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Nutrition 2 (Semester I) > 5. GI Health > Flashcards

5. GI Health Flashcards

1
Q

What is hypochlorhydria?

A

Low stomach acid
Characterised by gastric pH above 3

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2
Q

What are the key signs/symptoms of hypochlorhydria?

A

Gas/bloating (less than 30 mins after eating)
Nutrient deficiencies (Fe, Zn, B9, B12)
Heartburn
Feeling of fullness
Foul smelling stools
Diarrhoea

Nausea after taking supplements
Food allergies
Brittle nails

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3
Q

What are the implications of hypochlorhydria?

A

Reduced mineral absorption (Ca, Fe)
Poor protein digestion = SI protein putrefaction
Reduced protection from bacterial infection (H. pylori in stomach, SIBO in SI
Poor pancreatic juice and bile flow
Less IF = reduced B12 absorption

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4
Q

Natural approach to hypochlorhydria

A

Chew thoroughly
Avoid overeating
Avoid drinking with meals
ACV (1-2 tsp) in water before meals
Zn/B6 rich foods
Bitter foods - rocket, dandelion leaf, watercress
Bitter herbs - dandelion, gentian
Herbs - fennel seed, cardamom, citrus peel

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5
Q

What is exocrine pancreatic insufficiency (EPI)?

A

Deficiency of exocrine pancreatic enzymes needed to maintain normal digestion

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6
Q

What does exocrine pancreatic insufficiency (EPI) lead to?

A

Nutrient (esp fat) malabsorption

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7
Q

Common signs/symptoms of exocrine pancreatic insufficiency?

A

Bloating/belching/flatulence (1-2hrs after food)
Greasy/floating stools
Drowsiness after meals
Food intolerances
Low Zn/B12/B9 absorption
Symptoms of IBS/candidiasis/SIBO

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8
Q

What can cause exocrine pancreatic insufficiency?

A

Chronic stress - reduced Vagus nerve activity
Hypochlorhydria - reduced CCK stimulation
Damaged SI wall - Coeliac, IBD
Chronic diseases - cystic fibrosis, pancreatitis, DM
Xenobiotics - can inactivate pancreatic enzymes
SIBO - can conjugate pancreatic enzymes
Dysbiosis

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9
Q

Natural approach to exocrine pancreatic insufficiency

A

Chew thoroughly
Avoid overeating
Avoid snacking between meals
Correct stomach acid levels - bitters
Stimulate Vagus nerve to activate PSNS
Deep breathing, gargle, hum
Pancreatic enzyme replacement therapy

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10
Q

What types of pancreatic enzyme replacement therapies are there?

A

Animal-derived
Plant-based

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11
Q

What are animal derived PERTs made from?

A

Pork

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12
Q

Benefits of plant based PERT over animal derived

A

Better acid stability
Broader range of enzymes
Wider pH range
Suitable for veggies/vegans/Jewish/Islamic

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13
Q

When to take pancreatic enzymes

A

Start of meals
Add during the meal depending on meal size/duration

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14
Q

What is bile insufficiency?

A

A condition where bile synthesis or bile flow is compromised
(affects ability to digest, absorb and utilise fatty acids from diet)

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15
Q

What are the signs/symptoms of bile insufficiency?

A

Pale, fatty stools
Constipation
Diarrhoea
Intolerance to fatty foods/nausea when eating
Bloating
Excess flatulence
Cramping

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16
Q

What indicators for bile insufficiency would be found on a stool test?

A

Low/absent bile acids
High faecal fats
(indicates fat malabsorption)

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17
Q

Common causes of bile insufficiency

A

Low dietary fat intake
Impaired liver function
Obesity
Oestrogen dominance - increased liver production of cholesterol which thickens bile and also slows oestrogen excretion
Low HCl - reduces CCK and bile release
Gall bladder removal
Coeliac disease
Crohn’s disease
Chronic pancreatitis
SIBO

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18
Q

What are the implications of long-term bile insufficiency?

A

Deficiency of fat-soluble nutrients
Hormone imbalances
Compromised liver detoxification
SIBO/dysbiosis (bile has antimicrobial effects)
Hypercholesterolaemia
Gallstones

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19
Q

Natural approach to bile insufficiency

A

Adequate hydration
Avoid processed food, trans fats, refined sugar
Chew slowly and thoroughly until food is liquid
Diaphragmatic breathing - massages liver, increases bile production
Increase taurine and choline-rich foods
Support liver detoxification
Consume choleretic and cholagogue foods and herbs

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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 immune cells in the gut wall

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21
Q

What is the mucosal barrier made up of?

