Neurological and Immune Reactive
Conditions Affecting Kids:
The mercury connection to neurological pervasive developmental disorders
(autism, schizophrenia, dyslexia, ADD,
childhood depression, learning disabilities, OCD, etc.)
and developmental immune conditions (eczema, asthma, and allergies)
Bernard Windham- Chemical Engineer
http://www.home.earthlink.net/~berniew1/kidshg.html
The incidence of neurotoxic, allergic, and immune reactive
conditions such as autism, schizophrenia, ADD, dyslexia, allergies, asthma,
eczema, psoriasis, childhood diabetes, etc. have been increasing rapidly in
recent years(1,2,3,5,23,50,52,75,82,86).
A recent report by the National Research Council found that 50% of all
pregnancies in the U.S. are now resulting in prenatal or postnatal mortality,
significant birth defects, developmental disabilities or otherwise chronically
unhealthy babies(3). There has been a similar sharp increase in developmental
disabilities in Canadian children over the last 2 decades(71),
including learning disabilities and behavioral problems, asthma and allergies,
and childhood cancer. Exposure to toxic chemicals or environmental factors
appear to be a major factor in much of the developmental problems of the 4
million U.S. children born each year(3,1,2), with at least 1
in 6 having one of the neurological conditions previously listed(1-3).
U.S. EPA has estimated that over 3 million of these are
related to lead or mercury toxicity, with at least 25% of U.S. kids getting
mercury exposure at dangerous levels (1,81).
The U.S. Dept. Of Education indicates that over 5 million children attending
school have neurological related disabilities reported by state agencies, other
than ADD(2a). According to the American Academy of Pediatrics
between 4 to 12 % of all school age children are affected by ADHD(4) and a
similar number have some degree of dyslexia(1). However large
surveys of elementary level student records finds much higher levels- with over
20% of elementary school boys in some areas being treated for ADD(75).
Studies have found that long term use of stimulent drugs commonly causes
significant adverse neurological and health effects(76), and
options are available to deal with such conditions without such adverse effects
including dealing with the underlying causes. Estimates of the percentage of
children with mood or anxiety orders are as much as 20%. Studies indicate that
over 60,000 children are born each year with neurodevelopmental impairments due
to prenatal exposure to methyl mercury (45,46),
and two other sources of mercury exposure appear more common and at higher
levels than this, mercury from vaccines and amalgam dental fillings(22,50,81).
A study at the U.S. CDC found "statistically significant
associations" between neurologic developmental disorders such as autism,
attention deficit disorder(ADD) and speech disorders with exposure to mercury
from thiomersal-containing vaccines before the age of 6 months (62,80).
An analysis of the U.S. CDC VAERS database for adverse reactions from vaccines
regarding effects of the diptheria-tetanus-pertusis vaccine found that those
receiving DTaP and DTucP vaccines with thimerosal had significantly higher rates
of autism, speech disorders, and heart arrest than those receiving DtaP vaccine
without thimerosal, and that the rate of these increase exponentially with dose(81).
An analysis of the U.S. Dept. of Education report on the prevalence of various
childhood conditions among school children found that the rate of autism and
speech disorders increased with increasing levels of thimerosal exposure from
vaccines(81).
Changes in birth proceedures in hospitals such as
immediate cord clamping has also been found to be a factor in the increase in
neurological developmental problems(83).
Also according to the U.S. FDA, at least 26 million have
allergies, at least 17 million have asthma, 15 million have systemic eczema, and
childhood diabetes is increasing rapidly(82). Although Russian and U.S. studies
from the 1980s found that thimerosal was highly toxic and recommended thats its
use as a medical preservative should be discountinued(70,79) , its use was not
discontinued. One study(60a) found 5 times higher rate of allergy among a group
vaccinated with pertussis vaccine(DPT) as opposed to an unvaccinated group, and
2 other studies(60bc) found increased asthma, allergies, and eczema among the
vaccinated group. Over the last 20 years the percent of diabetes cases below 20
years old has increased from 2% to over 30%, and there was a 70% in cases under
40 years of age between 1990 and 1998(50,52,59). Studies in the U.S. and Sweden
have confirmed vaccinations to be a major factor in the increased diabetes
cases(52). Currently approx. 16 million have diabetes. DPT vaccinations have
also been linked to sudden enfant death syndrome(SIDS)(61). DPT vaccines are
mostly given at 2, 4, and 6 months of age and 85% of SIDS cases occur during
this age span. One study found babies die at a rate 8 times the normal rate
within 3 days of DPT shots(60a), while another found that among SIDS victims 61%
had DPT within the 2 previous weeks and 13% within 24 hours of DPT
vaccination(60c). A monitoring study of infant breathing patterns after DPT
vaccinations showed large increases in breathing difficulties including episodes
of ceased breathing, which continued for months after DPT in some cases(61b).
Some cases of seizures after DPT were also observed. Another study found
significantly higher rates of heart arrest in those getting DpaT vaccines with
mercury thimerosal compared to those without(81). Prenatal exposure to mercury
has also been found to predispose animals and infants to seizures and
epilepsy(85).
Mercury has been found to cause an increase in
inflammatory Th2 cytokines(58). In the pancreas, the cells responsible for
insulin production can be damaged or destroyed by the chronic high levels of
cytokines, with the potential of inducing type II diabetes - even in otherwise
healthy individuals with no other risk factors for diabetes(52). Mercury
inhibits production of insulin and is a factor in diabetes and hypoglycemia,
with significant reductions in insulin need after replacement of amalgam filings
and normalizing of blood sugar(52,22). In addition to this mechanism, other
links between vaccines and diabetes have also been found and there is evidence
vaccines are the number one cause of Type I diabetes in young children(52).
The largest increase in neurological and immune conditions
has been in infants (1,2,5-7,23,4,50,81), with an increase in autism cases to
over 500,000 (1,2,23,22,86), an over 900% increase to a level of approx. 1 per
500 infants in the last decade(2ab), making it the 3rd most common chronic
childhood condition. For 1999 through 2002, the number of professionally
diagnosed in California with full syndrome autism has doubled(2e,86). There have
been similar increases in ADD and dyslexia to over 10 million, similar large
numbers(over 10%) with childhood depression or anxiety, and over 10 % of
infants- approximately 15 million in the U.S. with systemic eczema(1,2,82).
Studies researching the reason for these rapid increases in infant reactive
conditions seem to implicate earlier and higher usage of vaccines containing
mercury(thimerisol) as a likely connection (2cd,23,30,40,80,81). A recent study
comparing pre- and post-vaccination mercury levels, found a significant increase
in both preterm and term infants after vaccination(42), with post-vaccination
mercury levels approximately 3 times higher in the preterm infants as compared
with term infants. The study found mercury blood levels up to 23.6 ug/L and
received an average dose of 16.7 ug/kg. Just this one vaccination gave an
exposure to mercury that is many times the U.S. ATSDR adult minimum risk
level(MRL) for mercury of .3/ug/kg body weight per day(41,81).
