Journal of Food & Nutritional Sciences
This case report details a functional nutrition approach for an 11-year-old male diagnosed with Crohn’s disease and elevated fecal calprotectin levels. The patient initially presented with gastrointestinal pain, bloating, fever, facial swelling, and blood in the stool. Early management emphasized removing inflammatory foods through an eight-to-nine-week elimination diet, followed by gradual transition to a whole-food, modified Paleo pattern. To further support intestinal healing, a targeted supplement protocol was implemented, including serum-derived immunoglobulins, gut barrier-restoring nutrients, probiotics, and high-potency omega-3 fatty acids. Together, these interventions aimed to reduce gastrointestinal inflammation, improve mucosal barrier integrity, and restore microbial balance. Over the following months, the patient experienced significant resolution of gastrointestinal pain, bloating, and facial swelling, along with cessation of rectal bleeding. Fecal calprotectin decreased to 0 µg/g, reflecting normalization of intestinal inflammation. A brief, asymptomatic elevation in early 2025 improved with reinforced dietary consistency, without the need for medication. Throughout two years of follow-up, the patient remained free of gastrointestinal symptoms while avoiding pharmacologic therapy. This case highlights the value of a comprehensive nutrition and supplement-based approach in supporting inflammatory balance and restoring proper gastrointestinal function in pediatric Crohn’s disease.
*Corresponding Author:
Frank Bodnar,
The Nutrient Fix, 12295 Blue Lake Ct., Noblesvile, IN 46060, USA; Email: thenutrientfix@gmail.com
DOI: http://www.10.1057/jfns.2025.000050
ABSTRACT
This case report details a functional nutrition approach for an 11-year-old male diagnosed with Crohn’s disease and elevated fecal calprotectin levels. The patient initially presented with gastrointestinal pain, bloating, fever, facial swelling, and blood in the stool. Early management emphasized removing inflammatory foods through an eight-to-nine-week elimination diet, followed by gradual transition to a whole-food, modified Paleo pattern. To further support intestinal healing, a targeted supplement protocol was implemented, including serum-derived immunoglobulins, gut barrier-restoring nutrients, probiotics, and high-potency omega-3 fatty acids. Together, these interventions aimed to reduce gastrointestinal inflammation, improve mucosal barrier integrity, and restore microbial balance. Over the following months, the patient experienced significant resolution of gastrointestinal pain, bloating, and facial swelling, along with cessation of rectal bleeding. Fecal calprotectin decreased to 0 µg/g, reflecting normalization of intestinal inflammation. A brief, asymptomatic elevation in early 2025 improved with reinforced dietary consistency, without the need for medication. Throughout two years of follow-up, the patient remained free of gastrointestinal symptoms while avoiding pharmacologic therapy. This case highlights the value of a comprehensive nutrition and supplement-based approach in supporting inflammatory balance and restoring proper gastrointestinal function in pediatric Crohn’s disease.
Keywords: Crohn’s disease; pediatric inflammatory bowel disease; fecal calprotectin; functional nutrition; elimination diet; gut barrier integrity; nutraceuticals; probiotics; omega-3 fatty acids; serum-derived immunoglobulins.
ABBREVIATIONS:
CD – Crohn’s disease
FC – Fecal calprotectin
IBD – Inflammatory bowel disease
CRP – C-reactive protein
ESR – Erythrocyte sedimentation rate
TNF-α – Tumor necrosis factor alpha
IL – Interleukin
SBI – Serum-derived bovine immunoglobulin
EPA – Eicosapentaenoic acid
DHA – Docosahexaenoic acid
CFU – Colony-forming units
GI – Gastrointestinal
INTRODUCTION
Crohn’s disease (CD) is a chronic inflammatory condition that can affect any region of the gastrointestinal tract, most commonly the terminal ileum and colon [1]. Typical manifestations include diarrhea, abdominal cramping, fatigue, and dermatologic changes [2], while disease progression may result in complications such as intestinal stenosis, fistula formation, or abscess development [1]. Endoscopy remains a primary diagnostic tool, providing direct visualization of the intestinal mucosa and permitting biopsy; however, it can be an invasive process especially for pediatric patients. Laboratory biomarkers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) [1] are also used to evaluate disease activity, though their sensitivity and specificity are limited. Fecal calprotectin (FC), a neutrophil-derived protein, has emerged as a useful non-invasive marker that correlates positively with intestinal inflammation and clinical flare-ups in CD [3].
