RESEARCH
There is abundant evidence from research, conducted through ‘RCTs’ (Randomised Control Trials), that our mind and body states are affected by our emotions. Imbalances in our bodies’ systems, which can be triggered by our emotions, lead to pain – and, in some instances, chronic pain.
Tension and stress, as well as emotional traumas that haven’t been healed, can create great disturbance in neural networks. Receptors attached to the membrane of virtually every cell wait for messenger molecules called ligands to come by. The binding of receptor to ligand is a vital part of the infrastructure for cellular dialogue. These receptors are present in all parts of the brain and the limbic system and are also present in the immune system, our defence mechanism, and the endocrine system. Emotions such as fear, anger, sadness, joy etc., have a biochemical response at the cellular level. The impact of stress and tension, as well as repressed emotional trauma, blocks the information molecules at the level of the receptors and disrupts cellular communication. When this disruption continues over an extended period the integrity of the cell is weakened.
Professor Lorimer Moseley and Dr David Butler at the School of Health Sciences, University of South Australia have undertaken many years of research into pain. Crucially, they believe much of the complex pain science and research outcomes over the last forty years can be reduced to a simple equation: “We will have pain when our brain has more credible evidence of danger to our body than credible evidence of safety to our body.” The definition of safety is: “the condition of being protected from harm”.
Stress and Pain
Psychological Stress
“Considerable evidence indicates bidirectional interactions between stress and pain. An acute injury serves as a prime example of this relationship. As is well known, pain is vital to the survival of the organism. It serves as a warning signal, signifying the presence of threat and enhancing motivation toward elimination of the threat or dampening its effects to prevent further injury. In the case of injury, and accompanying pain, the stress response is automatically activated, triggering a series of physiological events intended to help the organism adapt to the stressor and reach a level of homeostatic balance. Although this response system is adaptive, as it enables the body to acclimate to various environmental and internal challenges-a process known as allostasis (Logan and Barksdale, 2008), the continuous activation of the stress response may increase the health-related burden and facilitate progression of chronic disease, including persistent pain. (McEwen 1998).”
“Given the interconnectedness of emotion and pain systems it is no surprise that they influence one another. Pain can also have long-term consequences on emotions. For example chronic pain increases risk for affective disturbance and impairs emotional awareness and decision-making.” (ibid p54)
“In three innovative studies, Rainville, Bao, and Chretien (2005) used hypnotic suggestion to induce anger, fear, sadness, relief, and satisfaction about painfully hot water. They found that pain intensity and unpleasantness were increased by negative emotions and decreased by positive emotions (regardless of the emotion).” (Ibid, p55)
“Disorders of emotion (e.g.. depression) are often comorbid and there is evidence that affective disturbance might serve as a risk factor for chronic pain. Moreover, emerging evidence suggests that dysfunctions within emotion circuitry might promote disorders of both affect and pain. This could lead to higher thresholds to experience positive emotions, lower thresholds to experience negative emotions, prolongation of negative emotions or augmented levels of negative emotions in patients. In addition chronic pain patients may have a reduced capacity to engage pain inhibitory mechanisms….Three studies manipulated emotion and pain in patients with irritable bowel syndrome (IBS) Posserud et al. (2004) evoked stress (stroop test and mental arithmetic) in patients with IBS and controls and found patients had an abnormal stress response (e.g., higher reported stress, corticotropic releasing hormone) and experienced hyperalgesia in response to rectal distention. No controls experienced distention-related pain.” (Ibid p65)
“The relationship between psychiatry and stress relies on the diathesis stress model (Monroe and Simons 1991) While not necessarily being the cause of a psychiatric disorder, the stress response, in combination with other factors (genetic, developmental etc.) contributes to several disorders, particularly depression. Melancholic depression is associated with hyper-secretion of CRH, Corticotropin releasing hormone, HPA activation and immunosuppression….termination of the responses is necessary to avoid persistent wear and tear on the body. The stress response impinges on multiple systems, including reproduction, growth, immune function and pain.
al’Absi M and Flaten M
The Neuroscience of Pain, Stress and Emotion, Academic Press, 2016.
“A research team at Carnegie Mellon University in Pittsburgh found that chronic psychological stress is associated with the body losing its ability to regulate the inflammatory response. Research shows for the first time that the effects of psychological stress on the body’s ability to regulate inflammation can lead to the development and progression of disease.
Sheldon Cohen, professor of psychology at the university’s Dietrich College of Humanities and Social Sciences, said prolonged stress alters the effectiveness of cortisol to regulate the inflammatory response because it decreases tissue sensitivity to the hormone. Specifically, immune cells become insensitive to cortisol’s regulatory effect and in turn runaway inflammation is thought to promote the development and progression of many diseases. He said: “Inflammation is partly regulated by the hormone cortisol and when cortisol is not allowed to serve this function, inflammation can get out of control.”
