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11 November 2026

22 Pages

Medical Nutrition Therapy in Autoimmune Diseases: Clinical Roles, Patient Stratification, and Implementation

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School of Pharmacy, Harbin University of Commerce, Harbin 150076, China
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Author to whom correspondence should be addressed.
Nutrients2026, 18(22), 3746;https://doi.org/10.3390/nu18223746
This article belongs to the Section Nutritional Immunology
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Abstract

Autoimmune diseases are markedly heterogeneous in pathogenesis, target-organ injury, clinical state, and treatment context, while partial immunometabolic convergence and recurring nutrition-related phenotypes may occur in specific disease states. This narrative review synthesizes human evidence identified through a structured literature search to examine the clinical roles of medical nutrition therapy (MNT), patient stratification, and clinical implementation. The clearest disease-directed applications include a gluten-free diet for celiac disease and nutritional induction therapy for low-risk pediatric luminal Crohn’s disease, with separate evidence for cyclic exclusive enteral nutrition (EEN) as maintenance after EEN-induced remission. Adjunctive MNT addresses specific symptoms, nutritional or functional phenotypes, and comorbidity burden alongside standard treatment; supportive MNT prioritizes nutritional adequacy and physiological safety when organ dysfunction constrains intake or nutrient handling. Shared phenotypes provide common domains for cross-disease assessment and generate hypotheses for patient stratification; intervention selection must also account for disease state, nutritional phenotype, organ function, and background treatment. Candidate multi-omics biomarkers may help predict differential treatment responses, but their predictive performance and clinical utility for intervention selection remain to be validated. Future research should prospectively test patient–intervention matching and document actual intervention exposure alongside clinical outcomes, safety, and feasibility, with reassessment as disease state and treatment context change.

1. Introduction

Autoimmune diseases (ADs) are a heterogeneous group of disorders characterized by the loss of immune tolerance and impose a substantial disease burden worldwide [1]. The tissues and organs affected vary considerably across diseases and may include the central nervous system, intestinal mucosa, pancreatic beta cells, and neuromuscular junction. Their triggers, immune responses, and clinical manifestations also differ. Nevertheless, in some active disease states, immune cells and affected tissues may exhibit similar metabolic alterations involving glycolysis, mitochondrial function, and lipid and amino acid metabolism. Such convergence is partial and context-dependent, not evidence of a shared metabolic mechanism across ADs.
At the patient level, recurring nutrition-related phenotypes—including inadequate intake or malnutrition, altered body composition or physical function, and cardiometabolic risk—provide common domains for cross-disease nutritional assessment. Medical nutrition therapy (MNT) refers to individualized nutrition therapy based on clinical nutrition assessment and treatment goals. Specific diets, supplements, and nutrition support are components of MNT, not the full scope of MNT [2]. These phenotypes, together with disease state, organ function, and background treatment, can inform individualized MNT assessment and intervention selection [3]. Human evidence is needed to determine the clinical role and expected benefits of specific interventions in each disease context. Accordingly, this review synthesizes human evidence relevant to the disease-directed, adjunctive, and supportive roles of MNT and examines how shared phenotypes and candidate biomarkers may inform patient stratification and clinical implementation.

2. Materials and Methods

2.1. Literature Search

The literature search was updated on 25 October 2026 through focused searches in PubMed (https://pubmed.ncbi.nlm.nih.gov/) and ClinicalTrials.gov (https://clinicaltrials.gov/). PubMed searches were restricted to English-language publications and combined disease-specific terms with terms covering clinical nutrition interventions and dietary management, nutrition-related phenotypes and supportive care, nutrition-linked immune and immunometabolic mechanisms, and precision nutrition and candidate prediction of intervention response. ClinicalTrials.gov was searched for relevant registered interventional studies. The complete search strategies, filters, and retrieval counts are provided in the Supplementary Material. Registered studies without available results were not treated as evidence of efficacy. Because the search was limited to PubMed and ClinicalTrials.gov, relevant studies indexed exclusively in other databases or registries may have been missed.

