Running head: Anxiety Disorder Research and Breakthroughs1

2

Anxiety Disorder Research

Anxiety Disorder Research and Breakthroughs

Chase G. Parnell

Huntington University

OUTLINE

ABSTRACT…………………………………………………Page 3

ESSAY………………………………………………………Page 4-10

REFERENCES…………………………………………… Page 11

APENDIX A (First study data)……………………………..Page 12-15

APENDIX B (Second study data)………………………......Page 16-19

APENDIX C (third study data)……………………………..Page 20-23

APENDIX D (Interview)…………………………………...Page 24-25

Abstract

This paper introduces three original studies conducted in recent years in regards to anxiety disorders. The first study is a longitudinal research study, conducted for the purpose of determining the genetic stability of anxiety disorders within individuals between the ages of 12-30 years old. The second study aims to determine once and for all whether cognitive behavioral therapy (CBT) is effective at treating anxiety disorders or not. The final study analyzes the predictive validity of automatic self-associations for the onset of anxiety disorders. Throughout the paper, each study will be explained in a certain order. First, the study’s goals will be briefly explained. Next, the method and limitations will be acknowledged and briefly explained. Finally, the results of the study will be explained in the terms of the researchers themselves and also in the context of the writer of this paper. The introduction will briefly explain anxiety disorders, and end with the thesis for the paper. The conclusion will sum up the results of the research and explain what these studies have contributed to the world of psychological science.

“The most common mental disorder reported by adults in the United States is any kind of anxiety disorder” (Kessler et al., 2005). Anxiety disorders can be defined as “all disorders in which the most dominant symptom is excessive or unrealistic anxiety” (Cicerelli & Meyer, 2007 pg.530). Many types of anxiety disorders plague society today, including (but not limited to): social phobias, obsessive compulsive disorder (OCD), panic disorder, generalized anxiety disorder (GAD) and post traumatic stress disorder (PTSD) (Cicerelli & Meyer). Recent research has shed some light on facts about anxiety disorders in regards to its root causes and also in its treatments. The research following will tackle three different anxiety questions: (1) are anxiety disorders genetically stable over time? (2) Is cognitive behavioral therapy truly an effective form of treatment? And (3) are automatic and/or deliberate self-associations useful predictors of the onset of anxiety disorders? Each of these studies addresses anxiety as it develops during the adolescent-early adulthood years. These studies prove that anxiety disorders are stable over time, effectively treated by CBT, and predictable by automatic/deliberate self-associations.

The first study is a longitudinal genetic analysis of anxiety sensitivity, which aimed to examine the stability of anxiety disorders genetically in adolescence (Zavos et al., 2012). “Anxiety sensitivity refers to sensitivity to the physical and emotional symptoms of anxiety and the belief that these are harmful” (Zavos et al., 2012 pg. 1). These researchers wanted to know whether anxiety was genetically stable throughout adolescence-early adulthood or not. Previous to this research, knowledge about anxiety genetic markers and their stability was limited. The study sought to prove whether or not anxiety disorders were a repressed trait within particular individuals. Basically, anxiety disorders only surface when environmental influences trigger the disorders; however, the question was whether these repressed disorders would remain dormant in an individual throughout adolescence and early adulthood or not. If not, then anxiety disorders would not be traits, and the triggering of anxiety disorders would be specifically limited to adolescent development. However, this study proved that this is not the case.

This study used thousands of adolescent participants, primarily through questionnaires sent to the adolescents. The study involved mostly genetic twins, both monozygotic and dizygotic (Zavos et al., 2012). It used four time intervals, between 1-2 years difference, in order to measure the stability of the anxiety disorder using the questionnaires (Zavos et. al., 2012). They asked questions based on typical anxiety disorder symptoms, which determined when anxiety disorders seemed to begin (Zavos et al., 2012) (see Appendix A).

