Gastrointestinal Health Testing

What are the benefits of gastrointestinal (GI) health testing?

It’s been said, “You are what you eat.” A more accurate way to put it would be, “You are what you digest and absorb.” Essentially, your diet could be the healthiest diet in the world, chock full of the highest quality, nutrient dense foods, but if your gut isn’t functioning properly all of those high quality nutrients (and all that money spent on them) will get flushed down the toilet…literally!

With the hundreds of patients we have helped, we’ve found that gastrointestinal dysfunction is an underlying issue in diseases and disorders that affect nearly every area of the body. We consider GI health to be one of the most important components of overall health and wellness. Besides better digestion and absorption, a healthy gut means a stronger immune system, less inflammation, more energy, and more stable moods.

How do I know if I need gastrointestinal health testing?

If you experience any of the following symptoms on a regular basis, gastrointestinal health testing can reveal why you may be experiencing those symptoms and what to do about it:

Anal itching
Bad breath
Blood or mucous in the stool
Brain fog
Food sensitivities
Gas, bloating, and/or abdominal distension
Headache or migraines
Heart burn/acid reflux
Joint pain• Loose stools
Mood swings/depression
Nausea and vomiting
Nutritional deficiencies and malnutrition
Skin conditions including lumps, rashes, itchy patches, and ulcers

Gastrointestinal health testing can also reveal the causes of debilitating disorders like:

Crohn’s disease
Colitis and ulcerative colitis
Gastroesophageal reflux disease (GERD)
Inflammatory bowel disease (IBD)
Irritable bowel syndrome (IBS)
Food intolerances (allergies and sensitivities)

More information on different gastrointestinal diseases can be found at:

U.S. Department of Health and Human Services
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
National Institutes of Health (NIH)
National Digestive Diseases Information Clearinghouse (NDDIC)

What does your gastrointestinal health testing measure?

Our gastrointestinal health testing covers all areas of the gut including:

Levels of good/beneficial organisms
Levels of harmful/pathogenic organisms including bacteria, fungi, yeast, parasites, and worms
Digestion and absorption of nutrients
Immunological markers
Beneficial short-chain fatty acids (SCFAs) which are an important food source for beneficial bacteria
Occult blood and red blood cells in stool

What are the causes of poor gastrointestinal health?

There are many causes of poor gastrointestinal health, but the most common causes include:

Poor hygiene – They’re not kidding when they say to wash your hands for 30 seconds after you use the bathroom.
Travel – Traveling to foreign countries exposes you to foreign organisms that can make you seriously ill (but might have no effect on the locals).
Intestinal dysbiosis – This is a fancy way of saying you lack good/beneficial organisms in your gut and/or you have a pathogenic organism infection

Clostridium difficile

This is a common organism that can affect people in hospitals or be transmitted by people that work in hospitals [5] and also see www.cdc.gov. the CDc condiders this a healthcare-associated infections (HAIs). C. difficile causes diarrhea linked to 14,000 American deaths each year. Those most at risk are people, especially older adults, who take antibiotics and also get medical care. CDC provides guidelines and tools to the healthcare community to help prevent Clostridium difficile infections as well as provides resources to help the public safeguard their own health.

This is a bacteria associated with inflammatory bowel disease and colitis [6]. The use of anti-cancer chemotherapeutic drugs may result in high fatality rates in cancer patients susceptible to Clostridium difficile infection [7]. Symptoms of C. difficile include:

Watery diarrhea (at least three bowel movements per day for two or more days)
Loss of appetite
Abdominal pain/tenderness


Transmission of C. difficile (from CDC http://www.cdc.gov/hai/organisms/cdiff/Cdiff-patient.html)

Clostridium difficile is shed in feces. Any surface, device, or material (e.g., toilets, bathing tubs, and electronic rectal thermometers) that becomes contaminated with feces may serve as a reservoir for the Clostridium difficile spores. Clostridium difficile spores are transferred to patients mainly via the hands of healthcare personnel who have touched a contaminated surface or item. Clostridium difficile can live for long periods on surfaces.

Treatment of C. difficile (from CDC http://www.cdc.gov/hai/organisms/cdiff/Cdiff-patient.html)

In about one in four patients, Clostridium difficile infection will resolve within 2-3 days of discontinuing the antibiotic to which the patient was previously exposed. Clostridium difficile is generally treated for 10 days with antibiotics prescribed by your healthcare provider. The drugs are effective and appear to have few side-effects. In addition to what the CDC recommends, we also add natural antibiotics to our treatment strategies, make diet modifications (like increasing garlic, parsley and oregano consumption) and increasing probiotic intake.

