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FOOD AND DRUG / NUTRIENT INTERACTIONS 1. THE AUSTRALIAN DEATH CEREMONY  The death ceremony started as a crude ritual, back in the days of witch ‑ craft.

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Presentation on theme: "FOOD AND DRUG / NUTRIENT INTERACTIONS 1. THE AUSTRALIAN DEATH CEREMONY  The death ceremony started as a crude ritual, back in the days of witch ‑ craft."— Presentation transcript:

1 FOOD AND DRUG / NUTRIENT INTERACTIONS 1

2 THE AUSTRALIAN DEATH CEREMONY  The death ceremony started as a crude ritual, back in the days of witch ‑ craft. In recent years it has developed into a science. It usually takes from ten to fifteen years; however, modern advancements are shortening this period of time.  It starts with one simple aspirin for a simple headache. When one aspirin will no longer cover up the headache, take two. After a few months, when two aspirins will no longer cover up the headache, you take one of the stronger compounds.  By this time it becomes necessary to take something for the ulcers that have been caused by the aspirin. Now that you are taking two medicines, you have a good start. After a few more months, these medications will disrupt your liver functions. If a good infection develops, you can take some penicillin. Of course the penicillin will damage your red blood corpuscles and spleen so that you develop anaemia. 2

3  Another medication is then taken to cover up the anemia. By this time all of these medications will put such a strain on the kidneys, they should break down.  It is now time to take antibiotics. When these destroy your natural resistance to disease, you can expect a general flare-up of all your symptoms. The next step is to cover up all of these symptoms with sulpha drugs.  When the kidneys finally plug up, you can have them drained. Some poisons will build up in your system, but you can keep going for quite a while in this way. 3

4  By now the medications will be so confused they won't know what they are supposed to be doing, but it doesn't really matter. If you followed every step as directed, you can now make an appointment with the undertaker.  This game is played by practically all Australian people, except for the few ignorant souls who follow nature.  By Dr

5 WHAT IS AN INTERACTION ?  A drug-nutrient interaction is defined as the result of a physical, chemical, physiologic, or pathophysiologic relationship between a drug and nutrient status, a nutrient, multiple nutrients, or food in general (http://www.medscape.com/viewarticle/518759_2) 5

6  Nutrition can affect the body's response to drugs; conversely, drugs can affect the body's nutrition.  A drug-nutrient interaction is the effect of a medication on food or a nutrient in food. Medications interact with foods and nutrients in several ways. Medications can decrease appetite or change the way a nutrient is absorbed, metabolized, or excreted.  A food-drug interaction is the effect of food or a nutrient in food on a medication. Dietary nutrients can affect medications by altering their absorption or metabolism. The food you eat could make the medications you take work faster, slower, or even prevent them from working at all. 6

7  Such interactions raise concerns that medications may lead to nutritional deficiencies or that the diet may change how a medication works. This does not mean that if a person is taking a medication they will need to use a vitamin and or mineral supplement. What it does mean is that taking a medication for a short time, such as a ten-day treatment, will affect the nutritional status. However, use of some medications for months or years may affect nutritional health.  Changing the diet to include more foods rich in vitamins and minerals is preferred to taking vitamin or mineral supplements. In fact, vitamin and/or mineral supplements taken in excess can affect how a medication works. 7

8 Interactions Evaluation Guide  Interactions are by definition probable events. Probabilities assigned to the interactions are based on the following criteria of combined likelihood and clinical relevance.  Certain: Interaction occurrence is definite. Available research and clinical experience both indicate that:  Co-administration is likely to provide increased therapeutic effect  Concomitant use is to avoided with adverse reactions 8

9  Probable: A relatively high probability of an interaction occurring. Available research and clinical experience both indicate that:  Co-administration is likely to provide increased therapeutic effect  Concomitant use is to avoided with adverse reactions 9

10 Who is at Risk of Drug-Nutrient Interactions?  Those with a poor diet  People who have serious health problems  Growing children  Pregnant women  Older adults  People taking two or more medications at the same time  People using prescription and over-the counter medications together 10

11  People not following medication directions  People taking medications for a long periods of time  People who drink alcohol or smoke excessively 11

12 WHY DO INTERACTIONS OCCUR?  Medications can decrease appetite or cause nausea, vomiting, an unpleasant taste, or dry mouth. This can affect nutritional health by causing poor food intake. Appetite suppressants are medications that directly affect food intake by depressing appetite. Several cancer medications and treatments may cause nausea, vomiting, sore, or dry mouth resulting in poor food intake 12

