The Comprehensive Digestive Stool Analysis

Comprehensive Digestive Stool Analysis Digestive System

Nutrition and digestion are undeniably important to good health. We are, essentially, what we eat and then absorb. Over the long haul, excellent health is impossible without good nutrition. However, without adequate breakdown and assimilation, even the best diet offers little help. Additionally, incomplete or faulty digestive processes may lead to a variety of chronic disorders.

I often tell my patients that the gastrointestinal tract is much like a carburetor in a car. Your digestive tract tract must take gasoline (your food), and then mix it with air (enzymes and other digestive juices). If this mixing process goes well, your car runs and doesn't cough or sputter. How efficiently your fuel burns determines to a large extent how many years you're going to get out of your car. Although a rather crude analogy, this principle does hold true for the human digestive tract. There are many points along the digestive where some "burning" process can go awry and cause seemingly unrelated problems elsewhere in the body. This article will discuss those various places and give you a very good detail of what can go wrong.

Gastrointestinal disorders have a major impact on health. One recent study found that during a three-month period nearly 70% of American households experienced one or more gastrointestinal symptom.¹

Maldigestion, malabsorption and abnormal gut flora and ecology, as well as many complex chronic illnesses and symptoms, lie at the root of most common GI complaints. Thus, nutrition and digestive processes are central to long-term health. Great Smokies’ Comprehensive Digestive Stool Analysis (CDSA) provides clinicians with a critical tool for evaluating the status of the GI tract.

This test helps pinpoint imbalances, provide clues about current symptoms and warns of potential problems should the imbalances progress. With an accurate assessment, custom-tailored treatment can be easily applied, greatly increasing the chances for therapeutic success.

The CDSA is used in the evaluation of various gastrointestinal symptoms or systemic illnesses that may have started in the intestine.

Because illnesses are often not discernable from symptoms, the CDSA is a valuable means of identifying critical imbalances previously unsuspected.

As most food molecules can’t be absorbed or utilized in their native state, a primary function of the gastrointestinal system is to break down molecules and absorb nutrients. This is a complex process taking place primarily in the gastrointestinal mucosa, where the battle for health—to absorb nutrients and exclude toxins—is fought. The gastrointestinal mucosa does this through a combination of physical barriers to diffusion, mucosal fluids and active immune processes.²

Diseases Linked to Low Gastric Acidity

• Bloating, belching, burning and flatulence immediately after meals
• 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 cheeks and nose (in nonalcoholics)
• Post-adolescent acne
• Iron deficiency
• Chronic intestinal infections — parasites, yeast, bacteria
• Undigested food in stool

Table 1 (ref. 6,7)

Teeth break up food and mix it with saliva. Saliva in turn helps form a bolus and protects the pharyngeal and esophageal mucosa, primarily with secretory IgA antibodies. Saliva also helps remineralize the teeth with calcium salts. The enzymes lingual lipase, salivary amylase and ptyalin initiate fat and starch digestion.³

The stomach mechanically churns food, breaks up and emulsifies fats and exposes molecules to additional enzymes. In doing this, it produces one to two liters of gastric juices per day.⁴

Most digestion and absorption takes place in the small intestine and is mediated by pancreatic enzymes and bile.⁴

1. Secretion of pancreatic juices (about 2.5 liters/day) is controlled by the vagus nerve and the duodenal hormones secretin and cholecystokinin. Hormone production, in turn, is stimulated by the presence of fat, protein and acid chyme.
2. Bicarbonate begins the process of neutralizing stomach acid.
3. The proteases trypsinogen, chymotrypsinogen and procarboxypeptidase are activated to trypsin, chymotrypsin and carboxypeptidase. These enzymes digest proteins to oligopeptides and amino acids.
4. Amylase splits starch to maltose.
5. Lipase hydrolyzes diglycerides and triglycerides, producing long chain fatty acids.
6. Bile secreted by the liver (about 700 ml/ daily) is stored in the gall bladder. Bile salts solubilize and emulsify fats, enabling enzymatic hydrolysis.

The Crypts of Lieberkuhn of the intestinal mucosa also produce immunoglobulins and small amounts of digestive enzymes such as peptidase and disaccharidases.

