13. Integumentary System (Skin)

Question 1

What is the integumentary system? What is his role? x2

Answer 1

The skin, hair, nails, sebaceous and sweat glands and sensory receptors form the integumentary system.
1* Skin, the largest organ in the body, acts as a major protective barrier against chemicals, pathogens and other substances in the environment.
2* Has a major role in detoxification via the excretion of waste products. If the liver, kidneys, lungs or gut 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.

Question 2

What is acne vulgaris?

Answer 2

Acne vulgaris = inflammatory skin condition characterised by excess sebum production, follicular hyperkeratinisation of sebaceous ducts, follicular colonisation by Cutibacterium acnes and inflammation.

Question 3

Who and what is affected by acne?

Answer 3

Acne predominantly affects skin with dense sebaceous follicles — primarily the face, but also the chest and back.
* Commonly affects adolescents with incidence tending to decrease with age.
* More common in males than females due to hyper-responsiveness to androgen hormones.
* Microbial colonisation with Cutibacterium acnes implicated but not the causative factor.

Question 4

Acne clinical presentation?

Answer 4

• 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.

Question 5

Causes and RF for Acne ? x7

Answer 5

1. hormones
2. PCOS — association with hyperinsulinemia / insulin resistance.
3. Psychological stress via HPA-axis, release of CRH, promotes lipogenesis and induces cytokines (IL6 + IL11) in keratinocytes → inflammation.
4. 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.
5. insulin resistance
6. VitD deficiency
7. microbiome

Question 6

Causes and RF for Acne ? Hormones

Answer 6

Hormones: Increased androgens.
* Free testosterone — and particularly by its
potent metabolite dihydrotestosterone (DHT).
* DHEA — most abundant steroid in body.
* DHEAS — sulphated version of DHEA.

Stimulate hyperkeratinisation of follicles.
* Increase sebum production.
* Stimulate acne lesions.
* Greater activity of 5-alpha-reductase (converts testosterone to DHT) — associated with factors such as hyperinsulemia, obesity and low zinc).

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

DHEA = dehydroepiandrosterone DHEAS = dehydroepiandrosterone sulphate

• Hormone fluctuations e.g., puberty, menstruation and pregnancy.

Question 7

Causes and RF for Acne ? insulin resistance

Answer 7

Insulin resistance: Diet, obesity, inactivity.
* ↑ proliferation of keratinocytes, stimulates synthesis of androgens and ↑ sebum production.
* Hyperinsulinemia upregulates IGF-1 and downregulates insulin-growth factor-binding protein-3 (IGFBP-3). Net effect = ↑ androgen production and direct impact on keratinocyte hyperplasia and apoptosis.

• 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.
• Insulin resistance, smoking, low zinc levels, and the excess adipose tissue associated with obesity can lead to ↑ levels of DHT, and subsequently to acne.

Question 8

Causes and RF for Acne ? Foods x3

Answer 8

• Dairy and high GI / GL foods ↑ IGF-1.
• 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.

Question 9

Causes and RF for Acne ? VitD deficiency

Answer 9

• The role of factors such as vitamin D, diet, obesity, the microbiome and auto-inflammation is evolving.
• Vitamin D — a role in regulating proliferation and differentiation of keratinocytes and sebocytes ― anti-comedogenic properties.

Question 10

Causes and RF for Acne ? microbiome

Answer 10

• 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.

Question 11

TCM for acne

Answer 11

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

Question 12

Dietary exclusion for acne

Answer 12

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

Question 13

Dietary inclusion for acne x9

Answer 13

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

Question 14

What diet is effective for acne?

Answer 14

Fasting is highly effective — see popular dietary models nutrition 1

Question 15

Nutrients for Acne x5

Answer 15

1. Vitamin A 5000 iu / day
2. Vitamin B3 (niacinamide) 20–50 mg / day in B complex.
3. Vitamin D Optimise levels
4. Chromium 200–1000 mcg / day
5. Zinc: 15–30 mg

Question 16

Vit A for acne - functions

Answer 16

• 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.

