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Review

Genetic Predisposition and Nutritional Interactions in Gastroenterology: A Review of European Clinical Recommendations

by
Vaios Svolos
1,2,*,
Anastasia Triantafyllou
1,
Georgios Charmantzis
1,
Maria Delliou
1,
Maria-Nikoletta Nanti
1,
Melina Moustaka
1,
Eleni Bakasieta
1,
Evanthia Balafa
1,
Dimitra Eleftheria Strongylou
1 and
Odysseas Androutsos
1
1
Laboratory of Clinical Nutrition and Dietetics, Department of Nutrition and Dietetics, School of Physical Education, Sports Science and Dietetics, University of Thessaly, 42100 Trikala, Greece
2
School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QF, UK
*
Author to whom correspondence should be addressed.
Gastrointest. Disord. 2025, 7(4), 67; https://doi.org/10.3390/gidisord7040067
Submission received: 1 September 2025 / Revised: 6 October 2025 / Accepted: 10 October 2025 / Published: 17 October 2025
Browse Figure
Versions Notes

Abstract

Background/Objectives: Despite the growing understanding of the relationship between the genome and nutrition, clearly defined and evidence-based clinical guidelines remain insufficient. The objective of this review was to identify and compile all available European guidelines related to the impact of genetic predisposition on nutritional recommendations in the field of gastroenterology. Methods: A review of guidelines and position papers issued by four European organisations [the European Crohn’s and Colitis Organisation (ECCO), the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN), the European Society for Clinical Nutrition and Metabolism (ESPEN), and United European Gastroenterology (UEG)] was conducted for the past ten years. Results: Out of 5196 recommendations and statements extracted from 124 manuscripts, only 13 highlighted a link between genetic predisposition and dietary factors in clinical gastroenterology. From the available guidelines, there is no clear trend indicating an increased focus on genetic background and its association with nutrition in recent years. Conclusions: There is a critical opportunity for European organisations to develop an evidence-based information framework, guided by clinical protocols, in order to integrate the large volume of genetic data into clinical practice and personalised care of individuals with gastrointestinal disorders.

Graphical Abstract

1. Introduction

The complex interplay between genetic predisposition and nutritional factors acts as a catalyst in the development, diagnosis, and management of many gastrointestinal (GI) disorders. Advances in genomic research have revealed that individual genetic variations can influence susceptibility to GI diseases [1,2], modulate immune responses [3] and affect metabolism and absorption of nutrients [4,5,6]. These genetic influences are increasingly recognised as important determinants of disease phenotype and patient outcomes.
In conditions such as inflammatory bowel disease (IBD), coeliac disease (CoD), irritable bowel syndrome (IBS), colorectal cancer, and lactose intolerance, genetic factors contribute to diagnosis but also to individual variability in clinical presentation and treatment response. For instance, specific human leukocyte antigen (HLA) genotypes (HLA-DQ2 and HLA-DQ8) are central to the diagnosis of CoD, guiding decisions on gluten exclusion and monitoring. In IBD, gene variants like NOD2 have been linked to disease behaviour and complications, that in turn, can affect nutritional strategies to manage inflammation and maintain remission [7,8,9,10,11,12].
At the same time, two fields emerged at the intersection of genomics and nutrition that underpin precision nutrition: nutrigenetics and nutrigenomics. Nutrigenetics focuses on how genetic variants influence the absorption, metabolism, and utilisation of nutrients, thereby explaining interindividual variability in dietary requirements and responses [13,14]. An example of nutrigenetics is the lactase persistence polymorphism, where variation in the LCT gene determines whether lactose can be digested in adulthood [15]. In contrast, nutrigenomics explores how diet and food components regulate gene expression, protein synthesis, and metabolic pathways, thereby modulating physiological and pathological processes [13,14].
In GI disorders, these approaches form the basis of precision nutrition, which clarifies the impact of individuals’ genetic and metabolic characteristics in the effectiveness of dietary therapies [16,17]. For example, in IBS, sucrase-isomaltase mutations and distinct metabolomic or microbial signatures can predict responsiveness to a low-FODMAP diet, while in paediatric Crohn’s disease, exclusive enteral nutrition (EEN) demonstrates therapeutic benefit that may be optimised by integrating host genetics, microbiome composition, and metabolic biomarkers. At the same time, nutrigenomic research highlights the importance of preventing adverse effects of restrictive diets, such as nutrient deficiencies, by guiding reintroduction strategies and targeted supplementation [16,18,19]. Collectively, these advances point out the significance of tailoring dietary recommendations to individual genetic and microbial profiles. As such, enhancing treatment outcomes and establishing precision nutrition are presented as central to both therapeutic and preventative strategies in GI health.
European clinical guidelines developed by expert societies incorporate current evidence to standardise diagnosis and treatment. These guidelines increasingly acknowledge genetic factors as part of precision medicine approaches in gastroenterology and nutrition. However, the extent to which genetics informs nutritional recommendations across different GI disorders in these guidelines remains unclear. A thorough assessment of guidelines concerning genome–nutrition interactions is crucial for understanding existing approaches in clinical practice and identifying opportunities to integrate genetics into personalised care.
This review aimed at systematically identifying and synthesising European guideline statements that address genetic predisposition and host genome influence in the nutritional management of GI diseases. By collating and analysing these recommendations, we seek to clarify how genetics is currently incorporated into clinical nutrition for GI conditions and stress out gaps for future research and guideline development. Although advances in nutrigenetics and nutrigenomics show promise for personalising nutrition in GI disorders, their translation into European guidelines has been slow. A few initiatives have explored gene–diet applications, but limited reproducible evidence, uncertainty about clinical utility, and practical barriers to genetic testing have hindered formal recommendations.

