BU$TED?

Peter Bowditch wrote:

It likely does this by increasing
the rate that thimerosal breaks down releasing ethylmercury which is the
toxic material" -------Testimony Prof Boyd Haley, University of Kentucky,
Chair and Head of Chemistry.......

And there it is again - Haley being either ignorant of chemistry or
lying.

Why cannot he do both at the same time?

Of course, when he gets thrown out of the Omnibus Thimerosal claim
hearings after a Daubert examination, we could call him Haley the Comet.

"Mark Probert" wrote in message
...
Peter Bowditch wrote:

It likely does this by increasing
the rate that thimerosal breaks down releasing ethylmercury which is
the
toxic material" -------Testimony Prof Boyd Haley, University of
Kentucky,
Chair and Head of Chemistry.......

And there it is again - Haley being either ignorant of chemistry or
lying.

Why cannot he do both at the same time?

Of course, when he gets thrown out of the Omnibus Thimerosal claim
hearings after a Daubert examination, we could call him Haley the Comet.

I don't suppose *YOU* care to *PROVE* he was a paid witness?

Thrown out....What a HYPOCRITE!

In the Matter of Mark Probert (Admitted as Mark S. Probert), a
Suspended Attorney, Respondent.
Grievance Committee for the Tenth Judicial District, Petitioner.

92-02731

SUPREME COURT OF NEW YORK, APPELLATE DIVISION, SECOND DEPARTMENT

183 A.D.2d 282; 590 N.Y.S.2d 747

November 9, 1992, Decided

PRIOR HISTORY: [***1]

Disciplinary proceedings instituted by the Grievance Committee for the
Tenth Judicial District. Respondent was admitted to the Bar on
February 15, 1978, at a term of the Appellate Division of the Supreme
Court in the Second Judicial Department, under the name Mark S.
Probert.

DISPOSITION: Ordered that the petitioner's motion to impose discipline
upon the respondent based upon his failure to appear or answer is
granted; and it is further,

HEADNOTES: Attorney and Client - Disciplinary Proceedings

Respondent attorney, who is charged with 22 counts of failing to
cooperate with investigations of alleged misconduct by the Grievance
Committee, and who has failed to answer or appear, is disbarred.

COUNSEL:

Frank A. Finnerty, Jr., Westbury (Muriel L. Gennosa of counsel), for
petitioner.

JUDGES: Mangano, P. J., Thompson, Bracken, Sullivan and Harwood, JJ.,
concur.

Ordered that the petitioner's motion to impose discipline upon the
respondent based upon his failure to appear or answer is granted; and
it is further,

Ordered that pursuant to Judiciary Law § 90, effective immediately,
the respondent, Mark Probert, is disbarred and his name is stricken
from the roll of attorneys and counselors-at-law; and it is further,

Ordered that the respondent shall continue to comply with this Court's
rules governing the conduct of disbarred, suspended and resigned
attorneys (22 NYCRR 691.10); and it is further,

Ordered that pursuant to Judiciary [***2] Law § 90, the respondent,
Mark Probert, is commanded to continue to desist and refrain (1) from
practicing law in any form, either as principal or as agent, clerk or
employee of another, (2) from appearing as an attorney or
counselor-at-law before any court, Judge, Justice, board, commission
or other public authority, (3) from giving to another an opinion as to
the law or its application or any advice in relation thereto, and (4)
from holding himself out in any way as an attorney and
counselor-at-law.

OPINIONBY: Per Curiam.

OPINION: [*282]

[**747] By decision and order of this Court dated September 29,
1989, the respondent was suspended from the practice of law until the
further order of this Court based upon his failure to cooperate with
the Grievance Committee. By further order of this Court dated June 4,
1992, the Grievance Committee was authorized to institute and
prosecute a disciplinary proceeding [*283] against the respondent
and the Honorable Moses M. Weinstein was appointed as Special Referee.

[**748] A notice of petition and petition was personally served upon
the respondent on July 2, 1992. No answer was forthcoming. The
petitioner now moves to hold the [***3] respondent in default. The
motion was personally served upon the respondent on August 14, 1992.
The respondent has failed to submit any papers in response to the
default motion.

The charges involve 22 counts of the respondent's failure to cooperate
with the Grievance Committee in its investigations into complaints of
professional misconduct.

