Do I Have Anxiety or am I Just Worried? A Psychiatrist’s Perspective
Anxiety is a normal part of life and serves as a protective mechanism, but at what point is worry actually anxiety? The anxiety response can be conceptualized as part of the brain’s alarm system firing during times of perceived danger. Unfortunately, some individuals experience an overactive “alarm system” and have difficulty turning down their internal alarm system, causing them to experience this normal emotion in excess. The clinical diagnosis of generalized anxiety disorder (GAD) includes excessive worry and anxiety that is difficult to control, as well as three or more of the following symptoms: restlessness/on edge, easily fatigued, trouble concentrating, irritability, muscle tension, and/or sleep disturbance. Researchers have found multiple genetic variants of 5-HT1A (serotonin) that have been linked to decreased serotonin neurotransmission in individuals with GAD. In addition to this, researchers have also found a genetic variant of 5-HT1A that is seen more frequently in females with GAD.
One key diagnostic feature of GAD is chronic worry, which can be defined as persistent, repetitive, negative thoughts that are usually verbal in nature. Research has shown that individuals with GAD use worry to down-regulate anxiety and negative emotions triggered by uncontrollable and unpredictable situations. Worrying becomes reinforced early in life for individuals with GAD when their feared outcomes that are the focus of their worries end up rarely happening. This creates an illusion, in a sense, that worrying is effective in preventing bad things from happening, thus creating a maladaptive strategy for emotion regulation.
Individuals with GAD have difficulty controlling their worrying. According to findings from several neuroimaging studies, there is increased activity in the dorsal anterior cingulate cortex (dACC) and the dorsal medial prefrontal cortex (dmPFC) when subjects are given a task that induces worry. The difference between healthy controls and individuals with GAD is that, when the worry inducing tasks were stopped, individuals with GAD continued to have hyperactivation in the dACC and dmPFC, which suggests that these individuals become inflexible once they develop the habit of worrying as a way to manage their anxiety and negative emotions.
Another difference found in individuals with GAD is that they will attend to threatening stimuli more readily and will be slower to disengage their attention from threatening stimuli compared to healthy controls. This is referred to as Attention Threat Bias and plays a key role in causing and maintaining worry in GAD. Individuals with GAD will even be triggered by mildly threatening stimuli and are less likely to recognize cues in the environment that signal safety.
Attention threat bias in GAD leads to selective activation of the amygdala and different areas within the PFC, specifically the dACC and dmPFC. Research has shown that individuals with GAD not only activate the amygdala during brief threat exposure, but are also more likely to activate the amygdala simply through anticipation of a possible threat.
The brain is a powerful organ and has survival mechanisms designed to keep us safe. Normally, the ventral PFC (vPFC) will be activated to appropriately assess the significance of a threat and possible safety cues in the environment. In addition to this, the vPFC also acts to down-regulate the amygdala if it becomes hyperactive in response to a threat. However, individuals with GAD do not activate the vPFC and therefore are unable to appropriately assess a threat or down-regulate the amygdala. This results in a sustained sense of threat and chronic stress.
There are several FDA approved medications to treat GAD. While each individual responds differently to each medication, one of the more effective FDA approved medications for GAD is Venlafaxine (Effexor). This medication is classified as an SNRI (serotonin norepinephrine reuptake inhibitor) and works by essentially increasing the amount of serotonin and norepinephrine in the synapse. Specifically, venlafaxine blocks the serotonin transporter (SERT) and the norepinephrine transporter (NET), thereby keeping both in the synapse longer. In doing this, there is more serotonin and norepinephrine available in the synapse to bind to and activate G-Protein-Coupled postsynaptic receptors, which increases neurotransmission for both. The benefit of using an SNRI over an SSRI (selective serotonin reuptake inhibitor) is that the symptoms are targeted and treated from two angles rather than just one. Targeting serotonin affects the individuals mood, anxiety, and sleep-wake cycle, while norepinephrine helps control anxiety, alertness, and arousal.
While medications can be very helpful in treating anxiety, they should be used in combination with therapy and seen as something that augments therapy rather than being the sole source of treatment. Treatment based entirely on medication contributes to the adoption of a passive participant in your healing process and does not help to foster greater control over the anxiety. One useful coping mechanism that can not only help reduce anxiety but also improve one’s overall wellbeing is meditation. Practicing mindfulness meditation or guided imagery teaches you to fully attend to present moment experiences, which can lead to improved attentional control, self-regulation, and the ability to analyze an action before engaging in it.
When thinking about how worrying manifests in your life, do you wish you could press pause on the persistent negative thoughts or feel overwhelmed by the constant pit in your stomach? If you’re curious about your own relationship with anxiety beyond the psychoeducational parts, start on your healing journey by reaching out to our team here. As a Psychiatric Nurse Practitioner, I strive to bring focus back to treating you as a whole rather than an isolated disorder. My focus in treatment is to provide a holistically dynamic integration of therapy and medication management with the goal of helping you lead a life unhindered by your mental health.
Written by Mind Body Co-op Psychiatric Nurse Practitioner, Luke Swift, DNP, APN, PMHNP-BC, who specializes in Care Coordination & Interdisciplinary Collaboration, Initial Psychiatric Evaluations, Medication Management and Second Opinion Consultation. Luke received his Masters in Nursing and Doctorate of Nursing Practice (DNP) from Rush University specializing in Psychiatry and is a board-certified Psychiatric-Mental Health Nurse Practitioner. He has experience at the inpatient, residential, and outpatient psychiatric levels of care. His passion is working with individuals and groups coping with any and all psychiatric disorders.
Mind Body Co-op is Chicago’s only space for individuals to discover, explore, and heal what is occurring internally at the cognitive, emotional, and physical levels. This unique, holistic approach to treatment and wellness is born out of the belief that examining the cognitive, emotional, and physical pieces and how they intersect helps lead to uncovering your full potential by providing thoughtful, collaborative, and complete integrative mental health care. We offer a variety of clinical services, including individual psychotherapy, group psychotherapy, psychological/neuropsychological assessments, medication management, CPT (comprehensive transitional program), somatic mindfulness, somatic groups, DBT, adventure therapy, therapeutic yoga, and more. We provide culturally competent services in English, Mandarin, Spanish, French, Russian & Arabic.