COMPREHENSIVE DIGESTIVE STOOL ANALYSIS

Stephen Barrie, ND

Introduction
Proper digestion is a prerequisite for optimal health. Without adequate breakdown and assimilation, even the best dietary intake is of diminished benefit to the body. Additionally, incomplete breakdown may lead to the absorption of macromolecules (including whole bacteria), intestinal and systemic toxemia, and intestinal irritation, infection, and dysbiosis leading to food allergies (see Chapters II:Food Allergy Testing and IV:Food Allergy), toxemia (see Chapter IV:Bowel Toxemia), and many chronic degenerative and autoimmune diseases. The CSDA (Comprehensive Digestive Stool Analysis) is a battery of integrated tests that evaluate digestion and intestinal function, environment and absorption.

tion. Salivary enzymes (lingual lipase, salivary amylase, and ptyalin) initiate fat and starch digestion.3 Stomach: The stomach mechanically churns food, breaks up and emulsifies fats, exposes molecules to additional enzymes and produces 1 to 2 liters of gastric juices, consisting of:4 1. Hydrochloric acid: secreted by the parietal cells, which denatures proteins, converts pepsinogens to active form pepsin, renders some minerals (e.g., calcium) and iron more absorbable, and helps kill bacteria in ingested matter. The acid was previously thought to create a sterile environment; a recently discovered exception being the presence of Helicobacter pylori. 2. Mucus: forms an acid and pepsin resistant coating for the stomach. 3. Intrinsic factor: bonds with vitamin B12 and is necessary for intestinal absorption. 4. Rennin: clots milk. 5. Gastric lipase: has weak fat-splitting activity. 6. Miscellaneous enzymes: control gastric secretions. Small Intestine: Most digestion and absorption takes place in the small intestines through the action of enzymes secreted by the pancreas, Crypts of Lieberkuhn, and the liver.4 The primary enzymes and secretions include: 1. Pancreatic juices: (2.5 L/day) are secreted by the pancreas under the control of the vagus nerve, and the duodenal hormone secretin. Its production in turn is stimulated by the presence of fat and acid chyme. 2. Bicarbonate: neutralizes stomach acid. 3. Trypsinogen and chymotrypsinogen: are activated to trypsin and chymotrypsin. These enzymes digest proteins by cleaving polypeptides to oligopeptides and small amounts of free amino acids. Most dietary protein is absorbed in the upper jejunum. 4. Amylase: splits starch to maltose. 5. Maltase: splits maltose to glucose. 6. Lipase splits fats to monoglycerides and free fatty acids. 7. Bile: secreted by the liver (700 mL daily) is stored in the gall bladder. Bile salts emulsify fats to allow the action of water soluble lipases. The Crypts of Lieberkuhn of the intestinal mucosa also produce small amounts of digestive enzymes and immunoglobulins. In addition, small amounts of microbial-derived enzymes are found in the small intestine. Large Intestine: The major role of the large intestine is to absorb approximately a liter of water daily and provide a controlled route for excretion of waste products and toxic substances. The large intestine also provides an environment for microbial fermentation and degradation of carbohydrates (CHO) that results in the production of short chain fatty acids
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The Gastrointestinal Tract

The major function of the gastrointestinal system is to break down and absorb nutrients. Energy liberated by the digestive process is used by the body for repair and growth.1 The absorption of nutritional energy is inseparable from the process of complete digestion because the energy in foods consists mostly of polymers (e.g., starch, triglycerides, and proteins), whereas the actual absorbable and usable fuels released transported from the intestine to the body tissues are monomers or specially reconstituted polymers (e.g., chylomicrons). The digestive tract has the paradoxical dual role of discriminately allowing absorption (molecular uptake) while selectively functioning as a physical and immune barrier. The gastrointestinal tract has a surface area equal to two tennis courts due to the intestinal folds, villi, and macrovilli which increase its surface area 600 times as compared to a simple cylinder. Absorption is largely controlled by the membranes of intestinal epithelial cells. Molecules penetrate the protein /lipid membrane by various mechanisms: simple passive diffusion, facilitated diffusion, active transport, or pinocytosis. Gastrointestinal tract secretory IgA is also utilized for immune exclusion of undesirable molecules and provides an environment for microbial flora growth and activities.2 A startling aspect of digestion is that while the digestive process deals with the daily exogenous intake of approximately 100g of fat, 75g of protein, 350g of carbohydrates, and 2,300 mL of water, it also must digest, absorb or eliminate endogenous secretions of up to 100g of protein (primarily from sIgA), 30g of fat, 75g of protein, and 6,500 mL of water!

The Digestive Process

Mouth: In the mouth, chewing breaks up the food and mixes it with saliva. Saliva aids in bolus formation and protects the pharyngeal and esophageal mucosa, primarily with secretory IgA antibodies.3 Saliva also helps to remineralize the teeth with calcium salts and tags food molecules for better protein digesCopyright 1993 Pizzorno, Murray and Barrie

which are the main energy source for colonic epithelial cells. Bacterial hydrolases break down CHO polymers and bacterial amylases break down starch and glycogen.

gut. All factors within the GI tract are important to the ecological unit, with gut secretions, microflora, and nutrient material being the major components. Normal Intestinal Microflora: The microflora of the gastrointestinal tract constitute an enormously complex ecosystem of aerobic and anaerobic microorganisms.31 A human harbors more than 400 to 500 species of intestinal flora.49 The normal human is composed of over 1014 cells of which 90% are microbial cells, which mostly reside in the gastrointestinal tract.50 In other words there are more bacteria in the gut than the total number of human cells in the body and the flora possesses more metabolic activity than the host itself. However, flora content is surprisingly stable within an individual over time.51 In many ways, the gut flora can be viewed as an organ of the body in its own right, as these microbes profoundly influence many physiologic processes of the host. Certain normal metabolic functions and enzyme activities can be attributed to the microflora, which play a role in metabolizing nutrients, vitamins, drugs, endogenous hormones and carcinogens; synthesizing short chain fatty acids; preventing colonization of the intestines by pathogens; and stimulating maturation of the normal immune response.52,53 Short Chain Fatty Acids: A special property of colonic bacteria is their fermentation of carbohydrates to short chain fatty acids (acetate, propionate, butyrate and valerate).54 SCFAs provide up to 70% of the energy for colonic epithelial cells.52 The factors that influence SCFA production include: composition of colonic flora, transit time, diet, and ingestion of antimicrobial drugs.55 Intestinal Permeability: The association between intestinal inflammation, increased permeability and autoimmune diseases is emerging. A significant cause of increased intestinal permeability and maldigestion relates to disordered bowel flora.