The charges, if established, would require the imposition of a
disciplinary sanction against the respondent. Since the respondent has
chosen not to appear or answer in these proceedings, the charges must
be deemed established. The petitioner's motion to hold the respondent
in default and impose discipline is, therefore, granted. Accordingly,
the respondent is disbarred and his name is stricken from the roll of
attorneys and counselors-at-law, effective immediately

Source:

NY UNIFIED COURT SYSTEM, ATTORNEY REGIST. UNIT

Currency Status:

ARCHIVE RECORD

NAME & PROFESSIONAL INFORMATION

Name:

MARK PROBERT

Date Of Birth:

11/XX/1946

Gender:

MALE

Address:

1698 WEBSTER AVE

MERRICK, NY 11566

County:

NASSAU

Phone:

516-968-5572

EMPLOYER INFORMATION

Employer:

MARK S PROBERT ESQ

Organization:

PERSON

LICENSING INFORMATION

Licensing Agency:

NY STATE OFFICE OF COURT ADMINISTRATION

License/Certification Type:

ATTORNEY

License Number:

1253889

Issue Date:

00/00/1978

License Status:

DISBARRED

License State:

NY

Jason Johnson wrote:

Mark,
I know that ONE vaccine that contains alumninum is not likely to cause harm.
However, as you probably know, alumninum is in many different products
such as
antacids. If they started placing alumninum in all vaccines (to replace
mercury), it could cause high levels of alumninum to build up in the
bodies of people.

Why would you ASSUME that there would be a build up?

It could cause as much harm as high levels of mercury.

Why would you assume that? Different toxins act differently. Spend some
time learning the various types of "snake venom" and how they work.

It could lead to alumninum poisoning. Heavy metal poisoning and alumninum
poisoning are known medical issues. I was shocked when I noticed that
almost every brand of antacids contains high levels of alumninum.

Does the body absorb it, though? Does the body retain it?

One dose
of alumninum is NOT a problem--however, I hope that even you would agree
that 100 doses of alumninum is a problem--esp. in those people that have
an allergic reactions to alumninum.

Only if it accumulates to a toxic level.

People that have various types of
kidney diseases are advised not to use productes that contain alumninum.

Why?

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Mark,
You made some good points in your post. I have conducted some research
related to kidney diseases mainly by reading a book that was written by a
kidney specialist that is a professor at a medical college. I am NOT an
expert on kidney diseases. It's my understanding based upon what I read in
that book that diseased kidneys have a difficult time removing various
substances such as mercury, alumninum (and various types of medications),
and other heavy metals from the body. As a result, those things
accumuluate and cause great harm. For example, if you drank an entire
bottle of an antacid (and had normal kidneys), it probably would not harm
you. On the other hand, if someone that had weak or diseased kidneys,
drank a bottle of antacid, the alumninum in that bottle of antacid may
cause great harm and perhaps even alumninum poisoning.

Dear Jason, have you ever heard the expression: "the poison is in the
dosage"? Or: "one aspirin takes the headache away, a whole bottle takes
the patient away"? Are you aware that you can die from drinking too much
water. Yes, plain, good ol' H2O. Are you aware that aluminum is one of
the most ubiquitous element on the face of the earth and if it really
were that poisonous, life on earth as we know it would not exist? Are
you aware that aluminum is NOT a heavy metal, but in fact one of the
lightest metals that we know of?

You would be amazed
at the number of medications that have a warning that states: "People that
have kidney disease or liver disease should NOT take this medication."
Yes--I would agree that heavy metals may in some cases (e.g. kidney
disease) accumulate to a toxic level.
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ ~~~

In article , JohnDoe
wrote:

Jason Johnson wrote:

Mark,
I know that ONE vaccine that contains alumninum is not likely to
cause harm.
However, as you probably know, alumninum is in many different products
such as
antacids. If they started placing alumninum in all vaccines (to replace
mercury), it could cause high levels of alumninum to build up in the
bodies of people.

Why would you ASSUME that there would be a build up?

It could cause as much harm as high levels of mercury.

Why would you assume that? Different toxins act differently. Spend some
time learning the various types of "snake venom" and how they work.

It could lead to alumninum poisoning. Heavy metal poisoning and alumninum
poisoning are known medical issues. I was shocked when I noticed that
almost every brand of antacids contains high levels of alumninum.

Does the body absorb it, though? Does the body retain it?

One dose
of alumninum is NOT a problem--however, I hope that even you would agree
that 100 doses of alumninum is a problem--esp. in those people that have
an allergic reactions to alumninum.

Only if it accumulates to a toxic level.

People that have various types of
kidney diseases are advised not to use productes that contain alumninum.

Why?

