A Compilation of Documentation


Aluminum Involvement in the Progression of Alzheimer’s Disease.
Article in Journal of Alzheimer’s disease: JAD 35(1) · February 2013
DOI: 10.3233/JAD-121909 · Source: PubMed

1st J R Walton

The neuroanatomic specificity with which Alzheimer’s disease (AD) progresses could provide clues to AD etiopathology. Magnetic resonance imaging studies of AD clinical progression have confirmed general conclusions from earlier studies of AD neuropathological progression wherein neurofibrillary tangle pathology was observed to spread along a well-defined sequence of corticocortical and corticosubcortical connections, preferentially affecting certain cell types, while sparing others. Identical and non-identical twin studies have consistently shown AD has mixed (environmental and genetic) etiopathogenesis. The decades-long prodromal phase over which AD develops suggests slow but progressive accumulation of a toxic or infective agent over time. Major environmental candidates are reviewed to assess which best fits the profile of an agent that slowly accrues in susceptible cell types of AD-vulnerable brain regions to toxic levels by old age, giving rise to AD neuropathology without rapid neuronal lysis. Chronic aluminum neurotoxicity best matches this profile. Many humans routinely ingest aluminum salts as additives contained in processed foods and alum-treated drinking water. The physical properties of aluminum and ferric iron ions are similar, allowing aluminum to use mechanisms evolved for iron to enter vulnerable neurons involved in AD progression, accumulate in those neurons, and cause neurofibrillary damage. The genetic component of AD etiopathogenesis apparently involves a susceptibility gene, yet to be identified, that increases aluminum absorption because AD and Down syndrome patients have higher than normal plasma, and brain, aluminum levels. This review describes evidence for aluminum involvement in AD neuropathology and the clinical progression of sporadic AD.
The putative role of environmental aluminium in the development of chronic neuropathology in adults and children. How strong is the evidence and what could be the mechanisms involved?
Review article
Morris G, et al. Metab Brain Dis. 2017.
Show full citation
The conceptualisation of autistic spectrum disorder and Alzheimer’s disease has undergone something of a paradigm shift in recent years and rather than being viewed as single illnesses with a unitary pathogenesis and pathophysiology they are increasingly considered to be heterogeneous syndromes with a complex multifactorial aetiopathogenesis, involving a highly complex and diverse combination of genetic, epigenetic and environmental factors. One such environmental factor implicated as a potential cause in both syndromes is aluminium, as an element or as part of a salt, received, for example, in oral form or as an adjuvant. Such administration has the potential to induce pathology via several routes such as provoking dysfunction and/or activation of glial cells which play an indispensable role in the regulation of central nervous system homeostasis and neurodevelopment. Other routes include the generation of oxidative stress, depletion of reduced glutathione, direct and indirect reductions in mitochondrial performance and integrity, and increasing the production of proinflammatory cytokines in both the brain and peripherally. The mechanisms whereby environmental aluminium could contribute to the development of the highly specific pattern of neuropathology seen in Alzheimer’s disease are described. Also detailed are several mechanisms whereby significant quantities of aluminium introduced via immunisation could produce chronic neuropathology in genetically susceptible children. Accordingly, it is recommended that the use of aluminium salts in immunisations should be discontinued and that adults should take steps to minimise their exposure to environmental aluminium.

PMID 28752219 [PubMed – in process] PMCID PMC5596046

Aluminium based adjuvants and their effects on mitochondria and lysosomes of phagocytosing cells.
Ohlsson L, et al. J Inorg Biochem. 2013.
Show full citation
Aluminium oxyhydroxide, Al(OH)3 is one of few compounds approved as an adjuvant in human vaccines. However, the mechanism behind its immune stimulating properties is still poorly understood. In vitro co-culture of an aluminium adjuvant and the human monocytic cell line THP-1 resulted in reduced cell proliferation. Inhibition occurred at concentrations of adjuvant several times lower than would be found at the injection site using a vaccine formulation containing an aluminium adjuvant. Based on evaluation of the mitochondrial membrane potential, THP-1 cells showed no mitochondrial rupture after co-culture with the aluminium adjuvant, instead an increase in mitochondrial activity was seen. The THP-1 cells are phagocytosing cells and after co-culture with the aluminium adjuvant the phagosomal pathway was obstructed. Primary or early phagosomes mature into phagolysosomes with an internal pH of 4.5 – 5 and carry a wide variety of hydrolysing enzymes. Co-culture with the aluminium adjuvant yielded a reduced level of acidic vesicles and cathepsin L activity, a proteolytic enzyme of the phagolysosomes, was almost completely inhibited. THP-1 cells are an appropriate in vitro model in order to investigate the mechanism behind the induction of a phagocytosing antigen presenting cell into an inflammatory cell by aluminium adjuvants. Much information will be gained by investigating the phagosomal pathway and what occurs inside the phagosomes and to elucidate the ultimate fate of phagocytosed aluminium particles.

© 2013.
PMID 23992993 [PubMed – indexed for MEDLINE]
Oxidative stress and mitochondrial dysfunction in aluminium neurotoxicity and its amelioration: a review.
Review article
Kumar V, et al. Neurotoxicology. 2014.
Show full citation
Aluminium is light weight and toxic metal present ubiquitously on earth which has gained considerable attention due to its neurotoxic effects. The widespread use of products made from or containing aluminium is ensuring its presence in our body. There is prolonged retention of a fraction of aluminium that enters the brain, suggesting its potential for accumulation with repeated exposures. There is no known biological role for aluminium within the body but adverse physiological effects of this metal have been observed in mammals. The generation of oxidative stress may be attributed to its toxic consequences in animals and humans. The oxidative stress has been implicated in pathogenesis of various neurodegenerative conditions including Alzheimer’s disease and Parkinson’s disease. Though it remains unclear whether oxidative stress is a major cause or merely a consequence of cellular dysfunction associated with neurodegenerative diseases, an accumulating body of evidence implicates that impaired mitochondrial energy production and increased mitochondrial oxidative damage is associated with the pathogenesis of neurodegenerative disorders. Being involved in the production of reactive oxygen species, aluminium may impair mitochondrial bioenergetics and may lead to the generation of oxidative stress. In this review, we have discussed the oxidative stress and mitochondrial dysfunctions occurring in Al neurotoxicity. In addition, the ameliorative measures undertaken in aluminium induced oxidative stress and mitochondrial dysfunctions have also been highlighted.

Copyright © 2014 Elsevier Inc. All rights reserved.
PMID 24560992 [PubMed – indexed for MEDLINE]
Full text

Adaptive Downregulation of Mitochondrial Function in Down Syndrome
Pablo Helguera, Jaqueline Seiglie, […], and Jorge Busciglio

Additional article information

Mitochondrial dysfunction and oxidative stress are common features of Down syndrome (DS). However, the underlying mechanisms are not known. We investigated the relationship between abnormal energy metabolism and oxidative stress with transcriptional and functional changes in DS cells. Impaired mitochondrial activity correlated with altered mitochondrial morphology. Increasing fusion capacity prevented morphological but not functional alterations in DS mitochondria. Sustained stimulation restored mitochondrial functional parameters but increased ROS production and cell damage, suggesting that reduced DS mitochondrial activity is an adaptive response to avoid injury and preserve basic cellular functions. Network analysis of genes overexpressed in DS cells demonstrated functional integration in pathways involved in energy metabolism and oxidative stress. Thus, while preventing extensive oxidative damage, mitochondrial downregulation may contribute to increased susceptibility of DS individuals to clinical conditions in which altered energy metabolism may play a role such as Alzheimer’s disease, diabetes, and some types of autistic spectrum disorders.
Chronic oxidative stress and mitochondrial dysfunction are conspicuous features of DS (Arbuzova et al., 2002; Slonim et al., 2009). We found that mitochondrial morphology is consistently altered in DS cells, which exhibit increased fragmentation. Mitofusin overexpression reverted the fragmented phenotype. However, it did not improve MMP in DS cells. Consequently, we investigated whether DS mitochondria actually possessed the capacity to increase ATP production after metabolic stimulation. Creatine increased DS mitochondrial activity and mitochondrial anterograde movement, but it nearly doubled ROS levels, increased lipid peroxidation and reduced viability in DS cells. Thus, sustained stimulation resulted in increased DS cell damage and death, suggesting that the downregulation of DS mitochondria is part of an adaptive response to avoid excessive ROS generation and cellular injury.