13  Medications can decrease nutrient absorption. laxatives can decrease the absorption of many vitamins and minerals. Laxatives cause food to move rapidly through the body causing poor nutrient absorption. Aluminium hydroxide contained in some antacids can bind to phosphorus in food. This can prevent phosphorus from being absorbed and used by the bones. Over time this could result in phosphorus depletion. Mild phosphorus depletion causes muscle weakness and severe cases can cause osteomalacia and severe pain in walking. 13

14 Some anticonvulsants can decrease folate absorption. Folate deficiency can result in megaloblastic anaemia. Some cholesterol lowering medications reduce cholesterol by removing bile acids. Bile acids are needed to absorb the fat- soluble vitamins A, D, E, and K. As a result some cholesterol lowering medications can reduce absorption of fat- soluble vitamins 14

15  Medications can slow down nutrient production. Vitamin K is produced by bacteria in the intestines. Antibiotics kill harmful bacteria, but they can also kill helpful bacteria. Killing the helpful vitamin K producing bacteria decreases the amount of vitamin K produced in the intestine.  Medications can interfere with the body’s ability to metabolize nutrients. Birth control pills can lower levels of vitamin B 6 and folate in the body. 15

16  Medications can increase the loss of a nutrient. Diuretics remove excess fluid from the body. Some diuretics may also increase loss of potassium along with fluids. Potassium is very important in proper functioning of the heart and other muscles.  Some anticonvulsant medications can cause the liver to increase the removal of vitamin D from the body. Vitamin D is needed for calcium absorption 16

17 Large amounts of aspirin can cause increased loss of folate. Also, large amounts of aspirin over long periods of time may cause stomach bleeding that could result in iron deficiency. Over time iron deficiency can lead to anaemia.  Food and nutrients can also alter a medication’s effectiveness in many ways.  Dietary calcium can bind to the antibiotic tetracycline. As a result the body does not absorb the amount of antibiotic intended. 17

18  Food can increase or decrease the absorption of a drug. Absorbing less than the intended dose may decrease the effect of the drug. Absorbing more than the intended dose increases the chance for an overdose effect.  Drugs are absorbed more quickly into the body when the stomach is empty. Having food in the stomach will slow down a medication’s absorption. Sometimes a medication should be taken with food. Other medications should be taken on an empty stomach, one hour before or two hours after eating. 18

19  Drugs are absorbed more quickly into the body when the stomach is empty. Having food in the stomach will slow down a medication’s absorption. Sometimes a medication should be taken with food. Other medications should be taken on an empty stomach, one hour before or two hours after eating. It is important to read the directions to see if a medication should be taken with or without food 19

20  The type of food or beverage consumed with a medication can affect a medication’s absorption. Usually, medications should be taken with water. Acidic soft drinks, juices, and foods may produce excess stomach acidity which may destroy a medication or a cause a medication to dissolve in the stomach instead of the intestine. Acidic foods may dissolve a timed release medication all at once instead of over time. 20

21  Foods or nutrients may interfere with a drug’s metabolism or a drug’s action in the body. Aged and fermented foods contain a chemical called tyramine that interacts with a medication, monoamine oxidase inhibitor. This interaction can result in dangerously high blood pressure. Vitamin K can decrease the effectiveness of certain anticoagulant medications. 21

22  Foods or nutrients may be needed for the removal of a medication from the body. Liver enzymes prepare medications for removal from the body. These enzymes require nutrients to work properly. If required nutrients are not present, medications may stay active in the body longer than they are supposed to. This may cause an overdose effect 22

23  Alcohol and medications do not mix well. Alcohol can adversely affect medications as well as nutrients. Alcohol can slow down the body’s metabolism. As a result medications can stay active in the body longer than they were supposed to. In some cases, mixing alcohol and medications can be fatal. A rule of thumb is to avoid alcoholic beverages when taking prescription or over-the-counter medications.  Large amounts of zinc can interfere with copper and iron absorption. Similarly, large amounts of iron can interfere with zinc absorption. 23

24  Nutrient supplements themselves can result in drug-nutrient interactions. In excessive amounts, vitamins and minerals act like drugs instead of nutrients. Nutrients in excessive amounts may interact with other nutrients or may even be toxic. 24

25 Certain drugs affect vitamin absorption or metabolism.  Ethanol impairs thiamin utilization, and isoniazid interferes with niacin and pyridoxine metabolism.  Ethanol and oral contraceptives inhibit folate absorption.  Most patients receiving phenytoin, phenobarbital, primidone, or phenothiazines develop folate deficiency, probably because hepatic microsomal drug- metabolizing enzymes are affected. 25

