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FOOD-DRUG INTERACTION PRESENTED BY: DEEPIKA BARANWAL PhD SCHOLAR

Nutrient drug interaction

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Page 1: Nutrient drug interaction

FOOD-DRUG INTERACTION

PRESENTED BY:DEEPIKA BARANWALPhD SCHOLAR

Page 2: Nutrient drug interaction

DEFINITION Drug-nutrient interaction: the

result of the action between a drug and a nutrient that would not happen with the nutrient or the drug alone.

Food-drug interaction: a broad term that includes drug-nutrient interactions and the effect of a medication on nutritional status.

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Food-Drug InteractionFor example, a drug that causes chronic

nausea or mouth pain may result in poor intake and weight loss.

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BENEFITS OF MINIMISING DRUG INTERACTION

Medications achieve their intended effects.Patients do not discontinue their drug.The need for additional medication is minimized.Fewer caloric or nutrient supplements are

required.Adverse side effects are avoided.Optimal nutritional status is preserved.Accidents and injuries are avoided.Disease complications are minimized.The cost of health care services is reduced.There is less professional liability.Licensing agency requirements are met.

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DRUG EFFECTS ON FOOD INTAKE

Increased appetite (antihistamines, psychotropic drugs and steroids)

Decreased appetite(amphetamines, insulin and alcohol)

Taste changes(chelating agents and diuretics)

Nausea (cardiac glycosides )Bulking effects (methylcellulose and

other dietary fiber products)

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DRUG EFFECTS ON NUTRIENT ABSORPTION AND METABOLISM

Increased nutrient absorption (cimetidine and ranitidine)

Decrease nutrient absorption(colchicine, alcohol, laxatives, antibiotic neomycin)

Mineral depletion (diuretics, chelating agents, alcohol, antacids, aspirin)

Vitamin depletion(vitamin antagonists, oral contraceptives)

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OUTCOMES OF DRUG AND NUTRIENT INTERACTIONS

BENEFICIAL EFFECTS: Infectious disease controlControl of cancerPrevention of thrombosesTreatment of metabolic diseasePrevention of acute drug toxicity

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To be continued :

ADVERSE EFFECTS:Loss of drug efficacy Drug- induced nutritional deficiencies

Toxic reactionsBlocked feeding tubes

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Table 1. Drug Induced Nutritional DeficienciesDRUG AFFECTED

NUTRIENTSPOSSIBLE

MECHANISMEFFECT

ANORECTIC DRUGS(amphetamines)

All nutrients Anorexia Decreased food intake

ANTACIDS Phosphates Decreased absorption

Osteomalacia

ANTIEPILECTIC DRUGS (phenytion , phenobarbitone, primidone, valproic acid)

FolateVitamin DVitamin EZinc

SeleniumVitamin K

Decreased absorptionEnzyme induction Excess utilization ?Chelation

Peroxide damage?

Megaloblastic anemiaOsteomalacia Haemolysis Anorexia , celebellar dysfunctionHepatotoxicityHemorrhage

ANTIFOLATE DRUGS(e.g. methotrexate, pyrimethamine, trimethamine, trimethoprim)

Folate Dihydrofolate reductase inhibition

Megaloblastic anemia, cytopenia

BIGUANIDES (phenformin, metformin)

Vitamin B12 Decreased absorption

Megaloblastic anemia

CEPHALOSPORINS (Cefamendole, cefoperazone, latamoxef)

Vitamin K Decreased prothrombin synthesis

Bleeding episodes

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To be continued:DRUG AFFECTED

NUTRIENTSPOSSIBLE MECHANISM

EFFECT

CHOLESTYRAMINE Fat , vitamin A,D,K,B12,folate iron

Complex formation bleeding, steatorrhoea

Anaemia ,osteomalacia

COLCHICINE Fat, β-carotene, Na,K, vitamin B12

Mucosal damage Anaemia , lethargy

CORTICOSTEROIDS

Calcium Decreased Ca, vitamin D metabolism

Bone disorders

COUMARIN ANTICOGULANTS

Vitamin K ? Hemorrhage

DIURETICS Zn , Ca, K, Mg Urinary loss depression

Weakness , electrolyte imbalance

FRUSEMIDE Thiamin Urinary loss Cardiac muscle weakness

GLUTETHIMIDE Calcium Enzyme induction, altered calcium metabolism

Weakness, osteopenia

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To be continued:

DRUG AFFECTED NUTRIENTS

POSSIBLE MECHANISM

EFFECT

HARMONAL CONTRACEPATIVES STEROIDS

Riboflavin , Folate Enzyme induction, decreased absorption, competition for binding of the enzymes

Metabolic errors, depression

HYDRALAZINE Pyridoxine Complex formation Peripheral neuropathy

ISONIAZED (INH) Pyridoxine Complex formation Peripheral neuropathy, Convulsions, psychatric manifestation

LAXATIVE (MINERAL OILS)

Vitamin D Enzyme inhibition Osteopenia

LEVODOPA Nicotinic acid Competitive inhibition coenzyme and vitamin B6 deficiency

