Is depression an inflammatory disease?

Is depression an inflammatory disease?

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In the paper:

  • Michael Berk et al, So depression is an inflammatory disease, but where does the inflammation come from?, BMC Medicine 2013, 11:200, doi:10.1186/1741-7015-11-200

it is presented as an undisputed fact that depression is an inflammatory disease.

For example (the first sentence of the abstract):

We now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system.

However, AFAIK, we are far from understanding the etiology of depression (perhaps there is no universal one). Sure, there are many correlates (for example - levels of neurotransmitters), but I haven't heard that there a single, accepted cause (except for the cited paper). For the reference, Wikipedia mentions inflammation as one of multiple related conditions in the "Other hypotheses" section.

So, as of now, is it universally accepted that depression is an inflammatory disease? And if not, is it at least one of many mainstream opinions?

Discussion on HN, through which I've learnt about this paper

There certainly isn't a single cause of depression. Wikipedia does not list inflammation, so that seems to be sufficient disproof of universal acceptance, and at least one candidate for representative of mainstream opinions. Berk and colleagues (2013) make a pretty convincing case though, so it may only be a matter of time, exposure to the evidence, and someone bothering to update Wikipedia.

For another, partially independent (probably cites some of the same studies), preexisting reference on the matter, check out Psychology Today's article, "The Brain on Fire: Inflammation and Depression: Inflammation and Its Effects on Mood" (Greenblatt, 2011, November 23). It too supports the potentially causal relationship, though I don't see any direct evidence of inflammation causing depression here. You may want to scrutinize it more closely than I have; if you find anything, please comment or edit!

While it is indeed one of the theories, it is by no means not the mainstream one. Nowadays, it seems the neurogenic theory of depression is gaining a lot of support, if one looks at recent publications.

Briefly, the theory claims that impaired neurogenesis prevents replenishment of parahippocampal granule cells that normally inhibit the amygdala - a structure harboring fear and anxiety circuits.

The neurogenic theory also explains some of the correlations between inflammation and depression, namely the involvement of a factor known as NFkB.

If you're interested in knowing more, I'd be happy to recommend readings.

Inflammation, heart disease, and depression

Morbidity and mortality of cardiovascular disease is exceedingly high worldwide. Depressive illness afflicts a significant portion of the population worldwide. Epidemiological studies have confirmed the high co-morbidity between these two entities and the co-morbidity is bidirectional. Systems that contribute to this co-morbidity include the central and autonomic nervous systems, the neuroendocrine, immune, vascular and hematologic systems. Specific pathophysiologic factors include imbalance between the sympathetic and the parasympathetic systems, sympathoadrenal activation, hypothalamic-pituitary-adrenal axis activation, immune system dysregulation with release of pro-inflammatory cytokines and chemokines, platelet activation and hypercoaguability. Inflammation occurs in cardiac and cardiovascular pathology independent of the presence or absence of depression and in depression. Inflammation is closely associated with endothelial dysfunction which is a preamble to atherosclerosis and atherothrombosis. A likely common instigator underlying this co-morbidity is mental stress leading to sustained sympathetic overdrive and diminished vagal tone. Diminished vagal tone contributes to a pro-inflammatory status which affects neurotransmitter regulation, specifically serotonergic transmission. Stress hormones and certain pro-inflammatory substances released by macrophages and microglia upregulate the rate-limiting enzymes in the metabolic pathway of tryptophan. This results in a shunt in tryprophan metabolism away from serotonin formation and down the kynurenine pathway with resulting formation of neurotoxic metabolites.

Psychological Issues in Inflammatory Bowel Disease: An Overview

Inflammatory bowel disease (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC) is a chronic and disabling disease with unknown etiology. There have been some controversies regarding the role of psychological factors in the course of IBD. The purpose of this paper is to review that role. First the evidence on role of stress is reviewed focusing on perceived stress and patients’ beliefs about it in triggering or exacerbating the course of IBD. The possible mechanisms by which stress could be translated into IBD symptoms, including changes in motor, sensory and secretory gastrointestinal function, increase intestinal permeability, and changes in the immune system are, then reviewed. The role of patients’ concerns about psychological distress and their adjustment to disease, poor coping strategies, and some personality traits that are commonly associated with these diseases are introduced. The prevalence rate, the timing of onset, and the impact of anxiety and depression on health-related quality of life are then reviewed. Finally issues about illness behavior and the necessity of integrating psychological interventions with conventional treatment protocols are explained.

1. Introduction

Inflammatory Bowel Disease (IBD) describes a group of chronic gastrointestinal tract diseases that are relapsing and remitting the term primarily comprises Crohn’s disease (CD) and Ulcerative Colitis (UC). The prevalence of these diseases has increased in the past decades, up to 120–200/100000 and 50–200/100000 persons for UC and CD, respectively [1]. To date, there is no certain cure for IBD, and treatment is aimed at managing the inflammatory response during flares and maintaining remission with a focus on adhering to therapy [2]. The etiology of IBD is unknown, but genetic, immune, and environmental factors are each thought to play a role in its causation [1, 3, 4]. These factors interact together, so in a person who is predisposed genetically, environmental factors trigger immune dysfunction and bowel symptoms [5]. One of these environmental triggers may be psychological factors particularly psychological stress.

2. Role of Psychological Stress in IBD

A belief in the relevance of psychological factors to IBD is not new. Historically, it was first in the 1930s that gastroenterologists and psychiatrists suggested that emotional life events and experiences are likely related to exacerbation of intestinal symptoms [6]. At that time, IBD was considered as a psychosomatic disease, and its relation to stress and other psychological factors was thought so strong that researchers felt no need to use any control group in their studies. A few decades later, this finding was questioned mostly due to methodological weaknesses and uncontrolled studies published in this area. For a while IBD was considered as an organic disease, and psychological influences were discounted as contributing to it. But further anecdotal evidence and clinical observations indicated that stressful experiences could adversely affect the course of IBD.

Indeed many review articles have now emphasized the relationship between stress and IBD [6–10], concluding that confusions and controversies in published reports were partly due to differences in definitions of stress (e.g., stressful life events or hassles, daily stress) and partly due to inclusion of mixed groups of patients (CD versus UC) and/or mixed status of disease (active versus inactive) [6, 8]. Therefore, the major trends in recent studies were to differentiate between CD and UC patients, and to utilize the notion of perceived stress, which emphasizes on individual’s subjective perception of stress and his/her emotional response to it [11].

