Fibromyalgia and IBS Recovery Through out Polyvagal Lens

Fibromyalgia and IBS Recovery Through out Polyvagal Lens


Medically unexplained somatic problems including chronic diffuse pain and functional gastrointestinal disorders (FGIDs) are persistent, disabling, costly, and seen across all medical settings (1–3). However, their pathophysiology is poorly understood. Increasingly, there is a growing awareness that chronic diffuse pain and FGIDs are highly prevalent among those with a history of trauma or abuse (4, 5). Rates of abuse history tend to be highest among patients in pain and gastroenterology clinics (6) and one study found that of all females referred to a gastroenterology clinic, 67% had experienced sexual or physical abuse (7).


Sexual and physical abuse in both childhood and adulthood are a widespread problem. Based on a series of large-scale meta-analyses, international prevalence rates are estimated to be 13% for childhood sexual abuse (8% males, 18% females) and 23% for childhood physical abuse (19). In the US, the Centers for Disease Control and Prevention estimate that the lifetime prevalence of rape is 19% in women and 2% in men and intimate partner violence prevalence is 32% in women and 28% in men (with severe intimate partner violence prevalence at 22 and 14%, respectively) (20). Notably, these higher rates of sexual and physical abuse among women are paralleled in the gender-specific prevalence of fibromyalgia and irritable bowel syndrome. Women are about twice as likely to have a fibromyalgia diagnosis (13) and have 1.67 greater odds of having irritable bowel syndrome than men (18).

Converging evidence across many studies shows that abuse history is a strong predictor of fibromyalgia. In a meta-analysis of 18 studies with a total of over 13,000 combined participants, Häuser and colleagues found that sexual and physical abuse in both childhood and adulthood predicted greater odds of fibromyalgia (odds ratio point estimate range: 1.94–3.07) (21). In their meta-analysis, Paras and colleagues found that rape survivors have especially high odds of fibromyalgia diagnosis (OR = 3.27) (22). These risk factors are higher in fibromyalgia patients than those with rheumatoid arthritis, highlighting the specificity of the role of abuse and trauma in FM pathogenesis compared to a pain disorder with a known organic cause (23).

Rates of gastrointestinal problems such as irritable bowel syndrome are similarly elevated in survivors of abuse. Meta- analytic evidence supports this with childhood sexual abuse being associated with higher risk of gastrointestinal problems (24). It is estimated that individuals with a history of sexual abuse are about twice as likely to develop abdominal pain and gastrointestinal problems than those without an abuse history (25). As seen with fibromyalgia, rape survivors are among those with the highest risk, with meta-analytic methods suggesting their odds of having a functional gastrointestinal disorder are about four times greater than those without an abuse history (22). Those with an abuse history also have higher severity and quantity of GI symptoms and seek medical help more often (26).

Overall, these robust associations suggest that abuse and trauma experiences may be key to understanding the pathogenesis of fibromyalgia and irritable bowel syndrome. However, a comprehensive integrative model to explain the mechanisms through which traumatic experiences affect these chronic disorders is lacking.


The Polyvagal Theory proposes that the evolution and individual anatomical pathways of the DVC, SNS, and VVC give rise to an ordered response hierarchy that promotes coordinated responses to threats. Under normal homeostatic conditions, each system is involved in basal functions for organism maintenance. However, under threat conditions, the function of individual systems can be recruited to regulate metabolic resources as needed. Phylogenetically newer systems are primary responders; older systems are recruited as threat persists. This phylogenetically ordered response hierarchy is consistent with the Jacksonian principle of dissolution (35). First, under threat, the VVC, the most rapidly responsive system, withdraws its inhibitory influence on mobilization. Since a component of HRV, known as respiratory sinus arrhythmia (RSA; see below), is primarily a product of this circuit, it is often used as an index of the strength of this circuit. Second, the SNS can further ramp up mobilization and promote fight/flight behaviors. Finally, when recruited for defense responses, the DVC produces an efferent vagal surge that inhibits metabolic functions by slowing heart rate, reducing digestive processes, and promoting behavioral shut down. Notably, all three autonomic systems feature cardio- regulatory pathways; modulating cardiac function is key to altering metabolic resources for body responses. Calm, affiliative social engagement requires dampening of threat-related bodily mobilization (this mobilization brake must be removed for efficient body mobilization), fight/flight mobilization requires ratcheting up available resources, and behavioral shut down requires reduction of metabolic function.

