O Nutrition and Health

effects of endogenous opioid peptides in the brain. Naloxone has been
shown to retard weight gain in experimental animals (Reid 1985). Although
it also appears to reduce food intake in humans (Cohen et al. 1985), studies
exploring its clinical use in weight reduction have been disappointing
(Levine et al. 1985).

Digestion and Absorption
A variety of commonly used drugs impair the digestion and absorption of
certain nutrients.

Laxatives decrease gastrointestinal transit time and reduce the absorption
of glucose, calcium, protein, sodium, and potassium (Frier and Scott 1977).
It has been suggested that mineral oil solubilizes and sequesters fat-soluble
vitamins and prevents their absorption (Morgan 1941; Mahle and Patton
1947), but more recent data suggest this effect may be minimal. Cellulose
can decrease absorption of calcium and magnesium (Berstad et al. 1975;
F'ak 1973).

Excessive consumption of aluminum-containing antacids can induce a
phosphate depletion syndrome when dietary phosphate combines with
aluminum hydroxide to form aluminum phosphate, which is insoluble and
hence is completely excreted (Cooke, Teitelbaum, and Avioli 1978; Insogna
et al. 1980). The risk of acute phosphate depletion is greatest when the diet
is low in phosphate (Roe 1984). Antacids have been reported to have
induced a severe copper deficiency in a patient with decreased gastric
emptying time (Anonymous 1984a). Prolonged use of aluminum-containing
antacids by patients with impaired renal or biliary excretion should be
avoided, because the absorption and accumulation of aluminum under
these conditions may impair calcium metabolism and lead to bone disease
as is seen in kidney dialysis patients (Lemboke et al. 1982; Herzog et al.
1982).

Cholestyramine and colestipol prevent intestinal reabsorption ofbile acids;
they lower blood cholesterol levels by enhancing the conversion of choles-
terol to bile acids. These drugs, however, also alter bile acid activity and
may result in malabsorption of fat, vitamins A, D, K, and B,,, and folacin
(Whiteside et al. 1965; West and Lloyd 1975). However, use of cho-
lestyramine for 7 to 9 years in the Coronary Primary Prevention Trial by
men with high blood cholesterol did not appear to cause nutrient deficien-
cies. Fat-soluble vitamins are frequently prescribed along with cho-
lestyramine to eliminate any risk of deficiency.

676


Drug-Nutrient Interactions 0

Certain antibiotics, such as neomycin, may damage the intestinal mucosa
and also precipitate bile acids, thus decreasing the absorption of vitamin K,
carotene, and vitamin A, which are dependent on bile acid action for
absorption (Levine 1967; Thompson et al. 1971; Barrowman, D'Mello, and
Herxheimer 1973). Excessive amounts of broad-spectrum antibiotics can
also destroy the natural vitamin K-producing bacterial population of the
intestine, thus inducing bleeding conditions that can be reversed, if neces-
sary, by vitamin K administration (Ansell, Kumar, and Deykin 1977; Anon-
ymous 1984b).

The anti-inflammatory agent colchicine used to treat gout may alter intes-
tinal transport mechanisms, leading to sodium, potassium, lipid, and nitro-
gen fecal loss (R&e, Paes, and Faloon 1970; Webb et al. 1968).

Metabolism and Utilization

Oral Contraceptive Agents. Oral contraceptive agents are formulated from
synthetic estrogens and progesterones that can affect metabolic processes
involving essential vitamins and minerals. They are used by an estimated
10 million women in the United States (Ory, Forrest, and Lincoln 1983).
Although numerous studies have reported laboratory evidence of marginal
nutritional deficiencies among women taking these drugs, such evidence
has been inconsistent and has only rarely been confirmed by clinical
evidence. For example, blood levels of vitamin B, were found in some
studies to be reduced among 20 percent or more of women using oral
contraceptives, but other studies have failed to demonstrate such effects
(Thorp 1980). The clinical significance of these observations is uncertain
(Leklem 1986; Miller 1986). Circulating levels of zinc and release of zinc
from tissues have also been reported to be reduced among users of oral
contraceptives, but there is no evidence that such changes alter the dietary
requirement for this mineral (King 1987). As with other interactions yield-
ing minimal to moderate decreases in serum levels of micronutrients,
clinical manifestations of deficiencies are likely to be detected only when
nutritional status is below optimal levels before taking the drug.

Anticonvulsanfs. Various anticonvulsants accelerate the metabolism and
elimination of vitamin D (Harvey 1985) and have been associated with
clinical signs of rickets in children and osteomalacia in adults (Matheson et
al. 1976). Also, the anticonvulsants phenytoin, phenobarbital, and pri-
midone are capable of inducing a biochemical or clinical folate deficiency
state (Chanarin 1979; Lambie and Johnson 1985; Edeh and Toone 1985).
These drugs also interfere with metabolism of thiamin (Klein et al. 1977).

