Skin and Respiratory Flashcards

1
Q

What is asthma? Describe the pathophysiology?

A

A chronic respiratory disorder characterised by variable airway obstruction and hyper-responsiveness to stimuli.
Airways narrow due to:
– Bronchial smooth muscle spasm.
– Swelling of bronchial mucosa.
– Excess viscous mucus secretion

1) Mediated by immunoglobulin E (IgE), triggered by allergic response to an allergen (e.g., pollen, animal dander).

2) This leads to the release of inflammatory mediators such as histamine leukotrienes, and prostaglandins, causing
bronchospasm, triggering an attack.

3) Mucus production by goblet cells plugs the airway and, together with increased airway tone and hyper-responsiveness, causes the airway to narrow,

4) Airway remodelling — chronic inflammation causes bronchial smooth muscle hypertrophy, resulting in
persistent airflow obstruction, similar to COPD.

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2
Q

Discuss the main causes and risk factors in asthma?

A

1) Th1 / Th2 balance imbalance: excessive Th2 response encourages IgE release, ↑ inflammatory mediators.
(Heightened Th2 immune response during pregnancy predisposes infant to allergic disease)

2) inadequate antigen exposure: causes abnormal responses to innocuous stimuli- exposure supports neonatal exposure by increasing Th1 ‘hygiene hypothesis’

3) Antibiotics: Pre- or post-natal exposure
— gut dysbiosis linked to early disruption of the immune system - first year of life critical.

  • Compromised gut microbiome leads to antigen stimulation of antibody pathway causing heightened Th2 response with abnormal responses.

4) The presence of pathogenic bacteria and fungi (e.g., Candida albicans) in the gut and lungs of infants and children has been linked with development of allergic sensitisation and asthma.

5) Not breastfeeding: protective via several
mechanisms including immune development and gut microbiome.Longer breastfeeding shown to result in ↓ risk of wheeze and to have a protective effect until school age.
* Ideally, exclusively breastfeed for 6–9 months

6) Early weaning (< 6 months): ↑ risk of food allergy, including asthma.

7) Obesity:
* Lung function: Changes in mechanical properties of lungs and chest wall significantly ↓ ERV and FRC.
* Diets that promote obesity: (↑ saturated fat and sugar,
↑ omega 6:3, low fibre and antioxidants) increase asthma risk.
* Microbiome changes: Obesity is linked with low Bacteroidetes bacteria (major producer of SCFAs)- alterations increase allergic airway disease.
* Systemic inflammation: ↑ cytokines released from adipose tissue contribute to airway hyper-responsiveness and remodelling.

8) Preservatives — benzoates, sulphur dioxide, sulphites
in food / drink may aggravate asthma in children.* Food colourings — azo dyes (esp. tartrazine) may trigger attack.

9) Molybdenum deficiency — as its needed to convert sulphite to sulphate to enable safe excretion, therefore can contribute to sulphite sensitivity

10) Female sex hormone fluctuations:
* Raised oestrogen favours TH2 (HRT increases risk in studies)
* Perimenstrual asthma — a cyclical worsening of asthma during the luteal phase and / or first few days of menstruation, relates to fluctuation in oestrogen

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3
Q

What are the two classifications of asthma?

A
  • Extrinsic (allergic / atopic) asthma (60–90% of cases):
    – Involves an IgE mediated response.
    – Common triggers include pollen, mould, dust mites, pet dander.
  • Intrinsic (non-allergic) asthma (10–40% of cases):
    – More common in females, typically develops later in life.
    – Bronchial reaction, IgE can sometimes be involved.
    – Possible triggers cold temperatures, humidity, stress, exercise, pollution, irritants in air such as smoke, and respiratory infections.
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4
Q

Which naturopathic investigations might be appropriate for asthma?

A
  • Dietary / lifestyle evaluation: Diet diary, thorough case history, elimination diet, identification of triggers.

1) IgG / IgE food profile: e.g., York Test IgG foods and IgE foods test. to assess potential food allergy or intolerances.

2) IgG / IgE inhalant allergy profile: e.g., Genova’s inhalants / IgE moulds test. to Assess for chemical or environmental irritants.

3) Food / chemical intolerance test: e.g., Genova’s toxic element clearance profile, elemental analysis.
Assess specific food additives, colourings, pharmaco-active agents, environmental chemicals

4) GI profile or digestive analysis: e.g., Genova’s NutrEval.
To ensure optimal digestion, microflora colonisation and immune health.

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5
Q

Dietary approach to asthma?

A

1) Allergies and sensitivities: Reduce pre-disposition in child; consider nutritional status of parents and pre-conception toxin exposure.

