OSA severity was not related with depression while
patients. major depression disorder (MINI). obesity, EDS, symptoms of initial insomnia and sleep
medication use were. Sex difference in dystimia were
observed but not in major depression.
Bliwise et al., 1986 Elderly male subject with OSA presented higher No prevalence reported. Association not evaluated.
level of depressive symptoms than those without
OSA
Borak et al., 1996 Emotional status don’t improve after CPAP 55% of OSA patients presented depressive symptoms Association not evaluated.
treatment (BDI; no cutoff); 70% presented anxious symptoms
(MAS; no cutoff)
Cheshire et al., 1992 Anxious and depressive symptoms contribute to 24.1% of OSA patients presented depressive symptoms No association was observed between anxious and
daytime impairment in OSA patients. (HADS no cutoff); 34.5% presented anxious symptoms depressive symptoms and polysomnographic
(HADS no cutoff) variables.
Daabis et al., 2012 Anxiety and depression score were higher in 33% of patients with OSA presented anxious ESS and low QoL were the strongest predictors of
patients with OSA than in control (p < 0.01). symptoms; 51% presented depressive symptoms depression, while reduced QoL was predictor of
(HADS ≥ 11; prevalence of depressive and anxious anxiety. No association was observed between
symptoms in control group not showed). depression, sex, BMI or respiratory sleep parameters.
Dai et al., 2016 Depressive status have high comorbid rate in 47.4% of patients with OSA presented depressive Depressive status was related to female sex, AHI,
Chinese OSA patients symptoms (SDS > 53). hypoxemia but not with BMI.
Diamanti et al., 2013 CPAP treatment improve depressive symptoms. 53.6% of OSA patients presented depressive symptoms Depressive symptoms were related to AHI (p = 0.01)
(CES-D ≥ 16) but not to lower oxygen saturation (p = 0,13)
Dominici & Gomes, 2009 There is no association between OSA and No prevalence reported. Depression was related to gender but not to OSA.
depressive symptoms.
Edwards et al., 2015 Depressive symptoms are common in OSA and are 72.6% of OSA patients presented depressive symptoms AHI (p < 0,001) and BMI (p < 0,005) resulted
related to its severity. (PHQ-9 ≥ 10). associated with depressive symptoms, but not sex.
El-Sharbini et al., 2011 Depressive symptoms are common in OSA. 29.7% of OSA patients presented depression (SCID). Association not evaluated.
Gall et al., 1993 No difference between mild OSA group and No prevalence reported. Association not evaluated.
normal group for depressive symptoms.
Guglielmi et al., 2011 OSA patients presented higher level of depression No prevalence reported. Anxious symptoms were related to SaO2 basal and
and anxiety than control group (p < 0.01). BMI; depression was related to sleep quality and
quantity, polysomnographic variables, and BMI.
Guillelminault et al., 1977 Depressive symptoms are highly present in OSA 28% of OSA patients presented depressive symptoms Association not evaluated.
patients (MMPI > 70).
Gylen et al., 2014 OSA patients no differed in depression respect to No prevalence reported. Sleep duration was related to depression.
no OSA group.
Hashmi et al., 2006 Patients with OSA presented high prevalence of 58% of patients with OSA presented depressive No relation between depression, severity of OSA, EDS,
depression symptoms (BDI ≥ 10). or BMI were observed.
Hrubos-Strøm et al., 2012 OSA patients don’t showed higher levels of 9.1% of patients with OSA presented current major Disorders of axis I were not related to OSA. Female sex
depression than non-OSA group. depressive disorder (vs. 16.7 no OSA group; p = 0.055) was a risk factor for depression in OSA patients.
and current anxiety (14.3% vs. 15.8 no OSA group;
p = 0.726; SCID-I).
(Continued )
43
44
Husain et al., 1997 Symptoms of depression are commonly seen in No prevalence reported. Depressive symptoms were related with arousal
a sleep clinic. indices (p < 0.001) and inversely correlated with RDI
(p = 0.03).
Ishman et al., 2010 OSA patients presented a sixfold increased risk of 34% of OSA patients presented symptoms of Depression was related to EDS and sex but not with
depression when compared with control group depression (BDI II ≥ 14) vs. 8% in non-OSA group; OSA severity (RDI).
p < 0.01.
Ishman et al., 2014 Surgical treatment of OSA reduced significantly 27.3% of OSA patients presented depressive symptoms Depressive symptoms were not associated with RDI
S. GARBARINO ET AL.
depressive symptoms. (BDI-II ≥ 12). on univariate (p = 0.26) or multivariate analysis

