What causes anxiety in the brain?


Anxiety is a common mental health disorder that affects millions of people worldwide. It involves feelings of worry, fear, tension, and apprehension. While anxiety is a normal emotion that everyone experiences from time to time, some people suffer from excessive, persistent anxiety that disrupts their daily lives. Understanding what causes anxiety in the brain can help improve treatments and management strategies.

What causes anxiety in the brain?

The Biology Behind Anxiety

Several parts of the brain are involved in generating feelings of anxiety. The most important include:

The Amygdala

The amygdala is an almond-shaped set of neurons located deep in the temporal lobes. It plays a key role in processing emotions, emotional memories, and fear responses. The amygdala is responsible for triggering the “fight-or-flight” response to perceived threats. When the amygdala detects danger, it sends signals to other parts of the brain that control fear and anxiety responses like increased heart rate, sweating, and hyperventilation. Overactivity of the amygdala has been linked to anxiety disorders.

The Hippocampus

The hippocampus is located next to the amygdala and is also involved in processing emotional memories and controlling the stress response. It influences anxiety levels by interacting with the amygdala and regulating release of cortisol, the primary stress hormone. Impaired hippocampal function can lead to excessive cortisol release and increased anxiety.

The Prefrontal Cortex

The prefrontal cortex (PFC) regulates rational thinking and conscious decision making. It can override automatic fear responses from the amygdala. Poor PFC function leads to decreased inhibition of the amygdala, resulting in exaggerated anxiety reactions. The PFC also governs working memory processes tied to anxiety.

The Cingulate Gyrus

The cingulate gyrus coordinates signals between the amygdala, PFC, and other areas. Problems with cingulate gyrus connections to the PFC may play a role in anxiety disorders. Altered function in this region has been linked to excessive worry seen in generalized anxiety disorder.

Neurotransmitters and Anxiety

In addition to key brain regions, chemical messengers called neurotransmitters also influence anxiety levels. The main neurotransmitters implicated include:

Gamma-Aminobutyric Acid (GABA)

GABA is the brain’s primary inhibitory neurotransmitter, meaning it reduces neuronal activity and promotes calm. Low GABA levels leave the brain prone to excessive excitability. This can trigger increased anxiety, restlessness, and agitation. Many anti-anxiety medications work by increasing GABA activity.


Serotonin regulates mood, social behavior, appetite, digestion, sleep, and inhibition of anger and aggression. Low serotonin is associated with increased anxiety and decreased emotional control. Selective serotonin reuptake inhibitors (SSRIs) boost serotonin to treat anxiety.


Also called noradrenaline, norepinephrine influences the body’s fight-or-flight stress response via the sympathetic nervous system. Excess norepinephrine can cause anxiety, increased heart rate and blood pressure, insomnia, and restlessness. Some antidepressants work by blocking norepinephrine activity.


Dopamine is involved in pleasure, motivation, and reward pathways in the brain. Low dopamine is linked to loss of motivation, decreased enthusiasm, and avoidance behaviors seen in some anxiety disorders. Dopamine-targeting substances have shown promise for managing treatment-resistant anxiety symptoms.


Glutamate is the brain’s primary excitatory neurotransmitter. Too much glutamate can cause excessive neuronal firing and feelings of agitation, panic, and overwhelm. Research shows elevated glutamate levels in certain anxiety disorders. Glutamate-modulating drugs may benefit anxiety treatment.

Genetic Factors

Research shows that anxiety disorders tend to run in families, indicating a genetic component. Specific genes that may be implicated include:

  • Serotonin transporter gene (SERT)
  • Catechol-O-methyltransferase gene (COMT)
  • Brain-derived neurotrophic factor gene (BDNF)
  • FKBP5 gene

These genes are involved in neurotransmitter systems like serotonin that influence brain processes tied to stress reactivity, emotional regulation, and anxiety. Certain variants of these genes may predispose people to anxiety by altering neurotransmitter signaling pathways.

Environmental Triggers

In those genetically predisposed, certain environmental exposures can trigger problematic anxiety. Key contributors include:


Both acute and chronic stress disrupt neurotransmitter balance, impair PFC function, and sensitize the amygdala. This leads to exaggerated fear and anxiety responses to everyday challenges. Early life adversity may cause lasting neurological changes that manifest as anxiety later on.


Traumatic experiences like abuse, disasters, accidents, violence, or significant loss can alter the brain’s fear circuitry. PTSD involves overactivity of the amygdala along with too little PFC inhibition, causing severe anxiety reactions.

