Reduction of starch and sucrose intake is associated with less food-triggered symptoms. A randomized clinical trial

Abstract

Background

Patients with irritable bowel syndrome (IBS) often experience food-related symptoms. Both a diet low in fermentable oligo-, di-, monosaccharides, and polyols (FODMAP) and a starch- and sucrose-reduced diet (SSRD) alleviate symptoms.

Aims/Objectives

The aim of this randomized clinical trial was to evaluate the proportion of participants with symptoms and the type of food items triggering symptoms during intervention by either diet.

Methods/Methodology

Patients with IBS according to Rome IV were included for a four-week intervention. Participants completed a three-day food diary, study questionnaire, Rome IV questionnaire, IBS-severity scoring system (IBS-SSS), and visual analog scale for IBS (VAS-IBS) at baseline, after 4 weeks of either SSRD or low FODMAP, and at a six-month follow-up. The food items that triggered symptoms were registered along with the type of symptoms.

Results/Findings

Totally, 155 participants (84% women), 42 (32–55) years, were included; 77 were randomized to SSRD and 78 to low FODMAP. SSRD rendered a reduction of participants with symptoms triggered by food avoided/modified such as fast food (p < 0.001), snacks/cakes (p = 0.008), pasta (p = 0.034), and fruit (p = 0.046), and the reduction remained at follow-up for fast food (p = 0.021), when also symptoms were reduced for vegetables/legumes (p = 0.002) and potatoes (p = 0.046). In the low FODMAP group, the proportion of participants with symptoms decreased for onion week 4 and coffee/tea at follow-up (both p = 0.046). Trigger symptoms were associated with higher intake and/or impaired psychological well-being.

Conclusion

The proportion of participants with food-triggered symptoms was reduced for six food groups during/after the SSRD intervention and for two food groups during/after low FODMAP.

Keywords

Dietary intervention food triggers irritable bowel syndrome low FODMAP diet starch- and sucrose-reduced diet (SSRD)

Introduction

Irritable bowel syndrome (IBS) is a disorder of gut–brain interaction (DGBI) with a prevalence of 4.1% according to the Rome IV criteria (Lacy et al., 2016; Sperber et al., 2021). The entity is a multifactorial, chronic disorder of heterogeneous etiopathogenesis, pathophysiology, and clinical phenotype (Drossman, 2016), often associated with impaired psychological well-being (Bellini et al., 2014). Patients often experience aggravated gastrointestinal (GI) symptoms in relation to food intake (Hayes and Fraher, 2014). Therefore, dietary treatment is the first treatment of choice (Algera et al., 2019; Mitchell et al., 2019). The most established diets are the National Institute for Health and Care Excellence (NICE) guidelines and a diet low in fermentable oligo-, di-, monosaccharides, and polyols (FODMAP) (Gibson and Shepherd, 2010; McKenzie et al., 2012). Since IBS patients are predisposed to reduced activity of the sucrase-isomaltase (SI) enzyme (Henström et al., 2018), a starch- and sucrose-reduced diet (SSRD) with reduced intake of snacks, soda, cereals, pasta, rice, some starch-rich vegetables and fruits, and processed and ultra-processed food has been tested in IBS (www.csidcares.org; Danialifar et al., 2024; Nilholm et al., 2019a, 2019b; Roth et al., 2024).

The effect on symptoms was equivalent between low FODMAP and SSRD (Cuffe et al., 2025; Roth et al., 2024). Although both diets reduce carbohydrate intake, there are some differences between the diets. SSRD emphasizes the reduction of sugary products, and processed and ultra-processed food (Roth et al., 2024), in contrast to low FODMAP (Gibson and Shepherd, 2010; McKenzie et al., 2012). SSRD rendered more pronounced reductions of fructan and galacto-oligosaccharides (GOS) than low FODMAP, with a higher nutrient density (Al-Shiblawi et al., 2025). A modified, simpler low FODMAP, reducing only fructan and GOS, has been shown to be as efficient and easier to adhere to than the regular low FODMAP (Singh et al., 2025), which also may lead to increased risk of insufficient nutrient and fiber intake (Al-Shiblawi et al., 2025; Staudacher et al., 2020). The supposed mechanisms behind symptom alleviation are that food containing high amount of FODMAPs and malabsorption of disaccharides cause increased intestinal gas production and osmotic load (Gibson and Shepherd, 2010; Staudacher et al., 2017; Treem et al., 1995). However, the food items most important to trigger symptoms are not defined. Since SSRD and low FODMAP both have similarities and differences in food composition but similar effects on symptom relief, it is of great importance to identify the most important food triggers, especially since there is a difference between the diets regarding nutrient density and metabolic effects (Al-Shiblawi et al., 2025; Roth et al., 2025). Furthermore, previous studies have shown a close association between weight/body mass index (BMI) reduction, mental well-being, and symptom relief (Roth and Ohlsson, 2025). Therefore, we wanted to examine not only the overall symptom reduction but also the food items of interest to trigger symptoms, along with weight and psychological well-being.

The aim of the present study was to evaluate the number/proportion of participants with food-triggered symptoms in the two groups before, during, and after the dietary intervention, and which food items in each dietary group that triggered the symptoms.

Materials and methods

Patients

The inclusion criteria of this study were a diagnosis of IBS according to the ROME IV criteria (Lacy et al., 2016), age between 18 and 70 years, and irritable bowel syndrome-severity scoring system (IBS-SSS) score ≥ 175, without suffering from any other severe disease or already following a diet (Supplemental Figure 1). A comprehensive description of the recruitment process was previously published (Roth and Ohlsson, 2024a). In summary, patients were recruited from the County of Region Skane if they had received any of the diagnoses K58.1 (diarrhea-predominated IBS; IBS-D), K58.2 (constipation-predominated IBS; IBS-C), K58.3 (mixed IBS; IBS-M), and K58.8 (other and unspecified IBS; IBS-U) during 2019–2022. A total of 744 patients were informed about the study by letter and phone call. Furthermore, 203 primary healthcare centers in the county were informed about the study, and information leaflets were sent to them to distribute in waiting rooms. Several lectures were held for healthcare professionals. To further enhance recruitment, a professional recruitment agency (Trialy, Gothenburg, Sweden) used social media platforms to recruit patients with an IBS diagnosis. In total, 300 eligible patients were found, of whom 214 were randomized through block randomization to either the SSRD or low FODMAP dietary group (BR). After the initial screening, 155 participants (72.4% of randomized cases) proceeded with the dietary intervention. Exclusions occurred due to failure to attend the first visit or not meeting the inclusion or exclusion criteria (Supplemental Figure 1) (BO). Participants recruited via social media had an inclusion rate of 42.7%, whereas participants identified through medical records had an inclusion rate of 6.5%. Seven participants who were included had an IBS-SSS slightly below 175, but were still included due to a clear diagnosis of IBS.

