Digestion (week 2)

Question 1

Digestive Dysfunction

Answer 1

Overtly Digestive Complaints:
-gas
-bloating
-constipation
-heartburn
-diarrhea

Commonly related complaints:
-acne, eczema, skin conditions
-environmental allergies
-fatigue
-hormonal imbalance
-chronic inflammatory conditions
-autoimmune disease
-joint pain
-mental health challenges

Question 2

Digestive Dysfunction - the brain

Answer 2

the brain = northernmost point of the digestive process

sympathetic dominance:
-eating on the go, less chewing
-reduced saliva
-signals to increase gastric secretions are inhibited

encourage clients to balance sympathetic and parasympathetic tone before eating:
-sit down, take deep breaths, admire the food, put away devices, chew well, practice gratitude

Question 3

Digestive Dysfunction - the mouth

Answer 3

chewing:
-20-30 times per bite
-initial breakdown of food into smaller parts
-sends messages to brain and digestive organs: “food incoming, get ready”

salivary amylase and lingual lipase begin initial breakdown of carbohydrates and fats
-inadequate mechanical or chemical breakdown (chewing and saliva) can leave undigested food further down the chain
-feeds opportunistic microorganisms (candida, dysbiosis)

Question 4

Stomach dysfunction: Hypochlorhydria (low stomach acid)

Answer 4

Hydrochloric acid:
-too little = hypochlorhydria
-too much = hyperchlorhydria

Upper GI health is also about the context surrounding HCL production:
-where (reflux)
-when (empty stomach)
-what (what is driving it)

Question 5

Stomach dysfunction: Hypochlorhydria (low stomach acid)

Answer 5

Immune: predisposes someone to infections from food born and environmental microbes

Absorption: many vitamins and minerals are bound to proteins- HCL and pepsin help liberate. EX: B12, iron

Signaling: impaired north to south function impaired, cascading dysfunctions result in slow moving, poorly digested food feeding microbial populations

Question 6

Stomach dysfunction: Hypochlorhydria (low stomach acid)

Answer 6

Risk factors:
-age
-stress and fatigue
-nutrient deficiencies
-smoking and alcohol consumption
-food allergies, hypersensitivities, or intolerances
-low protein diets
-bariatric surgeries
-aid blocking medications
-H Pylori infection (hypo and hyper)

Question 7

H. pylori bacteria and Peptic Ulcer

Answer 7

~67% of humans have H. pylori normally - not associated disease

overgrowth can cause gastric ulcers

stomach acid & H. pylori:
-low stomach acid increases risk of overgrowth
-early/acute infections increases stomach acid
-long term infection decreases stomach acid, malabsorption

peptic ulcer - exacerbated by pepsin

can contribute to malabsorption, protein putrefaction, and lower levels of mood and metabolic-regulating amino acids

-acid blockers/antacids commonly used with antimicrobial therapy to reduce the H pylori populations

Question 8

Stomach dysfunction: Hyperchlorhydria

Answer 8

aka chlorhydria

pH of stomach is lower than the standard range (less than 2.0), especially outside of meals

context matters: timing, tissues, and conditions

contributing factors:
-stress
-increased histamine
-certain medical conditions
-H pylori infection

Leads to damaged mucosal membranes:
-gastritis (inflammation)
-esophageal or duodenal injury
-ulcers
-GERD
-GI bleeding

Question 9

Acid Reflux, Heartburn, and GERD

Answer 9

terms are often used interchangeably, but differ

Reflux: the movement of acid into the esophagus

Heartburn: the associated symptoms, pain and burning

GERD: gastroesophageal reflux disease

Question 10

LES function

Answer 10

Weakening of lower esophageal sphincter (LES):
-atrophy
-intra-abdominal pressure
-inversion
-hiatal hernia
-inflammation
-transient relaxants
-medications: antihistamine, pain relievers, antidepressants, sedatives, and some blood pressure medications
-damage to the vagus nerve
-stress
-hypo/hyper stomach acid production

Question 11

Low Stomach Acid and LES Function

Answer 11

low stomach acid levels:
-reduced signal to tighten LES
-delayed gastric emptying
-reduced signal for enzymatic secretions
-foods not broken down as well/fast = increases pressure in stomach

even if the pH is suboptimal for digestion, it can erode the tissue in the esophagus and drive inflammation

the LES itself gets the signal to tighten, in part, by an acidic pH in the stomach

