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  #31  
Old August 1st 06, 06:57 AM posted to misc.health.alternative,misc.kids.health,sci.med,uk.politics,uk.politics.misc
Jan Drew
external usenet poster
 
Posts: 2,707
Default 'the MMR10'.


"Mark Probert" wrote in message
...
Jason Johnson wrote:

http://www.laleva.cc/environment/alu...lzheimer2.html
Can Aluminum Cause Alzheimer's Dis
by Melvyn R. Werbach, M.D. Senile dementia is a progressive degenerative
brain disease associated
with old age. Its symptoms include short-term memory loss, slowness in
thought and movement, confusion, disorientation, depression,
difficulty communicating, and loss of physical function. Alzheimer's
disease accounts for about half of all senile dementia cases. Although
there are many theories about what causes Alzheimer's, the fact is,
its origins remain poorly understood. One theory proposed that the
common occurrence of being exposed to
aluminum could cause Alzheimer's dementia. Aluminum, the theory
postulated, becomes concentrated in the characteristic lesions (senile
plaques and neurofibrillary tangles) that develop in the brain during
the course of the disease. At first, medical scientists thought this
theory was absurd. Aluminum, they believed, accumulated merely as a
result of a destructive process caused by some other factor. In recent
years, however, the aluminum hypothesis has been gaining
respect. For example, studies have discovered a direct association
between the level of aluminum in municipal drinking water and the risk
of Alzheimer's dementia. One study found aluminum in drinking water
was related to only this specific type of dementia;1 another found
that the probability of the association being due to chance was only 1
in 24, with a 46 percent increased risk for people drinking water with
the highest aluminum levels.2 The use of aluminum-containing
antiperspirants--but not the use of
antiperspirants and deodorants in general--has also been associated
with a risk of Alzheimer's dementia, with a trend toward a higher risk
corresponding with increasing frequency of use.3 This relationship
does not extend to aluminum-containing antacids,4 which may simply be
evidence that the aluminum in antacids is not absorbed--the process of
absorption through the gut mucosa is quite different from absorption
through the skin. We also know that serum aluminum concentrations
increase with age.
Aluminum may accumulate slowly over our lifetimes or we may absorb it
more easily as we age. Moreover, there is evidence that people with
probable Alzheimer's disease have serum aluminum levels that are often
significantly higher than those of people with other types of
dementia, as well healthy people of similar ages.5 Further evidence that
aluminum fosters the development of Alzheimer's
dementia comes from a scientific (placebo-controlled) trial of
desferrioxamine, a drug that removes aluminum from the body by binding
with it. While regular administration of the drug failed to stop the
disease from progressing, desferrioxamine did significantly reduce the
rate of decline in the ability of a group of people with Alzheimer's
dementia to care for themselves.6 Although the aluminum/Alzheimer's link
remains unproven, I believe
that waiting for definitive proof before taking a few easy and
protective measures is foolhardy--and more scientists are starting to
agree.7,8 Perhaps one person in 10 age 65 or older suffers from
dementia; by age 80 that figure rises to one in five. This is too
common an illness to ignore preventive measures until we can know for
certain why it develops. Ways To Avoid Aluminum Here are my suggestions