Absorption of Specific Nutrients5

Carbohydrates: Salivary amylases initiate starch digestion in the mouth. However, this activity is short-lived, as the enzyme is denatured by low gastric pH. In the duodenum, oligo- and disaccharides undergo hydrolysis by pancreatic amylase. Further hydrolysis is carried out by brush border enzymes, specific disaccharides (lactase, sucrase, and maltase) located on the enterocyte microvilli. The resultant monosaccharides are absorbed by specific sodium-dependent transport carrier mechanisms. Carbohydrate malabsorption occurs when there is an insufficiency of any of the above processes. Clinical examples include: pancreatic insufficiency, specific brush border enzyme deficiency (e.g., lactase deficiency), disruption of the brush border (e.g., celiac disease, Crohn's disease), or total loss of intestinal mucosal surface area (e.g. resection). Proteins: Gastric acid and pepsin initiate the digestion of dietary protein. This is followed in the duodenum by hydrolysis into oligopeptides by proteolytic pancreatic enzymes. Final digestion is accomplished by intestinal brush border peptidases. Proteins are absorbed as dipeptides, tripeptides, free amino acids, and probably other short chain peptides. Like carbohydrate malabsorption, protein malabsorption can occur with pancreatic insufficiency, hypo- or achlorhydria, diseases affecting enterocyte function, and loss of absorptive surface. Fat: Processing of dietary fat is the most complex of the digestive and absorptive processes. As fat is water-insoluble, the GI tract must transform large water-insoluble particles into soluble, absorbable forms. Digestion begins in the mouth with secretion of lingual lipases. The stomach emulsifies fat, dispersing fat globules into an evenly divided phase. Pancreatic enzymes then split triglycerides into fatty acids and monoglycerides, and hydrolyze various polyesters. These then combine with bile acids and phospholipids secreted by the liver to form micelles. The process of micellar solubilization transforms water-insoluble fat into a water-soluble form that is absorbed in the proximal small intestine. After absorption, fatty acids and other fats are reesterified in the intestinal cells to form chylomicrons, which are then secreted into the lymphatic system. Medium-chain triglycerides can be absorbed directly in the jejunum without undergoing hydrolysis and micellar solulblization. Disruption of bile synthesis or flow, pancreatic insufficiency, or enterocyte disruption can lead to fat malabsorption. Thus biliary tract obstruction, chronic pancreatitis, Crohn's disease, celiac disease, or resection may all cause fat malabsorption.

Digestive Abnormalities
Malabsorption
Malabsorption results from intraluminal maldigestion or mucosal malabsorption. Malabsorption is characterized by abnormal fecal excretion of fat (steatorrhea) and variable malabsorption of fats, fat soluble vitamins, other vitamins, proteins, carbohydrates, minerals, and water. Some causes are listed in Table 1.6-9 In patients with maldigestion, the processing of nutrients in the gastrointestinal tract is impaired most commonly because of: insufficient mastication, gastric acid deficiency, pancreatic insufficiency, hepatobiliary disease, and intraluminal bacterial overgrowth.9

Intestinal Microecology
The contents of the gut lumen form a microecology that has profound effects on the host as well as the inhabitants of the
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Table 1. Causes of Malabsorption

Bowel mucosal damage Bacterial and viral infections Inadequate absorptive surface Insufficient concentrations of digestive enzymes Drug induced Multifactorial

Hypo- and Achlorhydria: Gastric acid secretion is a fundamental step in digestion and assimilation, particularly of proteins and mineral. Although much has been said about hyperacidity, little attention has been paid to hypochlorhydria. This deficiency of acid is a significant health problem, as many, or possibly more, health problems are caused by hypochlorhydria and achlorhydria than by hyperacidity. Many symptoms, signs and diseases are associated with low gastric acidity, particularly HLA B8 related autoimmune diseases (Table 2 and 3). Table 2. Common Signs and Symptoms of Low Gastric Acidity10,11
Bloating, belching, burning, and flatulence immediately after meals A sense of fullness after eating Indigestion, diarrhea or constipation Systemic reactions after eating Nausea after taking supplements Rectal itching Weak, peeling, or cracked fingernails Dilated capillaries in the cheek and nose (in nonalcoholic) Post adolescent acne Iron deficiency Chronic intestinal infections parasite, yeast, bacteria Undigested food in stool

was ineffective.14 The authors speculated that this was due to atrophy of various digestive organs. Intestinal peristalsis and gastric acid secretion normally prevent excessive proliferation of bacteria in the small intestine. Hypo- or achlorhydria can be a cause of bacterial overgrowth. Bacterial overgrowth leads to intraluminal maldigestion, interferes with fat digestion, and microbially-bound vitamin B12, which reduces its availability for absorption. Such overgrowth can cause damage to the intestinal mucosa through microbial cell walls and metabolic products (glycosides, proteases and toxins). Pancreatic Exocrine Insufficiency: Inadequate delivery of pancreatic lipase, proteases, and bicarbonate to the small intestine can result in intraluminal maldigestion. Pancreatic insufficiency leads to impaired absorption of dietary fat and protein with potential major negative systemic effects. The absorption of carbohydrates and water soluble vitamins, however, is only partially impaired. Mucosal Malabsorption: Disease-induced mucosal lesions impair the uptake and transport of available intraluminal nutrients across the mucosa of the small intestine. Table 4 lists diseases which damage the intestinal mucosa, while Table 5 lists drug which may cause malabsorption. Table 4. Diseases Which Damage the Intestinal Mucosa
Crohn's disease Cryptosporidiosis Eosinophilic gastroenteritis Giardiasis Lactose intolerance Sprue Whipple's disease

