12. Immune Health Flashcards

Question

4x Medicinal mushrooms for low immunity

Answer 1

1. Reishi — increases * immune cells incl. T-cells, macrophages and NK cells. Cytotoxic to cancer cells. 2. Chaga — immunomodulator, anti-viral. 3. Shiitake — increases phagocytes, T-cells, NK cells and interferons. 4. Maitake — increases in Th1. Stimulates macrophages and NK cells. Anti-cancer

Answer 2

1/ Vit A - Retinol acetate / palmitate Dose: 5000 iu. Vitamin A has anti-viral activity, including against measles and norovirus. It reduces infection associated with otitis media. 2/ Vit C - Buffered form e.g., magnesium ascorbate, ester-C. 1000 mg per hour for up to 6 hours. Treatment requires higher (gram) doses to decrease duration of cold symptoms. It inhibits virus multiplication and improves immune cell function. Gorton (1999) found an 85% improvement in symptoms at a dose of 1000 mg per hour for up to 6 hours. Possible to take 1 g / hr until bowel tolerance reached. 3/ Zinc - Chelated form e.g., zinc citrate. 15–30 mg / day. Zinc shows antiviral properties against many viruses, including Hep C, and HIV. In vitro, low levels inhibit replication of influenza and other viruses. 4/ Vit D - Dose: 5000 iu. 5/ Elderberry - Dose: 3–8 g. Contains phytochemicals (including cyanidin-3-glucoside and cyanidin-3-sambubioside) which ‘blunt’ hemagglutinin spikes, preventing viral cell entry. It strengthens the immune response against influenza, speeding recovery and decreases URT symptoms in general according to a recent metanalysis. 6/ Beta Glucans - Dose 900 mg.Reduce URTIs in elderly and children. 7/ Echinacea - Dose: 4000 mg. Immune enhancing / modulating (alkylamides); activates phagocytes and NK cells. Can decrease the duration / severity of acute RTIs. 8/ Lysine - Dose 1-3g.Inhibits viral replication. Especially for herpes simplex infection, so can help cold sores. Also avoid arginine and consider low arginine diet.

Answer 3

oregano, sage, garlic.

Answer 4

An excess of pro-inflammatory cytokines which can cause lung tissue damage, respiratory distress, pneumonia, or even death.

Answer 5

- Elderberry is actively antiviral, and so should reduce viral load, reducing overall inflammation. It is also a powerful antioxidant, reducing damage, so its overall effect is very likely beneficial. - Ensuring use of a combined nutrient protocol (rather than high dose single nutrient) will also help to ensure the effect on the immune system is synergistic. For example, vitamin D is supportive as deficiency may predispose to cytokine storm.

Answer 6

SARS-CoV-2 is defined as the causal agent in producing the Coronavirus disease of 2019 (COVID-19) The receptor-binding domain of the COVID virus is angiotensin converting enzyme-2 (ACE-2), which enables viral entry.

Answer 7

1. See earlier factors. More specifically: 2. Obesity, diabetes mellitus, CVD and non-alcoholic fatty liver disease negatively influence the progression and prognosis of COVID-19. – Metabolic dysfunction can lead to chronic inflammation — TNFα, IL-6 and IL-1β are upregulated in the adipose tissue. 3. Nutritional deficiencies: Vitamin D (immunomodulatory, ↓ inflamm. cytokines); vitamins C, B6, selenium, zinc, DHA and EPA. metaflammation = constant low-grade inflammatory state driven by metabolic state 4. Dysbiosis: Depletion of immunomodulatory gut bacteria such as Bifidobacterium spp., Faecalbacterium prausnitizii and Eubacterium rectale has been found in COVID-19 patients. Consider metabolic endotoxaemia — it has been shown that the spike protein and LPS interaction leads to aggravated inflammation.

Answer 8

1. CNM Naturopathic Diet with a focus on plant protein, less poultry / red meat, less sugar and alcohol (Kim et al. 2021). 2. ‘The basics’ i.e., adequate rest, avoid suppressing symptoms. * Support holistically — especially stress, sleep, blood glucose, toxic load, oxidative stress. Healthy weight management. 3. Support innate immunity — most neutralise COVID virus by mucosal IgA, with no / few symptoms. E.g., with probiotics, beta-glucans, vitamin C, etc. Support innate immunity as per 'treatment options during infection’ covered earlier. Ensure optimal ranges of vitamin D. 4. Microbiome support — restore diversity, gut barrier support, reduce inflammation (e.g., with prebiotics such as GOS which can raise Bifidobacterium; probiotics and polyphenols). See GI lecture.

