Irritable bowel syndrome (IBS) is a common gastrointestinal (GI) disorder that is characterized by recurrent abdominal pain together with an abnormal frequency and/or consistency of stools [1
]. The diagnosis is based on fulfilling the Rome criteria for IBS without any signs of an organic GI disease on limited diagnostic testing [1
]. Although IBS is associated with a large health care utilization [2
], efficient treatment options are still limited. As many patients with IBS report diet as a major factor in triggering or worsening GI symptoms [4
], dietary treatment is often considered as a first-line option. There is some evidence that intake of alcohol [8
], caffeine [5
], and spicy foods [4
], as well as foods rich in fat and carbohydrates [4
] might trigger symptoms and should thus be limited in intake, but not all patients respond to these dietary modifications. Patients with IBS differ from each other in symptom patterns and severity and have different underlying pathophysiology; there is still much to be done in developing dietary therapies that target different subtypes of IBS and with different underlying mechanisms of the disease.
Restricting intake of fermentable carbohydrates, FODMAPs (Fermentable Oligo-, Di-, Monosaccharides and Polyols) is increasingly recommended in the management of IBS. The low-FODMAP diet focuses on reducing intake of poorly digestible carbohydrates, such as galacto-oligosaccharides (GOS), fructans, lactose, fructose, and sorbitol [10
]. These carbohydrates are typically found in wheat-based products, onion, garlic, legumes, dairy, and a wide range of fruits and vegetables. The common trait among these carbohydrates is that they are incompletely absorbed in the small intestine, which can cause gas production due to rapid fermentation and to an osmotic action with increased water retention. Thus, reducing FODMAP intake could lead to less luminal distention and, thereby, less pain [10
]. However, as some FODMAPs also act as prebiotics [11
], a reduction in FODMAPs will concurrently reduce the prebiotic intake, and concerns have been raised if this will affect the gut microbiota in an unfavorable manner in the long term [12
To date, most dietary studies on FODMAP intake in patients with IBS have been focusing on restricting or limiting intake of all FODMAPs during a period of time, followed by a reintroduction of selected FODMAPs and evaluating the change in symptom severity and patterns. As a short-term dietary treatment, the low-FODMAP diet seems effective in reducing GI symptoms in around 50–80% of the treated patients in randomized controlled trials [13
]. In a previous study, we have reported that the habitual intake of FODMAPs varies largely between individuals with IBS, but there is also a large day-to-day variation within individuals [17
]. Little is still known about how the habitual FODMAP intake correlates to symptom generation and severity in this patient group, and if amounts, types, or intake patterns matter. In addition, not much is described regarding whether this relationship differs among IBS subtypes. The aim of this study was to evaluate the relationship between FODMAP intake and symptom severity and pattern in patients with IBS, taking advantage of existing detailed dietary intake data among well-characterized patients of different IBS subtypes.
In this cross-sectional study, using a well-characterized group of patients with IBS with detailed dietary data, we studied how habitual FODMAP intake relates to symptom severity in different IBS subtypes based on the predominant bowel habit. Our study showed large similarities in FODMAP intake among patients with different IBS subtypes, even though minor differences were noted. Furthermore, weak associations between FODMAP intake and IBS symptom severity were demonstrated with differences among subtypes, where excess fructose intake accounted for a large share of explained variance in symptom severity among women with IBS-U.
This study is one of few to link habitual FODMAP intake to symptom severity, and to study this relationship among different subtypes of IBS. A recent study published data on habitual FODMAP intake in a UK population, where the mean total FODMAP intake was 17 g/day [27
], which is well in line with our findings. Another study performed in a Dutch setting has investigated the habitual diet of patients with IBS, and although the total FODMAP intake was not reported, the authors also found dissimilar results among the different subtypes of IBS [28
]. For instance, a lower fiber intake correlated significantly with higher symptom scores among IBS-D, but this was not the case for the other subtypes. Furthermore, intake of apples significantly correlated to increased discomfort among IBS-C and IBS-M [28
]. In that cohort, only 4.6% of the participants were classified as IBS-U, which might explain the lack of statistically significant findings in that subtype.
In this study, reported intake of FODMAPs appeared quite similar among the different subtypes of IBS; the only significant difference was that women with IBS-D reported a lower daily lactose intake. This may be attributed to the higher proportion of women with IBS-D who appeared to exclude lactose from their diet. Lactose intolerance is a common condition among patients with IBS, as it is in the general adult population [29
]. Symptoms of lactose intolerance may arise from lactose malabsorption, i.e., from the inability to produce lactase at the brush border, but it may also arise from an unfavorable composition of the intestinal microbiome or a history of GI disorders [29
]. Symptoms of lactose intolerance include watery stools and bloating; hence, the symptoms of lactose intolerance overlap with symptoms of the diarrhea-predominant type of IBS. Notably, not all individuals that are lactose malabsorbers do experience symptoms after lactose intake, and on the other hand, individuals with visceral hypersensitivity may experience symptoms even at very low intakes [29
]. Our study showed that lactose accounts for approximately 50% of the total FODMAP intake among patients with IBS, whereby intake of lactose has the potential to affect symptom generation to a large degree depending on if lactose is well tolerated or not. Whether lactose malabsorption is more prevalent among IBS-D than among other subtypes of IBS is unclear, but it is likely that patients in our study attributed their symptoms to intake of lactose and had therefore reduced their lactose intakes prior to the study measurement.
