Nutrition should be high on the agenda for those who care for patients with inflammatory bowel disease (IBD), as well as those who have the condition. The Irish Society of Colitis and Crohn’s (ISCC) surveyed its members in 2015¹ and results showed that 34% were using some form of alternative non-medical treatment. Of the 34%, 71% were using dietary management and 57% felt diet could be a trigger of their symptoms. Some 61% believed that IBD specialists disregarded the importance of diet which is a worrying statistic given that many IBD patients still do not have access to a dietitian.  

In 2009 the UK IBD standards group stated that “all IBD patients should have access to a dietitian with a specialist interest in IBD”. This had not been met when reviewed in 2013.² In 2006 the group audited 75% of UK hospitals where the median number of dietitian sessions dedicated to gastroenterology was two per week. Only 52% of patients admitted with Crohn’s disease were weighed and only 37% were seen by a dietitian. 

The standards recommend minimum staffing of 0.5 WTE dietitians per 250,000 population. This works out at a caseload of 1,000 per 0.5 WTE dietitian for the 240,000 patients with IBD in the UK, which seems grossly inadequate given the nutritional consequences of this disease. 

In Ireland, there is only one clinical specialist dietitian post and a handful of senior dietitians specialising in gastroenterology so numbers here are also insufficient to deal with the rising incidence of IBD.  

Role of diet

Diet has two major roles in IBD – adjuvant and primary therapy. Basic nutrition support is used as an adjuvant or supportive therapy to prolong effects of drug therapy and prevent and treat malnutrition in both Crohn’s and ulcerative colitis. Exclusive enteral nutrition (EEN) can be used as primary therapy instead of medication to achieve remission in certain patients with an acute exacerbation of Crohn’s disease.³ Nutritional intervention is tailored to each individual and depends on disease type, location, phase, surgical history, comorbidities, therapeutic goals, patient preference and team consensus. There are many variables.  

Limitations

The limitations of diet should be outlined to patients to address any misconceptions. Diet can contribute to or ease symptoms but it does not cause a flare. It can induce remission in carefully selected cases but it must not replace medications if they are prescribed. Diet cannot cure IBD but there is evidence to show diet may prevent IBD developing in the first instance.^4,5,6,7 Our better understanding of the microbiome is also adding to the link between diet and IBD pathogenesis.

Using models or diagrams of the gastrointestinal tract can help patients understand how IBD impacts nutrition and vice versa. Not all dietary therapies used by patients are evidence based. Due to gaps in research, knowledge and dietetic services, some patients are seeking their own ‘cure’. Interest in diets such as the specific carbohydrate diet, gut and psychology syndrome and paleo is growing alongside gluten-free and low FODMAP diets, which may in time prove useful for functional symptoms or IBS overlap.

Malnutrition

It is well documented that there is an increased risk of developing malnutrition in IBD. Studies show that up to 85% of hospitalised patients suffer from protein energy malnutrition.⁸ A wide variation in rates of malnutrition is reported in the literature due to differences in assessment criteria, disease type, severity and phenotype. Crohn’s appears to have a greater nutritional insult than ulcerative colitis with higher rates attributed to it when we look at each condition separately – Crohn’s disease 80%,⁹ ulcerative colitis 18-62%.¹⁰ Up to 75% of our patients experience weight loss¹¹ and 50% present in negative nitrogen balance.¹² Healthcare professionals caring for patients with IBD should be aware of these risks and know when to refer their patients to a CORU-registered dietitian. 

It is easy for these patients to slip into a malnourished state. In the active phase, IBD is an anorexigenic disease due to increased pro-inflammatory cytokines IL-18 and TNF alpha¹³ which, along with altered gastrointestinal hunger hormones GLP and leptin,¹⁴ make it counterintuitive to eat.  

Food aversions and fear of eating, otherwise known as sitophobia, can occur which is understandable given that diet and the gastrointestinal tract are inextricably linked. Self-imposed dietary restrictions in an effort to control GI symptoms can compound malnutrition further.¹⁵

Fatigue is extreme and extra gastrointestinal manifestations such as arthritis¹⁶ can hinder food preparation. Odynophagia due to oral aphthous ulcers can also reduce oral intake.¹⁷ It can be helpful to measure and monitor food-related quality of life at each consultation.¹⁸ Increased nutrient, fluid and electrolyte losses due to malabsorptive symptoms, like diarrhoea, high output stomas or fistulae, lead to wide ranging deficiencies and deficits.     

