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Digestive Conditions / The Comprehensive Digestive Stool Analysis
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Carbohydrate Digestion: Salivary amylase initiates starch digestion in the mouth. However, this activity is short-lived as the enzyme is denatured by low gastric pH. In the duodenum, oligosaccharides and starch polymers undergo hydrolysis by pancreatic amylase. Specific disaccharides are hydrolyzed by brush border enzymes (lactase, maltase, sucrase) located on the enterocyte microvilli. Resulting monosaccharides are absorbed by specific sodium-dependent transport carrier mechanisms.
• Asthma • Celiac disease • Chronic autoimmune disorders • Dermatitis herpetiformis • Diabetes mellitus • Eczema • Food allergies • Gallbladder disease • Gastric carcinoma • Gastritis • Grave’s disease • Hepatitis • Lupus erythematosus • Osteoporosis • Pernicious anemia • Psoriasis • Rosacea • Thyrotoxicosis • Urticaria • Vitiligo
Table 2 (ref. 14-24) |
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Protein Digestion: Gastric acid and pepsin initiate the digestion of dietary protein. This is followed in the duodenum by hydrolysis into oligopeptides and amino acids by proteolytic pancreatic enzymes. Final protein digestion is accomplished by intestinal brush border peptidases. Dipeptides, tripeptides, free amino acids, and probably other short-chain peptides are then absorbed.
Fat Digestion: Processing of dietary fat is the most complex of the digestive and absorptive processes. Fat is water insoluble so the GI tract must transform large water-insoluble particles into a soluble, absorbable form.
Digestion begins in the mouth with secretion of enzymes called lipases. The stomach disperses fat globules into an evenly divided phase, called chyme. Pancreatic enzymes then split triglycerides into fatty acids and monoglycerides, which then combine with bile acids and phospholipids to form micelles. This process transforms waterinsoluble lipids into a water-soluble form absorbed in the proximal small intestine.
After absorption, fatty acids and other lipids are re-esterified in the intestinal cell to form chylomicrons, which are then secreted into the lymphatic system. Medium-chain triglycerides can be absorbed directly in the jejunum without forming chylomicrons.
Maldigestion: Gastric acid secretion is a fundamental step in digestion and assimilation. Many clinical conditions originate with decreased gastric acidity. Acid secretion decreases with age, and low stomach acidity is found in more than half of patients over age 60.11,12 Researchers speculate that malabsorption of nutrients in the elderly is due to atrophy of various digestive organs because of hypochlorhydria.13
Gastric acid has a fundamental role in activating pancreatic proenzymes and converting them from inactive precursors (chymotrypsinogen, trypsinogen, etc.) to their active forms (chymotrypsin, trypsin). Intestinal peristalsis and gastric acid secretion normally prevent excessive growth of bacteria in the small intestine. It has been suggested that bacterial overgrowth might interfere with fat digestion and irritate the intestinal mucosa.
Pancreatic Exocrine Insufficiency: Inadequate delivery of pancreatic lipases and proteases to the small intestine can lead to inadequate breakdown of fats and protein. The net effect is a failure to obtain nourishment from protein, carbohydrate and fiber foods and an unhealthy environment for the flora of the large colon. It has been argued that even small decreases in pancreatic output can contribute substantially to maldigestion and have far-reaching effects in chronically ill patients.
Malabsorption: Malabsorption is characterized by abnormal fecal excretion of fat (steatorrhea) and variable malabsorption of fats, fat-soluble vitamins, other vitamins, proteins, carbohydrates, minerals and water. Common causes include:
- Defective protein, fat or carbohydrate breakdown
- Inadequate solubility of fatty acids (inadequate bile salts)
- Rapid transit (e.g. diarrhea), which doesn’t allow sufficient time for absorption
- Mucosal cell abnormality and inadequate surface area
- Intestinal infection
A number of important clinical diseases are strongly associated with and may cause mucosal malabsorption. They include sprue, Whipple’s disease, Crohn’s disease, Giardiasis, Cryptosporidiosis, lactose intolerance and eosinophilic gastroenteritis.
Clinical Considerations of Malabsorption: The signs and symptoms of malabsorption are varied. Interestingly, malabsorption increases with age.25 Amino acids, carbohydrates, fats, vitamins and trace elements may be absorbed by different processes so an individual may suffer malabsorption for one nutrient but not for others. In fat malabsorption, essential fatty acid deficiency may result in addition to the loss of the highest dietary source of calories. Take this preliminary to see if your condition could respond to treatment.
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