Introduction
According to the National Institute of Health, primary anxiety disorders are very common, affecting almost one in every five people in the US in any given year. Anxiety serves to warn us of danger and to help us mobilize effective defenses. In some circumstances, anxiety can overwhelm us resulting in a variety of symptoms. According to the DSM-5 Anxiety disorders include disorders that share features of excessive fear and anxiety and related behavioral disturbances. Anxiety disorders often co-present with depression or depressive symptoms, personality disorder, or alcohol or drug misuse. Anxiety manifest in a variety of ways that include: phobic anxiety disorders, panic disorders, generalized anxiety disorder, and post-traumatic stress disorder. In the following paper I will explore the biological, genetic, psychological, cognitive and social paradigms that contribute to the understanding of anxiety disorders. I will also discuss evidence based interventions and approaches for effective treatment.
Anxiety Paradigms
Biological Paradigm
Unregulated stress can cause a change in the biochemistry of our brains. Extreme stress can inhibit learning and growth while moderate stress can stimulate the production of hormones. When a person experiences a traumatic experience, the neural networks do not function properly and neural integration is disrupted. Neural disruption affects learning, behavior, emotion, sensation and cognition. Under extreme stress, the integration of information processing may shut down, which causes dissociation. The role of medication and therapy is to restore neural network integration and coordination, so that emotion, cognition, sensation, and learning can occur without being overwhelmed by stressors from within or outside of the self. In each of the anxiety disorders, biological factors are implicated in their etiologies and treatments. In the case of generalized anxiety disorders heightened cortical activity accounts for intense arousal and hypervigilance (Berzoff 2016). this causes alterations in the amygdala, the part of the brain that controls emotions. In the case of panic disorders, there are a number of biological explanations. Noradrenergic neurons many misfire into the hippocampus and amygdala, affecting the limbic system and cerebral cortex. The misfires interfere with normal fight-flight responses, which increase cortisol and serotonin.
Genetic Paradigm
The genetic basis of mood and anxiety disorders have not yielded consistent findings due to specific symptom categories are shared across mood and anxiety disorders. Genetic links are modest, which suggest that environmental factors play a larger role in the development of generalized anxiety disorders than do biological (Wilson et al. 1995). Genetic epidemiology has assembled convincing evidence that anxiety and related mood disorders are influenced by genetic factors, however the genetic component is highly complex. Studies of the patterns of inheritance of personality indicate that various dimensions are likely to be influenced by genes and quantitative traits. The modes of inheritance of anxiety disorders are complex, it has been concluded that multiple genes of small effect, in interaction with each other and with non-genetic neurodevelopment events, produce vulnerability to anxiety disorders. Progress has been made in identifying relevant pathomechanisms for obsessive-compulsive and related disorders, however several factors need to be considered when evaluating the results of genetic association studies in mood and anxiety disorders such as: phenotype definition, functional annotation of associated variants and gene vs. environment interactions.
Psychological/Cognitive Paradigm
Processing stressful events requires executive functions that involve interpretation, attention, and memory. These functions are applied when threat and danger assessments and responsive actions are formed which creates the fight or flight response. When a person is aroused by stress, the individual tries to regulate their emotions by offsetting the unpleasant experience with emotions such as fear, worry, distress, terror, or despair. How the person perceives the stress provides the basis for an anxious responses. If any executive functions of the brain are impaired, then judgments and decisions become inaccurate. Severe levels of anxiety can include physiological reactions that stimulate the sympathetic and parasympathetic nervous systems, resulting in increased heart rate, trembling, sweating, nausea, shortness of breath, dizziness, headaches and diarrhea.
Social Paradigm
Anxiety can cause extreme self-consciousness in everyday social or performance situations. In these cases, anxiety about being scrutinized and negatively evaluated is so severe that the person becomes paralyzed with fear and panic. This occurs in situations others would consider non-threatening social interactions. Social anxiety disorder is not simply shyness. The symptoms of social anxiety disorder usually include: loneliness, low self-esteem, depression, and substance misuse. Clients with this disorder may hide the symptoms and not discuss them with others until they can no longer be hidden. In an effort to protect their current state, clients may minimize their subjective experiences.
Literature Review
A recent study tested whether social support served as a mediator of anxiety and depressive symptoms following evidence-based anxiety treatment. Gender, age and race were tested as moderators. Data was obtained from 1004 adult patients who participated in a randomized effectiveness trail comparing cognitive-behavioral therapy and/ psychopharmacology to coordinated anxiety skills management study. Patients were assessed with a battery of questionnaire at baseline, as well as at 6,12, an 18 moths following baseline. The measures used in this study included the abbreviated medical outcomes, social support survey and somatic an anxiety subscales. Based on the study’s findings, perceived social support may be central to anxiety and depressive symptom changes over time with evidence-based intervention. These findings possibly have important implications for development of anxiety interventions. The results are consistent with prior studies that found direct predictive relations among variables. This is the first study to demonstrate that perceived social support functions as a mediator of symptom improvement following evidence-based intervention for anxiety disorders. Many studies have examined social support as a moderator or outcome of treatment. Although this study highlights perceived social support as an agent of change, the results do not suggest that social support without evidence based interventions are effective. According to the study, behavioral changes following the intervention may possibly led to greater self-efficacy that contributes to stronger beliefs in ability to find support.
Discussion Section
Cognitive and behavioral therapies and pharmacotherapies are well established as efficacious anxiety treatments. Cognitive behavioral therapy has focused on the extent to which cognitions and beliefs around anxiety and depression and symptom changes, however many patients remain symptomatic. I believe there needs to be more emphasis on how certain treatments lead to change rather than the analysis of outcomes. I am interested in understanding the long-term effects of anxiety on the adrenal system. If the adrenal glands don’t properly regulate the stress how does the body effectively absorb the medication to regulate anxiety when taken over long periods of time.
