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Overview
Pathophysiology:
- Ulcerative colitis (UC) and Crohn's disease (CD) are chronic inflammatory bowel diseases that follow a relapsing and remitting course. [1] In both conditions, the intestinal wall is infiltrated by acute and chronic inflammatory cells that cause IBD lesions. [2]
- In UC, the inflammatory process is limited to the mucosa, sparing deeper layers of the bowel epithelium. [3]
- In CD, the entire wall of the bowel is oedematous and thickened, with deep ulcers. [4] These may penetrate through the bowel wall to initiate abscesses or fistulae [*] involving the bowel, bladder, uterus, vagina, and skin of the perineum. [5]
- These events may perpetuate chronic dysplasia that may lead to the development of colon cancer. [6]
- Nutrient malabsorption is a common clinical comorbidity as a result of intestinal damage. [7]
- UC involves only the colon, while CD can involve any part of the gastrointestinal tract from mouth to anus. [8]
- IBD develops in genetically susceptible individuals due to an abnormal inflammatory response. This may be triggered in response to emotional stress, infection, gastroenteritis, antibiotics, non-steroidal anti-inflammatory drug (NSAID) therapy or bacterial dysbiosis. [9] These factors may initiate intestinal damage either directly, or indirectly.
- Triggers that activate IBD are further amplified by T regulatory (Treg) cell activity. If Treg cells are impaired or reduced, this can disrupt the balance of downstream T-helper (Th) 1 and Th2 activity, resulting in excessive Th1 immune activation that generates unwarranted levels of inflammation, [10] resulting in chronic inflammatory damage seen in IBD.
- Gastrointestinal microbiota are strongly implicated in IBD, with dysbiosis linked to immune dysregulation. [11]
- Bacterial antigens are taken up by specialised M cells, pass between leaky epithelial cells or enter the lamina propria through ulcerated mucosa. [12]
- These are presented to antigen-presenting cells (APCs), resulting in T cell activation and differentiation to a Th1-mediated cytokine response via the release of interferon gamma (IFN-γ). This perpetuates the inflammatory process via the activation of non-immune cells and release of other cytokines, including interleukin 12 (IL-12), IL-23, IL-1, IL-6 and tumour necrosis factor alpha (TNF-α) in IBD [Figure 1]. [13]
- Reduced bacterial diversity or loss of protective species, such as Firmicutes and Faecalibacterium prausnitzii may result in a reduction of anti-inflammatory metabolites, such as butyrate and other short-chain fatty acids (SCFA) that protect intestinal mucosa. [14] As a result, individual microbial features can enhance recovery or perpetuate immune activation in IBD.
Figure 1: Pathogenesis of IBD involving bacterial dysbiosis and Th1 immune activation pathways. [15]
Key: APC: antigen-presenting cells; Th: T-helper cells; IL: interleukin; TNF-α: tumour necrosis factor alpha; IFN-γ: interferon gamma.
Key Drivers:
- Microbiome disruption/Intestinal permeability: A diverse gut microbiota moderates immune function through its interactions with the intestinal epithelia and mucosal immune responses. [34] The microbiota ensures the integrity of the gut barrier by releasing antibacterial molecules such as bacteriocins, anti-inflammatory SCFAs and other metabolites that modulate the immune response. Alterations in diversity or functional changes of the intestinal microbiota can result in dysbiosis (e.g. due to antibiotic use). This is associated with altering the immune response, increasing epithelial permeability and destabilising intestinal homeostasis, perpetuating conditions that may increase IBD activity. [35],[36] Commensal bacteria also help to shape the immune response by inducing specific Treg cells within the gastrointestinal-associated lymphoid tissue (GALT), needed to maintain peripheral tolerance and moderate aberrant Th1 activity. [37]
- Infectious agents: Infections can initiate both the onset and relapse of IBD. [38] This occurs as a result of infections stimulating the production of inflammatory cytokines that my overwhelm immune regulatory mechanisms. [39] The disease process itself also predisposes patients to an increased infection risk, and some IBD treatments may increase risk of infectious complications [40] (particularly thiopurine and anti-TNF therapies). [41] Enterohepatic helicobacter spp. (i.e. non – gastric Helicobacter pylori spp.) and campylobacter spp. have been associated with increased risk of IBD. [42] Latent viral infections such as cytomegalovirus (CMV) have also been shown to increase the rate of comorbid C. difficile infections in patients with IBD, demonstrating the negative and compounding effect of infections on IBD outcomes. [43]
- Vitamin D deficiency: Vitamin D is essential for regulatory Treg stimulation, which helps to regulate the immune response in autoimmune conditions such as IBD. Its key mechanism relates to the development of self- tolerance, as vitamin D regulates T cell and dendritic cell functions, which are involved in inducing Treg cells. This results in the moderation of Th1-driven autoimmune responses, promoting immune tolerance instead of reactive immune responses [44] against intestinal mucosa in IBD.