(p = 0,15)
Jackson et al., 2011 OSA patients reported more depression when 19.7% of OSA patients showed depressive symptoms Depression was related to EDS and BMI, but not with
compared with healthy control (p < 0.05). from moderate to severe (BDI II ≥ 20) vs. 5% of control polysomnographic variables.
group showed minimal depressive symptoms, p not
shown.
Kawahara et al., 2005 OSA patients showed higher depressive symptoms No prevalence reported. Depressive symptoms correlated with some domain of
than control group and CPAP improve those quality of life.
symptoms.
Klonoff et al., 1987 OSA patients showed elevated depressive No prevalence reported. Association not evaluated.
symptoms and the surgical treatment significantly
improve those symptoms.
LaGrotte et al., 2016 Patients with OSA don’t show higher levels of 11.9% of OSA patients showed depressive symptoms Overweight, obesity, and EDS were associated with
depression than no OSA group. (vs. 15.5% in non-OSA group). (MMPI) depression, while OSA was not.
Lee et al., 2012 OSA patients at baseline showed mild depressive No prevalence reported. Association not evaluated.
and anxious symptoms.
Lee et al., 2015a High rates of anxiety are present in the sample of 48.4% of OSA patients presented anxious symptoms Female sex, EDS, and lower education level were
OSA patients. (STAI ≥ 40); 46.4% of patients with OSA presented related to anxiety. No association with AHI.
depressive symptoms (BDI ≥ 10).
Lee et al., 2015b OSA severity indexes are not good predictors of 39% of patients with OSA presented depressive Depression was significantly related with BMI
depression in severe OSA patients. symptoms (BDI ≥ 10). (p = 0.004), EDS (p = 0.004), sleep quality (p < 0,001),
and total sleep time (p = 0,001), sleep efficiency
(p = 0.008) in severe OSA patients.
Lee et al., 2016 Patients with REM-related SDB reported higher 44.4% of patients with OSA presented depressive REM related SDB was significantly related with
depression rates than patients without REM- symptoms (BDI > 10). a higher level of depressive symptoms, but only in
related SDB (54.1% vs. 42.3%). men.
Lehto et al., 2013 An elevated AHI was associated with the presence 53.7% of OSA patients presented anxious symptoms The persistence of anxiety was associated with AHI
of persistent anxiety after 12-month lifestyle (15 D no data about cutoff) (p = 0.025).
modification program.
Luik et al., 2015 Men with severe OSA reported less depressive No prevalence reported. Severity of sleep apnea is not related to depressive
symptoms than those in the middle of the symptoms.
spectrum.
(Continued )
Macey et al., 2010 OSA severity should not be assumed to relate to No prevalence reported. OSA severity is not related with psychological
severity of accompanying psychological symptoms, nor with BMI or EDS.
symptoms.
McCall et al., 2006 Depression are more severe in woman with OSA 44.6% of patients with OSA presented depressive Depression in OSA patients is associated with sex and
than in men. symptoms (BDI ≥ 10). oxygen desaturation nadir. No association with EDS.
Means et al., 2003 OSA patients showed depressive symptoms that 35.9% of OSA patients presented depressive symptoms Depression score was associated with SaO2. No
improved after CPAP treatment. (BDI > 10) association with EDS.
Millman et al., 1989 Depressive symptoms are common in OSA 45% of OSA patients presented depressive symptoms Depressive symptoms were associated with AHI
patients. (SDS > 50). (p < 0.05).
Mysliwiec et al., 2015 CPAP improve depressive symptoms in military No prevalence reported. Association not evaluated.
personnel with OSA
Peppard et al., 2006 There is a high risk of developing depression for 15% in men and 27% in women of patients with OSA There is a causal link between depression and SDB.
patients with moderate or worse SDB (OR = 3.2, presented symptoms of depression (SDS ≥ 50 or
CI95% 1.8–5.8; p < 0.001). antidepressant use).
Pierobon et al., 2008 Obese patients with OSA presented levels of 33.6% of patients with OSA presented high rates in Association not evaluated.
depression higher than normative data. depression symptoms (> 85° percent) and a 20.3%
high rates in anxious symptoms (> 85%).
Pillar & Lavie, 1998 Women with severe OSA had higher symptoms of No prevalence reported. OSA was not associated with depressive or anxious
