PHQ-9 & GAD-7 Data in a National Survey about COVID-19 Restrictions in Australia

Research paper Title

Patient Health Questionnaire 9 (PHQ-9) and General Anxiety Disorder 7 (GAD-7) data contributed by 13,829 respondents to a national survey about COVID-19 restrictions in Australia.

Background

While the Patient Health Questionnaire 9 (PHQ-9) and General Anxiety Disorder 7 (GAD-7) are frequently used in mental health research, few studies have reported comprehensive data on these measures from population or community samples.

The aim of this study was to describe gender- and age-specific PHQ-9 and GAD-7 item and summary data contributed by those who completed this survey.

Methods

The PHQ-9 and GAD-7 were used as indicators of symptoms of depression and anxiety in a national online anonymous survey to assess the mental health of adults in Australia during the COVID-19 restrictions.

Data were analysed descriptively.

Results

Complete survey responses were contributed by 13,829 people.

For both measures, item-by-item results, summary statistics (mean, standard deviation, minimum, maximum, median and interquartile range) and prevalence of severity categories are reported for the whole sample, and disaggregated by gender and age groups.

Conclusions

These comprehensive data provide a useful point of comparison for future COVID-19-related or other research among population or community samples.

Other researchers are encouraged to report detailed PHQ-9 and GAD-7 data in the future, to enable and promote relevant between-group comparisons.

Reference

Stocker, R., Tran, T., Hammarberg, K., Nguyen, H., Rowe, H. & Fisher, J. (2021) Patient Health Questionnaire 9 (PHQ-9) and General Anxiety Disorder 7 (GAD-7) data contributed by 13,829 respondents to a national survey about COVID-19 restrictions in Australia. Psychiatry Research. doi: 10.1016/j.psychres.2021.113792. Online ahead of print.

What is Generalised Anxiety Disorder (GAD)?

Introduction

Generalised anxiety disorder (GAD) is an anxiety disorder characterised by excessive, uncontrollable and often irrational worry about events or activities. Worry often interferes with daily functioning, and sufferers are overly concerned about everyday matters such as health, finances, death, family, relationship concerns, or work difficulties. Symptoms may include excessive worry, restlessness, trouble sleeping, exhaustion, irritability, sweating, and trembling.

Symptoms must be consistent and ongoing, persisting at least six months, for a formal diagnosis of GAD. Individuals with GAD often suffer from other disorders including other psychiatric disorders (e.g. major depressive disorder), substance use disorder, obesity, and may have a history of trauma or family with GAD. Clinicians use screening tools such as the GAD-7 and GAD-2 questionnaires to determine if individuals may have GAD and warrant formal evaluation for the disorder. Additionally, sometimes screening tools may enable clinicians to evaluate the severity of GAD symptoms.

GAD is believed to have a hereditary or genetic basis (e.g. first-degree relatives of an individual who has GAD are themselves more likely to have GAD) but the exact nature of this relationship is not fully appreciated. Genetic studies of individuals who have anxiety disorders (including GAD) suggest that the hereditary contribution to developing anxiety disorders is only approximately 30-40%, which suggests that environmental factors may be more important to determining whether an individual develops GAD.

The pathophysiology of GAD implicates several regions of the brain that mediate the processing of stimuli associated with fear, anxiety, memory, and emotion (i.e. the amygdala, insula and the frontal cortex). It has been suggested that individuals with GAD have greater amygdala and medial prefrontal cortex (mPFC) activity in response to stimuli than individuals who do not have GAD. However, the relationship between GAD and activity levels in other parts of the frontal cortex is the subject of ongoing research with some literature suggesting greater activation in specific regions for individuals who have GAD but where other research suggests decreased activation levels in individuals who have GAD as compared to individuals who do not have GAD.

Traditional treatment modalities include variations on psychotherapy (e.g. cognitive-behavioural therapy (CBT)) and pharmacological intervention (e.g. citalopram, escitalopram, sertraline, duloxetine, and venlafaxine). CBT and selective serotonin reuptake inhibitors (SSRIs) are the respectively predominant psychological and pharmacological treatment modalities; other treatments (e.g. selective norepinephrine reuptake inhibitors (SNRIs)) are often considered depending on individual response to therapy. Areas of active investigation include the usefulness of complementary and alternative medications (CAMs), exercise, therapeutic massage and other interventions that have been proposed for study.

Estimates regarding prevalence of GAD or lifetime risk (i.e. lifetime morbid risk (LMR)) for GAD vary depending upon which criteria are used for diagnosing GAD (e.g. DSM-5 vs ICD-10) although estimates do not vary widely between diagnostic criteria. In general, ICD-10 is more inclusive than DSM-5, so estimates regarding prevalence and lifetime risk tend to be greater using ICD-10. In regard to prevalence, in a given year, about two (2%) percent of adults in the United States and Europe have been suggested to suffer GAD. However, the risk of developing GAD at any point in life has been estimated at 9.0%. Although it is possible to experience a single episode of GAD during one’s life, most people who experience GAD experience it repeatedly over the course of their lives as a chronic or ongoing condition. GAD is diagnosed twice as frequently in women as in men.

Diagnosis

DSM-5 Criteria

The diagnostic criteria for GAD as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (2013), published by the American Psychiatric Association, are paraphrased as follows:

  1. “Excessive anxiety or worry” experienced most days over at least six (6) month and which involve a plurality of concerns.
  2. Inability to manage worry.
  3. At least three (3) of the following occur:
    • Restlessness.
    • Fatigability.
    • Problems concentrating.
    • Irritability.
    • Muscle tension.
    • Difficulty with sleep.
    • Note that in children, only one (1) of the above items is required.
  4. One experiences significant distress in functioning (e.g. work, school, social life).
  5. Symptoms are not due to drug abuse, prescription medication or other medical condition(s).
  6. Symptoms do not fit better with another psychiatric condition such as panic disorder.

No major changes to GAD have occurred since publication of the Diagnostic and Statistical Manual of Mental Disorders (2004); minor changes include wording of diagnostic criteria.

ICD-10 Criteria

The 10th revision of the International Statistical Classification of Disease (ICD-10) provides a different set of diagnostic criteria for GAD than the DSM-5 criteria described above. In particular, ICD-10 allows diagnosis of GAD as follows:

  • A period of at least six months with prominent tension, worry, and feelings of apprehension, about everyday events and problems.
  • At least four symptoms out of the following list of items must be present, of which at least one from items (1) to (4).
    • Autonomic arousal symptoms:
      • (1) Palpitations or pounding heart, or accelerated heart rate.
      • (2) Sweating.
      • (3) Trembling or shaking.
      • (4) Dry mouth (not due to medication or dehydration).
    • Symptoms concerning chest and abdomen:
      • (5) Difficulty breathing.
      • (6) Feeling of choking.
      • (7) Chest pain or discomfort.
      • (8) Nausea or abdominal distress (e.g. churning in the stomach).
    • Symptoms concerning brain and mind:
      • (9) Feeling dizzy, unsteady, faint or light-headed.
      • (10) Feelings that objects are unreal (derealization), or that one’s self is distant or “not really here” (depersonalization).
      • (11) Fear of losing control, going crazy, or passing out.
      • (12) Fear of dying.
    • General symptoms:
      • (13) Hot flashes or cold chills.
      • (14) Numbness or tingling sensations.
    • Symptoms of tension:
      • (15) Muscle tension or aches and pains.
      • (16) Restlessness and inability to relax.
      • (17) Feeling keyed up, or on edge, or of mental tension.
      • (18) A sensation of a lump in the throat or difficulty with swallowing.
    • Other non-specific symptoms:
      • (19) Exaggerated response to minor surprises or being startled.
      • (20) Difficulty in concentrating or mind going blank, because of worrying or anxiety.
      • (21) Persistent irritability.
      • (22) Difficulty getting to sleep because of worrying.
  • The disorder does not meet the criteria for panic disorder (F41.0), phobic anxiety disorders (F40.-), obsessive-compulsive disorder (F42.-) or hypochondriacal disorder (F45.2).
  • Most commonly used exclusion criteria: not sustained by a physical disorder, such as hyperthyroidism, an organic mental disorder (F0) or psychoactive substance-related disorder (F1), such as excess consumption of amphetamine-like substances, or withdrawal from benzodiazepines.[21]

See ICD-10 F41.1

Note: For children different ICD-10 criteria may be applied for diagnosing GAD (see F93.80).

History of Diagnostic Criteria

The American Psychiatric Association introduced GAD as a diagnosis in the DSM-III in 1980, when anxiety neurosis was split into GAD and panic disorder. The definition in the DSM-III required uncontrollable and diffuse anxiety or worry that is excessive and unrealistic and persists for 1 month or longer. High rates in comorbidity of GAD and major depression led many commentators to suggest that GAD would be better conceptualised as an aspect of major depression instead of an independent disorder. Many critics stated that the diagnostic features of this disorder were not well established until the DSM-III-R. Since comorbidity of GAD and other disorders decreased with time, the DSM-III-R changed the time requirement for a GAD diagnosis to 6 months or longer. The DSM-IV changed the definition of excessive worry and the number of associated psychophysiological symptoms required for a diagnosis. Another aspect of the diagnosis the DSM-IV clarified was what constitutes a symptom as occurring “often”. The DSM-IV also required difficulty controlling the worry to be diagnosed with GAD. The DSM-5 emphasized that excessive worrying had to occur more days than not and on a number of different topics. It has been stated that the constant changes in the diagnostic features of the disorder have made assessing epidemiological statistics such as prevalence and incidence difficult, as well as increasing the difficulty for researchers in identifying the biological and psychological underpinnings of the disorder. Consequently, making specialized medications for the disorder is more difficult as well. This has led to the continuation of GAD being medicated heavily with SSRIs.

Risk Factors

Genetics, Family and Environment

The relationship between genetics and anxiety disorders is an ongoing area of research. It is broadly understood that there exists an hereditary basis for GAD, but the exact nature of this hereditary basis is not fully appreciated. While investigators have identified several genetic loci that are regions of interest for further study, there is no singular gene or set of genes that have been identified as causing GAD. Nevertheless, genetic factors may play a role in determining whether an individual is at greater risk for developing GAD, structural changes in the brain related to GAD, or whether an individual is more or less likely to respond to a particular treatment modality. Genetic factors that may play a role in development of GAD are usually discussed in view of environmental factors (e.g. life experience or ongoing stress) that might also play a role in development of GAD. The traditional methods of investigating the possible hereditary basis of GAD include using family studies and twin studies (there are no known adoption studies of individuals who suffer anxiety disorders, including GAD). Meta-analysis of family and twin studies suggests that there is strong evidence of a hereditary basis for GAD in that GAD is more likely to occur in first-degree relatives of individuals who have GAD than in non-related individuals in the same population. Twin studies also suggest that there may be a genetic linkage between GAD and major depressive disorder (MDD), which may explain the common occurrence of MDD in individuals who suffer GAD (e.g. comorbidity of MDD in individuals with GAD has been estimated at approximately 60%). When GAD is considered among all anxiety disorders (e.g. panic disorder, social anxiety disorder), genetic studies suggest that hereditary contribution to the development of anxiety disorders amounts to only approximately 30-40%, which suggests that environmental factors are likely more important to determining whether an individual may develop GAD. In regard to environmental influences in the development of GAD, it has been suggested that parenting behaviour may be an important influence since parents potentially model anxiety-related behaviours. It has also been suggested that individuals who suffer GAD have experienced a greater number of minor stress-related events in life and that the number of stress-related events may be important in development of GAD (irrespective of other individual characteristics).

Studies of possible genetic contributions to the development of GAD have examined relationships between genes implicated in brain structures involved in identifying potential threats (e.g. in the amygdala) and also implicated in neurotransmitters and neurotransmitter receptors known to be involved in anxiety disorders. More specifically, genes studied for their relationship to development of GAD or demonstrated to have had a relationship to treatment response include:

  • PACAP (A54G polymorphism): remission after 6 month treatment with Venlafaxine suggested to have a significant relationship with the A54G polymorphism (Cooper et al. (2013)).
  • HTR2A gene (rs7997012 SNP G allele): HTR2A allele suggested to be implicated in a significant decrease in anxiety symptoms associated with response to 6 months of Venlafaxine treatment (Lohoff et al. (2013)).
  • SLC6A4 promoter region (5-HTTLPR): Serotonin transporter gene suggested to be implicated in significant reduction in anxiety symptoms in response to 6 months of Venlafaxine treatment (Lohoff et al. (2013)).

Pathophysiology

The pathophysiology of GAD is an active and ongoing area of research often involving the intersection of genetics and neurological structures. GAD has been linked to changes in functional connectivity of the amygdala and its processing of fear and anxiety. Sensory information enters the amygdala through the nuclei of the basolateral complex (consisting of lateral, basal and accessory basal nuclei). The basolateral complex processes the sensory-related fear memories and communicates information regarding threat importance to memory and sensory processing elsewhere in the brain, such as the medial prefrontal cortex and sensory cortices. Neurological structures traditionally appreciated for their roles in anxiety include the amygdala, insula and orbitofrontal cortex (OFC). It is broadly postulated that changes in one or more of these neurological structures are believed to allow greater amygdala response to emotional stimuli in individuals who have GAD as compared to individuals who do not have GAD.

