Hypothalamo-Pituitary-Adrenal Axis
I touched on the Hypothalamo-pituitary-adrenal axis in the last post.
So what is the Hypothalamo-pituitary-adrenal (HPA) Axis and what do I think we need to know about it?
The HPA Axis is:
- a central control and regulatory system of the organism that connects the central nervous system (CNS) with the hormonal system. This stress-responsive system helps the organism:
- adapt to increased demands and maintain homeostasis after challenge.
- support normal physiological functioning.
- (Kudielkaa and Kirschbaum, 2005)
The end product of the HPA axis is cortisol (a glucocorticoid) which is a hormone that:
- plays a critical role in metabolism by mobilizing resources to provide energy.
- regulates or impacts on other important physiological systems, like the immune system, the sympathetic-adrenal-medullary (SAM) axis, the cardiovascular system, as well as affective and cognitive processes.
- (Kudielkaa and Kirschbaum, 2005)
As mentioned in the “Importance of Sleep” post:
- Subsequent increases in concentrations of cytokines and cortisol is most likely due to increased activation of the Hypothalamo-Pituitary-Adrenal (HPA) Axis (Balbo et al, 2010).
So we can see that if the HPA axis is “activated” by increased demands/stresses that the end result is likely to be increased levels of cytokines and cortisol.
What are cytokines and cortisol?
- Cytokines:
- Milligan and Watkins (2009)
- A chemical signal released by immune cells that significantly alters many cell types, including other immune cells.
- Lead to pro-inflammatory responses with effects, such as neuronal hyperexcitability, neurotoxicity and chronic inflammation.
- Milligan and Watkins (2009)
- Cortisol:
- Gatchel et al (2007)
- Main hormonal product of the HPA axis in humans. Although increased cortisol secretions are considered an adaptive response of the organism when stressed (for purposes of energy mobilization), prolonged secretion can lead to negative effects such as muscle atrophy, impairment of growth and tissue repair, immune system suppression, and so forth.
- Melzack (2001 and 2005)
- Cortisol is an essential hormone for survival after injury because it is responsible for producing and maintaining high levels of glucose for rapid response after injury, threat, or other emergency.
- Is potentially a highly destructive substance because, to ensure a high level of glucose, it breaks down the protein in muscle and inhibits the ongoing replacement of calcium in bone.
- Sustained cortisol release, therefore, can:
- Produce myopathy, weakness, fatigue, and decalcification of bone.
- Suppress the immune system.
- Gatchel et al (2007)
So basically my interpretation of the above is that:
- Disrupted/sustained activity of the HPA Axis by continued “stressors” such as fear, anxiety, depression, lack of sleep, pain etc may lead to increased levels of cytokines and cortisol.
- The combined effects of the increased levels of cytokines and cortisol can potentially lead to occurrences such as:
- Impairment of tissue/injury repair
- Loss of muscle mass
- Increased levels of inflammatory mediators
- All of these issues could potentially create Inflammatory signs and symptoms and/or heightened levels of tissue sensitivity i.e. Peripheral Sensitisation.
References:
Balbo M, Leproult R, Van Cauter E. Impact of Sleep and Its Disturbances on Hypothalamo-Pituitary-Adrenal Axis Activity. International Journal of Endocrinology (2010):1-16.
Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychological Bulletin (2007); 133 (4):581-624.
Melzack, RPain and the neuromatrix in the brain. Journal of Dental Education. (2001); 65:1378–1382.
Melzack, R. Evolution of the neuromatrix theory of pain. Pain Practice (2005); 5:85–94.
Milligan ED, Watkins LR. Pathological and protective roles of glia in chronic pain. Nat Rev Neurosci. (2009); 10(1): 23–36.
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