Table 5. Drugs Which Can Cause Malabsorption

Cholestyramine Neomycin Colchicine Irritant Laxatives

Table 3. Diseases Possibly Associated With Low Gastric Acidity15-24

Addison's disease Asthma Celiac disease Chronic autoimmune disorders Dermatitis herpetiformis Eczema Food allergies Gallbladder disease Gastric carcinoma

Decreased intrinsic factor production is associated with hypochlorhydria. Many studies have shown that acid secretory ability decreases with age, with low stomach acidity found in over half of those over age 60.12,13 One study of elderly people found that their tissue nutrient levels could be saturated only with intramuscular supplementation as oral supplementation
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Clinical Considerations: The signs and symptoms of malabsorption are varied. Some causes are: changes in stool osmolarity, unabsorbed CHO fermentation, physical accumulation of undigested materials, impaired vitamin or mineral absorption, protein malabsorption, intestinal wall irritation and decreased gut immune system.26 Malabsorption increases with age.27 Table 5 lists the common signs and symptoms of malabsorption. Amino acids, carbohydrates, fats, vitamins, and trace elements are all absorbed by different processes, so malabsorption for one nutrient does not necessarily imply malabsorption of others. In the case of fat malabsorption, besides the loss of the highest source of dietary calories, essential fatty acid deficiency may result. EFA's are the precursors for prostaglandins, leukotrienes and other active compounds.
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Table 6. Signs and Symptom of Malabsorption28

Abdominal cramps, distention, flatulence Anemia Chronic autoimmune diseases Chronic intestinal infections Diarrhea Easy bruisability Greasy stools Increased intestinal permeability Osteomalacia Weight loss

complaints.36 There should be no doubt of the profound relation between GI tract infections, malabsorption, permeability changes, and health. Yeast: In the last few years, Candida albicans has attracted considerable attention and controversy as a cause of chronic ecological illness.37 Many investigators have suggested that an intestinal overgrowth of Candida albicans (and other intestinal yeast) may be an etiologic factor in food allergy, migraine, irritable bowel, asthma, indigestion and gas, depression related to PMS, vaginitis, and chronic fatigue.38-42 Others have dismissed these claims as unproven speculation. While the normal GI tract harbors small amounts of yeast, overgrowth of yeast may be more common now as a consequence of the recent wide use of antibiotics, corticosteroids, birth control pills and increased dietary carbohydrates.43 Proponents of yeast as etiologic agents in disease believe that it is not its presence but its overgrowth and its effects on systemic processes in patients that characterize the disease state. Odds' text on Candida summarized over 20 papers showing that patients had C. albicans in their feces over twice as often as normal controls.44 Yeast overgrowth can result in increased mycotoxin activity in the intestines and systemic effects due to translocation of yeast antigens to body tissues. The resulting circulating immune complexes can have immunosuppressive effects and play a role in a variety of diseases such as systemic lupus, rheumatoid arthritis, chronic inflammatory bowel disease, and food allergies. One recent article reported that chronic diarrhea and abdominal cramps may be caused by large numbers of dead or damaged yeast found in feces.45 While the debate on pathogenicity of yeasts will continue, high quality lab work is essential. Yeast may be observed directly microscopically or indirectly through culture. Both are necessary for collection of good data on their occurrence. Viruses: Viruses that infect the GI tract can be divided into two groups: those that induce diseases within the GI tract (e.g., gastroenteritis) and those that initially replicate in the GI tract but induce disease in other organ systems (e.g., the myocardium or CNS).36 GI Tract and Arthritis: The link between enteritis and arthritis is becoming more accepted. In situations of altered bowel anatomy, chronic bacterial overgrowth can lead to the formation of circulating immune complexes that may result in synovitis.46 If the GI tract is the portal of entry of microbial antigens that are cross-reactive with endogenous host antigens, then an autoimmune reaction may follow. Changes in bowel permeability because of local gut inflammation may expose the host immune system to novel microbial or food antigens, allow bacterial translocation and result in synovitis.47,48 Finally, toxins derived from enteric organisms (e.g., C. difficile) may play a direct role in the introduction of arthritis.

