2 Free Articles Remaining (through 06/21/18)

The low-FODMAP diet is very popular among people with gastrointestinal illnesses, especially Irritable Bowel Syndrome (IBS)—an extremely common condition in today’s society. If you tell your gastroenterologist or dietitian that you suffer from IBS, chances are they’ll recommend a diet that’s low in fermentable oligo-, di-, and mono-saccharides and polyols (FODMAPs).

One of the primary reasons for this diet’s popularity, both among patients and clinicians, is that a solid body of clinical research supports its efficacy. Few diets have been subjected to as much scientific scrutiny as the low-FODMAP diet. Several clinical trials have examined its therapeutic potential, since it was specifically developed for the management and treatment of gastrointestinal illness. These studies’ results indicate that the low-FODMAP diet effectively reduces gastrointestinal symptoms such as diarrhea and bloating in patients with IBS, and may be useful in the treatment of organic gastrointestinal disorders such as Inflammatory Bowel Disease (IBD).5,7,8,15

Many people assume, after reading the results of these studies, that patients with gastrointestinal illnesses such as IBS should follow a low-FODMAP diet for an extended period, or even indefinitely. In today’s article, I’ll explain why this assumption can be problematic.

The Big Picture: An Overview of the Problem

It’s a huge mistake to base our understanding of nutrition and health solely on the results of clinical trials, meta-analyses, and other similar studies. These types of studies are undoubtedly informative; however, they only offer us part of the picture. Before we dig into the depths of PubMed, we must ensure that we are equipped with the knowledge and tools we need to make sense of the wealth of information therein. Most importantly, we need to understand the biological mechanisms underpinning the condition we’re researching.

The foods that we eat contain a broad range of nutrients, which are each digested in a specific manner and location within our GI tracts. Fats, proteins, simple sugars, and starches are primarily digested in the upper portion (the mouth, stomach, and small intestine), whereas oligosaccharides and non-starch polysaccharides are primarily digested in the large bowel (the colon). However, there are some exceptions to this rule. For example, in lactose-intolerant individuals, lactose may pass undigested through the small bowel and undergo microbial fermentation in the colon.  Moreover, some nutrients may be exposed to digestive enzymes in both the lower and upper parts of the gastrointestinal tract. However, in general, the aforementioned principle holds true, and it figures critically in the therapeutic value and optimal application of a low-FODMAP approach.

The low-FODMAP diet is a contradictory diet. It doesn’t exclude non-starch polysaccharides, although they pass undigested through the upper gut; yet it does exclude fructose and lactose, which many people’s small intestines absorb quite effectively. It is easy to be skeptical of such a carbohydrate-classification system.

That said, in general, the nutrients excluded from the low-FODMAP diet belong to the latter category of the above: carbohydrates that pass through the small intestine largely undigested. The human genome lacks genes that code for the digestive enzymes necessary to break down these carbohydrates; hence, our microbiota do the job for us. Gut microbes love FODMAPs.

FODMAPs are ubiquitous; they appear in a broad range of different plant foods. Hence, they have been a part of the human diet for millions of years. Actually, our ancient ancestors ate many more fermentable carbohydrates than most contemporary humans do.10,13 Some ancient peoples may have consumed as much as 135 grams of inulin-type fructans every day.12 Contemporary African hunter-gatherers, such as the Hadza, are also known to consume a lot of fermentable carbohydrates.14,19

We cannot assume a significant proportion of the human population has suddenly lost the ability to properly digest fermentable carbohydrates. There must be some other mechanism at work here, to cause such rampant dysfunction.

Getting to the Root of the Problem

Over the past few decades, it has become increasingly clear that gut dysbiosis—an imbalance in the gut microbiome—is central to the pathophysiology of many health conditions. Virtually all of the gastrointestinal problems that affect Homo sapiens have been linked with gut dysbiosis.12,18 Patients with IBS, the condition most often treated with the low-FODMAP diet, typically harbor an imbalanced gut microbiome.1,4,9,17 Hence, some researchers have suggested that a better name for the cluster of symptoms comprising IBS would be Dysbiotic Bowel Syndrome (DBS).1 Gut dysbiosis is not the sole factor in IBS, but it’s surely a central component.