Study design

The study was an open randomized, non-inferiority trial, with two parallel groups conducted from March 2022 until February 2024, at the Department of Internal Medicine, Skåne University Hospital in Malmö, Sweden (Roth et al., 2024). Following a 10-day run-in period (baseline), participants were randomized to a dietary intervention with either SSRD or low FODMAP for 4 weeks. Following the intervention completion, the participants were given information about the diet they had not been randomized to, which they were free to try without obligations. However, participants in the low FODMAP group had to reintroduce FODMAP-containing food according to clinical routines, between the intervention and the follow-up at 6 months (Staudacher et al., 2020, 2022). At baseline, week 4, and month 6, the participants had to complete the study questionnaire, food diary (www.livsmedelsverket.se Swedish Food Agency, , ), ROME IV questionnaire (Palsson et al., 2016), IBS-SSS (Francis et al., 1997), and visual analog scale for irritable bowel syndrome (VAS-IBS) (Bengtsson et al., 2007). Further, the participants underwent physical examinations and anthropometric measurements of weight, height, and waist circumference at each time point. All participants were informed to continue with their regular energy intake, degree of physical activity, medications, and probiotics. The participants could reach the investigators by phone or email whenever they wanted during the study.

Dietary advice

The participants received verbal and written information about their randomized diet (BO). The SSRD group focused on a diet with reduced starch and sucrose intake, avoiding all sucrose containing and processed food, with unrestricted intake of certain fruits, vegetables, fish, meat, egg, and dairy products. Participants were encouraged to buy raw food and make their own cooking. Participants received a list of fruits and vegetables with less starch content (Supplemental Tables S1 and S2). These advices were modified from the dietary guidelines developed for patients with CSID (www.csidcares.org; Danialifar et al., 2024) and have previously been described in detail (Nilholm et al., 2019a).

Briefly, participants were instructed to avoid all sucrose containing foods. Nuts and seeds were recommended as replacements for sugary snacks. One serving per day of whole-grain bread or oatmeal porridge was allowed. Instead of processed breakfast cereals, whole grains were recommended. Fiber-rich alternatives to rice or pasta were recommended. For participants who did not tolerate fiber, smaller amounts of regular processed rice and pasta were allowed. Proteins such as beef, lamb, pork, turkey, chicken, fish, and egg were allowed without restriction. However, processed meat, such as bacon, sausage, and ham, should be avoided if they contain starch or sugar. Unsweetened dairy products were allowed, but plant-based alternatives like soy milk or oat milk were not. Fats such as butter and oil were allowed. The intake of salt, pepper, and fresh herbs was unrestricted.

Participants were encouraged to chew food thoroughly and to increase their intakes of fat and/or protein to enhance salivary amylase breakdown of starch and to slow the GI transit time.

The low FODMAP group focused on a diet with a reduced intake of fructans (e.g. wheat, onion, and garlic), GOS (e.g. pulses), lactose (e.g. milk), fructose more than glucose (e.g. honey), and polyols (e.g. apples and pears). The greatest differences between the two diets are that SSRD aims to reduce starch, sucrose, and added sugar intake but allows intake of fructose, lactose, and sweeteners (Nilholm et al., 2019a), whereas low FODMAP is less restrictive regarding starch and sucrose (Gibson and Shepherd, 2010; Staudacher et al., 2022).

Questionnaires

A study questionnaire regarding sociodemographic factors, lifestyle habits, pregnancy and childbirth, medical history, drug treatments, and family history was completed. Any side effects during the study were registered. A platform called Riksmaten Flex, 2021 of the Swedish Food Agency was used to register food intake over 3 days (Wednesday–Friday) at baseline, week 4, and month 6 (www.livsmedelsverket.se Swedish Food Agency). Those who could not manage to complete the questionnaire digitally could complete the food diary manually in the forms included in the study questionnaire.

The digital platform system did not give any possibility to register symptoms. Thus, all participants were encouraged to register manually in the included empty forms of the study questionnaire when they experienced any GI symptoms in relation to food intake. They had to register the type and amount of food intake, the GI symptoms provoked, and the time point for debut of symptoms, as well as the duration of symptoms.

Questions Nos 40–48 in the Swedish version of the Rome IV questionnaire were used to diagnose IBS (Palsson et al., 2016). IBS-SSS estimates abdominal pain, abdominal distension, satisfaction with bowel habits, and the impact of bowel habits on daily life using a visual analog scale (VAS) ranging from absent (0 mm) to very severe (100 mm), and the number of days with abdominal pain in the last 10 days. Maximal score is 500 (Francis et al., 1997). VAS-IBS was used to estimate abdominal pain, diarrhea, constipation, bloating and flatulence, vomiting and nausea, intestinal symptoms’ influence on daily life, and psychological well-being on scales ranging from absent (0 mm) to very severe (100 mm) symptoms (Bengtsson et al., 2007, 2013).

Categorization

The number of participants with any food-related symptoms during the 3-day food registration was recorded. Thereafter, the number of participants who reported GI symptoms in relation to food at baseline, week 4, and month 6 was recorded according to various food items ingested before the trigger event. These items were selected due to most often being registered to induce symptoms and of greatest interest to change in the dietary intervention. The items were vegetables/legumes, potatoes, onions, fruits, cereals, rice, pasta, dairy products, eggs, meat, fish, fast food, snacks/cakes, and coffee/tea. If a meal that was composed of several food items had triggered symptoms, all items from the meal were recorded. Thus, one triggering event could lead to the registration of several food items leading to this event. To match the food intake with food items that had triggered symptoms, data from Riksmaten Flex 2021 is given as the median intake in grams per day of each food item (Swedish Food Agency). Fast food represents the sum of hamburger and pizza intake; dairy products represent the sum of sour milk, milk, cream, and hard cheese intake; snacks represent the sum of candies and chips intake; and coffee/tea intake was summarized into one category. The specific symptoms registered by the participants were abdominal pain, bloating, flatulence, diarrhea, nausea, and reflux.

Statistical analysis

The statistical analyses were performed using IBM SPSS, version 30. Power calculation is described previously (Roth et al., 2024). The Kolmogorov-Smirnov test was used to assess the normality of data. The data of anthropometry, symptoms, and food intakes were not normally distributed and presented as medians (interquartile ranges), whereas energy intake was normally distributed and presented as mean ± standard deviation (SD). The first research question was to examine whether the number/proportion of participants with symptoms provoked by certain food items differed between baseline (reference value) and after the 4-week dietary intervention. The second research question was to examine whether the number/proportion of participants with symptoms provoked by certain food items differed between baseline (reference value) and after the 6-month follow-up. The Wilcoxon signed-rank test and Mann-Whitney U-test were used to calculate data within and between groups when data was not normally distributed, and the paired T-test and independent-samples T-test were used for normally distributed data. Fisher’s exact test was used for dichotomous data at baseline. For changes in the proportion of participants with or without triggered symptoms over time, the paired-samples proportions test according to McNemar was used. Logistic regression was used on categorized variables to calculate the association between the intake of the food item (independent variable) and triggering symptoms due to that food (dependent variable). Crude odds ratio (OR) and 95% confidence interval (CI) were calculated, as well as adjusted OR after adjustments for weight and psychological well-being. All calculations were performed by protocol, and missing values were excluded from analyses. p ≤ 0.05 was considered statistically significant.

