13. SKIN & RESPIRATORY HEALTH - Lou Flashcards

This module covers: • Asthma. • Bronchitis. • Chronic obstructive pulmonary disease. • Integumentary system. • Acne vulgaris. • Rosacea. • Atopic dermatitis. • Psoriasis.

1
Q

What is asthma?

A

A chronic respiratory disorder characterised by variable airway obstruction and hyper-responsiveness to stimuli.

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2
Q

What could cause airway narrowing in asthma?

A
  • Bronchial smooth muscle spasm.
  • Swelling of bronchial mucosa.
  • Excess viscous mucus secretion.
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3
Q

What are the hallmark symptoms of asthma?

A

Wheeze, intermittent shortness of breath, chest tightness and dry cough.

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4
Q

List three signs / symptoms of asthma

A
  • Initially shortness of breath, coughing or chest tightness
  • Itching of chest or neck (especially in children)
  • Expiratory wheeze
  • Dry cough at night or while exercising
  • Anxiety and sweating
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5
Q

By which of the following glycoproteins is asthma usually mediated?
* IgM
* IgG
* IgA
* IgE
* IgD

A

IgE

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6
Q

List three examples of inflammatory mediators which can cause bronchospasm, triggering an asthma attack?

A
  • histamine
  • leukotrienes
  • prostaglandins
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7
Q

Following inflammatory mediators, what can cause further airway narrowing in asthma?

A

If inflammation is not adressed, eosinophils, T-helper cells and mast cells migrate into the airways.
Mucus production by goblet cells is increased, plugging the airway and
along with increased airway tone and hyper-responsiveness, causes the airway to narrow, further exacerbating symptoms.

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8
Q

What is ‘Airway remodelling’?

A

Bronchial smooth muscle hypertrophy, formation of new vessels and interstitial collagen deposition due to chronic inflammation. This results in persistent airflow obstruction, similar to COPD.

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9
Q

What is the relevance of arachidonic acid metabolism in asthmatics?

A

Asthmatics have an imbalance in arachidonic acid metabolism, leading to relative increases in lipoxygenase products.

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10
Q

What are lipoxygenase products?

A

They are the most potent chemical mediators in asthma. 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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11
Q

Why is disrupted Th1 / Th2 balance a risk factor for asthma?

A

Immune tolerance (Th1 / Th2 balance) is important as excessive Th2 response encourages IgE release, increasing inflammatory mediators.

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12
Q

What is the ‘Hygiene Hypothesis’?

A

Pathogen exposure is needed for the neonatal immune system to develop.
When inadequate, it is associated with increased atopic diseases and autoimmunity.
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.

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13
Q

Outline how pre- or post-natal exposure to antibiotics can be linked to asthma?

A

It can ↑ the risk and severity of asthma in children:

  • First year of life is critical in gut microbiome development — gut dysbiosis is linked to early disruption of the immune system and the development of chronic atopic and inflammatory diseases.
  • Compromised gut microbiome leads to antigen stimulation of antibody pathway causing heightened Th2 response with increased antigen sensitivity and abnormal responses.
  • 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.
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14
Q

What advice can be given to pregnant women and new mothers to reduce the risk of atopic conditions?

A
  1. Natural birth: Appropriate microbial innoculation of the neonatal microbiome reduces the chance of dysbiosis and immune imbalance.
  2. ** Breastfeeding:** is protective via several mechanisms including immune development and gut microbiome.
  3. Weaning: Longer breastfeeding ( > 6 months) is shown to result in ↓ risk of wheeze and to have a protective effect until school age.
    Ideally, exclusively breastfeed for 6–9 months. Early weaning and feeding infant formula, ↑ risk of food allergy, including asthma.
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15
Q

List three factors implicated in obese asthma

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

ERV = expiratory reserve volume
FRC = functional residual capacity

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16
Q

Which components in highly processed foods could aggravate or trigger asthma?

A
  • Preservatives — benzoates, sulphur dioxide, sulphites.
  • Food colourings — azo dyes, especially tartrazine (E102).
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17
Q

A deficiency in which essential trace mineral could contribute to asthma occurence?

A

Molybdenum deficiency
can contribute to sulphite sensitivity as it is a co-factor for sulphite oxidase (oxidises sulphite to sulphate, enabling safe urinary excretion).

or sulfites as they are known in most other countries

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18
Q

Why could female sex hormone fluctuations cause asthma?

A

Female sex hormone fluctuations can affect asthma:
* Raised oestrogen: Oestrogen favours Th2.
* HRT: linked with ↑ risk of severe exacerbations in asthmatic women. Greater risk with previous rather than current use.
* Perimenstrual asthma: a cyclical worsening of asthma during the luteal phase and / or first few days of menstruation.
* Hormone fluctuations: particularly the impact of oestrogen changes at ovulation and prior to menstruation.

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19
Q

What is the gold standard test for diagnosing asthma?

A

There is no gold standard test.
Medical history, physical examination, lung function tests (spirometry / peak expiratory flow) is taken.

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20
Q

Which percentage of asthma cases can be classified as extrinsic? What does this classification mean?

A

60–90% of cases

Extrinsic (allergic / atopic) asthma:
- Involves an IgE mediated response.
- Common triggers include pollen, mould, dust mites, pet dander.

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21
Q

What is intrinsic asthma?

A

Intrinsic (non-allergic) asthma (10–40% of cases):
- More common in females, typically develops later in life.
- Bronchial reaction, IgE sometimes involved.
- Possible triggers: cold temperatures, humidity, stress, exercise, pollution, irritants in air such as smoke, and respiratory infections.

