Content uploaded by Kristin Homme
Author content
All content in this area was uploaded by Kristin Homme on Apr 25, 2017
Content may be subject to copyright.
60 TOWNSEND LETTER – JANUARY 2017
Summary
• The chronic eects of cumulave,
low-dose mercury exposure
are underrecognized by both
mainstream and alternave health
authories and, consequently, by
the public. Mercury can cause or
contribute to most chronic illnesses,
including neurological disorders,
cardiovascular disease, metabolic
syndrome, chronic fague,
bromyalgia, adrenal and thyroid
problems, autoimmunity, digesve
disorders, allergies, chemical
sensivies, mental illness, sleep
disorders, and chronic infecons
such as Lyme and Candida. Mercury
toxicity should be suspected in
individuals experiencing mulple
health problems.
• Diagnosis of chronic mercury
toxicity is oen dicult because
the body’s natural defenses may
mask or delay symptoms. Natural
defenses are a funcon of genec
suscepbility, epigenec factors,
micronutrient status, and allostac
load (cumulave wear and tear
on the body). Furthermore,
individuals who retain mercury may
counterintuively show low levels in
blood, urine, and hair.
• The developmental window
from concepon through early
childhood is one of extreme
vulnerability to mercury. Mercury
is an epigenec toxicant (aecng
future gene expression) as well as
a neurotoxicant. Damage may be
permanent; therefore, prevenon is
key.
• For most people mercury is the
most signicant toxicant in the
body. By promong oxidave stress
and depleng anoxidant defenses,
including the glutathione system,
mercury impairs the body’s response
to toxicants in general including
mercury itself.
• Mercury toxicity creates a need
for extra nutrion, both to repair
damage and to provide ample
enzyme cofactors that can push
blocked enzymes. Carbohydrate
intolerance can be a symptom of
mercury toxicity, and fat can be a
preferred fuel. Many people with
chronic mercury toxicity have found
a nutrient-dense diet to be a useful
starng point for symptom relief.
Individualized supplementaon may
also be helpful to overcome the
extreme nutrional depleon and
unnatural toxic state.
Introducon
Mercury is an unusually insidious
toxicant that can cause or contribute
to most chronic illnesses. Its eects on
various body systems can be mutually
reinforcing, seng up a complex
process of damage and dysfuncon. For
example, by inhibing the glutathione
system, which is key to detoxicaon,
mercury perpetuates a vicious cycle
of suscepbility and toxicity. As a
result, mercury promotes nutrional
depleon, oxidave stress, hormonal
disrupon, immune alteraon, and
neurotransmier disturbances, which
in turn can cause poor digeson, leaky
gut, food allergies, altered gut ora,
and autoimmunity. Yet, despite its
pervasive ability to damage the body,
mercury easily eludes detecon; and
many aected individuals have no idea
that their unexplained health problems
are due to past or ongoing mercury
exposures.
Adding to the confusion, symptoms
may manifest dierently in each
person depending on exposures,
lifestyle, genecs, and micronutrient
status. For example, it may manifest
in one person as autoimmune issues
such as Hashimoto’s thyroidis,
mulple sclerosis, or systemic lupus
erythematosus and in someone else as
mood, behavior, learning, or psychiatric
problems. Long latencies may occur
with onset of symptoms somemes
occurring months or years aer the
exposure has ceased.1,2 Many symptoms
are vague, resembling premature
cellular aging. Other symptoms are
more disnct, a case in point being
erethism (a constellaon of personality
traits including midity, didence,
contenousness, insecurity, bluntness,
rigidity, excitability, and hypersensivity
to cricism and to sensory
smulaon).3–5 The term erethism, or
reddening, derives from the person’s
tendency to blush.6 Considering the
subtle but reproducible eects of
mercury on emoons, a number of
problems that are blamed on character,
personality, and stress may in fact be
caused or compounded by low-level
mercury toxicity.
Unfortunately, the public receives
mixed messages from health authories
and agencies about the risks of mercury
Mercury:
The Quintessential Anti-Nutrient
by Sara Russell, PhD, NTP, and
Kristin G. Homme, PE(ret.), MPP, MPH
TOWNSEND LETTER – JANUARY 2017 61
from roune exposures involving
denstry, sh, and vaccines. Certain
exposure risks are widely discounted by
the mainstream; yet according to the
US Environmental Protecon Agency,
approximately 2–7% of women of
childbearing age in the US have blood
mercury levels of concern.7 And there is
reason to believe that these regulatory
levels of concern are too lax.i,8 In fact,
neurodevelopmental disorders aect
almost 11% of all US births, up 30%
over the past decade;9 and subclinical
decrements in brain funcon are even
more common, aecng up to 15% of
births.10 However, health authories
are unlikely to provide useful guidance
on mercury risks for several reasons.
Mercury is technically and polically
dicult to study; thus, scienc
conclusions about risks remain couched
in uncertainty. Mercury’s eects are
non-specic and mul-factorial. Finally,
much exposure is iatrogenic – caused
by health care – making it an unpopular
topic.
Exposures
body. Being lipophilic, these forms of
mercury leave the bloodstream quickly,
passing through biological membranes
and concentrang in cells (including
brain cells).11 Mercury is especially
drawn to high-sulfur organelles such
as mitochondria. Once inside a cell,
mercury is soon oxidized to Hg2+. This
is a hydrophilic (lipophobic) form of
mercury and therefore cannot easily
pass through biological membranes.
This form of mercury thus becomes
trapped inside the cells, causing
ongoing damage.12 Mercury has a
parcular anity for the brain, where
it may be retained indenitely.13,14 It
also accumulates in epithelial ssues,
organs, and glands such as the salivary
glands, thyroid, liver, pancreas, tescles,
prostate, sweat glands, and kidneys as
well as the epithelium of the intesnal
tract and skin.15
Dental Amalgam
Dental amalgam, the material
used in “silver llings” beginning in
the nineteenth century, is about 50%
mercury. Mercury is highly volale;
consequently, amalgams connuously
o-gas in the mouth. Health authories
have deemed amalgam as safe based
on studies that were designed to detect
only obvious harm, not subtle or long-
term eects. New evidence indicates
that suscepbility (and resistance) to
mercury toxicity is driven by genes, only
a few of which have been idened.16
Furthermore, evidence indicates that
exposure from amalgams is sucient
to cause harm to suscepble people.17
The authors of the mercury chapter
in the most recent metals toxicology
textbook esmate that roughly 1% of
the populaon is incurring clinical illness
from their dental amalgams – and this
is likely to be a gross underesmate
because it excludes cases that have
another diagnosis such as mulple
sclerosis that may have a mercury
component.18
The World Health Organizaon
esmates that the typical absorbed
dose of mercury from amalgams is
1–22 micrograms per day with most
values in the range of 1–5 micrograms
per day.19 Various factors including gum
chewing and bruxism can increase these
exposures to an upper range of about
100 micrograms per day.20 Preliminary
evidence suggests that certain types
of electromagnec radiaon including
from mobile phones and from magnec
resonance imaging (MRI) may increase
the release of mercury vapor from
dental amalgams.21
In 2009, the US Food and Drug
Administraon (FDA) reiterated the
safety of dental amalgam despite much
scienc evidence to the contrary.
As of 2016, public interest groups
are challenging this “nal amalgam
rule” in federal court. Issues to be
ligated include whether amalgam
is deemed an implant, which would
require manufacturers to provide proof
of safety, and whether the toxicity
warnings that are given to densts via
labeling requirements should also be
given to paents. Norway, Denmark,
and Sweden have banned dental
amalgam; and, as of May 2015, a
scienc commiee of the European
Commission recommends that non-
mercury alternaves be used in llings
for pregnant women and children.22
As if the cumulave eects of
ongoing amalgam exposure were not
enough, unsafe amalgam removal can
cause acute exposures to mercury
vapor. Thus, paents wishing to
replace amalgam llings with less toxic
alternaves must evaluate densts’ use
of adequate protecve measures. The
Internaonal Academy of Oral Medicine
and Toxicology (IAOMT), a professional
dental organizaon, has developed
a protocol and training program that
aempts to minimize the exposure to
mercury vapor to the paent, denst,
and sta during amalgam removal. In
women of childbearing age, removal of
amalgam should be med to avoid the
12–18 months preceding concepon as
a well as pregnancy and breaseeding.