2. Results

2.1. Distribution of Total, Nutrition, and Genetic Related Statements per European Organisation

A total of 124 manuscripts were identified issued by four European organisations: the European Crohn’s and Colitis Organisation (ECCO), the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN), the European Society for Clinical Nutrition and Metabolism (ESPEN), and United European Gastroenterology (UEG). The identified manuscripts included 42 ECCO [20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61], 52 ESPGHAN [61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96,97,98,99,100,101,102,103,104,105,106,107,108,109,110,111,112], 14 UEG [112,113,114,115,116,117,118,119,120,121,122,123,124,125] and 16 ESPEN manuscripts [112,126,127,128,129,130,131,132,133,134,135,136,137,138,139,140] (Table 1).
A total of 5196 statements were extracted (Supplementary Table S1). ECCO provided 1363 statements, with 13.1% addressing nutrition and 1.5% referring to genetic factors. ESPGHAN issued 1639 statements, of which 36.9% focused on nutrition and 2.7% on genetics. UEG provided 873 statements, including 15.7% nutrition-related and 1.8% genetics-related content. ESPEN contributed 1321 statements, 67.5% of which had nutrition guidelines, while only 0.2% referred to genetic factors (Table 1). The UEG and ESPGHAN organisations had five and six statements linking genetics with nutrition, respectively, while ESPEN had much fewer and ECCO had none. The results show considerable variability among organisations in the extent to which they have incorporated nutrition and genetics into gastroenterology guidelines.

