Dysbiosis is a condition characterized by increased bacterial overgrowth in the small intestine. Normally, the small intestine is not infested by bacteria like the colon due to intestinal motility and gastric secretions. Bacteroial overgrowth arises mainly due to:

a. Low digestive secretion (low gastric HCL, uses of antacids, pancreatic insufficiency, and/or decreased bile acids secretions due to liver or gallbladder disease)

b. Intestinal hypomotility (low-fiber diet, scleroderma, SLE, and high refined sugar diet. Since glucose is primarily absorbed in the duodenum and jejunum, intake of high refined sugar food induces intestinal hypomotility to allow the sugar to be absorbed in the jejunum and duodenum)

Symptoms of intestinal dysbiosis include (Abdominal cramps, bloating, steatorrhea, gases, weight loss, and vitamin B12 malabsorption). Intestinal dysbiosis can occur with or causes (Diabetes mellitus, colon cancer, allergies due to IgA deficiency, inflammatory bowel diseases, obesity, chronic pancreatitis, GERD, SLE, and giardiasis or parasitic infestation)

Bacteria functions as small biochemical factories containing enzymes that act upon digested food substrates. Gut flora metabolize bile acids, which contributes to the diarrhea seen in bacterial overgrowth and may contribute to colon cancer formation 

Diseases related to dysbiosis

1. Metabolic disorders: one hypothesis that explains how dysbiosis can cause metabolic disturbances mentions that metabolic disease arises due to autoimmune inflammation as a consequence of their endotoxins. Lipopolysaccharides (LPS) are a part of the gram-negative bacteria cell wall, and they are potent endotoxin. In dysbiosis, gram-negative bacteria thrive in the gut; by shedding their cell wall after death or recurrent antibiotic use, the absorbed LPS by the leaky gut will evoke a powerful inflammatory reaction and insulin tolerance (Metabolic endotoxemia). The body attempts to reduce the LPS endotoxemia by binding the LPS via the lipoproteins like HDL (60%), LDL (25%), and VLDL (12%), which might partially explain the raised cholesterol level in patients with dysbiosis

2. Ulcerative colitis: in dysbiosis, sulfur-containing food particles can be digested by “Sulfate-reducing bacteria”, resulting in the formation of “Hydrogen sulfide – H2S”, a bacterial toxin. Excess intra-luminal colonic hydrogen sulfide impairs butyrate oxidation and results in colonic epithelial inflammation   

3. Obesity: obese patients typically have deficiency in Bacteriodetes; dysbiosis contribute to obesity via increase food fermentation and increased production level of “Short-chained fatty acids – SCFAs”, which work as a source of energy production for many organs such as the liver (Fatty liver), muscles, and adipose tissues (High fat content). The increased SCFAs content in the colon can lead to increased lipogenesis in the liver and increased VLDL production (High serum cholesterol level)

4. Leaky gut syndrome: the term “Leaky gut syndrome” refers to a condition in which emotional of physical stress to the intestine causes increase cortisol level, which will results in vascular leakiness and gut-lining hypoxia, including the blood brain barrier. The vascular leakiness will allow the bacterial endotoxins within the intestinal lumen to “Leak” into the systemic circulation in large amounts. Endotoxins are powerful inducers of “Aromatase” and “Nitric oxide synthase”, which will increase estrogen and nitric oxide formation in the body. Both nitric oxide and estrogen will induce the formation of: cortisol, fibrinogen, and inflammatory cytokines, which all will causes the blood to spontaneously coagulate and the capillary to be leaky


Selected references

1. Carding S et al. Dysbiosis of the gut microbiota in disease. Microbial Biology in Health & Disease 2015; 26: 26191

2. Hawrelak JA et al. The causes of intestinal dysbiosis: a review. Altern Med Rev 2004; 9(2):180-197

3. Greiner T eta l. Effects of the gut microbiota on obesity and glucose homeostasis. Trends in Endocrinology and Metabolism 2011; 22(4): 117-123

4. Cani PD et al. The role of the gut microbiota in energy metabolism and metabolic disease. Current Pharmaceutical Design 2009, 15: 1546-1558

5. Rohmer L et al. Are pathogenic bacteria just looking for food? Metabolism and microbial pathogenesis. Trends in Microbiology 2011; 19(7): 341-348