Anxiety Disorder: Causes, Aspects, and Treatment

Introduction

Anxiety is usually a normal reaction to stress and is even essential in certain situations. For example, anxiety can signal pending danger, alerting and preparing an individual to remain attentive. Anxiety disorder, however, is distinct from ordinary feelings of nervousness — it involves excessive and persistent fear or worry. Anxiety disorder is the most common mental health condition, affecting around 30% of adults at some point during their lifetime (Craske et al., 2011). The positive side is that anxiety disorder is treatable, and several effective treatment mechanisms exist that enable people to live full, functional lives.

Anxiety involves excessive worry or anticipation about the future, and it is primarily associated with avoidance behavior and muscle tension. Anxiety disorders may prompt individuals to avoid situations that worsen or trigger their symptoms, which can impair personal relationships, job performance, and academic work. For a diagnosis of anxiety disorder, the anxiety must be disproportionate to the individual's age or situation and must meaningfully impair their ability to function. There are several kinds of anxiety disorders, including panic disorder, generalized anxiety disorder (GAD), social anxiety disorder, separation anxiety disorder, specific phobias, and agoraphobia, among others.

Some of the risk factors for anxiety disorders are not fully understood; however, they may include environmental, genetic, developmental, and psychological factors (Rowa & Antony, 2008). In some cases, anxiety disorders run in families, suggesting that a combination of genetic predisposition and environmental stress can cause these conditions.

To diagnose and treat anxiety disorders, the first step is consulting a doctor to rule out any underlying physical problem. Once an anxiety disorder is diagnosed, a mental health professional can guide the patient in finding appropriate treatment. Regrettably, many people suffering from anxiety disorders never seek help — some fail to recognize that they have a treatable illness. Most anxiety disorders respond well to two primary treatment types: medication and psychotherapy, which can be administered separately or in combination (Craske et al., 2011). Cognitive-behavioral therapy (CBT) can also help individuals learn new ways of thinking, reacting, and behaving in order to feel less anxious.

While medication cannot cure anxiety disorders, it can provide significant symptom relief. Anti-anxiety medications and antidepressants are commonly prescribed, usually for a short period of use (Rowa & Antony, 2008). Beta-blockers, typically used for heart conditions, are occasionally used to manage the physical symptoms of anxiety as well.

For those unable to access professional help, several self-help strategies can assist in managing anxiety disorder symptoms. Meditation and stress management techniques can be particularly beneficial. Support groups — both online and in person — provide opportunities to share coping strategies and experiences. Learning more about one's specific anxiety disorder, and helping friends and family understand the condition, has also been found to be helpful.

Neuroscience Aspect of Anxiety

Symptoms of anxiety disorders are believed to partly result from a disruption in the balance of activity between the brain's emotional centers and its higher cognitive centers. The higher cognitive brain centers are situated within the frontal lobe, the most phylogenetically recent brain region. Historically, the emotional-processing brain structures were collectively referred to as the "limbic system." The limbic cortex forms part of the phylogenetically ancient cortex and integrates the cognitive, affective, and sensory components of pain, while also processing data about the internal state of the body (Grecucci et al., 2020). Another key limbic system structure is the hippocampus, which exerts tonic inhibitory control over the hypothalamic stress-response system and plays a role in negative feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis.

The growth of new cells and hippocampal volume within the limbic system have been implicated in both stress resilience and stress sensitivity in anxiety disorders. The amygdala — an evolutionarily ancient limbic structure — processes emotionally salient external stimuli and generates appropriate behavioral responses. The amygdala is essential for the expression of fear and aggression, as well as specific defensive behaviors. It also plays a role in the retrieval and formation of emotional and fear-linked memories (LeDoux & Pine, 2016). The amygdala nucleus is interconnected with cortical regions — including the limbic cortex — to function correctly, and also receives input from the thalamus, hypothalamus, and hippocampus.

Heightened activity in brain regions that process emotion — as observed in anxiety disorder patients — may result from increased excitatory neurotransmission via glutamate or from decreased inhibitory signaling via γ-aminobutyric acid (GABA). The well-established antidepressant and anxiolytic effects of drugs that act on monoaminergic systems have implicated serotonin, dopamine, and norepinephrine in the pathogenesis of anxiety disorders. Consequently, genes that regulate monoaminergic signaling have become a major area of research interest in understanding the pathophysiology of anxiety disorders, as they are believed to be central to the mechanism of action of antidepressant drugs.

Classic neurotransmitters are often packaged and released together with neuropeptides within the central nervous system. These neuropeptides are predominantly expressed in limbic regions and exert substantial effects on emotion and stress circuitry. Neuropeptides with strong connections to psychopathology include galanin, cholecystokinin, vasopressin, neuropeptide Y, and oxytocin. Cholecystokinin is present in multiple limbic regions, as well as in the vagus nerve and the gastrointestinal system (Pine, 2001). Galanin regulates feeding behavior, pain processing, and the cardiovascular and neuroendocrine systems.

