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Mercury: The Quintessential Anti-Nutrient


Abstract and Figures

The chronic effects of cumulative, low-dose mercury exposure are underrecognized by both mainstream and alternative health authorities and, consequently, by the public. Mercury can cause or contribute to most chronic illnesses, including neurological disorders, cardiovascular disease, metabolic syndrome, chronic fatigue, fibromyalgia, adrenal and thyroid problems, autoimmunity, digestive disorders, allergies, chemical sensitivities, mental illness, sleep disorders, and chronic infections such as Lyme and Candida. Mercury toxicity should be suspected in individuals experiencing multiple health problems. Diagnosis of chronic mercury toxicity is often difficult because the body's natural defenses may mask or delay symptoms. Natural defenses are a function of genetic susceptibility, epigenetic factors, micronutrient status, and allostatic load (cumulative wear and tear on the body). Furthermore, individuals who retain mercury may counterintuitively show low levels in blood, urine, and hair. The developmental window from conception through early childhood is one of extreme vulnerability to mercury. Mercury is an epigenetic toxicant (affecting future gene expression) as well as a neurotoxicant. Damage may be permanent; therefore, prevention is key. For most people mercury is the most significant toxicant in the body. By promoting oxidative stress and depleting antioxidant 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 nutrition, 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 starting point for symptom relief. Individualized supplementation may also be helpful to overcome the extreme nutritional depletion and unnatural toxic state.
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• The chronic eects of cumulave,
low-dose mercury exposure
are underrecognized by both
mainstream and alternave health
authories and, consequently, by
the public. Mercury can cause or
contribute to most chronic illnesses,
including neurological disorders,
cardiovascular disease, metabolic
syndrome, chronic fague,
bromyalgia, adrenal and thyroid
problems, autoimmunity, digesve
disorders, allergies, chemical
sensivies, mental illness, sleep
disorders, and chronic infecons
such as Lyme and Candida. Mercury
toxicity should be suspected in
individuals experiencing mulple
health problems.
• Diagnosis of chronic mercury
toxicity is oen dicult because
the body’s natural defenses may
mask or delay symptoms. Natural
defenses are a funcon of genec
suscepbility, epigenec factors,
micronutrient status, and allostac
load (cumulave wear and tear
on the body). Furthermore,
individuals who retain mercury may
counterintuively show low levels in
blood, urine, and hair.
• The developmental window
from concepon through early
childhood is one of extreme
vulnerability to mercury. Mercury
is an epigenec toxicant (aecng
future gene expression) as well as
a neurotoxicant. Damage may be
permanent; therefore, prevenon is
• For most people mercury is the
most signicant toxicant in the
body. By promong oxidave stress
and depleng anoxidant 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 nutrion, 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
starng point for symptom relief.
Individualized supplementaon may
also be helpful to overcome the
extreme nutrional depleon and
unnatural toxic state.
Mercury is an unusually insidious
toxicant that can cause or contribute
to most chronic illnesses. Its eects on
various body systems can be mutually
reinforcing, seng up a complex
process of damage and dysfuncon. For
example, by inhibing the glutathione
system, which is key to detoxicaon,
mercury perpetuates a vicious cycle
of suscepbility and toxicity. As a
result, mercury promotes nutrional
depleon, oxidave stress, hormonal
disrupon, immune alteraon, and
neurotransmier disturbances, which
in turn can cause poor digeson, leaky
gut, food allergies, altered gut ora,
and autoimmunity. Yet, despite its
pervasive ability to damage the body,
mercury easily eludes detecon; and
many aected individuals have no idea
that their unexplained health problems
are due to past or ongoing mercury
Adding to the confusion, symptoms
may manifest dierently in each
person depending on exposures,
lifestyle, genecs, and micronutrient
status. For example, it may manifest
in one person as autoimmune issues
such as Hashimoto’s thyroidis,
mulple sclerosis, or systemic lupus
erythematosus and in someone else as
mood, behavior, learning, or psychiatric
problems. Long latencies may occur
with onset of symptoms somemes
occurring months or years aer the
exposure has ceased.1,2 Many symptoms
are vague, resembling premature
cellular aging. Other symptoms are
more disnct, a case in point being
erethism (a constellaon of personality
traits including midity, didence,
contenousness, insecurity, bluntness,
rigidity, excitability, and hypersensivity
to cricism and to sensory
smulaon).3–5 The term erethism, or
reddening, derives from the person’s
tendency to blush.6 Considering the
subtle but reproducible eects of
mercury on emoons, 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 authories
and agencies about the risks of mercury
The Quintessential Anti-Nutrient
by Sara Russell, PhD, NTP, and
Kristin G. Homme, PE(ret.), MPP, MPH
from roune exposures involving
denstry, sh, and vaccines. Certain
exposure risks are widely discounted by
the mainstream; yet according to the
US Environmental Protecon 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 aect
almost 11% of all US births, up 30%
over the past decade;9 and subclinical
decrements in brain funcon are even
more common, aecng up to 15% of
births.10 However, health authories
are unlikely to provide useful guidance
on mercury risks for several reasons.
Mercury is technically and polically
dicult to study; thus, scienc
conclusions about risks remain couched
in uncertainty. Mercury’s eects are
non-specic and mul-factorial. Finally,
much exposure is iatrogenic – caused
by health care making it an unpopular
body. Being lipophilic, these forms of
mercury leave the bloodstream quickly,
passing through biological membranes
and concentrang 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
parcular anity for the brain, where
it may be retained indenitely.13,14 It
also accumulates in epithelial ssues,
organs, and glands such as the salivary
glands, thyroid, liver, pancreas, tescles,
prostate, sweat glands, and kidneys as
well as the epithelium of the intesnal
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 volale;
consequently, amalgams connuously
o-gas in the mouth. Health authories
have deemed amalgam as safe based
on studies that were designed to detect
only obvious harm, not subtle or long-
term eects. New evidence indicates
that suscepbility (and resistance) to
mercury toxicity is driven by genes, only
a few of which have been idened.16
Furthermore, evidence indicates that
exposure from amalgams is sucient
to cause harm to suscepble people.17
The authors of the mercury chapter
in the most recent metals toxicology
textbook esmate that roughly 1% of
the populaon is incurring clinical illness
from their dental amalgams – and this
is likely to be a gross underesmate
because it excludes cases that have
another diagnosis such as mulple
sclerosis that may have a mercury
The World Health Organizaon
esmates 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 electromagnec radiaon including
from mobile phones and from magnec
resonance imaging (MRI) may increase
the release of mercury vapor from
dental amalgams.21
In 2009, the US Food and Drug
Administraon (FDA) reiterated the
safety of dental amalgam despite much
scienc evidence to the contrary.