677


O Nutrition and Health

Newborn infants of mothers taking barbiturates or phenytoin are more
likely to have coagulation defects because of reduced availability of vitamin
K (Keith, Gundberg, and Gallop 1980; Keith et al. 1983). Osteomalacia
secondary to phenytoin may require replenishment of vitamin K as well as
vitamin D to restore the vitamin K-dependent proteins that are important
for normal calcium metabolism in bone. Camitine may be depleted by
therapy with the anticonvulsant valproic acid, resulting in hepatic injury
and a Reyes-like syndrome (Bohles et al. 1982; Coulter 1984; Murphy,
Marquardt, and Shug 1985).

Vitumin Antagonists. Several drugs used as cancer chemotherapeutic
agents (e.g., methotrexate), as diuretics (triamterene), or as antimalarial or
antibacterial drugs (pyrimethamine) are antagonists of folic acid (Lambie
and Johnson 1985). These drugs bind to the enzyme dihydrofolate reduc-
tase, preventing the conversion of folic acid to tetrahydrofolate, the vi-
tamin form that is required for synthesis of purines. As a result, DNA
synthesis is arrested and the cells die (Anderson, Smith, and Hutchinson
1966; Kahn, Fein, and Brodsky 1968; Lieberman and Bateman 1968;
Myatt, Hemandez, and Coatney 1953). The drug sulfasalazine, used to
treat ulcerative colitis, inhibits intestinal transport of folic acid and has
been associated with the clinical signs of deficiency of this vitamin often
seen in persons with inflammatory bowel disease (Halsted, Gandhi, and
Tamura 1981).

The vitamin K antagonists-dicumarol, phenprocoumon, and warfarin-
are used as anticoagulants; they block a specific carboxylation step in the
activation of six vitamin K-dependent clotting factors (Wessler and Gitel
1984; O'Reilly 1985). Parkinsonian patients, whose tremors are controlled
by L-dopa, may experience a precipitation of their symptoms if they ingest
large doses of vitamin B, because of an interaction between L-dopa and
pyridoxal-5 phosphate, the active form of this vitamin (Evered 1971; Mars
1974).

The antitubercular drug isoniazid binds and inactivates vitamin B,, induc-
ing pyridoxine deficiency and its resulting neuropathy (Biehl and Vilter
1954). Consequently, vitamin B, is often given to individuals receiving this
therapy. One benefit of this interaction is that overdoses of isoniazid can be
treated successfully by administration of vitamin B, (Wason, Lacouture,
and Lovejoy 1981). A similar vitamin B,-responsive neuropathy occurs in
patients taking hydralazine, a hypotensive agent (Raskin and Fishman
1965). Cycloserine, another antitubercular drug, impairs niacin synthesis
and absorption and may lead to a niacin deficiency (Heinivaara and Plava
1964).

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Drug-Nutrient Interactions O

Vitamin B,, metabolism is also affected by a variety of drugs. For example,
the antitubercular drug paraminosalicyclic acid affects intestinal transport
mechanisms for vitamin B,, (Toskes and Deren 1972), and prolonged
exposure to nitrous oxide has been reported to produce a megaloblastosis
(Chanarin 1982) and a myeloneuropathy similar to symptoms typical of
vitamin B,, deficiency (Layzer 1978) perhaps because of binding and
inactivation of the cobalt present in that vitamin.

Antihypertensive Drugs. These drugs produce disturbances of mac-
ronutrient metabolism, resulting in glucose intolerance and hyper-
lipidemia. Beta blockers increase blood levels of triglycerides but decrease
levels of high density lipoprotein cholesterol (Helgeland 1984; Weinberger
1985). Thiazide diuretics decrease glucose tolerance (Amery et al. 1978;
Murphy et al. 1982; Perez-Stable and Caralis 1983; Helderman et al. 1983;
Ames 1984), increase serum levels of low density lipoprotein cholesterol
(Goldman et al. 1980; Grimm et al. 1981; Weinberger 1985) and decrease
losses of calcium in urine (McCarron 1985; Stier and Itskovitz 1986).
Spironolactone lowers serum levels of high density lipoprotein cholesterol
and increases serum levels of insulin (Falch and Schreiner 1983).

Excretion

Diuretics. Diuretics, such as the thiazides and furosemide, decrease the
resorption of potassium and other minerals by the kidneys, thereby in-
creasing their excretion (Dyckner and Webster 1979; Morgan,
Murkinshaw, and Davidson 1978). Patients on long-term diuretic therapy
are usually advised to consume foods rich in potassium.