- Dietary factors: Dietary factors influence IBD symptoms, an effect largely associated with its influence on gut microbiota. [45] CD is associated with a lower fibre and high-sugar diet, [46] consistent with diminished microbiome health. Similar diet trends have been observed in other autoimmune conditions, where lower intake of antioxidants, as well as higher intake of sugar, sodium, red meats, protein, and iron have been associated with AI development. [47] Moreover, these risk factors have been linked to an increased risk of colorectal cancer, which IBD patients are at the higher risk of developing. [48] Dietary habits that support a healthy microbiome (i.e. high levels of antioxidants and soluble fibre from fruit and vegetable intake) may therefore support IBD management.
- Chronic stress: Chronic stress alters the hypothalamic-pituitary-adrenal (HPA) axis response, which promotes excessive release of pro-inflammatory cytokines, therefore altering the immune response and increasing the susceptibility to immune dysfunction and infectious development. Chronic stress has been linked to a greater risk of developing AI disease due to its disruptive effects on the autonomic nervous system, resulting in the dysregulation of the inflammatory response. [49]
- Smoking: Cigarette smoking is causally linked with the development of both UC and CD. [50] Mechanisms purported to trigger inflammation include tissue damage induced by production of free radicals and lipid peroxidation, increased production of inflammatory cytokines such as IL-6 and CRP, and the suppression of normal immune activity by T cells and natural killer (NK) cells. [51]
Red Flags:
- Life-threatening colonic inflammation/toxic megacolon: In extreme cases, the colon dilates and bacterial toxins pass freely across the diseased mucosa into the portal and then systemic circulation. This in turn triggers an extreme inflammatory response similar to sepsis. This complication arises most commonly during the first attack of colitis. Severe colonic inflammation with toxic dilatation is a surgical emergency and most often requires colectomy. [52] If suspected, immediately refer the patient for assessment by an overseeing medical Practitioner/General Practitioner or call triple zero (000) in case of emergency.
- Haemorrhage: Due to erosion of a major artery is rare but can occur in both UC and CD. [53] Hemorrhagic shock occurs when the body begins to shut down due to large amounts of blood loss, resulting in low blood pressure, rapid heart rate, weak pulse, shallow breathing, dizziness, or loss of consciousness. If suspected, immediately refer the patient for assessment by an overseeing medical Practitioner/General Practitioner or call triple zero (000) in case of emergency.
- Bowel cancer: The risk of dysplasia and cancer increases with the duration and extent of uncontrolled colonic inflammation, thus patients who have long-standing, extensive colitis are at highest risk. [54] In patients experiencing bloody or nocturnal diarrhoea and unexplained weight loss (i.e. >5% of body weight in previous six months) and unexplained iron deficiency, this may indicate underlying malignant disease within the digestive tract. If suspected, immediately refer the patient for assessment by an overseeing medical Practitioner/General Practitioner for endoscopic investigation to rule out cancer.
