5. GASTROINTESTINAL HEALTH Flashcards

This module covers: • Digestive insufficiencies. • The mucosal barrier. • Elimination diet. • The 5R protocol. • Dysbiosis. • Metabolic endotoxaemia. • GI disorders.

1
Q

Define the following:
* Hypochlorhydria
* Achlorhydria
* Hyperchlorhydria

A
  • Hypochlorhydria = low stomach acid production characterised by a fasting gastric pH above 3.0 (1.5–3.0 is considered normal).
  • Achlorhydria = absence of stomach acid→gastric pH >7.0
  • Hyperchlorhydria = a gastric pH <1.5, normally without consequences unless other conditions present; e.g., GORD.
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2
Q

Signs & symptoms of hypochlorhydria

A

Gas and bloating < 30 minutes after eating
Heartburn
Sensation of fullness
Foul smelling stools
Diarrhoea
Nausea after taking supplements
Food allergies
Brittle nails

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3
Q

Nutrient deficiencies that could result from hypochlorhydria

A

Iron
Zinc
Folate
B12

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4
Q

Implications of hypochlorhydria

A
  • Reduced calcium absorption affecting bone density
  • Reduced iron absorption => anaemia
  • Protein putrification creating polyamides which are implicated in colorectal cancer
  • Reduced protection from bacterial infection (H.pylori, SIBO)
  • Poor pancreatic juice and bile flow
  • Less intrinsic factor, reducing B12 absorption
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5
Q

What cancer is associated with hypochlorhydia?

A

Colorectal cancer

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6
Q

Natural approach to addressing hypochlorhydria

A
  • Good food hygiene
  • ACV (1 or 2tsp) diluted in a little water before meals
  • Zinc and B6-rich foods
  • Bitter foods - rocket, chickory, dandelion leaf, watercress
  • Herbs that are cold and stimulate the vagus nerve - gentian, dandelion, goldenseal, barberry bark (berberine)
  • ‘Warming bitters’ for excess cold/aggrevated agni or spleen Qi - fennel seed, cardamon, citrus peel, ginger
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7
Q

What is exocrine pancreatic insufficiency (EPI)?

A

A deficiency of exocrine pancreatic enzymes needed to maintain normal digestion resulting in nutrient (especially fat) malabsorption.

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8
Q

Common symptoms of exocrine pancreatic insufficiency?

A
  • Bloating/belching/flatulence 1-2 hours after eating
  • Steatorrhoea
  • Drowsiness after meals
  • Food intolerances
  • Low zinc, B12 and folate absorption
  • symptoms of IBS, candidiasis or SIBO
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9
Q

What is steatorrhea?

A

Excessive fat in faeces. Greasy or floating stools.

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10
Q

Name the causes of pancreatic insufficiency

A
  • Chronic stress => Decreased vagus nerve activity
  • Hypochlorhydria => Reduced CCK stimulation
  • Chronic diseases - cyctic fibrosis, pancreatitis, obstructive pancreatic tumours, GI surgery, diabetes mellitus
  • Damaged small intestinal wall (coeliac, IBD) - ↓ CCK production and pancreatic stimulation
  • Xenobiotics can inactivate pancreatic enzymes
  • Microbial interaction - SIBO can deconjugate pancreatic enzymes; dysbiosis
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11
Q

Naturopathic approach to pancreatic insufficiency

A
  • Food hygiene
  • Correct stomach acid levels
  • Stimulate the vagus nerve to activate the parasympthetic nervous system
  • Pancreatic enzyme replacement
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12
Q

How can the Vagus nerve be activated?

A
  • Diaphragmatic breathing before meals
  • Gargle, hum or sing
  • Laughter and social enrichment
  • Using bitters – gentian, artichoke and dandelion
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13
Q

What is Pancreatic Enzyme Replacement Therapy (PERT)?

A
  • Animal derived enzymes (pork pancreatin) used in conventional medicine - amylase, lipase and protease
  • Plant based and microbe-derived enzymes - better acid stability, broader range of enzymes, more variants, wider pH range
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14
Q

What is bile insufficiency?

A

A condition where bile synthesis and/or bile flow is compromised.
This affects the ability to digest, absorb and utilise fatty acids from the diet.

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15
Q

What are the signs & symptoms of bile insufficiency?

A
  • Steatorrhea
  • Intolerance to fatty foods/nausea when eaten
  • Bloating, excess flatulence and cramping
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16
Q

What are the stool test indicators of bile insufficiency?

A
  • Low/absent bile acids
  • High faecal fats – indicate fat malabsorption
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17
Q

Bile insufficiency causes

A
  • Low dietary fat intake
  • Impaired liver function and obstructed bile ducts
  • Obesity (↓ postprandial bile acid response)
  • Oestrogen dominance
  • Other GI conditions - Cholecystectomy, coeliac disease, crohn’s disease, chronic pancreatitis, SIBO
  • Low HCl (↓ CCK and bile release)
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18
Q

What are the implications of long-term bile insufficiency?