In sum, drugs cause little nutrient-related difficulty for the great majority of
individuals taking medications. Adverse effects are usually limited to per-
sons who consume relatively high doses over prolonged periods, or to
persons who have clinical conditions that interfere with normal drug me-
tabolism and excretion or that make them unusually susceptible to drug-
induced nutritional deficiencies (Smith and Bidlack 1982).

Effects of Diet on Drug Metabolism

Nutritional factors affect the activity of drugs by altering their rates of
absorption, metabolism, or excretion.

Absorption
Dietary factors can decrease, delay, or enhance the absorption of drugs,
primarily by altering their availability, their solubility, or the amount of time

679


O Nutrition and Health

they spend in the stomach or intestine (Hathcock 1985). Calcium, for
example, can bind tetracycline antibiotics and form a complex that renders
both the drug and nutrient unavailable (Roe 1985). Dietary fat enhances the
absorption of fat-soluble drugs, but the absorption of drugs that bind to
fiber is reduced by high-fiber diets. Drugs such as L-dopa and penicillin G
that are metabolized or degraded in the stomach may be partially destroyed
when gastric emptying is delayed. The bioavailability of certain drugs, such
as the antibacterial nitrofurantoin, the cardiovascular drug propranolol,
and the hypotensive drug hydralazine, is enhanced when gastric emptying
is delayed and more of the agent can be dissolved in the gastric juice
(Melander 1978; Toothaker and Welling 1980). Digitalis absorption is
slowed by the presence of food in the gastrointestinal tract. Instructions to
take drugs with or between meals, or the coating of drugs to prevent
dissolution, attempt to take advantage of these gastric properties, although
it is uncertain how well patients adhere to such instructions. The acidity of
the gastrointestinal tract also affects drug disposition. A more acidic en-
vironment reduces the bioavailability of penicillin and isoniazid but in-
creases the absorption of tetracyclines (Roe 1985).

Food decreases, delays, or enhances the absorption of certain antibiotics
(Hathcock 1985). The complexity of the diet and of drug responses makes
the clinical implications of such interactions difficult to predict.

Metabolism and Utilization

The effects of drugs are modulated by their rates of metabolism by the liver
and other tissues. Drugs that are metabolized slowly do not need to be
taken as frequently or in as high doses as those that are rapidly eliminated
by the body. Drugs are metabolized by two basic processes. The first
(Phase I) metabolic step is usually an oxidation reaction that alters a
functional group in the drug. This alteration may either activate the drug or
deactivate it. The most common example of this process involves the same
mixed-function oxidase enzyme systems that metabolize many other en-
dogenous or foreign (xenobiotic) compounds. These systems contain
cytochrome P-450 and other cytochromes and employ reduced nicotina-
mide adenine dinucleotide phosphate (NADPH) and molecular oxygen in
their reactions. A second step (Phase II) conjugates the oxidized drug to an
inactive, water-soluble form that can be readily excreted (Bidlack 1982;
Meydani 1987; Hathcock 1987a). Most effects of diet on drug metabolism
affect the oxidation reactions, whereas relatively little is known about the
ways in which nutritional factors affect conjugation reactions (Hathcock
1986).

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Drug-Nutrient Interactions O

The rate of drug metabolism by mixed-function oxidase systems can be
accelerated (induced) by the drugs themselves as well as by a variety of
dietary factors. Such factors include protein, cruciferous vegetables such
as broccoli or cabbage, and charcoal-broiled meats (Bidlack 1982). Thiamin
deficiency also increases drug metabolism-it has been shown to increase
the demethylation of mestranol, for example (Hoyumpa and Schenker
1982).

On the other hand, low-protein, high-carbohydrate diets and deficiencies of
several vitamins and minerals reduce levels of drug-metabolizing enzymes
and, consequently, the rate of drug metabolism, so that drug concentrations
may decline slowly. Thus, in many cases, the net effect of nutritional
deficiency is to increase drug potency (Hathcock 1987a). In starved individ-
uals, for example, the activities of the mixed-function oxidase enzymes are
reduced and the clearance of drugs such as chloramphenicol and sul-
fadiazine is impaired. The metabolism of other drugs is unaffected by
starvation (Bidlack 1982).

Excretion

High-fiber diets interfere with the enterohepatic circulation of drugs ex-
creted in bile (Hathcock 1985). Urinary acidity, which can be affected by
diet, also influences drug elimination. Aspirin, for example, is resorbed in
acidic urine, whereas amphetamines are resorbed under more alkaline
conditions (Welling and Tse 1983).

Effects of Drug-Food lncompetibilities

Certain drugs can interact with specific nutrients or non-nutrient compo-
nents in foods to cause acute adverse reactions. Such reactions can be
prevented by avoiding the foods when taking the medication. Examples
include interactions between monoamine oxidase inhibitors and foods
containing tyramine, and between alcohol and disulfiram, hypoglycemic
agents, and many other drugs (Taylor 1987).