These trends have contributed to resolving controversies, and illuminating the role of psychological stress in IBD. Thus, while the role of stress in the onset of IBD has not been established, there is no doubt that stress is a triggering and exacerbating factor in relation to the course and symptoms of IBD [8, 10, 12, 13]. Indeed it can be considered as one of the determinants of disease relapse [12, 14, 15]. However, there are some discordant reports about a relation between stress and disease onset, like that of Li et al. [16] who, based on a follow-up study on the onset of IBD in parents who lost a child in Denmark, found a negative relationship between psychological stress and development of IBD. These conclusions provide support for the beliefs of almost 75% of patients with IBD that stress, or their own personality is a major contributor to the development of their disease [10, 12], and of more than 90% that it influences their disease activity [13, 17].

3. Possible Mechanisms of the Effects of Psychological Stress on Patients with IBD

In the light of recent advances in psychobiological research, what are the mechanisms by which the course of IBD can be influenced by stress?

3.1. Nonspecific Effects

Many of the IBD symptoms experienced by patients may be due to stress-induced changes in gastrointestinal (GI) function. There is a richly innervated nerve plexus between the enteric nervous system (ENS) and its spinal and autonomic connections to the central nervous system, known as the brain-gut axis. GI motor, sensory and secretory function as well as thresholds for the perception of pain [13], can be affected by psychological and emotional stress directly or indirectly through this axis. These effects are mediated by substance P (SP), vasoactive intestinal protein (VIP) [18], several neuropeptides, neurotransmitters, and hormones [12, 19]. Stress stimulates the secretion of corticotropin-releasing factor (CRF) either from central or peripheral parts of CNS (hypothalamus and adrenal cortex, resp.). While central CRF regulates the ACTH-cortisol system, peripheral CRF directly influences gastrointestinal motility. Endogenous CRF mediates the stress-induced inhibition of the upper GI tract motility and stimulation of colonic motility [12, 20]. Thus when symptoms such as abdominal pain and change in bowel function occur in IBD without significant disease activity, they may be attributed, at least in some instances, to alterations in motor and sensory function as a result of psychological stress.

3.2. Intestinal Permeability

Psychological stress can also increase intestinal permeability, probably as a result of alterations in the cholinergic nervous system and mucosal mast cell function [21]. Söderholm and Perdue [22] pointed out that various types of physical and psychological stress have an impact on several components of intestinal barrier function such as increasing intestinal permeability and stimulating secretion of ions, water, mucus, and even IgA. This increased permeability in turn reduces mucosal barrier function and alters bacteria-host interaction [12, 23]. However, based mainly on animal studies, these observations are likely to play a role in the pathophysiology of human IBD.

3.3. Immunological Mechanisms

Finally, stress is also likely to mediate its effect on IBD through the immune system [15, 19]. On the one hand, it is believed that an inadequately controlled response within the intestinal mucosa leads to inflammation in patients who are genetically predisposed to IBD. Dysfunction of the intestinal immune system and cross-reactivity of its cells against host epithelial cells have been implicated as major mechanisms by which the inflammatory response occurs [5]. On the other hand, it is increasingly recognized that the (hypothalamus-pituarity-adrenal) HPA axis, autonomic nervous system (ANS), and ENS can interact directly with the immune system. Cytokines are essential immune molecules in the pathogenesis of IBD [24, 25]. Many researchers [15, 20, 26, 27] reported that chronic or acute stress can alter profiles of cytokines (e.g., IL-1β, IL6, IL10, IL4, and TNFα) or of hormones such as cortisol, which may contribute to the pathophysiology of IBD. There is a bidirectional communication between neurons and mast cells within the gastrointestinal tract [28], and mucosal mast cells can be activated by stress [15, 29]. Stress-induced activation of mast cells, through release of mediators such as eicosanoids, serotonin, and IL6 could contribute to the pathogenesis of IBD [29].

3.4. Indirect Effects

In addition to the above-mentioned direct pathways, stress can also indirectly affect clinical course of IBD. These indirect effects are exerted through behaviors known to promote relapse [14] and include poor medication adherence [30] and smoking [31]. Direct and indirect mechanisms by which the course of IBD can be influenced by stress are shown in Figure 1.

4. Coping with IBD

Once IBD develops, the unpredictability, uncertainty, and chronic course of the disease can cause a wide range of psychological and interpersonal concerns to patients. These include loss of control of the bowel, fatigue, impairment of body image, a fear of sexual inadequacy, social isolation of dependency, a concern about not reaching to one’s full potential, and feeling dirty [13, 32]. Indeed, symptoms, such as faecal incontinence or soiling and lack of bowel control, can lead to a loss of self-unworthiness or cause stigmatization in patients [33, 34].

Dealing with these concerns needs appropriate coping strategies and good adaptation. Unfortunately, however, a variety of studies suggest that IBD patients rely significantly on passive coping strategies [34, 35], utilizing fewer purposeful problem solving and positive reappraisal, and more escape-avoidance strategies [36, 37]. Concerns such as those listed above on the one hand, and passive and/or avoidant coping on the other hand, lead to psychological distress [38] with maladaptation and poor adjustment to the disease.

Sewitch et al. [39] and Mikocka-Walus et al. [40] using Symptom Checklist-90-R (SCL-90) indicated that IBD patients had impaired psychological functioning. When patients receive a new diagnosis of IBD, a series of psychological adaptive steps occurs. For example, the patient may do an initial evaluation of the disease’s likely impact on his/her life, subsequently showing emotional reactions such as distress, grief, and sometimes guilt, exhibiting a behavioral response involving taking new medications, seeking social support, and modifying their diet various degrees of denial and or disease acceptance may occur. This adaptive process is complex it is likely to be influenced by a range of factors including severity of disease, age of onset of disease, its extent of interference in the patient’s life and future plans [32], beliefs and thoughts about illness and health, illness attribution [37], emotional status [41], and previous experiences.

Among these, factors such as social support and affective state (in the frame of personality trait) have been studied in detail. Sewitch et al. [39] revealed that the relationship between psychological distress and perceived stress changes according to the level of satisfaction with social support. For patients who experienced moderate-to-high levels of perceived stress, high satisfaction with social support decreased the level of psychological distress and facilitated adjustment to the disease, a point which highlights the importance of social support in maintaining mental health in and adjustment to IBD. Moreover, Pellissier et al. [41] suggested that negative effect was associated with poorer coping to IBD.