A
  • Deficiency of fat soluble nutrients (A, D, E, K, EFAs, beta-carotene)
  • Hormone imbalances (poor oestrogen clearance)
  • Hypercholesterolemia
  • Compromised liver detox
  • SIBO and dysbiosis (bile has antimicrobial and detoxifying effects, stimulates peristalsis)
  • Gallstones or inflammation of the liver or pancreas
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19
Q

Natural approach to bile insufficiency?

A
  • Adequate hydration
  • Avoid processed foods, trans fats and refined sugar
  • Chew slowly and thoroughly
  • Diaphragmatic breathing (massages liver, ↑bile production)
  • ↑ taurine (seaweed, seafood, chicken thighs) and choline foods (kidney beans, broccoli, eggs) or supplement
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20
Q

What is the mucosal barrier?

A

Mucus covering the entire GIT provides a thick barrier between the immune-stimulating contents of the outer world and the multitude of immune cells in the gut wall (1st line of defence)

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21
Q

What does mucus contain?

A
  • Water 96-98%
  • Glycoproteins called mucins
  • IgA and anti-microbial peptides
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22
Q

How is the mucosal barrier implicated in ulcerative colitis?

A

In UC the inner mucosal lining becomes permeable, resulting in a large amount of bacteria in close contact with host tissue => inflammation

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23
Q

What can result from a disturbed mucosal barrier?

A

A bacterial translocation and the leakage of LPS-> metabolic endotoxemia

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24
Q

Outline how to support the mucosal barrier.

A
  • Optimise dietary fibre
  • A diet rich in polyphenols - feeds commensal bacteria (Akkermansia spp.) and protects the mucin lining; reduces inflammation (green tea, blueberries, pomegranates)
  • Mucopolysaccharides - slippery elm, marshmallow root, liquorice, flaxseeds
  • Fucoidans (polysaccharides) - seaweeds, algaes.
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25
Q

Why is adressing intestinal tight junction permeability important?

A

Intestinal tight junction disassembly contributes to ↑ LPS load and excessive immune reactions

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26
Q

How could intestinal tight junction integrity be supported?

A
  • Glutamine (cabbage juice, spirulina, asparagus)
  • Zinc carnosine
  • Vitamin A
  • N-Acetyl glucosamine
  • Bone broth (rich in glycine)
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27
Q

Which diagnostic tests could confirm intestinal permeability?

A
  • test for zonulin in stool
  • Cyrex Labs Array 2 (serum antibodies)
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28
Q

What is secretory IgA?

A

Immunoglobulins residing in the mucosal lining and protects the intestinal epithelium from toxins and pathogenic microbes through a process called immune exclusion (promoting the clearance of antigens by blocking their access to epithelial receptors)

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29
Q

What can cause low secretory IgA ?

A
  • Ongoing emotional/physical stress
  • NSAIDs
  • Antibiotics
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30
Q

How can secretory IgA secretion be supported?

A
  • Address stress
  • Saccharomyces boulardii
  • Mushrooms (esp. medicinal)
  • Vitamin A - transports SIgA over the mucosal lining
  • Vitamin D3 - upregulates SIgA expression
  • Polyphenols
  • Chlorella
  • Probiotics and prebiotics
  • Echinacea spp
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31
Q

What is an elimination diet?

A

It is a diet where suspected foods are removed for a period of time and changes in symptoms monitored. Then the food is reintroduced and symptoms are monitored again to confirm sensitivity.
It is a cost effective way of identifying food allergies or intolerances.

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32
Q

What are the most probable foods causing an immune reaction?

A

gluten
dairy
corn and soy
eggs
nuts
beef
pork
yeast
citrus
nightshades
chocolate
coffee

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33
Q

How many days does stage 1 last in the elimination diet?

A

1-2. This is the detox stage.

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34
Q

How many days does stage 2 last in the elimination diet?

A

Days 3-14 (± 12 days).
This is the elimination stage.
If symptoms don’t improve by 3rd week, consider other possible triggers.

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35
Q

How many days does stage 3 last in the elimination diet?

A

Day 15 onwards.
This is the reintroduction stage. One food is reintroduced for 1-3 days and any symptoms monitored.

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36
Q

What are the stages of the 5R Protocol?

A
  1. Remove
  2. Replace
  3. Reinoculate
  4. Repair
  5. Rebalance
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37
Q

Describe Stage 1 of the 5R Protocol

A

What needs to be removed to support healthy GI function?

  • Dietary irritants
  • allergens/intolerances
  • toxins
  • unnecessary drugs
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38
Q

Which antimicrobial herbs are recommended in stage 1 of the 5R protocol?

A
  • berberine
  • garlic
  • oregano
  • uva ursi
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39
Q

Which anti-bacterials could be recommended in stage 1 of the 5R protocol?

A

oregano oil
berberine
garlic
neem

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40
Q

Which anti-parasitics are recommended in stage 1 of the 5R protocol?

A

black walnut hulls
wormwood
oregano
neem
clove buds
pumpkin seeds

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41
Q

What anti-fungals are recommended in stage 1 of the 5R protocol?