Monoamine Oxidase Inhibitors

Monoamine oxidase (MAO) inhibitors are mood-elevating agents that were
formerly used with great frequency to treat severe depression. Their nutri-
tion-related problems stem from metabolism of the potentially toxic amine
tyramine. Tyramine is formed when intestinal bacteria degrade the amino
acid tyrosine; it is also found in fermented foods such as cheese, wine,

681


O Nutrition and Health

yogurt, some kinds of sausages, and beer. Under ordinary circumstances,
the enzyme MAO converts tyramine to soluble products that can be
excreted in urine. Inhibition of MAO in the presence of foods containing
tyramine permits this toxic amine to increase in blood to the point where it
causes severe-and occasionally fatal-hypertension (Asatoor, Levi, and
Mime 1963). Because the use of MAO inhibitors by people who ingest foods
containing tyramine can induce a severe hypertensive crisis, they are now
prescribed less frequently (Roe 1984).

Alcohol

Acetaldehyde-induced nausea and vomiting can occur within 15 minutes
after the consumption of alcohol by persons taking the drugs disulfiram
(Antabuse), metronidazole (Plagyl), and chlorpropamide (Diabinese). Di-
sulfiram inhibits the enzyme acetaldehyde dehydrogenase, which oxidizes
acetaldehyde, a product derived from the metabolism of alcohol (Hald and
Johnson 1948). This interaction, which is so unpleasant as to deter the use
of alcohol, is the basis for the use of Antabuse in detoxification programs
(for reviews see Roe 1984; Seitz and Simanowski 1987).

Alcohol consumption can cause hypoglycemia in persons with diabetes
who are using agents such as the sulfonylureas to lower blood sugar levels
(Harris 1971; Carulli, Manenti, and Gal10 1971). It also potentiates the
prolongation of bleeding time induced by aspirin (Deykin, Janson, and
McMahon 1982), an interaction that can have serious consequences in
alcoholic patients who suffer from gastritis, esophageal varices, or peptic
ulcers.

Acutely, alcohol inhibits the activity of drug-metabolizing enzymes by
displacing other drugs bound to cytochrome P-450, by decreasing the
availability of NADPH, or by disturbing the lipid bilayer membrane that
provides the microenvironment for drug-metabolizing enzymes (Hoyumpa
and Schenker 1982). Chronic alcohol consumption enhances oxidation and
toxicity of many substances, for example, acetominophen (Seitz and Sim-
anowski 1987). It increases the toxic side effects of analgesics, anesthetics,
anticoagulants, anticonvulsants, antihistamines, antimicrobials, tran-
quilizers, and narcotics (Anonymous 1979). Meprobamate, chloral hy-
drate, and barbiturates are also metabolized and excreted more slowly
when alcohol is taken simultaneously (Hoyumpa and Schenker 1982).
Ingestion of benzodiazepines and alcohol together results in higher plasma
concentration of the drugs and enhanced sedative effects due to decreased
hepatic clearance. The postural hypotension produced by organic nitrates
for angina is accentuated by alcohol (Needleman, Corn and Johnson 1985).

682


Drug-Nutrient Interactions 0

As a general rule, any toxic side effect of a medication will be potentiated if
alcohol is consumed along with it (Anonymous 1979; Seitz and Simanowski
1987).

Effects of Drugs Used in Food Production

Antibiotics such as tetracycline and penicillin are fed to livestock to pre-
vent infections and to promote growth. Because the genetic information
that controls some kinds of resistance to antibiotics is carried on transposa-
ble genetic elements (plasmids) that can be transferred from one organism
to another, questions have been raised as to whether subtherapeutic doses
of livestock with antibiotics (a procedure that enhances growth and feed
utilization) might encourage the proliferation of antibiotic-resistant micro-
organisms that are human pathogens or are capable of transferring antibiot-
ic resistance to human pathogens (Stallones 1982).

In 1980, a National Academy of Sciences (NAS) report concluded that the
research necessary to establish and to measure potential risks of antibiotic
use in animals had not yet been conducted (NAS 1980). Since then, human
infections with drug-resistant Salmonella have been documented, both as a
result of eating hamburger originating from cattle that had been fed sub-
therapeutic doses of tetracyclines (Holmberg et al. 1984) and from drinking
raw cow milk infected with Salmonella resistant to chloramphenicol and
several other antimicrobial agents (Tacket et al. 1985). As a result of these
studies, the Center for Veterinary Medicine of the Food and Drug Adminis-
tration, with the counsel of a new NAS committee, is reviewing the avail-
able research findings on the hazards and benefits of this use of drugs. At
issue is whether to institute procedures to suspend low-level uses of pen-
icillins and tetracyclines in animal feeds (Goodman-Malamuth 1986).