Lean body mass and muscle function are significantly reduced in all stages of disease, a known predictor for the development of osteoporosis.¹⁹ Body fat distribution differs too – a depletion of visible fat and increase in intra-abdominal fat over time may play a role in the inflammatory process. Screening tools and BMI do not detect these changes. Useful anthropometric methods include skinfold thickness, mid-upper arm circumference, dynamometry and newer generation bioelectric impedance analysis technology.  

The use of DEXA reports and CT should be explored for this purpose too given that many IBD patients undergo these investigations routinely.²⁰ Positive or negative changes in body composition may be due to IBD medications. Although there are many reports of weight gain, fluid retention and false appetite from taking steroids, more recent studies have not found a dose-response relationship of oral glucocorticoid therapy on energy intake, appetite, body weight or body composition.²¹ Infliximab causes weight gain by inducing remission, a welcomed side effect in an undernourished person.²² It is important that patients receive counselling on these side effects prior to starting, particularly in those who are already overweight or obese and are keen to reduce or maintain weight.

Consequences of undernutrition in IBD are similar to other chronic diseases. Patients should be optimised at all times but particular emphasis should be put on their status pre surgery to ensure best outcomes. PEM leads to increased septic complications following gastrointestinal resections,²³ and post-operative anastomotic leakage has been cited in those who lose greater than 5kg weight prior to surgery.²⁴

If malnutrition is identified at pre-surgical assessment, the dietitian must recommend that surgery is delayed for seven to 14 days for intensive nutrition support to prevent such consequences. If however surgery cannot be delayed, as is the reality for cases of toxic megacolon, total obstruction, ischaemia or other emergencies, nutrition support should be given immediately post-op.²⁵

Malnutrition occurs in quiescent disease or remission too with approximately 40% of patients overweight.²⁶ This trend is a concern and patients should no longer be encouraged to have a buffer of excess weight between flares. Studies show those with high BMIs are more prone to developing active Crohn’s disease²⁷ and requiring surgery sooner²⁸ than those in the ideal range. 

Healthy eating and micronutrients

It is important to recommend healthy eating for weight management and to be explicit when prescribing exercise. A twice-weekly programme of resistance training is required to correct changes in body composition.²⁹ IBD patients require ongoing and regular monitoring of their nutritional status after they are discharged from hospital. This currently takes place in specialist hospital outpatient clinics if a dietitian service exists. Alternative models of care in primary care should be explored.  

Assessment of micronutrients should be measured routinely due to the impact that deficiencies can have on outcomes. Supplementation is required due to some drug food interactions, such as with sulfasalazine.³

Low vitamin D is associated with increased risk of surgery and hospitalisation in IBD.³¹ The literature also mentions that deficiency alters efficacy of medication.³² Vitamin D was the most common micronutrient deficiency noted in an Irish cohort, followed closely by haematinics such as iron, folate and B12.³³ Optimising zinc levels may improve gut integrity in Crohn’s disease.³⁴

One caveat in the interpretation of micronutrients is the degree of inflammation at time of sampling, so not only should a clinician check if inflammatory markers such as C-reactive protein (CRP) are raised but note how much they are raised.³⁵ An accurate vitamin D level for example may not be attained until CRP is less than 10, which for many with acute IBD will not be during an inpatient stay. Similar CRP thresholds are suggested for other micronutrients. Seek and treat all deficiencies using local guidelines. Calcium should also be supplemented if intake is low. Beware of the possibility of transient lactose intolerance³⁶ in those with small bowel Crohn’s and recommend dairy alternatives to meet calcium needs until resolved.  

