Aluminum in Vaccines

[RobinN]

This research was done by Stan Kurtz. He graciously allowed me to bring it to CWE if I linked to his site. Stan also moderates the progressive online Health group that collaborates with 2,000 families and professionals helping to improving chronic illness and autism using the techniques Stan developed while recovering himself from IBS and ADHD and his son Ethan from Autism. It can be found at:
http://health.groups.yahoo.com/group/mb12valtrex/

I am a believer of Stan's methods. Who wouldn't be after looking at his recovery videos. I am touched each time I view them. I thank him for the use of his research.

Stan has researched over 20 medical articles and prefaces his post by this statement:

This is a bit much for anyone to read, but let's just say that aluminum in vaccines is probably not a good idea as far as toxicity, brain and central nervous system cell death, motor, memory issues, oxidative stress, neurodegenerative disease and more.

Aluminum is well studied as being a toxin. Here are 20 or so peer-reviewed citation summaries relating to aluminum. I have put together a draft of information to add to my anti-infection document.

My best,

- Stan

Effects of aluminum on the nervous system and its possible link with neurodegenerative
diseases.

Kawahara M.

Department of Analytical Chemistry, School of Pharmaceutical Sciences, Kyushu University
of Health and Welfare, Nobeoka-city, Miyazaki, 882-8508, Japan.
kawamasa@phoenix.ac.jp

Aluminum is environmentally abundant, but not an essential element. Aluminum has been associated with several neurodegenerative diseases, such as dialysis encephalopathy, amyotrophic lateral sclerosis and Parkinsonism dementia in the Kii peninsula and Guam, and in particular, Alzheimer's disease. Although this association remains controversial, there is increasing evidence which suggests the implication of metal homeostasis in the
pathogenesis of Alzheimer's disease. Aluminum, zinc, copper, and iron cause the conformational changes of Alzheimer's amyloid-beta protein. Al causes the accumulation of tau protein and amyloid-beta protein in experimental animals. Aluminum induces neuronal apoptosis in vivo as well as in vitro. Furthermore, a relationship between
aluminum and the iron-homeostasis or calcium-homeostasis has been suggested. Based
on these findings, the characteristics of aluminum neurotoxicity are reviewed, and the potential link between aluminum and neurodegenerative diseases is reconsidered.

Aluminum: new recognition of an old problem.

Klein GL.

Children's Hospital Room 3.270, University of Texas Medical Branch, 301 University
Boulevard, Galveston TX 77555-0352, USA. gklein@utmb.edu

The aluminum problem is now over 25 years old, but has remained a neglected concern. Data indicate that aluminum contaminates much of the raw material used to manufacture solutions used for intravenous nutritional support of hospitalized and ambulatory patients, and that pharmaceutical manufacturers have only recently obtained the technology necessary to detect aluminum contamination of their products. As a result, aluminum bypassed normal barriers and entered the blood, accumulating in tissues such as bone, liver and the central nervous system with toxic consequences. Now that the FDA has finally issued a rule governing aluminum contamination in these solutions, manufacturers
will need to develop methods to minimize such contamination; scientists should also realize that when data they obtain indicate a serious problem in the manufacturing sector they should be sure that the problem is properly addressed.

Aluminum as a toxicant.

Becaria A, Campbell A, Bondy SC.

Department of Community and Environmental Medicine, Center for Occupational and
Environmental Health Sciences, Irvine, CA 92697-1820, USA. abecaria@uci.edu

Although aluminum is the most abundant metal in nature, it has no known biological function. However, it is known that there is a causal role for aluminum in dialysis encephalopathy, microcytic anemia, and osteomalacia. Aluminum has also been proposed
to play a role in the pathogenesis of Alzheimer's disease (AD) even though this issue is controversial. The exact mechanism of aluminum toxicity is not known but accumulating evidence suggests that the metal can potentiate oxidative and inflammatory events, eventually leading to tissue damage. This review encompasses the general toxicology of aluminum with emphasis on the potential mechanisms by which it may accelerate the progression of chronic age-related neurodegenerative disorders.

Aluminum inclusion macrophagic myofasciitis: a recently identified condition.

Gherardi RK, Authier FJ.

Muscle and Nerve Group, Henri Mondor University Hospital, Créteil, France. lauret@univ-
paris12.fr

The authors conclude that the persistence of aluminum hydroxide at the site of intramuscular injection is a novel finding which has an exact significance that remains to be established fully. It seems mandatory to evaluate possible long-term adverse effects induced by this compound, because this issue has not been addressed (in the past,
aluminum hydroxide was believed to be cleared quickly from the body). If safety concerns about the long-term effects of aluminum hydroxide are confirmed, novel and alternative vaccine adjuvants to rescue vaccine-based strategies should be proposed to ensure the enormous benefit for public health that these vaccines provide worldwide.

 

[RobinN]

Aluminum salts in vaccines--US perspective.

Baylor NW, Egan W, Richman P.

Food and Drug Administration, Center for Biologics Evaluation and Research, Office of Vaccines Research and Review, Bethesda, MD, USA. baylor@cber.fda.gov

Aluminum in the form of aluminum hydroxide, aluminum phosphate or alum has been commonly used as an adjuvant in many vaccines licensed by the US Food and Drug Administration. Chapter 21 of the US Code of Federal Regulations [610.15(a)] limits the amount of aluminum in biological products, including vaccines, to 0.85 mg/dose. The amount of aluminum in vaccines currently licensed in the US ranges from 0.85-0.125 mg/dose. Clinical studies have demonstrated that aluminum enhances the antigenicity of some vaccines such as diphtheria and tetanus toxoids. Moreover, aluminum-adsorbed
diphtheria and tetanus toxoids are distinctly more effective than plain fluid toxoids for primary immunization of children. There is little difference between plain and adsorbed toxoids for booster immunization. Aluminum adjuvants have a demonstrated safety profile of over six decades; however, these adjuvants have been associated with severe local reactions such as erythema, subcutaneous nodules and contact hypersensitivity.

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

Szutowicz A.

Chair of Clinical Biochemistry, Department of Laboratory Medicine, Medical University of
Gdańsk, Debinki 7, 80-211 Gdańsk, Poland. aszut@amg.gda.pl

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.

College of Pharmacy and Graduate Center for Toxicology, University of Kentucky Medical
Center, Lexington, USA. ryokel1@pop.uky.edu

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.

Stan has researched about 20 medical articles on the subject.

 

[RobinN]

After all the literature I just sent regarding one vaccine ingredient, aluminum, here is a
citation from the Pediatrics Journal and the Division of Infectious Diseases who says....

"...quantities of mercury, aluminum, formaldehyde, human serum albumin, antibiotics, and
yeast proteins in vaccines have not been found to be harmful in humans or experimental
animals."

They use the word quantities in case they are sued they might say "I meant quantities less
than 1:1,000,000,000,000,000,000"

----
Of course mercury, aluminum, formaldehyde, antibiotics, and yeast have been found to
cause harm in humans or animals....

This type of behavior is just gross to me.

- Stan

Once again I thank Stan for this info. Please visit his website or come ask a few questions at the Yahoo group.