A primary role of the large intestine is absorption of water—about one liter daily. The large intestine also provides an environment for microbial fermentation of soluble fiber, starch and undigested carbohydrates.

Anaerobic colonic fermentation results in production of short chain fatty acids, the main energy source for colonic epithelial cells. It is largely these SCFAs, in combination with amines derived from protein degradation, that provide buffering and create the slightly acidic pH of fecal matter.

Carbohydrate Digestion: Salivary amylase initiates starch digestion in the mouth. However, this activity is short-lived as the enzyme is denatured by low gastric pH. In the duodenum, oligosaccharides and starch polymers undergo hydrolysis by pancreatic amylase. Specific disaccharides are hydrolyzed by brush border enzymes (lactase, maltase, sucrase) located on the enterocyte microvilli. Resulting monosaccharides are absorbed by specific sodium-dependent transport carrier mechanisms.

Diseases Linked to Low Gastric Acidity

• Asthma
• Celiac disease
• Chronic autoimmune disorders
• Dermatitis herpetiformis
• Diabetes mellitus
• Eczema
• Food allergies
• Gallbladder disease
• Gastric carcinoma
• Gastritis
• Grave’s disease
• Hepatitis
• Lupus erythematosus
• Osteoporosis
• Pernicious anemia
• Psoriasis
• Rosacea
• Thyrotoxicosis
• Urticaria
• Vitiligo

Table 2 (ref. 14-24)

Protein Digestion: Gastric acid and pepsin initiate the digestion of dietary protein. This is followed in the duodenum by hydrolysis into oligopeptides and amino acids by proteolytic pancreatic enzymes. Final protein digestion is accomplished by intestinal brush border peptidases. Dipeptides, tripeptides, free amino acids, and probably other short-chain peptides are then absorbed.

Fat Digestion: Processing of dietary fat is the most complex of the digestive and absorptive processes. Fat is water insoluble so the GI tract must transform large water-insoluble particles into a soluble, absorbable form.

Digestion begins in the mouth with secretion of enzymes called lipases. The stomach disperses fat globules into an evenly divided phase, called chyme. Pancreatic enzymes then split triglycerides into fatty acids and monoglycerides, which then combine with bile acids and phospholipids to form micelles. This process transforms waterinsoluble lipids into a water-soluble form absorbed in the proximal small intestine.

After absorption, fatty acids and other lipids are re-esterified in the intestinal cell to form chylomicrons, which are then secreted into the lymphatic system. Medium-chain triglycerides can be absorbed directly in the jejunum without forming chylomicrons.

Maldigestion: Gastric acid secretion is a fundamental step in digestion and assimilation. Many clinical conditions originate with decreased gastric acidity. Acid secretion decreases with age, and low stomach acidity is found in more than half of patients over age 60.^11,12 Researchers speculate that malabsorption of nutrients in the elderly is due to atrophy of various digestive organs because of hypochlorhydria.¹³

Gastric acid has a fundamental role in activating pancreatic proenzymes and converting them from inactive precursors (chymotrypsinogen, trypsinogen, etc.) to their active forms (chymotrypsin, trypsin). Intestinal peristalsis and gastric acid secretion normally prevent excessive growth of bacteria in the small intestine. It has been suggested that bacterial overgrowth might interfere with fat digestion and irritate the intestinal mucosa.

Pancreatic Exocrine Insufficiency: Inadequate delivery of pancreatic lipases and proteases to the small intestine can lead to inadequate breakdown of fats and protein. The net effect is a failure to obtain nourishment from protein, carbohydrate and fiber foods and an unhealthy environment for the flora of the large colon. It has been argued that even small decreases in pancreatic output can contribute substantially to maldigestion and have far-reaching effects in chronically ill patients.

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. Common causes include:

A number of important clinical diseases are strongly associated with and may cause mucosal malabsorption. They include sprue, Whipple’s disease, {crohns} Crohn’s disease, Giardiasis, Cryptosporidiosis, lactose intolerance and eosinophilic gastroenteritis.

