Comorbidity in social phobia by mikeholy



                                       Comorbidity in social anxiety disorder

                                                    Lydia Fehm

                                               Hans-Ulrich Wittchen

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Comorbidity                             18        12      Fehm, Lydia, Dresden, Germany
Other anxiety disorders, depression,                      Wittchen, H.U., Dresden, Germany
alcohol and substance abuse, eating
disorders, essential tremor…

Dr. Lydia Fehm, Dipl.-Psych.
Dresden University of Technology
Clinical Psychology and Psychotherapy
Chemnitzer Str. 46
D - 01187 Dresden
Phone: +49 - (0)351 - 463-36989
Fax: +49 - (0)351 - 463-36984

Prof. Dr. Hans-Ulrich Wittchen; Dipl.-Psych.
Dresden University of Technology
Clinical Psychology and Psychotherapy
Chemnitzer Str. 46
D - 01187 Dresden
Phone: +49 - (0)351 - 463-36983
Fax: +49 - (0)351 - 463-36984

I. Concepts and Definitions

During the last two decades comorbidity of psychiatric disorders has gained increasing

interest both on the scientific level as well as on the therapeutic. On a very broad level

comorbidity can be defined as the co-occurrence of problems in a person. Having been poorly

conceptualized and lacking clear definitions at first, there seems to be growing convergence in

definitions and operationalizations of the term - at least there is convergence in the statement

that a clear and differentiated definition is essential for yielding meaningful and interpretable

results. Many sources of possibly influential factors have to be considered:

1) the unit in question: Does comorbidity relate to disorders according to a defined

classification system (e.g. ICD-10 or DSM-IV) or subthreshold or other syndromes or

symptoms? Are subtypes of diagnoses taken into consideration? When classification systems

are used, which of the possible diagnoses are included, e.g. are only axis-I disorders included

or is the focus extended to personality disorders and somatic disorders as well? Are

hierarchical rules applied within the classification system?

2) time window: What is the time frame for stating co-occurrence, e.g. two weeks, two years

or the whole lifespan?

3) assessment: How are the units in question determined, e.g. by loosely structured clinical

diagnoses or by standardized diagnostic instruments?

4) methodological issues during statistical analyses and interpretation: What were the

sampling procedures? Were differing base rates corrected? How were possible confounding

factors be dealt with?

Existing definitions of comorbidity differ in at least some of the issues described above: A

first definition referred to treatment outcome of specific disease entities and follow-up studies

(1). A focus on methodological aspects was laid in the definition of comorbidity as the

relative risk for a person with one disorder to acquire another disorder (2). Burke et al. (3)

provided an influential definition of comorbidity comprising a clear definition of the unit in

question, enlarging the time-frame to a possible lifetime perspective, but concretely defining

the inspected interval for each statement. Accordingly, comorbidity is defined as "the

presence of more than one specific disorder in a person in a defined period of time" (3). More

recently even more detailed definitions emerged, e.g. by separating co-occurrence from

lifetime comorbidity (4) or delimiting as much as four different forms of comorbidity (5). For

the present contribution we will rely on the definition provided by Burke et al. (3).

It should be noted that the definition does not provide an explanation for the pattern of co-

occurrence. Three possible approaches can be differentiated:

1) Disorder X is an explicit cause for disorder Y, so disorder Y would be a direct consequence

of disorder X. In the ongoing discussion of possible causal patterns of comorbidity this would

be called the "splitters perspective" (e.g. (6).

2) Disorder X is an indirect cause for disorder Y, for example by lowering the threshold for

disorder Y.

3) Disorder X as well as disorder Y are caused by a third common factor, e.g. a genetic

vulnerability for XY-disorders. This variant is proposed with the "lumpers perspective" (see


To explore these patterns is a great challenge and it should also be noted that the three

patterns are not exclusive but may also overlap or interact as well as that different causal

patterns may be responsible during the course of the disorder (e.g onset versus fluctuations in


In the present contribution we will first present cross-sectional results assessing lifetime

comorbidity retrospectively. Few but very interesting studies using longitudinal designs allow

to determine temporal patterns of comorbidity, which will be presented in section IV. In a last

section we will discuss implications of comorbidity for the course of social anxiety disorder

as well as for treatment outcome.