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22
Q

How could dietary / lifestyle evaluation be applied to establish a possible asthma diagnosis?

A
  • Diet diary
  • thorough case history
  • elimination diet
  • identification of triggers.
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23
Q

Which functional tests would you consider for a client with suspected asthma?

A
  • IgG / IgE food profile: e.g., York Test IgG foods and IgE foods test.
    Assess potential food allergy or intolerances.
  • IgG / IgE inhalant allergy profile: e.g., Genova’s inhalants / IgE moulds test.
    Assess for chemical or environmental irritants.
  • Food / chemical intolerance test: e.g., Genova’s toxic element clearance profile, elemental analysis.
    Assess specific food additives, colourings, pharmaco-active agents, environmental chemicals
  • GI profile or digestive analysis: e.g., Genova’s NutrEval.
    To ensure optimal digestion, microflora colonisation and immune health.
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24
Q

Suggest five dietary exclusions that might be recommended in the treatment protocol of an asthmatic client.

A
  1. Remove allergens and foods triggering sensitivities: most common foods associated with asthma are cows’ milk, eggs, chocolate, rice, soy, corn, citrus fruit, apple. Consider an elimination diet or Cyrex array 10 to identify trigger foods.
  2. Reduce red meat intake: arachidonic acid link to ↑ series 2 prostaglandins and leukotrienes, causing transient airway hyper-responsiveness.
  3. Avoid dietary sulphites: alcohol, dried fruits, bagged / prepared salads.
  4. Avoid nitrates: Cured meat ↑ symptoms.
  5. MSG and its derivatives can trigger symptoms.
  6. Reduce excess salt: potentially increases bronchial reactivity.
  7. Avoid very cold drinks: can trigger bronchial spasm.
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25
Q

What pre-conception advice can be given to reduce the risk of asthma in the child?

A
  • Allergies and sensitivities: Reduce pre-disposition in child; consider nutritional status of parents and pre-conception toxin exposure.
  • Follow CNM Naturopathic Diet: Eat only fresh, natural, unprocessed organic food pre-conception / pregnancy. Eliminate / reduce common allergenic foods. Eat fish / purified fish oil supplement (during pregnancy / lactation).
  • Breastfeeding: reduces incidence and severity of asthma.
  • 1st year of child’s life critical: minimise chemical exposure as immature liver is unable to detoxify many compounds.
  • Ensure good sleep
  • Minimise stress
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26
Q

Recommend five dietary inclusions to reduce oxidative stress and address asthma.

A
  • Antioxidants: Include vitamins A, C, E, carotenes, co-factors — zinc, selenium, copper, and flavonoids (particularly quercetin).
  • Increase selenium: A co-factor of GPO which is often low in asthmatics.
  • Increase vitamin E: A potent antioxidant, improves lung function, optimises Th1 & suppresses Th2, ↓ IgE and atopy.
  • Flavonoids: Such as quercetin inhibit histamine release from mast cells and basophils when stimulated by antigens. Quercetin decreases
    airway inflammation and hyper-responsiveness. Increase in diet and/or supplement up to 3 g / day (adult dose) before meals.
  • Support SIgA levels: Probiotics incl. S. boulardii, zinc, A, D, colostrum for immune tolerance and reduced food reactions.
  • Optimise omega-6:3 ratio: An inflammatory omega 6:3 profile causes ↑ prostaglandin E2 (PGE2)➔IgE = atopy and inflammation.
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27
Q

Why is ensuring optimal digestive function key in addressing asthma, especially in children?
Make one dietary recommendation to this effect.

A

Low HCl and protein maldigestion is linked to asthma in children.

Increase dietary fibre
- Associated with improvements in lung function — anti-oxidant and anti-inflammatory effects (25g / d women; 35g / d men).
- Studies show an 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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28
Q

Give three lifestyle recommendations to support the asthmatic client

A
  • Avoid potential triggers: Environmental pollutants (incl. tobacco smoke), household chemicals (e.g., cleaning products, paint), moulds, pollens, dust mites etc.
  • Buteyko breathing: Exercises using shallow breathing through the nose to correct the breathing pattern.
  • Stress reduction: Stress and anxiety contribute to asthma exacerbations.
    Occurs through various mechanisms e.g., oxidative stress pathways, glucocorticoid resistance, nerve-mast cell interaction.
  • Address posture: compression of lungs exacerbates symptoms. Smartphones ― development of forward head posture.
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29
Q

Which supplemental nutrients could be considered to enhance immune tolerance and address asthma?

A
  • Vit C
  • Vit D
  • Magnesium
  • Zinc
  • Probiotics
  • Fish oil
  • CoQ10
  • Boswellia
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30
Q

List two spices that an asthmatic client can include in their daily diet to inhibit arachidonic acid metabolism?

A

Ginger and turmeric

Include in meals, add to fresh vegetable juices, freshly grate and infuse in boiling water or take powdered as a supplement.

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31
Q

Which herb can be recommended for asthma. Include rationale and dosage.

A

Boswellia

Inhibits leukotriene production. Shown to improve shortness of breath, number of attacks, respiratory capacity and indicators of inflammation in asthmatics.

200 mg–500 mg / day

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32
Q

Outline the rationale and dosage for Vitamin C supplementation in asthma

A
  • Vit C is an 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).
  • 2–3 g / day in divided doses
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33
Q

Why is it important to optimise Vitamin D levels in the client with asthma?