Question 12

Acid Reflux & Heartburn

Answer 12

Heartburn: sensation of burning in the chest and throat
Other symptoms:
-sour taste, regurgitation, difficulty swallowing, lump in throat, sore throat, cough, postnasal drip, hoarseness, general indigestion (bloating, excessive burping, feeling overly full)

Hypo/hyperchlorhydria can overlap
-Hyper: may produce more severe heartburn and changes in esophageal tissue
Hypo: may be less painful or even silent

excessive and ongoing contact of gastric juices with esophagus and tissues in the throat can increase risk for cancer and other serious conditions and needs to be addressed

Question 13

Gastroesophageal Reflux Disease (GERD)

Answer 13

GERD:
-severe form of acid reflux
-occurs more than twice per week
-damage to esophagus has occurred

Symptoms:
-more advanced acid reflux
-bad breath, damage to dental enamel, persistent dry cough, hoarse voice, asthma, frequent respiratory infections, difficulty swallowing, regurgitation, chest pain
-if left untreated, ulcers, esophageal bleeding, cancer

risk factors:
-overweight, hiatal hernia, smoking, alcohol consumption, medication use
-common in pregnancy

Question 14

Gastroesophageal Reflux Disease (GERD)

Answer 14

medically treated with acid blockers to stop production and/pr acid reducers that neutralize acid + antibiotics if H. pylori is present

Natural approaches aim to:
-strengthen mucosal lining
-improve LES function
-increase parasympathetic tone
-avoid food allergies, hypersensitivities and intolerances
-increase nutrient density
-support commensal bacteria populations
-support the optimal production of HCL or supplement
-investigative common triggers: alcohol, coffee, spicy foods, fatty or greasy foods, tomatoes, sugar, chocolate

Question 15

Stomach Dysfunction: Gastroparesis

Answer 15

Diagnostic criteria: more than 10% of stoach contents remain after 4 hours

Poor upper GI function + extended time in stomach can result in stomachache, bloating, reflux

Maldigested foods:
-protein - putrefy
-carbs - ferment
-fats - rancidify

underlying mechanisms and risk factors

vagal nerve damage or dysfunction

diabetes = increased risk for gastroparesis

stress: ineffective communication via vagus nerve

large amounts of fat and protein trigger CCK, which slows gastric emptying. some is good, too much is not

pH:
-hypochlorhydria: impaired signaling north to south
-hyperchlorhydria: acidic chyme in duodenum can trigger pyloric valve to shut and slows emptying
-inflamed duodenum = reduced secretin and bicarbonates = damage to duodenal tissue

medications that impact motility: opioids, antidepressants, blood pressure meds, allergy meds

Question 16

Digestive Dysfunction: the pancreas

Answer 16

Review:
1. chyme enters the duodenum
2. mechanical and chemical cues release secretin and CCK
3. tells exocrine cells of pancreas to bicarbonate and pancreatic enzymes

Poor regulation of cascade = increased risk for inflammation, dysbiosis, indigestion

Generalize suboptimal pancreatic function and indigestion vs Exocrine pancreatic insufficiency

Question 17

Digestive Dysfunction: the liver and gallbladder

Answer 17

Bile = emulsify fats
-thickening of the bile and./or reduced emptying of bile can lead to gallbladder inflammation, stones, and lipid/fat indigestion

Bile acts as an antimicrobial for small intestine

removes toxins and metabolic waste

Nutrients needed for bile production:
-water
-cholesterol
-phospholipids
-bile acids
-amino acids
-bilirubin
-cofactor nutrients (Vit C, electrolytes, minerals)

Question 18

Digestive Dysfunction: Biliary Stasis

Answer 18

Contributing Factors:
-physical obstruction
-blood sugar regulation: association between impaired bile excretion and type 2 diabetes and metabolic disorders
-low fat diets = reduces CCK = reduces the signal for gallbladder to contract (ex: low fat weight loss diets)
-trans fatty acids / hydrogenated oils
-cholesterol: bile is one of several ways to maintain cholesterol homeostasis. the majority of gallbladder stones are composed of solidified cholesterol
-elevated bilirubin levels
-hormones, ex: elevated estrogen and estrogen dominance

