Complete Digestive Stool Analysis (CDSA)

Transcription

1 Complete Digestive Stool Analysis (CDSA) C l i n i c a l G u i d e This Clinical guide: Provides the practitioner with information to enhance understanding and interpretation of the Complete Digestive Stool Analysis (CDSA) results. Provides information about digestion, absorption, intestinal function and the microbial flora which may help in the management of acute and chronic gastrointestinal complaints. Introduction You are what you eat is commonly referred to in the context of general health. However, it is often an over simplification of an individual s potential to achieve their optimal health. It assumes one consumes a balanced nutritional diet, lives and works in a clean environment, and is stress, infection free and has no significant inherited predisposition to disease. The manifestation of chronic ill-health may be determined by the low-level impact of prevailing factors causing a cascade of interrelated stresses on physiological processes and organ function, possibly resulting in critical disturbances to homeostasis and health. Two of the major organs governing the initiation and progression of these processes are the gastro-intestinal tract (GIT) and the liver respectively. 1 The GIT should digest/process food, selectively absorb essential nutrients and eliminate toxic/allergenic compounds. Gastro-intestinal Tract Function The GIT, for the purposes of understanding the process of digestion and absorption, can be divided into four main areas: Mouth Mastication and the physical break up of food. Saliva and enzymes mix with food to facilitate transit, digestion and protection of the pharyngeal and oesophageal mucosa. 2 Stomach Mixing and digestion of food by gastric juices (emulsifiers, enzymes, acids etc) and ordered delivery to the small intestine. 2 Small Intestine Major site for digestion and absorption, mediated by pancreatic enzymes and bile acids. The residency time of nutrients is crucial to the efficiency of absorption. 2 Large Intestine Absorption of water and microbial fermentation of soluble 1 fibre, resistant starch and other undigested or unabsorbed carbohydrates. Production of short chain fatty acids (SCFA) and control of faeces. 3 The gut ecology in the small and large intestine must be in balance to ensure the healthy and normal function of the intestinal mucosa. Microflora imbalance can alter the immunological and mechanical integrity of the mucosa ( leaky gut ), thus permitting absorption of inflammatory, allergenic and toxic molecules. 3,4 In cases where patients suffer from food sensitivities and liver dysfunction, increased intestinal permeability or nutrient deficiencies, some practitioners use the CDSA to explore possible underlying causes. Remember, further investigation may be necessary to look for other possible causes. CDSA Tests: CDSA Level 1 CDSA Level 2 CDSA Level 3 CDSA Level 4 CDSA Level 5 Qualified By Performance Since 1974

2 The Importance of Making a Diagnosis The CDSA can be a very informative and clinically relevant test for many patients with suboptimal digestive function. Scientific studies continue to highlight the importance of looking for the underlying cause of disease rather than simply treating its manifestations. In a recently published report, it is advised to test for Dientamoeba fragilis in patients before a diagnosis of Irritable Bowel Syndrome (IBS) is made. A pilot study of patients with IBS showed 14 out of 21 patients diagnosed with D. fragilis experienced immediate resolution of their symptoms after successful eradication of the parasite. 5 This small study illustrates two important points: 1. The importance of understanding underlying causes of disease (i.e. possible diagnoses / differential diagnoses). 2. The importance of having and utilising diagnostic tests to investigate the possible causes (i.e. make an exact diagnosis). CDSA Markers: The CDSA provides an overview of the components of digestion, absorption, intestinal function and microbial flora. The following CDSA markers are detailed below. Digestion and absorption Macroscopic/microscopic appearance The colour, form, consistency and digestive markers of faeces may provide an important insight into a number of various conditions. An unformed stool may indicate maldigestion, malabsorption, inflammation or infection. Elevated food remnants or food fibres may reflect inadequate digestion. 