Prof Cohen, whose early work showed that people suffering from psychological stress are more susceptible to developing colds, used the common cold as the model for testing his theory. With the common cold, symptoms are not caused by the virus. They are instead a side effect of the inflammatory response that is triggered as part of the body’s effort to fight infection. The greater the body’s inflammatory response to the virus, the greater is the likelihood of experiencing the symptoms of a cold.
In Cohen’s first study 276 healthy adults completed an intensive stress interview and were then exposed to a virus that causes the common cold and monitored in quarantine for five days for signs of infection and illness. It was found that experiencing a prolonged stressful event was associated with the inability of immune cells to respond to hormonal signals that normally regulate inflammation. In turn, those with the inability to regulate the inflammatory response were more likely to develop colds when exposed to the virus.
In the second study, 79 healthy participants were assessed for their ability to regulate the inflammatory response and then exposed to a cold virus and monitored for the production of pro-inflammatory cytokines, the chemical messengers that trigger inflammation. Prof Cohen found that those who were less able to regulate the inflammatory response as assessed before being exposed to the virus produced more of these inflammation-inducing chemical messengers when they were infected. He said: “The immune system’s ability to regulate inflammation predicts who will develop a cold, but more importantly it provides an explanation of how stress can promote disease. “When under stress, cells of the immune system are unable to respond to hormonal control, and consequently, produce levels of inflammation that promote disease. Because inflammation plays a role in many diseases such as cardiovascular, asthma and autoimmune disorders, this model suggests why stress impacts them as well. “Knowing this is important for identifying which diseases may be influenced by stress and for preventing disease in chronically stressed people.”
Proceedings of the National Academy of Sciences April 2012,
Emotions
The Brain and Pain
“Emotions are strong modulators of pain…. On the one hand effects of emotions on pain appear to be implemented by descending pain-modulatory systems which involve pathways from the cerebral cortex down to the spinal cord…. On the other hand, it has to be noted that ascending nociceptive signals – as soon as they enter the cerebral cortex – are subjected to a multi-sensory integration process in which various external stimuli, including emotional stimuli, can influence the perception of pain: i.e. its localisation, intensity and unpleasantness. “
Haggard P, Iannetti GD, and Longo MR Spatial sensory organisation and body representation in pain perceptions (2013)
“The supraspinal modulation of pain by higher order cognition in a top-down manner is nicely supported by studies in which the threat value of nociceptive stimuli is manipulated by suggesting that they may cause injury. This manipulation increases pain perception through preactivation of the anterior midcingulate cortex and anterior INS, during anticipation of the nociceptive stimulation and of the aMCC during actual stimulation (Wiech and Tracey, 2009)…these findings provide compelling evidence that higher-order brain areas exert influences on pain experience, but that fundamentally distinct brain mechanisms can result in similar modulations of the experience of pain.”
Ploner M, Bingel U, and Wiech K (2015)
The Impact of Stress on Wound Healing
“Wound healing is a critical process involved in the recovery from injury and surgical procedures. Poor healing increases the risk for wound infections or complications, lengthens hospital stays, magnifies patient discomfort, and slows down a return to normal activities. Converging and replicated evidence indicate that psychological stress can modulate wound healing processes. This article reviews the methods and findings of experimental models of wound healing. Psychological stress can have a substantial and clinically relevant impact on wound repair. Physiological stress responses can directly influence wound healing processes. Furthermore, psychological stress can indirectly modulate the repair process by promoting the adoption of health-damaging behaviours. Translational work is needed to develop innovative treatments able to attenuate stress-induced delays in wound healing.”
“Converging evidence from different research paradigms suggest that psychological stress and other behavioural factors can affect wound healing. A meta-analytic study using diverse wound healing models and outcomes found that across studies there was an average correlation of −.42 between psychological stress and wound healing. This suggests that the relationship between stress and wound repair is not only statistically significant, but also clinically relevant. This review presents data and methods from observational, experimental, and interventional studies corroborating the impact of stress on wound healing.”
“Psychological factors can also modulate healing of chronic wounds. Fifty-three older adults with chronic lower leg wounds were followed longitudinally to assess speed of wound repair. Patients who experienced the highest levels of depression and anxiety (based on a median split of the Hospital Anxiety and Depression Scale) were 4 times more likely to be categorized in the delayed healing group, compared to individuals who reported less distress. Importantly, in these observational studies, distress predicted wound healing outcomes over and above differences in sociodemographic variables and medical status. Psychological distress thus appears to influence recovery from medical procedures and healing of chronic wounds in clinical settings.” The US National Library of Medicine. National Institute of Health
“Intervention studies that improve healing outcomes by reducing psychological stress provide further evidence of the impact of psychological and behavioural factors in wound repair. Meta-analyses of clinical studies show that behavioural stress management interventions before surgery have been associated with improved post-operative outcomes, including fewer medical complications and shorter hospital stays.”