Individuals who GAD have been suggested to have greater amygdala and medial prefrontal cortex (mPFC) activation in response to stimuli than individuals who do not have GAD. However, the exact relationship between the amygdala and the frontal cortex (e.g. prefrontal cortex or the orbitofrontal cortex (OFC)) is not fully understood because there are studies that suggest increased or decreased activity in the frontal cortex in individuals who have GAD. Consequently, because of the tenuous understanding of the frontal cortex as it relates to the amygdala in individuals who have GAD, it’s an open question as to whether individuals who have GAD bear an amygdala that is more sensitive than an amygdala in an individual without GAD or whether frontal cortex hyperactivity is responsible for changes in amygdala responsiveness to various stimuli. Recent studies have attempted to identify specific regions of the frontal cortex (e.g. dorsomedial prefrontal cortex (dmPFC)) that may be more or less reactive in individuals who have GAD or specific networks that may be differentially implicated in individuals who have GAD. Other lines of study investigate whether activation patterns vary in individuals who have GAD at different ages with respect to individuals who do not have GAD at the same age (e.g. amygdala activation in adolescents with GAD).

Treatment

Traditional treatment modalities broadly fall into two (2) categories:

  • Psychotherapeutic; and
  • Pharmacological intervention.

In addition to these two conventional therapeutic approaches, areas of active investigation include complementary and alternative medications (CAMs), brain stimulation, exercise, therapeutic massage and other interventions that have been proposed for further study. Treatment modalities can, and often are utilised concurrently so that an individual may pursue psychological therapy (i.e. psychotherapy) and pharmacological therapy. Both cognitive behavioural therapy (CBT) and medications (such as SSRIs) have been shown to be effective in reducing anxiety. A combination of both CBT and medication is generally seen as the most desirable approach to treatment. Use of medication to lower extreme anxiety levels can be important in enabling patients to engage effectively in CBT.

Psychotherapy

Psychotherapeutic interventions include a plurality of therapy types that vary based upon their specific methodologies for enabling individuals to gain insight into the working of the conscious and subconscious mind and which sometimes focus on the relationship between cognition and behaviour. Cognitive behavioural therapy (CBT) is widely regarded as the first-line psychological therapy for treating GAD. Additionally, many of these psychological interventions may be delivered in an individual or group therapy setting. While individual and group settings are broadly both considered effective for treating GAD, individual therapy tends to promote longer-lasting engagement in therapy (i.e. lower attrition over time).

Psychodynamic Therapy

Psychodynamic therapy is a type of therapy premised upon Freudian psychology in which a psychologist enables an individual explore various elements in their subconscious mind to resolve conflicts that may exist between the conscious and subconscious elements of the mind. In the context of GAD, the psychodynamic theory of anxiety suggests that the unconscious mind engages in worry as a defence mechanism to avoid feelings of anger or hostility because such feelings might cause social isolation or other negative attribution toward oneself. Accordingly, the various psychodynamic therapies attempt to explore the nature of worry as it functions in GAD in order to enable individuals to alter the subconscious practice of using worry as a defence mechanism and to thereby diminish GAD symptoms. Variations of psychotherapy include a near-term version of therapy, “short-term anxiety-provoking psychotherapy (STAPP).

Behavioural Therapy

Behavioural therapy is therapeutic intervention premised upon the concept that anxiety is learned through classical conditioning (e.g., in view of one or more negative experiences) and maintained through operant conditioning (e.g. one finds that by avoiding a feared experience that one avoids anxiety). Thus, behavioural therapy enables an individual to re-learn conditioned responses (behaviours) and to thereby challenge behaviours that have become conditioned responses to fear and anxiety, and which have previously given rise to further maladaptive behaviours.

Cognitive Therapy

Cognitive therapy (CT) is premised upon the idea that anxiety is the result of maladaptive beliefs and methods of thinking. Thus, CT involves assisting individuals to identify more rational ways of thinking and to replace maladaptive thinking patterns (i.e. cognitive distortions) with healthier thinking patterns (e.g. replacing the cognitive distortion of catastrophising with a more productive pattern of thinking). Individuals in CT learn how to identify objective evidence, test hypotheses, and ultimately identify maladaptive thinking patterns so that these patterns can be challenged and replaced.

Acceptance and Commitment Therapy

Acceptance and commitment therapy (ACT) is a behavioural treatment based on acceptance-based models. ACT is designed with the purpose to target three therapeutic goals:

  1. Reduce the use of avoiding strategies intended to avoid feelings, thoughts, memories, and sensations;
  2. Decreasing a person’s literal response to their thoughts (e.g., understanding that thinking “I’m hopeless” does not mean that the person’s life is truly hopeless); and
  3. Increasing the person’s ability to keep commitments to changing their behaviours.

These goals are attained by switching the person’s attempt to control events to working towards changing their behaviour and focusing on valued directions and goals in their lives as well as committing to behaviours that help the individual accomplish those personal goals. This psychological therapy teaches mindfulness (paying attention on purpose, in the present, and in a non-judgemental manner) and acceptance (openness and willingness to sustain contact) skills for responding to uncontrollable events and therefore manifesting behaviours that enact personal values. Like many other psychological therapies, ACT works best in combination with pharmacology treatments.

Intolerance of Uncertainty Therapy

Intolerance of uncertainty (IU) refers to a consistent negative reaction to uncertain and ambiguous events regardless of their likelihood of occurrence. Intolerance of uncertainty therapy (IUT) is used as a stand-alone treatment for GAD patients. Thus, IUT focuses on helping patients in developing the ability to tolerate, cope with and accept uncertainty in their life in order to reduce anxiety. IUT is based on the psychological components of psychoeducation, awareness of worry, problem-solving training, re-evaluation of the usefulness of worry, imagining virtual exposure, recognition of uncertainty, and behavioural exposure. Studies have shown support for the efficacy of this therapy with GAD patients with continued improvements in follow-up periods.

Motivational Interviewing

A promising innovative approach to improving recovery rates for the treatment of GAD is to combine CBT with motivational interviewing (MI). Motivational interviewing is a strategy centred on the patient that aims to increase intrinsic motivation and decrease ambivalence about change due to the treatment. MI contains four key elements:

  • Express empathy;
  • Heighten dissonance between behaviours that are not desired and values that are not consistent with those behaviours;
  • Move with resistance rather than direct confrontation; and
  • Encourage self-efficacy.

It is based on asking open-ended questions and listening carefully and reflectively to patients’ answers, eliciting “change talk”, and talking with patients about the pros and cons of change. Some studies have shown the combination of CBT with MI to be more effective than CBT alone.

Cognitive Behavioural Therapy

Cognitive behavioural therapy (CBT) is an evidence-based type of psychotherapy that demonstrates efficacy in treating GAD and which integrates the cognitive and behavioural therapeutic approaches. The objective of CBT is to enable individuals to identify irrational thoughts that cause anxiety and to challenge dysfunctional thinking patterns by engaging in awareness techniques such as hypothesis testing and journaling. Because CBT involves the practice of worry and anxiety management, CBT includes a plurality of intervention techniques that enable individuals to explore worry, anxiety and automatic negative thinking patterns. These interventions include anxiety management training, cognitive restructuring, progressive relaxation, situational exposure and self-controlled desensitisation.

Other forms of psychological therapy include:

  • Relaxation techniques (e.g. relaxing imagery, meditational relaxation).
  • Metacognitive Therapy (MCT):
    • The objective of MCT is to alter thinking patterns regarding worry so that worry is no longer used as a coping strategy.
  • Mindfulness based stress reduction (MBSR).
  • Mindfulness based cognitive therapy (MBCT).
  • Supportive therapy:
    • This is a Rogerian method of therapy in which subjects experience empathy and acceptance from their therapist to facilitate increasing awareness.
    • Variations of active supportive therapy include Gestalt therapy, Transactional analysis and Counselling.

Pharmacotherapy

Historically, benzodiazepines (BZs) were used prominently to treat anxiety starting in the 1970s but support for this use attenuated in view of the risk for dependence and tolerance to the medication. BZs can have a plurality of effects that made them a seemingly desirable option for treating anxiety – i.e. BZs have anxiolytic, hypnotic (induce sleep), myorelaxant (relax muscles), anticonvulsant and amnestic (impair short-term memory) properties. While BZs are well appreciated for their ability to alleviate anxiety (i.e. their anxiolytic properties) shortly after administration, they are also known for their ability to promote dependence and are frequently abused. Current recommendations for using BZs to treat anxiety in GAD allow no more than 2-4 weeks of BZ exposure. Antidepressants (e.g. SSRIs/SNRIs) have become a mainstay in treating GAD in adults. First-line mediations from any drug category often include drugs that have been approved by the US Food and Drug Administration (FDA) for treating GAD because these medications have been proven safe and effective for treating GAD.

FDA-Approved Medications for Treating GAD

FDA-approved medications for treating GAD include:

  • SSRIs:
    • Paroxetine.
    • Escitalopram.
  • SNRIs:
    • Venlafaxine.
    • Duloxetine.
  • Benzodiazepines (BZs):
    • Alprazolam: Alprazolam is the only FDA-approved BZ for treating GAD.
  • Azapirones:
    • Buspirone.

Non-FDA Approved Medications

While certain medications are not specifically FDA approved for treatment of GAD, there are a number of medications that historically have been used or studied for treating GAD. Other medications that have been used or evaluated for treating GAD include:

  • SSRIs (antidepressants):
    • Citalopram.
    • Fluoxetine.
    • Sertraline.
    • Fluvoxamine (SSRI).
  • Benzodiazepines:
    • Clonazepam.
    • Lorazepam.
    • Diazepam.
  • GABA analogs:
    • Pregabalin (atypical anxiolytic, GABA analog).
    • Tiagabine.
  • Second-generation antipsychotics (SGAs):
    • Olanzapine (evidence of effectiveness is merely a trend).
    • Ziprasidone.
    • Risperidone.
    • Aripiprazole (studied as an adjunctive measure in concert with other treatment).
    • Quetiapine (atypical antipsychotic studied as an adjunctive measure in adults and geriatric patients).
  • Antihistamines:
    • Hydroxyzine (H1 receptor antagonist).
  • Vilazodone (atypical antidepressant).
  • Agomelatine (antidepressant, MT1/2 receptor agonist, 5HT2c antagonist).
  • Clonidine (noted to cause decreased blood pressure and other AEs).
  • Guanfacine (a2A receptor agonist, studied in paediatric patients with GAD).
  • Mirtazapine (atypical antidepressant having 5HT2A and 5HT2c receptor affinity).
  • Vortioxetine (multimodal antidepressant).
  • Eszopiclone (non-benzodiazepine hypnotic).
  • Tricyclic antidepressants:
    • Amitriptyline.
    • Clomipramine.
    • Doxepin.
    • Imipramine.
    • Trimipramine.
    • Desipramine.
    • Nortriptyline.
    • Protriptyline.
  • Opipramol (atypical TCA).]
  • Trazodone.
  • Monamine oxidase inhibitors (MAOIs):
    • Tranylcypromine.
    • Phenelzine.
  • Homeopathic preparations (discussed below, see complementary and alternative medications (CAMs))

Selective Serotonin Reuptake Inhibitors

Pharmaceutical treatments for GAD include selective serotonin reuptake inhibitors (SSRIs).[50] SSRIs increase serotonin levels through inhibition of serotonin reuptake receptors.

FDA approved SSRIs used for this purpose include escitalopram and paroxetine. However, guidelines suggest using sertraline first due to its cost-effectiveness compared to other SSRIs used for GAD and a lower risk of withdrawal compared to SNRIs. If sertraline is found to be ineffective, then it is recommended to try another SSRI or SNRI.

Common side effects include nausea, sexual dysfunction, headache, diarrhoea, constipation, restlessness, increased risk of suicide in young adults and adolescents, among others. Sexual side effects, weight gain, and higher risk of withdrawal are more common in paroxetine than escitalopram and sertraline. In older populations or those taking concomitant medications that increase risk of bleeding, SSRIs may further increase the risk of bleeding. Overdose of an SSRI or concomitant use with another agent that causes increased levels of serotonin can result in serotonin syndrome, which can be life-threatening.

Serotonin Norepinephrine Reuptake Inhibitors

First line pharmaceutical treatments for GAD also include serotonin-norepinephrine reuptake inhibitors (SNRIs). These inhibit the reuptake of serotonin and noradrenaline to increase their levels in the CNS.

FDA approved SNRIs used for this purpose include duloxetine (Cymbalta) and venlafaxine (Effexor). While SNRIs have similar efficacy as SSRIs, many psychiatrists prefer to use SSRIs first in the treatment of GAD The slightly higher preference for SSRIs over SNRIs as a first choice for treatment of anxiety disorders may have been influenced by the observation of poorer tolerability of the SNRIs in comparison to SSRIs in systematic reviews of studies of depressed patients.