2.2. Number of Total Statements per European Organisation and Publication Year

The data, organised by European organisation and year of publication, provide an overview of the volume and focus of the extracted information. Over the ten-year study period, ECCO demonstrates the most consistent output of relevant statements, providing a steady number of publications. In contrast, two of the other organisations, UEG and ESPEN, seem to have a more recent involvement, since their first relevant publications appear after 2019 (Table 2).
A total of 1363 statements were extracted from ECCO publications between 2015 and 2025. The number of statements extracted each year varies, with the highest number observed in 2017 (194 statements) and the lowest in 2025 (85 statements).
The data for ESPGHAN does not maintain a consistent stream of publications over the decade. Unlike ECCO, which has a more stable output, ESPGHAN’s activity is characterised by significant variability. The number of extracted statements ranges from a low of just seven in 2015 to a remarkable peak of 476 in 2018 and 418 in 2024. A stable trend is observed in the remaining years.
The data for UEG indicate a later start to its publishing activity on the topics of nutrition and genetic factors compared to the remaining organisations. From 2015 to 2018, there are no relevant statements extracted (0%). In 2019, the number of statements is 80 and it increases significantly in 2020 (265 statements). This peak in 2020 is followed by a slight decrease in the following years.
The data for the ESPEN reveals a pattern of activity that began in 2019, with no relevant statements extracted from 2016 to 2018. The organisation has only three statements in 2015 but has a significant increase in output, particularly in 2020 (352 statements) and 2022 (270 statements). While ESPEN did not consistently publish on these topics throughout the entire decade, its activity from 2019 onwards shows an important focus, with a consistently high number of extracted statements in the later years of the study. The total number of statements is lower in 2025; however, it should be noted that the relevant research was conducted only up until the end of July 2025.

2.3. Distribution of Total, Nutrition, and Genetic Related Statements per Publication Year

The analysis of the total number of extracted statements related to nutrition from all four organisations from 2015 to 2025 reveals a fluctuating pattern (Table 3). The number of nutrition-related statements varies significantly, ranging from a low of 18 in 2015 to a high of 308 in 2023. A notable increase in activity is observed since 2018, with a peak in 2023, where 59.3% of the total extracted statements for that year were related to nutrition. While the total number of relevant statements shows some year-to-year variation, the overall trend suggests a growing focus on nutrition-related topics in the publications of these European organisations, especially in the later years of the study period.
The analysis of statements with genetic-related content reveals a significantly different pattern compared to those with nutrition content. Across all four organisations, the volume of genetic-related statements is considerably lower and exhibits less consistency. Over the decade, the total number of statements on this topic did not exceed 20 in any single year between 2015 and 2019. Despite a slight increase in 2020, the overall trend indicates that genetic factors received far less attention in the publications of these European organisations compared to nutritional topics.
The analysis of statements that link genetics with nutrition reveals a very limited and sporadic pattern of activity. For many years, specifically from 2015 to 2018 and then in 2020 and 2023, there are no extracted statements on this combined topic (0%). Statements addressing both nutrition and genetic factors appear in publications from 2019, 2022, 2024, and 2025. The highest count is six statements in 2019.

2.4. Qualitative Analysis of Statements on Nutrition and Genetic Factors

This section presents a detailed qualitative analysis of the 13 extracted statements that link nutrition to genetic factors. The analysis reveals a clear focus on a specific disease area, CoD. A significant portion of the statements, primarily from UEG and ESPGHAN, addresses the relationship between HLA-DQ2/DQ8 genes and gluten intake in the diagnosis and management of CoD. These statements emphasise the utilisation of genetic testing to either rule out the disease or to guide further diagnostic steps, such as a gluten challenge, in patients who are already on a gluten-free diet. The data highlights a shared understanding among these organisations that genetic predisposition plays a crucial role in CoD, influencing both diagnostic protocols and dietary recommendations (Table 4).
Moreover, a few statements address other genetic conditions. ESPEN links genetic causes of Carbohydrate Malabsorption (CarbMal) to dietary restrictions, while ESPGHAN states that congenital sucrase-isomaltase deficiency is usually diagnosed by genetic testing after symptoms of malabsorption appear with the introduction of sucrose and starch in the diet. There is only one statement from ESPEN that recommends nutritional support for patients with Cystic Fibrosis (CF) who are not growing according to their “genetic potential” (Table 4).

