Putrefaction dysbiosis and the GI tract digestion and absorption of food

Putrefaction dysbiosis and the GI tract digestion and absorption of food

The GI tract, for the purposes of understanding the process of digestion and absorption, can be divided into four main areas: the mouth, stomach, small intestine, and large intestine. The mouth is responsible for mastication and the physical break up of food. Saliva and enzymes mix with food to facilitate transit, digestion, and protection of the pharyngeal and esophageal mucosa.

The stomach mixes and digests food by gastric juices (emulsifiers, enzymes, acids) and orders delivery to the small intestine. In turn, the small intestine is the major site for digestion and absorption, mediated by pancreatic enzymes and bile acids. Residency time of nutrients is crucial to efficiency of absorption. The large intestine is responsible for the absorption of water and microbial fermentation of soluble fiber, resistant starch, and undigested carbohydrates, as well as the production of short-chain fatty acids (SCFA) and pH control of feces.

The GI tract provides an ideal environment for a vast and diverse array of normal flora. These bacteria exert positive effects and are vital for well-being and health. As a consequence of their metabolic activities and when dysbiosis occurs, they may also 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 in the stomach. 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.

Putrefactive dysbiosis is more likely when diets high in animal protein and fat and low in fiber are consumed. Significant imbalances in stool bacteria populations occur (i.e., increased Bacteroides sp. and decreased Bifidobacterium sp.) with consequent major disturbances to enzyme activity and metabolism, causing the following: decarboxylation of amino acids (production of vasoactive and neurotoxic amines like histamine, octopamine, tyramine), catalysis of tryptophan by bacterial enzyme tryptophanase (production of indoles, skatoles, phenols, etc.), hydrolysis of urea to
ammonia by increased bacterial urease (Bacteroides sp., Proteus sp., Klebsiella sp. activity) that results in raised stool pH and yeast/fungal overgrowth, hydrolysis of conjugated bile acids and hormones by bacterial enzymes (increased stool levels of bile acids and increased plasma levels of estrogens), bacterial reduction of primary bile acids (production of secondary bile acids such as deoxycholate), reduced production of SCFAs (impaired energy synthesis in colonic epithelial cells), and compromised liver detoxification enzyme systems.

Putrefactive dysbiosis is strongly implicated in the pathogenesis of colon and breast cancer.