ORIGINAL ARTICLE Psychiatry and Clinical Psychopharmacology 2020;30(1):3-9
DOI:10.5455/PCP.20200212045154
KEYWORDS: ADHD, functional
impairment, mental disorders,
ADHD comorbidity
ARTICLE HISTORY
Received: Jan 12, 2020
Accepted: Feb 18, 2020
Corresponding author: Pratap R. Chokka, E-Mail: pratapchokka@chokkacenter.com
To cite this article: Hankey JR, Liu YS, Chokka PR. Adult ADHD: Prevalence, Comorbidities, and Patient-Reported Dysfunction in a Tertiary
Mental Health Clinic. Psychiatry and Clinical Psychopharmacology 2020;30(1):3-9, DOI: 10.5455/PCP.20200212045154
often persist even after symptoms have remitted, which
may be attributable, at least in part, to the cumulative
effects of social isolation and the development of ADHDrelated deficits in self-efficacy and self-esteem [5, 7].
The negative outcomes associated with ADHD are diverse,
including physical health problems such as higher rates
of obesity, smoking, asthma, migraines, emergency
room visits, and injury-related insurance claims and
accidental death [7, 11–13]. ADHD is also correlated with
lower academic performance, including lower grades
and higher rates of academic probation and drop-out
[2, 14], and ADHD-associated impulsivity and diminished
in-job engagement may precipitate financial problems
stemming from higher rates of unemployment and debt,
fewer saving behaviours, and lower credit ratings [4, 15,
16].
ADHD is also linked to poorer mental health outcomes,
including higher rates of depression, anxiety, and
suicidality [17, 18], as well as substance use and addictions,
including cannabis, alcohol, illicit drugs, gambling, and
problematic technology use [19–21]. Additionally, ADHD is
Jeffrey R. Hankeya,b, Yang S. Liub,c, Pratap R. Chokkab,c
a
Department of Educational Psychology, University of Alberta, Canada, b
Chokka Center for Integrative Health, Edmonton
Alberta, Canada, c
Department of Psychiatry, University of Alberta, Canada
Adult ADHD: Prevalence, Comorbidities, and PatientReported Dysfunction in a Tertiary Mental Health Clinic
Abstract
Background: To investigate patient-reported dysfunction associated with ADHD and three common
comorbidities—major depressive disorder (MDD), generalized anxiety disorder (GAD), and bipolar
disorder (BPD)—as well as their prevalence.
Methods: Dysfunction was measured using the Sheehan Disability Scale (SDS). Diagnosis was attained
by a certified psychiatrist using DSM-5 criteria.
Results: In all, 46.7% of our sample (432/925) was diagnosed with ADHD. The most common
comorbidities, in ascending order, were MDD (21.99%), BPD (24.77%), and GAD (31.48%). Sorted by
ascending SDS score, the most functionally debilitating diagnoses in our sample were GAD < ADHD <
ADHD + GAD < BPD < ADHD + BPD < MDD < ADHD + MDD.
Conclusions: Our sample of adults with ADHD, GAD, BPD, and particularly MDD report significant
daily dysfunction. Comorbid ADHD is associated with increased dysfunction, particularly with GAD. The
prevalence of adult ADHD in our study was higher than in previous studies.
INTRODUCTION
Attention-deficit/hyperactivity disorder (ADHD) is a
heritable, neurodevelopmental disorder marked by
difficulties in executive function, impulse control, and
emotional dysregulation that can result in distractibility,
inattention, impulsivity, and hyperactivity [1, 2]. Though
typically regarded as a childhood-onset disorder, ADHD
persists into adulthood in approximately half of cases [3,
4] and there is evidence for heterogeneity in the etiology
of adult ADHD, a disorder that may be masked in one’s
childhood by protective factors or mistaken for laziness
and rebelliousness [5, 6], or which may be, as some
researchers have suggested, neurologically distinct from
childhood ADHD [4, 7].
