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.
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