5. Personality Traits

Perhaps these factors can be integrated together and attributed to personality traits. Indeed, some patients with IBD believe that their own personality is a major contributor to the development of their disease [17]. In this context, Thornton and Andersen [42] suggest that personality traits can modulate the relationship between stress and the immunological reaction to it.

5.1. Neuroticism and Perfectionism

In IBD patients, the commonest personality trait is reported to be neuroticism [17, 43, 44] furthermore, high neuroticism scores appear to reduce psychological wellbeing, psychological adjustment, and quality of life in patients with IBD [44, 45]. Another personality characteristic, emphasized in IBD patients, is perfectionism [46] its negative impact in IBD is probably explained by its relationship with negative cognitive biases, heightened reactivity to stressors, and feeling pressured to be and look perfect. The latter may be particularly detrimental for IBD patients because these conditions are often accompanied by stigma, shame, feeling of dirty, and a burden [47]. The above investigators have shown a relationship between perfectionism and the psychological impact of IBD, so as the trait was associated with emotional preoccupation coping a maladaptive coping way with disease.

5.2. Alexithymia

Some studies have shown alexithymia to be another common personality characteristic in IBD patients. Patients with alexithymia have difficulty in recognizing and verbalizing emotions, and their ability to regulate emotions and express them to others is usually reduced [48]. Numerous studies [36, 44, 45, 49] have shown that IBD patients have higher scores for alexithymia than controls. In Jones, Wessinger, and Crowell’s study [36], the scores of 74 IBS patients, 55 healthy control subjects, and 48 IBD patients compared on Toronto Alexithymia Scale and results showed that the IBS and IBD patients had higher scores on measures of alexithymia than controls but did not differ from one another. Porcelli et al. [49] in an epidemiological study compared 121 functional gastrointestinal disorders patients, 116 IBD patients, and a group of 112 healthy subjects using Toronto Alexithymia Scale. Their results showed that the FGID group was significantly more alexithymic than the IBD group, and the scores of two gastrointestinal groups were higher than the normal healthy group. Even after controlling for the influence of education, gender, anxiety, depression and gastrointestinal symptoms, these differences remained significant. Moreno-Jiménez et al. [44] did not use any control group. In their sample comprised of 60 UC and 60 CD patients, they have tried to address this question that, which personality factors may predict HRQOL in IBD patients. They showed that difficulty in describing one’s feelings was significant on predicting two dimensions of HRQOL, that is, systemic symptoms and social functioning. Difficulty in describing one’s feelings negatively predicted systemic symptoms and social functioning. Patients experiencing more difficulty in describing their feelings reported lower HRQOL.

However, Drossman and Ringel [13] reemphasized that while alexithymia is not specific to IBD, it may lead patients to communicate their psychological distress through somatic and behavioral symptoms rather than verbal communication this might occur particularly when patients have limited perceived social support or personality traits such as introversion. Whether alexithymia is specific to IBD or not, it has been reported that affected patients have greater difficulty in describing their feelings to others, have poorer disease outcome, lower psychological functioning, and worse health-related quality of life [44, 46, 50].

Although discrete personality traits have been studied among IBD patients, no certain personality type matches this disease to date. It is recommended that future research considers discrete personality traits observed in these patients and integrates them in such a way that the traits will be addressed to new personality types such as type D [51, 52] and C [53], which are well matched with unregulated immune and hormonal systems that are characteristics of IBD.

6. Anxiety and Depression

The numerous concerns and worries mentioned above, together with patients’ awareness of its incurability and uncertain course and prognosis, and their fear of surgery or the development of cancer, are all likely to contribute to a risk of anxiety in people with IBD [54, 55]. Once a patient develops IBD, he/she usually might form adaptive adjustment to it and accept the condition. Sometimes when patient has weak coping skills or social support or he/she may be personally predisposed (some personality trait such as neuroticism), he/she may feel frustrated, sad, and avoid social events. According to Seligman’s theory [56], unpredictable and incurable course of disease impaired individual’s belief about self-control [33] and self-efficacy [23, 32, 57] and thereby caused helplessness and predisposed the patient to depression.

There are some controversies about the comorbidity of clinical anxiety and depression in IBD patients. While some researchers [38, 58, 59] found no evidence of any association between these psychiatric disorders and either UC or CD, others [60–63] confirmed that depression and anxiety are common in IBD patients. The prevalence of anxiety and/or depression has been estimated to be as high as 29–35% during remission [64] and 80% for anxiety and 60% for depression during relapse [65]. Robertson et al. [17] and Mikocka-Walus et al. [40] distinguished between these disorders and reported that anxiety is more prevalent than depression in IBD.

Another source of controversy lies in the question of whether psychological disorders precede and/or follow after onset of the IBD? Some researchers have considered the psychological disorders as a consequence of a new diagnosis [6, 20] and emphasized that IBD is not caused by a psychological condition. However, Kurina et al. [66], using a database of linked hospital records abstracts, in a retrospective nested case-control study on 12499 patients (7268 UC and 5231 CD) and 800000 controls with minor medical conditions not related to the conditions of interest, found that both depression and anxiety preceded UC (but not CD) significantly more often than would be predicted by chance the relationships were strongest when the mental conditions were diagnosed shortly before UC. However, these disorders were significantly more common after the diagnosis of CD, and UC was followed by anxiety, not by depression. In contrast, Tarter et al. [67] reported that anxiety prior to diagnosis was common, in CD, but found no significant antecedent psychological disorder in UC. These researchers studied 53 consecutive IBD patients including 26 CD and 27 UC patients and 28 healthy controls. In this study compared to normal controls, CD patients manifest an increased prevalence of anxiety, depression, and panic disorder occurring at any time in their life. Only panic disorder had an excess prevalence in CD relative to community dwelling normals prior to the time of disease onset. Individuals with UC did not demonstrate an increased prevalence of psychiatric disorder before or after disease onset. Mikocka-Walus et al. [7] suggested that it is difficult to reconcile these two divergent findings, as neither study was appropriately controlled. However, the sample size of the Kurina et al.’s [66] group was substantially larger than of the Tarter et al. [67], and it is a methodological strength that partly facilitates the conclusion.

