No.

94 January 2006

Herbs and Heavy Metal Detoxification

by Kerry Bone and Michelle Morgan
meaning crab or lobster claw, suggested by the way in
which the metal is gripped in at least two places by the
organic groups.) Chelating agents are used to produce
stable compounds with relatively low toxicity and also to
enhance the excretion of metals.2,3 Heavy metals can also
exist covalently bound to organic molecules. In the case of
As this substantially reduces its toxicity. For Hg it
substantially increases toxicity, eg methyl mercury.
Aluminium is not a heavy metal and considerations related
to aluminium exposure, health effects and its
detoxification are not always the same as for heavy
metals.

What is a Heavy Metal?

Heavy metals are metallic elements which have a high
atomic weight and a density much greater (at least 5
times) than water. There are more than 20 heavy metals,
but four are of particular concern to human health: lead
(Pb), cadmium (Cd), mercury (Hg) and inorganic arsenic
(As).1 According to the US Agency for Toxic Substances and
Disease Registry, these four heavy metals are four of the
top six hazards present in toxic waste sites. They are
highly toxic and can cause damaging effects even at very
low concentrations. They tend to accumulate in the food
chain and in the body and can be stored in soft (eg kidney)
and hard tissues (eg bone). Being metals, they often exist
in a positively charged form and can bind on to negatively
charged organic molecules to form complexes. Chelates
are a special type of complex where the organic molecule
binds to the metal at two or more points (and hence quite
strongly). (The term chelation comes from the Greek chl

Sources of Heavy Metals

The following table (Table 1) lists for the four major heavy
metals the main types and sources of exposure, together
with specific details of absorption and elimination.

Lead
types

elemental lead, inorganic lead compounds, organic lead

sources

industrial and household products: paints, cans, plumbing fixtures, leaded petrol/gasoline, lead crystal
contaminated food: leafy vegetables grown in lead-contaminated soil, via improperly glazed ceramics
occupational/environmental exposure (eg living near industry): battery manufacturing, demolition, painting and paint
removal, ceramics

absorption

ingestion or inhalation
skin (organic lead in additives to gasoline)
children absorb up to 50% of lead ingested, adults absorb 1020%
gastrointestinal absorption is enhanced by fasting and by dietary deficiencies in calcium, iron and zinc
absorbed into blood plasma and extracellular fluid, crosses membranes (eg blood-brain barrier, placenta), accumulates in
soft and hard tissues
largest proportion of absorbed lead is incorporated into the skeleton (90% of the body's total burden)

elimination

mainly in urine (depends on glomerular filtration and tubular secretion) and feces
can appear in hair, nails, sweat, saliva, breast milk
half-life of lead in blood is approx. 25 days, in soft tissue about 40 days, in the nonlabile portion of bone more than 25
years so blood lead levels may decline significantly while the body's total burden remains heavy
Mercury

types

metallic mercury (Hg0)

mercurous mercury (Hg+) (a form of inorganic mercury)
mercuric mercury (Hg2+) (the other form of inorganic mercury)
organic mercury compounds such as methyl mercury (slowly broken down to form inorganic compounds)
inorganic mercury can be converted by microorganisms in soil and water into methyl mercury

Not for Public Distribution. For Education of Health Care Professionals Only.

sources

absorption

metallic mercury (Hg0): thermometers, dental amalgams (typically containing about 50%), some batteries
inorganic mercury compounds: occupational exposure in some chemical, metal-processing, electrical-equipment,
automotive and building industries; medical and dental services

methyl mercury: contaminated fish especially tuna and swordfish

other possible environmental exposure (controversial): contaminated drinking water, inhalation of fumes from incinerators
burning mercury-contaminated waste products

estimates of daily intake (for people in the USA and Canada) of elemental mercury form amalgam restorations ranges from
1 to 27 g/day; the majority of dental amalgam holders being exposed to less than 5 g/day

the precise exposure from amalgam may not only be a function of amalgam-filled teeth, but may also be a function of the
size and location of these fillings

ethyl mercury: in the form of thimerosal added as an antiseptic to widely used vaccines; has been assumed that the
toxicology of ethyl mercury is similar to methyl mercury
elemental mercury

