The participant is a 33-year-old male diagnosed with CD in early adulthood, with an otherwise unremarkable medical history except for a torn knee meniscus in 2009. There was no family history of IBD, although his maternal grandfather had irritable bowel syndrome. Diagnosis followed recurrent rectal bleeding, with colonoscopy and biopsy confirming inflammation. At age 20 in 2012, after being rejected as a blood donor for low haematocrit, he developed diarrhoea with haematochezia, averaging six to seven episodes daily. Flexible sigmoidoscopy revealed superficial rectal ulceration, and biopsy confirmed acute chronic colitis. Rectal 5-aminosalicylic acid (5-ASA) therapy resulted in partial improvement; however, adherence was poor.

By mid-2014, the participant’s symptoms worsened with recurrent haematochezia and diarrhoea, prompting a repeat colonoscopy that revealed terminal ileal ulceration and stellate colonic ulcers consistent with CD. He was treated with prednisone and azathioprine; however, the participant was hospitalised later that year for a partial small-bowel obstruction. In December 2014, infliximab (Remicade) was initiated, followed by methotrexate supplementation and intermittent corticosteroid therapy. Despite these therapies, disease control remained ineffective from 2014 to 2018, with ongoing inflammation, terminal ileal narrowing, fibrostenotic component deemed not reversible (noted on colonoscopy, see Table 1), frequent flares, decreased appetite because of constant nausea, significant fatigue, significant weight loss (decreased weight from 79 kgs to 65.77 kgs), multiple hospitalisations, one bowel obstruction episode, and culminating in a partial colectomy in early 2019.

The Crohn’s Disease Elimination Diet (CDED) is a structured dietary approach designed to reduce exposure to foods thought to exacerbate intestinal inflammation.¹⁷ The Whole30 diet represents a related elimination framework grounded in ketogenic and Paleo principles that exclude sugar, alcohol, grains, legumes, dairy and processed foods for a defined period.¹⁸ At the same time, low-FODMAP strategies focus on reducing fermentable carbohydrates through staged elimination and reintroduction.¹⁸ These approaches are commonly explored by patients with Crohn’s disease seeking symptom control through dietary modification.¹⁹

In late 2016, the patient implemented a Whole30-style elimination diet combined with a low-FODMAP approach, resulting in short-term symptomatic improvement lasting approximately 6 months. Following relapse, a GF diet was attempted, but provided minimal sustained benefit. After recurrent flares characterised by diarrhoea and cramping and progression to partial colectomy, the patient transitioned to a self-directed LCK dietary pattern. Total carbohydrate intake was consistently limited to fewer than 50 total grams per day with stable protein intake and increased dietary fats from foods such as butter, cream and bacon drippings. Non-starchy vegetables were eaten freely with added fats, without macro tracking or fasting. Although ketosis was expected, ketone levels were not measured (Figure 1).

This study is a single retrospective case report (n = 1) describing an individual with CD. Data were obtained from both the electronic medical record, including radiology findings, colonoscopy results, laboratory values, and the participant’s self-reported observations. Written informed consent was obtained from the patient for the publication of de-identified data. The Institutional Review Board at Liberty University reviewed this study and deemed it exempt per their guidelines.

The participant had a confirmed diagnosis of CD based on colonoscopy and histopathology, with disease involvement of the terminal ileum and colon. Recurrent flares, steroid dependence, escalation to biologic therapy, hospitalisation and surgical intervention, including partial colectomy in 2019, characterised the disease course before the DI. This clinical profile reflects moderate-to-severe, treatment-refractory disease prior to the initiation of the DI.

The DI was self-initiated and self-directed by the participant and was not prescribed as part of a formal clinical nutrition programme. Gastroenterology care, including medication management, laboratory monitoring, imaging, and endoscopic evaluation, continued under physician supervision during the DI period. No registered dietitian formally supervised the DI. However, the participant consulted regularly with a Metabolic Health Practitioner (MHP), well-versed in the use of TCR for chronic diseases like CD and its applications for symptom mitigation.