Dietary Fish
Mercury released into the
atmosphere through natural and human
acvies is deposited in soil and water
where it enters the food chain. Mercury
accumulates in sh, parcularly large,
long-lived ocean sh. Natural releases
from the Earth’s crust and the oceans
Table I:
Common Exposures to Mercury
Dental amalgams – a few
micrograms of mercury vapor per
lling per day.
Dietary sh – depending on species,
a poron may contain roughly 1–100
micrograms of methylmercury.
Certain vaccines – 12.5 to 25
micrograms of ethylmercury per
shot.
Prenatal exposures – levels are
unknown but clinically signicant.
➤
For most people, the major sources
of mercury exposure are elemental
mercury vapor from dental amalgams
and methylmercury from dietary
sh. Ethylmercury in certain vaccines
provides smaller amounts, but
these can be highly toxic during the
vulnerable window of gestaon and
early childhood. These three forms of
mercury are all easily absorbed and
readily distributed throughout the
iA 2012 study showed blunted corsol response and higher
inammatory markers at blood mercury levels well below the 5.8
microgram per deciliter level of concern.
62 TOWNSEND LETTER – JANUARY 2017
account for 60–70% of the annual
releases of mercury to the atmosphere.
The remaining 30–40% is aributable to
human acvies.23 Thus, humans have
always encountered some mercury in
certain sh; and, as long as the natural
defense systems are working, one can
consume mercury-containing sh in
moderaon. In healthy individuals,
intesnal metallothioneins (a class of
metal-storage molecules that can be
cumulavely damaged by mercury) can
sequester ingested mercury and slowly
allow its excreon. Selenium, discussed
below, is a micronutrient that oers
some protecon against mercury and is
found in sh as well as other foods.
Mercury levels in sh vary widely by
species and by individual, ranging from
less than 0.1 part per million (ppm)
for salmon and sardines to more than
1 ppm for some samples of lesh,
shark, swordsh, and king mackerel.
This means that a typical 3.5-ounce
(100 gram) serving of sh could contain
anywhere from a few micrograms to
more than 100 micrograms of mercury.
Tuna contains moderate levels, which
vary by species. The FDA sets an Acon
Level for mercury contaminaon in
commercial sh of 1.0 ppm; this means
that federal ocials are allowed to
conscate the product but not that they
actually do so.
Vaccines
One of the most controversial
aspects surrounding vaccines is their
mercury content. Prior to about 2004,
many childhood vaccines contained
thimerosal, a preservave and adjuvant
that is 50% ethylmercury.ii Childhood
exposure to thimerosal rose sharply in
the US during the 1990s as new vaccines
were added to the childhood vaccine
schedule set by the US Centers for
Disease Control and Prevenon (CDC).
Infants subjected to the CDC vaccine
schedule during this me typically
received up to 187.5 micrograms of
mercury in the rst six months of life.24
No regulatory safety standard exists
for ethylmercury. Because ethylmercury
is chemically similar to methylmercury,
the above-menoned 187.5-microgram
dose can be compared to the safe
reference dose for methylmercury (the
form present in dietary sh) set by the
US Environmental Protecon Agency
(EPA) of 0.1 microgram per kilogram
of body weight per day for chronic
exposure, equivalent to about 0.3
micrograms per day for a newborn, and
0.6 micrograms per day for a 6-month
old baby. Even if the 187.5-microgram
exposure, delivered in a number of
concentrated doses, is averaged over
the six-month period, the resulng
dose of 1.04 micrograms per day is sll
signicantly higher than the EPA’s safe
reference dose of 0.3–0.6 micrograms
total per day for methylmercury. In
addion, the EPA safe reference dose for
methylmercury may be too lax,25,26 es-
pecially when applied to ethylmercury.
Indeed, there may be no threshold that
precludes adverse neuropsychological
eects in children,27,28 whose brains are
rapidly developing. Furthermore, unlike
methylmercury from ingested sh,
injected ethylmercury is not subject to
the natural defense mechanisms related
to ingeson, including metallothioneins
and selenium, discussed later.
In 1999, the US Public Health Service
called for the eliminaon of thimerosal
from childhood vaccines. Nonetheless,
due to supply and demand issues, it took
several years to transion to reduced-
thimerosal and then thimerosal-free
alternaves.29
Addionally, during the period
in which thimerosal began to be
phased out of pediatric vaccines, the
thimerosal-containing inuenza vaccine
became an important exposure source
for fetuses and children. In 2002, the
CDC began recommending that the
inuenza vaccine be given to children
aged 6-23 months, as well as pregnant
women in their second and third
trimester, even though the only vaccine
approved for these groups at the me
was preserved with thimerosal.30
Furthermore, the CDC aggressively
increased the dosing and expanded
the target groups for the inuenza
vaccine, recommending a double dose
for infants at both 6 and 7 months plus
subsequent annual doses and a dose for
all pregnant women, no longer limited
as they previously had been to the
second and third trimester.31 As of 2013,
more than half of inuenza vaccines
were sll preserved with thimerosal,32
with the availability of non-thimerosal
versions subject to supply-and-demand
dynamics. For example, the thimerosal-
free u vaccine shortage during
the 2015 u season led California’s
governor to sign an excepon allowing
thimerosal-containing vaccines to be
administered to infants and children
despite a previous statewide restricon.
Some mul-dose meningococcal
meningis vaccines and tetanus toxoid
(booster) vaccines (not recommended
for children under six years of age), like
the mul-dose inuenza vaccines, also
contain thimerosal as a preservave
in amounts ranging from 12.5 to 25
micrograms per dose.33 As of 2016,
some childhood vaccine preparaons
sll ulize thimerosal. In these vaccines,
such as the mul-dose DTaP and the
DTaP/Hib combinaon vaccines, most
of the thimerosal is then ltered out,
reducing thimerosal to “trace” amounts,
according to the CDC.34
Other Exposures
Up to the early 2000s, broken
mercury thermometers were a common
exposure risk in many countries. Unl
the 1960s, teething powders for babies
contained mercury in the form of
calomel. Thimerosal was used in contact
lens soluons. Merbromin was once
widely used as an ansepc under the
trade name Mercurochrome. In 1998,
such products were banned when
the FDA declared that mercury as an
acve ingredient in over-the-counter
products was not “generally recognized
as safe (GRAS).” Nevertheless, the use
of mercury as an inacve ingredient is
allowed by the FDA provided its content
is under 65 ppm, and FDA regulaons
regarding cosmecs do not obligate
ingredients that make up less than 1%
of the product to be disclosed on the
Mercury
➤
iiApproximate mercury content of 1990s-era vaccines: Diphtheria-
Tetanus-Pertussis (DTP and DTaP): 4 doses totaling 100 mcg;
Haemophilus inuenzae type B (HIB): 4 doses totaling 100 mcg;
and Hepas B, 3 doses totaling 37.5 mcg. Mul-dose inuenza
vaccines given annually: 25 mcg. Tetanus vaccine: 25 mcg.
TOWNSEND LETTER – JANUARY 2017 63
label. For instance, some brands of
mascara sll contain thimerosal as an
anmicrobial and preservave.
Compact uorescent lamps (CFLs)
typically contain about 4 milligrams
(4,000 micrograms) of mercury, some
of which is released upon breakage
in the form of mercury vapor. The
concentraon of this toxic release is
compared to various regulatory safety
standards in Table II. CFL proponents
argue that the energy savings oered by
CFLs, which includes reduced mercury
emissions from coal power plants,
makes them desirable; but this debate is
beyond the scope of this arcle.