not well absorbed by GIT

when volatilized (eg upon standing at room temperature, or from dental amalgam) the vapour is well absorbed by
inhalation, is then lipid soluble and crosses blood-brain barrier and placenta, oxidized into mercuric chloride which is
retained in kidney and brain for years

half-life of elemental mercury as such: approx. 60 days

inorganic mercury

GIT and dermal

large overdoses disrupt GIT barriers, further enhancing absorption

breaks down into metallic and mercuric forms

half-life: approx. 40 days

organic mercury (especially methyl mercury)

when evaporates, can be absorbed by inhalation

well absorbed when ingested (eg contaminated fish)

only small amount absorbed via skin

when absorbed is lipid soluble, crosses the blood-brain barrier and placenta, appears in breast milk, concentrates in the
kidneys and CNS

half-life of organic mercury compounds: approx. 70 days

elimination

elemental mercury: mainly in urine and feces

inorganic mercury: mainly in urine and feces, some retained in kidney as mercuric mercury
organic mercury (especially methyl mercury): detoxified by the liver and excreted in urine (only 1% is excreted
unchanged)
Cadmium

sources

contaminated food: especially grains, cereals and leafy vegetables which readily absorb cadmium occurring naturally or in
soil contaminated by sewage sludge, fertilizers and polluted groundwater
contaminated water eg by mining effluents
environmental exposure: airborne cadmium from smelting or incineration of waste containing plastics and nickel-cadmium
batteries or from wear on car tires
cigarette smoke
occupation exposure: metal-plating, pigment, battery and plastics industries

absorption

ingestion or inhalation, only 5-10% absorbed

concentrates in liver and kidneys
half-life of 1030 years
GI absorption may be influenced by nutritional factors, such as iron status

elimination

lack of effective elimination pathway: reabsorbed in kidney

Arsenic

sources

natural processes (eg volcanoes, deep-water wells), industrial processes, contaminated food and tobacco

absorption

ingestion: inorganic form (more toxic) accumulates in organs

elimination

organic form: in urine (rapidly excreted)

inorganic form: somewhat metabolised in liver but leaves residue in skin, hair, nails
Table 1. Types, Sources, Absorption and Elimination for Lead, Cadmium, Mercury and Arsenic.1,2,4,5,6

Not for Public Distribution. For Education of Health Care Professionals Only.

Signs and Symptoms of Heavy Metal

Exposure7
The typical signs and symptoms of heavy metal exposure
are listed below:
Arsenic - Fatigue, headaches, dermatitis, increased
salivation, muscular weakness, loss of hair and nails,
hypopigmentation of skin, anemia, skin rashes, skin
cancer.
Cadmium - Loss of sense of smell, anemia, dried scaly
skin, hair loss, hypertension, kidney problems, skeletal
damage, cancer.

"behavioral signature" for lead toxicity. The bases for the

substantial individual variability in vulnerability to lead are
uncertain, although they might include genetic
polymorphisms and contextual factors. The current Centers
for Disease Control and Prevention screening guideline of
10 g/dL is a risk management tool and should not be
interpreted as a threshold for toxicity. No threshold has
been identified, and some data are consistent with effects
well below 10. Historically, most studies have
concentrated on neurocognitive effects of lead, but higher
exposures have recently been associated with morbidities
such as antisocial behavior and delinquency.9

Mercury - Reduced sensory abilities (taste, touch, vision

and hearing), metallic taste with increased salivation,
fatigue, anorexia, irritability and excitability, psychoses,
mania, anemia, paresthesias, tremors, incoordination,
cardiovascular disease, hypertension with renal
dysfunction.

A study in Poland found that increased average levels of

lead in the hair of children suffering from "rheumatic"
disease as compared with controls. The difference in the
magnesium/lead ratio between the controls and
rheumatic volunteers was statistically significant.10 Traffic
policemen in Egypt had higher lead levels in blood, urine,
hair and nails compared to healthy (non-exposed) controls.
Lead levels in blood, hair and nails showed significant and
positive correlations with the duration of exposure to lead
which was measured as the duration of employment.
Urinary excretion of NAG (a marker of tubular damage)
was positively correlated with duration of employment,
blood lead and nail lead. Urinary albumin (a marker of
glomerular injury) was positively correlated with duration
of employment, blood lead and hair lead.11

There is a general consensus that high level exposure to

heavy metals can cause the symptoms described above.
What is more controversial is whether these same toxic
effects and symptoms can result from chronic, low level
exposure in sensitive individuals. In addition other more
subtle effects might result from such low level exposure.