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Mark,
You made some good points in your post. I have conducted some research
related to kidney diseases mainly by reading a book that was written by a
kidney specialist that is a professor at a medical college. I am NOT an
expert on kidney diseases. It's my understanding based upon what I read in
that book that diseased kidneys have a difficult time removing various
substances such as mercury, alumninum (and various types of medications),
and other heavy metals from the body. As a result, those things
accumuluate and cause great harm. For example, if you drank an entire
bottle of an antacid (and had normal kidneys), it probably would not harm
you. On the other hand, if someone that had weak or diseased kidneys,
drank a bottle of antacid, the alumninum in that bottle of antacid may
cause great harm and perhaps even alumninum poisoning.

Dear Jason, have you ever heard the expression: "the poison is in the
dosage"? Or: "one aspirin takes the headache away, a whole bottle takes
the patient away"? Are you aware that you can die from drinking too much
water. Yes, plain, good ol' H2O. Are you aware that aluminum is one of
the most ubiquitous element on the face of the earth and if it really
were that poisonous, life on earth as we know it would not exist? Are
you aware that aluminum is NOT a heavy metal, but in fact one of the
lightest metals that we know of?

You would be amazed
at the number of medications that have a warning that states: "People that
have kidney disease or liver disease should NOT take this medication."
Yes--I would agree that heavy metals may in some cases (e.g. kidney
disease) accumulate to a toxic level.
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ ~~~

JohnDoe,
True or False:
Is alumninum poisoning a know medical issue?

Do babies ever develop reactions to the Hep-B vaccine that contains alumninum?


Jason

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ ~~~~~~~~~

Jason Johnson wrote:
In article , JohnDoe
wrote:

JohnDoe,
True or False:
Is alumninum poisoning a know medical issue?
Is H2O poisoning a know medical issue?

Do babies ever develop reactions to the Hep-B vaccine that contains aluminum?
Do babies ever develop reactions to the Hep-B vaccine that contains
H2O?

I was fascinated to learn that "buffered" aspirin contains a
significant amount of aluminum. Is this also the same situation vis a
vis 'enteric coated' aspirin?

Assuming that enteric coated aspirin does NOT contain a significant
amount of aluminum, is it easy to mistake coated and buffered aspirin?

Cordially,

RL

"JohnDoe" wrote in message
. ..
Jason Johnson wrote:

Mark,
I know that ONE vaccine that contains alumninum is not likely to cause
harm.
However, as you probably know, alumninum is in many different products
such as antacids. If they started placing alumninum in all vaccines (to
replace
mercury), it could cause high levels of alumninum to build up in the
bodies of people. Why would you ASSUME that there would be a build up?
It could cause as much harm as high levels of mercury.
Why would you assume that? Different toxins act differently. Spend some
time learning the various types of "snake venom" and how they work.
It could lead to alumninum poisoning. Heavy metal poisoning and
alumninum
poisoning are known medical issues. I was shocked when I noticed that
almost every brand of antacids contains high levels of alumninum. Does
the body absorb it, though? Does the body retain it?
One dose
of alumninum is NOT a problem--however, I hope that even you would
agree
that 100 doses of alumninum is a problem--esp. in those people that
have
an allergic reactions to alumninum. Only if it accumulates to a toxic
level.
People that have various types of
kidney diseases are advised not to use productes that contain
alumninum. Why?

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Mark,
You made some good points in your post. I have conducted some research
related to kidney diseases mainly by reading a book that was written by a
kidney specialist that is a professor at a medical college. I am NOT an
expert on kidney diseases. It's my understanding based upon what I read
in
that book that diseased kidneys have a difficult time removing various
substances such as mercury, alumninum (and various types of medications),
and other heavy metals from the body. As a result, those things
accumuluate and cause great harm. For example, if you drank an entire
bottle of an antacid (and had normal kidneys), it probably would not harm
you. On the other hand, if someone that had weak or diseased kidneys,
drank a bottle of antacid, the alumninum in that bottle of antacid may
cause great harm and perhaps even alumninum poisoning.

Dear Jason, have you ever heard the expression: "the poison is in the
dosage"?

If he has been around here very long. He most certainly has.

It is an OLD excuse..used by those who wish to derail the subject.
In some cases it is also untrue.

Or: "one aspirin takes the headache away, a whole bottle takes
the patient away"? Are you aware that you can die from drinking too much
water. Yes, plain, good ol' H2O.

Oh..yes. Here comes what most often follows the dose is the poison.
Which has nothing to do with the subject.

There's the derailing and stupid skeptic tricks.

Are you aware that aluminum is one of
the most ubiquitous element on the face of the earth and if it really were
that poisonous, life on earth as we know it would not exist? Are you aware
that aluminum is NOT a heavy metal, but in fact one of the lightest metals
that we know of?

Yes, he is. Did you actually read what he stated?

Heavy metal poisoning and alumninum
poisoning are known medical issues

See the word *and*.

What John overlooks....