Clostridium Difficile is a major cause of antibiotic associated diarrhea and colitis and is the most likely cause for virtually all cases of pseudomembranous colitis. We use an assay for testing that will directly detect toxins A & B which are associated with disease caused by C. Difficile.

Reference Sites:

Centers for Disease Control and Prevention


U.S. National Library of Medicine

National Institutes of Health


Escherichia coli (E. coli)

Escherichia coli (E. coli) is a diverse group of bacteria that includes harmless bacteria and pathogenic bacteria that can cause illness. E. coli normally live in the intestines of people and animals. The types of E. coli that can cause diarrhea can be transmitted through contaminated water or food, or through contact with animals or persons.

The pathogenic forms of E. coli strains are categorized into six pathotypes that are associated with diarrhea and collectively referred to as diarrheagenic E. coli:

Shiga toxin-producing E. coli (STEC)—STEC may also be referred to as Verocytotoxin-producing E. coli (VTEC) or enterohemorrhagic E. coli (EHEC). This pathotype is the one most commonly heard about in the news in association with foodborne outbreaks. About 3-4 days after being infected (with a range of 1-10 days), symptoms often include severe stomach cramps, diarrhea (often bloody), and vomiting. There may also be a low-grade fever (less than 101˚F/less than 38.5˚C). Most people get better within 5–7 days. Some infections are very mild, but others are severe or even life-threatening. This type of E. coli can cause colitis [8] if not treated properly. Shiga toxins are a family of related toxins with two major groups, Stx1 & Stx2. STEC can cause diarrhea often accompanied by cramping, fever and vomiting. STEC strains have been traced to undercooked meat, unpasteurized fruit juices or milk, alfalfa sprouts, lettuce, dry-cured salami, and cheese curds. For more information see: http://www.cdc.gov/ecoli/general/index.html
Enterotoxigenic E. coli (ETEC) – is a major cause of travelers’ diarrhea and diarrheal disease in underdeveloped nations [9]. Infection with ETEC can cause profuse watery diarrhea, abdominal cramping, fever, nausea with or without vomiting, chills, loss of appetite, headache, muscle aches and bloating. Illness develops 1-3 days after exposure and usually lasts 3-4 days, but it may take a week or longer to resolve. Symptoms rarely last more than 3 weeks. For more information see: http://www.cdc.gov/nczved/divisions/dfbmd/diseases/enterotoxigenic_ecoli/
• Enteropathogenic Escherichia coli (EPEC) – is a major cause of diarrheal disease worldwide [10]. EPEC infection of the human small intestine results in severe watery diarrhea linked to a weak inflammatory response. EPEC inhibits the capacity of the intestinal cells to secrete the inflammatory cytokine IL-8 in response to bacterial antigens and inflammatory cytokines while allowing damage to the barrier function [11].
• Enteroaggregative E. coli (EAEC) – another form of of E. coli that causes diarrhea. It is thought to induce inflammation by stimulating the migration of polymorphonuclear leukocytes into the lining of the digestive tract [12].
• Enteroinvasive E. coli (EIEC) – EIEC strains possess some of the biochemical characteristics of E. coli and have the ability to cause dysentery using the same method of invasion as Shigella does [13].
• Diffusely adherent E. coli (DAEC) – This type is thought to be linked to Crohn’s disease and cancer [14-25].

In addition to what the CDC recommends to treat the various forms of pathogenic E. coli, we also add natural antibiotics to our treatment strategies, make diet modifications (like increasing garlic, parsley and oregano consumption) and increasing probiotic intake.

Helicobacter pylori – This bacterium is associated with ulcers [26], cancers of the digestive tract [27-29], and homocysteine levels [30-32] which may predispose people to cardiovascular disease. The HpSA enzyme immunoassay (EIA) is an invitro qualitative procedure for the detection of H. Pylori antigens in the stool. Test results are intended to aid the diagnosis of H. Pylori infection, and to monitor the response during and post therapy.

For more information see: http://www.cdc.gov/ulcer/index.htm

In the United States, the recommended treatment protocol is 14 days of clarithromycin-based triple therapy (proton pump inhibitor [PPI] + clarithromycin + amoxicillin or metronidazole) or 10–14 days of bismuth quadruple therapy (PPI or H2-blocker + bismuth + metronidazole + tetracycline). Detailed information about these and other recommended treatment regimens by the American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection can be found here: (www.acg.gi.org/physicians/guidelines/ManagementofHpylori.pdf)

In addition to what the CDC recommends to treat the various forms of pathogenic E. coli, we also add natural antibiotics to our treatment strategies, make diet modifications (like increasing garlic, parsley and oregano consumption) and increasing probiotic intake. (Link to Gut Cleanse Supplement Strategy)

Macro Exam –This is a test for worms. The test involves direct macroscopic examination for worms, (Cestodes, Nematodes, Trematodes) that may be shed in stool.