Answer 9

- Quercetin (500–1000 mg, twice daily) ― impairs spike protein binding to ACE2; inhibits viral replication; possibly anti-coagulation. - Resveratrol (200 mg / day or eat resveratrol-rich foods) — inhibits SARS CoV-2 in vitro; a potent antioxidant. - Turmeric (Curcuma longa) 1.5 g daily — appears to have cytoprotective effects of type II alveolar cells; decreases the population of inflammatory macrophages; ACE2 blocking. Reducing pulmonary and cardiovascular complications. - Berberine 400 mg twice daily — interferes with viral replication. Insulin sensitivity; microbiome-balancing.

Answer 10

- Cease smoking — associated with more severe COVID symptoms. - N-acetyl cysteine (NAC) 1.5 g daily — protects lung tissue; mucolytic, glutathione synthesis (antioxidant effects). - Vitamin D — inhibits microbial entry into lungs (↓ lung permeability). - Anti-microbial herbs — oregano, garlic, thyme, sage. - Diluted grapefruit seed oil, colloidal silver, saline gargled or via nasal douche to clear nose (including biofilms). Lugol’s solution (iodine) inhaled in a salt pipe.

Answer 11

Inflammation is a normal immune response to tissue damage to localise, eliminate and heal the affected area. - Involves: Vasodilation, increased tissue permeability, blood clotting, accumulation of fluid, recruitment of immune cells. - Cardinal signs: Redness, heat, oedema, pain, loss of function. - It acts as a signal to protect the affected area, rest and allow repair. As an acute response (i.e., acute inflammation), it therefore provides an important immune function

Answer 12

Inflammation should be targeted, time-limited and proportionate.

Answer 13

Inflammation directed at self tissue (autoimmunity) or non-harmful antigens (allergy), or not fully resolved (latent infection, scar tissue), it can lead to local or systemic dysfunction. Chronic inflammation may play a key part in many clients’ clinical issues but is particularly linked to chronic diseases such as neurodegenerative disease, cardiovascular disease and cancer.

Answer 14

Symptoms / signs, e.g., pain, swelling, aches, joint stiffness, redness and heat. Diagnosis / symptoms of an inflammatory condition, e.g., IBD, CVD. Related conditions with inflammatory element, e.g., depression. + History of latent / unresolved infection (e.g., periodontal disease), high stress, sports ‘overtraining’, use of steroids and analgesics. GP tests — High CRP, WBC, ESR, fibrinogen, low vitamin D. Imaging e.g., ultrasound, MRI may show local tissue inflammation. Functional tests — hsCRP, high omega 6:3 ratio, low omega-3. Genetics — FADS1/2, IL-6, IL-13, TNF-⍺, HLA, VDR.

Answer 15

* Cytokines — TNF⍺, IL-6, IL-1 (e.g., IL-1β) upregulate inflammation. * Histamine — promotes vasodilation and vascular permeability. * Kinins — (e.g., bradykinin) ↑ vasodilation / permeability and ‘pain’. * Nuclear Factor-Kappa B (NF-kB) — activates gene transcription, upregulating a range of inflammatory processes.

Answer 16

It is activated by: – Cytokines (e.g., TNF-⍺); reactive oxygen and nitrogen species. – LPS (consider disturbed gut mucosal barrier). – Homocysteine. – Heavy metals (e.g., arsenic); polycyclic aromatic hydrocarbons.

Answer 17

NFкB dysregulation has been linked to cancer and autoimmune / inflammatory disorders such rheumatoid arthritis and IBD.

Answer 18

Eicosanoids = locally-acting hormone-like messengers made by the oxidation of omega-3 and 6 fats in cell membranes. * They can exert different degrees of pro-inflammatory activity depending on the fatty acid precursor used. * Include prostaglandins, thromboxanes, leukotrienes, prostacyclins, and lipoxins. E.g.: – Prostaglandin E2 (PGE-2) ↑ vasodilation, platelet aggregation, histamine and kinins. Certain cytokines (e.g., TNF, IL-1) activate COX and convert arachidonic acid to PGE-2. – Leukotriene B4 (LTB-4) is inflammatory (converted by 5-LOX).