for minimizing your exposure to aluminum. * Drinking water should be low
in aluminum. Some bottled-water
companies provide an analysis of the aluminum content of their water.
You might also find out from your public water company what the
aluminum level is in the local drinking water. * Aluminum-containing
antiperspirants can easily be avoided, as can
aluminum utensils and even, to play it safe, aluminum-containing
antacids. * Commercially processed foods such as cake and pancake mixes,
frozen
doughs and self-rising flour are sources of dietary aluminum, so their
ingestion should be minimized. Watch for and avoid sodium aluminum
phosphate, an ingredient in baking powder. Pickles and cheese should
also be avoided. * There is a close relationship between silicon and
aluminum in
Alzheimer brain lesions, as the two substances bind together to form
aluminosilicates.9 High levels of silica in drinking water in the form
of silicic acid do seem to protect against the adverse effects of
aluminum ingestion, and silicic acid ingestion increases urinary
aluminum excretion.10,11 Whether silica supplements protect against
the development of dementia has yet to be determined. * Besides
minimizing aluminum exposure, taking the Recommended Dietary
Allowance (RDA) of calcium, magnesium and zinc should help to protect
against aluminum accumulation.12-14 Deficiencies of these important
minerals are common among the elderly.15 Yet, unless there is
laboratory evidence of a zinc deficiency, I would not recommend zinc
supplementation to help prevent Alzheimer's disease, for two reasons.
First, beta-amyloid protein, the major substance found in the brain
lesions (usually in a liquid form), binds with zinc. At concentrations
only slightly higher than those normally found in the brain, excess
zinc may convert the protein to the solid form that is found in
Alzheimer lesions.16 This suggests that, at least in theory, excess
zinc could actually promote the development of the disease. Second,
there is a lack of adequate research demonstrating the efficacy of
zinc supplementation in preventing Alzheimer's, although in one study
all six relatively young dementia victims had some memory improvement
following supplementation with zinc aspartate.17 References 1. Martyn,
C.N., et al. Lancet, 1: 59-62, 1989. 2. Neri, L.C., & Hewitt, D. Letter.
Lancet, 338: 390, 1991. 3. Graves, A.B., et al. J Clin Epidemio,l 43(1):
35-44, 1990. 4. Ibid. 5. Zapatero, M.D. Biol Trace Elem Res, 47: 235-40,
1995. 6. McLachlan, D.R., et al. Lancet, 337: 1304-8, 1991. 7. Lukiw,
W.J. Mineral and Metal Neurotoxicology. 113-26. CRC Press,
1997. 8. McLachlan, D.R., et al. Can Med Assoc J, 145(7): 793-804, 1991.
9. Candy, J.M., et al. Lancet, i: 354-57, 1986. 10. Jacqmin-Gadda, H., et
al. Epidemiology 7(3): 281-85, 1996. 11. Bellia, J.P., et al. Ann Clin
Lab Sci, 26: 227-33, 1996. 12. Foster, H.D. Health, Disease and the
Environment. 311-16. Boca
Raton, Fla.: CRC Press, 1992: 13. Durlach, J. Magnes Res, 3(3): 217-18,
1990. 14. Wenk, G.L., & Stemmer, K.L. Brain Res 288: 393-95, 1983. 15.
Werbach, M.R. Foundations of Nutritional Medicine: Common
nutritional deficiencies. Tarzana, Calif.: Third Line Press, 1997. 16.
Bush, A.I., et al. Science, 265: 1464-67, 1994. 17. Constantinidis, J.
Schweiz Arch Neurol Neurochir Psychiatr,
141(6): 523-56, 1990. Melvyn R. Werbach, M.D., is a faculty member at
the UCLA School of
Medicine and the author of Nutritional Influences on Illness (Third
Line Press Inc., 1993). Melvyn R. Werbach, M.D., is a faculty member at
the UCLA School of
Medicine and the author of Nutritional Influences on Illness (Third
Line Press Inc., 1993).


