Immune Health Flashcards

1
Q

What is the Role of the immune system?

A

Identify and neutralise pathogens.

Distinguish self vs non-self antigens.
.
Distinguish pathological vs. non-harmful antigens.

Repair the site of any injury or damage.

Tumour surveillance.
.

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2
Q

What are some signs of immune system dysfunction?

A
  • Inability to identify and destroy abnormal cancer cells
  • Increased susceptibility to infection
  • increased susceptibility to autoimmunity
    -Insufficient — incomplete repair, scarring, Cancer, Re-activated
    viruses
    (e.g., shingles).
    Excessive — cell damage, chronic inflammation, autoimmunity , allergic reactions
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3
Q

What is the germ/ terrain theory?

A

Pasteur’s ‘Germ Theory’: pathogens cause disease

Antoine Béchamp’s Terrain Theory: germs are ‘attracted to the environment of diseased tissue’.
(explain why some people become unwell and others don’t despite the same pathogen exposure)
* Pathogens become harmful in a certain context, depending on the overall health and resilience, immune function, stress levels, emotional state, gut function, microbiome etc.

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4
Q

5 things that effective immunity is dependent on?

A
  • Healthy barrier tissue integrity, pathogens first contact — skin, gut, lungs etc.
  • Presence of secretions — tears, saliva etc., which have antimicrobial properties. Healthy mucus production
  • Probiotic bacteria occupy space on epithelial surfaces, secreting lactic acid and natural antibiotics.
  • Immune activity is concentrated at key points of entry — MALT / GALT (e.g., tonsils, Peyer’s patches), large numbers of immune cells (B cells, secreting sIgA)
  • Inflammation — ‘quarantines’ a specific area and ↑ immune activity.
  • Many innate immune cells then act as antigen presenting cells (APCs) to the adaptive immune system, which can support with a more tailored response to a specific threat.
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5
Q

What is the function of a TH1 cell, and what triggers it’s differentiation ?

A

Defence against intracellular pathogens (e.g., viruses). Anti-cancer / tumour. Production of cytotoxic (CD8) T-cells, macrophages, IFN-γ and TNF-⍺/β.

IL-12 promotes differentiation into Th1.

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6
Q

What is the function of a Th2 cell and what triggers it?

A

Defence against extracellular threats (e.g., parasites).
IL-2, 4 and 5 promote Th2.Production of IL-4, -5, -10 and - 13, ↑ B-cell antibody production (e.g., IgE). Induces eosinophils.

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7
Q

What do Th17 cells trigger, and what are their function?

A

Produce pro-inflammatory IL-17, IL-6, IL-22 and TNF-α, often involved in the chronic stage of inflammatory diseases incl. allergies and some autoimmune disease.

Cytokine IL-1. IL-6 and TNF-B promote, Defence against extracellular pathogens.

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8
Q

What do T-reg cells do? where do they originate?

A

Modulate and deactivate the immune response. produce ‘transforming growth factor- beta’ (TGF-β) and IL-10. Both cytokines are inhibitory to helper T-cells.
The majority of peripherally produced T-reg cells originate in the GALT.

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9
Q

What clinical signs and tests would indicate low immunity?

A
  • History of increased susceptibility prolonged infections, e.g., respiratory, urogenital, skin etc.
  • Fatigue, loss of appetite, weight loss, fevers, chills, aches and pains, enlarged lymph nodes. soreness / pain, coughing, runny nose, phlegm.

Tests:
* Low WBC count (blood); low sIgA (stool or saliva test).
* Positive test for pathogen or antibodies — e.g., blood antigen test for hepatitis and EBV antibodies, urine testing for STDs, stool testing for gut pathogens, other microbiome testing (e.g., vaginal).

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10
Q

Discuss causes and risk factors for low immunity

A
  • ‘Hygiene hypothesis’ — pathogen exposure is needed for the neonatal immune system to develop

-Poor nutrition (e.g., high refined sugars, alcohol) / nutrient deficiencies, especially zinc and vitamin A, D and C.