3. Discussion

Our findings reflect this gap: although clinical need and early initiatives exist, variable evidence strength, regulatory concerns, and lack of consensus tools likely explain the slow uptake of gene–diet guidance in European recommendations. Our review revealed that out of more than 5000 statements, published by four European organisations (ECCO, ESPGHAN, ESPEN and UEG), only 13 explicitly linked genetics with nutrition in gastroenterology. While statements focusing exclusively on nutrition were numerous, statements incorporating genetic predisposition were far fewer, underscoring the limited integration of genomics into current dietary recommendations. The lack of consistent output indicates that the joint topic of nutrition and genetics is not a primary focus for these European organisations, at least not in a way that is clearly addressed in their publications.
Most gene–diet statements are related to HLA typing in CoD, confirming that genetic testing is well established in this context. CoD is a multifactorial disease that triggers an abnormal immune response upon gluten intake in genetically predisposed individuals, particularly those carrying specific class II human leukocyte antigen (HLA) variants within the major histocompatibility complex (MHC) [141]. The majority of CοD patients are carriers of HLA-DQ2 and/or HLA-DQ8, and the value of HLA genotyping in suspected coeliac disease lies mainly in its strong negative predictive value [142]. In susceptible individuals, gluten can lead to gut inflammation and villous atrophy, so extensive studies have shown that adherence to a strict gluten-free diet (GFD) can restore normal small bowel histology [141,143]. According to the new ESPGHAN guideline, there is insufficient evidence to associate high gluten intake with different HLA risk types [84].
Regarding the diagnosis of CoD, standard tests of serology and conventional histology are often adequate to reach a diagnosis of CoD, but HLA-DQ2/8 testing can help exclude individuals without genetic risk for CoD, reducing unnecessary repeated testing in symptomatic patients with a first-degree relative affected by the disease. It can also be used in patients with suspected CoD but who fail to respond to a GFD [142]. As reported in the new UEG guideline, HLA-DQ2/DQ8 typing has an important but supportive role in the diagnosis of CoD. Although HLA-DQ2/DQ8 typing should not be used as a routine initial test, it can be valuable for excluding the disease when negative and for clarifying ambiguous cases such as seronegative CoD, patients already on a gluten-free diet, or those with discordant serology and histology. Diagnosis, thus, relies on a combination of serology, histology (on a gluten-containing diet), and genetics [122].
However, other GI disorders where genetics are increasingly relevant—such as IBD, IBS—were scarcely addressed, showing a limited scope of current recommendations. Recent work has highlighted progress in understanding the genetic architecture of IBD, including pharmacogenetic applications. In parallel, new bioinformatics and multi-omics platforms can integrate genomic, transcriptomic, proteomic, metabolomic and microbiome data to build comprehensive molecular maps of disease, creating opportunities for future gene–diet guidance once evidence matures [144,145]. Existing research suggests [146,147] the potential use of specific loci as diagnostic biomarkers for IBD and IBS through genome-wide association studies (GWAS), providing new insights into the aetiology of these diseases. However, since the underlying genes remain insufficiently characterised, further progress is necessary for therapeutic approaches, including nutritional interventions.
While scientific evidence supports the role of genetic polymorphisms in nutrient metabolism and disease susceptibility, our findings suggest that European guidelines still lag in incorporating this knowledge. This gap points out the need for systematic frameworks to integrate genetic data into dietary recommendations, as highlighted in recent precision nutrition research [148,149,150,151,152]. According to the Academy of Nutrition and Dietetics, “nutritional genomics provides insight into how diet and genotype interactions affect phenotype. The practical application of nutritional genomics for complex chronic disease is an emerging science, and the use of nutrigenetic testing to provide dietary advice is not ready for routine dietetics practice” [153]. At present, advances in high-throughput genotyping, machine learning, and artificial intelligence enable the collection and analysis of vast amounts of genetic data [150]. However, further research is needed before these tools can provide rigorous evidence to support dietary recommendations for either groups or individuals [151,152]. In fact, heterogeneity in genetic associations, insufficient clinical trial evidence, and the absence of validated clinical tools for translating nutrigenetic findings into practice might explain the limited inclusion of gene–nutrition guidance. Guideline committees are often cautious about issuing recommendations in areas where the evidence remains preliminary or inconsistent. Therefore, the absence of clear, evidence-based guidance leaves clinicians with limited support for integrating genetic data into nutritional care. This gap risks slowing the adoption of precision nutrition approaches, despite their potential to improve patient outcomes in gastroenterology.
We observed significant differences across societies; ESPEN produced many nutrition-related guidelines but almost no genetic content, while ESPGHAN and UEG provided only a handful of gene–diet statements. This variability may reflect differences in target populations and in the thresholds of evidence required for guideline development. Additional reasons might well be variations in methodological approaches to evidence appraisal, the pace at which each society integrates emerging research, and the degree of collaboration between geneticists, nutritionists, and clinicians.
A strength of our study is the comprehensive, systematic search across major European gastroenterology and nutrition organisations, which enhances the robustness of our findings. However, we may have missed relevant guidelines issued by other professional bodies, smaller societies, or those published only in non-English languages. Furthermore, global organisations were not included, and therefore the statements reported here are restricted to the European context. Our analysis focused only on explicit gene–diet references, which may underestimate the extent of indirect genetic considerations. Finally, the aim of this paper was to collect and map existing statements, without evaluating the strength or quality of the relevant recommendations.
There is a critical opportunity for expert societies to expand guideline development by incorporating emerging gene-nutrition interaction evidence, particularly in IBD, IBS, and metabolic GI disorders. Multidisciplinary collaboration, standardisation of genetic testing protocols, endorsing robust methodological designs, such as longitudinal studies and clinical trials, will be key to building an evidence-based framework for precision nutrition in gastroenterology.

