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The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
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Panic disorder is an anxiety disorder characterized by recurrent and sudden minutes-long episodes of intense fear, known as panic attacks. These attacks may feel like heart attacks and often happen without warning or a specific cause. They can include symptoms such as rapid heart rate, shortness of breath, chest pain, trembling, sweating, dizziness, and a sense of helplessness. During a panic attack, individuals may feel as though they are experiencing a heart attack or are in a...
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CO2 challenge induced HPA axis activation in panic.

Marlies A van Duinen1, Koen R J Schruers, Michael Maes

  • 1Maastricht University, Department of Psychiatry & Neuropsychology, and Vijverdal Academic Anxiety Center, The Netherlands.

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The hypothalamic-pituitary-adrenal (HPA) axis shows a similar response to CO(2) inhalation in panic disorder patients and controls. This suggests panic disorder may not involve initial HPA axis overactivation during panic attacks.

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Area of Science:

  • Neuroendocrinology
  • Psychiatry
  • Stress Physiology

Background:

  • The hypothalamic-pituitary-adrenal (HPA) axis is crucial for stress response.
  • Its role in panic disorder (PD) is debated, with prior studies showing inconsistent cortisol responses to CO(2) challenges.
  • Cortisol alone may not fully represent HPA axis activity.

Purpose of the Study:

  • To investigate the HPA axis response to CO(2) inhalation in PD patients compared to healthy controls.
  • To measure both cortisol and adrenocorticotropic hormone (ACTH) levels.
  • To clarify the HPA axis's involvement in the pathophysiology of panic disorder.

Main Methods:

  • Double-blind, placebo-controlled study with 16 PD patients and 16 healthy controls.
  • Participants underwent 35% CO(2) inhalation and placebo inhalation on separate days.
  • Serum and salivary cortisol and ACTH levels were measured at regular intervals.

Main Results:

  • Both PD patients and controls exhibited increased cortisol and ACTH levels after CO(2) inhalation.
  • The magnitude of the HPA axis response was similar between groups, irrespective of anxiety levels.
  • This is the first study to demonstrate a clear HPA response to CO(2) in both PD patients and controls.

Conclusions:

  • CO(2) inhalation reliably activates the HPA axis in both panic disorder patients and healthy individuals.
  • This HPA axis activation appears independent of the panicogenic effects of CO(2).
  • Further research is needed to determine if panic originates from HPA axis activation or other stress systems.