From a broader perspective, the relation between mitochondrial morphology and function appears to be context-specific, depending on the cell’s state and the factors affecting it. For example, in insulinoma cells, ATP-dependent hormone secretion is not affected by induced mitochondrial fragmentation with a dominant negative form of mfn1 but is significantly reduced by hFis1 overexpression, which also generates a fragmented phenotype (Park et al., 2008). In the case of DS primary cells, mitochondria are more fragmented and both energy production and some cellular functions are impaired. Thus, the balance between mitochondrial morphology and function is complex and it is influenced by multiple factors.

We found 92 genes differentially expressed in DS cells. Ingenuity analysis generated a network of overexpressed genes indicative of a transcriptional response to oxidative stress (SFig 2). These changes in gene expression may orchestrate the cellular adaptations required to preserve homeostasis in DS cells, including downregulation of energy metabolism. This possibility is further supported by similar although less pronounced changes in the expression of “DS signature genes” in NL astrocytes under mild oxidative stress (Fig 4B). Under basal culture conditions, which are nevertheless pro-oxidant, and where DS energy metabolism is already impaired (Coskun and Busciglio, 2012; Valenti et al., 2011), the adaptive response would stabilize cell homeostasis at the expense of compromising cellular functions dependent on particular energy requirements, e.g. insulin secretion in β cells or axonal transport in neurons. At the organismal level, this adaptation may contribute to the increased susceptibility of DS individuals to pathologies in which energy metabolism appears to be compromised such as Alzheimer’s disease, diabetes, and some forms of autism (Capone et al., 2005; Esbensen, 2010; Lott and Head, 2005).

Recent studies have underscored the critical role of chronic superoxide production leading to mitochondrial dysfunction, telomere shortening and replicative senescence in human cells (Passos et al., 2007), further suggesting that the accelerated senescence phenotype characteristic of DS cells (Pallardo et al., 2010) may also be a direct result of cumulative oxidative damage and mitochondrial mutations (Coskun and Busciglio, 2012). Aneuploidies in general are detrimental to organismal and cellular function, altering cell metabolism and decreasing cell proliferation in yeast, mice and humans, regardless of which chromosome is affected (Williams et al., 2008). In fact, human fibroblasts harboring different aneuploidies display similar increased sensitivity and common cellular responses to chronic oxidative stress (Helguera and Busciglio, unpublished result). In this context, DS phenotypes at both cellular and system levels would arise from the interplay between specific changes in chromosome 21-gene expression operating on a background of generalized metabolic perturbations set off by the aneuploid state.

In summary, DS cells exhibit chronic energy deficits that appear to be part of an adaptive response to minimize oxidative damage and preserve cellular homeostasis. Depending on particular energy requirements, specific cellular functions will be affected in different cell types. In the case of DS pancreatic β cells, insulin secretion and proinsulin processing were significantly improved only when antioxidant treatment and mitochondrial stimulation were applied together. Thus, combined therapeutic strategies directed to prevent free radical damage while modulating energy metabolism may prove valuable for managing some of the clinical manifestations commonly associated with DS.

Myelination defects in Down syndrome

Pamela J. Hines
Science 06 May 2016:
Vol. 352, Issue 6286, pp. 669-670
DOI: 10.1126/science.352.6286.669-e
In Down syndrome (DS), an extra chromosome 21 causes a variety of developmental and cognitive disabilities. Olmos-Serrano et al., have compared the transcriptome of postmortem brains from normal donors as well as those with DS, surveying developmental stages from prenatal to adult. Of over 17,000 genes profiled from two regions of the brain, about 4% revealed abnormal expression. Dysregulated genes, found across the whole genome and throughout the age range, grouped by function. One group of genes affected oligodendrocytes and myelination. Indeed, myelination was deficient in a mouse model of DS, contributing to defective transmission of neural signals. The authors speculate that poor myelination may underlie the problems with learning, memory, and age-related neurodegeneration that characterize DS.
Neuron 89, 1208–1222 (2016).
Science: 352 (6286)

Medication-induced mitochondrial damage and disease.
Review article
Neustadt J, et al. Mol Nutr Food Res. 2008.
Show full citation
Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer’s disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson’s disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
PMID 18626887 [PubMed – indexed for MEDLINE]

Inhibition of Drp1-mediated mitochondrial fission improves mitochondrial dynamics and bioenergetics stimulating neurogenesis in hippocampal progenitor cells from a Down syndrome mouse model.
Valenti D, et al. Biochim Biophys Acta. 2017.
Functional and structural damages to mitochondria have been critically associated with the pathogenesis of Down syndrome (DS), a human multifactorial disease caused by trisomy of chromosome 21 and associated with neurodevelopmental delay, intellectual disability and early neurodegeneration. Recently, we demonstrated in neural progenitor cells (NPCs) isolated from the hippocampus of Ts65Dn mice -a widely used model of DS – a severe impairment of mitochondrial bioenergetics and biogenesis and reduced NPC proliferation. Here we further investigated the origin of mitochondrial dysfunction in DS and explored a possible mechanistic link among alteration of mitochondrial dynamics, mitochondrial dysfunctions and defective neurogenesis in DS. We first analyzed mitochondrial network and structure by both confocal and transmission electron microscopy as well as by evaluating the levels of key proteins involved in the fission and fusion machinery. We found a fragmentation of mitochondria due to an increase in mitochondrial fission associated with an up-regulation of dynamin-related protein 1 (Drp1), and a decrease in mitochondrial fusion associated with a down-regulation of mitofusin 2 (Mnf2) and increased proteolysis of optic atrophy 1 (Opa1). Next, using the well-known neuroprotective agent mitochondrial division inhibitor 1 (Mdivi-1), we assessed whether the inhibition of mitochondrial fission might reverse alteration of mitochondrial dynamics and mitochondrial dysfunctions in DS neural progenitors cells. We demonstrate here for the first time, that Mdivi-1 restores mitochondrial network organization, mitochondrial energy production and ultimately improves proliferation and neuronal differentiation of NPCs. This research paves the way for the discovery of new therapeutic tools in managing some DS-associated clinical manifestations.
Copyright © 2017 Elsevier B.V. All rights reserved.
PMID 28939434 [PubMed – in process]
Intrinsic defect of the immune system in children with Down syndrome: a review.
Review article
Kusters MA, et al. Clin Exp Immunol. 2009.

Down syndrome (DS) is the most frequent cause of mental retardation in man. Immunological changes in DS have been observed since the 1970s. The neurological system appears to be ageing precociously, with early occurrence of Alzheimer disease; until now, the observed immunological differences have been interpreted in the same context. Looking back at past and present results of immunological studies in DS children in relation to the clinical consequences they suffer, we conclude that it is more likely that the DS immune system is intrinsically deficient from the very beginning.
PMID 19250275 [PubMed – indexed for MEDLINE] PMCID PMC2759463
Non-efficacy of low-dose intradermal vaccination against hepatitis B in Down’s syndrome.

Ahman L1, Bäck E, Bensch K, Olcén P.
Author information
Persons with Down’s syndrome (DS) constitute a risk group for hepatitis B (HB) and are recommended to be immunized. Of 123 persons with DS in Orebro county screened for markers of HB, 31% had such markers; 16% were potentially contagious. 83 persons without markers participated in a comparative trial of the immunogenicity of a recombinant HB vaccine given either intramuscularly (IM) or in a lower dose intradermally (ID). Immunity developed in 73% after IM vaccination as compared to 29% of those given ID vaccination (p < 0.005). At 3-year follow-up half and two-thirds of the immune persons, respectively, had lost their immunity. Those > 30 years had a poor immunization response compared to the younger ones (p < 0.01). Only 19% of the non-responders developed immunity after an IM booster dose given 10 months after the third injection. Intradermal vaccination is not warranted in persons with DS, especially not in middle aged and older persons. A booster dose of vaccine does not ascertain immunity in those who do not respond with immunity to the ordinary immunization schedule. Post-vaccination immunity should therefore be controlled.

Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia
Pinar E. Coskun1,2 and Jorge Busciglio1,2
1Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders (iMIND), University of California, Irvine, CA 92697, USA
2Center for the Neurobiology of Learning and Memory (CNLM), University of California, Irvine, CA 92697, USA
Received 1 November 2011; Accepted 13 February 2012
Academic Editor: Elizabeth Head

Genome-wide gene deregulation and oxidative stress appear to be critical factors determining the high variability of phenotypes in Down’s syndrome (DS). Even though individuals with trisomy 21 exhibit a higher survival rate compared to other aneuploidies, most of them die in utero or early during postnatal life. While the survivors are currently predicted to live past 60 years, they suffer higher incidence of age-related conditions including Alzheimer’s disease (AD). This paper is centered on the mechanisms by which mitochondrial factors and oxidative stress may orchestrate an adaptive response directed to maintain basic cellular functions and survival in DS. In this context, the timing of therapeutic interventions should be carefully considered for the successful treatment of chronic disorders in the DS population.
Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia.
Perluigi M, et al. Curr Gerontol Geriatr Res. 2012.
Show full citation
Down syndrome (DS) is one of the most frequent genetic abnormalities characterized by multiple pathological phenotypes. Indeed, currently life expectancy and quality of life for DS patients have improved, although with increasing age pathological dysfunctions are exacerbated and intellectual disability may lead to the development of Alzheimer’s type dementia (AD). The neuropathology of DS is complex and includes the development of AD by middle age, altered free radical metabolism, and impaired mitochondrial function, both of which contribute to neuronal degeneration. Understanding the molecular basis that drives the development of AD is an intense field of research. Our laboratories are interested in understanding the role of oxidative stress as link between DS and AD. This review examines the current literature that showed oxidative damage in DS by identifying putative molecular pathways that play a central role in the neurodegenerative processes. In addition, considering the role of mitochondrial dysfunction in neurodegenerative phenomena, results demonstrating the involvement of impaired mitochondria in DS pathology could contribute a direct link between normal aging and development of AD-like dementia in DS patients.
PMID 22203843 [PubMed] PMCID PMC3235450

Oxidative stress and mitochondrial dysfunction in Down syndrome.
Pagano G, et al. Adv Exp Med Biol. 2012.
Down syndrome (DS) or trisomy 21 is the genetic disease with highest prevalence displaying phenotypic features that both include neurologic deficiencies and a number of clinical outcomes. DS-associated neurodegeneration recalls the clinical course of Alzheimer disease (AD), due to DS progression toward dementia and amyloid plaques reminiscent of AD clinical course. Moreover, DS represents one of the best documented cases of a human disorder aetiologically related to the redox imbalance that has long been attributed to overexpression of Cu,Zn-superoxide dismutase (SOD-1), encoded by trisomic chromosome 21. The involvement of oxidative stress has been reported both in genes located else than at chromosome 21 and in transcriptional regulation of genes located at other chromosomes. Another well documented hallmark of DS phenotype is represented by a set of immunologic defects encompassing a number of B and T-cell functions and cytokine production, together prompting a proinflammatory state. In turn, this condition can be directly interrelated with an in vivo prooxidant state. As an essential link to oxidative stress, mitochondrial dysfunctions are observed whenever redox imbalances occur, due to the main roles of mitochondria in oxygen metabolism and this is the case for DS. Ultrastructural and biochemical abnormalities were reported in mitochondria from human DS patients and from trisomy 16 (Ts16) mice, to be reviewed in this chapter. Together, in vivo alterations of mitochondrial function are consistent with a prooxidant state as a phenotypic hallmark in DS.
PMID 22411251 [PubMed – indexed for MEDLINE]
Antibody response to pneumococcal vaccine in patients with trisomy-21 (Down’s syndrome).

Nurmi T, Leinonen M, Häivä VM, Tiilikainen A, Kouvalainen K.
The antibody response to pneumococcal vaccine was lower in adults with trisomy-21 (Down’s syndrome) than in controls. Males gave lower response than females, significantly so among the 21-trisomic patients. The antibody response to different polysaccharides differed between the groups.
Immune evaluation and vaccine responses in Down syndrome: evidence of immunodeficiency?
Joshi AY, et al. Vaccine. 2011.
Show full citation
BACKGROUND: Patients with Down syndrome (DS) appear to be at a greater risk for serious infections, but it is unclear whether this is due to anatomic variations or intrinsic immune defects.

OBJECTIVE: We assessed a cohort of pediatric subjects with DS to determine if immunological abnormalities indeed account for the excess infections.
METHODS: We performed quantitative assessment of T-independent (type 2 – pneumococcal polysaccharide vaccine) and T-dependent Ab responses (with inactivated seasonal influenza vaccine) along with numerical quantitation of lymphocyte subpopulations and thymic output in a random population sample of children with DS (cases) along with family-matched sibling or community controls.
RESULTS: Median serum IgG levels were significantly higher in cases (1090 mg/dL) as compared with controls (808 mg/dL, P=0.02). Cases had significantly lower median CD4 T cell counts than the controls (636 cells/μL, P=0.01). Cases had reduced CD19 B cell counts and CD19% than the controls (P=0.009 and 0.006 respectively). Cases also showed decreased total memory (CD19+CD27+, P=0.002) and class-switched memory (CD19+CD27+IgM-IgD-, P=0.004) B cells. The median CD4 recent thymic emigrant (RTE) in females and males cases was lower than controls (P=0.007 and 0.07 respectively). Cases had a lower median T cell receptor excision circle (TREC) count of 2556 as compared to the controls count of 5216, P<0.006 although both the cases and controls were within the established reference range. There were no differences in the percentage of cases and controls who responded to inactivated influenza vaccine, but the response to polysaccharide pneumococcal vaccine was suboptimal in cases.
CONCLUSIONS: Our study suggests that there are subtle abnormalities in both humoral and cellular arms of the immune response in children with DS as compared to the control subjects.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID 21596078 [PubMed – indexed for MEDLINE] PMCID PMC3909669

Infections and immunodeficiency in Down syndrome
G Ram and J Chinen
Down syndrome (DS) is the most common genetic disease and presents with cognitive impairment, cardiac and gastrointestinal abnormalities, in addition to other miscellaneous clinical conditions. DS individuals may have a high frequency of infections, usually of the upper respiratory tract, characterized by increased severity and prolonged course of disease, which are partially attributed to defects of the immune system. The abnormalities of the immune system associated with DS include: mild to moderate T and B cell lymphopenia, with marked decrease of naive lymphocytes, impaired mitogen-induced T cell proliferation, reduced specific antibody responses to immunizations and defects of neutrophil chemotaxis. Limited evidence of genetic abnormalities secondary to trisomy of chromosome 21 and affecting the immune system is available, such as the potential consequences of gene over-expression, most significantly SOD1 and RCAN1. Secondary immunodeficiency due to metabolic or nutritional factors in DS, particularly zinc deficiency, has been postulated. Non-immunological factors, including abnormal anatomical structures (e.g. small ear canal, tracheomalacia) and gastro-oesophageal reflux, may play a role in the increased frequency of respiratory tract infections. The molecular mechanisms leading to the immune defects observed in DS individuals and the contribution of these immunological abnormalities to the increased risk of infections require further investigation. Addressing immunological and non-immunological factors involved in the pathogenesis of infectious diseases may reduce the susceptibility to infections in DS subjects.
Vaccination and autoimmune diseases: is prevention of adverse health effects on the horizon?

Vadalà M, et al. EPMA J. 2017.
Autoimmune diseases, including multiple sclerosis and type 1 diabetes mellitus, affect about 5% of the worldwide population. In the last decade, reports have accumulated on various autoimmune disorders, such as idiopathic thrombocytopenia purpura, myopericarditis, primary ovarian failure, and systemic lupus erythematosus (SLE), following vaccination. In this review, we discuss the possible underlying mechanisms of autoimmune reactions following vaccinations and review cases of autoimmune diseases that have been correlated with vaccination. Molecular mimicry and bystander activation are reported as possible mechanisms by which vaccines can cause autoimmune reactions. The individuals who might be susceptible to develop these reactions could be especially not only those with previous post-vaccination phenomena and those with allergies but also in individuals who are prone to develop autoimmune diseases, such as those with a family history of autoimmunity or with known autoantibodies, and the genetic predisposed individuals. Further research is encouraged into the direct associations between vaccines and autoimmune conditions, and the biological mechanisms behind them.
PMID 29021840 [PubMed] PMCID PMC560715

Trisomy 21 and the brain.
Review article
Mrak RE, et al. J Neuropathol Exp Neurol. 2004.
In fetuses with Down syndrome, neurons fail to show normal dendritic development, yielding a “tree in winter” appearance. This developmental failure is thought to result in mental retardation. In adults with Down syndrome, neuronal loss is dramatic and neurofibrillary and neuritic Abeta plaque pathologies are consistent with Alzheimer disease. These pathological changes are thought to underlie the neuropsychological and physiological changes in older individuals with Down syndrome. Two chromosome 21-based gene products, beta-amyloid precursor protein (betaAPP) and S100B, have been implicated in these neuronal and interstitial changes. Although not necessary for mental retardation and other features, betaAPP gene triplication is necessary, although perhaps not sufficient, for development of Alzheimer pathology. S100B is overexpressed throughout life in Down patients, and mice with extra copies of the S100B gene have dendritic abnormalities. S100B overexpression correlates with Alzheimer pathology in post-adolescent Down syndrome patients and has been implicated in Abeta plaque pathogenesis. Interleukin-1 (IL-1) is a non-chromosome-21-based cytokine that is also overexpressed throughout life in Down syndrome. IL-1 upregulates betaAPP and S100B expression and drives numerous neurodegenerative and self-amplifying cascades that support a neuroinflammatory component in the pathogenesis of sporadic and Down syndrome-related Alzheimer disease.
PMID 15290893 [PubMed – indexed for MEDLINE] PMCID PMC3833615