Given this correlation, achieving and maintaining optimal fecal calprotectin levels is a key therapeutic goal, as it closely reflects mucosal inflammation and disease activity. Dietary and nutraceutical interventions that address intestinal permeability, microbial imbalance, and immune activation may serve as effective adjuncts to traditional care, particularly in pediatric cases where minimizing pharmaceutical exposure is desired.
Emerging evidence suggests that nutrition-focused interventions can play a meaningful role in supporting long-term healing and symptom stability in Crohn’s disease by influencing key physiologic processes involved in the disease progression. Nutritional choices significantly affect intestinal permeability, microbial composition, and immune signaling, all of which contribute to inflammatory activity in the gastrointestinal tract. Targeted nutritional interventions may reduce exposure to dietary antigens, support mucosal repair, and promote immune tolerance, leading to a significant reduction in inflammation over time.
In pediatric populations, where lifelong medication exposure is especially concerning, nutrition-centered approaches may offer additional value by supporting gut barrier integrity and immune regulation while minimizing reliance on pharmaceutical therapy. Evidence examining individualized dietary and nutraceutical interventions helps clarify how functional nutrition strategies may contribute to sustained remission and long-term symptom stability in Crohn’s disease.
In this case, a functional nutrition approach was implemented to modulate inflammatory pathways and restore intestinal integrity using targeted supplementation and dietary modification. The intervention included Designs for Health’s OmegAvail™ Hi-Po, IgGI Shield™, GI Revive®, and ProbioMed™ 50, each selected to support specific aspects of gut and immune health. OmegAvail™ Hi-Po provides high-potency omega-3 fatty acids to help regulate inflammatory mediators; IgGI Shield™ supplies serum-derived immunoglobulins that bind and neutralize microbial antigens; GI Revive® delivers nutrients that promote epithelial repair and mucosal barrier function; and ProbioMed™ 50 replenishes beneficial commensal bacteria essential for maintaining intestinal balance.
This case report examines the implementation of a comprehensive, integrative intervention combining dietary modification, gut health restoration, and targeted supplementation to reduce inflammation and support clinical improvement in a male diagnosed with Crohn’s disease. The study aims to evaluate the impact of an evidence-based functional approach on intestinal inflammation, gut barrier integrity, and quality of life in pediatric Crohn’s disease.
NARRATIVE
An 11-year-old male presented in early 2023 with abdominal pain related to eating and physical activity, along with bloating, intermittent fever, facial swelling, and blood in the stool. A pediatric gastroenterologist performed endoscopy and colonoscopy with biopsies showing active ileitis with ulceration and poorly formed non-necrotizing granulomas in several segments of the colon, consistent with early Crohn’s disease. Other possible causes, including immune disorders and infection, were evaluated but not confirmed. The physician recommended infliximab (REMICADE®), a tumor necrosis factor-alpha (TNF-α) inhibitor, dosed at 200 mg at weeks 0, 2, and 6, followed by every eight weeks. After reviewing potential side effects, the parent decided to delay medication and pursue a functional nutrition plan first.
The child’s medical history was unremarkable until late 2022, when gastrointestinal symptoms began. Baseline labs in January 2023 showed normal T-cell and NK-cell levels, slightly elevated absolute CD19 B-cells (1,374/mm³), and a CD4:CD8 ratio of 2.62, findings consistent with normal cellular immunity and mild B-cell activation. Screening for HIV, hepatitis B, infection, and tuberculosis was negative, and no medications were started at that time. Surgical pathology confirmed granulomatous inflammation in both the ileum and colon, consistent with Crohn’s disease. Fecal calprotectin was elevated at 260 µg/g. Despite the gastroenterologist’s advice to begin biologic therapy, the family chose a nutritional and supplemental plan emphasizing gut healing and immune modulation.
The initial approach used a strict carnivore diet for approximately nine weeks to remove dietary antigens and calm intestinal inflammation. During this time, the child began daily supplementation with IgGI Shield™, GI Revive®, ProbioMed™ 50, and OmegAvail™ Hi-Po. These products were chosen to support mucosal repair, microbiome balance, and anti-inflammatory activity through immunoglobulins, targeted probiotics, and omega-3 fatty acids. Within several weeks, abdominal pain, bloating, and facial swelling resolved completely. Blood in the stool stopped, and energy, appetite, and physical activity returned to normal.
