MNT Exam #2

gallbladder overview/functions

lies underneath right lobe of liver

main functions: concentrate, store, and excrete bile (bile emulsifies fat)

bile must be excreted

cholesterol and bile relation

bile is made up of cholesterol, bilirubin, and bile salts

bile can be used to reduce cholesterol in body — we can produce cholesterol in body

more cholesterol = more bile = lower serum cholesterol

cholesterol is needed to excrete bile*

RDA for cholesterol = 300mg; CVD cholesterol = 200mg

cholecystitis

inflammation of the gallbladder

usually caused by gallstones blocking bile ducts — less common and less severe however

acute: critically ill patients with flow of bile is impaired

chronic: multiple, repeated, mild attacks of acute cholecystitis

• leads to thickening of gallbladder walls and gallbladder shrinks and diminishes function

aggravated by a HIGH FAT diet

cholecystitis MNT

acute: oral feedings stop, PN may be implemented, when feedings resume a low fat diet is recommended (30-45g/day or low fat formula)

chronic: long term, low fat diet (25-30%), water soluble forms of fat soluble vitamins

cholelithiasis (gallstones)

gallstones = calculi — composed of cholesterol, bilirubin, and calcium salts

3 types: cholesterol (80%, most common, consist of ~10% cholesterol), pigment, and mixed stones

generally asymptomatic until it blocks bile ducts causing obstruction, pain, and cramping (cholangitis)

formation of gallstones: too much absorption of water or bile acids from bile, too much cholesterol in bile, or epithelium inflammation

increased risk with: high fat diet, obesity, insulin resistance, diabetes, IBD, cystic fibrosis, and rapid weight loss

cholelithiasis MNT

Reduce risk:

• vegetarian diets

• low fat (<30%) and modest protein

• Small frequent meals

• During acute attack, NPO, complete bowel rest

Increase risk:

• low-fiber, high fat, westernized diet

• high CHO consumption

• fasting (bile secretion decreases)

cholangitis

inflammation of biliary ducts secondary to obstruction of common bile duct

initial treatment: fluids and broad spectrum antibiotics

then, surgery: cholecystectomy (removal of gallbladder) and NPO 12 hours before surgery

pancreas

Elongated, flattened gland that lies in upper abdomen behind the stomach

endocrine functions: produce glucagon and insulin for absorption into blood stream

exocrine functions: secrete enzymes and other substances for metabolism of macronutrients

tests to evaluate pancreatic function

secretin stimulation test — measures pancreatic secretion, particularly bicarbonate (to neutralize stomach acid) in response to secretin secretion

glucose tolerance test — assess endocrine function by measuring insulin response to a glucose load

72-hour stool fat test — assess exocrine function by measuring fat absorption that reflects pancreatic lipase secretion

pancreatitis (overview)

inflammation of the pancreas — way more severe and common than gallbladder diseases

characterized by edema and fat necrosis

can result in: autodigestion (autoimmune), necrosis, and hemorrhage of pancreatic tissue

symptoms: severe upper abdominal pain that may radiate to back, nausea, vomiting, abdominal distension, and steatorrhea

pancreatitis (acute)

risk factors: gallstones (~40%), chronic alcoholism (35%), trauma, genetics, certain drugs

asymptomatic OR upper abdominal pain radiating to back worsening with ingestion of food

diagnosed based on clinical symptoms, elevated lipase, and/or serum amylase

lipase and amylase are elevated with pancreatitis due to pancreatic tissue damage

pancreatitis (chronic)

chronic, irreversible inflammation leading to fibrosis with tissue calcification

symptoms: chronic abdominal pain, elevated pancreatic enzyme levels, weight loss, malnutrition, and/or steatorrhea

diabetes in 30-50% of patients

acute pancreatitis MNT

withhold oral feedings; maintain hydration intravenously

progress diet to as tolerated to clear liquids and then low fat diet, ~6 small meals

