FOOD-DRUG INTERACTION

PRESENTED BY:
DEEPIKA BARANWAL
PhD SCHOLAR
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.
Food-Drug Interaction
 For example, a drug that causes chronic nausea or
mouth pain may result in poor intake and weight
loss.
 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.
 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)
 DRUG EFFECTS ON NUTRIENT
ABSORPTION AND METABOLISM
 Increased nutrient absorption (cimetidine
and ranitidine)
 Decrease nutrient
absorption(colchicine, alcohol, laxatives, an
tibiotic neomycin)
 Mineral depletion (diuretics, chelating
agents, alcohol, antacids, aspirin)
 Vitamin depletion(vitamin antagonists, oral
contraceptives)
OUTCOMES OF DRUG AND NUTRIENT
INTERACTIONS
 BENEFICIAL EFFECTS:
 Infectious disease control
 Control of cancer
 Prevention of thromboses
 Treatment of metabolic disease
 Prevention of acute drug toxicity
To be continued :

ADVERSE EFFECTS:
 Loss of drug efficacy
 Drug- induced nutritional deficiencies
 Toxic reactions
 Blocked feeding tubes
 Table 1. Drug Induced Nutritional Deficiencies
DRUG AFFECTED POSSIBLE EFFECT
NUTRIENTS MECHANISM
ANORECTIC DRUGS All nutrients Anorexia Decreased food intake
(amphetamines)
ANTACIDS Phosphates Decreased absorption Osteomalacia
ANTIEPILECTIC Folate Decreased absorption Megaloblastic anemia
DRUGS Vitamin D Enzyme induction Osteomalacia
(phenytion , Vitamin E Excess utilization ? Haemolysis
phenobarbitone, Zinc Chelation Anorexia , celebellar
primidone, dysfunction
valproic acid) Selenium Peroxide damage Hepatotoxicity
Vitamin K ? Hemorrhage
ANTIFOLATE DRUGS Folate Dihydrofolate reductase Megaloblastic anemia,
(e.g. methotrexate, inhibition cytopenia
pyrimethamine,
trimethamine,
trimethoprim)
BIGUANIDES Vitamin B12 Decreased absorption Megaloblastic anemia
(phenformin,
metformin)
 To be continued:
DRUG AFFECTED POSSIBLE EFFECT
NUTRIENTS MECHANISM
CHOLESTYRAMINE Fat , vitamin Complex formation Anaemia ,osteomalacia
A,D,K,B12,folate iron bleeding, steatorrhoea

COLCHICINE Fat, β-carotene, Na,K, Mucosal damage Anaemia , lethargy

vitamin B12

CORTICOSTEROIDS Calcium Decreased Ca, vitamin Bone disorders

D metabolism

COUMARIN Vitamin K ? Hemorrhage

ANTICOGULANTS

DIURETICS Zn , Ca, K, Mg Urinary loss depression Weakness , electrolyte

imbalance

FRUSEMIDE Thiamin Urinary loss Cardiac muscle

weakness

GLUTETHIMIDE Calcium Enzyme induction, Weakness, osteopenia

altered calcium
metabolism
 To be continued:

DRUG AFFECTED POSSIBLE EFFECT

NUTRIENTS MECHANISM
HARMONAL Riboflavin , Folate Enzyme induction, Metabolic errors,
CONTRACEPATIVES decreased absorption, depression
STEROIDS competition for binding
of the enzymes

HYDRALAZINE Pyridoxine Complex formation Peripheral neuropathy

ISONIAZED (INH) Pyridoxine Complex formation Peripheral neuropathy,
Convulsions, psychatric
manifestation
LAXATIVE (MINERAL Vitamin D Enzyme inhibition Osteopenia
OILS)
LEVODOPA Nicotinic acid Competitive inhibition Pellagra
coenzyme and vitamin
B6 deficiency
NEOMYCIN Vitamin A,D,E,K, Mal-absorption, Osteomalacia,
B12,Ca, complex formation, Peripheral neuropathy
pyridoxine Mucosal damage,
binding of bile salts
 To be continued:

DRUG AFFECTED POSSIBLE EFFECT

NUTRIENTS MECHANISM
PARA – AMINO Vitamin B12 decreased absorption Megaloblastic anaemia
SALICYCLIC (PAS)
D-PENICILLAMINE Pyridoxine ,Zn, Cu Complex formation Peripheral neuropathy,
Anemia
POTASSIUM Vitamin B12 decreased ileal Ph Decreased absorption
CHLORIDE
RIFAMPCIN Vitamin D Enzyme induction Osteomalacia
SALICYLATES Vitamin C, Folate Increased excretion, Anemia ,infection
decreased uptake
NEOMYCIN Vitamin A,D,E,K, Mal-absorption, Osteomalacia,
B12,Ca, complex formation, Peripheral neuropathy
pyridoxine Mucosal damage,
binding of bile salts

SULPHASALAZINE Folate Mucosal block Decreased absorption

TETRACYCLINE Iron , vitamin C Chelation Decreased absorption
TYPES:
1. Pharmacodynamic Interactions: which
affect the pharmacologic action of the
drug.

1. Pharmacokinetic Interaction: which

affect the movement of the drug
into, around, out of the body.
PHARMACODYNAMICS
Pharmaco-dynamics is the study of the biochemical
and physiologic effects of a drug.
 The mechanism of action, e.g. how a drug works
 Often the drug molecule binds to a receptor, enzyme,
or ion channel, producing a physiological response
PHARMACOKINETICS
 Pharmacokinetics is the study of the
time course of a drug in the body
involving absorption, distribution,
metabolism (biotransformation), and
excretion of the drug.
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.
Absorption
 Swallowing
 Disintegration
 tablet swells
 breaks up
 Dissolution
 reactions with acid
 faster when ionized
 Absorption
 most post pyloric
 in basic environment
 require non-ionized state
Food Interactions with Absorption
 Milk products alter pH
 Metals chelate some medications
 Some foods compete for same absorption sites
 Food speeds GI speed – reduced absorption
 Degree of significance is important
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
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
Metabolism – Interaction with food
 Cytochrome 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
EXCRETION
 Drugs are eliminated from the body as an
unchanged drug or metabolite
 Renal excretion the major route of elimination;
affected by renal function and urinary pH
 Some drugs eliminated in bile and other body
fluids
Excretion
 Urine acidity will
change drug
excretion
 Cranberry juice
will alter pH and
cause higher
dissolution. This
occurs with
sulfonamides
 Lime juice is most
acidic
PHARMACOGENOMICS
 Genetically determined variations that are
revealed solely by the effects of drugs
 Affect only a subset of people
 Examples include G6PD (glucose-6-phosphate
dehydrogenase) enzyme deficiency, warfarin
resistance, and slow inactivation of isoniazid
(IHN) or phenelzine
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.
G6PD (GLUCOSE-6-PHOSPHATE
DEHYDROGENASE) ENZYME DEFICIENCY
 It 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 beans
 Vitamin C
 Vitamin K
Warfarin
 Anticoagulant used to reduce strokes
 Inactivated by Vitamin K - broccoli
 Enteral nutrition products contain Vitamin K.
 Warfarin activity drops when nutrition given
 Study shows warfarin binds to protein at pH 8