Intestinal Infections
Organisms which may infect the intestines and cause pathology include: bacteria, yeasts, parasites and viruses. The normal host defense mechanisms include: acid and enzymatic degradation, secretory IgA antibody attack, normal flora antibacterial enzymes, peristalsis, and competitive growth inhibition by normal flora.29-32 The better the quality of the composition of the indigenous microflora, the higher the colonization resistance.33 Besides the acute symptoms of abdominal cramps and diarrhea, intestinal infections can cause a wide range of systemic and chronic effects stemming from increased intestinal permeability; translocation of bacteria, antigens, and parasites; and the disruption of normal flora. Bacteria: Common bacteria that can cause diarrhea in the United States include: Salmonella, Shigella, Campylobacter jejuni, Yersinia, Clostridium, Citrobacter and 5 forms of E. coli (enterotoxigenic, enteropathogenic, enteroinvasive, enterohemorrhagic, and enteroadherent). Intestinal pathogens can cause epithelial inflammation that can lead to mucosal lesions and damage. This may cause clinical and subclinical malabsorption of nutrients. The morphological changes in the mucosa can alter the barrier to macromolecular absorption and increase bowel permeability to large macromolecules and antigens resulting in food and chemical sensitivities and intolerance. Pathogens can produce endotoxins that can lead to immunologic reactions. These reactions activate the alternate complement pathway, releasing chemotactic factors leading to chronic systemic inflammatory conditions (e.g., psoriasis and lupus). There is evidence that some microflora share antigenic determinants with normal tissues and produce cross-reactive antibodies (See Chapter IV:Bowel Toxemia). These have been shown in diabetes mellitus, meningitis, thyroid disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, pernicious anemia, and systemic lupus.34,35 Whipple's disease, although rare, presents an interesting model of the interaction of bacterial infection, absorptive processes and systemic health. This disease is known to be caused by an unusual bacteria, which has resisted attempts to culture in vitro. Patients suffer severe alterations in intestinal permeability and suffer chronic fatigue along with a list of other systemic
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induce disease by altering the nutrition or immune responses of their host.70 Disorder Mechanisms: The mechanisms for these disorders are varied: Bacteroides cause B12 deficiency by uncoupling the B12-intrinsic factor complex; Klebsiella and Proteus are thought to precipitate ankylosing spondylitis and rheumatoid arthritis in genetically susceptible individuals through mimicry of human HLA antigens;35 the arthritis by protozoan infestation is probably caused by circulating immune complexes;76 aerobic bacteria may cause irritable bowel syndrome by increasing prostaglandin synthesis and Candida albicans may do so because of Type I hypersensitivity.77 Alterations in gut fermentation patterns and bile salt metabolism seem involved in colon carcinogenesis;78 estrogen metabolism by gut flora may account for dietary effects on mammary carcinogenesis.73 Activation of the alternate pathway of complement by bacterial endotoxin or yeast zymosan because of increased permeability may underlie the pathophysiology of Crohn's disease, psoriasis, and cystic acne.79,80 Recent Observations and Major Causes: Recent observations that the colonic flora produce important nutrients for colon epithelial cells, and that colonic flora may also attack and degrade mucus support the theory that colonic flora are involved in colonic pathophysiology. Table 8. Some Major Causes of Intestinal Dysbiosis70,81,82
Antibiotic/drug therapy Decreased gut motility Decreased immune function Increased intestinal pH Intestinal infection Maldigestion Poor diet/nutritional status fat, simple CHOs Presence of xenobiotics Stress

m Sto

Es op ha gu s

Foods
Nutrients Minerals Vitamins Herbs

Gut Secretions
Electrolytes Enzymes Protein Water Fat

Digestion Absorption Immune Function Detoxification Hormone Production

h ac

I all Sm

Mo uth

stin nte

Colon Microflora
Bacteria Viruses Fungi Parasites

Figure 1. Microecology Relationships

Dysbiosis
Recognition that intestinal flora has a major impact on human health first developed during the birth of microbiology in the late nineteenth century. It became generally accepted that our healthy relationship with indigenous gut flora is "Eusymbiotic." Early this century, Metchnikoff popularized the idea of "Dys-symbiosis" or "Dysbiosis" a state of living with intestinal flora that has harmful effects. He postulated that toxic amines produced by bacterial putrefaction of food were the cause of degenerative disease.69 This hypothesis has recently gained increasing experimental and clinical support. With the widespread use in the past 30 years of antibiotics that profoundly disrupt the normal flora, the role and interaction of normal microflora in health and disease has become of more critical importance. Table 7. Diseases in Which Dysbiosis Is Implicated31,7175

Autoimmune arthropathies Chronic fatigue syndrome Colon and breast cancer Cystic acne Eczema Inflammatory bowel disease Irritable bowel syndrome Psoriasis Steatorrhea Vitamin B12 deficiency

Food Allergy: Food allergy is, of course, a well known phenomena. However, its prevalence, lab methods for testing, and treating modalities remain controversial. Hunter recently proposed that food allergy is not an immunological disease, but a disorder of bacterial fermentation in the colon. He theorized in The Lancet that the combined mechanisms of reduced gut enzyme concentrations, imbalanced bacterial flora, and increased permeability account for many cases of food intolerance.83 Dysbiosis Patterns: In his recent research, Galland has advanced the idea of four interlocking patterns of bacterial dysbiosis: 1. Putrefaction: Putrefaction dysbiosis results from diets high in fat and animal flesh and low in insoluble fiber. This type of diet produces an increased concentration of Bacteroides sp. and a decreased concentration of Bifidobacteria sp. in stool. It also increases bile flow and induces bacterial urease activity.
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Dysbiosis is defined as a disordered microbial ecology that causes disease. This state may exist in the oral cavity, gastrointestinal tract, or vaginal cavity. In dysbiosis, organisms of low intrinsic virulence, including bacteria, yeasts and protozoa,
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The microbial changes occur primarily among anaerobes, but the effects are measured as an increase in stool pH (partly caused by elevated ammonia production), an increase in bile or urobilinogen, and possibly by a decrease in short chain fatty acids, especially in butyrate. A putrefaction dysbiosis is accompanied by an increase in fecal concentration of various bacterial enzymes which metabolize bile acids to tumor promoters and deconjugate excreted estrogens, raising the plasma estrogen level. Epidemiologic and experimental data implicate this type of dysbiosis in the pathogenesis of colon cancer and breast cancer. Putrefaction dysbiosis is corrected by decreasing dietary fat and flesh, increasing fiber consumption and supplementing with Bifidobacteria and Lactobacillus preparations. 2. Fermentation excess: This is a condition of carbohydrate intolerance induced by an excess of normal bacterial fermentation. Small intestinal or fecal bacterial overgrowth is the usual cause. Products of bacterial fermentation of dietary starch or sugar include short chain fatty acids, lactic acids, and ethanol. Abdominal distention, flatulence, diarrhea, constipation and feelings of malaise or fatigue are commonly described. If d-lactic acid is a by-product, neurological dysfunction can occur. In small bowel bacterial overgrowth, degradation of intestinal brush border enzymes and of pancreatic enzymes by bacterial proteases can cause maldigestion. Fermentation excess is suggested by elevated fecal short chain fatty acids and evidence of maldigestion accompanying the appropriate clinical syndrome. Patients with fermentation excess are usually intolerant of fiber supplementation and often benefit from reduction or alteration of carbohydrate consumption and from anti-microbials. 3. Deficiency: Exposure to antibiotics or a diet depleted of soluble fiber may create an absolute deficiency of normal fecal flora, including Bifidobacteria, Lactobacillus and E. coli. Direct evidence of this condition is seen on stool culture when concentration of Lactobacillus or E. coli are reduced. Low concentrations of fecal short chain fatty acids provides presumptive evidence. This condition has been described in patients with irritable bowel syndrome and food intolerance. Deficiency and putrefaction dysbiosis are complementary conditions which often occur together and have the same treatment. Sometimes feeding vegetable extracts rich in fructose-containing oligosaccharides is more effective than feeding on fiber to help re-establish a normal flora. 4. Sensitization: Aggravation or abnormal immune responses to components of the normal indigenous intestinal microflora may contribute to the pathogenesis of inflammatory bowel disease, spondyloarthropathies and other connective tissue diseases, and skin disorders
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like psoriasis or acne. The responsible bacterial components include endotoxins, which can activate the alternative complement pathway, and antigens, some of which may cross-react with mammalian antigens. Treatment studies in ankylosing spondylitis and inflammatory bowel disease suggest that sensitization may complement fermentation excess and that similar treatments may benefit both conditions. It would be inappropriate to consider dysbiosis a "disease". Rather, it is the result of interactions between various aspects of the intestinal environment. It is a "marker" concept, indicating an imbalance. When identified, it should trigger a series of actions by the clinician to rebalance the bowel and therefore eliminate the possible cause of much ill health.