Though acute neural threat reactions are adaptive and necessary, chronic state shifts that maintain threat responses can be a risk factor for body dysfunction and disease. The brain- body connection is composed of multiple integrated feedback loops and the chronic maintenance of threat responses can lead to a “compromised” functional state. Chronic compromised states may give rise to the emergence of functional gastrointestinal disorders and altered pain signaling as part of a chronic systemic, rather than an event related organ- specific, pathophysiology. These changes in homeostatic functions may be self-maintaining or cascading even after the threat has been lifted due to long-term alterations in set points, learned responses to threat cues, and the symptoms themselves propagating threat-reaction.


Neural Pain Regulation in the Periphery

The detection and appropriate responses to noxious or dangerous stimuli from without and within relies partly on the propagation of pain signals through the nervous system (nociception). Mechanisms integrating nociceptive sensory signaling, spinal pathways, and central regulation allow dynamic flexibility for acute and long-term safety- and danger-related

functions. Pain signal regulation is a normal part of a nervous system defense response, such as the body’s illness reaction that activates and sensitizes afferent nociceptive neurons (36). This adaptive pain signal modulation, which relies on integrated afferent-efferent brain-body feedback loops may be compromised in chronic-long term states of threat response.

Spinal nociceptive pathways are not passive conveyors of information from the body to brain, but rather under dynamic endogenous regulatory control that includes mechanisms contributing to sensitization and inhibition. During typical homeostatic states, active inhibition of pain signals modulates the strength of nociceptive response levels, silences nociceptive neurons in the absence of noxious stimuli, and impedes the spread of excitatory signals between sensory modalities and somatotopic borders (37). These inhibitory signals are prepotent, typically tonically active, crucial for constraining spinal nociceptive signaling, and have a large portion of the spinal neural architecture dedicated to them (38, 39). Dampening of these inhibitory mechanisms or facilitation of pain-related signaling can lead to hyperalgesia, allodynia, or spontaneous pain (37, 39). Somatic and interoceptive systems provide constant dynamic input from the body to the brain, and pain signaling from these system is highly integrated with homeostatic threat- responsive systems (40). Changes in homeostatic and threat- response feedback loops thus may interact with these incoming afferent signals, altering efferent (motor) output and perceptual qualities.

The sensitization and inhibition of spinal pain pathways is under the influence of brain-body feedback loops. These include multiple brain areas related to survival and threat related functions as well as the sympatho-adrenal system and vagal afferent pathways in the periphery. Descending modulation from the brain includes the periaqueductal gray, the rostroventral medulla, the lateral and caudal dorsal reticular nucleus, and the ventrolateral medulla (39, 41). Notably, several of the brainstem areas that are involved in pain modulation–including the medullary raphe and ventromedial reticular region-are also involved in the regulation of autonomic sexual functions and defense behavior (42), providing the substrate for functional coupling of survival- and threat-related states with pain.

Peripheral mechanisms that include vagal and spinal pathways are also involved in regulating nociception. Under normal homeostatic conditions, active nociceptive inhibitory control is maintained by spontaneous tonic vagal afferent activity (36, 43). Threat-related subdiaphragmatic vagal afferent signaling or disruption of tonic activity to the brain can trigger defense reactions that affect pain not just in the viscera but in the superficial and deep somatic tissues as well (36, 44). These signals can activate second-order NTS neurons, leading to an illness response cascade that facilitates nonciceptive impulse transmission in the spinal cord, inhibition of digestion, and biobehavioral state changes including immobility and sleep increase (36). In rodents, the nociceptive sensitivity

induced by severing vagal afferents shows an extended time delay, with maximum sensitization of the paw-withdrawal threshold being reached by about 1–3 weeks post-surgery and involving interactions with the sympatho-adrenal system (45). In this study, this level sensitization endured over the course of the study, which lasted 8 weeks, indicating that the sensitization was chronic. In light of the present model, vagal afferent severance may mimic an extreme loss of vagal afferent flow and feedback loop, promoting a state of heightened autonomic threat response. This slow time frame to reach maximum sensitization may reflect complex, slow acting processes that give rise to latent sensitization emerging some time after the initial traumatic insult.

