Chapter 1
What is it and does psyche have anything to do with it?
Jane M. Andrews
Introduction
Inflammatory bowel disease (IBD) is named for its effects on the gut, however, due to the centrality of gastrointestinal (GI) health on the whole person, a purely GI centric view of the illness fails to conceive the full spectrum of the patients’ experiences and concerns (Andrews et al. 2009). The gut is essential for nutrition and also contributes to the pleasure experienced through taste, food satisfaction, satiety and the emotional, community aspects of shared meals, in addition to serving ritual purposes, both social and religious. Disturbances in GI function and the inability of people to participate fully in this food/meal-based aspect of life that is usually ‘taken for granted’ can cause much distress. In addition, IBD is a chronic illness, the onset of which is usually before mid-life, meaning that most people affected have a long exposure time, are affected at a time when they expect to be well, and have a long-term illness with an uncertain future, whereas other illnesses affecting this age bracket are usually acute and self-limiting. All of these factors make IBD a difficult disease/illness from a psychological/societal viewpoint. Hence, the importance of considering the psychological dimension of IBD.
Moreover, it also appears likely that psychological status itself may exert an influence on IBD inflammatory activity/behaviour, although this is an area of contention and is difficult to study. Many patients with IBD are convinced of the relationship, at a personal level, between stress, anxiety, depression and flares. However, due to recall biases, and symptom-based measurement tools, the data to date here is still unclear (Andrews et al. 2009; Bernstein et al. 2010; Singh et al. 2009). Despite the uncertainty in humans, in animals where models of inflammation, stress and depression can be manipulated, there is a clear effect of psychological status (and CNS disturbances) on GI inflammation, moreover, treating these disturbances has been shown to ameliorate GI inflammation (Ghia et al. 2009). These data form the basis for the emerging neuro-immune model of inflammation with regard to IBD and provides another major reason we should consider the psychological dimension of IBD.
Current concepts of IBD aetiology, epidemiology and treatment
Aetiology
The precise aetiology of IBD is unknown, although microbial, genetic, dietary and other environmental factors are all implicated. It is generally conceived as a group of autoimmune diseases, as the affected person’s own immune system is activated (inappropriately and persistently or recurrently), with a focus on/in GI tissues, which leads to tissue damage. It is, as yet, uncertain whether there is a specific GI tissue/molecular target for the inflammation, although this appears likely due to the relative stability over time of the physical location of the inflammation within an individual. Inflammation can also be seen in other tissues, predominantly the skin and joints; however, the main focus of the disease is GI, which is what distinguishes it from other autoimmune disorders.
The importance of microbial factors will be reviewed in detail in Chapter 4, however, it should be noted here that IBD cannot be induced in germ-free animal models. In humans, luminal disease improves with antibiotics and when luminal contents are diverted (removing the interaction between luminal contents – mainly bacteria – and the mucosa). Genetic risk loci associated with IBD risk and behaviour are now well described, and interestingly, many of these are functional receptors or modulators in pathways that interact with host microbial and immunoregulatory responses and are also noted in other autoimmune diseases (Jostins et al. 2012). Despite the large numbers of genes associated with IBD, none of them are either necessary nor sufficient to lead to IBD development in an individual, and concordance, even in identical twins, is not 100 per cent. Significantly, many important genes described in Caucasian populations have not been replicated as risk factors in other racial groups, emphasizing the likelihood that it is the interaction between genes and the environment that lies at the crux of IBD aetiology, rather than a single factor in isolation.
Several environmental factors are also associated with IBD (Gearry et al. 2010), and interestingly, these do not always associate with both Crohn’s disease (CD) and ulcerative colitis (UC) equally. For example, smoking is more common in CD and has been linked with worse disease behaviour (Lawrance et al. 2013), whereas in UC, smokers are less likely to be affected and smoking cessation worsens UC course. Other environmental factors implicated, but not always validated, as either increasing or decreasing risk include: dietary fat and sugar intake, breast feeding in infancy, socioeconomic status, latitude, vitamin D, sun exposure, metropolitan or rural birthplace and having a childhood vegetable garden.
Epidemiology
IBD has increased substantially in incidence since its initial recognition. Both CD and UC became more common in developed countries in the second half of the 1900s and are now rapidly increasing in the developing world (Ng et al. 2013). In the developed world, CD is now more common than UC, whereas, in Asia, UC is currently twice as common as UC. Disease onset, in general, is prior to 40 years of age, with −25 per cent having onset during childhood. While the incidence is low, making them ‘uncommon’ disorders, they are chronic disorders and their prevalence is much more substantial as each affected person has the disorder ‘for life’. Recent prevalence estimates in Western countries sit between 300–480/100,000 (Burisch et al. 2013; Rocchi et al. 2012), meaning that from an economic and healthcare delivery viewpoint (Access-Economics 2007), this patient group is important to care for well so as to ensure minimal morbidity. As is outlined below, both physical and psychological aspects of care need to be optimal to ensure those affected by IBD are able to enjoy a healthy, productive life.
