FODMAPS are a group of carbohydrates that have in common that they are poorly absorbed (malabsorbed) in the small bowel, but can serve as a feedstock for our colonic bacteria. FODMAP stands for fermentable – oligo- di- and monosaccharides and polyols. And fermentation means that bacteria or fungi can anaerobically digest the substance in our colons.
Fermentation of undigested leftovers happens normally in the colon, and although there is a gradient of bacterial colonization in the more proximal (closer to the mouth) gut, significant fermentation in the small bowel is abnormal and is referred to as SIBO – small intestinal bacterial overgrowth. FODMAPs, especially free fructose, may contribute to SIBO. SIBO may be what turns H.Pylori in the stomach from a harmless commensal into an ulcer-causing pathogen. Excess fructose may be the real “cause” of peptic ulcer disease.
Now, technically, most non-cellulose carbohydrates can be fermented in the colon. What FODMAPs have in common is that they make it to the colon without being hydrolysed and absorbed in the small bowel, like our fuel-source starches and regular sugars. They can all thus be considered “prebiotics”. However, unlike longer molecules like inulin that are also fermented in the colon, the FODMAPs tend to be rapidly fermented in the proximal parts of the colon, rather than slowly fermented more distally. It is this rapid proximal fermentation that can lead to increased growth of bacteria in the terminal ileum – the distal part of the small bowel that attaches to the proximal colon – then you have SIBO.
So what are they exactly? Oligosaccharides (OS) are short polymers (chains) of simple sugars. Short polymers of glucose are just glucose oligosaccharides – they are hydrolysed and absorbed just like starch. To be a FODMAP, the OS must have a bond or bonds that we have no enzyme to hydrolyse (break apart). Examples include raffinose, which is galactose (milk sugar) joined to the fructose sugar of the disaccharide sucrose by an alpha bond. Galactose – Fructose –Glucose. Alpha galactosidase (a-gal) is the enzyme used to break the alpha bond. Humans and hindgut fermenting mammals don’t make it, but bacteria do. The best illustration of the effects of eating a lot of raffinose remains the campfire scene in Blazing Saddles. Raffinose is one of the main OS found in beans. A-gal is also the active ingredient in “Beano”.
Fructans and fructo-oligosaccharides (FOS) are FODMAPs found in wheat and may account for much of the GI distress encountered on high-wheat diets, as well as for much of the relief obtained by eliminating wheat.
Fructose is a monosaccharide FODMAP functionally. By this I mean, if you absorb it all in your small bowel, it is not a FODMAP. But if you get a big dose of free fructose - fructose in excess of glucose in the same meal - or if you get a very large bolus even with the same amount of glucose - two coca-colas in a row, a binge on glazed donuts, a bunch of Christmas cookies at the office party – it is likely that some of the fructose, or even a lot of it, will escape digestion and absorption in the small bowel and make it to the colon. There it will serve as food for bacteria, similar to the way the raffinose would, and with similar effects. As I’ve suggested, I view this as part of an evolutionary adaptation – part of a defense against fructose poisoning. The first line of defense is this limitation on our ability to absorb too much of it at once, sending the excess to the colonic compost pile for the bacteria to eat. The second line of defense is the liver, where the fructose we do absorb is sequestered by combustion or conversion into fat to keep it out of the circulation. (I sometimes wonder how many of those who think concerns about excess fructose reflect “alarmism” are aware of these simple facts about fructose metabolism.)
Examples of polyol FODMAPs include xylitol and sorbitol. These are sugar alcohols. Xylitol is used in “sugarless” gum as it is not fermentable by mouth bacteria and so does not encourage dental caries. Sugar alcohols are not broken down in the small bowel, so they do not cause significant blood glucose elevation when eaten. They do get fermented in the colon, though, and it is possible to exacerbate irritable bowel syndrome or get osmotic diarrhea from, say, compulsively chewing sugarless gum or eating “diabetic” chocolates. Polyols are also very abundant in apples, pears and peaches naturally.
Inulin, polyols and FOS are all very common additives found in the junk marketed as “sugar-free”, “low carb”, or “diabetic”. Many are not aware of how much intestinal upset they can cause. Another reason to stick with real food and not eat anything that comes in a box, whether it says “low fat” or “low carb” or “sugar free”.
How else to avoid excess FODMAPs ? Minimize excess fructose, onions, jerusalem artichokes, wheat, tomatoes, apples, peaches, pears. And minimize fruits with fructose substantially in excess of glucose (watermelon, apple).
Dr. Peter Gibson is the originator of the FODMAP concept. You can plug his name into pubmed and find quite a lot, but here are two links to good papers by him for further reading. Dr. Gibson has done research showing symptomatic relief in irritable bowel syndrome sufferers with FODMAP restriction and also speculates that they could play a role in development of the very serious inflammatory bowel diseases - such as Crohn's disease.
As many of the FODMAPs are soluble fiber "prebiotics", and there seem to be a lot of people advising you to eat more of these on purpose or even supplement with them as a "health" measure, Dr. Gibson's ideas might be something to consider. Even it you don't mind the additional gas they might give you.
FODMAP and crohns
FODMAP and functional bowel