Side effects common to both SNRIs include anxiety, restlessness, nausea, weight loss, insomnia, dizziness, drowsiness, sweating, dry mouth, sexual dysfunction and weakness. In comparison to SSRIs, the SNRIs have a higher prevalence of the side effects of insomnia, dry mouth, nausea and high blood pressure. Both SNRIs have the potential for discontinuation syndrome after abrupt cessation, which can precipitate symptoms including motor disturbances and anxiety and may require tapering. Like other serotonergic agents, SNRIs have the potential to cause serotonin syndrome, a potentially fatal systemic response to serotonergic excess that causes symptoms including agitation, restlessness, confusion, tachycardia, hypertension, mydriasis, ataxia, myoclonus, muscle rigidity, diaphoresis, diarrhoea, headache, shivering, goose bumps, high fever, seizures, arrhythmia and unconsciousness. SNRIs like SSRIs carry a black box warning for suicidal ideation, but it is generally considered that the risk of suicide in untreated depression is far higher than the risk of suicide when depression is properly treated.

Pregabalin and Gabapentin

Pregabalin (Lyrica) acts on the voltage-dependent calcium channel to decrease the release of neurotransmitters such as glutamate, norepinephrine and substance P. Its therapeutic effect appears after 1 week of use and is similar in effectiveness to lorazepam, alprazolam and venlafaxine but pregabalin has demonstrated superiority by producing more consistent therapeutic effects for psychic and somatic anxiety symptoms. Long-term trials have shown continued effectiveness without the development of tolerance and additionally, unlike benzodiazepines, it does not disrupt sleep architecture and produces less severe cognitive and psychomotor impairment. It also has a low potential for abuse and dependency and may be preferred over the benzodiazepines for these reasons. The anxiolytic effects of pregabalin appear to persist for at least six months continuous use, suggesting tolerance is less of a concern; this gives pregabalin an advantage over certain anxiolytic medications such as benzodiazepines.

Gabapentin (Neurontin), a closely related medication to pregabalin with the same mechanism of action, has also demonstrated effectiveness in the treatment of GAD, though unlike pregabalin, it has not been approved specifically for this indication. Nonetheless, it is likely to be of similar usefulness in the management of this condition, and by virtue of being off-patent, it has the advantage of being significantly less expensive in comparison. In accordance, gabapentin is frequently prescribed off-label to treat GAD.

Complementary and Alternative Medicines Studied for Potential in Treating GAD

Complementary and alternative medicines (CAMs) are widely used by individuals who suffer GAD despite having no evidence or varied evidence regarding efficacy. Efficacy trials for CAM medications often suffer from various types of bias and low quality reporting in regard to safety. In regard to efficacy, critics point out that CAM trials sometimes predicate claims of efficacy based on a comparison of a CAM against a known drug after which no difference in subjects is found by investigators and which is used to suggest an equivalence between a CAM and a drug. Because this equates a lack of evidence with the positive assertion of efficacy, a “lack of difference” assertion is not a proper claim for efficacy. Moreover, an absence of strict definitions and standards for CAM compounds further burdens the literature regarding CAM efficacy in treating GAD. CAMs academically studied for their potential in treating GAD or GAD symptoms along with a summary of academic findings are given below. What follows is a summary of academic findings. Accordingly, none of the following should be taken as offering medical guidance or an opinion as to the safety or efficacy of any of the following CAMs.

  • Kava Kava (Piper methysticum) extracts:
    • Meta analysis does not suggest efficacy of Kava Kava extracts due to few data available yielding inconclusive results or non-statistically significant results.
    • Nearly a quarter (25.8%) of subjects experienced adverse effects (AEs) from Kava Kava extracts during six (6) trials.
    • Kava Kava may cause liver toxicity.
  • Lavender (Lavandula angustifolia) extracts:
    • Small and varied studies may suggest some level of efficacy as compared to placebo or other medication; claims of efficacy are regarded as needing further evaluation.
    • Silexan is an oil derivative of Lavender studied in paediatric patients with GAD.
    • Concern exists regarding the question as to whether Silexan may cause unopposed oestrogen exposure in boys due to disruption of steroid signalling.
  • Galphimia glauca extracts:
    • While Galphima glauca extracts have been the subject of two (2) randomised controlled trials (RCTs) comparing Galphima glauca extracts to lorazepam, efficacy claims are regarded as “highly uncertain.”
  • Chamomile (Matricaria chamomilla) extracts:
    • Poor quality trials have trends that may suggest efficacy but further study is needed to establish any claim of efficacy.
  • Crataegus oxycantha and Eschscholtzia californica extracts combined with magnesium:
    • A single12-week trial of Crataegus oxycantha and Eschscholtzia californica compared to placebo has been used to suggest efficacy.
    • However, efficacy claims require confirmation studies.
    • For the minority of subjects who experienced AEs from extracts, most AEs implicated gastrointestinal tract (GIT) intolerance.
  • Echium amoneum extract:
    • A single, small trial used this extract as a supplement to fluoxetine (vs using a placebo to supplement fluoxetine); larger studies are needed to substantiate efficacy claims.
  • Gamisoyo-San:
    • Small trials of this herbal mixture compared to placebo have suggested no efficacy of the herbal mixture over placebo but further study is necessary to allow definitive conclusion of a lack of efficacy.
  • Passiflora incarnata extract:
    • Claims of efficacy or benzodiazepam equivalence are regarded as “highly uncertain.”
  • Valeriana extract:
    • A single 4-week trial suggests no effect of Valeriana extract on GAD but is regarded as “uninformative” on the topic of efficacy in view of its finding that the benzodiazepine diazepam also had no effect.
    • Further study may be warranted.

Other Possible Modalities Discussed in Literature for Potential in Treating GAD

Other modalities that have been academically studied for their potential in treating GAD or symptoms of GAD are summarised below. What follows is a summary of academic findings. Accordingly, none of the following should be taken as offering medical guidance or an opinion as to the safety or efficacy of any of the following modalities.

  • Acupuncture:
    • A single, very small trial revealed a trend toward efficacy but flaws in the trial design suggest uncertainty regarding efficacy.
  • Balneotherapy:
    • Data from a single non-blinded study suggested possible efficacy of balneotherapy as compared to paroxetine.
    • However, efficacy claims need confirmation.
  • Therapeutic massage:
    • A single, small, possibly biased study revealed inconclusive results.
  • Resistance and aerobic exercise:
    • When compared to no treatment, a single, small, potentially unrepresentative trial suggested a trend toward GAD remission and reduction of worry.
  • Chinese bloodletting:
    • When added to paroxetine, a single, small, imprecise trial that lacked a sham procedure for comparison suggested efficacy at 4-weeks.
    • However, larger trials are needed to evaluate this technique as compared to a sham procedure.
  • Floating in water:
    • When compared to no treatment, a single, imprecise, non-blinded trial suggested a trend toward efficacy (findings were statistically insignificant).
  • Swedish massage:
    • When compared to a sham procedure, a single trial showed a trend toward efficacy (i.e. findings were statistically insignificant).
  • Ayurvedic medications:
    • A single non-blinded trial was inconclusive as to whether Ayurvedic medications were effective in treating GAD.
  • Multi-faith spiritually-based intervention:
    • A single, small, non-blinded study was inconclusive regarding efficacy.

Lifestyle

Lifestyle factors including: stress management, stress reduction, relaxation, exercise, sleep hygiene, and caffeine and alcohol reduction can influence anxiety levels. Physical activity has shown to have a positive impact whereas low physical activity may be a risk factor for anxiety disorders.

Substances and Anxiety in GAD

While there are no substances that are known to cause GAD, certain substances or the withdrawal from certain substances have been implicated in promoting the experience of anxiety. For example, even while benzodiazepines may afford individuals with GAD relief from anxiety, withdrawal from benzodiazepines is associated with the experience of anxiety among other adverse events like sweating and tremor.

Tobacco withdrawal symptoms may provoke anxiety in smokers and excessive caffeine use has been linked to aggravating and maintaining anxiety.

Comorbidity

Depression

In the National Comorbidity Survey (2005), 58% of patients diagnosed with major depression were found to have an anxiety disorder; among these patients, the rate of comorbidity with GAD was 17.2%, and with panic disorder, 9.9%. Patients with a diagnosed anxiety disorder also had high rates of comorbid depression, including 22.4% of patients with social phobia, 9.4% with agoraphobia, and 2.3% with panic disorder. A longitudinal cohort study found 12% of the 972 participants had GAD comorbid with MDD. Accumulating evidence indicates that patients with comorbid depression and anxiety tend to have greater illness severity and a lower treatment response than those with either disorder alone. In addition, social function and quality of life are more greatly impaired.

For many, the symptoms of both depression and anxiety are not severe enough (i.e. are subsyndromal) to justify a primary diagnosis of either major depressive disorder (MDD) or an anxiety disorder. However, dysthymia is the most prevalent comorbid diagnosis of GAD clients. Patients can also be categorised as having mixed anxiety-depressive disorder, and they are at significantly increased risk of developing full-blown depression or anxiety.

Various explanations for the high comorbidity between GAD and depressive disorders have been suggested, including genetic pleiotropy, meaning that GAD and nonbipolar depression might represent different phenotypic expressions of a common aetiology.

Comorbidity and Treatment

Therapy has been shown to have equal efficacy in patients with GAD and patients with GAD and comorbid disorders. Patients with comorbid disorders have more severe symptoms when starting therapy but demonstrated a greater improvement than patients with simple GAD.

Pharmacological approaches i.e. the use of antidepressants must be adapted for different comorbidities. For example, serotonin reuptake inhibitors and short acting benzodiazepines (BZDs) are used for depression and anxiety. However, for patients with anxiety and substance abuse, BZDs should be avoided due to their abuse liability. CBT has been found an effective treatment since it improves symptoms of GAD and substance abuse.

Compared to the general population, patients with internalising disorders such as depression, GAD and post-traumatic stress disorder (PTSD) have higher mortality rates, but die of the same age-related diseases as the population, such as heart disease, cerebrovascular disease and cancer.

GAD often coexists with conditions associated with stress, such as muscle tension and irritable bowel syndrome.

Patients with GAD can sometimes present with symptoms such as insomnia or headaches as well as pain and interpersonal problems.

Further research suggests that about 20% to 40% of individuals with attention deficit hyperactivity disorder have comorbid anxiety disorders, with GAD being the most prevalent.

Those with GAD have a lifetime comorbidity prevalence of 30% to 35% with alcohol use disorder and 25% to 30% for another substance use disorder. People with both GAD and a substance use disorder also have a higher lifetime prevalence for other comorbidities. A study found that GAD was the primary disorder in slightly more than half of the 18 participants that were comorbid with alcohol use disorder.

Epidemiology

GAD is often estimated to affect approximately 3-6% of adults and 5% of children and adolescents. Although estimates have varied to suggest a GAD prevalence of 3% in children and 10.8% in adolescents. When GAD manifests in children and adolescents, it typically begins around 8 to 9 years of age.

Estimates regarding prevalence of GAD or lifetime risk (i.e. lifetime morbid risk (LMR)) for GAD vary depending upon which criteria are used for diagnosing GAD (e.g. DSM-5 vs ICD-10) although estimates do not vary widely between diagnostic criteria. In general, ICD-10 is more inclusive than DSM-5, so estimates regarding prevalence and lifetime risk tend to be greater using ICD-10. In regard to prevalence, in a given year, about two (2%) percent of adults in the United States and Europe have been suggested to suffer GAD. However, the risk of developing GAD at any point in life has been estimated at 9.0%. Although it is possible to experience a single episode of GAD during one’s life, most people who experience GAD experience it repeatedly over the course of their lives as a chronic or ongoing condition. GAD is diagnosed twice as frequently in women as in men and is more often diagnosed in those who are separated, divorced, unemployed, widowed or have low levels of education, and among those with low socioeconomic status. African Americans have higher odds of having GAD and the disorder often manifests itself in different patterns. It has been suggested that greater prevalence of GAD in women may be because women are more likely than men to live in poverty, are more frequently the subject of discrimination, and be sexually and physically abused more often than men. In regard to the first incidence of GAD in an individual’s life course, a first manifestation of GAD usually occurs between the late teenage years and the early twenties with the median age of onset being approximately 31 and mean age of onset being 32.7. However, GAD can begin or reoccur at any point in life. Indeed, GAD is common in the elderly population.

  • US: Approximately 3.1% of people age 18 and over in a given year (9.5 million).
  • UK: 5.9% of adults were affected by GAD in 2019.
  • Australia: 3% of adults
  • Canada: 2.5%.
  • Italy: 2.9%
  • Taiwan: 0.4%.

What is Exposure Therapy?

Introduction

Exposure therapy is a technique in behaviour therapy to treat anxiety disorders. Exposure therapy involves exposing the target patient to the anxiety source or its context without the intention to cause any danger. Doing so is thought to help them overcome their anxiety or distress. Procedurally, it is similar to the fear extinction paradigm developed studying laboratory rodents. Numerous studies have demonstrated its effectiveness in the treatment of disorders such as generalised anxiety disorder (GAD), social anxiety disorder, obsessive-compulsive disorder (OCD), post traumatic stress disorder (PTSD), and specific phobias.