Impaired myelination of the human hippocampal formation in Down syndrome.
Ábrahám H, et al. Int J Dev Neurosci. 2012.
Myelination is considered as one of the last steps of neuronal development and is essential to the physiologically matured function of afferent and efferent pathways. In the present study, myelin formation was examined in the human fetal, postnatal and adult hippocampal formation in Down syndrome and in age-matched controls with immunohistochemistry detecting a protein component of the myelin sheath, the myelin basic protein synthesized by oligodendroglial cells. Myelination is mainly a postnatal event in the hippocampal formation of both healthy controls and in patients with Down syndrome. In patients with Down syndrome the sequence of myelination of the hippocampal formation followed a similar developmental pattern to that in controls. However, myelin formation was generally delayed in Down syndrome compared to age-matched controls. In addition, in the hilus of the dentate gyrus a decreased density of myelinated axons was detected from the start of myelination until adulthood. The majority of local axons (mossy fibers) are not myelinated in the hilar region and myelinated fibers arriving in the hilus come mainly from the subcortical septal nuclei. Since intact septo-hippocampal connections are necessary for memory formation, we hypothesize that decreased myelination in the hilus may contribute to the mental retardation of Down syndrome patients.
Copyright © 2011 ISDN. Published by Elsevier Ltd. All rights reserved.
PMID 22155002 [PubMed – indexed for MEDLINE

Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria.
Murakami K, et al. J Cell Biochem. 2004.
Effect of aluminum on the NADPH supply and glutathione regeneration in mitochondria was analyzed. Reduced glutathione acted as a principal scavenger of reactive oxygen species in mitochondria. Aluminum inhibited the regeneration of glutathione from the oxidized form, and the effect was due to the inhibition of NADP-isocitrate dehydrogenase the only enzyme supplying NADPH in mitochondria. In cytosol, aluminum inhibited the glutathione regeneration dependent on NADPH supply by malic enzyme and NADP-isocitrate dehydrogenase, but did not affect the glucose 6-phosphate dehydrogenase dependent glutathione formation. Aluminum can cause oxidative damage on cellular biological processes by inhibiting glutathione regeneration through the inhibition of NADPH supply in mitochondria, but only a little inhibitory effect on the glutathione generation in cytosol.

Copyright 2004 Wiley-Liss, Inc.
PMID 15486972 [PubMed – indexed for MEDLINE
Aluminum-Induced Entropy in Biological Systems: Implications for Neurological Disease


Over the last 200 years, mining, smelting, and refining of aluminum (Al) in various forms have increasingly exposed living species to this naturally abundant metal. Because of its prevalence in the earth’s crust, prior to its recent uses it was regarded as inert and therefore harmless. However, Al is invariably toxic to living systems and has no known beneficial role in any biological systems. Humans are increasingly exposed to Al from food, water, medicinals, vaccines, and cosmetics, as well as from industrial occupational exposure. Al disrupts biological self-ordering, energy transduction, and signaling systems, thus increasing biosemiotic entropy. Beginning with the biophysics of water, disruption progresses through the macromolecules that are crucial to living processes (DNAs, RNAs, proteoglycans, and proteins). It injures cells, circuits, and subsystems and can cause catastrophic failures ending in death. Al forms toxic complexes with other elements, such as fluorine, and interacts negatively with mercury, lead, and glyphosate. Al negatively impacts the central nervous system in all species that have been studied, including humans. Because of the global impacts of Al on water dynamics and biosemiotic systems, CNS disorders in humans are sensitive indicators of the Al toxicants to which we are being exposed.

Myelin is a preferential target of aluminum-mediated oxidative damage.
Verstraeten SV, et al. Arch Biochem Biophys. 1997.
The capacity of Al3+ to promote oxidative damage to brain membranes was investigated both in vitro and in vivo. In vitro, Al3+ and related metals (Sc3+, Ga3+, In3+, Be2+, Y3+, and La3+) stimulated Fe2+-initiated lipid and protein oxidation in brain myelin and synaptic membranes. Al3+, Sc3+, Y3+, and La3+ significantly promoted protein-associated carbonyl production in myelin, while in synaptic membranes, the stimulatory effect was observed in the presence of Ga3+, In3+, Y3+, Sc3+, and La3+. In myelin the magnitude of the stimulation of lipid oxidation followed the order Sc3+, Y3+, La3+ > Al3+, Ga3+, In3+ > Be2+. When compared to mitochondria and microsomal and synaptic membranes, myelin showed a marked susceptibility to Al3+-mediated lipid peroxidation. The differential susceptibility of myelin compared to synaptic membranes could not be explained by differences in membrane composition, since the relative content of negatively charged phospholipids (binding sites) was similar for both membranes, and myelin had a lower content of poly-unsaturated fatty acids (substrates of lipid oxidation) and a higher concentration of alpha-tocopherol compared to synaptic membranes. In a model of Al3+ intoxication imposed to mice during pregnancy and early development, a 72% higher content of lipid peroxidation products was found in brain myelin. The fluidity of myelin evaluated by the polarization fluorescence of 1,3-diphenylhexatriene was significantly higher in the Al3+-intoxicated mice than in controls. Since myelin has a high relative content of lipid:protein compared to other membranes, these results support our hypothesis that ions without redox capacity can stimulate in vitro and in vivo lipid oxidation by promoting phase separation and membrane rigidification, thus accelerating lipid oxidation.
PMID 9264541 [PubMed – indexed for MEDLINE]

Microglial activation and chronic neurodegeneration.
Lull ME, et al. Neurotherapeutics. 2010.
Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurodegenerative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-α, nitric oxide, interleukin-1β, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson’s disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype.

Copyright © 2010 The American Society for Experimental NeuroTherapeutics, Inc. Published by
PMID 20880500 [PubMed – indexed for MEDLINE] PMCID PMC2951017
Polysorbate-80 coating enhances uptake of polybutylcyanoacrylate (PBCA)-nanoparticles by human and bovine primary brain capillary endothelial cells
© European Neuroscience Association
Issue European Journal of Neuroscience
European Journal of Neuroscience
Volume 12, Issue 6, pages 1931–1940, June 2000

Certain drugs such as dalargin, loperamide or tubocurarine are not transported across the blood–brain barrier (BBB) and therefore exhibit no effects on the central nervous system. However, effects on the central nervous system can be observed when these drugs are loaded onto polybutylcyanoacrylate (PBCA)-nanoparticles and coated with polysorbate 80. The mechanism by which these complexed nanoparticles cross the BBB and exhibit their effects has not been elucidated. Cultured microvessel brain endothelial cells of human and bovine origin were used as an in vitro model for the BBB to gain further insight into the mechanism of uptake of nanoparticles. With cells from these species we were able to show that polysorbate 80-coated nanoparticles were taken up by brain endothelial cells much more rapidly and in significantly higher amounts (20-fold) than uncoated nanoparticles. The process of uptake was followed by fluorescence and confocal laser scanning microscopy. The results demonstrate that the nanoparticles are taken up by cells and that this uptake occurs via an endocytotic mechanism.

Aluminum adjuvants of vaccines injected into the muscle: Normal fate, pathology and associated disease.
Aluminum oxyhydroxide (Alhydrogel(®)) is a nano-crystalline compound forming aggregates that has been introduced in vaccine for its immunologic adjuvant effect in 1926. It is the most commonly used adjuvant in human and veterinary vaccines but mechanisms by which it stimulates immune responses remain ill-defined. Although generally well tolerated on the short term, it has been suspected to occasionally cause delayed neurologic problems in susceptible individuals. In particular, the long-term persistence of aluminic granuloma also termed macrophagic myofasciitis is associated with chronic arthromyalgias and fatigue and cognitive dysfunction. Safety concerns largely depend on the long biopersistence time inherent to this adjuvant, which may be related to its quick withdrawal from the interstitial fluid by avid cellular uptake; and the capacity of adjuvant particles to migrate and slowly accumulate in lymphoid organs and the brain, a phenomenon documented in animal models and resulting from MCP1/CCL2-dependant translocation of adjuvant-loaded monocyte-lineage cells (Trojan horse phenomenon). These novel insights strongly suggest that serious re-evaluation of long-term aluminum adjuvant phamacokinetics and safety should be carried out.

