The gut is home to trillions of bacteria and other microbes (the gut microbiota) that support digestion and absorption of food, regulate the integrity and function of the gut lining (mucosa), train and modulate the immune system, and communicate with the brain about energy uptake (via hormones and neurotransmitters) that affects mood and overall well-being.
In the healthy state, this ecosystem maintains a delicate balance to protect the body against infection while preventing tissue-damaging immune overreactions and inflammatory responses to numerous bacterial and foreign food antigens. Disturbance of this homeostatic coexistence in the gut is associated with many chronic diseases, at least partly stemming from inflammation or immune system dysregulation triggered by infections, food sensitivity, maldigestion/malabsorption of food, intestinal dysbiosis, and/or intestinal permeability.
A recent explosion of scientific research worldwide, including the Human Microbiome Project (HMP),13 is providing new insights into the importance of the gut as the “gateway to good health” and giving new meaning to the phrase “you are what you eat.”
In fact, most functional GI disorders, including IBS, comprise a number of different, often treatable, conditions that can be diagnosed or ruled out with the use of serum and fecal biomarkers.14-16 Such biomarkers give important clues into the underlying causes, e.g., intestinal dysbiosis, celiac disease/gluten sensitivity, maldigestion/malabsorption of food, inflammatory bowel disease (IBD), food allergies or other immune dysregulation, and bacterial/fungal/parasitic infections. This information is critical to being able to effectively treat the disorder and restore the patient (and their gut) to a state of health, by means of dietary interventions, specific supplements, medications, and/or more targeted tests.
Salveo Diagnostics and its team of medical experts have created a streamlined program that incorporates scientifically supported, evidence-based tests along with an intuitive and informative lab report, and a professionally-trained network of nutritional health counselors, to help you personalize diagnosis and tackle this growing challenge head on. Our Gut Health Assessment will provide clinical information to help you treat the underlying cause of the disease rather than just the symptoms. The tests assess several broad areas of potential dysfunction:
Schematic showing bacteria surrounding the intestinal villi.
Most chronic disease sufferers have a disorder of the microbiota that can be related to the disease pathophysiology.17,18 The microbiota is the collective term for all the microorganisms that inhabit the human body; a mixture of bacteria, viruses, fungi, and yeasts. These microbes reside in communities specific to different regions such as the skin, mouth, genitals, and intestines. The human microbiome refers to the genes and genomes of all the organisms that make up the microbiota. The gut microbiome is vital to our survival and functions to establish and maintain our immune system, fend off opportunistic pathogens, and help extract nutrients from our food. It is key to the structural integrity of the gut lining and preventing inflammation. Dysbiosis is an undesirable shift in the composition of the microbiota resulting in an imbalance between protective and harmful bacteria that can lead to a plethora of chronic diseases if left unchecked.17,18 However, pathogenic bacteria may coexist peacefully with beneficial bacteria if the overall balance of the microbiota is healthy. A high-fat, high-sugar (standard Western) diet may induce dysbiosis in the gut through the actions of bile which can affect the growth of some microbes. Chronic dysbiosis can alter the environment (e.g., pH) in the gut and thus invite pathogenic bacteria, fungi, or parasites to flourish. This can result in lower levels of beneficial short-chain-fatty-acid (SCFA)-producing bacteria, promoting intestinal hyperpermeability (“leaky gut”) and inflammation.