anxiety and depression than men. symptoms.
Pochat et al., 1993 OSA patients showed elevated symptoms of 33% of OSA patients presented moderate depressive IAH was associated with depressive symptoms
anxiety and depression. symptoms (MADRS> 25); 35.7% of OSA patients (p = 0,04).
presented anxious symptoms (HARS> 15).
Quam et al., 2014 Individuals with mild OSA doesn’t present higher No prevalence reported. There were no significant correlations between age,
level of depression than normal group (p > 0.05). EDS, and depression rate.
Ramos-Platón et al., 1992 OSA patients showed significantly higher 78% of OSA patients presented depressive symptoms Association not evaluated.
depressive symptoms than control group. (MMPI > 70) vs. 53% in control group.
Razaeitalab et al., 2014 The frequency of anxiety and depression in OSA 53.9% of patients with OSA presented anxious OSA severity was associated with the frequency of
patients is higher than in the general population symptoms (BAI ≥ 8); 46.1% of patients with OSA anxiety but not of the depression.
regardless of the gender. presented depressive symptoms (BDI II ≥ 10).
Rey de Castro & Rosales- There was no difference in depression between 18% of patients with OSA with depressive symptoms Depression was related to age, sex, ESS, and
Mayor, 2013 OSA and no OSA patients (p = 0.216). (BDI ≥ 14). Prevalence of depression in no OSA group comorbidities. No association was found with OSA
not showed. severity, nor with BMI.
Reyes Zuñiga & Rosales- OSA patients show a prevalence of anxiety or 18.5% of patients with OSA presented anxious Anxiety and depression were associated with sex, BMI,
Mayor, 2012 depression higher than general population in symptoms (HADS ≥ 8); 7.6% of patients with OSA and ESS. SDB severity was not related with anxiety or
Mexico. presented depressive symptoms (HADS ≥ 8). depression.
Reynolds et al., 1984 A considerable portion of OSA patients met No prevalence reported. Depressive symptoms were associated with age, EDS,
research diagnostic criteria for an affective longer REM latency. AHI was not associated with
disorder. depressive symptoms.
Ruberto & Liotti, 2011 OSA patients showed higher levels of depression No prevalence reported. AHI was associated with depression score.
than control group (p < 0.001).
(Continued )
45
46
Sampaio et al., 2012 Women with OSA show more depression and No prevalence reported. Depression and anxiety in OSA is associated with sex
anxiety than men with OSA. and QoL.
Sanchez et al., 2001 Anxiety and depressive symptoms decreased after No prevalence reported. Association not evaluated.
3 months of CPAP treatment.
Schwartz et al., 2005 OSA often presents depressive symptoms than can 50% of OSA patients presented depressive symptoms RDI was associated with depressive symptoms among
ameliorate after CPAP therapy. (BDI-SF ≥ 4). depressive OSA patients (p = 0,02)
S. GARBARINO ET AL.
Schwartz et al., 2007 Depressive symptoms improve after CPAP 30% of OSA patients presented depressive symptoms Association not evaluated.
treatment. (BDI-SF ≥ 4)
Sforza et al., 2002 Mood disorders in OSA patients could be related No prevalence reported. Depression is related to ESS and shorter sleep latency
to misinterpretation of EDS. at the MWT.
Sforza et al., 2016 Women have higher anxiety and depression score 38% of patients with OSA presented anxious symptoms Depression was associated with sex. No association
than men. (Goldberg ≥ 5) and 8% depressive symptoms founded between depression, anxiety and OSA
(QD2A > 7). existence or severity.
Surani et al., 2013 Patients with OSA presented high levels of 52.9% of patients with OSA presented anxious Sex is related to anxiety but not to depression.
depression and anxiety. symptoms and 39.2% depressive symptoms
(HADS ≥ 10).
Vandeputte et al., 2003 Prevalence of depressive symptoms in patients 41% of OSA patients presented depressive symptoms Association not evaluated.
with sleep disorders was high, especially in (BDI > 10).
insomnia and OSA groups.
Wells et al., 2004 Depression is a better predictor of self-reported No prevalence reported. Depression is not related with polysomnographic
sleep quality than are polysomnographic measures but it is related with self-reported sleep
measures of sleep in patients with OSA. quality and BMI.
Wells et al., 2007 Patients with higher symptoms of OSA after CPAP No prevalence reported. Association not evaluated.
