GIT - Lecture 5 Flashcards
1
Q
What is HYPOCHLORHYDRIA ?
At what pH is it considered to be HYPOCHLORHYDRIA?
A
Hypochlorhydria = low stomach acid production characterised by a fasting gastric pH above 3.0 (1.5–3.0 is considered normal). Stomach acid does not get acidic enough to break down food coming in.
2
Q
What are the key signs and symptoms of hypochlorhydria?
A
- Gas and bloating (often <30 minutes after eating), heartburn, sensation of fullness after meals (food is coming back up because the stomach is churning too hard), foul smelling stools (protein not digested well – trucker stools), diarrhoea, nausea after taking supplements (because when you put a stomach in and you cannot break down the mineral from its bond it create nausea), food allergies, atopic conditions, brittle nails (not absorbing mineral very well).
- Nutrient deficiencies (malabsorption) e.g., iron, zinc, folate and B12 – stomach acid role with IF to absorb B12.
3
Q
What are the key nutrient deficiencies of hypochlorhydria?
A
Nutrient deficiencies (malabsorption) e.g., iron, zinc, folate and B12 – stomach acid role with IF to absorb B12.
4
Q
What is the pH for achlorhydria, hypochlorhydria and hyperchlorhydria?
A
- 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.
- Hypochlorhydria = a gastric pH >3.0
5
Q
What are the consequences of hypochlorhydria? x6
A
- Reduced mineral absorption - calcium ↓ bone density, iron → anaemia
- Protein putrefaction - colorectal cancer
- H. pylori infection
- SIBO
- poor pancreatic juice and bile flow (lipase, amylase, elastase)
- B12 deficiency (IF)
6
Q
Causes to hypochlorhydria?
A
Chronic stress – excessive fight and flight
Anorexia, starvation – stomach damage (the stomach wall atrophies and the cell that make the stomach wall might die and never grow back which make these person at risk of low stomach acid for the rest of their lives).
Stomach surgery, PPI LT use
7
Q
Natural approach to hypochlorhydria?
A
- Chew thoroughly, avoid overeating and drinking with meals. Smell food, observe it, cook the food with strong herbs and spices for aroma.
- Avoid lots of water with meal
- Take slightly acid things with the meal like ACV and lemon juice
- Slow cooking proteins (so they are already pre-digested
- Apple cider vinegar (1–2 tsp) diluted in a little water before meals.
- Zinc and B6-rich foods – essential to make stomach acid
- Bitter reflex – when we taste something bitter we start producing digestive juices and saliva to start the digestive process.
- Bitter foods and herbs stimulate digestive secretions (incl. HCl):
- Bitter greens e.g., rocket, chicory, dandelion leaf, watercress.
- Herbs: Gentian, dandelion, goldenseal, barberry bark — stimulate the Vagus nerve (although energetically cold).
- Alternative herbs: Fennel seed, cardamon, citrus peel, ginger (these are energetically ‘warming bitters’, so good if excess cold / aggravated Agni / Spleen Qi deficiency) + clear gases.
8
Q
Supplement for hypochlorhydria?
A
Supplementing with Betaine HCl: a basic protocol for suspected meal-time hypochlorhydria. Betaine come from ACV – provide more acidity for digesting meal. Often found with pepsin that helps protein digestion.
If we chose to use this, use natural processes first.
* Begin by taking 1 capsule containing 350–750 mg Betaine HCl with a protein-containing meal (>500 kcal+).
* If no discomfort (tingling / burning), increase mealtime dose by 1 capsule every 2 days (max. 3 g) until dose results in tingling or warm sensation (it is not a discomfort!), then reduce dose by 1 capsule.
* Use this dose at subsequent meals with the correct dose
9
Q
What cautions with Betaine HCl?
A
Betaine HCl/ Pepsin is contraindicated with some drugs and peptic ulcers
HCl irritate sensitive tissues and is irritative to the teeth
Capsule should not be emptied in food or dissolve in a glass
Should not be given on an empty stomach unless food follow immediately
smaller meals require smaller doses
10
Q
What is Exocrine pancreatic insufficiency (EPI)? What is the result of that?
A
A deficiency of exocrine pancreatic enzymes needed to maintain normal digestion resulting in nutrient (especially fat) malabsorption.
Lipase, amylase and protease
11
Q
What are the common signs and symptoms of Exocrine pancreatic insufficiency (EPI)?
A
- Bloating / belching / flatulence 1–2 hours after eating.
- Steatorrhoea (excessive fat in faeces; i.e., greasy or floating stools). A type of diarrhoea (frothing, foul smelling, pale, floating and break on contact with the bowl).
- Drowsiness after meals.
- Food intolerances.
- Low zinc, B12 and folate absorption.
- Symptoms of IBS, candidiasis or SIBO
12
Q
What are the common causes of Exocrine pancreatic insufficiency (EPI)?
A
- Chronic stress — ↓ Vagus nerve activity. If you are in chronic stress dysfunction you’ll get digestive disturbances (low stomach acid, low pancreatic juices, low motility that can become high motility because of enzyme probles), IBS is linked with poor vagus nerve activity.
- Hypochlorhydria — ↓ CCK stimulation.
- Chronic diseases: cystic fibrosis (very low pancreatic enzyme function and have to take supplement for the rest of their life), chronic pancreatitis, obstructive pancreatic tumours, GI surgery (resection), diabetes mellitus type 1 especially (some autoimmune samage can also damage the exocrine functions).
- Damaged small intestinal wall (e.g., coeliac, IBD) — ↓ CCK production and ↓ pancreatic stimulation.
- Xenobiotics (pesticides, herbicides, phthalates, BPA) can inactivate pancreatic enzymes.
- Microbial interactions: SIBO (although it could be a cause or effect) can deconjugate pancreatic enzymes; dysbiosis. If you have SIBO they can deconjugate pancreatic enzyme and make them work not very well.
- If you do a stool test you can measure pancreatic elastase 1 – if come up low it shoes the person need digging to work out why it is low and support.
13
Q
what is the stool test indicator for Low pancreatic function?
A
Low pancreatic function is indicated by low pancreatic elastase-1, a marker found in most comprehensive stool tests.
14
Q
Naturopathic approach to pancreatic insufficiency
A
- Don’t overeat, chew adequately, avoid snacking between meals (to give anough time for the process to work well).