Whether anxiety and depression appear before or after the onset of IBD, physiological data [68, 69], suggest that these mood disorders can stimulate production of proinflammatory cytokines and thereby adversely affect the course of IBD, a conclusion supported by clinical observations [64]. Drossman and Ringel. [13] suggest that psychological disturbances as a component of the illness may modulate its clinical expression, rather than being etiologic or specific to IBD. It is, therefore, a priority to pay careful attention to the possibility of mood disorders in patients with IBD.

7. Quality of Life (QOL)

IBD generally begins in child- or young adulthood and lasts life-long. Although the life expectancy of IBD patients approximates to that of healthy people, IBD substantially impairs patients’ health-related quality of life (HRQOL) [70, 71]. Relevant factors include those discussed above, the chronicity of IBD, its complications, associated physician visits and hospitalizations, and side effects of medical treatment or surgery. It is not surprising, therefore, those patients with active IBD have poorer disease-specific quality of life relative than those with inactive disease [35, 72–74]. Of course, poor HRQOL is not restricted to active episodes, and the negative impact of IBD on patients quality of life continues even when it is inactive. Considering disease type, Mikocka-Walus et al. [40] and Farmer et al. [75] pointed out that impairment in psychosocial dimensions of HRQOL is greater for CD than UC. Mikocka-Walus et al. [40] compared psychological problems such as anxiety and depression and impairment of quality of life in IBD, IBS and Hepatitis C, and general population. These researchers found that each of three groups had significantly lower quality of life than the general population. In IBD group, 31 participants with CD had poorer physical quality of life in Physical Component Summary (PSC) subscales of SF-12 than 33 UC patients (

). Farmer et al. [75], using an interview consisted of four categories: functional/economic, social/recreational, affect/life in general, and medical/symptoms, studied quality of life on 94 patients with ulcerative colitis and 70 patients with Crohn's disease. They found that Patients with ulcerative colitis had better scores on medical/symptoms’ category in the interview than those with Crohn's disease. These researchers believed that perhaps these findings could be attributable to experiencing more severe disease by CD patients than UC patients. Drossman and Ringel [13] have pointed out to this conclusion, as well. However, others have suggested that after severity of disease was taken into account, there were no significant differences between CD and UC in terms of HRQOL [57, 70].

However, the physical symptoms of IBD do not completely explain the reductions of HRQOL in affected patients because disease activity and the intensity of patients’ symptoms do not significantly correlate with their subjective impairments [77]. Indeed, sociodemographic variables influence quality of life. For example, Sainsbury and Heatley [35], Casellas et al. [70], and Haapamaki [71] listed the effects of gender (women had poorer QOL than men), level of education, socioeconomic status, and older age on HRQOL in IBD patients. In addition to sociodemographic variables, others have noted that psychological factors can also affect HRQOL in these diseases. In this regard, more psychological disturbance and the presence of anxiety or depression contribute to poorer HRQOL, regardless of severity of the IBD [43, 59, 74]. Furthermore, Moreno-Jiménez et al. [44] and Boye et al. [45] suggest that factors such as personality traits may influence psychological well-being and HRQOL in their studies, neuroticism and greater difficulty in describing feelings to others were related to poorer HRQOL. Overall, because of its influence on patients’ psychological well-being, social adjustment to their IBD and health care utilization, integrating HRQOL into the routine clinical assessment of patients with IBD, and targeting it as a treatment aim is strongly recommended. The factors affecting QOL of patients with IBD summarized in Table 1.

8. Illness Behavior

The personal meaning of the illness, the individual’s attitudes and expectations, and illness attributions to internal or external factors may all affect disease-related concerns and consequently a patient’s adjustment to an illness. Since patients differ in social context, cultural heritage, value systems, family structure, prior experiences with illness, and psychological status, each individual is likely to respond differently to the challenge of a chronic illness such as IBD. Levenstein et al. [78] suggested that because of the impact of sociocultural beliefs and values about the illness, the impact of a given disease may also vary significantly between one country and another, even if its biological behavior is uniform.

For example, a patient with ulcerative colitis who suffers from abdominal pain may not go to the physician if he/she has previously experienced those symptoms without serious consequences, or if he/she has grown up in a family where attention to illness has been minimal, or if he/she believes that complaining might be regarded as weakness. Another patient with the same disease activity and symptoms may frequently utilize healthcare services if he/she perceives symptoms to have dangerous consequences and is seeking disability or comes from a family where greater attention has been paid to illness. In this context, Drossman et al. [79] found that the number of physician visits in IBD patients was related to both psychological and physical health factors, so that the presence of psychological distress such as depression may lead to more frequent physician visits.

For the above reasons, physicians need to establish a close and effective therapeutic relationship with their patients, be sensitive and responsive to their patients’ concerns about IBD, provide information consistent with the patients’ questions and needs, and educate their patients properly about their condition and planned treatment, thereby reducing patients’ concerns and uncertainties and their dependency on the healthcare system.

9. Management of Psychological Disorders in Patients with IBD

As mentioned earlier, psychological disorders such as anxiety and depression are common among IBD patients. Even if the severity of these psychological problems does not reach the clinical definition of psychiatric disease, psychological distress, concerns, worries, fears, and poor coping strategies which may lead to reduced quality of life fully justify professional attention. Most current conventional medical treatments for IBD are associated with potential side effects, some of which are psychological (e.g., mood changes, mania, or depression induced by corticosteroids), and none of them pay attention to patient’s psychological status or concerns or QOL [63]. Therefore, integrating psychological treatment with conventional medical therapy to improve psychological distress and coping strategies and when necessary to alleviate depression or anxiety is likely to be beneficial.

9.1. Effect of Psychological Interventions on IBD Activity

It has been suggested that if psychological stress, for example, by worsening mucosal barrier and immune function, is a pathogenic factor in IBD (see above), then psychological intervention aimed at stress reduction and may potentially reduce disease activity [9, 15]. Specifically, Niess et al. [19] and Thornton and Andersen [42] proposed that psychological interventions such as relaxation training influence stress-mediated alterations of the immune system. Furthermore, psychological interventions can reportedly improve the course of some immune-mediated diseases such as cancer and HIV [93, 94]. More work is needed to assess the proposal that psychological approaches could affect the course of IBD itself.