Answer 19

Inflammation resolution: A co-ordinated response to prevent secondary tissue damage. It involves: * The production of receptor antagonists to proinflammatory mediators. * T-reg cells produce TGF-β and IL-10 — both are inhibitory to helper T-cells (i.e. inhibiting Th1 and 2 activity). * Production of ‘less inflammatory’ PGE-1, PGE-3, resolvins and protectins from omega-3 fatty acids in cell membranes. * Increase in lipoxins — downregulate NFkB and many aspects of immune response. Formed from AA or LTB-4 by LOX enzymes.

Answer 20

1. Predisposed to high inflammation = We have a high inflammatory load to start with. 2. Inadequate inflammatory response = We don’t have the resource to resolve it properly, so it persists. 3. Inadequate resolution = We raise inflammation, but can’t switch it off. 4. Ongoing damage = Continual exposure to source of damage e.g., RSI, oxidised Tgs. 5. Inadequate recovery / repair = We don’t have time / resources to get better.

Answer 21

1. The Western diet and lifestyle drives chronic inflammation. – High refined sugar (increases free radicals and AGE), high omega-6 / low omega-3 (increases PGE-2), trans fats. – Pathogen associated molecular patterns (PAMPS) of dead bacteria in poor-quality processed, pre-chopped foods. 2. FADS1, FADS2 polymorphisms (genes that code for delta-5 and delta-6 desaturase) — lead to increased inflammation. 3 SNPs on pro-inflammatory genes (e.g., TNF, IL-6) — associated with an upregulated inflammatory response. 4 Obesity / overweight — as discussed earlier. 5 Chronic stress — results in glucocorticoid receptor resistance = failure to downregulate inflammatory responses. Low cortisol / cortisol resistance can ↑ inflammation. 6 Poor sleep quality / short sleep duration — studies show this ↑ levels of CRP, IL-6, fibrinogen and TNF-⍺, especially in women. 7 Excess exercise with inadequate recovery (‘overtraining’) can increase inflammation via oxidative stress, impact on sleep, etc. 8 Oxidative stress — results in inflammation and vice versa e.g., from air pollution, smoking, alcohol, etc. Low anti-oxidant status. 9 High toxic load — can drive chronic low-grade inflammation. 10 Metabolic endotoxaemia — raises LPS in the blood and interacts with toll-like receptors = chronic low-grade inflammation. 11 Sex hormone imbalance – oestrogen is anti-inflammatory, but in excess can be pro-inflammatory. Low testosterone promotes inflammation in men. Maintaining healthy sex hormone levels reduces the risk of several inflammatory diseases. 12 Persistent or latent infection (e.g., viral, parasitic, etc.) — inadequate immune response. 13 Excess myeloid derived suppressor cells — normally downregulate inflammation to prevent tissue damage.

Answer 22

* NSAIDs: E.g., ibuprofen, naproxen. Inhibit COX-1 / COX-2 and ↓ prostaglandin synthesis. Side effects: GIT bleeding (esp. > 65 years), peptic ulceration, renal damage, CVD, agranulocytosis (naproxen). * Corticosteroids: E.g., prednisolone. Inhibit inflammatory proteins blocking NF-kB, induce expression of anti-inflammatory proteins and inhibit 5-LOX and COX-2. Side effects: Weight gain, diabetes, hypertension, visual disturbances (blurring), osteoporosis. HPA and immune suppression (increased risk of serious infections). * DMARDS: E.g., methotrexate, azathioprine. Side effects: Bone marrow depression, agranulocytosis, increased risk of infection, throat ulcers.

Answer 23

1 Blood glucose — dietary support to stabilise glucose and insulin. 2 Gut health — high fibre, low allergen / PAMP diet, protocols for dysbiosis / permeability as appropriate. 3 Oxidative stress — high antioxidant diet or supplement support. 4 Stress, sleep and recovery support. 5 Immune function — you may need to support the immune system to deal with latent infections, periodontal disease, etc. 6 Methylation — background support for wide range of functions.

Answer 24

1. Turmeric - Dose: 500–2000 mg 2. Curcumin - Dose: Up to 1000 mg; less if absorption ↑ via emulsification, liposomal or piperine (200‒400 mg). 3. Ginger - Dose: 500–1000 mg. 4. Plant sterols - Dose: 3 g 5. Boswellia - Dose: 250‒500 mg 6. OPCs - Dose: 100–500 mg 7. EFAs esp. EPA - Dose: 1 g of actual EPA or higher as required. 8. Vitamin D - Dose: 2000‒10000 iu

Answer 25

Whole root — numerous therapeutic applications (see herbal medicine). Anti-inflammatory — blocks NF-κB activation and inhibits pro-inflammatory cytokines like IL-1β and −6. May be better than curcumin for antimicrobial support and cancer. Turmeric Dose: 500–2000 mg

Answer 26

Key antioxidant in turmeric, with antioxidant and anti-inflammatory properties. It regulates cytokines such as IL-1β, IL-6, IL-12, TNF-α, and IFN-γ and reduces PGE-2 and 5-LOX. Reduces joint inflammation / osteoarthritic pain. Curcumin Dose: Up to 1000 mg; less if absorption ↑ via emulsification, liposomal or piperine (200‒400 mg).

