GI health Flashcards
What are the symptoms of Hypochlorhydria?
Gas and bloating < 30 minutes after eating, heartburn, foul smelling stools, diarrhoea, nausea after supplements due mineral bonds not being broken apart , sensation of fullness after meals, nutrient deficiencies (malabsorption) eg iron, zinc, folate, B12- stomach acid isnt acidic enough to break down proteins and foods.
What is considered a normal fasting gastric pH?
1.5- 3.0. Above 3.0 is considered low stomach acid production (hypochlorhydria)
What are the implications of hypochlorhydria?
1) Reduced mineral absorption eg less calcium can lead to decrease in bone density, less iron= anaemia
2) Poor protein digestion can lead to small intestinal protein putrefaction, can create polyamines which are implicated in colorectal cancer.
3) Higher pH means less protection from bacterial infection , facilitating H.pylori survival in the stomach= bacteria may proliferate in SI (SIBO)
4) Poor pancreatic juice and bile flow- the acidity of the chyme from the the stomach into the SI triggers both of these
5) Less intrinsic factor can lead to reduced B12 absorption
Discuss 5 natural approaches to hypochlorhydria
1) Chew food thouroughly and eat mindfully- initiates the parasympathetic nervous system (rest and digest) and digestive secretions
2) Eat bitter foods and herbs to stimulate digestive secretions including HCL- dandelion leaf, rocket, chicory, gentian, goldenseal, watercress
3) Reduce stress- biggest reason is excessive SNS response in body
4) Include B6 and zinc rich foods (seafood, poultry, legumes, wholegrains, nuts and seeds
5) Apple cider vinegar 1-2 tsp diluted in a little water before meals
How would you supplement Betaine HCL for suspected mealtime hypochlorhydria?
Start with one capsule (350-750mg) with a protein containing meal, if no tingling/ burning increase mealtime dose by 1 capsule every 2 days until tingling or warm sensation then reduce by 1 capsule. Use this dose
What is exocrine pancreatic insufficiency (EPI) ?
A deficiency of exocrine pancreatic enzymes (Protease, lipase, amylase) needed for normal digestion, resulting in nutrient (especially fat) malabsorption
What are 5 common symptoms of EPI?
1) Bloating/belching/flatulence 1-2 hours after eating
2) Steatorrhoea (excessive fat in faeces, fat isn’t getting emulsified so enzymes can’t work on it)
3) Drowsiness after meals
4) Food intolerances
5) Symptoms of IBS, candidiasis or SIBO
5 causes of pancreatic insufficiency?
1) Chronic stress- decreased vagus nerve activity (important to switch off fight or flight)
2) Hypochlorhydria - decreased cholecystokinin
3) xenobiotics (pesticides, herbicides, phylates, BPA can inactivate pancreatic enzymes
4) SIBO can deconjugate pancreatic enzymes; dysbiosis but low pancreatic enzymes can also cause SIBO
5) Damaged SI wall eg coeliac, IBD = decreased CCK production and pancreatic stimulation
What are 4 natural approaches to pancreatic insufficiency?
1) Chew adequately and avoid snacking between meals
2) Stimulate the vagus nerve to activate the parasympathetic nervous system - deep diaphragmatic breathing before meals, gargle, hum, sing, laughter and social enrichment
3) Bitters such as gentian, artichoke and dandelion
4) Pancreatic enzyme replacement therapy (PERT) - pork derived or plant based. Meal <15 minutes= take all at start of meal, 15-30 half at start half in middle, >30 beginning, middle and end.
What is a bile insufficiency? What is the primary role of bile?
Condition whereby bile synthesis and or bile flow (should be thin) is compromised, affecting someones ability to digest, absorb and utilise fatty acids from the diet.
- Bile is needed to emulsify the fat so that pancreatic enzymes have enough surface area to work on them
What are the key signs and symptoms of bile insufficiency?