  • Immunosuppressants e.g., corticosteroids, methotrexate, azathioprine.
  • Gut / microbiome — commensals
    offer direct immune protection
    and programme a healthy
    immune response. Compromised
    with c-section, formula-fed,
    antibiotics, overly hygienic upbringing,
    dysbiosis / low sIgA, PPIs, NSAIDs, steroids
  • Impaired barrier defences — poor skin quality (e.g., topical steroids / irritants, nutrient deficiencies such as zinc and EFAs),damaged lungs, gut permeability, tonsillectomy, adenoidectomy, appendectomy.
  • Stress: Emotional, chemical and physical(e.g., overtraining) – ↑ cortisol inhibits phagocytes, NK cells and lymphocyte activity.
  • Poor sleep — ↓ immune memory, ↓ anti-viral cytokines ↑ inflammatory cytokines (e.g., IL-6), ↓ lymphocyte blastogenesis.
  • Heavy metal toxicity can inhibit lymphocyte proliferation.
  • Blood glucose dysregulation — hyperglycaemia activates protein kinase C (PKC), inhibits phagocytosis and superoxide production, altering the innate immune response.
    – Blood glucose spikes = ↑ cortisol = gluconeogenesis and so on…).
  • Poor energy delivery mechanisms (e.g., CFS)
  • Disrupted methylation
    impairs leukocyte differentiation and maturation. The folate cycle is
    important for DNA synthesis and repair (requiring folate, B2 and B3).
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11
Q

How does neonate exposure impact the immune system?

A
  • Neonates are born with a TH2 immune bias, and exposure to pathogens increases TH1, achieving immune learning and balance, in parallel with acquisition of gut microflora. Lack of exposure is linked to increased atopic allergy- Hygiene hypothesis’ — pathogen exposure is needed for the neonatal immune system to develop-
  • Additionally, breast feeding (GOS, other prebiotics, colostrum, growth factors, maternal immune cells)
    enhance the maturation of immunity and the microflora
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12
Q

Which genes regulate vitamin D, and can cause lo immunity?

A
  • Genetic polymorphisms / SNPs.
    Vitamin D regulation with key genes:
  • VDBP = less effective binding / transport of vitamin D. Likely to require more s sun / food / supplements
    to attain adequate levels.
  • VDR = lower sensitivity to vitamin D. Likely to require higher levels in order to receive / respond to vitamin D.
  • Induces ‘cathelicidin antibacterial peptide’
  • Represses inflammatory cytokines IFN-γ, TNF, IL6
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13
Q

Nutrients to support immunity?

A

Vitamin A 2500–5000 iu / day.
- Supports lymphatic tissues and immune cells, maintains lung barrier function. Deficiency associated with RTIs

Vitamin C- Buffered form e.g., magnesium ascorbate, ester-C 1–5000 mg / day.
- Supports the innate and adaptive immune systems and epithelial barrier.

Zinc Chelated form e.g., zinc citrate, gluconate 10–15 mg / day.
Inhibits viral replication, permeability of barriers, and↑ specific anti-viral immune defenses.

Probiotics
1–30 billion, depending on strain.
Act as a ’low level’ challenge to the immune system, Various probiotics boost sIgA, incl. several Lactobacilli spp. and Saccharomyces boulardii.

Vitamin D
Cholecalciferol (D3) 1000‒2000 iu / or test
- Enhances innate immune system, increases regulatory T-cells and downregulates T-cell-driven IgG production.
Shifts towards Th2.
-maintains self-tolerance by dampening excessive immune responses.

Beta glucans 900 mg
1,3 and 1,6 support innate and adaptive immunity and are particularly supportive against upper respiratory tract infections.
-They exert immune-modulating and anti-tumour effects.

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14
Q

Good nutrient options during an infection?

A

-Vitamin A: 5000 iu.
anti-viral activity, including against measles and norovirus. It reduces infection associated with otitis media.

-Vitamin C Buffered form e.g., magnesium ascorbate, ester-C. 1000 mg per hour for up to 6 hours until bowel tolerance reached
- It inhibits virus multiplication and improves immune cell function.

  • Zinc Chelated form e.g., zinc citrate. 15–30 mg / day.
    antiviral properties against many
    viruses, including Hep C, and HIV. In vitro, low levels inhibit replication of influenza and other viruses.

Vitamin D 5000 iu.
- upregulates production of antimicrobial peptides.

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,

Echinacea : 4000 mg
Immune enhancing / modulating (alkylamides); activates phagocytes and NK cells. Can decrease the duration / severity of acute RTIs.

Lysine Dose: 1–3 g
Inhibits viral replication. Especially for herpes simplex infection, Also avoid arginine and consider low arginine diet.