Effects of Pharmacologic Doses of Nutrients

Nutrients are sometimes used in unusually high doses for their phar-
macologic effect. Niacin, for example, is used pharmacologically to reduce
blood cholesterol levels (Grundy et al. 1981; Blankenhorn et al. 1987).
Retinoid derivatives of vitamin A have been used successfully to treat
severe acne and other conditions (Bollag 1983). All pharmacologic
therapies induce side effects (pharmacology has been described as "applied
toxicology" because even the desirable effects of drugs are obtained by
altering-poisoning-normal metabolic function), and high-dose nutri-
tional therapies are no exception. Although excess water-soluble vitamins
are excreted and usually cause little difficulty, side effects have been

683


O Nutrition and Health

reported in cases of excessively high doses (Miller and Hayes 1982). High-
dose niacin induces flushing, and neurologic symptoms have been reported
from excessive intake of vitamin B, (Schaumburg et al. 1983). Excessive
intake of fat-soluble vitamins or their derivatives is well known to induce
toxic symptoms. Excess vitamin A, for example, causes birth dkfects in
animals, and, possibly, in humans; caution has been urged in its use for
women who are pregnant or likely to become pregnant (Teratology Society
1987).

Individuals born without the genes to produce key functional enzymes may
require amounts of certain nutrients greatly in excess of those required by
most people. Such inborn metabolic errors have been identified for en-
zymes necessary for absorption, metabolism, or storage of nearly all of the
vitamins (Stanbury et al. 1985). In some cases, higher-than-normal intake
of the vitamin will restore activity. A classic example of such a vitamin-
responsive syndrome is pernicious anemia, a condition of impaired absorp-
tion of vitamin B,,. Patients with this condition must have exceedingly high
doses of the vitamin from food or supplements, or lower doses by injection.
Another example is homocystinuria, a condition that results from a defi-
ciency of the enzyme cystathione beta synthetase. Lack of this enzyme
leads to the accumulation of methionine, the appearance of homocystine in
urine, and clinical symptoms ranging from thromboses and osteoporosis to
mental retardation. About 40 percent of individuals with this condition
respond favorably to doses of vitamin B, that are 50 to 500 times higher than
levels defined by Recommended Dietary Allowances (Mudd and Levy
1983).

Acrodermatitis enteropathica, a severe skin and gastrointestinal disorder,
is caused by a deficiency in zinc absorption, but it can be overcome by zinc
administration at levels greatly in excess of those normally required (Prasad
1983). An inborn error of metabolism resulting in systemic camitine defi-
ciency, with clinical manifestations of excessive ketone production, has
been treated successfully with supplemental camitine (Wolff et al. 1986).

In other conditions, certain metabolic products cannot be degraded and,
therefore, accumulate to toxic levels. In some cases, such disorders can be
treated with carefully designed dietary preparations having a very low
content of the poorly metabolized nutrient. An example of this type of
condition is phenylketonuria, a genetic lack of the enzyme that converts
the amino acid phenylalanine to tyrosine. Patients with phenylketonuria
accumulate phenylalanine and other metabolites that, at high levels, are
toxic and cause mental retardation and other neurologic damage (Anony-

684


Drug-Nutrient Interactions O

mous 1986d). Dietary treatment is designed to reduce the phenylalanine
content of the diet to levels below those that cause symptoms. The special
infant formula product Lofenelac, for example, contains sufficient quan-
tities of all of the essential amino acids with the exception of phenylalanine
(Tourian and Sidbury 1983).

Implications for Public Health Policy

Dietary Guidance

General Public

Although drugs interact with dietary factors in many ways that impair
nutrient availability, evidence about the public health significance of such
interactions is insufficient to recommend general shifts in the pattern of use
of any particular drug on the basis of its adverse effects on nutritional
status. Nor may any implications be drawn at this time for the general
public on intake of specific nutrients with relation to nonprescription drug
interactions.

Special Populations

Studies of patients consuming multiple drugs for prolonged time periods,
especially those patients who are older, suggest that dietary intakes may
need to be adjusted to compensate for adverse interactions of specific
nutrients with medications and that information should be provided to such
patients by qualified health professionals on appropriate use of such diets.
Patients taking drugs that induce acute reactions in the presence of dietary
factors such as tyramines or alcohol should be instructed on appropriate
means to avoid those factors.

Persons with inborn metabolic errors that respond to pharmacologic doses
of nutrients or to special products designed to minimize toxic symptoms
should be advised on the safe and effective use of such therapies. Health
professionals should receive instruction about drug-nutrient interactions to
understand how best to maximize drug efficacy and minimize adverse
reactions.

Nutrition Programs and Services

Food Labels

Evidence related to the role of diet in drug interactions currently holds no
special implications for change in policy related to food labeling.