The Developmental Aspect of Anxiety

Anxiety disorders are among the first psychiatric disorders to manifest during development. For example, while the average age of onset for depression is 29, the average age of onset for anxiety disorder is 11. This early emergence is consistent with research showing that individual levels of trait anxiety are established at an early age and remain relatively stable throughout a person's lifetime. Anxiety disorders and trait anxiety are therefore likely influenced by early developmental processes or experiences that shape brain development (Berenson, 1991). There is also a significant genetic component to the development of anxiety circuitry; studies suggest that genetic factors may account for 30–40% of the variance in generalized anxiety disorder (GAD).

However, the genetic component is not specific to anxiety: the genetic risk for developing anxiety largely overlaps with the genetic risk for depression. The phenotypic differences observed between the two disorders are likely driven by interactions between a shared set of genetic risk factors and differing environmental conditions (La Greca et al., 1988). The concept of critical developmental periods further supports the idea that environmental exposures during periods of heightened brain plasticity can significantly influence the development of baseline brain function.

As the nervous system matures and the brain develops, neural systems interact and become receptive to particular environmental inputs, helping the organism expand its behavioral repertoire. Such developmental patterns can be observed shortly after birth. For instance, most infants show distress when taken from their mothers by an unfamiliar person between the ages of 7 and 9 months. The onset of stranger anxiety is relatively rapid and typically resolves within a few months (Berenson, 1991). By age 2, children develop consistent response patterns to novel environments — as evidenced by behavioral inhibition — which remain stable across several years and may predict future risk of anxiety disorders.

Early life anxiety, particularly generalized anxiety, appears to predict both anxiety and depression later in life. This is not surprising given the evidence that both disorders share underlying genetic vulnerabilities. However, less is known about how temporal and environmental factors shape the expression of these vulnerabilities. Evidence suggests that early life risk factors mediate both anxiety risk and later depression (Pratt & Hill, 2011), while psychological factors may subsequently moderate the development of depression.

Conclusion

Anxiety disorder is the most common among mental disorders, contributing to a significant percentage of adults experiencing mental health difficulties at some point in their lifetime. Anxiety disorders may prompt individuals to avoid situations that worsen or trigger their symptoms (Craske et al., 2011), impairing personal relationships, job performance, and academic work. Anxiety can be understood through several distinct perspectives, including neuroscience, developmental psychology, cognitive-behavioral theory, and biblical theology. From the neuroscience perspective, symptoms of anxiety disorders partly result from disruptions in the balance of activity between the brain's emotional centers and higher cognitive regions (Grecucci et al., 2020). From the biblical perspective, anxiety should not define the life of a Christian believer; instead, believers are called to turn to God in every challenge they face.

References

Beidel, D. C., Turner, S. M., & Dancu, C. V. (1985). Physiological, cognitive, and behavioral aspects of social anxiety. Behaviour Research and Therapy, 23(2), 109–117.

Berenson, C. K. (1996). Anxiety and the developing child. American Psychiatric Press Review of Psychiatry.

Butler, G., Fennell, M., Robson, P., & Gelder, M. (1991). Comparison of behavior therapy and cognitive behavior therapy in the treatment of generalized anxiety disorder. Journal of Consulting and Clinical Psychology, 59(1), 167.

Cantz, P., & Castle, M. (2013). A psycho-biblical response to death anxiety: Separation and individuation dynamics in the Babel narrative. Journal of Psychology and Theology, 41(4), 327–339.

Colbert, D. (1999). The Bible cure for depression and anxiety. Charisma Media.

Craske, M. G., Rauch, S. L., Ursano, R., Prenoveau, J., Pine, D. S., & Zinbarg, R. E. (2011). What is an anxiety disorder? Focus, 9(3), 369–388.

Grecucci, A., Sırçı, H., Lapomarda, G., Amodeo, L., Messina, I., & Frederickson, J. (2020). Anxiety regulation: From affective neuroscience to clinical practice. Brain Sciences, 10(11), 846.

Ingram, R. E., & Kendall, P. C. (1987). The cognitive side of anxiety. Cognitive Therapy and Research, 11(5), 523–536.

James, D., & Moggach, D. (2017). Bruno Bauer: Biblical narrative, freedom and anxiety. In Volume 6, Tome II: Kierkegaard and His German Contemporaries — Theology (pp. 13–34). Routledge.

La Greca, A. M., Dandes, S. K., Wick, P., Shaw, K., & Stone, W. L. (1988). Development of the Social Anxiety Scale for Children: Reliability and concurrent validity. Journal of Clinical Child Psychology, 17(1), 84–91.

LeDoux, J. E., & Pine, D. S. (2016). Using neuroscience to help understand fear and anxiety: A two-system framework. American Journal of Psychiatry.

Pine, D. S. (2001). Affective neuroscience and the development of social anxiety disorder. Psychiatric Clinics, 24(4), 689–705.

Pratt, M. L., & Hill, E. L. (2011). Anxiety profiles in children with and without developmental coordination disorder. Research in Developmental Disabilities, 32(4), 1253–1259.

Rowa, K., & Antony, M. M. (2008). Generalized anxiety disorder.