There were many flaws in the design that are formally acknowledged by the writers of the study. Firstly, the “waves” of participants differed significantly in age, which made it “difficult to attribute the emergence of developmental influences to specific ages or stages of development” (Zavos et al., 2012 pg. 6). The second flaw lies in the reliance on questionnaires. The researchers admitted that questionnaires “may therefore fail to capture the intricacy of the phenotype in question” (Zavos et al., 2012 pg. 6). Despite their best efforts to recruit different study members for different waves, “there was also evidence of selective attrition. This was taken into account to some extent by using a weight that assigned greater value to those who were underrepresented in the sample and less to those who were overrepresented” (Zavos et al., 2012 pg. 6). Finally, their study was limited by the use of only twins. Issues with using only twins include: “chorionicity, the equal environments assumption, and generalizability” (Zavos et al., 2012 pg. 7).

The results of the study concluded that genetic factors involved with the development and blooming of anxiety disorders are stable and continuous throughout adolescent-young adulthood stages. They also proved that anxiety disorders are rooted in trait theory.

“Our finding of genetic continuity in individual measures of anxiety sensitivity and a latent factor of trait anxiety sensitivity suggests that genes are shared across development to a greater extent than they are specific. This supports the “generalist genes hypothesis” (Eley, 1997). This hypothesis posits that genetic factors act as general influences, with environmental factors resulting in specific manifestations of symptoms. Continuity of genetic influences and the overall influence of genes at each time point can be taken as support for trait theories of anxiety sensitivity.” (Zavos et al., 2012 pg. 7)

The research concludes that anxiety disorders are ultimately stable genetically, and only bloom from specific environmental forces that influence the individual’s anxiety to fluctuate out of control. Whether or not anxiety disorders are primarily genetic or environmental has not been determined by this study. The study also does not analyze anxiety disorder stability throughout all the stages, but merely proves the stability between the early stages of adolescence and early adulthood.

The second study tests the effectiveness of cognitive-behavioral therapy (CBT) on patients suffering from anxiety disorders (Chambless & Stewart, 2009). Cognitive-behavioral therapy, previous to this study, was supposedly proven to be very effective at treating anxiety disorders. However, the research did not test CBT effectiveness within the clinical environment that most CBT takes place. The previous studies used research treatments in controlled environments, not in clinical practice settings, which beg the question as to whether CBT is truly effective (Chambless & Stewart, 2009).

The method to the experiment involved using complex mathematical sequences to determine the effectiveness of CBT using certain codes. The mathematical equations and further details to the experiment can be found on Appendix B. Flaws to the experiment involve a “construct validity issue”. The specific way the researchers chose to use the coding sequence could be disagreed upon, and therefore subject to bias. “Another concern in meta-analysis is the quality of included research studies and the measures utilized to represent constructs” (Chambless & Stewart, 2009, pg. 8). In other words, the researchers are concerned that the studies they chose to base their research on and the measures they used to analyze the effectiveness of cognitive behavioral therapy might not be empirically valid. This suggests that the study must be further researched before a proper conclusion can take place. Finally, some researchers failed to report key characteristics of the patients, which are a key foundation for the research (Chambless & Steward, 2009, pg. 8).

This study managed to prove two important facts about cognitive-behavioral therapy. First of all, “These results are consistent with prior controlled research indicating that patients with anxiety disorders may improve more with standardized treatments than with therapist-generated treatment plans (Schulte, Kunzel, Pepping, & Schulte-Bahrenberg, 1992) and that therapists become more skilled at delivering an EST when they receive supervised training (Sholomskas et al., 2005)” (Chambless & Steward, 2009, pg. 7). In other words, standardized cognitive behavioral therapy has been proven to be more effective by this study. Therefore, any therapist using self-generated cognitive-behavioral therapy techniques or tests would not be as effective as a therapy conducted by a psychological association first.