A
  • caprylic acid
  • grapefruit seed extract
  • garlic
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42
Q

What anti-virals are recommended in stage 1 of the 5R protocol

A

olive leaf extract
nano silver
elderberry

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43
Q

In stage 2 of the 5R protocol, what needs to be replaced in support of healthy gut function?

A

Replenish digestive factors that may be lacking:

  • Stomach acid secretions e.g., digestive bitters, HCI
  • Pancreatic support e.g., bitters, pancreatic enzymes (PERT)
  • Bile support e.g., choleretics / cholagogues
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44
Q

In stage 3 of the 5R protocol, how can beneficial bacteria be encouraged to flourish?

A
  • Probiotic foods (cultrued vegetables, fermented foods and drinks)
  • Probiotic supplements
  • Prebiotic foods (foods rich in fructans, FOS and inulin)
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45
Q

What can be used to encourage the repair of the GI mucosa?

A

Epithelial & tight junction support:

  • L-glutamine
  • N-acetyl glucosamine
  • quercetin
  • zinc
  • EFAs
  • B vitamins
  • Vitamin A
  • collagen
  • bone broth
  • aloe vera

Mucous barrrier support:

  • mucilage rich demulcent herbs (slippery elm, liquorice, marshmallow root, meadowsweet)
  • fibre
  • polyphenols

Increase SIgA and reduce inflammation:

  • S. Boulardii
  • Curcumin
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46
Q

What lifestyle changes are required to support gut healing?

A
  • adressing stress
  • good sleep hygiene
  • regular exercise
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47
Q

What is dysbiosis?

A

Dysbiosis is an imbalance in the colonies of the bowel flora, leading to a potential disruption in both local and systemic health.

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48
Q

What causes dysbiosis?

A
  • poor diet (highly processed, high refined carbs, ↓ fibre, ↓ polyphenols)
  • intestinal/oral infections
  • medications (antibiotics, antacids, OCP)
  • chronic stress (= ↓ digestive secretions)
  • low digestive secretions (HCI, bile)
  • C-section, non-breastfed
  • GI suregry and abdominal scar tissue
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49
Q

What is metabolic syndrome?

A

A combination of hypertension, insulin resistance and obesity.

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50
Q

What diseases can dysbiosis lead to?

A
  • Atopic diseases
  • Metabolic syndrome
    -Associated with less Bifidobacteria and Akkermansia spp.
    A diet rich in fibre and SCFA-producing bacteria (probiotics) has shown improvements in metabolic syndrome.
  • Colorectal Cancer
    -Fibrous diets ↑ abundance of SCFA-producers and beneficial bacteria.
  • Neurodegenerative diseases
    -Alzheimer’s, Parkinson’s and MND
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51
Q

What is metabolic endotoxaemia?

A

A subclinical rise in bacterial LPS in the blood, resulting in chronic low-grade inflammation.

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52
Q

What increases serum LPS?

A

Dysbiosis, mucosal degradation and permeability of the GI tight junctions (often interlinked).

53
Q

Which chronic diseases are associated with endotoxaemia?

A
  • CVD
  • Diabetes Mellitus
  • Autoimmune diseases
  • Degenerative disorders
54
Q

Outline the natural approach to metabolic endotoxaemia.

A
  • Avoid alcohol (↑ LPS transport across the intestinal epithelium), other dietary irritants/toxins/NSAIDs
  • Avoid western or ketogenic diet
  • Increase dietary fibre (to bind and clear LPS via the bowel and to feed butyrate producing species - Roseburia, Akkermansia spp.)
  • Focus on the rainbow of colour to feed keystone bacterial species, ↓ inflammation and discourage growth of gram-negative bacteria
  • Reinoculate and support GI barrier (stage 3 and 4 of 5R)
  • Support liver function, bile production/flow to aid LPS clearance (milk thistle, burdock root, artichoke, dandelion, spirulina, chlorella)
  • A variety of dietary antioxidants (E, C, carotenoids, Se)
  • NAC, cruciferous veg and resveratrol to ↑ glutathione
  • Nrf2 inducers (to scavenge ROS) - broccoli sprouts, green tea
  • Breathing techniques and cold exposure reduce systemic LPS load.
55
Q

What is SIBO?

A

An overgrowth of non-pathogenic bacteria in the small intestine. It is the most common cause of IBS (60-70%)

56
Q

What are the symptoms of SIBO?

A
  • Bloating
  • Abdominal pain or discomfort
  • Constipation/diarrhoea
  • Flatulence
  • All symptoms must be chronic and happen after every meal
57
Q

In SIBO what gas causes diarrhoea?

A

Hydrogen

58
Q

In SIBO what gas causes constipation?

A

Methane

59
Q

What are the clinical indicators of SIBO?