- Correct stomach acid levels.
- Stimulate the Vagus nerve to activate the parasympathetic nervous system:
- Deep (diaphragmatic) breathing before meals.
- Osteopathy
- Gargle, hum or sing. Activation of the back of the throat – 5min a day.
- Laughter and social enrichment.
- Using bitters such as gentian, artichoke and dandelion.
- Pancreatic enzyme replacement therapy (PERT)
15
Q
What 2 types of Pancreatic Enzyme Replacement Therapy (PERT) exist and how they differ?
How do you take the enzymes?
When to avoid PERT?
A
- A wide range of enzyme formulations are available on the market, each different in terms of type, origin and dosage.
- Animal-derived (pork pancreatin) has been the standard of care in conventional medicine providing amylase, lipase and protease. Stronger.
- Plant-based and microbe-derived enzymes appear to offer advantages, e.g., better acid stability, broader range of enzymes, more variants and wider pH range.
- Take enzymes with the first bite of a meal and consider adding extra enzymes during, or at the end of a meal depending on the meal size and duration, e.g., if the meal is:
‒ <15 minutes — take all at the start of the meal.
‒ 15–30 minutes — take half the enzymes at the start and half in the middle of the meal.
‒ >30 minutes — take a third at the beginning, middle and end of the meal. - The rationale is to mimic endogenous secretion whereby enzyme secretion increases as more food is ingested.
Avoid digestive enzymes in cases of ulceration
16
Q
What is bile insufficiency ?
A
Bile insufficiency = a condition whereby bile synthesis and / or bile flow (note — bile should be quite ‘thin’) is compromised affecting one’s ability to digest, absorb and utilise fatty acids from the diet. Similar to low pancreatic function symptoms.
17
Q
Key signs and symptoms of bile insufficiency?
A
- Steatorrhoea: Constipation or diarrhoea. Might have a yellow colour.
- Intolerance to fatty foods / nausea when eaten. How does the client feel after a fatty meal.
- Bloating, excess flatulence and cramping around small intestine area (look similar to IBS).
- When bile is into the small intestine the bacteria start deconjugating it and then it is put back in circulation and recycled. But create metabolites. Bile acts as a laxative – too much => diarrhoea and not enough => constipation and methane producing becterias.
18
Q
Stool test indicators (accompanying key symptoms) of bile insufficiency?
A
- Low / absent bile acids (accompanied by key signs / symptoms — as zero can be normal if very efficient at resorbing bile salts). Can be normal or abnormal – depends on the signs coming with it could be bile insufficiency and you want to support bile production.
- High faecal fats (steatocrit – hard to measure and depend on meal) — indicates fat malabsorption. Can be a guide if you look at the whole picture.
19
Q
Common causes of bile insufficiency?
A
- Long Term Low dietary fat intake => train the body not to release bile
- Impaired liver function and obstructed bile ducts (gallstones, NASH (fatty liver), inflammation of the liver).
- Obesity (shown to have ↓ postprandial bile acid response)
- Oestrogen dominance (↑ liver production of cholesterol which thickens bile and also slows the excretion of oestrogen — a viscous cycle!) – if bile is too thick it does not work very well.
- Other GI conditions e.g., cholecystectomy (gall bladder removal – not enough bile production in meal because you cannot store the meal or have bile dropping between meal on empty intestine – have more small meals), coeliac disease, Crohn’s disease, chronic pancreatitis, SIBO (chicken or egg – could be low bile create SIBO or SIBO prevent the proper feedback system).
- Low HCl (reducing CCK and hence bile release) – needs the trigger
20
Q
Implications of long-term bile insufficiency?
A
- Deficiency of fat-soluble nutrients:
– Vitamins A, D, E, K; essential fatty acids, phytonutrients (e.g., beta-carotene) – low vit D despite supplementation. - Hormone imbalances (i.e., associated with poor oestrogen clearance).
- Hypercholesterolaemia. You can get rid of excess cholesterol in the bile and then binds to fibre and gets excreted
- Compromised liver detoxification. Some toxins stay fat soluble and need exit via the bile and if bile function is impaired create backlog in the liver and create inflammation in the liver and a vicious circle. Over exposure to toxins in the liver.
- SIBO and dysbiosis (bile has antimicrobial effects, detoxifies bacterial endotoxins and stimulates peristalsis). When someone has SIBO can get a bile insufficiency.
- Gallstones or inflammation of the liver or pancreas. Will create issue with bile flow.
21
Q
Natural approach to bile insufficiency?
A
– Adequate hydration — at least 6‒8 glasses per day. You need water to make bile.
– Avoid processed food, trans fats and refined sugar. Saturated fat and trans fats create stress on bile production as will induce a lot of bile flow – will sometimes not be enough for what is there. Refined sugar can interrupt the whole metabolic process.
– Chew slowly and thoroughly (until food is liquid). DO the bitter foods, smelling meal, not too much fat in the meal.
– Diaphragmatic breathing — massages the liver, ↑ bile production. Help move the liver and the gallbladder. See an osteopath if diaphragm is blocked.
22
Q
What 2 nutrients are key bile component + what food source?
A
↑ taurine and choline foods (key bile components – bile salts get conjugated to these to work), or supplement.
Taurine rich food : Seaweed, scallops,
clams, tuna, salmon, turkey / chicken thighs.
Choline rich food: Wheat germ, kidney beans, broccoli, Brussel sprouts, quinoa, beef liver, eggs,
23
Q
What are choleretic and cholagogue-rich foods and herbs for bile insufficiency?
A
choleretic = ↑ bile production
Foods: Radish, cucumber, bitter melon, onion, kidney beans, ACV.
Herbs: Gentian, artichoke leaf,
barberry bark, dandelion root.
cholagogue = ↑ bile flow
Foods: Apples, artichoke, beets, bitter greens, celery, fennel.
Herbs: Milk thistle, turmeric,
ginger, dandelion greens, fenugreek (fenugreek removes cholesterol from bile to ↑ bile acid concentration by 4x).
Take herbal choleretics and cholagogues within 30 mins of starting a meal
24
Q
What is the mucosal barrier ?
A
Mucosal barrier = 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). Mucous in different parts of the GIT has different thickness
24
What is the mucosal barrier ?