- Kidney stones (nephrolithiasis): Kidney stones are more prevalent in patients with IBD than in the general population. [55] Crohn’s disease of the small intestine decreases the body’s ability to absorb fat, leading to oxalate retention and stone formation. [56] Risk is increased with the number of small bowel resections, with recurrent calcium oxalate stone formation occurring more frequently after surgery (15% to 30%) compared to before surgery (4% to 5%). [57] Symptoms may include sharp pain, nausea, vomiting, and blood in the urine. If suspected, refer the patient for assessment by an overseeing medical Practitioner/General Practitioner for endoscopic investigation or surgical removal. Practitioners may support patients by prescribing a low-oxalate diet to reduce intakes and thus limit oxalate kidney stone formation.
Treatment Recommendations
Core Recommendations
Glutamine & Boswellia (Bospure ® Boswellia) for Intestinal Integrity
Dosage: Add 2 level scoops (7.7 g) to 200 mL water twice daily with food, or as directed by your healthcare professional.
A combination of glutamine, Bospure ® Boswellia, aloe vera, larch, zinc and vitamin A to support and maintain healthy intestinal integrity, protect the gastrointestinal mucosa and assist overall gut and microbiome health in IBD.
Mechanism of Action/Clinical Research:
-
Aloe has been shown to promote the rapid repair of damaged membranes in the gastrointestinal tract. [58]
- In a randomised double-blind controlled trial, aloe vera juice administered over a four-week period in 44 UC patients demonstrated significant improvements including increased clinical remission (p<0.05). [59]
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900 mg/d [†] of Boswellia has been shown to be as effective as conventional medication, sulfasalazine, in a randomised controlled study providing a daily dose of 6.3 mg/d of boswellia constituent, AKBA, in patients with colitis. [60]
-
Similarly, in 102 CD patients, boswellia was found to be as effective as conventional medication in providing symptomatic relief. [61]
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Larch arabinogalactans fermented within the digestive tract by gut bacteria create SCFAs, particularly butyrate, act as a fuel source for epithelial cells. [62 ]
- Several protective mechanisms have been linked to butyrate in IBD including the restoration of the intestinal barrier, reduction of inflammatory meditators IL-8 and NF-kB, Treg cell formation, and the upregulation of mucin-gene, which restores levels of protective mucin production within the small and large intestines. [63]
- Glutamine is an amino acid that is fundamental to epithelial integrity. Low glutamine availability due to reduced protein intake results in atrophy of the intestinal epithelial cells, leading to intestinal permeability (IP). [64]
- Zinc is an essential nutrient for the survival and function of epithelial cells, with its deficiency resulting in increased IP. [65] Zinc deficiency is common in patients with IBD in active and remission disease states, with a prevalence ranging from 15% to 40%. [66]
-
Vitamin A promotes mucosal immunity via induction of Tregs and increases secretory immunoglobulin A (sIgA), which protects the mucosal barrier and modulates the immune response. [67]
- The combined effects of glutamine, zinc and vitamin A have been shown to significantly decreased IP compared to glutamine alone over 12 months (p<0.041). [68]
-
Vitamin D deficiency has been shown to compromise intestinal barrier function and promote IP. [69]
- Vitamin D has been demonstrated to reduce markers of inflammation associated with an abnormal immune response in IBD children with low vitamin D status (<50 nmol/L) [70] and in adults with adequate status (83 nmol/L). [71]
BCM-95™ Turmeric & Devil's Claw to Treat Chronic Inflammation
Dosage: Acute dose: 3 capsules twice daily, reducing to the maintenance dose of 1 capsule morning and two capsules evening, once symptoms have improved.
A combination of herbs to reduce production of inflammatory mediators at multiple points of the inflammatory cascade, reducing inflammation and corresponding tissue damage occurring with AI disease activity.