26  Folate supplements may make phenytoin less effective.  Anticonvulsants can cause vitamin D deficiency.  Malabsorption of vitamin B 12 can occur with use of aminosalicylic acid, slow-release K iodide, colchicine, trifluoperazine, ethanol, and oral contraceptives.  Oral contraceptives with a high progestin dose can cause depression, probably because of metabolically induced tryptophan deficiency 26

27 Effects of some drugs on nutrition: EFFECTDRUGS Increases appetiteAlcohol, antihistamines, corticosteroids, dronabinol, insulin, megestrol acetate, mirtazapine, many psychoactive drugs, sulfonylureas, thyroid hormone Decreases appetiteAntibiotics, bulk agents (methylcellulose, guar gum), cyclophosphamide, digoxin, glucagon, indomethacin, morphine, fluoxetine Decreases absorption of fats Orlistat Increases plasma glucose levels Octreotide, opioids, phenothiazines, phenytoin, probenecid, thiazide diuretics, corticosteroids, warfarin Decreases plasma glucose levels ACE inhibitors, aspirin, barbiturates, β-blockers, insulin, monoamine oxidase inhibitors (MAOIs), oral antihyperglycemic drugs, phenacetin, phenylbutazone, sulfonamides Increases plasma lipid levels Adrenal corticosteroids, chlorpromazine, ethanol, growth hormone, oral contraceptives (estrogen-progestin type), thiouracil, vitamin D Decreases protein metabolism Chloramphenicol, tetracycline 27

28  Now refer to the relevant section of your Griffith Handbook text. 28

29 INTERACTIONS: POSITIVE AND NEGATIVE 29

30 GRAPEFRUIT JUICE  Grapefruit became quite famous because of the acclaimed Hollywood grapefruit diet; yet, this fruit can cause dramatic increases drops in blood levels of many substances, including a number of pharmaceuticals, because it inhibits the liver- metabolism pathway, cytochrome 450.  Because of this effect on cytochrome 450, many levels of pharmaceuticals may be increased and will affect serum/plasma measurements. 30

31  The drugs that are most affected by this phenomenon are those with a typical high first- pass degradation. Among these are felodipine, nitrendipine, nisoldipine, and saquinavir. (Meletis, C. 2002, ‘Some Natural Medicines may alter Laboratory Tests Results’, Alternative and Complementary Therapies, December)  This study demonstrated that consumption of 250 mL of grapefruit juice caused a 115% increase in plasma drug concentration for a single oral dose of 5 mg of amlodipine taken with the juice. (Josefson, M, Zackrisson, AL, Ahlner J ‘Effect of grapefruit juice on the pharmacokinetics of amlopidine in healthy volunteers’ European Journal of Clinical Pharmacology, 51(2):189–193) 31

32  The effects of the juice on buspirone were tested in a randomized, phase-2 crossover study. For this study, 10 healthy volunteers took either 200 mL of double-strength grapefruit juice or water, 3 times per day, for 2 days. The mean increase resulting from the grapefruit juice consumption was 4.3-fold. (Melitis 2002)  Co-administration of grapefruit juice and lipophilic statins, in patients with primary dyslipidaemia, increases the drugs levels and causes toxic effects in liver and muscle function and must be avoided. (Paschalidou, H, Efthimiadis, A et al, 2006, ‘THE EFFECT OF GRAPEFRUIT JUICE CONSUMPTION ON METABOLISM OF STATINS IN PATIENTS WITH PRIMARY DYSLIPIDEMIA’, The Pharmacological control of lipids and lipoproteins, p.576) 32

33  Co-administration of the calcium antagonist felodipine (used for hypertension) with usual doses of commercially available grapefruit juice substantially decreased the pre-systemic clearance of felodipine. This interaction substantially increased the systemic exposure to felodipine and by this amplified its pharmacodynamic effects. (Sica,D, 2006, ‘Juice and Calcium Channel Blockers, American Journal of Hypertension, vol 19, pp ) 33

34  Grapefruit juice furocoumarins are responsible for marked increase in the oral bioavailability of many drugs with unintended consequences and risk of toxicity. Furocoumarins increase the bioavailability of drugs mainly by reducing the first pass metabolism of drugs by inhibiting the CYP3A4 enzyme and modulating the activity of transporter proteins in the gut. (Girennavar, B., Jayaprakasha, K et al, 2007, ‘Radical scavenging and cytochrome P450 3A4 inhibitory activity of bergaptol and geranylcoumarin from grapefruit’, Bioorganic & Medicinal Chemistry vol.15, pp.3684–3691) 34