It has been estimated that if all of the vaccines
recommended by the American Assoc. of Pediatrics are given and contain
thimerisol, then by age 6 months an infant would have received 187 micrograms of
ethyl mercury which is more than the EPA/ATSDR health standard for organic
mercury(33,41,81) and by age 3 the typical child has received over 235
micrograms of mercury thimerisol from vaccinations which is considerably more
than Federal mercury safety guidelines(41,81), in addition to significant levels
from other sources for many(23). Infants during this period have undeveloped
blood brain barriers and much of the mercury goes to the brain, resulting in
significant adverse neurological effects in those that are most susceptible
(43,3). The bioaccumulation in the brain and toxic effects of ethyl mercury are
comparable to that of methyl, with mercury accumulation in the brain and
physical effects actually being more extensive(79).
Because of the evidence the FDA has completed a study and
written a letter to vaccine manufacturers asking that mercury be removed from
vaccines. The updated letter stated, "The Center for Biologics Evaluation and
Research (CBER) has completed its evaluation of the use of thimerisol in
vaccines.. Our review concluded that reducing or eliminating thimerisol from
vaccines is merited(44). The letter pointed to a joint
statement by the American Academy of Pediatrics and the United States Public
Health Service in 1999, which "called for the
removal of thimerisol from vaccines as soon as possible."
A Congressional Committee after holding a hearing has also called for
elimination of mercury in vaccines as soon as possible.
Many thousands of parents have reported that their child
got such conditions after vaccination, and tests have confirmed high levels of
mercury in Many of those tested, along with other toxic exposures. An additional
source of thimerisol to the fetus of women who are RH negative is the 30
micrograms in the RhoGAM shot they receive, which has been found to be a
significant factor in autism incidence(86). Underweight infants that get the
same dose of thimerisol as other infants have also been found to be at special
risk. Many of those diagnosed with high mercury levels have also been found to
have significant improvement after mercury detoxification(23,30,40,11,35,51).
Thimerisol had been previously removed from similar preservative uses in eye
drops and eye medications after evidence of a connection to chronic degenerative
eye conditions. After over 15,000 law suits were filed in France over adverse
effects of the Hepatitis B vaccine, the French Minister of Health ended the
mandatory hepatitis B vaccination program for all school children. Adverse
effects included neurological disorders and autoimmune disorders such as
multiple sclerosis and lupus. Some hospitals in the U.S. also quit recommending
certain vaccinations.
Although vaccinations appear to be the largest source of
mercury in infants, mercury has been found to be transmitted from the mother to
the fetus through the placenta and accumulate in the fetus to higher levels than
in the mother's blood(22). Infants of mothers who had dental work involving
amalgam during pregnancy had significantly higher levels of mercury in hair
tests(78,86). Breast milk of women who have amalgam fillings is the 2nd largest
source of mercury in infants and young children(22,69), but eating a lot of fish
has also been found to be a significant source(45). Milk increases the
bioavailability and retention of mercury by as much as double(22,68,69) and
mercury is often stored in breast milk and the fetus at much higher levels than
that in the mother's tissues (22,69). Mercury is transferred mainly by binding
to cassein(68,24). The level of mercury in breast milk was found to be
significantly correlated with the number of amalgam fillings(69), with milk from
mothers with 7 or more fillings having levels in milk approx. 10 times that of
amalgam-free mothers. The mercury in milk sampled ranged from 0.2 to 6.9 ug/L.
Prenatal mercury exposure can also developmentally damage the metals detox
system of the liver which can lead to accumulation and toxicity of later metals
exposure(22).
A recent study found that prenatal mercury exposures and
susceptability factors such as ability to excrete mercury appear to be a major
factors in those with chronic neurological conditions like autism(86). Infants
whose mothers received prenatal Rho D immunoglbulin injections containing
mercury thimerosal or whose mother's had high levels of amalgam fillings had a
much higher incidence of autism. While the hair test levels of mercury of
infants without chronic health conditions like autism were positively correlated
with the number of the mother's amalgam fillings, vaccination thimerosal
exposure, and mercury from fish, the hair test levels of those with chronic
neurological conditions such as autism were much lower than the levels of
controls and those with the most severe effects had the lowest hair test levels,
even though they had high body mercury levels. This is consistent with past
experience of those treating children with autism and other chronic neurological
conditions(23). Very low levels of exposure have been found to seriously affect
relatively large groups of individuals who are immune sensitive to toxic
metals(11,35), or have an inability to detoxify metals due to such as deficient
sulfoxidation or metallothionein function(18,36,51) or other inhibited enzymatic
processes related to detoxification(15-24,30) or excretion of metals(87). Those
with the genetic allele ApoE4 protein in the blood have been found to detox
metals poorly and to be much more susceptable to chronic neurological conditions
than those with types ApoE2 or E3(87).
A direct mechanism involving mercury's inhibition of
cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino
acids appears to be a major part of the connection to these allergic/immune
reactive conditions(15-23,36,47,51). For example mercury has been found to
strongly inhibit the activity of xanthine oxidase and dipeptyl peptidase (DPP
IV) which are required in the digestion of the milk protein
casein(15,16,17,19,20,22), and the same protein that is cluster differentiation
antigen 26 (CD26) which helps T lymphocyte activation. CD26 or DPPIV is a cell
surface glycoprotein that is very susceptible to inactivation by mercury binding
to its cysteinyl domain.
Mercury and other toxic metals also inhibit binding of
opioid receptor agonists to opioid receptors, while magnesium stimulates binding
to opioid receptors(15). Studies involving a large sample of patients with
autism, schizophrenia, or mania found that over 90 % of those tested had high
levels of the milk protein beta-casomorphine-7 in their blood and urine and
defective enzymatic processes for digesting milk protein(24,25,27), and
similarly for the corresponding enzyme needed to digest wheat gluten(24,26).The
studies found high levels of Ig A antigen specific antibodies for casein,
lactalbumin and beta-lactoglobulin and IgG and IgM for casein.
Beta-casomorphine-7 is a morphine like compound that results in neural
disfunction (24,25), as well as being a direct histamine releaser in humans and
inducing skin reactions (14,21,25c). Similarly many also had a corresponding
form of gluten protein(26). Elimination of milk and wheat products and sulfur
foods from the diet has been found to improve the condition. A double blind
study using a potent opiate antagonist, naltrexone(NAL), produced significant
reduction in autistic symptomology among the 56% most responsive to opioid
effects(28). The behavioral improvements was accompanied by alterations in the
distribution of the major lymphocyte subsets, with a significant increase in the
T-helper-inducers and a significant reduction of the T-cytotoxic-suppressors and
a normalization of the CD4/CD8 ratio.