Copyright © 2016 Elsevier Masson SAS. All rights reserved.
PMID 26948677 [PubMed – indexed for MEDLINE]


Subcutaneous injections of aluminum at vaccine adjuvant levels activate innate immune genes in mouse brain that are homologous with biomarkers of autism
sciencedirect.com | December 1, 2017

Autism is a neurobehavioral disorder characterized by immune dysfunction. It is manifested in early childhood, during a window of early developmental vulnerability where the normal developmental trajectory is most susceptible to xenobiotic insults. Aluminum (Al) vaccine adjuvants are xenobiotics with immunostimulating and neurotoxic properties to which infants worldwide are routinely exposed. To investigate Al′s immune and neurotoxic impact in vivo, we tested the expression of 17 genes which are implicated in both autism and innate immune response in brain samples of Al-injected mice in comparison to control mice. Several key players of innate immunity, such as cytokines CCL2, IFNG and TNFA, were significantly upregulated, while the nuclear factor-kappa beta (NF-κB) inhibitor NFKBIB, and the enzyme controlling the degradation of the neurotransmitter acetylcholine (ACHE), were downregulated in Al-injected male mice. Further, the decrease of the NF-κB inhibitor and the consequent increase in inflammatory signals, led to the activation of the NF-κB signaling pathway resulting in the release of chemokine MIP-1A and cytokines IL-4 and IL-6. It thus appears that Al triggered innate immune system activation and altered cholinergic activity in male mice, observations which are consistent with those in autism. Female mice were less susceptible to Al exposure as only the expression levels of NF-κB inhibitor and TNFA were altered. Regional patterns of gene expression alterations also exhibited gender differences, as frontal cortex was the most affected area in males and cerebellum in females. Thus, Al adjuvant promotes brain inflammation and males appear to be more susceptible to Al′s toxic effects.

Autism spectrum disorders (ASD) is a heterogeneous group of neurodevelopmental disorders characterized by impairment in social interaction, verbal communication and repetitive/stereotypic behaviors [1] ; [2]. A growing body of scientific literature shows that general immune dysfunction including various neuroimmune abnormalities (i.e., abnormal cytokine profiles, neuroinflammation and presence of autoantibodies against brain proteins) are key pathological biomarkers in ASD patients [3]; [4]; [5]; [6]; [7]; [8]; [9]; [10]; [11]; [12]; [13]; [14] ; [15]. Other key characteristics of autistic brains include abnormal neural connectivity [16]; [17]; [18] ; [19], decreased number of cerebellar Purkinje cells [20]; [21] ; [22], small cell size and increased cell packing density at all ages in the limbic system (the hippocampus, amygdala and entorhinal cortex) suggesting a curtailment in normal neuronal development [20].

It is also generally acknowledged that ASDs are complex disorders resulting from the combination of genetic and environmental factors with multiple gene–gene and gene–environmental interactions, although there is still uncertainty about the exact proportions of each component [23]. Moreover, the molecular mechanisms of these gene-environmental interactions which result in autistic pathology remain to be discovered. Aluminum (Al) is an environmental toxin with demonstrated negative impact on human health, especially the nervous system, to which humans are regularly exposed. In particular, Al can enter the human body through various sources including food, drinking water, cosmetic products, cooking utensils and pharmaceutical products including antacids and vaccines [24]; [25]; [26]; [27]; [28]; [29]; [30]; [31]; [32] ; [33]. In addition, Al is also present in many infant formulas [34]. However, compared to dietary Al of which only ~ 0.25% is absorbed into systemic circulation, Al from vaccines may be absorbed at over 50% efficiency in the short term [35] and at nearly 100% efficiency long-term [36]. Thus, vaccine-derived Al has a much greater potential to produce toxic effects in the body than that obtained through diet. Nonetheless, even dietary Al has been shown to accumulate in the central nervous system (CNS) over time, producing Alzheimer’s disease type outcomes in experimental animals fed equivalent amounts of Al to those humans consume through a typical Western diet [26] ; [37].

VRM: The Problem With Vaccines Part 2 – Synergistic Effect of Heavy Metal Toxicity On The Body
by Joel Lord

October 20, 2010

Toxicity is defined in the Medical lexicon as “a condition that results from exposure to a toxin or to toxic amounts of a substance that does not cause adverse effects in smaller amounts.” Vaccine-induced toxicity, while similar in some respects to this model, requires a deeper understanding in terms of its overall effect on the human body.
Most practicing MD’s recognize Mercury & Aluminum to be severe neuro-toxins. Still, pediatricians & family doctors routinely recommend their patients (including babies, young children, pregnant women & the elderly) receive the full/partial schedule of standard immunization shots available.

How many of these doctors have examined the package inserts accompanying each vaccine? And if so how many have considered the synergy factor that occurs when combining multiple ingredients such as heavy metals, live viruses (or strands of DNA/RNA “heat treated virus”), mycoplasma, anti-biotics, formaldehyde, detergent, diploid cells, phenol dye & excipient buffers; their synergistic long-term impact on the body’s delicate network of immune, endocrine, nervous, circulatory, lymphatic & digestive system operations?

In a closed door meeting conducted by the CDC in 2000, known as the Simpsonwood Retreat, doctors alluded to their concerns over heavy metal toxicity in vaccines; while acknowledging a glaring void in scientific research on this neglected aspect of synergy,

“Aluminum & mercury are often simultaneously administered to infants, both at the same site & at different sites. However, there is absolutely no data, including animal data, about the potential for SYNERGY, additively or antagonism, all of which can occur in binary metal mixtures that relate and allow us to draw any conclusions from the simultaneous exposure to these two salts in vaccines.” Dr. Dick Johnston/Immunologist & Pediatrician, University of Colorado School of Medicine (see transcript – page 20)
In the same breath, Johnston also stressed the necessity of using aluminum as an adjuvant (immune stimulant) in vaccines,

“Aluminum salts are important in the formulating process of vaccines, both in antigen stabilization and absorption of endotoxin.” (see transcript – page 19)

“But from all of the other studies of toxic substances, the earlier you work with the central nervous system, the more likely you are to run into a sensitive period for one of these effects, so that moving from one month or one day of birth to six months of birth changes enormously the potential for toxicity. There are just a host of neurodevelopmental data that would suggest that we’ve got a serious problem. The earlier we go, the more serious the problem.

The second point I could make is that in relationship to aluminum, being a nephrologist for a long time, the potential for aluminum and central nervous system toxicity was established by dialysis data. To think there isn’t some possible problem here is unreal.” Dr. Bill Weil/Pediatrician, Academy of Pediatricians Committee on Environmental Health (see transcript – page 24)

‎“I got called out at eight o’clock for an emergency call and my daughter-in-law delivered a son by C-section. Our first male in the line of the next generation, and I do not want that grandson to get a Thimerosal containing vaccine until we know better what is going on. It will probably take a long time. In the meantime, and I know there are probably implications for this internationally, but in the meanwhile I think I want that grandson to only be given Thimerosal-free vaccines.” Dr. Johnston (see transcript – page 200)

These are glaring examples of medical hypocrisy in action – such rampant blind trust in long-held beliefs ingrained in medical students throughout their formal training; which thus extends in real practice to the clinics & hospitals we frequent as trusting patients.

Compare this to another professionally held viewpoint:

‘In 1927, Dr. Victor Vaughn, a toxicologist with the University of Michigan, testified before the Federal Trade Commission that “all salts of aluminum are poisonous when injected subcutaneously or intravenously”. According to the American Academy of Pediatrics, “Aluminum is now being implicated as interfering with a variety of cellular & metabolic processes in the nervous system and in other tissues. In 1997 The New England Journal of Medicine published data showing that premature babies injected with aluminum build up toxic levels in the blood, bones and brain, and that aluminum toxicity can lead to neurological damage, including mental handicaps at 18 months of age.” Neil Miller

This wide gulf in understanding can be explained. According to Dr. Russell Blaylock, world renowned former brain surgeon, the average doctor receives the equivalent of a weekend seminar, in their first year only, on the specific topic of the neurological side-effects & disorders associated with vaccine uptake; approximately seven hours of careful, focused study into the complex strata of auto-immune breakdown type complexities. Without this fundamental bedrock of knowledge a critical component is missing from any doctor’s arsenal, considering the widespread impact neurological side-effects to vaccines have had on the community at large.

‎‘No medical man during his student days is taught to think. He is expected to assimilate the thoughts of others and to bow to authority. Throughout the whole of his medical career he must accept the current medical fashions of the day or suffer the loss of prestige and place. No public appointments, no coveted preferments are open to the medical man who declines to parrot the popular shibboleths of his profession. His qualifications may be beyond reproach, he may in himself possess qualities that command respect, but unless prepared to think and act within the narrow circle of accepted dogmas, he must be prepared for a more or less isolated path.’ Dr. Walter Hadwen, M.D., UK

Precisely what is aluminum and why is it so deadly in terms of vaccines?

