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Is anxiety high or low dopamine?

Anxiety is a complex condition that involves both psychological and biological factors. Dopamine is a neurotransmitter that plays a key role in the brain’s reward and pleasure pathways. There has been much debate around whether anxiety is characterized by abnormally high or low levels of dopamine.

The role of dopamine

Dopamine is one of the key neurotransmitters involved in anxiety. It is synthesized in the brain and plays a major role in the regulation of cognition, motivation, pleasure, and emotional arousal. Dopamine is released from neurons and binds to dopamine receptors on neighboring neurons to propagate signals between brain cells.

Dopamine is commonly associated with the brain’s reward system. When we engage in pleasurable activities like eating, having sex, or taking drugs, dopamine is released, reinforcing those behaviors. Dopamine is also involved in focus, attention, learning, and memory.

Given dopamine’s role in regulating mood and emotional states, it is closely linked to anxiety disorders. However, there are conflicting theories on whether anxiety is caused by excessive or deficient dopamine signaling.

The case for high dopamine and anxiety

Some research suggests that abnormally high dopamine levels may contribute to anxiety. Evidence for this theory includes:

  • Stress and anxiety increase dopamine release and turnover in animal studies.
  • Drugs that increase dopamine like amphetamines and cocaine can induce anxiety.
  • Antipsychotic medications that block dopamine receptors can reduce anxiety.
  • People with anxiety disorders may have enhanced dopamine transmission.

In conditions of acute, high stress, dopamine firing increases. This prepares the body to respond to perceived threats. However, chronically high dopamine activity may put the body in a constant state of stress and hyperarousal, leading to anxiety disorders.

Animal studies on dopamine and anxiety

Animal studies have found that exposing rodents to stressors causes a release of dopamine in brain regions like the prefrontal cortex, nucleus accumbens, and amygdala. These areas are involved in processing emotions, reward, and fear.

For example, one study exposed rats to the elevated plus maze test, which generates anxiety-like behaviors. Stressed rats showed increased dopamine levels and turnover in the prefrontal cortex and amygdala compared to controls. Drugs that blocked dopamine signaling prevented anxiety behaviors, suggesting high dopamine mediates anxiety.

Effects of dopaminergic drugs on anxiety

If dopamine contributes to anxiety, drugs that increase dopamine signaling should also increase anxiety. Studies have found supporting evidence for this:

  • Cocaine, which elevates extracellular dopamine levels, can induce panic attacks and anxiety in humans.
  • Amphetamines like Adderall, which increase dopamine release, are linked to heightened anxiety as a side effect.
  • Parkinson’s patients treated with levodopa/carbidopa, which increases dopamine, report increased anxiety.

Additionally, anti-psychotic medications used to treat schizophrenia act as dopamine receptor antagonists – blocking dopamine activity. These drugs, like haloperidol and chlorpromazine, have anti-anxiety effects in humans.

Therefore, artificially raising dopamine seems to induce anxiety, while lowering dopamine reduces it. This is consistent with the high dopamine theory.

Evidence for low dopamine and anxiety

On the other hand, some studies have found associations between anxiety and reduced dopamine activity:

  • People with anxiety may have lower baseline dopamine.
  • Some genetic polymorphisms linked to anxiety alter dopamine signaling.
  • Mice engineered to lack dopamine have severe anxiety behaviors.
  • Dopamine-enhancing drugs can relieve anxiety in some cases.

This suggests that an inherent deficiency in dopamine neurotransmission could predispose individuals to developing anxiety disorders.

Baseline dopamine differences

Neuroimaging studies using positron emission tomography (PET) have found that patients with social anxiety disorder, PTSD, and generalized anxiety disorder tend to show reduced dopamine receptor binding at baseline compared to healthy controls.

This implies they may have chronically low dopamine signaling, especially in the striatum area of the brain.

Dopamine-related genetic mutations

Variations in genes that control dopamine signaling have been linked to anxiety disorders:

  • COMT is involved in breaking down dopamine. The Val158Met polymorphism impairs COMT activity and increases dopamine. This variant is associated with anxiety in some populations.
  • DRD2 codes for the D2 dopamine receptor. Mutations linked to reduced D2 receptor density increase susceptibility to anxiety.

These mutations suggest altered dopaminergic neurotransmission arising from genetic factors may contribute to anxiety risk.

Dopamine deficiency in animal models

Selectively deleting dopamine receptors and transporters in mice is used to model dopamine deficiency. These genetic manipulations produce severe anxiety-like behaviors:

  • Mice without D1 receptors have impaired dopamine postsynaptic signaling. They show heightened anxiety across multiple behavioral tests.
  • Mice lacking the dopamine transporter DAT cannot clear released dopamine. They display anxious and depressed-like behaviors.

This indicates that lifelong dopamine signaling deficits can lead to anxious phenotypes in animals.

Anxiety involves dopamine system dysregulation

Rather than being strictly a high or low dopamine disorder, research indicates anxiety arises from improper dopamine regulation and dysfunction in dopamine neurotransmission pathways.

Evidence suggests individuals with anxiety cannot appropriately modulate their dopamine signaling. They may have:

  • Abnormally low tonic/baseline dopamine activity
  • Exaggerated dopamine release in response to stress
  • Impaired ability to terminate dopamine signals
  • Altered post-synaptic dopamine receptor sensitivity

Furthermore, dopamine dysfunction in anxiety may be region-specific. Some areas like the prefrontal cortex may be hyperdopaminergic, while others are hypodopaminergic.

In summary, anxiety involves dysregulation of dopamine neurotransmission rather than overall high or low dopamine levels.

Dopamine’s relationship to anxiety symptoms

Beyond contributing to anxiety risk, dopamine activity specifically influences anxiety’s physical and psychological symptoms:

Physiological arousal

The sympathetic nervous system controls the body’s fight-or-flight response. Dopamine modulates sympathetic outflow from the brain, increasing heart rate, blood pressure, sweating, and breathing rate. Through this mechanism, dopamine drives anxiety’s physical symptoms.

Fear and apprehension

Anxiety disorders are characterized by irrational fear and worry. As a neurotransmitter involved in emotional processing, dopamine signaling modulates the brain’s fear reactions. Abnormal dopamine function leads to a heightened threat response.

Cognitive patterns

Dopamine regulates working memory, concentration, and decision-making, which are often impaired in anxiety. Furthermore, altered dopamine activity contributes to the negative thought patterns, rumination, and cognitive biases of anxiety disorders.

Avoidance behaviors

Through its role in reward pathways, dopamine also motivates avoidance behaviors. People with anxiety excessively avoid perceived threats. Low dopamine function reduces motivation for pleasurable activities, furthering avoidance and withdrawal.

Therefore, proper dopamine signaling is essential for appropriate behavioral responses to potential threats versus non-threats.


Research indicates dopamine dysregulation is central to anxiety, however the exact nature of the relationship is complex. While some findings associate anxiety with exaggerated dopamine activity and reactivity to stress, other evidence points to deficient baseline dopamine levels.

Rather than being characterized by purely high or low dopamine, anxiety likely arises from improper modulation of the dopamine system that leads to dysfunctional neurotransmission. Dopamine imbalance contributes to both the psychological symptoms like irrational fear and cognitive distortions as well as physiological arousal in anxiety disorders.

Overall, dopamine signaling plays a crucial yet complex role in anxiety pathogenesis. More research is needed to elucidate the nuances of how dopamine dysfunction manifests in anxiety disorders in order to improve treatment.