As of 2016, public interest groups
are challenging this “nal amalgam
rule” in federal court. Issues to be
ligated 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 densts via
labeling requirements should also be
given to paents. Norway, Denmark,
and Sweden have banned dental
amalgam; and, as of May 2015, a
scienc commiee of the European
Commission recommends that non-
mercury alternaves be used in llings
for pregnant women and children.22
As if the cumulave eects of
ongoing amalgam exposure were not
enough, unsafe amalgam removal can
cause acute exposures to mercury
vapor. Thus, paents wishing to
replace amalgam llings with less toxic
alternaves must evaluate densts’ use
of adequate protecve measures. The
Internaonal Academy of Oral Medicine
and Toxicology (IAOMT), a professional
dental organizaon, has developed
a protocol and training program that
aempts to minimize the exposure to
mercury vapor to the paent, denst,
and sta during amalgam removal. In
women of childbearing age, removal of
amalgam should be med to avoid the
12–18 months preceding concepon as
a well as pregnancy and breaseeding.
Dietary Fish
Mercury released into the
atmosphere through natural and human
acvies is deposited in soil and water
where it enters the food chain. Mercury
accumulates in sh, parcularly 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 poron may contain roughly 1–100
micrograms of methylmercury.
Certain vaccines – 12.5 to 25
micrograms of ethylmercury per
Prenatal exposures – levels are
unknown but clinically signicant.
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 gestaon and
early childhood. These three forms of
mercury are all easily absorbed and
readily distributed throughout the
iA 2012 study showed blunted corsol response and higher
inammatory markers at blood mercury levels well below the 5.8
microgram per deciliter level of concern.
account for 60–70% of the annual
releases of mercury to the atmosphere.
The remaining 30–40% is aributable to
human acvies.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
moderaon. In healthy individuals,
intesnal metallothioneins (a class of
metal-storage molecules that can be
cumulavely damaged by mercury) can
sequester ingested mercury and slowly
allow its excreon. Selenium, discussed
below, is a micronutrient that oers
some protecon 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 lesh,
shark, swordsh, 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 Acon
Level for mercury contaminaon in
commercial sh of 1.0 ppm; this means
that federal ocials are allowed to
conscate the product but not that they
actually do so.
One of the most controversial
aspects surrounding vaccines is their
mercury content. Prior to about 2004,
many childhood vaccines contained
thimerosal, a preservave 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 Prevenon (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-menoned 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 Protecon 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 resulng
dose of 1.04 micrograms per day is sll
signicantly higher than the EPA’s safe
reference dose of 0.3–0.6 micrograms
total per day for methylmercury. In
addion, 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
eects 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 ingeson, including metallothioneins
and selenium, discussed later.
In 1999, the US Public Health Service
called for the eliminaon of thimerosal
from childhood vaccines. Nonetheless,
due to supply and demand issues, it took
several years to transion to reduced-
thimerosal and then thimerosal-free
Addionally, during the period
in which thimerosal began to be
phased out of pediatric vaccines, the
thimerosal-containing inuenza vaccine
became an important exposure source
for fetuses and children. In 2002, the
CDC began recommending that the
inuenza 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 inuenza
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 inuenza vaccines
were sll 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 excepon allowing
thimerosal-containing vaccines to be
administered to infants and children
despite a previous statewide restricon.
Some mul-dose meningococcal
meningis vaccines and tetanus toxoid
(booster) vaccines (not recommended
for children under six years of age), like
the mul-dose inuenza vaccines, also
contain thimerosal as a preservave
in amounts ranging from 12.5 to 25
micrograms per dose.33 As of 2016,
some childhood vaccine preparaons
sll ulize thimerosal. In these vaccines,
such as the mul-dose DTaP and the
DTaP/Hib combinaon 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. Unl
the 1960s, teething powders for babies
contained mercury in the form of
calomel. Thimerosal was used in contact
lens soluons. Merbromin was once
widely used as an ansepc under the
trade name Mercurochrome. In 1998,
such products were banned when
the FDA declared that mercury as an
acve ingredient in over-the-counter
products was not “generally recognized
as safe (GRAS).” Nevertheless, the use
of mercury as an inacve ingredient is
allowed by the FDA provided its content
is under 65 ppm, and FDA regulaons
regarding cosmecs do not obligate
ingredients that make up less than 1%
of the product to be disclosed on the
iiApproximate mercury content of 1990s-era vaccines: Diphtheria-
Tetanus-Pertussis (DTP and DTaP): 4 doses totaling 100 mcg;
Haemophilus inuenzae type B (HIB): 4 doses totaling 100 mcg;
and Hepas B, 3 doses totaling 37.5 mcg. Mul-dose inuenza
vaccines given annually: 25 mcg. Tetanus vaccine: 25 mcg.
label. For instance, some brands of
mascara sll contain thimerosal as an
anmicrobial and preservave.
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
concentraon of this toxic release is
compared to various regulatory safety
standards in Table II. CFL proponents
argue that the energy savings oered by
CFLs, which includes reduced mercury
emissions from coal power plants,
makes them desirable; but this debate is
beyond the scope of this arcle.
Incinerators, coal-red power
plants, crematoria, and other industrial
processes may be signicant 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 amnioc uid, cord
blood, placental ssue, and breast
milk are signicantly 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 Epigenec Toxicity
The developmental period
spanning from concepon through
early childhood is a window of
vulnerability in which both epigenec
and neurological damage can occur
unfortunately, when either parent
is exposed to mercury, even prior to
concepon, the child’s own genec
expression can be aected.