Question 19

Liver/Gallbladder Dysfunction

Answer 19

-pain in right side of abdomen
-chronic biliary stasis can lead to gallbladder stones, severe inflammation, pain and illness
-fat maldigestion, increase in bile and waste products backing up into blood stream
-cholecystectomy: surgical removal of gallbladder
-bile is still produced in the liver, but decreased storage and delivery at meals
-loose, floating, foul smelling, pale colored stool

Question 20

Digestive Dysfunction: Dysbiosis

Answer 20

an umbrella term pointing to any alteration in the intestinal microbiome

a complex imbalance of the many different types of microorganisms - as many variations as there are individuals

Two common themes:
-changes in ratios between bacteroides and firmicutes
-conditions in the intestines leading to overgrowth of “opportunistic” species and strains. Ex: candida albicans overgrowth following antibiotics, or gram-negative bacteria following an acute illness

Question 21

Digestive dysfunction: Gram negative bacteria & LPS

Answer 21

gram-negative cell walls contain lipopolysaccharide (LPS or endotoxin)

elicits inflammatory response

contributes to intestinal hype-permeability of the small intestine

increased intestinal permeability allows more LPS to move into the bloodstream
-severe cases = metabolic endotoxemia

stress can make dysbiotic strains more virulent

Question 22

Small intestine dysfunction: hyperpermeability

Answer 22

aka leaky gut

single cell layer of epithelial cells held together by tight junctions

a selective barrier to absorb nutrients, but keep out harmful substances

cells become inflamed, tight junctions become hyperpermeable

increased absorption of antigens - microbial bodies or byproducts, food particles, environmental particles, or reabsorption of liver’s waste

systemic inflammation, toxic burden, and leaky brain

autoimmune does not equal hyperpermeability

many possible contributing factors: north to south dysfunction (dysbiosis, undigested foods, etc), nutrient deficiencies, some medications, stress, elevated zonulin

Question 23

small intestine dysfunction: zonulin

Answer 23

produced by liver and enterocytes

higher levels induce disassembly of tight junction proteins

many chronic inflammatory diseases are associated with elevated zonulin levels

especially associated with celiac disease, with higher levels found during celiac flare ups

gluten and gliadin proteins found in wheat, barley, and rye can increase zonulin, even in non-celiac

Question 24

Food allergies & intolerances

Answer 24

two categories of food reactions:

Immunologic:
-characterized by the production of antibodies, also called immunoglobulins
-subtypes: classical allergies (IgE), hypersensitivity (IgG and other pathways)

Non-immunologic intolerances:
-often related to our ability to digest certain dietary components. ex: lactose indigestion
-adverse reactions to specific compounds. ex: histamine, oxalates, lectins

loss of selectivity of the intestinal barrier = an increased allowance of larger food particles = increased immune activation and food reactions

Question 25

small intestine dysfunction: ileum and ileocecal valve

Answer 25

furthest south portion of small intestine, connects to colon

opening/closing can become impaired
+stuck closed
–delaying evacuation
–toxins reabsorbed, liver burden

+stuck open
–weakness or compaction causes it to remain open
–bacteria and waste from large intestine can back flow (SIBO)

vagus nerve involvement

Question 26

digestive dysfunction: the large intestine

Answer 26

lack of fiber in chyme
-less preferential feeding of beneficial bacteria
-diminished levels of SCFAs, which nourish the cells of the colon
-diverticula, ulcerative colitis, and chrohn’s disease associated with low levels of butyrate
-SCFA stimulate production of serotonin in the END
-sensitivity to giber will be addressed with specialized diets

Question 27

large intestine dysfunction: bowel transit time

Answer 27

Constipation:
-lack of fiber
-metabolites of bacterial fermentation are needed for motility (SCFAs, bile acids, methane)
-magnesium deficiency, excessive iron supplementation
-biliary stasis
-hypothyroidism
-sedentary lifestyle and structural issues

Diarrhea:
-irritation and inflammation
-water is pulled into intestines to speed defecation
-infections, dysbiosis
-food reactions
-malabsorption of dietary fats of certain sugars
-certain medications
-stress

Question 28

Common digestive disorders

Answer 28

Irritable bowel syndrome (IBS)

inflammatory bowel disease (IBD)
-crohn’s disease
-ulcerative colitis

celiac disease

small intestinal bacterial overgrowth (SIBO)

candida overgrowth

Question 29

Irritable bowel syndrome (IBS)