Question 17

Vit B3 for acne - functions

Answer 17

• 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.
• Topical niacinamide gel 4% as effective as antibiotic gel ↓ number and severity of acne lesions.

Question 18

Vit D for acne - functions

Answer 18

• Regulates metabolism of keratinocytes and sebocytes.
• Supports glycaemic control by increasing
  cellular sensitivity to insulin.

Question 19

Chromium for acne - functions

Answer 19

• 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.

Question 20

Zinc for acne - functions

Answer 20

• Modulates immune and inflammatory processes.
• Inhibits 5α reductase, ↓ DHT.
• Antimicrobial activity against C. acnes.
• May ↓ number and severity of acneiform lesions.

Question 21

Herbs for acne x5

Answer 21

• Herbs that modulate androgens: 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).

Question 22

Tissue salts for acne x4

Answer 22

Tissue salt support: 1 tab 3 x daily for 4–6 months.
* 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.

Question 23

Back flower for acne

Answer 23

• Bach flower remedies e.g., larch (lacks confidence, low self- esteem), crab apple (feels unclean, unattractive, self-repulsion).

Bach flowers: 4 drops, 4 times daily

Question 24

Other recommendations natural for acne ? x4

Answer 24

• 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.

Question 25

What is Rosacea?

Answer 25

Rosacea = a chronic inflammatory skin condition associated with capillary hyper-reactivity presenting as an erythematous (red) rash or flush across the cheeks and nose.

Question 26

In what population is rosacea more common?

Answer 26

• Predominantly manifests in women aged 30–50 years.
• More common in fair-skinned people, less incidence in darker skins although people of African descent may have a granulomatous form of the condition.
• Can occur in children ― paediatric rosacea.

Question 27

Clinical presentation of rosacea?

Answer 27

Clinical presentation:

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

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

Question 28

Causes and risk factors for rosacea? x4

Answer 28

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

Gut-skin axis: Gut microbiota- produced SCFAs impact the predominance of skin microbiota and subsequently affect the cutaneous immune response

Question 29

Natural approach to rosacea?

Answer 29

Natural approach:
1. Apply the CNM Naturopathic Diet.
2* Identify and avoid dietary triggers: Food diary, elimination diet.
3* Capsaicin (peppers) and cinnamaldehyde (e.g., tomatoes, citrus, chocolate, cinnamon) are identified as common triggers.
4* Focus on cooling, anti-inflammatory foods.
5* Reduce high-histamine foods and support detoxification pathways (see immune lecture).
6* Support gut health as needed (e.g., H pylori) — see GI lecture.
Low stomach acid is common — use bitters, HCl, digestive enzymes.
7* Ensure good intake of omega-3 fatty acids to reduce inflammation and maintain integrity of the skin barrier.
8* Include foods rich in vitamin C and proanthocyanidins (flavonoid compounds) that improve integrity of blood vessels e.g., grapes, blueberries and cranberries.
9* 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.
10* Stress is a major trigger — see stress lecture for recommendations.
11* Protect the face from UV light.
12* Care should be taken with cosmetic and personal care products.

Question 30

What is atopic dermatitis/eczema?

Answer 30

Atopic dermatitis (AD) / eczema = a disorder of altered skin barrier integrity and immune dysregulation that presents as a chronic relapsing inflammatory skin disease.

Question 31

Clinical presentation of atopic dermatitis?

Answer 31

• 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.

Question 32

what is the atopic triad?

Answer 32

Atopic triad present in 30%–50% of cases ― atopic dermatitis, allergic rhinitis, asthma

Question 33

what are the 2 types of atopic dermatitis?

Answer 33

AD is divided into: Exogenous / extrinsic (IgE-mediated — 70–80%) and endogenous / intrinsic (non IgE-mediated — 20–30%).

Question 34

what are the two pathways implicated in atopic dermatitis and how they work?