35  In the case of simvastatin, a cholesterol- lowering drug, grapefruit juice increased mean peak serum concentrations approximately ninefold and researchers concluded that concomitant use should be avoided and also mentioned the possibility of greatly reducing simvastatin in therapy. (Sorenson, JM ‘Herb–Drug, Food–Drug, Nutrient–Drug, and Drug–Drug Interactions: Mechanisms Involved and Their Medical Implications’, THE JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE Vol, 8. No. 3, pp. 293–308) 35

36 PHYTOSTEROLS  The effects of natural phytosterols found in foods, herbs, and dietary supplements such as b-sitosterol, campesterol, stigmasterol, fucosterol, and z- guggulsterone were investigated. The accumulation of substrates of P-gp, increased in the presence of guggulsterone. The efflux of a further substrate was inhibited by guggulsterone. The activities of P-gp and MRP1 were stimulated by guggulsterone. These results suggest that guggulsterone, a natural dietary hypolipidemic agent have dual inhibitory effects on P-gp and MRP1 and the potencies to cause food–drug interactions. ( Nabekura,T, Yamake, T et al, 2008, ‘Effects of plant sterols on human multidrug transporters ABCB1 and ABCC1’, Biochemical and Biophysical Research Communications 369 pp.363–368) 36

37  A combination of statin therapy with a phytosterol regimen has been the topic of intervention trials. (de Jong, N, et al, 2004, ‘The combined use of cholesterol-lowering drugs and cholesterol-lowering bread spreads: health behaviour data from Finland’, Preventive Medicine vol.39, pp.849–855)  In the study of Blair et al. total cholesterol was typically reduced an extra 7% and LDL cholesterol an extra 10% in patients taking both phytosterols and statins compared to the placebo group taking statins only. 37

38  A triple treatment of simvastatin, BAS (bile acid sequestrants) and phytostanols (cholesterol lowering margarine) resulted in a total LDL cholesterol reduction of 67%. Plant sterol esters block the intestinal absorption of cholesterol, statins block the synthesis of cholesterol and BAS increase the conversion of cholesterol into bile acids. 38

39  In a placebo-controlled double-blind study, we examined the effects of dressing containing plant sterol (PS) on blood lipids and the safety in Japanese borderline or mildly hypercholesterolemic subjects. 59 subjects were randomly divided into two groups and tested for serum Total Cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (ApoB) concentrations over a 12 week period. The results indicated that PS-containing dressing decreased serum TC, LDL-C and ApoB concentrations in borderline or mildly hypercholesterolemic subjects. It is therefore proved that the dressing containing PS is helpful in maintaining blood cholesterol level normal and hence, the health of Japanese. (Kurokawa, M, Masuda. Y, Noda, M. 2008, ‘Effects of dressing containing plant sterol on serum cholesterol concentration and the safety evaluation in borderline or mildly hypercholesterolemic Japanese subjects’, Journal of Oleo Science. 57(1):35-45) 39

40  Phytosterol/-stanol-enriched margarines can modestly reduce serum total cholesterol in the community. These margarines cannot equal the effect of cholesterol-lowering drugs, but may act additively. Further investigation of the health effects that may occur during simultaneous cholesterol lowering drugs and phytosterol-or - stanol-enriched margarines usage is important, as well as community education about the cholesterol lowering foods and drugs. (de Jong N, Zuur A, Wolfs MC. 2007, ‘Exposure and effectiveness of phytosterol/-stanol-enriched margarines’ European Journal of Clinical Nutrition, 61(12): ) 40

41 DIETARY FATS  Administration of cyclosporine together with verapamil increased the absorption compared to the control (1.6 times) suggesting an effect on jejunal permeability. However, addition of dietary lipids to the media led to a 50% reduction in the absorption of cyclosporine indicating lack of major effects by P-gp inhibition by lipids in vivo. (Perssona, EM, Norfgrenb, P, Forsell,B et al, 2008, ‘Improved understanding of the effect of food on drug absorption and bioavailability for lipophilic compounds using an intestinal pig perfusion model’, European Journal of Pharmaceutical Sciences vol.3 4, pp.22–29) 41

42  Meals that were rich in fat caused a reduction in the maximum serum concentration of indinavir by an astonishing 84% compared to low-fat meals that included toast, coffee, cornflakes, jelly, and low-fat milk. However, administration of saquinavir with a high-fat diet increased bioavailability by 30%. (Sorenson 2002) 42