The latest WHO evaluation concludes that As (inorganic)

exposure via drinking water is causally related to cancer in
the lungs, kidney, bladder and skin (for drinking water
levels >50 g/L). There is also relatively strong evidence
between As exposure and risk for hypertension and
cardiovascular disease.1

Effects of Chronic Low Level Exposure

A link between Cd and skeletal damage was first reported

from Japan in the 1950s due to
Cd-contaminated water used for irrigation of rice fields
(itai-itai disease). However, during recent years new data
have emerged suggesting that relatively low Cd exposure
may give rise to osteoporosis and fractures.1 The levels of
Cd in organs increase with age because of the lack of an
active biochemical process for its elimination coupled with
renal reabsorption. Cd-linked bone and kidney toxicities
were observed in people whose intake was well within
the provisional tolerable weekly intake (PTWI) set by
FAO/WHO (see later). Also evidence for the carcinogenic
risk of chronic Cd exposure is accumulating and effects on
reproduction have begun to emerge.12

Lead - In children: delayed mental development,

hyperactivity, delayed learning, behavioral problems.
Children and adults: fatigue, anemia, metallic taste, loss of
appetite, weight loss and headaches, insomnia,
nervousness, decreased nerve conduction, possibly motor
neuron disorders.

A selection of these issues in the mainstream peer review

literature is presented in the following paragraphs. These
studies are confirming what has long been suspected: that
heavy metal exposure can cause subtle endocrine,
neurological and immunological dysfunctions, even at low
exposure levels.
It is well documented that low level exposure to Pb in
children can lead to intellectual deficit.8 On this topic, and
the more general issue of lead exposure in children, one
researcher suggested the following:
Children differ from adults in the relative importance of
lead sources and pathways, lead metabolism, and the
toxicities expressed. The central nervous system effects of
lead on children seem not to be reversible. Periods of
enhanced vulnerability within childhood have not
consistently been identified. The period of greatest
vulnerability might be endpoint specific, perhaps
accounting for the failure to identify a coherent
Not for Public Distribution. For Education of Health Care Professionals Only.

111 women with repeated miscarriages had their urinary

excretion of heavy metals evaluated after challenge (with
a chelating drug). Heavy metal excretion was significantly
correlated to different immune and hormonal phenomena.
The authors concluded that heavy metals appear to have a
negative impact on ovarian and pituitary function and that
3

the induced immunological changes may lead to

miscarriages.13
A high dietary intake of methyl mercury from consumption
of fish has been shown to increase the risk of coronary
artery disease. This has been confirmed in one study but
challenged in another.1
A case-controlled study involving multiple sclerosis
patients conducted between 1991 and 1994 found a
suggestive elevated risk for those individuals with a large
number of dental amalgams and for a long period of time.
However the difference between cases and controls was
not statistically significant.14 A larger and more recent
epidemiological study found some evidence of an
association between dental amalgam and disease.
(Disorders of the nervous system and kidney were
examined in particular.) Multiple sclerosis had an adjusted
hazard ratio of 1.24, but there was no association with
chronic fatigue syndrome or kidney disease.15
One US study examined the effect of Hg and high-end fish
intake. 89 patients with high-end fish intake or showing
symptoms suggestive of Hg toxicity were assessed for Hg
exposure (in San Francisco). 89% had whole blood Hg
levels exceeding the recent US EPA and NAS recommended
maximum of 5.0 g/L. Swordfish intake was significantly
and positively correlated with Hg blood levels, red snapper
was negatively correlated. A significant decline in Hg
levels was shown when fish intake was stopped. Some
children were >40 times the national average.16 This study
also provided details of average methyl mercury levels in
fish which are provided in Table 2.
High
Shark
Swordfish
Ahi
Snapper
Halibut
Lobster
Tuna

1.33
0.95
0.38
0.25
0.25
0.23
0.21
Medium

Sea bass
Crab
Flounder

0.16
0.12
0.09

Low
Shrimp
0.047
Scallops
0.042
Salmon
0.035
Table 2. Average Methyl Mercury Levels in Fish.16
Note: All units in g/g