Brief History

The use of exposure as a mode of therapy began in the 1950s, at a time when psychodynamic views dominated Western clinical practice and behavioural therapy was first emerging. South African psychologists and psychiatrists first used exposure as a way to reduce pathological fears, such as phobias and anxiety-related problems, and they brought their methods to England in the Maudsley Hospital training programme.

Joseph Wolpe (1915-1997) was one of the first psychiatrists to spark interest in treating psychiatric problems as behavioural issues. He sought consultation with other behavioural psychologists, among them James G. Taylor (1897-1973), who worked in the psychology department of the University of Cape Town in South Africa. Although most of his work went unpublished, Taylor was the first psychologist known to use exposure therapy treatment for anxiety, including methods of situational exposure with response prevention – a common exposure therapy technique still being used. Since the 1950s several sorts of exposure therapy have been developed, including systematic desensitisation, flooding, implosive therapy, prolonged exposure therapy, in vivo exposure therapy, and imaginal exposure therapy.

Medical Uses

Generalised Anxiety Disorder

There is empirical evidence that exposure therapy can be an effective treatment for people with generalised anxiety disorder, citing specifically in vivo exposure therapy, which has greater effectiveness than imaginal exposure in regards to generalized anxiety disorder. The aim of in vivo exposure treatment is to promote emotional regulation using systematic and controlled therapeutic exposure to traumatic stimuli.

Phobia

Exposure therapy is the most successful known treatment for phobias. Several published meta-analyses included studies of one-to-three hour single-session treatments of phobias, using imaginal exposure. At a post-treatment follow-up four years later 90% of people retained a considerable reduction in fear, avoidance, and overall level of impairment, while 65% no longer experienced any symptoms of a specific phobia.

Agoraphobia and social anxiety disorder are examples of phobias that have been successfully treated by exposure therapy.

Post Traumatic Stress Disorder

Virtual reality exposure (VRE) therapy is a modern but effective treatment of post-traumatic stress disorder (PTSD). This method was tested on several active duty Army soldiers, using an immersive computer simulation of military settings over six sessions. Self-reported PTSD symptoms of these soldiers were greatly diminished following the treatment. Exposure therapy has shown promise in the treatment of co-morbid PTSD and substance abuse.

Obsessive Compulsive Disorder

Exposure and response prevention (also known as exposure and ritual prevention; ERP or EX/RP) is a variant of exposure therapy that is recommended by the American Academy of Child and Adolescent Psychiatry (AACAP), the American Psychiatric Association (APA), and the Mayo Clinic as first-line treatment of obsessive compulsive disorder (OCD) citing that it has the richest empirical support for both youth and adolescent outcomes.

ERP is predicated on the idea that a therapeutic effect is achieved as subjects confront their fears, but refrain from engaging in the escape response or ritual that delays or eliminates distress. In the case of individuals with OCD or an anxiety disorder, there is a thought or situation that causes distress. Individuals usually combat this distress through specific behaviours that include avoidance or rituals. However, ERP involves purposefully evoking fear, anxiety, and or distress in the individual by exposing him/her to the feared stimulus. The response prevention then involves having the individual refrain from the ritualistic or otherwise compulsive behaviour that functions to decrease distress. The patient is then taught to tolerate distress until it fades away on its own, thereby learning that rituals are not always necessary to decrease distress or anxiety. Over repeated practice of ERP, patients with OCD expect to find that they can have obsessive thoughts and images but not have the need to engage in compulsive rituals to decrease distress.

The AACAP’s practise parameters for OCD recommends cognitive behavioural therapy, and more specifically ERP, as first line treatment for youth with mild to moderate severity OCD and combination psychotherapy and pharmacotherapy for severe OCD. The Cochrane Review’s examinations of different randomised control trials echoes repeated findings of the superiority of ERP over waitlist control or pill-placebos, the superiority of combination ERP and pharmacotherapy, but similar effect sizes of efficacy between ERP or pharmacotherapy alone.

Techniques

Exposure therapy is based on the principle of respondent conditioning often termed Pavlovian extinction. The exposure therapist identifies the cognitions, emotions and physiological arousal that accompany a fear-inducing stimulus and then tries to break the pattern of escape that maintains the fear. This is done by exposing the patient to progressively stronger fear-inducing stimuli. Fear is minimised at each of a series of steadily escalating steps or challenges (a hierarchy), which can be explicit (“static”) or implicit (“dynamic” – refer to Method of Factors) until the fear is finally gone. The patient is able to terminate the procedure at any time.

There are three types of exposure procedures. The first is in vivo or “real life.” This type exposes the patient to actual fear-inducing situations. For example, if someone fears public speaking, the person may be asked to give a speech to a small group of people. The second type of exposure is imaginal, where patients are asked to imagine a situation that they are afraid of. This procedure is helpful for people who need to confront feared thoughts and memories. The third type of exposure is interoceptive, which may be used for more specific disorders such as panic or post-traumatic stress disorder. Patients confront feared bodily symptoms such as increased heart rate and shortness of breath. All types of exposure may be used together or separately.

While evidence clearly supports the effectiveness of exposure therapy, some clinicians are uncomfortable using imaginal exposure therapy, especially in cases of PTSD. They may not understand it, are not confident in their own ability to use it, or more commonly, they see significant contraindications for their client.

Flooding therapy also exposes the patient to feared stimuli, but it is quite distinct in that flooding starts at the most feared item in a fear hierarchy, while exposure starts at the least fear-inducing.

Exposure and Response Prevention

In the exposure and response prevention (ERP or EX/RP) variation of exposure therapy, the resolution to refrain from the escape response is to be maintained at all times and not just during specific practice sessions. Thus, not only does the subject experience habituation to the feared stimulus, but they also practice a fear-incompatible behavioural response to the stimulus. The distinctive feature is that individuals confront their fears and discontinue their escape response. The American Psychiatric Association recommends ERP for the treatment of OCD, citing that ERP has the richest empirical support.

While this type of therapy typically causes some short-term anxiety, this facilitates long-term reduction in obsessive and compulsive symptoms. Generally, ERP incorporates a relapse prevention plan toward the end of the course of therapy.

Mindfulness

A 2015 review pointed out parallels between exposure therapy and mindfulness, stating that mindful meditation “resembles an exposure situation because [mindfulness] practitioners ‘turn towards their emotional experience’, bring acceptance to bodily and affective responses, and refrain from engaging in internal reactivity towards it.” Imaging studies have shown that the ventromedial prefrontal cortex, hippocampus, and the amygdala are all affected by exposure therapy; imaging studies have shown similar activity in these regions with mindfulness training.

Research

Exposure therapy can be investigated in the laboratory using Pavlovian extinction paradigms. Using rodents such as rats or mice to study extinction allows for the investigation of underlying neurobiological mechanisms involved, as well as testing of pharmacological adjuncts to improve extinction learning.

Is It Useful to Screen for Anxiety using the GAD-7 in Pregnant Women?

Research Paper Title

Validation of the Generalised Anxiety Disorder Screener (GAD-7) in Spanish Pregnant Women.

Background

Anxiety during pregnancy is one of the most common mental health problems and a significant risk factor for postpartum depression. The Generalised Anxiety Disorder-7 (GAD-7) is one of the most widely used self-report measures of anxiety symptoms available in multiple languages. This study evaluates the psychometric properties and underlying factor structures of the Spanish GAD-7 among pregnant women in Spain.

Methods

Spanish-speaking pregnant women (N = 385) were recruited from an urban obstetrics setting in Northern Spain. Women completed the GAD-7 and the anxiety subscale of the Symptom Checklist (SCL90-R) at three time points, once per trimester. The reliability, concurrent validity, and factor analyses were conducted to evaluate the psychometric properties and factor structure, respectively.

Results

In the first trimester, the GAD-7 demonstrated good internal consistency (a = 0.89). GAD-7 is positively correlated with SCL90-R (anxiety subscale; r=0.75; p < 0.001). The proposed one-factor structure is found using exploratory factor analysis -FACTOR programme – with Unweighted Least Squares procedure and optimal implementation of parallel analysis (GFI = 0.99).

Conclusions

Health providers should screen for anxiety using the GAD-7 during pregnancy among urban Spanish-speaking samples to provide appropriate follow-up care.

Reference

Soto-Balbuena, C. Rodriguez-Munoz, M.F. & Le, H-N. (2021) Validation of the Generalized Anxiety Disorder Screener (GAD-7) in Spanish Pregnant Women. Psicothema. 33(1), pp.164-170. doi: 10.7334/psicothema2020.167.

What is Panic Disorder?

Introduction

Panic disorder is an anxiety disorder characterised by reoccurring unexpected panic attacks. Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something terrible is going to happen. The maximum degree of symptoms occurs within minutes. There may be ongoing worries about having further attacks and avoidance of places where attacks have occurred in the past.

The cause of panic disorder is unknown. Panic disorder often runs in families. Risk factors include smoking, psychological stress, and a history of child abuse. Diagnosis involves ruling out other potential causes of anxiety including other mental disorders, medical conditions such as heart disease or hyperthyroidism, and drug use. Screening for the condition may be done using a questionnaire.

Panic disorder is usually treated with counselling and medications. The type of counselling used is typically cognitive behavioural therapy (CBT) which is effective in more than half of people. Medications used include antidepressants and occasionally benzodiazepines or beta blockers. Following stopping treatment up to 30% of people have a recurrence.

Panic disorder affects about 2.5% of people at some point in their life. It usually begins during adolescence or early adulthood but any age can be affected. It is less common in children and older people. Women are more often affected than men.

Signs and Symptoms

Panic disorder sufferers usually have a series of intense episodes of extreme anxiety during panic attacks. These attacks typically last about ten minutes, and can be as short-lived as 1-5 minutes, but can last twenty minutes to more than an hour, or until helpful intervention is made. Panic attacks can wax and wane for a period of hours (panic attacks rolling into one another), and the intensity and specific symptoms of panic may vary over the duration.

In some cases, the attack may continue at unabated high intensity or seem to be increasing in severity. Common symptoms of an attack include rapid heartbeat, perspiration, dizziness, dyspnoea, trembling, uncontrollable fear such as: the fear of losing control and going crazy, the fear of dying and hyperventilation. Other symptoms are a sensation of choking, paralysis, chest pain, nausea, numbness or tingling, chills or hot flashes, faintness, crying and some sense of altered reality. In addition, the person usually has thoughts of impending doom. Individuals suffering from an episode have often a strong wish of escaping from the situation that provoked the attack. The anxiety of panic disorder is particularly severe and noticeably episodic compared to that from generalised anxiety disorder. Panic attacks may be provoked by exposure to certain stimuli (e.g. seeing a mouse) or settings (e.g. the dentist’s office). Nocturnal panic attacks are common in people with panic disorder. Other attacks may appear unprovoked. Some individuals deal with these events on a regular basis, sometimes daily or weekly.

Limited symptom attacks are similar to panic attacks but have fewer symptoms. Most people with PD experience both panic attacks and limited symptom attacks.

Interoceptive

Studies investigating the relationship between interoception and panic disorder have shown that people with panic disorder feel heartbeat sensations more intensely when stimulated by pharmacological agents, suggesting that they experience heightened interoceptive awareness compared to subjects without PD.

Causes

Psychological Models

While there is not just one explanation for the cause of panic disorder, there are certain perspectives researchers use to explain the disorder. The first one is the biological perspective. Past research concluded that there is irregular norepinephrine activity in people who have panic attacks. Current research also supports this perspective as it has been found that those with panic disorder also have a brain circuit that performs improperly. This circuit consists of the amygdala, central gray matter, ventromedial nucleus of the hypothalamus, and the locus ceruleus.

There is also a cognitive perspective. Theorists believe that people with panic disorder may experience panic reactions because they mistake their bodily sensations for life-threatening situations. These bodily sensations cause some people to feel as though are out of control which may lead to feelings of panic. This misconception of bodily sensations is referred to as anxiety sensitivity, and studies suggest that people who score higher on anxiety sensitivity surveys are fives times more likely to be diagnosed with panic disorder.

Panic disorder has been found to run in families, which suggests that inheritance plays a strong role in determining who will get it.

Psychological factors, stressful life events, life transitions, and environment as well as often thinking in a way that exaggerates relatively normal bodily reactions are also believed to play a role in the onset of panic disorder. Often the first attacks are triggered by physical illnesses, major stress, or certain medications. People who tend to take on excessive responsibilities may develop a tendency to suffer panic attacks. Post-traumatic stress disorder (PTSD) patients also show a much higher rate of panic disorder than the general population.

Prepulse inhibition has been found to be reduced in patients with panic disorder.

Substance Misuse

Substance abuse is often correlated with panic attacks. In a study, 39% of people with panic disorder had abused substances. Of those who used alcohol, 63% reported that the alcohol use began prior to the onset of panic, and 59% of those abusing illicit drugs reported that drug use began first. The study that was conducted documented the panic-substance abuse relationship. Substance abuse began prior to the onset of panic and substances were used to self-medicate for panic attacks by only a few subjects.