Incinerators, coal-red power
plants, crematoria, and other industrial
processes may be signicant sources
of local exposures to mercury. For over
those found in newborns of amalgam-
bearing mothers with no other
known exposures.37 Furthermore,
mercury levels in amnioc uid, cord
blood, placental ssue, and breast
milk are signicantly associated in
a dose-dependent manner with the
number of maternal dental amalgam
llings.38,39 Human and animal studies
show increased rates of miscarriage,
neonatal death, low birth weight, and
developmental disorders associated
with mercury exposure.40
Developmental and Epigenec Toxicity
The developmental period
spanning from concepon through
early childhood is a window of
vulnerability in which both epigenec
and neurological damage can occur
unfortunately, when either parent
is exposed to mercury, even prior to
concepon, the child’s own genec
expression can be aected.
Such epigenec damage may range
from mild to severe, and the resulng
phenotype may include characteriscs
such as dental deformies, myopia,
asymmetries of the face, and
disproporons of the body. Such
characteriscs are described in Weston
A. Price’s pioneering Nutrion and
Physical Degeneraon,42 whose ideas
have subsequently been developed
in Chris Masterjohn’s research on fat-
soluble vitamins; in Sally Fallon Morell
and Thomas Cowan’s Nourishing
Tradions Book of Baby and Child
Care43; and in the more epigenecally-
focused Deep Nutrion by Catherine
and Luke Shanahan.44 Within the
alternave health community, the role
of micronutrients is well recognized to
promote physical and mental health as
well as opmal child development. Less
well recognized is the role of toxicity
in depleng one’s micronutrient status
and the analogous role of micronutrient
status in exacerbang or alleviang
toxicies.
Genec Suscepbilies
A loose scienc consensus has
long discounted the idea of mercury
toxicity from dental amalgams because
populaon studies have shown that
people with high exposures and even
people with a high body burden do not
necessarily have toxicity symptoms.
Therefore, those who blame amalgams
for their illnesses have been viewed
askance. But within the past ten years,
over a dozen common genec variants
that convey increased suscepbility to
mercury toxicity have been documented
in human studies.45,46 Moreover,
hundreds more variants are likely to
exist. Mercury aacks sulfur in proteins;
and since the body has tens of thousands
of genecally determined sulfur-
containing proteins, many of these
proteins are likely to include variants
that contribute to suscepbility.47
Mercury
➤
Esmated inial release from typical broken CFL (Johnson et al. 2008)
Some regulatory standards for inhalaon of mercury vapor
US Naonal Instute for Occupaonal Safety and Health (NIOSH)
“Immediately Dangerous to Life or Health” (NIOSH 1994)
US Occupaonal Safety and Health Administraon (OSHA) “Permissible
Exposure Limit” for healthy workers exposed 40 hours per week (OSHA 1998)
US Agency for Toxic Substances and Disease Registry “Minimal Risk Level”
(the safe limit for connuous exposure) (ATSDR 1999)
Table II: Mercury Exposure from Compact Fluorescent
Lamps (CFLs)
micrograms per
meter3 of air
200–800
10,000
100
0.2
a decade, the EPA has aempted to
restrict mercury emissions from coal
plants in the US by about 90%; but the
rule is under ligaon, and legal experts
predict that enforcement is years away.
In some countries, gold mining
techniques that employ mercury
(which were historically employed in
the US during the Gold Rush) remain
a signicant source of exposure for
miners and local populaons.
Fetal and Childhood Exposures
Fetal neurons are more sensive
to the toxic eects of mercury than
any other cell type.35 Mercury from
the mother’s body readily crosses the
placenta and accumulates in the fetus,
as revealed in post-mortem human
and animal studies.36 In ssue culture,
clear eects on nerve growth arise at
mercury concentraons equivalent to
at exposures far lower than those
known to cause toxicity in adults.
Epigenecs refers to the alteraon of
gene expression (turning genes on and
o), usually via environmental factors,
in a manner that can be passed to
ospring without alteraon of the DNA
nucleode sequence itself. Mercury
is a potent epigenec toxicant of
alarming scope with both direct and
indirect eects on gene expression.
Mercury directly targets the cysteine
that comprises the DNA-binding sites
on most gene transcripon factors. In
addion, it targets the cysteine in DNA
methyltransferase enzymes, which play
a role (DNA methylaon) in normal
gene expression. Indirectly, mercury
promotes severe oxidave stress – and
early-life stressors are known to induce
changes in gene expression that set the
stage for disease in later life.41 Thus,
64 TOWNSEND LETTER – JANUARY 2017
Candidate genes are involved not only
in methylaon and detoxicaon but
in vitamin and mineral (i.e., enzyme
cofactor) absorpon, transport, and
metabolism. Yet genec suscepbilies
have yet to be considered by policy
makers, health authories, or the dental
industry. Indeed, for millions of children
and adults covered by subsidized dental
programs, military family dental care,
and Nave American services, for
example, amalgam is virtually the only
opon for dental restoraons.
Regarding genec suscepbilies to
vaccine injury, a few isolated court cases
in the US and elsewhere have recognized
post facto that a limited number of well-
documented genec suscepbilies
including some mitochondrial disorders
have caused certain children to suer
permanent neurological damage. But
genec suscepbilies are a connuum,
and the growing movement to mandate
vaccines has so far failed to recognize
this complex reality.
Mercury as An-Nutrient
Mercury’s toxicity is uniquely far-
reaching. It disrupts fundamental
biochemical processes, promotes
oxidave stress, depletes anoxidant
defenses, and destroys biological
barriers. It causes numerous interacng
eects across mulple organ systems,48
leading to a gamut of health issues
ranging from fague and inammaon
to endocrine and immune dysregulaon
and mood disorders.
Mercury readily binds to sulydryl
(-S-H), a type of sulfur also called a
thiol. The thiol is the major reacve site
within the amino acid, cysteine, which
is ubiquitous in biochemically acve
proteins such as enzymes. The human
body contains tens of thousands of
enzymes, which drive most fundamental
biological processes. Mercury also
binds strongly to selenium, a cofactor
for several dozen enzymes involved in
vital tasks such as thyroid funcon and
brain anoxidant protecon. Selenium
is said to protect against mercury
toxicity, but its protecve scope is
limited by its intracellular availability.
This is governed by kidney processes
that limit the amount of such minerals
in the bloodstream and by specialized
channels within the cell membrane
that control mineral transport from
the bloodstream into cells. Lipophilic
mercury, on the other hand, has no such
limits when entering cells. Moreover,
selenoprotein P, a substance that stores
and transports selenium to cells,49 can
become blocked by mercury. Therefore,
selenium oers only limited protecon
against mercury exposure.
The body’s most important
intracellular anoxidant mechanism is
the glutathione system. Because the
glutathione molecule and its related
enzymes employ cysteine, they are
targets for mercury. Specically,
mercury damages the body’s
glutathione system both by depleng
the glutathione molecule itself and by
blocking the enzymes that synthesize
and recycle glutathione and facilitate
its use. Glutathione detoxies mercury
by binding it (in a process called
glutathione conjugaon) into a less
toxic form suitable for excreon through
the bile. Incidentally, the glutathione
system has been found to be crucial in
the detoxicaon of thimerosal.50 By
depleng glutathione and disabling the
glutathione-related enzymes, mercury
impairs the detoxicaon of many
toxicants, including mercury itself,
leading to increased toxicity.
By damaging methylaon enzymes,
including methionine synthase,
mercury dysregulates the methylaon
cycle, a biochemical pathway in
which the sulfur-containing amino
acid methionine is recycled, creang
two important products: s-adenosyl
methionine (SAMe), the body’s universal
methylator; and cysteine, the precursor
for the transsulfuraon pathway,
which in turn produces glutathione,
sulfate, and taurine. By impairing the
methionine synthase enzyme, mercury
blocks not only detoxicaon via the
transsulfuraon pathway that produces
glutathione but also the producon of
many hormones and neurotransmiers
that require methyl donors like SAMe. A
lack of methyl donors also inhibits the
acvity of the DNA methyltransferase
enzymes, which regulate gene
expression.
