MNT Gastrointestinal disorders Flashcards
Bloating or distention?
Is it bloating, or distension?
Bloating - do they describe fullness, swelling,
trapped gas, tightness, or “inflammation”? Are the
symptoms subjective?
Distension - do they have a visible increase in the
size of their gut that they may describe as “looks
pregnant” or “looks like I swallowed a bowling ball”
Bloating
Lactose intolerance
Fructose intolerance
Other carbohydrate intolerances,
inc. FODMAPs
Sugar alcohol consumption
Too much fiber
Specific food: Aka lettuce
Bloating conditions
SIBO/IMO
Celiac
Exocrine pancreatic
insufficiency
Gastroparesis
Hypothyroid
Diverticulosis
IBDPelvic floor dysfunction
Functional dyspepsia
Functional bloating
IBS
Constipation
Diarrhea
H pylori
Abdominophrenic
Dysynergia (APD)
Chronic stress
Abdominal bloating and distention
IS constipation present? (Yes) -1. Detailed history with rectal exam.
2. Rome IV critieria for IBS-C or chronic constipation
3. ARM to diagnose pelvic floor dyssynergia
Treatment:
1. Treat the constipation
2. Biofeedback therapy if dyssynergic defecation is present
Food intolerance? (Yes)
1. DX: Carbohydrate intolerance CD NCGS or food allergies
TX: Carbohydrate or FODMAP restriction
Alarm symptoms (vomiting, weight loss>10 %, Gi bleeding, FHx IBD) or recent worsening nausea or pain present?
1. DX: consider CBC, CMP, other labs as indicated, KUB, abdominal ultrasound, CT/MRI, endoscopy to exclude structural abnormalities.
Motility studies to diagnose gastroparesis, CIP, or other motility disorders.
2. TX: treatment based on clinical findings.
Prokinetics for motility disorders.
SIBO risk factors present?
1. DX: Hydrogen based breath testing with glucoseor lactulose or small bowel aspirates
2. TX: Antibiotics
Abdominophrenic dyssnergia (APD) or visceral hypersensitivity (VH) suspected
1. DX: APD: abdominal distention not explained by increased intestinal gas, worse after meals,
VH: abdominal pain, severe bloating
2. TX: Diaphragmatic breathing
-central neuromodulators
-Brain-gut behavior therapies.
Bloating is constipation
Fiber (up or down)
Fluids
Meal structure
Insufficient kcal
Exercise
Cheese intake :)
Warm liquids within 3
hours of waking
2 kiwi fruit/day
12 prunes/2 oz prune juice
Psyllium
Magnesium citrate
Pro-kinetic (Motil Pro,
Motility Activator)
Referral to pelvic floor
therapy
Bloating is Abdominophrenic Dyssynergia (APD)
No great evidence, but good guesses:
Diaphragmatic breathing
Gut directed CBT and gut directed hypnotherapy
Happy Inside
Nerva
GI Psychology
Foundation of Eating
Any food, eaten too fast, can lead to sx.
Any food, eaten under stress, can lead to sx
Meals that are imbalanced can lead to sx
Start with the basics
Start with basics
At the bottom of the house:
Eat slowly and mindfully
Use personalized nutrition
Chew your food
Eat balanced meals
Belly breathing before/after meals
Rome IV Criteria for IBS dx:
Recurrent abdominal pain on average at least 1 day/week in the
last 3 months, associated with two or more of the following
criteria:
1.Related to defecation
2.Associated with a change in frequency of stool
3.Associated with a change in form (appearance) of stool
Criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to dx.
Gut Brain Axis
Influences:
secretion, motility, delivery of nutrients, Microbial balance, immune function.
Brain-vagus nerve -Gut- ENS, CNS, Gut Wall, HPA axis -Brain
Gut to HPA Axis: Influences: Mood and behavior, stress and anxiety, Neurotransmitter
IBS Etiology
ACEs
Diet
GI InfectionGenetics
Epigenetics: methylation, histone
modifications
Microbiome alterations including
histamine
Gut brain interactions
Corticotropin-releasing factor
HPA Axis and CRF
Hypothalamus–Corticotropin releasing factor (CRF)-CRF receptor (pituitarygland)–Adrenocoricotropic hormone release -Melanocortin receptor (adrenal cortex) –cortisol release—intestinal target.
