Deconstructing stigma as a barrier to treating DGBI: Lessons for clinicians

Abstract

Stigma, defined as social devaluation based on negative stereotypes toward a particular population, is prevalent within health care and is a common phenomenon in disorders of gut-brain interaction (DGBI). Characteristically, DGBI including functional dyspepsia (FD) lack a structural etiology to explain symptoms, have high psychiatric co-morbidity, and respond to neuromodulators traditionally used to treat psychopathology. As a result, these disorders are frequently and wrongly presumed to be psychiatric and carry a great deal of stigma. Stigma has profound adverse consequences for patients, including emotional distress, medication non-adherence, barriers to accessing care, and increased symptoms. The basis for stigma dates back to the 17th Century concept of mind-body dualism. Patients and health care providers need to understand the factors that promote stigma and methods to ameliorate it. In this minireview, we address the data presented in Yan et al.’s (Neurogastroenterol Motil, 2020, e13956). We offer concrete solutions for clinicians to mitigate the impact of stigma to optimize treatment adherence and clinical outcomes for patients with DGBI.

1 |. STIGMA AND FUNCTIONAL DYSPEPSIA

Stigma, defined as “social devaluation/discrimination based on negative stereotypes toward a particular population” or “an attribute that is deeply discrediting,”¹ is a common phenomenon in health care that undermines the quality of care and caring for patients with chronic illnesses. Indeed, in various clinical contexts, stigma is associated with increased depression and anxiety,² treatment non-adherence,³ more clinical symptoms, lower quality of life,² reduced self-esteem and self-efficacy, and less access to medical care.⁴

The concept of stigma falls into three unique but inter-related domains: perceived, enacted, and internalized.⁵ Perceived stigma refers to an individual’s experience of being treated negatively because of a particular condition or attribute. Enacted stigma refers to the discriminatory behaviors that an individual might receive because of a specific attribute. Finally, internalized stigma, perhaps the most damaging, is when individuals align with or believe the negative stereotypes put on them by others due to a particular condition. While there is a limited body of literature describing the impact of perceived,⁶ internalized,⁷ and enacted⁴ stigma in gastrointestinal disorders, little is known about the impact of stigma with functional dyspepsia (FD) or of being prescribed neuromodulators to treat the symptoms.

In their non-randomized prospective study “The impact of stigma on medication adherence in patients with Functional Dyspepsia,” Yan et al. sought to evaluate the prevalence of internalized (IS) and perceived stigma (PS), among patients with FD refractory to first-line treatments (e.g., anti-secretory therapy and prokinetic agents). They explored the impact of stigma on treatment adherence to neuromodulators, which have shown clinical efficacy in treating this condition.

FD is a disorder of gut-brain interaction (DGBI),⁸ previously referred to as a “functional gastrointestinal disorder” (FGID).⁹ It is one of 33 adult and 20 pediatric disorders classified by the Rome IV Diagnostic Criteria. These disorders lacking a known “organic” or structural basis due to negative endoscopy, laboratory, histopathological, or radiographic findings are considered “functional.” FD is defined by bothersome symptoms of epigastric burning or pain, postprandial fullness, or early satiety with two overlapping but pathophysiologically diverse and clinically relevant subtypes¹⁰ (see http://romedross.video/38wyrHe for an overview). These include Epigastric pain syndrome (EPS—bothersome epigastric pain or burning) and postprandial distress syndrome (PDS—bothersome postprandial fullness or early satiety). To make a diagnosis of FD the patient must (1) fulfill the Rome IV diagnostic criteria for at least 3 months, (2) have other causes that might explain the symptoms excluded, and (3) have symptoms that began at least 6 months before the diagnosis.

The American College of Gastroenterology¹¹ and the Rome IV⁸ guidelines recommend using antidepressant medications, which we now designate as “neuromodulators” (to reduce stigma)¹² as a treatment for moderate-to-severe symptoms. Certain medications including tricyclic antidepressants (TCAs), serotonin-norepinephrine reuptake inhibitors (SNRIs), mirtazapine, and buspirone can reduce pain signals and bloating and treat early satiety and nausea.¹³ Importantly, EPS and PDS may respond differently to neuromodulator treatments based on their pathophysiology and the medications’ targeted actions. For example, in PDS, the stomach fails to relax postprandially, and buspirone, a gastric relaxing agent, reduces early satiety. At the same time, mirtazapine has a central effect reducing dyspeptic symptoms, weight loss, and nausea. EPS, which appears to be associated with visceral hypersensitivity, may be treated with acid blockers and TCAs to control pain via central analgesia.¹³ Additionally, given the high prevalence of often undiagnosed comorbid psychiatric disturbances¹⁴ these medications also treat underlying mood symptoms. Psychological therapies, such as cognitive-behavioral therapies (CBTs), have also shown benefits.¹³

