Dietary interactions with

Hatton RC. Dietary interaction with phenytoin. Clin Pharm (1984) 3, 110-11. 

As of the mid-1990s, use of MAOIs for the treatment of depression is severely restricted because of potential side effects, the most serious of which is hypertensive crisis, which results primarily from the presence of dietary tyramine. Tyramine, a naturally occurring amine present in cheese, beer, wine, and other foods, is an indirecdy acting sympathomimetic, that is, it potently causes the release of norepinephrine from sympathetic neurons. The norepinephrine that is released interacts with adrenoceptors and, by interacting with a-adrenoceptors, causes a marked increase in blood pressure the resultant hypertension may be so severe as to cause death. 

M AO Is. The MAOIs are not widely used because of their potential for serious adverse reactions. Fhtients receiving MAOIs require strict dietary control because foods containing tyramine should not be eaten because of the danger of a hypertensive crisis. (See Home Care Checklist Avoiding Drug-Food Interactions With MAOIs). 

Because of their lack of selectivity and their irreversible inhibition of MAO, the first MAOIs to be developed presented a high risk of adverse interactions with dietary tyramine (see Chapter 20). However, more recently, drugs which are selective for and, more importantly, reversible inhibitors of MAO-A (RIMAs) have been developed (e.g. moclobemide). These drugs are proving to be highly effective antidepressants which avoid the need for a tyramine-free diet. 

The main problems with early, irreversible MAOIs were adverse interactions with other drugs (notably sympathomimetics, such as ephedrine, phenylpropanolamine and tricyclic antidepressants) and the infamous "cheese reaction". The cheese reaction is a consequence of accumulation of the dietary and trace amine, tyramine, in noradrenergic neurons when MAO is inhibited. Tyramine, which is found in cheese and certain other foods (particularly fermented food products and dried meats), is normally metabolised by MAO in the gut wall and liver and so little ever reaches the systemic circulation. MAOIs, by inactivating this enzymic shield, enable tyramine to reach the bloodstream and eventually to be taken up by the monoamine transporters on serotonergic and noradrenergic neurons. Fike amphetamine, tyramine reduces the pH gradient across the vesicle membrane which, in turn, causes the vesicular transporter to fail. Transmitter that leaks out of the vesicles into the neuronal cytosol cannot be metabolised because... 

Dietary consumption of polyphenols is associated with a lower risk of degenerative diseases. In particular, protection of serum lipids from oxidation, which is a major step in the development of arteriosclerosis, has been demonstrated. More recently, new avenues have been explored in the capacity of polyphenols to interact with the expression of the human genetic potential. The understanding of the interaction between this heterogeneous class of compounds and cellular responses, due either to their ability to interplay in the cellular antioxidant network or directly to affect gene expression, has increased. 

PIETTA p G and siMONETTi p (1998) Dietary flavonoids and interaction with endogenous antioxidant , Biochem Molec Biol Int, 44(5), 1069-74. 

MORTENSEN A, SKIBSTED L H and TRUscoTT T G (2001) The interaction of dietary carotenoids with radical species , Arch Biochem Biophys, 385, 13-19. 

Similarly, dietary fibers are known to interact with bile acids in the intestinal limien and thus increase bile salt excretion in feces, resulting in decreased munbers... 

Inform the patient about the potential drug-drug interactions with warfarin, including over-the-counter medications and dietary supplements (Tables 7-8, 7-9, and 7-10). Instruct the patient to call the health care practitioner responsible for monitoring warfarin therapy before starting any new medications or dietary supplements. 

Several studies have evaluated dietary supplements such as isoflavones, which are found in soy products and red clover. A well-controlled trial in more than 400 postmenopausal women evaluating a specific isoflavone, ipriflavone, found no benefits on bone mineral density or fracture rates after 3 years.47 Nevertheless, because these therapies are available without prescription and are not regulated by the FDA, patients may choose to self-medicate with isoflavones. Lymphocytopenia appeared in several patients treated with ipriflavone in clinical trials. Additionally, ipriflavone should be used with caution in immunocompromised patients or those with renal disease. It may inhibit CYP1A2 and CYP2C9 and may interact with drugs metabolized by those pathways, such as warfarin. 