In addion to aacking the sulfur
in enzymes, mercury aacks the sulfur
in the funconal proteins within cell
membranes. These include membrane
transport channels that allow
micronutrients into cells. One result,
for example, is altered homeostasis
of many essenal minerals, which can
appear abnormally high or low on
tesng and is an aspect of many chronic
illnesses that has no other obvious
explanaon. Addionally, mercury may
target the disulde bonds in collagen,
the connecve ssue found in blood
vessels, in the gut, and throughout
the body. More importantly, mercury
impairs the ongoing synthesis and repair
of collagen, bone, and carlage, both by
impairing the necessary enzymes and by
depleng a required cofactor – vitamin
C. Thus mercury can be implicated in
arthris, osteoporosis, and connecve
ssue disorders.
Mercury promotes oxidave stress
in several mutually reinforcing ways.
Within cells, mercury concentrates
in mitochondria, the organelles that
synthesize ATP energy. There, it
displaces iron and copper, converng
them to free radicals with the potenal
to cause ongoing oxidave stress unless
buered by anoxidants. Mercury
also blocks mitochondrial enzymes,
creang an overproducon of reacve
oxygen species, including free radicals.
The resulng oxidave stress further
damages mitochondrial enzymes
as well as harming mitochondrial
membranes and mitochondrial DNA.
Mitochondrial dysfuncon can result in
overproducon of lacc acid, yielding
metabolic acidosis, which depletes
minerals and may promote certain
pathogens. Mitochondrial damage
further drains cellular energy by
creang a disproporonate need for
repair, perpetuang a vicious cycle.51
Mitochondrial dysfuncon aects
immunity, digeson, cognion, and
any energy-intensive system within the
body and is a key component of many
chronic illnesses.
Oxidave stress perpetuates another
vicious cycle in which free radicals cause
lipid peroxidaon, a self-propagang
Mercury
➤
TOWNSEND LETTER – JANUARY 2017 65
chain reacon in which the unsaturated
fay acids in cell membranes are
aacked, becoming free radicals
themselves, and ulmately leading to
excess permeability in membranes and
other barriers, thus provoking sll more
damage.
Metallothioneins are cysteine-rich
metal storage molecules that appear to
play a role in storing zinc and copper and
are found in high levels in the intesnes.
When metallothioneins become
saturated with mercury, they can no
longer store zinc or copper or protect
the body from mercury. It is much more
common for mercury-aected people
to suer from low zinc than from low
copper for several reasons. Dietary
sources of zinc are more limited than for
copper. Excess copper is excreted into
the bile and removed from the body
via the feces, but many people have
sluggish bile ow and/or conspaon,
causing copper to accumulate in the
liver. Addionally, estrogen dominance,
which may be amplied in mercury-
aected individuals due to common
hormonal imbalances, causes copper
retenon. Estrogen dominance is
common, especially in women, due to
exposure to plascs, soy, ax, and other
estrogenic foods as well as hormonal
birth control products. Copper pipes,
copper IUDs, and copper sulfate sprayed
on crops as an an-fungal (even on
many organic crops) add to the overall
copper load. Because copper and zinc
are antagonisc, the more that copper
is retained by the body, the more that
zinc tends to be depleted.
Mercury-induced anomalies in
the transport of essenal minerals
such as magnesium and zinc cause
an extra need for these minerals in
the diet. Furthermore, many health
condions caused by mercury toxicity
are aggravated by low magnesium
and/or zinc including cardiovascular
disease, bromyalgia, ausm spectrum
disorders, aenon decits, and
depression. Not every person with a
history of mercury exposure is decient
in all of these nutrients, however; and it
is important to note that minerals have
complex synergisc and antagonisc
relaonships. For example, low zinc is
oen accompanied by high copper, and
low magnesium is oen accompanied
by high calcium in so ssues.
Mercury’s toxicity may be amplied
by exposure to other toxic metals,
including lead, cadmium, and aluminum.
Mercury and lead, in parcular, are
highly synergisc. In fact, in one study,
a dose of mercury sucient to kill 1%
of the lab rats (lethal dose “LD01”)
when combined with a dose of lead
sucient to kill 1% of the rats resulted
in killing 100% of the rats.52 A similar
test involving mercury and aluminum in
cultured neurons killed 60% of the cells
when the two low-dose toxicants (LD01)
were combined.53 Even anbiocs have
been shown to enhance the uptake,
retenon, and toxicity of mercury.54
Mercury
➤
66 TOWNSEND LETTER – JANUARY 2017
Addionally, testosterone appears
to aggravate mercury toxicity during
development while estrogen protects
against it.55 In fact, more boys than girls
are diagnosed with ausm spectrum
disorders and aenon decit.
Ausm, Aenon Decit and Other
Neurological Disorders
Many scienc studies suggest
a connecon between mercury and
ausm spectrum disorder (ASD), yet
the subset of studies cited by health
authories fails to nd a causal
link.56 Such a link is widely viewed as
biologically plausible,57 yet remains a
taboo subject in mainstream medicine
and the media. Ausm is documented to
involve oxidave stress, mitochondrial
dysfuncon, immune or inammatory
processes, impaired sensory processing,
and abnormal mineral homeostasis, all
of which are consistent with mercury
toxicity.58 Ausc children have been
found to have signicantly higher
exposure to mercury during fetal
development and early infancy, as
measured by metals in baby teeth.59 The
element most frequently decient in
ASD is zinc.60 Other commonly observed
mineral imbalances in ASD include low
calcium, iron, magnesium, manganese,
and selenium as well as high copper
and elevated toxic metals, which can
somemes be dicult to detect through
tesng, as described later.
Aenon decit disorder (ADD) and
aenon decit hyperacvity disorder
(ADHD) are common early ndings
in mercury-exposed children.61 Zinc
deciency has been idened as a
biomarker for ADHD62; and the abnormal
mineral prole for ADHD appears quite
similar to that for ausm and mood
disorders, with the excepon that
ADHD typically includes iron overload.
Addionally, copper dysregulaon is a
key factor in ADHD.63
Many studies report a close
associaon between clinical depression
and zinc deciency with severity of
symptoms inversely correlated with
serum zinc levels. Decreased levels
of zinc, calcium, iron, and selenium
have been reported as risk factors
for postpartum depression.64 Other
neurological and psychiatric disorders
associated with mercury include
narcolepsy, obsessive-compulsive
disorder, schizophrenia, bipolar
disorder, Touree syndrome, and
borderline personality disorder as
well as neurodegenerave disorders –
Alzheimer’s, Parkinson’s and Mulple
Sclerosis, for example. Each has been
documented to involve oxidave
stress, inammaon, mitochondrial
dysfuncon, and mineral imbalances; all
of which can be aributed to mercury.
These diseases are complex, such that
human studies are unlikely to nd a
direct causal link with any one risk factor
that is strong enough to sasfy skepcs;
but a growing body of evidence suggests
that mercury plays a major role.65
Exacerbang the mineral
dysregulaon associated with
these many condions are the
neurotransmier imbalances provoked
by mercury. For example, mercury
increases extracellular levels of the
excitatory neurotransmier glutamate,
thus overacvang glutamate receptors
on cell surfaces.66 The amplicaon
of glutamate is further exacerbated
by mercury’s inhibion of the
calming neurotransmier GABA67:
Mercury blocks GABA receptors; it
disproporonately destroys GABA-
producing Purkinje neurons; and it
impairs glutamate decarboxylase (GAD),
the enzyme responsible for converng
glutamate to GABA. Furthermore,
mercury’s dysregulaon of glutamate
and GABA is associated with depression
and suicide.68–70
Altered Microbiota, Digesve
Dysfuncon and Immune Health
Mercury is known to alter the
intesnal microbiota, yielding increased
levels of undesirable mercury-resistant
bacterial species, which may also
develop resistance to anbiocs.71–73
For example, the opportunisc yeast
Candida albicans may overgrow, causing
a host of unpleasant symptoms. This
dysbiosis may be exacerbated by
mercury’s dysregulaon of the immune
system as well as its promoon of
metabolic acidosis. All this has negave
implicaons for digeson, immunity,
and mental health.74–76
Mercury also inhibits several
enzymes aecng digeson including
gastric hydrogen-potassium-ATPase,
the enzyme that allows the synthesis
of hydrochloric acid via the stomach’s
proton pump. In addion, by
promong oxidave stress, mercury
moves the autonomic nervous system
into sympathec (stress) mode,
inhibing digeson. Furthermore, the
mitochondrial dysfuncon from which
many mercury-aected individuals
suer impairs digeson as well as other
bodily funcons. By damaging both
the gut and the blood-brain barrier,
mercury leads to leaky gut, which in
turn leads to food allergies and brain
disorders caused by maldigested
proteins entering the bloodstream. As
a fairly common case in point, parally
digested proteins in foods containing
gluten and casein may be metabolized
into the opioid pepdes gluteomorphin
and casomorphin.77 This is oen seen in
children with ausm spectrum disorder
and explains many parental reports of
symptom relief on a gluten-free, casein-
free diet.