Maldigestion of food can cause GI symptoms such as bloating, abdominal pain, gas, constipation, and diarrhea. It can stem from a variety of problems, including low stomach acid, abnormal GI motility (either rapid or slow transit times), lack of bile acids, and pancreatic exocrine insufficiency (reduced secretion of digestive enzymes from the pancreas).19 Chronic maldigestion can promote bacterial/fungal overgrowth (small intestinal bacterial overgrowth or SIBO), which can compromise the intestinal barrier, allowing toxins, bacteria, and undigested food particles to enter the circulation and increase risk for food allergies, autoimmune disorders, and an overburdened liver.20 Malabsorption of nutrients can be a consequence of maldigestion and can also occur when infection or inflammation damages the intestinal mucosa or increases transit times.19 The resulting nutrient deficiencies can lead to malnutrition and other health complications such as anemia, skin and cognitive/mood disorders, impaired vision, and osteoporosis.21
Dysregulation of the normal homeostatic relationships between gut bacteria and host immune responses can lead to intestinal inflammation, and evidence suggests that luminal flora may be a central factor in the development of inflammatory bowel disease (IBD).22 Crohn’s disease and ulcerative colitis are immune-mediated conditions characterized by chronic inflammation of the small intestine (ileum) and large intestine (colon). The pathogenesis of these conditions is multifactorial, but they are generally thought to result from “an exaggerated immune response towards the gut microbiome/toxic luminal substances in a genetically susceptible individual.”23 Ulcerative colitis is characterized by inflammation that is limited to the colon—typically the superficial mucosa and submucosal layers, whereas Crohn’s disease involves any part of the GI tract and commonly involves complications such as strictures, abscesses, and fistulas.
Possible triggers may include:
Candida (yeast) overgrowth — intestinal dysbiosis (imbalance) favoring yeast overgrowth disrupts the intestinal epithelium, causing hyperpermeability
Certain medications — chronic use of drugs such as antibiotics, aspirin, acid-reducing drugs, or nonsteroidal anti-inflammatory drugs (NSAIDs)
Food additives and inflammatory foods — gluten, emulsifiers, excess sugar/alcohol consumption, and dairy
Stress and age
The intestinal epithelium is the largest exposed surface area of the human body and its ability to act as a barrier against potentially harmful molecules, bacteria, and foreign substances is critical to gut immune homeostasis. The permeability of this barrier is finely regulated by the presence of tight junctions—molecular complexes that seal the spaces between the epithelial cells, guiding passage of select molecules (e.g., nutrients) through the transcellular spaces. The epithelial cells produce mucus and antimicrobial molecules to further protect against noxious or infectious agents. Breakdown of this barrier can cause a disruption of normal mucosal immune homeostasis that can lead to uncontrolled chronic intestinal inflammation, allowing increased passage of undigested food particles, microorganisms, and their immune-stimulating antigenic products (e.g., lipopolysaccharide) to the circulation.24 The integrity and function of the epithelial cells themselves can also affect intestinal barrier function; if disrupted, tight-junction components and regulatory proteins will appear in the stool.
Intestinal parasites can be a significant source of gastrointestinal illness.25 If the immune system does not manage to clear them or keep them in check, they may start to cause patient symptoms.26
The immunochemical fecal occult blood test (iFOBT) detects the presence of hidden blood in the stool, which may indicate a benign or cancerous growth, IBD, or other damage to the gut lining.27,28
Autoimmune disorders are often triggered or made worse in genetically susceptible individuals by intestinal dysbiosis and a dysregulated gut inflammtory response (often with increased intestinal permeability) to stress, toxins, infections, nutrient insufficiencies, and various foods.29,30
- Ward BW, et al. Multiple chronic conditions among US adults: a 2012 update. Prev Chronic Dis. 2014;11:130389.
- Centers for Disease Control and Prevention. Death and mortality. NCHS FastStats Web site. http://www.cdc.gov/nchs/fastats/deaths.htm. Accessed Mar 6, 2016.
- Gerteis J, et al. Multiple Chronic Conditions Chartbook. [PDF – 10.62 MB] AHRQ Publications No, Q14-0038. Rockville, MD: Agency for Healthcare Research and Quality; 2014. Accessed Mar 9, 2016.
- Anderson J. Chronic care: Making the case for ongoing care. 2010 Chartbook. Robert Wood Johnson Foundation. www.rwjf.org/pr/product.jsp?id=50968. Accessed Mar 6, 2016.