Aluminium: A silvery-white, ductile metallic element, the most abundant in the earth’s crust but found only in combination, chiefly in bauxite. Having good conductive and thermal properties, it is used to form many hard, light, corrosion-resistant alloys. Atomic number 13; atomic weight 26.98; melting point 660.2°C; boiling point 2,467°C; specific gravity 2.69; valence 3.

‘Aluminium is mined in huge scales as bauxite (typically Al2O3.2H2O). Bauxite contains Fe2O3, SiO2, and other impurities. In order to isolate pure aluminium, these impurities must be removed from the bauxite. This is done by the Bayer process. This involves treatment with sodium hydroxide (NaOH) solution, which results in a solution of sodium aluminate and sodium silicate. The iron remains behind as a solid. When CO2 is blown through the resulting solution, the sodium silicate stays in solution while the aluminium is precipitated out as aluminium hydroxide. The hydroxide can be filtered off, washed, and heated to form pure alumina, Al2O3. The next stage is formation of pure aluminium. This is obtained from the pure Al2O3 by an electrolytic method. Electrolysis is necessary as aluminium is so electropositive. It seems these days that electrolysis of the hot oxide in a carbon lined steel cell acting as the cathode with carbon anodes is most common.’

Aluminum is a highly conductive metal. Note the scientific description: “aluminium is so electropositive”. The human body is also charged with electromagnetic, bio-conductive energy. Essentially we are bio-electric beings. Certain storehouses are concentrated with higher degrees of “conductivity”; in particular the brain which consists primarily of neurons.

‘Under a microscope a neuron looks like an octopus with many tentacles. A neuron can transmit an electrical impulse to the next neuron. The network of electrical impulses enables us to receive information from the physical world and then send it to our brains, and vice versa. Without the neuron circuits our bodies would completely shut down, like turning off the power supply to a city. If it were possible to describe the nervous system as a circuit diagram, with each neuron represented by a single pinhead, such a circuit diagram would require an area of several square kilometres it would be several hundred times more complex than the entire global telephone network.’

Aluminum (Aluminum Hydroxide/Potassium Sulfate) use in vaccines traces back to the early 1920’s. Alum (Sodium Potassium Sulfate) had already been used in Industrial applications for generations, mainly as a fix-it in dyes. In new trials they discovered it would also generate a prolonged immune response when injected into the body as an adjuvant; whereupon aluminum was immediately introduced on the vaccine market. However no studies were done to ascertain its effects on the nervous system or behavior. The Regulatory Agencies quietly rubber stamped & fast tracked the product for approval, merely ‘grandfathering’ it into widespread use, without any precautionary clinical safety analysis. To this day, aside from Squaline (shark oil), aluminum remains the primary immune stimulating component in all ‘heat-treated virus’ type vaccines.

It is important to note Mercury use in vaccines was similarly rubber-stamped into service. ‘Invented in the 1920’s by Eli Lilly (Thimerosal is 49.6% ethlymercury by weight, a neurotoxin known to be more than a hundreds times more lethal to tissue than lead) safety testing consisted of a 1930 study of 22 patients dying from mengiococcal meningitis in an Indiana hospital. Patients were injected with the solutions and followed until their death, which was within days. Because the patients died of meningitis, they were declared to show no adverse reaction to thimerosal and the product was declared safe for use.’

Eli Lilly and Company: Thimerosal/Material Safety Data Sheet – ‘Thimerosal contains 49.6% w/w organically-bound mercury. Exposure Guidelines: Thimerosal – No known occupational exposure limits established. Early signs of mercury poisoning in adults are nervous system effects, including narrowing of the visual field and numbness in the extremities. Exposure to mercury in utero and in children may cause mild to severe mental retardation and mild to severe motor coordination impairment.’

, and blood samples in 2-month-old infants, obtained 3–20 days after vaccination, contain 3.8–20.6 nM ethylmercury. Our studies therefore indicate the potential for thimerosal to cause adverse effects on MS (methionine synthase – determines the viability of cells) activity at concentrations well below the levels produced by individual thimerosal-containing vaccines.‘ M Waly, H Olteanu, R Banerjee, S-W Choi, JB Mason, BS Parker, S Sukumar, S Shim, A Sharma, JM Benzecry, V-A Power-Charnitsky, RC Deth – See page 10

‘Autistic children have much lower Hg (Hemoglobin – Oxygen supplier/iron-containing oxygen-transport metalloprotein in the red blood cells) levels in their birth hair, yet numerous physicians have reported that autistic children carry a higher mercury body burden than control children. The obvious explanation is micro-mercuralism & genetic susceptibility to retention toxicity. There is an obvious gender difference. This is explained by testosterone (male sex hormone) effects on T-toxicity. Estrogen (female sex hormone) decreases Thimerosal toxicity (species defense mechanism equipped in female body) whereas Testosterone increases the toxicity. Gender effects are involved.‘ Dr. Boyd E. Hayley

There is also a myth, perpetrated by the Vaccine Industry, suggesting the alternative use of a muted or heat-treated virus negates any direct infection of the immune system. ‘Attenuated or killed vaccines are not dead or neutral, since they must retain immunising power if they are to produce a reaction from the immune system. Their active principle is therefore to cause disease and insofar as the sought-after effect is to provoke the malady, vaccines represent a traumatizing jolt to the organism.’ Whether you’re receiving a live virus or so called “dead strands of RNA/DNA”, the adjuvant accelerates any lessening which may occur in tempering down the original virus. It is, in essence, super-charged, re-ivigorated by the metal salts or Squaline otherwise added to the concoction; generating a robust immune response.

Immune suppression has everything to do with point of entry into the body; in addition to the timing of exposure to these toxic elements. As mentioned in part one of this article, the vast majority of infections enter the body through the nasal passages (mucous membrane) & the Gastro-Intestinal Tract or the guts (gut flora). Accordingly 80% of the body’s immune system is stationed at these junctures – the first line of defence.

Vaccines are injected into deep muscle tissue, a route which literally bypasses one’s natural defences altogether. Inadvertently, heavy metals & live viruses that would otherwise be sequestered & chelated out of the body, will unnaturally accumulate in the bloodstream. The very young (babies and small children) are at a high risk because their brains are undergoing the most rapid development at the very time they receive the greatest number of vaccinations.

Early onset autism occurs anywhere from 12-18 months, potentially even earlier. It is significant that autism coincides precisely with most intense period of standard immunization. According to the CDC’S ‘Recommended Immunization Schedule for Persons Aged 0 Through 6 Years—United States • 2010’ by 15 months the average child has received 25 injections including: 3 doses of Hepatitis B, Rotavirus, HIB (Haemophilus Influenzae Type b), IPV (Inactivated Polio Vaccine) & Hepatitis A, 4 doses of DPT (Diphtheria, Pertussis, Tetanus) & PCV (Pneumococcal Conjugate Vaccine), 1 dose of Varicella & Meningococcal and 2 doses of MMR (Measles, Mumps, Rubella).

‘Aluminum is now being implicated as interfering with a variety of cellular and metabolic processes in the nervous system and in other tissues.‘ Aluminum Toxicity in Infants and Children (RE9607), Pediatrics Volume 97, Number 3 March, 1996, pp. 413-416

As Dr. Gary Tunsky illustrates, Aluminum is a coagulant which inherently binds to any toxin in its path. In fact its primarily industrial use is to bond debris in water treatment centers; whereupon it is then scraped out of the cylinders during the filtration process.

“Your blood has no method of excretion; Heavy metals & live viruses, formaldehyde are redistributed by the blood to areas of fatty tissue (highly conductive/electrical tissues) – found in the gray matter of the brain, the Myelin Sheath, neurons, the meninges/spine, cardiac cells, breasts & ovaries (in women), prostate (in men). Blood is made of water. When you stick aluminum in your blood, anything that’s toxic debris is going to bond to and coagulate and cause a congestive coccidiosis and this stuff gets caught in the tiny highways & byways.

So you have the big gushing arteries & veins but they byfricate and branch into streams like a river; and they branch in again to the tiny arterial & capillary bits. That’s where the blockages are occurring, the brain, the spine, (the intestines/bowel) fingers & toes – which turn blue, choking of the micro-vessels from all the sludge that gets caught from all these repetitive hits/vaccinations, over & over. There are 60,000 miles of blood-vessels in one body. They run through every part of your muscle, your bone, your brain. Anywhere you stick an inter-muscular injection it goes into the blood. ” Dr. Gary Tunsky

Aluminum is a positively charged bio-conductive element, 64 times more positive than colloidal blood products (ie. anything suspended in your blood) are negative; with the properties of a coagulant. It literally draws in all other metals & toxins in its path. When injected into deep muscle tissue or subcutaneously, this neurotoxin gets redistributed via the bloodstream (consisting of 90% water) to areas of fatty tissue (highly electrical tissues – negatively charged) throughout the body, builds up over time in these delicate centers; primarily in the Brain, Spinal cord, Myelin sheath, Meninges, cardiac cells, breasts & ovaries (in women), prostate (in men), kidneys, liver, gut & bowels.