2) Follow CNM Naturopathic Diet, Eat only fresh, natural, unprocessed organic food pre-conception / pregnancy.
Reduce intake of sugar, dairy, processed foods,
wheat, additives, preservatives, colourings.

3) Eliminate / reduce common allergenic foods: most common foods associated with asthma
are cows’ milk, eggs, chocolate, rice, soy, corn, citrus fruit, apple.

4) Assess salicylate sensitivity — may cause delayed intolerance reaction. Assess client tolerance.

5) Avoid dietary sulphites — alcohol, dried fruits, bagged / prepared salads.
* Avoid nitrates: Cured meat ↑ symptoms.

6)Reduce red meat — arachidonic acid link to ↑ series 2 prostaglandins and leukotrienes (transient airway hyper-responsiveness).

7) Dehydration — may exacerbate exercise-induced asthma.

8) Excess salt — potentially increases bronchial reactivity.

9) Include Antioxidants: Include vitamins A, C, E, carotenes, co-factors — zinc, selenium, copper, and flavonoids (particularly quercetin). These:
– Inhibit leukotriene formation and histamine release.
– Increase epithelial lining integrity.
– Protect lung against free radicals and oxidising agents that may stimulate bronchial constriction
* Increase selenium (a co-factor of GPO) — often low in asthmatics.
* vitamin E — potent antioxidant, improves lung
function, optimises Th1 and suppresses Th2, ↓ IgE and atopy.

10) include Flavonoids — such as quercetin inhibit histamine
release from mast cells and basophils when
stimulated by antigens, decreases
airway inflammation and hyper-responsiveness.

11) Optimise omega-6:3 ratio — an inflammatory
omega 6:3 profile causes ↑ prostaglandin E2
(PGE2)IgE = atopy and inflammation.

12) increase Dietary fibre- anti-oxidant and anti-inflammatory effects (25 g / d women; 35 g / d man).
* inverse association between fibre
intake and pro-inflammatory interleukin-6 (IL-6),
tumour necrosis factor-α receptor-2, and C-reactive protein.
* Fibre is metabolised by gut bacteria into SCFAs which positively influence immune and metabolic responses.

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6
Q

Specific nutrients for asthma?

A

1) Vitamin B complex 50–150 mg / day
* B3 decreases histamine release — calms the allergic response.
* B5 beneficial for those with allergies and asthma.
Reduces secretion of cortisol in times of stress.
* B6 reduces frequency and severity of asthma
(25–30 mg / day).
* B12 helps in the oxidation and metabolism of sulphites
and may help reduce inflammatory reactions.

2) Vitamin C: 2–3 g / day in divided doses
* Antioxidant, anti-histamine, stimulates neutrophils, increases lymphocyte and interferon production.
* ↓ release of arachidonic acid which impedes prostaglandin E2 (PGE2) synthesis = ↓ inflammation and bronchoconstriction.
* ↓ bronchial spasm (1 g daily), prevents exercise-induced asthma (500 mg).

3) Vitamin D:Optimise levels
* Modulates genes for asthma / allergy. Maternal levels linked to allergy — higher levels protective against asthmatic wheezing in young children.
* Inhibits eosinophils (involved in pathogenesis of asthma).

4) Magnesium: 200‒400 mg / day
* Improves lung function, reduces bronchial reactivity.
* Antagonises movement of calcium across membranes, ↓ calcium uptake in bronchial smooth muscles
leads to relaxation / dilation bronchial airways.

5) Zinc: 15‒30 mg / day
* Improves cell-mediated immunity — increases production of T-lymphocytes, regulates function of white blood cells.
* Deficiency may shift Th1 / Th2 response, favouring Th2 response characteristic of asthma.

6) Probiotics: L. rhamnosus GG and GR-1 Dosage as per label
* Balance Th1 / Th2 immunity — ↑Th1 cytokines profile (IL-12, IFN-γ, and TGF-β), ↓Th2 cytokine profile (IL-4, IL-5, IL-10, and IL-13).
* ↓ eosinophil and lymphocytes infiltration to the respiratory tract, ↓ IgE, IgG1, IgG2a production.
* ↑ butyrate / IgA production, alleviate symptoms, ↑ quality life.

7) Fish oils:1 g of actual EPA or higher as required.
* Improves respiratory health, reduces inflammatory markers
* Needed for production of anti-inflammatory prostaglandins.

8) Coenzyme Q10: 150 mg / day
* Antioxidant — ↓ oxidative stress and asthma symptoms.
* May ↓ long-term side-effects of glucocorticoid medications.