The above illustration should be a clear caution that components of food may interact with drugs, resulting in substantial positive or negative therapeutic effects. As will be noted later, this principle also applies to so-called dietary supplements, including bo-tanicals, used for the treatment of numerous medical conditions. 

Although many patients believe that dietary supplements will not interact with medications, recent literature suggests otherwise. Recently, many St. John s wort-drug interactions have been reported in the literature. Cases of patients developing symptoms of serotonin syndrome have been reported with St. John s wort alone and in concomitant therapy with other antidepressants such as monoamine oxidase inhibitors, serotonin reuptake inhibitors, and venlafaxine. St. John s wort may exacerbate the sedative effects of benzodiazepines, alcohol, narcotics, and other sedatives. St. John s wort may decrease the levels of protease inhibitors, cyclosporine, digoxin, and theophylline. 

Many dietary supplements have antiplatelet activity, which may increase the risk of bleeding when used concurrently with anticoagulants. Feverfew inhibits cyclooxygenase and phospholipase A2 and may interact with anticoagulants and potentiate the antiplatelet effect of aspirin. Other supplements that possess antiplatelet activity include but are not limited to garlic, ginkgo, vitamin E, vitamin A, and selenium. 

Hsu FS, Krook L, Pond WG, et al. 1975. Interactions of dietary calcium with toxic levels of lead and zinc in pigs. J Nutr 105 112-118. 

Spin trapping methods were also used to show that when carotenoid-P-cyclodextrin 1 1 inclusion complex is formed (Polyakov et al. 2004), cyclodextrin does not prevent the reaction of carotenoids with Fe3+ ions but does reduce their scavenging rate toward OOH radicals. This implies that different sites of the carotenoid interact with free radicals and the Fe3+ ions. Presumably, the OOH radical attacks only the cyclohexene ring of the carotenoid. This indicates that the torus-shaped cyclodextrins, Scheme 9.6, protects the incorporated carotenoids from reactive oxygen species. Since cyclodextrins are widely used as carriers and stabilizers of dietary carotenoids, this demonstrates a mechanism for their safe delivery to the cell membrane before reaction with oxygen species occurs. 

Brownlee IA, Dettmar PW, Strugala V and Pearson JP. 2006. The interaction of dietary fibres with the colon. Curr Nutr Food Sci 2 243-264. 

The concept of bioavailability was developed to explain the difference between the total amount of mineral in a food and the amount which was used by the individual consuming the food. Over the past sixty years or more, there have been numerous studies related to dietary calcium requirements and bioavailability (1,2). As a result, much is known about non-calcium food components which influence the absorption and utilization of dietary calcium under experimental conditions. What now is lacking is a detailed knowledge of how these factors interact with calcium under normal conditions of ingestion in meals. 

Very little published information is available about the interaction of endrin with other chemicals. The toxicity of endrin may be influenced by interactions with other chemicals and physical agents. Quails treated with endrin and chlordane had significantly lower endrin residues in brain tissue (p<0.025) than birds treated with endrin alone (Ludke 1976). The authors attributed this difference to the presence and accumulative toxic action of one or more of the chlordane components in the nervous system. Dietary endrin pretreatment potentiated CC14 hepatotoxicity, producing slight elevation of the serum enzymes... 

P. Pavek, G. Merino, E. Wagenaar, E. Bolscher, M. Novotna, J.W. Jonker, and A.H. Schinkel. Human breast cancer resistance protein Interactions with steroid drugs, hormones, the dietary carcinogen 2-amino-l-methyl-6-phenylimidazo(4,5-b)pyridine, and transport of cimetidine. J Pharmacol Exp Ther. 312 144—152... 

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