Studies have found mercury causes increased levels of the
CD8 T-cytotoxic-suppressors(29). As noted previously, such populations of
patients have also been found to have high levels of mercury and to recover
after mercury detox(23,11,22,30,40). As mercury levels are reduced the protein
binding is reduced and improvement in the enzymatic process occurs(22,11).
Studies have also found heavy metals to deplete
glutathione and bind to protein-bound sulfhydryl SH groups, resulting in
inhibiting SH-containing enzymes and production of reactive oxygen species such
as superoxide ion, hydrogen peroxide, and hydroxyl radical(39,43,45-47,
63-65,22). In addition to forming strong bonds with SH and other groups like
OH,NH2, and Cl in amino acids which interfere with basic enzymatic processes,
toxic metals exert part of their toxic effects by replacing essential metals
such as zinc at their sites in enzymes.
An example of this is mercury's disabling of the
metallothionein protein, which is necessary for the transport and detoxification
of metals. Mercury inhibits sulfur ligands in MT and in the case of intestinal
cell membranes inactivates MT that normally bind cuprous ions(66), thus allowing
buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD
function. Another large study(51) found a high percentage of autistic and PDD
children are especially susceptible to metals due to the improper functioning of
their metallothionein detoxification process, and that with proper treatment
most recover. Mercury has also been found to play a part in neuronal problems
through blockage of the P-450 enzymatic process(67). Mercury induced reactive
oxygen species and lipid peroxidation has been found to be a major factor in
mercury's neurotoxicity, along with leading to decreased levels of glutathione
peroxidation and superoxide dismustase(SOD) (63). This has been found to be a
major factor in neurological and immune damage caused by the heavy metals,
including damage to mitochondria and DNA(63,22) , as well as chronic
autoimmune conditions and diseases(35)
Additional cellular level enzymatic effects of mercury's
binding with proteins include blockage of sulfur oxidation processes such as
cysteine dioxygenase, gamma- glutamyltranspeptidase(GGT), and sulfite oxydase,
along with neurotransmitter amino acids which have been found to be significant
factors in many autistics(18,36,47,17), plus enzymatic processes involving
vitamins B6 and B12, with effects on the cytochrome-C energy processes as well.
For example, the Vitamin B6 activating enzyme, B6-kenase, is totally inhibited
in the intestine at extremely low(nanamolar) concentrations(56). Epson
salts(magnesium sulfate)baths, supplementation with the p5p form of Vit B6 and
vit B12 shots are methods of dealing with these enzymatic blockages that have
been found effective by those treating such conditions. Mercury has also been
found to have adverse effects on cellular mineral levels of calcium, magnesium,
zinc, and lithium(39,22,47,50). Supplementing with these minerals has also been
found to be effective in the majority of cases(39,50), and lithium has even been
found to cause regeneration of neurons in damaged areas of the brain such as the
hippocampus. Another of the results of these toxic exposures and enzymatic
blockages is the effect on the liver and disfunction of the liver detoxification
processes which autistic children have been found to have(30,36,51,22). All of
the autistic cases tested were found to have high toxic exposures/effects and
liver detoxification profiles outside of normal(30a).
Another aspect of gastrointestinal dysfunction that is
found in the majority of autism cases are intestinal inflammation,
enterocolalitis, lymphondular hyperplsia, abnormal intestinal permeability, or
malabsorption(17,53). Such damage to the intestines and gastrointestinal
processes are known from animal studies to be caused by mercury(54). Inorganic
mercury is the predominant excretionary form in the intestines,whatever the
source form. All forms are absorbed by the intestines and inorganic mercury
accumulates in intestinal tissues, especially in young animals or infants(55),
which are known to have poor biliary excretion of mercury. As noted previously
children in the U.S. are exposed to high levels of mercury thimerisol, a highly
toxic organic form of mercury. Organic mercury in primate studies is found to
cause paneth cells in the intestines to be enlarged and packed with secretionary
granules(57). This is also common in autistic children(17c).
Along with these blockages of cellular enzymatic
processes, mercury has been found to cause additional neurological and immune
system effects in many through immune/autoimmune reactions(11,12,35).
Mercury(22) as well as thimerisol(31,32) and other toxic metals(50) also have
direct neurotoxic effects on brain nucleoid binding proteins through their
effect on Ca2+ATPase and Na+/K+ATPase activity. But the effects on the
neurological and immune systems of exposure to various toxic substances such as
toxic metals and environmental pollutants has also been found to have additive
or synergistic effects and to be a factor in increasing eczema, allergies,
asthma, delayed food allergies, and sensitivity to other lesser
allergens(14-22,35,50).
Most of the children tested for toxic exposures have found
high or reactive levels of other toxic metals, and organochlorine compounds
(30,40,11,12,35,48). Other than the organochlorines or toxic metals which are
discussed later, three common pollutants that have been documented to have
effects on such conditions are traffic and industrial pollutants nitrogen oxide,
power plant residual oil fly ash, and organochlorine pollutants(48).
Mercury has also been found to cause reduced
acetylycholine levels(77) and to be a factor in autism. When the author
succeeded in removing excessive metal deposits using cilantro and upregulation
techniques, he found Acetylcholine suddenly increased towards a normal level,
short-term memory, the ability to concentrate and think clearly improved
significantly; and often those who had abnormal or anti-social and irritable
behavior returned to more acceptable behavior.
Another effect of mercury and toxic metals is a reduction
in B- lymphocytes (37,38,50,22). One of these studies(37a) dealing with autistic
patients and further work with such patients has found this causes a tendency to
be more seriously affected by viruses and to develop intestinal disorders
including leaky gut, lymphoid modular hyperplasia, and a high incidence of
parasites. Metals by binding to SH radicals in proteins and other such groups
can cause autoimmunity by modifying proteins which via T-cells activate B-cells
that target the altered proteins inducing autoimmunity as well as causing
aberrant MHC II expression on altered target cells(72). Studies have also found
mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and
myelin basic protein (73,74). While zinc binding with MBP stabilizes the
association with brain myelin, mercury and cadmium have been found to intefere
with zinc binding to MBP and thus cause disfunction and autoimmunities(74). Dr.
Stejskal(11) recently began testing children with autism. Her preliminary
results on 18 autistic children and 11 controls, found that 5 of 18 autistic
children had a positive proliferative ("allergic") response on MELISA to
Thimerosal, vs. 1/11 controls. Similar results were recently found for methyl
mercury (6/10 autistics vs 0/11 controls) and inorganic mercury (6/18 autistics,
vs 0/11 controls). Most importantly, 13/16 autistics tested positive for
reactivity to the mercury-MBP vs. only 3/10 controls. The mercury-MBP reactivity
is presumed to be caused by the mercury reconfiguring the three-dimensional MBP,
to which the body generates the allergic (autoimmune) response.