2.2. Study Selection and Narrative Synthesis

The structured searches identified publications for consideration; a representative, question-driven subset was selected for narrative synthesis according to disease context, clinical state, nutritional intervention or phenotype, and outcomes assessed. The literature search and initial study selection were conducted by X.-W.Z., with the search results and eligibility decisions verified by K.X. A total of 120 sources were included in the narrative synthesis. Human intervention studies reporting disease-related, symptom, functional, nutritional, or safety outcomes were prioritized when assessing clinical effects. Guidelines and observational studies informed nutritional assessment and supportive care. Mechanistic studies informed biological interpretation and were not used as stand-alone evidence of clinical efficacy. Publications unrelated to these clinical and nutritional questions were outside the scope of the clinical synthesis. The evidence was synthesized narratively without quantitative meta-analysis.

3. Disease-Specific Immune Initiation, Effector Mechanisms, and Target-Organ Context in Autoimmune Diseases

3.1. Disease-Specific Triggers and Immune Initiation

Genetic predisposition, environmental or infectious exposures, breach of barrier and disruption of immune regulation may be the trigger for autoimmune responses. However, the relative contribution and sequence of these factors vary from disease to disease [4]. Genetic background can influence antigen presentation, immune recognition, and cellular activation thresholds [5], whereas external exposures, such as infection and smoking, or tissue injury may alter the local inflammatory environment, barrier integrity, and self-antigen exposure. In certain diseases, immune induction may be initiated by molecular mimicry, post-translational modifications, or presentation of cryptic epitopes, but the evidence for this is of variable strength and extent [6,7]. These factors, as well as the effector mechanisms involved and the patterns of target-organ injury, are also modulated by the tissue environment and disease context.

3.2. Disease-Specific Immune Effector Mechanisms and Target-Organ Injury

Differences in the predominant immune effector mechanisms and their targets further illustrate the heterogeneity of ADs (Figure 1). Systemic lupus erythematosus (SLE) is characterized by multisystem injury involving autoantibodies, immune complexes, and complement [8]. In systemic sclerosis (SSc), autoimmunity, microvascular injury, and fibrosis collectively shape cutaneous and internal-organ involvement [9]. Type 1 diabetes mellitus (T1DM) is defined by immune-mediated destruction of pancreatic beta cells [10], whereas myasthenia gravis (MG) is primarily caused by pathogenic autoantibodies that impair neuromuscular junction function [11]. Crohn’s disease (CD) is an immune-mediated inflammatory disease characterized by barrier dysfunction, dysregulated mucosal immunity, and transmural intestinal inflammation [12].
Figure 1. Heterogeneous pathways to disease-specific target-tissue injury. Diverse initiating contexts may produce distinct patterns of immune dysregulation, effector activity, and tissue injury, with their relative contributions varying across diseases and clinical states. Arrows indicate the direction of the pathways and interactions shown; labeled symbols identify the relevant cells and mediators, while colors distinguish the illustrated components.
These distinct immune–target-organ patterns can give rise to multisystem injury, impaired gastrointestinal motility or absorption, loss of glycemic homeostasis, swallowing dysfunction, or structural intestinal complications. Across diseases, these injury patterns can produce partially overlapping nutrition-related phenotypes, which are summarized in Table 1.
Table 1. Disease context and nutrition-relevant features across selected autoimmune and immune-mediated inflammatory diseases.

4. Disease Heterogeneity, Shared Clinical Phenotypes, and a Cross-Disease Framework for MNT

Across the autoimmune diseases reviewed, nutrition-related phenotypes reflect disease activity, target-organ involvement, and treatment exposure [45,46]. The following sections examine these clinical domains alongside selected immunometabolic findings to establish practical assessment principles and define testable clinical roles for MNT.