4. Materials and Methods

4.1. Guideline Identification

A comprehensive systematic search was conducted to identify clinical practice guidelines, original research articles, and review articles—including consensus papers, topical reviews, and position statements—published between 1 January 2015 and 30 July 2025 by leading European organisations addressing nutrition and/or gastroenterology. The search included PubMed and the official repositories of the following European organisation: ECCO, ESPGHAN, ESPEN and UEG.
The search was performed in July 2025 using combinations of keywords such as “guideline”, “clinical practice”, “gastroenterology”, “nutrition”, and disease-specific terms (e.g., “inflammatory bowel disease”, “coeliac disease”, “irritable bowel syndrome”, “Crohn’s disease”, “lactose intolerance”). To ensure completeness, additional manual searches were conducted in the guideline databases available on each organisation’s website. Articles focusing on surgical interventions or oncology were not included, as this was outside the scope of the current study.

4.2. Eligibility Criteria

The eligibility criteria included guideline, consensus or other guidance manuscripts that were published or endorsed by the aforementioned European associations. The included manuscripts addressed topics related to gastroenterology and gastrointestinal disorders, including IBD, CoD, IBS, lactose intolerance, and any other GI condition. Publications were in English.

4.3. Data Extraction and Review Process

All statements, recommendations, and consensus points from the identified guidelines were systematically extracted into a dedicated database. Extracted statements were categorised by issuing organisation and publication year.
Two independent researchers (V.S. and A.T.) reviewed all extracted statements to identify statements referring to nutrition in gastroenterology, including references to specific nutrients, diet, enteral nutrition, and parenteral nutrition. By utilising the same approach, they also identified the statements referring to genetic predisposition. This included explicit references to genes, genetic polymorphisms, genotypes, genetic testing, and familial history. From the classified statements, we further extracted those that referred to both nutrition and genetic elements.

4.4. Data Synthesis

Quantitative summaries were generated to indicate the number and proportion of statements addressing nutrition or/and genetic factors within each guideline source and by publication year. Comparative analyses were performed to identify trends across different guideline-producing organisations and over time, providing insight into evolving emphasis on genetics in nutrition-related gastroenterology guidance.
Extracted statements involving nutrition and genetics in gastroenterology were collated in tabular form, organised by disease area, guideline source, and publication year. A narrative synthesis described the scope and depth of genetic considerations in nutrition-related gastroenterology recommendations, highlighting areas with robust evidence and gaps needing further research.

