This essay explores the potential mechanisms that may account for functional gastrointestinal disorders (FGIDs), and how that correlates to the stress levels of the individual. With a brief introduction on the complexity of visceral pain, the paper explores theories of how and why chronic gastrointestinal develops using two research papers that center around the relationship between stress and FGIDs, specifically irritable bowel syndrome (IBS). The essay also contextualizes how this correlation between stress and chronic gastrointestinal pain plays a role in the overlap between patients who also suffer from trauma or mental health disorders and those who suffer from FGIDs.
Chronic Gastrointestinal Pain: How Stress affects it and why it Matters
Chronic gastrointestinal pain is a common phenomena that comes in different forms; however many of the disorders are still not quite understood. Yet with 20% of the world suffering from Irritable Bowel Syndrome, (“Mechanisms of Stress-Induced Visceral Pain” 2015.), and an estimate of 11-29.2% of people globally living with functional dyspepsia (“Epidemiology of functional dyspepsia: A global perspective”, 2006.), there is far too little understanding for the basic causes and correlations of chronic abdominal pain. The effects of stress on chronic gastrointestinal pain reveal the foundation of this phenomena occurs on neurochemical level between the gut and brain, and thus applying that correlation can potentially lead the future of treating and understanding chronic gastrointestinal pain disorders.
To bring perspective on the complex nature of gastrointestinal visceral pain and why it still remains such a mystery in the medical community, it should be noted the significant differences between visceral and somatic sensory. For instance, visceral nociceptors respond to different stimuli than somatic; an example is visceral nociceptors usually do not respond to a cut on a hollow organ, but will respond to a contraction of a hollow organ. Another fundamental characteristic is visceral pain tends to be poorly localized, and even occasionally diffuses outside of the abdominal region (“Behavioral Neurobiology of Chronic Pain”,2016). These differences in how visceral pain is how processed makes it difficult to study and translate it based what is already known about somatic sensory.
What is known about the mechanisms of the gastrointestinal pain is the visceral afferents (i.e. the vagal afferents, nucleus tractus solitarius, and spinoparabrachial projections) of the enteric system converge to the dorsal column (Visceral Pain – the Ins and Outs, the Ups and Downs, 2012.). From there, the message passes through the thalamus, up to the somatosensory cortex for pain localization, and then to the cingulate cortex, insular cortex, and limbic system (specifically the amygdala) for additional autonomic, neuroendocrine, and emotional processing (“Mechanisms of Stress-Induced Visceral Pain”, 2016). The visceral afferents that sense noxious visceral stimuli are called visceral nociceptors (pain receptors). Visceral receptors are unique in having insensitive nociceptors which can obtain sensitivity to specific mechanisms such as inflammation (although not a very well understood type of nociceptor, the notion implies they play a crucial role in chronic gastrointestinal pain) (“Mechanisms of Stress-Induced Visceral Pain”, 2016). Between this lack of understanding of these insensitive nociceptors and the lack of understanding of the exact neurological processing of visceral pain the cerebral cortex and limbic system, there is still a long way to go in decoding the neurotransmission that accounts for chronic visceral pain.