Mechanism of Action/Clinical Research:
-
Curcumin has broad anti-inflammatory effects, decreasing many inflammatory mediators including phospholipase, lipoxygenase (LOX), cyclooxygenase–2 (COX-2), leukotrienes (LTs), thromboxane, prostaglandins (PGs), nitric oxide (NO), collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1, interferon-inducible protein, TNF-α, and IL-12. [72] , [73]
- As an example of curcumin’s effect on AI pathologies, 45 patients with rheumatoid arthritis were randomised into three equal groups to receive either BCM-95™ Turmeric (25 g/d), NSAID medication diclofenac sodium (50 mg/d), or a combination of both. BCM-95™ Turmeric was found to be as effective or superior to diclofenac sodium for reducing RA symptoms. [74]
- 900 mg/d of Boswellia has been shown to be as effective as conventional medication, sulfasalazine, in a randomised controlled study providing a daily dose of 6.3 mg/d of boswellia constituent, AKBA, in patients with colitis. [75]
- Boswellic acid, acetyl-11-keto-beta-boswellic acid (AKBA), demonstrates anti-inflammatory actions via allosteric regulation of 5-LOX, resulting in LT inhibition. [76] Additionally, boswellia exerts anti-inflammatory activity further up the inflammatory cascade, inhibiting the activation of proinflammatory signaling pathway, nuclear factor kappa B (NFĸB). [77]
- Devil’s claw provides significant analgesic effects by reducing pain sensations in the brain via increasing gamma-aminobutyric acid (GABA) levels and opioid activity, while also reducing glutamate signaling. [78]
Lactobacillus plantarum 299v
Dosage: Take 1-2 capsules daily.
Highly-researched probiotic strain, L.plantarum (299v), which may assist in the reduction of colonic inflammation and support IBD remission.
Mechanism of Action/Clinical Research:
- In a randomised placebo-controlled study in patients with mild to moderate UC, daily intake of 200 million colony forming units (CFUs) of L.plantarum 299V in combination with dietary fibre (oats and barley malt) consumed as probiotic beverage over eight weeks was shown to reduce clinical colitis activity by 50% compared to a placebo (p<0.04). [79] Further, 299V was shown to positively influence UC remission in 31% of participants compared to 15% in the placebo group (p<0.048).
- Similar findings in an open-label study in 39 patients with mild to moderate UC using the same treatment over 24 weeks indicated a 56.5% reduction in colitis scores, with 46% of patients achieving UC remission. [80]
- In vivo research reveals the protective effective of L.plantarum 299V in mitigating inflammatory mediators associated with IBD and colitis (i.e. IL-12 and IFN-γ), resulting in a protective effect that decreased histologic colitis scores in animals. [81]
- In animal models, L.plantarum 299V was demonstrated to regulate the expression of genes that repress inflammatory mediators within the gastrointestinal mucosa, such as nuclear factor kappa-B (NF-κB), as well as downregulate enzyme adenosine deaminase, responsible for the breakdown of the anti-inflammatory adenosine, a mechanism that may temper intestinal inflammation. [82]
OR
To promote immune regulation via the microbiome
Lactobacillus paracasei LP-33 ® and Lactobacillus rhamnosus (LGG ®) for Immune Control
Dosage: 1 capsule daily.
Clinically trialled probiotic strains to restore promote immune tolerance and moderate over-active immune responses associated with AI disease progression.
Mechanism of Action/Clinical Research:
- Lactobacillus paracasei LP-33 ® and Lactobacillus rhamnosus (LGG ®) have been shown to induce Treg cell production, which provides immunoregulatory support via promoting Th1 and Th2 cytokine balance to dampen inflammation in autoimmune disorders. [83] , [84]
- Lactobacillus rhamnosus (LGG ®) has the capacity to induce IL-10, a key anti-inflammatory and immunoregulatory cytokine that is expressed by Tregs and Th2 cells. [85]
To manage acute pain episodes associated with IBD activity
Highly Bioavailable PEA and Magnesium for Neuromuscular Support and Pain
Dosage: Add 1 level scoop (5 g) to 200 mL of water twice daily, with food.