treatment tended to have more depressive
symptoms after CPAP treatment.
Yamamoto et al., 2000 A high percentage of OSA patients presented 63.4% of OSA patients presented depressive symptoms Association not evaluated.
depressive symptoms that improved after CPAP (SDS ≥ 41).
treatment.
Yue et al., 2003 OSA patients suffered from psychosomatic No prevalence reported. Psychological status was associated with sleep
symptoms more than control. fragmentation, % S1, NREM latency, and EDS.
Yusunkaya et al., 2016 OSA patients reported a higher level of depression 16.4% of patients with OSA presented moderate Depression symptoms were associated with sleep
than subjects without OSA. depressive symptoms (BDI ≥ 17). . disruption, arousal, and T90 in OSA patients.
OSA: Obstructive Sleep Apnea; MMPI: Minnesota Multiphasic Personality inventory; SCL-90: Symptoms Check List-90; BDI: Beck Depression Scale; SCID: Structured clinical Interview for DSM-IV;
SDS: Zung Self-rating Depression Scale; PS: Primary Snorers; IPD:; HADS: Hospital Anxiety and Depression Scale; CES-D: Center for Epidemiological Studies Depression Scale; PLMD: Periodic Limb
Movement Disorder; IPD: Insomnia with psychiatric disorders; PHQ-9: Patients Health Questionnaire; MAS: Taylor’s Manifest Anxiety Scale; HARS: Hamilton Anxiety Rating Scale; MADRS:
Montgomery-Asberg Depression Rating Scale; QoL: Quality of Life; EDS: Excessive daytime sleepiness; STAI: State-Trait Anxiety Inventory; MINI: The Mini-International Neuropsychiatric Interview;
BMI: Body Mass Index; AHI: Apnea Hypopnea Index; SaO2:oxygen saturation; RDI: Respiratory Disturbance Index; SDB: Sleep Disordered Breathing; BAI: Beck Anxiety Inventory; QD2A: Self-Report
Inventory on Depressive Symptomatology; %S1: % of stage 1 of sleep; NREM: non-REM sleep.
Figure 1. Article selection algorithm.
analysis showed high heterogeneity, both for depression (I2 = 97.3%), and for anxiety (I2 = 95.5%) (see
Figure 2 and Figure 3).
Most of the case-series studies included in the pooled analysis lacked a control group of non-OSA
patients. In studies that included a control group, OSA patients showed a higher prevalence of
depression (Akashiba et al., 2002; Dai et al., 2016; Guglielmi et al., 2011; Ishman, Cavey, Mettel, &
Gourin, 2010; Jackson et al., 2011; Ramos-Platón & Espinar-Sierra, 1992; Ruberto & Liotti, 2011) or
of anxiety disorder (Daabis & Gharraf, 2012; Guglielmi et al., 2011) than control patients.
Figure 2. Prevalence of depressive symptoms in OSA patients.
Figure 3. Prevalence of anxiety symptoms in OSA patients.
The cumulative odds ratio of self-diagnosed depression in OSA patients versus non-OSA controls,
based upon the four studies with no sufficient data (Bardwell, Moore, Ancoli-Israel, & Dimsdale,
2000; Hrubos-Strøm et al., 2012; Ishman et al., 2010; Ramos-Platón & Espinar-Sierra, 1992), showed
a nonsignificant increase (OR = 1.47; 95% CI, 0.48–4.52).
Some cross-sectional studies observed that the prevalence of depression and anxiety was higher in
OSA patients than in the general population (Pierobon et al., 2008; Razaeitalab, Moharrari, Saberi,
Asadpour, & Rezaeetalab, 2014; Reyes Zuñiga et al., 2012). Nevertheless, other studies failed to observe
significant differences in the prevalence of depressive symptoms between OSA and non-OSA groups
(Bardwell et al., 2000; Dominici & Gomes, 2009; Gylen et al., 2014; Hrubos-Strøm et al., 2012; Luik et al.,
2015; Quan et al., 2014; Rey de Castro & Rosales-Mayor, 2013). In a longitudinal study with a follow-up
of 7.5 years, LaGrotte et al. (2016) did not find any association between OSA and depression.
Which OSA-related risk factors are associated with depressive and anxious symptoms?
Many studies have also investigated which clinical factors might be associated with psychiatric
symptoms. In those studies in which the association between sex and depression in OSA patients
was analyzed, depression was more prevalent in female than in male OSA patients (Ashagary et al.,
2012; Dai et al., 2016; Dominici & Gomes, 2009; Hrubos-Strom et al., 2012; Ishman et al., 2014, 2010;
Pillar & Lavie, 1998; Rey de Castro & Rosales-Mayor, 2013; Sampaio et al., 2012; Sforza, Saint
Martin, Barthélémy, & Roche, 2016), while in two articles, this difference was not observed or did
not reach the statistically significance (Daabis & Gharraf, 2012; Edwards et al., 2015). Similarly,