Clinical Considerations of Malabsorption: The signs and symptoms of malabsorption are varied. Interestingly, malabsorption increases with age.²⁵ Amino acids, carbohydrates, fats, vitamins and trace elements may be absorbed by different processes so an individual may suffer malabsorption for one nutrient but not for others. In fat malabsorption, essential fatty acid deficiency may result in addition to the loss of the highest dietary source of calories.

Because the oxygen content of the colon is low, the vast majority of bacteria are anaerobes. There are, however, hundreds of varieties of anaerobic flora in vastly different concentrations, all growing very slowly. The significance of most of these flora remains largely unknown. Most researchers, therefore, utilize the aerobic flora as an indication of bacterial health.

Three frequently identified organisms, Lactobacilli, Bifidobacteria, and Escherichia coli, are employed as indicators of eubiosis or healthy overall flora. Lactobacilli and Bifidobacteria are well established as offering intrinsic benefit and aiding digestion while helping to prevent overgrowth of abnormal flora.

Bacterial cultures also identify and show potential pathogens. We utilize the term “potential pathogens” because individuals may harbor traditional pathogens and appear healthy, while others harbor weak or questionable pathogens and have gastrointestinal complaints.

For a full list of pathogenic and potentially pathogenic organisms, see the following chart. For a complete ist of parasitic organisms, see this chart.

While they are sometimes found linked to GI tract disturbances, some intestinal bacteria may also be involvedin the etiology of various chronic or systemic problems seemingly unrelated to GI function. These include Klebsiella, Proteus, Pseudomonas, and Citrobacter. These organisms may be involved, through molecular mimicry, in various autoimmune diseases. This has been reported in diabetes mellitus, meningitis, thyroid disease, ulcerative colitis, arthritis, ankylosing spondylitis and systemic lupus.^26,27

Some potential pathogens may cause clinical and subclinical malabsorption of nutrients and increase bowel permeability to large macromolecules. A number of clinicians speculate that this is directly related to the etiology of food and chemical sensitivity and intolerance.

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 resists attempts to culture it in vitro. Symptoms include severe alterations in intestinal permeability and chronic fatigue.²⁸ There is strong scientific support for the profound relation between GI tract flora, malabsorption, permeability changes and overall health.

Yeast: In the last few years, colonic yeast infections have attracted attention and controversy as a possible cause of chronic complex illness.²⁹ Many investigators suggest that an intestinal overgrowth of Candida albicans (and other intestinal yeast) may be involved in food allergy, migraine, irritable bowel, asthma, indigestion and gas, depression related to PMS, vaginitis and chronic fatigue.^30-35

Although others have dismissed these claims as speculation, we suggest that part of the problem is focusing on the terms “pathogen” and “commensal.” It may be more accurate to use the terms “strong pathogen” and “weak pathogen.” A significant and surprising amount of peer-reviewed literature supports yeast as a weak pathogen.^36-38

While the normal GI tract harbors small amounts of yeast, overgrowth as a consequence of the wide use of antibiotics, corticosteroids, birth control pills and increased dietary carbohydrates may be abnormal.³⁹ Odds’ text on Candida summarized more than 20 papers that found patients had a frequency of C. albicans in their feces more than twice as often as normal controls.⁴⁰ One study reported that chronic diarrhea and abdominal cramps may be caused by large numbers of dead or damaged yeast, as found in feces.⁴¹ Other research indicates Candida as a cause of colitis in patients with AIDS, neoplastic disease and renal transplants.^42-44

While the yeast pathogenicity debate continues, high-quality lab work is essential. Yeast may be observed directly via a microscope or indirectly through a culture. Both are necessary for proper analysis.

GI Tract and Arthritis: Researchers increasingly acknowledge that there is a link between digestive processes and arthritis. In patients with altered bowel anatomy, chronic bacterial overgrowth can lead to theformation of circulating immune complexes and synovitis.⁴⁵ Changes in bowel permeability due to local gut inflammation may expose the host immune system to microbial or food antigens and even bacterial translocation. ^46,47 In some cases, toxins derived from enteric organisms (e.g., Clostridium difficile) may play a direct role in the induction of arthritis.