Despite their efficacy in treating FD,^12,15–19 prior literature and the current study reveal that stigma may hinder the use of or adherence to neuromodulators, thereby undermining the treatments, impact.²⁰ Additionally, in FD, stigma may operate for at least three different reasons. There is stigma related to having a diagnosis of a DGBI because lacking a structural or “organic” basis, FD may be considered “psychosomatic.”^21,22 Stigma may also relate to the patient having a known comorbid psychiatric diagnosis²³ or to using a neuromodulator, especially when these medications are labeled as “antidepressants.”²⁴

In their study,²⁵ the authors prospectively evaluated 138 refractory FD patients, 18–70 years old, seen in the clinic with mild to moderate anxiety or depression. Those who did not achieve a 50% reduction in symptoms when initially treated with anti-secretory or prokinetic therapies were prescribed by a psychiatrist and gastroenterologist 8 weeks of a neuromodulator medication. The authors studied FD-related IS and PS, the severity of FD symptoms, symptoms of depression and anxiety, neuromodulator-related stigma, and neuromodulator medication adherence.

They found that both perceived and internalized stigma had adverse effects for patients with FD through the association with reduced neuromodulator adherence and less symptom improvement. Those with the highest stigma levels were less likely to adhere to their neuromodulator prescriptions or show improvements in FD symptoms, depression, or anxiety after treatment. Interestingly, the stigma scores of the sample increased after treatment. A substantial portion of participants also endorsed stigma related to using neuromodulators, indicating that the disease and medication-related stigma were obstacles to treatment adherence and efficacy. Additionally, benefitting from treatment was associated with lower levels of stigma. It is not clear whether this effect was driven by higher medication adherence or perhaps the perception that these medications were “right” for the patient. These findings highlight the importance of pre-emptively managing stigma when treating patients with FD and prescribing neuromodulators. Further research is needed to disentangle these relationships and effects.

There are several limitations of this study that may influence the interpretation of the results. First, several publications^26–29 report higher stigma levels for individuals with mental illness from Eastern (China, Korea, Japan) vs. Western (Australia, Great Britain, United States) countries.³⁰ Given that this study was conducted in China, the findings may not be generalizable to Western cultural groups, and validation in Western populations is warranted.

Second, participants with FD were not sub-classified by subtype (EPS vs. PDS), which respond differently to neuromodulators. While the analyses did not detect differences in cessation among the different medications, the lack of stratification by subtype could have masked a potential effect.

Third, the choice of treatments is problematic. With no treatment protocol, these decisions left to the clinicians were not consistent with existing data; For example, about half of the participants (67/138) were prescribed selective serotonin reuptake inhibitors (SSRIs), which have been shown not useful for FD.¹⁷ Additionally, prescribing 75 mg of venlafaxine, a serotonin-norepinephrine reuptake inhibitor (SNRI), may be too low a dose to achieve analgesia from the needed noradrenergic effect.¹² Finally, mirtazapine was prescribed in only 15% and none were prescribed a TCA. These are two treatments known to benefit patients with FD.¹² Furthermore, a non-response may also introduce stigma, with patients believing they have an untreatable and possibly not a legitimate condition.

Merely being prescribed an “antidepressant” may introduce perceived stigma by suggesting that participants have a psychiatric problem, perhaps not previously considered. Finally, investigator bias may have influenced positive responses, primarily due to placebo effects with no treatment protocol.

A fourth limitation involves the choice to exclude patients with normal psychometric scores for anxiety and depression. This exclusion begs the question as to whether the researchers were aiming to treat dyspepsia or mental illness. Indeed, prescribing SSRIs to half the study population might indicate that treatment was directed more at psychiatric than FD symptoms, given their lack of evidence for treating dyspepsia. Additionally, this exclusion also limits the study results’ generalizability to a large proportion of patients with FD who lack psychiatric symptoms.

Overall, the study findings are relatively intuitive and recapitulate the idea that both internalized and perceived stigma relate to having a diagnosis of functional dyspepsia, being prescribed “antidepressants,” and, potentially, the presumption of having symptoms of depression and anxiety. The associations between stigma and adverse outcomes were not only evident, but we could consider this study as a proof-of-concept that prescribing “antidepressants” for DGBI increases stigma. Furthermore, until we can identify and prevent stigma, its presence may impede neuromodulators’ benefit in treating FD and comorbid psychiatric symptoms. Clinicians need to recognize that treating patients with psychiatric co-morbidities and DGBI may be associated with stigma within themselves and with their patients and reducing stigma may improve clinical outcomes.