anxiety was more prevalent in female than in male patients in three studies (Lee, Paek, & Han, 2016;
Sampaio et al., 2012; Surani, Rao, Surani, Guntupalli, & Subramanina, 2013).
Some studies investigate the influence of BMI on the presence of depressive symptoms in OSA
patients. In many studies, obesity, expressed as excessive body mass index (BMI), emerged as an
important factor associated with depression (Aloia et al., 2005; Bardwell, Moore, Ancoli-Israel, &
Dimsdale, 2003; Björnsdóttir et al., 2016; Edwards et al., 2015; Guglielmi et al., 2011; Jackson et al.,
2011; LaGrotte et al., 2016; Lee, Han, & Ryu, 2015a; Reyes Zuñiga et al., 2012; Wells et al., 2004) and
with anxiety (Guglielmi et al., 2011; Reyes Zuñiga et al., 2012) in OSA patients. Others researchers did
not observe this association (Aikens, Caruana-Montaldo, Vanable, Tadimeti, & Mendelson, 1999a;
Daabis & Gharraf, 2012; Macey et al., 2010; Razaeitalab et al., 2014). Another clinical variable that is
commonly associated with mental disorders due to the influence it has on everyday life is excessive
daytime sleepiness (EDS). In fact, EDS, which is generally self-evaluated with the Epworth Sleepiness
Scale, appeared to be associated with depressive symptoms in 11 studies (Aloia et al., 2005; Björnsdóttir
et al., 2016; Daabis & Garraf, 2012; Ishman et al., 2010; Jackson et al., 2011; LaGrotte et al., 2016; Lee
et al., 2015a; Rey de Castro & Rosales-Mayor, 2013; Reyes Zuñiga et al., 2012; Reynolds et al., 1984;
Sforza et al., 2002) and with anxiety in 2 studies (Lee et al., 2015a; Reyes Zuñiga et al., 2012). A lack of
association between EDS and depression in OSA patients was reported only by Macey et al. (2010). An
association between OSA severity (expressed by the AHI) and depressive symptoms was found in 8
studies (Dai et al., 2016; Diamanti et al., 2013; Edwards et al., 2015; Millman, Fogel, McNamara, &
Carlisle, 1989; Pochat et al., 1993; Ruberto & Liotti, 2011; Schwartz, Kohler, & Karatinos, 2005; Yue
et al., 2003). Conversely, most studies failed to find an association between OSA severity and
depression prevalence or severity (Aikens et al., 1999a; Akashiba et al., 2002; Ashgary et al., 2012;
Björnsdóttir et al., 2016; Cheshire et al., 1992; Daabis & Garraf et al., 2012; Hashmi, Giray, &
Hirshkowitz, 2006; Ishaman et al., 2014; Ishman et al., 2010; Jackson et al., 2011; LaGrotte et al.,
2016; Luik et al., 2015; Macey et al., 2010; Razaeitalab et al., 2014; Reyes Zuñiga et al., 2012; Reynolds
et al., 1984; Sforza et al., 2016). Similarly, no association was found between OSA severity and anxiety
symptoms (Lee et al., 2016; Lehto et al., 2013; Reyes Zuñiga et al., 2012; Sforza et al., 2016).
We also evaluated if any of the above-reported factors could explain the observed hetero-
geneity between studies. However, moderator analysis failed to find a significant association
between the type of questionnaire used to evaluate depressive symptoms (p = .40) and the
prevalence of self-assessed depression. Similarly, no significant association was found between
OSA severity (p = .10), age (p = .30), obesity (p = .90), EDS (p = .70), sex (p = .09), or country
where the study was performed (p = .40) and the observed prevalence rates of depression. We
also disaggregated the data about depressive symptoms prevalence by sex in the 10 articles
(Bjornsdottir et al., 2016; Daabis & Gharraf, 2012; Dai et al., 2016; El-Sherbini et al., 2011;
Ishman et al., 2014, 2010; McCall, Harding, & O’Donovan, 2006; Peppard et al., 2006; Razaeitalab
et al., 2014; Sforza et al., 2016) in which the percentages of men and women that showed at least
a mild level of this disorder were provided. The pooled prevalence of depressive symptoms was
34% in OSA women and 26% in OSA men. This gender difference did not reach statistical
significance (p = 0.4).
In the subgroup of studies about OSA and anxious symptoms, no association between type of
questionnaire (p = .08) or country where the study had been conducted (p = .80) and anxiety
prevalence was observed.
Publication bias was also assessed. The funnel plot and Egger’s test were used to evaluate asymmetry
in negative and positive effect size. Since the results of Egger’s test were not significant (p = .07;
p = .98), there was no conclusive evidence of publication bias in the selected sample of articles.
Discussion