Mucosal barrier = 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). Mucous in different parts of the GIT has different thickness
25
What is the composition of the mucosal barrier?
Mucus contains water (96–98%), glycoproteins called mucins (give structure to the water – viscosity and stickiness and trap, IgA (made by epithelial cells) and anti-microbial peptides such as α and β defensins (innate immune system)
26
in which condition does the mucosal barrier becomes very thin causing inflammation?
* In ulcerative colitis, it has been observed that the inner mucosal lining becomes permeable (thin) = large amount of bacteria in close contact with host tissues = inflammation.
27
what is metabolic endotoxaemia ?
* A disturbed mucosal barrier can lead to bacterial translocation and the leakage of LPS → metabolic endotoxaemia – too many LPS (outter cell wall of bacteria ending up in the system => inflammatory response – linked with diabetes, autoimmune, Alzheimer’s, Neurodegenerative disease, depression). It can be the start of intestinal permeability.
28
How to support the mucosal barrier ?
* Feed the correct bacteria and avoid things that are detrimental on the mucosal barrier.
* Optimise dietary fibre (because if you don’t feed the bacteria, they can eat your mucins!). Dysbiosis.
* A diet rich in polyphenols (plant chemicals associated with all the colours of the rainbow) — feeds commensal bacteria (including the important ‘keystone’ bacteria Akkermansia spp.) and protects the mucin lining; reduces inflammation.
‒ Green tea, blueberries, cranberry, blackcurrants, pomegranates. Blue and red colours.
* Mucopolysaccharides (carbs with a mucous component in them) such as slippery elm, marshmallow root, liquorice and flaxseeds, seaweed.
* Fucoidans, which are polysaccharides, in seaweeds and algaes
29
What is mucin?
glycoproteins found in mucus
30
What is Intestinal tight junction permeability ?
Intestinal tight junction disassembly contributes to ↑ LPS load and excessive immune reactions.
31
How to support the intestinal epithelial barrier? x3 nutrients
‒ Glutamine — supplemented or from food, e.g., cabbage juice, spirulina, asparagus.
‒ Zinc carnosine (for epithelial cells), vitamin A, vit D (for epithelial barrier) and N-acetyl glucosamine (tightness of gut barrier).
‒ Bone broth (rich in glycine), collagen.
32
What to look for on test for in Intestinal tight junction permeability ?
* Look for the missing of Akkermansia because if missing it gives you a risk factor of poor mucosal balance.
* Look for Ruminococcus gnavus (R.gnavus) or R.torques in high amount
* Absence of diversity in Bacteriodes sub-groups can cause the bacteria to become more mucin-degrading – eat the mucosal barrier if no source of fibre in the diet! If you are on a Keto diet you must take fibre supplements to protect your mucosal barrier and avoid metabolic endotoxemia.
* Zonulin (stool) – protein marker when the gut junctions are open -> intestinal permeability – but could also be negative on test… Zonulin can be tested via the serum.
* ‘Cyrex Labs Array 2’ (serum antibodies) – gives an idea if there is intestinal permeability
* Drinks a small sugar and if gets through intestinal barrier will show in urine
* You will get in clinics first a lot of sign and symptoms:
* Is the client presenting a chronic disease
* Metabolic endotoxemia
* C reactive protein raise between 2.5 and 5
33
What is secretory IgA in the mucosal barrier? What is its role ?
Secretory IgA = resides 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). SIgA can also communicate with our immune system to monitor diseases and microbes.
34
what is the process that promotes the clearance of antigens by blocking their access to epithelial receptors? what immunoglobulin is responsible for the process in the mucosal barrier?
immune exclusion
Secretory IgA
35
What is the issue with low IgA
Low SIgA: Increases the risk of GI infections including SIBO. Covid, etc. Viruses can get deeper faster because the mucosal barrier is not there to prevent that.
36
What can low IgA be caused by?
* Low SIgA can be caused by: Ongoing emotional / physical stress, NSAIDs and antibiotics. Often the reason is chronic stress, toxic stress, problem with the mucosal barrier, celiac disease. Constant exposure to antibiotics
37
How to naturally increase IgA?
* Address stress.
* Address poor mucosal barrier
* Saccharomyces boulardii (a non-pathogenic yeast) – beneficial yeast for travellers diarrhea, fungal infection, etc. Increase secretory IgA production and is anti-inflammatory – pro biotic.
* Mushrooms (esp. medicinal varieties due to the ↑ beta-glucans).
* Vitamin A (needed for the transport of SIgA over the mucosal lining).
* Vitamin D3 (upregulates SIgA expression).
* Zinc
* Polyphenols (e.g., green tea, cocoa, pomegranate) – increase SIgA and protect mucosal barrier
* Chlorella and Spirulina.
* Probiotics and prebiotics.
* Echinacea spp. Andrographis, Astragalus
38
What is the elimination diet ?
The elimination diet is the most cost-effective way of identifying a food allergy or intolerance.
* It involves first removing the suspected food(s) from the diet for a period of time and monitoring any change in symptoms.
* The potential offending food is then reintroduced and symptoms are monitored to confirm sensitivity.
39
What are the most common food causing immune reaction?
gluten (sometimes it might be the fodmap the issue and not the gluten itself) and dairy, corn and soy, eggs, nuts, beef, pork, yeast, citrus, nightshades, chocolate and coffee
40
What are the 3 stages of the elimination diet and what is their respective length?
Stage 1 (days 1–2) Detox * Increase fruits, vegetables, gluten-free wholegrains, healthy fats, water intake, herbal teas.
* Remove processed foods, confectionary, chocolate, additives, caffeine, etc.
Stage 2 (days 3–14) Elimination * Above, plus remove all suspected foods for 2 weeks (can be done one at a time). If symptoms don’t improve by 3rd week consider other possible triggers.
Stage 3 (days 15 onwards) Reintroduction
(one food at a time!) * Eat the ‘challenge’ food 2–3 times a day for 1–3 days.
* If you notice any symptoms, remove the food and wait for symptoms to completely disappear before challenging the next food.
* If the food does not cause a reaction, it is safe to keep in your diet for the rest of the programme.
* If a food causes a reaction, keep out of the diet for 3 months before challenging again.
41
What is the 5 stages of the 5R protocol?
Remove What may need to be removed to support healthy GI function? (e.g., offending foods or pathogenic bacteria).