Immune mechanisms are thus seen to be a major factor in
neurotoxicity of metals seen in conditions such as autism and ADD(37b,63,72-74).
Parathyroid Hypertensive Factor (PHF) is produced by the
parathyroid gland and is measurable by the University of Alberta. Preliminary
PHF determinations on over 100 patients through the Pfieffer Treatment Center
have revealed very high levels for autistic patients . Heavy metals are known to
block calcium L-channels at the cell membrane, whereas PHF is known to open
calcium L-channels [84a] and stimulate phosphodiesterase [84b]. Calcium
L-channels perform numerous functions, including initiation of transcriptional
events which support learning, memory and endocrine secretion. Mercury inhibits
L-channels at micromolar concentration [84c] in an irreversible manner in
hippocampal neurons. Hypothetically, elevated PHF may serve to at least
partially compensate Hg-inhibition of L-channels. Mercury is also a potent
inhibitor of cAMP [84d], cellular levels of which presumably further decrease
with PHF-stimulation of phosphodiesterase. Thus, in the context of mercury
toxicity, PHF may play both adaptive and maladaptive roles. The very mechanism
of mercury-induced auto-immune disease in mercury-sensitive rats is related to
L-channel signaling. This process involves induction of interleukin-4 gene
expression, which is mediated by protein kinase C-dependent calcium influx
through L-channels [84e]. PHF hypothetically may affect the auto-immune response
In addition to large numbers of cases affecting infants,
allergic contact eczema is the most frequent occupational disease(1,22,82); and
the most common cause of contact eczema is exposure to toxic metals(1, 6-12,22).
The metals most commonly causing allergic immune reactivity are nickel, mercury,
chromium, cobalt, and palladium(1,6-14,22). The highest level of sensitization
is to Infants, who are most reactive to thimerisol, a form of mercury that has
been used as a preservative in vaccines and eye drops(6,7). Many with immune
reactive conditions like eczema and psoriasis recover after tests and treatment
for the cause of the immune reactivity(11,22 ).
There has been strong suggestive and clinical evidence for
a connection between toxic metals and autism spectrum conditions(2bcd,15-40,50)
and recent studies using government databases have confirmed the
connection(80,91). There also appear to be subgroups of exposure and symptom
patterns among the many different types of persuasive developmental disorders
(PDD) including autism, Asperger's syndrome, obsessive compulsive disorder(OCD),
dyslexia, ADD/ADHD, learning disabilities, childhood
depression, etc. Some of the apparent subgroups of autism include one group of
general brain-related encephalies and/or immune effects of toxic exposures(23),
the Singh subgroup of autoimmune reactions to brain myelin sheath(37b), the
Wakefield/MMR subgroup with intestional leaky gut and involvement of measles
virus(37a), and the Megson/DPT visual abnormality related group(49). Since most
children have been been found to have high levels of toxic exposure, most of
those affected appear to have symptoms related to both the first subgroup plus
often one or more of the other exposures/subgroups. The Megson group are often
helped significantly by treatment with Vitamin A from cod liver oil an
urocholine. Thousands of autistic children are being treated for metals toxicity
using chelation protocols after tests have documented high exposures to mercury
and other toxic metals, and the majority have shown significant
improvement(23,40,51).
References
(1) (a)Weiss B, Landrigan PJ.
The developing brain and the Environment. Environmental Health Perspectives,
Volume 107, Supp 3, June 2000; & EPA spokesman, U.S.News & World Report, "Kids
at Risk"(cover story), 6-19-2000; & Frith CD et al, More Dyslexia in English
Speaking Countries, Science, Mar 2001; & EPA spokesman, U.S.News & World Report,
"In the Air that they Breathe", Science & News, 12-20-99; & U.S. EPA, Region
I, 2001, www.epa.gov/region01/children/outdoors.html; & Dr. Fionta Stanley,
Department of Paediatrics, the University of Western Australia "Before the bough
breaks: 21st Centry kids in crisis" Zonta International Conference,
Gothenburg Sweden, July 2, 2002
www.zonta.org/Member_Resource_Center/StanleySpeech.pdf
& (b) ATSDR/EPA Priority List for 2001: Top 20
Hazardous Substances, Agency for Toxic Substances and Disease Registry,U.S.
Department of Health and Human Services, www.atsdr.cdc.gov/clist.html
(2) (a)The Center for
Education Statistics, http://nces.ed.gov/ ; & Annual Report to Congress on the
implementation of the Individuals with disabilities act.
http://www.ed.gov/offices/OSERS/OSEP/ (1994 to 1998); & U.S. Dept. of Education,
Office of Special Education Programs, Data Analysis Section, partB, Chapter1:
1990-1997; & (b) State government agency reports on autism incidence trends for
the last decade for California, New Jersey, Maryland, Rhode Island, Illinois,
Pennsylvania, Colorado, Washington, etc. in: Autism 99 : A National Emergency,
http://www.garynull.com/documents/autism_99.htm; & © Gary Null, Second
Opinion: Vaccinations, Gary Null and Associates, Inc. 2000,
http://www.garynull.com/marketplace/documents.asp & (d) Bernard Rimland, Ph.D,
Autism Research Institute,
The Autism Epidemic Is Real, and Excessive
Vaccinations Are the Cause,
www.autismcanada.org/News/RimlandstatementJuly2003.htm
(e) California Department of Developmental Services (DDS), "Autistic Spectrum
Disorders, Changes in the California Caseload: 1999-2002". May 2003.
(3) National Academy of
Sciences, National Research Council, Committee on Developmental Toxicology,
Scientific Frontiers in Developmental Toxicology and Risk Assessment, June
1, 2000, 313 pages. & Press Release; Evaluating Chemical and Other Agent
Exposures for Reproductive and Developmental Toxicity Subcommittee on
Reproductive and Developmental Toxicity, Committee on Toxicology, Board on
Environmental Studies and Toxicology, National Research Council National Academy
Press, 262 pages, 6 x 9, 2001; & National Environmental Trust (NET), Physicians
for Social Responsibility and the Learning Disabilities Association of America,
"Polluting Our Future: Chemical Pollution in the U.S. that Affects Child
Development and Learning" Sept 2000; http://www.safekidsinfo.org
(4) American Acadamy of
Pediatrics, American J of Psychiatry, 2000, 157:1077-1083; & American Acadamy of
Pediatrics, Report to Clinicians; http://www.aap.org/policy/autism.html; & James
A Kaye, Maria del Mar
Melero-Montes, Hershel Jick; Boston
Collaborative Drug Surveillance Program, Boston University School of Medicine,
11 Muzzey Street, Lexington, MA 02421, USA, 2000, National Vaccine Information
Center
http://www.909shot.com
(5) American Academy of
Dermatology, Press Release, February, 2000; & Silhan P, Arenberger P. Standard
epicutaneous tests in ambulatory care of patients. Cas Lek Cesk 1999,
138(15):469-73..