Worms are parasites that can have negative effects on human health [33-41]. You can get them from undercooked foods. Worm infections occur primarily in developing countries and can be picked up by people traveling to those countries. About one-quarter of the world’s population, 1.5 billion, are infected with one or more of the major soil-transmitted worms, including hookworms, ascarids, and whipworms [42]. They infect more than 200 million people worldwide with 600 million at risk in 74 countries [42]. Worms can blunt the immune response and allow themselves to infect individuals for years. They might also impair the immunological response to bacterial, viral, and protozoal pathogens and to vaccination [42]. Treatment of worms usually involves taking albendazole or mebendazole for 1-3 days. For more information: http://www.cdc.gov/parasites/sth/


Click here to purchase the Digestive Health Supplement Package



1. Katayama, K., et al., Supplemental treatment of rheumatoid arthritis with natural milk antibodies against enteromicrobes and their toxins: results of an open-labelled pilot study. Nutr J, 2011. 10: p. 2.

2. Haroon, E., C.L. Raison, and A.H. Miller, Psychoneuroimmunology meets neuropsychopharmacology: translational implications of the impact of inflammation on behavior. Neuropsychopharmacology, 2012. 37(1): p. 137-62.

3. Maes, M., The cytokine hypothesis of depression: inflammation, oxidative & nitrosative stress (IO&NS) and leaky gut as new targets for adjunctive treatments in depression. Neuro Endocrinol Lett, 2008. 29(3): p. 287-91.

4. Maes, M., M. Kubera, and J.C. Leunis, The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuro Endocrinol Lett, 2008. 29(1): p. 117-24.

5. Pochapin, M., The effect of probiotics on Clostridium difficile diarrhea. Am J Gastroenterol, 2000. 95(1 Suppl): p. S11-3.

6. Navaneethan, U., et al., Clostridium difficile infection is associated with worse long term outcome in patients with ulcerative colitis. J Crohns Colitis, 2012. 6(3): p. 330-6.

7. Khan, A., et al., The evolution of Clostridium difficile infection in cancer patients: epidemiology, pathophysiology, and guidelines for prevention and management. Recent Pat Antiinfect Drug Discov, 2012. 7(2): p. 157-70.

8. Golan, L., et al., Enterohemorrhagic Escherichia coli induce attaching and effacing lesions and hemorrhagic colitis in human and bovine intestinal xenograft models. Dis Model Mech, 2011. 4(1): p. 86-94.

9. Levine, M.M., Escherichia coli that cause diarrhea: enterotoxigenic, enteropathogenic, enteroinvasive, enterohemorrhagic, and enteroadherent. J Infect Dis, 1987. 155(3): p. 377-89.

10. Glotfelty, L.G. and G.A. Hecht, Enteropathogenic E. coli effectors EspG1/G2 disrupt tight junctions: new roles and mechanisms. Ann N Y Acad Sci, 2012. 1258: p. 149-58.

11. Ruchaud-Sparagano, M.H., M. Maresca, and B. Kenny, Enteropathogenic Escherichia coli (EPEC) inactivate innate immune responses prior to compromising epithelial barrier function. Cell Microbiol, 2007. 9(8): p. 1909-21.

12. Boll, E.J. and B.A. McCormick, A new understanding of enteroaggregative Escherichia coli as an inflammatory pathogen. Cell Adh Migr, 2012. 6(5): p. 413-8.

13. van den Beld, M.J. and F.A. Reubsaet, Differentiation between Shigella, enteroinvasive Escherichia coli (EIEC) and noninvasive Escherichia coli. Eur J Clin Microbiol Infect Dis, 2012. 31(6): p. 899-904.

14. Boudeau, J., et al., Invasive ability of an Escherichia coli strain isolated from the ileal mucosa of a patient with Crohn’s disease. Infect Immun, 1999. 67(9): p. 4499-509.

15. Bringer, M.A., et al., Replication of Crohn’s disease-associated AIEC within macrophages is dependent on TNF-alpha secretion. Lab Invest, 2012. 92(3): p. 411-9.

16. Cane, G., et al., Up-regulation of intestinal vascular endothelial growth factor by Afa/Dr diffusely adhering Escherichia coli. PLoS One, 2007. 2(12): p. e1359.