9.2. Improving Personal Control

Another reason for incorporating these interventions as complementary options in the treatment protocol relates to establishing and highlighting for the patient a sense of personal control. Compared to medical therapy that emphasizes patient’s obedience to their doctor in relation, for example, to medication adherence, psychological interventions engage the patient in the treatment process and increase a sense of personal control of their illness. These interventions do this by educating patients about cues for managing stress and relaxing them, assist the patients to solve their problems rather than avoiding them or surrendering them to others, and restructuring their cognitions rather than trying to alter their external environment. Many researchers [95] in sociology and psychology have indicated that personal control is important to psychological functioning and can be regarded as a robust predictor of physical and mental well-being. Furthermore, psychological interventions may increase self-efficacy in patients and thereby improve their capacity for coping and managing their distress.

9.3. Potential Psychological Therapies

Numerous psychological interventions have been developed and studied in IBD, with a range of outcomes. Keller et al. [80] and Wietersheim et al. [81] reported that supportive-expressive and psychodynamic therapy may be ineffective in the treatment of psychological comorbidities and somatic course of IBD. Some studies [43, 82–86] showed that although cognitive-behavioral therapy or stress management may lead to significant improvements in anxiety, depression, and quality of life, they have no effect on the course of patients’ IBD. In contrast, others [87–89] suggested that stress management, relaxation training, and IBD-focused counseling have been useful both for psychological problems and the clinical symptoms of IBD. A comprehensive lifestyle modification program [90] and mind-body therapy [91] have also been studied in IBD patients and revealed significant improvements in quality of life, anxiety, and psychological well-being.

9.4. Antidepressants

High prevalence of psychological disorders, such as anxiety and depression in patients with IBD, may recommend psychopharmacological therapies specially antidepressants as an alternative treatment for these patients. Although a qualitative study [92], based on interviewing with gastroenterologists, showed that some gastroenterologists use antidepressants for treating pain, anxiety and/or depression, and insomnia in patients with IBD, to date application of these drugs is not straightforward. Mikocka-Walus et al. [96], based on their systematic review about antidepressants and IBD, reported that tricyclic antidepressants (e.g., Amitriptylin, dothiepin, prothiaden, doxepin, imipramin, and nortriptyline) not only alleviate psychological distress, but also have some positive effects on somatic status of IBD patients through reducing pain, gut irritability, and urgency of defecation. Newer antidepressants are not prescribed as much as TCAs by physicians. Recent systematic review by Mikocka-Walus et al. [97] even reported that antidepressants have positive effect on inflammation of the bowel in IBD patients. Since the most published data in this area have not been randomized and have methodological weaknesses, Hardt et al. [63] concluded that it is impossible to make a definitive statement of efficacy of antidepressants on mental and somatic status of IBD patients.

Overall, while there are contradictory reports on the effect of psychological interventions on clinical course of IBD, most show a positive effect on psychological and emotional status and HRQOL. Contradictory findings may be in part due to difference in trial design, the components of the tested treatment protocols, outcome measures assessed, and other confounding variables. Undoubtedly, more rigorous better designed studies in this field are needed. With regard to recent findings about the effect of psychological interventions on immune modification [97, 98] and reducing the likelihood of relapse [57], the necessity of incorporating them to conventional treatment protocol of IBD is more illustrated. Options for management of psychological disorders in patients with IBD are listed in Table 2.

10. Conclusion

Current evidence indicates that psychological factors play a role both in the pathophysiology and course of IBD and in how patients deal with these chronic and disabling diseases. Over the two last decades, improvements in study design and methodology, along with advances in psychoneuroendocrinology and psychoneuroimmunology, have led to improved, if still incomplete, understanding of the relevant pathophysiological mechanisms. The contribution of some psychological factors such as predisposing personality remains uncertain and requires further study. Most importantly, in view of the importance of psychological dysfunction in modifying illness behavior and its negative impact on symptoms and QOL, the integration of psychological interventions into conventional medical therapy, seems advisable. Where further study is most urgently needed, however, it lies in the analysis of the precise effects of these interventions on not only psychological state and quality of life, but also on the physiological parameters and the course of IBD itself. Such research should investigate also which is the most effective component, or combination of components for the psychological management of IBD.

Auther Contributions

All authers have contributed equally to this work.

Supportive Foundations

Supported by Iran National Science Foundation: INSF, No. 89002451


The authers thank Professor David Rampton for his advice on the manuscript.


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Copyright © 2012 M. S. Sajadinejad et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

What Is Inflammation?

Inflammation is the body’s response to a threat, whether it's a foreign invader, such as a bacteria, virus, or cancer, a transplanted organ (which the body sees as “foreign”), or even a psychological or emotional stressor. In response, the immune system sends out an army of chemicals, called pro-inflammatory cytokines, to attack the invaders.

“Think of inflammation as a ‘sickness behavior,’” says Madhukar Trivedi, MD, director of the Center for Depression Research and Clinical Care at UT Southwestern Medical Center in Dallas. Inflammation, he says, "causes your body to act fluish, even in the absence of the flu virus.”

Pro-inflammatory cytokines usually do their job and then disappear, but when stress is chronic, they are “upregulated” in your system — meaning the cycle of stress and inflammatory response gets habituated in the body, explains Gupta. Over time, these cytokines may perpetuate themselves. That’s when inflammation starts to cause deleterious effects on the body. And while no one is completely sure why — there are many mechanisms responsible for diseases — what many conditions have in common is chronic, low-level inflammation.


If a cut on your skin swells up, turns red, and hurts, those symptoms are signs of acute, or short-lived, inflammation. Feeling hot or losing function may be signs of inflammation from other harm to your body. Some inflammation that occurs in your body&rsquos cells or tissues may not have outward symptoms.

Inflammation is a normal part of the body&rsquos defense to injury or infection, and, in this way, it is beneficial. But inflammation is damaging when it occurs in healthy tissues or lasts too long. Known as chronic inflammation, it may persist for months or years.