Replace What may need to be replaced to support healthy GI function? (e.g., digestive enzymes, bile salts, stomach acid).
Reinoculation What may be needed to reestablish a healthy balance of microflora? (e.g., reinoculation with pre- and / or probiotics).
Repair What may be needed to regenerate and repair a healthy mucosal layer? (e.g., specific nutrients / phytonutrients).
Rebalance What lifestyle changes may be needed to support gut healing? (e.g., stress reduction, addressing work / life balance).
42
Describe the Remove stage 1 of the 5R protocol
Remove – 2-3 weeks:
* Foods may be the most important offending agents.
* Remove dietary irritants; i.e., processed food, food additives, sugar, alcohol, caffeine, carrageenan (quite irritant to the guts) etc. => like a simple detox in a way
* Personalised diet; i.e., remove food allergens / foods that trigger an intolerance (e.g., dairy, gluten), low FODMAP, low histamine, specific carbohydrate diet etc.
* Avoid toxins; i.e., pesticides (eat organic), plastic / tinned packaging, non-filtered / distilled water, chemically-laden beauty products.
* Avoid unnecessary drugs; (e.g., NSAIDs) which can damage the GI mucosa / function.
43
Give an example of herbs that are for the Remove phase of the 5R protocol
o Anti-microbial
o Anti-bacterials
o Anti-parasitics
o Anti-fungals
o Anti-viral
o Anti-microbial herbs (i.e., broad spectrum) — berberine (goldenseal), garlic, oregano, uva ursi.
o Anti-bacterials — e.g., oregano oil, berberine, garlic, neem.
o Anti-parasitics — e.g., black walnut hulls, wormwood, oregano, neem, clove buds, pumpkin seeds.
o Anti-fungals — e.g., oregano oil, caprylic acid, grapefruit seed extract, garlic.
o Anti-viral — e.g., olive leaf extract, nano silver, elderberry, echinacea.
44
What digestive secretion to replenish during phase II (REPLACE) of the 5R protocol ? x3
* Stomach acid secretions — e.g., digestive bitters, betaine HCl.
* Pancreatic support — e.g., bitters, pancreatic enzymes, plant-based enzyme formulas, less frequent meals.
* Bile support — e.g., choleretics / cholagogues, ox bile.
45
Give pre/probiotics example for the 5R protocol phase III Reinoculate ? What are SIBO Safe prebiotics?
* Probiotics: Cultured vegetables, fermented foods and drinks (such as sauerkraut, kimchi, kefir – if not on a non-histamine diet), probiotic supplements e.g., Lactobacillus and Bifidobacterium spp.
* Prebiotics: Foods rich in fructans, fructooligosaccharides (FOS), inulin e.g., chicory, leeks, onions, Jerusalem artichokes. SIBO safe prebiotics – PHGG, galacto-oligosaccharides.
* Use the prebiotics for the targeted bacteria you want to repair
46
In phase 4 (Repair) of the 5R protocol, which nutrients for the epithelial tight junctions?
* For epithelial and tight junction support: L-glutamine, N-acetyl glucosamine, quercetin, zinc, EFAs (incl. EPA / DHA), B vitamins, D vitamins, vitamin A, collagen, bone broth, aloe vera (↑ fibroblast collagen synthesis and inhibits COX).
47
In phase 4 (Repair) of the 5R protocol, which nutrients for the mucous barrier?
* Supporting the mucous barrier: Demulcent herbs rich in mucilage. slippery elm, liquorice, marshmallow root, oats, aloe vera juice, meadowsweet. Fibre. Polyphenols (↑ keystone bacterial species = ↑ mucin + SIgA). Polyphenols rich food.
48
In phase 4 (Repair) of the 5R protocol, which nutrients for increasing IgA?
* Increase SIgA where needed (e.g., S. boulardii) and reduce inflammation (e.g., curcumin – amazing for the gut). Vit A and D, Zinc.
49
What lifestyle choices x3 to pay attention to in phase 5 of the 5R protocol, rebalance?
* Address stress; breathing exercises, nervines and adaptogens, e.g., passionflower, ashwagandha, etc.
* Practise good sleep hygiene.
* Undertake regular exercise.
50
What specific conditions (x4) need more time for the 5R protocol?
* Parasites or worms often need a second phase of antimicrobials to prevent eggs hatching. Either do 10 days on, 10 days off, then repeat or hold out the treatment for a whole 4 weeks. So repeat 2x because eggs can hatch in that time. That is the minimum. OR you could do a straight 4 weeks to make sure you get the eggs.
* SIBO / strong dysbiosis may need 4 weeks of anti-microbials and also a repeat.
* Deficient microbiomes will take time to repair / re-inoculate, so do for a minimum of 4 weeks.
* Food intolerances need the gut wall to be repaired before reintroducing; a minimum of 6-week intervention is often needed.
51
What is dysbiosis?
‘Dysbiosis’ = an imbalance in the colonies of the bowel flora, leading to a potential disruption in both local and systemic health.
52
what is the causes of dysbiosis (Aetiology)?
* Poor diet (highly processed, ↑ refined carbs, ↓ fibre, ↓ polyphenols).
* Intestinal / oral infections. A pathogen can cause an imbalance with the rest of our gut microbes – need to be removed before finding the balance again.
* Medications: Antibiotics / antacids / OCP.
* Chronic stress (e.g. = ↓ digestive secretions).
* Low digestive secretions (e.g. HCl, bile).
* C-section, non-breastfed.
* GI surgery and abdominal scar tissue.
* Note: These factors should be extracted from your case taking.
53
What 4 types of diseases are the result of dysbiosis? Which microbes is missing in each?
* Atopic diseases — C-section infants who received formula milk instead of breastmilk have a lower abundance of Bifidobacteria and Lactobacilli. This has been associated with atopic diseases in later life. The administration of both bacteria as probiotics reduces incidence and symptoms.
* Metabolic syndrome ― has been associated with less Bidifobacteria, Akkermansia spp.; increased E coli and a high Firmicutes to Bacteroidetes ratio.
– A diet rich in fibre and SCFA-producing bacteria (probiotics) has shown improvements in metabolic syndrome.