A
  • Worsening GI symptoms from probiotics (try for 3-7 days to be sure)
  • Fibre worsening GI symptoms
  • Chronic GI symptoms following long term broad spectrum antibiotics/PPIs/opiates
  • Chronic low ferritin/iron with no other causes
  • Developing IBS following GI infection
  • When a coeliac patient reports insufficient improvement from strict GF diet.
60
Q

SIBO aetiology

A
  • Hypochlorhydria and bile insufficiency (HCI + bile are anti-microbial)
  • Low SIgA
  • Prolonged stress (↓ SIgA and HCI)
  • Scar tissue adhesions from surgery
  • Hypothyroidism (slows motility)
  • Poor oral health
  • Ileocecal valve dysfunction
  • Opioid pain medications (slows motility) and antibiotics
  • Acute gastroenteritis
61
Q

Describe the process of how food poisoning can contribute to SIBO

A

Pathogenic bacteria release a toxin called cytolethal distending toxin (CDT).
A small portion of CDT resembles nerve cells in the small intestine called interstitial cells of Cahal (ICC).
The ICC are responsible for the MMC - a peristaltic movement that sweeps bacteria into the colon.
Through the autoimmune process of molecular mimicry, in response to CDT-B, the ICC can incur enough damage to negatively affect the MMC, resulting in SIBO.

62
Q

What is the link between SIBO and food sensitivities?

A

SIBO can damage the villi of the small intestine, reducing enzymes like lactase (=lactose intolerance) and diamine oxidase (DAO) that are produced in these finger-like projections.
DAO metabolises histamine in the GIT, therefore less DAO can result in reactions to high histamine foods (hives, migraines).
A client presenting with multiple intolerances, including to histamine, should be automatically screened for SIBO.

63
Q

What is the dietary approach to SIBO?

A

Reduce food sources for the bacteria

  • Low FODMAP for up to 6 weeks
  • Specific Carbohydrate Diet (SCD) preferable to FODMAP if there is intestinal inflammation
  • May combine dietary models in severe cases.
64
Q

Which natural anti-microbials are useful in a SIBO protocol?

A

Use 1-3 of the following anti-microbials in the initial phase of a SIBO plan. Use for 4-8 weeks:

* Berberine – inhibits protein synthesis of bacteria, blocks TLR4 pathway
* Oregano oil - affects bacterial cell membrane permeability
* Allicin – for methane producing bacteria
* Neem
* Uva ursi and cinnamon
65
Q

In what way can digestive and MMC support be used in a client with SIBO?

A

Digestive support

  • Digestive bitters (dandelion, rocket, watercress)
  • Betaine HCl, digestive enzymes, ACV

MMC support

  • 12 hour overnight fast
  • Meal spacing (4 hours minimum), no snacks
  • Pro-kinetic agents before bed (ginger, artichoke)
  • Mindful eating, diaphragmatic breathing exercises
66
Q

What are the signs and symptoms of candidiasis?

A
  • Frequent UTIs
  • Fatigue
  • Digestive symptoms
  • Sugar cravings
  • Joint pain
  • Depression
  • Anxiety
  • Brain fog
  • Food sensitivities
  • Skin and nail fungal infections
67
Q

Candidiasis pathophysiology

A
  • Candida is usually kept under control by native bacteria and the immune defences but Disruption of the host bacterial environment or immune dysfunction can allow opportunistic candida to proliferate (terrain theory).
  • C. albicans (produces many toxins and can suppress immune function) then penetrate epithelial cells and switch morphology from commensal to pathogen.
  • Infections are usually limited to the mouth or genitals and skin.
68
Q

Key risks factors for candidiasis

A
  • Antibiotic use
  • Low immunity (↓ SIgA)
  • Chronic stress (↑ cortisol)
  • ↓ digestive secretions
  • High sugar intake
  • Dysbiosis
  • Impaired liver function
  • Exposure to toxins
69
Q

How to test for candidiasis

A
  • Stool test
  • Organic acids test (↑ arabinose)
  • Saliva test (candida antibodies)
  • Blood test (candida antigens)
70
Q

At home candida test

A

Upon waking spit into a glass of water. Healthy saliva floats but if you see strings coming down or it sinks, you may have candida overgrowth.

71
Q

Naturopathic approach to candidiasis

A

Create an environment where candida cannot overgrow while optimising the body’s ability to heal naturally
1. Optimise elimination and detoxification
2. Adopt an anti-candida diet
3. Use natural antifungals and address biofilms
4. Address predisposing risk factors
5. Support the microbiome
6. Restore nutrient deficiencies

72
Q

How to promote detoxification and elimination for candidiasis

A
  • Resolve any constipation
  • Stay hydrated
  • ↑ intake of soluble fibre and eat foods rich in mucilage
    • Flaxseeds, chia seeds, psyllium husk
  • If necessary, milk thistle to enhance liver function (protects against phase I metabolites - increases glutathione and SOD)
  • Consider a binding agent to mop up potential candida die off
73
Q

What binding agents can be used to mop up candida die off?

A
  • Lactoferrin
  • Lactoglobulin
  • Chlorella
74
Q

Describe the anti-candidia diet

A
  • Eliminate refined sugars and minimise carbohydrates
  • Go gluten/dairy free
  • Eat lots of non starchy vegetables and low sugar fruit
  • Eliminate yeast or mould-containing foods (alcohol, cheese, dried fruit, vinegar, peanuts)
  • Opt for organic where possible
  • Reduce oxalates (impair enzymes which help the body to eliminate candida).
75
Q

How long should antifungal and biofilm disruptors be taken for?