Mercury’s eects on the gut can
exacerbate mercury’s eects on the
immune system. Mercury is known
to cause allergies, reduced immunity,
and autoimmunity78; and such immune
dysfuncon plays a role in many chronic
illnesses. Reduced immunity yields
suscepbility to chronic infecons
such as Lyme and Candida. Finally,
although technically not an allergy,
mulple chemical sensivies can result
from mercury overloading the body’s
detoxicaon system and blocking
metabolic enzymes in the liver and other
ssues so that common but undesirable
chemicals such as fragrances are
metabolized incompletely, yielding toxic
intermediates.
Thyroid Disorders, Hypothalamus-
Pituitary-Adrenal Dysfuncon, and
Stress-Related Disorders
Mercury is known to concentrate
in glands, including the thyroid
and pituitary, and to impair the
hypothalamus-pituitary-adrenal
Mercury
➤
TOWNSEND LETTER – JANUARY 2017 67
(HPA) axis. HPA funcon and thyroid
funcon are ghtly interrelated, with
impairment of one system oen causing
impairment of the other. Mercury blocks
the selenium-dependent enzyme that
converts the thyroid hormone, thyroxine
(T4), to its acve form, triiodothyronine
(T3). Unfortunately, despite symptoms,
the resulng hypothyroidism oen goes
undetected by roune blood work,
which typically only tests levels of TSH,
the hormone secreted by the pituitary
that signals the thyroid gland to produce
T4. Further suppressing thyroid funcon
is the mercury-induced depleon of
selenium and zinc, which are cofactors
for thyroid enzymes.
The oxidave stress caused by
mercury is a type of chronic stress
that depletes the HPA axis; thus,
mercury is implicated in the cluster
of symptoms referred to as adrenal
fague. Incidentally, an evolving view
of this condion suggests that it is not
a glandular problem, but rather a brain-
stress problem.79 Early-life exposure to
mercury also causes epigenec damage
to the HPA axis, which can dysregulate
the stress response throughout life.
This may involve a tendency toward
either high or low baseline corsol as
well as a loss of the dynamic corsol
response to stress.80 The laer yields
a disabling feeling of unwellness
and stress intolerance. High baseline
corsol, on the other hand, may feel
less debilitang, but this is a catabolic
state that can promote degeneraon of
otherwise healthy ssues.
Metabolic Disorders, Obesity, and
Cardiovascular Disease
HPA dysregulaon and thyroid
dysfuncon strongly impact metabolism
and weight. As an epigenec toxicant,
mercury can cause a host of metabolic
issues, including blood sugar problems,
insulin resistance, and stress intolerance.
These symptoms can persist throughout
life and into future generaons. In
addion, mercury impairs many
enzymes needed to metabolize
food into energy including pyruvate
dehydrogenase, which is required for
metabolism of carbohydrates but not fat
or proteins. Hypoglycemic symptoms,
which are common in mercury toxicity,
may not reect true low blood sugar
but may indicate impaired enzymes
within the brain and/or HPA axis. Other
enzymes impaired by mercury include
those of the citric acid cycle and the
electron transport chain, leading to low
ATP energy. Mercury also blocks the
insulin receptor, promong high insulin
and thus fat storage. Mercury can cause
weight gain or weight loss, depending
on whether metabolic dysregulaon or
gut dysfuncon predominates.
Regarding mercury’s role in
cardiovascular disease, mercury oxidizes
blood vessels as well as cholesterol,
leading to arterial plaque. Mercury
promotes thrombosis and endothelial
dysfuncon in blood vessels.81
Mercury can cause high or low blood
pressure depending on whether artery
calcicaon or artery deterioraon and
HPA dysfuncon predominate. Finally, in
a remarkable example of how mercury
accumulates in certain ssues, a biopsy
study of 13 paents with a type of heart
failure found that mercury levels in the
myocardium were 22,000 mes higher
than normal.82
Nutrion
Mercury damage creates a need for
extra nutrion, both to repair damage
and to prod blocked enzymes. Nutrient-
dense diets are of crical importance,
and targeted supplementaon may help
to overcome the unnatural toxic state.
Because everyone’s nutrient status is
uniquely aected by mercury, it is wise
to take an individual approach rather
than supplement all potenally depleted
nutrients across the board. In addion,
dietary modicaons are somemes
necessary to control the inammaon
and other symptoms that result from
food sensivies, which are common in
aected individuals. Also, eang foods
to which we are allergic or intolerant
impairs detoxicaon by placing undue
stress on the organs of digeson and
eliminaon, pung the HPA axis
on alert, and increasing the level of
inammaon in the body. It is common
for people with mercury toxicity to have
mulple food sensivies, parcularly
to gluten, casein, and soy.
High-quality fat is a preferred fuel
in mercury toxicity, because it supplies
much-needed fat-soluble vitamins
and helps stabilize blood sugar levels.
Addionally, because both brain ssue
and the phospholipid bilayer of the cell
membrane are built in large part from
saturated fat, consumpon of grass-fed
animal fats such as lard, tallow, ghee,
and buer contributes to repair. Cod
liver oil, liver, extra-virgin organic olive
oil, red palm oil, and lard are important
sources of fat-soluble vitamins; and it is
important to eat a variety of healthy fats
from both animal and plant sources. Fat
metabolism requires fewer enzymes
than carbohydrate metabolism, thus
has less opportunity to be blocked
by mercury. In addion to slowing
energy producon, impaired enzymes
can create toxic intermediates, which
can yield food intolerances to some
carbohydrate foods. Carbohydrates
can raise insulin, the fat-storage
hormone, which may already be high
due to mercury toxicity. Finally, high-
carbohydrate foods are more likely than
high-fat foods to contain an-nutrients
such as phytates, oxalates, and lecns.
Bone broth is ideal for repairing the
digesve lining and connecve ssue,
and for supplying easily assimilated
amino acids and other nutrients.
Daily consumpon of bone broth
can help repair the excessive gut
permeability that oen leads mercury-
toxic individuals to food allergies and
autoimmunity. Glutamine is one of the
most important amino acids needed
to repair the lining of the gut; and
glutamine and glycine, both abundant
in bone broth, are precursors to the
body’s producon of glutathione.
Vitamin B6 and magnesium may ease
the conversion of glutamate to GABA.83
In the event of sensivity to glutamate,
it is advisable to simmer the broth for
no longer than 3-4 hours.
Beet kvass can improve the ow
of bile and thus improve excreon of
mercury and other toxicants through
the bile, parcularly in individuals who
tend to be conspated. Other probioc
foods, such as sauerkraut, are also
helpful as part of a healing program.
Mercury
➤
68 TOWNSEND LETTER – JANUARY 2017
It is a good idea to start with a small
amount of probioc foods and to
increase gradually as tolerated. Organ
meats are nutrient-dense and can help
supply vitamins and minerals depleted
by mercury. For example, liver is high
in vitamins A and B-12 as well as zinc,
magnesium, and selenium.
Foods high in vitamins A, C, D and
E confer important anoxidant and
immune-modulang benets. Vitamin
C helps rebuild damaged collagen and
can be obtained from a variety of food
sources as tolerated, taking care not
to rely enrely on the sweeter fruits,
which can be problemac for people
with blood sugar issues. Good sources
of the vitamin include rose hips, guava,
acerola cherry, lemons, limes, oranges,
grapefruit, kale, broccoli, cauliower,
Brussels sprouts, papaya, mango,
pineapple, kiwi, and strawberries.