* Colorectal cancer (CRC) — fibrous diets increase the abundance of SCFA-producers and beneficial bacteria like Roseburia, Eubacterium, Bifidobacterium. Pathogens known to promote CRC are enterotoxigenic B. fragilis, E. coli, Fusobacterium spp. and Campylobacter spp.
* Neurodegenerative diseases:
– Alzheimer’s, Parkinson's and MND sufferers often have ↑ pro-inflammatory bacterial species.
– Periodontal pathogens, P. gingivalis and T. denticola are also associated with the development of Alzheimer’s disease. LPS of P. gingivalis were detected in the brain tissue of AD patients.
54
What is metabolic endotoxaemia?
Metabolic endotoxaemia = a subclinical rise in bacterial LPS in the blood, resulting in chronic low-grade inflammation.
55
which which Chronic disease is metabolic endotoxaemia associated with?
CVD, diabetes mellitus, autoimmunity and degenerative disorders.
56
Pathogenesis of metabolic endotoxaemia ?
* Dysbiosis, mucosal degradation and permeability of the GI tight junctions (often interlinked), increase serum LPS, which triggers the production of pro-inflammatory cytokines (e.g., TNF-α, IL-β).
57
Which diets are linked to increase LPS?
* High fat diets (incl. ketogenic) ↑ LPS transport across the intestinal membrane; be cautious if a tendency to metabolic endotoxemia. You want to make sure that someone who goes on the Keto diet does not have intestinal permeability or metabolic endotoxemia before starting keto and that they have lots of fibres
58
What are LPS?
* LPS are from the cell walls of gram-negative bacteria and
interact with toll-like receptors (esp. TLR4) in the immune system.
59
Natural approach to metabolic endotoxaemia ?
* Avoid alcohol (↑ LPS transport across intestinal epithelium), other dietary irritants / toxins / NSAIDs (see full stage 1 of 5R).
* ↑ dietary fibre ― to bind and clear LPS via the bowel, and to feed butyrate producing species (e.g., Roseburia, Akkermansia spp.).
* Avoid a Western or ketogenic diet.
* Focus on a rainbow of colour (esp. polyphenol-rich foods) to feed the keystone bacterial species, ↓ inflammation and discourage growth of gram-negative bacteria).
* Breathing techniques and cold exposure (e.g., cold showers, swimming in cold water) have been shown to help reduce systemic LPS load.
* Reinoculate and support the GI barrier (stage 3 and 4 of ‘5R’).
60
How to naturally support the liver in metabolic endotoxaemia ?
Support liver function, bile production / flow to aid LPS clearance:
* Milk thistle (hepatoprotective, ↑ glutathione), burdock root, artichoke, dandelion, artichoke, spirulina and chlorella (has an LPS-blocking effect at the TLR4).
* A variety of dietary antioxidants (e.g., vitamin C, E, carotenoids). Selenium — for glutathione peroxidase.
* NAC, cruciferous vegetables and resveratrol to ↑ glutathione.
* Nrf2 inducers (to scavenge ROS) — e.g., broccoli sprouts, green tea, lycopene (tomatoes), rosemary, curcumin.
61
What is SIBO?
SIBO = an overgrowth of non-pathogenic bacteria in the small intestine. It is the most common cause of IBS (60‒70%).
62
What are the two gases in SIBO and associated bowel symptoms?
* Hydrogen dominant gas production tends to cause diarrhoea;
* Methane dominant gas production can cause severe constipation. (more likely – there are exception to this rule and can also be alternating)
63
Why does SIBO created gas, bloating and discomfort?
Overpopulation of microflora in the small intestine leading to production of hydrogen and methane
* The small intestines are not normally densely populated by microflora. In SIBO, bacterial growth is excessive and can lead to the production of hydrogen and methane gases as a result of carbohydrate use.
64
What are the key symptoms of SIBO?
* Hallmark symptoms: Bloating, abdominal pain or discomfort, constipation and / or diarrhoea and flatulence. Has to happen at every single meal! Chronic and ongoing.
* Others symptoms include: nausea, GORD (due to excessive amount of gas in the SI), excessive burping, prolonged feeling of fullness, malabsorption (e.g., anaemia symptoms – can damage the micro villi in the small intestine especially like B12 and Iron), insomnia and brain fog.
- diarrhoea, constipation, unintentional weight loss
- worsening GI symptoms from probiotics and/or fibre
- Chronic GI symptoms after long term antibiotics
- chronic low ferritin/iron even when supplemented
- Coeliac symptoms on a Gluten free diet
65
What nutrients can be depleted in SIBO?
B12 and Iron
66
What food and supplement can worsen the symptoms of SIBO?
- probiotics
- fibre
67
What are the main causes of SIBO?
- Hypochlorhydria and Bile insufficiency (HCl + bile are anti-microbial. Allow bacteria to flourish more than they should)
- Low SIgA (low immune system in the gut)
- Prolonged stress (shut off the MMC, lower SIgA and HCl)
- Scar tissue from surgery (C-section)
- Hypothyroidism (slow motility)
- Poor oral health
- Ileocaecal valve dysfunction (where the large and small intestine join)
- opioids and antibiotics
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What is a common trigger of SIBO?
- acute gastroenteritis ==> food poisoning ==> Some food poisoning pathogens can release a toxin which can damage the MMC – local nerve damage.
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What pathogenic bacteria is released by salmonella? Explain the link with MMC and SIBO.
cytolethal distending toxin (CDT).
* A 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 sweep 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.
* After you clear the SIBO work with the MMC and prevent exposure to other pathogens.
food poisoning -> bacterial toxins -> auto immunity -> gut nerve cell damage -> SIBO
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Explain how SIBO can cause food sensitivities/intolerances? What are two food intolerance linked with SIBO?
SIBO and food sensitivities: SIBO can damage the villi of the small intestine, reducing enzymes like lactase and diamine oxidase (DAO – breaks apart histamine to make sure we don’t get an excessive immune response) that are produced in these finger-like projections.
* A loss of lactase = possible lactose intolerance.
* A loss of DAO = possible histamine intolerance.
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What are the two common dietary approach to SIBO? Which one is better if there is intestinal inflammation?
* Low FODMAP — generally advisable to follow this for up to 6 weeks before gradually reintroducing FODMAPs.
* Specific carbohydrate diet (SCD) — may be preferable to low FODMAPs, especially if there is intestinal inflammation.