Yet, what can be induced by the fact that pain is processed in the insular cortex (which is thought to process consciousness and self-awareness), the cingulate cortex (which is involved in emotion processing, learning, and memory), and limbic system (which controls emotion and memory), is that visceral pain is not something exclusively sensed at face value, but the result of sensation, cognition, memory, and emotion. Evidence of how one’s psychological state can affect gastrointestinal pain can be seen in the fact that irritable bowel syndrome (IBS) is correlated to veterans (“Mechanisms of Stress-Induced Visceral Pain”, 2016.), as well as those with anxiety, depression, childhood trauma (The relationship between irritable bowel syndrome and psychiatric disorders, 2014). At the very least the correlation suggests those who have experienced or regularly acute anxiety may have a lower threshold to gastrointestinal pain, if not more prone to gastrointestinal hyperalgesia. Furthermore, it is commonly known stress is a trigger or consistently worsens the symptoms of gastrointestinal disorders such as IBS and ulcerative colitis. Thus, this research indicates stress not only may be correlated to the development of gastrointestinal disorders but actively evokes the symptoms. A more psychological theory in response to this evidence is that those with higher levels of stress merely have a tendency to focus or notice their gastrointestinal motion or pain more than those without (“Stress-Induced Chronic Visceral Pain of Gastrointestinal Origin”, 2017), and thus they may be propelling their symptoms. The process is illustrated as the patient experiences gastrointestinal discomfort, their stress levels rise in response, thus their gastrointestinal symptoms worsen in responses, creating a positive feedback cycle (“Stress-Induced Chronic Visceral Pain of Gastrointestinal Origin”, 2017). This view of chronic gastrointestinal pain as more of psychologically charged phenomena can explain some of the more biologically daunting questions such as “how does the pain diffuse” and “how does stress and trauma influence it.” To deviate more on the theoretical perspective of how pain is consciously located, philosopher Murat Ayede in the (“The Stanford Encyclopedia of Philosophy” 2013.) elaborates:
“[Pain location] is represented by pain experiences…even though there is an attribution of pain to a bodily location, the proposed analysis says that this is not what is going on…I attribute to myself a feeling state (an experience) which has an intentional content to the effect that a certain region of my body is in a physical condition of a certain sort.”
Ayed’s point is that pain is a sensation formed in our minds, and from there, our mind creates the location and experience based on context. In terms of chronic visceral pain and why it localizes so poorly, why it diffuses, and why it is triggered at times by little to no stimuli, this philosophy may be explain how our minds may be potentially misrepresenting the pain experience it is having, thus misattributing the pain to another location, or even fabricating the feeling state in order to suit the whatever it may be experiencing internally.
With all this information currently known about gastrointestinal pain, one can begin to understand the difficulty in attempting to decipher the mechanisms of FGIDs. Unlike other abdominal pains, FGIDs have no known cause of symptoms. As of now, there is no answer in the medical community as to how exactly these functional gastrointestinal disorders develop. However, due to the correlation of those with mental disorders and trauma and those who suffer from FGID, there have been more research conducted specifically investigating the comorbidities of these gastrointestinal disorders and how stress may be the link to all of it.
An example of this can be found in “Combined effect of early life stress and acute stress on colonic sensory and motor responses,” 2011. The research centers on the effects of neonatal maternal separation and acute stress on a rat’s gastrointestinal pain threshold. The groups were: the control group, a group separated from their mothers for 2-14 days, a group put on plank above floating water for an hour, a group subjected to both scenarios, and then two other groups also put under both scenarios, however were also given two different doses of Parachlorophenylalanine (PCPA), a chemical that promotes serotonin reuptake. They recorded the sensitivity of the intestinal tract by placing an abdominal distention balloon inside their colon, then expanding it until they detected an abdominal contraction. Through the time it took for their abdomen to contact, they determined their pain thresholds. The results proved the first two experimental groups experienced both had significantly lower pain thresholds, and what is more is that the two groups treated with PCPA had significantly higher thresholds. The findings reveal both acute stress and early life stress result in gastrointestinal hyperalgesia, and that the stress that causes this gastrointestinal hyperalgesia is correlated with serotonin pathways.
Another example of research focusing on the effects of cortisol on the gastrointestinal tract is “Cortisol Levels and Gastrointestinal Disorders After Stressful Surgery in Rabbits” (2017). The experiment displays the effects of heightened cortisol levels in rabbits who just operated on for allogeneic tracheal surgery, proving how “rabbits with [gastrointestinal disturbance] GI disturbance had higher cortisol levels than the otherwise healthy rabbits.” Because rabbits have a much more intensified reaction to stress, immediately after surgery the majority of the rabbits experienced symptoms of gastrointestinal disorders such as diarrhea, weight loss, and depression. Their autopsies in the end corresponded to the fact they were suffering from gastrointestinal dysfunctions such as pockets of gas, fatty livers, and high levels of bile. The report also suggests due to the nature of the cortisol slowing down the digestive tract, extensive periods of cortisol in the digestive tract causes food to build up in the digestive tract, thus cortisol is likely the causing the pockets of gas, high levels of stomach acid, etc…
Discussion
The evidence reveals that the brain-gut axis that accounts for chronic pain is governed by hormones and psychological perception, which ultimately explains how extended periods of stress inevitably increase the likelihood of FGIDs. This concept also accounts for the reason why victims of trauma and mental disorders (specifically the ones with symptoms of acute stress such as anxiety disorders and depression) are more like to suffer from FGID. Lastly, this correlation may further be used to promote treating those FGID’s and some of the stress-related comorbidities listed above with antidepressants and anxiety medication, with the hope of alleviating a significant portion of their symptoms.