Pellagra

NEOMYCIN Vitamin A,D,E,K, B12,Ca,pyridoxine

Mal-absorption, complex formation, Mucosal damage, binding of bile salts

Osteomalacia, Peripheral neuropathy

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To be continued:

DRUG AFFECTED NUTRIENTS

POSSIBLE MECHANISM

EFFECT

PARA – AMINO SALICYCLIC (PAS)

Vitamin B12 decreased absorption

Megaloblastic anaemia

D-PENICILLAMINE Pyridoxine ,Zn, Cu Complex formation Peripheral neuropathy, Anemia

POTASSIUM CHLORIDE

Vitamin B12 decreased ileal Ph Decreased absorption

RIFAMPCIN Vitamin D Enzyme induction Osteomalacia

SALICYLATES Vitamin C, Folate Increased excretion, decreased uptake

Anemia ,infection

NEOMYCIN Vitamin A,D,E,K, B12,Ca,pyridoxine

Mal-absorption, complex formation, Mucosal damage, binding of bile salts

Osteomalacia, Peripheral neuropathy

SULPHASALAZINE Folate Mucosal block Decreased absorption

TETRACYCLINE Iron , vitamin C Chelation Decreased absorption

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TYPES:1. Pharmacodynamic Interactions:

which affect the pharmacologic action of the drug.

2. Pharmacokinetic Interaction: which affect the movement of the drug into, around, out of the body.

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PHARMACODYNAMICS Pharmaco-dynamics is the study of the

biochemical and physiologic effects of a drug. The mechanism of action, e.g. how a drug

worksOften the drug molecule binds to a receptor,

enzyme, or ion channel, producing a physiological response

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PHARMACOKINETICSPharmacokinetics is the study of the time course of a drug in the body involving absorption, distribution, metabolism (biotransformation), and excretion of the drug.

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ABSORPTION : Absorption is the process of the movement of the drug

from the site of administration to the blood-stream. This process is dependent on the (1) route of administration, (2) the chemistry of the drug and its ability to cross

biologic membranes, (3.) the rate of gastric emptying & gastrointestinal

movement, and (4.) the quality of product formulation

Food, food components and nutritional supplements can interfere with the absorption process, especially when the drug is administered orally.

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AbsorptionSwallowingDisintegration

tablet swellsbreaks up

Dissolutionreactions with acid faster when ionized

Absorptionmost post pyloric in basic environmentrequire non-ionized

state

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Food Interactions with AbsorptionMilk products alter pHMetals chelate some medicationsSome foods compete for same absorption

sitesFood speeds GI speed – reduced absorptionDegree of significance is important

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DISTRIBUTION:Distribution occurs when the drug leaves

the systemic circulation and moves to various parts of the body

Drugs in the bloodstream are often bound to plasma proteins; only unbound drugs can leave the blood and affect target organs

Low serum albumin can increase availability of drugs and potentiate their effects

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Metabolism (biotransformation)Primarily in the liver; cytochrome P-450

enzyme system facilitates drug metabolism; metabolism generally changes fat soluble compounds to water soluble compounds that can be excreted

Foods or dietary supplements that increase or inhibit these enzyme systems can change the rate or extent of drug metabolism

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Metabolism – Interaction with foodCytochrome P-450

in GI, liver Grapefruit juice made from frozen concentrate will alter this enzyme

Many drugs for AIDS, HTN

Effects occur 24 hours after ingestion

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EXCRETIONDrugs are eliminated from the body as an

unchanged drug or metaboliteRenal excretion the major route of

elimination; affected by renal function and urinary pH

Some drugs eliminated in bile and other body fluids

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ExcretionUrine acidity

will change drug excretion

Cranberry juice will alter pH and cause higher dissolution. This occurs with sulfonamides

Lime juice is most acidic

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PHARMACOGENOMICSGenetically determined variations that are

revealed solely by the effects of drugsAffect only a subset of peopleExamples include G6PD (glucose-6-

phosphate dehydrogenase) enzyme deficiency, warfarin resistance, and slow inactivation of isoniazid (IHN) or phenelzine

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SLOW INACTIVATION OF ISONIAZID OR PHENEIZINE:

Increases the risk of pyridoxine deficiency and peripheral neuropathy.

Slow inactivation of phenelzine, a monoamine oxidase inhibitor (MAOI), increases the risk for hypertensive crisis if foods high in tyramine are consumed.

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G6PD (GLUCOSE-6-PHOSPHATE DEHYDROGENASE) ENZYME DEFICIENCYIt can lead to : Neonatal jaundice, hemolytic

anemia or acute hemolysis.It is also called favism.Drugs included: aspirin, sulfonamides and

antimalerial drugs caused hemolysis and acute anemia.

Food –drug interactions in G6PD deficiency :Ingestion of fava beansVitamin CVitamin K

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WarfarinAnticoagulant used to reduce strokesInactivated by Vitamin K - broccoliEnteral nutrition products contain Vitamin

K.Warfarin activity drops when nutrition

givenStudy shows warfarin binds to protein at

pH 8

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