6 Biochemistry : a useful and important biochemical parameter to analyse Indicates: physico-chemical environment / of bowel is essentially determined by gut ecology (the production of acid or alkali) and transit time (acid consumption), therefore when it is abnormal think of dysbiosis total acid = Short Chain Fatty Acids (SCFAs) + other organic acids (fermentation products) Significance: is an important marker from two perspectives: a) Cause: altered is an important marker reflecting underlying problems including maldigestion, malabsorption, abnormal transit time, unhealthy diet and, most importantly, dysbiosis b) Effect: altered has a dramatic effect on the function of the entire gut including enterocyte damage, enzyme inactivation, decreased bile acid conjugation, deranged symbiotic metabolism, smooth muscle activity Influences: Acid production (gut microbial fermentation) - SCFA production - prebiotics / fibre intake / carbohydrate digestion - probiotics / gut ecology / dysbiosis Acid consumption - SCFA consumption (bowel transit time) Alkali production - Ammonia Elevated (alkaline) DECREASED ACID decreased SCFA - production - prebiotics - probiotics - consumption - slow transit time INCREASED ALKALI excess ammonia production - putrefactive dysbiosis ( meat fibres) Lowered (acidic) INCREASED ACID increased SCFA - production - prebiotics - probiotics - consumption - rapid transit time DECREASED ALKALI acidic inhibits putrefaction of the stool is more influenced by events further down the gastrointestinal tract i.e. regions closer to the anus where the stool composition is finally completed. This means that the distal small bowel and the large bowel have a far greater influence on stool than the stomach and proximal small bowel. 6 Valerate and iso-butyrate: These SCFAs are produced by the fermentation of dietary protein. 1 Elevated Valerate / Iso-Butyrate increased bacteria fermenting (bacterial : compete with host for food) increased protein / amino acids to ferment - protein maldigestion - hypochlorhydria - pancreatic insufficiency DECREASED CONSUMPTION malabsorption (especially if other indicators of malabsorption) Chymotrypsin: Chymotrypsin is a proteolytic enzyme produced by the exocrine pancreas. Maldigestion is important in the genesis of many GIT disorders and the pancreas is one of the main organs in the GIT. The level of chymotrypsin seen in the stool is a reflection of the balance between production (from pancreas) and consumption (intestinal absorption). 1 Decreased Chymotrypsin INCREASED CONSUMPTION slow gut motility ( absorption) DECREASED PRODUCTION chronic pancreatitis pancreatic insufficiency hypochlorhydria Elevated Chymotrypsin DECREASED COMSUMPTION rapid gut motility ( absorption) acute pancreatitis pancreatic hypersecretion (rare) Triglycerides: Triglycerides are a major component of dietary fat. An increased level reflects incomplete fat hydrolysis i.e. maldigestion. 1 Elevated Triglycerides hypochlorhydria pancreatic insufficiency bile salt insufficiency - production and / or secretion: hepatobiliary disease - deactivation: bacterial high fat diet (uncommon cause) Absorption Total Long Chain Fatty Acids: Normal digestion of fats involves the hydrolysis of fatty acids (some of which are long chain) from triglycerides. As free fatty acids, they should be easily absorbed by the intestinal mucosa, and therefore elevated levels represent fat malabsorption. Chronic fat malabsorption can impede the assimilation of fat-soluble nutrients such as vitamin A, E and essential fatty acids. 7 It should be noted that malabsorption syndromes are complex and beyond the scope of this guide. Cholesterol: Faecal cholesterol is derived from both dietary sources and mucosal epithelial cell breakdown, although levels generally remain constant despite fluctuating dietary intake. As well as representing malabsorption, a high level of cholesterol can also reflect rapid cell turnover as occurs in mucosal inflammation e.g. shigella infection. 7 Total Faecal Fat: This is the sum of all lipids, except short chain fatty acids. 7 Elevated Cholesterol, Long Chain Fatty Acids (LCFAs) and Total Faecal Fat deranged gut ecology - intestinal dysbiosis - small bowel bacterial - intestinal infection (bacteria, yeast or parasite), tropical sprue maldigestion - disaccharidase deficiency - pancreatic insufficiency - bile salt insufficiency - liver or gallbladder disease anatomical derangements - surgical interventions: resection, bypass intestinal mucosal disorders - Whipple disease, collagenous sprue, Crohn s, eosinophilic enteritis etc. food induced gut inflammation / immune damage - food sensitivities - gluten sensitivity / coeliac disease other mucosal irritants - chronic use of NSAIDs insufficiencies of mucosal nutrients - vitamin, mineral or EFA deficiency Total Short Chain Fatty Acids: Within the realms of the CDSA, SCFAs are a significant marker of intestinal health. Colonic bacteria produce SCFAs through the fermentation of dietary carbohydrate (CHO). They are readily absorbed by the intestinal epithelium and constitute an important source of energy. Faecal levels reflect a balance between production and consumption. 