IBS does not mean Mast cell activation syndrome
- Typical symptoms + response to drugs
leads to probable MCA - Symptoms are severe and episodic
A. Yes: MCAs are likely
-screen for MCAS criteria and clarifying etiology of MCAs.
Leads to MCAS criteria fulfilled
a. idopathic MCAS (established a management and treatment plan)
b. Primary MCAS (clonal MC disease : CM, SM, MMAS) –established a management and treatment plan.
c. Secondary MCAS (underlying condition: e.g. IgE-mediated allergy ) -established a management and treatment plan.
IBS Etiology
- Are there a larger number of mast cells with patients with
IBS than healthy controls? YES - Colonic biopsies from IBS pts released significantly greater
mast cell mediators compared to HCs. - If you give Cromalyn or antihistamines, you can decrease
visceral hypersensitivity that occurs with IBS. - IBS pts have leakier guts than healthy controls this appears
to be mast cell driven - Stress is one of the primary drivers of mast cell activation
IBS = a loss of oral tolerance?
IBS is a loss of oral tolerance - people become sensitive after GI
infections to foods they have previously been tolerant to.
Prescriptions:
Cromolyn (maybe, but unlikely)
H1 receptor antagonist (Cyproheptadine)
Tricyclic antidepressant
IBS + histamine mechanisms
- Histamine in environment
- Histamine in food
- Histamine in microbiome (from histidine)
- Lack of DAO (diamine oxide enzyme)
Anamnasis
symptoms of histamine intolerance?
symptoms triggered by histamine rich foods?
Drugs liberating histamine or inhibiting DAO?
Allergies?
Concomitent diseases?
a. mastocytosis? Tryptase
b. food allergies? Skin prick test, RAST, provocation.
c. Exclusion of underlying disease?
-eg. endoscopy for gastrointestinal symptoms.
Diet Diary: Improvement by histamine free diet, antihistamines, mast cell stabilizers, substitution of DAO?
> = 2 symptoms of histamine intolerance + improvement by histamine free diet.
a. double blind placebo controlled histamine provocation.
b. Measurement of DAO + histamine
Histamine free diet, antihistamines, mast cell stabilizers, DAO substitution,
certification of medication before exposure to drugs liberating histamine or inhibiting DAO.
Histamine and histamine intolerance image
Histidine
1. Histamine (H+ leads to Co2) /L-Histadine carboxylase (HDC)
2. DAO
3. S-adenosyl-methionine 4.
(HNMT)
4. Imidazole acetaldehyde >Aldehyde dehydrogenase > Imidazole acetate
*Histamine> N-Methylhistamine > 5. MAO-B Aldehyde dehydrogenase >N-Methylimidazole acetate
*N-Methylhistamine >6. DAO>N-MEthylimidazole acetaldehyde>Imidazole acetaldehyde > aldehyde dehydrogenase >Imidazole acetate
What is really causing the SX
Gluten
FODMAPS
Insoluble fiber
wheat
other ingredient
amylase trypsin inhibitor
Top down vs bottom down approach
IFM way Bottom Down
a. Multi food elimination diet for all clients
b. Re introduce one food or one food category (FODMAP) at a time.
c. Assess symptoms before adding another food.
CI recommends/prevents disordered eating.
a. Eliminate more if necessary
b. Assess symptoms
c. Eliminate the most likely culprit
Orthorexia nervosa
conditions requiring diet modification for therapy (celiac disease) > screen for disordered eating > disordered eating traits identified >
No> Trial of dietary modification therapy > Ongoing dietary support with ongoing screening for disordered eating.
