Sunday, January 27, 2013

Bad Colon Prep Can Be Hazardous To Your Heath

Exploding bowels!
This sounds like a topic more suited to the Weekly World News than an evidence-based blog on inflammatory bowel disease, but unfortunately it is a real phenomenon.  From 1952 to 2006, twenty cases of intestines exploding during GI exams occurred.  As you can well imagine, having your intestines go nuclear and breach the barrier of the abdomen creates an immediate, life-threatening emergency.  While not common, it does highlight the need for good colon preparation before the frequent colonoscopy/sigmoidoscopy sessions needed by those with Crohn's disease and Ulcerative Colitis. (1)

How exactly does the bowel explode?  There are three items necessary for a bowel explosion.  Remove any one of the three, and things can’t go boom:
·         Fuel.  In this case, the explosive is either methane or hydrogen gas.  Both are produced naturally as byproducts of bacteria in the intestine (or archea, for those tri-domain pedants out there).  In the normal, unevacuated bowel, they can reach concentrations of 40% or higher.  If a proper preparation is performed, they should be present in only minimal amounts.  It only takes a 5% concentration of methane or 4% of hydrogen to reach the critical point for explosion.
·         An oxidizer.  Things don’t burn without oxygen, which means good old O2 is necessary for explosions as well.  The atmosphere has approximately 21% oxygen, and only 5% or so is needed to cause the methane/hydrogen to go boom.*
·         An ignition source.  Generally, this is either an electrical spark or a heat source.  Electricity (or the capacity for a spark) is present through any electronics associate with the scope.  The heat source comes from the cauterization tip used in cauterization after polyp removal or biopsy.

In general, the third factor is outside the control of both the doctor and the patient.  The other two factors are well within their control, though.  First is preparation.  During a colon prep, the patient needs to fully evacuate their bowels – lowering the gas content of the bowels to subcritical levels (and making it viable to visualize the colon walls).  In the 1980s, substances like mannitol and sorbitol were used as more tolerable bowel preparation tools (these, along with xylitol, are sugar alcohols now most likely to be found in chewing gum).  They worked by drawing water into the colon, but had the side effect of fermenting into less favorable gaseous byproducts.  As such, they are no longer used.(2)

Current bowel preps don’t have the issue of generating dangerous gas byproducts – as long as they are followed!  Approximately 22% of colonoscopies find inadequate preparation.  Of these, 18% of patients reported they did not follow preparation protocols (because this is self-reporting, the actual number is likely a bit higher).  While the preparation isn’t fun, it is an easy way to ensure you don’t go out with a bang.  The added benefits include shorter colonoscopy times and better imaging results.  As with the sorbitol and mannitol above, patients should follow their doctor’s instructions as to what they can mix and not mix with their prep – mixing drinks with the wrong artificial sweetener can cause the unwanted fermentation.  (3)

The other factor is the presence of oxygen.  While this is not up to the patient, the doctor can take certain precautions.  First, performing appropriate suction during the procedure will reduce the presence of unwanted gases and solids.  Second, insufflation (blowing air into the intestines) can be done using CO2 instead of air (remember the 21% O2 concentration noted above).  CO2 is inert and has the side benefit of reducing bloating and discomfort during and after the procedure.(4)

Bottom Line

·         Follow colonoscopy preparation guidelines carefully.  If you can’t complete the prep, be honest with your doctor.  Though very rare, bad complications can occur.
·         Doctors should consider CO2 insufflation where available instead of air insufflation.

* Technically, many explosives have bound oxygen as part of their chemical makeup, so gaseous O2 isn’t really needed.  As for nuclear reactions – don’t even go there.  This is a blog on medicine, and if there is a fusion and/or fission reaction as a result of your colonoscopy, you have bigger problems than bowel prep.
1.       Spiros D Ladas, George Karamanolis, Emmanuel Ben-Soussan.  Colonic gas explosion during therapeutic colonoscopy with electrocautery.  World Journal of Gastroenterology.  2007.
2.       A Avgerinos, N Kalantzis, G Rekoumis, G Pallikaris, G Arapakis, and T Kanaghinis.  Bowel preparation and the risk of explosion during colonoscopic polypectomy.  Gut. 1984.
3.       Reid M Ness MD, MPH, Raj Manam B, Helena Hoen M and Naga Chalasani MD.  Predictors of inadequate bowel preparation for colonoscopy.  American Journal of Gastroenterology. 2001.
4.       Wu J, Hu B. The role of carbon dioxide insufflation in colonoscopy: a systematic review and meta-analysis.  Endoscopy.  2012.

Sunday, January 20, 2013

Fecal transplants and IBD

Brother can I borrow some feces?