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What anti-microbial herbs to use in the initial phase of SIBO? for how long?
Use 1‒3 of the following anti-microbials (or a specialised formulated herbal formula) for 4‒8 weeks depending on the case.
* Berberine (or barberry bark and goldenseal, e.g., as a tincture) — inhibits protein synthesis of bacteria; blocks TLR4 pathway.
* Oregano oil (affects bacterial cell membrane permeability). Very strong so not use with mucosal barrier dysfunction cannot tolerate
* Allicin (extract of garlic) — mostly just for methane-producing bacteria.
* Neem.
* Also, uva ursi and cinnamon.
Do 4 weeks of antimicrobial, retest, wait for a week, redo the 4 weeks and to a low fodmap diet at the same time.
Consider rotating the anti-microbials to avoid any resistance
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What digestive support looks like in SIBO?
* Digestive support:
* Digestive bitters at the start of meals (e.g., greens such as dandelion, rocket, watercress; herbs such as gentian, fennel, barberry bark).
* Betaine HCl, digestive enzymes, ACV.
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What MMC support looks like in SIBO?
* MMC support:
* 12-hour overnight fast (minimum) / intermittent fasting. Meal spacing (at least 4 hours) with no snacks. To allow the MMC to activate and happen.
* Pro-kinetic agents before bed, e.g., ginger root, artichoke. Botanicals that help the MMC to move – in the evening before bed to help the MMC before bed.
* Practise mindful eating; diaphragmatic breathing exercises.
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What mushroom is recommended for SIBO
Lion's mane = promotes regeneration of neurons if suspected autoimmune (also promotes regeneration of GI mucosa).
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What are biofilms? When consider biofilm in SIBO?
Biofilms: A biofilm is an extracellular matrix that can protect bacteria and fungus from our immune system. If antimicrobial protocols / dietary changes are not working, consider biofilm production.
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What is the natural approach to biofilms? Food x4 and supplements x3
Natural approach: Coconut oil, ACV, garlic, curcumin.
Biofilm disruptors, e.g., NAC, nano silver, serrapeptase.
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What pathologies x2 are associated with SIBO?
100% fibromyalgia patient have SIBO (SIBO cause fibromyalgia) LPS cause inflammation and increase pain sensitization and impair mitochondrial function, + bacteria produce neurotoxins that cause fatigue ans muscle pain.
Thyroid dysfunction (because 21% of T4 to T3 conversion happens in he gut, and slow thyroid means low stomach acid and motility disorder)
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Which commensal yeast is involved in candidiasis?
Candida albicans is the most common commensal yeast that asymptomatically inhabits mucosal surfaces.
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How is Candida albicans kept under control in Candidiasis?
* Candida is usually kept under control by native bacteria and the immune defences (especially by neutrophils, macrophages and T helper 1 cells. Lowering of immune system and damage of mucosal membrane => opportunity for candidiasis to grow out of way.
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What can cause Candidiasis? which body parts?
Infections are usually limited to the mouth (people taking asthma inhaler) or genitals (thrush) and skin, but infections can become systemic in severe immunocompromise.
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Signs and symptoms of candidiasis?
- Frequent UTIs
- fatigue
- digestive symptoms (e.g., bloating)
- sugar cravings
- joint pain
- depression
- anxiety
- brain fog
- food sensitivities
- skin and nail fungal infections, etc.
- Mouth Tongue white coating with redness under, also coating on the gums in little circles – redness and harshness to it
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Causes of candidiasis?
* Disruption of the host bacterial environment or immune dysfunction can allow opportunistic candida to proliferate (terrain theory).
* C. albicans can then penetrate epithelial cells and switch morphology from commensal to pathogen.
* Some candida can be harsh than others – careful with starving it for food because it can cause more damage when starved and dig deeper in the mucosal membrane
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8 key risk factors of candidiasis?
- Antibiotic use
- High sugar intake can worsen it (hence sugar dysregulation in type 1 diabetes => candidiasis)
- Low immunity (↓ sIgA) – LT corticosteroid use, type 1 diabetes, HIV patients
- Dysbiosis
- Chronic stress (↑ cortisol), sleep depravation
- Impaired liver function
↓ digestive secretions
- Exposure to toxins – lower immune response and make us more prone to infections like candida
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What testings for candidiasis ? x4
Candida infections can be measured in several ways. Stool testing is very common.
* Stool test — if suspect it is in the GIT - mycology culture (see below) – careful might look positive when not.
* Organic acids test — elevated arabinose is indicative of yeast infection.
* Saliva test — candida antibodies.
* Blood test — circulating candida antigens.
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What elevated value to look for in the organic acid test for candidiasis?
elevated arabinose is indicative of yeast infection.
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How to do the saliva test for candidiasis?
Upon waking, spit into a glass of water. Healthy saliva floats but if you see strings coming down or it sinks, you may have a candida overgrowth.
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What is the 6 steps natural approach to candidiasis?
Naturopathic approach to candidiasis: Create an environment where candida cannot overgrow (optimise the terrain) while optimising the body’s ability to heal itself naturally.
1. Optimise elimination and detoxification. Optimise the terrain think about the whole picture of the microbiota (stress, digestive capacity, dysbiosis) – support digestive enzymes and bile function, rich fibre and water, poop properly.
2. Adopt an anti-candida diet – careful
3. Use natural antifungals and address biofilms – N-Acetyl Cysteine (NAC)
4. Address predisposing risk factors – stress, what got someone there in the first place
5. Support the microbiome.
6. Restore nutrient deficiencies.
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How to promote detox and elimination in the treatment of Candidiasis (Step 1)?
1. Promote detoxification and elimination:
* Resolve constipation if necessary. Water + fibre + probiotics
* Drink plenty of water (>1.5 L / day).
* Increase intake of soluble fibre and eat foods rich in mucilage (e.g., flaxseeds, chia seeds, psyllium husk, apple pectin).
* If necessary, silymarin (milk thistle) to enhance liver function (protects against phase I metabolites — increases glutathione and SOD).
* Consider a binding agent (e.g., lactoferrin and lactoglobulin or chlorella) to ‘mop up’ potential candida ‘die off’ (Herxheimer reaction). Use this with any dysbiosis plan and person is not strong enough to deal with the LPS when the microbe dies off, add with the antimicrobial a binding agent to make sure the LPS is eliminated via the bowel. Fibre is a great binding agent. Activated charcoal on a short period of time (careful can prevent other minerals absorption).