Answer 27

Ginger inhibits TNF-α and PGE-2 through inhibition of COX-2 and reduces inflammatory joint pain. Ginger Dose: 500–1000 mg.

Answer 28

In some studies reduces inflammation — lowering IL-6, CRP, TNF-α. Plant sterols Dose: 3 g

Answer 29

Inhibits inflammation by reducing 5-LOX activity. Reduces pain and shown to improve knee-joint function. Boswellia Dose: 250‒500 mg

Answer 30

Oligomeric proanthocyanadins from pine bark / grapeseed reduce inflammation by inhibiting COX-2, ↓ ROS and ↓ matrix metalloproteinase (MMP) activity, supporting tissue structure. OPCs Dose: 100–500 mg

Answer 31

High potency omega-3 from fish oil can reduce inflammation by inhibition of the PGE2 pathway. Inhibiting NFκB, TNF-α and Interleukin-6. EFAs esp. EPA Dose: 1 g of actual EPA or higher as required.

Answer 32

Inhibits eosinophils, ↑ tolerogenic factors in dendritic cells. Improves T-reg function, decreases proliferation of all T-helper cells but with an accompanying shift away from Th1 and towards Th2. Reduces inflammatory cytokines (e.g., IL-6 and TNF-α) Vitamin D Dose: 2000‒10000 iu.

Answer 33

1. Quercetin (250‒1500 mg / day) — inhibits LOX and COX; a potent down-regulator of NF-κB. 2. To optimise the conversion of ALA into EPA, ensure adequate co-factors for delta-6 and -5 desaturase, i.e., zinc, magnesium, B3, B6, vitamin C. 3. Reishi (Ganoderma lucidum) (3–9 g / day) — triterpenes are anti-inflammatory — reduces the activity of NF-kB. 4. Probiotics — reduce inflammatory markers such as TNF-α and IL-6.

Answer 34

Autoimmune (AI) disease: Involves the immune system mistakenly attacking the body’s own cells, resulting in ill-health and disease. * AI is present in healthy individuals to eliminate degraded self antigens but becomes pathological if there is a breakdown in self tolerance. * The tissue / system targeted will dictate the manifestation, resulting in different disorders such as coeliac disease, RA, psoriasis and MS. * There are nearly 100 distinct autoimmune diseases — some are organ specific and some systemic, such as SLE. * Prevalence is approximately 3–5% in the global population. * Having one AI condition increases the risk of developing more.

Answer 35

* A number of mechanisms regulate self tolerance to prevent AI. * ‘Central tolerance’ ensures self-reactive lymphocytes are deleted in the thymus. * Mature self-reactive T-cells are also deleted in peripheral tissues. * However, T-cells may not be fully exposed to self antigens or are released early into circulation, and so are not fully ‘trained’. * Also ‘peripheral regulation’ may be inadequate — there may be too few T-reg cells to manage any autoreactive Th cells. * So, we have a potential loss of self-tolerance due to dysregulation of autoreactive T-cells.

Answer 36

* Both Th1 and Th17 cells are important drivers of the inflammatory process in tissue or organ-specific autoimmunity. * E.g., Th1 increases macrophages via cytokine IFN-γ in Crohn’s disease. Th17 also increases inflammatory cells, especially neutrophils. * However, systemic AI conditions, like SLE and Sjögren's are characterised by Th2 dominant cytokine production. * In pregnancy, Th2 immunity predominates, sometimes resulting in relief of Th1 type AI, but symptoms can rebound post-partum.

Answer 37

The presence of an autoantigen (or mimic) may trigger a reaction against specific self tissues. This could be: – Mimicry — an antigen looks like a self antigen e.g., foods or pathogens. – Tissue damage / injury from previous bacterial or viral infection which releases self-antigens.

Answer 38

The Major Histocompatibility Complex (MHC) encodes cell surface proteins (human leukocyte antigens / HLAs) and plays a key role in antigen presentation and prevention of the immune system targeting its own cells. Dysfunction of this is associated with AI disease.