A
  • Vitamin D modulates genes for asthma / allergy. Maternal levels linked to allergy — higher levels protective against asthmatic wheezing in young children.
  • It inhibits eosinophils (involved in pathogenesis of asthma).
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34
Q

Outline the rationale and dosage for supplementating the following minerals in asthma:
1. Magnesium
2. Zinc

A
  1. Magnesium
    * Improves lung function, reduces bronchial reactivity.
    * Antagonises movement of calcium across membranes: ↓ calcium uptake in bronchial smooth muscles = relaxation / dilation of bronchial airways.
    * Used as bronchodilator in acute asthma attacks. Linked with↓ bronchial reactivity.
    200‒400 mg / day
  2. Zinc
    * 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.
    15‒30 mg / day
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35
Q

How is probiotic supplementation helpful for supporting immune tolerance to improve asthma symptoms?
Which two specific strands have been found especially beneficial?

A
  • Probiotics can 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 lymphocyte infiltration to the respiratory tract, ↓ IgE, IgG1, IgG2a production.
  • ↑ butyrate / IgA production alleviate symptoms, ↑ quality life.
  • L. rhamnosus GG and GR-1
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36
Q

Outline the rationale and dosage for fish oil supplementation in asthma

A
  • Fish oil reduces inflammatory markers, improving respiratory health and symptoms in children (in combination with vitamin C and zinc).
  • Needed for production of anti-inflammatory prostaglandins.
  • 1 g of actual EPA or higher as required.
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37
Q

Outline the rationale and dosage for CoQ10 supplementation in asthma

A
  • Antioxidant: ↓ oxidative stress and asthma symptoms.
  • May ↓ long-term side-effects of glucocorticoid medications.
  • 150 mg / day
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38
Q

Which two tissue salts could be recommended for asthma?

A

Kali. mur. & Mag. phos.
2 pills x 2 daily.

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39
Q

Recommend one way in which to use essential oils to alleviate asthma symptoms.

A

Adding a few drops of lavender oil to a diffuser or
humidifier may reduce airway inflammation and help alleviate stress.

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40
Q

What is ‘bronchitis’?

A

Acute or chronic inflammation of the bronchi associated with environmental irritants, inducing:
- 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.

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41
Q

What are the hallmark symptoms of bronchitis?

A
  • 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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42
Q

Which Dietary exclusions could be considered in adressing bronchitis?

A
  • Reduce intake of sugar, salt, saturated fats, cows’ dairy, wheat, processed foods, additives, preservatives, colourings.
  • 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.
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43
Q

What dietary inclusions can be recommended for the client with bronchitis?

A
  • Follow the principles of the CNM Naturopathic Diet and include easy-to-digest foods e.g., soups.
  • Ensure adequate fluid intake; water, herbal teas, juices, broths.
  • Increase intake of mucolytic foods (changes the viscosity of mucus enabling easier expulsion) e.g., garlic, onions; decrease catarrh; horseradish (not for dry cough); ginger reduces inflammation, has antiseptic properties; cinnamon — a warming expectorant.
  • Bromelain, a proteolytic enzyme from pineapple decreases airway inflammation, is mucolytic and has potential as an anti-viral agent.
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44
Q

What is a common aetiological factor in chronic bronchitis?

A

Acute bronchitis is most commonly associated with a weak terrain and subsequent infection. Support immunity to assist recovery.

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45
Q

Optimal levels of vitamin A function to maintain \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ integrity and promote \_\_\_\_\_\_\_\_ secretion, contributing to mucociliary defence.
It enhances \_\_\_\_\_\_\_ proliferation and interleukin-2 secretion reducing lung inflammation.

A

mucous membrane
mucin
T-cell

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46
Q

What dosage of vitamin A can be recommended in bronchitis?

A

5000 iu daily

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47
Q

Name the nutrient for bronchitis:

  • Increases T-cells, interferons and natural killer cells.
  • Reduces oxidative stress and inflammation of airways.
  • High plasma concentrations are associated with reduced risk of acute and chronic respiratory illness and shorter duration of existing infection.
A

vitamin C

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48
Q

Name the vitamin for bronchitis:

  • Deficiency is associated with increased risk of respiratory infection.
  • Moderates pulmonary inflammatory responses.
  • Enhances innate immune responses to pathogens.
A

Vitamin D

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49
Q

Outline the rationale for supplementation of 15-30mg zinc/day for bronchitis

A
  • Zinc modulates antiviral and antibacterial immunity and regulates the inflammatory response.
  • Helps maintain mucous membrane integrity.
  • Maintains phagocytic and NK cell function.
  • Supports aspects of cellular and humoral immunity
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50
Q

What is COPD?

A

COPD is 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.

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51
Q

How does COPD differ from asthma?

A

Unlike asthma, the airflow obstruction in COPD is only partially (or not at all) reversible, and the disease process is progressive.

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52
Q

COPD is considered a combination of which two main pathologies?

A
  • 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.
53
Q

What percentage of COPD is caused by smoking?

A

Approximately 90%

54
Q

List two causes / risk factors for COPD apart from smoking

A
  • Exposure to lung irritants: Air pollution, industrial chemicals, dusts, etc.
  • Genetic susceptibility.
55
Q

In terms of COPD:

Why is healthy weight management important?

A
  • 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).
56
Q

Which dietary inclusions could be recommended for COPD?