Dysbiosis is the state of disordered microbial ecology that causes disease. It may exist in the oral cavity, gastrointestinal tract or vaginal cavity. In dysbiosis, organisms of low intrinsic virulence, including bacteria, yeasts and protozoa, induce disease by altering the nutrition or immune responses of their host.⁴⁸

The concept of intestinal flora having a major impact on human health has increasingly gained support, particularly as the widespread use of antibiotics has been observed to disrupt the normal flora.

Published research has implicated intestinal dysbiosis as contributing to vitamin B12 deficiency, steatorrhea, irritable bowel syndrome, inflammatory bowel disease, autoimmune arthropathies, colon and breast cancer, psoriasis, eczema, cystic acne and chronic fatigue.^49-54

Normal Intestinal Microflora: The microflora of the GI tract constitute a complex ecosystem of aerobic and anaerobic microorganisms.⁴⁹ There are more bacteria in the gut than human cells in the body, and the flora possess more metabolic activity than the host itself.

Flora content is surprisingly stable over time but is affected by diet, antibiotic use and health status.⁵⁵ In many ways, the gut flora can be viewed as an organ of the body, as these microbes profoundly influence physiologic processes of the host.

Certain normal metabolic functions and enzyme activities can be attributed to the microflora, and these play a role in metabolizing nutrients, vitamins, drugs, endogenous hormones and carcinogens; synthesizing short chain fatty acids; preventing colonization of pathogens; and stimulating maturation of the normal immune response.^56,57

Food allergy: Food allergy is a well documented problem, although its prevalence, testing methods and treatment modalities are controversial. J.O. Hunter 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.⁶⁰

Leo Galland, M.D., has advanced the idea of four interlocking patterns of bacterial dysbiosis:

This is the Western degenerative disease pattern which results from diets high in fat and meat and low in fiber. This type of diet produces increased concentrations of Bacteroides sp. and induces bacterial urease and beta-glucuronidase activity. These enzymes may then metabolize bile acids to tumor promoters and deconjugate excreted estrogens, raising the plasma estrogen level. The fecal pH may increase as a result of increased ammonia production. Epidemiologic data implicates this type of dysbiosis in the pathogenesis of colon cancer and breast cancer. It is usually corrected by decreasing dietary fat and flesh, increasing fiber consumption and consuming probiotic preparations.

This is a condition of carbohydrate intolerance induced by an excess of normal bacterial fermentation usually resulting from small bowel bacterial overgrowth. Abdominal distention, flatulence, diarrhea, constipation and feelings of malaise are commonly described. In small bowel bacterial overgrowth, degradation of intestinal brushborder and pancreatic enzymes by bacterial proteases may cause maldigestion. Fecal short chain fatty acids may be elevated. Patients with fermentation excess are usually intolerant of soluble fiber supplements and often benefit from antimicrobials and a reduction of carbohydrate consumption.

Exposure to antibiotics or a diet depleted of soluble fiber may create a deficiency ofnormal fecal flora, including Bifidobacteria, Lactobacillus and E. coli. Direct evidence of this condition is seen in stool cultures when concentrations of any of these organisms are reduced. This condition has been described in patients with irritable bowel syndrome and food intolerance. Deficiency and putrefaction dysbiosis often occur together and respond to the same treatment. Probiotic supplementation as well as fructooligosaccharides are often helpful in reestablishing a normal flora.

Abnormal immune responses to components of the normal indigenous intestinal microflora may contribute to the development of inflammatory bowel disease, spondyloarthropathies and other connective tissue diseases or skin disorders such as psoriasis or acne. Endotoxins may activate the alternative complement pathway, and sensitization may complement fermentation excess. Similar treatments may benefit both conditions.

The Comprehensive Digestive Stool Analysis provides diagnostic tools for analysis of digestion, colonic environment and absorption.

Great Smokies has developed unique detergent extraction and enzymatic analysis procedures that allow quantitative, precise and accurate measurements.^61,62 These methods give physicians the tools for differential diagnosis of digestive conditions as they relate to acute and chronic illness.

Common Potential Pathogens

• Aeromonas
• Bacillus cereus
• Campylobacter
• Citrobacter
• Klebsiella
• Proteus
• Pseudomonas
• Salmonella
• Shigella
• Staphylococcus aureus
• Vibrio

Table 4

Triglycerides: Triglycerides are the major dietary fat component. Elevated fecal amounts reflect incomplete fat hydrolysis and suggest pancreatic insufficiency.