Despite a high symptom burden, adult ADHD is widely underrecognized and under-treated [8, 9]. This shortcoming
may be due to a lack of training and familiarity among
practitioners with the typical onset and course of adult
ADHD, as well as difficulty in distinguishing ADHD from
other mental health conditions, particularly borderline
personality disorder and bipolar disorder [1, 10]. ADHD
can have lasting socioeconomic and health effects that
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associated with poorer psychosocial outcomes, including
life satisfaction and subjective wellbeing, psychological
distress, social isolation, and difficulties maintaining
healthy relationships [4, 22, 23]. All of these outcomes
may be linked to the internalizing effects of stigma and
perceived health discrimination [6, 10, 24]. Compounding
these stressors and risks, ADHD is also associated with
insomnia and sleep disorders, nightmares, fatigue, and
exhaustion [25–27]. As well as personal ramifications for
individuals and their families, work-related impairments
and increased healthcare costs present a substantial
economic burden on society [1, 18]. The prevalence of
adult ADHD in the general population has been estimated
at 2.5-5.4% [4, 28–30] and is typically more frequent in
high-income than low-income countries [29]. However,
the tendency toward underdiagnosis means the overall
prevalence could be higher, particularly when using DSM-IV
criteria [5, 6, 10].
To date there are few studies of daily functioning in adults
with ADHD, with and without comorbidities. Accordingly,
the primary aim of this study was to measure and
compare self-reported dysfunction in patients diagnosed
with pure (mutually exclusive) ADHD, major depressive
disorder (MDD), generalized anxiety disorder (GAD),
bipolar disorder (BPD), or alcohol use disorder (AUD), and
those with MDD, GAD, BPD, or AUD and comorbid ADHD.
Our secondary aim was to ascertain the prevalence of
ADHD and its comorbidities in a sample of nonpsychotic
psychiatric outpatients. A small number of AUD diagnoses
precluded a full analysis of AUD dysfunction; as a result we
did not generate hypotheses for AUD or comorbid ADHDAUD dysfunction.
Our hypotheses regarding patient-reported dysfunction
in ADHD and non-ADHD patients with and without
comorbidities were informed by neurocognitive hypotheses
of anxiety, depression, bipolar, and ADHD, according to
which deficits in executive function and biases in emotional
processing specific to MDD, and to a lesser extent BPD, are
more likely to elevate self-reported dysfunction in those
patients compared to those with GAD and ADHD [31–34].
Our hypotheses were as follows:
• Patient-reported dysfunction in pure (mutually
exclusive) cases would fall into the following
quantitative hierarchy: MDD > BPD > GAD > ADHD.
• The addition of comorbid ADHD in patients with
MDD would not significantly increase dysfunction
scores. We anticipated that the additive effects on
dysfunction introduced by comorbid ADHD would be
most pronounced in GAD patients, followed by BPD, and
least of all in MDD patients.
METHODS
In this single-centre, retrospective, naturalistic study
approved by University of Alberta Research Board, we
investigated the prevalence of ADHD, its comorbidities,
and associated patient-reported dysfunction at an
interdisciplinary, referral-based, tertiary care centre in a
large city in western Canada. From June 2016 to October
2018, new patients were invited to participate in the
study. Participants provided written informed consent
before completing the Sheehan Disability Scale (SDS) [35],
a short, simple, easy-to-score instrument that assesses
functional impairment on a 10-point scale—from 0 (not
at all) to 10 (extremely)—in the domains of work/school,
social life, and family life. To our knowledge, while the
SDS has been psychometrically validated for use with
adults with ADHD [36], it has not been used elsewhere
to measure functional impairment in adults with ADHD
outside of Morstedt, Corbisiero, Bitto, and Stieglitz’s
study of impairment due to emotional symptoms [37].
Upon completion of the SDS, patients were seen by one of
our centre’s certified psychiatrists, who was blinded to the
results of the SDS, for face-to-face assessment, diagnosis,
and treatment as usual. For this study we logged patients
who received a DSM-5 [38] diagnosis, not in remission, of
one or more of five common mental disorders observed
at our clinic—MDD, GAD, BPD, AUD, and ADHD—as well
as their SDS scores (total and work/school, social life,
and family life subscales). While there is emerging
evidence that adult ADHD may be neurologically distinct
from childhood ADHD [4, 7], for our diagnostic purposes
in this study, we used established DSM-5 criteria that
include adult experiences and require fewer symptoms
after age 17 but that nevertheless require the presence
of symptoms prior to the age of 12 [38].
Statistical Analysis
Statistical analyses were conducted using the IBM
SPSS Statistics for Macintosh, Version 25.0. To test our
hypotheses of differential dysfunction levels among pure
and comorbid diagnoses, we used factorial ANOVA followed
by two-tailed between-group t tests. Thirty participants
who had missing answers in SDS subscales were excluded
from analyses using SDS total score; SDS subscales were
analyzed using the full sample. Nine participants who
identified as “other” gender were also excluded from
factorial ANOVA analysis to prevent confounds in gender
analysis (n = 913).