Answer 34

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

2/ Immune-response defect (inside-out hypothesis):
* 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 → ↑ susceptibility to allergens, secondary to structural epidermal defects.

Question 35

atopic dermatitis causes and risk factors x7

Answer 35

1* See immune health lecture allergy section —
e.g., Th1 / Th2 imbalance (heightened Th2), hygiene hypothesis, C-section birth, vaccinations, antibiotics.
2* Stress (see immune lecture) — promoting chronic inflammation.
3* Filaggrin gene mutations — strongest known genetic risk factor.
Filaggrin facilitates the aggregation of keratin filaments.
4* Nutritional deficiencies — e.g., vitamin D, zinc (see later).
5* 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).
6. Dysbiosis
7. Excess histamine - disrupts tight junction integrity.

Question 36

Atopic Dermatitis risk factor - dysbiosis

Answer 36

• 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.

Question 37

lab testing for atopic dermatitis

Answer 37

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

Question 38

allopathic treatment of atopic dermatitis

Answer 38

Allopathic treatment examples:
* Topical corticosteroids (highly suppressive and promotes skin atrophy); antihistamines; immunosuppressants (AD commonly recurs when treatment stops).

Question 39

natural approach to atopic dermatitis - address triggers and mediators - elimination of exacerbating factors x9

Answer 39

1* Elimination or oligoantigenic diet (eliminate all foods that could provoke an allergic response) — see GI Health lecture.
2* Key allergens: Children should especially avoid cows’ milk, eggs, peanuts, wheat, soy, nuts and fish.
3* Older children / adults may be react to birch pollen- associated foods for e.g., apple, carrot, celery, hazelnut.
4* Avoid inflammatory foods: Sugar, saturated fat, refined carbohydrates (white rice, white pasta, white bread, etc.), processed meat, red meat, MSG, artificial sweeteners.
5* Environmental allergens: Airborne (e.g., pollutants), plants, dyes, medications.
6* 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.
7* Heat, humidity, excessive bathing.
8* Address skin infections, e.g., S. aureus (due to deficiencies in endogenous bactericidal peptides) or viruses e.g., HSV.
9* Stress management (see stress lecture).

Question 40

natural approach to atopic dermatitis - dietary inclusions x5

Answer 40

1* Follow the CNM Naturopathic Diet, with a focus on the inclusion of anti-inflammatory foods.
2* Eczema is often associated energetically with excess heat in the blood — focus on cooling foods / beverages.
3* Increase daily sources of omega-3 fatty acids (e.g., ‘SMASH’ fish, flaxseeds, chia seeds, spirulina, etc.).
4* Increase quercetin-rich foods (see mechanism later), e.g., apples, kale, blueberries, spinach, red onions.
5* Although AD is not considered autoimmune, it does ↑ the risk of other AI diseases. An AIP may be beneficial (see immune lecture).

Question 41

natural approach to atopic dermatitis - heal the gut x3

Answer 41

• 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 (see GI health lecture).
• Immunomodulatory / anti-inflammatory — help correct Th1 / Th2 imbalance (see immune lecture). E.g., echinacea (dampens Th2 — 4 g), turmeric (500–2000 mg), boswellia (250‒500 mg).

Question 42

Nutrients for Atopic Dermatitis x8 - see prints for functions of each nutrient

Answer 42

1. Vitamin A (retinol) 5000 iu / day
2. Vitamin C 1–2 g / day
3. Zinc 15–30 mg / day
4. Vitamin E: Up to 600 iu / day.
5. Quercetin Up to 3 g / day
6. Vitamin D Optimise levels
7. EFAs: EPA 1 g+; GLA (evening primrose oil 320g)
8. Selenium 200 μg

Question 43

Herbs/Homeopathy for Atopic Dermatitis x3

Answer 43

1. Nettle (leaf) Dose: 500 mg
2. Key homeopathic remedies (or referral): 30C x2 daily
   - Sulphur
   - Psorinum
   - Rhus. tox.
3. Bathing in Dead Sea salts — magnesium is likely to be responsible for improved barrier function, cell differentiation and hydration.

