Digestion (week 2) Flashcards
Digestive Dysfunction
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
Digestive Dysfunction - the brain
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
Digestive Dysfunction - the mouth
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)
Stomach dysfunction: Hypochlorhydria (low stomach acid)
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)
Stomach dysfunction: Hypochlorhydria (low stomach acid)
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
Stomach dysfunction: Hypochlorhydria (low stomach acid)
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)
H. pylori bacteria and Peptic Ulcer
~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
Stomach dysfunction: Hyperchlorhydria
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
Acid Reflux, Heartburn, and GERD
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
LES function
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
Low Stomach Acid and LES Function
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
Acid Reflux & Heartburn
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
Gastroesophageal Reflux Disease (GERD)
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
Gastroesophageal Reflux Disease (GERD)
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
Stomach Dysfunction: Gastroparesis
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
Digestive Dysfunction: the pancreas
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
Digestive Dysfunction: the liver and gallbladder
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)
Digestive Dysfunction: Biliary Stasis
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
Liver/Gallbladder Dysfunction
-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
Digestive Dysfunction: Dysbiosis
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
Digestive dysfunction: Gram negative bacteria & LPS
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
Small intestine dysfunction: hyperpermeability
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
small intestine dysfunction: zonulin
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
Food allergies & intolerances
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
small intestine dysfunction: ileum and ileocecal valve
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
digestive dysfunction: the large intestine
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
large intestine dysfunction: bowel transit time
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
Common digestive disorders
Irritable bowel syndrome (IBS)
inflammatory bowel disease (IBD)
-crohn’s disease
-ulcerative colitis
celiac disease
small intestinal bacterial overgrowth (SIBO)
candida overgrowth
Irritable bowel syndrome (IBS)
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
inflammatory bowel disease (IBD)
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
Types of adverse reaction to gluten
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
celiac disease
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
wheat allergy
allergy
IgE against gluten type proteins
systemic allergic responseI
non-celiac gluten sensitivity
hypersensitivity/intolerance
IgA, IgG, IgM mediated
widespread symptoms of inflammation
what is gluten?
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
Gluten cross reactivity / contamination
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
Sources of gluten
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
Client education
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
small intestinal bacterial overgrowth (SIBO)
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
SIBO 1
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
SIBO 2
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
SIBO 3
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
SIBO 4
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
Candidiasis
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
candida overgrowth drivers
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
Candida overgrowth symptoms
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
candida overgrowth intervention
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
what do we need to make bile?
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)
