FODMAPS: a review of the current literature and more…

Michael Bizeau, PhDMetropolitan State University of

Denver

Incidence of Lower GI tract Disorders

• Specifically we will address IBS for this discussion as FODMAP studies have used IBS patients.– Depending on criteria used incidence varies but on average

it is considered about 11% -15% of population has IBS.• Canavan et al 2014.

– Hypersensitivity of enteric nervous system is considered a primary factor.

• SSRIs and TCA used with some success for treatment.• Diet also receiving consideration

– Increased fiber diets commonly used although studies show no clear improvement over placebo. (Eswaran et al 2013.)

Linking diet to discomfort

• Anecdotal success with several elimination diets. – Both research based and non-research based.

• Lactose– We all understand lactase non-persistence

• Fructose-Latest data suggests fructose malabsorption occurs in about 30% of population.– Dose dependent as well as dependent on glucose in

the meal.• Gluten- Non Celiac gluten intolerance?

FODMAP Hypothesis• Gibson and Shepherd propose FODMAP hypothesis in 2005 paper

based upon some clinical observations and non-controlled trials. (Gibson 2005)

• Diet a likely candidate in symptoms associated with diseases of GI tract.

• An research based approach utilized.– Clinical observations– Non-controlled trials– Biological plausibility and proposed mechanisms

• Specific evidence is limited and current interventions marginally effective.

• FODMAP consumption potentially explains success of many popular diets with regards to improving GI symptoms.

Characteristics of FODMAPS

• Poorly absorbed in small intestine.– Low capacity or velocity transport systems.– Low enzymatic activity (lactase)– Lack of hydrolases – Large molecule size.

• Small, thus osmotically-active.• Rapidly Fermented – Perhaps dependent on GI microbiome.– Chain Length dependent

Fructose

• Increased fructose consumption.• Humans have a limited capacity to absorb free

fructose. (Rao et al 2007)• 100% can absorb 15g• 90% can absorb 25 g• 25% can absorb 50g• Estimated at 30% of population has dose

dependent fructose malabsorption.

Lactose

• Lactase non-persistence.• Positive hydrogen breath test for lactose.

Fructans• Non- digestible Oligo and poly saccharides of fructose

w/glucose terminal end.– Inulins and Levans– Inulins are most common dietary from and a common food

additive.– Short chain inulins commonly called fructooligosaccharides.

(FOS)– Long chain just called inulins.

• Commonly found in wheat and onions.• Not digested in SI but rapidly and almost completely

fermented in colon.• Average intake ~ 10g/day (Gibson 2005)

Galactooligosaccharies

• Contain both beta-fructosidic linkages as well as galactosidic linkages.

• Not digested and again fermented in colon.• Raffinose is primary dietary source.• Legumes, cabbages, brussels sprouts, onions.• Traditional preparations methods reduce

raffinose content in foods.

Polyols

• Sorbitol, xylitol, mannitol, malitol.• Poorly absorbed and again fermented in

colon.– Smaller chain length forms absorbed better than

longer chain length.– Erythritol for example.

• Apples, pears, stone fruits as well as artificial sweetener use.

Potential Mechanism of action• Current literature suggest increased A large load

of FODMAPS to colon will result in increased osmotic load.

• Rapid fermentation results in increased gas in colon.

• Gas as well as osmotic load result in distention and increased stimulation of enteric nervous system with already exhibits hypersensitive.– Pain, discomfort, dysregulation of bowel movement,

gas etc.-IBS

Mechanisms of action continued.

• Also increased fermentation leads to increase SCFA production. – Positives and negatives associated with this effect.

• Selective bacterial culture in colon.• Potential small intestinal bacterial overgrowth.• Increase in epithelial permeability.• Increased inflammation?

Well… does it work?

• Limited number of studies but evidence is accumulating.

Studies• Early studies uncontrolled but provided pilot data used in current studies.• Ong et al, 2010- single blind crossover study with healthy and IBS subjects.

High vs Low FODMAP diet. – High FODMAP diet resulted in increased breath hydrogen, great IBS symptoms (in

IBS group).• Staudacher et al, 2011. IBS patients given standard vs. Low FODMAP diet

counseling.– Low FODMAP diet group had lower reported symptoms.

• Roest et al. 2013- Prospective study of IBS patients demonstrated significant reduction in IBS symptoms with adherence to diet. Furthermore in this study adherence was 75%.

• Halmos et al. 2014-In a controlled, cross-over study of patients with IBS, a diet low in FODMAPs effectively reduced functional gastrointestinal symptoms

• Murray et al. 2014-healty subjects consumed high FODMAP test meals. Distention in both large and small bowel detected via MRI.

• Halmos et al. 2015-A low FODMAP diet alters GI microbiome.

Where does this leave us?

• There is an increasing albeit limited body of evidence suggesting that in IBS patients adoption of a low FODMAP diet may potentially reduce symptoms.

• Overall about 70% of patients respond with a 50% reduction in symptoms.

• Adherence is about 75%– Symptom reduction– Guidance of trained dieticians

Implementation of FODMAP diet

• Success in this diet is strongly associated with dietician based implementation with two major phases. Implementation and reintroduction.

• 1. Determine both lactase non-persistence and fructose malabsorption with challenge and hydrogen breath test.

• 2. Record patient eating habits to determine baseline FODMAP intake.

Implementation of FODMAP diet

• 3. Explain Physiology behind the diet.• 4. Counsel patient on high vs. low FODMAP foods

and provide lists of these foods.• 5. Explain the concept of low not no FODMAPS.• 6. Provide recipes/cookbooks/information on

eating outside the home.• 7. 6-8 weeks of full implementation.• 8. Reintroduction phase-the art. – Specific foods, specific doses etc….

Potential Adverse Consequences

• Nutritional adequacy-Should not be a problem when given guidance from a dietician.

• Altered GI microbiome.– ?????

What we need to know.

• Longer term studies needed in diverse populations.– i.e. beyond IBS

• Research conducted in other laboratories/clinical settings.• Both large and small intestine involved?• Efficacy in other GI diseases.

– Data suggests favorable response in IBD although more studies needed. (Charlebois 2015)

• Does diet work in upper bowel disease?• Two non controlled studies suggest possible relief from GERD with low

FODMAP diet.

• What is efficacy/adherence when diet and education not directly supervised by trained dieticians?

Resources

• http://fodmapmonash.blogspot.com.au• http://livinghappywithibs.com/category/low-f

odmap-diet/about-the-low-fodmap-diet/