43  The use of lipid-based dosage forms for enhancement of drug absorption or delivery has drawn considerable interest from pharmaceutical scientists. An important question for lipid formulation is whether the drug remains in solubilised form along the gastrointestinal (GI) tract after it is administered. Certain lipid excipients and surfactants have been reported to change intestinal permeability or interfere with enzyme/transporter activity, thereby affecting drug bioavailability. The potential influence of biopharmaceutical and/or pathophysiological factors on the drug or lipid excipient(s) needs to be explored. (Chen, M, 2008, ‘Lipid excipients and delivery systems for pharmaceutical development: A regulatory perspective’ Advanced Drug Delivery Reviews vol.60 pp.768–777) 43

44  Realisation that the oral bioavailability of poorly water soluble, lipophilic drugs may be enhanced when co- administered with a meal rich in fat has led to increasing recent interest in the formulation of poorly water-soluble drugs (PWSD) in lipids as a means to enhance drug solubilisation in the gastrointestinal tract. Lipid suspensions, solutions and emulsions have all been used to enhance the oral bioavailability of PWSD and more recently, there has been increasing focus on the utility of self-emulsifying lipid-based formulations. Some of these lipid-based products that have been commercialised are Neoral® (cyclosporine), Norvir® (ritonavir), Fortovase® (saquinavir) and Agenerase® (amprenavir). (Porter,C, et al, 2008, ‘Enhancing intestinal drug solubilisation using lipid-based delivery systems’, Advanced Drug Delivery Reviews vol.60, pp.673–691) 44

45  Rupatadine is an oral active antihistamine for the management of diseases with allergic inflammatory conditions, such as perennial and seasonal rhinitis and chronic idiopathic urticaria. The results of this study indicate that concomitant intake of food a high-fat meal on the pharmacokinetic profile and bioavailability of a single oral dose of rupatadine 20 mg exhibits a significant increase in rupatadine bioavailability. 45

46 IRON  Iron is a component of heme, which comprises haemoglobin and myoglobin. These are necessary for oxygen transport. Pharmaceuticals that may induce iron deficiency include aspirin, acid blockers, thyroxine, and quinolone antibiotics. (Meletis C, Lacobs T. Interactions Between Drugs and Natural Medicines: A Simple Guide to a Complex Subject, 2nd ed. Sandy, OR: Eclectic Medical Publications, 2005)  Supplemental iron salts may diminish absorption and bioavailability of ACE inhibitors and vice versa. This is most likely caused by its binding within the intestines to form a poorly absorbed complex. (Stargrove,M., Treasure,J., McKee,D. 2008, ‘ Herb, Nutrient and Drug Interactions: Clinical Implications and Therapeutic Strategies’, Mosby USA) 46

47  All iron-antacid interactions are affected by the physiological premise that hydrochloric acid in the stomach reduces ferric iron to ferrous iron, the required form for absorption. By inhibiting acid secretion or neutralising the normally acidic gastric environment, acid suppressive agents will reduce the absorption o f dietary iron. (Stargrove et al 2008)  NSAID’s can damage the epithelium of the stomach as well as the small and large intestines, causing ulceration, increased small intestine permeability, chronic bleeding and eventually iron deficiency.  Oral indomethacin is one of the most damaging NSAID’s in this regard. 47

48  It causes anaemia by 2 possible mechanisms: Peptic ulceration or GI bleeding Interference with normal iron metabolism and erythropoiesis  As both NSAID’s and iron can cause GIT irritation, concomitant use represents a potential additive adverse effect. (Stargrove et al 2008) 48

49  Limited but pharmacologically sound evidence indicates that thyroxine and iron (as ferrous sulfate) can bind to form a poorly soluble complex when ingested simultaneously. Thus, dietary and supplemental iron may reduce the GI absorption of oral thyroxine, potentially adversely affecting therapeutic response in patients being treated for primary hypothyroidism. (Stargrove et al 2008) 49

50  Tetracycline-class antibiotics are primarily absorbed in the stomach and upper small intestines. When ingested concurrently with iron salts, the tetracyclines form insoluble chelates. This pharmacokinetic interaction can impair absorption and bioavailability of both agents, reduce the therapeutic activity of the antibiotic, and adversely affect iron balance. (Stargrove et al 2008) 50

51  Concern has been raised that concomitant oral iron intake might alter absorption and therapeutic activity of methotrexate. However, more research is needed but it will be wise to monitor your clients and advise them to separate intake by at least 3 hours. (Stargrove et al 2008) 51