The viscosity of this toxic sludge resulting from vaccines which accumulates in the organs (ie. heart, liver, kidney, spleen), joints, meninges, intestines, along the neural pathways, veins & capillaries interlacing the entire body (resulting from “stagnant” blood), is comparable to the black paste-like build-up found over time in the lining of your drains – especially in terms of its impact on your vital health.

‘Approximately 25% of the total amount of the cholesterol present in humans is localized to this organ, most of it present in myelin. Almost all brain cholesterol is a product of local synthesis, with the blood-brain barrier efficiently protecting it from exchange with lipoprotein cholesterol in the circulation.

It has been estimated that up to 70% of the brain cholesterol is associated with myelin. Because up to half of the white matter may be composed of myelin, it is unsurprising that the brain is the most cholesterol-rich organ in the body. The concentration of cholesterol in the brain, and particularly in myelin, is consistent with an essential function related to its membrane properties.‘ Division of Clinical Chemistry, Huddinge University Hospital, Sweden

Within 72 hours of oxygen deprivation any cell can become cancerous. Cancer cells thrive in an oxygen-deprived environment. This will occur when bio-conductive aluminum (consisting of live virus, antibiotic, heavy metal, detergent coagulated sludge) clogs/singes the vast network of arterial veins & capillaries leading to the brain, inducing Ischemia.

‘Oxygen–glucose deprivation resulted in expression of apoptotic and necrotic cell death phenotypes, especially in neurons.’ ‘Following 72 hours incubation in the presence of 0.3% O2, cells were labeled with Annexin V/PI and the level of cell death was measured by flow cytometry. In 6 independent experiments, hypoxia increased levels of Annexin V-positive OC316 cells from 5.3 ± 1.0% to 19.2 ± 2.8%; …cell death under these conditions had predominant features of late apoptosis.’

Meanwhile bad food choices (casein, gluten, poly-saturated fats, iodized salts, sugars) produce a breeding ground in the body for long-term infections, thyroid disorder, disease & vaccine derived viruses. All viruses thrive in a non-alkaline, acidic environment. Overall the impact of of Ischemia & excessive alkalinity serve as a double-edged sword, critically damaging our vital health.

‘The human blood is a colloidal suspension. Proteins, Amino acids, heavy metals etc., are carried in suspension within the blood as a function of the net negative charge within the system. Drop the net negative charge, flow pressures in tiny end blood vessel “pipes” will start to sludge, agglomerate, and increase viscosity of blood in circumscribed microscopic vascular areas.

This “sludging” is activated when Aluminum (64 times more positive than colloidal blood products are negative) interacts with Hemoglobin in flow, in the negatively charged environment. This causes the negatively charged blood products to “attract” towards the larger, more massive positively charged Aluminum, causing clumping or “sludging”. This restricts blood flow, and it changes the Zeta Potential to change from -15mv (minus 15 milivolts) towards -10 mv (minus 10 milivolts), or possibly closer to zero. This is an increase in Zeta Potential, from a negatively charge towards neutral. (This is somewhat analogous to a change in state of water as it turns to ice – it’s a change in viscosity, affecting blood flow).

Agglomerates of sludged blood products cannot traverse microscopic blood vessels designed to carry oxygen transporting red blood cells, in single file. Capillary blood vessels oriented against gravity are uniquely susceptible. Forward blood flow momentum is a function of the negative charge and “spin” in fluid dynamics which keeps particles with mass separated from one another. For the brain, and body, this causes hypoxia (low oxygen), anoxia (no oxygen) and ischemia (impaired blood flow). This is bodily harm when vaccine induced.’ Dr. Andrew Moulden
‘It is well known and published in the scientific literature that combinations of two chemicals may be 10 times as toxic as either separately, or 3 chemicals 100 times as toxic…The levels of mercury Thimerosal in vaccines has been shown to be highly neurotoxic, but the effect was found to be much larger due to the synergistic effect with aluminum, which is also in most vaccines.

In an unpublished paper by Frank Hartman entitled, ‘Vaccination. Toxicity. Infection and Science’ Hartman proposed a plausible theory implicating aluminum toxicity as one of the prime agents in vaccines leading to intravascular coagulation. There are over 7000 references to the toxicity of aluminum, he noted. In regard to the procoagulant effects he quoted a simple experiment of making a mixture of flour and water (in which the flour readily goes into the solution). When one drop of an antiperspirant (contains aluminum) is added, the flour immediately clumps and settles to the bottom. Touching on areas of physics, Hartman went on to explain,

“All trace minerals, metals, inorganic materials, proteins and amino acids are held in suspension in liquids as microscopic and submicroscopic particles like dust particles in the air. The very small particles are called colloids. Colloids are held in suspension via a very slight electronegative charge on the surface of each particle. This charge is called a Zeta Potential. The ability of a liquid to carry material in suspension is a function of these minute electrical charges. As the electronegative charge increases, more material can be carried in suspension. As the charge decreases the particles move closer to each other and the liquid is unable to carry the same amount of materials. Calcium and heavy metals drop out first, adhering to the vessel wall or organ surface.

The quantity of positive and negative charges from chemical elements in suspension as colloids has a major effect on carrying capacity. Electropositive ions decrease carrying capacity while electronegative ions increase it. Elements with only one excess positive or one excess negative have little effect on suspensions. Elements with two positive or two negative ions (divalent) such as magnesium or beryllium (+2) have 3000 times more effect on coagulation or dispersion than elements with single ions. Elements with a valence of 3, such as aluminum (+3) and nitrogen and phosphorous (-3) have 6000 times more effect on carrying capacity due to the three extra positive charges. vaccines contain aluminum salts which greater exacerbate coagulation.‘ Excerpt from ‘Medical Veritas: The Journal of Medical Truth’ By Gary S. Goldman, Ph.D P. 133-134

Note: ‘Elements with a valence of 3, such as aluminum (+3), have 6000 times more effect on carrying capacity (sludging toxicity) due to the three extra positive charges.’

The United States Food & Drug Administration ‘Drug Labeling Regulations Guide’ states unequivocally,

“Aluminum may reach toxic levels with prolonged parenteral administration if kidney function is impaired. Premature neonates are particularly at risk because their kidneys are immature, and they require large amounts of calcium and phosphate solutions, which contain aluminum. Research indicates that patients with impaired kidney function, including premature neonates, who receive parenteral levels of aluminum at greater than 4 to 5 [micro]g/kg/day accumulate aluminum at levels associated with central nervous system and bone toxicity. Tissue loading may occur at even lower rates of administration.”

This means that for a 6 pound baby, 11-14 mcg would be toxic. The Hepatitis B vaccine given at birth contains 250 mcg of aluminum – 20 times higher than safety levels allow. Babies weigh about 12 pounds (5.5 kg) at 2 months of age when they receive 1225 mcg of aluminum from their vaccines – 50 times higher than safety levels.’

Currently children are getting 17 shots containing aluminum, a quadrupling of the amount given since the 1970’s. It is found in Hepatitis A, Hepatitis B, DTaP (diphtheria, tetanus, pertussis), Hib (Haemophilus influenzae type b), Pneumococcal & Gardasil (HPV) vaccines.

‘Since the 2002 gradual phase-out of the Thimerosal Mercury in vaccines, the use of aluminum has increased by 20%. Babies receive multiple doses of aluminum-containing shots. For example the Hepatitis B vaccine (Energix-B) is given at birth, 2 and 6 months of age. Each dose contains 250 micrograms (mcg) of aluminum. The DTaP shot (Infanrix) is given at 2, 4, 6, and 15 months. Each dose contains 625 mcg of aluminum. the Hib vaccine (Pedvax) is given at 2, 4, and 12 months. Each dose contains 125 mcg of aluminum. The Hepatitis A vaccine (Havrix) is given at 12 and 18 months. each dose contains 250 mcg of aluminum. Thus babies who follow the CDC immunization schedule are injected with nearly 5000 mcg (50 mg) of aluminum by 18 months of age.‘

Based on Dr. David Ayoub’s findings children, on average, receive 2-400 micrograms per vaccine, over a milligram of Aluminum; a concentration & dosage that is 10 – 20 times more toxic than Mercury. Multiple vaccines are far worse, over a 1000 micrograms on average for a triple set shot. Compounding the problem even more aluminum gets in during the manufacturing process. An indicator that the tools and/or machinery used are not properly monitored for safety.