Assessing Heavy Metal Exposure

Heavy metal exposure can be assessed by measuring
levels in body tissues or excretions. Hair analysis is
Not for Public Distribution. For Education of Health Care Professionals Only.

commonly used because it has some distinct advantages,

it is easier and safer to collect, ship and store and is less
expensive. It also can represent a record of long-term
exposure. Whole blood is a good measure of current
exposure and some examples of reference levels are
provided in Table 3. Urine can be unreliable, but after
provocation with a chelating agent such as EDTA or DMSA,
24-hour urine levels can give an indication of body stores.
Lead
Reporting limit
Normal
Exposed

1.0 g/dL
<10 g/dL

Children (0-6 years)

>10 g/dL

Adults (OSHA action level)

Toxic

40 g/dL

Children (0-6 years)

>70 g/dL

Adults (OSHA action level)

>80 g/dL

Arsenic
Reporting limit
10 ng/mL
Reference range
up to 10 ng/mL
Table 3. Example of Reference Levels for Heavy Metals in
Blood.17

Hair analysis can be interfered with by some shampoos,

hair dyes and dust exposure. There can be considerable
variability in heavy metal levels from sample to sample of
the same persons hair. Heavy metal analysis is tricky and
the lab needs to have expert chemists using validated
methods in a certified lab. As a consequence results can
vary considerably. Reference ranges are different from lab
to lab which can make interpretation of results difficult.18,19
Hair analysis for Hg is, however, a very good indication of
methyl mercury exposure (reference limit 1.0 g/g).

A Strategy of Using Herbs for Heavy

Metal Exposure
As outlined previously, we are exposed to heavy metal
intake mainly through the environment, via the air, water
and food. Occupational exposure can also be an issue in
some instances, for example lead smelter workers. In
terms of minimizing these exposures one can drink only
purified water and choose to live in an area with less air
pollution, but there is less that can be done from an
avoidance perspective about dietary exposure. Also for
individuals who unavoidably have a higher intake via the
air they breathe, their daily heavy metal load can be
managed by reducing their gastrointestinal intake. Both
these considerations argue for an approach which is
capable of minimizing heavy metal exposure via the
inhibition of absorption from the gastrointestinal tract
(GIT).
Hence any herbs which are capable of binding to heavy
metals, but not making them more soluble as a result, are
4

likely to have a key role in reducing the GIT absorption of

these elements. This will help to free up the bodys
excretion mechanisms (which can be overloaded if there is
a high intake). In addition, any herbs which can actively
encourage mobilization and excretion of heavy metals will
also further assist in reducing an individuals overall
exposure. Both the FAO and WHO have set provisional
tolerable weekly intake (PTWI) values for lead, cadmium
and mercury. These are as follows:20 lead 50 g/kg/week;
cadmium 7 g/kg/week; mercury 5 g/kg/week.
Assuming a 70 kg (154 lb) person, these values translate
to: lead 3.5 mg/week; cadmium 490 g/week; mercury
350 g/week (EPA 49 g/week).
These are small quantities and it is quite feasible that an
herbal product taken regularly with each meal could
selectively inhibit a substantial amount of this weekly
intake. Hence the rationale behind using herbs is as
follows:
reduce gastrointestinal uptake of heavy metals (when
the herbs are taken with meals)
thereby help to free up the bodys excretion
mechanisms (which can be overloaded if there is a
high intake or high stores)
as an added factor, actively facilitate excretion of
heavy metals from the body
Two key herbs which can act in this way are discussed in
detail below, namely garlic and milk thistle. In addition
cilantro is briefly discussed since it seems so popular for
this application (perhaps undeservedly).

Garlic
Allium sativum contains alliin as the main sulfur-containing

mercury (but not for those treated with phenyl mercury).