Our meta-analysis showed that the pooled prevalence of depressive and anxious symptoms in OSA
patients is 35.0% and 32.0%, respectively. The observed prevalence rates are considerable, confirming
the prevalent scientific opinion that includes anxiety and depression among the OSA comorbidities.
Nevertheless, the data observed in the systematic review of the literature and the meta-analytic
analysis, albeit realized on a limited number of articles that presented the data of interest, do not
support the existence of an association between OSA severity and presence of depressive symptoms.
This finding could indicate that AHI is not the most appropriate polysomnographic measure of
clinical impact of OSA and that factors other than respiratory events could contribute to mood
disturbances. EDS, sleep disruption, fatigue, or other objective indices of OSA severity could be
better predictors of depression in OSA patients; nevertheless, due to the lack of data and the quality
of studies included, we are unable to give more precise explanations about this association throw the
quantitative analysis.
The range of variation of anxiety or depression among OSA patients is very large in these studies,
which refer exclusively to patients with an instrumentally confirmed diagnosis and therefore come
mainly from sleep centers. A large number of factors, like sex, EDS, age, BDI distribution, and sleep
quality could contribute to this variability.
The substantial heterogeneity between studies may also be due to the variability in the character-
istics of the underlying populations, which differed by age, gender, severity of OSA, and prevalence
of obesity or sleepiness. Nevertheless, none of the factors considered in the moderator analysis was
significantly associated with the prevalence of mood disorders in patients with OSA. The most
important factor that could explain variability between studies was, however, the choice of the
questionnaire used for the diagnosis of depression or anxiety and, of course, the chosen cutoff level.
Mood scales tend to overestimate complaints as compared to psychiatric consultation (Acker et al.,
2017). In the present study, no significant differences were observed in prevalence of symptoms of
anxiety and depression between the studies in which this assessment was completed using
a questionnaire and those in which clinical diagnosis was performed. It is important to note that
diagnosis of anxiety or depression was confirmed by psychiatric examination only in very few
studies, and this may overestimate their prevalence. In a very recent study the subsequent specialist
examination led to a clinical diagnosis of depression in 21.5% of OSA patients (Acker et al., 2017).
This prevalence rate was similar to that observed in other studies relying on clinical diagnosis
(Sharafkhaneh, Giray, Richardson, Young, & Hirshkowitz, 2005).
In our study, the moderator analysis performed did not show significant differences in anxiety or
depression in relation to the different questionnaires used. A recent meta-analytic study suggests that
the frequency of reported symptoms that are common in both diseases is associated with the resulting
estimated prevalence of depression in OSA patients (Nanthakumar, Bucks, & Skinner, 2016). This
indicates that when using depression questionnaires to assess the prevalence of depression in OSA,
questionnaires that have a lower proportion of symptom overlap between OSA and depression as well
as a higher proportion of anhedonia symptoms, reduce the likelihood of overestimating the prevalence
of depression in OSA (Nanthakumar et al., 2016). Results from several studies show that there is
a strong correlation between depression and EDS in OSA patients; however, this association did not
emerge in our analysis. As previously explained, these results should be interpreted with caution due to
the lack of data. Fatigue and EDS are the cardinal symptoms of OSA and at the same time are among
the most common complaints in psychiatric patients.
The selected studies often had other methodological shortcomings, such as the lack of a control
group. Because of this methodological limitation it was only possible to calculate the pooled risk of
depressive symptoms in the OSA group compared with the non-OSA group in four studies that
contained the necessary data. The cumulated odds ratio of depressive symptoms in OSA patients