2 |. UNDERSTANDING THE ORIGINS OF STIGMA AND ITS IMPLICATIONS FOR DGBI

Research reveals that while stigma may operate in various social contexts, it is particularly harmful within health care settings, as stigma serves as a barrier to accessing the health care necessary to control symptoms of illness.⁵ Given the findings of Yan et al., which revealed that stigma increased once patients initiated treatment with neuromodulators, it is valuable to review the concept of stigma in DGBI and provide clinicians with practical strategies to reduce stigma around these disorders’ diagnoses and treatments.

The origins of stigma may be attributed to the western medical paradigm of mind-body dualism, a concept popularized by Rene Descartes in the 17th Century that still exists in medical practice today.³¹ Prior to Descartes’ postulation that the mind and body are distinct and separate entities, the church forbade human dissection, proposing that the spirit resided within the body. Therefore, with Descartes’ new paradigm of dualism, the human body could now be dissected or subject to surgical intervention, without consequence for the human soul. With dissection came the morphological basis for medicine, through pathology, histology, as well as imaging methods. This idea became the foundation of the modern biomedical model: That medical diagnoses were observable phenomena, diagnosed and legitimized by physical evidence. See this link for further information on Cartesian dualism and the concept of stigma in DGBI: http://bit.ly/2HbpVDy, as well as a recent conversation from experts on stigma in DGBI: https://www.facebook.com/TuesdayNightIBS/videos/603069907073484.

Patients having illnesses like DGBI, without physical findings, do not fit neatly into the biomedical model. This concept, perceived as “illness without the disease,” is a catalyst for stigma.¹³ Without structural or pathological evidence, DGBI are frequently misunderstood by patient and doctor alike as stress-related and may be seen as illegitimate.³² Clinicians adhering to the biomedical model will see these patients as challenging to treat.^7,31–34 Further, the high degree of psychiatric co-morbidity with DGBI¹⁴ also carries a stigma, which may further interfere with and undermine a therapeutic patient-physician relationship critical to treating these disorders.^35,36 Dualistically-oriented medical providers not trained in an integrated biopsychosocial model of care³⁷ may perceive the DGBI diagnosis as out of their realm of responsibility and authority. They may then seek to order other investigations (e.g., laboratory tests, imaging, diagnostic procedures) to find a “legitimate” cause and, failing this, attribute the symptoms to being “in the patient’s head.” As a result, proper diagnosis using the Rome symptom-based criteria⁸ and implementing appropriate, well-targeted treatments that exist for effective care does not occur.¹³ Also, these perceptions and behaviors interfere with the patient-provider relationship because the physician may, wittingly or unwittingly, communicate uncertainty, negative attributions, and stigma to the patient.

Studies support this contention and reveal that physicians demonstrate a preference for patients with organic versus functional diagnoses and treat them differently.^4,38 For example, they consider after-hours calls by patients with DGBI to have less severe symptoms and the patients to be less reasonable than calls from patients with organic complaints even for the same symptoms.³⁸ Additionally, patients with underlying organic diseases, compared to those with DGBI, were rated by physicians as having more severe complaints, being more disabled, having more reasonable requests, and even being more likable.³⁸ Another study compared perceived stigma in patients with a functional vs. organic disease [i.e., IBS vs. Inflammatory Bowel Disease (IBD)]. The IBS patients were more likely to report high levels of perceived stigma from a broader range of sources, with the largest difference from health care providers. Additionally, 27% of IBS patients reported moderate-to-high levels of PS compared with 8% of IBD patients.²

Relating to the stigma of mental illness and prescribing neuromodulators, Yan et al.’s study showed a correlation between low adherence and low recovery from FD and psychological symptoms. A review of 32 studies examining “antidepressant”-specific stigma found that perceived emotional weakness, high severity of illness, a perceived inability to deal with problems, and a lack of belief in these medications’ efficacy significantly correlate with stigma.²⁰ Although internalized stigma against mental illness did not impact therapeutic adherence to medications, antidepressant-specific stigma did undermine adherence. Thus, specifically addressing medication-related stigma in the clinical setting, as it relates to the treatment of mental health disorders and DGBI, is critical for optimizing treatment efficacy.