30-35 kcal/kg/day — use IBW if obese (usually normal or overweight)

nutrition support as needed (NG tube, EN)

enteral nutrition for severe acute pancreatitis — use of GI tract decreases stress response, less infection complications, decreased length of hospital stay, less expensive, associated with faster return to oral diet

chronic pancreatitis MNT

high risk for protein-energy malnutrition (PEM) due to malabsorption

35 kcal/kg/day with 1-1.5g/kg/day of protein

antioxidants, medium chain triglycerides

pancreatic enzyme replacements if fat malabsorption present

low fiber diet is recommended = fiber may bind the enzymes

pulmonary system overview

major function = gas exchange (provide oxygen, remove CO2)

other functions: immune defense system, regulate acid-base balance (respiratory acidosis — excess CO2), lungs convert angiotensin I to angiotensin II by ACE (angiotensin II increases blood pressure)

mucus in lungs = keeps lungs moist and traps microorganisms and particles for immune defense

anatomy of pulmonary system

includes: nose, pharynx, larynx (voice box), trachea, bronchus, bronchioles, alveolar ducts, and alveoli

alveolar cells secrete surfactant which maintains the stability of pulmonary tissue

no new alveoli are produced after age 20, and lungs lose elasticity and lung capillaries during aging

phagocytosis

alveolar macrophages engulf inhaled inert materials and microorganisms and digest them

cholestasis MNT

reduced or blocked bile flow

occurs when no enteral feedings (no food); need stimulation of biliary motility and secretions by EN if NPO

most pulmonary disease = __________________

require more kcal due to increased effort to eat

key nutrients with pulmonary disorders

protein, iron, calcium, magnesium, phosphorus, potassium

low protein and iron = low hemoglobin

surfactant is also synthesized from protein and phospholipids

vitamin C = required for collagen production for supporting lung tissues

pulmonary assessments to test function

physical exam — percussion and auscultation

diagnostic and monitoring tests — imaging procedures, arterial blood gas, sputum cultures, biopsies

pulmonary function tests — spirometry (breathing to measure lung volume and rate of air inhalation and exhalation)

pulse oximetry used to measure oxygen status of arterial blood OR oxygen saturation using light waves; measures respiratory system’s ability to exchange O2 and CO2 — normal range is 95-99%

cystic fibrosis

inherited autosomal recessive disorder that causes persistent lung infections and limits ability to breathe over time

all exocrine glands persistently secrete abnormally thick mucus that obstructs glands and ducts in organs; thick layer of mucus in airways

most common lethal genetic disorder in white population

epithelial cells and exocrine glands secrete abnormal mucus (thick); >1700 mutations noted

affects respiratory tract, sweat, salivary, intestine, pancreas, liver, reproductive tract

acute or chronic bronchitis, pneumonia, may cause cor pulmonale or infections in advanced stage

a backpack was invented to shake the mucus out of the respiratory tract

most significant organs affected: lungs and pancreas

cystic fibrosis diagnosis

neonatal screening = opportunity to prevent malnutrition in CF infants

sweat test (Cl >60) = gold standard for diagnosing CF (explains increased sodium needs)

>75% of people are diagnosed with CF by age 2

malabsorption — pancreatic insufficiency causes maldigestion of food and malabsorption of nutrients; mucus may interfere with nutrient absorption by microvilli

family history, genotyping

cystic fibrosis MNT

high risk for malnutrition due to maldigestion and malabsorption

individualize throughout life

high risk populations: infants/children (may have growth failure), adolescents, and pregnant/lactating women

factors that influence adequate intake: dyspnea, coughing, coughing-induced vomiting, GI discomfort, anorexia

general recommendations:

• High fat, high calorie diet

• BMI (males <23 and females <22)

• 15-20% from protein or 1.5-2.0x the DRI for age

• 35-45% from fat (MCT)

• increased sodium needs due to losses in sweat

• water soluble formed fat soluble vitamins supplementation (WSV are usually adequate)

  • check annually: vitamins A, D, E, and K; iron, zinc, and albumin

• may start tube feedings at night to maintain high kcal intake

May need pancreatic enzyme replacement therapy (PERT) — individualize

aspiration

movement of food or fluid into lungs

can cause pneumonia or death

proper positioning during eating

high risk populations: infants, toddlers, and older adults and persons with oral, upper GI, neurologic, or muscular abnormalities

foods easy to aspirate: liquids, round foods (nuts, popcorn, hotdogs), chunks of poorly chewed foods (meat or raw vegetables)