In another study, 100 methamphetamine-dependent individuals were analysed for co-morbid psychiatric disorders; of the 100 individuals, 36% were categorised as having co-morbid psychiatric disorders. Mood and Psychotic disorders were more prevalent than anxiety disorders, which accounted for 7% of the 100 sampled individuals.

Smoking

Tobacco smoking increases the risk of developing panic disorder with or without agoraphobia and panic attacks; smoking started in adolescence or early adulthood particularly increases this risk of developing panic disorder. While the mechanism of how smoking increases panic attacks is not fully understood, a few hypotheses have been derived. Smoking cigarettes may lead to panic attacks by causing changes in respiratory function (e.g. feeling short of breath). These respiratory changes in turn can lead to the formation of panic attacks, as respiratory symptoms are a prominent feature of panic. Respiratory abnormalities have been found in children with high levels of anxiety, which suggests that a person with these difficulties may be susceptible to panic attacks, and thus more likely to subsequently develop panic disorder. Nicotine, a stimulant, could contribute to panic attacks. However, nicotine withdrawal may also cause significant anxiety which could contribute to panic attacks.

It is also possible that panic disorder patients smoke cigarettes as a form of self-medication to lessen anxiety. Nicotine and other psychoactive compounds with antidepressant properties in tobacco smoke which act as monoamine oxidase inhibitors in the brain can alter mood and have a calming effect, depending on dose.

Stimulants

A number of clinical studies have shown a positive association between caffeine ingestion and panic disorder and/or anxiogenic effects. People who have panic disorder are more sensitive to the anxiety-provoking effects of caffeine. One of the major anxiety-provoking effects of caffeine is an increase in heart rate.

Certain cold and flu medications containing decongestants may also contain pseudoephedrine, ephedrine, phenylephrine, naphazoline and oxymetazoline. These may be avoided by the use of decongestants formulated to prevent causing high blood pressure.

Alcohol and Sedatives

About 30% of people with panic disorder use alcohol and 17% use other psychoactive drugs. This is in comparison with 61% (alcohol) and 7.9% (other psychoactive drugs) of the general population who use alcohol and psychoactive drugs, respectively. Utilisation of recreational drugs or alcohol generally make symptoms worse. Most stimulant drugs (caffeine, nicotine, cocaine) would be expected to worsen the condition, since they directly increase the symptoms of panic, such as heart rate.

Deacon and Valentiner (2000) conducted a study that examined co-morbid panic attacks and substance use in a non-clinical sample of young adults who experienced regular panic attacks. The authors found that compared to healthy controls, sedative use was greater for non-clinical participants who experienced panic attacks. These findings are consistent with the suggestion made by Cox, Norton, Dorward, and Fergusson (1989) that panic disorder patients self-medicate if they believe that certain substances will be successful in alleviating their symptoms. If panic disorder patients are indeed self-medicating, there may be a portion of the population with undiagnosed panic disorder who will not seek professional help as a result of their own self-medication. In fact, for some patients panic disorder is only diagnosed after they seek treatment for their self-medication habit.

While alcohol initially helps ease panic disorder symptoms, medium- or long-term alcohol abuse can cause panic disorder to develop or worsen during alcohol intoxication, especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long-term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquilisers to people with alcohol problems. The reason chronic alcohol misuse worsens panic disorder is due to distortion of the brain chemistry and function.

Approximately 10% of patients will experience notable protracted withdrawal symptoms, which can include panic disorder, after discontinuation of benzodiazepines. Protracted withdrawal symptoms tend to resemble those seen during the first couple of months of withdrawal but usually are of a subacute level of severity compared to the symptoms seen during the first 2 or 3 months of withdrawal. It is not known definitively whether such symptoms persisting long after withdrawal are related to true pharmacological withdrawal or whether they are due to structural neuronal damage as a result of chronic use of benzodiazepines or withdrawal. Nevertheless, such symptoms do typically lessen as the months and years go by eventually disappearing altogether.

A significant proportion of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia have developed these conditions as a result of alcohol or sedative abuse. Anxiety may pre-exist alcohol or sedative dependence, which then acts to perpetuate or worsen the underlying anxiety disorder. Someone suffering the toxic effects of alcohol abuse or chronic sedative use or abuse will not benefit from other therapies or medications for underlying psychiatric conditions as they do not address the root cause of the symptoms. Recovery from sedative symptoms may temporarily worsen during alcohol withdrawal or benzodiazepine withdrawal.

Mechanism

The neuroanatomy of panic disorder largely overlaps with that of most anxiety disorders. Neuropsychological, neurosurgical, and neuroimaging studies implicate the insula, amygdala, hippocampus, anterior cingulate cortex (ACC), lateral prefrontal cortex, and periaqueductal grey. During acute panic attacks, viewing emotionally charged words, and rest, most studies find elevated blood flow or metabolism. However, the observation of amygdala hyperactivity is not entirely consistent, especially in studies that evoke panic attacks chemically. Hippocampus hyperactivity has been observed during rest and viewing emotionally charged pictures, which has been hypothesized to be related to memory retrieval bias towards anxious memories. Insula hyperactivity during the onset of and over the course of acute panic episodes is thought to be related to abnormal introceptive processes; the perception that bodily sensations are “wrong” is a transdiagnostic finding(i.e. found across multiple anxiety disorders), and may be related to insula dysfunction. Rodent and human studies heavily implicate the periaqueductal grey in generating fear responses, and abnormalities related to the structure and metabolism in the PAG have been reported in panic disorder. The frontal cortex is implicated in panic disorder by multiple lines of evidence. Damage to the dorsal ACC has been reported to lead to panic disorder. Elevated ventral ACC and dorsolateral prefrontal cortex during symptom provocation and viewing emotional stimuli have also been reported, although findings are not consistent.

Researchers studying some individuals with panic disorder propose they may have a chemical imbalance within the limbic system and one of its regulatory chemicals gamma-aminobutyric acid (GABA-A). The reduced production of GABA-A sends false information to the amygdala which regulates the body’s “fight or flight” response mechanism and, in return, produces the physiological symptoms that lead to the disorder. Clonazepam, an anticonvulsant benzodiazepine with a long half-life, has been successful in keeping the condition under control.

Recently, researchers have begun to identify mediators and moderators of aspects of panic disorder. One such mediator is the partial pressure of carbon dioxide, which mediates the relationship between panic disorder patients receiving breathing training and anxiety sensitivity; thus, breathing training affects the partial pressure of carbon dioxide in a patient’s arterial blood, which in turn lowers anxiety sensitivity. Another mediator is hypochondriacal concerns, which mediate the relationship between anxiety sensitivity and panic symptomatology; thus, anxiety sensitivity affects hypochondriacal concerns which, in turn, affect panic symptomatology.

Perceived threat control has been identified as a moderator within panic disorder, moderating the relationship between anxiety sensitivity and agoraphobia; thus, the level of perceived threat control dictates the degree to which anxiety sensitivity results in agoraphobia. Another recently identified moderator of panic disorder is genetic variations in the gene coding for galanin; these genetic variations moderate the relationship between females suffering from panic disorder and the level of severity of panic disorder symptomatology.

Diagnosis

The DSM-IV-TR diagnostic criteria for panic disorder require unexpected, recurrent panic attacks, followed in at least one instance by at least a month of a significant and related behaviour change, a persistent concern of more attacks, or a worry about the attack’s consequences. There are two types, one with and one without agoraphobia. Diagnosis is excluded by attacks due to a drug or medical condition, or by panic attacks that are better accounted for by other mental disorders.

The ICD-10 diagnostic criteria:

  • The essential feature is recurrent attacks of severe anxiety (panic), which are not restricted to any particular situation or set of circumstances and are therefore unpredictable.

The dominant symptoms include:

  • Sudden onset of palpitations.
  • Chest pain.
  • Choking sensations.
  • Dizziness.
  • Feelings of unreality (depersonalisation or derealisation).
  • Secondary fear of dying, losing control, or going mad.
  • Panic disorder should not be given as the main diagnosis if the person has a depressive disorder at the time the attacks start; in these circumstances, the panic attacks are probably secondary to depression.

The Panic Disorder Severity Scale (PDSS) is a questionnaire for measuring the severity of panic disorder.

Treatment

Panic disorder is a serious health problem that in many cases can be successfully treated, although there is no known cure. Identification of treatments that engender as full a response as possible, and can minimise relapse, is imperative. CBT and positive self-talk specific for panic are the treatments of choice for panic disorder. Several studies show that 85% to 90% of panic disorder patients treated with CBT recover completely from their panic attacks within 12 weeks. When CBT is not an option, pharmacotherapy can be used. SSRIs are considered a first-line pharmacotherapeutic option.

Psychotherapy

Panic disorder is not the same as phobic symptoms, although phobias commonly result from panic disorder. CBT and one tested form of psychodynamic psychotherapy have been shown efficacious in treating panic disorder with and without agoraphobia. A number of randomized clinical trials have shown that CBT achieves reported panic-free status in 70-90% of patients about 2 years after treatment.

A 2009 Cochrane review found little evidence concerning the efficacy of psychotherapy in combination with benzodiazepines such that recommendations could not be made.

Symptom inductions generally occur for one minute and may include:

  • Intentional hyperventilation creates lightheadedness, derealisation, blurred vision, and dizziness.
  • Spinning in a chair creates dizziness and disorientation.
  • Straw breathing creates dyspnoea and airway constriction.
  • Breath holding creates sensation of being out of breath.
  • Running in place creates increased heart rate, respiration, and perspiration.
  • Body tensing creates feelings of being tense and vigilant.

Another form of psychotherapy that has shown effectiveness in controlled clinical trials is panic-focused psychodynamic psychotherapy, which focuses on the role of dependency, separation anxiety, and anger in causing panic disorder. The underlying theory posits that due to biochemical vulnerability, traumatic early experiences, or both, people with panic disorder have a fearful dependence on others for their sense of security, which leads to separation anxiety and defensive anger. Therapy involves first exploring the stressors that lead to panic episodes, then probing the psychodynamics of the conflicts underlying panic disorder and the defence mechanisms that contribute to the attacks, with attention to transference and separation anxiety issues implicated in the therapist-patient relationship.

Comparative clinical studies suggest that muscle relaxation techniques and breathing exercises are not efficacious in reducing panic attacks. In fact, breathing exercises may actually increase the risk of relapse.

Appropriate treatment by an experienced professional can prevent panic attacks or at least substantially reduce their severity and frequency – bringing significant relief to 70% to 90% of people with panic disorder. Relapses may occur, but they can often be effectively treated just like the initial episode.

vanApeldoorn, F.J. et al. (2011) demonstrated the additive value of a combined treatment incorporating an SSRI treatment intervention with CBT. Gloster et al. (2011) went on to examine the role of the therapist in CBT. They randomised patients into two groups: one being treated with CBT in a therapist guided environment, and the second receiving CBT through instruction only, with no therapist guided sessions. The findings indicated that the first group had a somewhat better response rate, but that both groups demonstrated a significant improvement in reduction of panic symptomatology. These findings lend credibility to the application of CBT programs to patients who are unable to access therapeutic services due to financial, or geographic inaccessibility. Koszycky et al. (2011) discuss the efficacy of self-administered CBT (SCBT) in situations where patients are unable to retain the services of a therapist. Their study demonstrates that it is possible for SCBT in combination with an SSRI to be as effective as therapist-guided CBT with SSRI. Each of these studies contributes to a new avenue of research that allows effective treatment interventions to be made more easily accessible to the population.

Cognitive Behavioural Therapy (CBT)

CBT encourages patients to confront the triggers that induce their anxiety. By facing the very cause of the anxiety, it is thought to help diminish the irrational fears that are causing the issues to begin with. The therapy begins with calming breathing exercises, followed by noting the changes in physical sensations felt as soon as anxiety begins to enter the body. Many clients are encouraged to keep journals. In other cases, therapists may try and induce feelings of anxiety so that the root of the fear can be identified.

Comorbid clinical depression, personality disorders and alcohol abuse are known risk factors for treatment failure.

As with many disorders, having a support structure of family and friends who understand the condition can help increase the rate of recovery. During an attack, it is not uncommon for the sufferer to develop irrational, immediate fear, which can often be dispelled by a supporter who is familiar with the condition. For more serious or active treatment, there are support groups for anxiety sufferers which can help people understand and deal with the disorder.

Current treatment guidelines American Psychiatric Association and the American Medical Association primarily recommend either CBT or one of a variety of psychopharmacological interventions. Some evidence exists supporting the superiority of combined treatment approaches.

Another option is self-help based on principles of CBT. Using a book or a website, a person does the kinds of exercises that would be used in therapy, but they do it on their own, perhaps with some email or phone support from a therapist. A systematic analysis of trials testing this kind of self-help found that websites, books, and other materials based on CBT could help some people. The best-studied conditions are panic disorder and social phobia.