Steatorrhea, constipation or diarrhoea, intolerance to fatty foods and nausea when eaten, bloating, excess flatulence and cramping
How may bile insufficiency be indicated in a stool test?
1) Low or absent bile acids- accompanied with key signs and symptoms otherwise zero may be normal
2) High faecal fats (steatocrit) indicates fat malabsorption
Discuss 5 common causes of bile insufficiency
1) Low dietary fat intake- body becomes trained to not release bile
2) Impaired liver function and obstructed bile ducts (gallstones and any liver inflammation including fatty liver disease)
3) Obesity - shown to decrease postprandial bile acid response
4) Oestrogen dominance- liver produces extra cholesterol which can thicken bile and also slows excretion of oestrogen- viscous cycle
5) Low HCI- needed to trigger CCK and bile release
Name 5 implications of long- term bile insufficiency
1) Deficiency of fat soluble nutrients - Vitamins A, D, E, K, beta carotene needs fat for absorption, essential fatty acids.
2) Hormone imbalances due to reduced oestrogen clearance
3) Compromised liver detoxifaction
4) Hypercholesterolemia
5) SIBO and dysbiosis- bile has antimicrobial effects and stimulates peristalsis
Discuss natural approaches to bile insufficiency
1) Adequate hydration
2) Avoid processed foods- trans fats ( will induce excessive bile release) and refined sugars
3) Chew slowly and thoroughly until food is liquid
4) Diaphragmatic breathing- massages the liver and increases bile production
5) Taurine and choline foods (Bile components) - seaweed, scallops, salmon, chicken, kidney beans, broccoli, quinoa, eggs
6) Support liver detoxification with cruciferous veg and fibre
Which choleretic - rich foods and herbs may increase bile production?
Radish, cucumber, melon, onion, kidney beans, apple cider vinegar, gentian, artichoke leaf, barberry, dandelion root
Which cholagogue rich foods and herbs may increase the release of bile?
Apples, artichokes, beets, bitter greens, celery, fennel, , milk thistle, turmeric, ginger, dandelion greens, fenugreek
What is the mucosal barrier and what is its composition?
The mucus covering the entire GIT, providing a thick barrier between the immune stimulating contents of the outside world and the immune cells of the gut wall (1st line of defence) . It can also provide an adhesion site/ nutrient source for commensal bacteria.
- composed of 96-98% water, glycoproteins called mucins, IgA (made by epithelial cells to create barrier to prevent overactive immune response), and anti- microbial peptides
How can a disturbed mucosal barrier lead to metabolic endotoxemia?
Low mucosal integrity can be associated with bacterial translocation, leakage of LPS and too much cross talk coming through the thin mucosal barrier, leading to low grade inflammation and metabolic endotoxemia
How can you support the mucosal barrier?
1) optimise dietary fibre to feed the bacteria so they don’t eat your mucins
2) Increase polyphenols to feed commensal bacteria including important Akkermansia spp. and protect mucin lining- green tea, blueberries, cranberry, blackcurrants, pomegranates
3) Include mucopolysaccharides such as slippery elm, marshmallow root, flaxseeds and liquorice
Why is it important to decrease intestinal tight junction permeability?
Intestinal tight junction disassembly can increase LPS load and excessive immune reactions
How can you naturally support the intestinal epithelial barrier (tight junctions) ?
1) Glutamine - supplemented or cabbage juice, spirulina, asparagus
2) Zinc carnosine
3) vitamin A
4) N acetyl glucosamine
5) Bone broth (rich in glycine)
Name a test which would indicate intestinal permeability
Zonulin may be present in a stool test. Present when gap junctions are open so indicates intestinal permeability
What is metabolic endotoxemia?
When too many lipopolysaccharides (LPS) (found on outer cell wall of bacteria) end up in our system and trigger an inflammatory response. This is linked to chronic diseases including autoimmune and diabetes
What is secretory IgA and what is its role?