Interestingly, we found no correlation between FODMAP intake and severity of bloating, which has been suggested as one of the main symptoms influenced by FODMAPs through bowel distension [30
]. Again, this might be explained by a foregoing reduction in FODMAPs among individuals who experience FODMAP containing foods to cause bloating.
We did not see any effect of CVw on symptom severity score, which indicates that individuals who report consuming regular amounts of FODMAPs experience the same grade of symptom severity as individuals who report a more irregular consumption. From this, we can conclude that regular FODMAP consumption is not clearly more beneficial over occasional intakes.
There was a weak but statistically significant correlation between quartiles of energy-adjusted FODMAP intake and IBS symptom severity. This relationship was mainly driven by the subgroup IBS-U, where FODMAP intake correlated to a higher pain frequency and more bowel habit dissatisfaction. This was further studied in the regression models, and of all individual FODMAPs, excess fructose was clearly the most potent in generating symptoms. As much as 20% of all variance in IBS symptom severity was explained by excess fructose intake in IBS-U, which is remarkable. Fructose malabsorption is common both among healthy subjects as well as among individuals with functional GI disorders [31
], and up to one-third of patients with IBS is thought to have insufficient fructose absorption [32
]. Fructose is mainly absorbed in the small intestine by facilitated diffusion via glucose transporter (GLUT) 5 receptors, but it can also be absorbed by co-transport with glucose through GLUT2 receptors [25
]. Symptoms of fructose malabsorption resemble those of lactose intolerance, i.e., increased flatulence and loose stools [33
]. However, it is not apparent why patients with IBS-U in particular would have such increased symptom burden after ingestion of excess fructose. Whether fructose malabsorption is more common among IBS-U, or if the lack of abnormal stools makes the association between food intake and symptom generation more difficult to link, would be interesting for future research.
In the regression analyses, we also demonstrated that reported energy intake was weakly, but statistically significantly, related to lower IBS symptom severity, meaning that individuals who reported a low intake of energy experienced having more GI symptoms than individuals who reported a higher energy intake. This could reflect that individuals who experience a lot of symptoms have reduced their food intake in an attempt to reduce pain. We have previously shown that the higher number of food items a person attributes to trigger symptoms, the more severe the IBS symptoms [34
]. A qualitative study has described how women with IBS have developed “self-care strategies” to cope with their GI symptoms, which include a “trial and error” method to exclude foods believed to trigger symptoms, and to reintroduce them again if the symptoms did not improve [35
]. Consequently, patients experiencing a heavy IBS symptom burden may exclude more foods from their diet, leading to a lower energy intake.
In the multivariable regression model, when FODMAP intake was adjusted for energy intake, age, BMI, and other somatic symptoms, the final full model remained statistically significant for IBS-U and also became statistically significant for IBS-M. However, women with IBS-M had less symptoms with increasing FODMAP intake, whereas women with IBS-U had increasing symptom burden with higher intake. From the bivariate regression models, one can note that intake of lactose (although not statistically significant) seems to contribute to less severe symptoms in IBS-M, and that the reported lactose intake was highest in this group. In the second full model, where lactose was removed from the total sum of FODMAPs, symptom severity was no longer related to FODMAP intake in IBS-M. One can assume that this reflects that lactose absorbers have continued to consume lactose and, when tolerable, lactose does not yield negative effects on symptom severity.
A strength of this study was the inclusion of a large number of well-characterized IBS patients, covering a wide range of IBS symptoms. However, there were too few male participants in this study to be able to perform correlation or regression analyses with sufficient power in women and men separately; thus, these analyses were performed on women only. As participants were recruited both at regular outpatient clinics as well as through advertisement in the local newspaper, the study participants likely represent an IBS population where the results can be generalizable. The use of validated and well-established questionnaires to characterize participants and symptoms is also a key strength. On the negative side is the lack of longitudinal data; as we only have access to one measurement of food intake and symptom severity taken concurrently, we do not know whether patients have already changed their diet in order to manage symptoms. Therefore, we cannot rule out reversed causality, and the results must be interpreted with caution regarding cause and effect.
In summary, the intake of FODMAPs seems to exert varying effects in individuals with IBS, and there might be some similar traits within patients with the same subtype of IBS. As the different types of FODMAPs seem to be more or less potent in generating symptoms, it is warranted to study the effect of each FODMAP separately and among the different subtypes of IBS, in longitudinal studies or randomized controlled trials.