4.1. How Disease State and Target-Organ Involvement Shape Nutrition-Related Clinical Phenotypes

Disease state, target-organ function, and treatment context jointly shape patients’ nutrition-related phenotypes [32,47,48]. These problems can be broadly grouped into three categories: intake, absorption, and nutritional adequacy; altered body composition, physical function, and cardiometabolic burden; and nutritional constraints related to organ function or treatment. Both SSc and CD may be accompanied by malnutrition. In SSc, malnutrition is more closely associated with gastrointestinal dysmotility and fibrosis, whereas nutritional risk in CD is influenced by active inflammation, strictures, previous surgery, and residual intestinal function [12,32,49]. In MG, swallowing impairment and aspiration risk require particular attention [50]. In patients with renal involvement, nutritional intake and related restrictions should be assessed in relation to proteinuria, volume status, and kidney function [51]. Changes in body composition and physical function in RA and MS may likewise be influenced by inflammation, disability, and treatment [22,46]. Table 1 summarizes disease/target-organ contexts, nutrition-related phenotypes, and MNT roles across selected ADs.

4.2. Partial Immunometabolic Convergence and Its Clinical Significance

Immunometabolic features relevant to cross-disease comparison can be examined at three levels: intracellular metabolism in immune cells, the target-tissue microenvironment, and the patient’s overall nutritional and metabolic state [52,53,54]. Cellular metabolic alterations, such as increased glycolysis or changes in mTOR activity, are highly dependent on cell type, tissue environment, and disease state.
Reported features also include alterations in oxidative phosphorylation and fatty-acid oxidation, while metabolomic studies have identified disease-associated changes in amino-acid and lipid metabolism [55,56] (Figure 2). In rheumatoid arthritis (RA), a meta-analysis of randomized trials found that omega-3 supplementation increased circulating eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and reduced the omega-6/omega-3 ratio, demonstrating that nutritional exposure can measurably alter systemic lipid profiles [57]. EPA and DHA are also precursors of lipid mediators involved in the regulation and resolution of inflammation, providing a plausible biological link between dietary fatty-acid exposure and immune function [58]. To determine whether these changes are related to immune-cell or target-tissue metabolism and clinical responses, studies need to assess actual nutritional exposure, relevant lipid and immune mediators, and clinical outcomes within the same intervention context. Metabolomics can identify candidate metabolic features for patient stratification, but their ability to predict differential responses to specific nutritional interventions remains to be established [59,60,61].
Figure 2. Context-dependent immunometabolic features across immune-cell lineages. Selected metabolic processes in T cells, B cells, and myeloid cells vary with cellular, disease, treatment, and tissue contexts. Linking these features to MNT requires human intervention evidence relating nutritional exposure to relevant immune or metabolic measures and clinical outcomes. Arrows indicate relationships among the illustrated components, and different colors distinguish the major immune-cell types.

4.3. From Shared Clinical Phenotypes to Shared MNT Assessment Principles

When similar nutrition-related phenotypes occur across different diseases, shared assessment domains can provide a common starting point. After nutritional-risk screening, malnutrition can be diagnosed using GLIM criteria [62,63]. The Eating Assessment Tool-10 (EAT-10) and SARC-F (Strength, Assistance with walking, Rise from a chair, Climb stairs, and Falls) can be used to screen for dysphagia and sarcopenia, respectively [64,65]. Nutritional risk warrants evaluation of dietary intake and absorption, whereas abnormal body composition requires assessment of muscle mass and physical function [62,66]. In patients with excess adiposity or cardiometabolic risk, body weight and relevant metabolic indicators should also be considered [2].
Assessment components should be selected according to disease activity, organ function, and current treatment. For example, although gastrointestinal malabsorption, impaired swallowing, and inflammation- or disuse-related deterioration in body composition may all manifest as malnutrition, they require different measurements and follow-up priorities [50,66,67]. Shared clinical phenotypes can therefore guide initial assessment and risk-management priorities.