Such epigenec damage may range
from mild to severe, and the resulng
phenotype may include characteriscs
such as dental deformies, myopia,
asymmetries of the face, and
disproporons of the body. Such
characteriscs are described in Weston
A. Price’s pioneering Nutrion and
Physical Degeneraon,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
Tradions Book of Baby and Child
Care43; and in the more epigenecally-
focused Deep Nutrion by Catherine
and Luke Shanahan.44 Within the
alternave health community, the role
of micronutrients is well recognized to
promote physical and mental health as
well as opmal child development. Less
well recognized is the role of toxicity
in depleng one’s micronutrient status
and the analogous role of micronutrient
status in exacerbang or alleviang
Genec Suscepbilies
A loose scienc consensus has
long discounted the idea of mercury
toxicity from dental amalgams because
populaon 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 genec variants
that convey increased suscepbility to
mercury toxicity have been documented
in human studies.45,46 Moreover,
hundreds more variants are likely to
exist. Mercury aacks sulfur in proteins;
and since the body has tens of thousands
of genecally determined sulfur-
containing proteins, many of these
proteins are likely to include variants
that contribute to suscepbility.47
Esmated inial release from typical broken CFL (Johnson et al. 2008)
Some regulatory standards for inhalaon of mercury vapor
US Naonal Instute for Occupaonal Safety and Health (NIOSH)
“Immediately Dangerous to Life or Health” (NIOSH 1994)
US Occupaonal Safety and Health Administraon (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 connuous exposure) (ATSDR 1999)
Table II: Mercury Exposure from Compact Fluorescent
Lamps (CFLs)
micrograms per
meter3 of air
a decade, the EPA has aempted to
restrict mercury emissions from coal
plants in the US by about 90%; but the
rule is under ligaon, 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 signicant source of exposure for
miners and local populaons.
Fetal and Childhood Exposures
Fetal neurons are more sensive
to the toxic eects 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 eects on nerve growth arise at
mercury concentraons equivalent to
at exposures far lower than those
known to cause toxicity in adults.
Epigenecs refers to the alteraon of
gene expression (turning genes on and
o), usually via environmental factors,
in a manner that can be passed to
ospring without alteraon of the DNA
nucleode sequence itself. Mercury
is a potent epigenec toxicant of
alarming scope with both direct and
indirect eects on gene expression.
Mercury directly targets the cysteine
that comprises the DNA-binding sites
on most gene transcripon factors. In
addion, it targets the cysteine in DNA
methyltransferase enzymes, which play
a role (DNA methylaon) in normal
gene expression. Indirectly, mercury
promotes severe oxidave stress and
early-life stressors are known to induce
changes in gene expression that set the
stage for disease in later life.41 Thus,
Candidate genes are involved not only
in methylaon and detoxicaon but
in vitamin and mineral (i.e., enzyme
cofactor) absorpon, transport, and
metabolism. Yet genec suscepbilies
have yet to be considered by policy
makers, health authories, or the dental
industry. Indeed, for millions of children
and adults covered by subsidized dental
programs, military family dental care,
and Nave American services, for
example, amalgam is virtually the only
opon for dental restoraons.
Regarding genec suscepbilies to
vaccine injury, a few isolated court cases
in the US and elsewhere have recognized
post facto that a limited number of well-
documented genec suscepbilies
including some mitochondrial disorders
have caused certain children to suer
permanent neurological damage. But
genec suscepbilies are a connuum,
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
oxidave stress, depletes anoxidant
defenses, and destroys biological
barriers. It causes numerous interacng
eects across mulple organ systems,48
leading to a gamut of health issues
ranging from fague and inammaon
to endocrine and immune dysregulaon
and mood disorders.
Mercury readily binds to sulydryl
(-S-H), a type of sulfur also called a
thiol. The thiol is the major reacve site
within the amino acid, cysteine, which
is ubiquitous in biochemically acve
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 funcon and
brain anoxidant protecon. Selenium
is said to protect against mercury
toxicity, but its protecve 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 oers only limited protecon
against mercury exposure.
The body’s most important
intracellular anoxidant mechanism is
the glutathione system. Because the
glutathione molecule and its related
enzymes employ cysteine, they are
targets for mercury. Specically,
mercury damages the body’s
glutathione system both by depleng
the glutathione molecule itself and by
blocking the enzymes that synthesize
and recycle glutathione and facilitate
its use. Glutathione detoxies mercury
by binding it (in a process called
glutathione conjugaon) into a less
toxic form suitable for excreon through
the bile. Incidentally, the glutathione
system has been found to be crucial in
the detoxicaon of thimerosal.50 By
depleng glutathione and disabling the
glutathione-related enzymes, mercury
impairs the detoxicaon of many
toxicants, including mercury itself,
leading to increased toxicity.
By damaging methylaon enzymes,
including methionine synthase,
mercury dysregulates the methylaon
cycle, a biochemical pathway in
which the sulfur-containing amino
acid methionine is recycled, creang
two important products: s-adenosyl
methionine (SAMe), the body’s universal
methylator; and cysteine, the precursor
for the transsulfuraon pathway,
which in turn produces glutathione,
sulfate, and taurine. By impairing the
methionine synthase enzyme, mercury
blocks not only detoxicaon via the
transsulfuraon pathway that produces
glutathione but also the producon of
many hormones and neurotransmiers
that require methyl donors like SAMe. A
lack of methyl donors also inhibits the
acvity of the DNA methyltransferase
enzymes, which regulate gene
In addion to aacking the sulfur
in enzymes, mercury aacks the sulfur
in the funconal proteins within cell
membranes. These include membrane
transport channels that allow
micronutrients into cells. One result,
for example, is altered homeostasis
of many essenal minerals, which can
appear abnormally high or low on
tesng and is an aspect of many chronic
illnesses that has no other obvious
explanaon. Addionally, mercury may
target the disulde bonds in collagen,
the connecve 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 carlage, both by
impairing the necessary enzymes and by
depleng a required cofactor vitamin
C. Thus mercury can be implicated in
arthris, osteoporosis, and connecve
ssue disorders.
Mercury promotes oxidave stress
in several mutually reinforcing ways.