More importantly, this study proved that cognitive-behavioral therapy is “robustly effective” at treating individuals with anxiety disorders (Chambless & Steward, 2009, pg. 8). However, the study did not test the effectiveness of cognitive-behavioral therapy on children with anxiety disorders or on individuals with other mental disorders (Chambless & Steward, 2009, pg. 8). Therefore, it’s safe to assume that cognitive-behavioral therapy has yet to be proven to be universally effective in mental disorder treatments. However, it’s also safe to assume that CBT is relatively useful in treating anxiety disorders, just as psychologists previously concluded.

The final study tests the predictive validity of automatic self-associations for the onset of anxiety disorders. This study researched the concept that automatic self-associations might predict the blooming of anxiety disorders later in life. For example, if an individual unconsciously assumes that snakes are dangerous, then the automatic self-association would be that physical closeness with a snake is scary, and someone would jump or instantly feel fear while being near a snake. Therefore, these self-associations would evolve into anxiety disorders eventually.

“In recent dual-process models, emphasis has been placed on the importance of distinguishing between more deliberate, rule-based (i.e., explicit) self-beliefs and more automatically activated associations (e.g., Gawronski & Bodenhausen, 2006). Automatic self-associations are assumed to be simple links between self and associated concepts in memory, which can be activated directly in response to relevant stimuli. Thus, it is thought that when an anxiety-relevant stimulus appears, it directly activates anxiety-related self-associations via the spreading of activation from one concept to associated concepts. These automatic associations are thought to influence more spontaneous behavioral responses toward threatening stimuli (e.g., Huijding & de Jong, 2006).” (Glashouwer et al., 2011, pg. 1)

The researchers also considered the possibility of deliberate self-associations in the onset of anxiety disorders. In other words, individuals who consciously teach themselves to fear something might unintentionally create an anxiety disorder out of that deliberate self-association. For example, if someone was bitten by a dog, they might learn to stay away from dogs. However, deliberate avoidance of dogs might trigger anxiety-related reactions to being in the presence of dogs. Therefore, the deliberate avoidance of dogs in response to being bitten will predict a future anxiety disorder relevant to the event with the dog. “These deliberate cognitions are thought to guide more controlled behaviors. Considering that anxiety symptoms include spontaneous as well as controlled behaviors, both deliberate and more automatic dysfunctional self-associations might play an important role in the cognitive vulnerability for developing anxious symptoms” (Glashouwer et al., 2011, pg. 1-2).

The researchers used a study sample, measuring both automatic and deliberate self-associations. “A total of 2,981 persons ages 18 through 65 years were included, including healthy controls; individuals at risk because of prior episodes, subthreshold symptoms, or family history; and individuals with a current first or recurrent depressive or anxiety disorder. The inclusion was restricted to major depressive disorder, dysthymia, general anxiety disorder, panic disorder, social phobia, and agoraphobia” (Glashouwer et al., 2011, pg. 2).

The results of the study conclude that “In line with what we expected, results showed that automatic as well as deliberate self-anxious associations were predictive of the onset of anxiety disorders between baseline and 2-year follow-up. Deliberate self-anxious associations predicted the onset of anxiety disorders in all groups, whereas automatic self-anxious associations were related to the onset of anxiety disorders in the remitted depression group and in currently depressed individuals” (Glashouwer et al, 2011, pg. 5). Therefore, deliberate self-associations actually proved to be more relevant to all types of anxiety disorders, whereas automatic self-anxious associations were only related to those with depression.

In conclusion, anxiety disorders are genetically stable over time, effectively treated by cognitive-behavioral therapy, and predictable through automatic and deliberate self-associations. These studies have substantially influenced perceptions about anxiety disorders as a whole. However, limitations to the experiments imply that none of the studies was perfect; therefore, these studies ought to be perceived as a glimpse into the complex reality of the science of anxiety disorders.