685


O Nutrition and Health

Drug Labels
Evidence related to the role of diet in drug interactions suggests that drug
manufacturers should provide information in the package insert on the
potential effects of the medication on nutritional status, and vice versa.

Food Services

Evidence related to the role of diet in drug interactions currently holds no
special implications for change in policy related to food service programs.

Food Products

Evidence related to the role of diet in drug interactions currently holds no
special implications for change in policy related to packaged food products.
Preliminary evidence relating human infections to antibiotic-resistant
micro-organisms derived from animals treated with subtherapeutic doses
of antibiotics suggests the need for close scrutiny of this practice.

Special Populations

Persons-especially older persons-who consume drugs should be pro-
vided with counseling and assistance on dietary methods to avoid adverse
drug-nutrient interactions. Persons with inborn metabolic errors requiring
therapy with pharmacologic doses of nutrients should be provided with
counseling and assistance on appropriate and safe use of such supple-
ments.

Research and Surveillance

Research and surveillance issues of special priority related to the role of
diet in drug interactions should include investigations into:
o The extent of drug taking (prescription, over the counter, and illegal)
  among the population.

o The extent of adverse drug-nutrient interactions in the population and
their clinical significance.

o Age-related changes in nutrient metabolism with special implications
for pharmaceutical use.

o Effects of medications on the nutritional status of older persons.
o Drug effects on nutrient intake, absorption, metabolism, and excre-
tion.

o Effects of diet, including alcohol, on drug absorption, metabolism, and
excretion.

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Drug-Nutrient Interactions O

o The effects of antibiotics, hormones, or other drugs in animal feeds on
human health.
0 The levels of intake of essential nutrients that induce toxic symptoms.
o The most effective means to educate health professionals and the
general public about drug-nutrient interactions.

687


u Nutrition and Health

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Chapter 19

Dietary Fads and Frauds

The advertising quack . . . is the black wolf,
aye, the Bengal tiger of the profession. . . .
He is full of shrewdness and cunning, and
knows the poor weak human nature like a
           book.
     Dr. Willis P. King, 1882
  Quacks and Quackery in Missouri

Introduction

Historical Perspective

Food, an indispensable ingredient of life, has long been endowed with
metaphysical, moral, and theological meanings. The folklore and supersti-
tions of cultures throughout history have attributed healing or harmful
properties to certain foods. This tendency has not disappeared with the
advent of the sciences of nutrition and medicine. Food folklore continues
today, although in many instances it is inconsistent with scientific evidence
(Young 1978).

Contemporary food fads often make one or more of the following claims,
none of which are substantiated by available scientific evidence (Bitensky
1973; Darby 1974; Shifflett 1976; Deutsch 1977; Stare 1980; Miller 1980;
Jarvis 1983, 1984b):

0 Some foods have magical, life-promoting properties.
o Modern foods are grown on depleted soil, are overprocessed, and,
therefore, cannot provide good nutrition.
o Food supplements are always necessary to ensure good nutrition, and
megadoses of nutrients provide "supernutrition."

Definitions

Nutrition fraud is a comprehensive term used by the U.S. Food and Drug
Administration (FDA) to describe the abuses that occur as the result of the
misleading claims for traditional foods, dietary supplements, and dietary

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products and of the deceptive promotion of other food substances, proc-
esses, and devices (Nightingale 1984). Nutrition fraud has long been recog-
nized as the leading example of health fraud (Larrick 1963). Food faddism
and quackery describe two types of nutrition fraud commonly purveyed to
the public (Huenemann 1956; Todhunter 1973; Jarvis 1984a).

Food faddism is a dietary practice based upon an exaggerated belief in the
effects of food or nutrition on health and disease. Food fads derive from
three beliefs: (1) that special attributes of a particular food may cure
disease, (2) that certain foods should be eliminated from the diet because
they are harmful, and (3) that certain foods convey special health benefits
(McBean and Speckmann 1974). Unlike more transitory fads, many key
concepts associated with food faddism persist or reappear periodically.
Food faddists are those who follow a particular nutritional practice with
excessive zeal and whose claims for its benefits are substantially more than
science has substantiated. In most instances, foods praised as beneficial,
such as special products or vitamin supplements, are not as good as
faddists claim, and those foods condemned as harmful, such as white flour
or sugar, are not as bad (Jarvis 1983).

Food quackery, which involves the exploitive, entrepreneurial aspects of
food faddism, is the promotion for profit of special foods, products, proc-
esses, or appliances with false or misleading health or therapeutic claims.
A food quack is one who pretends to have medical or nutritional knowledge
and who promotes special foods, products, processes, or appliances with
false or misleading claims, usually for personal financial gain.