Question 44

Topical applications for atopic dermatitis

Answer 44

• 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.

Question 45

What is psoriasis?

Answer 45

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

Question 46

Clinical presentation of psoriasis

Answer 46

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), 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.

Question 47

Pathogenesis of psoriasis and the two phases?

Answer 47

Autoimmune — associated with 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.

Question 48

Complications of psoriasis ?

Answer 48

1. Psoriatic arthritis (30%),
2. CVD
3. IBD
4. depression
5. ocular disorders (e.g., uveitis).

Question 49

Causes and risk factors of psoriasis x14

Answer 49

1* Genetic predisposition — key susceptibility genes include 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 — Koebner phenomenon. The mechanism is thought to be 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 as a trigger / exacerbating factor. TNF-α and IFN-γ may explain the pathophysiological link with COVID-19 vaccination.
4* Air pollution — particulate matter and cadmium can promote pathogenesis.
5* Medications — commonly lithium, beta-blockers, antimalarials, TNF-alpha inhibitors, corticosteroids and NSAIDs. Occur with direct and indirect mechanisms.
6* Infectious agents — e.g., Streptococcus pyogenes (strep. tonsilitis)triggering T-cell and TNF-α activation epidermal inflammation and hyperproliferation.
HIV and candida (fungal infections) are also linked.
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:
- Inflammation — ↑ adipose tissue
↑ adipokines, chemokines, cytokines and abnormal fatty acid metabolism.
- High serum FFAs sensitises dendritic cells to amplify Th1 / Th17 responses.
10* Gut dysbiosis — linked to ↓ Akkermansia muciniphila and Bacteroidetes phylum, and ↑ Firmicutes phylum.
11* High toxic load (e.g., alcohol) and impaired detoxification/ elimination pathways — contributing to ‘autotoxaemia’.
12* Poor protein digestion — producing polyamines which can induce excess cell proliferation through inhibition of cAMP.
13* NAFLD — twice as prevalent in psoriasis. Insulin resistance is likely a contributory factor.
14* Chronic high-level stress — ↓ cortisol and ↑ epinephrine and norepinephrine stimulate mast cells, affect skin barrier function and upregulate proinflammatory cytokines.

Question 50

Natural approach to Psoriasis x9

Answer 50

CNM Naturopathic Diet with a focus on:
1* Fibre (and adequate water) to facilitate bowel elimination; to support gut commensals and SCFA production.
2* Antioxidant-rich fruit and vegetables to reduce inflammation and support liver detoxification.
3* EPA / DHA — inhibit inflammatory mechanisms, e.g.,leukocyte chemotaxis, prostaglandin and leukotriene production from arachidonic acid and the production of inflammatory cytokines.
4* Detox protocol (detox lecture). Consider a juice cleanse, fasting etc.
5* Consider applying specific AI protocols (e.g., AIP).
6* Digestive support — e.g., bitters, digestive enzymes.
7* Probiotics and prebiotics to support commensals.
8* Weight loss as needed — ↓ inflammatory mediators.
9* Stress management (see stress lecture).

Question 51

Natural approach (Psoriasis): address triggers and mediators x4

Answer 51

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

Question 52

Topical applications for Psoriasis x3

Answer 52

Topical applications (also see eczema):
* ‒ 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).

Also soak in dead sea salt or Epsom Bath

Question 53

Nutrients for psoriasis x6

Answer 53

1. Vitamin A (retinol) 5000 iu / day
2. Vitamin D Optimise levels
3. Vitamin E 400–800 iu / day
4. Selenium 100‒200 ug / day
5. Omega-3 oil 6 g / day (720 mg DHA / 1080 mg EPA)
6. Zinc 15‒30 mg / day

Question 54

Herbs for psoriasis x3

Answer 54

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