Within cells, mercury concentrates
in mitochondria, the organelles that
synthesize ATP energy. There, it
displaces iron and copper, converng
them to free radicals with the potenal
to cause ongoing oxidave stress unless
buered by anoxidants. Mercury
also blocks mitochondrial enzymes,
creang an overproducon of reacve
oxygen species, including free radicals.
The resulng oxidave stress further
damages mitochondrial enzymes
as well as harming mitochondrial
membranes and mitochondrial DNA.
Mitochondrial dysfuncon can result in
overproducon of lacc acid, yielding
metabolic acidosis, which depletes
minerals and may promote certain
pathogens. Mitochondrial damage
further drains cellular energy by
creang a disproporonate need for
repair, perpetuang a vicious cycle.51
Mitochondrial dysfuncon aects
immunity, digeson, cognion, and
any energy-intensive system within the
body and is a key component of many
chronic illnesses.
Oxidave stress perpetuates another
vicious cycle in which free radicals cause
lipid peroxidaon, a self-propagang
chain reacon in which the unsaturated
fay acids in cell membranes are
aacked, becoming free radicals
themselves, and ulmately leading to
excess permeability in membranes and
other barriers, thus provoking sll more
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 intesnes.
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-aected people
to suer 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 conspaon,
causing copper to accumulate in the
liver. Addionally, estrogen dominance,
which may be amplied in mercury-
aected individuals due to common
hormonal imbalances, causes copper
retenon. Estrogen dominance is
common, especially in women, due to
exposure to plascs, 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 antagonisc, the more that copper
is retained by the body, the more that
zinc tends to be depleted.
Mercury-induced anomalies in
the transport of essenal minerals
such as magnesium and zinc cause
an extra need for these minerals in
the diet. Furthermore, many health
condions caused by mercury toxicity
are aggravated by low magnesium
and/or zinc including cardiovascular
disease, bromyalgia, ausm spectrum
disorders, aenon decits, and
depression. Not every person with a
history of mercury exposure is decient
in all of these nutrients, however; and it
is important to note that minerals have
complex synergisc and antagonisc
relaonships. For example, low zinc is
oen accompanied by high copper, and
low magnesium is oen accompanied
by high calcium in so ssues.
Mercury’s toxicity may be amplied
by exposure to other toxic metals,
including lead, cadmium, and aluminum.
Mercury and lead, in parcular, are
highly synergisc. In fact, in one study,
a dose of mercury sucient to kill 1%
of the lab rats (lethal dose “LD01”)
when combined with a dose of lead
sucient 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 anbiocs have
been shown to enhance the uptake,
retenon, and toxicity of mercury.54
Addionally, testosterone appears
to aggravate mercury toxicity during
development while estrogen protects
against it.55 In fact, more boys than girls
are diagnosed with ausm spectrum
disorders and aenon decit.
Ausm, Aenon Decit and Other
Neurological Disorders
Many scienc studies suggest
a connecon between mercury and
ausm spectrum disorder (ASD), yet
the subset of studies cited by health
authories 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. Ausm is documented to
involve oxidave stress, mitochondrial
dysfuncon, immune or inammatory
processes, impaired sensory processing,
and abnormal mineral homeostasis, all
of which are consistent with mercury
toxicity.58 Ausc children have been
found to have signicantly higher
exposure to mercury during fetal
development and early infancy, as
measured by metals in baby teeth.59 The
element most frequently decient 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
somemes be dicult to detect through
tesng, as described later.
Aenon decit disorder (ADD) and
aenon decit hyperacvity disorder
(ADHD) are common early ndings
in mercury-exposed children.61 Zinc
deciency has been idened as a
biomarker for ADHD62; and the abnormal
mineral prole for ADHD appears quite
similar to that for ausm and mood
disorders, with the excepon that
ADHD typically includes iron overload.
Addionally, copper dysregulaon is a
key factor in ADHD.63
Many studies report a close
associaon between clinical depression
and zinc deciency 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, Touree syndrome, and
borderline personality disorder as
well as neurodegenerave disorders –
Alzheimer’s, Parkinson’s and Mulple
Sclerosis, for example. Each has been
documented to involve oxidave
stress, inammaon, mitochondrial
dysfuncon, and mineral imbalances; all
of which can be aributed 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 sasfy skepcs;
but a growing body of evidence suggests
that mercury plays a major role.65
Exacerbang the mineral
dysregulaon associated with
these many condions are the
neurotransmier imbalances provoked
by mercury. For example, mercury
increases extracellular levels of the
excitatory neurotransmier glutamate,
thus overacvang glutamate receptors
on cell surfaces.66 The amplicaon
of glutamate is further exacerbated
by mercury’s inhibion of the
calming neurotransmier GABA67:
Mercury blocks GABA receptors; it
disproporonately destroys GABA-
producing Purkinje neurons; and it
impairs glutamate decarboxylase (GAD),
the enzyme responsible for converng
glutamate to GABA. Furthermore,
mercury’s dysregulaon of glutamate
and GABA is associated with depression
and suicide.68–70
Altered Microbiota, Digesve
Dysfuncon and Immune Health
Mercury is known to alter the
intesnal microbiota, yielding increased
levels of undesirable mercury-resistant
bacterial species, which may also
develop resistance to anbiocs.71–73
For example, the opportunisc yeast
Candida albicans may overgrow, causing
a host of unpleasant symptoms. This
dysbiosis may be exacerbated by
mercury’s dysregulaon of the immune
system as well as its promoon of
metabolic acidosis. All this has negave
implicaons for digeson, immunity,
and mental health.74–76
Mercury also inhibits several
enzymes aecng digeson including
gastric hydrogen-potassium-ATPase,
the enzyme that allows the synthesis
of hydrochloric acid via the stomach’s
proton pump. In addion, by
promong oxidave stress, mercury
moves the autonomic nervous system
into sympathec (stress) mode,
inhibing digeson. Furthermore, the
mitochondrial dysfuncon from which
many mercury-aected individuals
suer impairs digeson as well as other
bodily funcons. 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, parally
digested proteins in foods containing
gluten and casein may be metabolized
into the opioid pepdes gluteomorphin
and casomorphin.77 This is oen seen in
children with ausm spectrum disorder
and explains many parental reports of
symptom relief on a gluten-free, casein-
free diet.