Iron deficiency anaemia increases morbidity and mortality but treating it improves quality of life independent of disease activity. The anaemia seen in IBD patients is usually a combination of iron deficiency anaemia and anaemia of chronic disease. Anaemia of chronic disease is caused by blood loss, disease severity or phenotype and focus should be on resolving the underlying cause such as giving RCC or treating the disease without giving iron. Iron supplementation should only be given in cases of anaemia. There is no evidence for treating iron deficiency without anaemia in IBD but a decision may be made to supplement on a case by case basis 

Excess iron is not absorbed in inflammatory states. CRP is a surrogate marker for hepcidin – a peptide that regulates iron absorption. If high, give intravenously as enteral absorption is blocked, hence difficulties tolerating oral iron.³⁷ Iron deficiency anaemia recurs quickly following IV replacement so restart when ferritin < 100 or HB < 12. Check levels at three-monthly intervals in active disease.³⁸ There is a useful reference table for iron requirements based on weight and haemaglobin level cited in ESPEN guidelines 2017.³⁹

Levels of albumin are important to assess response to medical treatment and the inflammatory process rather than nutritional status. It is unknown if patients lose response to biologics due to reduced nutritional status or vice versa but we know that biologics are carried on albumin. For example, enteral nutrition providing more than 600kcals of nutritional requirements daily leads to a sustained response to infliximab.⁴⁰

In the acute phase and if malnourished a high-calorie high-protein diet is recommended for most with careful consideration of hydration and micronutrients. Fibre may be restricted temporarily or long term in the case of stricturing disease.⁴¹ In remission and in well nourished states there are no blanket restrictions and patients are advised to follow healthy eating and lifestyle advice to maintain nutritional status between flares.⁴²

If nutrition is chosen as the primary treatment for Crohn’s, exclusive enteral nutrition in the form of a polymeric formula is administered orally or via nasogastric tube for a minimum of 10 days for a duration of four to six weeks with close dietetic supervision.⁴³ Exclusive enteral nutrition can be used as a bridging treatment until a medication takes effect or during medication-free periods pre and perioperatively.⁴⁴

Parenteral nutrition should not be used as primary treatment of inflammatory luminal Crohn’s disease. Bowel rest has not been proven to be more efficacious than nutrition per se. The most common indication is the presence of short bowel syndrome. Parenteral nutrition is indicated for those who are malnourished, have inadequate or unsafe oral intake, or a non-functioning, inaccessible or perforated gut. Specific indications include obstruction, high intestinal or fistulae output.⁴⁵

Future considerations

One size does not fit all and nutritional intervention must be tailored to the individual. Dietary advice depends on type of IBD, phenotype, location, severity, previous surgeries, symptoms, nutritional status and comorbidities. 

As in other chronic diseases, obesity is the new face of IBD. We are seeing less of the classic underweight presentations, therefore it is harder to spot malnutrition, but it is there and most certainly worsening the disease course of patients. Implementing nutrition focused physical findings as part of the nutrition care process will only help to identify patients most in need of support. Assessment of nutritional status at regular intervals regardless of disease phase or care setting is key to optimising the patient throughout the course of their disease. 

Emerging research in areas such as fibre, pre- and probiotics, curcumin and emulsifiers mean advancements in the nutritional management of IBD are on the horizon. Service infrastructure needs to be improved however, so that all those with IBD can access a CORU-registered dietitian.  