8 Abnormalities Decreased Total SCFA DECREASED PRODUCTION prebiotic deficiency (lack dietary fibre) probiotic numbers low (deficiency dysbiosis) probiotic function low (high ) INCREASED CONSUMPTION slow transit time / constipation Elevated Total SCFA small bowel bacterial maldigestion (increased substrate for fermentation) DECREASED CONSUMPTION rapid transit time / diarrhoea Abnormal SCFA Distribution dysbiosis - altered gut ecology causes patterns of abnormal gut fermentation - overall measure of dysbiosis where specific opportunistic pathogens (potentially pathogenic organisms) not detected N.B. It is impossible to assess the vast majority of gut symbiotes and therefore rather than directly quantifying organisms, indirect markers such as metabolic products are used to indicate eubiosis or dysbiosis. 2 3

3 Metabolic Markers Short Chain Fatty Acids (SCFAs): SCFAs contribute to normal large bowel function and are thought to prevent pathology through their actions in the lumen and on the colonic musculature and vasculature through their metabolism by colonocytes. The SCFAs (acetate, propionate, butyrate) are the principal products of CHO fermentation with stool levels reflecting fermentation in the large bowel to a greater degree than that in the small bowel. These three SCFAs are the predominant anions in the colon representing 75% of the total amount. 8 In contra-distinction to these SCFAs, the branch chain SCFAs iso-butyrate, iso-valerate represent fermentation of amino acids, rather than carbohydrates. Ratios: The ratios of the various SCFAs remain relatively constant in the healthy gut, but become imbalanced in certain disease states i.e. dysbiosis. For example, high levels of acetate together with low levels of butyrate relative to total are associated with an increased risk of bowel cancer. 1,9 With several hundred species of probiotic organisms in the gut it is not feasible to measure all of them, therefore measuring the metabolic markers is a more practical way of detecting disturbed gut ecology, e.g. dysbiosis. Starch gives the highest SCFAs yield and the most butyrate, whilst non-starch polysaccharides (e.g. pectins) produce mostly acetate and propionate. Butyrate is thought to be protective against colorectal cancers and ulcerative colitis. 9 Butyrate: This is the preferred fuel for the colonic epithelium. Low butyrate (and n-butyrate) is thought to be associated with an increased risk of ulcerative colitis, colon cancer, and diarrhoea (since butyrate stimulates sodium and water absorption by the colonic mucosa). 1,9 Propionate and Acetate These by-product SCFAs are thought to stimulate biomass and effect faecal bulk. 1 Additional Markers Detection of mucous, occult blood, pus, white blood cells or red blood cells should be investigated as appropriate. The GIT provides an ideal environment for a vast and diverse array of flora. These bacteria exert various effects and are considered vital for wellbeing and health. As a consequence of dysbiosis their metabolic activity may exert negative effects. Few of the bacteria ingested with food or drink or which originate in the nose, mouth or oropharynx survive the very acidic conditions of the stomach, with this being an important control of small intestinal bacterial numbers. Hence colonization of the stomach is an infrequent event (<10 viable organisms/ml of stomach contents is the norm) although it may occur when Helicobacter pylori invade the stomach mucosa. 3 Gut Symbiotes The gut contains over 400 different species of organisms 20 species account for around 75% of the population. The gut contains trillion organisms very significant metabolic activity. Anaerobes outweigh aerobes 5000:1 (fermentation predominates over respiration). 10 Maintaining the delicate balance of intestinal microflora is critical. 10 is a state of imbalance of intestinal microbial flora which is implicated in the genesis of many diseases. 