A
  • Take 1 biofilm and 2 antifungal agents for 3 months
  • Start slow and build up to prevent die off symptoms
76
Q

Natural antifungal agents

A

Berberine
caprylic acid
Pau d’Arco
oregano
thyme
rosemary
allicin

77
Q

Biofilm disrupters

A
  • Proteolytic enzymes
    • Serrapeptatse
  • Plant based
    • Allicin, curcumin, berberine
78
Q

What are the predisposing factors for candidiasis?

A
  • stress
  • poor sleep
  • alcohol, sugar smoking
  • some medications
79
Q

What are gallstones?

A

Crystalline calculi formed within the gallbladder from a build up of bile components.

80
Q

What percentage of gallstones contain cholesterol?

A

80%

81
Q

What causes gallstones to form (cholelithiasis)?

A
  • Gallstones form when bile becomes supersaturated with cholesterol, either because there is too much cholesterol or because there are not enough bile salts and phospholipids to keep it dissolved.
  • Biles stasis or delayed gallbladder emptying due to ↓ gallbladder motility
82
Q

Key risk factors of gallstones

A
  • T2D
  • OCP
  • HRT
  • Typical western diet
  • Sedentary
  • Obesity
  • High alcohol
83
Q

Natural approach to gallstones

A
  • ↑fibre
  • ↓ refined sugar, trans fats, saturated fats and alcohol
  • Consume choleretic and cholagogue-rich foods and herbs to support bile flow
    • ACV
    • Bitter greens
    • Globe artichoke
  • Weight loss
  • ↑ PUFAs as found in oily fish
  • Peppermint (terpenes help to dissolve stones)
84
Q

Supplements for gallstones

A
  • Vitamin C (500-2000mg/day)
  • Lecithin (high phospholipid content; keeps cholesterol in solution)
  • Purified bile salts (ox bile)
85
Q

Describe the gall bladder flush

A
  1. Perform the liver flush for 10 days
  2. On the evening of the 10th day, mix ½ pint of lemon juice with ½ pint olive oil. The cycloartenol content of olive oil is thought to aid bile flow.
  3. Lying on your sofa on the right side, drink this mixture in small sips until it is finished
  4. Prepare a castor oil pack and place over liver region
  5. Go to bed with a hot pack over the castor oil pack
  6. In the morning, sift your first bowel motion and look for stones
    Do not perform with active cholecystitis

Liver Flush: Make a smoothie with the following ingredients, drinking it first thing every morning for 10 days (do not eat for two hours after drinking):
- Juice of a whole lemon or lime
- 1 garlic clove
- 1⁄2 pint / 1⁄4 litre fresh pressed apple juice (or carrot, celery or beetroot juice)
- Tbsp extra virgin cold pressed olive oil
- Small piece of grated fresh ginger.
- Optional: Pinch of cayenne powder.

86
Q

What are peptic ulcers?

A

Peptic ulcers = ulcers of the stomach (gastric) or duodenum characterised by a breakdown of the mucosal barrier and erosion of the regions wall by HCl.

87
Q

What are the symptoms of peptic ulcers?

A
  • epigastric pain (may radiate to the back)
  • gnawing / pain between meals
  • nausea, vomiting
  • ↓ appetite
  • dyspepsia
88
Q

What are the complications of peptic ulcers? When to seek medical attention?

A
  • GIT bleed (persistent small loss of blood or large haemorrhage)
  • perforation (→ peritonitis).

Seek urgent medical attention if:
- sudden sharp worsening abdominal pain
- haematemesis (vomiting blood)
- melaena.

89
Q

Peptic ulcer risk factors

A
  • Stress (sympathetic dominance) - can lead to vasoconstriction and inadequate blood supply which interferes with mucus production and reduces the secretion of protective prostaglandins.
  • Low antioxidant status and low gastric output - may predispose H. pylori colonisation.
  • NSAID use (↓ gastric prostaglandin synthesis, ↓ gastric mucosal blood flow and mucus production; interferes with the repair of superficial injury).
  • Smoking, caffeine, alcohol (damage the mucosa).
90
Q

What conditions are H. pylori infection in the stomach associated with?

A

peptic ulceration
chronic gastritis
gastric cancer

91
Q

What are the effects of H. pylori in the stomach?

A

Its corkscrew shape enables it to burrow through the protective mucus layer into the stomach lining, causing inflammation.

H. pylori secretes cytotoxins and enzymes; e.g., protease, phospholipase and urease (releases ammonia) and damages the mucosal barrier.

Numerous strains vary in their ability to trigger inflammation (virulence factors CagA and VacA carry greatest risk).

92
Q

Natural approach to peptic ulcers. Include dietary, lifestyle and herbal support.

