The GI microbial world is comprised of 3 very different compartments: Gastric, Small Intestinal & Colonic. Each has a distinct biochemical and physiologic “climate.”
The Gastric Ecoystem is characterized by a low pH environment that kills most external bacteria coming in with food. Gastric contents are emptied relatively rapidly (usually within 60-90 min), and there is a thick mucus barrier between the gastric mucosa and gastric contents. The high acidity is one of the body’s major defense systems against exogenous pathogens.
It is important to appreciate that a healthy human stomach produces roughly 2 liters of acidic gastric juice daily. Aging typically slows gastric re-acidification after meals, but normally this won’t change fasting or fed gastric pH. However, acid suppressive drugs can have a major disruptive effect on this defense system, setting the stage for downstream dysregulation of the small intestinal microenvironment. Other drugs, like clonidine can also cause problems, as can diseases like diabetes.
Helicobacter pylori is a very common inhabitant of the human stomach. While in many people it is pathogenic, in others it is not. Recently, a debate has emerged about the merits and down-sides of eradicating H. pylori. Like many aspects of the GI microflora, the role of H. pylori is complex (read, Must We Always Eradicate H. Pylori?)
The Small Intestinal Ecosystem is an entirely different world from the gastric compartment. It is characterized by great length (roughly 25 feet), immense surface area (approximately the size of a tennis court), and an alkaline pH owing to duodenal and pancreatic bicarbonate secretion.
The small intestine is a major locus of immune system activity; it is loaded with intraepithelial lymphocytes (CD8 cells) as well as Peyer’s patch lymphocytes (CD4 cells) that interact in complex ways with the commensal microflora.
Disruptions of small intestinal ecology can be caused by infections, overgrowth of particular bacterial species, excessive fermentation of food, exuberant immune system responses, mucosal hyperpermeability, changes in motility, and malnutrition (as seen in patients receiving parenteral feeding or those on low fiber diets). Gastric achlorhydria or hypochlorhydria certainly can set the stage for small intestinal disruptons.
Signs and symptoms include: carbohydrate/fiber intolerance, bloating, altered bowel habits, constant fatigue, and vitamin B12 deficiency. Overgrowth of pathogens can result in mucosal damage by bacterial enzymes, which will show up as blunted, broadened villi, with loss of brush borders. Histological exam will show increased mononuclear cells in the lamina propria. If the condition becomes chronic, it can cause liver damage, arthritis, myalgias and depression.
Small intestinal dysbiosis is common in people who’ve undergone surgical resection or blind loops, those with strictures, fistulae or diverticulosis. Think about it in anyone with intestinal giardiasis, tropical sprue or immunodeficiency.
Small bowel bacterial overgrowth is much more common than previously suspected, especially in people with irritable bowel syndrome. A study of 202 IBS patients showed that 157 of them (78%) had SBBO as indicated by breath-testing.
The Colonic Ecosystem is characterized by its slow motility (48 hours is typical for emptying), and its immense bacterial count. On average, a human colon hosts about 100 trillion organisms, which together weigh about 3 pounds! The colon has a pH in the range of between 6-8.
Many things can affect the complex ecology of the colon. Common disruptors include: antibiotics, unabsorbed bile acids, unabsorbed fructose from the small intestine, bacterial putrefaction, altered intestinal motility, a host of different drugs, and chronic stress.
The fructose factor is very important clinically. Humans have a limited ability to absorb fructose, and this ability varies greatly between people. Fructose not absorbed in the small bowel undergoes fermentation in the colon. Think about this in any patient experiencing refractory flatulence.
People with fructose malabsorption are affected by foods high in fructose or fructans (polymers of fructose found in wheat and in vegetables like onions and leeks). High levels of fructose are found in apples, pears, melons, grapes, sucrose, honey, coconut, most dried fruits, fruit juices and sweet wines. For many reasons such people should avoid high fructose corn syrup.
END