References

1. Irish Society for Colitis and Crohns. Gut Responses: Crohns and Colitis in Ireland Survey 2015. www.iscc.ie/policy-positions 
2. IBD standards group. IBD standards. UK: Crohns and Colitis UK; 2009 [updated 2013]. www.crohnsandcolitis.org.uk/improving-care-services/health-services/ibd-standards
3. O Sullivan M, O Morain C. Nutrition in inflammatory bowel disease. Best Pract Res Clin Gastroenterol 2006; 20:561-573 
4. Hou JK, Abraham B, El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol 2011;106:563-573
5. Racine A, Carbonnel F, Chan SS et al. Dietary patterns and risk of inflammatory bowel disease in Europe: results from the EPIC study. Inflamm Bowel Dis  2016; 22:345-354
6. Ananthakrishnan AN, Khalili H, Konijeti GG et al. Long-term intake of dietary fat and risk of ulcerative colitis and Crohn’s disease. Gut 2013; 63(5):776-784
7. Ananthakrishnan AN, Khalili H, Konijeti GG et al. Prospective study of long-term intake of dietary fiber and risk of Crohn’s disease and ulcerative colitis. Gastroenterology 2013; 145(5):970-977
8. Vagianos, K, Bector, S, McConnell J et al. Nutrition assessment of patients with inflammatory bowel disease. J Parenter Enteral Nutr 2007; 31:311-319
9. Gerasimidis K, McGrogan P, Edwards CA. J Hum Nutr Diet. The aetiology and impact of malnutrition in paediatric inflammatory bowel disease. J Hum Nutr 2011; 24(4):313-26
10. Bannerman E, Davidson I, Conway C et al. Altered subjective appetite parameters in Crohn’s disease patients. Clin Nutr 20; 2001: 399-405
11. Lochs H, Dejongb C, Hammarqvistc F et al. ESPEN guidelines on enteral nutrition: gastroenterology. Clin Nutr 2006; 25; 2: 260-274 
12. Royall D, Greenberg GR, Allard JP, Baker JP, Jeejeebhoy KN. Total enteral nutrition support improves body composition of patients with active Crohn’s disease. J Parenter Enteral Nutr 1995; 19:95-99
13. Murch SH. Local and systemic effects of macrophage cytokines in intestinal inflammation. Nutrition 1998; 14:780-783
14. Karmiris K, Koutroubakis IE, Xidakis C et al. Circulating levels of leptin, adiponectin, resistin, and ghrelin in inflammatory bowel disease. Inflamm Bowel Dis 2006; 12:100-105
15. Palant A, Koschack J, Rassmann S et al. And then you start to lose it because you think about Nutella: The significance of food for people with inflammatory bowel disease - a qualitative study. BMC Gastroenterology 2015; 15:93
16. Orchard TR. Management of arthritis in patients with inflammatory bowel disease. Gastroenterol Hepatol 2012; 8(5):327-329
17. Muhvic-Urek M, Tomac-Stojmenovic M, Mijandruic-Sincic B. Oral pathology in inflammatory bowel disease. World J Gastroenterol 2016 Jul 7; 22(25):5655-67
18. Hughes LD, King L, Morgan M et al. Food-related quality of life in inflammatory bowel disease: development and validation of a Questionnaire. Gut 2016; 10(2): 194-201 
19. Byrant RV, Ooi S, Schultz CG et al. Low muscle mass and sarcopenia: common and predictive of osteopenia in inflammatory bowel disease. Aliment Pharmacol Ther 2015; 41(9):895-906
20. Bryant RV, Schultz CG, Ooi S, Goess C, Costello SP et al. Obesity in Inflammatory Bowel Disease: gains in adiposity despite high prevalence of myopenia and osteopenia. Nutrients 2018 Sep; 10(9):1192
21. Berthon BS, MAcDonald-Wicks LK, Wood LG. A systematic review of the effect of oral glucocorticoids on energy intake, appetite and body weight in humans. Nutr Res 2014; 34(3):179-90 
22. Vadan R, Gheorghe LS, Constantinescu A, Gheorghe C. The prevalence of malnutrition and the evolution of nutritional status in patients with moderate to severe forms of Crohn’s disease treated with Infliximab. Clin Nutr 2011; 30(1):86-91
23. Alves A, Panis Y, Bouhnik Y, Pocard M, Vicaut E, Valleur P. Risk factors for intra-abdominal septic complications after a first ileocecal resection for Crohn’s disease: a multivariate analysis in 161 consecutive patients. Dis Colon Rectum 2007; 50(3):331-6