Mercury’s eects on the gut can
exacerbate mercury’s eects on the
immune system. Mercury is known
to cause allergies, reduced immunity,
and autoimmunity78; and such immune
dysfuncon plays a role in many chronic
illnesses. Reduced immunity yields
suscepbility to chronic infecons
such as Lyme and Candida. Finally,
although technically not an allergy,
mulple chemical sensivies can result
from mercury overloading the body’s
detoxicaon 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
Thyroid Disorders, Hypothalamus-
Pituitary-Adrenal Dysfuncon, and
Stress-Related Disorders
Mercury is known to concentrate
in glands, including the thyroid
and pituitary, and to impair the
(HPA) axis. HPA funcon and thyroid
funcon are ghtly interrelated, with
impairment of one system oen causing
impairment of the other. Mercury blocks
the selenium-dependent enzyme that
converts the thyroid hormone, thyroxine
(T4), to its acve form, triiodothyronine
(T3). Unfortunately, despite symptoms,
the resulng hypothyroidism oen goes
undetected by roune 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 funcon
is the mercury-induced depleon of
selenium and zinc, which are cofactors
for thyroid enzymes.
The oxidave 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
fague. Incidentally, an evolving view
of this condion suggests that it is not
a glandular problem, but rather a brain-
stress problem.79 Early-life exposure to
mercury also causes epigenec damage
to the HPA axis, which can dysregulate
the stress response throughout life.
This may involve a tendency toward
either high or low baseline corsol as
well as a loss of the dynamic corsol
response to stress.80 The laer yields
a disabling feeling of unwellness
and stress intolerance. High baseline
corsol, on the other hand, may feel
less debilitang, but this is a catabolic
state that can promote degeneraon of
otherwise healthy ssues.
Metabolic Disorders, Obesity, and
Cardiovascular Disease
HPA dysregulaon and thyroid
dysfuncon strongly impact metabolism
and weight. As an epigenec 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 generaons. In
addion, 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 reect 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, promong high insulin
and thus fat storage. Mercury can cause
weight gain or weight loss, depending
on whether metabolic dysregulaon or
gut dysfuncon 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
dysfuncon in blood vessels.81
Mercury can cause high or low blood
pressure depending on whether artery
calcicaon or artery deterioraon and
HPA dysfuncon predominate. Finally, in
a remarkable example of how mercury
accumulates in certain ssues, a biopsy
study of 13 paents with a type of heart
failure found that mercury levels in the
myocardium were 22,000 mes higher
than normal.82
Mercury damage creates a need for
extra nutrion, both to repair damage
and to prod blocked enzymes. Nutrient-
dense diets are of crical importance,
and targeted supplementaon may help
to overcome the unnatural toxic state.
Because everyone’s nutrient status is
uniquely aected by mercury, it is wise
to take an individual approach rather
than supplement all potenally depleted
nutrients across the board. In addion,
dietary modicaons are somemes
necessary to control the inammaon
and other symptoms that result from
food sensivies, which are common in
aected individuals. Also, eang foods
to which we are allergic or intolerant
impairs detoxicaon by placing undue
stress on the organs of digeson and
eliminaon, pung the HPA axis
on alert, and increasing the level of
inammaon in the body. It is common
for people with mercury toxicity to have
mulple food sensivies, parcularly
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.
Addionally, because both brain ssue
and the phospholipid bilayer of the cell
membrane are built in large part from
saturated fat, consumpon of grass-fed
animal fats such as lard, tallow, ghee,
and buer 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 addion to slowing
energy producon, 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 lecns.
Bone broth is ideal for repairing the
digesve lining and connecve ssue,
and for supplying easily assimilated
amino acids and other nutrients.
Daily consumpon of bone broth
can help repair the excessive gut
permeability that oen 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 producon of glutathione.
Vitamin B6 and magnesium may ease
the conversion of glutamate to GABA.83
In the event of sensivity 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 excreon of
mercury and other toxicants through
the bile, parcularly in individuals who
tend to be conspated. Other probioc
foods, such as sauerkraut, are also
helpful as part of a healing program.
It is a good idea to start with a small
amount of probioc 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 anoxidant and
immune-modulang benets. Vitamin
C helps rebuild damaged collagen and
can be obtained from a variety of food
sources as tolerated, taking care not
to rely enrely on the sweeter fruits,
which can be problemac for people
with blood sugar issues. Good sources
of the vitamin include rose hips, guava,
acerola cherry, lemons, limes, oranges,
grapefruit, kale, broccoli, cauliower,
Brussels sprouts, papaya, mango,
pineapple, kiwi, and strawberries.
People who suer from thiol sensivity,
discussed below, will need to avoid or
limit the vegetables included on the list.
Because grapefruit can smulate phase
II of the liver’s detoxicaon and slow
down phase I, it is wise to consume
grapefruit only occasionally unless
phase I is already known to be overly
acve with respect to phase II.
The two minerals most commonly
depleted by mercury are magnesium
and zinc. Liver, leafy green vegetables,
neles, properly soaked lenls (if
tolerated), and properly prepared
almonds are good sources of
magnesium. Neles 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 crical, 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-aected people, keeping in
mind that we absorb zinc much more
eciently 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
potenally problemac 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 consumpon of sh, the
evidence suggests that once the body’s
natural defenses have been overrun by
mercury the selenium in seafood is less
eecve in buering the mercury. Thus,
people who know or suspect a mercury
problem must consider the benets
and the risks in determining their sh
consumpon 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 nutrional benets of sh while
keeping mercury exposure as low as
Eliminaon and reintroducon of
suspect foods is the best way to assess
whether these foods are problemac
for an individual. The goal is the least
restricve nutrient-dense diet. For
example, many children and adults
with mercury toxicity benet from
a gluten-free, casein-free diet while
others can tolerate one or both of
these foods. Addional intolerances
too numerous to list aect certain
mercury-toxic individuals to varying
degrees. The intake of alcohol, sugar,
rened starches, processed foods,
caeine, medicaons, etc. reduces
the body’s ability to detoxify, causing
unpleasant symptoms in many aected
individuals. Addionally, the common
intolerance to sultes in wine suggests
impairment of the sulte oxidase
enzyme needed to convert toxic sulte
to benecial sulfate. This enzyme
can be boosted by supplemenng its
cofactor, molybdenum. Also, because
mercury blocks metabolic enzymes
such as phenolsulfotransferases, certain
food compounds, such as phenols,
become parally metabolized into
toxic intermediates, oen resulng in
reacons such as red cheeks and/or ears
and hyperacvity aer consuming foods
high in phenol.84 Addionally, yeast
overgrowth can increase sensivity 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-aected individuals,
parcularly if the transsulfuraon
pathway is compromised, as can occur
with molybdenum deciency. 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
essenal amino acids, including those
that contain sulfur. Andrew Cutler,
author of Amalgam Illness: Diagnosis
and Treatment (see Resources, below)
and Hair Test Interpretaon: Finding
Hidden Toxicies notes that foods high
in free thiol can provoke symptoms in a
signicant subset of mercury-aected
people, in part by increasing plasma
cysteine, which may rise in response
to mercury and its biochemical eects.