Inflammation may result from many factors, such as:

  • Environmental chemicals
  • Injuries like scrapes, insect stings, or a splinter in your finger
  • Pathogens (germs) like bacteria, viruses, or fungi
  • Radiation

Inflammation plays a key role in many diseases, some of which are becoming more common and severe. Chronic inflammatory diseases contribute to more than half of deaths worldwide. 1

Inflammation is associated with diseases such as the following:

  • Autoimmune diseases like rheumatoid arthritis
  • Cardiovascular diseases like high blood pressure and heart disease
  • Gastrointestinal disorders like inflammatory bowel disease
  • Lung diseases like asthma
  • Mental illnesses like depression
  • Metabolic diseases like Type 2 diabetes
  • Neurodegenerative diseases like Parkinson&rsquos disease
  • Some types of cancer, like colon cancer

What is NIEHS Doing?

Increasing evidence suggests environmental factors contribute to chronic inflammation. A review 2 of scientific literature conducted by NIEHS-funded researchers affiliated with the National Toxicology Program found the environment plays a role in inflammation in both positive and negative ways, such as:

  • Environmental chemicals &ndash The federal Toxicology in the 21st Century, or Tox21 , program shows how chemicals we commonly encounter may alter molecular pathways that underlie inflammation.
  • Nutrition &ndash Diets high in refined grains, alcohol, and processed foods can alter gut microbiota and lead to intestinal and immune changes.
  • Microbiome &ndash Studies of various microbiome imbalances and disease states show connections to inflammation.
  • Social and cultural changes &ndash Disrupted sleep patterns, psychosocial stress, artificial light, and other factors influence the immune system.
  • Developmental origins &ndash Childhood obesity, psychological stress, exposure to microbes in infancy, and prenatal conditions are linked to inflammation.
  • Physical activity &ndash When skeletal muscles contract, they release proteins that can reduce inflammation throughout the body.

NIEHS researchers and grantees are exploring ways to predict, prevent, and treat inflammatory diseases. They are studying the underlying causes of inflammatory diseases, developing experiments to examine the inflammatory effects of current and emerging environmental threats, and testing novel strategies to treat environmentally-induced inflammation. Below are examples of recent findings:

  • Chronic liver inflammation and cancer &ndash By suppressing one of the body&rsquos natural mechanisms to fight cancer, chronic liver inflammation can lead to a new tumor-promoting pathway. This discovery may inform liver cancer treatments. 3
  • Nanotechnology and lung inflammation &ndash Silver nanowires, which are used in personal care products, food storage boxes, and computers, were taken up by cells in the lungs of rats, leading to lung inflammation. 4
  • Ozone and cardiovascular disease &ndash Exposure to ozone, even at levels lower than the current U.S. Environmental Protection Agency (EPA) air quality standard, may lead to cardiovascular disease. 5
  • Air pollution and diabetes &ndash The diabetes drug metformin may reduce inflammation triggered by air pollution exposure by preventing immune cells known as macrophages from releasing an inflammatory molecule called interleukin-6. 6
  • Inflammation and Parkinson&rsquos disease &ndash Blocking a brain enzyme called soluble epoxide hydrolase in mice helped curb the inflammation associated with the development and progression of Parkinson&rsquos Disease. 7
  • Environmental stressors and lifespan &ndash NIEHS scientists demonstrated that inflammatory responses to environmental stressors can reduce lifespan, supporting a theory that longevity depends on a balance between pro- and anti-inflammatory proteins. 8
  • B vitamins and air pollution &ndash Taking B vitamins may help lessen the effects of fine particles, a common air pollutant. 9
  • Prostate cancer among first responders &ndash Changes in inflammation and immune regulation from exposure to World Trade Center dust may have increased prostate cancer progression among those first responders. 10

Future Directions

NIEHS continues to support a wide variety of research projects focused on inflammation and its role in wellness and disease. Questions NIEHS researchers and grantees are addressing include:


While there has been a great deal of speculation over the years on the importance of emotional factors in inflammatory bowel disease (IBD), it is only in the last decade or so that studies with stronger designs have been available to clarify the nature of this relationship. This review considers recent evidence on the prevalence of anxiety and depressive disorders in IBD, the role of these disorders as a risk factor for IBD onset, the degree to which they affect the course of the IBD, and the contribution of corticosteroid treatment to psychiatric symptom onset. There is evidence that anxiety and depression are more common in patients with IBD and that the symptoms of these conditions are more severe during periods of active disease. The few studies that address the issue of anxiety and depression as risk factors for IBD do not yet provide enough information to support definite conclusions. There is evidence, however, that the course of the disease is worse in depressed patients. Treatment with corticosteroids can induce mood disorders or other psychiatric symptoms. The second part of the review focuses on patient management issues for those with comorbid anxiety or depression. Practical approaches to screening are discussed, and are recommended for routine use in the IBD clinic, especially during periods of active disease. We review evidence-based pharmacological and psychological treatments for anxiety and depression and discuss practical considerations in treating these conditions in the context of IBD to facilitate overall management of the IBD patient.

The etiology of Crohn's disease (CD) and ulcerative colitis (UC) is not well delineated, but is currently understood to relate to the complex interaction between genetic and environmental variables resulting in an inappropriate and exaggerated intestinal inflammatory response in vulnerable individuals. 1 , – 3 The chronic clinical course often results in reduced quality of life. 4 Given that the disease has both early life onset and does not typically contribute to shortened life span, addressing how the individual manages with and is impacted by the disease is an important aspect of care.

The presence of a chronic medical condition is often associated with higher rates of anxiety and mood disorders compared to the general population. 5 , – 7 Potentially, there are reciprocal influential processes, such that the experience of the disease is sufficiently stressful to trigger or intensify the psychiatric condition or conversely anxiety or depression may be sufficient to trigger or exacerbate the health condition. 8 , – 10 Alternatively, there has been significant discussion about potential common pathways, particularly between depression and inflammatory conditions such as inflammatory bowel disease (IBD), related to dysfunctioning immunoregulatory circuits. 11 , – 13

Regardless, the comorbidity can complicate functioning as well as disease outcomes. 7 , 14 , 15 A great deal of disability and functional impairment that occurs in chronic health problems is associated with anxiety and depression more so than the features of the disease. 14 , 15 Depression has been projected to be the second leading cause of disability worldwide by 2020, 16 and yet it often goes unrecognized and untreated.