9) Ginger 400–500 mg with Turmeric 500–2000 mg
(or curcumin)
* Gingerols (ginger) and curcumin (turmeric) are dual inhibitors of arachidonic acid metabolism (↓ leukotrienes).

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7
Q

What are the most common chemical mediators in asthma and why ?

A
  • Because Asthmatics have an imbalance in arachidonic acid metabolism, this leads to increases in lipoxygenase products, Leukotrienes are 1000 times more potent stimulators of bronchial constriction than histamine.
  • COX is downregulated in favour of LOX leading to ↑ leukotrienes.
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8
Q

Lifestyle factors for ashtma

A

1) Stress and anxiety contribute to asthma exacerbations.
Occurs through various mechanisms e.g., oxidative stress pathways, glucocorticoid resistance, nerve-mast cell interaction.

2) Avoid potential triggers: Environmental pollutants
(incl. tobacco smoke), household chemicals (e.g., cleaning products, paint), moulds, pollens, dust mites etc.

3) Buteyko breathing exercises — uses shallow breathing through the nose to correct the breathing pattern.

4) Posture — compression of the lungs exacerbating symptoms. Smartphones ― development of forward head posture.

5) Essential oils — adding a few drops of lavender oil to a diffuser or
humidifier may reduce airway inflammation and help alleviate stress.

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9
Q

What is bronchitis with hallmark symptoms?

A

Acute or chronic inflammation of the bronchi:
* Associated with:
– Mucosal oedema, infiltration with macrophages and neutrophils.
– Hypertrophy of bronchial glands.
– Hypertrophy / hyperplasia of bronchial smooth muscle.
– Irreversible scarring of the airway walls, reducing airflow.

Hallmark symptoms:
* Hacking unproductive cough, becoming productive within days (thick, yellowy mucus).
* Fever, sore throat, shortness of breath,
headache, runny or blocked nose, muscle pain.

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10
Q

Natural approach to bronchitis?

A

1) Reduce bronchial irritants:
* Stop smoking, avoid dust / smoky atmospheres, avoid environmental irritants.

2) Reduce intake of sugar, salt, saturated fats, cows’ dairy, wheat, processed foods, additives, preservatives, colourings, , Follow the principles of the CNM Naturopathic Diet

3) avoid mucus-forming foods: Known allergens / intolerances; histamine-rich foods e.g., processed meats, dried fruit cheese, fermented foods, smoked fish, alcohol,
avocado, tomato, spinach, mushrooms.

4) Ensure adequate fluid intake; water, herbal teas, juices, broths.

5) Increase intake of mucolytic foods e.g., garlic, onions; decrease catarrh; horseradish (not for dry cough); ginger reduces inflammation, has antiseptic properties; cinnamon — a warming expectorant.

6) Bromelain, a proteolytic enzyme from pineapple decreases airway inflammation, is mucolytic and has potential as an anti-viral agent.

7) Onion Thyme Manuka Honey Combo:
Onions — contain phytonutrients and vitamin C that support immunity; the sulphur compounds are mucolytic. Thyme — antimicrobial, expectorant.
Manuka honey — antibacterial, anti-inflammatory, soothing.

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11
Q

Nutrients for bronchitis

A

1) Vitamin A 5000 iu daily
* Maintains mucous membrane integrity and promotes mucin secretion, contributing to mucociliary defence.
* Enhances T-cell proliferation and interleukin-2 secretion; reduces lung inflammation.

2) Vitamin C 3–10 g / day in small frequent doses.
* Increases T-cells, interferons and natural killer cells.
* Reduces oxidative stress and inflammation of airways.

3) Vitamin D Optimise levels
* Deficiency is associated with increased risk of respiratory infection.
* Moderates pulmonary inflammatory responses.
* Enhances innate immune responses to pathogens.

4) Zinc 15–30 mg / day
* Modulates antiviral and antibacterial immunity and regulates the inflammatory response.
* Helps maintain mucous membrane integrity.
* Maintains phagocytic and NK cell function.

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12
Q

What is COPD with main causes and risk factors?

A

a chronic inflammatory response of the lungs causing airflow limitation due to airway and functional lung tissue damage that is progressive and not fully reversible.

Combination of two main pathologies:
* Emphysema: Dilation of alveolar sacs by destruction of alveolar wall, leading to collapse of alveoli during expiration = breathlessness.

  • Chronic bronchitis: Inflammation and thickening of bronchial lining with mucus hyper-secretion = cough and wheezing.

Causes and risk factors:
* Smoking: Predominant cause (approx. 90%).
* Exposure to lung irritants: Air pollution, industrial
chemicals, dusts, etc., genetic susceptibility.

