Inflammatory bowel disease (IBD) is a group of chronic, multisystem, immune-mediated diseases of the gastrointestinal tract (GIT), mainly comprising Crohn’s disease (CD) and ulcerative colitis (UC). The diseases are typically manifesting in a remitting and relapsing course.
The intestinal manifestation of the disease differs, CD causes a transmural inflammation with oedema and ulceration in any part of the GIT (from mouth to anus). UC result in a superficial inflammation of the mucosa and submucosa of the colon with subsequent erosion and ulceration, starting distally and in an ascending manner. CD may manifest with a non-bloody chronic diarrhoea and abdominal pain, whereas UC patients typically present with crampy abdominal pain with bloody diarrhoea containing mucoid material.
The mucosal barrier seems to be disrupted in patients with IBD, which leads to increased permeability to microbial particles, and they in turn when displaced, may cause an inflammation .
The resultant inflammation will be uninhibited and continued due to pro-inflammatory mediators release such as tumour necrosis factor (TNF)-α and interleukins 6 and 10 (IL-6 and IL10). The inflammation response can be detected by blood samples, including IL, SR, CRP and LPK as well as anemia.
Depression could provoke IBD development . Depression is a complex disorder, proposed to involve genetic, epigenetic, psychological, and environmental factors that decreases a person’s capacity to tolerate stress . The symptoms characteristic for the syndrome is persistent feeling of sadness, worthlessness, and hopelessness. Patients typically show changes in cognitive function (commonly concentration disturbances), appetite, sleep-pattern, they tend to become more easily irritable, and lose interest in previously pleasurable activities, also known as anhedonia. This may further lead to social withdrawal, suicidal thoughts and in worst case, suicide .
Several mechanisms have been implicated in the pathophysiology of depression, including alterations in brain neurotransmission, decreased neuroplasticity and neurogenesis in the limbic system (among others), as well as vascular and inflammatory changes in the CNS. All mentioned changes are not seen in every patient, but it is believed that the different pathophysiological mechanisms are interconnected, and alteration in any part may initiate a series of events and biological effects causing depressive symptomatology .
Up to 80% of patients with IBD and comorbid depression were diagnosed with depression more than two years before they were diagnosed with IBD. Of them, a higher proportion had an earlier onset of IBD than those without depression. This suggest that the illness itself may not only be a trigger of depression, but also that an underlying depression may be a trigger to develop IBD .
Studies have shown that patients with IBD that had active disease , increased amounts of exacerbations , higher disability related to bowel disease  and who were using corticosteroids [3,7, 8] had higher rates of comorbid depression, and patients with inactive disease had approximately the same rate as in healthy controls . This further leads towards the thought that biological mechanisms in the active inflammation play a big role in the development of depression in these patients.
Studies of the U.S. population have shown that the prevalence of depression in IBD subjects was as high as 49% compared to 23% in non-IBD subjects. The rates increased with female gender, older age and if the patient was separated, divorced or widowed . In addition, it was also possible to see a connection with higher rates of depression in patients who were less physically active and those who had lower educational level , or lack of family support .
The relationship between depression and IBD seem to be bidirectional, as suggested by the two-fold increased risk of developing CD in patients with depression, compared to that of non-depressed individuals.
An active inflammation in the gut leads to stress response, which is an important contributor to the development of depression. Both emotional and physical stress triggers the noradrenergic system (NE) which in turn activate the hypothalamic-pituitary-adrenal (HPA) axis. . Other causes of a stress response include early childhood negative events (such as reject or neglect), as well as ‘loss of autonomy’, a state that may occur when a person falls ill in a medical illness . Major depressive disorder is associated with increased CRP and TNF-α. Antidepressants such as selective serotonin reuptake inhibitors (SSRIs) normalize levels of CRP and IL-6 according to a meta-analysis .
Quality of life (QoL) is decreased in patients with IBD, which leads to poorer compliance to treatment and thus worse outcome of disease . It has been shown in the Canadian population that decreased QoL, depression and anxiety in patients with IBD were associated with younger age, female sex, and those who were single .
In addition, the chronic course of the disease requires life-long contact with the health care system, tight adherence to medical treatment and an ability of self-management. The perceived disability and psychological stress may therefore trigger negative mental well-being and reduced ability in coping with the disease . Over time, the ability of self-management may be reduced leading to more symptoms, more pain, more stress, and less ability to engage in activities, which may eventually further intensify negative emotions. In this aspect, good control of symptoms is exceedingly important for the physical as well as the mental well-being [5, 7].
Previous studies have concluded that having a medical illness increased the risk of developing depression by 5-10 times compared to that of healthy subjects .
Due to this knowledge, it can be concluded that depression and decreased mental well-being in patients with IBD should be identified, in order to minimize further harm to the patient, to inprove the disease outcome and quality of life, and to decrease the burden of the healthcare system.