Yes> referral to psychologist for further screening> Trial of dietary therapy > ongoing psychology support
Conditions where diet modification is one type of therapy (IBS)
> Screen for disordered eating
>Disordered eating traits identified
a. No: Trial of dietary modification therapy> ongoing dietary support with ongoing screening for disordered eating.
b. Yes: Referral to psychologist for further screening
1. deemed suitable for diet therapy with ongoing psychology support.
- Ongoing dietary support with rescreening for for disordered eating.
1. deemed suitable for dietary therapy
-Refer other therapies, (pharmacotherapy, CBT, gut directed hypnotherapy).
So what to do?
A. Consider lowering histamine load from environment
B. Consider low histamine diet (no RCT’s done yet)
C. Consider DAO supplementation + mast cell stabilization such as quercetin, P5P
D. Be aware: Klebsiella aerogenes produces histamine.
-Push Lactobacillus to counteract
E.If lactose intolerant, be strict as lactose exposure increases
mast cells
a. Consider a low FODMAP diet to reduce histamine production.
Small intestine: FODMAPS>
pull water into the small intestine>
Colon> Increase gas and acid content
-dysbiosis
-microbe derived metabolites
-immune activation
-intestine permeability
Supplement suggestions
-5 g glutamine/day w/o food
-Peppermint oil - 180-225 mgs 1-3x/daily
-Iberogast
-Probiotics (make sure to think about strains for diarrhea vs constipation)
SWIFT PROTOCOL
Start with the basics
work with differentials
integrative care for stress
foods that fit, but not unnecessary restrictions.
Top to most effective, least invasive
stomach acid (baking soda)
Testing - baking soda
¼ tsp baking soda with 4 oz water.
Drink first thing in the a.m.
Time onset of burps
Testing HCL
1, 350-750 mg capsule of HCl with protein-containing meal for 48 hours. No
reaction?
2, 350-750 mg capsules with protein -containing meal.
Continue up to 5 caps until you get burning, heat, etc.
Stay with that dose as you eat - note that smaller meals may require less . . .
Remember SWIFT
SIBO SYMPTOM INTERVENTIONS NEEDS
Anemia
Fat soluble
water soluble
predisposing factors
Anemia: Feeds high in Vitamin B12 (megoblastic anemia possible in SIBO)
Foods high in iron
Meg(Klaire Labs chewable iron Chelate)
2. Fat soluble: vitamin A, D, E, (K may be elevated)
3. water soluble: B12, Thiamine, nicotinamide (folate may be elevated)
4. Predisposing factors: use MNT to support
SWIFT FOR SIBO (SYMPTOM RELIEF)
Anemia
Vitamin D, E, A
Vitamin B12, thiamine
predisposing factors
K is often high
Folate is often High
Safety and necessity of special SIBO diets
HX of ED
Family Hx of ED
current anxiety, OCD
ability to follow diet
GUT BRAIN AXIS
stress
traumatic brain injury
vagal tone
sleep
motility
Migrating motor complex
Food Hygiene
Hypochlorhydria/PPI
Resistant starch
fiber
ferments
prebiotics
Binders:
Charcoal
clay
modified citrus pectin
Immune/LSP support
IgG SBIs
BIOFILM DISRUPTORS:
specific enzyme blends
N
SEED: probiotic (Caution)
WEED: presence of hydrogen producing bacteria: streptococcus, Escherchia coli, Bacteroides, staphlycoccus, clostridium , Micrococcus, Klebsiella pneumoniea,
preptstreptococcus,
-presence of methane producing bacteria/archaea: Methanobrevibacter smithii
-presence of sulfur producing bacteria: Desulfovibrio
Reintroduce foods: Follow plan guidelines,
Ensure sustainability:
reconsider nutrition
reconsider sleep
reconsider movement
reconsider stress practices
TAPER SUPPLEMENTATIONS
symptom relief last
Make long term plan
SIBO symptoms interventions
a. first approach
b. treatment resistant
NEED: FIRST APPROACH; Approach: SCD, GAPS, low FODMAP
NEED: First Approach Approach: Cedars-Sinai Diet (C-SD),
NEED: treatment resistance; Approach: SSFG (Siebecker)
NEED: treatment resistance; Exclusive Enteral Nutrition, Polymeric, peptide, or elemental.