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15
Q

What is cytokine storm and how can we avoid it?

A

Some people are susceptible to immune hyperresponsiveness: ‘Cytokine Storm Syndrome’.
* An excess of pro-inflammatory cytokines which can cause lung tissue damage, respiratory distress, pneumonia, or even death.

  • 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.
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16
Q

6 risk factors for covid 19?

A
  • Obesity,
    -diabetes mellitus,
    -CVD
    -non-alcoholic fatty liver disease
    – Metabolic dysfunction can lead to chronic inflammation — TNFα, IL-6 and IL-1β are upregulated in the adipose tissue.
  • Vitamin D deficiency (immunomodulatory, ↓ inflamm.
    cytokines)
  • vitamins C, B6, selenium, zinc, DHA and EPA.
  • dysbiosis = infection, and infection = dysbiosis.
  • Depletion of immunomodulatory gut bacteria such as Bifidobacterium spp., Faecalbacterium prausnitizii and Eubacterium rectale has been found in COVID-19 patients.
  • metabolic endotoxaemia — the spike protein and LPS interaction leads to aggravated inflammation.
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17
Q

What is the naturopathic approach to covid?

A

Naturopathic Diet, focus on plant protein, less poultry / red meat, less sugar and alcohol
* adequate rest, avoid suppressing symptoms.
* Support holistically — especially stress, sleep, blood glucose,
toxic load, oxidative stress. Healthy weight management.
* Support innate immunity — neutralise
COVID virus by mucosal IgA, E.g., with probiotics, beta-glucans, vitamin C

Support innate immunity as per ‘treatment options during
infection’ covered earlier.

  • Ensure optimal ranges of vitamin D.
  • For severe or ‘long COVID’ issues, focus on wider system support, esp. supporting inflammation, mitochondrial function, gut, lung dysfunction etc.
  • Microbiome support — restore diversity, gut barrier support, reduce inflammation (e.g., with prebiotics such as GOS which can raise Bifidobacterium; probiotics and polyphenols).
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18
Q

How could you specifically support the lungs in covid 19?

A

Lung tissue contains protective antioxidants, including SOD and GPO: N-acetyl cysteine (NAC) 1.5 g daily — protects lung tissue;
mucolytic, glutathione synthesis (antioxidant effects).

  • Cease smoking — associated with more severe COVID symptoms.
  • 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).
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19
Q

Specific nutrients to support Covid 19?

A
  • Quercetin (500–1000 mg, twice daily) ― impairs spike protein binding to ACE2; inhibits viral replication
  • Resveratrol (200 mg / day 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.
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20
Q

What is the difference between a normal immune response, and chronic inflammation?

A

As an acute response, inflammation
is a normal immune response to tissue damage to localise, protect, eliminate and heal the affected area. It is time-limited, proportionate and targetted

  • Involves: Vasodilation, increased tissue permeability, blood clotting, accumulation of fluid, recruitment of immune cells.
  • Cardinal signs: Redness, heat, oedema, pain, loss of function.
    • If 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 plays a
    part in neurodegenerative disease, cardiovascular disease and cancer.
21
Q

Clinical signs of chronic inflammation?

A
  • pain, swelling, aches, joint stiffness, redness and heat.
  • inflammatory condition, e.g., IBD, CVD.
  • Related conditions with inflammatory element, e.g., depression.
  • History of latent infection (e.g., periodontal disease)
  • high stress, sports ‘overtraining’,
  • use of steroids and analgesics.
  • GP tests — High CRP, WBC, ESR, fibrinogen low vitamin D.
  • Functional tests — hsCRP, high omega 6:3 ratio, low omega-3.
  • Genetics — FADS1/2, IL-6, IL-13, TNF-⍺, HLA, VDR.
22
Q

4 mediators of chronic inflammation?

A

1) Cytokines — TNF⍺, IL-6, IL-1 upregulate inflammation.

2) Histamine — promotes vasodilation and vascular permeability.

3) Kinins — (e.g., bradykinin) ↑ vasodilation / permeability and ‘pain’.

4) Nuclear Factor-Kappa B (NF-kB) — activates gene transcription, upregulating a range of inflammatory processes. (activated by: Cytokines (e.g., TNF-⍺); reactive oxygen and nitrogen species. – LPS (consider disturbed gut mucosal barrier).