A

Water
Mucins
IgA
Anti-microbial peptides

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22
Q

What does the mucosal barrier provide an adhesion site for?

A

Commensal bacteria

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23
Q

What can disturbed mucosal barrier lead to?

A

Bacterial translocation
Leakage of LPS
Metabolic endotoxaemia

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24
Q

Natural approach to supporting the mucosal barrier

A

Optimise dietary fibre (to feed the bacteria)
Diet rich in polyphenols (feeds commensal bacteria, protects mucin lining, reduces inflammation)
Mucopolysaccharides - slippery elm, marshmallow root, liquorice, flaxseeds, seaweed

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25
Q

What does intestinal tight junction disassembly lead to?

A

Increased LPS load
Excessive immune reactions

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26
Q

Natural approach to supporting the intestinal tight junctions

A

Glutamine
Zinc carosine
Vit A
NAC
Bone broth (rich in glycine)

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27
Q

How can intestinal permeability be tested?

A

Stool test (Zonulin)
Serum antibodies (Cyrex Labs Array 2)

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28
Q

What is secretory IgA?

A

Resides in mucosal lining
Protects intestinal epithelium from toxins and pathogenic microbes through immune exclusion

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29
Q

What is immune exclusion?

A

SIgA promoting the clearance of antigens by blocking their access to epithelial receptors

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30
Q

What does low SIgA increase the risk of?

A

GI infections including SIBO

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31
Q

What can low SIgA be caused by?

A

Ongoing emotional/physical stress
NSAIDs
Antibiotics

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32
Q

How can we increase SIgA?

A

Address stress
Vit A (transport of SIgA over mucosal lining)
Vit D (upregulates SIgA expression)
Probiotics
Prebiotics
Saccharomyces boulardi
Mushrooms
Echinacea spp

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33
Q

What can an elimination diet be used for?

A

Identifying a food allergy or intolerance

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34
Q

What sorts of foods can cause reactions?

A

Gluten
Dairy
Corn
Soy
Eggs
Nuts
Beef
Pork
Yeast
Citrus
Nightshades
Chocolate
Coffee

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35
Q

What are the stages of an elimination diet?

A

Detox - days 1-2
Elimination - days 3-14
Reintroduction - days 15 onwards

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36
Q

What does stage 1 of an elimination diet involve?

A

Detox
Increase fruits, vegs, GF whole grains, healthy fats, water
Remove processed foods, confectionary, additives, caffeine, alcohol

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37
Q

What does stage 2 of an elimination diet involve?

A

Elimination
As per the detox and remove all suspected foods for 2 weeks (can be done one at a time

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38
Q

What does stage 3 of an elimination diet involve?

A

Reintroduction
Eat the suspect food 2-3 x/day for 1-3 days
If symptoms appear, remove the food again and wait for symptoms to disappear before trying the next suspect food
If a food causes a reaction, keep out of diet for 3 months
Need to also heal the gut

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39
Q

What are the stages of the 5R protocol?

A

Remove
Replace
Repopulate
Repair
Rebalance

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40
Q

What does the Remove stage of the 5R protocol involve?

A

Removing dietary irritants
Removing food allergens/triggers
Avoiding toxins
Avoiding unnecessary drugs/supplements
Removing potentially pathogenic bacteria, parasites etc

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41
Q

What does the Replace stage of the 5R protocol involve?

A

Replace digestive factors that may be lacking: Stomach acid secretions (bitters, reduce stress)
Pancreatic enzymes (bitters, enzymes)
Bile support (cholerectics, cholagogues)

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42
Q

What does the Repopulate stage of the 5R protocol involve?

A

Repopulating microbiome with probiotics and prebiotics

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43
Q

What does the Repair stage of the 5R protocol involve?

A

Repairing gut mucosa
Tight junction support
Supporting the mucosal barrier
Increasing SIgA
Reducing inflammation

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44
Q

What does the Rebalance stage of the 5R protocol involve?

A

Paying attention to lifestyle choices
Address stress
Sleep hygiene
Regular exercise

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45
Q

Does the 5R protocol have to be done in the same order each time and same duration?