versus non-OSA controls showed a nonsignificant increase. This data must be interpreted with
caution, given the scarcity of studies. Our quantitative and qualitative analyses show that, despite the
methodological differences, depressive and anxious symptoms are more frequent in OSA patients
than in the general population. Nevertheless, the qualitative and the quantitative analysis, with its
previously mentioned methodological limits, does not support a causal link between OSA and
depression. Current evidence is in line with the results obtained in this study. Evidence includes
a recent, very relevant 10-year cohort study by Kendzerska, Gershon, Hawker, Tomlinson, and
Leung (2017), demonstrating that OSA and related severity measures are not related to the risk of
hospitalization for depression. Based on the clinical and psychological profiles of patients with OSA,
and on the observation that severity of OSA, obesity, and EDS are strong risk factors for prevalent
and incident depression, it is likely that depressive symptoms are a consequence, rather than a cause,
of the disorder (Bixler, Gaines, & Vgontzas, 2017). This statement, however, does not exclude the
possibility that the two diseases may be interlinked. Given the current uncertainty, a possible
neurophysiological link between OSA, anxiety, and depression should be evaluated.
A growing body of evidence has suggested that the more frequently observed comorbidities of
OSA, such as cardiovascular diseases or metabolic imbalance, could be associated with elevated levels
of mental distress. It could be argued that additional mechanisms observed in OSA patients, such as
inflammation (Finnel & Wood, 2016), oxidative stress (Luppino et al., 2010), or immune system
function issues (Steiropoulos et al., 2009), could be involved in this link. Poor mental health in OSA
patients may be due to the aforementioned comorbidity and their underlying mechanisms.
Nevertheless, a recent study did not find any association between depression severity and presence
of inflammatory and cardiovascular biomarkers in persons at high risk for OSA (Einvik et al., 2011).
In a similar vein, a recent review highlighted how OSA affects endothelial dysfunction and neuroin-
flammation and this may initiate or amplify several microvascular and neurovascular pathologic
processes that could mediate the association with depression (Kerner & Roose, 2016). Future studies
could investigate the influence of comorbidity, such as cardiovascular or metabolic disease, on the
variation of depression prevalence in patients with OSA.
The association of OSA with depression or anxiety is clinically relevant. OSA patients with
depression could experience higher levels of fatigue and lower quality of life than OSA patients
without mood disorders. Depression and anxiety could also make CPAP therapy difficult. A recent
study showed that depression was independently associated with poorer adherence and that a focus
on improvement of depressive symptoms could be a strategy to increase the treatment efficacy (Law,
Naughton, Ho, Roebuck, & Dabscheck, 2014). In current practice, however, physicians generally give
more attention to only one of the two diseases.
The current study is the first to present a meta-analytical estimate of the comorbidity rate of
anxiety and depression in OSA patients. Analysis is based on very wide bibliographic examination of
the most qualitatively valid studies published in the literature investigating the presence of anxiety or
depression in patients accurately diagnosed using instrumental methods. Nevertheless, this study
presents several limitations. Many studies included in the systematic review were not used in the
meta-analysis because data about prevalence of depression or anxiety in OSA patients were not
available, or because it was not clear which questionnaire’s cutoff was adopted, or the value chosen
was too different from that used in the other studies included. From an epidemiological point of
view, the overall result is unsatisfactory. The fact that most studies are of low quality indicates that
the scientific literature has so far overlooked this important topic. From a clinical point of view,
finding that the interplay of OSA and mental illness has been overlooked is worrying. This means
that today many patients are not adequately being diagnosed or treated. The questionnaires chosen