4.4. From Shared Assessment to Testable Clinical Roles for MNT

For this review, disease-directed MNT refers to a nutritional intervention intended as a primary treatment strategy for a defined disease or clinical state, with its effects assessed primarily through disease-related outcomes in human studies [68]. Adjunctive MNT is delivered alongside standard treatment and primarily addresses body weight, nutrient deficiencies, symptoms, physical function, or comorbidity risk. Its additional effects on disease-related outcomes may also be evaluated [57]. Supportive MNT focuses on maintaining nutritional intake, ensuring feeding safety, or managing constraints imposed by organ dysfunction or essential treatment requirements. Its clinical necessity and any disease-modifying effect should be evaluated separately [69]. When roles overlap, classification should follow the intervention’s primary clinical objective within the treatment plan: disease control for disease-directed MNT, phenotype or symptom management alongside standard care for adjunctive MNT, and nutritional adequacy or physiological safety for supportive MNT.
These roles organize interventions according to their primary clinical objectives. Disease-related outcomes, changes in symptoms or clinical phenotypes, and nutritional or safety outcomes address different clinical questions [70,71]. Studies of specific diets or supplements are included when they address a defined clinical or nutritional target relevant to an MNT role; they provide evidence for individual intervention components and do not necessarily evaluate comprehensive, individualized MNT programs. Mechanistic findings inform biological hypotheses, whereas clinical roles are assessed using relevant human outcomes.

5. Human Evidence Defining the Clinical Roles of MNT in Autoimmune Diseases

Human evidence is unevenly distributed across ADs [72]. A small number of nutritional interventions directly target disease-related outcomes, whereas more studies assess improvements in specific clinical phenotypes alongside standard treatment [73]. Other interventions primarily aim to improve or maintain nutritional status in patients with disease-related nutritional impairment [74].

5.1. Disease-Directed MNT: Evidence from Disease-Related Outcomes in Defined Clinical States

Current pediatric guidelines recommend exclusive enteral nutrition (EEN) as first-line nutritional induction therapy for low-risk luminal CD, with CDED + PEN as an alternative [75]. Network meta-analyses also support EEN-based induction, although the comparative evidence remains limited and heterogeneous [68,76]. In a small 2006 open-label RCT (n = 37), clinical remission did not differ significantly between EEN and corticosteroids, whereas mucosal healing was more frequent with EEN [77,78]. In a multicenter RCT, CDED + PEN was better tolerated than EEN; week-6 remission did not differ significantly, while week-12 sustained remission favored the CDED + PEN sequence, although regimens differed after week 6 [79]. For maintenance after EEN-induced remission, a pediatric trial found a lower 12-month relapse rate with cyclic EEN than with daily PEN (49% vs. 76%); this finding does not establish efficacy of adult CDED regimens [80].
In adults, the open-label CDED-AD pilot randomized trial (44 participants randomized; 40 analyzed) found no statistically significant difference in week-6 remission rate between CDED+PEN and CDED alone (68% vs. 57%; p = 0.46); 80% of week-6 responders remained in remission at week 24 [81]. In celiac disease (CeD), lifelong adherence to a strict GFD is the established disease-directed treatment [34]. In a 5-year adult cohort (99 patients enrolled; 52 reassessed at 1 year and 46 at 5 years), tissue transglutaminase IgA remained elevated in 44% and 30% of patients at 1 and 5 years, respectively; mucosal remission (Marsh 0) increased from 37% to 50%, while remission/response (Marsh 0/1) increased from 54% to 85% [82]. In a separate 2-year prospective cohort, persistent villous atrophy was present in 40 of 76 patients (53%); 72.5% of these 40 patients were asymptomatic and 75% had negative serology. At least one fecal sample was positive for gluten immunogenic peptides in 69% of the cohort, suggesting intermittent gluten exposure. However, median fecal peptide levels did not differ significantly between patients with persistent atrophy and those with mucosal recovery [83].