5. Conclusions

A large number of nutrition-focused guidelines was identified, particularly from ESPEN. However, our study revealed that out of more than 5000 statements issued by four European scientific societies (ECCO, ESPGHAN, ESPEN, and UEG), only 13 explicitly linked genetic predisposition with nutrition in gastroenterology, highlighting a significant gap in the literature. The emerging scientific field of precision nutrition provides the opportunity to apply genomic knowledge to the nutritional prevention of multifactorial diseases. Although clinicians are faced with a growing volume of nutrigenetic data, evidence-based guidelines for patient counselling—at least from the organisations mentioned in this paper—remain limited.

Supplementary Materials

The following supporting information can be downloaded at https://www.mdpi.com/article/10.3390/gidisord7040067/s1: Table S1: Extracted statements for gastrointestinal health mentioned within ESPEN, ECCO, UEG and ESPGHAN manuscripts between 2015–2025.

Author Contributions

Conceptualization, V.S., A.T. and O.A.; methodology, V.S. and A.T.; formal analysis, A.T. and G.C.; data curation, A.T., G.C., M.D., M.-N.N., M.M., E.B. (Eleni Bakasieta), E.B. (Eleni Balafa) and D.E.S.; writing—original draft preparation, V.S. and A.T.; writing—review and editing, V.S., A.T., G.C., M.D., M.-N.N., M.M., E.B. (Eleni Bakasieta), E.B. (Eleni Balafa) and D.E.S.; supervision, V.S. and O.A.; project administration, A.T. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
CarbMalCarbohydrate Malabsorption
CDCrohn’s Disease
CDACeliac Disease Autoimmunity
CFCystic Fibrosis
CoDCoeliac Disease
CSIDCongenital sucrase-isomaltase deficiency
DGPDeamidated gliadin peptides
ECCOEuropean Crohn’s and Colitis Organisation
EENExclusive enteral nutrition
EMAEndomysial antibodies
ENEnteral nutrition
ESPEN European Society for Clinical Nutrition and Metabolism
ESPGHANEuropean Society for Paediatric Gastroenterology, Hepatology and Nutrition
FODMAPFermentable Oligosaccharides Disaccharides Monosaccharides And Polyols
GFDGluten free diet
GIGastrointestinal
HLAHuman Leukocyte Antigen
IBDInflammatory Bowel Disease
IBSIrritable Bowel Syndrome
LCT geneLactase gene
NCGSNon-Celiac Gluten Sensitivity
NOD2Nucleotide-binding oligomerization domain 2
TG2Tissue transglutaminase 2
TGPDeamidated gliadin peptides
UCUlcerative Colitis
UEGUnited European Gastroenterology
ULNUpper Limit of Normal
VAVillous Atrophy