- Tally NJ. Functional gastrointestinal disorders as a public health problem. Neurogastroenterol Motil 2008;20 Suppl 1:121–129.
- Canavan C, et al. The epidemiology of irritable bowel syndrome. Clin Epidemiol 2014;6:71–80.
- Peery AF, et al. Burden of gastrointestinal disease in the United States: 2012 update. Gastroenterology 2012;143:1179–1187.
- Levy S, et al. Perceptions of gastroenterologists and patients regarding irritable bowel syndrome and inflammatory bowel disease. Eur J Gastroenterol Hepatol 2014;26:40–46.
- Gikas A, Triantafillidis JK. The role of primary care physicians in early diagnosis and treatment of chronic gastrointestinal diseases. Intern J Gen Med 2014;7:159–173.
- Spiegel BMR. Do physicians follow evidence-based guidelines in the diagnostic work-up of IBS? Nat Clin Prac 2007;4(6):296–297.
- Drossman DA, et al. International survey of patients with IBS: symptom features and their severity, health status, treatments, and risk taking to achieve clinical benefit. J Clin Gastroenterol 2009;43(6):541–550.
- Camilleri M, et al. Irritable bowel syndrome: methods, mechanisms, and pathophysiology. The confluence of increased permeability, inflammation, and pain in irritable bowel syndrome. Am J Physiol Gastrointest Liver Physiol 2012;303:G775-G785.
- NIH HMP Working Group. The NIH Human Microbiome Project. Genome Res 2009; 19(12): 2317–2323.
- Habba SF. Diarrhea predominant irritable bowel syndrome (IBS-D): Fact of fiction. Medical Hypotheses 2011;76:97–99.
- Ayling RM. New faecal tests in gastroenterology. Ann Clin Biochem 2012;49:44–54.
- Alibrahim B, et al. Fecal calprotectin use in inflammatory bowel disease and beyond: A mini-review. Can J Gastroenterol Hepatol 2015;29(3):157–163.
- Sekirov I, et al. Gut microbiota in health and disease. Physiol Rev 2010;90:859–904.
- Carding S, et al. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis 2015;26:26191.
- Keller J, Layer P. The pathophysiology of malabsorption. Viszeralmedizin 2014;30:150–154.
- Sachdev AH, Pimentel M. Gastrointestinal bacterial overgrowth: pathogenesis and clinical significance. Ther Adv Chronic Dis 2013;4(5):223-231.
- Ward E. Addressing nutritional gaps with multivitamin and mineral supplements. Nutr J 2014;13:72.
- Bellaguarda E, Chang EB. IBD and the gut microbiota—from bench to personalized medicine. Curr Gastroenterol Rep 2015;17:15.
- Michielan A, D’Inca R. Intestinal permeability in inflammatory bowel disease: Pathogenesis, clinical evaluation, and therapy of leaky gut. Mediators Inflamm 2015; 2015:628157.
- Bischoff S, et al. Intestinal permeability – a new target for disease prevention and therapy. BMC Gastroenterology 2014;14:189.
- Amin OM. Seasonal prevalence of intestinal parasites in the United States during 2000. Am J Trop Med Hyg 2002;66(6):799–803.
- Painter et al 2015. Cryptosporidiosis Surveillance—United States, 2011–2012; Giardiasis Surveillance—United States 2011–2012. MMWR 64(3):1-25.
- Shah R, et al. Biomarkers for early detection of colorectal cancer and polyps. Cancer Epidemiol Biomarkers Prev 2014;23(9):1712–1728.
- Allison JE, et al. Population screening for colorectal cancer means getting FIT: the past, present, and future of colorectal cancer screening using the immunochemical test for hemoglobin (FIT). Gut Liver 2014;8(2):117–130.
- Campbell AW. Autoimmunity and the gut. Autoimmune Dis 2014;2014:152428.
- Lerner A, Matthias T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmune rev 2015;14(6):479–489.