Evidence for Dampened RSA in

Fibromyalgia and Irritable Bowel Syndrome

In accordance with this prediction, several reviews and meta-analytic analyses document that fibromyalgia is associated with depressed heart rate variability including RSA, which is often reported as high frequency HRV (59–61). Furthermore, there is mounting evidence that interventions that decrease pain in fibromyalgia also result in increased HRV. A recent study reported that individuals whose fibromyalgia symptoms benefited from resistance training also responded with an increase in HRV (62), while an intervention that used breathing biofeedback documented that practice increased participant RSA and decreased pain (63).

Similarly, irritable bowel syndrome has also been linked to reduced VVC control of the heart as indexed by RSA. A meta-analysis based on 7 studies found that RSA was depressed in irritable bowel syndrome patients compared to healthy controls (64). This dampened VVC control may be especially pronounced in the subtype of irritable bowel syndrome characterized by predominant constipation, severe abdominal pain, and a comorbidity of anxiety or depression (65).

That both fibromyalgia and irritable bowel syndrome are marked by low amplitude RSA supports the hypothesized role of dampened VVC control in these disorders and suggests these disorders are associated with a state of heightened threat-related autonomic state. This link is so consistently observed that low heart rate variability has even been proposed as a “biomarker” of fibromyalgia (61, 66). However, the lack of specificity of low HRV as unique to fibromyalgia and the functional relation between VVC function to broad safety- and threat-related functions warrants a more systemic autonomic interpretation of this link.

Polyvagal Theory proposes an alternative interpretation of the covariation of HRV with both fibromyalgia and irritable bowel syndrome. Consistent with the integrated model of the autonomic nervous system described in the theory, atypical heart rate variability is not interpreted as a biomarker of any specific disease. Rather, depressed respiratory sinus arrhythmia (high frequency heart rate variability) is proposed as a neurophysiological marker of a diffuse recalibration of the autonomic nervous system following an adaptive complex autonomic reaction to threat. We propose that an initially adaptive neural response to threat, via visceral afferent feedback from the visceral organs to the brainstem, may result in a chronic reorganization of autonomic regulation observed in vagal regulation of the heart (i.e., depressed RSA) in conjunction with altered

subdiaphragmatic organ function and afferent pain signaling (see Figure 1).


In addition to the shared VVC dampening in both fibromyalgia and irritable bowel syndrome, these disorders also share a high co-morbidity and overlap in autonomic symptoms. Fibromyalgia occurs in about 49% of irritable bowel syndrome cases (17). Both diagnoses are also associated with other autonomic and state-regulation problems. Irritable bowel syndrome patients have increased rates of non-digestive pelvic pain, chronic fatigue, sleep problems, syncope and dizziness (67), as well as heightened visceral and cutaneous pain perception (68). Fibromyalgia co- morbidities are similar and include chronic fatigue, sleep problems, elevated rates of visceral pain and sensory hypersensitivities (13). Furthermore, self-reported autonomic problems – including issues with subdiaphragmatic organs, orthostatic, vasomotor, and secretomotor functions – are elevated in fibromyalgia patients and overall severity of fibromyalgia symptoms is associated with severity of these problems (69).