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13
Q

What lifestyle interventions may help COPD?

A

1) Smoking cessation is essential!
* Cigarette toxins initiate inflammatory effects
by activating the NFκB pathway leading to an inflammatory cascade in the airway epithelial
cells and recruitment of macrophages and neutrophils.

2) Healthy weight management:
* Overweight puts greater pressure on the heart and lungs.
* Underweight impedes ability to maintain normal body function. COPD is associated with weight loss and ↑ risk of sarcopenia and pulmonary cachexia (↓ physical activity, metabolic changes).

4) A combination of eucalyptus and peppermint essential oils inhaled, can loosen mucus and dilate the airways.

5) Exercise improves bodyweight, muscle strength and quality of life.

6) Manual therapy (e.g., osteopathy, physio) and
breathing exercises support breathing mechanics.

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14
Q

What dietary support may help with COPD?

A

1) Avoid refined grains and sugar, fast foods, processed foods, saturated fats, take-aways, soft drinks, alcohol.

2) Avoid mucus-producing foods: Known intolerances, cows’ dairy.

3) Include nutrient-rich, easily digested foods e.g., fresh juices, broths to improve anorexia ( increased work of breathing can impact this)

4) include Fruits / vegetables ― ↑ antioxidant and anti-inflammatory nutrients. Have vegetables lightly cooked rather than raw.

5) Include antioxidant, anti-inflammatory and warming herbs such as turmeric, ginger and garlic.

6) Ensure good intake of beneficial fats omega-3 fatty acids (↑ energy, anti-inflammatory).

7) Good intake of quality protein is essential (sarcopenia risk) with specific focus on leucine,

8) Consider all nutrients outlined for bronchitis noting that:
* Vitamin D deficiency in COPD is associated with ↑ risk of exacerbations

9) Combining bioflavonoids with vitamin C enhances utilisation and free radical scavenging capacity, positively associated with forced expiratory volume (FEV)
* Increased oxidative stress during disease exacerbation is linked to lowered serum levels of vitamin A and E.

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15
Q

What specific nutrients may help with COPD?

A

1) N-acetyl cysteine 400–1200 mg / day
* Mucolytic (breaks disulphide bonds in mucoproteins) enabling expulsion of mucus.
* Increases glutathione and decreases the oxidative damage associated with inflammation
* Increases mean forced expiratory flow.

2) Fish oils EPA 800– 1000 mg DHA: 300 mg
* associated with reduced COPD morbidity (↓ exacerbation risk, fewer respiratory symptoms and ↑ quality of life).
* Reduces inflammation, improves body composition and enhances exercise performance.

3) Shiitake 1.5–10 g / day- powder or include in the diet
* Heightens immune vigilance against potential pathogens: ↑ phagocytes, T- and B-lymphocytes and NK cells.
* Enhances interferon synthesis (anti-viral proteins).
* Increases SIgA.

4) Cordyceps 2–5 g / day
* Improves FEV1% and FEV1 / FVC ratio
* Improves exercise tolerance (antioxidant and anti- fatigue mechanisms e.g., ↓ lactate accumulation).
* Strengthens the immune system.

5) Thyme - expectorant with mucolytic and antibacterial activities. Has antioxidant properties, downregulates activated NF-kB in COPD.

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16
Q

What is acne vulgaris, how is it characterised, who is it more common in, and what are the main clinical presentations?

A
  • inflammatory skin condition characterised by excess sebum production, follicular hyperkeratinisation of sebaceous ducts, follicular colonisation by Cutibacterium acnes and inflammation.
  • predominantly affects skin with dense sebaceous follicles — primarily the face, but also the chest and back.
    • Commonly affects adolescents, More common in males than females due to hyper-responsiveness to androgen hormones.

Clinical presentation:
* Comedones (pimples) mainly affect face, shoulders, upper chest, back.
* Dilated pores with dark plugs of keratin (a protein found in skin) and sebum (secretion of sebaceous glands).
* Open (blackheads), closed (whiteheads).
* Dome-shaped papules formed through sebum
and keratin accumulations deeper in the ducts.
* Bacterial infection causes inflammatory cysts (granulomas) beneath the skin, which result in scarring.
* Low self esteem: Link to anxiety and depression.

17
Q

Discuss the causes and risk factors for acne vulgaris?

A

1) Increased androgens stimulate hyperkeratinisation of follicles, Increase sebum production and Stimulate acne lesions.
* Free testosterone - mostly potent metabolite (DHT).Greater activity of 5-alpha-reductase (converts testosterone to DHT) — associated with factors such as hyperinsulemia, obesity and low zinc).
* DHEA — most abundant steroid in body and DHEAS — sulphated version of DHEA.

