The Pain Effect

Posted: May 2022
Author: Sharlene Bennett |  BHSc, AdvDip Nat, AdvDip Med Herb
 

The development of chronic pain conditions in the body easily becomes a complex and misunderstood issue in-clinic. Pain in its acute form is designed to alert us that something is wrong and then encourages the repair and recovery processes in the body, both physically and mentally. When pain develops into a more chronic condition, it can become a long-term debilitating illness and commonly accompanies or initiates other chronic diseases.

The pain effect – how it all begins?

Long term pain can result from systemic inflammation and pro-inflammatory mediators including cytokines and molecular release of certain compounds such as cox 1 and 2, cytokine production and the pain neuro pathways, including NF-KB. This all helps to drive the genetic expression of disease and inflammation in the body, acting on a cellular level. One of the core drivers of any chronic disease, from diabetes to cardiovascular to joint mobility conditions, is believed to be widespread body inflammation.^1,5

The pain neurotransmitters – helping solve the mystery

Our neurotransmitters like serotonin, dopamine and GABA all play a pivotal role in the release of pro-inflammatory or anti-inflammatory compounds. It is an intrinsic and delicate balancing act, with just enough neurotransmitter release helping in recovery and is essential for mood. Whereas too much neurotransmitter production and release can act as an opposing force, hindering recovery and contributing to the picture of chronic pain in the body.^1,5

The dual action of serotonin

The release of serotonin within our neural pathways and axon terminals can contribute to our pain response for better or worse. Any excessive release of serotonin through the nervous system can result in overstimulation of the pain and inflammatory pathways. While just enough serotonin production and release is helpful. The same rules apply to our reward neurons, dopamine and GABA, to help with a healthy pain response in the body. Just like the serotonin effect, too much or an imbalanced production of dopamine and GABA may cause and become a driving factor for chronic inflammatory conditions in the body.⁵

The brain centres – achieving equilibrium

Normal serotonergic activity helps to modulate pain, alongside GABAergic neuronal endings, these both have descending projections into the spinal nervous system. From there the neuronal communication reaches and is interlinked via the bi-directional gut/brain axis and brain regions which largely process and respond to pain stimuli or messengers. The periaqueductal gray (PAG) is a vital brain region, that has been shown to act as a pain inhibitory system. The PAG receives the processing information from the higher brain centres around it, such as the rostroventromedial medulla (RVM) which also communicates with the thalamus, making it an end messenger and supports the PAG brain area to act as a potent analgesic.^1,2

These brain centres are all interlinked and cross communicate with serotonergic receptor sites and neurotransmitter pathways, including adrenergic receptors that modulate the adrenal response in the body, such as cortisol, adrenaline and noradrenaline. The brain centres help to act either with an analgesic effect or as an innate inflammatory driver. In cases where excessive neurotransmitter function and release occurs, the result can be overstimulated and overactivated dorsal spinal nerve endings, which encourages an overactive pain response.^1,5

Helping the pain effect – finding the off switch

The ongoing dysfunction and chronic nature of endogenous pain inhibition in the body is largely reliant on multiple contributing factors such as generic neurotransmitter release and production, alongside multiple shared neuro-pathways such as brain-gut and many other bi-directional pathways.

The chronic disease state drives dysfunction and may be part of the picture in well-known chronic conditions such as IBS, IBD or osteoarthritis. The involved brain centres exposed to long term stress may experience or encourage neuroplastic changes, thus becoming an end driver for chronic pain and the cycle of systemic inflammation.

Phytotherapy – helping homeostasis

The inclusion of phytotherapy may help in supporting and managing a healthy pain response. Some top therapeutic botanicals can include Turmeric, White Willow bark, California Poppy, Jamaican Dogwood, Kava, and Ginger.

Where there is neuropathic pain, California Poppy and Jamaican Dogwood support the inhibition of neural pain pathways and inflammation. Turmeric and Willow bark offer options for systemic inflammation, and if back or muscular pain is indicated, Willow can be a consideration. Kava is a relevant choice when pain, sleeplessness and stress are part of the overall picture. While Ginger is suitable for IBS or IBD disorders as a conjunctive herbal botanical for easing digestion and body inflammation.

Herbal botanicals can help in addressing the drivers of chronic disease alongside everyday management of symptoms, helping in-clinic results and the whole effect, from pain relief to wellbeing.  

References:

1. Ossipov, M. H., Morimura, K., & Porreca, F. (2014). Descending pain modulation and chronification of pain. Current opinion in supportive and palliative care, 8(2), 143–15 https://doi.org/10.1097/SPC.0000000000000055
2. Szok, D., Tajti, J., Nyári, A., & Vécsei, L. (2019). Therapeutic Approaches for Peripheral and Central Neuropathic Pain. Behavioural neurology, 2019, 8685954. https://doi.org/10.1155/2019/8685954
3. Lee, J. W., & Park, H. S. (2015). Relation of the factor to menstrual pain and musculoskeletal pain. Journal of exercise rehabilitation, 11(2), 108–111. https://doi.org/10.12965/jer.150188
4. Sommer C. (2004). Serotonin in pain and analgesia: actions in the periphery. Molecular neurobiology, 30(2), 117–125. https://doi.org/10.1385/MN:30:2:117
5. Cortes-Altamirano, J. L., Olmos-Hernandez, A., Jaime, H. B., Carrillo-Mora, P., Bandala, C., Reyes-Long, S., & Alfaro-Rodríguez, A. (2018). Review: 5-HT1, 5-HT2, 5-HT3 and 5-HT7 Receptors and their Role in the Modulation of Pain Response in the Central Nervous System. Current neuropharmacology, 16(2), 210–221. https://doi.org/10.2174/1570159X15666170911121027
6. Roth, W., Zadeh, K., Vekariya, R., Ge, Y., & Mohamadzadeh, M. (2021). Tryptophan Metabolism and Gut-Brain Homeostasis. International journal of molecular sciences, 22(6), 2973. https://doi.org/10.3390/ijms22062973