Results

Basal characteristics

In total, 155 participants (130 women, 84%) were included in the study. Twenty-six participants (16.8%) had IBS-C, 44 participants (28.4%) had IBS-D, 54 participants (34.8%) had IBS-M, seven participants (4.5%) had IBS-U, and 24 participants (15.5%) had functional bowel disorder (FBD) with abdominal pain weekly but with less association (<30%) with altered bowel habits. Seventy-seven participants were randomized to SSRD, and 78 were randomized to low FODMAP.

There was no difference between the groups regarding sex distribution, age, weight, BMI, sociodemographic factors, or lifestyle habits (Table 1). The weight decreased from 71.5 (63.6–82.8) kg to 70.0 (63.2–81.0) kg in the SSRD group after 4 weeks (p < 0.001) and from 68.6 (63.0–83.4) kg to 67.8 (62.5–82.7) kg in the low FODMAP group at week 4 (p < 0.001). There was no difference at baseline between the two groups in specific GI symptoms, psychological well-being, or total GI symptoms, and the symptom improvements after 4 weeks and 6 months were equal. Although symptoms slightly increased after 6 months, the symptoms were still significantly decreased compared to baseline, except for constipation in the SSRD group (Figure 1 and Supplemental Table S3).

Figure 1.

Total IBS-SSS before and after dietary intervention. Participants were randomized to a starch- and sucrose-reduced diet (SSRD; N = 77) or low content of fermentable oligo-, di, and monosaccharides and polyols (FODMAP; N = 78). Box plots of total scores of irritable bowel syndrome-severity scoring system (IBS-SSS) (Francis et al., 1997), showing vaules from baseline, week 4 and month 6 from each diet group. There were values for 72 participants at week 4 and 53 at month 6 in the SSRD group, and 71 at week 4 and 49 at month 6 in the low FODMAP group. The Wilcoxon signed-rank test was used for comparison from baseline at 4 weeks and 6 months. p < 0.001 for all.

Table 1.

Basal characteristics.

Parameters	SSRDN = 77	Low FODMAPN = 78	p-value
Age (year)	41.0 (29.5–53.0)	43.0 (33.8–56.0)	0.227
Gender (male/female) (n, %)	15 (19.5)/62 (80.5)	10 (12.8)/68 (87.2)	0.283
Weight (kg)	71.5 (63.6–82.8)	68.6 (63.0–83.4)	0.389
BMI (kg/m²)	25.1 (22.6–28.4)	24.7 (22.1–27.6)	0.479
Disease duration (year)	16 (7–27)	20 (10–30)	0.261
Education (n, %)			0.585
Primary school	5 (6.5)	2 (2.6)
Secondary school	10 (13.0)	13 (16.7)
Education after secondary school	20 (26.0)	17 (21.8)
Examination at university	42 (54.5)	46 (59.0)
Occupation (n, %)			0.963
Working full-time	48 (62.3)	46 (59.0)
Working 99%–51%	6 (7.8)	9 (11.5)
Working 50%	1 (1.3)	1 (1.3)
Studying	10 (13.0)	10 (12.8)
Sick leave	3 (3.9)	2 (2.6)
Unemployment	3 (3.9)	2 (2.6)
Retirement	6 (7.8)	8 (10.3)
Marital status (n, %)			0.837
Living alone	16 (20.8)	14 (17.9)
Living together	55 (71.4)	56 (71.8)
Other	6 (7.8)	8 (10.3)
Smoking (n, %)			0.086
Never	42 (54.5)	43 (55.1)
Former	26 (33.8)	28 (35.9)
Present un regular	2 (2.6)	6 (7.7)
Present regular	7 (9.1)	1 (1.3)
Alcohol intake for 1 week (standard glass) (n, %) Missing		1	1.000
< 1	34 (44.2)	33 (42.3)
1–4	28 (36.4)	29 (37.2)
5–9	13 (16.9)	13 (16.7)
10–14	1 (1.3)	2 (2.6)
≥.6)	1 (1.3)	0
Physical activity for 1 week (n, %) Missing		1	0.475
No time	10 (13.0)	8 (10.4)
<30 min	11 (14.3)	14 (18.2)
30–60 min	16 (20.8)	14 (18.2
60–90 min	8 (10.4)	16 (20.8)
90–120 min	8 (10.4)	8 (10.4)
>120 min	24 (31.2)	17 (22.1)

SSRD: starch-and sucrose-reduced diet; Low FODMAP: low content of fermentable oligo-, di-, and monosaccharides and polyols; n: number; BMI: body mass index. Physical activity refers to activity that leads to shortness of breath. Values are presented as numbers and percentages or median and interquartile values. Fisher’s exact test and Mann-Whitney U test. p ≤ 0.05 was considered statistically significant.

The most common comorbidities were eczema (n = 19, 12.3%), allergies (n = 17, 11.0%), and reflux/hiatus hernia (n = 18, 11.6%). The most used medications were paracetamol (n = 54, 34.8%), proton pump inhibitors (n = 48, 31.0%), allergy medications (n = 24, 15.5%), and hormonal contraceptives (n = 24, 15.5%). Dietary supplements of vitamins and minerals were used by 55 participants (35.5%). Probiotics were ingested by 15 participants (9.7%).

Seventy-eight participants (50.3%) were already following a restricted diet; 63 (40.6%) were on a lactose-free diet, 19 (12.3%) on a gluten-reduced diet, and 14 (9%) were vegetarians.

Food intake

There was no difference in food intake between the two intervention groups at baseline. After 4 weeks of SSRD, there was an increased intake of vegetables (52 (15–91) g vs. 146 (76–231) g, p < 0.001) and dairy products (35 (10–86) g vs. 66 (27–154) g, p = 0.002). The intakes of potatoes, bread, fast food, and snacks were significantly decreased after 4 weeks (p < 0.001 for all), with no changes in food intake at follow-up compared to baseline. In the low FODMAP group, no food intake was increased after 4 weeks. The intake of fast food and coffee/tea was decreased after 4 weeks (p < 0.001 for both), and intake of fast food was still slightly decreased at follow-up (Table 2).

Table 2.

Intake of food items before, during, and after dietary intervention in participants with IBS.