EN may be recommended

pulmonary treatments and suctioning of excessive lung secretions = critical to prevent aspirations

asthma

bronchial hyperresponsiveness

increased mucus secretion that obstructs airways; inflammation and swelling; smooth muscle tightening that results in smaller airways

leading cause of hospitalization and death

caused by genetics, immunologic, and environmental factors; respiratory infections by viruses may play a role

decreased risk in childhood with healthy diet during pregnancy and early life and prolonged breastfeeding

allergic (extrinsic): common, triggered by pollen, pet dander, air pollution, smoke, etc

non-allergic (intrinsic): triggered by stress, anxiety, virus, exercise, cold/dry air, smoke, etc

symptoms: cough, dyspnea, tight chest

medical treatment: acute is immediate airway dilation and for chronic use steroids

asthma MNT

weight management

omega 3 > omega 6 fatty acids (decrease production of bronchoconstrictive leukotrienes); need more research

omega 3, zinc, and vitamin C supplementation = improves asthma in kids

nutritionally adequate diet

side effects of asthma medication: dry mouth/throat, nausea, early satiety, vomiting, diarrhea, increased blood glucose, sodium retention

bronchopulmonary dysplasia (BPD)

chronic lung disease of prematurity (often occurs in premature or low birth rate infants); inflammation, impaired growth, and alveoli development

etiology is complex and multifaceted — proinflammatory cytokines, oxygen toxicity, ventilator trauma, and vitamin A status associations

immature lungs cannot synthesize surfactant that permits inflation for gas exchange

prevention and treatment: mechanical ventilation, PN and EN support, good prenatal care to prevent premature delivery, and use of prenatal steroids if premature delivery is expected

bronchopulmonary dysplasia (BPD) MNT

15-20% higher than healthy infants

120-130 kcal/kg/day or higher

3-4g/kg/day of protein

vitamin A supplementation

closely monitor electrolyte balance

sufficient minerals for bone growth — inadequate stores due to prematurity

Chronic obstructive pulmonary disease (COPD)

slow, progressive obstruction of airways

1. emphysema — abnormal, permanent enlargement and destruction of alveoli

2. chronic bronchitis — productive cough with inflammation of bronchi and other lung changes

3rd leading cause of death; it kills 1 life every 4 minutes; half of Americans remain undiagnosed

causes: smoking, secondhand smoke, environmental air pollution, and genetic susceptibility

clinical manifestations: decreased airflow rates, dyspnea, mild hypoxemia (inadequate oxygenation of arterial blood—cyanosis), decreased ventilation due to CO2 retention and respiratory acidosis

cor pulmonale (right ventricular enlargement and heart failure) in late course of emphysema and early in chronic bronchitis

Chronic obstructive pulmonary disease (COPD) management and treatment

4 main goals:

1. assess/monitor disease

2. reduce risk factors

3. manage stable COPD

4. manage exacerbations

treatment:

• pulmonary rehabilitation programs

• oxygen therapy

• medications (bronchodilators, glucocorticosteroids, mucolytic agents, antibiotics)

• surgery (lung transplantation)

Chronic obstructive pulmonary disease (COPD) MNT

calories:

• 1.33 x REE / 25-35 kcal/kg (maintenance)

• 1.5 x REE / 35-45 kcal/kg (repletion)

• replete but DO NOT overfed (excess kcal = excess CO2)

macronutrients

• 1.2-1.7 g/kg of protein to maintain/restore lung and muscle strength and promote immune function

• maintain RQ

15-20% protein

35-45% fat

40-55% CHO

vitamins and minerals

• vitamin C supplementation for smokers

• magnesium and calcium for muscle contraction/relaxation

• vitamin D and K for those with low bone mineral density

• sodium and fluid restriction for those with fluid retention and cor pulmonale

• potassium and calcium if diuretics are prescribed

Respiratory Quotient (RQ)

RQ = CO2 eliminated / O2 consumed

Range: 0.7-1

0.7 = 100% fat diet (fat ratio is 2:1)

1.0 = 100% CHO diet (CHO ratio is 1:1)

lung cancer

occurs in bronchi with metastases in other organs (bone, brain, liver, skin)

risk factors: tobacco smoke, secondhand smoke, exposure to radon or asbestos (radiation, in old houses), air pollution, personal or family history

side effects of chemotherapy, radiation therapy, and surgery: weight loss, cancer cachexia, and anorexia

MNT:

• calorie and protein dense foods, beverages, and nutrition supplements

• manage nutrition-impact symptoms

pneumonia

acute infection (bacteria, virus, fungi) or from aspiration of food, fluid, or secretions (saliva)

results in inflamed alveoli and fluid or pus accumulation; symptoms: coughing, fever, chills, and labored breathing

MNT:

• EFAs = possibly protective (anti-inflammatory)

• goals are to provide adequate fluids, energy, and protein

• small, frequent meals may be better tolerated

• proper positioning during eating

liver physiology and functions

largest solid, internal organ (~1.5 kg or the size of a football)

two functional lobes: right and left

functional unit: lobule

we cannot live without a liver but only ~10-20% function is needed to sustain life

hepatocytes = resilient and regenerative

functions: produces bile; bilirubin elimination; metabolizes hormones and drugs; synthesizes proteins, glucose, and clotting factors; stores vitamins/minerals; changes ammonia → urea; converts fatty acids → ketones, metabolizes macronutrients

common lab values to test liver function

blood test (ammonia: increased with cirrhosis and liver failure)

protein studies (albumin and total protein: decrease with hepatic disease and inflammation)

enzymes (increase with hepatic injuries):

• alkaline phosphatase (ALP): increased with hepatic disease, chronic obstruction of biliary duct, increased levels suggest cholestasis

• aspartate aminotransferase (AST): less specific enzyme to detect hepatic disease secondary to cellular necrosis

• alkaline aminotransferase (ALT): most SENSITIVE test for hepatocellular injury secondary to exacerbation of hepatitis

• AST:ALT ratio of 2:1 or higher may indicate alcohol injury

pigment studies (total serum bilirubin: reflects liver ability to conjugate/excrete bilirubin; increased in liver and biliary disease, causing clinical jaundice (yellow tint to body tissues caused by excess bilirubin in extracellular fluid))

bilirubin elimination process

reticuloendothelial — red blood cells → heme → unconjugated bilirubin (oxygen binds to heme on hemoglobin to transport oxygen)

bloodstream — albumin → unconjugated bilirubin-albumin complex (indirect bilirubin)

liver — uridine glucouranyl transferase → conjugated bilirubin (direct bilirubin)

gut — gut bacteria → urobilinogen (80% excreted in feces, stercobilin; 2% excreted in urine, urobilin; 18% enterohepatic circulation)

hepatitis types (liver disease)

Hepatitis A — transmitted via fecal-oral route; contaminated water, food, sewage

Hepatitis B — aka serum hepatitis; transmitted via blood, blood products, semen, and saliva; acute or chronic; development of cirrhosis and liver cancer

Hepatitis C — exposure to blood or body fluids from infected person; associated with chronic liver disease, cirrhosis, and need for liver transplant

Hepatitis D and E — uncommon, acute infection, rare in US

viral hepatitis MNT

nutritional implication: weight loss and nutritional deficiencies (inadequate intake typically)

nutrition assessment: weight/weight history, food intake, lifestyle factors

nutrients needed for liver regeneration:

• 30-35 kcal/kg/day

• 1.2-1.5 g/kg/day of protein

• avoid alcohol

nonalcoholic fatty liver disease (NAFLD)

spectrum of liver disease ranging from steatosis → steatohepatitis

• Steatosis: accumulation of fat within the liver; fatty liver

• Nonalcoholic steatohepatitis (NASH): liver inflammation; accumulation of fibrous tissue within the liver (progressive due to oxidative stress); related to excessive energy intake

affects ~25% of population; commonly associated with obesity, dyslipidemia, metabolic syndrome, T2DM, and insulin resistance

liver diseases chart

healthy liver → NAFLD (fatty liver) → NASH (inflammation) → NASH with fibrosis (reversible) OR NASH with cirrhosis (irreversible except transplantation)

NASH (inflammation) → NASH with cancer without cirrhosis

NASH with cirrhosis → NASH with cancer and cirrhosis

Key takeaway: cirrhosis is irreversible and severe

MNT for NAFLD and NASH

weight management (moderate-lower kcal; NO high kcal as they are usually overweight already)

1-1.2 g/kg/day of protein

low fat diet, limit saturated fats; use mono- or poly- unsaturated fatty acids instead

manage diabetes if present (CHO controlled)

NAFLD vs NASH

NAFLD: fatty liver

NASH: acute inflammation/viral

alcoholic liver disease

important in cirrhosis etiology; most common liver disease in the US

alcoholism defined: 5 drinks for men (15 drinks per week) and 4 drinks for women (8 drinks per week)