Vegetarian diets are parcularly
deleterious to a signicant subset of
people suering from mercury toxicity
because it is virtually impossible to
obtain sucient protein on a vegetarian
diet that is modied to reduce free-thiol
A problemac food for many
mercury-toxic individuals is cilantro leaf,
which contains a chelang substance
capable of redistribung mercury, thus
exacerbang symptoms in sensive
individuals. Unfortunately, within the
alternave health community, cilantro
leaf is somemes recommended
in large amounts in both food
and supplement form. Also oen
recommended is chlorella, which is
inadvisable as a supplement due to its
potenal for contaminaon from the
environment in which it is grown and
to its lipopolysaccharide content, which
can cause inammatory stress.85
Each mercury-toxic person has
a unique combinaon of mineral
imbalances that aect how mercury
toxicity is expressed and what parcular
nutrient combinaon is likely to
provide relief. Mineral dysregulaon
is signicantly more pronounced in
people with chronic mercury toxicity
than in the general populaon,86 as are
other nutrional deciencies and food
Tesng for mercury toxicity is
not straighorward. 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 administraon
of a chelator in a dosage high enough to
cause signicant oxidave stress due to
redistribuon 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
negaves is high unless the sample is
handled carefully. A hair elements test
can reveal apparent dysregulaon of
essenal mineral homeostasis i.e.,
essenal 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 essenal minerals are
dysregulated, a high level of an essenal
mineral may not indicate adequate
intracellular status but may simply
mean high excreon in hair.
It is beyond the scope of this
nutrion-focused arcle to discuss
mercury treatment opons, but we
recommend cauon when considering
detoxicaon 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 nutrional
supplements without warning about
its metal chelang properes. 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 aempt 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 detoxicaon
read the books by Andrew Cutler listed
in the Resources secon. Cutler’s work is
the most useful compilaon of science-
based explanaons of mercury toxicity
and its myriad eects. It should be
noted that Cutler’s chelaon protocol,
though grounded in scienc theory, is
controversial and is not without risk.
Because of mercury’s powerful
an-nutrient eects, a nutrient-dense
diet may alleviate many symptoms of
chronic mercury toxicity. Moreover,
the nutrional depleon caused by
mercury is so pervasive that aected
individuals oen require nutrional
supplementaon as well as a nutrient-
dense diet. At the same me, it’s
important to note that many mercury-
aected individuals are quite sensive to
a large number of foods, supplements,
and medicaons. 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 mulple health problems may
suer from undiagnosed chronic
mercury poisoning. Mercury depletes
nutrients needed for vital funcons
and dysregulates mineral and
neurotransmier metabolism to a
greater extent than any other common
Yet chronic mercury toxicity
remains underrecognized by both
mainstream and alternave health
authories for a number of reasons.
The scienc literature on mercury is
complicated, incomplete, and easily
misinterpreted. Mercury demonstrates
a complex, nonlinear toxicity. Mercury
suscepbility depends on genecs,
epigenecs, and micronutrient status.
The body’s natural defenses may mask
toxicity, creang long latencies between
exposures and symptoms. Symptoms
are varied and nonspecic and may be
intermient in the early stages. Mercury
research is controversial because much
exposure has been iatrogenic, via dental
amalgams and vaccine preservaves.
Toxicity tesng is not straighorward,
as described above. In summary, the
combinaon of ubiquitous exposures,
iatrogenic involvement, long latencies,
broad toxic eects, nonspecic
symptoms, and potenally irreversible
damage renders chronic mercury
toxicity an underrecognized epidemic.
• - Internaonal Academy of Oral Medicine
and Toxicology, a professional dental associaon that
provides fact sheets about mercury and describes the
Academy’s safe amalgam removal protocol
• - a joint project of IAOMT and
CoMeD (Coalion for Mercury-Free Drugs), which
advocates removal of mercury from all vaccines
• - Dental Amalgam Mercury Soluons,
a non-prot organizaon dedicated to educang
consumers about unhealthy dental pracces
• Amalgam Illness: Diagnosis and Treatment (1999) by
Andrew Hall Cutler. This book is sll the most complete,
science-based, self-help book on chronic mercury
toxicity to date. Available through the author’s website
at 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 rendion
some may nd more readable.
sulfur-sulphur-food-list/ - a resource that explains why
some people with mercury toxicity cannot tolerate thiols
and how to idenfy thiol intolerance.
Sara Russell is a Nutrional Therapy Praconer, Cered GAPS
Praconer, and Weston A. Price chapter leader residing in Italy.
Sara works via phone and Skype with clients worldwide, specializing
in ferlity, pregnancy, and young children. You can learn more about
Sara’s work at hp://
Krisn Homme, MPP, MPH, is a rered engineer turned science writer who has authored
several scienc arcles in peer-reviewed journals.
• hp:// - 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 cosmecs.
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 arcle at various stages of its draing and revision.
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G. Amalgam studies: disregarding basic principles of
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17. Ibid.