RESULTS
In total, 955 patients participated in our study. Of those
who provided a total SDS score from all three subscales (n
= 925), 46.70% (n=432) were diagnosed with ADHD by one
of our clinic’s psychiatrist using DSM-5 criteria. To test our
hypotheses, we first conducted a full factorial ANOVA using
SDS total score as a dependent variable, and age, gender,
and diagnostic label (e.g., MDD), including all pairwise
comorbid diagnoses (e.g., ADHD comorbid with MDD) and
two or more comorbid diagnoses (e.g., ADHD comorbid
with MDD and GAD), as independent variables. We found
a null effect of age and gender and their associated
interaction effects (see Table 1), so we followed up with a
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series of two-tailed independent sample t-tests to directly
investigate our hypotheses. Our results generally confirm
our first hypothesis—MDD > BPD > GAD > ADHD—with the
exception that we did not find a statistically significant
difference between GAD and ADHD (see Table 2).
Table 1. Summary of factorial ANOVA results.
df F(df, 913) p ηpartial
2
Intercept 1 238.52 0.000** 0.38
Diagnosis Label 11 6.01 0.000** 0.15
Age 55 1.23 0.139 0.03
Gender 4 1.59 0.177 0.15
Diagnosis Label x Age 290 0.95 0.673 0.09
Diagnosis Label x Gender 12 0.46 0.936 0.43
Age x Gender 47 0.84 0.759 0.01
Diagnosis Label x Age x Gender 100 0.91 0.709 0.19
Mutually exclusive diagnosis labels used in ANOVA model include the
following: ADHD only, BPD only, GAD only, MDD only, AUD only, ADHD
and BPD, ADHD and GAD, ADHD and MDD, ADHD and AUD, ADHD with
2 and more comorbidity, two and more comorbidity but no ADHD, and
No diagnosed disorders.
Table 2. Between sample t-test summary
Diagnosis 1 Diagnosis 2 t df p
MDD BPD 2.56 79.72 .013*
BPD GAD 2.57 98.45 .012*
GAD ADHD -.86 119.47 .393
BPD ADHD 2.19 76.06 .031*
*denotes statistical significance (p<0.05)
Our AUD sample size was too small for an analysis of
dysfunction. The mean total dysfunction, out of 30, as
measured by the SDS for ADHD-only patients (n=163)
was 15.85 (Standard Deviation [SD]=7.83), for GAD-only
(n=64) was 14.89 (SD=7.53), for BPD-only (n=50) was 18.82
(SD=8.53) , and for MDD-only (n=111) was 22.33 (SD=6.97)
(see Figure 1). Mean total dysfunction for comorbid ADHD
and GAD-only (only one comorbidity) (n=55) was 18.11
(SD=7.25), comorbid ADHD and BPD-only (n=69) was 20.39
(SD=7.44), and comorbid ADHD and MDD-only (n=36) was
23.36 (SD=4.66) (see also Figure 2).
Figure 1. SDS total score as a function of psychiatric
diagnosis, sorted by ascending SDS score.
Table 3 contains subscale scores by diagnostic category.
While the relative magnitudes of the subscales generally
reflect those of the total scores, it may be worth noting
that all diagnoses that included ADHD had the highest
patient-reported dysfunction in the domain of Work/
School.
Table 3. Descriptive statistics of SUS subscales
Diagnosis Social Life Work and School Family Life
N Mean SD N Mean SD N Mean SD
Single
GAD 69 5.42 3.08 64 5.08 3.28 69 4.55 2.74
ADHD 166 4.73 3.13 163 5.90 3.02 166 5.22 2.96
BPD 51 6.35 3.06 50 6.36 3.20 51 6.25 3.17
MDD 115 7.59 2.63 111 7.49 2.72 115 7.33 2.53
Comorbid
ADHD
and GAD 57 5.82 2.92 55 6.76 2.45 57 5.63 2.87
ADHD
and BPD 71 6.46 2.60 69 7.00 2.90 70 6.69 2.88
ADHD
and MDD 39 7.46 2.42 37 8.14 2.02 39 7.69 2.20
SD stands for standard deviation
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Of the 432 ADHD-diagnosed patients, 37.73% (n=163) had
no comorbidities, 21.99% (n=95) had comorbid MDD, 31.48%
(n=136) had comorbid GAD, 24.77% (n=107) had comorbid
BPD, and 5.79% (n=25) had comorbid AUD (see Table 4).
Table 4. Comorbidity of psychiatric illness among ADHD
patients. Due to some patients having multiple comorbidities,
total proportion will not equal 100%.