Montgomery GH, David D, Winkel G, Silverstein JH, Bovbjerg DHAnesth. Analg. The effectiveness of adjunctive hypnosis with surgical patients: a meta-analysis 2002 Jun; 94(6):1639-45
“Prospective studies examining wound healing-related complications following surgery provide evidence for the impact of stress on wound repair. Greater fear or distress prior to surgery has been associated with poorer outcomes including longer hospital stays, more postoperative complications, and higher rates of re-hospitalisation. For example, among 111 patients undergoing gallstone removal surgery, those who reported more stress on the third postoperative day had a longer hospital stay, compared to less anxious individuals. Among 309 consenting consecutive patients who underwent an elective coronary artery bypass graft surgery, patients who were more optimistic were less likely to be re-hospitalised than less optimistic individuals. Conversely, patients who experienced more depressive symptoms were more likely to require re-hospitalisation for infection-related complications than individuals reporting less distress. This result was replicated in a study of 72 patients undergoing coronary artery bypass surgery. Patients who had more depressive symptoms at discharge had more infections and poorer wound healing in the following 6 weeks after surgery, compared to participants who reported less distress.
Doering LV, Moser DK, Lemankiewicz W, Luper C, Khan S Am J Crit Care. 2005 Depression, healing, and recovery from coronary artery bypass surgery
“In summary, a wide array of acute and chronic stressors can disrupt the healing process. Furthermore, the impact of stress on wound repair has been observed across different methodologies and with different healing outcomes and most results have bee replicated in at least two independent laboratories. Collectively, results from observation, experimental, and intervention studies provide strong evidence that psychological stress can influence wound healing. Psychological stress leads to the activation of the hypothalamic-pituitary-adrenal and the sympathetic-adrenal-medullary axes.” Padgett DA, Glaser R How stress influences the immune response. Trends Immunol. 2003 Aug; 24(8):444-8.
“The impact of negative emotions on mucosal wound healing was replicated in a larger study. Among 193 healthy undergraduate students who received a 3.5 mm wound on the hard palate, individuals reporting high levels of depressive symptoms were almost 3.6 times more likely to be classified as slow healers, compared to less dysphoric students.
Depressive symptoms also predict mucosal wound healing. A 2 mm full thickness wound was placed on the back of one upper arm of obese women prior to receiving elective gastric bypass surgery. Greater acute pain immediately after surgery and persistent pain in the 4 weeks following surgery were associated with slower healing of the experimental wound. Pain generates psychological distress, and, when compounded by the presence of other stressors, can put a person at increased risk for delayed wound repair. Hostility and pain are related to inflammation in older adults.”
Graham JE, Robles TF, Kiecolt-Glaser JK, Malarkey WB, Bissell MG, Glaser R
Brain Behav Immun. 2006 Bosch JA, Engeland CG, Cacioppo JT, Marucha PT Psychosom Med. 2007 Sep-Oct
“Stress can also impede healing of a punch biopsy wound among younger people who experienced less intense stress. Twenty-four healthy young men were followed for 21 days after a standard 4 mm punch biopsy was performed on their forearm. In that study, wound healing was assessed using ultrasound biomicroscopy. Stress levels were measured using a self-report questionnaire, the Perceived Stress Scale. Higher perceived stress on the day of the biopsy was associated with slower wound healing. A substantial correlation of −.59 was found between perceived stress and healing progress between the days 7 and 21 after the biopsy.”
Ebrecht M, Hextall J, Kirtley LG, Taylor A, Dyson M, Weinman J
Perceived stress and cortisol levels predict speed of wound healing in healthy male adults. Psychoneuroendocrinology. 2004
Temporomandibular Disorder (TMD)
“Despite an increase in studies related to TMD over the last century, the mechanisms of TMD pathogenesis remain controversial. It is commonly believed that both occlusal abnormalities and psychological stress are strongly related to the occurrence of TMD. In recent years, with the transformation of the medical mode from the simple biomedical mode to the biological-psychological-social medical mode, more researchers have paid attention to the role of psychological factors in the etiology of TMD. Studies conducted by List et al. have shown psychological factors such as high stress levels, somatic complaints, and emotional problems play a more important role than dental factors in TMD. Similarly, using data from questionnaires, clinical histories and dental panoramic tomography, Kafas and Leeson have demonstrated that TMD are closely related to the mood of the patients.”
Slade GD, Diatchenko L, Bhalang K, Sigurdsson A, Fillingim RB, Belfer I, Max MB, Goldman D, Maixner WJ Dent Res. 2007 et al.
Mood Disorders and Functional Illnesses
Mood disorders and functional illnesses
“The HPA axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function. Pariante CM (August 2003).”
Journal of Neuroendocrinology “Depression, stress and the adrenal axis”
“One risk factor that may prime the person’s susceptibility to pain disorders and hypersensitivity in the pain pathways is the role of early life stress in programming the HPA axis, which has been well-studied in animal models. Exposure to extreme or prolonged stress in childhood can induce a hyper-reactive HPA axis and may contribute to lifelong vulnerability to stress.”
Flinn MV, Nepomnaschy PA, Muehlenbein MP and Ponzi D Evolutionary functions of early social modulation of hypothalamic–pituitary–adrenal axis development in humans. Neuroscience and Biobehavioral Reviews (June 2011)