Interoceptive Techniques

Interoceptive exposure is sometimes used for panic disorder. People’s interoceptive triggers of anxiety are evaluated one-by-one before conducting interoceptive exposures, such as addressing palpitation sensitivity via light exercise. Despite evidence of its clinical efficacy, this practice is reportedly used by only 12-20% of psychotherapists. Potential reasons for this underutilisation include “lack of training sites, logistical hurdles (e.g. occasional need for exposure durations longer than a standard therapy session), policies against conducting exposures outside of the workplace setting, and perhaps most tellingly, negative therapist beliefs (e.g. that interoceptive exposures are unethical, intolerable, or even harmful).”

Medication

Appropriate medications are effective for panic disorder. Selective serotonin reuptake inhibitors are first line treatments rather than benzodiazepines due to concerns with the latter regarding tolerance, dependence and abuse. Although there is little evidence that pharmacological interventions can directly alter phobias, few studies have been performed, and medication treatment of panic makes phobia treatment far easier (an example in Europe where only 8% of patients receive appropriate treatment).

Medications can include:

  • Antidepressants (SSRIs, MAOIs, tricyclic antidepressants and norepinephrine reuptake inhibitors).
  • Antianxiety agents (benzodiazepines):
    • Use of benzodiazepines for panic disorder is controversial.
    • The American Psychiatric Association states that benzodiazepines can be effective for the treatment of panic disorder and recommends that the choice of whether to use benzodiazepines, antidepressants with anti-panic properties or psychotherapy should be based on the individual patient’s history and characteristics.
    • Other experts believe that benzodiazepines are best avoided due to the risks of the development of tolerance and physical dependence.
    • The World Federation of Societies of Biological Psychiatry, say that benzodiazepines should not be used as a first-line treatment option but are an option for treatment-resistant cases of panic disorder.
    • Despite increasing focus on the use of antidepressants and other agents for the treatment of anxiety as recommended best practice, benzodiazepines have remained a commonly used medication for panic disorder.
    • They reported that in their view there is insufficient evidence to recommend one treatment over another for panic disorder.
    • The APA noted that while benzodiazepines have the advantage of a rapid onset of action, that this is offset by the risk of developing a benzodiazepine dependence.
    • The UKs National Institute of Clinical Excellence (NICE) came to a different conclusion, they pointed out the problems of using uncontrolled clinical trials to assess the effectiveness of pharmacotherapy and based on placebo-controlled research they concluded that benzodiazepines were not effective in the long-term for panic disorder and recommended that benzodiazepines not be used for longer than 4 weeks for panic disorder.
    • Instead NICE clinical guidelines recommend alternative pharmacotherapeutic or psychotherapeutic interventions.
    • When compared to placebos, benzodiazepines demonstrate possible superiority in the short term but the evidence is low quality with limited applicability to clinical practice.

Other Treatments

For some people, anxiety can be greatly reduced by discontinuing the use of caffeine. Anxiety can temporarily increase during caffeine withdrawal.

Epidemiology

Panic disorder typically begins during early adulthood; roughly half of all people who have panic disorder develop the condition between the ages of 17 and 24, especially those subjected to traumatic experiences. However, some studies suggest that the majority of young people affected for the first time are between the ages of 25 and 30. Women are twice as likely as men to develop panic disorder and it occurs far more often in people with above average intelligence.

Panic disorder can continue for months or years, depending on how and when treatment is sought. If left untreated, it may worsen to the point where one’s life is seriously affected by panic attacks and by attempts to avoid or conceal the condition. In fact, many people have had problems with personal relationships, education and employment while struggling to cope with panic disorder. Some people with panic disorder may conceal their condition because of the stigma of mental illness. In some individuals, symptoms may occur frequently for a period of months or years, then many years may pass with little or no symptoms. In some cases, the symptoms persist at the same level indefinitely. There is also some evidence that many individuals (especially those who develop symptoms at an early age) may experience symptom cessation later in life (e.g. past age 50).

In 2000, the World Health Organisation found prevalence and incidence rates for panic disorder to be very similar across the globe. Age-standardised prevalence per 100,000 ranged from 309 in Africa to 330 in East Asia for men and from 613 in Africa to 649 in North America, Oceania, and Europe for women.

Children

A retrospective study has shown that 40% of adult panic disorder patients reported that their disorder began before the age of 20. In an article examining the phenomenon of panic disorder in youth, Diler et al. (2004) found that only a few past studies have examined the occurrence of juvenile panic disorder. They report that these studies have found that the symptoms of juvenile panic disorder almost replicate those found in adults (e.g. heart palpitations, sweating, trembling, hot flashes, nausea, abdominal distress, and chills). The anxiety disorders co-exist with staggeringly high numbers of other mental disorders in adults. The same comorbid disorders that are seen in adults are also reported in children with juvenile panic disorder. Last and Strauss (1989) examined a sample of 17 adolescents with panic disorder and found high rates of comorbid anxiety disorders, major depressive disorder, and conduct disorders. Eassau et al. (1999) also found a high number of comorbid disorders in a community-based sample of adolescents with panic attacks or juvenile panic disorder. Within the sample, adolescents were found to have the following comorbid disorders: major depressive disorder (80%), dysthymic disorder (40%), generalised anxiety disorder (40%), somatoform disorders (40%), substance abuse (40%), and specific phobia (20%). Consistent with this previous work, Diler et al. (2004) found similar results in their study in which 42 youths with juvenile panic disorder were examined. Compared to non-panic anxiety disordered youths, children with panic disorder had higher rates of comorbid major depressive disorder and bipolar disorder.

Children differ from adolescents and adults in their interpretation and ability to express their experience. Like adults, children experience physical symptoms including accelerated heart rate, sweating, trembling or shaking, shortness of breath, nausea or stomach pain, dizziness or light-headedness. In addition, children also experience cognitive symptoms like fear of dying, feelings of being detached from oneself, feelings of losing control or going crazy, but they are unable to vocalize these higher-order manifestations of fear. They simply know that something is going wrong and that they are very afraid. Children can only describe physical symptoms. They have not yet developed the constructs to put these symptoms together and label them as fear. Parents often feel helpless when they watch a child suffer. They can help children give a name to their experience, and empower them to overcome the fear they are experiencing.

The role of the parent in treatment and intervention for children diagnosed with panic disorder is discussed by McKay & Starch (2011). They point out that there are several levels at which parental involvement should be considered. The first involves the initial assessment. Parents, as well as the child, should be screened for attitudes and treatment goals, as well as for levels of anxiety or conflict in the home. The second involves the treatment process in which the therapist should meet with the family as a unit as frequently as possible. Ideally, all family members should be aware and trained in the process of CBT in order to encourage the child to rationalize and face fears rather than employ avoidant safety behaviours. McKay & Storch (2011) suggest training/modelling of therapeutic techniques and in-session involvement of the parents in the treatment of children to enhance treatment efficacy.

Despite the evidence pointing to the existence of early-onset panic disorder, the DSM-IV-TR currently only recognizes six anxiety disorders in children: separation anxiety disorder, generalised anxiety disorder, specific phobia, obsessive-compulsive disorder, social anxiety disorder (a.k.a. social phobia), and post-traumatic stress disorder. Panic disorder is notably excluded from this list.

What is Anxiety?

Introduction

Anxiety is an emotion characterised by an unpleasant state of inner turmoil, often accompanied by nervous behaviour such as pacing back and forth, somatic complaints, and rumination. It includes subjectively unpleasant feelings of dread over anticipated events.

Anxiety is a feeling of uneasiness and worry, usually generalised and unfocused as an overreaction to a situation that is only subjectively seen as menacing. It is often accompanied by muscular tension, restlessness, fatigue and problems in concentration. Anxiety is closely related to fear, which is a response to a real or perceived immediate threat; anxiety involves the expectation of future threat. People facing anxiety may withdraw from situations which have provoked anxiety in the past.

Anxiety disorders differ from developmentally normative fear or anxiety by being excessive or persisting beyond developmentally appropriate periods. They differ from transient fear or anxiety, often stress-induced, by being persistent (e.g. typically lasting 6 months or more), although the criterion for duration is intended as a general guide with allowance for some degree of flexibility and is sometimes of shorter duration in children.

Anxiety vs Fear

Anxiety is distinguished from fear, which is an appropriate cognitive and emotional response to a perceived threat. Anxiety is related to the specific behaviours of fight-or-flight responses, defensive behaviour or escape. It occurs in situations only perceived as uncontrollable or unavoidable, but not realistically so. David Barlow defines anxiety as “a future-oriented mood state in which one is not ready or prepared to attempt to cope with upcoming negative events,” and that it is a distinction between future and present dangers which divides anxiety and fear. Another description of anxiety is agony, dread, terror, or even apprehension. In positive psychology, anxiety is described as the mental state that results from a difficult challenge for which the subject has insufficient coping skills.

Fear and anxiety can be differentiated in four domains:

  1. Duration of emotional experience;
  2. Temporal focus;
  3. Specificity of the threat; and
  4. Motivated direction.

Fear is short-lived, present-focused, geared towards a specific threat, and facilitating escape from threat; anxiety, on the other hand, is long-acting, future-focused, broadly focused towards a diffuse threat, and promoting excessive caution while approaching a potential threat and interferes with constructive coping.

Joseph E. LeDoux and Lisa Feldman Barrett have both sought to separate automatic threat responses from additional associated cognitive activity within anxiety.

Symptoms

Anxiety can be experienced with long, drawn-out daily symptoms that reduce quality of life, known as chronic (or generalised) anxiety, or it can be experienced in short spurts with sporadic, stressful panic attacks, known as acute anxiety. Symptoms of anxiety can range in number, intensity, and frequency, depending on the person. While almost everyone has experienced anxiety at some point in their lives, most do not develop long-term problems with anxiety.

Anxiety may cause psychiatric and physiological symptoms.

The risk of anxiety leading to depression could possibly even lead to an individual harming themselves, which is why there are many 24-hour suicide prevention hotlines.

The behavioural effects of anxiety may include withdrawal from situations which have provoked anxiety or negative feelings in the past. Other effects may include changes in sleeping patterns, changes in habits, increase or decrease in food intake, and increased motor tension (such as foot tapping).

The emotional effects of anxiety may include “feelings of apprehension or dread, trouble concentrating, feeling tense or jumpy, anticipating the worst, irritability, restlessness, watching (and waiting) for signs (and occurrences) of danger, and, feeling like your mind’s gone blank” as well as “nightmares/bad dreams, obsessions about sensations, déjà vu, a trapped-in-your-mind feeling, and feeling like everything is scary.” It may include a vague experience and feeling of helplessness.

The cognitive effects of anxiety may include thoughts about suspected dangers, such as fear of dying. “You may … fear that the chest pains are a deadly heart attack or that the shooting pains in your head are the result of a tumour or an aneurysm. You feel an intense fear when you think of dying, or you may think of it more often than normal, or can’t get it out of your mind.”

The physiological symptoms of anxiety may include:

  • Neurological, as headache, paraesthesia’s, fasciculations, vertigo, or presyncope.
  • Digestive, as abdominal pain, nausea, diarrhoea, indigestion, dry mouth, or bolus.
  • Respiratory, as shortness of breath or sighing breathing.
  • Cardiac, as palpitations, tachycardia, or chest pain.
  • Muscular, as fatigue, tremors, or tetany.
  • Cutaneous, as perspiration, or itchy skin.
  • Uro-genital, as frequent urination, urinary urgency, dyspareunia, or impotence, chronic pelvic pain syndrome. Stress hormones released in an anxious state have an impact on bowel function and can manifest physical symptoms that may contribute to or exacerbate IBS.

Types of Anxiety

There are various types of anxiety. Existential anxiety can occur when a person faces angst, an existential crisis, or nihilistic feelings. People can also face mathematical anxiety, somatic anxiety, stage fright, or test anxiety. Social anxiety refers to a fear of rejection and negative evaluation by other people.

Existential

The philosopher Søren Kierkegaard, in The Concept of Anxiety (1844), described anxiety or dread associated with the “dizziness of freedom” and suggested the possibility for positive resolution of anxiety through the self-conscious exercise of responsibility and choosing. In Art and Artist (1932), the psychologist Otto Rank wrote that the psychological trauma of birth was the pre-eminent human symbol of existential anxiety and encompasses the creative person’s simultaneous fear of – and desire for – separation, individuation, and differentiation.

The theologian Paul Tillich characterised existential anxiety as “the state in which a being is aware of its possible nonbeing” and he listed three categories for the nonbeing and resulting anxiety: ontic (fate and death), moral (guilt and condemnation), and spiritual (emptiness and meaninglessness). According to Tillich, the last of these three types of existential anxiety, i.e. spiritual anxiety, is predominant in modern times while the others were predominant in earlier periods. Tillich argues that this anxiety can be accepted as part of the human condition or it can be resisted but with negative consequences. In its pathological form, spiritual anxiety may tend to “drive the person toward the creation of certitude in systems of meaning which are supported by tradition and authority” even though such “undoubted certitude is not built on the rock of reality”.

According to Viktor Frankl, the author of Man’s Search for Meaning, when a person is faced with extreme mortal dangers, the most basic of all human wishes is to find a meaning of life to combat the “trauma of nonbeing” as death is near.