II. Cross-sectional designs

Overall, comorbidity seems to be rather the rule than the exception - which is true not only for

social anxiety disorder but also for the majority of other psychiatric disorders. For social

anxiety disorder, epidemiological studies yield lifetime comorbidity rates with any other

psychiatric disorder between 69% (7) and 81% (8). A primary care study provided

comparable results (81%, (9)). Data drawn from clinical samples are hampered by a help-

seeking bias, as it is well known that especially for social anxiety disorder patients

comorbidity is a major cause for seeking professional help ((7), (10) .

Three groups of disorders proved to be strongly associated with social anxiety disorder: other

anxiety disorders, affective disorders and substance problems, which will be presented in the


A. other anxiety disorders

Epidemological studies find as much as about 50% of persons with social anxiety disorder

reporting at least one other anxiety disorder (57%, (8); 50%, (11)). Much lower rates are

reported for the ECA (9.1, (12)) and in the French primary care study (19.2, (13).

On the level of single disorders, high comorbidity rates are reported for specific phobia

("Zürich Study": 50%, OR: 5.8, (14), (15); ECA: 60.8%, OR: 8.3, (16); ECA": 59.0%, OR:

9.2, (7); NCS: 37.6%; OR: 7.6, (8); EDSP: 43.6%; OR: 3.7, (11), as well as for agoraphobia

("Zürich Study": 29%, OR: 16.7, (15); ECA: 45%, OR: 6.3, (16); ECA2: 45%, OR: 11.8, (7);

NCS: 23.3%, OR: 7.1, (8); "Bremer Jugendstudie": 23.5%, OR not reported, (17); EDSP:

8.8%, 5.5, (11)) and panic disorder ("Zürich study": 26.9%, OR: 3.1, (14); (15); ECA: 11.6%,

OR: 10.6, (16), ECA2: 4.7%, OR: 3.2, (7); NCS: 10.9%, OR: 4.8, (8); EDSP: 6.2%, OR: 4.7,

(11)). Somewhat lower rates are reported for generalized anxiety disorder (2 - 27%; (11), (8);

(16)), obessessive-compulsive disorder (2 - 19%; (11), (16), (7)), and post-traumatic stress

disorder (5 - 16%; (11), (8); (16)).

When differentiating between the generalized and non-generalized subtype of social anxiety

disorder, it can be noted that the generalized subtype is characterized not only by higher

degrees of impairment and higher help-seeking rates (18) but also by stronger comorbidity


B. Affective disorders

Affective disorders are found to be the second most important group of comorbid disorders

with a comorbidity rate of 41% (8) when social anxiety disorder is taken as the index

disorder. When differentiating the respective single disorders, major depression and

dysthymia exert a more prominent influence than disorders of the bipolar spectrum (e.g.

16.6% of all respondents having lifetime comorbid major depression, 12.5% comorbid

dysthymia, but only 4.7% bipolar disorder (7), similar relations are reported within the NCS:

37.2% major depression, 14.6% dysthymia, 5.1% Mania (8); EDSP: 25.5% Major depression,

10.9% dysthymia (11);

But also studies examining social anxiety disorder as comorbid condition within affective

disorders point to social anxiety disorder as intimately associated especially with depression

((10),(20), (21), (22).

As for other anxiety disorders pure speaking phobias, corresponding to the non-generalized

subtype of social anxiety disorder, are associated with a significant lower risk for comorbidity

((18); (19)).

C. alcohol and substance abuse

Alcohol and substance use problems have been idenitified as a third group of disorders

frequently associated with social anxiety disorder. We will also include nicotine problems in

this section, but most studies are available for alcohol problems. In epidemiological samples

those reporting alcohol misuse or dependence at any time in their life add up to 12 to 28%

((23); (7); (16); (24); (8)). For illegal substances somewhat lower percentages are found

ranging between 5 and 13% ((23), (7), (8)). As expected, in clinical samples associations

between social anxiety disorder and alcohol dependence are even stronger, resulting in an

average rate of 25% of patients with social anxiety disorder showing lifetime alcohol

dependence (25).