6 The main patterns of dysbiosis can be categorised as putrefaction, fermentation, deficiency and sensitization. Patterns of Putrefaction Western diet of high animal fat and flesh and low insoluble dietary fibre Poor diet: junk food, saturated fats, excess meat, lack fruit / vegetables / whole foods Poor digestion: rushed, stressed, lack chewing, overeating, eating late at night Bad breath: despite good oral hygiene Pathology: constipation, diverticular disease, hemorrhoids, colonic polyps / cancer Macroscopic Appearance Possibly excess food remnants / food fibres Microscopic Appearance Possibly excess meat fibres Chymotrypsin Possibly decreased Valerate and Iso-butyrate Possibly elevated Increased Bacteroides but cannot be quantified therefore look at metabolic markers Decreased Bifidobacteria Elevated due to ammonia production from: - Bacteroides - Induction of bacterial urease enzymes by high meat intake (found in Bacteroides, Proteus and Klebsiella species) hydrolyzing urea to ammonia - Lack of inhibition of urease by acid fermentation products - Lack prebiotics and/or probiotics in large bowel SCFA Possibly decrease in total SCFA level Abnormal SCFA distribution: low butyrate Management of Putrefactive Increase gut acidity, especially in the colon Lifestyle Eat smaller meals more often and avoid eating late at night or just prior to sleeping Increase dietary fibre: soluble, insoluble and particularly resistant starch (see prebiotics) Decrease meat and saturated fat in diet. Follow general healthy dietary principles Digestion Correct any hypochlorhydria and / or pancreatic insufficiency. As with any gut condition, and especially with dysbiosis, maximising digestion is critical to effective management Prebiotics Supplement with fibre, such as resistant starch, that is fermented in the colon and is bifidogenic. Together with fermentative probiotics (most significantly Bifidobacteria) these are essential to acidify the colon: Fructo-oligosaccharides, arabinogalactans, inulin, lactulose Probiotics Be guided by CDSA report and replace appropriate probiotics. All probiotics ferment and produce organic acids and will therefore treat this type of dysbiosis but the single most important is Bifidobacteria. Some probiotic supplements also contain powerful bifidogenic substances that are even more beneficial Repeat testing 2-3 months 7 Patterns of Fermentation Bacterial of endogenous bacteria in stomach, small intestine and caecum due to hypochlorhydria, stasis due to abnormal motility, strictures, fistulae and surgical blind loops, immune deficiency or malnutrition Classic picture of elderly as hypo-/achlorhydria becomes universal Common irritable bowel pattern of excess gas and bloating soon after meals, especially carbohydrate intolerance carbohydrate intolerance may be the only symptom of bacterial making it indistinguishable from intestinal candidiasis Multiple food sensitivities, very sensitive to dietary changes Multiple nutrient deficiencies even if adequate intake: esp. B group / B12, Zn, Mg Maybe associated with yeast Often slightly elevated antigliaden IgG (sometimes marked elevation) Macroscopic Appearance Possibly excess food remnants / food fibres Microscopic Appearance Possibly excess fat globules, meat fibres, vegetable fibres, starch cells Chymotrypsin Possibly decreased secondary to hypochlorhydria High probiotic counts (but may have deficiency of some probiotics) Possible yeast or candida Increased association with parasitosis (cause and effect) SCFA Increased total SCFA (not always: remember other acid fermentation products) Abnormal SCFA distribution Lowered due excess SCFA AND other organic acids (e.g. lactic acid) LCFAs / Cholesterol Possibly elevated due to small bowel inflammation and enterocyte dysfunction from endotoxins (lipopolysaccharides), exotoxins (metabolic products), and acidity 4 5

4 Management of Fermentative It is critical to break the vicious cycle between maldigestion and bacterial, and / or decrease small bowel acidity Diagnose and Manage Underlying Causes It is important to address the underlying causes of bacterial, the most common being hypochlorhydria. In this instance address factors such as acid suppressive medication, zinc status and general nutrition, leaky gut, stress levels, food sensitivities, H. pylori and Avoid high carbohydrate diet, and minimise sugar. In the short term decrease all starchy carbohydrates to decrease the extent of fermentation. Follow general healthy dietary principles Digestion In this form of dysbiosis maximising digestion is the key to management. The vicious