Answer 39

1. Micro-organism 2. Foods

Answer 40

* Peptide sequences in foods may be similar to human tissues. This ‘molecular mimicry’ can induce or exacerbate autoimmune diseases. * Peptide sequences in dairy and wheat are similar to certain molecules, such as myelin oligodendrocyte glycoprotein and human islet cell tissue, so may be a factor in MS and other conditions. * Food proteins may be modified by toxins, making them more reactive. * Gliadin is a molecular mimic of transglutaminase, which is abundant in the thyroid gland. * Gluten-free diet improves thyroid antibodies in Hashimoto's. * In several studies, gluten-free diet improves disease in MS.

Answer 41

* Epitope spreading — antibody or cellular response to a given antigen may extend from one ‘epitope’ on the antigen to other epitopes of the antigen, or adjacent antigens, increasing damage. * Bystander activation — infections activate APCs such as dendritic cells, which then activate autoreactive T-cells. * Cryptic epitopes — some self-epitopes are 'hidden’ from immune recognition, reducing autoantigenicity. If produced in large quantities or freed (e.g., damage), autoimmune T-cell reactions may occur. Epitope = part of an antigen, to which a single antibody can bind

Answer 42

1. Genetics: * SNPs predisposing to inflammation increase AI risk, e.g., TNF-⍺ IL-2, IL-12, IFNɣ in Graves’ disease. * Methylation SNPs and alterations in DNA methylation have been linked to many AI conditions, including RA and MS. * HLA (MHC) SNPs — disruption of antigen recognition and self-tolerance. e.g., HLA-DRB1 in RA and MS; HLA-DQA1 / HLA‐DQ8 in coeliac disease. * VDR, CYP24A1 and CYP27B1 (vitamin D conversion) SNPs are associated with increased incidence of AI. 2. Emotional trauma (resulting in immune dysregulation) or infection is a preceding factor in 80% of autoimmune sufferers. 3. Gluten is a key food source of molecular mimicry and inducer of intestinal permeability. 4. Environmental toxins — induce oxidative stress, contributing to loss of immune tolerance e.g., heavy metals, pesticides, mycotoxins. 5. Vitamin D def. — vit. D ↑ T-reg cells and maintains self-tolerance. Deficiency ↑ risk of MS and pancreatic β cell destruction (T1DM). 6. Many AI diseases show a geographical latitude-dependent prevalence, potentially related to vitamin D levels and VDR SNPs. 7. GIT * Dysbiosis and a thinning of the mucosal barrier — causes too much cross talk between GI microbes and the wider immune system. This is how coding for antibodies to seemingly commensal bacteria can happen. * Intestinal permeability — because the intestinal epithelial barrier controls the equilibrium between tolerance and immunity to non-self antigens. 8. Sex: * 78% of autoimmune patients are female. * Variations in disease activity are often observed throughout the menstrual cycle, pregnancy and breast-feeding. * The immune system of females tends to skew towards Th2 dominance and high oestrogen also has immune- stimulatory, pro-inflammatory properties. * High exposure to oestrogen through contraception, HRT and xenoestrogens may increase autoimmunity risk e.g., SLE.

Answer 43

1. Genetics: HLA SNP 2. Immune regulation: Vit D deficiency, Hormonal imbalance, Intestinal permeability/mucosal degradation, dysbiosis/lack of diverse microbiome 3. Environment: poor nutrition/deficiencies, gluten, infectious agents, environmental toxins, smoking, alcohol, drugs

Answer 44

1. Diagnosis of an AI condition or expressing symptoms, suggesting an AI disease e.g., bilateral joint pains, hand deformities — RA. 2. History of pathogen exposure, gut issues (dysbiosis, food reactions, esp. gluten), high toxic exposure, family history, stress. 3. GP tests — inflammatory markers (raised CRP, ESR). Fluorescent antinuclear antibody test (FANA) — diagnostic of specific autoantibodies, e.g., RA: Rheumatoid factor. Low vitamin D. 4. Functional tests — Cyrex Array 5 Multiple AI Reactivity Screen. comprehensive gut profiling e.g., GI effects, GI EcologiX. 5. SNPs — predisposing to inflammation (e.g., TNFα), VDR, HLA0).