A consequence of these behaviors and the stigma imposed is the creation of a “vicious cycle” of health care seeking¹³ (see Figure 1). In essence, the physician’s lack of training to accept the diagnosis of a DGBI and the reliance on laboratory tests, imaging, and histopathologic findings may have several consequences. It can exacerbate patient’s distress, leave them chronically dissatisfied without a diagnosis or treatment, and, in the process, restrict physician satisfaction and meaningfulness, even fueling clinician burnout.³¹

FIGURE 1.

Patients with symptoms of DGBI come to their physicians looking for a cure for their distressing physical sensations. Physicians perform a workup that turns out to be negative for organic disease and are subsequently frustrated that they did not find anything (the well-intentioned doctor wants an answer, and research shows that physicians have a difficult time managing uncertainty in clinical practice). Perhaps this physician opts to send their patient to another doctor for another workup or the patient self-selects another clinician. In the meanwhile the patient, who is suffering, may develop illness-related anxiety, become preoccupied with these mysterious symptoms, develop hypervigilance around sensations in the gut, and feel frustrated, invalidated, dissatisfied, and helpless. In fact, as emotional distress increases, pain thresholds decrease. More pain results in more referrals, more tests, surgical exploration, the potential for iatrogenic harm, and high financial, time, and emotional burden for the patient

3 |. REVERSING THE VICIOUS CYCLE

The first step to breaking the stigma and improving patients’ outcomes with DGBI is to become personally aware. This relates to (1) recognizing the role and impact that stigma has on personal and patient perceptions and behaviors that interfere with treatment (“Am I thinking about and treating this patient with functional dyspepsia differently than with my patient with Ulcerative Colitis? If so, why?”), and (2) reversing these behaviors by improving the patient-doctor relationship and prescribing treatments such as neuromodulators. This awareness can open the door for further inquiry, for example: “If I am thinking about this patient differently, I wonder how other clinicians must have treated them before they ended up in my office…”.

After recognizing and acknowledging potential sources of bias toward these patients, we can confront and mitigate them by actively listening and aligning ourselves with the patient by understanding their stigmatization experience. We should not hesitate to ask patients about their experience of stigma in their lives, how it occurs, by whom, and how they are dealing with it. We should also ask about their thoughts about their mental distress and their views on neuromodulators’ use. Anticipating that internalized stigma might already exist, asking about it, validating their perspective, and then challenging the stigma with the use of evidence can help foster a therapeutic alliance—which, in DGBI, is the cornerstone of therapy.³¹

At this point, we can convey to our patients the new scientific knowledge about the brain-gut axis. There is a bidirectional relationship between symptoms generated in the gut that impact the brain that produce distress. It is easier to begin the discussion by explaining that chronic and severe symptoms cause psychological distress, as this concept is almost universally accepted. We then present that the distress reciprocates back to affect symptom severity through dysmotility and lower pain thresholds due to visceral and central hypersensitivity. So we shift from a dualistic to a biopsychosocial construct to illustrate that the DGBIs are not psychiatric.³⁹ This understanding clarifies why it is possible to have pain and other GI symptoms without structural abnormalities and emotional distress without it being causative.

Doctor and patient can then focus on treatments to reverse the brain-gut dysregulation inherent to these disorders. Even using the terms “neuromodulators” instead of “antidepressants” and “DGBI” instead of “functional disorders” may help to de-stigmatize, break down dualistic thinking, and lower barriers leading to a willingness to accept brain-gut treatments (See https://romedross.video/Q_A_fgid_dgbi). This video shows how to explain the brain-gut axis and the gate control theory of pain: https://romedross.video/3b8jcVz. When physicians communicate this information, they now have the opportunity to prescribe either neuromodulators (https://romedross.video/Q_ANeuromod4), or brain-gut therapies, including cognitive-behavioral treatment or hypnosis (http://romedross.video/350lyDN), and patients feel validated.

Table 1 offers concrete skills to improve the patient-doctor relationship, reduce stigma, and optimize care plans. (See https://romedross.video/Q_A_10tips.) These strategies are summarized.⁴⁰

TABLE 1.