A

No - depends on your case
Food intolerances - need to Repair gut before reintroducing (6 weeks)
Deficient microbiome (4 weeks)
SIBO/dysbiosis (4 weeks)
Parasites/worms - may need 2nd lot of antimicrobials before Repopulating

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46
Q

What is dysbiosis?

A

An imbalance in the colonies of bowel microflora

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47
Q

What can cause dysbiosis?

A

Poor diet - high in processed food, refined sugars, low in fibre
Intestinal/oral infections
Medications - antibiotics, OCP, antacids
Chronic stress
Low digestive secretions
C section

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48
Q

What can dysbiosis lead to?

A

Potential disruption in both local and systemic health
Atopic diseases
Metabolic syndrome
Colorectal cancer
Neurodegenerative diseases

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49
Q

Why can dysbiosis lead to atopic diseases?

A

C section infants with formula milk = lower levels of Bifidobacteria and Lactobacilli

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50
Q

Why can dysbiosis lead to metabolic syndrome?

A

Associated with less Bifidobacteria and Akkermansia
Increased E coli
Increased Firmicutes to Bacteroidetes ratio

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51
Q

Why can dysbiosis lead to colorectal cancer?

A

Low fibre diets increase pathogenic bacteria like E coli, Campylobacter spp

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52
Q

Why can dysbiosis lead to neurodegenerative diseases?

A

AZD, Parkinson’s, MND sufferers often have increased pro-inflammatory bacterial species
Periodontal pathogens - P. gingivalis also associated with AZD

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53
Q

What is metabolic endotoxaemia?

A

Subclinical rise in bacterial LPS
Results in low grade inflammation

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54
Q

Which conditions is metabolic endotoxaemia associated with?

A

CVD
DM
AI
Degenerative disorders

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55
Q

What are LPS?

A

From the cell walls of gram negative bacteria

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56
Q

What GI dysfunctions can lead to an increase in LPS?

A

Dysbiosis
Mucosal degradation
Permeability of tight junctions

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57
Q

What do LPS do?

A

Interact with toll-like receptors (TLR4) in the immune system
Triggers the production of pro-inflammatory cytokines

58
Q

What type of diets can increase LPS transport across the intestinal membrane?

A

High fat
Keto

59
Q

Natural approach to metabolic endotoxaemia

A

Remove (5R)
Avoid Western or keto diet
Increase dietary fibre (bind and clear LPS - and to feed bacteria)
Focus on rainbow of colour to feed beneficial bacteria
Repopulate (5R)
Repair (5R)
Support liver/bile function - cruc, NAC, milk thistle
Breathing techniques
Cold showers/swimming

60
Q

What is SIBO?

A

Overgrowth of non-pathogenic bacteria in SI

61
Q

What are the main symptoms of SIBO?

A

Bloating (higher up)
Abdominal pain/discomfort
Constipation
Diarrhoea
Flatulence

62
Q

What are other symptoms of SIBO?

A

Nausea
GORD
Excessive burping
Prolonged feeling of fullness
Malabsorption
Insomnia
Brain fog

63
Q

What does hydrogen dominant gas in SIBO cause?

A

Diarrhoea

64
Q

What does methane dominant gas in SIBO cause?

A

Constipation

65
Q

What are the key clinical indicators of SIBO?

A

Worsening of GI symptoms from probiotics
Worsening of GI symptoms from fibre
Chronic GI symptoms following long term meds
Chronic low ferritin/Fe with no other cause
Developing IBS following GI infection
Coeliac not improved following GF diet

66
Q

What are the main causes of SIBO?

A

Hypochlorhydria (see reasons for that)
Low SIgA (see reasons for that)
Prolonged stress (shuts off MMC, lowers SIgA/HCl)
Scar tissue
Hypothyroidism (slows motility)
Poor oral health
Ileocaecal valve dysfunction
Opioids/antibiotics
Acute gastroenteritis

67
Q

How does acute gastroenteritis cause SIBO?

A

Food poisoning
Bacteria release a toxin (CDT)
A part of the CDT resembles nerve cells in the SI called interstitial cells of Cahal (ICC)
ICC are responsible for the MMC
Through AI process of molecular mimicry, ICC gets damaged, affecting the MMC
Results in SIBO

68
Q

Why can SIBO lead to food sensitivities?