24. Mäkelä JT, Kiviniemi H, Laitinen S. Risk factors for anastomotic leakage after left-sided colorectal resection with rectal anastomosis. Dis Colon Rectum 2003; 46(5):653-60
25. Forbes A, Escher J, Hébuterne X et al. ESPEN guideline: clinical nutrition in inflammatory bowel disease. Clinical Nutrition 2017; 36(2):321-347
26. Nic Suibhne T, Raftery TC, McMahon O, Walsh C, O’Morain C, O’Sullivan M. High prevalence of overweight and obesity in adults with Crohn’s disease: Associations with disease and lifestyle factors. Journal of Crohn’s and Colitis 2013; 7(1):e241-e248
27. Blain A, Cattan S, Beaugerie L, Carbonnel F, Gendre JP, Cosnes J. Crohn’s disease clinical course and severity in obese patients. Clin Nutr 2002 Feb; 21(1):51-7
28. Hass DJ, Brensinger CM, Lewis JD, Lichtenstein GR. The impact of increased body mass index on the clinical course of Crohn’s disease. Clin Gastroenterol Hepatol 2006; 4(4):482-8
29. Carlos Ayán Perez Pérez. Prescription of physical exercise in Crohn’s disease. Journal of Crohn’s and Colitis 2009; 3(4):225-231
30. Jansen G, van der Heijden J, Oerlemans R et al. Sulfasalazine is a potent inhibitor of the reduced folate carrier: implications for combination therapies with methotrexate in rheumatoid arthritis. Arthritis Rheum 2004; 50(7):2130-9
31. Ananthakrishnan AN, Cagan A, Gainer VS et al. Normalization of plasma 25-hydroxy vitamin D is associated with reduced risk of surgery in Crohn’s disease. Inflamm Bowel Dis 2013; 19(9):1921-7
32. Dai C, Jiang M, Sun M. Role of vitamin D in infliximab-induced remission in adult patients with Crohn’s disease. Inflamm Bowel Dis 2016; 22(1): E3
33. O’Sullivan M, O’Morain C. Nutritional therapy in Crohn’s disease. Inflamm Bowel Dis 1998; 4:45-53
34. Sturniolo GC, Di Leo V, Ferronato A et al. Zinc supplementation tightens ‘leaky gut’ in Crohn’s disease. Inflamm Bowel Dis 2001; 7(2):94-8
35. Duncan A, Talwar D, McMillan DC, Stefanowicz F, O’Reilly DS. Quantitative data on the magnitude of the systemic inflammatory response and its effect on micronutrient status based on plasma measurements. Am J Clin Nutr 2012 Jan; 95(1):64-71
36. Von Tirpitz C, Kohn C, Steinkamp M et al. Lactose intolerance in active Crohn’s disease: clinical value of duodenal lactase analysis. J Clin Gastroenterol 2002 Jan; 34(1):49-53
37. Dignass AU, Gasche C, Bettenworth D et al. European Crohn’s and Colitis Organisation [ECCO]. European consensus on the diagnosis and management of iron deficiency and anaemia in inflammatory bowel diseases. J Crohns Colitis 2015; 9:211e22
38. Kulnigg S, Teischinger L, Dejaco C, Waldhor T, Gasche C. Rapid recurrence of IBD-associated anemia and iron deficiency after intravenous iron sucrose and erythropoietin treatment. Am J Gastroenterol 2009; 104:1460e7
39. Evstatiev R, Marteau P, Iqbal T, Khalif IL, Stein J, Bokemeyer B et al. FERGIcor, a randomized controlled trial on ferric carboxymaltose for iron deficiency anemia in inflammatory bowel disease. Gastroenterology 2011; 141:846e53
40. Sazuka S, Katsuno T, Nakagawa T et al. Concomitant use of enteral nutrition therapy is associated with sustained response to infliximab in patients with Crohn’s disease. Eur J Clin Nutr 2012; 66:1219-1223
41. Inflammatory bowel disease: a global perspective. World Gastroenterology Organisation Global Guidelines. June 2009 
42. NICE Guidance. Crohn’s disease: Management in adults, children and young people. National Clinical Guideline Centre: October; 2012
43. Lee J, Allen R, Ashley S, Becker S et al. Gastroenterology Specialist Group of the British Dietetic Association. British Dietetic Association evidence-based guidelines for the dietary management of Crohn’s disease in adults. J Hum Nutr Diet. 2014; 27(3):207-18
44. Heerasing N, Thompson B, Hendy P et al. Exclusive enteral nutrition provides an effective bridge to safer interval elective surgery for adults with Crohn’s disease. Aliment Pharmacol Ther 2017; 45:660-669
45. Gossum A, Cabre E, Hebuterne X et al. ESPEN Guidelines on Parenteral Nutrition: Gastroenterology. Clin Nutr 2009; 28:415-42