5.2. Adjunctive MNT: Phenotype-Targeted Benefits Alongside Standard Treatment

Adjunctive MNT has been studied more extensively, but the intervention targets and outcomes vary considerably. Its principal role is to improve specific phenotypes, symptoms, or comorbidity burden alongside standard treatment. In patients with psoriasis (PsO) who are overweight or obese, hypocaloric diets primarily support weight loss. Some studies have also reported improvements in skin lesions, although disease-related benefits must be interpreted in the context of background pharmacotherapy [84,85].
In RA, higher-dose omega-3 supplementation added to treat-to-target disease-modifying antirheumatic drug (DMARD) therapy was associated with a lower rate of treatment failure and a shorter time to American College of Rheumatology (ACR) remission, illustrating that adjunctive MNT can also influence disease-related outcomes [86]. A meta-analysis of 23 randomized placebo-controlled trials found limited clinical benefit, with predominantly low- or very-low-certainty evidence and uncertain effects on non-steroidal anti-inflammatory drug (NSAID) use [87]. In the small MEDRA randomized trial, physical function and quality of life improved within both the Mediterranean-diet and healthy-eating-guideline groups; between-group differences in change from baseline were not significant, although week-12 endpoint scores favored the Mediterranean-diet group [73].
In a 24-week randomized trial involving 87 participants with relapsing–remitting multiple sclerosis (MS), fatigue improved in both the Swank and Wahls diet groups, with no between-group difference in Fatigue Severity Scale (FSS) change. The Wahls group had a greater reduction in Modified Fatigue Impact Scale (MFIS) scores at 24 weeks (p = 0.02), and mental and physical Multiple Sclerosis Quality of Life-54 (MSQoL-54) scores improved more with Wahls at weeks 12 and 24 (between-group p ≤ 0.05) [88].
In SLE, findings from vitamin D interventions have been inconsistent. A trial in adults with inactive disease improved vitamin D status but did not improve the prespecified interferon (IFN) signature [89], whereas a smaller trial in juvenile-onset SLE reported signals of improvement in disease activity and fatigue [90]. In quiescent inflammatory bowel disease (IBD), a low-FODMAP diet enabled more patients to report adequate symptom relief and improved quality of life. However, the between-group change in the main symptom-severity score was not statistically significant, and inflammatory markers did not improve [91].

5.3. Supportive MNT: Evidence for Physiological Safety Under Organ-Function Constraints

When disease impairs eating, swallowing, digestion, absorption, or an organ’s capacity to handle nutrients, the primary goals of MNT shift toward maintaining nutritional adequacy and physiological safety. The supporting rationale is therefore derived mainly from organ function, clinical physiology, and practical nutritional requirements. A small single-arm study of patients with gastrointestinal involvement in SSc reported reductions in nutrition-related symptom scores and improvements in some body-composition measures, although energy intake did not increase significantly [92]. A subsequent uncontrolled intervention study reported improvements in nutritional status and lean-tissue measures following high-protein oral nutritional supplementation in malnourished patients with SSc [74].
In complicated CD with severe malnutrition or intestinal failure, oral nutrition support, enteral nutrition (EN), or parenteral nutrition (PN), including home PN when needed, may be selected according to residual intestinal function [66,93]. Dysphagia and silent aspiration in MG require swallowing-risk assessment to guide individualized feeding texture and route [23].
In membranous nephropathy (MN), protein and sodium intake should be adjusted according to proteinuria, volume status, kidney function, and nutritional risk [41]. The cited crossover trial, published in 1991 and involving only nine patients, found no significant improvement in glomerular filtration rate (GFR) or proteinuria with protein restriction; its findings predate contemporary immunosuppressive treatment strategies for MN [94].

5.4. Clinical Boundaries of the Current Human Evidence

Figure 3 illustrates how clinical context shapes MNT objectives and the interpretation of disease-related outcomes. In T1DM, coordinating carbohydrate intake with exogenous insulin is a core component of supportive MNT for safe glycemic management [28]. This management role addresses glycemic safety rather than reversal of autoimmune pancreatic β-cell destruction. Table 2 summarizes representative human studies, their designs and sample sizes, corresponding MNT roles, and key clinical findings.
Figure 3. Clinical coupling and evidence boundaries of MNT in autoimmune diseases. Disease activity, organ injury, and treatment exposure can affect nutritional physiology and safety. MNT primarily targets nutrition-related outcomes, whereas effects on disease-related outcomes require matched human evidence in the relevant disease and clinical state. Arrow colors distinguish disease-related pathways (red), MNT effects (green), and treatment-related influences (blue); the dashed red arrow indicates disease-directed effects of MNT.
Table 2. Human evidence and interpretive boundaries of MNT across selected autoimmune disease contexts.