People who suer from thiol sensivity,
discussed below, will need to avoid or
limit the vegetables included on the list.
Because grapefruit can smulate phase
II of the liver’s detoxicaon and slow
down phase I, it is wise to consume
grapefruit only occasionally unless
phase I is already known to be overly
acve with respect to phase II.
The two minerals most commonly
depleted by mercury are magnesium
and zinc. Liver, leafy green vegetables,
neles, properly soaked lenls (if
tolerated), and properly prepared
almonds are good sources of
magnesium. Neles are a great source
of numerous vitamins and minerals,
including magnesium, and can be added
to soups or enjoyed as a tea. Zinc-rich
foods are crical, but unfortunately
oysters, the richest source of zinc, also
tend to be high in cadmium and other
heavy metals. Thus, red meat and
poultry, along with properly soaked
sesame and pumpkin seeds and pine
nuts, are important sources of zinc for
mercury-aected people, keeping in
mind that we absorb zinc much more
eciently from animal foods than from
plant sources.
Brazil nuts are a good source of
selenium, and, unlike sh that are
also high in selenium, do not contain
potenally problemac levels of
mercury. The selenium content of Brazil
nuts varies according to the soil where
the nuts are grown, as is the case for all
foods. Brazil nuts are high in unsaturated
fat and may not keep well if soaked
extensively, but overnight soaking
works well in temperate climates.
Regarding the consumpon of sh, the
evidence suggests that once the body’s
natural defenses have been overrun by
mercury the selenium in seafood is less
eecve in buering the mercury. Thus,
people who know or suspect a mercury
problem must consider the benets
and the risks in determining their sh
consumpon level. For example, those
who limit their seafood intake should
consider taking cod liver oil and perhaps
sh oil as well in order to derive some
of the nutrional benets of sh while
keeping mercury exposure as low as
possible.
Eliminaon and reintroducon of
suspect foods is the best way to assess
whether these foods are problemac
for an individual. The goal is the least
restricve nutrient-dense diet. For
example, many children and adults
with mercury toxicity benet from
a gluten-free, casein-free diet while
others can tolerate one or both of
these foods. Addional intolerances
too numerous to list aect certain
mercury-toxic individuals to varying
degrees. The intake of alcohol, sugar,
rened starches, processed foods,
caeine, medicaons, etc. reduces
the body’s ability to detoxify, causing
unpleasant symptoms in many aected
individuals. Addionally, the common
intolerance to sultes in wine suggests
impairment of the sulte oxidase
enzyme needed to convert toxic sulte
to benecial sulfate. This enzyme
can be boosted by supplemenng its
cofactor, molybdenum. Also, because
mercury blocks metabolic enzymes
such as phenolsulfotransferases, certain
food compounds, such as phenols,
become parally metabolized into
toxic intermediates, oen resulng in
reacons such as red cheeks and/or ears
and hyperacvity aer consuming foods
high in phenol.84 Addionally, yeast
overgrowth can increase sensivity to
high-thiol and high-oxalate foods.
Foods high in free thiols (which
include legumes, dairy, the cabbage
family, eggs) may be poorly tolerated
by some mercury-aected individuals,
parcularly if the transsulfuraon
pathway is compromised, as can occur
with molybdenum deciency. Other
sulfur-rich foods, such as red meat
and organ meats, do not cause such
problems. Of course it is important to
consume a diet that includes all the
essenal amino acids, including those
that contain sulfur. Andrew Cutler,
author of Amalgam Illness: Diagnosis
and Treatment (see Resources, below)
and Hair Test Interpretaon: Finding
Hidden Toxicies notes that foods high
in free thiol can provoke symptoms in a
signicant subset of mercury-aected
people, in part by increasing plasma
cysteine, which may rise in response
to mercury and its biochemical eects.
Vegetarian diets are parcularly
deleterious to a signicant subset of
people suering from mercury toxicity
because it is virtually impossible to
obtain sucient protein on a vegetarian
diet that is modied to reduce free-thiol
sources.
A problemac food for many
mercury-toxic individuals is cilantro leaf,
which contains a chelang substance
capable of redistribung mercury, thus
exacerbang symptoms in sensive
individuals. Unfortunately, within the
alternave health community, cilantro
leaf is somemes recommended
in large amounts in both food
and supplement form. Also oen
recommended is chlorella, which is
inadvisable as a supplement due to its
potenal for contaminaon from the
environment in which it is grown and
to its lipopolysaccharide content, which
can cause inammatory stress.85
Each mercury-toxic person has
a unique combinaon of mineral
imbalances that aect how mercury
toxicity is expressed and what parcular
nutrient combinaon is likely to
provide relief. Mineral dysregulaon
is signicantly more pronounced in
people with chronic mercury toxicity
than in the general populaon,86 as are
Mercury
➤
TOWNSEND LETTER – JANUARY 2017 69
other nutrional deciencies and food
intolerances.
Tesng
Tesng for mercury toxicity is
not straighorward. Mercury may
accumulate in organs like the brain even
while blood, urine, fecal and hair levels
are low. Urine challenge tests should be
avoided. They involve the administraon
of a chelator in a dosage high enough to
cause signicant oxidave stress due to
redistribuon of toxic metals to target
organs such as the brain and kidneys. A
porphyrin panel can reveal the footprint
of toxic metals including mercury.
Porphyrins are undesirable byproducts
that occur when enzymes are blocked
by toxicants. But since porphyrins are
easily destroyed,87 the risk of false
negaves is high unless the sample is
handled carefully. A hair elements test
can reveal apparent dysregulaon of
essenal mineral homeostasis – i.e.,
essenal hair minerals will appear
abnormally high and/or low – and thus
may serve as an economical screening
test for chronic mercury toxicity. Note
that when hair essenal minerals are
dysregulated, a high level of an essenal
mineral may not indicate adequate
intracellular status but may simply
mean high excreon in hair.
It is beyond the scope of this
nutrion-focused arcle to discuss
mercury treatment opons, but we
recommend cauon when considering
detoxicaon protocols. For the highly
mercury toxic, many products may be
either unsafe (such as chlorella and
cilantro) or may be used in an unsafe
manner (such as alpha lipoic acid). Alpha
lipoic acid is added to many nutrional
supplements without warning about
its metal chelang properes. When
taken by individuals who have mercury
dental amalgams or a body burden of
mercury, it can pull mercury from the
teeth and other ssues in an aempt to
equilibrate levels throughout the body
and brain. This is especially tragic when
fetal exposure is involved. We suggest
that anyone wishing to deepen their
knowledge of mercury detoxicaon
read the books by Andrew Cutler listed
in the Resources secon. Cutler’s work is
the most useful compilaon of science-
based explanaons of mercury toxicity
and its myriad eects. It should be
noted that Cutler’s chelaon protocol,
though grounded in scienc theory, is
controversial and is not without risk.
Conclusions
Because of mercury’s powerful
an-nutrient eects, a nutrient-dense
diet may alleviate many symptoms of
chronic mercury toxicity. Moreover,
the nutrional depleon caused by
mercury is so pervasive that aected
individuals oen require nutrional
supplementaon as well as a nutrient-
dense diet. At the same me, it’s
important to note that many mercury-
aected individuals are quite sensive to
a large number of foods, supplements,
and medicaons. Many people with a
hidden mercury burden nd relief by
following a nutrient-dense diet, adapted
as necessary to avoid gluten and/or
dairy and to limit sugars and starches.
Mercury creates a biochemical
train wreck in the body and has the
toxic power to cause or contribute to
most chronic illnesses. People who
have mulple health problems may
suer from undiagnosed chronic
mercury poisoning. Mercury depletes
nutrients needed for vital funcons
and dysregulates mineral and
neurotransmier metabolism to a
greater extent than any other common
toxicant.
Yet chronic mercury toxicity
remains underrecognized by both
mainstream and alternave health
authories for a number of reasons.