NEED: treatment resistance; Approach: Sibo-Bi phasic (B-PD)
SIBO Digestive competency
a. Gut Brain Axis
a. Gut brain axis:
>Eat with the client in session,
>frequent appointments
>Referral to therapist
>Referral to club/social groups
>Encourage social eating
>TBI protocols when warranted
MEg:
>Happy inside APP & virtual services
> Nerva
> Safe and sound protocol
>Accessing the healing power of the Vagus
>Nerve by Stanley Rosenberg
SIBO Digestive Competency
a. migrating motor complex
Ideally 5 hours between meals, clear liquids inbetween,
SIBO DIgestive Competency
Food Hygiene
Are they eating and bunch prebiotic, fiber rich foods that are feeding the overgrowth.
SIBO Digestive competency
Low stomach acid
Low stomach acid
If the client is on the PPI, you should not add HCL.
If not on a PPI, you can add bitters or HCL. as long as the client doesnt have GERD, Barrett’s esophagus or a stomach ulcer. but may be warranted for SIBO for hypochlorhydria. But also look for root cause of hypochlorhydria- which is often stress.
SIBO improve inflammation
A. Binder: charcoal, clay, modified citrus pectin
>quicksilver ultrabinder, Biocidin GI Detox
B. Immune/LPS support: Serum bovine IgGs
>Orthomolecular SBI protect
>Microbiome Labs MegaMucosa and IgG2000
C. Biofilm disruptor: specific enzyme blends, NAC, curcumin
>Klaire labs interfase
>Klaire labs interfase plus (caution with anemia)
SIBO FEED MICROBIOME
Seed: Bacillus based probiotics
MIcrobiome Labs megaspore
Weed Hydrogen: certain herbals, garlic, neem, oregano
>Biocedin liquid capsules, LSF, metagenics candibactin AR/BR
Weed Methane: Bitter Orange, bile acids, wormwood, quebracho, horse chestnut,
>Atrantil
Weed Sulfur: Bisthmuth, green tea, curcumin, Molybdenum + temporary elimination of aliums and cruciferous.
> Priority One Biofilm Phase 2 Advanced
SIBO Taper and reintroduce
Welcome, improve and Feed interventions first
Symptom interventions last
Food reintroduction: follow reintroduction guidelines.
Celiac disease
Celiac disease is an autoimmune disease that is triggered through consumption of gluten (a protein in wheat, rye, barley).
Antecedents: Increased risk with family hx of celiac, type 1 diabetes, Down syndrome.
Medical Testing (recommendations from Dynamed):
1. Use IgA antitissue transglutaminase antibody (tTG) as the initial test in patients
2. IgA or add immunoglobulin G (IgG)-based deamidated gliadin peptides (DGPs) if very low IgA anti-tTG levels suggest IgA deficiency
3. IgA anti-tTG and IgA- and IgG-DGPs in children < 2 years old
If IgA tTG > 10 times upper limit of normal, consider testing endomysial antibody (EMA) and human leukocyte antigen (HLA)-DQ serotyping to diagnose celiac disease without endoscopy and biopsy.
4. Obtain HLA-DQ2 or DQ8 genotyping to rule out celiac disease in selected situations if other testing is indeterminate
5. Obtain an upper endoscopy with small-bowel biopsy (with multiple biopsies from distal duodenum and duodenal bulb) to confirm the diagnosis in patients with suspected celiac disease.
6. Consider testing for nutritional deficiencies with hemoglobin, iron, folate, vitamin B12, calcium, and vitamin D levels.
Bone mineral density tests for osteoporosis
Diet:
1. Life-long gluten free diet - be sure to complete all blood testing and biopsies BEFORE starting gluten restriction
- Monitor oat consumption for oat intolerance or cross reactions to gluten.