The participant implemented a TCR nutrition plan with clinical guidance. The macronutrient distribution consisted of total calories from fats (70% – 75%), protein (20% – 25%), and carbohydrates (5% – 10%), with total grams of carbohydrates strictly limited to 50 grams per day.²⁰ Each day, total carbohydrate intake was tracked by reviewing food labels and consulting publicly available online nutrition resources. (e.g. Google). The participant’s diet emphasised animal proteins (meats, fish, poultry, eggs), low-glycaemic vegetables, nuts and healthy fats such as olive oil, avocado, heavy cream, and butter, while avoiding grains, refined sugars, processed carbohydrates, and most starchy vegetables. Meal frequency was 2–3 meals per day, with an estimated caloric intake of approximately 1800–2000 calories per day. Intermittent fasting was not incorporated. Over the following year (2019–2020), adherence to the TCR plan was maintained.

Beginning in 2017, the participant adopted a CDED, followed by a GF dietary approach after disease relapses. Both interventions resulted in limited durability of symptom control, and disease progression ultimately required partial colectomy in January 2019. After surgery, the participant initiated an LCK DI.

The LCK DI consisted of restricting total daily carbohydrate intake to fewer than 50 total grams while maintaining stable protein intake. Dietary fats increased to satiety through foods such as butter, heavy cream, sour cream, and bacon drippings, and non-starchy vegetables were consumed freely with added fats. Simple carbohydrates were significantly limited or eliminated.

The participant consumed two to three meals per day with very-low-carbohydrate snacks as needed, including meat and cheese. Intermittent fasting was not incorporated, and no nutrition applications were used for macronutrient tracking. Daily total carbohydrate intake was monitored by reading nutrition labels to track carbohydrate grams in selected foods, using Google to look up nutrition information when labels were unavailable, and keeping either a mental or written log of carbohydrate intake at each meal. This approach helped the participant remain under 50 grams per day, following guidance provided during consultations with the MHP.

Clinical information was abstracted from records provided by the participant, including chart notes, colonoscopy and pathology reports, radiologic imaging results, laboratory values (including haematocrit and C-reactive protein [CRP]), and infusion records from 2012 to 2023. Patient-reported dietary history and lifestyle factors were also recorded, particularly with the transition to an LCK diet. These sources were used to construct a longitudinal clinical timeline spanning diagnosis, treatment escalation, surgical intervention and dietary modification.

The clinical course was evaluated using multiple data sources. Symptom reporting was conducted using the Crohn’s and Colitis Foundation Inflammatory Bowel Disease (CCF-IBD) Symptom Tracker, a standardised tool widely used to identify CD symptoms that focuses on symptom frequency, including diarrhoea, haematochezia and abdominal pain²¹ (see Table 2). Objective findings were obtained from colonoscopy, imaging and biopsy reports, while laboratory monitoring focused on inflammatory markers, particularly high-sensitivity C-reactive protein (hs-CRP). Records of medication use, hospitalisations and surgical interventions were reviewed to track disease management and clinical progression. In addition, patient-reported outcomes were documented, including weight, number of emergency room visits, colonoscopy results, diet type, medications used, QoL measures and functional status. Clinical remission was defined as sustained absence of GI symptoms, discontinuation of Crohn’s-related pharmacologic therapy, and a lack of active inflammation measured by the number of flare-up episodes, and results on follow-up colonoscopies. The participant continued an LCK diet using TCR as a long-term maintenance strategy through 2025.

Ethical clearance to conduct this study was obtained from the Liberty University Institutional Review Board (No. IRB-FY25-26-656).

The subject reports his CD symptoms started in his junior year of high school with upset stomach, and through his senior year, when his symptoms were increasing. He became aware of his chronic fatigue during his senior year of high school. In the two years following high school, his fatigue became debilitating. He states, ‘I was unable to focus. Having conversations took effort’. He avoided any romantic relationships because ‘I didn’t even have the energy to carry on a conversation’. ‘I was living day-to-day. I had to drop out of community college. My life took a completely different path. Instead of going toward my intended career in healthcare, I have worked as a welder, groundskeeper at golf courses, and now as a mechanic’.