The scienc literature on mercury is
complicated, incomplete, and easily
misinterpreted. Mercury demonstrates
a complex, nonlinear toxicity. Mercury
suscepbility depends on genecs,
epigenecs, and micronutrient status.
The body’s natural defenses may mask
toxicity, creang long latencies between
exposures and symptoms. Symptoms
are varied and nonspecic and may be
intermient in the early stages. Mercury
research is controversial because much
exposure has been iatrogenic, via dental
amalgams and vaccine preservaves.
Toxicity tesng is not straighorward,
as described above. In summary, the
combinaon of ubiquitous exposures,
iatrogenic involvement, long latencies,
broad toxic eects, nonspecic
symptoms, and potenally irreversible
damage renders chronic mercury
toxicity an underrecognized epidemic.
Resources
• IAOMT.org - Internaonal Academy of Oral Medicine
and Toxicology, a professional dental associaon that
provides fact sheets about mercury and describes the
Academy’s safe amalgam removal protocol
• MercuryFreeBaby.org - a joint project of IAOMT and
CoMeD (Coalion for Mercury-Free Drugs), which
advocates removal of mercury from all vaccines
• Amalgam.org - Dental Amalgam Mercury Soluons,
a non-prot organizaon dedicated to educang
consumers about unhealthy dental pracces
• Amalgam Illness: Diagnosis and Treatment (1999) by
Andrew Hall Cutler. This book is sll the most complete,
science-based, self-help book on chronic mercury
toxicity to date. Available through the author’s website
at www.noamalgam.com as well as online bookstores: .
• Mercury Poisoning: The Undiagnosed Epidemic (2013)
by David Hammond. This book provides more context
and less physiology than Cutler’s book in a rendion
some may nd more readable.
• livingnetwork.co.za/chelaonnetwork/food/high-
sulfur-sulphur-food-list/ - a resource that explains why
some people with mercury toxicity cannot tolerate thiols
and how to idenfy thiol intolerance.
Mercury
Sara Russell is a Nutrional Therapy Praconer, Cered GAPS
Praconer, and Weston A. Price chapter leader residing in Italy.
Sara works via phone and Skype with clients worldwide, specializing
in ferlity, pregnancy, and young children. You can learn more about
Sara’s work at hp://buildnurturerestore.com.
➤
Krisn Homme, MPP, MPH, is a rered engineer turned science writer who has authored
several scienc arcles in peer-reviewed journals.
70 TOWNSEND LETTER – JANUARY 2017
• hp://www.ewg.org/skindeep/ - the Environmental
Working Group’s Skin Deep® searchable online consumer
database of body care products ranging from basics such
as soap and shampoo to sunscreen and cosmecs.
Acknowledgements
The authors would like to thank Nori Hudson, NC, Andrew
Hall Cutler, PhD, PE, Janet Kern, PhD, Marco Prina, PhD,
Rebecca Rust Lee, and Lana Russell for their input and reading
of the arcle at various stages of its draing and revision.
References
1. Muer J, Naumann J, Sadaghian C, Walach H, Drasch
G. Amalgam studies: disregarding basic principles of
mercury toxicity. Int J Hyg Environ Health. 2004;207:391–
397.
2. Weiss B, Clarkson TW, Simon W. Silent latency periods
in methylmercury poisoning and in neurodegenerave
disease. Environ Health Perspect. 2002;110 (Suppl
5):851–4.
3. Waldron HA. Did the Mad Haer have mercury
poisoning? Br Med J. 1983;287 (6409):1961.
4. Grum, DK, Kobal AB, Arnerič N, et al. Personality Traits
in Miners with Past Occupaonal Elemental Mercury
Exposure. Environ Health Perspect. 2006;114(2):290-296.
5. Clarkson, TW, Magos, L. The toxicology of mercury and its
chemical compounds. Crit Rev Toxicol. 2006;36:609–662.
6. Gerstner HB, Hu JE. Clinical toxicology of mercury. J
Toxicol Environ Health. 1977;2(3):491–526.
7. Mahaey KR, Clickner RP, Jeries RA. Adult women’s
blood mercury concentraons vary regionally in
the United States: associaon with paerns of sh
consumpon (NHANES 1999-2004). Environ Health
Perspect. 2009;117(1):47-53.
8. Gump BB, MacKenzie JA, Dumas AK, et al. Fish
Consumpon, Low-Level Mercury, Lipids, and
Inammatory Markers in Children. Environ Research.
2012;112:204-211.
9. Boyle CA , Boulet S, Schieve LA, et al. Trends in the
prevalence of developmental disabilies in US children,
1997-2008. Pediatrics. 2011;127(6):1034-42. The authors
provide the following gures: ADHD + Ausm + seizures +
stuer = 7.57% + 0.74% + 0.72% + 1.68% = 10.71%.
10. Grandjean P, Landrigan PJ. Neurobehavioural eects of
developmental toxicity. Lancet Neurol. 2014;13(3):330–8.
11. Berlin M, Zalups RK, Fowler BA. Mercury. In: Nordberg GF,
Fowler BA, Nordberg M, eds. Handbook on the Toxicology
of Metals. 4th ed. Amsterdam [etc.]: Elsevier/Academic
Press; 2015. pp. 1013–75.
12. Berlin Ibid.
13. Berlin Ibid.
14. Rooney JP. The retenon me of inorganic mercury in the
brain – a systemac review of the evidence. Toxicol Appl
Pharmacol. 2014;274(3):425-35.
15. Berlin, et al. 2015, op. cit.
16. Homme K, Kern JK, Haley B, et al. New Science Challenges
Old Noon that Dental Amalgam is Safe. Biometals.
2014:27;19-24.
17. Ibid.
18. Berlin, et al. 2015, op. cit.
19. IPCS (Internaonal Programme on Chemical Safety).
Elemental mercury and inorganic mercury compounds:
human health aspects. World Health Organizaon,
United Naons Environment Programme; 2003. Accessed
Dec. 29, 2015.
20. Berlin et al. 2015, op. cit.
21. Mortazavi G, Mortazavi SM. Increased mercury release
from dental amalgam restoraons aer exposure
to electromagnec elds as a potenal hazard for
hypersensive people and pregnant women. Rev Environ
Health. 2015;30(4):287-92.
22. EC European Commission Health and Food Safety
Scienc Commiee. Final opinion on dental amalgam.
May 2015. ,hp://ec.europa.eu/health/scienc_
committees/consultations/public_consultations/
scenihr_consultaon_24_en.htm. 29 April 29, 2015.
Accessed June 18, 2015.
23. Berlin, et al. 2015, op cit.
24. Geier DA, King PG, Hooker BS, et al. Thimerosal: Clinical,
epidemiologic and biochemical studies. Clinica Chimica
Acta. 2015;444:212–20.
25. Rice DC. The US EPA reference dose for methylmercury:
sources of uncertainty. Environ Res. 2004;95(3):406-13.
26. Budtz-Jørgensen E, Grandjean P, Weihe P. Separaon
of risks and benets of seafood intake. Environ Health
Perspect. 2007;115(3):323-7.
27. Rice 2004, op. cit.
28. World Health Organizaon. Mercury in Health Care,
Policy Paper. August 2005. hp://www.who.int/water_
sanitation_health/medicalwaste/mercurypolpaper.pdf.
Accessed April 28, 2016.
29. Geier et al. 2015, op. cit.
30. Ibid.
31. Ibid.
32. Ibid.
33. See for example the FDA’s chart on “Vaccine
Safety and Availability” at hp://www.fda.gov/
BiologicsBloodVaccines/SafetyAvailability/VaccineSafety/
UCM096228#t1 and the Naonal Vaccine Informaon
Center (NVIC) Frequently Asked Quesons on the topic
of “Thimerosal in Vaccines” at hp://www.nvic.org/faqs/
mercury-thimerosal.aspx (both accessed Jan 12, 2016).
34. CDC brochure: Understanding Thimerosal, Mercury
and Vaccine Safety. Revised 2013. hp://www.cdc. gov/
vaccines/hcp/patient-ed/conversations/downloads/
vacsafe-thimerosal-color-oce.pdf. Accessed January 12,
2016.