A

SIBO can damage villi
This reduces enzymes like lactase and diamine oxidase (DAO)
Leads to lactose intolerance
Leads to histamine intolerance

69
Q

Natural approach for SIBO

A

Restricting carbs for the bacteria to feed off
Low FODMAP and/or SCD
Anti-microbials to kill off bacteria
Bitters at start of meals
MMC support - fasting, prokinetics before bed, mindful eating, diaphragmatic breathing
Repopulate microflora
Lion’s Mane - promotes regeneration of GI mucosa
Visceral manipulation for IC valve

70
Q

What is a biofilm?

A

Extracellular matrix protecting bacteria and fungus from our immune system

71
Q

When should you consider using biofilm disruptors?

A

If anti-microbial or dietary changes aren’t working to remove SIBO

72
Q

Examples of biofilm disruptors

A

Allicin
Curcumin
NAC
Berberine
Serrapeptase

73
Q

Examples of anti-fungal agents

A

Coconut oil
Berberine
Oregano oil
Thyme
Rosemary
Allicin

74
Q

What is candidiasis?

A

Fungal infection caused by Candida albicans
Commensal yeast
Inhabits mucosal surfaces

75
Q

Why is candidiasis usually asymptomatic?

A

Candida usually kept under control by native bacteria and immune defences

76
Q

Where are candida infections usually found?

A

Mouth
Genitals
Skin

77
Q

What are the signs and symptoms of candidiasis?

A

Digestive symptoms i.e. bloating
Sugar cravings
Joint pain
Food sensitivities
Frequent UTIs
Fatigue
Anxiety
Brain fog
Skin/nail fungal infections

78
Q

What is the pathophysiology of candidiasis?

A

Disruption to the host bacterial environment or immune dysfunction which allows opportunistic candida to proliferate
C. albicans can then penetrate epithelial cells and switch from commensal to pathogenic

79
Q

What are the risk factors for candidiasis?

A

Antibiotics
Low immunity (reduced SIgA)
Chronic stress (increased cortisol)
Reduced digestive secretions
High sugar intake
Dysbiosis

80
Q

How can candidiasis be tested?

A

Stool test (mycology culture)
OAT (elevated arabinose)
Saliva (candida antibodies
Blood (circulating candida antigens)

81
Q

Natural approach to candidiasis

A

Optimise elimination and detoxification
Remove sugar from diet + gluten, dairy
Incorporate anti-fungals and address biofilms
Address risk factors
Support microbiome
Restore nutrient deficiencies (derived from testing)

82
Q

What are gallstones?

A

Small stones, usually formed from cholesterol, that form in the gallbladder

83
Q

What can cause gallstones?

A

Chemical imbalance in bile composition resulting in either excessive cholesterol concentration or a deficiency of substances that keep cholesterol in solution (bile salts, phospholipids)

Bile stasis or delayed gallbladder emptying due to reduced bile motility

84
Q

Natural approach to gallstones

A

Increase fibre
Reduce refined sugar, trans fats, saturated fats, alcohol
Consume choleretic and cholagogue foods/herbs to support bile flow
Weight loss in obese individuals
Increase polyunsaturated fats - oily fish
Peppermint - to dissolve stones

85
Q

Risk factors for gallstones

A

5Fs - Fat, Female, Forty, Fair, Fertile
Obesity
Women
HRT
OCP
Western diet
Sedentary lifestyle
High alcohol
DM

86
Q

What is a peptic ulcer?

A

Ulcer in stomach or duodenum
Characterised by breakdown of the mucosal barrier and wall of GIT by HCl

87
Q

Signs/symptoms of a peptic ulcer

A

Epigastric pain (may radiate to back)
Gnawing pain between meals
Nausea
Vomiting
Reduced appetite
Dyspepsia

88
Q

Complications of a peptic ulcer

A

GIT bleed
Peritonitis (perforation)

89
Q

What are the red flags for a peptic ulcer?

A

Sudden, sharp worsening abdominal pain
Vomiting blood
Black, tarry stools

90
Q

Risk factors for a peptic ulcer

A

Stress - vasodilation and inadequate blood supply which interferes with mucus production
H. pylori - low gastric output
NSAID use - disrupts mucosal barrier
Smoking/caffeine/alcohol - damages the mucosa

91
Q

Natural approach to peptic ulcers

A

Avoid alcohol, fizzy drinks, spicy foods, caffeine
Avoid NSAIDs
Increase fibre - slows gastric emptying
Address stress - nervine teas
Support mucosal barrier - slippery elm, cabbage juice, turmeric, aloe vera juice, liquorice
Identify and address H. pylori

92
Q

What does cabbage juice contain that makes it good for peptic ulcers?