- Assess for deficiencies of: folate, iron, vitamin B12, vitamin D
- Avoid lactose initially after diagnosis, can add back once gut is in better shape.
Celiac disease Things to know
Celiac disease is a chronic autoimmune disease
1 in 100 people worldwide have celiac disease, or 3 million Americans.
80% of Americans with celiac are undiagnosed.
Reaction to gluten only - found in wheat, rye, barley. Do not remove all grains only gluten-containing ones.
Oats can be contaminated - GF certified only
Family hx matters: people with first degree relative with celiac have a 1 in 10
chance of developing.
Incidence of celiac in children = Crohn’s, Ulcerative Colitis, and Cystic Fibrosis combined.
Celiac disease can affect every organ in your body.
Lifelong, gluten free diet is the ONLY treatment.
Approximately 20% of people with celiac disease do not respond to the gluten-free (refractory celiac)
Celiac diagnosis
Diagnosis typically takes 6-10 YEARS, during which time the following diseases
correlated with undiagnosed celiac can develop:
● intestinal cancers
● type 1 diabetes
● osteoporosis
● thyroid disease
● multiple sclerosis
● Infertility and miscarriage
● anemia
More than 300 symptoms associated with celiac, BUT 20% of people
asymptomatic
Even if they are asymptomatic, they are at risk for lifelong complications
Celiac Blood test and Malabsorption
Blood test, endoscopy.
Commonly co-occurring diseases include: microscopic colitis, IBD
Lactose and/or fructose intolerance
Malabsorption in celiac often comes with deficiencies in:
● Iron
● Calcium
● Magnesium
● Zinc
● Folate
● Niacin
● Riboflavin
● B12
● Vitamin D
refractory celiac (stubborn, unmanageable)
Incidence and risk:
2-20%, depending on the study
Risk: malnutrition (duh), as well as T-cell lymphoma and small bowel
adenocarcinoma.
Getting “Glutened”
● Supplements and Medications (inactive ingredients)
● Dental products (toothpaste, rinse, even bands used for braces)
● Lipstick and make up
● Communion wafers
● Play dough
● Stamps (lickable)
SWIFT Celiac
- Support: social wellness, positive mood, movement, sleep, gentle nutrition, hygiene, food life skills,
knowledge, self-compassion, stress reduction - Welcome: supportive gut bacterial balance through use of prebiotic/probiotics, antimicrobials/parasitics,
fiber-filled foods, SCFA, and dietary interventions - Improve: digestive competency with HCL, digestive enzymes, bile, fiber, vagal stim
- Feed: the gut with supportive nutrients including zinc, Vitamins A and D, glutamine, cabbage juice, collagen, NAC, marshmallow, etc.
- Taper: reintroduce any foods that were removed, ensure sustainability, and work to bring down
supplementation to most effective, least invasive.
Common micronutrient deficiencies in IBD (calcium, cobalamin:B12, Vitamin D, Folate B9, Iron, Magnesium, Pyridoxine (B6), Zinc
Calcium
Signs of deficiency: Hypotension, prolonged QT interval,
distal extremity, parasthesias, Chvostek sign, Trousseau sign,
muscle cramps, tetany, seizures
Risk factors:
Vitamin D deficiency,
decreased PTH activity,2
corticosteroid use
Biochemical Assessment:
Serum calcium does not
fluctuate with changes in
calcium intake
Recommended Replacement for deficiency:
Gender and age specific:
*9-18 yrs: 1300 mg
*19-50 yrs: 1000 mg
*51-70 yrs:
1000 mg (male),
1200 mg (female)
*71+ years: 1200 mg
IBD micronutrient deficiencies (cobalamin B12)
Cognitive decline,
cardiovascular disease,
bone fractures; megaloblastic anemia with macrocytosis; glossitis,
constipation, diarrhea;
hand/feet paresthesia; confusion, poor memory
Risk Factors for deficiency:
Crohn’s disease affecting
the terminal ileum; ileal
resection >20cm; significant gastric resection; small intestinal bacterial
overgrowth (SIBO); vegetarian diet
Biochemical assessment:
High serum Methylmalonic Acid, low plasma or serum B12, elevated MCV
Recommended replacement for deficiency: oral B12 supplementation >1000 mcg daily.Prophylaxis: IM B12 1000 mcg monthly with >60cm
ileum resected
Vitamin D IBD micronutrient defiency:
signs of defiency:Hypocalcemia, osteomalacia, osteoporosis
risk factor for deficiency:
Malabsorptive disorders,
small intestinal bacterial
overgrowth (SIBO), corticosteroid use
Biochemical assessment:
25-(OH)D <20 ng/mL
deficiency; 25-(OH)D
<21-29 ng/mL insufficiency
Recommended replacement for deficiency:
If level<20: 50,000 IU D25
or D3 for 12 weeks;
recheck levels and continue
supplementation if still
deficient.