This review considers the most recent literature on the nature of the relationship between IBD and 2 common psychiatric disorders, depression and anxiety. It emphasizes these disorders rather than more general distress or stress impact in order to more consistently link the psychiatric condition to appropriate clinical intervention. We examine the evidence on co-occurrence, the potential contribution of these psychiatric conditions as risk factors for IBD onset and disease course, and summarize the converse relationship of psychiatric symptoms as an adverse outcome of IBD treatment. Finally, we discuss strategies for screening and treating anxiety and depression in the context of IBD, considering both evidence-based pharmacological and nonpharmacological interventions.

The Impact of Anxiety and Depression on Patients with Inflammatory Bowel Diseases

Acknowledgement: This article is a summary of “Influences and Impact of Anxiety and Depression in the Setting of Inflammatory Bowel Disease” recently published in Inflammatory Bowel Diseases by Seyedehsan Navabi, MD, Venkata Subhash Gorrepati, MD, MPH, Sanjay Yadav, MD, Jaykrishna Chintanaboina, MD, Sarah Maher, MD, Peter Demuth, Benjamin Stern, MD, August Stuart, Andrew Tinsley, MD, Kofi Clarke, MD, Emmanuelle D Williams, MD, and Matthew D Coates, MD, PHD. This summary article was written by Catherine Soto, Director, Patient Education & Support at the Crohn’s & Colitis Foundation.

People with inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, are at increased risk of developing anxiety and/or depression. Some research has found that anxiety and depression are two to three times more likely to occur in IBD patients, compared with the general population. [1],[2],[3],[4],[5],[6],[7]

It is important for doctors, and other healthcare professionals to understand how IBD and anxiety and depression can affect each other. It is important to address this relationship between mental health and IBD because:

  1. Managing IBD can be even more challenging when patients have anxiety and depression.
  2. IBD patients who also experience anxiety and depression are more likely to report having symptoms, even with no inflammation.
  3. Anxiety and depression in IBD patients may heighten disease flares or other complications and lower the likelihood that a treatment will be successful. [8]
  4. IBD patients with anxiety and depression tend to show lower scores when asked to report on or rate their quality of life. [9],[10],[11],[12],[13],[14]

While IBD is a chronic condition, not all patients develop anxiety or depression. This has brought many researchers to try to understand why anxiety and depression occur among certain patients. Are there specific medical factors that can be connected to having anxiety and/or depression? How might these medical factors affect how a patient is using the healthcare system in the management of their disease?

A study was performed at Pennsylvania State University Hershey Medical Center looking at the data of patients who consented to be included in the Intestinal Diseases Natural History Database. The study was done as a retrospective analysis, a type of scientific approach that looks back at existing information in order to identify patterns or learn more about an issue or question. The data from this study was filtered to review patients seen between January 2015 and August 2016. The two objectives were to:

  1. Identify any medical information that could help us understand what types of patient experiences are more likely to be associated with anxiety and depression.
  2. Determine how anxiety and depression may affect a patient’s experience of symptoms, and their use of healthcare.

The results

Researchers looked closely at the data of 432 IBD patients within the Intestinal Diseases Natural History Database at the Pennsylvania State College of Medicine in Hershey, PA. Of these patients, approximately 44 percent were found to have significant scores on a scale for anxiety or depression, with a majority of them (59 percent) female. About 20 percent had both anxiety and depression. The medical factors that were associated with having anxiety or depression included:

  • Smoking
  • Extra-intestinal manifestations (symptoms outside of the gastrointestinal tract)
  • Previous surgery (or surgeries)

In addition, IBD patients with anxiety and/or depression showed these connections:

  • Had more imaging studies (such as x-rays, scans, endoscopies)
  • Visited the emergency room more often
  • Were more often hospitalized
  • Were on corticosteroids more frequently
  • Were taking a biologic (example: anti-TNF)

The study also found that patients with anxiety and/or depression reported their symptoms to be more severe compared to those that did not have anxiety or depression. Symptoms such as abdominal pain, fatigue, fecal urgency, excess gas, and blood in the stool, were more commonly reported. In addition, the level of inflammation shown through endoscopy was also scored higher among IBD patients with anxiety and depression.

This retrospective analysis highlights the importance of addressing mental health, specifically anxiety and depression as it relates to the patient’s disease management. Those who had anxiety and/or depression symptoms demonstrated higher likelihood of disease-related complications, and experienced a greater burden of their disease. There is a need to improve the access to mental health professionals and resources which could help reduce the risk of complications, flares, progression of IBD, and help improve a patient’s quality of life.

[1] Panara AG, Yarur AG, Rieders B, et al. The incidence and risk factors for developing depression after being diagnosed with inflammatory bowel disease: a cohort study. Aliment Pharmacol Ther. 201439:802-10

[2]Addolorato G, CapristoE, StefaniniGF, et al. Inflammatory bowel disease: a study of the association between anxiety and depression, physical morbidity, and nutritional status. Scand J Gastroenterol . 199732:1013–21.

[3] Fuller-ThomsonE, SulmanJ. Depression and inflammatory bowel disease: findings from two nationally representative canadian surveys. Inflamm Bowel Dis . 200612:697–707.

[4] KesslerRC, BerglundP, DemlerO, et al. National Comorbidity Survey Replication.

The epidemiology of major depressive disorder: results from the national comorbidity survey replication (NCS-R). Jama . 2003289:3095–105

[5] BhandariS, LarsonME, KumarN, et al. Association of inflammatory bowel disease (IBD) with depressive symptoms in the United States population and independent predictors of depressive symptoms in an IBD population: a NHANES study. Gut Liver . 201711:512–9.

[6] NeuendorfR, HardingA, StelloN, et al. Depression and anxiety in patients with inflammatory bowel disease: a systematic review. J Psychosom Res . 201687:70–80.

[7] Mikocka-WalusA, KnowlesSR, KeeferL, et al. Controversies revisited: a systematic review of the comorbidity of depression and anxiety with inflammatory bowel diseases. Inflamm Bowel Dis . 201622:752–62.

[8] PersoonsP, VermeireS, DemyttenaereK, et al. The impact of major depressive disorder on the short- and long-term outcome of crohn’s disease treatment with infliximab. Aliment Pharmacol Ther . 200522:101–10.

[9] SimrénM, AxelssonJ, GillbergR, et al. Quality of life in inflammatory bowel disease in remission: the impact of IBS-like symptoms and associated psychological factors. Am J Gastroenterol. 200297:389–96.