3 Stages (similar to CKD):

1. Hepatic Steatosis — reversible with abstinence from alcohol

2. Alcoholic Hepatitis — reversible with abstinence from alcohol

   toxic liver injury associated with chronic ethanol consumption (increase susceptibility to infections); symptoms are fatigue, anorexia, nausea, vomiting, weakness, diarrhea, fever, weight loss

3. Cirrhosis — irreversible

MNT for alcoholic dependency/alcoholic hepatitis/alcoholic liver disease

nutritional implications

• imbalanced diet and/or anorexia

• intestinal maldigestion and malabsorption

• increased energy expenditure and inadequate intake is typical

MNT

• abstinence from alcohol

• manage malnutrition

• manage vitamin deficiency (thiamin)

malnutrition in the alcoholic

displacing intake of adequate calories and nutrients

• light drinker: alcohol addition

• heavy drinker: alcohol substitution

Lipid and CHO metabolism is compromised

• impaired triglyceride oxidation = fat present in liver cells

Reduced intake and alterations in absorption, storage of vitamins/minerals: vitamin A, thiamin, and folate

Thiamin deficiency is the most common (occurs in ~80% of alcoholics) = responsible for Wernicke Encephalopathy

cirrhosis

end stage of chronic liver disease (similar to CKD); may be clinically silent and irreversible

the normal architecture of liver is replaced by fibrous tissue, blocking the flow of blood through the liver

blockage of blood flow; blood is forced backwards; blood cells essentially die (no blood flow through)

symptoms: fatigue, anorexia, nausea, weakness, poor appetite, weight loss (masked by ascites which is the accumulation of fluid, proteins, and electrolytes caused by increased pressure from hypertension and decreased albumin; only caused by alcohol), portal hypertension/liver failure, hepatic encephalopathy (brain disease caused by cirrhosis)

common causes: hepatitis C, alcoholic liver disease, NAFLD, hepatitis B+D, misc.

portal hypertension/ascites

elevated BP in portal venous system caused by obstruction of blood flow through the liver; usually solved with a brace to open esophagus

major cause of portal hypertension: alcoholic cirrhosis

characterized by:

• ascites — solved by draining

• varices — blood flow is forced backwards, causing veins to enlarge and varices develop across esophagus and stomach from pressure in portal vein

• encephalopathy — decreased mental capacity and consciousness

nutrition assessment of cirrhosis

moderate-severe malnutrition is common

causes: inadequate intake caused by anorexia, dysgeusia, early satiety, nausea and vomiting; dietary restriction (decrease blood volume = decrease sodium); maldigestion and malabsorption; altered metabolism secondary to liver dysfunction; increased energy expenditure; protein losses from paracentesis (draining of fluid/ascites)

MNT for cirrhosis

energy: 35-40 kcal/kg/day (depends on weight, obesity; use dry weight)

CHO: treat as diabetes (CHO controlled)

fat: <30% of total kcal; low fat (~40g/day) for significant stool fat loss; MCT may be beneficial for fat malabsorption; fat soluble vitamins may be a concern

protein: should NOT be restricted, even with encephalopathy; up to 1.6g/kg/day depending on malnutrition degree

ONLY restrict sodium (to decrease blood volume)

vitamins and minerals: supplementation is needed in all patients; deficiencies in fat soluble vitamins specifically (A, D, E, K) as well as vitamins B1, B3, B6, iron, magnesium, phosphorus, and zinc

caused by steatorrhea, alcoholism, diuretics, diarrhea, GI bleeding

sodium restriction with ascites (<2g/day Na) — fluid restriction is also normally recommended

common feeding problems: anorexia, nausea, dysgeusia, etc

other aspects of cirrhosis

portal hypertension

• PN if needed for at least 5 days

• EN contraindicated with bleeding varices

  • esophageal varices; may prescribe soft diet

• ascites

  • sodium restriction/diuretics

  • paracentesis: to relieve abdominal pressure (draining)

• hyponatremia

  • sodium losses via paracentesis, excessive diuretic use, or extreme sodium restriction

hepatic encephalopathy

syndrome characterized by impaired mentation, neuromuscular disturbances, and altered consciousness — complication of cirrhosis

pathogenesis is unknown; inability to eliminate cerebral toxin

3 Major Hypotheses:

1. ammonia accumulation

2. Synergistic neurotoxin (ammonia)

3. False neurotransmitter

Associated with urea cycle (in the liver) and protein (ammonia)