6. Patient Stratification and Future Research: Registered Trials, Clinical Phenotypes, and Biomarker Validation

Most human studies continue to estimate the effects of MNT in populations defined by disease labels and prespecified criteria. However, patients with the same AD differ in disease state, nutritional phenotype, organ function, and treatment context [95]. Research should therefore examine which stratification principles can be shared across diseases and validate intervention responses within specific diseases and clinical states [96,97].

6.1. Registered Human Trials and Gaps in the Current Evidence

Three trials were selected from the registry search as illustrative examples of human MNT in ADs, based on their defined dietary interventions and prespecified outcomes: adjunctive dietary therapy in pediatric CD, Mediterranean-diet counseling in MS, and microbiota-focused dietary intervention in CD (Table 3). A pediatric CD trial compares a modified Crohn’s disease exclusion diet (mCDED) combined with the anti-tumor necrosis factor (TNF) biologic infliximab against infliximab alone at treatment initiation. Its primary outcome is clinical and biochemical response at week 12; additional clinical, biochemical, and endoscopic outcomes are assessed through week 52, alongside adherence [98]. This trial is classified as adjunctive in Table 3 because mCDED is added to infliximab, whereas the CDED-based regimens in Table 2 are evaluated as primary nutritional treatment strategies. A trial of Mediterranean-diet counseling in MS uses quality of life as its primary outcome and also assesses fatigue and disability [99]. A third CD trial compares cranberry powder with placebo, using changes in the relative abundance of butyrate-producing Clostridia at week 15 as its primary outcome [100]. This microbiota endpoint assesses a biological response rather than a direct clinical outcome. Of the three trials listed in Table 3, none specifies biomarker-guided treatment allocation. The registry search also identified a separate SLE trial (NCT07183007), which uses HLA-DQ2/DQ8 status to determine eligibility for a low-gluten diet intervention; genotype-specific treatment effects remain untested [101].
Table 3. Representative Registered Human Nutrition-Intervention Trials in Autoimmune Diseases.

6.2. From Disease Labels to Stratification by Clinical State and Phenotype

Clinical stratification for MNT begins with assessment of disease state and nutritional phenotype. Within the same disease diagnosis, nutritional problems may be related to current immune activity, cumulative organ damage, or long-term immunomodulatory treatment. Disease state, nutritional phenotype, organ function, and treatment context should therefore jointly shape the goals, safety, and feasibility of MNT [95,96,97,102]. A characteristic has practical value for stratification only if it can alter intervention selection, risk assessment, or expected outcomes.
Adapting a diet to a patient’s preferences, culture, and lifestyle is part of individualized care [3]. Selecting MNT according to measurable clinical characteristics represents a further level of clinical stratification. Predicting differential benefit from a specific intervention requires validation of the relationship between the relevant characteristic and treatment response [60,103].

6.3. Multi-Omics Biomarkers: From Descriptive Associations to Predictive Stratification

Although different ADs may exhibit partially overlapping multi-omics features related to immunometabolism [104], biomarkers proposed to guide treatment selection must identify differential responses to a defined intervention within a specific disease and clinical state, rather than merely predict disease activity, progression, or relapse.
The biomarker evidence reviewed here includes a single proof-of-concept study predicting response to EEN; whether these biomarkers identify differential benefit from EEN versus alternative treatments remains untested. Established clinical applications also include serological and genetic testing for CeD diagnosis and glucose-guided carbohydrate–insulin adjustment in T1DM. A multi-omics model was developed to predict response to EEN, with an area under the receiver operating characteristic curve of 0.81 in an independent prospective cohort of 21 children and young adults (95% CI, 0.60–1.00) [59]. Although the model showed predictive potential, the study did not establish that selecting EEN according to the model improves patient outcomes [61]. Clinical translation requires replication in larger cohorts and prospective evaluation using biomarker-stratified or biomarker-strategy trials, with formal treatment-by-biomarker interaction testing and adequate sample sizes.