Depending on the source of the threat, psychoanalytic theory distinguishes the following types of anxiety:

  • Realistic.
  • Neurotic.
  • Moral.

Test and Performance

According to Yerkes-Dodson law, an optimal level of arousal is necessary to best complete a task such as an exam, performance, or competitive event. However, when the anxiety or level of arousal exceeds that optimum, the result is a decline in performance.

Test anxiety is the uneasiness, apprehension, or nervousness felt by students who have a fear of failing an exam. Students who have test anxiety may experience any of the following: the association of grades with personal worth; fear of embarrassment by a teacher; fear of alienation from parents or friends; time pressures; or feeling a loss of control. Sweating, dizziness, headaches, racing heartbeats, nausea, fidgeting, uncontrollable crying or laughing and drumming on a desk are all common. Because test anxiety hinges on fear of negative evaluation, debate exists as to whether test anxiety is itself a unique anxiety disorder or whether it is a specific type of social phobia. The DSM-IV classifies test anxiety as a type of social phobia.

While the term “test anxiety” refers specifically to students, many workers share the same experience with regard to their career or profession. The fear of failing at a task and being negatively evaluated for failure can have a similarly negative effect on the adult. Management of test anxiety focuses on achieving relaxation and developing mechanisms to manage anxiety.

Stranger, Social, and Intergroup Anxiety

Humans generally require social acceptance and thus sometimes dread the disapproval of others. Apprehension of being judged by others may cause anxiety in social environments.

Anxiety during social interactions, particularly between strangers, is common among young people. It may persist into adulthood and become social anxiety or social phobia. “Stranger anxiety” in small children is not considered a phobia. In adults, an excessive fear of other people is not a developmentally common stage; it is called social anxiety. According to Cutting, social phobics do not fear the crowd but the fact that they may be judged negatively.

Social anxiety varies in degree and severity. For some people, it is characterised by experiencing discomfort or awkwardness during physical social contact (e.g. embracing, shaking hands, etc.), while in other cases it can lead to a fear of interacting with unfamiliar people altogether. Those suffering from this condition may restrict their lifestyles to accommodate the anxiety, minimising social interaction whenever possible. Social anxiety also forms a core aspect of certain personality disorders, including avoidant personality disorder.

To the extent that a person is fearful of social encounters with unfamiliar others, some people may experience anxiety particularly during interactions with outgroup members, or people who share different group memberships (i.e. by race, ethnicity, class, gender, etc.). Depending on the nature of the antecedent relations, cognitions, and situational factors, intergroup contact may be stressful and lead to feelings of anxiety. This apprehension or fear of contact with outgroup members is often called interracial or intergroup anxiety.

As is the case with the more generalised forms of social anxiety, intergroup anxiety has behavioural, cognitive, and affective effects. For instance, increases in schematic processing and simplified information processing can occur when anxiety is high. Indeed, such is consistent with related work on attentional bias in implicit memory. Additionally recent research has found that implicit racial evaluations (i.e. automatic prejudiced attitudes) can be amplified during intergroup interaction. Negative experiences have been illustrated in producing not only negative expectations, but also avoidant, or antagonistic, behaviour such as hostility. Furthermore, when compared to anxiety levels and cognitive effort (e.g. impression management and self-presentation) in intragroup contexts, levels and depletion of resources may be exacerbated in the intergroup situation.

Trait

Anxiety can be either a short-term ‘state’ or a long-term personality “trait”. Trait anxiety reflects a stable tendency across the lifespan of responding with acute, state anxiety in the anticipation of threatening situations (whether they are actually deemed threatening or not). A meta-analysis showed that a high level of neuroticism is a risk factor for development of anxiety symptoms and disorders. Such anxiety may be conscious or unconscious.

Personality can also be a trait leading to anxiety and depression. Through experience, many find it difficult to collect themselves due to their own personal nature.

Choice or Decision

Anxiety induced by the need to choose between similar options is increasingly being recognised as a problem for individuals and for organisations. In 2004, Capgemini wrote: “Today we’re all faced with greater choice, more competition and less time to consider our options or seek out the right advice.”

In a decision context, unpredictability or uncertainty may trigger emotional responses in anxious individuals that systematically alter decision-making. There are primarily two forms of this anxiety type. The first form refers to a choice in which there are multiple potential outcomes with known or calculable probabilities. The second form refers to the uncertainty and ambiguity related to a decision context in which there are multiple possible outcomes with unknown probabilities.

Panic Disorder

Panic disorder may share symptoms of stress and anxiety, but it is actually very different. Panic disorder is an anxiety disorder that occurs without any triggers. According to the US Department of Health and Human Services, this disorder can be distinguished by unexpected and repeated episodes of intense fear. Someone who suffers from panic disorder will eventually develop constant fear of another attack and as this progresses it will begin to affect daily functioning and an individual’s general quality of life. It is reported by the Cleveland Clinic that panic disorder affects 2% to 3% of adult Americans and can begin around the time of the teenage and early adult years. Some symptoms include: difficulty breathing, chest pain, dizziness, trembling or shaking, feeling faint, nausea, fear that you are losing control or are about to die. Even though they suffer from these symptoms during an attack, the main symptom is the persistent fear of having future panic attacks.

Anxiety Disorders

Anxiety disorders are a group of mental disorders characterised by exaggerated feelings of anxiety and fear responses. Anxiety is a worry about future events and fear is a reaction to current events. These feelings may cause physical symptoms, such as a fast heart rate and shakiness. There are a number of anxiety disorders: including generalised anxiety disorder, specific phobia, social anxiety disorder, separation anxiety disorder, agoraphobia, panic disorder, and selective mutism. The disorder differs by what results in the symptoms. People often have more than one anxiety disorder.

Anxiety disorders are caused by a complex combination of genetic and environmental factors. To be diagnosed, symptoms typically need to be present for at least six months, be more than would be expected for the situation, and decrease a person’s ability to function in their daily lives. Other problems that may result in similar symptoms include hyperthyroidism, heart disease, caffeine, alcohol, or cannabis use, and withdrawal from certain drugs, among others.

Without treatment, anxiety disorders tend to remain. Treatment may include lifestyle changes, counselling, and medications. Counselling is typically with a type of cognitive behavioural therapy. Medications, such as antidepressants or beta blockers, may improve symptoms.

About 12% of people are affected by an anxiety disorder in a given year and between 5%-30% are affected at some point in their life. They occur about twice as often in women than they do in men, and generally begin before the age of 25. The most common are specific phobia which affects nearly 12% and social anxiety disorder which affects 10% at some point in their life. They affect those between the ages of 15 and 35 the most and become less common after the age of 55. Rates appear to be higher in the United States and Europe.

Short- and Long-Term Anxiety

Anxiety can be either a short-term “state” or a long-term “trait”. Whereas trait anxiety represents worrying about future events, anxiety disorders are a group of mental disorders characterized by feelings of anxiety and fear.

Co-Morbidity

Anxiety disorders often occur with other mental health disorders, particularly major depressive disorder, bipolar disorder, eating disorders, or certain personality disorders. It also commonly occurs with personality traits such as neuroticism. This observed co-occurrence is partly due to genetic and environmental influences shared between these traits and anxiety.

Anxiety is often experienced by those with obsessive compulsive disorder and is an acute presence in panic disorder.

Risk Factors

Anxiety disorders are partly genetic, with twin studies suggesting 30-40% genetic influence on individual differences in anxiety. Environmental factors are also important. Twin studies show that individual-specific environments have a large influence on anxiety, whereas shared environmental influences (environments that affect twins in the same way) operate during childhood but decline through adolescence. Specific measured ‘environments’ that have been associated with anxiety include child abuse, family history of mental health disorders, and poverty. Anxiety is also associated with drug use, including alcohol, caffeine, and benzodiazepines (which are often prescribed to treat anxiety).

Neuroanatomy

Neural circuitry involving the amygdala (which regulates emotions like anxiety and fear, stimulating the HPA Axis and sympathetic nervous system) and hippocampus (which is implicated in emotional memory along with the amygdala) is thought to underlie anxiety. People who have anxiety tend to show high activity in response to emotional stimuli in the amygdala. Some writers believe that excessive anxiety can lead to an overpotentiation of the limbic system (which includes the amygdala and nucleus accumbens), giving increased future anxiety, but this does not appear to have been proven.

Research upon adolescents who as infants had been highly apprehensive, vigilant, and fearful finds that their nucleus accumbens is more sensitive than that in other people when deciding to make an action that determined whether they received a reward. This suggests a link between circuits responsible for fear and also reward in anxious people. As researchers note, “a sense of ‘responsibility’, or self-agency, in a context of uncertainty (probabilistic outcomes) drives the neural system underlying appetitive motivation (i.e. nucleus accumbens) more strongly in temperamentally inhibited than noninhibited adolescents”.

The Gut-Brain Axis

The microbes of the gut can connect with the brain to affect anxiety. There are various pathways along which this communication can take place. One is through the major neurotransmitters. The gut microbes such as Bifidobacterium and Bacillus produce the neurotransmitters GABA and dopamine, respectively. The neurotransmitters signal to the nervous system of the gastrointestinal tract, and those signals will be carried to the brain through the vagus nerve or the spinal system. This is demonstrated by the fact that altering the microbiome has shown anxiety- and depression-reducing effects in mice, but not in subjects without vagus nerves.

Another key pathway is the HPA axis, as mentioned above. The microbes can control the levels of cytokines in the body, and altering cytokine levels creates direct effects on areas of the brain such as the hypothalmus, the area that triggers HPA axis activity. The HPA axis regulates production of cortisol, a hormone that takes part in the body’s stress response. When HPA activity spikes, cortisol levels increase, processing and reducing anxiety in stressful situations. These pathways, as well as the specific effects of individual taxa of microbes, are not yet completely clear, but the communication between the gut microbiome and the brain is undeniable, as is the ability of these pathways to alter anxiety levels.

With this communication comes the potential to treat anxiety. Prebiotics and probiotics have been shown to reduced anxiety. For example, experiments in which mice were given fructo- and galacto-oligosaccharide prebiotics and Lactobacillus probiotics have both demonstrated a capability to reduce anxiety. In humans, results are not as concrete, but promising.

Genetics

Genetics and family history (e.g. parental anxiety) may put an individual at increased risk of an anxiety disorder, but generally external stimuli will trigger its onset or exacerbation. Estimates of genetic influence on anxiety, based on studies of twins, range from 25%-40% depending on the specific type and age-group under study. For example, genetic differences account for about 43% of variance in panic disorder and 28% in generalised anxiety disorder. Longitudinal twin studies have shown the moderate stability of anxiety from childhood through to adulthood is mainly influenced by stability in genetic influence. When investigating how anxiety is passed on from parents to children, it is important to account for sharing of genes as well as environments, for example using the intergenerational children-of-twins design.

Many studies in the past used a candidate gene approach to test whether single genes were associated with anxiety. These investigations were based on hypotheses about how certain known genes influence neurotransmitters (such as serotonin and norepinephrine) and hormones (such as cortisol) that are implicated in anxiety. None of these findings are well replicated, with the possible exception of TMEM132D, COMT and MAO-A. The epigenetic signature of BDNF, a gene that codes for a protein called brain derived neurotrophic factor that is found in the brain, has also been associated with anxiety and specific patterns of neural activity. and a receptor gene for BDNF called NTRK2 was associated with anxiety in a large genome-wide investigation. The reason that most candidate gene findings have not replicated is that anxiety is a complex trait that is influenced by many genomic variants, each of which has a small effect on its own. Increasingly, studies of anxiety are using a hypothesis-free approach to look for parts of the genome that are implicated in anxiety using big enough samples to find associations with variants that have small effects. The largest explorations of the common genetic architecture of anxiety have been facilitated by the UK Biobank, the ANGST consortium and the CRC Fear, Anxiety and Anxiety Disorders.

Medical Conditions

Many medical conditions can cause anxiety. This includes conditions that affect the ability to breathe, like COPD and asthma, and the difficulty in breathing that often occurs near death. Conditions that cause abdominal pain or chest pain can cause anxiety and may in some cases be a somatisation of anxiety; the same is true for some sexual dysfunctions. Conditions that affect the face or the skin can cause social anxiety especially among adolescents, and developmental disabilities often lead to social anxiety for children as well. Life-threatening conditions like cancer also cause anxiety.

Furthermore, certain organic diseases may present with anxiety or symptoms that mimic anxiety. These disorders include certain endocrine diseases (hypo- and hyperthyroidism, hyperprolactinemia), metabolic disorders (diabetes), deficiency states (low levels of vitamin D, B2, B12, folic acid), gastrointestinal diseases (celiac disease, non-celiac gluten sensitivity, inflammatory bowel disease), heart diseases, blood diseases (anaemia), cerebral vascular accidents (transient ischemic attack, stroke), and brain degenerative diseases (Parkinson’s disease, dementia, multiple sclerosis, Huntington’s disease), among others.