Factors Contributing to Nutrition Fraud
Nutrition fraud flourishes in the United States today because of the diver-
sity of cultures, the historical tradition of concern for health and the use of
natural remedies, and the introduction of advanced communication tech-
nologies. Some frauds derive from traditional folklore inherited from the
many cultures populating this country, while others are uniquely American
(Young 1978; Deutsch 1977).

Food faddism in America had its roots in Great Britain, where patent
medicines were advertised and sold by everyone from hairdressers to
goldsmiths. In the colonies, legal protection of consumers against fraudu-
lent claims was first recorded in Massachusetts Bay in 1630. A citizen,
Nicholas Knopp, was whipped and fined five pounds for selling a cure for
scurvy that had "no worth nor value" and was "solde att a very deare rate"
(Young 1961).


Dietary Fads and Frauds Cl

Food faddism was very common in 19th-century America, perhaps as a
result of the high literacy rate and the proliferation of newspapers that
provided a medium for advertising. Claims for health benefits were an
integral part of the promotion of foods and food components sold by patent
medicine men and women and popular health reformers (Whorton 1982).
One of the earliest nutrition faddists was Sylvester Graham, a "back to
nature" reformer who was suspicious of any food, such as white flour,
altered from its "natural" condition (Young 1978; Whorton 1982). His
legacy continues among those who question whether processed food of any
type can provide adequate nutrition (Deutsch 1977; Stare 1980; Miller
1980).

Popular interest in nutrition, coupled with concern about food shortages
during World War I, was fostered by the increasing promotion of the health
properties of foods in the early 20th century (Young 1%7). Vitamins, by the
very nature of their discovery, became associated with the prevention or
cure of disease (Todhunter 1973) and were soon promoted as curative
agents (Young 1967). George I? Larrick (1959), then Commissioner of Food
and Drugs, explained this trend:

In the wake of scientific advances there often follows a host of persons who
misinterpret them and exploit them for private gain. That has been true in the
field of nutrition. The nutritionist studies the long-range benefits to the public
health from new scientific findings, withholds premature endorsement, and
has confidence that future research holds great promise. . . . The promoter

  does not wait for the facts or the possibility of different findings in the
&ire. He hastens to cash in before all the facts are known. Those interested
only in profit employ clever copywriters to promote products by pseudoscien-
tific statements, using half-truths and gross exaggeration to build up a scare
psychology. . . .

Today, the traveling patent medicine man has been largely replaced by the
highly skilled and organized use of electronic means to promote fraudulent
marketing-computers, customized mailing lists, national advertisements,
WATS banks of telephone lines, and other mass media. The medium and
the details have changed, but the message and the goals remain. It is
difficult for consumers to evaluate the validity of the health claims perpe-
trated by quacks and faddists (Tiemey 1984).

Background

Regulation of Nutrition Fraud
The need for public protection from fraud was recognized over a century
ago, when Congress enacted statutes to combat mail fraud (Nelson 1984).

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The first Federal legislation, the Pure Food and Drug Act of 1906, made it
unlawful to manufacture or introduce into interstate commerce adulterated
or misbranded food or drug products (Anderson 1964). This Act was passed
in response to an intensive campaign against patent medicines and food
abuses stimulated by the work of Dr. Harvey Washington Wiley, chief
chemist at the U.S. Department of Agriculture. Because of this, it soon
became known as "Dr. Wiley's Law."

The Federal Trade Commission Act of 1914 established Federal authority
for regulation of false advertising in interstate commerce, including adver-
tising of foods for human consumption. The 1938 Federal Food, Drug, and
Cosmetic (FD&C) Act gave the FDA new and more effective authority
over health food claims. Under the FD&C Act, a food is considered a drug
if therapeutic claims are made for it, and the burden of proving claims
fraudulent is less demanding than under the earlier law (Young 1967).

Currently, numerous Government, medical, and consumer-oriented orga-
nizations are responsible for preventing and controlling fraud (U.S. Con-
gress 1984b). At the Federal level, the FDA, the U.S. Postal Service
(USPS), and the Federal Trade Commission (FTC) have authority to act
against various kinds of illicit food and health-related practices. These
agencies work cooperatively, and their antifraud activities have become
more visible in recent years (Barrett 1985). The regulatory roles of these
various Federal agencies are reviewed below.

State enforcement activities against fraud are largely the responsibility of
the State attorneys general and offrces of consumer affairs and aging.
County consumer affairs offices and metropolitan police may also become
involved in regulation.

Private agencies and organizations such as the Better Business Bureau, the
American Dietetic Association, the American Heart Association, the Ar-
thritis Foundation, the American Cancer Society, the American Medical
Association, the National Council Against Health Fraud, and other health
professional groups are also active against food fraud. These organizations
often maintain informal liaison with each other and actively cooperate with
Federal regulatory agencies.