23
Q

What are eicosanoids and what is their function? Give examples

A

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- eg certain cytokines (TNF, IL-1) activate COX to convert AA to PGE-2- this prostaglandin increases vasodilation, platelet aggregation, histamine and kinins
  • Include prostaglandins, thromboxanes, leukotrienes, prostacyclins, and lipoxins.

– Leukotriene B4 (LTB-4) is inflammatory (converted by 5-LOX).

24
Q

How is inflammation resolved successfully?

A

A co-ordinated response to prevent secondary tissue damage involves:

  • The production of receptor antagonists to proinflammatory mediators.
  • T-reg cells produce TGF-β and IL-10 — both are inhibitory to 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 . Formed from AA or LTB-4 by LOX enzymes.
25
Q

Discuss causes and risk factors involved with chronic inflammation?

A
  • Western diet- 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.
  • Polymorphisms in FADS1, FADS2 (genes that code for delta-5 and delta-6 desaturase) — lead to increased inflammation.
  • SNPs on pro-inflammatory genes (e.g., TNF, IL-6) — upregulated inflammatory response.
    • Obesity / overweight
  • Chronic stress — glucocorticoid receptor resistance = failure to downregulate inflammatory
    responses. Low cortisol / cortisol resistance can ↑ inflammation.
  • Poor sleep quality ↑ levels of CRP, IL-6, fibrinogen and TNF-⍺, especially in women.
  • Excess exercise with inadequate recovery (‘overtraining’) can increase inflammation via oxidative stress, impact on sleep,
  • Oxidative stress — results in inflammation and vice versa e.g., from air pollution, smoking, alcohol, etc. Low anti-oxidant status.
  • High toxic load — can drive chronic low-grade inflammation.
  • Metabolic endotoxaemia — raises LPS in the blood and interacts
    with toll-like receptors = chronic low-grade inflammation.
  • Sex hormone imbalance – oestrogen is anti-inflammatory, but in excess can be pro-inflammatory. Low testosterone promotes inflammation in men.
  • Persistent or latent infection (e.g., viral, parasitic, etc.) — inadequate immune response.
26
Q

What is the main medical management for inflammation with side effects?

A

1) 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).

2) 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

3) DMARDS: E.g., methotrexate, azathioprine. Side effects: Bone marrow
depression, agranulocytosis, increased risk of infection, throat ulcers.

27
Q

Nutrients to support chronic inflammation?

A

1) Turmeric 500–2000 mg
Whole root — Anti-inflammatory — blocks NF-κB activation and inhibits pro-inflammatory cytokines like IL-1β and −6.

2) Curcumin Up to 1000 mg; less if absorption ↑ via emulsification, liposomal or piperine (200‒400 mg).
- 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.

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

4) Boswellia 250‒500 mg
reduces 5-LOX activity. Reduces pain and shown to improve knee-joint function.

5) EFAs esp. EPA 1 g of actual EPA or higher as required.
- inhibition of the PGE2 pathway. Inhibiting NFκB, TNF-α and Interleukin-6.

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

7) Quercetin (250‒1500 mg / day) — inhibits LOX and COX; a potent down-regulator of NF-κB.

28
Q

Why does autoimmunity occur?

A
  • the immune system mistakenly attacks 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
29
Q

How does a dysregulation of autoreactive T-cells lead to a loss of self tolerance?

A
  • ‘Central tolerance’ ensures self-reactive lymphocytes are deleted in the thymus.
  • Mature self-reactive T-cells are also deleted in peripheral tissues.
  • If T-cells are not fully exposed to self antigens or are released early into circulation, they are not fully ‘trained’.
  • Also ‘peripheral regulation’ may be inadequate — there may
    be too few T-reg cells to manage any autoreactive Th cells.
30
Q

Why does autoimmunity sometimes subside in pregnancy?

A
  • In pregnancy, Th2 immunity predominates, sometimes resulting in relief of Th1 type AI, E.g.Th1 increases macrophages via cytokine IFN-γ in Crohn’s disease. Th17 also increases inflammatory cells, especially neutrophils.

but symptoms can rebound post-partum.

31
Q

How can cross- reactivity result in autoimmunity?

A

– Mimicry — an antigen looks like a self antigen e.g., foods or pathogens and may trigger a reaction against specific self-tissues

– Tissue damage / injury from previous bacterial or viral infection can release self-antigens.