A

Vit C
Substance U
(stimulates mucin production)

93
Q

What is H. pylori?

A

Infection of stomach associated with peptic ulceration, chronic gastritis, gastric cancer

94
Q

How does H. pylori infect the stomach?

A

Burrows through protective mucus layer with its corkscrew shape, into the stomach lining
Causes inflammation by secreting cytokines and enzymes which damage the mucosal barrier

95
Q

Examples of enzymes secreted by H. pylori

A

Protease
Phospholipase
Urease
(releases ammonia)

96
Q

Natural approach to H. pylori

A

Saccharomyces boulardii - increases SIgA, inhibits colonisation and adhesion
Mastic gum - anti-bacterial
Liquorice - inhibits H. pylori protein synthesis
Cinnamon - inhibits urease
Curcumin - inhibits H. pylori growth

97
Q

Most common symptom of GORD

A

Heartburn

98
Q

What happens during GORD?

A

Relaxation of lower oesophageal sphincter

99
Q

Risk factors for GORD

A

Obesity/pregnancy - increased abdominal pressure
Hiatus hernia
Large amounts of fatty foods
Spicy food
Carbonated drinks
Alcohol
Coffee
Peppermint, tomatoes, chocolate - relax LOS
Smoking
Stress/anxiety
Meds - NSAIDs, nitrates, Ca channel blockers

100
Q

Natural approach for GORD

A

Avoid trigger foods/drinks
Med diet - shown to be protective
Increase fibre to avoid straining
Slow down, chew food thoroughly, eat mindfully, don’t overeat or too late
Avoid lying down post meal
When sleeping raise head
Address stress/anxiety
Visceral manipulation of hiatus hernia
Consider testing for H. pylori
Consider low stomach acid test
(fermentation of digested food leads to gas in stomach)
Support mucosal barrier

101
Q

What are the most common gluten-related disorders?

A

Coeliac disease (AI)
Wheat allergy (allergic)
Non-coeliac gluten sensitivity

102
Q

Proteins in gluten that cause symptoms

A

Gliadins
Glutenins

103
Q

What is a wheat allergy?

A

An IgE-mediated allergic response due to exposure to wheat
Can develop within minutes to hours

104
Q

Who is more commonly affected by a wheat allergy?

A

Children

105
Q

Signs/symptoms of a wheat allergy

A

Irritation/swelling of mouth/throat
Hives
Itchy rash
Nasal congestion
Headache
Nausea
Vomiting
GORD
Anaphylaxis

106
Q

What are people with a severe wheat allergy likely to carry?

A

EpiPen

107
Q

What is Coeliac disease?

A

Autoimmune condition where the body’s immune system attacks its own mucosa tissue in the SI in response to ingestion of gluten

108
Q

How many people are affected by Coeliac disease?

A

1 in 133

109
Q

What are the symptoms of Coeliac disease?

A

Abdominal pain
Nausea
Vomiting
Diarrhoea
Fatty stools
Fatigue
Weight loss
Malnutrition
Osteoporosis

110
Q

What are the complications from Coeliac disease?

A

Malabsorption - B12, B9, Fe, Ca
Osteoporosis
Anaemia

111
Q

What is the pathophysiology of Coeliac disease?

A

Gliadin in gluten is modified by tTG, an enzyme found in the mucosa of the SI
This modification allows it to be presented to the immune system
Immune system mistakenly identifies gliadin as foreign
Antigen presenting cells target gliadin and produce an inflammatory response that produces autoantibodies that damage the villi, causing atrophy
Zonulin also upregulated - dissembling tight gut junctions

112
Q

How is Coeliac disease tested?

A

Blood test - IgA anti-tissue transglutaminase (tTG) antibodies
Blood or saliva test - HLA-DQ2 or HLA-DQ8 genes
Duodenal biopsy

113
Q

Natural approach for Coeliac disease

A

Gluten free diet
Address nutritional deficiencies
Repair intestinal barrier

114
Q

Why might a gluten-associated cross-reactive foods and foods sensitivity panel be useful in Coeliac disease?