Answer 45

See section on inflammation, but additional considerations include: 1. Particular focus on gut / food sensitivity — digestion, microbiome balance and intestinal / mucosal barrier (see GI Health lecture). 2- Diet — blood glucose balancing / low GL (see Endocrine lecture), omega 3-rich (optimising the omega-3 to -6 ratio). 3- Eliminate gluten and remove / reduce other allergenic foods (check with test, food diary or exclusion). 4. Specific therapeutic diets such as paleo or autoimmune protocols (AIP / Wahl’s), depending on the individual. 5. Test and support optimal vitamin D levels. 6 Support methylation (see Nutrigenomics lecture). 7* Support pathways of detoxification and elimination. 8* Stress support (see Stress lecture) and optimise sleep. 9* Natural anti-virals if potential viral trigger (assume it is still there), e.g ., L-lysine, olive leaf, St John’s wort (Hypericum perforatum). As well as zinc and vitamin C. Combine with a low arginine diet.

Answer 46

Emphasises nutrient-dense foods and eliminates foods that may stimulate the immune system, cause hormone dysregulation, or harm the GI environment. * Focuses on dietary / lifestyle factors known to modulate immune function, gut health, and hormone health including adequate sleep, managing stress, being active (not over-training). * After a period of time, some of the excluded foods (see next slide) can be reintroduced usually if the disease is in remission (or not progressing); the GIT is working effectively or a person can manage without DMARDs, steroids or NSAIDs.

Answer 47

1* Vegetables (8 portions a day) esp. green leafy veg, a rainbow of colours, cruciferous, onions and garlic, sea vegetables. 2* Grass-fed organic meat. 3* Fish and shellfish. 4* Herbs and spices. 5* Healthy fats (e.g., oily fish, EVOO, avocado) 6* Probiotic / fermented foods e.g., sauerkraut.

Answer 48

1* Alcohol, dairy, grains, legumes, refined sugar / oils. 2* Eggs (esp. the whites). 3* Nuts (incl. butters, flours, oils). * Seeds (incl. seed oils). 4* Nightshades. 5* Sweeteners (even stevia). 6* Emulsifiers, thickeners and food additives. 7* Potentially gluten-cross reactive foods.

Answer 49

1* Green leafy vegetables and sulphur-rich vegetables e.g., cauliflower. 2* Brightly-coloured fruit, like berries (phytonutrient content). 3* Grass-fed meat and oily fish. 4* Fat from plant and animal sources, especially omega-3s

Answer 50

1* Dairy products and eggs. 2* Grains (including wheat, rice and oatmeal) — due to lectin content. 3* Legumes (beans and lentils) — due to lectin content. 4* Nightshade vegetables (e.g., tomatoes, aubergine, potatoes) ― due to their solanine content. 5* Sugar.

Answer 51

1. Vitamin D Dose: 2000–10000 iu 2. EFAs especially EPA Dose: 1 g of actual EPA or higher as required. 3. Curcumin Dose: up to 1000 mg, 200–400 mg if absorption increased . 4. Resveratrol (200 mg / day) 5. Alpha lipoic acid (200 mg / day) 6. Medicinal mushrooms

Answer 52

Interacts with VDR which modulates gene transcription, resulting in functional changes in multiple immune cells: * Inhibits CD4 Th1 cells, and their production of cytokines such as IL-2, interferon (IFN)-γ, and TNFα. * Increases T-reg activity and suppresses Th17. Vitamin D Dose: 2000–10000 iu

Answer 53

High potency omega-3 from fish oil can reduce inflammation by inhibition of the PGE2 pathway. High dose EPA reduces pain in RA. EFAs especially EPA Dose: 1 g of actual EPA or higher as required.

Answer 54

Improves clinical outcomes in ulcerative colitis, with potential for MS, lupus and RA. Curcumin Dose: up to 1000 mg, 200–400 mg if absorption increased .

Answer 55

Resveratrol (200 mg / day) — a polyphenol that has been shown to reduce Th17 cellular lines; downregulates NF-KB and COX-2.

Answer 56

Alpha lipoic acid (200 mg / day) — antioxidant, raises intracellular glutathione levels, and anti-inflammatory (reduces inflammatory markers such as CRP, IL-6 and TNF-α.

Answer 57

beta-glucans exert immune-modulating effects. – For example, ‘cordycepin’ in Cordyceps (Cordyceps sinensis) has been shown to inhibit IB-1β-induced MMP expression in rheumatoid arthritis synovial fibroblasts.