2) Hyperinsulinemia:
-decreases sex hormone binding globulin (SHBG), increasing levels of free testosterone.
- upregulates IGF-1 and downregulates insulin-growth factor-binding protein-3 (IGFBP-3). Net effect = ↑ androgen production

3) Hormone fluctuations e.g., puberty, menstruation and pregnancy.
* PCOS — association with hyperinsulinemia / insulin resistance.

4) Psychological stress via HPA-axis, release of CRH, promotes lipogenesis and induces cytokines (IL6 + IL11) in keratinocytes → inflammation.

5) Depression / anxiety:
psychodermatology (mind / skin link). Skin and nerve cells
are connected at the embryonic level through ectoderm and continue affect each other throughout life.

6) Insulin resistance: Diet, obesity, inactivity.
* ↑ proliferation of keratinocytes, stimulates synthesis of androgens and ↑ sebum production.

7) IGF-1 decreases FoxO1, leads to activation of mTORC1.
mTORC1 mediates sebaceous gland hyperproliferation, lipid synthesis, and hyperplasia of keratinocytes.
* Dairy and high GI / GL foods ↑ IGF-1.
* Dairy also increases circulating levels of insulin

trans fats activate mTORC1. Palmitate: Major FA = 32% milk TGs.

8) low Vitamin D — a role in regulating proliferation and differentiation of keratinocytes and sebocytes ― anti-comedogenic properties.

9) Microbiome — higher levels of bacteriodes implicated. Acne lesions are associated with increased
proportion of C. acnes as a skin commensal bacterium.

18
Q

Dietary suggestions for acne vulgaris

A

1) Avoid dairy, trans fats, saturated fat, red meat (↑ BCAAs), sugar, refined foods, high GI / GL foods, excess omega-6 fatty acids, alcohol, spicy foods.

2) Consume low GI / GL foods: Balance blood sugar levels to regulate insulin.* Include cinnamon in the diet to improve glycaemic control. ↑ insulin receptor sensitivity, facilitating transport of glucose into the cells.
3) Increase fibre to improve glycaemic control. Helps reduce toxic overload

4) Omega-3 (walnuts, flaxseed, chia seeds, fish) decrease IGF-1. EPA reduces inflammation and inhibits mTORC1 activation.
* Flaxseeds contain enterolactone, which has shown to decrease circulating free androgens.

5) Increase low GI fruit and vegetables — alkalising, ↑ antioxidant and anti-inflammatory nutrients.
* Include green tea, turmeric, berries — contain polyphenol compounds that decrease mTORC1.

6) Ensure a healthy microbiota by targeting harmful bacteria and / or enriching beneficial bacteria. See GI lecture.

7) Ensure good water intake to support elimination channels.

19
Q

Supplements for acne vulgaris?

A

1) Vitamin A 5000 iu / day
* Plays a role in collagen synthesis and supports integrity of the skin barrier. Supports immune function.
* Reduces sebum production and hyperkeratosis of follicles.
* Supports immune function and inhibits growth of C. acnes.

2) Vitamin B3 (niacinamide) 20–50 mg / day in B complex.
* Works alongside chromium in insulin regulation.
* Anti-inflammatory and reduces histamine release.
* Inhibits C. acnes-induced IL-8 production in keratinocytes through the NF-κB and MAPK pathways.

3) Vitamin D Optimise levels
* Regulates metabolism of keratinocytes and sebocytes.
* Supports glycaemic control by increasing
cellular sensitivity to insulin.

4) Chromium 200–1000 mcg / day
* A component of chromodulin — a protein that increases sensitivity of the enzyme tyrosine kinase, facilitating insulin receptor activity and entry of glucose into the cell.

5) Zinc: 15–30 mg
* Modulates immune and inflammatory processes.
* Inhibits 5α reductase, ↓ DHT.
* Antimicrobial activity against C. acnes.

20
Q

Which herbs might support acne vulgaris?

A

Saw palmetto and stinging nettle root inhibit 5α-reductase
(↓ conversion of testosterone to DHT).

  • Cleavers (Galium aparine) dried herb as a tea (2 tsp per cup). Supports lymphatic function, assisting in the removal of wastes.
  • Assess need for liver detoxification. Herbal support includes milk thistle, rosemary, green tea, turmeric. Antioxidant and upregulates phase II detoxification.
  • Anxiety / depression: Passionflower (anxiolytic, promotes restful sleep), lavender (helps elevate mood, calms agitation).
21
Q

Other recommendations for acne vulgaris?