Diagnosis Frequency Proportion (%)
ADHD only 163 37.73
Comorbid with MDD 95 21.99
Comorbid with GAD 136 31.48
Comorbid with BPD 107 24.77
Comorbid with AUD 25 5.79
DISCUSSION
This retrospective, naturalistic study examined patientreported dysfunction using the Sheehan Disability Scale
among individuals with pure (non-comorbid) ADHD, MDD,
GAD, or BPD, as well as those with ADHD and comorbid
conditions. Consistent with our first hypothesis, noncomorbid patient-reported dysfunction was highest for
MDD. We attribute these findings to hippocampal-related
executive function, memory, attention, concentration,
and motivation deficits common to MDD contributing
to actual daily dysfunction, as well as the potential for
habitual negative thinking and rumination associated with
a hyperactive limbic system [32–34], which could lead to
recall bias and inflated reports of dysfunction. Self-reported
dysfunction in BPD patients was also relatively high, which
makes sense in light of associated neurocognitive deficits
around executive function and verbal memory [39, 40].
However, also consistent with our first hypothesis, BPDassociated patient-reported dysfunction was lower than
that for MDD; we attribute these findings to the cyclical
nature of bipolar disorder, its cognitive heterogeneity,
the potential for recent or current hypomanic episodes
to ameliorate dysfunction and/or mitigate appraisals
of dysfunction, and the tendency for bipolar patients to
overestimate their own cognitive performance [31, 41].
Also consistent with our first hypothesis, self-reported
dysfunction in pure ADHD and GAD patients was significantly
lower than MDD and BPD patients. Compared to MDD and
BPD, GAD and ADHD are typically early-onset disorders
[3, 4, 32], which we anticipated could lead to inoculation
effects whereby dysfunction becomes normalized and less
salient to the patient during recall. Moreover, compared to
studies of MDD and BPD, the literature on neurocognitive
deficits associated with anxiety is less conclusive, with
Leonard and Abramovitch [42] finding that elevated
primary anxiety may not impact cognitive functioning in
the absence of threat or substantial cognitive load. As
noted above, ADHD is associated with marked cognitive
deficits that may impair daily functioning; we nevertheless
hypothesized that self-reported dysfunction in pure ADHD
patients would be lower than those with GAD only, due to the
particularly inoculating effects of childhood onset and the
unlikelihood of mood symptoms and emotional processing
biases artificially inflating self-report at the moment of
data collection, as may be common with MDD, BPD, and
GAD patients. Our findings, which show comparatively low
dysfunction scores for pure ADHD patients, are consistent
with studies that have found ADHD symptomatology is not
always and only debilitating. Some adults with ADHD do
function well, thanks to adaptive and compensatory skills
and traits such as high intelligence, finding work that is well
suited to their symptom profile, and the potential likeability
of their chaotic and unpredictable personas, including the
tendency for some to divert their attention from individual
tasks toward helping behaviours [1, 10, 16]. Contrary to
our hypothesis, we did not find a statistically significant
difference in patient-reported dysfunction between pure
ADHD and GAD patients, but the difference in dysfunction
between GAD/ADHD and BPD/MDD was substantive.
In line with our second hypothesis, the compounding effect
of a comorbid ADHD diagnosis on dysfunction in patients
with MDD and BPD was relatively small compared to those
with GAD. We attribute this to a ceiling effect whereby
pure MDD and BPD dysfunction scores approach the peak
of the numeric scale (total score of 30, or 10 on each
subscale) and therefore the additive effects of typically
early-onset symptoms of ADHD—which, in line with
neurocognitive hypotheses of dysfunction, may also be less
likely to emotionally bias recall—might not significantly
register. Patients with anxiety, on the other hand, whose
self-rated dysfunction is relatively moderate, have more
room to experience and report additional dysfunction due
to the additive effects of ADHD symptoms. We expect a
ceiling effect would have tempered our results using other
disability scales as well; the World Health Organization
Disability Assessment Schedule (WHODAS 2.0), which
has demonstrated internal consistency and reliability,
nevertheless offers less granularity than the SDS with its
five-point Likert scale [43].
Moreover, the symptom profiles of GAD and ADHD are
complementary, and we might expect them to act
synergistically to increase dysfunction in comorbid
patients. For instance, some patients with both ADHD and
GAD may experience enhanced anxiety due to their selfperceived inability to control their impulses and refrain
from engaging in risky or socially unacceptable behaviour.
While there is evolutionary advantage to approach and
avoidance tendencies working in equilibrium to keep
behaviours in check, it seems reasonable that an excess of
both may create a short circuit of distress and dysfunction.