A
  • Nutrient-rich, easily digested foods e.g., fresh juices, broths.
  • Fruits / vegetables: ↑ antioxidant and anti-inflammatory nutrients. Have vegetables lightly cooked rather than raw.
  • Herbs: with antioxidant, anti-inflammatory and warming properties such as turmeric, ginger and garlic.
  • Beneficial fats: with emphasis on omega-3 fatty acids (↑ energy, anti-inflammatory).
  • Quality protein: is essential (sarcopenia risk) with specific focus on leucine, a significantly stronger stimulator of anabolic signalling in skeletal muscle than other amino acids.
57
Q

Which nutrients should be optimised in a COPD protocol?

A
  • Vitamin A & E
  • Vitamin C + bioflavonoids
  • Vitamin D
  • Zinc
58
Q

Which nutraceutical for COPD does the following describe:

  • Mucolytic (breaks disulphide bonds in mucoproteins) enabling easier expulsion of mucus.
  • Increases glutathione and ↓ oxidative damage associated with inflammation and changes to respiratory architecture.
  • ↓ exacerbations and ↑ mean forced expiratory flow.
  • Inhibits bacterial adherence.
  • Can be supplemented at 400–1200 mg / day
A

N-acetyl cysteine

59
Q

Outline the benefits of fish oil for COPD. Also give the dosage for supplementation

A
  • Increased omega-3 intake is associated with reduced COPD morbidity (↓ exacerbation risk, fewer respiratory symptoms and ↑ quality of life).
  • Reduces inflammation, improves body composition and enhances exercise performance.
  • Dosage: Fish oil equiv. to EPA: 800– 1000 mg; DHA: 300 mg
60
Q

How could mycotherapy be applied to COPD?

A
  • Shiitake:
    1.5–10 g / day
    Use as a powder or include in the diet (raw or lightly cooked)
  • Heightens immune vigilance against potential pathogens: ↑ phagocytes, T- and B-lymphocytes and NK cells.
  • Enhances interferon synthesis (anti-viral proteins).
  • Increases SIgA.
  • Has tonic properties, helping to restore energy.
  • Cordyceps:
    2–5 g / day
  • Improves FEV1% and FEV1 / FVC ratio — important markers for disease progression.
  • Improves exercise tolerance (antioxidant and anti- fatigue mechanisms e.g., ↓ lactate accumulation).
  • Strengthens the immune system.

FEV1:FVC = how much air can be forcefully exhaled.

61
Q

Name the nutraceutical:

Increased intake is associated with reduced COPD morbidity (↓ exacerbation risk, fewer respiratory symptoms and ↑ quality of life).
Reduces inflammation, improves body composition and enhances exercise performance.

A

Omega-3

62
Q

Name the herb:

An expectorant with mucolytic and antibacterial activities. Has antioxidant properties and has shown to downregulate activated NF-kB in COPD.

A

Thyme
(Thymus vulgaris)

63
Q

Which essential oils have been found to be useful in COPD?

A

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

64
Q

Make two lifestyle suggestions in the case of COPD

A
  • Exercise (adjusted to the ability of the individual) alongside nutritional support improves bodyweight, muscle strength and quality of life.
  • Breathing exercises support breathing mechanics.
65
Q

What referral might be good for a client with COPD?

A

Manual therapy
(e.g., osteopathy, physio)

66
Q

If the liver, kidneys, lungs or gut are under stress, what could be the effect on the skin?

A

The skin has a major role in detoxification via the excretion of waste products. If the other detoxification routes are under stress, the resultant irritation and inflammation can contribute to skin dysfunction.
Any underlying dysfunction, such as toxic overload, must be considered when seeking to address common skin disorders including acne, eczema, rosacea and psoriasis.

67
Q

What is ‘Acne vulgaris’?

A

Acne vulgaris is an inflammatory skin condition characterised by:
1. excess sebum production,
2. follicular hyperkeratinisation of sebaceous ducts,
3. follicular colonisation by Cutibacterium acnes
4. and inflammation.

68
Q

TRUE OR FALSE:

Microbial colonisation with Propionibacterium acnes is the predominant causative factor of acne.

A

FALSE
Although implicated, it is NOT the causative factor.

Although Propionibacterium acnes has been reclassified as Cutibacterium acnes, this name is often still used.

69
Q

Which areas of the body are predominantly affected by acne and why?

A

Acne predominantly affects skin with dense sebaceous follicles — primarily the face, but also the chest and back.

70
Q

Which demographic is most affected by acne?

A

Acne commonly affects adolescents with incidence tending to decrease with age.
It is more common in males than females due to hyper-responsiveness to androgen hormones.

71
Q

Outline the clinical presentation of acne vulgaris

A
  • 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.
72
Q

Outline how increased androgens can cause acne

A

Increased androgens free testosterone (particularly DHT), DHEA (most abundant steroid in body) and DHEAS:
* Stimulate hyperkeratinisation of follicles.
* Increase sebum production.
* Stimulate acne lesions.

73
Q

What increases 5-alpha-reductase activity and why is this pertinent in acne?

A

Greater activity of 5-alpha-reductase (converts testosterone to DHT) is associated with factors such as hyperinsulemia, obesity and low zinc.
DHT is a potent androgen that stimulates acne formation through hyperkeratinisation of follicles and increased sebum production.

74
Q

How does hyperinsulinemia affect acne formation?

A

Hyperinsulinemia decreases sex hormone binding globulin (SHBG), increasing levels of free testosterone.