Chymotrypsin: Fecal chymotrypsin is a sensitive, specific measure of proteolytic enzyme activity.^63,64

Decreased values suggest diminished pancreatic output (pancreatic insufficiency), hypoacidity of the stomach or cystic fibrosis. Elevated chymotrypsin values suggest rapid transit time, or less likely, a large output of chymotrypsin from the pancreas.

Iso-butyrate, iso-valerate and n-valerate: New research suggests that these short chain fatty acids can be produced through bacterial fermentation of protein, thus reflecting the presence of undigested protein in the bowel. In a healthy colon, these SCFAs constitute less than 10% of the total concentrations of SCFAs due to the sparse amounts of polypeptides present in the large intestine compared to undigestible carbohydrates. However, an increase in the load of protein in the colon will alter these concentrations. Causes may include pancreatic insufficiency (insufficient proteases), malabsorption or gastrointestinal disease, leading to mucosal desquamation.⁶⁵

Long Chain Fatty Acids: These free fatty acids are readily absorbed by healthy mucosa. In cases of malabsorption, however,they accumulate and reach substantially elevated levels in the feces. They can also indicate pancreatic insufficiency.

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, but some is excreted. The fecal cholesterol level remains surprisingly constant during fluctuating exogenous intake. An elevated cholesterol level in feces is abnormal and may reflect mucosal malabsorption.

Common Imbalanced Flora

• Beta hemolytic strep
• Enterobacter
• Hafnia alvei
• Hemolytic E. coli
• Mucoid E. coli

Table 5

Total Fecal Fat: This parameter is the sum of all the lipids except SCFAs. It can be indicative of maldigestion or malabsorption. It has been suggested that elevated long chain fatty acid levels reflect malabsorption, and elevated triglyceride levels reflect maldigestion.

Total Short Chain Fatty Acids: A special property of colonic bacteria is their fermentation of soluble fibers to short chain fatty acids (acetate, propionate, butyrate and valerate).⁶⁶ These molecules normally are readily absorbed so that fecal levels reflect a balance between production and absorption. SCFAs provide up to 70% of the energy for colonic epithelial cells.⁵⁶ SCFA production may be an important factor in establishing and maintaining a balanced ecosystem in the colon and may prevent establishment of pathogenic microbes such as Salmonella and Shigella species.

One interesting report suggests that diversion colitis might be successfully treated with rectal irrigations of SCFAs, specifically butyrate.⁶⁷ Elevated levels of the four main SCFAs may reflect colonic malabsorption or bacterial overgrowth. Elevated levels are also found in active colitis.⁶⁸ Decreased levels may reflect insufficient dietary fiber or disruption of the normal colonic flora.

Healthy amounts of Lactobacilli, Bifidobacteria, and E. coli are essential to the maintenance of a healthy system. Lactobacilli and Bifidobacteria species, in particular, have long been noted for their contributions to intestinal health—from the inhibition of gut pathogens and carcinogens, control of intestinal pH and the reduction of cholesterol tothe synthesis of vitamins and disaccharidase enzymes.

In a healthy gut, these organisms make up a substantial portion of the 400-plus species of bacteria; Bifidobacteria alone comprises up to one-quarter of the total flora in a healthy adult. Reduced numbers of these organisms, resulting from the use of broadspectrum antibiotics, chronic maldigestion or bacterial overgrowth, leave the intestine susceptible to invasion by pathogens and production of carcinogens. Measurement of their levels may indicate the need to supplement with “friendly bacteria” to restore these important properties. While E. coli do not share some of these direct beneficial effects, clinical observation suggests ample amounts of these organisms are present in healthy intestines.⁶⁹

Bacteriology cultures quantitate normal flora (Lactobacilli, Bifidobacteria, E. coli and other frequently isolated organisms), imbalanced flora and potential pathogens. Sero-typing for toxigenic E. coli and Campylobacter cultures is performed on diarrhetic specimens.