Additionally, as Michelini, Eley, Gregory, and McAdams
[44], ADHD may precipitate attention biases (worry,
rumination) toward threat stimuli and thereby reduce the
ability to attend to everyday activities in already-anxious
individuals.
While lower than that of MDD and BPD, the level of
dysfunction associated with ADHD among patients at our
clinic, as measured using the SDS, still represents significant
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Psychiatry and Clinical Psychopharmacology
impairment in daily life. These findings are consistent
with the literature, synthesized above, that suggests
ADHD symptoms can make daily tasks difficult. In addition,
dysfunction may not tell the whole story. Individuals with
ADHD who appear or claim to be functioning at a high level
may be chronically struggling to cope, particularly with
the exhaustion from lack of sleep and the effort required
to focus their thoughts [1, 5]. Moreover, while the early
onset of ADHD may inoculate individuals against selfperceived functional impairments due to ADHD symptoms,
the chronic course of these symptoms over many years may
nevertheless lead to low self-esteem and self-confidence,
subjective distress, and substance misuse [10, 20]. Plus,
while ADHD symptom severity typically declines with age,
adjustment difficulties often persist, even after remission
[4, 7].
At 46.7%, the overall prevalence of ADHD in our nonpsychotic clinical outpatients sample was higher than that
found in similar studies (14-22% [6, 45–48]). These elevated
rates may be partly attributable to the local reputation
of our clinic’s psychiatrists as experts in assessing and
treating ADHD and the concomitantly high referral rate
from general practitioners in the area seeking assessment
for suspected ADHD. These high rates may also reflect an
enhanced recognition of and sensitivity to adult ADHD
using DSM-5 criteria [5, 6, 10]. Overall, 60.9% of ADHD
patients had at least one comorbid condition, which is
comparable to the 65-89% found in previous studies [6,
49, 50], particularly considering that other potential
comorbidities, such as personality disorders, were not
included in our analysis. At 31.48%, GAD was the most
common comorbidity, followed by BPD (24.77%), MDD
(21.99%), and AUD (5.79%). Our prevalence of comorbid
GAD is comparable to other studies in the literature (23-
45% [6, 49, 51–54]), while BPD is significantly higher (8-14%
[6, 49, 51]) and MDD significantly lower (40-53% [6, 51, 52,
54]). Substance use disorder is difficult to compare, as we
only measured for alcohol use.
This study has several limitations. While a naturalistic
study is advantageous in its ability to capture dysfunction
in the real world without stringent exclusion criteria,
the main limitation is the lack of a healthy control group
with which to conduct a full factorial analysis. We were
also unable to control for confounding variables such as
medication use, and our prevalence measures may have
been biased by the potential for inflated referral rates
from general practitioners with a knowledge of our clinic’s
specialization in ADHD. This study was also cross-sectional
and correlational, and thus temporal factors such as the
age of onset of ADHD and its comorbidities could not be
accounted for, precluding causal inferences. Additionally,
we did not differentiate between subtypes of ADHD and
BPD, and this collapsing of subtypes limited the depth of
our analysis. As the clinic in which this study was conducted
is a non-urgent, tertiary centre, bipolar patients seen at
this clinic tend more often to exhibit BPD type-II than
type-I symptoms; we would expect BPD-II patients’ selfreports to moderate SDS scores, as BPD-II is associated
with less severe cognitive deficits compared to BPD-I [31].
We also did not log other, less common comorbidities, such
as personality disorders. Finally, while this was accounted
for in our hypotheses, self-report may be unreliable.
Despite these limitations, to our knowledge this is one of
the first studies to use a psychometrically validated scale
to measure patient-reported dysfunction in non-psychotic
clinical outpatients and to compare dysfunction between
pure and comorbid conditions.
CONCLUSION
Canadian adults with one of ADHD, GAD, BPD, or MDD
report significant illness-related dysfunction in their
daily lives, and this dysfunction is especially pronounced
in patients with MDD. Comorbid MDD, GAD, and BPD is
common alongside ADHD, and while the presence of ADHD
exacerbates dysfunction for those with MDD, GAD, or BPD,
these compounding effects appear to be most significant in
those with GAD and least pronounced in those with MDD.
These disparities may, in part, be attributable to ceiling
effects in self-report and the inoculating effects of earlyonset ADHD and GAD. With an increased awareness of,
and enhanced ability to detect, adult ADHD using DSM-5
criteria, the prevalence of diagnosed adult ADHD may be
on the rise.
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