Tetracycline is a calcium chelator
Dynamis said:
Why can't you consume dairy products while on antibiotics?
Tetracycline and similar drugs are calcium chelators. When you eat tetracycline and calcium at the same time, some of the tetracycline binds (chelates) to the calcium in your stomach. When it is bound like that, your body can't use it.
http://home.caregroup.org/clinical/altmed/interactions/Drug_Classes/Tetracyclines.htm
--
nutrient/diet affecting drug performance: Calcium and Milk-containing Foods
• mechanism: Absorption of tetracycline class drugs takes place mainly in the stomach and upper small intestine. Calcium, as well as food and dairy products containing high concentrations of calcium, may decrease the absorption of tetracyclines due to chelate formation in the gut. This binding of the drug to the mineral may also lead to growth retardation and pigmented teeth. Furthermore, tetracycline increases urinary calcium excretion. Thus, with prolonged use, tetracycline can adversely effect bone formation and contribute to calcium depletion.
The interaction between tetracycline and calcium-rich foods such as milk products exerts adverse effects on bones and teeth that are well documented and widely recognized. Tetracyclines form a stable calcium complex in any bone-forming tissue. Unwanted pigmentation and other problems with tooth development due to tetracycline are well known to dentists and the general public. The tetracyclines also tend to localize in tumors, necrotic or ischemic tissue, liver and spleen and form tetracycline-calcium orthophosphate complexes at sites of new bone formation.
Tetracyclines are potent inhibitors of osteoclast function (i.e., anti-resorptive). Vernillo and Rifkin described the processes by which tetracyclines can affect several parameters of osteoclast function and consequently inhibit bone resorption: (1) altering intracellular calcium concentration and interacting with the putative calcium receptor; (2) decreasing ruffled border area; (3) diminishing acid production; (4) diminishing the secretion of lysosomal cysteine proteinases (cathepsins); (5) inducing cell retraction by affecting podosomes; (6) inhibiting osteoclast gelatinase activity; (7) selectively inhibiting osteoclast ontogeny or development; and (8) inducing apoptosis or programmed cell death of osteoclasts.
(Vernillo AT, Rifkin BR. Adv Dent Res 1998 Nov;12(2):56-62; Roe DA. 1989:87.)
--