The CDSA includes a mycology culture that identifies and quantitates fecal yeast. Some of the more commonly identified species are C. albicans, C. tropicalis, Rhodotorula and Geotrichum. Broth dilution sensitivity analyses are performed on all yeast cultures of 2+ or greater utilizing both pharmaceutical and natural substances. Quantitative MIC analysis determines the relative potency of differing antimycotic agents. This provides more information on the effective agents and dosages for each yeast. MIC analysis is available by request for yeasts reporting below 2+.

n-Butyrate: Butyric acid is a key SCFA because it is the main energy source for colonic epithelial cells. Adequate amounts are necessary for healthy metabolism of the colonic mucosa. A possible mechanism for the anticancer action of dietary fiber is the increased fermentation of fiber to butyrate. It has been suggested that failure to use butyric acid by colonic mucosal cells or inadequate amounts available in the colon could be a primary factor in the etiology ofulcerative colitis, inflammatory bowel disease and colon cancer.^66,70,71

Beta-glucuronidase: Beta-glucuronidase is a bacterial enzyme elaborated by several microorganisms, including E. coli, Bacteroides and Clostridium. Via the uncoupling of glucuronides (compounds detoxified through the hepatic glucuronidation pathway), this enzyme catalyzes reactions which may result in the formation of carcinogens in the bowel as well as the persistence of certain hormones and drugs in the body. Thus, excess betaglucuronidase activity may possibly contribute to the pathogenesis of colon cancer, as well as estrogen-related cancers via enhanced enterohepatic recirculation of estrogen in the body. The activity of this enzyme is strongly influenced by diet, levels of Lactobacilli and Bifidobacteria, intestinal pH and nutrients such as calcium glucarate.^72-75

pH: Fecal pH appears to be an indicator of the health or status of colonic digestive processes. Abnormally acidic or alkaline pH usually reflects an abnormality in either acid production or its absorption. Increasing evidence supports fecal pH as a useful biomarker linked to the development of colon cancer.^76-78 We have observed a correlation between alkaline pH and decreased short chain fatty acids (particularly butyrate).⁷⁹ Elevated fecal pH and diminished SCFAs suggest inadequate digestion of fiber and/or inadequate intake of dietary fiber.

Short Chain Fatty Acid Distribution: Adequate amount and proportions of the different SCFAs reflect the basic status of intestinal metabolism. The ratios of the individual SCFAs remains relatively constant in healthy colons but becomes imbalanced in various disease states. Imbalanced ratios of the SCFAs reflect imbalanced metabolic processes due to disordered bowel flora—a state called “dysbiosis”. Researchers are beginning to identify unique SCFA “fingerprints” with specific bacterial infections.⁷⁰ Hoverstad proposed that the ratio among SCFAs has diagnostic value for intestinal infections.⁷¹ A significantly higher ratio of acetate/total SCFAs and lower ratio of butyrate/total SCFAs has been found in the feces of patients with large bowel adenomas and cancer compared to control groups.⁷⁰

The fecal leukocyte test identifies the presence of lactoferrin, a marker for fecal leukocytes. This test is more sensitive than microscopy for identifying leukocytes and discriminates between inflammatory and non-inflammatory bowel processes.

Ulcerative colitis, Crohn’s disease, diverticulitis, and bacterial or parasitic infection will result in a positive result. Patients who have diarrhea on the basis of IBS, virus, and noninvasive parasites will have a negative result.⁸⁰

The presence of mucus or pus can indicate irritable bowel syndrome, intestinal wall inflammation (caused by infection—typhoid, Shigella or amoebic), diverticulitis or other intestinal abscess. Absence of mucus and pus is normal.

The CDSA also includes an occult blood test, which is a monoclonal antibody test that is highly specific for intact human hemoglobin. A positive result indicates blood loss from a lower GI source and warrants further imaging investigation.

Intestinal dysbiosis is marked by many indicators. For our Dysbiosis Risk Index, relevant results are weighed and an index is calculated to provide a quick assessment of the patient’s GI tract in terms of flora imbalance. Factors used to determine the index include digestive, absorptive, metabolic, and microbiological markers.

The CDSA’s battery of integrated tests evaluates digestion, colonic environmentand absorption. It enables therapeutic intervention based not only on single test results, but also on patterns and relationships.

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