[10] FarrokhyarF, MarshallJK, EasterbrookB, et al. Functional gastrointestinal disorders and mood disorders in patients with inactive inflammatory bowel disease: prevalence and impact on health. Inflamm Bowel Dis . 200612:38–46.

[11] Iglesias-ReyM, Barreiro-de AcostaM, Caamaño-IsornaF, et al. Psychological factors are associated with changes in the health-related quality of life in inflammatory bowel disease.

Inflamm Bowel Dis . 2014 20:92–102.

[12] KimES, ChoKB, ParkKS, et al. Daegukyungbook Gastrointestinal Study Group (DGSG). Predictive factors of impaired quality of life in Korean patients with inactive inflammatory bowel disease: association with functional gastrointestinal disorders and mood disorders. J Clin Gastroenterol . 201347:e38–44.

[13] VidalA, Gómez-GilE, SansM, et al. Health-related quality of life in inflammatory bowel disease patients: the role of psychopathology and personality. Inflamm Bowel Dis . 200814:977–83.

[14] ZhangCK, HewettJ, HemmingJ, et al. The influence of depression on quality of life in patients with inflammatory bowel disease. Inflamm Bowel Dis . 201319: 1732–9.

Inflammation and Diseases

Classically, inflammation is classically known as the crucial response to microbe invasion or tissue injury to keep maintenance of tissue homeostasis. In recent years, our knowledge of the inflammation role is greatly enlarged. Inflammatory pathway has been recognized as a pivotal molecular basis in the pathogenesis of many chronic diseases. By far, increasing literatures have shown that excessive inflammation play critical roles in the progression, and/or onset of stress-related diseases. There has been a growing number of evidence supporting that inflammatory response constitutes the 𠇌ommon soil” of the multifactorial diseases, including cardiovascular and metabolic diseases, psychotic neurodegenerative disorders and cancer (Scrivo et al., 2011).

Ways to Feel Better

Breathe. You can trigger the body to relax when you take slow breaths that fill your belly with air. Called diaphragmatic breathing, some research shows that it can reduce anxious and depressed feelings. Here’s how you do it:

  1. Breathe in through your nose for 4 or 5 seconds.
  2. Place your handon your belly. Only your stomach should expand.
  3. Hold your breath for a couple of seconds.
  4. Breathe out through your mouth for about 6 seconds.
  5. Repeat for 5-15 minutes.

Focus your mind. Some studies found that mindfulness-based meditation, like paying attention to your breath, may:

Brain scans show that people who pay attention to the moment tend to hurt less because the pain center in their brain is less active.

Intestinal behavioral therapy. You don’t have to have a mental illness to benefit from this kind of treatment. It's designed for anyone who wants to deal with the stress around UC.


  • Cognitive behavioral therapy (CBT)
  • Gut-directed hypnotherapy
  • Stress-management therapy

Get moving. You probably already know that exercise is good for your mood. Studies show it works just as well as antidepressants for some people. But listen to your body. If you are really active for a long time, it can cause more inflammation and make some IBD symptoms worse. Marathon runners sometimes get diarrhea or intestinal bleeding. That might not be a great activity to do if you have UC.

  • Moderate-intensity exercise like walking or yoga
  • High-intensity interval training (HIIT) is also safe for people with IBD
  • Weight training, also called resistance exercise, is another option that may lessen depression symptoms.

Reach out to someone. You might feel better if you talk to a therapist, especially one who's familiar with UC. You can also meet up with people who know what you are going through. The Crohn’s & Colitis Foundation can help you find a support group in your area.

Antidepressants may help. There is evidence they might boost your spirits and ease the pain of your gut symptoms at the same time. But talk to your UC doctor before trying any mediations for your mood. Some can cause side effects that worsen IBD.


Get enough sleep. You should try to snooze long enough that you aren’t tired during the day. That’s probably somewhere between 7-9 hours for adults. Talk to a specialist if you have trouble getting or staying asleep. Insomnia is linked to depression and higher levels of inflammation.

Go outside. Exercising out in nature may lower anxiety more than sweating it out in the gym. There is also evidence that walking in trees or looking at greenery can help lower stress levels in general.

Give yourself a break. You don’t have to pretend everything is fine. Along with all the other things that help you manage your emotions, experts say you will probably feel better sooner if you sit with your bad feelings for a little while instead of trying to make them go away.

Depression Predicts Increases In Inflammatory Protein Linked To Heart Disease

To help solve this long standing chicken and egg conundrum, researchers led by Jesse Stewart, Ph.D., assistant professor of psychology at Indiana University-Purdue University Indianapolis asked two critical questions. Does depression lead to elevated inflammatory proteins in the human body? Or does an increase in these proteins lead to depression? They found that the answer to the first question appears to be "yes," and the answer to the second question may be "no" among healthy adults.

The researchers report that depressive symptoms are associated with increases over time in interleukin-6, an inflammatory protein that predicts cardiovascular events. In contrast, levels of interleukin-6 were not related to later increases in depressive symptoms.

The new study, published in the October 2009 issue of the journal Brain, Behavior and Immunity, is the first to examine both directions of the depression-inflammation connection and to measure the physical symptoms of depression, such as fatigue and sleep disturbance, in addition to the cognitive-emotional symptoms, such as pessimism and sadness.

Several previous studies have linked depression to increased inflammatory protein levels measured at the same time. These studies, however, cannot speak to which is the cause and which is the effect. "There is two-way communication between the brain and the immune system, so we had to determine whether activation of the body's immune system sent a signal to the brain to affect mood and behavior or whether the depression activated the immune system," said Dr. Stewart, a clinical health psychologist in IUPUI's School of Science and an IU Center for Aging Research affiliated scientist.

Participants in the study were 263 healthy men and women aged 50-70 years at the start of the study. They were tested at baseline and again six years later to determine their levels of depressive symptoms and interleukin-6. Levels of C-reactive protein, another inflammatory protein, were also measured but were not related to depression.

The strength of the association of depression with future heart disease is similar to that of traditional risk factors like smoking, high blood pressure and elevated cholesterol, according to Dr. Stewart.

"Promotion of inflammation may be one pathway through which depression may 'get under the skin' to negatively influence cardiovascular health. The link to cardiovascular disease demonstrates that there may be physical as well as mental health reasons to treat depression," said Dr. Stewart.


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