Answer 58

* Probiotics improve GI symptoms and inflammation in RA, UC, and MS. Lactobacillus / Bifidobacterium combination improves disease and CRP in RA. * Evidence of dysbiosis (low Lactobacillus, Prevotella) in MS; and L. reuteri may improve symptoms. * L. salivarius and L. rhamnosus GG reduce inflammatory cytokines in IBD. * Also gut permeability support (vitamin A, C, zinc, glutamine, NAG, collagen etc), If persistent pathogens, we might consider a dysbiosis protocol — oregano, garlic, berberine etc. (see GI Health lecture).

Answer 59

SLE: A chronic inflammatory disease characterised by autoantibody response to nuclear and cytoplasmic antigens, causing multi-system dysfunction.

Answer 60

Signs / symptoms: Fatigue, joint inflammation, seizures, renal damage, photosensitivity; pulmonary, cardiac, cytopenia and digestive issues. Butterfly skin rash. Malaise, fever.

Answer 61

Diagnosed by presence of anti-nuclear (ANA) and double-stranded DNA (dsDNA) antibodies.

Answer 62

1* Genetics (HLA DR-3/2 — sibling risk 8 to 29-fold higher). 2* Sex hormone imbalance: More common in women in reproductive years. Oestrogen dominance pattern? 3* Not breastfed — formula feeding linked. Reduction in microbiome diversity — lower levels of Bacteroidetes and Proteobacteria. 4* Infectious trigger (e.g., EBV, periodontal disease). 5* Toxins — silica dust exposure (construction), smoking, drugs. 6* Stress—low DHEA levels linked to relapses. 7* Low vitamin D levels — linked to B-cell hyperactivity.

Answer 63

1* Tissue damage occurs through widespread cellular apoptosis and cell debris. Defective clearance allows for the persistence of antigen and immune complex production that deposit in the microvasculature, skin and kidneys. 2* Consequent ↓ glycolysis, β oxidation, glucogenic and ketogenic amino acid metabolism impairing energy production (= fatigue). 3* Consequent increased blood lipids, oxidative stress and inflammation. Reduced EFA, phospholipid synthesis, methylation, glutathione.

Answer 64

Allergy: An immune hypersensitivity reaction caused by exposure to a normally harmless substance, such as pollen, cat dander, food, and includes diagnoses like asthma, allergic rhinitis, and atopic eczema. Symptoms are due to the high level of dysfunctional immune activity and consequent inflammation and oxidative stress

Answer 65

These conditions may co-exist or progress from eczema in infancy to asthma and hay fever in later childhood (‘the allergic march’). They are often related to illnesses that have been suppressed by drugs.

Answer 66

For allergy to exist, allergen sensitisation must first occur. * Babies are born with a heightened Th2 response — potentially predisposing them to allergic reactions. * Exposure to the normal microbial environment including via vaginal birthing, and the development of the microbiome, promotes a Th1 response, rebalancing the immune response. * The ‘hygiene hypothesis’ proposes a lack of exposure to sufficient antigens in the first year of life is thought to be one reason for the increase in atopic dermatitis and AI disease. * The microbiome is vital to ‘training’ immune response through ‘bystander suppression’, whereby the presence of probiotic bacteria induce tolerance to allergens via T-reg cells.

Answer 67

Heightened Th2 response is the key mechanism in allergic disease. IL-4 promotes differentiation of Th cells into Th2 cells. * The Th2 cells secrete IL-4, IL-5, IL-6, IL-13 cytokines to regulate IgE antibody producing B cells, mast cells and eosinophils. * IgE antibody’s main function is immunity to parasites such as helminths and protozoa. * IgE is the least common Ig but elicits the most powerful response. * Binds to mast cells triggering degranulation and histamine release. * Mast Cell Activation Syndrome (MCAS) = mast cells inappropriately and excessively release chemical mediators, resulting in a range of chronic symptoms, sometimes including anaphylaxis.

Answer 68

Mast Cell Activation Syndrome (MCAS) = mast cells inappropriately and excessively release chemical mediators, resulting in a range of chronic symptoms, sometimes including anaphylaxis.

Answer 69

* Histamine upregulates inflammation, increases oxidative stress, and induces IL-31 production, triggering pruritus and altering skin barrier function in allergic dermatitis * High histamine may be exacerbated by poor detoxification or high ‘histamine loading’ (e.g., histamine-rich foods like cheese). * SNPs in histamine detoxification genes can slow its breakdown: Diamine oxidase (DAO), histamine-N-methyltransferase (HNMT), monoamine oxidase B (MAO-B), alcohol dehydrogenase (ADH), and N-acetyltransferase 2 (NAT2).