Maintenance dose of 1500-2000 IU/d
D3;7 higher maintenance
doses of 3000-6000 IU/d
are recommended for patients on glucocorticoids, anticonvulsants, those with malabsorption
BMI>30, or in those with
small bowel involvement.
Folate B9 deficiency (IBD)
SOD: Megaloblastic, macrocytic anemia; diarrhea,
smooth, sore tongue;
weight loss; nervous
instability; dementia
Risk factor for defiency:
GI resections; patient on
restrictive diet; use of
sulfasalazine, methotrexate, cholestyramine; achlorhydria; small intestinal bacterial overgrowth(SIBO)
Biochemical assessment:
Low plasma or serum
folate (will be elevated
if +SIBO), elevated MCV
and homocysteine, low
red blood cell folate
Recommended replacement for deficiency:
1 mg folic acid daily
Iron deficiency (IBD)
- SOD: Microcytic, hypochromic anemia; tachycardia; poor capillary refil, fatigue, sleepiness, headache, anorexia, nausea, pallor,
impaired behavioral
performance - Risk factor for deficiency:GI bleeding, UC, achlorhydria, small intestinal bacterial overgrowth
(SIBO) - Biochemical assessment: Hb 10-12 g/dL (women), 11-13 g/dL (men); Serum ferritin <100 ng/mL,
transferrin saturation
<20%, elevated transferrin receptor levels - In inactive IBD/normal
CRP: 100 mg oral iron daily in divided doses. Additional vitamin C may help
enhance iron absorption.
In active IBD, chronic iron
deficiency anemia, Hb <10
g/dL (women), <11 g/dL
men: consider parenteral iron.
Magnesium
Signs of defiency:Neuromuscular hyperexcitability, latent tetany, frank seizures,arrhythmias
Risk factor for defiency:Chronic or severe acute diarrhea, short gut
Biochemical assessment: Low serum magnesium
150 mg elemental Mg four times daily
Pyridoxine B6
signs of deficiency: Seborrheic dermatitis, microcytic anemia,
confusion, depression,
angular stomatitis,
glossitis, cheilosis
Risk factor for deficiency:
Restrictive diets, poor
oral intake, corticosteroid
or isoniazid use
Biochemical assessment:
Low mean plasma pyridoxal-5-phosphate (PLP)
concentration
50-100 mg/day OR
10 to 20 mg/day IM or IV
for 3 wk; then 2 to 5 mg/
day ORALLY for several
Zinc Deficiency for IBD
Signs of deficiency: Inadequate growth, acrodermatitis enteropathica, hypogonadism, impaired night vision, anorexia,
diarrhea alterations in
taste and smell, alopecia, impaired wound healing
Risk factors for deficiency:
PPI/H2 blockers, protein deficiency, malabsorptive disorders, diarrhea, fistulizing disease; vegetarian
diet,
Biochemical assessment: Low plasma or serum zinc
Recommended replacement for deficiency: 50 mg elemental zinc for
10 days. Caution copper
deficiency for those on
long term zinc supplementation.