Food groups	SSRD N = 77	p-value	Low FODMAP N = 78	p-value	p-value*
Energy (kcal)
Baseline	1813 ± 535		1783 ± 510		0.718
Week 4	1534 ± 478	<0.001	1667 ± 500	0.036	0.115
Month 6	1792 ± 600	0.535	1676 ± 739	0.069	0.409
Vegetables (g)
Baseline	52 (15–91)		67 (32–109)		0.094
Week 4	146 (76–231)	<0.001	70 (31–148)	0.047
Month 6	49 (8–109)	0.565	54 (24–123)	0.706
Legumes (g)
Baseline	0 (0–0)		0 (0–10)		0.312
Week 4	0 (0–0)	0.151	0 (0–4)	0.975	0.182
Month 6	0 (0–0)	0.615	0 (0–0)	0.083	0.347
Potatoes (g)
Baseline	30 (0–72)		27 (0–70)		0.974
Week 4	0 (0–0)	<0.001	60 (0–102)	0.072
Month 6	30 (0–70)	0.120	24 (0–77)	0.403
Fruit (g)
Baseline	57 (0–138)		75 (17–130)		0.503
Week 4	31 (0–111)	0.090	58 (0–119)	0.081
Month 6	60 (0–132)	0.986	40 (0–104)	0.062
Bread (g)
Baseline	37 (13–78)		28 (0–59)		0.122
Week 4	10 (0–40)	<0.001	19 (0–51)	0.250
Month 6	40 (5–78)	0.219	27 (0–57)	0.291
Pasta (g)
Baseline	0 (0–38)		0 (0–38)		0.880
Week 4	0 (0–13)	0.176	0 (0–34)	0.231
Month 6	0 (0–3)	0.100	0 (0–38)	0.195
Dairy products (g)
Baseline	35 (10–86)		41 (11–108)		0.406
Week 4	66 (27–154)	0.002	60 (23–112)	0.072
Month 6	48 (16–96)	0.718	60 (17–121)	0.396
Meat (g)
Baseline	0 (0–20)		0 (0–16)		0.816
Week 4	0 (0–32)	0.135	0 (0–28)	0.898
Month 6	0 (0–23)	0.604	0 (0–8)	0.817
Fast food (g)
Baseline	82 (0–153)		38 (0–132)		0.187
Week 4	0 (0–0)	<0.001	0 (0–39)	<0.001
Month 6	53 (0–138)	0.519	43 (0–98)	0.046
Snacks (g)
Baseline	6 (0–32)		6 (0–32)		0.612
Week 4	0 (0–0)	<0.001	4 (0–23)	0.840
Month 6	2 (0–18)	0.614	0 (0–17)	0.266
Coffee/tea (g)
Baseline	333 (142–625)		417 (217–627)		0.259
Week 4	424 (71–662)	0.466	292 (210–500)	<0.001
Month 6	367 (112–698)	0.531	350 (208–583)	0.135

IBS: irritable bowel syndrome; SSRD: starch-and sucrose-reduced diet with nine missing values at week 4 and 31 at month 6; Low FODMAP: low content of fermentable oligo-, di-, and monosaccharides and polyols with two missing values at baseline, 10 at week 4, and 31 at month 6. Food intake was registered for 3 days (Wednesday to Friday) at baseline, week 4, and month 6 at a digital platform called Riksmaten Flex 2021 of the Swedish Food Agency (www.livsmedelsverket.se). Values are given as median and interquartile range or mean ± standard deviation (SD). Calculations were performed according to the protocol. Wilcoxon signed-rank test for comparisons within the groups and Mann-Whitney U test* for comparison between baseline of the two groups. Paired T-test and independent-samples T-test* were used for normally distributed data. p ≤ 0.05 was considered statistically significant.

Food-triggered symptom occasions

Half of the participants registered food-triggered symptoms upon food intake. The proportion of participants with any triggered symptoms was lowered non-significantly over time (Table 3). The most often evoked symptoms were abdominal pain at all three times, followed by bloating, diarrhea, and flatulence. Only sporadic cases of nausea and reflux were observed. There was no difference in the number and type of symptoms between groups at any time points (Table 4).

Table 3.

Number and proportion of participants with food-triggered symptoms in relation to specific food groups before, during, and after dietary intervention.

Triggering factors	SSRDN = 77	p-value	Low FODMAPN = 78	p-value	p-value*
Symptoms triggered by food
Baseline (n = 155)	40 (51.9)		30 (38.5)		0.145
Week 4 (n = 144)	34 (47.2)	0.732	24 (33.3)	0.443
Month 6 (n = 102)	17 (32.1)	0.083	13 (26.5)	0.197
Vegetables/legumes
Baseline	18 (23.4)		11 (14.1)		0.154
Week 4	16 (22.2)	0.593	11 (15.3)	0.796
Month 6	5 (9.4)	0.002	4 (8.2)	0.206
Potatoes
Baseline	7 (9.1)		7 (9.0)		1.000
Week 4	3 (4.2)	0.206	4 (5.6)	0.705
Month 6	2 (3.8)	0.046	4 (8.2)	0.655
Onion
Baseline	5 (6.5)		5 (6.4)		0.619
Week 4	8 (11.1)	0.317	0 (0)	0.046
Month 6	1 (1.9)	0.180	2 (4.1)	0.655
Fruit
Baseline	7 (9.1)		5 (6.4)		0.374
Week 4	3 (4.2)	0.046	2 (2.8)	0.317
Month 6	3 (5.7)	0.705	1 (2.0)	0.317
Cereals
Baseline	19 (24.7)		17 (21.8)		0.707
Week 4	12 (16.7)	0.180	11 (15.3)	0.297
Month 6	9 (17.0)	0.371	5 (10.2)	0.071
Pasta
Baseline	9 (11.7)		2 (2.6)		0.032
Week 4	2 (2.8)	0.034	3 (4.2)	0.655
Month 6	3 (5.7)	0.480	1 (2.0)	1.000
Dairy products
Baseline	11 (14.3)		7 (9.0)		0.328
Week 4	9 (12.5)	0.782	10 (13.9)	0.439
Month 6	6 (11.3)	1.000	1 (2.0)	0.317
Meat
Baseline	6 (7.8)		7 (9.0)		1.000
Week 4	7 (9.7)	0.705	6 (8.3)	0.763
Month 6	4 (7.5)	0.705	4 (8.2)	0.527
Fast food
Baseline	14 (18.2)		7 (9.0)		0.106
Week 4	1 (1.4)	<0.001	5 (6.9)	0.763
Month 6	3 (5.7)	0.021	2 (4.1)	0.257
Snacks/cakes
Baseline	15 (19.5)		11 (14.1)		0.398
Week 4	4 (5.6)	0.008	9 (12.5)	0.782
Month 6	3 (5.7)	0.052	9 (18.4)	0.206
Coffee/tea
Baseline	10 (13.0)		6 (7.7)		0.304
Week 4	5 (6.9)	0.132	3.(4.2)	0.317
Month 6	3 (5.7)	0.132	0 (0)	0.046

SSRD: starch-and sucrose-reduced diet; Low FODMAP: low content of fermentable oligo-, di-, and monosaccharides and polyols. Number (percentages) of participants who registered any symptoms triggered by food or symptoms specific to any food group during the three-day diary book registration. Calculations were performed according to the protocol. Paired-samples proportions test for comparison between baseline and week 4 and month 6. * Fisher’s exact test for comparison between groups at baseline. p ≤ 0.05 was considered statistically significant.