This protective effect is due to a smaller amount of
mercury absorbed into the brain as a result of the
enhanced excretion of mercury from the body by garlic. In
another series of tests, administration of garlic (6.4% of
the diet) enhanced the excretion of cadmium, more
through feces than urine. In this test, administration of
diallyl disulfide (30 mg/kg), a sulfur constituent of garlic,
was inferior to whole garlic treatment. (In these tests,
cadmium was administered by injection.) The protective
effect of garlic is probably caused by the sulfur compounds
combining with the heavy metals in the body and
promoting excretion through bile to the feces.22 Several
other studies have confirmed a protective effect for garlic
against cadmium and mercury poisoning in rats.23
Garlic juice almost doubled the survival of rabbits exposed
to severe lead poisoning.24 Concomitant use of garlic juice
(100400 mg/kg) prevented the accumulation of lead in
liver, kidneys, brain, bone and blood in rats. The protective
effect may be due to the combined effects of reduced
absorption of the metal from the gastrointestinal tract and
increased excretion.25
The oral feeding of fresh garlic to rats during the
intraperitoneal injection of lead or cadmium reduced the
accumulation of these metals and the biochemical
alterations in the blood, liver and kidney. The antioxidant
property of garlic may also protect against oxidative
damage by these metals.26 Lead concentrations were
reduced in muscle and liver tissues of chickens given lead
and garlic simultaneously, and also when given lead
followed by garlic treatment. The reduction was in fact
greater in birds given garlic as a post-treatment.27

amino acid. In the presence of the enzyme alliinase (for

example, when the bulb is crushed), alliin is converted to
allicin (an odorous compound), which then produces a
range of other constituents including ajoenes,
vinyldithiines and polysulfides.21 The sulfur-containing
constituents are responsible for the characteristic smell of
garlic.

Oral administration of aqueous extract of fresh garlic

reduced the clastogenic (gene damaging) effect caused by
exposure to inorganic arsenic in mice. At the lowest
dosage of 25 mg/kg of garlic, at least 30 days of
treatment was required.28,29

Garlic demonstrated a protective effect against heavy

metal poisoning in rats. Oral co-administration of garlic
with cadmium or organic mercury compounds for 12
weeks resulted in a decrease in the accumulation of heavy
metals in liver, kidneys, bone and testes. (These are the
target organs of cadmium poisoning.) Histopathological
damage and the inhibition of serum alkaline phosphatase
were also decreased. The effective doses of fresh garlic
were 3.35% and 6.7% of the diet, which provided 100 and
200 ppm of allicin, respectively. (The protective effect
began to appear in the 3.35% group, and the heavy metal
accumulation decreased more than 40% in the 6.7% group
compared to the group exposed only to the metal.) Garlic
at the higher dosage produced a decrease in mercury
accumulation in the brain for animals treated with methyl

The effect of a garlic supplement on workers in a lead

smelter endangered by chronic lead poisoning was
investigated in the 1960s in Europe. Clinical and
pharmacological tests showed that under the influence of
the garlic preparation the number of workers already
exhibiting signs of early lead toxicity (such as damaged
red blood cells) fell by 83% after one to three months. The
amount of porphyrin still remaining in the urine was much
decreased, and there was a statistically significant increase
in the number of erythrocytes and in the amount of
haemoglobin. Of the workers who were not showing signs
of early lead toxicity at the beginning of the trial, 28% of
these developed signs after three months compared to
only 3% in the group given garlic. The authors suggested
that some of the lead in the gastrointestinal tract may

Not for Public Distribution. For Education of Health Care Professionals Only.

Clinical Study

have reacted with the sulfur compounds in garlic and was

excreted via the feces in the form of insoluble sulfides.
They also proposed that the removal of some of the garlic
sulfides via the respiratory air may also restrict the
absorption of lead powder in the respiratory tract.24

demonstrated in granulocytes taken from healthy

volunteers who had taken 240 mg of silybin. Silymarin
(240 mg/day) also improved liver function in patients with
liver disease caused by exposure to toxic levels of toluene
or xylene.36