SIBO
44% of SIBO reoccurs
Symptom relief: Assess for Anemia, Vitamin D, E, A, Vitamin B12, Thiamine, Predisposing factors, K is often high, Folate is often high,
Predisposing factors: Hypothyroid, IBS, IBD, chronic pancreatitis, celiac disease, T2DM, gastroparesis, medications (opiods, anticholinergics, PPIs), hypochlorhydia, ETOH abuse, gastric bypass,
Safety and Necessity of Special SIBO Diets: Hx of ED, Family history of ED, Current anxiety, OCD, Ability to follow diet,
Mechanisms contributing to nutrient deficiencies in small intestinal bacterial overgrowth.
Fat:
1. Deconjugation of bile acids resulting in decreased bile acids available for micelle formation.
2. Production of toxins such as lithocholic acid that may directly inhibit absorption.
Carbohydrates: Production of toxins such as lithocholic acid that may directly infhibit absorption.
2. decradation of sugars by bacteria
3. Impaired acitivity of brush border disaccharidase and hydrolase
Protein: Production of toxins such as lithocholic acid that may directly inhibit absorption.
Vitamin B12: Consumption of B12 by bacteria.
2. Inhibition of B12 absorption in the terminal ileum.
Vitamin A, D, E: Deconjugation of bile acids resulting in decreased bile acids available for fat absorption.
Risk factors for small intestinal bacterial overgrowth
- Failure of gastric acid barrier:
a. atrophic gastritis
b. Hypochlorhydria
c. gastric bypass
d. proton pump inhibitors - Failure of small bowel clearance
a. Primary visceral neuropathy or myopathy
b. Connective tissue disease (scleroderma, polymositis)
c. Amyloidosis
d. Gastroparesis
E. Radiation enteropathy
F. Paraneoplastic syndrome
G. Medications (opiods, anticholinergics) - Small bowel anatomic alteration:
a. short bowel syndrome
b. small bowel diverticulitis
c. small bowel strictures or fistulas
d. small bowel obstruction
e. Blind loops (Roux-en Y)
f. ileocecal valve resection - Immunodeficiency:
a. IgA deficiency
b. combined variable immune deficiency
c. T cell Deficiency - Multifactorial
a. irritable bowel syndrome
b. Cirrhosis
c. Chronic pancreatitis
d. obesity
e. Cystic fibrosis
f. celiac disease
g. Diabetes mellitus
h. hypothyroidism
SIBO symptom intervention
Anemia: Foods high in vitamin B12 (megoblastic anemia possible in sibo), foods high in iron.
+Klaire labs chewable iron chelate
Fat Soluble : Foods: Vitamin A, D, E (K may be elevated)
Water soluble: Foods: B12, Thiamine, nicotinamide (folate may be elevated)
PRedisposing factors: USe MNT to support
NEED: First approach
a. SCD, GAPS, low FODMAP
b. Cedars- Sinai Diet (CSD)
NEED: Treatment resistant
a. SSFG (Siebecker)
b. Exclusive, Enteral Nutrition, polymeric, peptide, or elemental
SWIFT FOR SIBO (Digestive competency)
Gut BRain Axis: Stress, Traumatic brain injury, Vagal tone, Sleep, motility, migrating motor complex.
Food Hygiene:
>Hydrochlorhydria/PPI
>Resistant starch:+
>Fiber +
>ferments+
>prebiotics +
+ may be problematic temporarily as can increase bacterial proliferation
NEED: Gut Brain Axis: Eat with cleint, frequent appointments, referrals to therapist, clubs, social groups, Encourage social eating, TBO protocols when warranted.
NEED: Migrating motor complex: 5 hours between meals, clear liquids ok.
NEED: If client is on PPI, do not add HCL . If NOT ON PPI, possible HCL as long as no risk of Barrett’s esophagus, stomach ulcer.
Food Hygiene: Are they eating prebiotics, fiber rich foods? May be feeding the overgrowth.