4 stages of hepatic encephalopathy

1. mild confusion, agitation, irritability, sleep disturbances, decreased attention

2. lethargy, disorientation, inappropriate behavior, drowsiness

3. somnolence but arousable, incomprehensible speech, confusion, aggression when awake

4. coma

MNT for hepatic encephalopathy

AVOID unnecessary protein restriction, despite past research — patients often have inadequate protein intake

most patients with cirrhosis can tolerate mixed-protein diets up to 1.6 g/kg/day

vegetable proteins may be beneficial (amino acid composition)

may use probiotics and synbiotics — decreases ammonia in portal blood; prevents production/uptake of lipopolysaccharides (LPS) in gut (AKA endotoxins)

Wernicke’s Encephalopathy

results from thiamin deficiency (most commonly associated with alcoholism)

thiamin = most important/common deficiency

WE: triad of acute mental confusion, ataxia (clumsiness), and ophthalmoplegia (eye issues)

True or False: we are more microbes than human cells

True

factors that influence microbiome

• diet

• pharmaceuticals

• geography

• life cycle stages

• stress (exercise, metabolic, psychological)

• birthing process

  • infant feeding method (breast fed vs formula, which is sterile)

microbiome definition

immensely diverse, dense, dynamic, complex, and resilient community of trillions of microbes belonging to thousands of species that dwell inside the gut

what happens when the microbiome is imbalanced?

eubiosis (homeostasis) → dysbiosis (non-homeostasis)

specific foods that influence gut microbiome

• whole grains

• fruits and nuts

• vegetables and legumes

As well as:

• fiber/CHO

• fat

• protein

  • phytochemicals

Mediterranean diet and gut microbiome

fiber rich boosts gut microbiome diversity and fosters beneficial microbes; flourishment of indigenous probiotics and other beneficial bacteria

• microbiota diversity = beneficial

Mediterranean diet = very beneficial for microbiome (most beneficial probably)

Mediterranean diet improves gut microbiome in older adults who followed a western diet previously (takeaway: it is NEVER too late)

microbiome modulation with diet reduces AD markers via gut-blood-brain axis

strategies to alter gut microbiome

1. FMT (fecal matter transplant — bacteria)

2. Diet, prebiotics and probiotics

   1. Microbial consortia, probiotics

probiotics

live microorganisms that provide health benefit when adequate amounts are consumed

help support our bacteria, especially with imbalances

present in many foods and dietary supplements

can support health by:

• ensure proper immune function

• aid digestion by breaking down foods we can’t digest

• keep harmful microorganisms in check

• contribute to vitamin biosynthesis and nutrient absorption

prebiotics

substrate selectively utilized by host microorganisms conferring a health benefit — essentially food for microbes

must confer a beneficial physiological effect on host and effect should derive at least in part from utilization of the compound by resident microbes

frequently equated with fiber, but only a subset of dietary fibers actually qualify as prebiotics

may be derived from non-fiber substances, like polyphenols

may be present naturally or in synthesized forms

distinguishing what is a prebiotic and what is not based on official definition

**not just fiber

prebiotics: CLAs, PUFAs, human milk oligosaccharides, oligosaccharides (FOS, inulin, GOS, MOS, XOS), phenolics and phytochemicals, readily fermentable dietary fiber

not prebiotics: antibiotics, proteins and fats, vitamins, probiotics, less fermentable dietary fiber

synbiotics

prebiotic + probiotic = synbiotic

mix of live microorganisms and substrates selectively utilized by host microorganisms that confer a health benefit on the host

complementary AND synergistic effects

complementary = prebiotic and postbiotic

synergistic = live microorganism and substrate

they go on to produce health benefit(s)

Postbiotics

preparation of inanimate microorganisms and/or their components that confer a health benefit on the host

must include some non-living microbial biomass, whether its whole cells or cell components

components: intact inanimate microbial cells, microbial cell fragments/structures, with or without metabolites/end products

microbiome take home messages:

we are what our gut bugs eat

we share a candid relationship with our gut microbiome

eat prudently, workout moderately, destress often, and relish gratitude