IBD is often linked to abnormal gut flora – the presence of “bad” bacteria, the absence of “good” bacteria, or an unhealthy bacterial cocktail are potentially associated with Crohns and Ulcerative Colitis.  Those with IBD have fewer bacteria in their intestines overall, and Clostridium coccoides, Clostridium Leptum and Lactobacillus are less prevalent.  Other bacterial species appear to be more prevalent, including Bacteroides vulgatus and certain E. Coli strains.  While none of this proves that bacterial abnormalities cause IBD, there is a correlation. (1,2)

Fecal microbiota transplantation (FMT), more commonly known as fecal transplants.  FMT is receiving a lot of recent press, but it has been around since the 1950’s.  FMT involves finding a healthy donor, who has their feces removed and made into a slurry for transplantation.  The donor can be a close relative, though for genetically predisposed conditions often a non-relative is chosen.  The slurry is then delivered to the bowels of the patient – generally through either enema or nasogastric tube.  Current research is looking into capsule-based delivery, and the storage of an individual’s own feces prior to antibiotic treatment to repopulate the gut and “reboot” following the wipeout of the resident species by the antibiotics.

Nothing sounds more like snake oil than a tube snaked through your nose into your gut that is injected with poo, but there is a sound medical basis for the treatment.  When a bacterial infection of the intestines occurs, the offending bacteria generally displaces the helpful (or benign) bacteria.  Once a more amenable species takes over again, the symptoms abate.  FMT seeks to speed up this process by the introduction of helpful bacteria.  This has been studied as a potential treatment for IBD since at least 1989. (3)

Before looking at the efficacy of FMT for IBD, let’s look at the better studied applications.  Perhaps the best studied (and most recent headline grabbing) application is the use in treating Clostridium Difficile (or C. Diff) infections.  C. Diff is notoriously difficult to treat using antibiotics, frequently causes diarrhea, and has been known to recur when not fully addressed.  Standard antibiotic treatments generally result in a temporary increase in diarrhea, which can necessitate additional treatment to replenish fluids and prevent dehydration.  Alternative treatments have shown promise (, but the dance card is still open for better ways to address the issue.

FMT has been studied on numerous occasions as a treatment for C. Diff infection.  Overall, the results are impressive – 87% of individuals had successful outcomes with FMT treatment, with minimal adverse side effects.  The results show a better response than typical antibiotic treatment on both fulminant and refractory C. Diff infections.  While the results come from multiple studies and are impressive, there haven’t been any large scale studies and none of the current studies were double blinded.  Given the diversity of the studies, however, FMT has at least been proven to have very strong preliminary evidence of being effective, and should be a consideration for those with difficult to treat C. Diff infections.(4)  There appear to be no major differences in methods of administration – either nasogastric (or nasojejunal), by colonoscopic implantation, or via enema.  In one small scale study, even home administration by enema from a donor that was mixed in a blender had positive results (though I would question the reuse of the same blender for milkshakes later that evening). (5)

What about Crohn’s Disease and Ulcerative Colitis with FMT?  A recent study in Gastroenterologie showed minimal effect on severe Ulcerative Colitis (there was a small initial effect, but a 12 week followup showed no statistically significant difference) (6).  A similar, small study with Crohn’s disease patients showed little impact 8 weeks after treatment, with mixed short-term effect and some minor adverse reactions (fever, diarrhea).  (7)  The only large review study likewise showed mixed results – some self-reporting and small studies showed promise, but over seventeen articles there were only 41 patients that met the inclusion criteria, and several of those has C. Diff infections.  As such, there is no good clinical evidence to support the use of FMT in treating IBD, however the matter has not been fully studied and because of the efficacy with C. Diff and the sound theory behind it, there is ample opportunity for larger scale, controlled studies to evaluate the technique. 

Bottom Line

·         Fecal transplants are a viable treatment for C. Diff.  The mechanism of delivery is largely irrelevant, and adverse results are minimal.
·         FMT has not been statistically shown to be effective in IBD, but the data is limited and larger trials are underway.
·         FMT studies should be monitored over the next couple of years to see if better studies show efficacy. 