  • Dysfunction of The Major Histocompatibility Complex (MHC) (encodes cell surface proteins (HLAs) and plays a key role in antigen presentation
32
Q

How is food cross-reactivity implicated in AI? Give an example?

A
  • Peptide sequences in foods may be similar to human tissues: molecular mimicry’ can induce or exacerbate autoimmune diseases. eg dairy and wheat are similar to 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 therefore Gluten-free diet improves thyroid antibodies in Hashimoto’s.
33
Q

Discuss causes and risk factors for autoimmunity

A

Genetics:

  • SNPs predisposing to inflammation e.g., TNF-⍺ IL-2, IL-12, IFNɣ in Graves’ disease.
  • DNA Methylation SNPs (RA and MS)
  • HLA (MHC) SNPs — disruption of antigen recognition and self-tolerance. e.g., HLA-DQA1 / HLA‐DQ8 in coeliac disease.
  • VDR, CYP24A1 and CYP27B1 (vitamin D conversion) SNPs
  • Emotional trauma (resulting in immune dysregulation) or infection is a preceding factor in 80% of autoimmune sufferers.
  • Gluten is a key food source of molecular mimicry and inducer of intestinal permeability.
  • Environmental toxins e.g., heavy metals, pesticides, mycotoxins. induce oxidative stress = loss of immune tolerance
  • Vitamin D def. — vit. D ↑ T-reg cells and maintains self-tolerance. Deficiency ↑ risk of MS and pancreatic β cell destruction (T1DM).
  • Many AI diseases show a geographical latitude-dependent
    prevalence, potentially related to vitamin D levels and VDR SNPs.
  • Dysbiosis and a thinning of the mucosal barrier — too much cross talk between GI microbes and the wider immune system.
  • Intestinal permeability — because the intestinal epithelial barrier controls tolerance and immunity to non-self antigens.
  • 78% of autoimmune patients are female.
  • females tend to skew towards Th2 dominance and high oestrogen has immune- stimulatory, pro-inflammatory properties- may increase risk eg SLE
    .
34
Q

What is a typical clinical presentation of autoimmunity?

A
  • Diagnosis of an AI condition or expressing symptoms, suggesting an AI disease e.g., bilateral joint pains, hand deformities — RA.
  • History of pathogen exposure, gut issues (dysbiosis, food reactions, esp. gluten), high toxic exposure, family history, stress.
  • GP tests — inflammatory markers (raised CRP, ESR). Fluorescent antinuclear antibody test (FANA) — diagnostic of specific autoantibodies, e.g., RA: Rheumatoid factor. Low vitamin D.
  • Functional tests — Cyrex Array 5 Multiple AI Reactivity Screen. comprehensive gut profiling e.g., GI effects, GI EcologiX.
  • SNPs — predisposing to inflammation (e.g., TNFα), VDR, HLA0).
35
Q

What is the auto-immune protocol ? (AIP)

A

-emphasises nutrient-dense foods and eliminates foods that may stimulate the immune system, cause hormone dysregulation, or harm the GI environment.

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

(some of the excluded foods 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)

Include:
* Vegetables (8 portions a day) esp. green leafy veg, a rainbow of colours, cruciferous, onions and garlic, sea vegetables.
* Grass-fed organic meat.
* Fish and shellfish.
* Herbs and spices.
* Healthy fats (e.g., oily fish, EVOO, avocado).
* Probiotic / fermented foods e.g., sauerkraut.
* Glycine-rich foods (e.g., bone broth).

36
Q

What is a general AI naturopathic approach?

A

Anti-inflammatory diet and:
* focus on gut / food sensitivity
— digestion, microbiome balance and intestinal / mucosal barrier

  • blood glucose balancing / low GL omega 3-rich (optimising the omega-3 to -6 ratio).
  • Eliminate gluten and remove / reduce other allergenic foods (check with test, food diary or exclusion).
  • Specific therapeutic diets such as paleo or autoimmune protocols (AIP / Wahl’s), depending on the individual.

Address the cause:
* Test and support optimal vitamin D levels.
* Support methylation
* Support pathways of detoxification
and elimination.
* Stress support and optimise sleep.
* 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.

37
Q

What is wahls protocol, used for MS?

A

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

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

38
Q

Name some supplements for autoimmunity

A

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

2) EFAs especially EPA 1 g of actual EPA
reduces inflammation by inhibition of the PGE2 pathway. High dose EPA reduces pain in RA.