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Table 1. Distribution of extracted statements on nutrition and genetic predisposition in guideline and position papers by European organisations.
Table 1. Distribution of extracted statements on nutrition and genetic predisposition in guideline and position papers by European organisations.
Name of OrganisationManuscripts Identified
n		Total Statements
n		Nutrition Statements
n (%) 1		Genetic Statements
n (%) 1		Nutrition and Genetic Statements
n (%) 1
ECCO421363179 (13.1%)21 (1.5%)0 (0%)
ESPGHAN521639605 (36.9%)44 (2.7%)5 (0.3%)
UEG14873137 (15.7%)16 (1.8%)6 (0.6%)
ESPEN161321892 (67.5%)2 (0.2%)2 (0.2%)
Total12451961813 (34.9%)83 (1.6%)13 (0.3%)
1 n = number; % = percentage.
Table 2. Number of total extracted statements from manuscripts of European organisations per year of publication.
Table 2. Number of total extracted statements from manuscripts of European organisations per year of publication.
YearECCO
n (%) 1		ESPGHAN
n (%) 1		UEG
n (%) 1		ESPEN
n (%) 1		Total
2015118 (92.2%)7 (5.5%)0 (0.0%)3 (2.3%)128
2016148 (77.9%)42 (22.1%)0 (0.0%)0 (0.0%)190
2017194 (70.5%)81 (29.5%)0 (0.0%)0 (0.0%)275
2018109 (18.6%)476 (81.4%)0 (0.0%)0 (0.0%)585
201978 (21.1%)110 (29.7%)80 (21.6%)102 (27.6%)370
202087 (11.0%)88 (11.1%)265 (33.5%)352 (44.4%)792
2021178 (34.8%)124 (24.3%)97 (19.0%)112 (21.9%)511
2022129 (20.2%)99 (15.5%)142 (22.2%)270 (42.2%)640
202392 (17.7%)190 (36.6%)0 (0.0%)237 (45.7%)519
202485 (9.7%)418 (47.9%)160 (18.3%)210 (24.1%)873
2025 *145 (46.3%)4 (1.3%)129 (41.2%)35 (11.2%)313
Total1363 (26.2%)1639(31.5%)873 (16.8%)1321 (25.4%)5196
1 n = number; % = percentage; * = lower n of statements, search conducted till July 2025.
Table 3. Number of total, nutrition and genetic related extracted statements from manuscripts of European organisations related to nutrition and/or genetics, reported per year of publication.
Table 3. Number of total, nutrition and genetic related extracted statements from manuscripts of European organisations related to nutrition and/or genetics, reported per year of publication.
YearManuscripts Identified
n		Total Statements
n		Nutrition Statements
n (%) 1		Genetic Statements
n (%) 1		Nutrition and Genetic Statements
n (%) 1
2015612818 (14.1%)2 (1.6%)0 (0.0%)
2016919039 (20.5%)5 (2.6%)0 (0.0%)
2017827557 (20.7%)5 (1.8%)0 (0.0%)
201811585165 (28.2%)11 (1.9%)0 (0.0%)
201914370176 (47.6%)20 (5.4%)6 (1.6%)
202017792297 (37.5%)7 (0.9%)0 (0.0%)
20211451174 (14.5%)13 (2.5%)0 (0.0%)
202212640268 (41.9%)7 (1.1%)1 (0.2%)
202311519308 (59.3%)0 (0.0%)0 (0.0%)
202415873274 (31.4%)7 (0.8%)5 (0.6%)
2025 *7313137 (43.8%)6 (1.9%)1 (0.3%)
Total12451961813 (34.9%)83 (1.6%)13 (0.3%)
1 n = number; % = percentage; * = lower n of statements, search conducted till July 2025.
Table 4. Extracted statements on gene–diet interactions from guideline documents.
Table 4. Extracted statements on gene–diet interactions from guideline documents.
Organisation
(Year; Condition)		Nutrition and Genetic Statement
ESPEN
(2025; CarbMal)		Genetic and non-genetic causes of carbohydrate malabsorption can be quite common in childhood and adolescence, and children and adolescents may show symptoms after ingestion of the respective carbohydrate, depending on the ingested dose and concurrent diseases like irritable bowel syndrome. Dietary restriction of the specific carbohydrate(s) is recommended when the intolerance to the specific carbohydrate is proven by validated symptom assessment [112].
ESPGHAN
(2024; CoD)		Observational and case–control studies suggest that the consumption of a higher amount of gluten at weaning and/or thereafter may increase the risk of CDA and CoD in genetically at-risk children [84].
ESPGHAN
(2024; CoD)		Observational studies, including cohort and case–control studies, do not provide evidence that the effect of high gluten intake on CoD and CDA development is related to different HLA risk types [84].
ESPGHAN
(2024; CoD)		Recommendations on breastfeeding for infants with known or unknown genetic risk should not be modified due to considerations regarding prevention of CoD [84].
ESPGHAN
(2024; CoD)		There is not enough evidence to give differentiated recommendations on gluten consumption for various HLA risk types [84].
ESPEN
(2024; CF)		We recommend clinicians should discuss use of EN in a timely manner with the patient and family when patients do not grow according to their genetic potential [126].
ESPGHAN
(2022; CSID)		The ESPGHAN GIC recommends that the diagnosis of congenital sucrase-isomaltase deficiency is usually made with genetic testing after appearance of a malabsorption syndrome when firstly exposed to sucrose and starch in the diet [64].
UEG
(2019; CoD)		HLA-DQ2/DQ8 testing should not be used routinely in the initial diagnosis of CoD. It is recommended that the results of such testing should be included along with a caution that patients at risk should be serologically tested for CoD without changing their diet [122].
UEG
(2019; CoD)		In case of elevated TG2-titre and normal histology: biopsies should be reviewed by a pathologist familiar with CoD. It is recommended to repeat biopsy after gluten challenge if the patient was not on gluten-containing diet before testing. HLA-DQ2/8 typing is mandatory. Testing for other antibodies, e.g., DGP and/or EMA, may be of added value [122].
UEG
(2019; CoD)		Seronegative CoD requires careful assessment with HLA-DQ2/8 testing and a response to a GFD after excluding other causes of seronegative VA. Coeliac serology, both IgA- and IgG based, should be negative [122].
UEG
(2019; CoD)		In patients who are already following GFD prior to testing, serology and HLA typing are needed. If serology is positive, then biopsy is the next step. Gluten challenge should be undertaken when serology is negative but HLA DQ2/DQ8 positive [122].
UEG
(2019; CoD)		CoD diagnosis may be made without duodenal biopsy in symptomatic children with high TG2 levels (>10 times ULN) and EMA in the presence of HLA-DQ2/8. The diagnosis is confirmed by an antibody decline and preferably a clinical response to a GFD [122].
UEG
(2019; CoD)		Serology and small-bowel histology (while the patient is on a gluten-containing diet) and HLA-DQ typing (to rule out CoD if negative) are needed to differentiate between CoD and NCGS [122].
CSID: congenital sucrase-isomaltase deficiency; CDA: Celiac Disease Autoimmunity, CoD: coeliac disease; CarbMal: carbohydrate malabsorption; CF: Cystic Fibrosis; GFD: strict gluten-free diet; NCGS: non-coeliac gluten sensitivity; HLA: Human Leukocyte Antigen; DGP: deamidated gliadin peptides; EMA: endomysial antibodies; TG2: tissue transglutaminase 2; EN: enteral nutrition;ULN: upper limit of normal; VA: Villous Atrophy.
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Svolos, V.; Triantafyllou, A.; Charmantzis, G.; Delliou, M.; Nanti, M.-N.; Moustaka, M.; Bakasieta, E.; Balafa, E.; Strongylou, D.E.; Androutsos, O. Genetic Predisposition and Nutritional Interactions in Gastroenterology: A Review of European Clinical Recommendations. Gastrointest. Disord. 2025, 7, 67. https://doi.org/10.3390/gidisord7040067