1.       SEKSIK, P., SOKOL, H., LEPAGE, P., VASQUEZ, N., MANICHANH, C., MANGIN, I., POCHART, P., DORÉ, J. and MARTEAU, P. Review article: the role of bacteria in onset and perpetuation of inflammatory bowel disease.  Alimentary Pharmacology & Therapeutics.  2006.
2.       Sokol, H., Seksik, P., Rigottier-Gois, L., Lay, C., Lepage, P., Podglajen, I., Marteau, P. and DorĂ©, J.  Specificities of the fecal microbiota in inflammatory bowel disease.  Inflammatory Bowel Disease.  2006.
3.       Borody, TJ; George, L; Andrews, P; Brandl, S; Noonan, S; Cole, P; Hyland, L; Morgan, A; Maysey, J; Moore-Jones, D. Bowel-flora alteration: a potential cure for inflammatory bowel disease and irritable bowel syndrome?. The Medical journal of Australia1989.
4.       Landy, J., Al-Hassi, H. O., McLaughlin, S. D., Walker, A. W., Ciclitira, P. J., Nicholls, R. J., Clark, S. K. and Hart, A. L.  Review article: faecal transplantation therapy for gastrointestinal disease. Alimentary Pharmacology & Therapeutics.  2011.
5.       Michael S. Silverman, Ian Davis, Dylan R. Pillai.  Success of Self-Administered Home Fecal Transplantation for Chronic Clostridium difficile Infection.  Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.  2010.
6.       S Angelberger, C Lichtenberger, C Gratzer, P Papay, C Primas, A Eser, A Mikulits, C Dejaco, G Novacek, H Vogelsang, W Reinisch.  Fecal transplantation in patients with moderately to severely chronic active ulcerative colitis (UC).  Gastroenterologie.  2012.
7.       Vermeire S , Joossens M , Verbeke K , et al. Pilot study on the safety and efficacy of faecal microbiota transplantation in refractory crohn's disease. Gastroenterology 2012.
8.       Anderson, J. L., Edney, R. J. and Whelan, K., Systematic review: faecal microbiota transplantation in the management of inflammatory bowel disease. Alimentary Pharmacology & Therapeutics, 2012.

Monday, January 14, 2013

What about diet and evidence-based IBD?

IBD and Diet

Despite claims to the contrary, there is no one diet that will provide universal symptom relief for IBD.  I’d like to say that the nutritional portions of this blog present a silver bullet approach to diet and IBD, but they don't.  There is no –I repeat no – clinical evidence for a one-size-fits-all diet plan that addresses everyone with these diseases.  Additionally, traditionally recommended diets such as the BRAT diet (bananas, rice, apple sauce, toast) don’t address long-term nutritional needs and may be unnecessarily restrictive.

Much of the information presented as authoritative ranges from harmless to outright dangerous.  Well meaning individuals provide anecdotal stories as evidence (“ I don’t know – my cousin has UC and ever since he started taking fish oil pills he’s been fine”) and health care providers repeat dietary guidance that they were taught in medical school (sometimes decades earlier) that has little to no clinical basis.  Even worse, for-profit enterprises promote diets that rely on magical thinking to work and can even go so far as to claim to “cure” IBD (unfortunately, with the exception of a complete colectomy for UC, there is no known cure for IBD as of this writing).

How do we differentiate between the myriad of sources offering dietary tips (and why is this blog any different)?  Everywhere else in medicine the gold standard for evaluating treatments is a concept called science-based medicine.  Science-based medicine is the application of the scientific method to evaluate various treatment modalities.  The process is straightforward, repeatable, based on sound principles of chemistry, biologic, and physics and open to professional review and scrutiny. 

In science-based medicine, a theory is put forth regarding a specific treatment (or, in this case diet) approach.  The theory should be based on solid scientific principles to differentiate it from “magical” theories based on physical impossibilities.  The theory is then tested in a double-blind fashion against a control group.  In double-blind studies, neither the evaluator nor the subject knows which group the subject is in.  The results are published in a peer-reviewed forum, and if the treatment is found to be more effective than the control (efficacy) in an objectively measurable fashion and to have minimal harmful side effects (safety), it is adopted as a new approach.  Ideally, the studies are confirmed by other, independent researchers and on a large scale. 

Contrast this approach to the way many dietary approaches are proposed.  An individual poses a theory that may be based on scientific principles or it may not.  They try that theory on themselves (or in the case of physicians, a few patients) and ask the subjects if they believe it works.  If so, they provide it to more patients and inform them a priori that they have had success with the treatment.  In these cases, there is no way to know if the diet is effective or if the placebo effect* is responsible for the results.  Additionally, even if there is efficacy, because the diet itself hasn't been isolated as a factor there is no way of knowing if the diet is responsible for or just correlated with positive results.

This blog attempts to provide science-based guidance, including dietary advice.  The guidance is provided based on high quality, peer reviewed research.  Where there are gaps in the research and unanswered questions, these are addressed as well.  

The information provided represents the consensus of the nutrition-based evidence at the time of writing.  Because we refine our scientific understanding over time, the studies and information presented may be refined (or in some cases even overturned with substantial evidence) over time.  To address this, I'll cover in a future post the ways for you to personally evaluate new evidence as it become available and incorporate it into your own  nutritional planning.

The placebo effect is only partially people feeling better because they believe they are being treated.  The effect is, in actuality, a multi-faceted effect.  It includes the provider selectively looking for evidence to support their theories and not looking at the negative results, choosing which evidence to include, other actions taken by people being treated, and the desire to “self-report” positive effects on subjective factors.