Therefore, it shouldn’t be surprising that IBS sufferers have trouble digesting fermentable carbohydrates. We depend on the genetic capabilities of the microbes that dwell deep in our gut to digest the great variety of carbohydrates in our plant foods. By ourselves, we’re only capable of digesting starches and some simple sugars. The rest are handled by our bacteria.

A diverse panoply of genes is required to produce the various enzymes necessary to break down all the carbohydrate types that pass into the large intestine. If the microbial community of the lower gut is undersized and/or imbalanced, digestion will obviously be compromised. Some nutrients that pass into the gut may only be partially digested, lacking the microbes capable of processing them; further, certain pathogenic bacteria, allowed to proliferate in the absence of their beneficial counterparts, could harness these nutrients to produce various toxins. This in turn would promote symptoms of food intolerance, such as bloating, loose stools, and flatulence, which are stereotypical of IBS.

Hence, it becomes apparent why studies show symptom improvement in IBS patients who undertake a low-FODMAP diet. Dramatically reducing fermentable carbohydrate consumption eliminates much of the colonic microbes’ food supply. There’s a big problem, though. Cutting out fermentable carbohydrates keeps gastrointestinal symptoms at bay, but does nothing about the underlying foundations of the condition. It may actually aggravate the problem long-term; when starved of food, the beneficial bacterial strains may wither and die, or they may end up digesting the mucus of the intestinal wall.3,20,21

Snuffing Out the Fire

Instead of trying to tame the fire via a low-FODMAP diet, it seems more productive to extinguish it completely, by fixing the microbial community of the gut. This strategy may not be effective in all IBS and IBD cases; genetic/epigenetic factors leave some patients with a severely inflamed gut that precludes development of a healthy, diverse microbiota; however, it should serve well in many cases.

Indeed, recent evidence shows that gut-microbiota manipulation (e.g. fecal microbiota transplantation, probiotics) is an effective treatment for many gut disorders, including IBS and IBD.1,4,11,16,17 The literature remains unclear as to the best approach for repairing a damaged gut microbiome; however, the science is constantly advancing. As long as we adhere to the evolutionary principles of Darwinian medicine, we should be on safe grounds.

The low-FODMAP diet may be useful during the first stages of treatment for certain gut disorders; however, it doesn’t represent an appropriate long-term intervention, unless repairing the gut microbiome and improving fermentable-carbohydrate tolerance have proven very difficult or impossible.

A diet that limits naturally occurring fermentable carbohydrates is evolutionarily novel; as a species, we have evolved to digest such carbohydrates effectively. The fact that many of us now struggle with this process cannot be explained by genetic change, but rather by shifts within the human microbiome.

A modern lifestyle, saturated with antibiotics, processed foods, and other microbial disruptors, has perturbed our bodies’ microbial communities, making us sick and fragile.6 We’re increasingly becoming allergic to pollen and other substances that are a normal part of our environment, and we’re suddenly struggling to digest nutrients that we’ve consumed for ages.

The solution is not merely to erect barriers to exclude the environmental inputs with which our bodies now struggle. Rather, we must restore our bodies to a fully functional state, so that we’re no longer allergic or intolerant to substances that, evolutionarily, weren’t so problematic. Again, this approach may not work universally; yet it should bear fruit in many cases. Removal of the “offenders” should only be a last resort, after exploring all other avenues.