Comprehensive Digestive Stool Analysis

The comprehensive digestive stool analysis offered by the Great Smokies Diagnostic Laboratory (copyrighted as CDSA) is a battery of 18 integrated diagnostic laboratory tests that evaluate digestion, intestinal function, intestinal environment and absorption. The CDSA provides information that is useful in leading to the correct diagnosis and development of appropriate therapeutic resources. Many physicians consider it a "foundation" screening test that consistently provides valuable clinical information. The CDSA can uncover the causes of both acute and chronic illnesses.

Digestion
Chymotrypsin: Fecal chymotrypsin is a measure of proteolytic enzyme activity that is both sensitive and specific.59,60 Amman reports a close correlation between duodenal and fecal enzyme activity.61 Decreased quantitative fecal values reflect pancreatic insufficiency and potential maldigestion of proteins.62 Elevated levels suggest rapid transit time. Reference range: 6.2 to 41.0 IU/g Triglycerides: Triglycerides are the major dietary fat component. Elevated quantitative fecal amounts reflect incomplete fat hydrolysis and suggest pancreatic insufficiency. Reference range: <0.6% Meat and Vegetable Fibers: These are microscopic qualitative indirect indicators of maldigestion from either HCI/pepsin insufficiency or pancreatic exocrine dysfunction. Several studies have reported that fecal meat fibers were as good as other methods for recognition of nonspecific maldigestion.59,63,64 Some studies have shown an excellent correlation between excessive fecal meat fibers and hypo- or achlorhydria as measured by direct radio telemetry. Reference range for meat fibers: 0 (none seen) Reference range for vegetable fibers: 0 to 4 fibers pH: There is considerable interest in fecal pH in relation to risk of colon cancer, especially as affected by fiber intake and the subsequent production of short and long chain fatty acids.65 A correlation between alkaline pH and decreased short chain fatty
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acid (particularly butyrate) values has been observed.66 Clinical studies have also shown a relationship between elevated fecal pH hypochlorhydria. Elevated pH values with diminished SCFA levels together support inadequate flora digestion of fiber and/or inadequate dietary fiber. Reference range: 6.0 to 7.2 pH

Microbiology
Normal Bacteria: The benefits of an ecologically balanced intestinal flora have already been discussed. There are several important resident bacteria that should always be present for optimal intestinal health and function. They are also important in preventing colonization by intestinal pathogens. They are: Escherichia coli (aerobic, non-pathogenic resident strain) Lactobacillus sp (aerobic) Bifidobacteria (anaerobic) These three organisms are cultured and growth is quantitatively measured. Reference range: 2+ to 4+ (within a 0 to 4+ scale) Pathogenic Bacteria: Alterations in the composition of the intestinal flora often accompany acute diarrheal illness. The CDSA reports the presence of bacterial pathogens, by type and amount. Some more common pathogens found include: Aeromonas Campylobacter Salmonella Shigella Staphylococcus aureus Vibrio Yersinia There are intestinal bacteria that, while not causing acute GI tract disturbances, may be involved in the etiology of various chronic or systemic problems and, through molecular mimicry, in several autoimmune diseases. These "possible pathogens" are quantified and reported and may include: Klebsiella Proteus Pseudomonas Citrobacter The CDSA also reports organisms that are characteristic of "imbalanced flora." It is important to know if bacteria are present that are markers of an imbalanced intestinal ecology. Some bacteria reported in this category include: Enterobacter Beta hemolytic Streptococci Hemolytic E. coli Hafnia Mucoid E. coli Gram Stain Ratio: From a gram stain, the percentage Gram negative versus Gram positive bacteria are reported. This ratio is another indication of bowel flora balance. Reference range: 70-80% gram -; 30-20% gram + Mycology: The identification and amount cultured of various yeast species is reported in this section. The common species reported are: C. albicans, C. tropicalis, Rhodotorula, and Geotrichum. Reference range: 2+ to 4+ is considered abnormal Dysbiosis Index: An intestinal state of "dysbiosis" is marked by many varied indicators. The CDSA weighs all the relevant results and computes an Index.. This helps in analyzing the multiple data and provides a quick assessment of the GI tract.
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Absorption
Long Chain Fatty Acids: These free fatty acids are normally readily absorbed by healthy intestines. In cases of mucosal malabsorption they accumulate and reach substantial fecal levels. Elevated levels of free fatty acids may reflect malabsorption. Reference range: <1.6% Cholesterol: Fecal cholesterol comes from both dietary sources and mucosal epithelial cell breakdown. Some of this cholesterol is absorbed, stored and used by the body, while some is excreted. Fecal cholesterol levels remains surprisingly constant during fluctuating exogenous intake. An elevated cholesterol level in feces is abnormal, and may reflect mucosal malabsorption. Reference range: <0.3% Total Short Chain Fatty Acids: SCFAs are the end products of microbial flora fermentation of fibers. Elevated total levels of the four main SCFAs may reflect malabsorption or bacterial overgrowth. Raised levels are found in active colitis.68 Increased levels also suggest disordered fluid, electrolyte and acid/base balances of the body. Decreased levels reflect disruption of the normal colonic flora, possibly due to use of antimicrobial drugs. Reference range: 25 to 155 mole/g