6.4. Translational Priorities for Precision MNT

Future trials should define the disease and treatment context for each MNT intervention, prespecify clinically meaningful goals and endpoints, and document actual intervention exposure, adherence, safety, and feasibility [102,105]. Where patient characteristics or biomarkers are proposed to guide treatment selection, trials should test whether these factors modify responses to the defined intervention and whether the resulting patient–intervention match yields clinically meaningful benefit [103,106].

7. Clinical Implementation of MNT and Interpretation of Treatment Effects

Clinical effects must be interpreted alongside implementation: whether an intervention is safe, feasible, and delivered at the intended level of exposure [107,108].

7.1. Treatment Context and Dynamic Changes in Nutrition-Related Phenotypes

Nutrition-related phenotypes are jointly influenced by disease activity, cumulative organ damage, functional status, and treatment exposure. Glucocorticoids can cause weight gain and increase the risks of hyperglycemia, dyslipidemia, and adverse bone outcomes [109,110]. Disease control and medication exposure may also affect appetite, body weight, and body composition. MNT outcomes should therefore be interpreted in relation to the treatment phase. In T1DM, carbohydrate intake must also be coordinated with exogenous insulin [111]. These treatment-related risks support early nutritional screening and ongoing monitoring, but medication exposure alone does not determine the nutritional prescription.

7.2. Risk–Benefit Balance and Safety Boundaries of MNT

MNT should aim to achieve a favorable net clinical benefit rather than the greatest theoretical immunological or metabolic effect. Expected benefits must be weighed against nutritional adequacy, physiological safety, practical feasibility, and treatment burden. For restrictive approaches, such as a strict low-FODMAP diet or the elimination of multiple foods, criteria for reassessment, food reintroduction, or gradual liberalization should be defined at the outset [112,113]. Protein restriction and supplement use should be adjusted according to organ function, nutritional risk, and the strength of evidence, avoiding excessive restriction or unsupported escalation [114,115].

7.3. Actual Intervention Exposure and Interpretation of Treatment Effects

Prescribing a dietary intervention does not mean that the intended exposure has been achieved. Actual intervention exposure depends on the intensity and duration of the intervention, as well as adherence and the extent of deviation from the prescribed regimen [116]. It can be estimated using dietary records, adherence scores, appropriate digital recording tools, and validated objective markers of exposure where available [117,118]. Treatment effects should be interpreted in relation to actual exposure. A negative result supports biological non-response only when actual exposure is both sufficient and adequately characterized; otherwise, implementation difficulties should be considered, with limited feasibility treated as an implementation outcome. Positive outcomes should likewise be assessed against actual exposure to determine whether the observed response is consistent with the planned intervention.

7.4. Dynamic Implementation and Reassessment of MNT

Implementation begins with nutritional-risk screening and definition of the clinical problem and treatment goal, followed by characterization of the relevant nutritional phenotype, organ-function constraints, and background treatment. An MNT intervention supported by relevant clinical evidence is selected in light of these factors, with nutritional safety, clinically meaningful benefit, and practical feasibility assessed before implementation [119,120]. Before implementation, the intended intervention exposure and the target clinical outcomes and adverse effects to be monitored should be specified. During follow-up, actual exposure, target outcomes, and adverse effects should be assessed together; these findings should guide whether to continue or modify the regimen, relax dietary restrictions, or discontinue the intervention.