Aluminum Neurotoxicity

Redhead K, Quinlan GJ, Das RG, Gutteridge JM. Pharmacol Toxicol 1992
Apr;70(4):278-80.

Aluminium-adjuvanted vaccines transiently increase aluminium levels in
murine brain tissue.

Division of Bacteriology, National Institute for Biological Standards and
Control, Herts., UK.

Aluminum is widely used as an adjuvant in human vaccines, and children can
often receive up to 3.75 mg of parenteral aluminum during the first six
months of life. We show that intraperitoneal injection of aluminum adsorbed
vaccines into mice causes a transient rise in brain tissue aluminum levels
peaking around the second and third day after injection. This rise is not
seen in the saline control group of animals or with vaccine not containing
aluminum. It is likely that aluminum is transported to the brain by the
iron-binding protein transferrin and enters the brain via specific
transferrin receptors. PMID: 1608913, UI: 92302160

http://www.ncbi.nlm.nih.gov/htbin-po...=6&db=m&Dopt=b

Gupta RK, Relyveld EH.

Adverse reactions after injection of adsorbed diphtheria-pertussis-tetanus
(DPT) vaccine are not due only to pertussis organisms or pertussis
components in the vaccine.

Vaccine. 1991 Oct;9(10):699-702. Review.PMID: 1759487; UI: 92101590

Aluminum compounds such as aluminum phosphate and aluminum hydroxide are the
most commonly used adjuvants with vaccines for human use. Due to the
increasing concern about the toxicity of aluminum, other adjuvants like
calcium phosphate may be evaluated as an alternative to aluminum adjuvants.
To minimize reactions after immunization with DPT vaccine due to impurities
in the toxoids, the use of toxoided purified toxins is suggested.

Neurotoxicology of the brain barrier system: new implications.

Zheng W.

J Toxicol Clin Toxicol. 2001;39(7):711-9.

College of Physicians and Surgeons, Columbia University, New York, New York
10032, USA.

The concept of a barrier system in the brain has existed for nearly a
century. The barrier that separates the blood from the cerebral interstitial
fluid is defined as the blood-brain barrier, while the one that discontinues
the circulation between the blood and cerebrospinal fluid is named the
blood-cerebrospinal fluid barrier. Evidence in the past decades suggests
that brain barriers are subject to toxic insults from neurotoxic chemicals
circulating in blood. The aging process and some disease states render
barriers more vulnerable to insults arising inside and outside the barriers.
The implication of brain barriers in certain neurodegenerative diseases is
compelling, although the contribution of chemical-induced barrier
dysfunction in the etiology of any of these disorders remains poorly
understood. This review examines what is currently understood about brain
barrier systems in central nervous system disorders by focusing on
chemical-induced neurotoxicities including those associated with
nitrobenzenes, N-methyl-D-aspartate, cyclosporin A, pyridostigmine bromide,
aluminum, lead, manganese, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and
3-nitropropionic acid. Contemporary research questions arising from this
growing understanding show enormous promises for brain researchers,
toxicologists, and clinicians.

Aluminum, NO, and nerve growth factor neurotoxicity in cholinergic neurons.

Szutowicz A.

J Neurosci Res. 2001 Dec 1;66(5):1009-18.

Chair of Clinical Biochemistry, Department of Laboratory Medicine, Medical
University of GdaÅ"sk, Debinki 7, 80-211 GdaÅ"sk, Poland.

Several neurotoxic compounds, including Al, NO, and beta-amyloid may
contribute to the impairment or loss of brain cholinergic neurons in the
course of various neurodegenerative diseases. Genotype and phenotypic
modifications of cholinergic neurons may determine their variable functional
competency and susceptibility to reported neurotoxic insults. Hybrid,
immortalized SN56 cholinergic cells from mouse septum may serve as a model
for in vitro cholinotoxicity studies. Differentiation by various
combinations of cAMP, retinoic acid, and nerve growth factor may provide
cells of different morphologic maturity as well as activities of
acetylcholine and acetyl-CoA metabolism. In general, differentiated cells
appear to be more susceptible to neurotoxic signals than the
non-differentiated ones, as evidenced by loss of sprouting and connectivity,
decreases in choline acetyltransferase and pyruvate dehydrogenase
activities, disturbances in acetyl-CoA compartmentation and metabolism,
insufficient or excessive acetylcholine release, as well as increased
expression of apoptosis markers. Each neurotoxin impaired both acetylcholine
and acetyl-CoA metabolism of these cells. Activation of p75 or trkA
receptors made either acetyl-CoA or cholinergic metabolism more susceptible
to neurotoxic influences, respectively. Neurotoxins aggravated detrimental
effects of each other, particularly in differentiated cells. Thus brain
cholinergic neurons might display a differential susceptibility to Al and
other neurotoxins depending on their genotype or phenotype-dependent
variability of the cholinergic and acetyl-CoA metabolism.