Intestinal Metabolism Markers

The amount and proportion of the different short chain fatty acids reflect the basic health of the intestinal metabolism.55,57 Intestinal microbes have a complex metabolic activity which is of great importance to the host. If one looks upon the flora as an "organ," then the total metabolic functions and by-products of the flora may be used to characterize the flora. The most important SCFAs are acetic, proprionic, butyric, and valeric. Imbalanced ratios of the SCFA reflect unbalanced metabolic processes because of disordered bowel flora, i.e., dysbiosis. Specific SCFA "fingerprints" have been shown to reflect specific bacterial infections. Butyric Acid: Butyric acid is the most important of the SCFAs and is the main energy source for colonic epithelial cells.54 Adequate amounts are necessary for healthy metabolism and welfare of the colonic mucosa. Butyrate has been shown to have protective effects against colorectal cancers, it has been suggested that decreased levels of butyric acid may play a part in the pathogenesis of human colonic carcinoma and ulcerative colitis. Elevated levels are associated with active colitis and inflammatory bowel diseases. Reference range: 10 to 50m/gww
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The factors used in determining the index include digestive, metabolic, and microbiological markers. Reference range: Dysbiosis Index <3 Microbial Sensitivities: Sensitivity analysis accompany possible pathogenic and pathogenic bacteria and pathogenic yeast. These sensitivities are conducted using pharmaceutical and botanical substances.

Macroscopic Observations
Fecal Color: The color of feces is observed and can be indicative of various conditions. Possible indications of abnormality are: Yellow to green: diarrhea, bowel sterilized by antibiotics Black - usually the result of upper tract bleeding Tan or gray: blockage of the common bile duct, pancreatic insufficiency (greasy stool), steatorrhea Red: possible result of lower tract bleeding Blood mixed in stool: colonic bleeding (including hemorrhoids) Reference range: light brown to brown Pus and Mucus: The presence of mucus or pus can be an indication of irritable bowel syndrome, intestinal wall inflammation (caused by infection, e.g., typhoid, Shigella, or amoebas), diverticulitis, or other intestinal abscess. Reference range: absence of mucus and pus Occult Blood: The CDSA notes the presence of fecal occult blood. Occult blood is a possible indicator of colon cancer and represents GI tract bleeding. Follow up with a second test and possible sigmoidoscope exam is recommended. Reference range: occult blood negative

Infections: Various antimicrobial agents, ranging from antibiotics to natural substances, can be used for eradication. Natural therapies include berberine, citrus seed extract, gentian formulas, garlic, and other agents. Additionally, immune support is recommended. This might include: Saccharomyces boulardii supplementation to stimulate sIgA secretion, fructooligosaccharides to stimulate Bifidobacteria, and Lactobacillusand Bifidobacteria preparations for their colonization competition and antimicrobial properties (lactic acid production). Yeast overgrowth can be treated through the use of various antifungal agents, including Nystatin, Nizoril, Diflucan, and natural substances such as undycelenic and caprylic acids, berberine and garlic. Elimination of dietary simple sugars is also helpful. Imbalanced Flora: Stimulating the growth of beneficial flora through the same measures as above is useful. A diet high in both soluble and insoluble fiber and low in saturated fat and animal protein is very helpful. These dietary changes work to lower the concentrations of Bacteroides and increase concentrations of lactic acid-producing bacteria. Fermented dairy products are also helpful.

References
1. Roberts, A: Systems of Life: the digestive system part 1. Nursing Times (March 13):87(11):45. 1991 2. Doe WF: An overview of intestinal immunity and malabsorption. Am J Med 67:1077, 1979 3. Valdez IH, Fox PC: Interactions of the salivary and gastrointestinal systems: The role of saliva in digestion. Dig Dis (Switzerland) 9:125-32, 1991 4. Davenport HW: A Digest of Digestion; 2nd Edition, 1994 5. Caspary WF: Physiology and pathophysiology of intestinal absorption. Am J Clin Nutr 55:299S-308S, 1992 6. Heizer WD: Normal and abnormal intestinal absorption by humans. In: Intestinal Toxicology: Raven Press, NY, 1984 7. Trier J: Intestinal malabsorption: differential of cause. Hosp Pract May 15 pp195-211, 1988 8. Cooke WT and Holmes GKT: Coeliac Disease. 1984 9. Schiller CM: Intestinal Toxicology. Raven Press, NY, 1984 10. Wright JV: Healing with Nutrition. Rodell Press, 1985 11. Rappaport EM: Achlorhydria. NEJM May 12 802-5, 1955 12. Vellas B, Belas D and Albarede JL: Effects of aging process on digestive functions. Comprehensive Therapy 17:46-52, 1991 13. Rafsky HA and Weingarten M: A study of the gastric secretory response in the aged. Gastroent (May):348-352, 1946 14. Baker H, Frank O and Jaslow SP: Oral versus intramuscular vitamin supplementation for hypovitaminosis in the elderly. J AM Geriat Soc 48:42-45, 1980 15. Howitz J and Scwartz M: Vitiligo, achlorhydria and pernicious anemia. Lancet 1331-4, 1971 16. Bray GW: The hypochlorhydria of asthma of childhood. Br Med J 588-90, 1930 17. Atkinsn M, Hosking DJ, Moody F, and Stewart IM: Vagal impairment of gastric secretion in diabetic autonomic neuropathy. Br Med J 588-90, 1975 18. Rabinowitch IM: Achlorhydria and its clinical significance in diabetes mellitus. Am J Dig Dis 18:322-33, 1949 19. Carper WM, Butler TJ, Kilby JO and Gibson MJ: Gallstones, gastric secretion and flatulent dyspepsia. Lancet 413-5, 1967 20. Rawls WB and Ancona VC: Chronic urticaria associated with hypochlorhydria or achlorhydria. Rev Gastroent 267-71, 1950 21. Gianella RA, Broitman SA and Zamcheck N: Influence of gastric acidity on bacterial and parasitic enter infections. Ann Int med 78:271-6, 1979 A TEXTBOOK OF NATURAL MEDICINE

