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Inflammatory bowel disease (IBD) encompasses both ulcerative colitis (UC) and Crohns disease (CD). Both of these diagnoses likely have similar etiologies, but they each affect different locations and layers within the lower GI system. Unlike UC, CD can affect the upper GI tract as well.

The following focuses on the Whole Health approach to IBD. When possible, it will be specified whether a given study focused on UC, CD, or both disorders.

In the U.S. military population, prevalence of IBD is estimated to be 202 and 146 cases out of 100,000 individuals for UC and CD, respectively. Three main demographic variables in this population incur a higher risk: age, female sex, and Caucasian ethnicity.[1] However, inflammatory bowel diseases have been increasing in minority populations; in addition, those who identify as Hispanic or Asian have increased rates of pan-colonic inflammation.[2] The incidence of IBD has been increasing with increasing industrialization and marked dietary changes over recent decades.[3][4]

IBD is complex and multifactorial. Environmental factors (especially nutrition, smoking, and infections) and genetic factors interact, leading to a dysfunctional relationship between ones intestinal microbiome and immune system due to abnormal intestinal barrier function (reference Figure 1).

An increased immune response to antigens (including foods) at the mucosal surface of the intestines leads to inflammation. With this inflammation, it becomes more possible for larger-sized molecules to cross from the gut into the bloodstream, which can precipitate even more of an immune response and inflammation. Interrupting this process should form the basis for a Personal Health Plan (PHP) that specifically focuses on regulating the immune system by decreasing inflammation and by rebalancing and healing the gut microbiome. Every individual and his or her disease is unique; thus, a personalized, rather than a one-size-fits-all, approach may be most effective.

The following recommendations focus on the best available evidence. Although general healthy living recommendations are not included, it should be assumed that health-promoting behaviors are the default treatment for any PHP.

Increasing physical activity leads to improved quality of life, increased muscle mass, and decreased rates of osteoporosis in those with IBD.[6] This is important given that those with IBD have a 40%-60% increased rate of osteoporotic fractures. This may be due to a combination of increased inflammation, steroid treatment, and micronutrient deficiencies.[7]

How important are our genes relative to our surroundings in determining our genetic susceptibility to IBD? There is a low concordance rate in identical twins for both CD (about 50%) and UC (about 10%), confirming that the environment is an important variable.[4]

Given that IBD is unevenly distributed around the world and in different socioeconomic strata in the United States, some hypothesize that the hygiene hypothesis may have an explanatory role. Humans living in industrialized countries of higher socioeconomic status are exposed to fewer microbes at an early age. This may cause them to have an immune system that is less able to tolerate microbial exposures later in life and which inappropriately activates, causing inflammation and possibly IBD.[3]

Given that shifts toward more Western diets are likely the most significant variable increasing IBD rates worldwide, what one eats likely plays a major role in both developing and controlling IBD.

Our diets are directly associated with the characteristics of our intestinal bacterial community (our microbiome), which likely play a role in the development of IBD as well. The microbiome stays relatively stable throughout life, starting at the ages of 2 or 3, but it can be modified through significant dietary changes.[3] For more information, refer to the Whole Health tool Promoting a Healthy Microbiome with Food and Probiotics.

Although research supports a higher rate of food allergies and sensitivities in those with CD (approximately 61%), no recommended diet exists, save eating liquid diets, during disease flares.[8] Some studies support use of specific diets, such as the Specific Carbohydrate Diet or a Low Sulfur Diet, but control groups often were eating a more Westernized diet. It may be that these IBD diets are actually just less Western and therefore all have similar effects.

However, most with IBD change their diets after diagnosis. Several small studies have shown that personalized elimination diets can be helpful, and this dietary approach has the best clinical evidence for both symptom and histological improvements for CD.[3] For guidance, refer to The Elimination Diet Whole Health tool. Given that micronutrient deficiencies are common in those with IBD, one must ensure that elimination diets do not become overly restrictive.