Answer 70

Genetic susceptibility: Certain SNPs can increase susceptibility to allergies in the presence of environmental triggers and impaired immune tolerance. 1* The gene FLG encodes profilaggrin may lead to increased permeability of the epithelium, increasing atopic dermatitis risk. 2* VDR SNPs are linked to asthma. 3* HLA SNPs: Many variants incl. HLA-DQB1 are implicated in allergy. 4* TNF-α and IL-13 SNPs ↑ the risk of asthma and more inflammation. 5* Glutathione SNPs e.g., GSTP1 and GSTM1 can increase oxidative stress in allergies and ↑ susceptibility to damage caused by toxins.

Answer 71

* Birth — c-section-born babies have reduced microbial diversity and have higher levels of IgA, IgG and IgM until at least 1 year of age, with twice the risk of developing egg and milk sensitisation, a factor in both eczema and asthma. * Formula-fed infants — have lower bacterial diversity associated with an increased risk of eczema and asthma. * Maternal atopy, vaccinations and early antibiotic use, also disrupt gut flora, increasing risk of allergy.

Answer 72

Introduction of dietary allergens (e.g., peanut, eggs) to breastfed infants from three months of age may help reduce food allergies.

Answer 73

* Diagnosis of an allergy or expressing symptoms of an allergy. * Family history of atopy; history of CS birth, formula-feeding, overly hygienic environment, hospitalisation, antibiotics, childhood stress. * Dysbiosis, food allergy / sensitivity, ↑ histamine foods, ↑ stress, ↓ sleep * GP Test — peak flow (asthma), patch testing, ELISA (enzyme-linked immunosorbent assay) — allergen-specific antibodies in your blood. * Functional tests — food sensitivity testing e.g., Cyrex 10, York test, Cambridge Foodprint, chemical sensitivity test e.g., Cyrex 11. * SNPs — MTHFR, HNMT, DAO, ADH, ALDH, NAT2, MAO-B, VDR, GSTM1/GSTP1 HLA-DQB1, IL-13, TNF-α, FLG.

Answer 74

See section on inflammation, but additional considerations include: 1* ↓ exposure to environmental triggers (symptom diary / Ig testing). 2* Particular focus on food sensitivity / gut — digestion, microbiome balance and gut permeability (see GI Health lecture). 3* Diet — blood glucose balancing, low GL, omega 3-rich, reduce allergenic foods especially considering dairy / eggs, (check with Ig test, food diary or exclusion). Consider reduction of high histamine foods. 4* Test and support optimal vitamin D levels. 5* Support stress and oxidative stress. Buteyko breathing (asthma).

Answer 75

1. Quercetin Dose: 250‒750 mg 2. Nettle (leaf) Dose: 500 mg 3. EFAs especially EPA Dose: 1 g of actual EPA or higher as required 4. Probiotics Lactobacillus and Bifidobacterium 5. Vitamin D Dose: 2000–10000 iu 6. Magnesium Dose: 200–400 mg 8. Vitamin C Dose: 2 g or higher as required

Answer 76

Inhibits LOX, stabilises mast cells, downregulates NF-KB and IL-4. Reduces allergic rhinitis symptoms, skin damage in eczema and relaxes smooth muscles in bronchi in asthma.

Answer 77

Reduces effect of histamine, inhibits COX-1 and 2, associated with allergic rhinitis. Fresh nettle tea can be takin 3+time daily

Answer 78

High potency omega-3 from fish oil can reduce inflammation by inhibition of the PGE2 pathway. Reduces asthma incidence and eczema symptoms.

Answer 79

Lactobacillus and Bifidobacterium combination reduced incidence of atopic eczema in infants, and reduces eczema symptoms.

Answer 80

Low maternal vitamin D status is linked to the development of allergy. Vitamin D increases T-reg activity and regulates antigen presentation.

Answer 81

Magnesium citrate improves bronchial reactivity in asthma.

Answer 82

Supports histamine detoxification — it acts as a co-factor for the enzyme ‘diamine oxidase’ (DAO), which degrades histamine in the gut.

Answer 83

* Reduce / avoid ― fermented foods / drinks such as dairy (especially cheese), alcohol, dried fruits, avocados, aubergine, spinach, processed meats, shellfish.

Answer 84

* Support detoxification of histamine via methylation (HNMT) with folate and B12. DAO (diamine oxidase), which helps break down histamine in gut, with copper, vitamin C and B6. Acetylation (vitamin B5), MAO-B (vitamin B2), ADH (zinc and vitamin B3). Reduce toxins that are also detoxified in the same pathways.

12. Immune Health Flashcards

(109 cards)