75
Q

Explain the link between dairy and acne

A
  • Dairy and high GI / GL foods ↑ IGF-1.
  • IGF-1 has been shown to ↓ FoxO1, which leads to activation of mTORC1.
  • In acne, mTORC1 mediates sebaceous gland hyperproliferation, lipid synthesis, and hyperplasia of keratinocytes.
  • Dairy also increases circulating levels of insulin with similar consequences to a high GL meal.
  • Dairy and meat (high BCAAs), saturated fats (esp. palmitic acid) and trans fats activate mTORC1. Palmitate: Major FA = 32% milk TGs.

mTORC1 = mammalian target of rapamycin complex 1, a signalling protein that regulates cell growth.
Fox01 = forkhead box protein 01,
a transcription factor that influences glucose metabolism and insulin signalling.

76
Q

Apart from insulin resistance, outline five possible causes and risk factors for acne vulgaris

A
  • Hormone fluctuations e.g., puberty, menstruation and pregnancy.
  • PCOS — association with hyperinsulinemia / insulin resistance.
  • Psychological stress via HPA-axis, release of CRH, promotes lipogenesis and induces cytokines (IL6 + IL11) in keratinocytes → inflammation.
  • Depression / anxiety: Emerging studies in psychodermatology (mind / skin link). Skin and nerve cells are connected at the embryonic level through ectoderm and continue to communicate and affect each other throughout life.
  • ↑ Corticosteroids e.g., Cushing’s disease.
  • Dairy and high GI / GL foods ↑ IGF-1: IGF-1 has been shown to ↓ FoxO1, which leads to activation of mTORC1. In acne, mTORC1 mediates sebaceous gland hyperproliferation, lipid synthesis, and hyperplasia of keratinocytes.
  • Microbiome: patients have a distinct gut microbiome with higher levels of bacteriodes. Acne lesions are associated with increased proportion of C. acnes as a skin commensal bacterium.
  • Vitamin D deficiency: Vit D plays a role in regulating proliferation and differentiation of keratinocytes and sebocytes ― anti-comedogenic properties.
77
Q

Outline the TCM view of acne along with the treatment

A

In TCM, acne is a manifestation of dampness and heat in the body, which tends to rise to the head.
On the face the location of spots can be a clue to the location of the cause — use the facial reflex zone chart.
Treatment is aimed at clearing damp heat. Damp clearing foods include whole grains, warming / drying spices e.g., cinnamon, ginger. Heat clearing foods incl. bitter foods e.g., dandelion, rocket.

78
Q

How is acne viewed from an Ayurvedic perspective?

A

In Ayurveda, acne is an outward sign of inward bodily distress caused by eating too many spicy, sweet and greasy foods.

79
Q

Which dietary exclusions are to be recommended for a client with acne?

A

Avoid foods linked with acne pathogenesis:
* sugar
* dairy
* trans fats
* ↑ saturated fat
* ↑ red meat (↑ BCAAs)
* refined foods
* high GI / GL foods
* excess omega-6 fatty acids
* alcohol
* spicy foods.

80
Q

Outline the dietary inclusions that could be recommended for a client with acne

A
  • Consume low GI / GL foods: Balance blood sugar levels to regulate insulin.
  • Increase low GI fruit and vegetables — alkalising, ↑ antioxidant and anti-inflammatory nutrients.
  • Increase fibre to improve glycaemic control. Helps reduce toxic overload and supports sluggish digestive system.
  • Omega-3 (walnuts, flaxseed, chia seeds, fish) decrease IGF-1. EPA reduces inflammation and inhibits mTORC1 activation. Has an acne-protective effect.
  • Flaxseeds contain enterolactone, which has shown to decrease circulating free androgens.
  • Include green tea, turmeric, berries — contain polyphenol compounds that decrease mTORC1.
  • Ensure a healthy microbiota by targeting harmful bacteria and / or enriching beneficial bacteria.
  • Include cinnamon in the diet to improve glycaemic control. ↑ insulin receptor sensitivity, facilitating transport of glucose into the cells.
  • Ensure good water intake to support elimination channels.
81
Q

Identify the nutrient for acne vulgaris:

Plays a role in collagen synthesis and supports integrity of the skin barrier.
Reduces sebum production and hyperkeratosis of follicles.
Supports immune function and inhibits growth of C. acnes.

A

Vitamin A

82
Q

Which B vitamin works alongside chromium in insulin regulation?

A

Vitamin B3
(niacinamide)

83
Q

Why should vitamin D levels be tested and optimised in a client with acne?

A

Vitamin D regulates the metabolism of keratinocytes and sebocytes.
It supports glycaemic control by increasing
cellular sensitivity to insulin.

84
Q

Which mineral can inhibit 5α reductase to lower DHT levels?

A

Zinc
15-30mg/day

85
Q

Which of the following are androgen modulating herbs, useful in acne vulgaris?
a. Slippery elm and berberine
b. Craetagus and dandelion root
c. Saw palmetto and stinging nettle root

A

c. Saw palmetto and stinging nettle root

86
Q

How is Cleavers (Galium aparine) tea useful in acne vulgaris?

A

Cleavers (Galium aparine) dried herb as a tea (2 tsp per cup). Supports lymphatic function, assisting in the removal of wastes.

87
Q

How is the microbiome of acne patients distinct?

A

Acne patients have a distinct gut microbiome with higher levels of bacteriodes. Acne lesions are associated with increased proportion of C. acnes as a skin commensal bacterium.

88
Q

What herbal support can be given for liver detoxification in acne?

A

Milk thistle, rosemary, green tea, turmeric.
They are ntioxidants and upregulates phase II detoxification.

89
Q

Which tissue salts can be given to support patients with acne vulgaris?