Sunday, January 6, 2013

Fiber and Low Residue Diets

IBD and Fiber

The intake of fiber is one of the cornerstones of most IBD diets.  The vast majority recommend that those suffering from IBD consume low-fiber foods.  At the extreme, the low residue diet recommends the removal of just about all fiber.  What is fiber and what does the evidence say about its effect on IBD?

Fiber is the part of plants that is indigestible, and is often broken up into two categories – soluble fiber and insoluble fiber.  Soluble fiber is broken down in the digestive system (through fermentation) and is believed to have cholesterol lowering effects and other health benefits.  Insoluble fiber, primarily cellulose, is not broken down and adds bulk to fecal output and absorbs water in the intestines.  Examples of foods with high fiber content in each category are as follows (1):*

Apple and Tomato Skins
Brussel Sprouts
Ripe Bananas
Sweet Potatoes
Chick Peas
Green beans
White Potatoes
Kidney Beans

Potato Skins


Whole grains

Fiber, specifically soluble fiber, has been shown to reduce cholesterol and assist in the absorption of vitamins and minerals.  Additionally, it has been shown to help regulate sugar intake in diabetics.  Insoluble fiber can assist in weight loss (because it is not digested, it gives a “full” feeling without the calories).

A high fiber diet was originally touted as reducing the risk of colon cancer.  Initially, several smaller studies showed a very small reduction in risk, between 10 and 20%, but the relative risk error bars crossed 1.0 in most of them.  Recent studies have found no link between overall fiber consumption and colon cancer development.

Negatively, a high fiber diet can cause bloating and associated abdominal discomfort, largely due to the fermentation that occurs when it is processed in the intestines.  This discomfort is cited as aggravating already inflamed intestinal tissue, exacerbating Crohn’s or UC symptoms.  When tested, though, does it really have that effect?

Specific to IBD, the low residue diet is a frequent recommendation, and can be carried over as a long term nutrition plan.  That said, the evidence for doing so is extremely weak.  A prospective study comparing a low fiber, low residue** diet with a normal diet concluded:

There was no difference in outcome between the two groups, including symptoms, need for hospitalisation, need for surgery, new complications, nutritional status, or postoperative recurrence.(4)

It should be noted that the comparison was between a low fiber diet and a normal fiber diet.  The study draws no conclusions about the impact of a high fiber diet.  Unfortunately, a high fiber diet has been shown to have no great impact on the course of the disease or symptoms either (5).

Despite the lack of clinical evidence, it is especially common to recommend a low fiber diet in those with active inflammation and structuring.  While there is no evidence to support this to promote healing, it is frequently recommended by physicians to avoid the potential life threatening formation of an obstruction.  

The most common reason for obstruction in adults is the formation of a bolus of fiber, or a phytobezoar (big ball of plant material).  These form from insoluble fiber that isn’t digested, usually in patients with deceased stomach acid production (a study of patients taking acid reducing drugs with their IBD may be warranted…).  Because of structuring and inflammation, the risk and impact of phytobezoar formation should theoretically be much higher in active IBD, though more study is required to confirm this.

Bottom Line

·         Fiber, especially soluble fiber, should not be avoided and normal amounts are acceptable if tolerated.
·         Neither high fiber diets nor low residue diets have been shown to have a positive impact on those already diagnosed with IBD.
·         Insoluble fiber should be limited for individuals with low stomach acid production, structuring, and extensive inflammation.

* Most foods contain both soluble and insoluble fiber – the foods listed represent high content sources in the listed category.
** While used synonymously, low residue and low fiber diets are not the same.  Low residue diets exclude fiber, but also other higher residue foods (such as milk products).

1.       JW Anderson and SR Bridges.  Dietary fiber content of selected foods.  American Journal of Clinical Nutrition.  1988.
2.       Fuchs CS, Giovannucci EL, Colditz GA, et al. Dietary fiber and the risk of colorectal cancer and adenoma in women. New England Journal of Medicine, 1999.
3.       Simons CCJM et al. Bowel Movement and Constipation Frequencies and the Risk of Colorectal Cancer Among Men in the Netherlands Cohort Study on Diet and Cancer. American Journal of Epidemiology, 2010.
4.       Levenstein, S., et al. Low residue or normal diet in Crohn's disease: a prospective controlled study in Italian patients. Gut, 1985.
5.       Russell, R. I. (1991), Review article: dietary and nutritional management of Crohn's disease. Alimentary Pharmacology & Therapeutics, 1991.
6.       Emerson, A. P. Foods high in fiber and phytobezoar formation. Journal of the American Dietetic Association, (1987): 1675.