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ ~~~~~~ Ilena,
Thanks for posting this interesting research study. The "gang" keeps
asking for studies and you posted an excellent study.


Jason, until you email me as I requested, I will merely comment on what
you post, and not engage in discussion with you.


http://groups.google.com/group/misc....db5f3991fe0575

Jul 30 2006 12:57 pm

BTW, just for your information, if wish to have further discussion with
me, I suggest that you email me.


mark{dot}probert{at}gmail{dot}com


No email, no further responses.
==

Poor Mark.

As for what is posted above, it is NOT a study by any means. It is an
article with annotations. IOW, it is expository writing providing the
writers point of view, which may or may not be correct. His citation of
the various articles are not necessarily accurate. Each must be checked.

For an example of how "leading researchers" can mis-cite and mis-state
information that they reference, you should read:

http://neurodiversity.comAGREES with Mark's BS.

[ ]




  #32  
Old August 1st 06, 07:32 AM posted to misc.health.alternative,misc.kids.health,sci.med,uk.politics.misc
cathyb
external usenet poster
 
Posts: 145
Default 'the MMR10'.

Jan Drew wrote:
You cannot be shown anything. Deaf, dumb, blind and brainwashed.

It is noted you did not show any proof.


It's noted that Jan couldn't provide any evidence that "the aluminum,
in the doses used, is a neurotoxin or an unacceptable risk" and that
she indulged in playground taunts instead. Plus ça change, plus c'est
la même chose.


"Jeff" wrote in message
ink.net...

"Jan Drew" wrote in message
...
(...)

I meant to say: "Water is a known poison. Yet, I consume liters of it
nearly every day."

The fact of the matter is that aluminum is in vaccines because it helps
the vaccine work better.

Jeff

Prove it.


http://www.nal.usda.gov/awic/pubs/antibody/overview.htm

The FACT is

Aluminum is an established neurotoxin.

Further fact, you dismissed all studies that have been posted.

You are a waste of time.


Please show that the aluminum, in the doses used, is a neurotoxin or an
unacceptable risk.

Jeff


  #33  
Old August 1st 06, 12:37 PM posted to misc.health.alternative,misc.kids.health,sci.med,uk.politics,uk.politics.misc
Jeff
external usenet poster
 
Posts: 780
Default 'the MMR10'.


"Jan Drew" wrote in message
.. .
You cannot be shown anything. Deaf, dumb, blind and brainwashed.


I saw a thread about a "true gentleman."

Thanks for showing how to be a true lady.

It is noted you did not show any proof.


I had a link to a US Drug Administration site about the use of many
different compounds in vaccines, including aluminum. This backed my
statement that aluminum is used to help vaccines work better.

My deepest apologies if the USDA is not good enough evidence for you on why
aluminum is used in vaccines.

Jeff

"Jeff" wrote in message
ink.net...

"Jan Drew" wrote in message
...
(...)

I meant to say: "Water is a known poison. Yet, I consume liters of it
nearly every day."

The fact of the matter is that aluminum is in vaccines because it helps
the vaccine work better.

Jeff

Prove it.


http://www.nal.usda.gov/awic/pubs/antibody/overview.htm

The FACT is

Aluminum is an established neurotoxin.

Further fact, you dismissed all studies that have been posted.

You are a waste of time.


Please show that the aluminum, in the doses used, is a neurotoxin or an
unacceptable risk.

Jeff





  #34  
Old August 1st 06, 04:22 PM posted to misc.health.alternative,misc.kids.health,sci.med,uk.politics,uk.politics.misc
john
external usenet poster
 
Posts: 265
Default 'the MMR10'.


"Jeff" wrote in message
k.net...


No child can escape poisons.


Wrong again. Children can escape vaccine poisons by not being vaccinated.


  #35  
Old August 1st 06, 08:03 PM posted to misc.health.alternative,misc.kids.health,sci.med,uk.politics,uk.politics.misc
Jan Drew
external usenet poster
 
Posts: 2,707
Default 'the MMR10'.


"Jeff" wrote in message
k.net...

"Jan Drew" wrote in message
.. .
You cannot be shown anything. Deaf, dumb, blind and brainwashed.


I saw a thread about a "true gentleman."


Good. WE *ALL* should take a lesson from him.


Thanks for showing how to be a true lady.


Got a problem with truth?

It is noted you did not show any proof.


I had a link to a US Drug Administration site about the use of many
different compounds in vaccines, including aluminum. This backed my
statement that aluminum is used to help vaccines work better.

My deepest apologies if the USDA is not good enough evidence for you on
why aluminum is used in vaccines.

Jeff


Sure, Jeff. How deep?

The USDA. No, they are not good enough for me.

I do not trust *organized medicine*. Neither do I trust the government.

But--you knew that.

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

==

Health Health Archives
Vaccines show sinister side
By pieta woolley


Publish Date: 23-Mar-2006


If two dozen once-jittery mice at UBC are telling the truth
postmortem, the world's governments may soon be facing one hell of a
lawsuit. New, so-far-unpublished research led by Vancouver
neuroscientist Chris Shaw shows a link between the aluminum hydroxide
used in vaccines, and symptoms associated with Parkinson's,
amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease), and
Alzheimer's.