A
  • Regular exercise — lowers insulin and IGF-1.
  • Neat essential oil of lavender can be applied to individual
    comedones. Is a strong antiseptic and dries out the lesion.
  • Contrast hydrotherapy to support lymphatic function. Alternating hot to cold acts as a ‘lymphatic pump’ helping to filter and carry away toxic substances. Start with hot and finish with cold.
    Hot application should be approx. 3 times longer.
    © CNM: Nutrition 2: Skin & Respiratory Health. MC. 57
    Bach flowers:
    4 drops, 4 times daily
22
Q

What is Rosacea and how is it characterised? Who is it most common in?

A

a chronic inflammatory skin condition associated with capillary hyper-reactivity presenting as an erythematous (red) rash or flush across the cheeks and nose, flushing, papules, pustules, telangiectasia and ocular manifestations.

  • Predominantly manifests in women aged 30–50 years.
  • More common in fair-skinned people,
  • Can occur in children ― paediatric rosacea.
23
Q

Causes and risk factors for rosacea?

A

1) Gastric H. pylori infection — can stimulate the immune system to produce a large number of inflammatory mediators, increases NO levels leading to vasodilation and inflammation.

2) SIBO — associated with increased intestinal permeability and systemic inflammation.

3) Vascular hyperactivity — triggered by exercise, hot weather, alcohol, spicy food, hot drinks, caffeine and stress.

4) Food allergy / intolerances; e.g., excess histamine

24
Q

How can you naturally support rosacea?

A

Apply the CNM Naturopathic Diet.
* Identify and avoid triggers: Capsaicin (peppers) and cinnamaldehyde (e.g., tomatoes, citrus, chocolate, cinnamon) are identified as common triggers. also stress and UV exposure

  • Focus on cooling, anti-inflammatory foods.
  • Reduce high-histamine foods and support
    detoxification pathways
  • Support gut health as needed (e.g., H pylori)
    Low stomach acid is common — use bitters, HCl, digestive enzymes.
  • Ensure good intake of omega-3 fatty acids to reduce inflammation and maintain integrity of the skin barrier.
  • Include foods rich in vitamin C and proanthocyanidins (flavonoid compounds) that improve integrity of blood vessels e.g., grapes, blueberries and cranberries.
  • Aloe vera gel applied topically can decrease inflammation and irritation. Inhibits COX and PG2 production.
  • Zinc has demonstrated benefits for rosacea — 25 mg / day.
  • Care should be taken with cosmetic and personal care products.
25
Q

What is atopic dermatitis and how does it commonly present?

A

a disorder of altered skin barrier integrity and immune dysregulation, presents as a chronic relapsing inflammatory skin disease.

Clinical presentation:

  • Pruritis with dry, erythematous areas — often occurs on flexor (or extensor) surfaces, face, scalp, neck, wrists or ankles.
  • Lichenification — hyperpigmented plaques of thickened skin caused by scratching or rubbing.
  • Can manifest with papulovesicular lesions, patches of erythema, exudation, scaling with small vesicles formed within the epidermis.
26
Q

Describe the inside-out and outside- on hypothesis in AD

A

1)Primary epithelial barrier disruption (outside-in hypothesis):

  • Disruption of tight junctions leading to permeability of stratum corneum and increased trans-epidermal water loss.
  • Structural protein defects (filaggrin).
  • Barrier disruption may
    be caused by microbial colonisation and release of inflammatory cytokines.

2) Immune-response defect (inside-out hypothesis): Secondary immune dysregulation.

  • Defects in TLRs- loss of epidermal innate immunity. Colonisation with S. aureus is linked to inflammation.
  • IgE-mediated allergic sensitisation leads to increased susceptibility to allergens, secondary to structural epidermal defects.
27
Q

Causes and risk factors of AD?

A

1) immune dysfunction: Th1 / Th2 imbalance (heightened Th2), hygiene hypothesis, C-section birth, vaccinations, antibiotics.

2) Stress promoting chronic inflammation.

3) Filaggrin gene mutations, facilitates the aggregation of keratin filaments.

4) Nutritional deficiencies — e.g., vitamin D, zinc, EFA deficiency / altered EFA metabolism — linoleic acid levels tend to be increased, Gamma-linolenic acid, EPA and DHA tend to be relatively low.

Reduced delta-6-desaturase activity (e.g., FADS2 SNP, Mg / B6 / Zn deficiency, IR, alcohol, high stress).

5) family history of atopy

6) dysbiosis: early life antibiotics, ↑ Clostridia spp., E. coli, S. aureus and Candida albicans, and less Bifidobacteria, Bacteroidetes and Bacteroides. Clostridia and E.coli
may be associated with AD via eosinophilic inflammation.