(6) Brasch J, Geier J, Schnuch
A. Differentiated contact allergy lists serve in quality improvement. Hautarzt
1998; 49(3): 184-0
(7) Manzini BM, Ferdani G,
Simonetti V, Donini M, Sedernari S. Contact sensitization in children. Pediatr
Dermatol 1998; 15(1): 12-17; & Romaguera C, Vilaplana J. Contact dermatitis in
children: 6 years experience. Contact Dermatitis 1998; 39(6): 277-80.
(8) Sun CC. Allergic contact
dermatitis of the face from contact with nickel and ammoniated mercury. Contact
Dermatitis 1987, 17(5):306-9.
(9) Xue C, He Z, Zhang H, Li
S. Study on the contact allergen in patients with dermatitis and eczema. Wei
Sheng Yen Chiu 1997, 26(5): 296-8.
(10) Aberer W, Holub H,
Strohal R, Slavicek R. Palladium in dental alloys- the dermatologists
responsibility to warn? Contact Dermatitis 1993. 28(3): 163-5.
(11) V.D.M.Stejskal, Dept. Of
Clinical Chemistry, Karolinska Institute, Stockholm, Sweden LYMPHOCYTE
IMMUNO-STIMULATION ASSAY -MELISA" & "Mercury-specific Lymphocytes: an indication
of mercury allergy in man", J. Of Clinical Immunology, 1996, Vol 16(1);31-40;
see: www.melisa.org
(12) Sterzl I, Prochazkova J,
Stejaskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and
autoimmunity. Neuroendocrinology Letters 1999; 20:221-228; & V.Stejskal,
"MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity",
Proceedings: 33rd Annual Meeting of American Academy of Environmental Medicine,
Nov. 1998, Baltimore, Maryland.
(13) Redhe O, Pleva J.
Recovery from asthma, allergies,ALS after removal of dental amalgam fillings.
Int J of Risk & Safety in Medicine 1994; 4:229-236.
(14) Kurek M, Przybilla B,
Hermann K, Ring J. An opioid peptide from cows milk, beta-casomorphine-7, is a
direct histamine releaser in man. Int Arch Allergy immunol 1992; 97(2): 115-20.
(15) Tejwani GA, Hanissian
SH. Modulation of mu, delta, and kappa opioid receptors in rat brain by metal
ions and histidine. Neuropharmology 1990; 29(5): 445-52.
(16) Mondal MS, Mitra S.
Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. J
Inorg Biochem 1996; 62(4): 271-9.
(17) Sastry KV, Gupta PK. In
vitro inhibition of digestive enzymes by heavy metals and their reversal by
chelating agents: Part 1, mercuric chloride intoxication. Bull Environ Contam
Toxicol 1978; 20(6): 729-35; & W.Y.Boadi et al, Dept. Of Food Engineering and
Biotechnology, T-I Inst of Tech., Haifa, Israel, "In vitro effect of mercury on
enzyme activities", Environ Res, 1992, 57(1):96-106; & Horvath K, Papadimitriou
JC, Rabsztyn A, Drachenberg C, Tildon JT; Gastrointestinal abnormalities in
children with autistic disorder. J Pediatr 1999, 135:559-63.
(18) Mc Fadden SA, Phenotypic
variation in xenobiotic metabolism and adverse environmental response: focus on
sulfur-dependent detoxification pathways. Toxicology, 1996, 111(1-3):43-65; &
Markovich et al, "Heavy metals (Hg,Cd) inhibit the activity of the liver and
kidney sulfate transporter Sat-1", Toxicol Appl Pharmacol, 1999,154(2):181-7; &
Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction
of disulfide bonds. J Biol Chem 1991; 266(19): 12695-702; & T.L. Perry et al,
"Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase
defieciency", Ann Neural, 1985, 18(4):482-489; & Ceaurriz et al, Role of gamma-
glutamyltraspeptidase(GGC) and extracellular glutathione in disposition of
inorganic mercury",J Appl Toxicol,1994, 14(3): 201-
(19) Shibuya-Saruta H,
Kasahara Y, Hashimoto Y.
Human serum dipeptidyl peptidase IV (DPPIV) and its
unique properties.
J Clin Lab Anal. 1996;10(6):435-40; & Blais A,
Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit
proximal tubules as a cellular model to study nephrotoxicity of xenobiotics.
Kidney Int. 1993 Jul;44(1):13-8; & Puschel G, Mentlein R, Heymann E, 'Isolation
and characterization of dipeptidyl peptidase IV from human placenta', Eur J
Biochem 1982 Aug;126(2):359-65; & Kar NC, Pearson CM. Dipeptyl Peptidases
in human muscle disease. Clin Chim Acta 1978; 82(1-2): 185-92; & Seroussi K,
Autism and Pervasive Developmental Disorders , 1998, p174,etc.,
www.autismndi.com/
(20) Stefanovic V. et al,
Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol
Biochem 1998; 8(5): 278-84.
(21) Crinnion WJ.
Environmental toxins and their common health effects. Altern Med Rev 2000,
5(1):52-63.
(22) Windham, B. Annotated
Bibliography: Adverse health effects related to mercury and amalgam fillings and
clinically documented recoveries after amalgam
replacement. (over 1500 peer-reviewed references);
www.home.earthlink.net/~berniew1/amalg6.html &
(b) U.S. EPA,
www.epa.gov/grtlakes/seahome/mercury/src/ways.htm
(23) Bernard S, Enayati A,
Redwood L, Roger H, Binstock T. Autism: a novel form of mercury poisoning. Med
Hypotheses 2001 Apr;56(4):462-71 www.autism.com/ari/mercurylong.html; &(b)Dr. A
Holmes, Autism Treatment Center,Baton Rouge, La,
http://healing-arts.org/children/holmes.htm; &(c) Jaquelyn McCandless, M.D.,
Autism Spectrum Treatment Center, Woodland Hills, CA,
&
Jaquelyn McCandless, M.D, Children with Starving
Brains, A Medical Treatment Guide for Autism Spectrum Disorder, 2003
www.autism-rxguidebook.com/DesktopDefault.aspx?tabindex=11&tabid=15; &
(d)L.Redwood, Mercury and Autism, Vitamin Research News, May 2001, 15(5):1-12;
&(e) Andrew H. Cutler, PhD, PE; Amalgam Illness:Diagnosis and
Treatment; 1996 , www.noamalgam.com/
(24) J.R. Cade et al, Autism
and schizophrenia linked to malfunctioning enzyme for milk protein digestion.
Autism, Mar 1999. http://www.hsc.ufl.edu/post/post0399/post03_19/1.html; &
Application of the Exorphin Hypothesis to Attention Deficit Hyperactivity
Disorder: A Theoretical Framework by Ronald Hoggan A Thesis Submitted To The
Faculty Of Graduate Studies In Partial Fulfilment Of The Requirements For The
Degree Of Master Of Arts, Graduate Division Of Educational Research,Calgary,
April, 1998 University of Calgary
(25) Reichelt KL.
Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen
1994, 114(12):1432-4; & Reichelt KL et al, Biologically active
peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem
Psychopharmocol 1981; 28: 627-43; Lucarelli S, Cardi E, et al, Food allergy and
infantile autism. Panminerva Med 1995; 37(3):137-41; & Shel L, Autistic disorder
and the endogenous opioid system. Med Hypotheses 1997, 48(5): 413-4.
(26) Huebner FR, Lieberman
KW, Rubino RP, Wall JS. Demonstration of high opioid-like activity in isolated
peptides from wheat gluten hydrolysates. Peptides 1984; 5(6):1139-47.
(27) Willemsen-Swinkels SH,
Buitelaar JK, Weijnen FG, Thisjssen JH, Van Engeland H. Plasma beta-endorphin
concentrations in people with learning disability and self-injurious and/or
autistic behavior. Br J Psychiary 1996; 168(1): 105-9; & Leboyer M, Launay JM et
al. Difference between plasma N- and C-terminally directed beta-endorphin
immunoreactivity in infantile autism. Am J Psychiatry 1994; 151(12): 1797-1801.
(28) Scifo R, Marchetti B, et
al. Opioid-immune interactions in autism: behavioral and immunological
assessment during a double-blind treatment with naltexone. Ann Ist Super Sanita
1996; 32(3): 351-9.
(29) Eedy DJ, Burrows D,
Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J prosthet
Dent 1990; 63(5):593-6; & & Yonk LJ et al, CD+4 helper T-cell depression in
autism. Immunol Lett, 1990, 25(4):341-5.
(30) Edelson SB, Cantor DS.
Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-63; &
Liska, DJ. The detoxification enzyme systems.
Altern Med Rev 1998. 3(3):187-98; & © HRI-Pfeiffer Center Autism Study; paper
presented to Dan Conference, Jan 2001; www.hriptc.ort/Publish0900/index.html.
(31) Sayers LG; Brown GR;
Michell RH; Michelangeli F. The effects of thimerisol on calcium uptake and
inositol1,4,5-trisphosphate-induced calcium release in cerebellar microsomes.
Biochem J 1993 Feb 1;289
( Pt 3):883-7; & Elferink JG. Thimerisol: a
versatile sulfhydryl reagent, calcium mobilizer, and cell function-modulating
agent. Gen Pharmacol 1999 Jul;33(1):1-6
(32) Lewis RN; Bowler K. Rat
brain (Na+-K+)ATPase: modulation of its ouabain-sensitive K+-PNPPase activity by
thimerisol. Int J Biochem 1983;15(1):5-7; & Anner BM, Moosmayer M. Mercury
inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5
Pt2):F84308.
(33) Halsey, NA. Limiting
Infant Exposure to Thimerisol in vaccines. J. of the Amer. Medical Assoc., 282:
1763-66.
(34) Wecker L, Miller SB,
Cochran SR, Dugger DL, Johnson WD. Trace element concentrations in hair from
autistic children. Defic Res 1985; 29(Pt 1): 15-22.
(35) Stejskal VDM, Danersund
A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al, Metal-specific memory
lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters, 1999;
& V.D.M.Stejskal et al, "Mercury-specific Lymphocytes: an indication of mercury
allergy in man", J. Of Clinical Immunology, 1996, Vol 16(1);31-40, & V.Stejskal,
"MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity",
Proceedings: 33rd Annual Meeting of American Academy of Environmental Medicine,
Nov. 1998, Baltimore, Maryland. See http://www.melisa.org
(36) Alberti A, Pirrone P,
Elia M, Waring RH, Romano C. Sulphation deficit in "low-functioning" autistic
children.
Biol Psychiatry 1999, 46(3):420-4.
(37) (a)Wakefield A et al,
Ileal-lymphoid-nodular hyperplasia and pervasive developmental disorder in
children.
Lancet 1998, 351(9103):637-41; & Kawashima H,
Mori T, Kashiwagi Y, Takekuma K, Hoshika A, Wakefield A. Detection and
sequencing of measles virus from peripheral mononuclear cells from patinets with
inflamatory bowel and autism. Dig Dis Sci 2000 45(4):723-9; & Wakefield A et al,
Inflammatory bowel disease syndrome and autism, Lancet, Feb 27, 2000; & (b)Singh
VK; Lin SX; Yang VC. Serological association of measles virus and human
herpesvirus-6 with brain autoantibodies in autism. Clin Immunol Immunopathol
1998 Oct;89(1):105-8; & G. Bell, Sterling Univ., Evidence of Toxic Metals/MMR
connection in Autism, Autism Research Trust, 2002
(38) B.J.Shenker et
al,"Immunotoxic effects of mercuric compounds on human lymphocytes and
monocytes: Alterations in B-cell function and viability" Immunopharmacol
Immunotoxicol, 1993, 15(1):87-112; & J.R.Daum,"Immunotoxicology of mercury and
cadmium on B-lymphocytes", Int J Immunopharmacol, 1993, 15(3):383-94.
(39) Pfieffer SI; Norton J;
Nelson L; Shott S. Efficacy of vitamin B6 and magnesium in the treatment of
autism. J Autism Dev Disord 1995 Oct;25(5):481-93; & Chuang D. Et al, National
Institute of Mental Health, Science News, Nov 11, 2000, 158:309; & Lithium
Protects Against Neuron Damage by Glutamate, Science News, 3-14-98, p164; &
Moore G.J.et al, Lancet Oct 7, 2000; & Science News, 10-31-98, p276.
(40)
Autism-Mercury@egroups.com, web group of parents with autistic kids and autism
doctors and researchers; &(b)Dr. SB Edelson, http://www.edelsoncenter.com ; & ©
Eppright TD, Sanfacon JA, Horwitz EA. ADHD, infantile autism, and elevated
blood-lead: a possible relationship. (case study) Mo Med 1996; 93(3):136-8.
(41) Agency for Toxic
Substances and Disease Registry, U.S. Public Health Service, Apr 19,1999 Media
Advisory, New MRLs for toxic substances, MRL: methy mercury/ oral/acute; &
www.atsdr.cdc.gov/mrls.html.
(42) Stajich GV, Lopez GP,
Harry SW, Sexson WR, Iatrogenic exposure to mercury after hepatitis B
vaccination in preterm infants. Journal of Pediatrics, May 2000, 136(5):679-81.
(43) Rodier P.M. Developing
brain as a target of toxicity. Environ Health Perspect 1995; 103(Supp 6): 73-76;
&
Rice DC, Barone S, Critical Periods of
Vulnerability for the Developing Nervous System: Evidence from human and animal
models. Environ Health Persect 2000, 108(supp 3):511-533.
