The etiology and pathogenesis of anxiety disorders

The etiology and pathogenesis of anxiety disorders mainly involve the interaction of multiple factors, such as genetic factors, neurotransmitter imbalances, psychosocial factors, abnormal brain function, and endocrine system disorders.

1. Genetic factors

Family studies have shown that anxiety disorders have a significant genetic predisposition, with a significantly higher probability of first-degree relatives being affected than the general population. Specific genes such as serotonin transporter gene polymorphism may affect an individual's sensitivity to stress. Twin studies have confirmed a high genetic contribution, but environmental factors still play a key regulatory role.

2. Neurotransmitter imbalance

The dysfunction of the gamma aminobutyric acid system is associated with excessive alertness, while the hyperactivity of the noradrenergic system leads to enhanced physiological arousal. Abnormal regulation of the serotonin system affects emotional stability. When the dynamic balance of these neurotransmitters is disrupted, it may trigger sustained pathological anxiety reactions.

3. Psychosocial factors

Childhood traumatic experiences such as emotional neglect or abuse may form unsafe psychological representations, long-term chronic stress may consume psychological resources, and major life events such as unemployment or bereavement may become acute triggers. Catastrophic thinking and excessive control tendencies in cognitive patterns can maintain anxiety states.

4. Abnormal brain function

Overactivation of the amygdala enhances threat perception, weakened regulation of the prefrontal cortex leads to emotional regulation disorders, and changes in hippocampal volume affect situational assessment ability. Functional magnetic resonance imaging shows that abnormal activity patterns in these brain regions are correlated with the severity of clinical symptoms.

5. Endocrine system disorders

Overactivation of the hypothalamic pituitary adrenal axis leads to abnormal cortisol levels, thyroid dysfunction may induce somatic anxiety, and fluctuations in sex hormones are associated with the onset of specific types of anxiety disorders. Endocrine changes participate in the pathogenesis process by affecting neural plasticity.

In response to the pathogenesis of anxiety disorders, it is recommended to establish a regular sleep schedule to ensure adequate sleep, use progressive muscle relaxation training to regulate autonomic nervous system function, maintain moderate aerobic exercise to promote endorphin secretion, improve brain default mode network activity through mindfulness meditation, and pay attention to reducing caffeine and alcohol intake to maintain neurotransmitter balance. When symptoms continue to affect daily life, professional psychological assessment and systematic treatment should be sought in a timely manner.