Milk Thistle

Cilantro

Silybum marianum fruit contains flavanolignans: silybin,

The reputation of cilantro (Coriandrum sativum) is based

on two published studies which purport to establish that it
helped to eliminate mercury from patients in a number of
cases.37,38 However, when these case studies are carefully
analysed it becomes clear that at no stage were mercury
or other heavy metal levels measured by normal
conventional means. Instead the authors used some kind
of subjective resonance methodology described as the
Bi-Digital ORing Test, which has not been adequately
described in this publication nor validated for heavy metal
assessment.* This fact, combined with an unpublished
study which found that cilantro possessed relatively weak
heavy metal binding capacity33 makes it a poor choice in
our view, compared to garlic and milk thistle. There is one
study that found that cilantro prevented localized lead
deposition in mice, but the data is weak because results
were only significant for bone and not for soft tissues and
a dose-response relationship was not observed.39

silychristin, silydianin and 2,3-dehydro derivatives.30 This

flavanolignan mixture is commonly referred to as
silymarin.
Oral administration of silybin (100 mg/kg/day,
administered as silybin--cyclodestrin complex) protected
against iron-induced hepatic toxicity in rats. Simultaneous
treatment with silybin decreased the accumulation of
malondialdehyde-protein adducts into iron-filled periportal
hepatocytes (ie it reduced oxidative damage/lipid
peroxidation). It also reduced the hepatic function
impairment (mitochondrial energy wasting). In addition to
the prominent antioxidant activity of silybin, this protective
effect may be due to its strong ability to chelate iron.31
A group of Italian scientists investigated the iron-binding
capacity of silybin, a component of the complex of
flavanolignans known as silymarin found in milk thistle
(Silybum marianum). Their motivation in doing so was to
find an orally-active, non-toxic alternative to the ironbinding synthetic drug desferrioxamine, which causes side
effects such as bone deformities, sensory abnormalities
and cerebral toxicity32 The scientists found that silybin
strongly binds the ferric ion (Fe(III)), even at acidic pH. The
complex of this molecule with iron demonstrated
remarkable stability. Our lab results have shown that
silymarin can also strongly bind heavy metals.33 Given the
bioavailability of silybin, it is probable that like garlic it can
also mobilize the excretion of heavy metals. One
important caveat is that iron-compromised individuals
would need to take an iron supplement at a different time
to this product. A combination of ascorbic acid (10 mg/kg)
and silymarin (10 mg/kg) ameliorated the Pb toxicity on
the liver of rats.34 In Pb and Cd poisoning in an
experimental model the structural and histochemical
hepatic changes were significantly prevented by
silymarin.35
Clinical Studies
The flavanolignans of Silybum marianum have
demonstrated antioxidant activity and protection against
drug-induced liver damage in clinical studies. The
antioxidant activity was shown for example, in patients
with cirrhosis or alcoholic liver damage by the increase in
superoxide dismutase activity of lymphocytes and
erythrocytes, and the increase in patient serum levels of
glutathione and glutathione peroxidase. Silymarin (280 or
420 mg/day) was prescribed. Antioxidant activity was also
Not for Public Distribution. For Education of Health Care Professionals Only.

* The Bi-Digital O-Ring Test is based on applied

kinesiology, and is similar to muscle testing. The theory is
that if there is a dysfunction in a certain organ, when a
point on the body representing that organ is stimulated
the force of the muscle tested (in this case an 'o-ring'
formed by touching the thumb and index finger of one
hand) is weakened through a brain response and the
muscle tone decreases.40 In the above study this test was
used to examine the presence of heavy metals in the
body, but it has not been validated by scientifically proven
methods of analysis. It cannot be credibly applied to the
quantification of heavy metals in tissues.
REFERENCES
1

Jrup L. Br Med Bull 2003; 68: 167-182

Harrison TR, Fauci AS (eds). Harrisons Principles of Internal Medicine,
14th Edn CD-ROM. McGraw-Hill, New York, 1998.
3
Gennaro AR et al. Blakiston's Gould Medical Dictionary: A modern
2

comprehensive dictionary of the terms used in all branches of medicine

and allied sciences, with illustrations and tables, 4th Edn. McGraw Hill,
New York, 1979.
4
Risher J, United Nations Environment Programme, International Labour
Organization, World Health Organization, Inter-Organization Programme
for the Sound Management of Chemicals. Elemental Mercury and
Inorganic Mercury Compounds: Human Health Aspects. Concise
International Chemical Assessment Document 50. World Health
Organization, 2003.
5
Richardson GM. Final Report: Assessment of Mercury Exposure and Risks
from Dental Amalgams. Medical Devices Bureau, Environmental Health
Directorate, Health Canada, 18 August 1995.
6
Clarkson TW, Magos L, Myers GJ. N Engl J Med 2003; 349(18): 1731-1737
7
Great Smokies Diagnostic Laboratory
8
WHO. Inorganic Lead. Environmental Health Criteria, Vol. 165. Geneva:
World Health Organization, 1995.