A
  • Kali. sulph. — skin is dirty in appearance, with susceptibility to pigmentation and scarring.
  • Calc. sulph. — skin suppurates easily, with thick yellow-green discharges.
  • Ferrum phos. — when there is marked inflammation present with limited suppuration.
  • Silica — cystic acne, where lesions take long to suppurate, if at all, and take long to heal.
90
Q

Make two lifestyle recommendations for a client with acne.

A
  • Regular exercise lowers insulin and IGF-1.
  • 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.
91
Q

What is ‘Rosacea’ and who is most likely to have it?

A

Rosacea is a chronic inflammatory skin condition associated with capillary hyper-reactivity presenting as an erythematous (red) rash or flush across the cheeks and nose.
It predominantly manifests in women aged 30–50 years.
It is more common in fair-skinned people, less incidence in darker skins although people of African descent may have a granulomatous form of the condition.

92
Q

What is the clinical presentation of Rosacea?

A

Facial erythema, flushing, papules, pustules, telangiectasia and ocular manifestations.

Telangiectasias (spider veins) = dilated or broken blood vessels located near the surface of the skin.

93
Q

List three possible causes and risk factors for Rosacea

A
  • Gastric H. pylori infection — can stimulate the immune system to produce a large number of inflammatory mediators and increase NO levels→vasodilation and inflammation.
  • SIBO — associated with increased intestinal permeability and systemic inflammation.
  • Vascular hyperactivity — prolonged flushing may be triggered by exercise, hot weather, alcohol, spicy food, hot drinks, caffeine and stress. Consider excess heat (energetic) states.
  • Food allergy / intolerances — e.g., excess histamine
94
Q

Outline a natural approach protocol to address Rosacea

A

Apply the CNM Naturopathic Diet.
* Identify and avoid dietary triggers: Food diary, elimination diet. Capsaicin (peppers) and cinnamaldehyde (e.g., tomatoes, citrus, chocolate, cinnamon) are identified as common triggers.
* 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 (patch test first). Inhibits COX and hence PG2 production.
* **Zinc **has demonstrated benefits for rosacea — 25 mg / day.
* Stress is a major trigger — guide client to reduce stress levels or build resilience.
* Protect the face from UV light.
* Care should be taken with cosmetic and personal care products.

95
Q

What is Atopic dermatitis and what is the common clinical presentation?

A

Atopic dermatitis, also known as eczema, is a disorder of altered skin barrier integrity and immune dysregulation that 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.

96
Q

How does exogenous and endogenous Atopic Dermatitis (AD) differ and which is more common?

A

Exogenous / extrinsic AD is IgE-mediated and more common, accounting for 70–80% of cases.
20–30% of cases are endogenous / intrinsic and are non IgE-mediated.

97
Q

Outline the immune-response defect pathway (inside-out hypothesis) of eczema

A
  • Secondary immune dysregulation.
  • Defects in TLRs has been implicated in the loss of epidermal innate immunity. Colonisation with S. aureus is linked to inflammation.
  • IgE-mediated allergic sensitisation → increased susceptibility to allergens, secondary to structural epidermal defects.
98
Q

Outline the primary epithelial barrier disruption pathway (outside-in hypothesis) of eczema

A
  • Disruption of tight junctions, ↑ permeability of stratum corneum.
  • ↑ trans-epidermal water loss.
  • Structural protein defects (filaggrin).
  • Barrier disruption may be caused by microbial colonisation and release of inflammatory cytokines.
99
Q

Discuss the causes and risk factors for Atopic Dermatitis in terms of immune regulation, gut health, nutrition, genetics and lifestyle.

A

Immune health:
* Th1 / Th2 imbalance (heightened Th2), hygiene hypothesis, C-section birth, vaccinations, antibiotics.
* Excess histamine (see immune) — disrupts tight junction integrity.

Gut dysbiosis:
* Significant associations with early life antibiotics.
* Associated with ↑ Clostridia spp., E. coli, S. aureus and Candida albicans in the gut microbiome, and ↓ Bifidobacteria, Bacteroidetes and Bacteroides. Interactions between specific microbes, the immune system, and the host are thought to drive AD. For example, Clostridia and E.coli may be associated with AD via eosinophilic inflammation.
* Gastric H.pylori infection — directly stimulates epidermal cells to secrete thymic stromal lymphopoietin (TSLP), a cytokine that induces dendritic cell-mediated inflammatory Th2 responses.

Nutrition:
* Nutritional deficiencies — e.g., vitamin D, zinc.
* EFA deficiency / altered EFA metabolism — a tendency for linoleic acid levels 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).

Genetics:
* Filaggrin gene mutations — strongest known genetic risk factor. Filaggrin facilitates the aggregation of keratin filaments.
* Family history of atopy.

Lifestyle:
Stress — promoting chronic inflammation.

100
Q

Which laboratory tests could be used to confirm a possible diagnosis of eczema?

A
  • Full blood count (eosinophils); serum IgE.
  • Allergy and food sensitivity testing (e.g., Cyrex).
  • Comprehensive stool testing.
  • Genetic panels (e.g., FADS2, VDR).
101
Q

What allopathic treatments are commonly used in Atopic Dermatitis?