Objective markers during this time improved in addition to physical symptoms. A stool calprotectin test in March 2024 showed full normalization at 0 µg/g, indicating remission. The diet was then expanded to a modified whole-food diet focused on organic produce, lean proteins, and avoidance of refined sugars and processed foods. Occasional deviations in the diet led only to slightly increased facial swelling without gastrointestinal pain or bleeding. The patient remained medication-free.
In January 2025, a routine stool calprotectin test increased to 806 µg/g, though the child remained nearly asymptomatic. The only change noted was mild morning puffiness around the eyes, with no reports of abdominal pain, diarrhea, or blood in the stool. Dietary compliance was reinforced, in a modified Paleo diet, while continuing the same supplement regimen. By May 2025, testing showed strong improvement as calprotectin reduced to 448 µg/g without any pharmacologic intervention. I ran another fecal calprotectin test in August 2025 that came back at 141 ug/g, building on the improvement from May.
Across the two-year period, no medications, hospitalizations, or emergency visits occurred. Energy and activity levels remained appropriate for age. The temporary biomarker elevation in early 2025 appeared to reflect a short-term inflammatory response rather than a significant clinical relapse. The child continued to follow an anti-inflammatory diet and supplement protocol consistently.
By mid-2025, the patient was fully asymptomatic, reporting normal digestion, no gastrointestinal discomfort, and stable energy levels. Calprotectin continued to trend downward. A modified Paleo diet was enforced, and the child continued to avoid processed or high-sugar foods, which had previously correlated with symptom recurrence. Regular physical activity was encouraged, and overall well-being was described as excellent.
The integration of immunoglobulins, targeted probiotics, and omega-3 fatty acids appeared to work synergistically to support mucosal healing and control inflammation. Improvements in fecal calprotectin provided objective confirmation of reduced intestinal inflammation and correlated closely with symptom recovery. Although a sharp rise in calprotectin occurred in early 2025, the absence of symptoms and fast improvement with dietary adherence suggest mild, reversible inflammation rather than a full-blown relapse. Continued monitoring and dietary consistency helped maintain stability without the need for pharmaceuticals.
This case demonstrates significant clinical remission of pediatric Crohn’s disease through a structured dietary and supplemental plan without pharmacologic therapy. The early decision to delay medication allowed for natural healing under a controlled nutrition protocol. Functional interventions that focused on removing antigenic foods, restoring mucosal integrity, and supporting microbial balance resulted in sustained remission and normalization of inflammatory markers. The intervention appeared safe and well-tolerated for over two years, with no adverse events reported and stable lab values throughout the observation period.
PATIENT PERSPECTIVE
When my son first started having stomach pain, fevers, and blood in his stool, we thought it was a passing virus. Hearing the words “inflammatory bowel disease” and then “Crohn’s” attached to an 11-year-old was overwhelming. The pediatric gastroenterologist recommended starting infliximab, and while I respect that approach, the potential side effects felt like too much for someone so young. I was also discouraged to hear that nutrition was unlikely to make a difference when, as a parent, food felt like one of the few things I could control.
We decided to pursue a functional medicine path first. As a family, we committed to a strict eight-to-nine-week carnivore-style elimination diet to remove as many potential GI triggers as possible, especially sugars and higher-fiber carbohydrates. At the same time, we began a targeted supplement regimen including IgGI Shield™, GI Revive®, ProbioMed™ 50, and OmegAvail™ Hi-Po, while encouraging him to stay as active as his energy and symptoms allowed.
It wasn’t easy, with social events and holidays, and the restrictions on a young boy’s diet were challenging for all of us. But the changes in his symptoms and labs made the effort feel worthwhile. His GI pain, bloating, facial swelling, and blood in the stool resolved, and his calprotectin levels improved dramatically. When his diet and supplements slipped over the holidays, we saw how quickly his markers and symptoms could flare again, which reinforced how important consistency is for him.
We’re not perfect, but today my son is active, off medication, and living a much more normal life. I’m incredibly grateful that we were able to find an approach that gave him relief and, at least for now, allowed us to avoid starting biologic therapy.