Answer 29

syndrome = collection of symptoms
often not visible
functional disorder: mediated by gut-brain axis and microbiome

Symptoms:
-constipation, diarrhea, gas, bloating, nausea, abdominal pain, cramping

visceral hypersensitivity

90% of IBS sufferers have at least one psychiatric conition

stress is major trigger

infections, ACEs, antibiotics and other medications, food intolerances

Question 30

inflammatory bowel disease (IBD)

Answer 30

disease = clear pathophysiology

visible damage and inflammation; significant inflammation and tissue damage

autoimmune disorder; considered autoimmune in nature

umbrella term for crohn’s and ulcerative colitis

evident upon examination

more frequent screening for colon cancer recommended

some genetic predisposition

profile of immune components that mediate the inflammation differ between types of IBD

primary symptoms:
-abdominal pain, cramping, changes to bowel frequency, diarrhea constipation, blood or mucus in stool, feeling of incomplete evacuation, nausea, vomiting

Secondary symptoms:
-body/joint pain, fatigue, loss of appetite, weight loss, delayed growth in kids/teens

complications can be severe

risk factors:
-genetic predisposition, first degree relatives
-other autoimmune conditions or disturbances to immune system
-environmental triggers like smoking, antibiotic use, NSAID use, childhood appendicitis

remitting and relapsing disease

therapeutic aim is to increase duration of remission

dietary approaches include specialized diets (gluten free, autoimmune paleo, specific carbohydrate diet, low FODMAP, autoimmune paleo)

therapeutic nutrients include vitamin D, omega 3, turmeric, probiotics

medical treatments: immune suppression, antibiotics, surgery

Question 31

Types of adverse reaction to gluten

Answer 31

celiac disease
wheat allergy
non-celiac gluten sensitivity (NCGS)

both CD and NCGS are increasing

1% of US population has CD vs 6% have NCGS

may be partly glysophate related based on impact to microbiome

Question 32

celiac disease

Answer 32

autoimmune
IgA antibodies against tissue transglutaminase
GI tissue destruction / villus atrophy

names: celiac sprue, gluten sensitive enteropathy, celiac disease

triggered by gluten exposure

genetic predisposition:
-more common in women, chromosomal abnormalities, other autoimmune diseases
-first degree relative increase chances from 1 in 100 to 1 in 10
-HLA-DQA1 and HLA-DQB1 gene alleles

Immune damage:
-lymphocytes infiltrated the epithelium
-gluten triggers the production of antibodies against tissue transglutaminase in the lamina propria connective tissue = unable to repair
-increased inflammation and damage to small intestine enterocytes

Digestive/inflammatory symptoms: bloating, diarrhea, constipation, gas, foul stool, nausea, vomiting, abdominal pain, joint pain, fatigue, anxiety

malabsorptive complications: anemia, fertility challenges, depression, skin irritation, osteoporosis

children: growth and structural issues

earlier life exposure to gluten:
-research is ongoing and mixed
-interest revolves around window of tolerance
-early high dose exposure while breastfeeding (4gram/day during months 4-6) may have protective effects
-increased consumption of gluten in first 5 years of life may increase risk
-many factors influence risk: maternal microbiome, rapid changes in an infants immune system during first two years of life, epigenetic factors, especially intestinal microbiota

Question 33

wheat allergy

Answer 33

allergy
IgE against gluten type proteins
systemic allergic responseI

Question 34

non-celiac gluten sensitivity

Answer 34

hypersensitivity/intolerance
IgA, IgG, IgM mediated
widespread symptoms of inflammation

Question 35

what is gluten?

Answer 35

prolamins and glutelins help store amino acids in the seeds that will be needed for the plant to develop after germination

gluten is an umbrella term used to describe the prolamins and glutelins in wheat, rye, or barley

Question 36

Gluten cross reactivity / contamination

Answer 36

sensitivity to non-gluten type prolamins/glutelins
ex: avenin and avenalin found in oats

risk for cross contamination during cultivation or processing

cross-reactivity can trigger pro inflammatory response

celiac disease increases risk for adverse response to dairy:
-lactose intolerance from villi damage
-casein (mammalian storage protein in dairy) cross reactivity