Substance Abuse

Drug or alcohol abuse can directly worsen anxiety as well as lead to withdrawal-related anxiety after stopping use. Substances also alter neurotransmitter systems linked to mood regulation over time, allowing anxiety to develop.

Medical Conditions

Various medical problems that affect neurotransmitter balance, brain function, or stress hormones can trigger anxiety as a symptom. Examples include thyroid disorders, hormone imbalances, gut issues, chronic pain, and neurodegenerative disorders.

The Vicious Cycle of Anxiety

Once present, anxiety can perpetuate itself through several vicious cycles that maintain and intensify symptoms:

  • Avoidance of anxiety-provoking situations prevents learning that feared outcomes are unlikely, keeping anxiety levels high.
  • Hypervigilance and scanning for threats strengthens neural pathways involving fear and anxiety.
  • Tense muscles, poor sleep, and bad habits like skipping meals keep the body stressed, feeding anxiety.
  • Anxious rumination (repeated worrying) strengthens associated thought patterns in the brain.
  • Social isolation and loneliness due to anxiety removes key social supports and outlets for stress.


In summary, anxiety arises in the brain when there is dysfunction in fear and emotion centers like the amygdala and PFC along with imbalances in neurotransmitters like serotonin, GABA, and norepinephrine. This may occur due to genetic vulnerabilities, stressful life experiences, medical issues, or substance abuse. Once present, anxiety symptoms tend to worsen through avoidance, rumination, isolation, and a stressed body state. Recognizing the neurological underpinnings of anxiety can lead to improved therapies targeting specific brain mechanisms over time.

Detailed Fact Section

  • The amygdala is the brain's emotional processing center and triggers the fight-or-flight response when danger is perceived. Overactivity of the amygdala is linked to excessive fear and anxiety.
  • The hippocampus regulates emotional memories and stress hormone release. Impaired hippocampal function can lead to high cortisol levels and increased anxiety.
  • The prefrontal cortex controls rational thinking, decision making, and inhibition of the amygdala. Poor PFC function results in an unchecked amygdala, heightening anxiety reactions.
  • The cingulate gyrus coordinates signals between emotion and thinking centers of the brain. Abnormalities here are tied to excessive worry in anxiety disorders.
  • Gamma-aminobutyric acid (GABA) is the brain's main inhibitory neurotransmitter. Low GABA allows excess neuronal excitability and anxiety.
  • Serotonin regulates mood, inhibition, digestion, sleep, and aggression. Low serotonin levels are linked to increased anxiety and emotional reactivity.
  • Norepinephrine mediates the fight-or-flight stress response. Too much norepinephrine can generate anxiety symptoms like rapid heart rate.
  • Dopamine influences motivation, pleasure, and reward pathways. Low dopamine is associated with loss of motivation and avoidance in anxiety disorders.
  • Glutamate is the brain’s main excitatory neurotransmitter. High glutamate levels may lead to excessive neuronal activity and anxious feelings.
  • Genetic variants in genes like SERT, COMT, BDNF, and FKBP5 may predispose people to anxiety by altering neurotransmitter systems.
  • Stress, trauma, medical issues, and substance abuse can trigger anxiety in those with genetic vulnerabilities by disrupting neurotransmitter balance.
  • Avoidance, hypervigilance, isolation, poor self-care, and rumination can worsen anxiety through negative reinforcement cycles in the brain.


  • Anxiety arises from a combination of genetic tendencies, environmental triggers, and vicious cycle effects in the brain.
  • Key brain regions involved include the amygdala, hippocampus, prefrontal cortex, and cingulate gyrus.
  • Imbalances in neurotransmitters like GABA, serotonin, norepinephrine, dopamine, and glutamate underlie anxiety's neurological basis.
  • Understanding the biological causes of anxiety informs treatment strategies targeting specific brain mechanisms and neurotransmitter systems.
  • Research into the neurobiology of anxiety holds promise for improving medications, psychotherapy techniques, and holistic management approaches over time.
  • A multifaceted approach addressing genetic vulnerabilities, thought and behavior patterns, lifestyle factors, and brain health is needed to fully overcome problematic anxiety.

Resources used to write this article

National Institute of Mental Health pages on Anxiety Disorders and The Brain and Anxiety

American Psychiatric Association pages on What Are Anxiety Disorders?

Anxiety and Depression Association of America pages on Understanding the Facts of Anxiety Disorders and Depression

Brain & Behavior Research Foundation pages on Anxiety Disorders

Cherry, K. (2020). How Does the Brain Work? VeryWell Mind.

Harvard Health Publishing. (2018). Understanding the stress response.

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