A combination of palmitoylethanolamide (PEA) and Magnesium bisglycinate with anti-inflammatory, glutamate-blocking and endocannabinoid-like actions to manage visceral pain in IBD caused associated with chronic inflammation and pain sensitivity. [86]
Mechanism of Action/Clinical Research:
-
Magnesium has been found to block glutamate via inhibition of the N-methyl-D-aspartate (NMDA) receptor and reduce excitatory neurotransmission associated with pain signalling and increased pain sensitisation. [87]
- Through enhancing endogenous cannabinoid system activity, PEA* reduces pain amplification driven by immune cells (i.e. microglial and astrocytes), [88],[89] and helps to downregulate TRPV1 nociceptor sensitivity. [90]
- Clinically, 600 mg/d of PEA has been shown to reduce chronic pain scores from 71% to 21% (p<0.05), [91] with numerous similar trials supporting the efficacy of 600 mg/d of PEA to reduce pain scores by >50% within four weeks. [92],[93]
MetaFibre™ and EpiCor ® for Gastrointestinal Health
Dosage: Add 2 level scoops (8.5 g) to 200mL of water once daily.
A blend of prebiotic compounds and fibre to promote intestinal integrity, enhance microbiome composition and enrich commensal species associated with SCFA production, in particular butyrate, which promotes epithelial repair in IBD.
Mechanism of Action/Clinical Research:
- MetaFibre ® has been shown to increase butyrate-producing phyla, including eubacterium and faecalibacterium. [94] These phyla are associated with improved tight junction adherence and stimulating luminal mucin secretion (which acts as a protective layer and limits epithelial contact with inflammatory mediators/triggers). [95]
- Human data indicates that butyrate concentrations increase after resistant maltodextrin supplementation (MetaFibre ®) [p<0.05]. [96]
- MetaFibre ® has been demonstrated to dose-dependently increase total bacterial numbers within the GIT (p<0.02). [97]
- Epicor ®has also been shown to increase butyrate-producing bifidobacteria. [98]
Additional Considerations
To manage chronic and perpetual inflammation
Specialised Pro-Resolving Mediators [†] [**]
Specialised Pro-resolving Mediators (SPMs) to manage underlying systemic inflammation and support immune regulation, which is associated with unresolved inflammation that may perpetuate conditions such as IBD.
Mechanism of Action/Clinical Research:
- SPMs encourage resolution by regulating macrophage polarisation. SPMs trigger the switch from pro-inflammatory M1 macrophages to anti-inflammatory M2 macrophages, reducing inflammation and tissue damage and promoting resolution. Additionally, M2 macrophages have been shown to inhibit polymorphonuclear neutrophils (PMNs) and promote efferocytosis and tissue repair. [102]
If presenting with low levels of vitamin D <100 nmol/L
Vitamin D3
Dosage: Take 1 capsule daily with food.
Vitamin D modulates the innate and adaptive immune response, regulating immune function in autoimmune conditions. Vitamin D deficiency has been shown to compromise intestinal barrier function [103] and may therefore perpetuate intestinal inflammation in IBD.
Mechanism of Action/Clinical Research:
- In a retrospective review in 68% patients that were deemed vitamin D deficient, 2,000 IU/d of vitamin D was found to be highly effective in reversing vitamin D deficiency. [104]
- Vitamin D has been demonstrated to reduce markers of inflammation associated with an abnormal immune response in IBD, in both children with low vitamin D status (<50 nmol/L) [105] and adults with adequate status (<83 nmol/L). [106]
- Vitamin D deficiency is associated with reduced Tregs activity. [107] , [108]
To enhance nutritional intake and offset impaired nutrient absorption in IBD:
Premium Strength Multivitamin with Activated B's and Bioavailable Minerals
Dosage: Take 1 tablet twice daily with food.