Copyright 2001 Wiley-Liss, Inc.

Aluminium impairs the glutamate-nitric oxide-cGMP pathway in cultured
neurons and in rat brain in vivo: molecular mechanisms and implications for
neuropathology.

Canales JJ, Corbalan R, Montoliu C, Llansola M, Monfort P, Erceg S,
Hernandez-Viadel M, Felipo V.

J Inorg Biochem. 2001 Nov;87(1-2):63-9.

Laboratory of Neurobiology, Instituto de Investigaciones Citológicas,
Fundación Valenciana de Investigaciones Biomédicas, Amadeo de Saboya 4,
46010 Valencia, Spain.

Aluminium (Al) is a neurotoxicant and appears as a possible etiological
factor in Alzheimer's disease and other neurological disorders. The
mechanisms of Al neurotoxicity are presently unclear but evidence has
emerged suggesting that Al accumulation in the brain can alter neuronal
signal transduction pathways associated with glutamate receptors. In
cerebellar neurons in culture, long term-exposure to Al added 'in vitro'
impaired the glutamate-nitric oxide (NO)-cyclic GMP (cGMP) pathway, reducing
glutamate-induced activation of NO synthase and NO-induced activation of the
cGMP generating enzyme, guanylate cyclase. Prenatal exposure to Al also
affected strongly the function of the glutamate-NO-cGMP pathway. In cultured
neurons from rats prenatally exposed to Al, we found reduced content of NO
synthase and of guanylate cyclase, and a dramatic decrease in the ability of
glutamate to increase cGMP formation. Activation of the glutamate-NO-cGMP
pathway was also strongly impaired in cerebellum of rats chronically treated
with Al, as assessed by in vivo brain microdialysis in freely moving rats.
These findings suggest that the impairment of the Glu-NO-cGMP pathway in the
brain may be responsible for some of the neurological alterations induced by
Al.

Effects of aluminium exposure on brain glutamate and GABA systems: an
experimental study in rats.

Nayak P, Chatterjee AK.

Food Chem Toxicol. 2001 Dec;39(12):1285-9.

Biochemistry and Nutrition Research Laboratory, Department of Physiology,
University of Calcutta, 92 A.P.C. Road, 700 009, Calcutta, India.


It has been postulated that the neurotoxic effects of aluminium could be
mediated through glutamate, an excitatory amino acid. Hence the effects of
aluminium administration (at a dose of 4.2mg/kg body weight daily as
aluminium chloride, hexahydrate, intraperitoneally, for 4 weeks) on
glutamate and gamma-amino butyrate (GABA), an inhibitory amino acid, and
related enzyme activities in different regions of the brain were studied in
albino rats. The glutamate level increased significantly in the cerebrum,
thalamic area, midbrain-hippocampal region and cerebellum in response to in
vivo aluminium exposure. The aluminium insult also caused significant
increases in glutamate alpha-decarboxylase activity in all the brain
regions. However, on aluminium insult, the GABA content was not
significantly changed except in the thalamic area, where it was elevated. On
the contrary, the GABA-T activities of all the regions were reduced
significantly in all regions except the midbrain-hippocampal region.
However, the succinic semi-aldehyde content of all brain regions increased,
often significantly. The aluminium-induced modification of the enzyme
activities may be either due to the direct impact of aluminium or due to
aluminium-induced changes in the cellular environment. The aluminium-induced
differential regional accumulation of glutamate or other alterations in
enzymes of the glutamate-GABA system may be one of the causes of
aluminium-induced neurotoxicity.

Dementia in patients undergoing long-term dialysis: aetiology, differential
diagnoses, epidemiology and management.

Rob PM, Niederstadt C, Reusche E.

CNS Drugs. 2001;15(9):691-9.

Nephrologisches Zentrum am Klinikum Süd, Kalhlhorststrasse 31, D-23552
Lübeck, Germany.

