#Nutritiontalk
Nutrient Absorption
Medication can decrease or prevent nutrient absorption. Chelation
reactions between medications and minerals (metal ions) reduce
the amount of mineral available for absorption. An example is
tetracycline and ciprofloxacin, which chelate calcium found in
supplements or in dairy products such as milk or yogurt. This is
also true for other divalent or trivalent cations such as iron, mag-
nesium, and zinc found in individual mineral supplements or
multivitamin-mineral supplements. Standard advice is to take the
minerals at least 2 to 6 hours apart from the drug.
Drugs can reduce nutrient absorption by influencing the
transit time of food and nutrients in the gut. Cathartic agents
and laxatives reduce transit time and may cause diarrhea, lead-
ing to losses of calcium and potassium. Diarrhea may be in-
duced by drugs containing sorbitol, such as syrup or solution forms of furosemide, valproic acid, carba-mazepine,
trimethoprim/sulfamethoxazole. Drugs that increase peristalsis
such as the gastric mucosaprotectant misoprostol or the
hyperosmotic, lactu-lose can also lead to this unpleasant side
effect.
Drugs can also prevent nutrient absorption by changing the GI
environment. H2-receptor antagonists, such as famotidine or
ranitidine, and proton pump inhibitors (PPIs), such as
omeprazole or esomeprazole, are antisecretory drugs used to
treat ulcer disease and GERD. They inhibit gastric acid secretion
and raise gastric pH. These effects mayimpair absorption of
vitamin B12 by reducing cleavage from its
dietary sources. Cimetidine is a H2-receptor antagonistthat also
reduces intrinsic factor secretion, which can be problem-
atic for vitamin B12 absorption, resulting in vitamin B12 deficiency
with long-term use. The effect on calcium absorption of proton
pump inhibitors may raise the risk of osteoporosis in at risk indi-
viduals, and the effect appears to be stronger with PPIs than with
H2-receptor antagonists. (Corley et al, 2010 and Kwok et al,
2011).
Aside from these well-known concerns, a number of recent studies
have also shown correlations between PPI therapy, Small Intestine
Bacterial Overgrowth (SIBO), and IBS (Chey and Spiegel, 2010).
Further studies of this type are needed to determine the long-term
effects of chronic disruption in the gastric environment and its
impact on gut health.
Drugs with the greatest effect on nutrient absorption are those
that damage the intestinal mucosa. Damage to the structure of
the villi and microvilli can inhibit the brush-border enzymes and
intestinal transport systems involved in nutrient absorption. The
result is varying degrees of specific malabsorption, which can
alter the ability of the GI tract to absorb minerals, specifically
iron and calcium. Damage to the gut mucosa commonly results
from chemotherapeutic agents, nonsteroidal antiinflammatory
drugs (NSAIDs), and long-term antibiotic therapy. NSAIDs may
adversely affect the colon by causing a nonspecific colitis or by
exacerbating a preexisting colonic disease (Tonolini, 2013). Pa-
tients with NSAID-induced colitis present with bloody diarrhea,
weight loss, and iron deficiency anemia; the pathogenesis of this
colitis is still controversial.
Drugs that affect intestinal transport mechanisms include
(1) colchicine, an antiinflammatory agent used totreat gout;
(2) sulfasalazine, used to treat ulcerativecolitis; (3)
trimethoprim (antibiotic in sulfamethoxazole-trim-ethoprim)
and (4) antiprotozoal agent pyrimeth-amine. The colchicine
impairs absorption of vita-min B12, while the others are
competitive inhibitors of folate transport mechanisms.
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