Table 4.

The prevalence of various symptoms triggered by food intake.

	SSRD	Low FODMAP	p-value
Baseline	N = 77	N = 78
Abdominal pain	28 (36.4)	23 (29.5)	0.396
Bloating	15 (19.5)	15 (19.2)	1.00
Flatulence	11 (14.3)	5 (6.4)	0.121
Diarrhea	7 (9.1)	6 (7.7)	0.780
Nausea	5 (6.5)	2 (2.6)	0.276
Reflux	1 (1.3)	1 (1.3)	1.00
Week 4	N = 72	N = 72
Abdominal pain	19 (26.4)	14 (19.4)	0.428
Bloating	9 (12.5)	7 (9.7)	0.792
Flatulence	6 (8.3)	3 (4.2)	0.494
Diarrhea	11 (15.3)	6 (8.3)	0.302
Nausea	1 (1.4)	2 (2.8)	1.00
Reflux	1 (1.4)	3 (4.2)	0.620
Month 6	N = 53	N = 49
Abdominal pain	12 (22.6)	6 (12.2)	0.201
Bloating	5 (9.4)	6 (12.2)	0.754
Flatulence	1 (1.9)	2 (4.1)	0.607
Diarrhea	6 (11.3)	4 (8.2)	0.491
Nausea	0	3 (6.1)	0.228
Reflux	1 (1.9)	1 (2.0)	1.00

SSRD: starch-and sucrose-reduced diet; Low FODMAP: low content of fermentable oligo-, di-, and monosaccharides and polyols. Number (percentages) of participants who experienced any symptoms triggered by specific food items. Calculations were performed according to the protocol. Fisher’s exact test. p ≤ 0.05 was considered statistically significant.

Regarding specific food items that triggered symptoms at baseline, pasta triggered symptoms in more participants in the SSRD group than in the low FODMAP group (p = 0.032). In SSRD, the proportion of participants with symptoms triggered by fast food (p < 0.001), snacks/cakes (p = 0.008), pasta (p = 0.034), and fruit (p = 0.046) decreased after 4 weeks, which remained at 6 months for fast food (p = 0.021) and tended to be significantly reduced for snack/cakes (p = 0.052). After 6 months, the proportion of participants with triggered symptoms was reduced also for vegetables/legumes (p = 0.002) and potatoes (p = 0.046). In the low FODMAP group, the proportion of participants with symptoms triggered by food was the same at 4 weeks as at baseline, except for onion (p = 0.046). Coffee and tea were the only foods that triggered symptoms in fewer participants at 6 months (p = 0.046) (Table 3).

When the association between specific food intake and trigger symptoms at baseline were adjusted for weight and psychological well-being, there was an association between trigger symptoms by vegetables/legumes and highest quartile of impaired psychological well-being (OR: 5.10; 95% CI: 1.45–17.88; p = 0.011), trigger symptoms by pasta and highest quartile of pasta intake (OR: 27.88; 95% CI: 3.17–245.00; p = 0.003), and trigger symptoms by dairy products and highest quartile of dairy product intake (OR: 4.74; 95% CI: 1.08–20.68; p = 0.039) and impaired psychological well-being (OR: 6.74; 95% CI: 1.22–37.25; p = 0.029). When calculations were stratified by diets, associations in the SSRD group were seen between trigger symptoms by pasta and highest pasta intake (OR: 29.11; 95% CI: 3.02–280.77; p = 0.004) and trigger symptoms by vegetables/legumes and highest intake of vegetables (OR: 5.29; 95% CI: 1.02–27.49); p = 0.047).

The only association found at 4 weeks was an association between trigger symptoms by snacks/cakes and the highest intake of snacks (OR: 3.90; 95% CI: 1.03–14.76; p = 0.045).

Egg (n = 3), fish (n = 3), and rice (n = 1) were triggering GI symptoms only sporadically and were thus not included in calculations.

Vegetables and legumes triggering symptoms

In both the SSRD and low FODMAP diets, patients are strongly encouraged to avoid several vegetables and legumes. Since the total intake of vegetables was increased in the SSRD group (Table 2), this warranted us to further examine the type of vegetables ingested. Only small amounts of legumes were ingested, but they were registered since they often were ingested together with vegetables (Table 2). Most of the vegetables/legumes that triggered GI symptoms were recommended for each diet, but still evoked symptoms. Among these can be mentioned asparagus, cabbage, cauliflower, and broccoli in the SSRD group and broccoli and cabbage in the low FODMAP group. Salad, tomatoes, and cucumber were often mentioned in the diary as triggering, but these food items are allowed by both diets. Some vegetables/legumes triggering symptoms were advised to avoid, but were still ingested, for example, beans and carrots in SSRD and avocado, cauliflower, and mushrooms in low FODMAP (Tables 5 and 6).

Table 5.

Vegetables and legumes that triggered symptoms in the SSRD group.

Participants	Baseline	Week 4	Month 6
1	Beetroot, salad, pepper, and tomato	Tomato
2	Salad, corn, and coleslaw
3	Chickpeas and pepper		Carrot, cucumber, and mushrooms
4	Vegetarian meat and sausage
5		Cauliflower and green beans
6		Beans and cucumber
7	Beans	Green beans, cauliflower, asparagus, and squash
8		Tomato, broccoli, and cauliflower
9		Cucumber and tomato
10		Cauliflower, pepper, and cabbage
11	Carrots, cauliflower, and pepper	Salad, tomato, cucumber, and olives	Kale
12	Raw food, cabbage, and white beans	Cabbage and pepper	Wok vegetables
13	Tomato and pepper	Cabbage
14	Cabbage	Tomato and pepper
15		Spinach
16	Vegetarian goulash
17	Salad	Salad and broccoli
18	Salad, cucumber, carrot, and tomato	Spinach
19	Salad, carrot, and green peas	Broccoli and mushrooms
20	Salad
21	Broccoli, pizza salad, avocado, parsnip, carrot, and cucumber	Tomato, coleslaw, and broccoli	Red cabbage
22	Cauliflower and avocado
23	Vegetables and vegetarian steaks
24	Vegetarian hamburger	Vegan buffet
25	Vegetables and salad

SSRD: starch-and sucrose-reduced diet. Twenty-five participants registered any symptom occasions triggered by specific food items.