In contrast to anxiety and affective disorders the generalized and non-generalized subtype

seem not to differ with regard to the degree of comorbidity with substance problems ((18);


D. Eating disorders

Eating disorders seem to deserve special interest, as among patients with eating disorders

social anxiety disorder seems to be the most prevalent comorbid condition (e.g. 55% among

patients with anorexia nervosa, 45 - 59% among bulimics, and 36.4% in obese binge eaters;

(26, 27). Epidemiological studies point to other relations: In a representative sample of

adolescents and young adults no significant relationship between social anxiety disorder and

eating disorders could be established (OR=1.99; 95%CI=0.93-4.27; (11)). The "Zürich-Study"

provided a similar association of social anxiety disorder and binge eating (OR = 2.8), but

provided not confidence interval to judge statistical significance (15).

E. bodydysmorphic disorder

Only recently attention was drawn to the relation of social anxiety disorder to body

dysmorphic disorder (BDD) (e.g. (28), (29). BDD is a debilitation and chronic disorder

characterized by imagined defect in appearance ((30, 31). Studies indicate a strong association

of BDD and social anxiety disorder, with a prevalence of social anxiety disorder among

BDD-subjects between 10 and 23% ((32); (29), (33)) and similarities to social anxiety

disorder even on the level of information processing (34). Social anxiety disorder was shown

to precede BDD in most to all cases (80% (35), 100% (33).

F. Somatic disorders

Only a fragmentary picture exists for the relation of social anxiety disorder and somatic

disorders. Results from the ECA (16) revealed elevated risks of participants with social

anxiety disorder for peptic ulcer disease (OR: 2.0, CI95%: 1.1 - 3.6) and neurological

disorders (OR: 3.0, CI 95%: 1.1 - 13.8). It should be noted that no significant association

emerged for the other eleven chronic medical conditions assessed in the study. As similar

picture emerges within a more recent study in an representative adult sample in the

community (YYFehm & Jacobi, unpublished data; for a description of the study see (36)).

Table XX reveals significant associations of social anxiety disorder with ulcers, endocrine

disorders and musculo-skeletal diseases. Whereas neurological disorders as a group showed

no significant association with social anxiety disorder, Parkinson´s disease alone was

significantly more prevalent in social anxiety disorder. It has to be noted that except for

Parkinson´s disease these associations may not be specific pathological patterns for social

anxiety disorder but may rather reflect a stronger association of mental and somatic problems

also inherent in other psychiatric disorders

Table XX

Comorbidity of social anxiety disorder and selected somatic disorders in a representative adult

sample (12-month prevalence rate; N = 4170)

Somatic disorder                                        prevalence (%) OR             CI 95%

                                                        no        SAD


Hypertension                                            13.1      11.0    .91         .43 - 1.90

Cardiac diseases, e.g. angina pectoris                  2.95      1.24    .46         .10 - 2.21

cerebrovascular diseases, e.g. stroke                   0.8       1.1     1.66        .21 - 13.13

chronic-obstructive pulmonal diseases, e.g. asthma      7.5       12.8    1.81        .93 - 3.53

ulcers, gastritis                                       7.5       15.7    2.24 **     1.23 - 4.10

Endocrine disorders, e.g. thyroid gland disesase        11.3      23.1    2.05 **     1.16 - 3.61

Metabolic syndromes, e.g. high cholesterol              14.5      20.7    1.93        .98 - 3.81

Neurological diseases, e.g. migraine                    10.7      17.2    1.50        .85 - 2.65

  Parkinson´s disease alone                             .07       .78     14.31 **    1.07 - 191.44

Musculo-skeletal diseases, e.g. different forms of      26.3      33.9    1.81 **     1.08 - 3.05


Allergies, e.g. hay fever, neurodermatitis              23.8      28.5    1.12        .68 - 1.84

Any somatic disorder                                    69.91     77.96 1.56          .83 - 2.94

Note. Abbreviations: SAD: Social Anxiety Disorder; OR: Odds Ratio; CI: Confidence

Interval; **: p < .05

A detailed analysis was made exploring the relationship between social anxiety disorder and

essential tremor, inspecting social anxiety disorder both preceding and following the onset of

essential tremor (37). Whereas 21.6% of essential tremor cases had a lifetime diagnosis of

social anxiety disorder, its onset occurred about as often before the onset of essential tremor

as after it. Much higher rates of social anxiety disorder were found among patients with

spasmodic torticollis, characterized by intermittent or sustained deviations of the head and

neck. As much as 41.3% of the patients with spasmodic torticollis also met criteria for current

social anxiety disorder (38). The vast majority (80%) reported the onset of social anxiety

disorder occurring after the onset of spasmodic torticollis.