Suggestions for Clinicians to Combat Stigma in DGBI through an Improved Doctor-Patient Relationship

Listen actively	Be fully present with your patient: make eye contact, avoid unnecessary interruptions, ask follow-up questions in response to what they are telling you “You mentioned that your symptoms act up when things are stressful at work. Can you tell me more about that?”
Identify your patient’s agenda	Ask questions that will enable you to see the patient’s perspective. This knowledge allows you to address these concerns upfront “What brought you here today?… What do you make of what’s going on with you? … What worries or concerns do you have?… What do you feel that I can do to help? … Based on what I’ve told you, what do you see as the pros and cons of trying this neuromodulator?”
Empathize	Practice empathy by understanding the patient’s perspective, being non-judgmental, recognizing their emotional response, and conveying it to them.41 Doing creates a connection while maintaining an objective perspective to help guide the patient’s pain and suffering toward solutions “This sounds incredibly challenging to deal with. I can understand that this is interfering with many aspects of your life.”
Validate	Establish that you hear what your patient is telling you and that their concerns are valid and real. Doing so can create a powerful bridge with your patient and serve as an antidote to shame they may have previously experienced “I can see that you are frustrated when people say that your pain is simply due to stress. What you’re experiencing is real, and I’m here to help you.” “It sounds like you have some hesitations about the potential side effects of neuromodulators. Let’s discuss this further so you can make the most informed decision.”
Set realistic expectations and goals	DGBIs are chronic conditions that take time to treat. Set your patients up for success by making this clear upfront “I know that you are suffering and are desperate for relief. I also want to be clear that these treatments can take time, and we might not eliminate all of your symptoms right away. What if we aim to get you 20% better by the time I see you next?”
Educate (an iterative process)	Education itself from a physician may be very therapeutic for patients, especially when the information is specific, relevant and thorough.42,43 One-on-one conversations in the office using diagrams to specify mechanisms of action, physiology, and treatment rationale are ideal ways of teaching that enhance adherence and empowers patients to develop self-management 44–46 Elicit your patient’s understandings → address any misunderstandings → provide information that is consistent with patient’s frame of reference → and check patient’s understanding of what was discussed
Reassure	Upon identifying the patient’s worries and concerns and validating them, respond to specific concerns while avoiding false reassurances “I know that you are worried that you are going to be in pain forever. We are going to work together to find solutions so that you find the relief that you deserve.”
Negotiate	Part of effectively treating DGBI is collaborating with your patient to develop solutions together as a shared responsibility. Doctors should encourage patients to take responsibility and ownership to build self-efficacy while also not shunting responsibility exclusively to the patient “We are in this together. Let’s think of a couple of strategies you might employ when you start to experience pain.”
Be there	Given the chronic and complex nature of DGBI, it is not the physician’s job to fix all of your patient’s problems. Being there means provide support and a listening ear and explicitly encouraging patients to schedule follow-up appointments, rather than asking them to “return if needed” which can be dismissive and stigmatizing. Communicating a plan of care tells patients that you care about their well-being and sets a foundation for positive future interactions42 “Please schedule a follow-up appointment with me in about 1 month so we can check-in and see how things are going. You should always feel free to call the office if you’d like to come in sooner.”
Practice self-awareness and compassion	Ultimately, caring for patients with DGBI can be challenging. We need to have the courage to challenge our own biases to reduce stigma. This requires that we meet ourselves where we are and learn to turn empathy inward. Practicing self-compassion as a physician involves treating ourselves kindly, removing any judgmental inner dialogue, recognizing that we are part of a shared human experience, and being mindful, without over-identifying with the patient’s suffering47 Take breaks in your day, practice self-care, set appropriate boundaries, seek support for your own mental and physical health

Ultimately, it is critical that physicians caring for patients with DGBI accept the reality of these illnesses, work with patients longitudinally on symptom reduction, and invest in effective communication to bolster the patient-physician relationship. Relationship-centered care requires that the patient is active and empowered. The doctor then responds to the patient’s cues, explicitly discusses psychosocial factors that influence symptoms, and employs patient-centered communication techniques (Table 1). Ultimately, treatment options are discussed and negotiated, leaving the final decision with the patient. This is the antidote to stigma. This model leads to improved diagnostic accuracy and clinical decision-making, establishes trust and collaboration in care, is time-efficient and leads to clear benefits for the patient, provider, and the ultimate clinical outcome.⁴⁰ For further information on learning to improve communication skills working with patients having DGBI, visit: https://romedross.video/3blx535.

Keypoints.

1. Yan et al. evaluated the prevalence of stigma among patients with refractory functional dyspepsia and comorbid depression/anxiety and the impact of stigma on adherence to neuromodulators (antidepressants) used to treat this disorder.

2. Stigma was present related to the condition itself and to neuromodulators and was associated with reduced neuromodulator adherence and less symptom improvement after intervention.

3. This study underscores the importance of identifying and intervening on stigma in order to optimize treatment and improve clinical outcomes.