Dementia in patients undergoing long-term dialysis has not been clearly
defined; however, four different entities have been described. Uraemic
encephalopathy is a complication of uraemia and responds well to dialysis.
Dialysis encephalopathy syndrome, the result of acute intoxication of
aluminium caused by the use of an aluminium-containing dialysate, was a
common occurrence prior to 1980. However, using modern techniques of water
purification, such acute intoxication can now be avoided.
Dialysis-associated encephalopathy/dementia (DAE) is always associated with
elevated serum aluminium levels. Pathognomonic morphological changes in the
brain have been described, but the mechanism for the entry of aluminium into
the CNS is incompletely understood. The mechanisms involved in the
pathogenesis of the neurotoxicity associated with aluminium are numerous.
Although only a very small fraction of ingested aluminium is absorbed, the
continuous oral aluminium intake from aluminium-based phosphate binders, and
also of dietary or environmental origin, is responsible for aluminium
overload in dialysis patients. Age-related dementia, especially vascular
dementia, occurs in patients undergoing long-term dialysis as frequently as
it does in the general population. The differential diagnoses of
dialysis-associated dementias should include investigation for metabolic
encephalopathies, heavy metal or trace element intoxications, and distinct
structural neurological lesions such as subdural haematoma, normal pressure
hydrocephalus, stroke and, particularly, hypertensive encephalopathy and
multi-infarct dementia. To prevent DAE, dietary training programmes should
aim to achieve the lowest phosphate intake and pharmacological tools should
be used to keep serum phosphate levels below 2 mmol/L. To prevent vascular
dementia, lifestyle modification should be undertaken, including optimal
physical activity and fat intake, nicotine abstinence, and targeting optimal
blood glucose, cholesterol and triglyceride levels, and blood pressure, to
those outlined in current recommendations.

The toxicology of aluminum in the brain: a review.

Yokel RA.

Neurotoxicology. 2000 Oct;21(5):813-28.

College of Pharmacy and Graduate Center for Toxicology, University of
Kentucky Medical Center, Lexington, USA.

Aluminum is environmentally ubiquitous, providing human exposure. Usual
human exposure is primarily dietary. The potential for significant Al
absorption from the nasal cavity and direct distribution into the brain
should be further investigated. Decreased renal function increases human
risk of Al-induced accumulation and toxicity. Brain Al entry from blood may
involve transferrin-receptor mediated endocytosis and a more rapid process
transporting small molecular weight Al species. There appears to be Al
efflux from the brain, probably as Al citrate. There is prolonged retention
of a fraction of Al that enters the brain, suggesting the potential for
accumulation with repeated exposure. Al is a neurotoxicant in animals and
humans. It has been implicated in the etiology of sporadic Alzheimer's
disease (AD) and other neurodegenerative disorders, although this is highly
controversial. This controversy has not been resolved by epidemiological
studies, as only some found a small association between increased incidence
of dementia and drinking water Al concentration. Studies of brain Al in AD
have not produced consistent findings and have not resolved the controversy.
Injections of Al to animals produce behavioral, neuropathological and
neurochemical changes that partially model AD. Aluminum has the ability to
produce neurotoxicity by many mechanisms. Excess, insoluble amyloid beta
protein (A beta) contributes to AD. Aluminum promotes formation and
accumulation of insoluble A beta and hyperphosphorylated tau. To some
extent, Al mimics the deficit of cortical cholinergic neurotransmission seen
in AD. Al increases Fe-induced oxidative injury. The toxicity of Al to
plants, aquatic life and humans may share common mechanisms, including
disruption of the inositol phosphate system and Ca regulation. Facilitation
of Fe-induced oxidative injury and disruption of basic cell processes may
mediate primary molecular mechanisms of Al-induced neurotoxicity. Avoidance
of Al exposure, when practical, seems prudent.

Aluminum neurotoxicity in preterm infants receiving intravenous-feeding
solutions.

Bishop NJ, Morley R, Day JP, Lucas A.

N Engl J Med. 1997 May 29;336(22):1557-61.

Comment in:

N Engl J Med. 1997 Oct 9;337(15):1090-1 PMID: 9324646

Medical Research Council (MRC) Dunn Nutrition Unit, Cambridge, United
Kingdom.

BACKGROUND: Aluminum, a contaminant of commercial intravenous-feeding
solutions, is potentially neurotoxic. We investigated the effect of
perinatal exposure to intravenous aluminum on the neurologic development of
infants born prematurely. METHODS: We randomly assigned 227 premature
infants with gestational ages of less than 34 weeks and birth weights of
less than 1850 g who required intravenous feeding before they could begin
enteral feeding to receive either standard or specially constituted,
aluminum-depleted intravenous-feeding solutions. The neurologic development
of the 182 surviving infants who could be tested was assessed by using the
Bayley Scales of Infant Development at 18 months of age. RESULTS: The 90
infants who received the standard feeding solutions had a mean (+/-SD)
Bayley Mental Development Index of 95+/-22, as compared with 98+/-20 for the
92 infants who received the aluminum-depleted solutions (P=0.39). In a
planned subgroup analysis of infants in whom the duration of intravenous
feeding exceeded the median and who did not have neuromotor impairment, the
mean values for the Bayley Mental Development Index for the 39 infants who
received the standard solutions and the 41 infants who received the
aluminum-depleted solutions were 92+/-20 and 102+/-17, respectively
(P=0.02). The former were significantly more likely (39 percent, vs. 17
percent of the latter group; P=0.03) to have a Mental Development Index of
less than 85, increasing their risk of subsequent educational problems. For
all 157 infants without neuromotor impairment, increasing aluminum exposure
was associated with a reduction in the Mental Development Index (P=0.03),
with an adjusted loss of one point per day of intravenous feeding for
infants receiving the standard solutions. CONCLUSIONS: In preterm infants,
prolonged intravenous feeding with solutions containing aluminum is
associated with impaired neurologic development.