Table 6.

Vegetables and legumes that triggered symptoms in the low FODMAP group.

Participants	Baseline	Week 4	Month 6
1		Lenses
2		Salad and mushrooms
3			Broccoli and salad
4		Avocado, aubergine, and tomato
5		Broccoli and tomato	Cooked vegetables
6			Cabbage, cauliflower, broccoli, and salad
7	Vegetables, salad, avocado, tomato, olives, cabbage, and broccoli	Salad	Spinach
8	Carrot
9		Broccoli
10	Spinach	Mushrooms
11	Chickpeas
12	Chickpeas
13	Salad and cucumber	Wok vegetables
14	Pepper, cucumber, tomato, and corn
15		Vegetable soup
16	Vegetables and lenses
17	Salad
18	Cucumber and vegetables
19		Vegetarian hamburger, carrot, and sprouts
20	Tomato and cabbage
21		Aubergine and tomato

Low FODMAP: low content of fermentable oligo-, di-, and monosaccharides and polyols. Twenty-one participants registered any symptom occasions triggered by specific food items.

GI symptom burden during the study

There was no difference in total IBS-SSS at baseline (287 (235–349) and 310 (238–354), respectively, p = 0.705) and 6 months (260 (161–328) and 210 (140–304), respectively, p = 0.248) between those with or without food-triggered symptoms. In contrast, at week 4, those with symptoms triggered by food had the highest total IBS-SSS (152 (79–250) and 106 (56–170), respectively, p = 0.031). The difference was due to the SSRD group, where those with food-triggered symptoms had the highest IBS-SSS (182 (81–278) and 112 (60–165), respectively, p = 0.048), with equal symptoms in the low FODMAP group between those with and without triggered symptoms (p = 0.305). Participants in the SSRD group with food-triggered symptoms at week 4 registered worse psychological well-being (28 (12–58) and 16 (3–24), respectively, p = 0.006) and tended to have significantly more abdominal pain (20 (10–36) and 13 (0–28), respectively, p = 0.078) and diarrhea (29 (84–65) and 14 (2–27), respectively, p = 0.052) compared to those who did not experience triggering symptoms.

Discussion

The proportion of participants with food-triggered symptoms was lowered for foods reduced during the SSRD intervention. Thus, fast food, pasta, potatoes, snacks/cakes, and fruit and vegetables high in starch rendered fewer symptoms during and after the intervention. The reduced intakes of these specific food items, along with increased intake of vegetables and dairy products, in both the current and a previous study (Nilholm et al., 2019A), suggest a reliable food change after given advice. Increased intake of vegetables with low starch content and dairy products did not increase triggering symptoms. Low FODMAP affected the proportion of participants with symptoms triggered by onion and coffee/tea.

The difference between SSRD and low FODMAP in the proportions of triggered symptoms following specific food items may depend on the fact that whole groups of food items are excluded in SSRD (www.csidcares.org, Danialifar et al., 2024), such as snacks, whereas low FODMAP more often recommend reduction of individual food items, for example, onion, and not whole groups (Gibson and Shepherd, 2010). Recent research has suggested that the reduction of fructan may be the most important factor to reduce trigger symptoms (Van den Houte et al., 2024), and a less restrictive variant of low FODMAP, only decreasing fructan and GOS, was as efficient as ordinary low FODMAP (Singh et al., 2025). From the current RCT, we have recently published that the intake of fructan and GOS was reduced to a greater extent by SSRD than by low FODMAP, with a correlation between decreased fructan intake and reduced bloating and flatulence (Al-Shiblawi et al., 2025). Thus, the high efficiency and tolerability of SSRD (Roth et al., 2024) may be explained by the reduction of starch and sucrose, but also by the reduction of important FODMAPs (Al-Shiblawi et al., 2025; Singh et al., 2025). Fewer participants with triggering symptoms at follow-up for vegetables and potatoes may depend on the ingestion of vegetables with less starch and continued lowered potato intake. Furthermore, the improved psychological well-being registered after the intervention may also affect the prevalence of trigger symptoms to vegetables/legumes and potatoes. An alteration of food habits may influence the symptom development and experience through several molecular mechanisms, for example, gut microbiota composition, concentration of short-chain fatty acids, and metabolomics, and is not as simple as just depending on the chemicals and texture of food (Cuomo et al., 2014; Ju et al., 2024).

Interestingly, several different diets have rather equal efficiency on IBS symptoms, such as low FODMAP (Mitchell et al., 2019), Mediterranean diet (Staudacher et al., 2024), low-carbohydrate diet with high fat and protein diet content (Nybacka et al., 2024), and SSRD (Roth et al., 2024). Possibly the core with reduced amounts of sugar and ultra-processed food is the most important, and the rest of the changes is of minor importance (Buscail et al., 2017; Khayyatzadeh et al., 2016; Wu et al., 2024). In a large French population cohort, IBS was associated with a Western diet, including fat and sugary products, sweetened beverages, and soda, and negatively associated with fruits, vegetables, dairy products, eggs, and fish (Buscail et al., 2017). In accordance, high consumption of fast food and ultra-processed food was associated with a higher risk to have and developing IBS (Khayyatzadeh et al., 2016; Wu et al., 2024). Besides IBS, ultra-processed food containing high amounts of starch and sucrose is also associated with several other globally escalating chronic diseases (Monteiro et al., 2025).

The healthier nutrient profile with increased intake of micronutrients in the SSRD group than in the low FODMAP group may depend on the increased intake of vegetables and dairy products in the SSRD (Al-Shiblawi et al., 2025). A similar presence of symptom occasions after low FODMAP, albeit a lower degree of symptoms, raises many questions. First, it might be low compliance, with participants continuing to ingest the same food items. However, dietary registration revealed changes in nutrient intake, suggesting compliance with the diet (Al-Shiblawi et al., 2025; Roth et al., 2024). Second, specific food items are not that important for symptom triggering. Third, the impaired psychological well-being may be important for the experience of symptoms triggered by food. Fourth, weight reduction may alleviate the symptom burden (Roth et al., 2024; Yu et al., 2025) and may explain some of the effect independently of food items.

Since several changes occur simultaneously after dietary interventions, such as changes in food intake and weight loss, it is difficult to trace the most causal factors of symptom relief. Previous studies have shown a closer association of symptom relief with weight/BMI reduction than with dietary changes (Roth and Ohlsson, 2025). In the present study, the regression calculations showed that both higher actual food intake and impaired psychological well-being were associated with trigger symptoms. The participants reported improved psychological well-being in both study groups. Thus, the similar responder rate by different diets may be partly explained by psychological mechanisms. Those in the current study who still experienced symptoms triggered by food had worse psychological well-being, which has been shown to predict a reduced response to dietary intervention (Colomier et al., 2022). The pain sensation is complex, and visceral hypersensitivity, impaired pain modulation, severe dysbiosis, higher energy intake, and impaired quality of life are other factors affecting treatment responses and self-reported food intolerance (Böhn et al., 2013; Colomier et al., 2022; Morris et al., 2016; Stabell et al., 2014). Thus, not only the actual food intake is of importance for self-reported symptoms. Psychological distress and perceived stress are closely related to reported food aversion reactions in IBS (Nasiri-Dehsorkhi et al., 2023).