7) Gastric H.pylori infection — directly stimulates epidermal cells to secrete thymic stromal lymphopoietin (TSLP),
induces dendritic cell-mediated inflammatory Th2 responses.

8) Excess histamine - disrupts tight junction integrity.

28
Q

Which environmental triggers and mediators could you remove in AD?

A

1) Environmental allergens: Airborne (e.g.,
pollutants), plants, dyes, medications.

2) Solvents, detergents, topical products, e.g., cosmetics. Especially avoid phthalates which promote a Th2 response.

3) Heat, humidity, excessive bathing.

4) Address skin infections, e.g., S. aureus (due to deficiencies in endogenous bactericidal peptides) or viruses e.g., HSV.

5) Stress management

29
Q

What exacerbating factors would you remove in AD?

A
  • Key allergens: Children should especially avoid cows’ milk, eggs, peanuts, wheat, soy, nuts and fish.
  • Older children / adults may be react to birch pollen- associated foods for e.g., apple, carrot, celery, hazelnut.
  • Avoid inflammatory foods: Sugar, saturated fat, refined
    carbohydrates (white rice, white pasta, white bread, etc.),
    processed meat, red meat, MSG, artificial sweeteners.
30
Q

Which dietary interventions would you use for AD?

A
  • Follow the CNM Naturopathic Diet, with a focus
    on the inclusion of anti-inflammatory foods.

1) Increase omega-3 fatty acids

2) Increase quercetin-rich foods
e.g., apples, kale, blueberries, spinach, red onions.

3) Pre and probiotics — support a healthy gut microbiome / correct dysbiosis, enhance SCFA production → anti-inflammatory (reduce inflammatory cytokine formation). Help maintain tight junctions. Researched strains include L. salivarius, L. rhamnosus, L. acidophilus and B. lactis.

  • 5R protocol / intestinal barrier support
    as needed
  • Immunomodulatory / anti-inflammatory — help correct

Th1 / Th2 imbalance . E.g., echinacea (dampens
Th2 — 4 g), turmeric (500–2000 mg), boswellia (250‒500 mg).

31
Q

Supplements for AD?

A

1) Vitamin A (retinol) 5000 iu / day
For epithelial cell differentiation and collagen synthesis. Deficiency potentiates Th2 inflammation and mast cell activation.

2) Vitamin C 1–2 g / day
Improves overall epidermal barrier function.
For keratinocyte differentiation; collagen synthesis; ceramide production in keratinocytes.

3) Zinc 15–30 mg / day
Promotes normal keratinocyte differentiation; reduces pro- inflammatory actions of keratinocytes; for EFA metabolism.

4) Vitamin E: Up to 600 iu / day.
Supports skin water barrier, epidermal barrier, ↓ oxidative stress. Can use a topical application of 5%.

5) Quercetin Up to 3 g / day
Bioactive effect on inflammation, oxidative stress,
and wound healing in keratinocytes.
Inhibits cytokines via NF-κB and other pathways. Stabilises mast cells.

6) Vitamin D Optimise levels
Normalising effect on Th1/Th2 cytokines seen in AD. Anti-allergic — reduces IgE production and dampens IgE-mediated mast cell activation.

7) EFAs: EPA 1 g+; GLA (evening primrose oil 320 g)
GLA ↑ PG1 which inhibits the synthesis of arachidonic acid metabolites. EPA ↑ the production of the anti-inflammatory PG3.

32
Q

Which topical applications might you use for AD?

A
  • aqueous creams and lotions e.g., chamomile, calendula, lavender, liquorice.
  • Herbal washes / baths eg Calendula — inhibits inflammatory cytokine / COX-2 production; inhibits NO production in several skin cells. Anti-microbial.

-Oatseed — its avenanthramides reduce histamine release from mast cells.

– Chickweed — its flavonoid glycosides have
anti-oxidant and anti-inflammatory effects.

33
Q

Describe the pathophysiology of psoriasis and how does it present?

A

Its a common T-cell-mediated, autoimmune inflammatory skin condition characterised by hyperkeratosis.

A deregulated T-cell-mediated inflammatory process leads to keratinocyte proliferation + dysfunctional differentiation.

1) Keratinocytes respond to a trigger → stimulate dendritic cells → cytokine production → T-helper cell differentiation.

2) T-helper cells release cytokines → keratinocyte proliferation → more inflammatory cells.