35. Berlin et al. 2015 op. cit.
36. Berlin Ibid.
37. Ibid.
38. Ibid.
39. Kern JK, Geier DS, Bjørklund G, et al. Evidence
supporng a link between dental amalgams and
chronic illness, fague, depression, anxiety, and suicide.
Neuroendocrinology Leers. 2014;35(7):537-52.
40. Berlin et al. 2015, op. cit.
41. Brigelius-Flohé R, Flohé L. Basic principles and emerging
concepts in the redox control of transcripon factors.
Anoxid Redox Signal. 2011;15(8):2335–81.
42. Price WA. Nutrion and Physical Degeneraon (8th
prinng). Lemon Grove, CA: The Price-Poenger
Nutrion Foundaon; 2011.
43. Fallon Morell S, Cowan TS. The Nourishing Tradions
Book of Baby and Child Care. Washington, DC: New
Trends Publishing; 2013.
44. Shanahan C and Shanahan H. Deep Nutrion: Why Your
Genes Need Tradional Food. Lawai, HI, Big Box Books;
2008.
45. Woods JS, Heyer NJ, Russo JE, Marn MD, Farin FM.
Genec polymorphisms aecng suscepbility to
mercury neurotoxicity in children: summary ndings
from the Casa Pia Children’s Amalgam clinical trial.
Neurotoxicology. 2014;44:288–302.
46. Muer et al. 2004, op. cit.
47. Berlin et al. 2015, op. cit.
48. Kern et al. 2014, op.cit.
49. Burk RF, Hill KE. Selenoprotein P: an extracellular
protein with unique physical characteriscs and a role in
selenium homeostasis. Annu Rev Nutr. 2005;25:215–35.
50. Westphal GA, Schmuch A, Schulz TG, et al. Homozygous
gene deleon of the glutathione S-transferases M1 and
T1 as associated with thimerosal sensizaon. Int Arch
Occup Environ Health 2000;73(6): 384-88.
51. Kern et al. 2014, op. cit.
52. Schubert J, Riley EJ, Tyler SA. Combined eects in
toxicology. A rapid systemac tesng procedure:
cadmium, mercury, and lead. Toxicol Environ Health.
1978;4(5/6):763-776.
53. Haley BE. Mercury toxicity: Genec suscepbility and
synergisc eects. Medical Veritas. 2005:2;535–542.
54. Ibid.
55. Geier DA, Kern JK, Geier MR. The biological basis of
ausm spectrum disorders: Understanding causaon
and treatment by clinical genecists. Acta Neurobiol Exp
(Wars). 2010;70(2):209-26.
56. Hooker B, Kern J, Geier D, et al. Methodological issues
and evidence of malfeasance in research purporng to
show thimerosal in vaccines is safe. Biomed Res Int. 2014.
57. Berlin et al. 2015, op cit.
58. Kern JK, Geier DA, Audhya T, King PG, Sykes LK, Geier MR.
Evidence of parallels between mercury intoxicaon and
the brain pathology in ausm. Acta Neurobiol Exp (Wars).
2012;72(2):113–53.
59. Adams JB, Romdalvik J, Ramanujam VM, Legator MS.
Mercury, lead, and zinc in baby teeth of children with
ausm versus controls. J Toxicol Environ Health A.
2007;70(12):1046-51.
60. Pfaender S, Grabrucker AM. Characterizaon of
biometal proles in neurological disorders. Metallomics.
2014;6(5):960–77.
61. Woods et al. 2014, op cit.
62. Pfaender S, Grabrucker AM. Characterizaon of
biometal proles in neurological disorders. Metallomics.
2014;6(5):960–77.
63. Malter, Richard. The Strands of Health: A Guide to
Understanding Hair Tissue Mineral Analysis. Coonwood,
AZ: Educaonal and Health Resources of Arizona, Inc.;
2002.
64. Pfaender S, Grabrucker AM. Characterizaon of
biometal proles in neurological disorders. Metallomics.
2014;6(5):960–77.
65. Carocci A, Rovito N, Sinicropi MS, Genchi G. Mercury
toxicity and neurodegenerave eects. Rev Environ
Contam Toxicol. 2014;229:1–18.
66. Farina M, Avila DS, da Rocha JBT, Aschner M. Metals,
oxidave stress and neurodegeneraon: a focus on
iron, manganese and mercury. Neurochem Int. 2013;
62(5):575–94.
67. Kern et al. 2012, op. cit.
68. Kern et al. 2014, op. cit.
69. Sowa-Kućma M, Szewczyk B, Sadlik K, et al. Zinc,
magnesium and NMDA receptor alteraons in the
hippocampus of suicide vicms. J Aecve Disord.
2013;151:924–931.
70. Zarate C, Duman RS, Liu G, Sartori S, Quiroz J, Murck H.
New paradigms for treatment-resistant depression. Ann
N Y Acad Sci. 2013;1292:21–31.
71. Kern et al. 2012, op. cit.
72. Lorscheider FL, Vimy MJ, Summers AO, Zwiers H. The
dental amalgam mercury controversy––inorganic
mercury and the CNS; genec linkage of mercury and
anbioc resistances in intesnal bacteria. Toxicology.
1995;97:19–22.
73. Summers AO, Wireman J, Vimy MJ, et al. Mercury
released from dental “silver” llings provokes an
increase in mercury- and anbioc- resistant bacteria in
oral and intesnal ora of primates. Anmicrob Agents
Chemother. 1993;37:825–834.
74. Diaz Heijtz R, Wang S, Anuar F, et al. Normal gut
microbiota modulates brain development and behavior.
Proc Natl Acad Sci USA. 2011;108:3047–3052.
75. Hansen CH, Nielsen DS, Kverka M, et al. Paerns of early
gut colonizaon shape future immune responses of the
host. PLOS One. 2012;7:e34043.
76. Tlaskalová-Hogenová H, Stepánková R, Hudcovic T, et
al. Commensal bacteria (normal microora), mucosal
immunity and chronic inammatory and autoimmune
diseases. Immunology Leers. 2004;93:97–108.
77. Campbell-McBride N. Gut and Psychology Syndrome.
Cambridge, MA: Medinform; 2010.
78. Vas J, Moneser M. Immunology of mercury. Ann N Y
Acad Sci. 2008;1143:240–267.
79. Gedgaudas N, Kharrazian D. Rethinking Fague: What
Your Adrenals Are Really Telling You and What You Can
Do about It (ebook). Primal Body Primal Mind Publishing;
2014.
80. Moisiadis VG, Mahews SG. Glucocorcoids and fetal
programming part 1: Outcomes. Nat Rev Endocrinol. July
2014; 10(7):391–402.
81. Houston MC. Role of mercury toxicity in hypertension,
cardiovascular disease, and stroke. J Clin Hypertens
(Greenwich). August 2011;13(8):621–7.
82. Frustaci A, Magnavita N, Chimen C, et al. Marked
elevaon of myocardial trace elements in idiopathic
dilated cardiomyopathy compared with secondary
cardiac dysfuncon. J Am Coll Cardiol. 1999;33(6):1578-
83.
83. Cutler AH, Amalgam Illness: Diagnosis and Treatment.
Sammamish, WA; 1999.
84. Mahews J. Nourishing Hope for Ausm: Nutrion and
Diet Guide for Healing Children. 3rd Ed. Healthful Living
Media; 2008.
85. Hsu HY, Jeyashoke N, Yeh CH, Song YJ, Hua KF, Chao LK,
Immunosmulatory bioacvity of algal polysaccharides
from Chlorella pyrenoidosa acvates macrophages via
Toll-like receptor 4, J Agric Food Chem. 2010;58(2):927-
36.
86. Cutler, AH, Hair Test Interpretaon: Finding Hidden
Toxicies. Sammamish, WA; 2004.
87. Woods JS. Urinary porphyrin proles and genec
suscepbility to mercury toxicity. Presentaon at the
Internaonal Academy of Oral Medicine and Toxicology
conference, San Antonio, Texas, March 2009. Available at
hp://www.youtube.com/watch?v=eW0kDV-jMF4.
Mercury
➤
u