DISCUSSION
Crohn’s disease is a chronic, relapsing inflammatory condition of the gastrointestinal tract driven by a heightened immune response to intestinal microbes in susceptible individuals. Loss of epithelial barrier integrity allows antigens and bacteria to penetrate the mucosa, activating macrophages and T-helper cells that release pro-inflammatory cytokines such as TNF-α, IL-6, and IL-23 [4]. This cascade may promote granulomatous inflammation, ulceration, and various characteristics of CD. Elevated fecal calprotectin (FC), a neutrophil-derived biomarker, closely reflects mucosal inflammation and often rises before clinical relapse [3]. In this case, the patient’s baseline FC of 260 µg/g reflected active inflammation, which normalized to 0 µg/g following nutritional interventions, eventually leading to mucosal healing and sustained clinical remission.
The patient’s clinical and FC response highlights how nutrition-based interventions can address multiple mechanisms underlying CD, including epithelial repair, microbial balance, and immune regulation. An initial carnivore-style elimination phase minimized dietary antigens and inflammation, giving the intestinal mucosa an opportunity to rest and recover. The gradual reintroduction of nutrient-dense, anti-inflammatory foods helped reduce both intestinal permeability and pro-inflammatory cytokine activity. The patient’s recovery demonstrates that targeted nutritional support can help restore gut and immune function in Crohn’s disease.
Supplement use targeted the key mechanisms underlying the patient’s presentation. Designs for Health’s IgGI Shield™, providing 2.5 g of serum-derived bovine immunoglobulin (SBI) per serving, was taken twice daily which supplies concentrated immunoglobulins that bind microbial components such as lipopolysaccharides and other bacterial antigens to support gut barrier integrity and immune homeostasis [5–7]. These immunoglobulins act within the intestinal lumen to neutralize antigens before they cross the mucosa, helping to maintain normal epithelial permeability and reduce immune activation [8,9]. By reducing exposure to bacterial antigens and supporting the production of short-chain fatty acids [10], SBI helps maintain mucosal balance and may lower the risk of relapse. The normalization of FC observed after SBI initiation is consistent with these mechanisms.
Designs for Health’s GI Revive® (8 g powder daily) provided key nutrients that support epithelial regeneration and intestinal barrier repair, including 1.5 g L-glutamine, 1 g N-acetyl-D-glucosamine, 17 mg zinc L-carnosine, 400 mg deglycyrrhizinated licorice, and 300 mg aloe vera. L-glutamine serves as the primary fuel source for enterocytes and helps maintain tight-junction integrity and reduce intestinal permeability, which helps support a healthy epithelial barrier [11,12]. N-acetyl-D-glucosamine supports healthy mucin production, a family of glycoproteins secreted by intestinal epithelial cells that play a role in mucosal protection, microbial balance, and lubrication of the GI tract [13]. Zinc L-carnosine aids in epithelial repair and helps maintain balanced inflammatory signaling within the mucosa [14]. Botanical demulcents such as slippery elm, aloe vera, and marshmallow root further aid mucosal recovery by coating and soothing the intestinal lining. Together, these compounds reinforce barrier integrity, reducing epithelial stress and downstream immune activation.
Restoring microbial balance was supported with ProbioMed™ 50 (50 billion CFUs daily), a probiotic containing Lactobacillus plantarum, L. acidophilus, L. rhamnosus GG, Bifidobacterium bifidum, B. longum, and other Bifidobacterium species. These species have been shown to support microbial diversity, promote colonization of beneficial bacteria, and regulate immune signaling within the intestinal environment [15,16]. Clinical studies on Bifidobacterium animalis demonstrate improvements in gastrointestinal comfort, immune function, and colonic transit [17,18]. Restoration of microbial diversity is especially important in CD, as depletion of beneficial bacteria can perpetuate dysbiosis and gut barrier dysfunction.
Systemic inflammation was addressed with OmegAvail™ Hi-Po, providing 1.6 g of EPA and DHA in a 1:1 ratio. Omega-3 fatty acids downregulate inflammatory signaling by reducing the production of pro-inflammatory eicosanoids and cytokines such as TNF-α, IL-1β, and IL-6, while also promoting the formation of specialized pro-resolving mediators that help downregulate inflammation. These actions aid in restoring immune balance and support the resolution of chronic inflammation [19].