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

4) Resveratrol (200 mg / day) —
reduces Th17 cellular lines; downregulates NF-KB and COX-2

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

6) Beta-glucans exert immune-modulating effects.
, ‘cordycepin’ in Cordyceps inhibits IB-1β-induced
MMP expression in rheumatoid arthritis synovial fibroblasts.

7) Probiotics
improve GI symptoms and inflammation in RA, UC, and MS. Lactobacillus / Bifidobacterium combination
* 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)
39
Q

What is SLE and it’s pathophysiology?

A

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

  • 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.
  • Consequent ↓ glycolysis, β oxidation, glucogenic and ketogenic amino acid metabolism impairing energy production (= fatigue).
  • Consequent increased blood lipids, oxidative stress and inflammation. Reduced EFA, phospholipid synthesis, methylation, glutathione
40
Q

What are the signs and symptoms of SLE?

A

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

  • Relapsing and remitting pattern.
  • 90% of sufferers are female.
  • Diagnosed by presence of anti-nuclear (ANA) and double-stranded DNA (dsDNA) antibodies.
41
Q

Causes and risk factors of systemic lupus erythematosus

A
  • Genetics (HLA DR-3/2
  • Sex hormone imbalance: women in
    reproductive years. Oestrogen dominance pattern?
  • Not breastfed — formula feeding linked. Reduction in microbiome diversity — lower levels of Bacteroidetes and Proteobacteria.
  • Infectious trigger (e.g., EBV, periodontal disease).
  • Toxins — silica dust exposure (construction), smoking, drugs.
  • Stress—low DHEA levels linked to relapses.
  • Low vitamin D levels — linked to B-cell hyperactivity.
42
Q

How can allergen sensitisation happen from birth?

A
  • Babies are born with a heightened Th2 response
    — potentially predisposing them to allergic reactions.
  • If no Exposure to the normal microbial environment including via vaginal birthing, and the development of the microbiome, which promotes a Th1 response, rebalancing the immune response or lack of exposure to sufficient antigens in first year of life ‘hygiene hypothesis’ = atopic and AI
  • 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.
43
Q

How does a heightened Th2 response promote allergic disease?

A

-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 is the least common Ig but elicits the most powerful response, it 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.
44
Q

How can high histamine be exacerbated?

A

-high ‘histamine loading’ (e.g., histamine-rich foods like cheese).

  • Poor detoxification eg SNPs in histamine detoxification genes slow its breakdown: Diamine oxidase
    (DAO), histamine-N-methyltransferase
    (HNMT), monoamine oxidase B (MAO-B), alcohol dehydrogenase (ADH), and N-acetyltransferase 2 (NAT2).
45
Q

What are some causes and risk factors for allergies?

A

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

  • 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 — 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.
  • Introduction of dietary allergens (e.g., peanut, eggs) to breastfed infants from three months of age may help reduce food allergies
46
Q

Supplements recommended for allergies?

A

1) Quercetin 250‒750 mg
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.

2) Nettle (leaf) 500 mg
Reduces effect of histamine, inhibits COX-1 and 2, associated with allergic rhinitis.

3) EFAs 1 g of actual EPA or higher
reduce inflammation by inhibition of the PGE2 pathway. Reduces asthma incidence and eczema symptoms.

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

5) Vitamin D 2000–10000 iu
Low maternal vitamin D status is linked to the development of allergy. increases T-reg activity and regulates antigen presentation.

6) Magnesium 200–400 mg
Magnesium citrate improves bronchial reactivity in asthma.

7) Vitamin C 2 g or higher
Supports histamine detoxification — co-factor for the enzyme ‘diamine oxidase’ (DAO), which degrades histamine in the gut.

47
Q

What are the main ways to reduce histamine?

A
  • ‘Histamine intolerance’ ― sensitivity to dietary histamine.
  • potential sensitivity too dietary histamine- Reduce / avoid ― fermented foods / drinks such as dairy (especially cheese), alcohol, dried fruits, avocados, aubergine, spinach, processed meats, shellfish.
  • 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.
48
Q

How does a healthy innate immune response take place?

A

Healthy innate immune response involves mobilisation of leukocytes such as macrophages, dendritic cells, neutrophils, mast cells etc. They recognise pathogens via pattern recognition (PAMPs, DAMPs) and neutralise them via phagocytosis,
production of reactive oxygen species, lactoferrin etc.