52 PSYLLIUM  Should be taken with plenty of water to avoid constipation; may increase excretion of nutritional supplements or medications, such as HMG CoA reductase inhibitors. (Horowitz, S. 2001, ‘Cholesterol Management: New Clinical Guidelines and Therapeutic Options’, Alternative and Complementary Therapies, October)  Psyllium is a bulk-forming laxative and is high in both fibre and mucilage. In this study 49 people were given either Plantago ovata., or placebo in combination with their anti-diabetic drugs and it was found that better gastric tolerance to metformin was recorded in the psyllium group. (Ziai, S., Larijani, B., Akhoondzadeh, S et al, 2005, ‘Psyllium decreased serum glucose and glycosylated hemoglobin significantly in diabetic outpatients’, Journal of Ethnopharmacology, vol.102, iss.2, pp.202-7) 52

53  A telephone survey was conducted that involved 77 HIV infected patients who had received nelfinavir treatment for at least 3 months to determine the prevalence of use and the efficacy of psyllium. Sixty-seven patients (87%) reported having diarrhoea while receiving nelfinavir treatment. Of all patients, 20 (25.9%) reported using psyllium during nelfinavir therapy. Doses reported ranged from 1 to 2 tablespoonfuls 1–3 times daily. Of the patients who had used psyllium, 55% said they had less frequent stools, 40% noted improvement in stool quality, and, when specifically asked, 55% said psyllium made it easier to adhere to nelfinavir therapy. (Sherman, D & Fish, D. 2000, ‘Management of Protease Inhibitor–Associated Diarrhoea’, Clinical Infectious Diseases, vol.30, pp ) 53

54  Psyllium is a soluble gel-forming fibre that has been shown to bind to the bile acids in the gut and prevent their normal reabsorption, similar to the bile acid sequestrant drugs. Psyllium is useful as an adjunct to dietary therapy (step 1 or step 2 American Heart Association [AHA] diet) in the treatment of patients with mild-to-moderate hypercholesterolemia. In combination with other cholesterol-lowering drugs, such as statins, psyllium provides an added benefit on cholesterol lowering, and is well tolerated and cost-effective. (Petchetti L, Frishman W et. al. 2007, Nutriceuticals in Cardiovascular Disease: Psyllium, Cardiology In Review, 15(3): ) 54

55 TYRAMINE  Potentially fatal food–drug interactions can occur between monoamine oxidase inhibitors (MAOIs), which are used to treat depressive disorders, tuberculosis, and high blood pressure, and foods that are rich in tyramine.  When MAOIs and tyramine-rich foods are combined, they can cause palpitations, sweating, severe headaches, or hypertensive crises that result in fatal cerebral haemorrhages and comas. 55

56  Tyramine is indirectly sympathomimetic and suppressing its metabolism by MAOIs results in markedly increased blood pressure, cardiac arrhythmia, and cerebral haemorrhage. (Sorenson 2002)  As a result of tyramine-content analyses in draught beer and the occurrence of several cases of hypertensive crises following the consumption of modest amounts of draught beer by patients on MAOIs, it has been concluded that all draught beer should be avoided by patients who take MAOIs. (Sorenson 2002) 56

57  The list of foods containing tyramine is long. The classes of foods that should strictly be avoided are broad bean pods; yeast concentrates (such as marmite, brewers yeast, or yeast supplements); salted, smoked, or pickled fish; and aged cheeses, including blue types, Camembert types, and hard types such as cheddar, Swiss cheese, or parmesan cheese. Overripe foods, fermented beverages, and chocolate contain tyramine.  Soy products, tofu, and soy sauces can contain significant amounts of tyramine and should also be avoided with MAOI therapy. 57

58 FOLATE  Review your knowledge and understanding of homocysteine and how hyperhomocysteinaemia is treated  Now follow the processes in the following slide. 58

59 59

60  Diabetic neuropathy / anti convulsant medications phenytoin, carbamazepine, and phenobarbital (cytochrome P450 enzyme inducers) are well known to induce folate deficiency.  As homocysteine is an established risk factor in atherosclerosis, this becomes an issue of concern in patients on long-term anticonvulsant therapy.  This may be particularly true in patients with diabetes, who may be on other medications with similar unfavourable effect, and as a baseline, are high risk for vascular disease  Importantly, homocysteine itself is a potential convulsant and may reduce seizure threshold and increase seizure frequency in these patients. (Bleich S, Degner D, Bandelow B, et al. 2000, ‘Plasma homocysteine is a predictor of alcohol withdrawal seizures’ Neuroreport 11:2749–2752) 60