Given the risk of nutritional deficiencies due to poor absorption or restrictive diets, consider ordering labs focused on determining ones nutritional health: red blood cell (RBC) magnesium, RBC zinc, serum albumin (or pre-albumin depending on context), serum iron, ferritin, transferrin, folate, B12, and 25-OH vitamin D (target levels >30 ng/mL). The most common deficiencies are folate, B12, and iron.[9]

In-vitro evidence supports considering using the following vitamin supplements[10]:

• Vitamin A, D, E, and K (fat-soluble vitamins)
• Selenium (anti-inflammatory)
• Iron (may need to be given IV, considering the difficulties with absorption)
• Zinc (vital for GI healing; consider short-term use with 2-3 week course if severe diarrhea; regular use can lead to copper deficiency)
• Calcium and vitamin D (optimize bone health; normalizing vitamin D levels also has been shown to decrease flares and improve the response to treatment[11])
• Folate and B12 (latter may need to be parenteral if the terminal ileum is involved or if there is a history of resection)

With the advent of newer biologic medications, specific diet formulas have become less frequently used for those with active CD. Such diets have traditionally been used in pediatric populations for whom chronic steroid therapy is undesirable.[12] Enteral nutrition with elemental, semi-elemental, and defined formula diets are nearly as effective in inducing remission as corticosteroids, and they are much better than placebo with a nearly 60% response rate.[13]

The type of formula does not seem to matter because it is not the protein or nitrogen source but likely the fat content that leads to benefit. It is believed to work through both an anti-inflammatory interaction of lipids with the intestinal mucosa as well as by changing the colonic microflora.[14] In UC, this approach does not seem to be effective.[3] However, relapses after discontinuing these diets are common, and the diets are often unpalatable. Although few supporting data exist, it seems reasonable to suggest an anti-inflammatory (or Mediterranean) diet given its better palatability and known positive effects on other aspects of health.

Finally, there are several plant-based compounds that have shown great promise as anti-inflammatory and antioxidants in basic science and animal studies. Clinical studies in those with IBD are lacking, and the following should be highlighted in ones diet until more is known[10]:

• This is naturally found in grapes, peanuts, and red wine.
• This is a mixture of enzymes derived from pineapples.
• Ingesting the whole fruit is best, but juice is reasonable.
• This is a polyphenolic flavonoid found in citrus fruits, tea, and buckwheat seeds.

Sleep modulates the immune response and therefore may affect the course of inflammatory diseases. Those with IBD often have disordered sleep, as exhibited by prolonged sleep latency, sleep fragmentation, higher sleep medication use, decreased daytime energy, and poor overall sleep quality. These observations are true even when IBD is not active.[15] Although there is likely a circular interplay between sleep dysfunction and inflammation, helping to restore healthy sleep patterns may improve quality of life and possibly disease severity.

The gut is the bodys emotional spinal cord.[16]

People with IBD are at a greater risk of anxiety, depression, and impaired quality of life. They also have altered sensory perceptions, as suggested by increased sensitivity to hot and cold.[15] A review of mind-body approaches concluded the following:

• Stress management techniques can have a modest benefit on disease severity and quality of life. Mindfulness-Based Stress Reduction (MBSR) has the most robust scientific evidence supporting its use. It has been shown to improve both mental health symptoms and surrogate markers of disease activity.[17]
• Cognitive Behavioral Therapy (CBT) improves mood but not IBD severity.
• Clinical Hypnosis has a positive impact on disease severity as well as mental health symptoms.[18] Gut-directed hypnotherapy, specifically, has been shown to decrease stress levels and increase self-efficacy. [19]

These may be best utilized with people who have concomitant mental health disorders.

Diet. Western diets are high in total fat, animal fats, and omega-6 polyunsaturated fats, as well as low in fiber and high in refined carbohydrates. High fiber and fruit intakes are associated with a decreased UC risk.[3] Retrospective data suggest that a high intake of fiber and fruit (but not vegetables) is associated with a reduced risk of CD.[4] Conversely, a high intake of vegetables (but not fruit) is associated with a reduced risk of UC.[4]

Tobacco use. Smoking increases the incidence of CD and worsens its course. However, smoking is protective against UC, and patients with UC who smoke should not necessarily be encouraged to stop depending on an overall assessment of the risks and benefits.[6] While 1 in 9 individuals with IBD smoke cannabis, this substance has not been shown to influence symptoms or levels of inflammation.[20]

Breastfeeding. This protects against IBD, especially if continued for 6 months after birth.[13]

Avoiding antibiotics. There is a possible association between long-term antibiotic use (especially doxycycline) for acne and CD. This suggests that long-term and repeated exposure to antibiotics should be avoided unless absolutely indicated.[21]

Other risk factors for IBD include family history, age 15-35 and 55-65, female sex, urban dweller, high stress, Jewish ancestry, high socioeconomic status. Possible risks include NSAIDs, oral contraceptives, antibiotics, and bacterial intestinal infections.[8]

Screening for colon cancer. UC is associated with an increased risk of colon cancer, though this risk varies based on the site(s) of disease and duration of symptoms (and not its activity). Epidemiologic data has shown that proctitis alone confers no additional risk, but pancolitis that began in childhood confers a 162 times higher colon cancer risk compared to those who do not have UC.[22] It is best to be screened when the disease is in remission. The frequency of screening has not been rigorously studied and should be individualized. Many guidelines recommend screening initiation 10 years after diagnosis with follow up every 1 to 5 years. Patients with CD do not appear to have an increased risk of colon cancer, though this is still being investigated; however, they may have an increased risk of small bowel cancer, though no reliable screening methods exist for this. Also, women taking immunosuppressive therapy may be at higher risk of cervical cancer, so close adherence to current screening guidelines is recommended.