cycle of maldigestion and bacterial must be broken from both sides 1. Acidifants 2. Digestive enzymes 3. Bile salts: in severe cases with significant maldigestion and malabsorption support hepatobiliary component of digestion Anti-microbials Antimicrobial therapy can have undesirable effects such as: i) Microbial resistance ii) Deficiency dysbiosis and iii) Yeast Therefore: 1. Use natural agents such as citrus seed extract, garlic and Golden seal. These antimicrobials also have antifungal properties 2. Monitor progress closely with regular patient review and follow up CDSA Prebiotics and Probiotics Generally avoid or at least until the above mentioned vicious cycle is broken. Even if Lactobacilli are decreased do not replace early on as these are a significant producer of lactic acid (homofermentative) within the small bowel and will aggravate hyperacidity Repeat testing 2-3 months Repeat testing sooner if poor progress, clinical progress difficult to assess, or if concerns of deficiency dysbiosis and / or yeast 7 Patterns of Deficiency Exposure to anti-microbials Lack of dietary fibre / prebiotics Often associated with other derangements in gut ecology such as parasitosis (e.g. Blastocystis hominis), and yeast Irritable bowel syndrome Food intolerances Decreased Lactobacilli, Bifidobacteria, E.Coli, Enteroccoci Total SCFA Decreased Elevated due to lack of SCFA Management of Deficiency Replace beneficial gut flora Address underlying causes of deficiency Similar management principles to putrefaction: both have lack of fermentation in common Increase dietary fibre: soluble, insoluble and particularly resistant starch (see prebiotics) General healthy dietary principles Lifestyle Avoid antibiotics - use other ways to treat infections. Assess and manage immune dysfunction where relevant why does the patient need antibiotics? Prebiotics Supplement with fibre, such as resistant starch, that is fermented in the colon and is bifidogenic. Together with fermentative probiotics (most significantly Bifidobacteria) these are essential to acidify the colon: Fructo-oligosaccharides, arabinogalactans, inulin, lactulose Probiotics Be guided by CDSA report and replace appropriate probiotics. Main species available are Lactobacilli, Bifidobacteria and E. Coli Repeat testing 2-3 months 7 Patterns of Sensitization An abnormal immune response to components of normal intestinal microbial flora, for example endotoxins production, may predispose to certain inflammatory conditions and to connective tissue diseases and this is referred to as sensitization dysbiosis. Sensitization dysbiosis may enhance the fermentation dysbiosis and similar treatments may benefit both conditions 6 Sensitization dysbiosis is a complex pattern and beyond the scope of this Clinical Guide Putting it Together to Make a Diagnosis - Suggested Approach 1. Have picture of patient in mind Think in terms of supporting or excluding differential diagnoses formed so far from the clinical data already obtained history, examination, other investigations. 2. Overview Quickly look over entire CDSA report and mark / note all abnormal results. You can also include results that are borderline or sub-optimal. Look thoroughly at areas where pathology is expected and be more critical here of sub-optimal results. 3. Choose a place to begin After noting all the abnormal parameters decide where the most significant pathology lies and start analysis there: macroscopic, microscopic, biochemistry, absorption, metabolic markers, additional markers, gut ecology 4. Analyse and think in terms of functional units The next step is to translate the above parameters into clinically meaningful areas. Work through each parameter to gain information about: diet, digestion, absorption, dysbiosis, pathogens, motility, other areas (See Table 1) where is abnormal or there is dysbiosis start analysis with patterns are complex and have been included in detail as they represent the most challenging patterns to recognise. 5. Use understanding to integrate data and make a working diagnosis Next combine all available information and use understanding of cause and effect, inter-relationships and vicious cycles of above functional units to arrive at a working diagnosis. look at all abnormal parameters and look for the pattern of best fit what is the simplest possible explanation? use clinical acumen to determine most likely diagnosis 6. Therapeutic trial Remember that therapeutic response can be diagnostic where unsure, test hypotheses with therapeutic trial. Follow up CDSA testing can also be used to confirm diagnostic and therapeutic accuracy. Reflecting on CDSA result in successful cases will help to improve understanding and interpretative skills. 