Shaw is most surprised that the research for his paper hadn't been
done before. For 80 years, doctors have injected patients with
aluminum hydroxide, he said, an adjuvant that stimulates immune
response.


"This is suspicious," he told the Georgia Straight in a phone
interview from his lab near Heather Street and West 12th Avenue.
"Either this [link] is known by industry and it was never made public,
or industry was never made to do these studies by Health Canada. I'm
not sure which is scarier."


Similar adjuvants are used in the following vaccines, according to
Shaw's paper: hepatitis A and B, and the Pentacel cocktail, which
vaccinates against diphtheria, pertussis, tetanus, polio, and a type
of meningitis.


To test the link theory, Shaw and his four-scientist team from UBC and
Louisiana State University injected mice with the anthrax vaccine
developed for the first Gulf War. Because Gulf War Syndrome looks a
lot like ALS, Shaw explained, the neuroscientists had a chance to
isolate a possible cause. All deployed troops were vaccinated with an
aluminum hydroxide compound. Vaccinated troops who were not deployed
to the Gulf developed similar symptoms at a similar rate, according to
Shaw.


After 20 weeks studying the mice, the team found statistically
significant increases in anxiety (38 percent); memory deficits (41
times the errors as in the sample group); and an allergic skin
reaction (20 percent). Tissue samples after the mice were "sacrificed"
showed neurological cells were dying. Inside the mice's brains, in a
part that controls movement, 35 percent of the cells were destroying
themselves.


"No one in my lab wants to get vaccinated," he said. "This totally
creeped us out. We weren't out there to poke holes in vaccines. But
all of a sudden, oh my God-we've got neuron death!"


At the end of the paper, Shaw warns that "whether the risk of
protection from a dreaded disease outweighs the risk of toxicity is a
question that demands our urgent attention."


He's not the only one considering that.


The charge that there's a sinister side to magic bullets isn't new.
With his pen blazing, celebrity journalist Robert F. Kennedy Jr.
popularized vaccine scepticism with his article arguing that mercury
in vaccines causes autism, which ran in the June 2005 Rolling Stone
and on-line at Salon.com. So did last year's vaccines-linked-to-
autism bestseller, Evidence of Harm by David Kirby (St. Martin's
Press). But there's a potential public-health cost to all the
controversy, according to the B.C. Centre for Disease Control.


"Vaccines have been a victim of their own success," spokesperson Ian
Roe told the Straight in a telephone interview from Ottawa. Diseases
such as polio, which killed his father-in-law, are almost eradicated
and therefore no longer serve as a warning to parents. But the
epidemic threat is still real. "If everyone decided to not get
vaccinated, we'd live in a very different world."


Canada's last national immunization conference, in December 2004,
heard a report that vaccine coverage is sometimes low. For diphtheria,
the Public Health Agency of Canada found that just 75 percent of
two-year-olds are immunized; the target is 99 percent. For tetanus,
just 66 percent of 17-year-olds are immunized, compared to a target of
97 percent.


Dr. Ronald Gold, the former head of the infectious-disease division at
Toronto's Hospital for Sick Children, told the conference that "we
will never be without an anti-vaccine movement," but "in reality,
there is no scientific evidence for these myths."


Shaw acknowledges that there's a lot of pressure on parents to
vaccinate their children. "You're considered to be a really bad parent
if you don't vaccinate," he said-and your child can't attend public
school. "But I don't think the safety of vaccines is demarcated. How
does a parent make a decision based on what's available? You can't
make an intelligent decision."


Conservatively, he said, if one percent of vaccinated humans develop
ALS from vaccine adjuvants, it would still constitute a health
emergency.


It's possible, he said, that there are 10,000 studies that show
aluminum hydroxide is safe for injections. But he hasn't been able to
find any that look beyond the first few weeks of injection. If anyone
has a study that shows something different, he said, please "put it on
the table. That's how you do science."