Since focusing on restricting his carbohydrates, the subject reports he has been symptom-free and medication-free (Table 1). He reports no CD flare-ups in the past two years (2023–2025). He also reported 6–7 episodes of diarrhoea per day before the intervention, which were reduced to 0 per day after initiating the intervention and have been maintained to the present time. His strength has returned, and he feels mentally clear. He has lost significant weight because of the severity of his condition in 2018 (reduced weight from a normal of 79 kgs to 65.77 kgs). The participant was able to increase his weight to 77.4 kg over the course of the year on LCK diet and, finally, to 79 kg (his normal body weight) with complete symptom remission to the present (see Table 2). The presence of rectal bleeding and rectal and ileal ulcerations has also resolved with colonoscopies reported as normal from 2020 to the present. He is now moving forward with his life. However, he regretfully states, ‘I lost ten years’. In addition to overall symptoms, the participant admits that occasionally, if he strayed from his LCK diet and indulged in pastries or bread for a day or two, he would experience a return of CD symptoms with stomach upset and diarrhoea. By promptly and aggressively eliminating carbohydrates, he reports that his symptoms would resolve in a couple of days. He reported overall changes in his CD symptoms using the CCF-IBD Symptom Tracker, as illustrated in Table 2.

Dietary modification has emerged as a promising therapeutic strategy for IBD. The 2024 AGA Clinical Practice Update on Diet and Nutritional Therapies in IBD identified four evidence-based dietary approaches: the Mediterranean Diet, the Specific Carbohydrate Diet (SCD), the low-FODMAP diet, and the CDED.²² Recent comparative trials have shown promising results for some of these dietary approaches.^8,10 The Dietary Inflammatory Nutrient Evaluation for Crohn’s Disease (DINE-CD) study demonstrated that both SCD and the Mediterranean diet can reduce symptoms and inflammation in CD.²³ The CDED, combined with partial enteral nutrition, has achieved remission and reduced faecal calprotectin levels, even as an add-on therapy to biologic medications.¹⁰ Despite this progress, most dietary studies have been limited by small sample sizes and heterogeneity in protocols, and many have shown symptomatic improvement without corresponding changes in objective inflammatory markers.⁴

Our subject tried various dietary approaches without much success, such as the SCD, the low-FODMAP diet, the CDED, and the Mediterranean Diet, before 2019, when he learned about the LCK diet. Notably, his 2020 and 2025 colonoscopy results indicated that his bowel appeared normal, with no signs of CD, despite many years of positive CD indications reported with colonoscopies and even a partial colectomy in 2019. These findings suggest that sustained adherence to an LCK dietary pattern may promote mucosal healing and durable remission in CD, pointing to carbohydrate restriction as a potential unifying mechanism across effective nutritional interventions.

The four AGA-recognised DIs share a common feature with LCK diets: the selective elimination of specific carbohydrates.² The low-FODMAP diet restricts FODMAP, which are short-chain carbohydrates that are poorly absorbed and rapidly fermented by gut bacteria.²⁴ The CDED restricts processed foods and gluten-containing grains while allowing certain whole-food carbohydrates.²⁵ The SCD eliminates complex carbohydrates, disaccharides and most grains.²⁶ Even the Mediterranean diet emphasises complex carbohydrates while minimising refined carbohydrates and added sugars.¹² The LCK approach represents a more comprehensive restriction, potentially amplifying therapeutic mechanisms of carbohydrate elimination while simultaneously inducing metabolic ketosis and attendant anti-inflammatory effects.⁷ Although the participant did not test his blood ketones during the intervention period, we can infer that the anti-inflammatory effects of the LCK diet contributed to the mitigation of his long-standing symptoms.

The elevation of circulating ketone bodies, particularly beta-hydroxybutyrate (BHB), is the primary metabolic hallmark of LCK diets and provides a mechanistic foundation for their therapeutic efficacy in IBD.⁹ Beta-hydroxybutyrate has demonstrated potent anti-inflammatory properties through multiple pathways. Research indicates that BHB directly inhibits the nucleotide-binding oligomerisation domain, Leucine-rich repeat-containing, Pyrin domain-containing 3 (NLRP3) inflammasome, a crucial component of innate immunity that regulates the production of inflammatory cytokines, including IL-1β and IL-18.² Additionally, BHB ameliorates colitis by promoting M2 macrophage polarisation through STAT6-dependent signalling, thereby shifting immune responses from a pro-inflammatory to an anti-inflammatory phenotype.²