Treatment
Investigations undertaken to diagnose and evaluate changing symptoms in those with IBD are described in Chapter 5. Here, a brief overview of the logic behind the approach to IBD treatment is presented. The treatment approach to IBD is necessarily tailored, as there are many different clinical scenarios, in terms of diagnosis (CD vs. UC), severity, location in the gut, patient preference, speed of progression of disease, complications and responses to previous therapies (including non-efficacy, allergy and/or side effects). Often, a dichotomy between medical (drug) and surgical therapies is presented, however, in reality, these approaches are often both required, either simultaneously or sequentially. Logically, surgery is the treatment of choice for mechanical complications, especially abscess, perforation, penetrating disease and strictures, whereas medical (anti-inflammatory) therapies are ideal for controlling inflammation. Surgery is discussed further in Chapter 12, however, it is important to emphasise that it should never be presented as a ‘last resort’, as this imbues the decision with a sense of failure for the patient and physician alike, and moreover, there is clearly a great benefit from proactive surgical management in certain IBD-related clinical scenarios.
Standard medical therapy and particular drug issues with regard to mental health and quality of life are discussed in detail in Chapter 13; here, the principles of therapy are outlined. Although physicians have become more comfortable in recent decades with escalating anti-inflammatory therapies more rapidly to control disease activity, there is still a hierarchy of therapies used. Commencing with those least likely to be associated with side effects, requiring least monitoring, and generally, costing less. When these agents are not sufficiently effective, others of greater potency should be promptly used to control inflammation.
In general, medications are used for two main reasons in IBD. First, they are used to bring new or acute inflammation under control, that is, to induce remission. Second, they are then used to prevent new episodes of inflammation, that is, to maintain remission. Some drugs act as both induction and maintenance agents, whilst others are only properly suited to be used as one or another. As IBD is a chronic disease, it is important that healthcare professionals move away from the out-dated concept that intermittent therapy of acute flares is acceptable management. It is now well accepted that this approach leads to long-term accumulation of damage to the bowel (Pariente et al. 2011) and avoidable complications, such as strictures, perforation and even cancer. As all maintenance agents are intended for long-term use, it is important that they are sufficiently safe and effective. It is also important that they are not associated with (or perceived to be) troublesome side effects, or undue risk, from the individual patient’s viewpoint.
Treatment, however, is more than simply the prescription of drugs or the performance of an operation (Andrews et al. 2009). It additionally involves a longer-term plan, and agreed goals between each patient and their chosen health care professionals (HCPs). Apart from controlling inflammation and preventing relapse, additional foci for longer-term management include minimising infection risk (with a focus on vaccinations and travel risks), bone health, colorectal cancer surveillance (Chapter 11), nutritional review (especially for iron deficiency), skin cancer prevention/surveillance, sexual health and fertility (Chapters 8 and 9) and general preventative health medicine, which is often overlooked in people suffering a chronic disease, presumably due to the distraction of HCPs by acute illness issues. For all these reasons, a chronic care model, wherein patients are seen when they are well, in addition to when needing acute care, is to be recommended in IBD. In this way, chronic disease ‘background’ issues can be managed without the distraction of acute illness. In the longer-term, this improves health-related quality of life and reduces avoidable morbidity; moreover it also appears to reduce healthcare costs (Sack et al. 2012).
Evidence of psychological comorbidity in IBD
It is well documented that any chronic disease leads to a greater burden of psychological stress, anxiety and depression than is seen in the background population and this is no different in IBD. There is also evidence that these are all more prevalent when IBD disease control is worse – with greater rates of psychological comorbidities seen with active disease (Graff et al. 2006; Mikocka-Walus et al. 2007). As referred to earlier, it is unclear whether this is a unidirectional association from illness leading to psychological problems, or whether there may be a closer inter-relationship between psychological status and inflammatory activity. This possible ‘brain-gut’ interaction will be more clearly explored in Chapter 3. From a practical clinical viewpoint, what is important about the psychological burden of IBD is that it is highly prevalent in a young patient group. As up to 25 per cent of those with IBD have an onset before 18 years of age, it means they are at risk of psychological disorders from a young age, during a time in which they would often be taking on their first adult roles with regard to education, relationships, sexuality and ...