A
  • Topical corticosteroids (highly suppressive and promotes skin atrophy)
  • antihistamines
  • immunosuppressants (AD commonly recurs when treatment stops)
102
Q

Outline the natural approach to addressing the triggers and mediators of Atopic Dermatitis

A
  • Elimination or oligoantigenic diet (eliminate all foods that could provoke an allergic response).
  • 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.
  • Environmental allergens: Airborne (e.g.,
    pollutants), plants, dyes, medications.
  • Solvents, detergents, topical products, e.g., cosmetics. Especially avoid phthalates (found in plastic and beauty products) which promote a Th2 response. Focus on natural skin / beauty products.
  • Heat, humidity, excessive bathing.
  • Address skin infections, e.g., S. aureus (due to deficiencies in endogenous bactericidal peptides) or viruses e.g., HSV.
  • Stress management
103
Q

Which dietary inclusions should form part of the natural protocol for Atopic Dermatitis?

A
  • CNM Naturopathic Diet, with a focus on the inclusion of anti-inflammatory foods.
  • Focus on cooling foods / beverages: Eczema is often associated energetically with excess heat in the blood.
  • Increase daily sources of omega-3 fatty acids (e.g., ‘SMASH’ fish, flaxseeds, chia seeds, spirulina, etc.).
  • Increase quercetin-rich foods e.g., apples, kale, blueberries, spinach, red onions.
104
Q

Which dietary models could be used to address immune and gastrointestinal health in order to support the client with eczema?

A
  • Autoimmune Protocol may be beneficial. Although AD is not considered autoimmune, it does ↑ the risk of other AI diseases.
  • An anti-histamine approach can also be applied
  • 5R protocol / intestinal barrier support as needed
  • Elimination or oligoantigenic diet (eliminate all foods that could provoke an allergic response)
  • CNM Naturopathic Diet, with a focus
    on the inclusion of anti-inflammatory foods.
105
Q

Why would you consider pre- and probiotics for a client with eczema. Which specific strains are well researched for this condition?

A

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
* B. lactis.

106
Q

Which herbs/spices can be used to help correct Th1 / Th2 imbalance usually seen in atopic dermatitis?

A

Immunomodulatory / anti-inflammatory herbs/spices such as:
* echinacea (dampens Th2 — 4 g)
* turmeric (500–2000 mg)
* boswellia (250‒500 mg).

107
Q

Provide rationale and dosage for supplementing the following for atopic dermatitis:
a) Vitamin A
b) Vitamin E
c) Zinc
d) Vitamin C

A

a) Vitamin A (retinol) – 5000 iu / day
For epithelial cell differentiation and collagen synthesis. Deficiency exacerbates extrinsic AD development by potentiating Th2 inflammation and mast cell activation.

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

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

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

108
Q

Name the nutrient for eczema:

Bioactive effect on inflammation, oxidative stress, and wound healing in keratinocytes. Inhibits cytokines via NF-κB and other pathways. Stabilises mast cells.

A

Quercetin

Up to 3 g / day

109
Q

Why is it a priority to optimise Vitamin D levels in clients with atopic dermatitis?

A

Vitamin D has a normalising effect on Th1/Th2 cytokines in AD. Anti-allergic — reduces IgE production and dampens IgE-mediated mast cell activation.

110
Q

How does EFAs benefit atopic dermatitis and what dosage can be recommended?

A
  • GLA increases PG1 which inhibits the synthesis of arachidonic acid metabolites.
  • EPA ↑ the production of the anti-inflammatory PG3.

Dosage: EPA 1 g+; GLA (evening primrose oil 320 g)

PG1 = Prostaglandin 1

111
Q

How is selenium useful for eczema? What dosage can be recommended?

A

Selenium inhibits NF-κB and may enhance T-cell function.

200 μg/day

112
Q

What herbal infusion can be recommended for eczema and why?

A

Nettle leaf

Reduces the effects of histamine, inhibits COX-1 and 2. Cooling energetics (clears heat). Use 2g dry leaf infusion 3 x per day or 500mg supplement.

113
Q

What topical applications can be recommended for eczema?

A
  • Focus on aqueous creams and lotions (oily preparations may increase heat), e.g., chamomile, calendula, lavender, liquorice.
  • Herbal washes / baths — place herbs in a muslin bag and place in bath as you run the water in. Cooling herbs that sooth pruritis:
    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.
114
Q

What is ‘psoriasis’?

A

Psoriasis is a common T-cell-mediated inflammatory skin condition characterised by hyperkeratosis.

115
Q

Outline the Clinical presentation of psoriasis

A

Psoriasis is characterised by:
* 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), umbilicus and sites of repeated trauma.
* Nail involvement is common; pitting and flaking, characteristic ‘oil drop’ stippling (yellowish brown spots under the nail plate).
* Often worse in winter; better in tropical climates.

116
Q

Give a brief outline of the pathogenesis of psoriasis

A

Psoriasis is an autoimmune condition associated with a deregulated T-cell-mediated inflammatory process → keratinocyte proliferation + dysfunctional differentiation.

  1. Initiation phase: Keratinocytes respond to a trigger → stimulate dendritic cells → cytokine production → T-helper cell differentiation.
  2. Maintenance phase: T-helper cells release cytokines → keratinocyte proliferation → more inflammatory cells.
117
Q

What complications could be seen in psoriasis

A

Complications:
* Psoriatic arthritis (30%)
* CVD
* IBD
* depression
* ocular disorders (e.g., uveitis).