The patient’s sustained resolution of gastrointestinal pain, bloating, fever, facial swelling, and rectal bleeding, along with normalization of stool frequency and stable biomarkers without pharmacologic therapy, illustrate that functional nutrition management can achieve clinically meaningful outcomes in select CD cases. While pharmaceutical interventions such as infliximab remain the standard of care for CD, they primarily act by suppressing immune-mediated inflammation rather than addressing underlying gut barrier or microbiome dysfunction. When implemented under clinical supervision and guided by laboratory monitoring, a functional nutrition approach may achieve comparable outcomes through non-pharmacologic means. Continued follow-up remains critical, as low-grade inflammation can persist and moderate FC elevations may precede a relapse [3].
Beyond symptom resolution, this case illustrates the larger physiological impact of addressing gut barrier repair, microbial balance, and inflammation through supplementation. By restoring mucosal integrity and supporting immune tolerance, these interventions can stop the inflammatory cascade that drives disease progression. Unlike pharmaceutical agents that primarily suppress immune activity, nutrition-based therapies work by enhancing epithelial resilience, microbial diversity, and mitochondrial function, which are essential to long-term gastrointestinal and overall health. Supporting these processes may offer benefits for both intestinal healing and overall recovery in Crohn’s disease.
Collectively, the selected interventions were designed to target multiple drivers of Crohn’s disease pathology rather than a single inflammatory pathway. By reducing the antigen burden, supporting epithelial barrier repair, restoring microbial balance, and modulating cytokine-driven immune responses, this targeted supplementation strategy aimed to interrupt the perpetual cycle of intestinal inflammation. The improvement in gastrointestinal symptoms and normalization of fecal calprotectin observed in this case suggests that addressing these mechanisms collectively may support both clinical improvement and objective reductions in intestinal inflammation.
CONCLUSION
This case illustrates how a functional nutrition intervention can support meaningful improvements in gastrointestinal function and inflammatory balance in a pediatric patient diagnosed with Crohn’s disease in January 2023. At presentation, the child experienced gastrointestinal pain with eating and physical activity, bloating, fever, facial swelling, and occasional blood in the stool. A baseline fecal calprotectin of 260 µg/g indicated active intestinal inflammation. Although pharmaceutical therapy was recommended after diagnosis, the family elected to begin a nutrition-based plan before starting medication.
The initial intervention period lasted approximately eight to nine weeks and focused on removing inflammatory and antigenic foods while supporting the intestinal lining and microbiome. Daily supplementation with immunoglobulins, probiotics, omega-3 fatty acids, and epithelial-repairing nutrients were introduced during this phase. These interventions targeted key mechanisms involved in CD pathology, including microbial dysbiosis, intestinal permeability, and cytokine-driven inflammation. Immunoglobulins helped bind microbial antigens, probiotics supported microbial diversity and immune regulation, and omega-3 fatty acids influenced the production of inflammatory mediators. Nutrients such as glutamine, N-acetyl-D-glucosamine, zinc-L-carnosine, and mucosal botanicals contributed additional support for epithelial integrity. As this plan was followed consistently, the patient experienced comprehensive relief of gastrointestinal symptoms and returned to both normal daily functioning and physical activity.
Laboratory testing reflected these clinical changes. Calprotectin decreased from 260 µg/g to 0 µg/g by March 2024, suggesting significant improvement in mucosal inflammation. A temporary increase to 806 µg/g in early 2025 occurred during a period of reduced dietary consistency but was not associated with symptom recurrence. Once the nutritional intervention was resumed, calprotectin returned to normal, indicating a reversible inflammatory fluctuation rather than a clinical relapse. No medications, emergency visits, or hospitalizations were required throughout the two-year observation period, and activity levels remained appropriate given the patient’s age.
Although this is a single case, the pattern of improvement suggests that early dietary modification, targeted support for barrier repair, and modulation of the microbiome may provide valuable support in pediatric CD. Additional research is warranted to explore how nutrition-focused strategies may contribute to long-term mucosal healing and symptom stability in Crohn’s disease cases.
Appreciation for editing by Jonathan Halcovage, and graduate student interns at the Notre Dame of Maryland University for research and development input. Dr. David Reilly for CARE guideline support in manuscript.
REFERENCES
1. Li J, Xu M, Qian W, et al. Clinical value of fecal calprotectin for evaluating disease activity in Crohn’s disease. Front Physiol. 2023; 14:1186665.
2. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Symptoms & causes of Crohn’s disease. National Institutes of Health. 2024.
https://www.niddk.nih.gov/health-information/digestive-diseases/crohns-disease/symptoms-causes
3. Kennedy NA, Jones GR, Plevris N, Patenden R, Arnott ID, Lees CW. Association between level of fecal calprotectin and progression of Crohn’s disease. Clin Gastroenterol Hepatol. 2019; 17(11):2269–2276.e4.
4. Baumgart DC, Sandborn WJ. Crohn’s disease. Lancet. 2012; 380(9853):1590–1605.
5. Pusztai A, Ewen SW, Grant G, et al. Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins. Br J Nutr. 1993; 70(1):313–321.
6. Detzel CJ, Horgan A, Henderson AL, et al. Bovine immunoglobulin/protein isolate binds pro-inflammatory bacterial compounds and prevents immune activation in an intestinal co-culture model. PLoS One. 2015; 10(4):e0120278.
7. Henderson AL, Brand MW, Darling RJ, et al. Attenuation of colitis by serum-derived bovine immunoglobulin/protein isolate in a defined microbiota mouse model. Dig Dis Sci. 2015; 60(11):3293–3303.
8. Petschow B, Burnett B, Shaw A, Weaver EM, Klein GL. Serum-derived bovine immunoglobulin/protein isolate: postulated mechanism of action for management of enteropathy. Clin Exp Gastroenterol. 2014; 7:181–190.
9. Petschow BW, Bilkslager AT, Weaver EM, et al. Bovine immunoglobulin protein isolates for the nutritional management of enteropathy. World J Gastroenterol. 2014; 20(33):11713–11726.
10. Van den Abbeele P, Kunkler CN, Poppe J, et al. Serum-derived bovine immunoglobulin promotes barrier integrity and lowers inflammation for 24 human adults ex vivo. Nutrients. 2024; 16(11):1585.
11. Kim MH, Kim H. The roles of glutamine in the intestine and its implication in intestinal diseases. Int J Mol Sci.2017; 18(5):1051.
12. Perna S, Alalwan TA, Alaali Z, et al. The role of glutamine in the complex interaction between gut microbiota and health: a narrative review. Int J Mol Sci. 2019; 20(20):5232.
13. Salvatore S, Heuschkel R, Tomlin S, et al. A pilot study of N-acetyl glucosamine in pediatric chronic inflammatory bowel disease. Aliment Pharmacol Ther. 2000; 14(12):1567–1579.
14. Hewlings S, Kalman D. A review of zinc-L-carnosine and its positive effects on oral mucositis, taste disorders, and gastrointestinal disorders. Nutrients. 2020; 12(3):665.
15. Elawadli I, Brisbin JT, Mallard BA, et al. Differential effects of lactobacilli on activation and maturation of mouse dendritic cells. Benef Microbes. 2014; 5(3):323–334.
16. Ibarra A, Latreille-Barbier M, Donazzolo Y, et al. Effects of 28-day Bifidobacterium animalis subsp. lactis HN019 supplementation on colonic transit time and gastrointestinal symptoms. Gut Microbes. 2018; 9(3):236–251.
17. Waller PA, Gopal PK, Leyer GJ, et al. Dose-response effect of Bifidobacterium lactis HN019 on whole gut transit time. Scand J Gastroenterol. 2011; 46:1057–1064.
18. Miller LE, Lehtoranta L, Lehtinen MJ. Effect of Bifidobacterium animalis ssp. lactis HN019 on cellular immune function. Nutrients. 2017; 9:191.
19. Calder PC. Marine omega-3 fatty acids and inflammatory processes: effects, mechanisms, and clinical relevance. Biochim Biophys Acta.
PEER REVIEW
Not commissioned. Externally peer reviewed.
1. Li J, Xu M, Qian W, et al. Clinical value of fecal calprotectin for evaluating disease activity in Crohn’s disease. Front Physiol. 2023; 14:1186665.
2. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Symptoms & causes of Crohn’s disease. National Institutes of Health. 2024.
https://www.niddk.nih.gov/health-information/digestive-diseases/crohns-disease/symptoms-causes
3. Kennedy NA, Jones GR, Plevris N, Patenden R, Arnott ID, Lees CW. Association between level of fecal calprotectin and progression of Crohn’s disease. Clin Gastroenterol Hepatol. 2019; 17(11):2269–2276.e4.
4. Baumgart DC, Sandborn WJ. Crohn’s disease. Lancet. 2012; 380(9853):1590–1605.
5. Pusztai A, Ewen SW, Grant G, et al. Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins. Br J Nutr. 1993; 70(1):313–321.