A
  • Avoid potential GI mucosal irritants: alcohol, smoking, fizzy drinks, spicy foods, caffeine, NSAID use.
  • Increase fibre - especially for duodenal ulcers as fibre slows gastric emptying.
  • Address stress. Consider calming nervine teas (e.g., chamomile, passionflower).
  • Support the mucosal / mucin barrier:
    ‒ Demulcent herbal powder - slippery elm, marshmallow, liquorice.
    ‒ ↑ dietary polyphenols and seaweeds / algaes (fucoidan content).
  • Raw cabbage juice - a traditional remedy for healing stomach ulcers. Contains vitamin C and ‘substance U’ which stimulates mucin production (250 ml 4 x / day showed ulcers healed in 7‒10 days).
  • Turmeric - anti-inflammatory - ↓ inflammatory cytokines and pro-inflammatory PGs (600 mg 5 x / day showed ulcers healed after 12 weeks).
  • Aloe vera juice - 20–30 ml 3 x daily. Inhibits COX (antiinflammatory), speeds up wound healing (↑ collagen synthesis).
  • Identify and address H. pylori.
93
Q

Strategies to eradicating H. pylori

A
  • Saccharomyces boulardii (↑ SIgA and mucosal barrier; inhibits colonisation and adhesion of H. pylori; inhibits IL‐8 and TNF‐α).
  • Mastic gum - dried sap from the mastic tree with ulcer-healing properties. It is anti-bacterial; thought to relate to its triterpenic acid content. 2 x 500 mg capsules before bed (30 days), then 1 x 500 mg capsule before bed (60 days).
  • Liquorice - contains flavonoids that inhibit H. pylori protein synthesis; it is anti-adhesive.
  • Cinnamon inhibits urease
  • Berberine containing herbs e.g., barberry bark
  • Curcumin from turmeric inhibit H. pylori growth
  • Also consider probiotics to outcompete H. Pylori.
94
Q

What is GORD, its symptoms and allopathic treatment?

A

Gastro-oesophageal reflux disease = the reflux of gastric juice (HCl, bile, pepsin) back into the oesophagus.

Associated with transient lower oesophageal sphincter (LOS) relaxation episodes and a decreased lower oesophageal sphincter pressure.

The most common symptom is heartburn (retrosternal pain).

Often treated conventionally with chronic PPI use.

95
Q

GORD risk factors

A
  • ↑ intra-abdominal pressure: Obesity, pregnancy.
  • Hiatus hernia (stomach protrudes through the diaphragm into the thoracic cavity).
  • Eating large amounts of fatty foods
    (acid remains in stomach longer).
  • Smoking, alcohol, coffee; peppermint, tomatoes and chocolate relax the LOS.
  • Certain medications: Calcium channel
    blockers, nitrates, NSAIDs, diazepam.
  • Stress, anxiety and family history.
96
Q

Dietary advice for GORD

A
  • Test for H.pylori.
  • Test for low stomach acid:
    ‒ Poor gastric digestion due to low HCl leads to fermentation of undigested food creating gas in the stomach and increasing pressure on the LOS.
    ‒ Correct low stomach acid using digestive bitters, ACV, bitters, betaine HCl. Consider digestive enzymes.
  • Avoid trigger foods / drinks and any foods associated with a food sensitivity or allergy, e.g., wheat.
  • A Mediterranean diet has been shown to be protective.
  • Use demulcent herbs to soothe and coat the oesophageal mucosa. Slippery elm (2–3 tsps. daily; mix into water (1 tsp:250 ml water). Can also use: marshmallow root, liquorice, meadowsweet, prickly pear.
97
Q

Lifestyle advice for GORD

A
  • Slow down, chew thoroughly, eat mindfully, don’t overeat (or too late - within 3 hours of bed), do not drink with meals.
  • Avoid lying down post meals; when sleeping elevate the head of the bed (by up to 20 cm).
  • Address stress and anxiety. Lose weight if applicable.
  • Visceral manipulation of hiatus hernia. Also ↑ fibre to ↓ straining.
98
Q

Name THREE most commonly recognised gluten-related disorders

A

– Coeliac disease (auto-immune).
– Wheat allergy (allergic).
– Non-coeliac gluten sensitivity (innate immunity).

99
Q

Why can consuming gluten be problematic?

A

Gluten is the main structural protein complex of wheat, rye and barley that is difficult for humans to digest and can lead to many symptoms within, and outside, the GIT.

The immune-trigger protein fractions of gluten include gliadins and glutenins.

100
Q

What is wheat allergy and its possible symptoms?

A

An IgE-mediated allergic response that can develop within minutes to hours of exposure to wheat (digestion or inhalation).
More common in children and many outgrow condition by aged 16.

Symptoms include irritation or swelling of the mouth and throat, hives, itchy rash, nasal congestion, headache, nausea, vomiting, GORD, difficulty breathing, diarrhoea and anaphylaxis.

101
Q

What is coeliac disease and its complications?

A

Coeliac disease (CD) = an autoimmune condition whereby the immune system can attack the mucosal lining of the small intestine in response to gluten, resulting in villous atrophy and malabsorption.

Complications: Malabsorption (e.g., B12, B9, iron, calcium), osteoporosis, anaemia (iron / megaloblastic).