Aluminum neurotoxicity in experimental animals.

Erasmus RT, Savory J, Wills MR, Herman MM.

Ther Drug Monit. 1993 Dec;15(6):588-92.

Department of Pathology, University of Virginia Health Sciences Center,
Charlottesville 22908.

Neurotoxic effects of aluminum (Al) were recognized 100 years ago, but
have only recently been studied in detail. By far, the most dramatic effect
of Al is that of producing intraneuronal perikaryal neurofilamentous
aggregates, which consist of phosphorylated neurofilaments. Several species
have been used to demonstrate this effect, rabbit being most common; the
effect also is seen in in vitro systems. Besides its role in producing
neurofibrillary pathology, Al appears to modify the blood-brain barrier and
exert cholinergic and noradrenergic effects. Possible mechanisms of Al
neurotoxicity could be related to cell damage via free radical production,
impairment of glucose metabolism, and effects on signal transduction.

Effects of metals on the nervous system of humans and animals.

Carpenter DO.

Int J Occup Med Environ Health. 2001;14(3):209-18.

School of Public Health University at Albany Rensselaer, NY 12144, USA.

Several metals have toxic actions on nerve cells and neurobehavorial
functioning. These toxic actions can be expressed either as developmental
effects or as an increased risk of neurodegenerative diseases in old age.
The major metals causing neurobehavioral effects after developmental
exposure are lead and methylmercury. Lead exposure in young children results
in a permanent loss of IQ of approximately 5 to 7 IQ points, and also
results in a shortened attention span and expression of anti-social
behaviors. There is a critical time period (2 years of age) for development
of these effects, after which the effects do not appear to be reversible
even if blood lead levels are lowered with chelation. Methylmercury has also
been found to have effects on cognition at low doses, and prenatal exposure
at higher levels can disrupt brain development. Metals have also been
implicated in neurodegenerative diseases, although it is unlikely that they
are the sole cause for any of them. Elevated aluminum levels in blood,
usually resulting from kidney dialysis at home with well water containing
high aluminum, result in dementia that is similar to but probably different
from that of Alzheimer's disease. However, there is some epidemiological
evidence for elevated risk of Alzheimer's in areas where there is high
concentration of aluminum in drinking water. Other metals, especially lead,
mercury, manganese and copper, have been implicated in amvotrophic lateral
sclerosis and Parkinson's disease.

http://www.altcorp.com/DentalInforma...umvaccines.htm



You would be amazed
at the number of medications that have a warning that states: "People
that
have kidney disease or liver disease should NOT take this medication."
Yes--I would agree that heavy metals may in some cases (e.g. kidney
disease) accumulate to a toxic level.
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ ~~~

In article . com, "Raving
Loonie" wrote:

Jason Johnson wrote:
In article , JohnDoe
wrote:

JohnDoe,
True or False:
Is alumninum poisoning a know medical issue?
Is H2O poisoning a know medical issue?

Do babies ever develop reactions to the Hep-B vaccine that contains aluminum?
Do babies ever develop reactions to the Hep-B vaccine that contains
H2O?

I was fascinated to learn that "buffered" aspirin contains a
significant amount of aluminum. Is this also the same situation vis a
vis 'enteric coated' aspirin?

Assuming that enteric coated aspirin does NOT contain a significant
amount of aluminum, is it easy to mistake coated and buffered aspirin?

Cordially,

RL

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

RL,
All subscribers (including RL) please note that the questions were not answered.
The correct answers are
Alumninum poisoning is a known medical issue.
Yes, some babies do develop reactions to the Hep-B vaccine.

Related to your questions to me:
Yes, if a person drinks huge amounts of water--it can kill them.