Clinical presentation:

  • Symmetric, well-defined, salmon-coloured plaques with overlapping thick, silvery scales.
  • Characteristically involves the scalp, the extensor surfaces (back of wrists, elbows, knees, buttocks and ankles), sites of repeated trauma.
  • Nail involvement is common; pitting and flaking, characteristic ‘oil drop’ stippling (yellowish brown spots under the nail plate).
34
Q

Discuss causes and risk factors or psoriasis

A

1) Genetic predisposition — HLA-Cw6 (with the most significant locus being PSORS1 — the ‘psoriasis susceptibility gene 1’).

2) Trauma — psoriatic skin lesions often appear in areas after injury — associated with various inflammatory mediators (e.g., IL-, IL-8), ↑ neuropeptides, nerve growth factor and vascular endothelial growth factor.

3) Vaccination — e.g., association with influenza and COVID-19 vaccination- TNF-α and IFN-γ may explain the pathophysiological

4) Air pollution — particulate matter and
cadmium can promote pathogenesis.

5) Medications — commonly lithium, beta-blockers, antimalarials, TNF-alpha inhibitors, corticosteroids
and NSAIDs.

6) Infectious agents — e.g., Streptococcus pyogenes (strep. tonsilitis) triggering T-cell and TNF-α activation epidermal inflammation and hyperproliferation.

7) Smoking ↑ ox. stress, NF-Κb & inflammatory cytokines (e.g., TNF).

8) Alcohol — ethanol ↑ TNF-α, ↑ lymphocyte
proliferation and mast cell histamine release.

9) Metabolic syndrome:
↑ adipokines= inflammation, chemokines, cytokines and abnormal fatty acid metabolism.
- High serum FFAs amplify Th1 / Th17 responses.

10) Gut dysbiosis — linked to ↓ Akkermansia
muciniphila and Bacteroidetes phylum, and ↑ Firmicutes phylum.

11) NAFLD — twice as prevalent in psoriasis.
Insulin resistance is likely a contributory factor.

12) Chronic high-level stress — ↓ cortisol and
↑ epinephrine and norepinephrine stimulate mast cells, affect skin barrier function and upregulate proinflammatory cytokines.

35
Q

Natural approach to psoriasis?

A

1) Reduce gluten foods — esp. when anti-gliadin antibodies present.

2) Restrict red meat — dietary SFAs amplify psoriatic inflammation.

3) Restrict simple sugars e.g., sucrose.

4) Reduce toxic load (e.g., stop
smoking, stop drinking alcohol, use
air filters, avoid unnecessary drugs,
avoid chemically-ridden cosmetics).

5) Digestive support — e.g., bitters, digestive enzymes. anti-microbial

6) Probiotics and prebiotics to support commensals.

7) Weight loss as needed — ↓ inflammatory mediators.

8) Stress management (see stress lecture).

9) Topical applications
‒ Coconut oil — anti-fungal and replenishing.
‒ Neem — anti-inflammatory (COX and LOX inhibition) and inhibitory effect on microbial growth.
‒ Aloe vera — inhibits COX and hence PG2 production. Vulnerary (activates fibroblast collagen synthesis).

36
Q

Supplements for psoriasis?

A

1) Vitamin A (retinol) 5000 iu / day For epithelial cell differentiation, collagen synthesis and intercellular adhesion. Inhibits bacterial decarboxylase

2) Vitamin D Optimise levels
Downregulates TNF-alpha, IL-1,IL-6, IL-8; anti-inflammatory and immunomodulatory effects. May help ↓ keratinocyte proliferation and ↑ cell differentiation.

3) Vitamin E 400–800 iu / day
↓ proinflammatory cytokines and ↓ monocyte adhesion to endothelial tissue.

4) Selenium 100‒200 ug / day
GPO and selenium levels are often low in psoriasis patients.

5) Omega-3 oil 6 g / day (720 mg DHA / 1080 mg EPA)
Arachidonic acid (AA) is high in psoriatic skin lesions, and its metabolite, leukotriene B4, is the principal mediator of inflammation. When COX or LOX (or both) metabolise EPA which has replaced AA in cell membranes, it can attenuate inflammation.

6) Zinc 15‒30 mg / day
A coenzyme for DNA and RNA polymerases — plays a key role in excessive keratinocyte proliferation in psoriasis.

7) Anti-inflammatory herbs: Turmeric (inhibits NFkB and COX-2 —500–2000 mg) and boswellia (inhibits LOX 200 mg–500 mg / day).

37
Q

Which functional tests might be used for AD?

A
  • Full blood count (eosinophils); serum IgE.
  • Allergy and food sensitivity testing (e.g., Cyrex).
  • Comprehensive stool testing.
  • Genetic panels (e.g., FADS2, VDR).