Question 37

Sources of gluten

Answer 37

primary treatment for CD is gluten-free diet

gluten free label = 20ppm or less

2019 study: gluten in celiac disease-more or less?
-50mg of gluten per = significant villous atrophy within 90 days
-10mg or less prevented significant changes to the villi
-10mg = 1/380th of a slice of bread, or about one grain of salt

Question 38

Client education

Answer 38

different types of wheat: durum, semolina, emmer, kamut, spelt, einkorn, barley, malt, rye

food additives and fillers

cross contamination

non-food related consumer goods

client: what kind do you want to make

Question 39

small intestinal bacterial overgrowth (SIBO)

Answer 39

imbalance in gut microbiota, specifically in the small intestine

opportunistic or pathogenic microbes proliferate into abnormal populations

most often originate from oral cavity or the lower bowel

nutrient competition and absorption issues

Question 40

SIBO 1

Answer 40

Factors impacting motility:
-poor signaling in North to south digestive process
-impaired vagus nerve
-gastroparesis
-scarring or obstructions
-disruptions to the migrating motor complex
-impaired peristalsis
-slowed bowel transit
-ileocecal valve dysfunction
-medications such as acid blockers, PPIs, pain medications

Other contributing factors:
-hypothyroidism
-low bile
-overuse of antibiotics
-food poisoning
-H pylori infection
-diverticulosis
-a diet high in refined sugars
-chronic stress
-gastric bypass surgery

Question 41

SIBO 2

Answer 41

North to south function:
-HCl directly inhibits overgrowth
-bile salts inhibit overgrowth
-enzymes break down bacterial cell walls
-undigested food = food for microbes
-ileocecal valve dysfunction:
+closed = delayed evacuation
+open = colonic bacteria reflux

Risk factors:
-advanced age
-diabetes
-celiac disease
-IBS/IBD, pancreatitis, and liver or kidney issues
-up to 80% of individuals with irritable bowel syndrome are likely to have SIBO

Question 42

SIBO 3

Answer 42

metabolism generates excess gass

SIBO thrives on simple carbohydrates, some proteins and B vitamins

low bile synthesis and metabolism

impairs nutrient absorption

symptoms:
-abdominal pain
-bloating
-disstension
-nausea
-reflux
-gas
-diarrhea
-constipation
-fatigue
-weight loss

Question 43

SIBO 4

Answer 43

markers:
-hydrogen/methane breath test
-stool and blood tests for comprehensive picture

triggering foods:
-sugar & sweeteners
-fruits
-starchy veggies
-dairy
-grains
-specific carbohydrate diet
-low FODMAP diet

concurrent use of probiotics improves outcomes with antimicrobials

investigate underlying contributors first

Question 44

Candidiasis

Answer 44

candida: genus of yeasts with over 200 species

candida albicans is the most implicated in candida overgrowth or candidiasis

normally found in the mouth, gut, and vagina

kept in balance by other beneficial microbes

Question 45

candida overgrowth drivers

Answer 45

damage to beneficial microbes = loss of symbiotic balance can lead to overgrowth

certain medications (oral contraceptives, immune suppressants like steroids)

diet high in sugars and/or high in blood glucose

candida releases mycotoxins:
-act as neurotoxins
-increase inflammation
-exacerbates IBS and IBD

Question 46

Candida overgrowth symptoms

Answer 46

Digestive symptoms:
-generalized GI symptoms (bloating, loose stools)
-light colored mucus, froth or foam in stools
-pain when swallowing
-sores in mouth
-coated tongue
-bad breath

Non-digestive symptoms:
-vaginal itching/burning
-fungal infections (athletes foot, jock itch, nail fungus)
-joint/body pains

Neurological:
-depression
-headaches
-fatigue
-muscle aches
-brain fog
-bizarre/vivid dreams

Question 47

candida overgrowth intervention

Answer 47

ay include stool test

treatment includes:
-reducing sugars, sweeteners, dried fruit, fruit juices, most grains, starchy veggies, non-fermented dairy
-repopulating the gut with beneficial bacterial
-possible anti-fungal medications or herbal protocols

Question 48

what do we need to make bile?

Answer 48

water (good hydration)
cholesterol
phospholipids (such as phosphatidylcholine)
amino acids (such as glycine and taurine)
bilirubin
other cofactor nutrients (such as Vitamin C, electrolytes and other key minerals)