Despite these efforts, misleading claims about foods and nutrients are
difftcult to regulate. As noted by the 1969 White House Conference on
Food, Nutrition, and Health, "No other areaof the national health probably
is as abused by deception and misinformation as nutrition. Many travesties

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Dietary Fads and Frauds O

cheat the public of enormous sums of money, and of good health as well. Yet
the American people falsely believe they are well-protected, both by Gov-
ernment and by the ethics of commerce" (White House Conference 1969).

Not only is regulation difficult because of the complexity of the science
base, the ease of exploiting the mails, and the special vulnerabilities of
people with health concerns, but in the United States, governments at all
levels are limited in what they can do about fraudulent nutrition practices
by an obligation to observe the constitutional rights to free speech and a
free press. Nutrition information, whether supported scientifically or not,
is guaranteed the same protection under the first amendment as any other
information (Stephenson 1978; Young 1%7). The right to say, write, or
publish anything one chooses is protected, as long as it is done without
intentional malice (Barrett 1977; Pennington 1984).

Regulatory Roles of Federal Agencies

Food and Drug Administration Aurhoriry. The FD&C Act empowers the
FDA to prohibit the introduction of any food, drug, device, or cosmetic
that is adulterated or misbranded. The Act does not include explicit author-
ity to address health fraud, but many of its general provisions enable
actions in these areas. Sections 702-704 authorize the gathering of informa-
tion about health fraud products and practices through inspections, collec-
tion of samples and records of interstate shipments, and gathering of
evidence such as photographs and copies of labeling. Many fraud cases are
based on misbranding charges resulting from false or misleading labeling of
products. Only factual and nonmisleading information is allowed on food
labels. Most false promotional claims, therefore, are not made on labels.
Instead, they appear in books, lectures, and mass media that are protected
by constitutional rights.

The FDA has the authority to use its food additive and drug approval
processes to control food products allowed on the market and to remove
fraudulent products. Although food products do not need to receive pre-
market approval as safe for human consumption, some food components
need either to be classified as "Generally Recognized As Safe" (GRAS) or
to have undergone the required FDA approval process for a food additive.
If one or more of a food product's ingredients are subject to these provi-
sions but is neither GRAS nor an approved additive, the product is consid-
ered adulterated and therefore illegal.

The FD&C Act defines drugs as articles that are intended for use in the
diagnosis, cure, mitigation, treatment, or prevention of diseases in hu-

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mans. Most fraudulent food products are classified as foods, but when
therapeutic claims are made for them, they are also considered to be drugs.
The Act's provisions require drug products to have (1) an approved New
Drug Application that demonstrates both safety and efficacy for its intend-
ed uses and (2) adequate directions for use. If a food product is also
classified as a drug and is considered by the FDA to be ineffective for its
claimed use, it will not have an approved New Drug Application. For
example, if it is promoted for treating a disease that is not amenable to lay
diagnosis, it cannot have adequate directions for use and will not be
approved. Recently, the FDA proposed a new policy on the appropriate use
of health-related messages on food labels (FDA 1987).

Educating the public on health fraud is complementary to the FDA's
regulatory activities. The Agency's magazine, FDA Consumer, devotes
editorial space to health fraud and includes major articles on the subject. In
addition, FDA consumer affairs officials across the country conduct a
health fraud consumer education program covering foods as well as medi-
cal devices and drugs. The objectives of this program are to increase public
knowledge and understanding of the FDA's statutory responsibilities and
the limitations of the FDA's authority in protecting consumers from misin-
formation about foods, dietary supplements, nutrition, and other FDA
concerns. The program provides guidance to enable consumers to recog-
nize fraud, evaluate product claims, make informed decisions, and register
complaints and concerns about fraudulent products.

U.S. Postal Service Authority. The authority of the USPS to control health
fraud is based on a general congressional mandate to protect the public
from marketing schemes conducted by mail. The purchaser is particularly
vulnerable to fraudulent inducements by mail because of the inability to
observe the product before payment (U.S. Congress 1984b). Specific au-
thority to protect the mail order consumer is vested in the criminal fraud
statute (18 U.S.C. 1341), the administrative false representation statute (39
U.S.C. 3005), and the supporting injunctive statute (39 U.S.C. 3007).

The mail fraud statute provides that any use of the mails in furtherance of an
intentional scheme to defraud is punishable by a fine of $1,000 and im-
prisonment of up to 5 years. Many nutrition-related schemes are pros-
ecuted under the mail fraud statute; they typically involve cure-ails, instant
weight reduction techniques, and a variety of substances falsely described
as having the ability to cure diseases or disabilities.

The false representation statute mandates that persons offering goods or
services for sale through the mail refrain from misrepresenting their prod-

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