As many as 12.3% of participants had reduced gluten intake, and 40.6% had excluded lactose (Roth et al., 2024). Nevertheless, the importance of non-celiac gluten sensitivity (NCGS) and lactose intolerance for IBS has not been confirmed (Molina-Infante et al., 2015; Pop et al., 2024). In the present study, we could show that impaired psychological well-being was associated with the prevalence of trigger symptoms by dairy products. The assumed lactose intolerance may lead to lower intake of vitamin D-containing food, rendering vitamin D deficiency (Nilholm et al., 2019a; Roth and Ohlsson, 2024b). Several items that evoked GI symptoms are well-known to evoke symptoms in all subjects, for example, cauliflower and cabbage, independently of IBS or not.

There are several limitations of the study, one being the complex combination of different food items in the same meal, making it difficult to estimate the most important trigger. Furthermore, the time relation between food intake and symptom debut may be difficult to register. Since it was an open RCT, bias from participants and investigators may occur. Participants wrote manually in a paper which food they ate when experiencing symptoms, but they had to mark in a pre-formatted list which food they ingested in the digital platform Riksmaten Flex (www.livsmedelsverket.se). The intake of food was delivered by the Swedish Food Agency on a standardized list. Thus, there was no exact concordance between the two registration forms. For example, the intake of onions and different kinds of fruits and vegetables was not delivered. The current categorization of food groups does not completely include all kinds of food, for example, snacks and fast food.

Conclusions

In conclusion, the proportion of participants with food-triggered symptoms was lowered for foods reduced during the SSRD intervention. Thus, fast food, fruit, pasta, and snacks/cakes induced fewer symptoms after 4 weeks, in addition to reduced symptoms from fast food, potatoes, and vegetables at follow-up. Those in the SSRD group who experienced symptoms in response to a meal after 4 weeks of dietary intervention had higher total GI symptom scores and worse psychological well-being than those without triggering symptoms. Low FODMAP did not affect the proportion of participants with symptoms triggered by food, except for onion and coffee/tea. Both the quantity of food intake and psychological well-being influenced the associations with trigger symptoms. The study supports that the reduction of foods rich in starch and sucrose is important in the treatment of IBS.

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Footnotes

Acknowledgements

The staff at the Clinical Research Unit at Skåne University Hospital are acknowledged for assistance during the recruitment process. Statistician Susann Ullén is acknowledged for statistical advice.

ORCID iD

Bodil Ohlsson

Ethical consideration

This study was performed in accordance with the Declaration of Helsinki and approved by the Swedish Ethical Review Authority (2021-05407-01, date of approval 10/11/2021). The study was registered at ClinicalTrials.gov, NCT05192603, 29/11/2021.

Consent to participate

Informed consent was obtained from all participants involved in the study.

Consent for publication

Not applicable.

Author contributions

BR and BO: conceptualization, methodology, formal analysis, and investigation; BO: software, validation, resources, data curation, writing–original draft preparation, visualization, project administration, and funding acquisition; BR: writing–review and editing.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: Development Foundation of Region Skane (BO); Foundation of Skane University Hospital (BO); and Dir Albert Påhlsson’s Foundation (BO).

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data availability statement

The data presented in this study are available on request from the corresponding author due to ethical reasons.

Supplemental material

Supplemental material for this article is available online.

References

Algera

Colomier

Simrén

(2019) The dietary management of patients with irritable bowel syndrome: A narrative review of the existing and emerging evidence. Nutrients 11: 2162.

Al-Shiblawi

Cullman

Roth

, et al. (2025) A starch- and sucrose-reduced diet leads to a more favorable nutrient profile than low FODMAP in patients with irritable bowel syndrome. A randomized clinical trial. Human Nutrition & Metabolism 42: 200337.

Bellini

Gambaccini

Stasi

, et al. (2014) Irritable bowel syndrome: A disease still searching for pathogenesis, diagnosis and therapy. World Journal of Gastroenterology 20: 8807–8820.

Bengtsson

Ohlsson

Ulander

(2007) Development and psychometric testing of the Visual Analogue Scale for Irritable Bowel Syndrome (VAS-IBS). BMC Gastroenterology 7: 16.

Bengtsson

Persson

Sjölund

, et al. (2013) Further validation of the visual analogue scale for irritable bowel syndrome after use in clinical practice. Gastroenterology Nursing 36: 188–198.

Böhn

Störsrud

Törnblom

, et al. (2013) Self-reported food-related gastrointestinal symptoms in IBS are common and associated with more severe symptoms and reduced quality of life. American Journal of Gastroenterology 108: 634–641. (Choosing Your Foods—CSID Cares) [accessed on 24 October 2024]. Available online: https://www.csidcares.org.

Buscail

Sabate

Bouchoucha

, et al. (2017) Western dietary pattern is associated with irritable bowel syndrome in the French NutriNet cohort. Nutrients 9: 986.

Colomier

Van Oudenhove

, et al. (2022) Predictors of symptom-specific treatment response to dietary interventions in irritable bowel syndrome. Nutrients 14: 97.

Cuffe

Staudacher

Aziz

, et al. (2025) Efficacy of dietary interventions in irritable bowel syndrome: Systematic review and network meta-analysis. The Lancet Gastroenterology & Hepatology 10: 520–536.

10.

Cuomo

Andreozzi

Zito

, et al. (2014) Irritable bowel syndrome and food interaction. World Journal of Gastroenterology 20: 8837–8845.

11.

Danialifar

Chumpitazi

Mehta

, et al. (2024) Genetic and acquired sucrase-isomaltase deficiency: A clinical review. Journal of Pediatric Gastroenterology and Nutrition 78: 774–782.

12.

Drossman

(2016) Functional gastrointestinal disorders: History, pathophysiology, clinical features and Rome IV. Gastroenterology 150(16): 1262–1279.

13.

Francis

Morris

Whorwell

(1997) The irritable bowel severity scoring system: A simple method of monitoring irritable bowel syndrome and its progress. Alimentary Pharmacology & Therapeutics 11: 395–402.

14.

Gibson

Shepherd

(2010) Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach. Journal of Gastroenterology and Hepatology 25: 252–258.

15.

Hayes

Fraher

Quigley

(2014) Irritable bowel syndrome: The role of food in pathogenesis and management. Gastroenterology and Hepatology 10: 164–174.

16.