Despite this promising evidence, there are still many questions unanswered. There is still no explanation to the exact mechanisms that cause of FGIDs. There is still no accounting for FGID patients who do not suffer from prolonged or acute stress, nor those who experience specific dietary triggers. There is still a lack of a clear explanation as to why women are more likely to suffer from FGIDs (“Mechanisms of Stress-Induced Visceral Pain”, 2016) and what that also means to the development of FGID. The evidence of women particularly struggling with chronic pain is deep-rooted in history, “Given their heightened sensibility, women were assumed to be especially vulnerable to the ill effects of immoderate ingestion and were sternly counseled to avoid extremes of eating and drinking” (“Neuroses of the Stomach”,2007.). The article goes on to say that women have been tied to stomach pains and “diseases of the will” as far back as the 1800s, yet doctors still struggle to find a psychopathological reason. And with IBS costing indirect US citizens approximately 30 million dollars annually (“Review article: epidemiology and quality of life in functional gastrointestinal disorders”, 2004.) as well as forcing patients patients with acute symptoms to bed rest 145 days of the years (“Health-related quality of life and health care costs in severe, refractory irritable bowel syndrome”,2001.), the situation of these millions of women, veterans, and patients of mental health disorders seem dire.
Without the proper cause of gastrointestinal disorders, effective generalized treatments are nowhere in sight. The medical community will have to further investigate the enteric system, the brain-gut axis, and psychological mechanisms for hyperalgesia before one can begin to effectively understand these chronic functional disorders. Given the time it took for research to progress this far, the odds of the medical community making this degree of progress in the near future slim.
References
Aydede, M. (2004). Pain. In Stanford encyclopedia of philosophy(Spring 2013 ed.). Stanford, CT: Stanford University, Metaphysics Research Lab.
Bian, Z., Qin, H., Tian, S., & Qi, S. (2011). Combined effect of early life stress and acute stress on colonic sensory and motor responses through serotonin pathways: Differences between proximal and distal colon in rats. Stress,14(4), 448-458. doi:10.3109/10253890.2011.558604
Chang, L. (2004). Review article: Epidemiology and quality of life in functional gastrointestinal disorders. Alimentary Pharmacology and Therapeutics,20(S7), 31-39. doi:10.1111/j.1365-2036.2004.02183.x
Creed, F. (2001). Health-Related Quality of Life and Health Care Costs in Severe, Refractory Irritable Bowel Syndrome. Annals of Internal Medicine,134(9_Part_2), 860. doi:10.7326/0003-4819-134-9_part_2-200105011-00010
Elizabeth A. Williams, "Neuroses of the Stomach: Eating, Gender, and Psychopathology in French Medicine, 1800–1870," Isis 98, no. 1 (March 2007): 54-79.
Fadgyas-Stanculete, M., Buga, A. M., Popa-Wagner, A., & Dumitrascu, D. L. (2014). The relationship between irritable bowel syndrome and psychiatric disorders: from molecular changes to clinical manifestations. Journal of molecular psychiatry, 2(1), 4. doi:10.1186/2049-9256-2-4
Furness, J. B. (2012). The enteric nervous system and neurogastroenterology. Nature Reviews Gastroenterology & Hepatology,9(5), 286-294. doi:10.1038/nrgastro.2012.32
Greenwood‐Van Meerveld, B. , Moloney, R. D., Johnson, A. C. and Vicario, M. (2015). Mechanisms of stress-induced visceral pain in irritable bowel syndrome. Psychoneuroendocrinology,61, 8-9. doi:10.1016/j.psyneuen.2015.07.410
Jang, S. J., Kang, S. S., Son, S. J., Lee, J. Y., Kim, G., & Choi, S. H. (2017). Cortisol Levels and Gastrointestinal Disorders After Stressful Surgery in Rabbits. In vivo (Athens, Greece), 31(4), 637-640.