Neuroscience research is difficult, Shaw said, because symptoms can
take years to manifest, so it's hard to prove what caused the
symptoms.


"To me, that calls for better testing, not blind faith."


He pointed out that George W. Bush passed legislation that opens the
door for the USA to order a nationwide anthrax immunization campaign,
with the threat of bioterrorism.


Shaw's paper is currently undergoing a peer review.

http://www.straight.com/content.cfm?id=16717


==

Safety of Aluminum Added to Vaccines as a Vaccine Adjuvant


E-mail from Dr. Philip Rudnick Ph.D.
Professor Emeritus, Chemistry
West Chester University of Pennsylvania


Date: Sun, 08 Dec 2002 15:08:06 -0500
From:
To:
Subject: Aluminum Neurotoxicity





http://www.altcorp.com/TESTFoundation/thimelililly.htm


Thimerosal is certainly a very potent neurotoxin. It should never have
been used in vaccines, particularly for infants and children. But what about
aluminum INJECTED into the body not as a vaccine preservative but as a
vaccine adjuvant? (Aluminum is not readily absorbed from the GI tract.)
Aluminum, also is a neurotoxin. This has been known for over 100 years. And
what safety studies have ever been done about the possible neurotoxic
interaction/synergism of thimerosal and aluminum?


Sincerely,


Philip Rudnick, PhD


Professor Emeritus, Chemistry


West Chester University of Pennsylvania


Some Refences:


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...=1608913&form=...


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.


==



Of course you have never read * A Dragon by the Tail*.................

http://www.hpakids.org/holistic-heal...Tail/print/183

Of course--you did. You were there in the thread

==

Posting..................

These experts include people
from the American Academy of Pediatrics, the CDC, FDA and Institute of
Medicine of the National Academy of Sciences.

You see that's what I don't trust --YOU.

You have never said your were an MD...............

Or --**Who is this Putz guy? Certainly, I have not seen someone with that
name
**here.


Jeffrey Peter, M.D.

"I no longer practice medicine. So I am no longer licensed." --Jeff Utz, MD
(Jeffrey Peter, M.D. )



Message 2 in thread From: Jeffrey Peter, M.D. ) Subject:
"Dr. Kid" ... Newsgroups: misc.kids.health, misc.health.alternative
Date: 2000/11/07 In article
, (Ilena
Rose) wrote:
Are you really a pediatrician ? What state are you licensed in, if so
and under what name?

I no longer practice medicine. So I am no longer licensed. Jeff Utz



Wed, May 2 2001 6:50 pm
Email: "Jeffrey Peter, M.D."

**Who is this Putz guy? Certainly, I have not seen someone with that name
**here.


Jeff P Utz


It's you ... and you are so deaf, dumb & blind ... you don't even
recognize yourself ... duh ........


Jeff PUtz 's Questions


For starters.




"Jeff" wrote in message
ink.net...

"Jan Drew" wrote in message
...
(...)

I meant to say: "Water is a known poison. Yet, I consume liters of it
nearly every day."

The fact of the matter is that aluminum is in vaccines because it
helps the vaccine work better.

Jeff

Prove it.

http://www.nal.usda.gov/awic/pubs/antibody/overview.htm

The FACT is

Aluminum is an established neurotoxin.

Further fact, you dismissed all studies that have been posted.

You are a waste of time.

Please show that the aluminum, in the doses used, is a neurotoxin or an
unacceptable risk.

Jeff







  #36  
Old August 1st 06, 11:22 PM posted to misc.health.alternative,misc.kids.health,sci.med,uk.politics,uk.politics.misc
Jeff
external usenet poster
 
Posts: 780
Default 'the MMR10'.


"john" wrote in message
...

"Jeff" wrote in message
k.net...


No child can escape poisons.


Wrong again. Children can escape vaccine poisons by not being vaccinated.


They also would have to not drink water, not eat cooked meat, not be around
electric motors, not be in a city, etc. Sorry, but there are poisons in very
small quantities all around us.

The benefits of vaccinations greatly outweigh the risks. The so-called
poisons are not toxic at the doses used and help the vaccines work better.

Jeff


 




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