Henström

Diekmann

Bonfiglio

, et al. (2018) Functional variants in the sucrase-isomaltase gene associate with increased risk of irritable bowel syndrome. Gut 67: 263–270.

17.

Jiang

, et al. (2024) Changes in fecal short-chain fatty acids in IBS patients and effects of different interventions: A systematic review and meta-analysis. Nutrients 16: 1727.

18.

Khayyatzadeh

Esmaillzadeh

Saneei

, et al. (2016) Dietary patterns and prevalence of irritable bowel syndrome in Iranian adults. Neurogastroenterology and Motility 28: 1921–1933.

19.

Lacy

Mearin

Chang

, et al. (2016) Bowel disorders. Gastroenterology 150: 1393–1407.

20.

McKenzie

Alder

Anderson

, et al. (2012) British dietetic association evidence-based guidelines for the dietary management of irritable bowel syndrome in adults. Journal of Human Nutrition and Dietetics 25: 260–274.

21.

Mitchell

Porter

Gibson

, et al. (2019) Review article: Implementation of a diet low in FODMAPs for patients with irritable bowel syndrome-directions for future research. Aliment Pharmacol. Ther 49: 124–139.

22.

Molina-Infante

Santolaria

Sanders

, et al. (2015) Systematic review: Noncoeliac gluten sensitivity. Alimentary Pharmacology & Therapeutics 41: 807–820.

23.

Monteiro

Louzada

Steele-Martinez

, et al. (2025) Ultra-processed foods and human health: The main thesis and the evidence. Lancet 406(10520): 2667–2684.

24.

Morris

Walker

Bruehl

, et al. (2016) Impaired conditioned pain modulation in youth with functional abdominal pain. Pain 157: 2375–2381.

25.

Nasiri-Dehsorkhi

Vaziri

Esmaillzadeh

, et al. (2023) Psychological distress, perceived stress and nocebo effect (multifood adverse reaction) in irritable bowel syndrome patients. Journal of Education and Health Promotion 12: n257.

26.

Nilholm

Larsson

Roth

, et al. (2019a) Irregular dietary habits with a high intake of cereals and sweets are associated with more severe gastrointestinal symptoms in IBS patients. Nutrients 11: 1279.

27.

Nilholm

Roth

Ohlsson

(2019b) A dietary intervention with reduction of starch and sucrose leads to reduced gastrointestinal and extra-intestinal symptoms in IBS patients. Nutrients 11: 1662.

28.

Nybacka

Törnblom

Josefsson

, et al. (2024) A low FODMAP diet plus traditional dietary advice versus a low-carbohydrate diet versus pharmacological treatment in irritable bowel syndrome (CARIBS): A single-centre, single-blind, randomised controlled trial. The Lancet Gastroenterology and Hepatology 9: 507–520.

29.

Palsson

Whitehead

Van Tilburg

MAL

, et al. (2016) Development and validation of the Rome IV diagnostic questionnaire for adults. Gastroenterology 150: 1481–1491.

30.

Pop

Popa

Pop

, et al. (2024) Self-perceived lactose intolerance versus confirmed lactose intolerance in irritable bowel syndrome: A systematic review. Journal of Gastrointestinal and Liver Diseases Sep 9: doi: 10.15403/jgld-5836. Epub ahead of print.

31.

Roth

D´Amato

Ohlsson

(2025) Improved lipid and glycemic profile and vitamin D levels after a dietary intervention with SSRD and low FODMAP in IBS patients. A randomized controlled trial. Nutrition, in press.

32.

Roth

Nseir

Jeppsson

, et al. (2024) A starch- and sucrose-reduced diet has similar efficiency as low FODMAP in IBS – A randomized non-inferiority study. Nutrients 6: 3039.

33.

Roth

Ohlsson

(2024a) Challenges of recruitment processes to a randomized dietary trial in irritable bowel syndrome. F1000Research 13: 323.

34.

Roth

Ohlsson

(2024b) Overweight and vitamin D deficiency are common in patients with irritable bowel syndrome – A cross-sectional study. BMC Gastroenterology 24: 296.

35.

Roth

Ohlsson

(2025) Dietary modifications in IBS leads to reduced symptoms, weight, and lipid levels: Two randomized clinical trials. Nutrients 17: 2966.

36.

Singh

Chey

Nee

, et al. (2025) Dietary Therapy in IBS Working Group; Lembo A, Chey WD. Is a Simplified, Less Restrictive Low FODMAP Diet Possible? Results From a Double-Blind, Pilot Randomized Controlled Trial. Clin Gastroenterol Hepatol 23: 362–364.

37.

Sperber

Bangdiwala

Drossman

, et al. (2021) Worldwide prevalence and burden of functional gastrointestinal disorders, results of Rome Foundation global study. Gastroenterology 160: 99–114.

38.

Stabell

Stubhaug

Flægstad

, et al. (2014) Widespread hyperalgesia in adolescents with symptoms of irritable bowel syndrome: Results from a large population-based study. J Pain 15: 898–906.

39.

Staudacher

Rossi

Kaminski

, et al. (2022) Long-term personalized low FODMAP diet improves symptoms and maintains luminal bifidobacteria abundance in irritable bowel syndrome. Neurogastroenterology and Motility 34: e14241.

40.

Staudacher

Mahoney

Canale

, et al. (2024) Clinical trial: A Mediterranean diet is feasible and improves gastrointestinal and psychological symptoms in irritable bowel syndrome. Alimentary Pharmacology & Therapeutics 59: 492–503.

41.

Staudacher

Ralph

FSE

Irving

, et al. (2020) Nutrient intake, diet quality, and diet diversity in irritable bowel syndrome and the impact of the low FODMAP diet. Journal of the Academy of Nutrition and Dietetics 120: 535–547.

42.

Staudacher

Whelan

(2017) The low FODMAP diet: Recent advances in understanding its mechanisms and efficacy in IBS. Gut 66: 1517–1527.

43.

Swedish Food Agency. [accessed on 22 October 2024]. Available online: www.livsmedelsverket.se.

44.

Treem

(1995) Congenital sucrase-isomaltase deficiency. Journal of Pediatric Gastroenterology and Nutrition 21: 1–14.

45.

Van den Houte

Colomier

Routhiaux

, et al. (2024) Efficacy and findings of a blinded randomized reintroduction phase for the low FODMAP diet in irritable bowel syndrome. Gastroenterology 167: 333–342.

46.

Yang

Liu

, et al. (2024) Ultra-processed food consumption and long-term risk of irritable bowel syndrome: A large-scale prospective cohort study. Clinical Gastroenterology and Hepatology 22: 1497–1507.e5.

47.

Zhou

Liu

, et al. (2025) Both general and central obesity are associated with increased risk of irritable bowel syndrome: A large-scale prospective cohort study. American Journal of Clinical Nutrition 121: 1054–1062.

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