Clinical Application
As the comprehensive digestive stool analysis is an integrated battery of tests, therapeutic intervention should be based not only on single test results, but also on patterns and interrelationships. The following presents a brief overview on the types of therapeutic interventions that may be appropriate. Maldigestion: Exogenous sources of enzymes can be supplemented, including HCl, pepsin, pancreatin, and various plant enzymes. Proper mastication and dietary habits should also be reviewed. Malabsorption: Reduction of inflammation through supplementation with glutamine, quercetin, and improved dietary habits. SFCA Imbalance: Increase consumption of the proper balance of soluble and insoluble dietary fiber. Also supplementation with fructooligosaccharides can increase growth of Bifidobacteria and help the fermentation process. As butyric acid is low, supplementation with butyrate may be of value. pH Imbalance: If alkaline, increase balanced fiber intake and supplement with butyric acid. If acidic, reduce fiber intake and treat bacterial overgrowth if present.
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22. De Witte TJ, Geerdink PJ and Lamaers CB: Hypochlorhydria and hypergastrinaemia in rheumatoid arthritis. Ann Rheum Dis 38:14-7, 1979 23. Ryle JA and Barber HW: Gastric analysis in acne rosacea. Lancet 11951196, 1920 24. Ayrea S: Gastric secretion in psoriasis, eczema and dermatitis herpetiformis. Arch Derm (July) 854-859, 1929 26. Webster ADB: The gut and immunodeficiency disorders. Clinics in Gastroent 5:323-340, 1976 27. Russel RM: Changes in gastrointestinal function attributed to aging. Am J Clin Nutr 55:1203S-1207S, 1992 29. Lenette E: Manual of Clinical Microbiology. 4th Edition, ASM, 1985 30. Petersdorf R, Adams R, Braunwald E, et al: Harrison's Principles of Internal Medicine. 10th Edition 31. Simon G and Gorbach S: The human intestinal microflora. Dig Dis and Sci 31:147S-62S, 1986 32. Walker W and Isselbacher K: Intestinal antibodies. Physiology in Med 297:767-72, 1977 33. Editorial: Evidence of immunoregulation of the composition of intestinal microflora and its practical consequences. Eur J Clin Microbiol Infect Dis (Feb) 103-6, 1988 34. Ebringer A, Khalapfour S and Wilson C: Rheumatoid arthritis and Proteus: a possible aetiological association. Rheumatol Int 9:223-8, 1989 35. Ebringer A, Cox N, Abuljadayel AI, et al: Klebsiella antibodies in ankylosing spondylitis and Proteus antibodies in rheumatoid arthritis. Br J Rheu 27:72-85, 1988 36. Robbins S and Cotran R: Pathologic Basis of Disease. 2nd Edition. Saunders, Philadelphia, PA, 1979 37. Crook WG: The Yeast Connection: A Medical Breakthrough. Prof Books, Jackson, TN, 1986 38. Palacios HJ: Hypersensitivity as a cause of dermatologic and vaginal moniliasis resistant to topical therapy. Ann allergy 37:110-3, 1976 39. Robinet RW: Asthma due to Candida albicans. Univ Mich Med Ctr Bull 34:12-5, 1968 40. Iwata K: A review of the literature on drunken symptoms due to yeast in the gastrointestinal tract. Proc 2nd Int Spec Symp on Yeasts Univ Tokyo Press p260-8, 1972 41. Truss CO: Tissue injury induced by Candida albicans: methyl and neurological manifestations. J Orthomol Pscyh 29:17-37, 1977 42. Kudelo NM: Allergy in chronic monilla vaginitis. Ann Allergy 29:266-7, 1971 43. Helstrom P and Balish E: Effects of oral Tetracycline, the microbial flora and the athymic state on gastrointestianl colonization and infection of BALB/c mice with Candida albicans. Infect Immun 23:764-74, 1979 44. Odds FC: Candida and Candidiosis. 2nd Edition. Baillire Tindall, 1991 45. Casseli M, Trevisani L, Bighi S, et al: Dead fecal yeast and chronic diarrhea. Digestion 41:142-9, 1988 46. Inman R: Antigens, the gastrointestinal tract and arthritis. Rheum Dis: Clin North AM 17:309-21, 1991 47. Wells CL, Jechorek RP and Gillingham KJ: Relative contributions of host and microbial factors in bacterial translocation. Arch Sur 126:247-52, 1991 48. Husby S, Jensenius JC and Svehag SE: Passage of undegraded dietary antigens into the blood of healthy adults: quantification, estimation of size distribution and relation of uptake levels to specific antibodies. Scand J Immunol 22:83-92, 1985 49. Hoverstad T: The normal microflora and short chain fatty acids, presented at 5th Bengt E. Gustafsson Symposium (Stockholm, Sweden) June 1st to 4th, 1988 50. Savage D: Microbial ecology of the gastrointestinal tract. Ann Rev Microbiol 31:107-33, 1977 51. Editorial: Soluble dietary fiber and short chain fatty acids; an advance in understanding the human bacterial flora. Am J Gastroent 85:1313-4, 1990 52. Grubb R, Midtevt T and Norin E: The regulatory and protective role of the normal microflora. Proceedings of the 5th Bengt E. Gustafsson Symposium (Stockholm, Sweden) June 1st to 4th, 1988 53. Hill MJ: Microbial metabolism in the digestive tract. CRC Press, Inc. London, 1986 54. Jeejeebhoy KN, Royall D and Wolever TMS: Clinical significance of colonic fermentation. Am J Gastroent 85:1307-2, 1990 55. Latella and Caprilli R: Metabolism of the large bowel mucosa in health and disease. Int J Colorectal Dis (Germany) 6:127-32, 1991 Copyright 1993 Pizzorno, Murray and Barrie