7. If in doubt keep going If still in doubt contact ARL, perform other diagnostic tests or refer to other clinicians use feedback from this to then review / reinterpret CDSA result so that you may improve future analysis. General Information Please refer to Table 2 on the following page for a list of the CDSA tests that ARL provides. Practitioner referral Contact ARL on to receive your request pad. References (1) Cummings JH. The Large Intestine in Nutrition and Disease, The Danone Chair Monographs, Institut Danone,1997 ( (2) Kaplan, L, et al, Clinical Chemistry Theory, Analysis, Correlation, Mosby, 3rd Edition, 1989 (3) Catto-Smith, A, Gut Flora and Mucosal Function, Asia Pacific Journal of Clinical Nutrition, Vol 5, pp 36-39, 1996 (4) Salminen, S et al, Probiotics and Stabilisation of the Gut Mucosal Barrier, Asia Pacific Journal of Clinical Nutrition, Vol 5, pp 53-56, 1996 (5) Rouse, R, Is it irritable bowel? Rule out parasites first, The Medical Observer, October 2002 Patients Give the patient a request form for a CDSA - they then contact ARL on to order a collection kit. The kit will be sent directly to the patient. Collection kits The functional pathology tests available from ARL, including the CDSA are non-invasive and designed so that the patient can collect specimens in the privacy of their home. This also allows for multiple specimen collection over a period of days if necessary. These kits can be dispatched anywhere within Australasia. The collection kit contains easy-to-follow instructions and a pre-paid airfreight satchel for its return to the laboratory. Results Patient results can be mailed, faxed or electronically downloaded. Practitioner support ARL has Regional Mangers in NSW, QLD and Victoria who are available for technical advice and on-going practitioner support. More information From within Australia call to find out more information. If calling from overseas call Web and ARL continually updates its web information pages, which can be accessed at All enquiries to info@arlaus.com.au (6) Galland, L, Barrie, S. Intestinal and the Causes of Disease. ( (7) James, S, Understanding Functional Pathology: Complete Digestive Stool Analysis Reference Guide, Analytical Reference Laboratories, 2003 (8) Topping, D. Short Chain Fatty Acids produced by Intestinal Bacteria, Asia Pacific Journal Clinical Nutrition, Vol 5, pp (9) Young, G, Prevention of Colon Cancer: Role of Short Chain Fatty Acids produced by Intestinal Flora, Asia Pacific Journal Clinical Nutrition, Vol 5, pp (10) Percival, M. Intestinal Health, Applied Nutritional Science Reports, Vol 5, No 5,

5 Table 1: Diagnostic and Patterns Chart 7 Parameter Digestion Absorption Motility Pathogens Other Macroscopic Colour ( ) ( ) ( ) Consistency ( ) ( ) ( ) Fibres ( ) Food remnants ( ) Microscopic Fat globules ( ) Meat fibres ( ) Vegetable fibres ( ) Starch cells ( ) Biochemistry PH ( ) ( ) Valerate / iso-butyrate ( ) Chymotrypsin Triglycerides ( ) Absorption Total LCFAs ( ) ( ) ( ) Cholesterol ( ) ( ) ( ) Total faecal fat ( ) ( ) ( ) Total SCFAs ( ) SCFAs n-butyrate ( ) ( ) Acetate ( ) ( ) Propionate ( ) ( ) Butyrate ( ) ( ) Additional Markers Mucus ( ) Pus ( ) Occult blood ( ) White blood cells ( ) Red blood cells ( ) E. coli ( ) Strep/Enterococci ( ) Lactobacilli ( ) Bifidobacteria ( ) Other Organisms Pathogens ( ) Key: = indicator of, or influenced by ( ) = possible indicator if present Table 2: Complete Digestive Stool Analysis (CDSA) Test CDSA Tests Bacteriology (Gut ecology) Mycology Parasitology Short Chain 3 Day Stool Sensitivities e.g. Lactobacilli & Bifidobacteria (Yeasts) e.g. Candida Fatty Acids Parasitology CDSA Level 1 CDSA Level 2 CDSA Level 3 CDSA Level 4 CDSA Level 5 NB: If clinically indicated, Helicobacter pylori antigen can be requested with any CDSA level. Please note all CDSAs include Microscopy and Macroscopy. Qualified By Performance Since 1974 Contact Ground Floor, 568 St Kilda Rd, Melbourne Victoria Australia T: (03) F: (03) info@arlaus.com.au ARL is registered for medical testing under the registration scheme of the National Association of Testing Authorities, Australia and The Royal College of Pathologists of Australasia. ARL 017 / HS 3795 Copyright 2003 ARL. All Rights Reserved. Reproduction in whole or part in any form or in any medium without the express permission of ARL is prohibited.