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Explain the anti candida diet (step 2)
Anti-candida diet:
* Eliminate refined / simple sugars and minimise carbohydrates. BUT – if you starve candida too strongly it will go deeper in the mucosal membrane – don’t remove all carbs. Whole food diet that remove sugar but still have some carbs going in.
* Go gluten / dairy free and avoid other suspected allergic foods.
* Eat lots of non-starchy vegetables and low-sugar fruit.
* Eliminate yeast or mould-containing foods (e.g., alcohol, cheese, dried fruit, vinegar, peanuts). If there is an immune reaction going-on.
* Opt for organic where possible.
* Oxalates impair carboxylase enzymes (CE), which help the body to eliminate candida. Research suggests that by reducing oxalates, CE increases and candida reduces. You still want a nice wholefood diet so still add some nice green vegetables.
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What is the role of oxalate compounds in candidiasis?
Oxalates impair carboxylase enzymes (CE), which help the body to eliminate candida. Research suggests that by reducing oxalates, CE increases and candida reduces. You still want a nice wholefood diet so still add some nice green vegetables.
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Which anti fungal agents in candidiasis? Step 3
Natural antifungal agents:
* Berberine containing herbs.
* Caprylic acid (in coconut oil; a fatty acid that is incorporated into candida membranes → rupture).
* Pau d’Arco (naphthoquinones have strong fungicidal effects).
* Oregano oil, thyme, rosemary, allicin.
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Which anti biofilm agents in candidiasis? Step 3
* Proteolytic enzymes (e.g., serrapeptase) — take away from meals.
* Plant-based biofilm disrupters e.g., allicin, curcumin, berberine. NAC – liver, glutathione, best for biofilm, affordable.
Take a biofilm disrupter along with two antifungal agents. 3 months is advised. Start slow, build up slowly to prevent die-off symptoms.
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What predisposing factors to address in candidiasis ? Step 4
Address predisposing factors:
* Help clients deal with stress and advise on sleep hygiene.
* Recommend avoiding alcohol, sugar, smoking.
* Review ongoing medications (with GP support).
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How to support the microbiome in Candidiasis ? (step 6)
Support the microbiome:
* Increase SIgA (mucosal immunity), e.g. Saccharomyces boulardii.
* Prebiotics (e.g., FOS) and probiotics with meals (e.g. multi-strain formula with Lactobacillus and Bifidobacteria strains).
* Prebiotics, polyphenols, probiotics – support the GIT bacteria + therapeutic yeast against fungal infections.
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What are gallstones?
What is the medical term for gallstone formation?
Gallstones = crystalline calculi formed within the gallbladder from a build up of bile components. 80% of gallstones contain cholesterol
‘Cholelithiasis’ (gallstone formation)
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Factors for gallstones formation?
* Supersaturation of bile with cholesterol.
– Cholesterol supersaturation can result from excessive cholesterol concentration in bile or a deficiency of substances that keep cholesterol in solution (i.e., bile salts and phospholipids).
* Bile stasis or delayed gallbladder emptying due to ↓ gallbladder motility.
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key risk factors for gallstones?
Key risk factors: Obesity, Type 2 diabetes, OCP, HRT, typical Western diet, sedentary, high alcohol.
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Natural approach to gallstones
Natural approach to gallstones: get the bile flowing well and eliminate built up cholesterol and bile salts so they are eliminated via the bowels
* ↑ fibre; ↓ refined sugar, trans-fats, saturated fats and alcohol. Cellulose and pectin (apples and pears) – high sat fat diet will provoke the gallbladder to spasm.
* Avoid dehydration because not enough water in system (too much tea and coffee and not enough water)
* Prevent excess cholesterol
* Lots of polyunsaturated fatty acids
* Consume choleretic and cholagogue-rich foods and herbs to support bile flow (e.g., ACV, bitter greens, globe artichoke).
* Weight loss may reduce gallstones in overweight individuals.
* Increase polyunsaturated fatty acids (PUFAs) as found in oily fish.
* Peppermint (its terpenes help to dissolve stones). Peppermint oil for spasm and cramping
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Supplements for gallstones x3
* Vitamin C (500–2000 mg / day) – in high doses to help flush things through and dissolve the stones
* Lecithin (high phospholipid content; keeps cholesterol in solution). Emulsify fats in digestive systems
* Purified bile salts (ox bile) – not for vegans.
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What is a peptic ulcer
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.
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Symptoms of peptic ulcer?
Epigastric pain (may radiate to the back), gnawing (feels like being eaten out from the inside) / pain between meals (because on a meal the stomach acid works on the food), nausea, vomiting, ↓ appetite, dyspepsia and reflux.
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Complication of peptic ulcer?
When to seek urgent medical attention?
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) or melaena. Need urgent medical attention => gastric bleed. Or very black stools => red flag
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Risk factors for peptic ulcer?
* Stress (sympathetic dominance) — can lead to vasoconstriction and inadequate blood supply which interferes with mucus production and reduces the secretion of protective prostaglandins. Stress (sympathetic dominance) reduce blood flow to digestive system which means your reduce the change to repair any damage that happen on a normal day to day basis and you don’t make enough mucous which protects the epithelial barrier.
* 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).
- H pylori infection
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Explain how H. Pylori infection can lead to peptic ulcer?
* H. pylori infection in the stomach is associated with peptic ulceration, chronic gastritis and gastric cancer. 80% of peptic ulcer cases have H. pylori colonisation.
* 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)
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Natural approach to peptic ulcer?
* Avoid alcohol, smoking, fizzy drinks, spicy foods and caffeine (potential GI mucosal irritants). Avoid NSAID use.
* Increase fibre — especially for duodenal ulcers as fibre slows gastric emptying.
* Address stress. Consider calming nervine teas (e.g., chamomile, passionflower).
* Supporting the mucosal / mucin barrier:
* Demulcent herbal powder — slippery elm, marshmallow, liquorice (see Nutrition 2, Herbal Medicine Lecture).
* ↑ 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). A study found that 600 mg given 5 x / day showed 76% were ulcer-free after 12 weeks.
* Aloe vera juice — 20–30 ml 3 x daily. Inhibits COX (anti- inflammatory), speeds up wound healing (↑ collagen synthesis).