A

Some grains and food contain proteins similar to gluten which may also need to be avoided

115
Q

What is non-coeliac gluten sensitivity (NCGS)?

A

The development of GI and extra-intestinal symptoms upon gluten ingestion in people not affected by coeliac disease or wheat allergy

116
Q

Signs/symptoms of NCGS?

A

Bloating
Abdominal pain
Diarrhoea
Nausea
GORD
Constipation
Tiredness
Headache
Brain fog
Joint pain
Anxiety
Depression

117
Q

What is the pathophysiology of NCGS?

A

Innate immunity
Gliadin causing release of zonulin from intestinal mucosa
Induces tight-junction disassembly and increase in gut permeability

118
Q

How can NCGS be diagnosed?

A

Resolution of symptoms when gluten is removed
Relapse of symptoms with gluten exposure

119
Q

What can the Cyrex Array 3 test for (Wheat/Gluten Proteome Reactivity and Autoimmunity)?

A

Reactions to other non-gluten proteins in wheat

120
Q

Examples of ‘unusual’ foods that may contain gluten

A

Sausages
Soy sauce
Malt vinegar

121
Q

What is IBS?

A

Umbrella diagnosis for chronic GI symptom when specific conditions have been ruled out

122
Q

Key symptoms of IBS

A

Abdominal pain/cramping relieved by passing a stool
Diarrhoea or constipation or both
Bloating
Flatulence
Incomplete emptying of bowels

123
Q

What could be the underlying causes of IBS?

A

Stress
Dysbiosis
SIBO
Candidiasis
Lactose intolerance
NCGS

124
Q

Natural support for diarrhoea

A

Increase soluble fibre to bulk out stool i.e. apple pectin
Digestive enzymes
S. boulardii - increase SIgA
Electrolyte replacement
Marshmallow root, slippery elm

125
Q

Natural support for constipation

A

Increase dietary fibre
Hydration
Magnesium citrate
B5/ginger - increase peristalsis
Psyllium husk/ground flaxseed
Prunes/figs

126
Q

What is inflammatory bowel disease?

A

Group of AI conditions of the SI and colon

127
Q

What are the principle types of IBD?

A

Crohn’s disease
Ulcerative colitis

128
Q

Key symptoms of IBD

A

Abdominal pain
Diarrhoea
Urgency to pass stools
Rectal bleeding
Weight loss
Fatigue (blood loss/malabsorption)

129
Q

Key complications of IBD

A

Colorectal cancer
Osteoporosis
Anaemia

130
Q

Which region of the GIT does Crohn’s affect?

A

Any but mostly terminal ileum

131
Q

Which regions of the GIT does UC affect?

A

Colon
Rectum

132
Q

How does Crohn’s distribute in the GIT?

A

Skip lesions

133
Q

How does UC distribute in the GIT?

A

Continuously

134
Q

Which layers of the GIT does Crohn’s affect?

A

All layers
(transmural)

135
Q

Which layers of the GIT does UC affect?

A

Mucosa

136
Q

Key symptoms of Crohn’s

A

Abdominal pain (right side)
Loose stools

137
Q

Key symptoms of UC

A

Abdominal pain (left side)
Bloody diarrhoea

138
Q

What is the pathophysiology of IBD?

A

Interaction between a genetically susceptible individual + environmental factors which have an impact on gut microbiota
Triggers aggressive T-cell responses

139
Q

What are the bacterial patterns commonly seen in IBD?

A

Low Akkermansia, increased R. gnavus/R. torques (mucus degradation)
Increased gram negative bacteria (which increases immune response)
Lack of commensal bacteria diversity (esp. SCFAs)

140
Q

Triggers for IBD

A

Medications (NSAIDs, OCP, antibiotics)
Smoking
Stress
Infections
Poor diet (low fibre/O3; high refined sugars)

141
Q

Natural approaches for IBD

A

Remove inflammatory foods/drinks/problematic foods
Consider SCD/low FODMAP
Easy to digest foods - soups, stews
Green juices - chlorophyll rich, anti-inflammatory
Vit D - tight junctions, mucosal inflammation, supports immune system
Fish oils - anti-inflammatory
Support mucosal and epithelial barrier
Ginger, turmeric, quercetin, chamomile - anti-inflammatory
Probiotics
Prebiotics
Address nutrient deficiencies

Nutrition 2 (Semester I) (15 decks)

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