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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 hp://
UCM096228#t1 and the Naonal Vaccine Informaon
Center (NVIC) Frequently Asked Quesons on the topic
of “Thimerosal in Vaccines” at hp://
mercury-thimerosal.aspx (both accessed Jan 12, 2016).
34. CDC brochure: Understanding Thimerosal, Mercury
and Vaccine Safety. Revised 2013. hp://www.cdc. gov/
vacsafe-thimerosal-color-oce.pdf. Accessed January 12,
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36. Berlin Ibid.
37. Ibid.
38. Ibid.
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ResearchGate has not been able to resolve any citations for this publication.
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We live in the world of unfolding epidemics. Autistic Spectrum Disorders, Attention Deficit Hyperactivity Disorder (ADHD/ADD), schizophrenia, dyslexia, dyspraxia, depression, obsessive -compulsive disorder, bipolar disorder and other neuro-psychological and psychiatric problems in children and adults are becoming more and more common. In clinical practice these conditions more often than not overlap with each other. A patient with autism often is hyperactive and dyspraxic. There is about 50% overlap between dyslexia and dyspraxia and 25-50% overlap between hyperactivity and dyslexia and dyspraxia. Children with these conditions are often diagnosed as being depressed and as they grow up they are more prone to drug abuse or alcoholism than their typically developing peers. A young person diagnosed with schizophrenia would often suffer from dyslexia, dyspraxia or/and ADHD/ADD in childhood. Schizophrenia and bipolar disorder are often described as two sides of one coin. We have created different diagnostic boxes to fit our patients in, but a modern patient does not fit into any one of them neatly. The modern patient in most cases fits into a rather lumpy picture of overlapping neurological and psychiatric conditions. This picture leads us to the fact that these conditions are related to each other by similar underlying causes. Let us discuss what these causes may be. What is a typical scenario we see in clinical practice? Before examining the patient it is very important to look at the health history of the parents. Whenever the parents are mentioned people immediately think about genetics. However, apart from genetics there is something very important the parents, mother in particular, pass to their child: their unique gut micro-flora. Not many people know that an adult on average carries 2 kg of bacteria in the gut. There are more cells in that microbial mass than there are cells in an entire human body. It is a highly organised micro-world, where certain species of bacteria have to predominate to keep us healthy physically and mentally. Their role in our health is so monumental, that we simply cannot afford to ignore them. We will talk in detail about the child's gut flora later. Now let us come back to the source of the child's gut flora - the parents. After studying hundreds of cases of neurological and psychiatric conditions in children and adults, a typical health picture of these children's mums has emerged.
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Thimerosal (or Thiomersal) is a trade name for an organomercurial compound (sodium ethyl-mercury (Hg) thiosalicylate) that is 49.55% Hg by weight, which rapidly decomposes in aqueous saline solutions into ethyl-Hg hydroxide and ethyl-Hg chloride. Developed in 1927, it has been and is still being used as a preservative in some cosmetics, topical pharmaceuticals, and biological drug products, including vaccines. Concerns have been voiced about its use because it is toxic to human cells. Although it is banned in several countries, it continues to be added to some vaccines in the United States and many vaccines in the developing world. This critical review focuses on the clinical, epidemiological, and biochemical studies of adverse effects from Thimerosal in developing humans. This review will include research that examines fetal, infant, and childhood death; birth defects; neurodevelopmental testing deficits in children; and neurodevelopmental disorders (attention deficit/hyperactivity disorder, autism spectrum disorder, tic disorder, and specific developmental delays). The review will also look at the research that examined the outcomes of acute accidental ethyl-Hg poisoning in humans. The studies that examine the underlying biochemical insights into the neuronal cellular damage will also be explored. The culmination of the research that examines the effects of Thimerosal in humans indicates that it is a poison at minute levels with a plethora of deleterious consequences, even at the levels currently administered in vaccines. Copyright © 2015. Published by Elsevier B.V.
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The purpose of this review is to examine the evidence for a relationship between mercury (Hg) exposure from dental amalgams and certain idiopathic chronic illnesses - chronic fatigue syndrome (CFS), fibromyalgia (FM), depression, anxiety, and suicide. Dental amalgam is a commonly used dental restorative material that contains approximately 50% elemental mercury (Hg0) by weight and releases Hg0 vapor. Studies have shown that chronic Hg exposure from various sources including dental amalgams is associated with numerous health complaints, including fatigue, anxiety, and depression - and these are among the main symptoms that are associated with CFS and FM. In addition, several studies have shown that the removal of amalgams is associated with improvement in these symptoms. Although the issue of amalgam safety is still under debate, the preponderance of evidence suggests that Hg exposure from dental amalgams may cause or contribute to many chronic conditions. Thus, consideration of Hg toxicity may be central to the effective clinical investigation of many chronic illnesses, particularly those involving fatigue and depression.
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Mercury (Hg) is neurotoxic, and children may be particularly susceptible to this effect. A current major challenge is identification of children who may be uniquely susceptible to Hg toxicity because of genetic predisposition. We examined the possibility that common genetic variants that are known to affect neurologic functions or Hg handling in adults would modify the adverse neurobehavioral effects of Hg exposure in children. Three hundred thirty subjects who participated as children in the recently completed Casa Pia Clinical Trial of Dental Amalgams in Children were genotyped for 27 variants of 13 genes that are reported to affect neurologic functions and/or Hg disposition in adults. Urinary Hg concentrations, reflecting Hg exposure from any source, served as the Hg exposure index. Regression modeling strategies were employed to evaluate potential associations between allelic status for individual genes or combinations of genes, Hg exposure, and neurobehavioral test outcomes assessed at baseline and for 7 subsequent years during the clinical trial. Among boys, significant modification of Hg effects on neurobehavioral outcomes over a broad range of neurologic domains was observed with variant genotypes for 4 of 13 genes evaluated. Modification of Hg effects on a more limited number of neurobehavioral outcomes was also observed for variants of another 8 genes. Cluster analyses suggested some genes interacting in common processes to affect Hg neurotoxicity. In contrast, significant modification of Hg effects on neurobehavioral functions among girls with the same genotypes was substantially more limited. These observations suggest increased susceptibility to the adverse neurobehavioral effects of Hg among children, particularly boys, with genetic variants that are relatively common to the general human population. These findings advance public health goals to identify factors underlying susceptibility to Hg toxicity and may contribute to strategies for preventing adverse health risks associated with Hg exposure.