6. Detzel CJ, Horgan A, Henderson AL, et al. Bovine immunoglobulin/protein isolate binds pro-inflammatory bacterial compounds and prevents immune activation in an intestinal co-culture model. PLoS One. 2015; 10(4):e0120278.
7. Henderson AL, Brand MW, Darling RJ, et al. Attenuation of colitis by serum-derived bovine immunoglobulin/protein isolate in a defined microbiota mouse model. Dig Dis Sci. 2015; 60(11):3293–3303.
8. Petschow B, Burnett B, Shaw A, Weaver EM, Klein GL. Serum-derived bovine immunoglobulin/protein isolate: postulated mechanism of action for management of enteropathy. Clin Exp Gastroenterol. 2014; 7:181–190.
9. Petschow BW, Bilkslager AT, Weaver EM, et al. Bovine immunoglobulin protein isolates for the nutritional management of enteropathy. World J Gastroenterol. 2014; 20(33):11713–11726.
10. Van den Abbeele P, Kunkler CN, Poppe J, et al. Serum-derived bovine immunoglobulin promotes barrier integrity and lowers inflammation for 24 human adults ex vivo. Nutrients. 2024; 16(11):1585.
11. Kim MH, Kim H. The roles of glutamine in the intestine and its implication in intestinal diseases. Int J Mol Sci.2017; 18(5):1051.
12. Perna S, Alalwan TA, Alaali Z, et al. The role of glutamine in the complex interaction between gut microbiota and health: a narrative review. Int J Mol Sci. 2019; 20(20):5232.
13. Salvatore S, Heuschkel R, Tomlin S, et al. A pilot study of N-acetyl glucosamine in pediatric chronic inflammatory bowel disease. Aliment Pharmacol Ther. 2000; 14(12):1567–1579.
14. Hewlings S, Kalman D. A review of zinc-L-carnosine and its positive effects on oral mucositis, taste disorders, and gastrointestinal disorders. Nutrients. 2020; 12(3):665.
15. Elawadli I, Brisbin JT, Mallard BA, et al. Differential effects of lactobacilli on activation and maturation of mouse dendritic cells. Benef Microbes. 2014; 5(3):323–334.
16. Ibarra A, Latreille-Barbier M, Donazzolo Y, et al. Effects of 28-day Bifidobacterium animalis subsp. lactis HN019 supplementation on colonic transit time and gastrointestinal symptoms. Gut Microbes. 2018; 9(3):236–251.
17. Waller PA, Gopal PK, Leyer GJ, et al. Dose-response effect of Bifidobacterium lactis HN019 on whole gut transit time. Scand J Gastroenterol. 2011; 46:1057–1064.
18. Miller LE, Lehtoranta L, Lehtinen MJ. Effect of Bifidobacterium animalis ssp. lactis HN019 on cellular immune function. Nutrients. 2017; 9:191.
19. Calder PC. Marine omega-3 fatty acids and inflammatory processes: effects, mechanisms, and clinical relevance. Biochim Biophys Acta.
The Roles of Choline in Maintaining Optimal Health
The Effects of Intake of Bread with Treated Corn Bran Inclusion on Postprandial Glyceamic Response
Food Waste throughout the Food Production Continuum – Water Food and Energy Nexus
Use of Lightly Potassium-Enriched Soy Sauce at Home Reduced Urinary Sodium-to-Potassium Ratio
A Different Type of Critical Migration
PRECEDE: A Conceptual Model to Assess Immigrant Health
Walking Together: Supporting Indigenous Student Success in University
Cosmetic Surgery and Body Image in Race/Ethnic Minorities
Our articles most useful
Adrian Taylor and Marica Bakovic*
Published : June 21, 2019
Journal of Food & Nutritional Sciences
Zhimin Cui, Lynne Kennedy, Weili Li*
Published : September 30, 2019
Journal of Food & Nutritional Sciences
Elena Castell-Perez*, Rosana G. Moreira, Hal S. Knowles, III
Published : October 01, 2019
Journal of Food & Nutritional Sciences
Nagako Okuda, Makoto Miura, Kazuyoshi Itai, Takuya Morikawa, Junko Sasaki, Tamami Asanuma, Mikako Fujii, Akira Okayama
Published : March 27, 2019
Journal of Food & Nutritional Sciences