Studies in murine colitis models have demonstrated that BHB administration reduces disease activity, improves colon length, and promotes intestinal tissue repair by inhibiting aberrantly activated NF-κB/NLRP3 signalling.²⁰ Importantly, IBD patients exhibit lower colonic mucosal BHB levels than healthy controls, suggesting that endogenous BHB production via dietary ketosis may restore a protective metabolic environment.⁹ In addition, a study by Barrea et al. investigated the effects of an LCK diet on hs-CRP and other inflammatory markers. The improvements in both hepatic insulin sensitivity and gut microbiome modulation seen in their subjects were influenced by carbohydrate restriction and the presence of dietary ketosis, with reductions in hs-CRP.²⁷ The results of the study by Barrea support the findings of our case report participant, who experiences significant reductions in hs-CRP post-LCK DI (see Table 1).

A recent case series of 10 patients by Norwitz et al., involving individuals with histologically confirmed IBD who achieved clinical remission on carnivore-ketogenic diets (a form of LCK) without medication, provides compelling clinical support for these mechanistic hypotheses, with observations showing an inverse association between intestinal ketone levels and IBD activity.⁹ Once the participant began reducing his daily carbohydrate intake, he noticed improvements in his diarrhoea and pain, and a reduction in flare-ups, supporting other studies on the beneficial effects of this dietary strategy on CD symptoms.⁹ His CCF-IBD Tracker reports demonstrated noticeable improvements in symptoms (see Table 2).

Low-carbohydrate ketogenic diets emphasise whole foods, exclude gluten and restrict processed and ultra-processed foods. This approach profoundly alters gut microbiome composition and metabolic activity, leading to therapeutic benefits. The low-residue profile may lessen fermentable substrates for bacterial metabolism, potentially decreasing pro-inflammatory metabolites and providing ‘bowel rest’.²⁴ The participant experienced fewer diarrhoea episodes after starting the diet while continuing Ustekinumab injections, making it difficult to determine which factor led to greater improvement. However, the positive effects became more apparent after discontinuing Ustekinumab in 2023, as symptoms remained absent for two years with LCK dietary management alone. This case, along with emerging evidence, indicates that structured LCK diets warrant further study in controlled trials to confirm their efficacy, safety and optimal management of IBD.

As with any study, certain limitations exist. The single-subject design (n = 1) limits generalisability, and characteristics such as age, comorbidities and adherence may have influenced the outcomes. The 7-year duration also raises the potential for recall bias, although hospital records verified the timeline, hospitalisations and medications.

Observer bias and reliance on self-reported dietary logs may have reduced accuracy, as the researcher’s familiarity with the participant could shape interpretation. The absence of a control group in this retrospective case report (n = 1) prevents the determination of causality, as changes could reflect placebo effects or concurrent treatments. These factors highlight the need for a cautious interpretation of the findings. As this was a retrospective report, not a study, there were no food logs, photo meal records, or blood ketone measurements.

Despite these limitations, the extended observation revealed consistent positive outcomes over time. Verification of dietary and symptom data would strengthen the validity of results. The influence of medication alongside DI remains an important consideration in assessing improvement in CD symptoms.

This study was a retrospective case report (n = 1) and can serve as a foundation for future research with a more robust study design. Future research should prioritise well-designed prospective trials to evaluate the efficacy, safety and sustainability of LCK diets in CD and other IBDs. Adequately powered randomised controlled trials are needed to determine whether TCR and nutritional ketosis (NK) independently promote healing of the gut lining, sustained remission, reduced flare frequency and improvements in objective inflammatory markers and hs-CRP. Mechanistic studies should further investigate the role of BHB in normalising intestinal immune responses, improving gut epithelial barrier function and assessing the role of gut microbiome composition in human IBD. Standardised dietary protocols and objective adherence indicators, such as blood or breath ketone monitoring, would strengthen the rigour of future studies. Comparative effectiveness research evaluating LCK diets alongside AGA-recommended approaches (including the CDED, the low-FODMAP diet and GF diets) could clarify whether TCR provides unique metabolic benefits. Long-term safety data are also needed to assess micronutrient adequacy, lipid changes and microbiome diversity. Finally, studies examining integration with biologic or immunomodulatory therapies, microbiome analysis, faecal calprotectin levels, and the addition of biomarker monitoring may help identify patients most likely to benefit from combined nutritional and pharmacologic strategies.