for screening and the cutoff levels chosen for diagnosis vary, suggesting that the cutoff values are not
standardized. All authors performed a screening of depression and of anxiety, but diagnoses were
generally not confirmed by a specialist. In most cases, we do not know if the symptoms of anxiety
and depression were independent, or if they occurred in the same person. Moreover, reports give no
data about the treatment of psychiatric illness. Rigorous longitudinal and case-control studies, using
clinician-administered semistructured diagnostic interviews, are thus needed in order to shed light
on the relationship between OSA and psychiatric disorders, and to identify which OSA-related
factors are involved in this association.
An indirect result of our study is the observation that depression and anxiety are associated with
OSA, but they are overlooked in common practice. Diagnosis and treatment of depression and
anxiety in OSA patients has room for important improvement. A physician focusing on symptoms
and treatment of the physical illness, to the exclusion of any associated mental illness, results in
incomplete care of the patient. In a disease like OSA, which has such a high percentage of
comorbidity of psychiatric disorders, this is unfortunate. This is contrary to the principles of person-
centered medicine and of rationalization of health care. Significant effort should be made to
personalize care for OSA patients, including early diagnosis and treatment of mental illnesses
(Lim, Sutherland, Cistulli, Pack, 2017; Sutherland, Almeida, de Chazal, & Cistulli, 2018).
Interdisciplinary cooperation is recommended for both OSA patients with symptoms of anxiety or
depression and depressed or anxious patients with treatment resistance. Future research direction
could address overlapping of OSA and mood disorders, because, on the one hand, OSA may
complicate diagnosis of depression and make treatment challenging, and treatment of OSA can
improve the response to standard therapy of depression or anxiety. Understanding the mechanisms
connecting OSA and psychiatric disorders may improve the choice of personalized treatment. This is
a new prospective that is in accordance with Personalized Medicine.
The study is strong due to the use of 73 articles investigating the presence of anxiety or depression
in patients accurately diagnosed using instrumental methods. It covers a very high span of scientific
literature and presents, for the first time, a precise meta-analytical estimate of the comorbidity rate of
anxiety and depression in OSA patients. The main limitation stems from the low methodological
quality of the selected studies which, being mainly of clinical interest, have dealt with the issue of
mental health with less attention with respect to OSA. This limit is at the same time one of the most
important results of this work, underlining the urgent need for high-quality research into psychiatric
comorbidities in OSA and their treatment.
Disclosure statement
No potential conflict of interest was reported by the authors.
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Behavioral Sleep Medicine

ISSN: 1540-2002 (Print) 1540-2010 (Online) Journal homepage: https://www.tandfonline.com/loi/hbsm20

Association of Anxiety and Depression in

Sergio Garbarino, Wayne A. Bardwell, Ottavia Guglielmi, Carlo Chiorri, Enrica

To link to this article: https://doi.org/10.1080/15402002.2018.1545649

Published online: 19 Nov 2018.

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Association of Anxiety and Depression in Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is a chronic condition characterized by sleep-related pauses in

CONTACT Ottavia Guglielmi ottavia.guglielmi@gmail.com Department of Neuroscience, Rehabilitation, Ophthalmology,

Data extraction, quality assessment, and meta-analysis

Table 1. Characteristics of the studies included in the systematic review.

How prevalent are symptoms of depression and anxiety in OSA patients?

patients with OSA showed anxious symptoms (SCL-90 T score

depressive symptoms. (BDI-II ≥ 12). on univariate (p = 0.26) or multivariate analysis

Figure 1. Article selection algorithm.

Figure 2. Prevalence of depressive symptoms in OSA patients.

Figure 3. Prevalence of anxiety symptoms in OSA patients.

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