Yes, buffered asperin contains aluminum. Thanks for pointing it out to me.
I just checked the label and confirmed that you are correct. I don't know
about enteric coated aspirin.

thanks for your post,
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Jason Johnson wrote:

In article , JohnDoe
wrote:

Jason Johnson wrote:

Mark,
I know that ONE vaccine that contains alumninum is not likely to
cause harm.
However, as you probably know, alumninum is in many different products
such as
antacids. If they started placing alumninum in all vaccines (to replace
mercury), it could cause high levels of alumninum to build up in the
bodies of people.

Why would you ASSUME that there would be a build up?

It could cause as much harm as high levels of mercury.

Why would you assume that? Different toxins act differently. Spend some
time learning the various types of "snake venom" and how they work.

It could lead to alumninum poisoning. Heavy metal poisoning and alumninum
poisoning are known medical issues. I was shocked when I noticed that
almost every brand of antacids contains high levels of alumninum.

Does the body absorb it, though? Does the body retain it?

One dose
of alumninum is NOT a problem--however, I hope that even you would agree
that 100 doses of alumninum is a problem--esp. in those people that have
an allergic reactions to alumninum.

Only if it accumulates to a toxic level.

People that have various types of
kidney diseases are advised not to use productes that contain alumninum.

Why?

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Mark,
You made some good points in your post. I have conducted some research
related to kidney diseases mainly by reading a book that was written by a
kidney specialist that is a professor at a medical college. I am NOT an
expert on kidney diseases. It's my understanding based upon what I read in
that book that diseased kidneys have a difficult time removing various
substances such as mercury, alumninum (and various types of medications),
and other heavy metals from the body. As a result, those things
accumuluate and cause great harm. For example, if you drank an entire
bottle of an antacid (and had normal kidneys), it probably would not harm
you. On the other hand, if someone that had weak or diseased kidneys,
drank a bottle of antacid, the alumninum in that bottle of antacid may
cause great harm and perhaps even alumninum poisoning.

Dear Jason, have you ever heard the expression: "the poison is in the
dosage"? Or: "one aspirin takes the headache away, a whole bottle takes
the patient away"? Are you aware that you can die from drinking too much
water. Yes, plain, good ol' H2O. Are you aware that aluminum is one of
the most ubiquitous element on the face of the earth and if it really
were that poisonous, life on earth as we know it would not exist? Are
you aware that aluminum is NOT a heavy metal, but in fact one of the
lightest metals that we know of?

You would be amazed
at the number of medications that have a warning that states: "People that
have kidney disease or liver disease should NOT take this medication."
Yes--I would agree that heavy metals may in some cases (e.g. kidney
disease) accumulate to a toxic level.
Jason
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ ~~~

JohnDoe,
True or False:
Is alumninum poisoning a know medical issue?

At what dose Jason, at what dose?

Do babies ever develop reactions to the Hep-B vaccine that contains alumninum?

And if they ever did, did aluminum cause it?
Dear Jason, the word 'metal' does not equal 'so poisonous it should be
wholly removed from the environment'. While you may not be an anti-vac
liar, you certainly seem to suffer from a degree of delusion with regard
to the toxicity of metals.

Jason

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ ~~~~~~~~~

"JohnDoe" wrote in message
. ..
Jason Johnson wrote:

..... And if they ever did, did aluminum cause it?
Dear Jason, the word 'metal' does not equal 'so poisonous it should be
wholly removed from the environment'. While you may not be an anti-vac
liar, you certainly seem to suffer from a degree of delusion with regard
to the toxicity of metals.

....

Hmmm... would that mean (according to those that equate metal to "bad") that
the following metals should never be ingested by humans:

calcium ...
http://www.theodoregray.com/Periodic.../index.s7.html
iron ...
http://www.theodoregray.com/Periodic.../index.s7.html
sodium ...
http://www.theodoregray.com/Periodic.../index.s7.html
potassium ...
http://www.theodoregray.com/Periodic.../index.s7.html

HCN wrote:
"JohnDoe" wrote in message
. ..
Jason Johnson wrote:

.... And if they ever did, did aluminum cause it?
Dear Jason, the word 'metal' does not equal 'so poisonous it should be
wholly removed from the environment'. While you may not be an anti-vac
liar, you certainly seem to suffer from a degree of delusion with regard
to the toxicity of metals.

...

Hmmm... would that mean (according to those that equate metal to "bad") that
the following metals should never be ingested by humans:

calcium ...
http://www.theodoregray.com/Periodic.../index.s7.html
iron ...
http://www.theodoregray.com/Periodic.../index.s7.html
sodium ...
http://www.theodoregray.com/Periodic.../index.s7.html
potassium ...
http://www.theodoregray.com/Periodic.../index.s7.html
http://www.theodoregray.com/Periodic.../index.s7.html