Fibromyalgia and irritable bowel syndrome are both associated with elevated sexual and reproductive system problems that may be a manifestation of general autonomic function. Individuals with irritable bowel syndrome have elevated rates of vulvodynia, dysmenorrhea, amenorrhea, and irregular menstruation (67). Likewise, fibromyalgia is related to increased incidence of dysmenorrhea (13). In addition, women with fibromyalgia experience blunted sexual desire and arousal, fewer experiences of orgasm, and increased pain during intercourse (70).

The co-occurrence of fibromyalgia and irritable bowel syndrome with their overlapping autonomic co-morbidities suggest a role for a general systemic dysfunction as an underlying pathophysiology that gives rise to chronic diffuse pain and functional gastrointestinal problems. This points to the possibility that integrated brain-body reactions may produce long-term systemic changes that give rise to chronic disease and dysfunction related to evolutionary threat responses. Abuse or psychological trauma provides an especially potent experience that may re-tune the nervous system toward a chronic threat response.


As reviewed above, the human autonomic nervous system is tuned to rapidly respond to a wide range of external and internal conditions. Many mild events that challenge the nervous system’s resources are part of everyday life and trigger adaptive acute reactions. However, traumatic

experiences may be especially potent in re-calibrating the autonomic nervous system toward a state that supports chronic defense responses. These long-term chronic changes, which affect autonomic regulation and the function of the brain and body, are observed across a range of traumatic events, including physical and sexual abuse in both childhood and adulthood.

These traumatic experiences may trigger a chronic threat- related brain-body response. A recent meta-analysis showed that RSA is dampened in individuals with Post-Traumatic Stress Disorder (PTSD) (71). This is consistent with a model of dampened VVC activity, as part of a chronic threat response, being implicated in long term effects following a trauma. Emerging evidence also suggests that a range of interventions including biofeedback and mindfulness that improve PTSD symptoms also increase heart rate variability (72–74). Importantly, however, VVC regulation may be dampened and trigger somatic problems even in the absence of a PTSD diagnosis. Although empirical research in this domain is currently scant, one study found that women with an abuse history have low RSA compared to health

controls even when they do not meet diagnostic criteria for PTSD (75).


Anxiety disorders and depression are common sequelae following traumatic events. Both fibromyalgia and irritable bowel syndrome co-occur with panic disorder, generalized anxiety disorder, and PTSD (13, 76). It is estimated that 30–50% of fibromyalgia patients also have anxiety and/or depression at the time of diagnosis (12). A meta-analysis shows that across studies, depression symptoms are elevated in fibromyalgia and irritable bowel syndrome and anxiety is elevated in irritable bowel syndrome (77). Patients with GI dysfunctions, who have an abuse history, have higher rates of panic symptoms and depression as well as autonomically-related somatic symptoms such as sleep disturbance and pelvic pain than those without abuse history (26), suggesting a higher likelihood of systemic brain-body dysfunction..

The evolutionary neurophysiological framework of the polyvagal theory provides a plausible model for post-traumatic chronic pain and functional gastrointestinal disorders based on systemic brain-body responses to safety and threat. This framework provides an integrative perspective that unites multiple co- occurring phenomena across perceptual and neurophysiological. eports, though much individual variability still remains. While FM and IBS share a neurophysiological substrate with threat- response systems, symptom heterogeneity is the rule rather than the exception, which likely reflects interactions with higher level brain structures, neuroendocrine, and immune processes [e.g., (89)]. However, this review highlights the potential for the autonomic nervous system to be the basis for the organization and synthesis of observations made made by physicians, mental health practitioners, and neuroscientists to piece together the mechanisms that link traumatic experiences, threat-related nervous system function, and multiple somatic disorders. Conversations about trauma history between patients and medical practitioners may be critical for interpreting symptoms and developing treatment plans, but these conversations are rare (26). By building a better understanding of the systemic chronic nervous system alterations that can be induced by trauma, the medical community can move toward explaining co-morbidities and developing targeted treatments.


Jacek Kolacz1* and Stephen W. Porges1,2

Traumatic Stress Research Consortium, Kinsey Institute, Indiana University, Bloomington, IN, United States, Department of Psychiatry, University of North Carolina, Chapel Hill, NC, United States

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