61  Aspirin and its metabolite, salicycle acid can inhibit folate-dependent enzymes and interfere with folate metabolism. Increased urinary excretion of folate has been associated with chronic aspirin use in patients with rheumatoid arthritis. (Stargrove et al 2008)  Medications that interfere with the normal pH of the GIT environment can impair folic acid absorption and may cause low or deficient plasma folate. (Stargrove et al 2008) 61

62  Methotrexate (used in oncology and rheumatology) is a folic acid antagonist. Many of the adverse effects associated with methotrexate are similar to those of severe folate deficiency. (Stargrove et al 2008)  Research suggests that while low folate do not characterise patients being treated with lithium, folate status may influence therapeutic response to lithium therapy. (Stargrove et al 2008) 62

63  Some NSAID’s such as sulindac and sulfasalazine, are known antifolates. With chronic use and when taken in high doses, many NSAID’s may exert antifolate activity by impairing folate absorption and transport, which could decrease serum folate concentrations and cause deficiency. (Stargrove et al 2008)  Decreased folic acid levels and increased homocysteine levels are associated with long- term use of furosemide therapy for hypertension. (Stargrove et al 2008) 63

64  Folic acid may interfere with the absorption and effectiveness of tetracycline antibiotics if ingested simultaneously and vice versa. As well, extended or recurrent use of antibiotics can cause folate depletion by eliminating the healthy intestinal flora, a major source of endogenous biosynthesis of folate. (Stargrove et al 2008) 64

65 THYROID / FOOD INTERACTIONS  It has long been known that thyroxine should not be taken with food, since foodstuffs adsorb the thyroid hormone, thereby decreasing its availability for intestinal absorption.  Hypothyroid patients taking thyroxine should be advised to take their thyroid medication well separated in time from chromium picolinate as chromium picolinate has been shown to decrease the absorption of thyroxine over a 6-hour period following co-administration of the drug. 65

66  Chromium picolinate is a salt of trivalent chromium, and it is similar in charge and ionic size to ferric ion, which is known to bind to thyroxine and cause malabsorption of the thyroid hormone.  Both in vivo and in vitro studies, have found that coffee ranks behind other known interferers of T4 absorption in that it acts to sequester the T4 thereby rendering less hormone available for uptake by the intestinal epithelium. (Benenga S, Martolone L, Pappalardo M et.al. 2008, ‘Altered Intestinal Absorption of L-Thyroxine Caused by Coffee’ Thyroid, vol.18, no.3)

67  Indeed, given the effects of food and the large number of medications that have not been tested for potential interactions with thyroxine absorption, it is suggested that patients be advised to take thyroxine only with water, at least 30 minutes before or 3– 4 hours after meals, or any other medications, if possible. (Kalarickal J, Pearlman G & Carlson H, 2007, ‘New Medications Which Decrease Levothyroxine Absorption’, Thyroid, Vol. 17, No. 8)  Selenium is important for detoxification reactions and for converting thyroxine to the more active form tri- iodothyronine. (Meletis C & Zabriskie, 2007, ‘Common Nutrient Depletions caused by Pharmaceuticals’, Alternative and Complementary Therapies, February) 67

68  Anecdotal evidence indicates a potential interaction between thyroxine and celery seed tablets. Although the validity of these anecdotal reports needs to be tested, as their number accumulates so too does the suspicion that the interaction is real. A pharmacokinetic study of the T 4 -celery interaction is under consideration by the Mater Hospital Pharmacy Services' Therapeutic Advisory Service. (http://www.australianprescriber.com/magazine/24/1/6/7/http://www.australianprescriber.com/magazine/24/1/6/7/ 68

69 VITAMIN K  Remind yourselves about vitamin K by referring pages 378 – 379 of Whitney  Vitamin K plays a key role in calcium transport and enhances bone formation. Oral corticosteroids can cause increased loss of vitamin K, as well as vitamin C, selenium and zinc. (Stargrove et al 2008) 69

70  Antimicrobial therapies, particularly chronic or recurrent courses of treatment, exert a detrimental and often devastating effect on beneficial bacterial flora naturally populating the human digestive tract. These micro- organisms that comprise the gut microflora play a critical role in the synthesis of vitamin K. When the intestinal flora are wiped out by antibiotics, their production of vitamin K diminishes. (Stargrove et al 2008) 70