SIBO Improve inflammation
Binders:
>Charcoal
>Clay
>Modified citrus pectin
Immune/LPS support:
IgG SIBIs
Biofilm disruptors:
Specific enzyme blends
NAC
curcumin
SEED: Probiotics (caution)
*Bascillus based (Microlabs Megaspore)
WEED: PResence of hydrogen producing bacteria; strep, Ecoli, Bacteroides, Staph, Clostridium, MIcrococcus, Klebsiella, Peptostreptococcus.
** Certain herbals, garlic, neem oregano ( Biocidin liquid capsules, LSF MEtagenics Candibactin AR/BR
> presence of methane producing bacteria/archea: MEthanobrevibacter
**Bitter orange, bile acids, wormwood, quebracho, horse chestnut (Atrantil)
> PResence of sulfure producing bacteria: Desulfovibrio.
** Bismuth green tea, curcumin, molybdenum + temporary elimination of aliums and cruciferous
(A. Biocidin Broad Spectrum liquid-titrate slowly;
B. Brain Octane Oil (contains caprylic acid), titrate
c. Metagenics Candibactin- AR/BR
- Reintroduce foods according to whatever plan you are using.
- Ensure sustainability
- Taper supplementation.
Taper:
Welcome, improve and Feed interventions First
symptom interventions last
IBD SWIFT PROTOCOL
ASSESS: Low Hemoglobin <12 g/dL Women <13 dL Men
>Low Ferritin <30 ng/ml
>Relationship to food
Dietary Triggers:
>IBS as well as IBD
>Fat malabsoprtion
>Insoluble Fiber
>Gluten
>Flares
>Treatment Resistance
IBD symptom intervention
ANEMIA:
-High iron foods (if client is anemic, you must supplement iron, food is not enough) 30-100 mg/day
REactivity to FODMAPS:
-Low Fodmap
Adults: AIP and SCD
Flare: Low residue, Exclusive Enteral Nutrition, Polymeric peptide, or elemental
Pediatrics: SCD
Treatment Resistance in Pediatric: Exclusive Enteral Nutrition, Polymeric, Peptide, or elemental
Crohn’s Disease: CDED
Fat Maldigestion: Low Fat
In Remission: MEditerranean
Crohn’s disease
Th1 and Th17 condition with elevated production of IL-12, IL-23, IFN-y, IL-17
SWIFT FOR IBD
Gut Brain Axis: Stress, mental health, QOL, Vagal tone
Food Hygiene: Dietary Diversity, Resistant starch, color in foods, omega’s, Fiber, Ferments, Prebiotics
GUT BRAIN AXIS: stress contributes to flares. Data on Vagal Stim.
Food hygiene: Watch Macros (protein and fat) and bioactive compounds such as ferments, omega’s : May be limited due to sumptoms.
Ulcerative Colitis
TH2 and Th9 condition with increased production of IL-13, IL-5, IL-9.
SWIFT PROTOCOL FOR IBD
- Look up everything, may be contraindicated
- repair the gut lining
- consider colostrum or IgG support when indicated
- BE curious about food intolerance
- consider anti-inflammatories
Contraindications: Melatonin (worsens clinical coarse) Glutamine (Be aware: may be harmful)
Repari Gut lining: Phosphatidylcholine in UC (improves mucosal lining) & Bone broth.
Immune/LPS support: Serum Bovine IgG , probiotics,
Food Intolerance: Repair gut lining, then consider elimination
Anti-Inflammatories:
>Curcumin
>Boswellia,
>Omega’s
>saffron (to reduce disease severity)
Taper: reintroduce foods:
make a plan, reintroduce 3x. repeat failed foods.
-Welcome, improve and feed interventions first.
-symptoms interventions last.
IBD FEED Microbiome
Feed:
Prebiotic foods: Garlic, onions, bananas, apples, oats, asparagus, resistant starches, such as cooked and cooled rice and potatoes.
Supplements: Psyllium and inulin in UC
FOS in CD,
Seed: Yogurt, kefir, sauerkraut, tempeh, kimchi, miso, kombucha, pickles.
Probiotic supplements
Weed: Posemary, sage, basil, oregano, parsley, olive leaves, nutmeg, citrus (anti-microbial herbal supplements)