102
Q

Name FIVE symptoms of coeliac disease

A
  • abdominal pain
  • nausea
  • vomiting
  • diarrhoea
  • steatorrhoea
  • fatigue, anxiety
  • anaemia
  • weight loss
  • failure to thrive
  • osteoporosis
  • malnutrition
  • dermatitis herpetiformis
  • ataxia
103
Q

Coeliac disease - pathophysiology

A
  • An inappropriate adaptive immune response to gluten-derived peptides (i.e., gliadin).
  • Gliadin is modified (cross-linked) by tissue transglutaminase (tTG) to allow gliadin to be presented to the immune system.
  • ‘Antigen presenting cells’ target gliadin and take up tTG-gliadin complexes producing autoantibodies and inflammation which damage the villi.
  • Gluten upregulates zonulin - a peptide known to reversibly regulate intestinal permeability by disassembling intercellular tight junctions.
104
Q

How is coeliac disease diagnosed?

A
  • Blood test for: IgA anti-tissue transglutaminase (tTG) antibodies (first choice). IgA anti-endomysial antibodies (EMAs).
  • Blood or saliva test for human leukocyte antigen (HLA) gene: HLA-DQ2 or HLA-DQ8.
  • The gold standard for a CD diagnosis is a duodenal biopsy of the small intestine to detect villous atrophy.

All tests (except HLA) requires a gluten-containing diet for > 6 weeks.

105
Q

Coeliac disease - natural support

A
  • Coeliacs must follow a completely gluten-free diet for life.
  • For optimum recovery, a gut-healing diet such as the specific carbohydrate diet (SCD) can also be used.
  • Address nutritional deficiencies.
  • Support the intestinal barrier (‘repair’).
106
Q

What is non-coeliac gluten sensitivity and its key symptoms?

A

Non-coeliac gluten sensitivity (NCGS) = the development of GI and extra-intestinal symptoms upon gluten ingestion in people not affected by coeliac disease or wheat allergy.

Intestinal:
Bloating
Abdominal pain
Diarrhoea
Nausea
GORD
Constipation

Extra-intestinal:
Tiredness
Headache
Anxiety
Brain fog
Joint pain
Depression

107
Q

Possible pathophysiology of non-coeliac gluten sensitivity.

A

the role of innate immunity is suspected (i.e., ⍺-gliadin causing the release of zonulin from intestinal mucosa, inducing tight-junction disassembly and an increase in gut permeability).

108
Q

How is non-coeliac gluten sensitivity diagnosed?

A

Diagnosis is by way of exclusion, i.e., the resolution of symptoms when gluten is withdrawn and the relapse of symptoms with gluten exposure.

109
Q

Name some foods that contain gluten

A

Bread
Breadcrumbs
Pasta
Cereal
Cake
Biscuits
Flour
Sausages
Soy sauce

110
Q

Define IBS

A

An umbrella diagnosis used to classify an individual with a constellation of chronic symptoms. It is not a ‘disease’.

It is the most common GI diagnosis globally — a prevalence of 11%.

111
Q

IBS symptoms

A

Key symptoms:
• Abdominal pain and cramping relieved by passing a stool.
• Diarrhoea, constipation or mixed.
• Bloating and flatulence.
• Incomplete emptying of bowels.

112
Q

What IBS subtypes are there?

A

IBS-C: Constipation
IBS-D: Diarrhoea
IBS-M: Mixed
IBS-U: Unclassified

113
Q

Natural support for constipation

A

1)↑ dietary fibre and stay hydrated.
2) Magnesium (e.g., magnesium citrate — increase dosage from 250 mg gradually until tolerance).
3) Vitamin B5 and ginger (↑ peristalsis).
4) Psyllium husk or ground flaxseed
(15‒30 g / day). 5-HTP (for some).
5) Natural laxatives e.g., prunes, figs. Pour prune juice over freshly ground flaxseeds (leave it in the fridge).

114
Q

Natural support for diarrhoea

A

• ↑ soluble fibre to help bulk stool e.g. apple pectin.
• Enteric-coated peppermint oil.
• Digestive enzymes.
• S. boulardii (↑ sIgA).
• Electrolyte replacement, juices and broths to account for fluid / electrolyte losses.
• Marshmallow root, slippery elm, meadowsweet (powder).

115
Q

Define IBD

A

a group of autoimmune conditions of the colon and small intestine. Crohn’s disease (CD) and ulcerative colitis (UC) are the principal types of IBD.

116
Q

IBD symptoms

A

Key symptoms (peaks 15‒35 years):
– Abdominal pain and diarrhoea.
– Urgency to pass stools.
– Rectal bleeding (more so in UC).
– Weight loss.
– Fatigue (blood loss and malabsorption).

117
Q

IBD complications

A

‒ colorectal cancer
- osteoporosis
- anaemia (e.g. iron, folate, B12).