8. Conclusions and Future Perspectives

Autoimmune diseases are markedly heterogeneous, yet they may exhibit partially overlapping nutrition-related phenotypes and limited immunometabolic commonalities. These features can inform cross-disease assessment and generate hypotheses for patient stratification. Current human evidence supports disease-directed MNT in selected settings, alongside adjunctive and supportive applications across other clinical contexts.
The current evidence is limited by small sample sizes, heterogeneity among interventions, incomplete reporting of adherence and actual intervention exposure, confounding by background treatment, and short follow-up periods. Future research should validate reproducible clinical phenotypes and multi-omics biomarkers, determine whether they predict differential responses to specific MNT interventions, and test the clinical utility of patient–intervention matching in prospective trials. Better reporting of actual intervention exposure, safety, and feasibility would support the evaluation and clinical implementation of MNT.

Supplementary Materials

The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/nu18223746/s1, Supplementary File S1: Detailed search strategies for PubMed and ClinicalTrials.gov, including search topics, disease and topic search blocks, search date, filters, and retrieval counts.

Author Contributions

X.-W.Z.: Writing—original draft, Conceptualization, Investigation, Visualization. H.S.: Investigation, Methodology. L.Y.: Investigation, Methodology. J.-Q.H.: Investigation, Validation. K.X.: Investigation, Validation. R.M.: Investigation, Validation. L.L.: Writing—review & editing, Conceptualization, Funding acquisition, Resources, Supervision. All authors have read and agreed to the published version of the manuscript.

Funding

This study was supported by the 2024 Heilongjiang Province “Double First Class” Discipline Collaborative Innovation Achievement Project (no. LJGXCG2024-P09) and Joint guidance project of Natural Science Foundation of Heilongjiang Province (no. PL2026H306).

Institutional Review Board 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:
25(OH)D25-hydroxyvitamin D
AAVANCA-associated vasculitis
ACRAmerican College of Rheumatology
ADsautoimmune diseases
AILDAutoimmune liver disease
AITDAutoimmune thyroid disease
ANCAAntineutrophil cytoplasmic antibody
APSAntiphospholipid syndrome
ASankylosing spondylitis
CDCrohn’s disease
CDEDCrohn’s disease exclusion diet
CDED-ADCrohn’s disease exclusion diet in adults
CeDceliac disease
CIConfidence interval
CNSCentral nervous system
DHAdocosahexaenoic acid
DMARDdisease-modifying antirheumatic drug
EAT-10Eating Assessment Tool-10
EENexclusive enteral nutrition
ENenteral nutrition
EPAeicosapentaenoic acid
FODMAPfermentable oligosaccharides, disaccharides, monosaccharides, and polyols
FSSFatigue Severity Scale
GFDgluten-free diet
GFRglomerular filtration rate
GIgastrointestinal
GLIMGlobal Leadership Initiative on Malnutrition
HLAhuman leukocyte antigen
IBDinflammatory bowel disease
IBSirritable bowel syndrome
IFNinterferon
mCDEDmodified Crohn’s disease exclusion diet
MedDietMediterranean diet
MEDRAMediterranean diet intervention in adults with rheumatoid arthritis
MFISModified Fatigue Impact Scale
MGmyasthenia gravis
MNmembranous nephropathy
MNTmedical nutrition therapy
MSmultiple sclerosis
MSQoL-54Multiple Sclerosis Quality of Life-54
mTORmechanistic target of rapamycin
NSnot statistically significant
NSAIDsnon-steroidal anti-inflammatory drugs
PASIPsoriasis Area and Severity Index
PENpartial enteral nutrition
PNparenteral nutrition
PsOpsoriasis
QoLquality of life
RArheumatoid arthritis
RCTrandomized controlled trial
RHDrheumatic heart disease
ROSreactive oxygen species
SARC-FStrength, Assistance with walking, Rise from a chair, Climb stairs, and Falls
SjSSjögren’s syndrome
SLEsystemic lupus erythematosus
SScsystemic sclerosis
T1DMtype 1 diabetes mellitus
TNFtumor necrosis factor
Tregregulatory T cell
UCulcerative colitis

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