17. Curova, K., et al., Enterovirulent E. coli in inflammatory and noninflammatory bowel diseases. Folia Microbiol (Praha), 2009. 54(1): p. 81-6.

18. Semiramoth, N., et al., Escherichia coli type 1 pili trigger late IL-8 production by neutrophil-like differentiated PLB-985 cells through a Src family kinase- and MAPK-dependent mechanism. J Leukoc Biol, 2009. 85(2): p. 310-21.

19. Sobieszczanska, B., et al., Virulence genes profiles and phylogenetic origin of Escherichia coli from acute and chronic intestinal diseases revealed by comparative genomic hybridization microarray. Pol J Microbiol, 2012. 61(2): p. 105-10.

20. Weber, P., et al., Microbic superinfection in relapse of inflammatory bowel disease. J Clin Gastroenterol, 1992. 14(4): p. 302-8.

21. Subramanian, S., et al., Characterization of epithelial IL-8 response to inflammatory bowel disease mucosal E. coli and its inhibition by mesalamine. Inflamm Bowel Dis, 2008. 14(2): p. 162-75.

22. Darfeuille-Michaud, A., et al., High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology, 2004. 127(2): p. 412-21.

23. El-Tawil, A.M., High incidence of Crohn’s disease in pre-menopausal women: Escherichia coli may be contributing. Int J Colorectal Dis, 2004. 19(5): p. 498.

24. Hunter, P.R., Drinking water and diarrhoeal disease due to Escherichia coli. J Water Health, 2003. 1(2): p. 65-72.

25. Martin, H.M., et al., Enhanced Escherichia coli adherence and invasion in Crohn’s disease and colon cancer. Gastroenterology, 2004. 127(1): p. 80-93.

26. Lin, M.H., et al., Histological examination of ulcer margin for diagnosing Helicobacter pylori infection in patients with gastric ulcers. Ann Diagn Pathol, 2013. 17(1): p. 63-6.

27. Hamajima, N., et al., Helicobacter pylori eradication as a preventive tool against gastric cancer. Asian Pac J Cancer Prev, 2004. 5(3): p. 246-52.

28. Li, Z., et al., HLA polymorphisms are associated with Helicobacter pylori infected gastric cancer in a high risk population, China. Immunogenetics, 2005.

29. Rothenbacher, D. and H. Brenner, Helicobacter pylori and gastric cancer. Gastroenterology, 2004. 126(7): p. 1927; author reply 1927-8.

30. Cenerelli, S., et al., Helicobacter pylori masks differences in homocysteine plasma levels between controls and type 2 diabetic patients. Eur J Clin Invest, 2002. 32(3): p. 158-62.

31. Dierkes, J., et al., Helicobacter pylori infection, vitamin B12 and homocysteine. A review. Dig Dis, 2003. 21(3): p. 237-44.

32. Evrengul, H., et al., Elevated homocysteine levels in patients with slow coronary flow: relationship with Helicobacter pylori infection. Helicobacter, 2007. 12(4): p. 298-305.

33. Adams, A.M., K.D. Murrell, and J.H. Cross, Parasites of fish and risks to public health. Rev Sci Tech, 1997. 16(2): p. 652-60.

34. Anantaphruti, M.T., Parasitic contaminants in food. Southeast Asian J Trop Med Public Health, 2001. 32 Suppl 2: p. 218-28.

35. Bruckner, D.A., Helminthic food-borne infections. Clin Lab Med, 1999. 19(3): p. 639-60.

36. Butt, A.A., K.E. Aldridge, and C.V. Sanders, Infections related to the ingestion of seafood. Part II: parasitic infections and food safety. Lancet Infect Dis, 2004. 4(5): p. 294-300.

37. Klein, S.L., Hormonal and immunological mechanisms mediating sex differences in parasite infection. Parasite Immunol, 2004. 26(6-7): p. 247-64.

38. Mao, S.P., Protozoan and helminth parasites of humans in mainland China. Int J Parasitol, 1991. 21(3): p. 347-51.

39. Read, C.P., Some aspects of nutrition in parasites. Am Zool, 1968. 8(1): p. 139-49.

40. Rees, P.H. and P.D. Marsden, Intestinal parasites. Br J Clin Pract, 1970. 24(1): p. 3-11.

41. Wilson, M.S. and R.M. Maizels, Regulation of allergy and autoimmunity in helminth infection. Clin Rev Allergy Immunol, 2004. 26(1): p. 35-50.

42. Kamal, S.M. and K. El Sayed Khalifa, Immune modulation by helminthic infections: worms and viral infections. Parasite Immunol, 2006. 28(10): p. 483-96.