- A non specific immunoglobulin that resides in the mucosal lining and protects the intestinal epithelium from toxins and pathogens by ‘immune exclusion’ .
- It communicates with macrophages and promotes clearance of antigens by blocking their access to epithelial receptors.
- Plays a role in immune tolerance by ‘tagging’ microbes
What can cause low SIgA and what risk can this pose?
-Low SIgA can be caused by chronic stress, NSAIDS and antibiotics.
- This increases the risk of GI infections including SIBO as in combination with a compromised mucosal barrier, pathogens can get in quicker and deeper.
How can you increase SIgA?
-Address stress
- saccharomyces boulardii (non pathogenic yeast)
- Vitamin A- needed to transport SIgA over the mucosal lining
- Vitamin D3- can upregulate SIgA expression
- polyphenols (green tea, pomegranate, cranberries)
- Chlorella and spirulina
- Probiotics and prebiotics
Which are the first foods to remove in an elimination diet?
Gluten, dairy, corn, soy, eggs, nuts, beef, pork, yeast, citrus, nightshades, chocolate and coffee
In the 5R protocol, discuss step 1 REMOVE
1) Remove dietary irritants ie processed foods, caffeine, sugar, alcohol, trans fats
2) Personalise diet, remove food allergens and intolerances eg dairy, gluten, low histamine diet, specific carbohydrate diet etc
3) Avoid toxins (pesticides, plastics, unfiltered water, chemicals in beauty products) and unnecessary drugs inc NSAIDS which can damage the GI mucosa
4) Eliminate pathogenic bacteria viruses, fungi and parasites using antimicrobials specific to the infection. Including berberine, oregano, garlic, neem, grapefruit seed extract, nano silver, elderberry
In the 5R protocol, discuss step 2 REPLACE
Replace digestive secretions that may be lacking -
- Stomach acid secretions (bitters, betaine HCL)
- Pancreatic support (Bitters, pancreatic enzymes, less frequent meals)
- Bile support (choleretics and cholagogues)
In the 5R protocol, discuss step 3 REINOCULATE
- Probiotics - fermented foods (saurkraut, kimchi, kefir) and supplements (lactobacillus and bifidobacterium spp.)
- Prebiotics to feed the good bacteria. Foods rich in fructooligosaccharides (FOS) and inulin eg chicory, leeks, onions, artichokes but not in case of low fodmap which takes these out and SIBO
In the 5R protocol, discuss step 4 REPAIR
Regeneration of the GIT mucosa.
- Support mucous barrier using demulcents such as slippery elm, marshmallow root, liquorice. polyphenols to feed commensal keystone bacteria
- Support tight junctions of the epithelium - L-glutamine in cabbage juice and asparagus, vitamin A , Zinc, EFAs, N-aceytl glucosamine, bone broth, collagen, aloe vera
- Increase SIgA where needed- saccharomyces boulardii, A, D, zinc
In the 5R protocol, discuss step 5 REBALANCE
How did the client get to this point and how can we get them back?
- Address stress. Nervines, adaptogens eg passionflower, ashwagandha, breathing exercises.
- Practise good sleep hygiene- migrating motor complex happens overnight
- undertake regular exercise
In the case of parasites or worms, how would you adapt the 5R protocol?
A second phase of antimicrobials may be needed to prevent eggs rehatching. Either 10 days on, 10 days off then repeat or hold out the treatment for a whole 4 weeks
What is ‘dysbiosis’?
An imbalance in the colonies of the bowel microflora, leading to a disruption in systemic and local health.
Discuss the aetiology of dysbiosis
1) Poor diet - highly processed, refined carbs, low fibre, low polyphenols
2) Medications- Antibiotics will upset colonies/ antacids/ OCP
3) Chronic stress can decrease digestive secretions
4) Low digestive secretions eg HCL, bile
5) C-section, non breastfed (breastmilk includes sugars for microbes)