Substance-Induced

Several drugs can cause or worsen anxiety, whether in intoxication, withdrawal or as side effect. These include alcohol, tobacco, cannabis, sedatives (including prescription benzodiazepines), opioids (including prescription pain killers and illicit drugs like heroin), stimulants (such as caffeine, cocaine and amphetamines), hallucinogens, and inhalants. While many often report self-medicating anxiety with these substances, improvements in anxiety from drugs are usually short-lived (with worsening of anxiety in the long term, sometimes with acute anxiety as soon as the drug effects wear off) and tend to be exaggerated. Acute exposure to toxic levels of benzene may cause euphoria, anxiety, and irritability lasting up to 2 weeks after the exposure.

Psychological

Poor coping skills (e.g. rigidity/inflexible problem solving, denial, avoidance, impulsivity, extreme self-expectation, negative thoughts, affective instability, and inability to focus on problems) are associated with anxiety. Anxiety is also linked and perpetuated by the person’s own pessimistic outcome expectancy and how they cope with feedback negativity. Temperament (e.g. neuroticism) and attitudes (e.g. pessimism) have been found to be risk factors for anxiety.

Cognitive distortions such as overgeneralising, catastrophising, mind reading, emotional reasoning, binocular trick, and mental filter can result in anxiety. For example, an overgeneralised belief that something bad “always” happens may lead someone to have excessive fears of even minimally risky situations and to avoid benign social situations due to anticipatory anxiety of embarrassment. In addition, those who have high anxiety can also create future stressful life events. Together, these findings suggest that anxious thoughts can lead to anticipatory anxiety as well as stressful events, which in turn cause more anxiety. Such unhealthy thoughts can be targets for successful treatment with cognitive therapy.

Psychodynamic theory posits that anxiety is often the result of opposing unconscious wishes or fears that manifest via maladaptive defence mechanisms (such as suppression, repression, anticipation, regression, somatisation, passive aggression, dissociation) that develop to adapt to problems with early objects (e.g. caregivers) and empathic failures in childhood. For example, persistent parental discouragement of anger may result in repression/suppression of angry feelings which manifests as gastrointestinal distress (somatisation) when provoked by another while the anger remains unconscious and outside the individual’s awareness. Such conflicts can be targets for successful treatment with psychodynamic therapy. While psychodynamic therapy tends to explore the underlying roots of anxiety, cognitive behavioural therapy has also been shown to be a successful treatment for anxiety by altering irrational thoughts and unwanted behaviours.

Evolutionary Psychology

An evolutionary psychology explanation is that increased anxiety serves the purpose of increased vigilance regarding potential threats in the environment as well as increased tendency to take proactive actions regarding such possible threats. This may cause false positive reactions but an individual suffering from anxiety may also avoid real threats. This may explain why anxious people are less likely to die due to accidents. There is ample empirical evidence that anxiety can have adaptive value. Within a school, timid fish are more likely than bold fish to survive a predator.

When people are confronted with unpleasant and potentially harmful stimuli such as foul odours or tastes, PET-scans show increased blood flow in the amygdala. In these studies, the participants also reported moderate anxiety. This might indicate that anxiety is a protective mechanism designed to prevent the organism from engaging in potentially harmful behaviours.

Social

Social risk factors for anxiety include a history of trauma (e.g. physical, sexual or emotional abuse or assault), bullying, early life experiences and parenting factors (e.g. rejection, lack of warmth, high hostility, harsh discipline, high parental negative affect, anxious childrearing, modelling of dysfunctional and drug-abusing behaviour, discouragement of emotions, poor socialisation, poor attachment, and child abuse and neglect), cultural factors (e.g. stoic families/cultures, persecuted minorities including the disabled), and socioeconomics (e.g. uneducated, unemployed, impoverished although developed countries have higher rates of anxiety disorders than developing countries). A 2019 comprehensive systematic review of over 50 studies showed that food insecurity in the United States is strongly associated with depression, anxiety, and sleep disorders. Food-insecure individuals had an almost three (3) fold risk increase of testing positive for anxiety when compared to food-secure individuals.

Gender Socialisation

Contextual factors that are thought to contribute to anxiety include gender socialisation and learning experiences. In particular, learning mastery (the degree to which people perceive their lives to be under their own control) and instrumentality, which includes such traits as self-confidence, self-efficacy, independence, and competitiveness fully mediate the relation between gender and anxiety. That is, though gender differences in anxiety exist, with higher levels of anxiety in women compared to men, gender socialisation and learning mastery explain these gender differences.

Treatment

The first step in the management of a person with anxiety symptoms involves evaluating the possible presence of an underlying medical cause, whose recognition is essential in order to decide the correct treatment. Anxiety symptoms may mask an organic disease, or appear associated with or as a result of a medical disorder.

Cognitive behavioural therapy (CBT) is effective for anxiety disorders and is a first line treatment. CBT appears to be equally effective when carried out via the internet. While evidence for mental health apps is promising, it is preliminary.

Psychopharmacological treatment can be used in parallel to CBT or can be used alone. As a general rule, most anxiety disorders respond well to first-line agents. First-line drugs are the selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors. Benzodiazepines are not recommended for routine use. Other treatment options include pregabalin, tricyclic antidepressants, buspirone, moclobemide, and seratriline, among others.

Prevention

The above risk factors give natural avenues for prevention. A 2017 review found that psychological or educational interventions have a small yet statistically significant benefit for the prevention of anxiety in varied population types.

Pathophysiology

Anxiety disorder appears to be a genetically inherited neurochemical dysfunction that may involve autonomic imbalance; decreased GABA-ergic tone; allelic polymorphism of the catechol-O-methyltransferase (COMT) gene; increased adenosine receptor function; increased cortisol.

In the central nervous system (CNS), the major mediators of the symptoms of anxiety disorders appear to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA). Other neurotransmitters and peptides, such as corticotropin-releasing factor, may be involved. Peripherally, the autonomic nervous system, especially the sympathetic nervous system, mediates many of the symptoms. Increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients are the diagnostic factors for prevalence of anxiety disorder.

The amygdala is central to the processing of fear and anxiety, and its function may be disrupted in anxiety disorders. Anxiety processing in the basolateral amygdala has been implicated with dendritic arborisation of the amygdaloid neurons. SK2 potassium channels mediate inhibitory influence on action potentials and reduce arborisation.

Book: The Anxiety and Phobia Workbook

Book Title:

The Anxiety and Phobia Workbook.

Author(s): Edmund J. Bourne, PhD.

Year: 2020.

Edition: Seventh (7th), Revised and Updated Edition.

Publisher: New Harbinger Publications.

Type(s): Paperback and Kindle.

Synopsis:

Celebrating 30 years as a classic in its field and recommended by therapists worldwide, The Anxiety and Phobia Workbook is an unparalleled, essential resource for people struggling with anxiety and phobias.

Living with anxiety, panic disorders, or phobias can make you feel like you aren’t in control of your life. Tackle the fears that hold you back with this go-to guide. Packed with the most effective skills for assessing and treating anxiety, this evidence-based workbook contains the latest clinical research. You’ll find an arsenal of tools for quieting worry, ending negative self-talk, and taking charge of your anxious thoughts, including:

  • Relaxation and breathing techniques; and
  • New research on exposure therapy for phobiasLifestyle, exercise, mindfulness and nutrition tips.

Written by a leading expert in cognitive behavioural therapy (CBT), this fully revised and updated seventh edition offers powerful, step-by-step treatment strategies for panic disorders, agoraphobia, generalised anxiety disorder (GAD), obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), worry, and fear.

You will also find new information on relapse prevention after successful treatment, and updates on medication, cannabis derivatives, ketamine, exposure, nutrition, spirituality, the latest research in neurobiology, and more.

Whether you suffer from anxiety and phobias yourself, or are a professional working with this population, this book provides the latest treatment solutions for overcoming the fears that stand in the way of living a meaningful and happy life.

This workbook can be used on its own or in conjunction with therapy.

Book: Embracing Anxiety – How to Access the Genius of This Vital Emotion

Book Title:

Embracing Anxiety – How to Access the Genius of This Vital Emotion.

Author(s): Karla McLaren.

Year: 2020.

Edition: First (1ed).

Publisher: Sounds True.

Type(s): Paperback and Kindle.

Synopsis:

An in-depth guide for engaging with anxiety–not as an affliction, but as an essential source of foresight, intuition, and energy for completing your tasks and projects.

If you are facing anxiety, you’ve probably got one thing on your mind – how to make it go away. But what if this challenging emotion were actually trying to help?

When we ignore or repress our anxiety,” teaches Karla McLaren, it can overwhelm us. But when we learn to welcome it with skill, we can access its remarkable gifts.

Engaged with wisely, anxiety is your task completion ally – it helps you to focus, plan, take action, and fulfill your goals. With Embracing Anxiety, you will join this acclaimed educator and researcher to explore:

  • Principles and practices to befriend your anxiety at every level of intensity (before it overwhelms you).
  • Strategies to engage with anxiety as a source of foresight, conscientiousness, and motivation.
  • Why fear, confusion, and panic are not the same as anxiety, and tools to work with each effectively.
  • How anxiety blends with anger, depression, and other emotions, and how to clarify these compounded states.
  • Using McLaren’s Conscious Questioning practice to engage with anxiety and garner its insights.
  • How to embrace procrastination and get things done.

When you identify, listen to, and act on anxiety skillfully, you support its purpose, teaches McLaren, and allow it to recede naturally until it is needed again. With Embracing Anxiety, you’ll learn how to get this powerful emotion on your side.

Does Comorbid GAD & Back Pain and GAD & Migraine have an Association with Non-Medical Opioid Use?

Research Paper Title

An Examination of Comorbid Generalized Anxiety Disorder and Chronic Pain on Substance Misuse in a Canadian Population-Based Survey.

Background

Chronic pain and generalised anxiety disorder (GAD) are co-occurring, and both conditions are independently associated with substance misuse. However, limited research has examined the impact of comorbid GAD and chronic pain on substance misuse.

The aim of this article was to examine the associations between comorbid GAD and chronic pain conditions compared to GAD only with non-medical opioid use, drug abuse/dependence, and alcohol abuse/dependence in a Canadian, population-based sample.

Methods

Data came from the 2012 Canadian Community Health Survey-Mental Health (N = 25,113).

Multiple logistic regressions assessed the associations between comorbid GAD and chronic pain conditions (migraine, back pain, and arthritis) on substance misuse.

Results

Comorbid GAD + back pain and GAD + migraine were associated with increased odds of nonmedical opioid use compared to GAD only. However, the relationship was no longer significant after controlling for additional chronic pain conditions.

No significant relationship was found between GAD + chronic pain conditions with drug or alcohol abuse/dependence.

Conclusions

Comorbid GAD + back pain and GAD + migraine have a unique association with non-medical opioid use in Canadians compared to GAD only, and chronic pain multi-morbidity may be driving this relationship.

Results emphasise the need for screening for substance misuse and prescription access in the context of GAD and comorbid chronic pain.

Reference

Bilevicius, E., Sommer, J.L., Keough, M.T. & El-Gabalawy, R. (2020) An Examination of Comorbid Generalized Anxiety Disorder and Chronic Pain on Substance Misuse in a Canadian Population-Based Survey. Canadian Journal of Psychiatry. doi: 10.1177/0706743719895340. [Epub ahead of print].

Feeling the Pain: Substance Misuse & Generalised Anxiety Disorder

Research Paper Title

An Examination of Comorbid Generalized Anxiety Disorder and Chronic Pain on Substance Misuse in a Canadian Population-Based Survey.

Background

Chronic pain and generalized anxiety disorder (GAD) are co-occurring, and both conditions are independently associated with substance misuse.

However, limited research has examined the impact of comorbid GAD and chronic pain on substance misuse.

The aim of this article was to examine the associations between comorbid GAD and chronic pain conditions compared to GAD only with non-medical opioid use, drug abuse/dependence, and alcohol abuse/dependence in a Canadian, population-based sample.

Methods

Data came from the 2012 Canadian Community Health Survey-Mental Health (N = 25,113). Multiple logistic regressions assessed the associations between comorbid GAD and chronic pain conditions (migraine, back pain, and arthritis) on substance misuse.

Results

Comorbid GAD + back pain and GAD + migraine were associated with increased odds of non-medical opioid use compared to GAD only.

However, the relationship was no longer significant after controlling for additional chronic pain conditions.

No significant relationship was found between GAD + chronic pain conditions with drug or alcohol abuse/dependence.

Conclusions

Comorbid GAD + back pain and GAD + migraine have a unique association with non-medical opioid use in Canadians compared to GAD only, and chronic pain multi-morbidity may be driving this relationship.

Results emphasise the need for screening for substance misuse and prescription access in the context of GAD and comorbid chronic pain.

Reference

Bilevicius, E., Sommer, J.L., Keough, M.T. & El-Gabalawy, R. (2020) An Examination of Comorbid Generalized Anxiety Disorder and Chronic Pain on Substance Misuse in a Canadian Population-Based Survey. Canadian Journal of Psychiatry. doi: 10.1177/0706743719895340. [Epub ahead of print].