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There are over 165 studies that have focused on Thimerosal, an organic-mercury (Hg) based compound, used as a preservative in many childhood vaccines, and found it to be harmful. Of these, 16 were conducted to specifically examine the effects of Thimerosal on human infants or children with reported outcomes of death; acrodynia; poisoning; allergic reaction; malformations; autoimmune reaction;Well’s syndrome; developmental delay; and neurodevelopmental disorders, including tics, speech delay, language delay, attention deficit disorder, and autism. In contrast, the United States Centers for Disease Control and Prevention states that Thimerosal is safe and there is “no relationship between [T]himerosal[-]containing vaccines and autism rates in children.” This is puzzling because, in a study conducted directly by CDC epidemiologists, a 7.6-fold increased risk of autism from exposure to Thimerosal during infancy was found.The CDC’s current stance that Thimerosal is safe and that there is no relationship between Thimerosal and autism is based on six specific published epidemiological studies co-authored and sponsored by the CDC. The purpose of this review is to examine these six publications and analyze possible reasons why their published outcomes are so different from the results of investigations by multiple independent research groups over the past 75+ years.
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Neurodegeneration is a broadly defined term that describes the loss of neuronal structure and function, and produces disorders known as neurodegenerative diseases. A common feature of neurodegeneration is the progressive cell loss in specific neuronal populations of the central nervous system (CNS), often associated with cytoskeletal protein changes that led to intracytoplasmic and/or intranuclear inclusions in neurons and/or glia. The neurological consequences of neurodegeneration in patients are often devastating and result in severe mental and physical effects, accounting for a large number of hospitalizations and disabilities. Although the causes of the majority of neurodegenerative diseases are still unknown, it has become increasingly clear that the major basic processes that induce neurodegeneration are multifactorial ones that are caused by genetic, endogenous, and environmental factors. Protein misfolding and aggregation, oxidative stress, mitochondrial dysfunction, and phosphorylation impairment are the major shared neurodegenerative pathogenic processes (Jellinger 2003).
Over the past decades, the use of common sources of electromagnetic fields such as Wi-Fi routers and mobile phones has been increased enormously all over the world. There is ongoing concern that exposure to electromagnetic fields can lead to adverse health effects. It has recently been shown that even low doses of mercury are capable of causing toxicity. Therefore, efforts are initiated to phase down or eliminate the use of mercury amalgam in dental restorations. Increased release of mercury from dental amalgam restorations after exposure to electromagnetic fields such as those generated by MRI and mobile phones has been reported by our team and other researchers. We have recently shown that some of the papers which reported no increased release of mercury after MRI, may have some methodological errors. Although it was previously believed that the amount of mercury released from dental amalgam cannot be hazardous, new findings indicate that mercury, even at low doses, may cause toxicity. Based on recent epidemiological findings, it can be claimed that the safety of mercury released from dental amalgam fillings is questionable. Therefore, as some individuals tend to be hypersensitive to the toxic effects of mercury, regulatory authorities should re-assess the safety of exposure to electromagnetic fields in individuals with amalgam restorations. On the other hand, we have reported that increased mercury release after exposure to electromagnetic fields may be risky for the pregnant women. It is worth mentioning that as a strong positive correlation between maternal and cord blood mercury levels has been found in some studies, our findings regarding the effect of exposure to electromagnetic fields on the release of mercury from dental amalgam fillings lead us to this conclusion that pregnant women with dental amalgam fillings should limit their exposure to electromagnetic fields to prevent toxic effects of mercury in their fetuses. Based on these findings, as infants and children are more vulnerable to mercury exposures, and as some individuals are routinely exposed to different sources of electromagnetic fields, we possibly need a paradigm shift in evaluating the health effects of amalgam fillings.
Fetal development is a critical period for shaping the lifelong health of an individual. However, the fetus is susceptible to internal and external stimuli that can lead to adverse long-term health consequences. Glucocorticoids are an important developmental switch, driving changes in gene regulation that are necessary for normal growth and maturation. The fetal hypothalamic-pituitary-adrenal (HPA) axis is particularly susceptible to long-term programming by glucocorticoids; these effects can persist throughout the life of an organism. Dysfunction of the HPA axis as a result of fetal programming has been associated with impaired brain growth, altered behaviour and increased susceptibility to chronic disease (such as metabolic and cardiovascular disease). Moreover, the effects of glucocorticoid-mediated programming are evident in subsequent generations, and transmission of these changes can occur through both maternal and paternal lineages.
Many neurodegenerative and neuropsychiatric disorders have been reported to coincide with the dysregulation of metal ions in the body and central nervous system. However, in most cases, it is not the imbalance of a single divalent metal ion but a plethora of metal ions reported to be altered. Given that different divalent metal ions are often able to bind to a protein in a competitive manner, although with different affinities, and that they might use similar transporters for uptake and regulation, it is likely that the imbalance of one metal ion will downstream affect the homeostasis of other metal ions. Thus, based on this assumption, we hypothesize that the dysregulation of a specific metal ion will lead to a characteristic biometal profile. Similar profiles might therefore be detected in various neurological disorders. Moreover, if such shared biometal profiles exist across different neurological disorders, it is possible that shared behavioural impairments in these disorders result from the imbalance in metal ion homeostasis. Thus, here, we evaluate the reported excess or deficiency of metal ions in various neurological disorders and aim to integrate reported alterations in metal ions to generate a characteristic biometal profile for the disorder. Based on this, we try to predict which alterations in biometals will be caused by the overload or deficiency of one particular metal ion. Moreover, investigating the behavioural phenotypes of rodent models suffering from alterations in biometals, we assess whether a shared behavioural phenotype exists for disorders with similar biometal profiles. Our results show that observed behavioural aspects of some neurological disorders are reflected in their specific biometal profile and mirrored by mouse models suffering from similar biometal deregulations.
Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children worldwide, and some diagnoses seem to be increasing in frequency. Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants-manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy. Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these efforts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.