(44) The Center for Biologics
Evaluation and Research (CBER), The US Food and Drug Administration(FDA), Jul 4,
2000.
(45) Grandjean P; Jurgensen
PJ; Weihe P. Milk as a Source of Methylmercury Exposure in Infants.
Milk as a Source of Methylmercury Exposure in
Infants. Environ Health Perspect 1994 Jan;102(1):74-7.
(46) (a)Science News,
Methylmercury's toxic toll. July 29, 2000, Vol 158, No.5, p77; & National
Research Council, Toxicological Effects of Methylmercury, National
Acadamy Press, Wash, DC, 2000; & U.S. CDC,
Second National Report on Human Exposure to
Environmental Chemicals, www.cdc.gov/exposurereport/
& U.S. Centers for Disease Control, Mar 2001,
Blood and Hair Mercury Levels in Young Children and Women of Childbearing Age
--- United States, 1999 www.cdc.gov/mmwr/preview/mmwrhtml/mm5008a2.htm;
& (b)Grandjean P, 2000, Health effects of
seafood contamination with methylmercury and PCBs in the Faroes.
Atlantic Coast Contaminants Workshop, June
22-25, 2000, Bar Harbor Maine; & Environ Res, 1998; 77: 165-72
(47) Moreno-Fuenmayor H,
Borjas L, Arrieta A, Valera V, Plasma excitatory amino acids in autism. Invest
Clin 1996, 37(2):113-28; & Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H.
Serotonin and amino acid content in platelets of autistic children. Acta
Psychiatr Scand 1993, 87(5): 312-6; & Naruse H, Hayashi T, Takesada M, Yamazaki
K. Metabolic changes in aromatic amino acids and monoamines in infantile autism
and a new related treatment, No To Hattatsu, 1989, 21(2):181-9; & Carlsson ML.
Is infantile autsim a hypoglutamatergic disorer? J Neural Transm 1998, 105(4-5):
525-35.
(48) Reichrtova E et al,
"Cord Serum Immunoglobulin E Related to Environmental Contamination of Human
Placentas with Oganochlorine Compounds", Envir Health Perspec, 1999,
107(11):895-99; & Gavett SH et al. Residual Oil Fly Ash Amplifies Allergic
Cytokines, Airway Responsiveness, and Inflammation in Mice. Am J Respir Crit
Care Med, 1999, 160(6):1897-1904; & Kramer U et al, Traffic-related air
pollution is associated with atopy in children living in urban areas
Epidemiology 2000, 11(1): 64-70.
(49) Megson MN, Is Autism A
G-Alpha Protein Defect Reversible with Natural Vitamin A? www.megson.com;
(50) B. Windham, Cognitive
and Behavioral Effects of Toxic Metals, (over 100 medical study references)
www.home.earthlink.net/~berniew1/tmlbn.html
(51) Walsh, WJ, Health
Research Institute, Autism and Metal Metabolism,www.hriptc.org/autism.htm, Oct
20, 2000; & Walsh WJ, Pfeiffer Treatment Center, Metal-Metabolism and Human
Functioning, 2000,http://www.hriptc.org/mhfres.htm;
& HRI-Pfeiffer Center Autism Study; paper
presented to Dan Conference, Jan 2001;
(52) Dr. Gerald Bernstein,
Beth Israel Medical Center, NY, past Pres., Amer. Diabetes Association; & U.S.
Centers for Disease Control, 2001,
www.mercola.com/2000/sept/17/diabetes_epidemic.htm; & Dr. Anthony Iacopino.
Conference Paper, American Academy of Periodontology ; & Dr. Bart Classen,
Vaccines are the largest cause of insulin-dependent diabetes in young children,
paper given at American College for Advancement in Medicine., Nashville, Tenn.,
May 14, 2001 ; Harris Coulter, Childhood Vaccinations and Juvenile-Onset
(Type-1) Diabetes, Testimony before the Congress of the United States, House of
Representatives, Committee on Appropriations, subcommittee on Labor, Health and
Human Services, Education, and Related Agencies, April 16, 1997,
www.909shot.com/hcdiabetes.htm & Classen B. ,Autoimmunity August 2002 Vol. 35
(4), pp. 247-253 & Swedish researchers, Ann. N.Y. Acad Sci. 958: 293-296, 2002
(53) Furlano RI, Anthony A,
Day R, Murch SH, et al, Colonic CD8 and gamma delta T-cell infiltration with
epithelial damage in children with autism. J Pediatr 138:366-72, 2001; &
D'Eufemia P, Celli M, Giardini O, et al, Abnormal intestinal permeability in
children with autism. Acta Paediatr 85:1076-9, 1996; & Goodwin MS, Cowen MA,
Goodwin TC. Malabsorption and cerebral dysfunction: a multivariate and
comparative sutudy of autistic children. J Austism Child Schizophr 1:48-52,
1971.
(54) Bamerjee S, Bhattacharya
S. Histopathological changes induced by chronic nonlethal levels of mercury and
ammonia in the small intestine of channa puntatus. Ecol Environ Safety 31:62-8
(1995); & Bohme M, Diener M, Mestres P, Rummel W. Direct and indirect actions of
HgCl2 and methyl mercury chloride on permeability and chloride secretion across
the rat colonic mucosa. Toxicol Appl Pharmacol 114:285-94 (1992); & Andres P.
IgA-IgG disease in the intestine of Brown-Norway rats ingesting mercuric
chloride. Clin Immunol and Immunopath 30:488-494
(1984).
(55) Sasser LB, Jarboe GE,
Walter BK, Kelman BJ. Absorption of mercury from ligated
segments of the rat gastrointestinal tract. Proc
Soc Exp Biol Med 157:57-60 (1978).; & Kostial K, Kargacin B, Landeka M. Gut
retention of metals in rats. Biol Trace Elem Res 21:213-218 (1989).
(56).Srikantaiah MV,
Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the
small intestine: Part III--purification and
properties of monkey intestinal pyridoxal
kinase. Indian J of Biochem 7:151-156 (1970).
(57) Chen W, Body RL, Mottet
NK. Biochemical and morphological studies of monkeys
chronically exposed to methylmercury. J Toxicol
Environ Hlth 12:407-416 (1983).
(58) P.W. Mathieson,
"Mercury: god of TH2 cells",1995, Clinical Exp Immunol
(59) Asthma, mercury, and
vaccines. http://www.whaleto.freeserve.co.uk/vaccines/asthma.html
(60) Odent MR, Culpin EE,
Kimmel T; Pertussis vaccination and asthma: is there a link? JAMA, 1994,
272:592-30; & (b) Dr. Julian Hopkn, Churchill Hospitial, Oxford, Asthma &
allergy risk increased by vaccination, paper at meeting of British Thoriac
Society, Dec 1997; & (c) Pertusiss vaccine associated with increased asthma and
allergies, Archives of Pediatrics and Adoloescent Medicine, 1998; 152:734-738.