* Identify and address H. pylori (next slide).
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Eradicating H. pylori naturally
* 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
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What is GORD?
Gastro-oesophageal reflux disease (GORD) = the reflux of gastric juice (HCl, bile, pepsin) back into the oesophagus.
* GORD is associated with transient lower oesophageal sphincter (LOS) relaxation episodes and a decreased lower oesophageal sphincter pressure.
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What is the most common symptom of GORD?
* The most common symptom is heartburn (retrosternal pain).
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GORD risk factors:
* ↑ 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 (can exacerbate the issue if sphincter tone is low in general), tomatoes and chocolate relax the LOS.
* Certain medications: Calcium channel blockers, nitrates, NSAIDs, diazepam.
* Stress, anxiety and family history.
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Natural approach to GORD:
* Consider testing for H.pylori.
* Consider low stomach acid (test it!):
* 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.
* 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.
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What are the 3 most common gluten related disorders?
* The most commonly recognised gluten-related disorders are:
* Coeliac disease (auto-immune).
* Wheat allergy (allergic).
* Non-coeliac gluten sensitivity (innate immunity).
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What are the two immune triggering proteins of gluten?
* The immune-trigger protein fractions of gluten include gliadins and glutenins.
114
Wheat allergy symptoms ?
Wheat allergy: 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.
* Diagnosis: Via a ‘skin prick’ test and managed by the strict avoidance of wheat.
* Those with severe wheat allergy may likely carry an adrenaline auto-injector (EpiPen) and wear an emergency card or bracelet with details of their allergy.
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Coeliac disease symptom and complications?
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.
* Affects 1 in 133 (10–20% diagnosed).
* Symptoms: Abdominal pain, nausea, vomiting, diarrhoea, steatorrhoea, fatigue, anxiety, anaemia, weight loss, failure to thrive, osteoporosis, malnutrition, dermatitis herpetiformis and ataxia.
* Complications: Malabsorption (e.g., B12, B9, iron, calcium), osteoporosis, anaemia (iron / megaloblastic).
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Coeliac disease — pathophysiology:
* It involves an inappropriate adaptive immune response to gluten-derived peptides (i.e., gliadin).
‒ It 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.
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Coeliac disease — diagnosis:
* 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. Note: 30‒40% of the global population carry at least one copy of this genetic variant but only 1% develop coeliac disease.
* 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
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Coeliac disease — natural support:
* Coeliacs must follow a completely gluten-free diet for life.
* Some grains and foods contain proteins similar to gluten (cross-reactive foods) that may also need to be avoided. Cyrex Labs provides an appropriate test: (Cyrex Array 4 — Gluten-associated cross-reactive foods and foods sensitivity panel).
* For optimum recovery, a gut-healing diet such as
the specific carbohydrate diet (SCD) can also be used.
* Nutritional deficiencies may also need to be addressed.
* Consider the need for supporting the intestinal barrier (‘repair’).
119
what is Non-coeliac gluten sensitivity (NCGS)?
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.
120
Key symptoms of Non-coeliac gluten sensitivity (NCGS) ?
Intestinal:
Bloating
Abdominal pain Constipation
Nausea
Diarrhoea
GORD
Extra-intestinal:
Tiredness
Headache
Anxiety
Brain fog
Joint pain
Depression
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Prevalence and pathophysiology of NCGS?
Prevalence and pathophysiology: Neither is clearly defined but 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).
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What is IBS?
IBS = an umbrella diagnosis used to classify an individual with a constellation of chronic symptoms. It is not a ‘disease’.
123
Key symptoms: IBS
* Abdominal pain and cramping relieved by passing a stool.
* Diarrhoea, constipation or mixed.
* Bloating and flatulence.
* Incomplete emptying of bowels.
* Feel worse after certain food or when stressed or anxious.
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What are the 4 sub-types of IBS?
IBS-C Constipation
IBS-D Diarrhoea
IBS-M Mixed
IBS-U Unclassified
125
Natural support for constipation in IBS-C
* ↑ dietary fibre and stay hydrated.
* Magnesium (e.g., magnesium citrate — increase dosage from 250 mg gradually until tolerance).
* Vitamin B5 and ginger, globe artichoke, 5-HTP (↑ peristalsis).
* Psyllium husk or ground flaxseed (15‒30 g / day). 5-HTP (for some).
* Natural laxatives e.g., prunes, figs. Pour prune juice over freshly ground flaxseeds (leave it in the fridge).
* Anthraquinone – laxative for emergency situation, not to use on ongoing basis because make the bowel lazy. Plant like Senna, rhubarb and some aloe vera
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Natural support for diarrhoea in IBS-D
* ↑ soluble fibre to help bulk stool e.g. apple pectin – help bind the stool.
* Enteric-coated peppermint oil – for pain to sooth the cramps and spasm.
* Digestive enzymes.
* S. boulardii (↑ sIgA).
* Electrolyte replacement, juices and broths to account for fluid / electrolyte losses.
* Marshmallow root, slippery elm, meadowsweet (powder).
* Stress play a role – nerve herbs to calm down the NS like camomile and lemon balm and work for the NS and the GIT
127
What is IBD?
Inflammatory bowel disease (IBD) = 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.
128
Key symptoms and onset age of IBD?
Key complications?
* 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).
Key complications: Colorectal cancer, osteoporosis, anaemia (e.g. iron, folate, B12).
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Present a differential diagnosis of CD and US including:
- region affected
- Distribution
- layers affected
- key symptoms
- complications
Region affected
CD: Any part of the GIT but mostly the terminal ileum.
UC: Colon and rectum.
Distribution:
CD = Skip lesions.
UC = Proximally continuous.
Layers affected:
CD = All layers (transmural).
UC = Mucosa only (‘ulcers’).
Symptoms:
CD = Crampy abdominal pain (right). Loose semi-solid stools.
UC = Abdominal pain (left side) Bloody diarrhoea.
Complications:
CD = Fistulas, abscess, obstruction, malabsorption
— B12 deficiency.
UC = Haemorrhage → anaemia.
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IBD aetiology and pathophysiology:
* 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 (see next slide).
131
Bacterial patterns commonly seen in IBD:
* 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.
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IBD triggers:
* 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
133
Dietary strategies for IBD:
* 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).
