From the Research
Yes, neural circuit dysfunction can increase cortisol levels in the body, as evidenced by the most recent and highest quality study available 1.
Background
Dysfunction in key brain regions like the hypothalamus, amygdala, and prefrontal cortex can disrupt the normal regulation of the hypothalamic-pituitary-adrenal (HPA) axis, which controls cortisol production.
- When neural circuits responsible for stress response become hyperactive or fail to properly inhibit stress signals, the hypothalamus releases excess corticotropin-releasing hormone (CRH), triggering a cascade that ultimately leads to increased cortisol secretion from the adrenal glands.
- This dysregulation can occur in various conditions including chronic stress, depression, anxiety disorders, post-traumatic stress disorder, and certain neurological conditions.
Clinical Implications
The elevated cortisol resulting from neural circuit dysfunction can have widespread effects throughout the body, including:
- Immune suppression
- Metabolic changes
- Cardiovascular effects
- Further impacts on brain function Treatment approaches often target these neural circuits through medications like selective serotonin reuptake inhibitors (SSRIs), cognitive behavioral therapy, mindfulness practices, or in some cases, medications that directly block cortisol production like ketoconazole or metyrapone for severe cases of hypercortisolism, as supported by studies such as 2 and 3.
Recent Findings
A recent study published in 2015 1 found that the neural regulation of the cortisol awakening response (CAR) is associated with reduced grey matter volume and increased stress-related brain activity in the perigenual anterior cingulate cortex (ACC), a region that inhibits HPA axis activity during stress.
- This study provides evidence for the role of the perigenual ACC in regulating the CAR in humans and may aid future research on the pathophysiology of stress-related illnesses, such as depression.
- The findings of this study are consistent with the idea that neural circuit dysfunction can contribute to increased cortisol levels, and highlight the importance of considering the neural mechanisms underlying HPA axis regulation in the development of treatments for stress-related disorders.