The core functions of the gastrointestinal (GI) system are digestion and absorption. This involves an orchestrated set of components that include digestive enzymes, hydrochloric acid, bile salts, small intestinal brush border transporters and disaccharidases, and microbes that break down complex food physically and biochemically into constituent parts of macronutrients and micronutrients for optimal absorption into the body.
The causes of poor digestion (maldigestion) and absorption (malabsorption) include:
- Nutrient poor diets
- Altered gut motility
- Enteropathy
- Small intestine bacterial overgrowth (SIBO)
- Altered neuroendocrine signaling
- Low endogenous levels of acid/enzymes/bile
In modern day living, nutrient poor diets composed of highly processed and fast foods are a major culprit for malnutrition. With emphasis on refined carbohydrates, fats, and protein, diets may be high in calories but fail to provide enriching nutrients to stabilize the terrain of the GI tract. This ultimately leads to malnourished microbes in the lower gut that rely heavily on non-digestible plant fiber for nourishment. The Standard American Diet (SAD) has contributed to “starving” beneficial bacteria that are critical in human physiologic processes and immune regulation. The consequences of maldigestion and malabsorption are far reaching and include reduced bioavailability of nutrients and increased availability of undigested food particles that lead to increased inflammation, immunogenicity, high detoxification burden, and increased fermentation by gut microbes.
Maldigestion can occur if any of these components are diminished, subsequently impacting the capacity to properly absorb nutrients:
- Hydrochloric Acid (HCl)
- Intrinsic factor
- Pancreas enzymes
- Bile Acids
- Disaccharidases
- Other enzymes that break down complex carbohydrates
Maldigestion can also ensue with small intestinal bacterial overgrowth (SIBO), which leads to bacterial consumption of nutrients that are subsequently unavailable for absorption. Maldigestion can be a consequence of mucosal disease with enteropathy or inflammation, such as Crohn’s disease or celiac disease, that can lead to disruption of brush border enzymes like disaccharidases that break down sugars.
Malabsorption is a consequence of an insult or injury to the small intestinal lining. The mechanism of malabsorption is divided into areas which constitute multiple specific diseases:
- Reduced small intestinal surface area due to inflammation or villous atrophy (Crohn’s disease, celiac disease, tropical sprue, Whipple’s disease, Collagenous Sprue, lymphoma, SIBO)
- Lymphatic obstruction (Lymphangiectasia, cirrhosis, amyloidosis, tuberculosis)
- Small intestinal surgery, which increases risk for short gut syndrome
- Rapid intestinal motility (hyperthyroidism, inflammatory bowel syndrome (IBS), or dumping syndrome from bariatric surgery)
- Mesenteric ischemia
- Loss of intrinsic factor due to autoimmune disease or pernicious anemia may lead to inability to absorb B12 in the terminal ileum
Both maldigestion and malabsorption may also be perpetuated by altered GI motility that can be seen with multiple disorders including gastroesophageal reflux disease (GERD), gastroparesis, IBS and functional GI disorders, intestinal pseudo-obstruction, and chronic constipation with slow transit. Hormonal imbalances, particularly thyroid disorders, can also alter gut motility.
Clinically, subjects with maldigestion and malabsorption present with GI symptoms, and the severity of macro- and micronutrient deficiencies will dictate presence of additional systemic manifestations. Typical gut symptoms associated with maldigestion and malabsorption include abdominal pain, gas/bloating, flatulence, early satiety, diarrhea, undigested food in the stool, and weight loss. Increased severity of malabsorption can lead to edema, ascites, and wasting. Depending on the severity of symptoms, additional biomarkers may include iron deficiency anemia, macrocytic anemia, hypoalbuminemia, and select micronutrient deficiencies.