  1. Benno P, Dahlgren AL, Befrits R, Norin E, Hellstrom PM, Midtvedt T. “From IBS to DBS: The Dysbiotic Bowel Syndrome.” J Investig Med High Impact Case Rep 4 (2016). 2324709616648458.
  1. Cho I, Blaser MJ. “’The Human Microbiome: At the Interface of Health and Disease.”  Nat Rev Genet 13 (2012): 260-70.
  1. Desai MS, Seekatz AM, Koropatkin NM, Kamada N, Hickey CA, Wolter M, Pudlo NA, Kitamoto S, Terrapon N, Muller A, Young VB, Henrissat B, Wilmes P, Stappenbeck TS, Nunez G, Martens EC. “A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility.” Cell 167 (2016): 1339-53.e21.
  1. Distrutti E, Monaldi L, Ricci P, Fiorucci S. “Gut Microbiota Role in Irritable Bowel Syndrome: New Therapeutic Strategies.” World Journal of Gastroenterology 22 (2016): 2219-41.
  1. Eswaran SL, Chey WD, Han-Markey T, Ball S, Jackson K. “A Randomized Controlled Trial Comparing the Low-FODMAP Diet vs. Modified Nice Guidelines in US Adults with IBS-D.” Am J Gastroenterol 111 (2016): 1824-32.
  1. Garnas E. “The Western Microbiome: How Our Modern Guts Make Us Sick, Fat, and Unhappy.” Darwinian-Medicine.com (2016). http://darwinian-medicine.com/the-western-microbiome-how-our-modern-guts-make-us-sick-fat-and-unhappy
  1. Gibson PR. “Use of the Low-FODMAP Diet in Inflammatory Bowel Disease.” J Gastroenterol Hepatol 32 Suppl 1 (2017): 40-42.
  1. Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG. “A Diet Low in FODMAPs Reduces Symptoms of Irritable Bowel Syndrome.” Gastroenterology 146 (2014): 67-75.e5.
  1. Kennedy PJ, Cryan JF, Dinan TG, Clarke G. “Irritable Bowel Syndrome: A Microbiome-Gut-Brain Axis Disorder?” World J Gastroenterol 20 (2014): 14105-25.
  1. Konner M, Eaton SB. “Paleolithic Nutrition: Twenty-Five Years Later.” Nutr Clin Pract 25 (2010): 594-602.
  1. Kruis W, Chrubasik S, Boehm S, Stange C, Schulze J. “A Double-Blind Placebo-Controlled Trial to Study Therapeutic Effects of Probiotic Escherichia Coli Nissle 1917 in Subgroups of Patients with Irritable Bowel Syndrome.” Int J Colorectal Dis 27 (2012): 467-74.
  1. Leach JD, Sobolik KD. “High Dietary Intake of Prebiotic Inulin-Type Fructans in the Prehistoric Chihuahuan Desert.” Br J Nutr 103 (2010): 1558-61.
  1. Lieberman D. The Story of the Human Body: Evolution, Health, and Disease (Vintage, 2014).
  1. Marlowe FW, Berbesque JC, Wood B, Crittenden A, Porter C, Mabulla A. “Honey, Hadza, Hunter-Gatherers, and Human Evolution.” J Hum Evol 71 (2014): 119-28.
  1. McIntosh K, Reed DE, Schneider T, Dang F, Keshteli AH, De Palma G, Madsen K, Bercik P, Vanner S. “Fodmaps Alter Symptoms and the Metabolome of Patients with IBS: A Randomised Controlled Trial.” Gut (2016).
  1. Moayyedi P, Surette MG, Kim PT, Libertucci J, Wolfe M, Onischi C, Armstrong D, Marshall JK, Kassam Z, Reinisch W, Lee C. “Fecal Microbiota Transplantation Induces Remission in Patients with Active Ulcerative Colitis in a Randomized Controlled Trial.” Gastroenterology 149 (2015): 102-09.e6.
  1. Ohman L, Simren M. “Intestinal Microbiota and Its Role in Irritable Bowel Syndrome (IBS).” Curr Gastroenterol Rep 15 (2013): 323.
  1. Round JL, Mazmanian SK. “The Gut Microbiome Shapes Intestinal Immune Responses During Health and Disease.” Nat Rev Immunol 9.5 (2009): 313-23.
  1. Schnorr SL, Candela M, Rampelli S, Centanni M, Consolandi C, Basaglia G, Turroni S, Biagi E, Peano C, Severgnini M, Fiori J, Gotti R, De Bellis G, Luiselli D, Brigidi P, Mabulla A, Marlowe F, Henry AG, Crittenden AN. “Gut Microbiome of the Hadza Hunter-Gatherers.” Nat Commun 5 (2014): 3654.
  1. Sonnenburg ED, Smits SA, Tikhonov M, Higginbottom SK, Wingreen NS, Sonnenburg JL. “Diet-Induced Extinctions in the Gut Microbiota Compound over Generations.” Nature 529 (2016): 212-5.
  1. Sonnenburg ED, Sonnenburg JL. “Starving Our Microbial Self: The Deleterious Consequences of a Diet Deficient in Microbiota-Accessible Carbohydrates.” Cell Metab 20 (2014): 779-86.