References

Chambless D. L., &, Stewart, R. E., (2009). Cognitive—Behavioral Therapy for Adult Anxiety

Disorders in Clinical Practice: A Meta-Analysis of Effectiveness Studies. Journal Of Consulting & Clinical Psychology, 77(4), 595-606. doi:10.1037/a0016032

Glashouwer, K. A., de Jong, P. J., & Penninx, B. H. (2011). Predictive Validity of Automatic Self-

Associations for the Onset of Anxiety Disorders. Journal Of Abnormal Psychology, 120(3), 607-616. doi:10.1037/a0023205

Kessler, R. C., Berglund, P., Demler, O., Jim, R., Merikangas, K. R., & Walters, E.E. (2005).

Lifetime prevalence and age0of-onset distributions of DSM-IV disorders in the national comorbidity survey replication. Archives of General Psychiatry, 62, 593-602

Zavos, H. S., Eley, T. C., & Gregory, A. M. (2012). Longitudinal Genetic Analysis of Anxiety

Sensitivity. Developmental Psychology, 48(1), 204-212. doi:10.1037/00024996

APENDIX A

Figure 1. Flow chart of participation in the G1219 study.

Phenotypic Correlations and Descriptive Statistics for Anxiety Sensitivity (Times 1– 3)

Within-Pair Twin and Sibling Correlations and Univariate Estimates for Anxiety Sensitivity at Times 1–3 [With 95% Confidence Intervals]

Model Fits for Multivariate Analysis

Parameter Estimates for Multivariate Longitudinal Genetic Models of Anxiety Sensitivity Between Times 1, 2, and 3 [With 95% Confidence Intervals]

Figure 2. Results for common pathway model. A = additive genetics; E = nonshared environment; T1, T2, and T3 = Time 1, Time 2, and Time 3.

APENDIX B

Effect Size Calculation and Statistical Procedures

Standardized mean gain

Standardized mean gain (pretest–posttest) effect sizes were computed for diagnosis-specific outcome measures. In addition, because generalized anxiety and depression symptoms are common complaints of patients with anxiety disorders and were often assessed, we computed effect sizes for these measures as well. For panic disorder, there were three disorder-specific symptom constructs: frequency of attacks, fear of fear, and avoidance measures. For OCD, social anxiety disorder, and PTSD, there was one disorder-specific construct. In the special case of GAD, generalized anxiety measures were used as diagnosis-specific outcome measures. Because of the paucity of intent-to-treat data (4 studies out of 56), completer data were used in this study. We calculated Cohen’s d for the pretest–posttest effect sizes using the pooled standard deviation (see Dunlap, Cortina, Vaslow, & Burke, 1996).

The effect size was adjusted to yield Hedges’s g (Hedges, 1981) and weighted to account for sample size. The weights were based on the standard errors of effect size (Lipsey & Wilson, 2001). The standard error formula for repeated measures requires the use of the correlation r between pretest and posttest measures. This value was never reported in the studies, although it is possible to derive a value of r from the means, standard deviations, and the paired t-test value with the following formula (D. Wilson, personal communication, February 27, 2008):  

However, only one fourth of the studies reported a paired t-test between pretest and posttest conditions. These rs were calculated, converted to z, averaged, and converted back to r to deduce an overall correlation r to be used in following calculations (r = .41). We also did a sensitivity analysis by repeating the analyses with correlation rs of .2 and .6, and we found that the results did not differ substantially. The results of the sensitivity analysis are presented in the supplemental materials on the journal’s website. On the basis of the averaged r, the standard error for each effect size for each study was calculated as follows (Lipsey & Wilson, 2001):  

Lastly, we calculated the weights of each effect size using the inverse variant weight, which is the reciprocal of the squared standard error:

 

Given the heterogeneity of the sample (see below), a priori random effects meta-analyses proceeded as follows. The effect size, standard error, and inverse variance weights were calculated for each construct measured in the study: the disorder-specific constructs, as well as generalized anxiety and depression. The weighted mean effect size for each construct was computed for each disorder, according to the formula:

 

The standard error of each weighted mean effect size was also calculated:

Effectiveness Pretest–Posttest Effect Sizes by Disorder

Benchmark Efficacy Studies by Disorder Versus Current Effectiveness Results: Pretest–Posttest Effect Sizes

APENDIX C

Arrangement of the Different Implicit Association Test Blocks

Means and Standard Deviations of the Self-Report and Automatic Measures at Baseline as a Function of Group

Correlation Matrix of Predictors at Baseline in Healthy Controls, Depressed Individuals, and Individuals With Remitted Anxiety Disorder (N = 1,279)

Single and Multiple Predictor Logistic Regression Models for Prediction of Onset of Anxiety Disorders Between Baseline and 2-Year Follow-Up in Healthy Controls and Individuals With Remitted Anxiety Disorder

Single and Multiple Predictor Logistic Regression Models for Prediction of Onset of Anxiety Disorders Between Baseline and 2-Year Follow-Up in Depressed Individuals With and Without a History of Anxiety Disorder

Single and Multiple Predictor Multinominal Regression Analyses for Prediction of Onset of Anxiety Disorders Between Baseline and 2-Year Follow-Up in Healthy Controls, Depressed Individuals and Individuals With Remitted Anxiety Disorder (N = 1,279)

single and Multiple Predictor Multinominal Regression Analyses for Prediction of Onset of Anxiety Disorders Between Baseline and 2-Year Follow-Up in Healthy Controls, Depressed Individuals and Individuals With Remitted Anxiety Disorder (N = 1,279)

Interview

Subject: Magdalena Silva

21 years old, Female

1. Q: What kind of anxiety do you have?

A: I’m not diagnosed, but I think I have a form of social anxiety

2. Q: When do you experience anxiety?

A: Around people, especially strangers. Acuintences still make me feel anxious or nervous too. I’m only comfortable around friends and family that know my secret, that I can trust.

3. Q: What makes you think your anxiety is unusual? Why do you think it is a disorder?

A: My thoughts when I experience anxiety are always irrational; I always think people are judging me, and I can’t stop worrying about their judgment. It’s a disorder because the symptoms are the same every time.

4. Q: What if you do make a bad first impression on people?A: I avoid that person as much as possible. If I have to be around them, I worry about making another bad impression.

5. Q: How does your anxiety impact your life at work and school?

A: It’s hard to make friends. It’s difficult if you don’t take risks that you need to in order to make new friends.

6. Q: How do you cope?

A: I avoid situations that involve meeting people as much as possible. I get depressed when I miss opportunities to make friends, or want to get information from a teacher and I’m afraid to ask the teacher.

7. Q: Do you think it’s irrational to worry so much about being judged?

A: Yes, I hate it. I know it’s irrational, but I can’t help but worry.

8. Q: What are the symptoms?

A: My heart races, I can’t organize my thoughts, stumble with words, shaking, sweating, goosebumps.

9. Q: Do you think you can get help for this?

A: I hope so, although I’m not really sure. I’m scared to get help for my anxiety because of my anxiety, so that makes it hard to know for sure.

10. Q: Do you have any plans in the future for trying to overcome your anxiety?

A: Yes, I’ve already bought some self-help books. I might visit a psychologist some day if my anxiety is still really bad later in life, but for not I’m trying to fix it on my own.

[Summary]

While interviewing Magdalena, she seemed a little nervous, even though I’ve known her for a very long time now. She wasn’t nervous because of me, though; she was nervous because she was worried what people reading this interview might think. I enjoyed talking to her about this, because it shed some light as to how people live with anxiety, and how much of a burden it is to people. She answered all of my questions extra-thoroughly, being very careful not to say anything that wasn’t 100% accurate.

I guess this goes to show how influential and inhibiting anxiety disorders can be in peoples’ lives. Magdalena surely has some kind of social anxiety, but I know that her anxiety could be a lot worse. Her answers have allowed me to visualize the burden of anxiety in everyday life. She was nervous throughout the interview, but in the end I think she was happy to share this with me, and the people who read this paper.