A scientifically formulated, high strength, multivitamin and mineral with activated B vitamins to help to meet the body’s nutritional needs and limit the development of nutritional deficiencies in IBD.
Mechanism of Action/Clinical Research:
- Micronutrient deficiencies occur in more than half of patients with IBD. Most common are deficiencies of iron, B12, vitamin D, vitamin K, folic acid, selenium, zinc, vitamin B6, and vitamin B1. [109]
- Deficiencies are more common in CD than in UC and more common in active disease states than in remission. [110]
- In a retrospective review of 61 patients with IBD provided a multivitamin supplement containing 1,000 IU of vitamin A, 7.5 IU of vitamin E, 2.5 mg of zinc, 200 µg of vitamin B12, multivitamin treatment was found to effectively correct deficiencies in patients with vitamin A deficiency (16%), vitamin E deficiency (6%) and zinc deficiency (35%). [111]
High Bioavailability Zinc with Vitamin C
Dosage: Adults and children over 14 years:
Acute: Add ½ metric teaspoon (1.9 g) to 200 mL water twice daily with food;
Maintenance: Add ½ metric teaspoon (1.9 g) to 200 mL water once daily with food.
Zinc and vitamin C to support immune function, promote epithelial repair and enhance treatment outcomes in IBD patients with zinc deficiency.
Mechanism of Action/Clinical Research:
- Zinc deficiency in common in IBD during disease and remission, with a prevalence ranging from 15% to 40%. [112]
- In a retrospective clinical study in 773 CD patients and 223 UC patients, individuals with serum zinc deficiency were at a greater risk of IBD-related hospitalisations (p<0.04) compared to those with normal zinc concentrations. [113]
- Zinc supplementation in patients with CD has demonstrated improvement in mucosal permeability that may reduce the risk of IBD relapse. [114]
- Vitamin C supplementation is highly efficacious in combination with zinc; with deficiencies of vitamin C and zinc both severely suppressing immune responses. [115] This in turn can assist in the management of compromised immune function in patients with IBD.
To support healthy immune function in immunocompromised patients
Cordyceps, Coriolus and Reishi for Immune Stimulation
Dosage:
Adults and children over 14 years:
Acute: 1 level metric teaspoon to 125 mL water, three times daily for five weeks
Chronic: 1 level metric teaspoon to 125 mL water daily
Medicinal mushrooms to modulate cellular and humoral immune processes, enhancing immune tolerance of self, whilst also increasing resistance to virulent infections and preventing infectious development in IBD.
Mechanism of Action/Clinical Research:
- Cordyceps, coriolus, reishi and shiitake activate the innate immune system, triggering the production of NK cells, lymphocytes, neutrophils, macrophages, and inflammatory cytokines. [116] Cytokine synthesis prompts adaptive immune processes to take effect, through the promotion of B cells for antibody production and stimulation of T cells, which mediate cellular and humoral immunity. [117]
- Cordycepin, from cordyceps, stimulates host defense mechanisms such as macrophage and phagocytic activity, and up-regulates inducible nitric oxide synthase (iNOS), involved in the cellular immune response. [118]
- Coriolus’ active constituent, polysaccharide krestin (PSK) exhibits immune-enhancing properties such as phagocytic stimulation and promotion of NO release, whilst also increasing cytokine and chemokine production in macrophages. [119]
- Reishi contains more than 150 biologically active polysaccharides that provide immune-enhancing, antiviral and antibacterial effects. Additionally, Ganoderma lucidum proteoglycans (GLPGs) have been found to modulate immune surveillance. [120]
- Shiitake’s active constituent, lentinan, enhances T helper cell activity, leading to the restoration of humoral immune responses. [121] The engulfing activity of macrophages has also been shown to increase in the presence of lentinan, prompting them to seek out pathogenic threats. [122]
Supportive Programs
The Metagenics Clinical Detoxification Program is designed to address gut pathogen-related issues and dysbiosis as a key driver of immune dysfunction in IBD. In particular, the Gut Pathogen Elimination Detoxification stream may be used to address imbalances in the gut microbiota involved in perpetuating intestinal inflammation in IBD. Full instructions and food lists are available for free download from www.metagenicsinstitude.com.au
Diet and Lifestyle Recommendations
Diet:
- Dietary patterns high in refined starches, sugar, and saturated and trans-fatty acids, poor in natural antioxidants and fibre from fruits, vegetables and wholegrains, and poor in omega-3 fatty acids may cause an activation of the innate immune system, most likely by excessive production of pro-inflammatory cytokines associated with a reduced production of anti-inflammatory cytokines. [123]
- Studies evaluating diet in IBD development support a varied intake of all food groups, with a focus on wholefoods instead of refined-foods, and plant-based instead of animal-derived foods. [124]
- The Mediterranean diet is inclusive of a wholefoods diet, and features high intake of fruits and vegetables, lean protein, quality essential fatty acids, and wholegrains (limiting starchy grains and vegetables).