118
Q

Discuss the following causes and risk factors of psoriasis:
a) Genetic predisposition
b) Trauma
c) Vaccination
d) Air pollution
e) Medications

A

a) Key susceptibility genes include HLA-Cw6 (with the most significant locus being PSORS1 — the ‘psoriasis susceptibility gene 1’).
b) Psoriatic skin lesions often appear in areas after injury — Koebner phenomenon. Mechanism possibly associated with various inflammatory mediators (e.g., IL-, IL-8), ↑ neuropeptides, nerve growth factor and vascular endothelial growth factor.
c) There is an association with influenza and COVID-19 vaccination as a trigger / exacerbating factor. TNF-α and IFN-γ
may explain the pathophysiological link with COVID-19 vaccination.
d) Particulate matter and cadmium can promote psoriasis pathogenesis.
e) Commonly lithium, beta-blockers, antimalarials, TNF-alpha inhibitors, corticosteroids and NSAIDs. Occur via direct and indirect mechanisms.

119
Q

Which infectious agents have been linked to the pathogenesis of psoriasis?

A
  • Streptococcus pyogenes (strep. tonsilitis) → triggering T-cell & TNF-α activation → epidermal inflammation & hyperproliferation.
  • HIV and candida (fungal infections) are also linked.
120
Q

How does smoking and alcohol consumption increase the risk of psoriasis?

A
  • Smoking increases ox. stress, NF-Κb & inflammatory cytokines (e.g., TNF).
  • Alcohol: The ethanol ↑ TNF-α, ↑ lymphocyte proliferation and mast cell histamine release.
121
Q

How is metabolic syndrome linked with psoriasis?

A

Metabolic syndrome:
* Inflammation — ↑ adipose tissue →
↑ adipokines, chemokines, cytokines and abnormal fatty acid metabolism.
* High serum FFAs sensitises dendritic cells to amplify Th1 / Th17 responses.

122
Q

Gut dysbiosis is often seen in psoriasis. Which species are commonly low and which are high?

A

Psoriasis is linked to low levels ofAkkermansia muciniphila and Bacteroidetes phylum and high Firmicutes phylum.

123
Q

What is the link between psoriasis and:
a) A high toxic load
b) Poor protein digestion
c) NAFLD

A

a) High toxic load (e.g., alcohol) and impaired detoxification / elimination pathways — contributing to ‘autotoxaemia’.
b) Poor protein digestion — producing polyamines which can induce excess cell proliferation through inhibition of cAMP.
c) NAFLD is twice as prevalent in psoriasis. Insulin resistance is likely a contributory factor.

124
Q

How can Chronic high-level stress be implicated in psoriasis?

A

Reduced cortisol and ↑ epinephrine and norepinephrine:
* stimulate mast cells
* affect skin barrier function
* upregulate proinflammatory cytokines.

125
Q

What can be include in a diet that supports the client with psoriasis?

A

CNM Naturopathic Diet with a focus on:
* Fibre (and adequate water) to facilitate bowel elimination; to support gut commensals and SCFA production.
* Antioxidant-rich fruit and vegetables to reduce inflammation and support liver detoxification.
* EPA / DHA — inhibit inflammatory mechanisms, e.g., leukocyte chemotaxis, prostaglandin and leukotriene production from arachidonic acid and the production of inflammatory cytokines.
* Detox protocol: consider a juice cleanse, fasting etc.
* Consider applying specific AI protocols (e.g., AIP).
* Digestive support — e.g., bitters, digestive enzymes. anti-microbial
* Probiotics and prebiotics to support commensals.

126
Q

What should be removed from the diet to support the client with psoriasis?

A

Address triggers and mediators:
* Reduce gluten foods — esp. when anti-gliadin antibodies present.
* Restrict red meat — dietary SFAs amplify psoriatic inflammation.
* Restrict simple sugars e.g., sucrose.
* Reduce toxic load:
stop smoking and drinking alcohol
use air filters
avoid unnecessary drugs
avoid chemically-ridden cosmetics

127
Q

What could be recommended for topical application in psoriasis?

A

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).

128
Q

Outline a potential supplement protocol for psoriasis. Include three supplements with rationale and dosage.

A

Any of the following:

    • Vitamin A (retinol)
      For epithelial cell differentiation, collagen synthesis and intercellular adhesion. Inhibits bacterial decarboxylase, the enzyme that converts undigested amino acids into polyamines. 5000 iu / day
  • Vitamin D
    Downregulates TNF-alpha, IL-1,IL-6, IL-8; anti-inflammatory and immunomodulatory effects. May help ↓ keratinocyte proliferation and ↑ cell differentiation. Optimise levels
  • Vitamin E
    ↓ proinflammatory cytokines and ↓ monocyte adhesion to endothelial tissue. 400–800 iu / day
  • Selenium
    GPO and selenium levels are often low in psoriasis patients. Possibly due to alcohol, malnutrition and excessive skin loss. 100‒200 ug / day
  • Omega-3 oil
    Arachidonic acid (AA) is found in high levels in psoriatic skin lesions, and its metabolite, leukotriene B4, is considered the principal mediator of inflammation in psoriasis. When COX or LOX (or both) metabolise EPA which has replaced AA in cell membranes, it can attenuate inflammation.
    6 g / day (720 mg DHA / 1080 mg EPA)
  • Zinc
    A coenzyme for DNA and RNA polymerases — plays a key role in excessive keratinocyte proliferation in psoriasis. 15‒30 mg / day
129
Q

List two herbs that can be useful in psoriasis

A
  • Liver herbs such as Milk thistle (↑ glutathione and SOD 3 x 100 mg daily).
  • Anti-inflammatory herbs such as Turmeric (inhibits NFkB and COX-2 —
    500–2000 mg) and boswellia (inhibits LOX 200 mg–500 mg / day).