56. Malhotra SL: Faecal urobilinogen levels and pH of stools in population groups with different incidence of cancer of the colon and their possible role in its aetiology. J Royal Soc Med 75:713, 1982 57. Roediger WE: The starved colon-diminished mucosal nutrition, diminished absorption and colitis. Dis Col Rect 75:713, 1982 58. Bistrian BR and ELsen RJ: Recent developments in short chain fatty acid metabolism. Department of Medicine. New England Deaconess Hospital. ACG mtg, Boston, 1992 59. Lankisch PG: Exocrine pancreatic function tests. Gut 23:777-98, 1982 60. Bode C and Bode JC: Usefulness of a simple photometric determination of chymotrypsin activity in stools - results of a multicenter study. Clin Biochem 19:333-7, 1986 61. Amman RW, Tagwergher E, Kashiwagi H and Rosenmund H: Diagnostic value of fecal chymotrypsin and trypsin assessment for detection of pancreatic disease. New Series 13:123-46, 1968 62. Haverback BJ, Dyce BJ, Gutentag PJ and Montgomery DW: Measurement of trypsin and chymotrypsin in stool. 44:588-596, 1963 63. Arvanitakis C, Cooke R: Diagnostic tests of exocrine pancreatic function and disease. Gastroent 74:932-48, 1978 64. Moore JG, Englert E, Bigler AH and Clark RW: Simple fecal tests of absorption: a prospective study and critique. Am J Dis Dig 16:97-105, 1971 65. Walker ARP, Walker BF and Walker AJ: Faecal pH, dietary fibre intake and proneness to colon cancer in four South African populations. Br J Cancer 53:489-95, 1986 66. Lee MJ and Barrie S: Relationship between butyrate pH and microbial flora in stool samples. Presented at the 16th International Congress on Microbial Ecology and Disease (Blacksburg, VA, USA) Sep 27-29, 1991 67. Newmark HL and Lupton JR: Determinants and consequences of colonic luminal pH: implications for colon cancer. Nutr Cancer 14:161-73, 1990 68. Roediger WEW, Heyworth M, Piris J, et al: Luminal ions and short chain fatty acids as markers of functional activity of the mucosa in ulcerative colitis. J Clin Pathol 35:323-6, 1982 69. Brown JP: Role of gut bacterial flora in nutrition and health: a review of recent advances in bacteriological techniques, metabolism and factors affecting flora composition. CRC Reviews in Food Sciences and Nutrition 8:229-336, 1977 70. Haenel JH and Bendig J: Intestinal flora in health and disease. Progress Food Nutrition Science 1:21-64, 1975 71. Gorbach SL: Estrogens, breast cancer and intestinal flora. Rev Infect Dis 61:S85-S90, 1984 72. Chung KT, Fulk GE and Slein MW: Tryptophase of fecal flora as a possible factor in the etiology of colon cancer. J Natl Cancer Inst 54:1073-8, 1975 73. Goldin BR: The metabolism of the intestinal microflora and its relationship to dietary fat, colon and breast cancer. Dietary Fat and Cancer 655-85, 1986 74. Ionescu G, Kiehl R, Ona L and Schuler R: Abnormal fecal microflora and malabsorption phenomena in atopic eczema patients. J Advan Med 3:71-89, 1990 75. Ionescu G, Kiehl R, Leimbeck R and Wichmann-Kunz F. Immunobiological significance of fungal and bacterial infections in atopic eczema. J Advan Med 3:47-58, 1990 76. Inman RD: Reactive arthritis, Reiter's syndrome and enteric pathogens. Infections in the Rheumatic Diseases. Espinosa L, Goldenberg D, Arnett F, Alacon G, Eds. Grune & Stratton, Orlando 273-80, 1988 77. Shorter RG, Hulzenga KA and Spencer RJ: A working hypothesis for the etiology and pathogenesis of nonspecific inflammatory bowel disease. Dig Dis 17:1024-32, 1972 78. Hill MJ, Melviulle DM, Lennard-Jones JE, et al: Faecal bile acids, dysplasia and carcinoma in ulcerative colitis. Lancet 2:185-6, 1987 79. Auer IO, Roder A, Wensinck F, et al: Selected bacterial antibodies in Crohn's disease and ulcerative colitis. Scand J Gastroenterol 18:217-23, 1983 80. Hollander D, Vadheim C, Brettholz E, et al: Increased intestinal permeability in patients with Crohn's disease and their relatives. Ann Int Med 105:883-5, 1986 83. Hunter JO: Food allergy or enterometabolic disorder? Lancet 2:338:495-6, 1991 84. Galland L: Dysbiotic relationships in the bowel. Am Coll Adv Med, 1992

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