- The Metagenics Wellness Diet reflects the wholefood principles of the Mediterranean diet and provides a simple guide to moderate portion size, and the overall balance of macronutrients.
- Current evidence suggests that the Mediterranean diet provides protection against several diseases associated with inflammation and immune activation. [125] The Mediterranean diet has also been found to improve disease-related fatigue by lowering the inflammatory load and simultaneously balancing gut microbiota. [126]
- Increase intake of microbiome-enhancing foods to nourish commensal gut flora and enhance gut-associated immunity. Refer to the Metagenics Microbiome Enhancing Foods list for dietary recommendations.
- In IBD patients with kidney stones/risk of hyperoxaluria, mitigating oxalate retention can be supported by implementing oxalate-reducing cooking methods, restricting dietary fat to 40-60 g/d per day and lowering dietary oxalate intake.
- Cooking methods that reduce oxalate absorption: Boiling, pairing with high calcium foods, soaking, steaming.
- Cooking methods that increase oxalate absorption: Baking, grilling, low-calcium diet, and roasting.
- Oxalate-rich foods sources: Beet greens, beet root, legumes, cereal grains, nuts, potatoes, rhubarb, sorrel, spinach, sweet potatoes, and Swiss chard.
Lifestyle:
- Ensure adequate sleep for cellular repair, achieving approximately eight hours of sleep each night. [127]
- Avoid alcohol, illicit drugs or additional stimulant substances (caffeine, nicotine), as these may negatively impact HPA axis activity and nervous system function, contributing to fatigue (a common symptom in IBD), and/or disturbing normal sleep patterns. [128]
- If indicated, provide patients with resources to support smoking cessation. Smoking is a strong risk factor in IBD development. [129]
- Engage in regular physical activity to improve fitness, health and wellbeing, and reduce stress. [130]
- Epidemiological evidence indicates that regular physical activity and frequent structured exercise reduces the incidence of many chronic diseases, including communicable diseases such as viral and bacterial infections, as well as non-communicable diseases such as AI.
- Regular physical activity and frequent exercise have been found to enhance immune competency and regulation. [131]
Clinical Investigation and Pathology:
Clinical Screening |
Rationale |
Health Appraisal Questionnaire (HAQ) |
The HAQ provides a comprehensive assessment of physical health, allowing Practitioners to gain insight into patient symptoms and evaluate overall health and wellbeing. |
Body Mass Index (BMI) |
An index employed to ascertain if a patient is within a healthy weight range, highlighting if their weight may be negatively impacted as a result of malabsorption in IBD. |
Footnotes
[*] A fistula is an abnormal connection between two epithelialised surfaces, such as blood vessels, intestines, or other hollow organs.
[†] 900mg/d is achieved using the recommended daily dose of Glutamine & Boswellia (Bospure ® Boswellia) for Intestinal Integrity combined with the maintenance dose of BCM-95™ Turmeric & Devil's Claw to Treat Chronic Inflammation.
References
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