118
Q

Crohns vs UC region affected

A

Crohns: Any part of the GIT but mostly the terminal ileum

UC: Colon and rectum

119
Q

Crohns vs UC distribution & layers affected

A

Crohns: skip lesions, all layers (transmural)
UC: proximally continuous, mucosa only (‘ulcers’)

120
Q

Crohns vs UC key symptoms

A

Crohns: crampy abdominal pain (right). Loose semi-solid stools
UC: Abdominal pain (left side), bloody diarrhoea

121
Q

Crohns vs UC key symptoms

A

Crohns: crampy abdominal pain (right). Loose semi-solid stools
UC: Abdominal pain (left side), bloody diarrhoea

122
Q

Crohns vs UC complications

A

Crohns: Fistulas, abscess, obstruction, malabsorption
- B12 deficiency.

UC: Haemorrhage ➡️ anaemia

123
Q

IBD aetiology and pathophysiology

A
  • IBD is characterised by the interaction between a genetically-susceptible individual and environmental factors, which have an impact on gut microbiota composition, triggering overly aggressive T-cell responses.
  • Genetics - there are at least 163 genes involved in IBD. Many are shared between UC and CD but some are unique to each.
  • Damage to the mucosal lining is very much associated with IBD.
124
Q

Bacterial patterns commonly seen in IBD:

A
  • Very low / missing Akkermansia spp.,
    ↑ R. gnavus and R. torques → mucus degradation.
  • Raised gram-negative bacteria (e.g., Fusobacterium nucleatum) create a high LPS load, which in itself ↑ immune response.
  • Bacteroides fragilis (enterotoxigenic) has also been associated as a trigger for IBD (its toxins destroy intestinal tight junctions).
  • A lack of commensal bacteria diversity (especially the SCFA- producers) - necessary in times of mucosal tissue repair. Lower numbers of F. prausnitzii, a bacterium that generates anti-inflammatory metabolic by-products, e.g., SCFAs incl. butyrate
125
Q

IBD triggers:

A

Certain environmental factors alter mucosal barrier integrity, the immune response, or GI ecology:
• Medication use: Antibiotics, NSAIDs, oral contraception.
• Smoking (particularly CD).
• Stress.
• Infections (e.g., viral).
• Poor diet (e.g., ↓ fibre = ↓ commensal substrates
and ↓ SCFAs; ↓ omega-3’s, ↑ arachidonic acid,
↑ refined sugars). Also, food additives such as carrageenan.

126
Q

Dietary strategies for IBD:

A
  • Remove inflammatory foods / beverages (e.g., dairy, gluten, refined sugars, coffee, alcohol, damaged oils).
  • Consider a low reactive dietary model such as SCD (especially for CD) or low FODMAP.
  • Include well-cooked foods (slow-cooked at a low temperature) as well as soups, stews and broths that are easy to digest and nourishing.
  • Consider an elimination diet to identify problematic foods.
  • Optimise omega-3 to 6 ratio (e.g., skinless oily fish) — can also be addressed via supplementation.
  • Fresh green juices (chlorophyll rich, anti-inflammatory).
127
Q

Other natural approaches for IBD:

A
  • Vitamin D - stabilises tight junctions, regulates mucosal inflammation and supports commensal bacterial colonisation. Supports immune function (↓ inflammatory cytokines, e.g., TNF-α).
  • Fish oils (4.5 g / day) - DHA and EPA have profound anti- inflammatory effects, inhibiting NFκB, TNF-α and IL-6.
  • Supporting the mucosal / epithelial barrier:
    – Demulcent herbs (marshmallow root, slippery elm).
    Green tea - catechins and epicatechins support
    the mucosal barrier; inhibits COX-1 and 5-LOX.
    Vitamin A, N-acetyl glucosamine, zinc carnosine, L-glutamine
128
Q

Other natural approaches for IBD

A
  • Ginger (e.g., fresh or powdered in food; grated ginger steeped in hot water) - inhibits LOX, COX and TNF-α.
  • Turmeric (2 g+ daily) - inhibits COX-2 and NF-kB.
  • Quercetin - inhibits LOX and COX; down-regulates NF-κB.
  • Aloe vera - inhibits COX and supports wound healing.
  • Bowellia serrata (frankincense) - inhibits 5-LOX.
  • Chamomile (infusion 2 tsp. dried herb) - inhibits COX-2 and NF-Κb inhibition).
  • Lion’s mane mushroom - promotes regeneration of the intestinal mucosa; acts as a prebiotic; immune-modulating.
129
Q

Other natural approaches for IBD

A
  • Probiotics - species of Lactobacilii (E.g., L. acidophilus, L. casei) and Bifidobacteria have been shown to strengthen the epithelial barrier function and reduce inflammation. Advisable not to use in a flare.
  • Prebiotics (e.g., FOS, psyllium) - bacterial fermentation of prebiotics = SCFAs, e.g., butyrate.
  • Prioritise nutrient deficiencies in IBD: Vitamin B12 (esp. in CD), folate (depleted by methotrexate), iron (bleeding), zinc (poor absorption and faecal loss), calcium (low absorption, vitamin D deficient), potassium (diarrhoea), magnesium, vitamin A / D / E / K.