AMA Style

Svolos V, Triantafyllou A, Charmantzis G, Delliou M, Nanti M-N, Moustaka M, Bakasieta E, Balafa E, Strongylou DE, Androutsos O. Genetic Predisposition and Nutritional Interactions in Gastroenterology: A Review of European Clinical Recommendations. Gastrointestinal Disorders. 2025; 7(4):67. https://doi.org/10.3390/gidisord7040067

Chicago/Turabian Style

Svolos, Vaios, Anastasia Triantafyllou, Georgios Charmantzis, Maria Delliou, Maria-Nikoletta Nanti, Melina Moustaka, Eleni Bakasieta, Evanthia Balafa, Dimitra Eleftheria Strongylou, and Odysseas Androutsos. 2025. "Genetic Predisposition and Nutritional Interactions in Gastroenterology: A Review of European Clinical Recommendations" Gastrointestinal Disorders 7, no. 4: 67. https://doi.org/10.3390/gidisord7040067

APA Style

Svolos, V., Triantafyllou, A., Charmantzis, G., Delliou, M., Nanti, M.-N., Moustaka, M., Bakasieta, E., Balafa, E., Strongylou, D. E., & Androutsos, O. (2025). Genetic Predisposition and Nutritional Interactions in Gastroenterology: A Review of European Clinical Recommendations. Gastrointestinal Disorders, 7(4), 67. https://doi.org/10.3390/gidisord7040067

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