(61) Fine JM, Chen LC;
"Confounding in studies of adverse reaction s to vaccines", Amer J Epidemiology,
1992, 136:
121-35; & (b) Dr. Vera Scheibner, Leif Karlsson;
"Association between DPT injections and Cot Death", 2nd Immuniztion Conference,
Canberra, Australia, May 27, 1991; & Torch WC, DPT Immunization: a potential
cause of sudden enfant death syndrome(SIDS), Amer Acad of Neurology, 34th Annual
Meeting, Apr 25, 1982; Neurology, 32(4), pt 2.
(62) Dr Thomas Verstraeten,
US Centres for Disease Control and Prevention, Summary Results: Vaccine Safety
Datalink Project - a database of 400,000 children , May 2000.
(63) P.Bulat, "Activity of
Gpx and SOD in workers occupationally exposed to mercury", Arch Occup Environ
Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bagchi D. Oxidative mechanisms
in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36.
(64) Spivey-Fox MR.
Nutritional influences on metal toxicity. Environ Health Perspect 1979; 29:
95-104; & Pfeiffer SI et al, Efficacy of vitamin B6 and magnesium in the
treatment of autism. J Autism Dev Disord 1995, 25(5):481-93.
(65) Hernberg S; & Moore MR.
in Lead Toxicity, R.Singhal & J.Thomas(eds), Urban & Schwarzenberg, Inc.
Baltimore, 1980; & Govani S, Memo M. "Chronic lead treatment differentially
affects dopamine synthesis", Toxicology 1979, 12:343-49; & Scheuhammer AM.
Cherian MG. Effects of heavy metal cations and sulfhydyl reagents on striatal D2
dopamine receptors. Biochem Pharmacol 1985, 34(19):3405-13.
(66) Lars Landner and Lennart
Lindestrom. Swedish Environmental Research Group(MFG), Copper in society and
the Environment, 2nd revised edition. 1999.
(67) J.C.Veltman et al,
"Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat
adrenal gland", Arch Biochem Biophys,1986, 248(2):467-78; & A.G.Riedl et al,
Neurodegenerative Disease Research
Center, King's College,UK, "P450 and
hemeoxygenase enzymes in the basal ganglia and their role's in Parkinson's
disease", Adv Neurol, 1999; 80:271-86
(68) Mata L, Sanchez L, Calvo
M, Interaction of mercury with human and bovine milk proteins. Biosci Biotechnol
Biochem 1997 Oct;61(10):1641-5; & Kostial K, Rabar I, Ciganovic M, Simonovic I,
Effect of milk on mercury absorption and gut retention in rats. Bull Environ
Contam Toxicol 1979, Nov;23(4-5) :566-7; & Rowland IR, Robinson RD, Doherty RA,
Effects of diet on mercury metabolism and excretion in mice given methylmercury:
role of gut flora, Arch Environ Health 1984 Nov-Dec;39(6):401-8
(69) E.Lutz et al,
"Concentrations of mercury in brain and kidney of fetuses and infants", Journal
of Trace Elements in Medicine and Biology, 1996,10:61-67; & G.Drasch et al,
"Mercury Burden of Human Fetal and Infant Tissues", Eur J Pediatr
153:607-610,1994; & A.Oskarsson et al, "Mercury in breast milk in relation to
fish consumption and amalgam", Arch environ Health, 1996,51(3):234-41; & Drasch
et al, "Mercury in human colostrum and early breast milk", J.Trace Elem.
Med.Biol., 1998,12:23-27
(70) Kravchenko AT, Dzagurov
SG, Chervonskaia GP. III. The detection of toxic properties in medical
biological preparations by the degree of cell damage in the L132 continuous cell
line. Zh Mikrobiol Epidemiol Immunobiol 1983 Mar;(3):87-92 [Article in Russian]
(71) The Health of Canada's
Children--A Canadian Institute of Child Health (CICH), Profile: 3rd Edition,
2000, 325 pages;
http://oncology.medscape.com/26856.rhtml
(72) (a) HultmanP, Johansson
U, Turley SJ; Adverse immunological effects and autoimmunity induced by dental
amalgam in mice. FASEB J 1994; 8: 1183-90; &.(b) Pollard KM, Lee DK, Casiano CA;
The autoimmunity-inducing xenobiotic mercury interacts with the autoantigen
fibrillarin and modifies its molecular structure ad antigenic properties. J
Immunol 1997; 158: 3421-8; &(c) P.L.Bigazzi, "Autoimmunity induced by metals",
in Chang, L., Toxicology of Metals, Lewis Publishers, CRC Press Inc.
1996., p835-52; & (d) Hu H; Moller G; Abedi-Valugerdi M. Major
histocompatibility complex class II antigens are required for both cytokine
production and proliferation induced by mercuric chloride in vitro. J Autoimmun
1997 Oct;10(5):441-6;
(73) (a)C.J.G.Robinson et al,
"Mercuric chloride induced anitnuclear antibodies In mice", Toxic Appl
Pharmacology, 1986, 86:159-169. & (b) El-Fawai HA, Waterman SJ, De Feo A, Shamy
MY. Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune
Mechanisms. Contact Dermatitis 1999; 41(1): 60-1;
& (c) Hu H; Moller G; Abedi-Valugerdi M.
Mechanism of mercury-induced autoimmunity: both T helper 1- and T helper 2-type
responses are involved. Immunology 1999 Mar;96(3):348-57;
(74) Earl C, Chantry A,
Mohammad N. Zinc ions stabilize the association of basic protein with brain
myelin membranes. J Neurochem 1988; 51:718-24; & Ricco P, Giovanneli S, Bobba A.
Specificity of zinc binding to myelin basic protein. Neurochem Res 1995;
20:1107-13.
(75) The extent of drug
therapy for attention deficit-hyperactivity disorder among children in public
schools. (American Journal of Public Health. 1999; 89(9):1359-64); &
www.niehs.hih.gov/oc/news.adhd.htm
(76) Adverse health effects
of Ritalin and other stimulant drugs:
http://users.cybercity.dk/~bbb9582/ritalin.htm; &
www.healthysource.com/ritalin.html; & www.breggin.com/RitalinNIHSPEECH.html; &
www.healthoptions.com/ritalin.html;
&
http://lifefellowship.org/-Updatables/Articles/40.html;
Michael R. Lyon, Healing the Hyperactive
Brain through the Science of Functional Medicine ,
www.pureliving.com/product.html
(77) Omura, Yoshiaki;
Abnormal Deposits of Al, Pb, and Hg in the Brain, Particularly in the
Hippocampus, as One of the Main Causes of Decreased Cerebral Acetylcholine,
Electromagnetic Field Hypersensitivity, Pre-Alzheimer's Disease, and Autism


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