IV. temporal patterns of comorbidity

When taking lifetime comorbidity as a basis, two stages of influence for comorbid disorders

can be delimited within the developmental model of social anxiety disorder (see figure 1):


please insert figure 1 about here


Pre-existing disorders may promote the development of social anxiety disorder at all as well

as its onset and presentation. Comorbid disorders beginning after the onset of social anxiety

disorder may influence the course of social anxiety disorder as well as presentation, general

impairment and help-seeking behaviour. As a third variant of course the concurrence of the

two disorders with or without a common etiological basis has to be considered. This

possibility is limited by the temporal resolution used in the study: As normally age of onset is

assessed in years, it is not possible to differentiate persons experiencing an onset of social

anxiety disorder in January and an onset of depression in November from those in the reverse

order. Some studies even use two years for assigning temporal co-occurrence (e.g. (39).

Data point to the second of the three possibilities to be the most frequent form of co-

occurrence: This is true for anxiety disorders ((7), (8), (40)), with the exception of specific

phobia developing more often before the onset of social anxiety disorder than after it (41) as

well as for depressive disorders (9); (42); (43); (7); (39); (10), (22)). Figure 2 shows results

from selected studies depicting temporal relations between the onsets of social phobia and



please insert figure 2 about here


As can be seen, social anxiety disorder precedes depressive disorders as well dysthymia in the

majority of cases, but which is not true for bipolar disorders.

Most studies providing insight in temporal patterns rely on retrospective data, which may be

object to recall biases. Only longitudinal studies allow to control those possible sources of

error. One of those studies compared cases with social anxiety disorder without current or

previous depression at baseline to persons with no mental disorders and found a significantly

higher risk (OR = 3.5, CI95%: 2.0 - 6.0) for cases with social anxiety disorder to develop a

depressive episode during the follow-up period of about for years (44). Persons with social

anxiety disorder and depressive disorder at baseline were at a significantly higher risk for

experiencing new depressive episodes or higher persistence of present episodes (OR = 2.3; CI

95%: 1.2 - 4.6). A prospective study examining the temporal pattern of social anxiety disorder

and alcohol problems found no significantly higher risk for individuals with social anxiety

disorder to develop alcohol abuse or dependence. But subthreshold social anxiety disorder

lead to significantly increased risks to develop heavy drinking (OR: 2.41) as well as alcohol

abuse/dependence (OR. 2.30; (12). This may point to alcohol as a means to cope with social

situations which are already avoided by individuals with full-blown social anxiety disorder. In

contrast to these findings in an adult sample, a prospective longitudinal study among

adolescents and young adults identified social anxiety disorder at baseline as a significant

predictor of regular as well as hazardous use of alcohol as well as of the persistence of already

existing alcohol dependence (45).

V: implications of comorbidity / prognostic issues

Comorbidity may influence the natural course of the disorder as well as help-seeking

behaviour and treatment response. In epidemiological studies retrospectively assessing

predictors of the course of social anxiety disorder comorbidity was associated with an

unfavourable course of social anxiety disorder ((46); (16), whereas follow-up studies

investigating treated patients could not affirm these relationships ((47); (48). In contrast,

comorbidity exerts a major influence on help-seeking behaviour ((10); (49). The role of

comorbidity for treatment response, in turn, has not been extensively researched. The level of

pretreatment depression was identified as predictor for treatment outcome (50) as well as

treatment groups with either comorbid anxiety or depressive disorders had higher post-

treatment scores in impairment (51). But when considering the fact that comorbid individuals

were more impaired already before treatment results inspecting differential treatment rates did

not differ accordingly.

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