71  Mineral oils (e.g. Agoral, Liquid Paraffin) absorb many substances and interfere with the normal absorption of vitamin K and other nutrients because, as fat soluble vitamins, these vitamins are dissolved in the mineral oil which is not absorbed from the intestines. This is especially problematic during pregnancy since the regular ingestion of mineral oil may reduce the assimilation of critical nutrients. The malabsorption of vitamin K can result in an increased anticoagulant activity by warfarin anticoagulants because of this adverse effect of mineral oil. (Stargrove et al 2008) 71

72 CALCIUM  The German Pharmacists Association (Apothekerverband) lists 315 pharmaceuticals that interact with foods. An important group is the tetracycline antibiotics that interact with calcium in dairy products resulting in lower, subtherapeutic plasma levels of these antibiotics. This does not only involve such calcium-rich dairy products as milk, yoghurt, and cheeses, but also calcium-containing nutritional supplements and calcium-fortified soymilk or juices. (Sorenson 2002) 72

73  Neomycin impairs calcium absorption when taken orally. (Stargrove et al 2008)  Many anticonvulsants, including phenobarbital, cause reduced calcium absorption with long term use. Some anticonvulsants, such as phenytoin and phenobarbital, adversely affect calcium metabolism by reducing serum levels of calcidol and thereby altering the hepatic metabolism of vitamin D. (Stargrove et al 2008) 73

74  Aluminium-based antacids may reduce calcium absorption and can complex with phosphates to cause a depletion of calcium stores. Aluminium hydroxide causes increased loss of calcium through urine and stool. (Stargrove et al 2008)  Corticosteroids can impair calcium absorption and interfere with both calcium and vitamin D metabolism, thereby adversely affecting bone density and potentially other calcium-related functions. Mechanisms involved include: 74

75  They interfere with the absorption of vitamin D  impairment of calcium absorption  secondary hyperparathyroidism.  The decrease in tubular calcium reabsorption  increase of urinary excretion of calcium.  They increase the risk for developing osteoporosis in 2 ways: By altering the normal calcium metabolism By reducing osteoblast activity 75

76 76

77  Inhibition of gastric acid secretion by H2 antagonists or proton pump inhibitors, particularly at high doses, can impair calcium absorption and increase risk of fractures since an acidic environment appears to enhance absorption of some forms of calcium. (Stargrove et al 2008)  Two human trials found that coffee intake, rather than caffeine, was associated with a negative balance shift of 4 – 6mg calcium per day for each 100mL coffee consumed. (Stargrove et al 2008) 77

78  Calcium compounds may form chelates with thyroid medication in the digestive tract, thereby reducing absorption, bioavailability and efficacy of both agents. Thyroid hormone medications are known to increase calcium excretion, suggesting that long term treatment was associated with decreased bone density of the spine and hip. (Stargrove et al 2008) 78

79 VITAMIN B12  Approximately 10%, but in some studies up to 30%, of patients taking metformin on a continuous basis have evidence of reduced vitamin B12 absorption. A number of reason have been postulated for this:  that metformin-induced B12 malabsorption is due to enhanced bacterial overgrowth, especially because diabetic patients are known to exhibit alterations in small bowel motility as well as bacterial overgrowth.  metformin could alter, bacterial flora through an effect on motility and/or facilitation of bacterial growth by delaying absorption of glucose. 79

80  Therefore, patients with type 2 diabetes treated with metformin, especially those who do not consume milk or milk products on a daily basis or do not take supplemental calcium should be encouraged to increase their intake of calcium as well as be closely monitored for vitamin B12 deficiency. (Sunilasnani,M., Chan,C., Murthy,S et al. 2003, ‘Effect of Pharmacological Treatments for Diabetes on Homocysteine’, Metabolic Syndrome and Related Disorders, vol.1, no.2) 80

81  Methotrexate’s intentional interference with normal functioning of folic acid metabolism creates problems with vitamin B 12 deficiency. As well, B 12 and folic acid work together to control homocysteine levels and prolonged methotrexate therapy has been shown to elevate homocysteine levels. (Stargrove et al 2008)  Excessive alcohol may reduce the absorption of B 12. (Stargrove et al 2008) 81

82  The use of oral contraceptives, especially those with higher oestrogen content, has been consistently associated with decreased levels of vitamin B12. (Stargrove et al 2008)  The proton pump inhibitor Omeprazole (Losec, Prilosec) leads to an inhibition of gastric acid secretion  interference with the cleavage of B12 from dietary proteins  decrease in protein absorption  a B 12 deficiency from malabsorption of protein-bound dietary vitamin B 12. (Stargrove et al 2008) 82

83  While these are considered major interactions, there are many others to consider when dealing with clients who are on medications. Refer to your Griffith Handbook for a comprehensive summary of nutrient / drug interactions. 83


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