Bellinger DC. Pediatrics 2004; 113(4): 1016-1022

Lech T. Biol Trace Elem Res 2002; 89(2): 111-125
11
Mortada WI, Sobh MA, El-Defrawy MM et al. Am J Nephrol 2001; 21(4):
274-279
12
Satarug S, Moore M. Environ Health Perspect 2004; 112(10): 1099-1103
13
Gerhard I, Waibel S, Daniel V et al. Hum Repro Update 1998; 4(3): 301309
14
Bangsi D, Ghadirian P, Ducic S et al. Int J Epidemiol 1998; 27(4): 667671
15
Bates MN, Fawcett J, Garrett N et al. Int J Epidemiol 2004; 33(4): 894902
16
Hightower JM, Moore D. Environ Health Persp 2003; 111(4) 604-608
17
University of Iowa, Department of Pathology, Laboratory Services
Handbook.
18
Wilhelm M, Idel H. Zbl Hyg 1996; 198: 485-501
19
Seidel S, Kreutzer R, Smith D et al. JAMA 2001; 285(1): 67-72
20
De Smet PAGM, Keller K, Hnsel R et al (eds). Adverse Effects of Herbal
Drugs Vol. 1. Springer-Verlag, Berlin. 1992
10

21

ESCOP Monographs: The Scientific Foundation for Herbal Medicinal

Products, 2nd Edn. ESCOP, European Scientific Cooperative on

Phytotherapy, Exeter, 2003.

22
Cha CW. J Korean Med Sci 1987; 2(4): 213-224
23
Koch PH, Lawson LD (eds). Garlic: The Science and Therapeutic
Application of Allium saltivum L. and Related Species, 2nd Edn. Williams &
Wilkins, Baltimore, 1996.
24
Petkov V. J Ethnopharmacol 1986; 15: 121-132
25
Senapati SK, Dey S, Dwivedi SK et al. J Ethnopharmacol 2001; 76(3):
229-232
26
Tandon SK, Singh S, Prasad S. Pharm Biol 2001; 39(6): 450-454
27
Hanafy MS, Shalaby SM, el-Fouly MS et al. Dtsch Tierarztl Wochenschr
1994; 101(4): 157-158
28
Choudhury AR, Das T, Sharma A. Cancer Lett 1997; 121(1): 45-52
29
Das T, Choudhury AR, Sharma A et al. Food Chem Toxicol 1996; 34(1):
43-47
30
Wagner H, Bladt S. Plant Drug Analysis: A Thin Layer Chromatography
Atlas, 2nd Edn. Springer-Verlag, Berlin, 1996.
31
Pietrangelo A, Borella F, Casalgrandi G et al. Gastroenterology 1995;
109(6): 1941-1999
32
Borsari M, Gabbi C, Ghelfi F et al. J Inorg Biochem 2001; 85: 123-129
33
Lehmann R, Private Communication, 2004.
34
Shalan MG, Mostafa MS, Hassouna MM et al. Toxicology 2005; 206(1):
1-15
35
Barbarino F, Neumann E, Deaciuc I et al. Med Interne 1981; 19(4): 347357
36
Wellington K, Jarvis B. BioDrugs 2001; 15(7): 465-489
37
Omura Y, Shimotsuura Y, Fukuoka A et al. Acupunct Electrother Res
1996; 21(2): 133-160
38
Omura Y, Beckman SL. Acupunct Electrother 1995; 20(3-4): 195-229
39
Aga M, Iwaki K, Ueda Y et al. J Ethnopharmacol 2001; 77(2-3): 203-208
40
Yamamoto S. The Formation and Basis of the Bi-Digital O-Ring Test.
Available from [Link]/~oring/e_basis.shtml. Accessed
October 2005.

This article was originally printed in the Townsend Letter for

Doctors and Patients, #270, January 2006.
See www. [Link]
Reprinted with permission.

Not for Public Distribution. For Education of Health Care Professionals Only.