Omega-3 fatty acids have not been shown to work in most studies and have had marginal benefit in others. While they have known anti-inflammatory properties in vitro and in vivo, they have not shown a clinical benefit in IBD. That said, they are often one of the most common supplements taken by those with IBD.[20][23][24][25][26][27][28]

Curcumin, a component of turmeric, has well-characterized anti-inflammatory and antioxidant effects.[24] It has been shown to objectively reduce measures of inflammation, increases response rate to treatment in those with mild to moderate UC by 50%, and it increases remission rates by 15%.[11][20] The dose is 500-1,500 mg twice per day with meals.[11][29] Curcumin has often been used in trials along with pharmaceuticals, so the current best evidence supports using it as an adjuvant therapy.[30]

Aloe vera gel is the mucilaginous aqueous extract of the aloe leaf. It is the most popular botanical used by those with IBD. One small but high-quality study supports its use in improving UC remission.[20] For UC, use 100 mL of a 50% solution twice daily. Be careful not to recommend aloe latex, as this acts as a laxative and can worsen diarrhea.[24]

Wheatgrass juice (Triticum aestivum) is better than placebo in inducing a clinical response for active distal UC in 23 patients over 4 weeks.[24] The amount used is 20 mL orally per day initially. This is increased by 20 mL per day to 100 mL total.

Boswellia serrata is a traditional Ayurvedic remedy and a component of incense. It is also known as Indian frankincense. It has been shown equal to sulfasalazine for moderately active UC and equal to mesalamine for CD in inducing a clinical response and/or remission. The dose used in the research was 300 mg three times daily for 6 weeks.[20][24]

Psyllium reduced symptoms and increased remission times in those with UC who took 20 gm with their mesalamine versus using mesalamine alone. Use caution, as taking this during flares can make symptoms worse.[31]

Probiotics Given that specific bacterial species exhibit anti-inflammatory effects and can positively alter the intestinal ecosystem, studying the effects of probiotics on IBD makes logical sense. Although significant research is being done, each individual likely has a uniquely dysfunctional gut microbiome, so individualized therapies will likely prove the most useful.[32][33] Novel, culture-independent DNA sequencing is revolutionizing our ability to understand this, and the research is becoming more positive over time. Several probiotic species alone or in combination have been studied and show the most promise in relapse prevention and remission induction in mild to moderate UC.[7][34] A meta-analysis examining probiotics effectiveness in CD revealed no overall benefit, but there is some suggestion that Lactobacillus rhamnosus GG or Saccharomyces boulardii may be beneficial.[35][36][37] The following can be considered:

• VSL#3 UC (improve flares and increases duration of remission; high-quality evidence for treatment of pouchitis).[20][38][39] One sachet twice per day. This contains eight strains of Bifidobacterium, Lactobacillus, and Streptococcus This product contains corn and is quite costly.
• Lactobacillus rhamnosus strain GG 10 to 20 billion colony-forming units (CFUs) per day.
• Saccharomyces boulardii 250 mg three times per day or 500 mg twice daily.

For more information, refer to Promoting a Healthy Microbiome with Food and Probiotics Whole Health tool.

Prebiotics. These are nonabsorbable carbohydrates that enhance the growth of beneficial intestinal bacteria (e.g., Lactobacillus). They provide a substrate for the generation of short-chain fatty acids (SCFAs), which possess anti-inflammatory properties; the most representative of these is butyrate.[5] Enteric-coated butyrate capsules (4 gm daily) in combination with mesalamine versus mesalamine alone improved symptoms in patients with mild to moderate UC.[31]

Table 1. Food Sources of Prebiotics [40]

In three meta-analyses, acupuncture with moxibustion and moxibustion alone demonstrated better efficacy than oral sulfasalazine in treating IBD. However, results were quite variable, and the studies were of low methodological quality. These therapies show promise, but research is insufficient to support making a strong recommendation.[41][42][43]

Nonpharmaceutical treatment recommendations for CD versus UC are summarized in Table 2.

Table 2. Summary of NonPharmaceutical Treatments