Dr. Mehl Madrona stresses the considerable dangers inherent to all adjuvants – “The vaccine-adjuvant complex can interfere with the development and integration of the immune, nervous, endocrine, and other body systems leading to profound neurological damage. Even today, adjuvants and adjuvant formulations which combine both immunoenhancing capacity and low toxicity are lacking.”

There is scant scientific literature covering the link between vaccine induced Aluminum toxicity in the brain & Alzheimer’s Disease. However scientists, generally, do concur that vulnerability to aluminum toxicity naturally increases with age as the body’s defences weaken; a common denominator amongst those coping with the disorder. ‘In both human Alzheimer’s disease and aluminum encephalopathy of animals, changes are observed in neurofibrillary structures. We have found that brains from Alzheimer patients contain approximately 1.4 times the aluminum level found in a control series.’

‘Changes of some elements in rat’s tissues except nerve centre with both ovariectomy and chronic aluminum toxication and the effects of estrogen supplement: “The content of Al (Aluminium) in kidney increased. Chronic aluminum toxication make Si (Silicon) transfer to heart of ovariectomized rats, and facilitate Zn (Zinc) in heart transfer to other tissues.”‘

Dr. Russell Blaylock goes even further, suggesting that vaccine derived viruses linger in the organs for decades to a lifetime. After 50 years of prolonged subcutaneous exposure to aluminum the gradual slide toward auto-immune failure, including a host of disorders such as Alzheimer’s, seems inevitable.

“Heavy metals & viruses in vaccines cause abnormal development in brain, long-term changes that put a child at high risk of neuro-degenerative diseases ie. Parkinson’s & Alzheimer’s for the rest of their life; also they become hyper-sensitive to environmental toxins (Pesticides, Herbicides). Live viruses in vaccines are incorporated into your genetic material & passed on to your children.”

‘One such study, in which autopsied elderly were examined for the presence of the measles virus, found that 20% of the brains had live measles viruses and 45% of other organs were infected. These viruses were highly mutated, meaning that they could be just as potent as other measles viruses, but could be even more virulent. Worse, is that in most cases they cause a smoldering destruction of tissues without the obvious symptoms of infection, which has been shown in a number of studies.’ Dr. Blaylock

A mutagenic Measles virus strain commonly infects the bowels of children with Autism. Merck package insert: Measles, Mumps, Rubella vaccine – ‘M-M-R II has not been evaluated for carcinogenic or mutagenic potential, or potential to impair fertility.’

Vaccine derived toxicity triggers intense cytokine reactions in children with Autism – Neuroglial activation and neuroinflammation in the brain of patients with autism: ‘Active neuroinflammatory process in the cerebral cortex, white matter & cerebellum of autistic patients, marked activation of microglia & astroglia. Cytokine profiling indicated that macrophage chemoattractant protein (MCP)-1 & tumor growth factor-beta1, derived from neuroglia, were most prevalent cytokines in brain tissues.’

‘Aluminum is one of the most abundant elements in the environment. Some human exposure is unavoidable — daily intake is largely oral and averages 30-50 mg ( 1 ). Of this, no more than about 7 mg is expected to come from water, based on the maximum reported concentration of aluminum in drinking water ( 2 ) and the average consumption of 2 l water/day. Inhalation exposure is generally negligible, though it can be significant in some occupational settings, as described below.

The contrast between widespread occurrence and relatively low intake underscores the importance of speciation in determining the bioavailability of aluminum, as this metal is of limited solubility in its environmentally occurring forms. Despite generally low exposures, the toxicity of aluminum, particularly to the nervous system, is of concern. Much research on aluminum in recent years has focused on its role in the etiology of Alzheimer’s disease (AD), but epidemiologic studies attempting to link aluminum with AD in drinking water have been inconclusive and contradictory.

Aluminum in pharmaceuticals has been reviewed by Yokel ( 22 ). Some over-the-counter pharmaceuticals such as antacids and buffered aspirin contain sufficient aluminum to increase the daily dose significantly. Many antacids consist of a mixture of Al(OH) 3 and other hydroxides, such as magnesium. Maalox Extra Strength tablets, for instance, contain 400 mg Al(OH) 3 and 400 mg Mg(OH) 2 . The recommended dose for relief from gastric discomfort is up to eight tablets per day; that is, 3.2 g Al(OH) 3 , or 1.1 g aluminum, which is a 30-fold increase over the average exposure from food and drinking water alone. Patients with renal insufficiency often take large quantities of aluminum-containing antacids to bind excess phosphate.

The resulting AlPO 4 is insoluble, making the phosphate more easily excretable via the feces. Other potentially significant exposures, though likely to be short term, can occur through use of intravenous solutions: 10% calcium gluconate and 3 M potassium phosphate were found to contain 5.1 mg aluminum/g and 17 mg/g, respectively. Diphtheria-pertussis-tetanus vaccine, administered widely in the United States to children and adults, contains an aluminum adjuvant ( 18 ).

Note: “the toxicity of aluminum, particularly to the nervous system, is of concern”.

Neuro-scientist Dr. Christopher Shaw has conducted rigorous independent studies to ascertain the connection between between aluminum in vaccines and the prevalence of dead motor neurons in mice; with indications of massive cell disruption. He has conclusive evidence verifying his theory.

‘In the first study, mice were subjected at regular intervals to specific behavioral tests of motor and cognitive function, including wire mesh hang (2×/week), open field (1×/week), and water maze (1×/week) over a 6 months post injection period (see [22]). The order in which the animals were tested was randomized for each trial. In the second study, we conducted a more detailed behavioural examination based on the automated EthoVision system (Noldus Information Technology, Seattle, WA) employing a video camera and tracking software (Noldus EthoVision® 3.1). Individual movements of the mice were tracked for 5 min in an open field at weekly intervals. The software allowed for quantitative measurements of a variety of motor functions, including distance moved, percentage of time moving, velocity, and a variety of others. These latter experiments continued for 28 weeks following the last injections.

Only mice injected with aluminum hydroxide showed significantly increased Morin labeling of cells in lumbar spinal cord compared to the other groups (Fig. 2A–E). Similarly, only aluminum-injected mice showed the presence of abnormal tau protein in motor neurons in lumbar cord (Fig. 3). Other regions of the cord were not tested in the current studies for either Morin or tau protein.The multiple aluminum hydroxide injections of experiment 2 showed profound effects on motor and other behaviours as shown in Figs. 4 and 5. Multiple aluminum injections produced significant behavioural outcomes including changes in locomotive behaviour, (Fig. 4) and induced memory deficits on water maze tasks (Fig. 5). Other behavioural measures including muscle strength and endurance as measured by the wire hang and motor coordination and balance as measured by rotarod were not significantly affected.

We speculate that the observed neurotoxic effects of aluminum hydroxide in the present study arise by both ‘direct’ and ‘indirect’ pathways, some of which are cited above. Direct toxicity refers to the physical presence (or close proximity) of aluminum and its potential for initiating cell death pathways.
Accumulation of aluminum into the cytoplasm via cellular uptake mechanisms or diffusion could cause alterations in glutaminase and glutamine synthetase and easily alter the availability of the neurotransmitter glutamate [47]. Aluminum acting to induce abnormal tau protein accumulation could also increase neurofibrillary tangles and impair cellular transport mechanisms [48]. Outside the cell, aluminum could affect neurons by altering synapses. For example, aluminum has been shown to decrease the thickness of post-synaptic density, increase the width of the synaptic cleft, and increase the number of flat synapses [49]. Aluminum could also block voltage-activated calcium channels [50], augment the activity of acetylcholinesterase [51], or interfere with synaptic transmission by merely accumulating in the synaptic cleft [52]. Aluminum can also induce apoptosis in astrocytes [53].

Since astrocytes are essential for maintaining neuronal health, any loss of astrocyte function could prove toxic to neurons. Indirect toxicity of aluminum could occur in various ways, including by activating various cytokines [54], releasing glutamate in an excitotoxic cascade, or by modifying various enzymatic pathways [55]. In addition to the above actions specifically on neural cells, aluminum might act indirectly by stimulating abnormal, generalized immune responses. This is, in fact, what adjuvants are placed in vaccines to do in the first place. Adjuvant neurotoxicity could thus be the result of an imbalanced immune response. Rook and Zumla [56] hypothesized that multiple vaccinations, stress, and the method of vaccination could lead to a shift in immune response [56,57]. Aluminum hydroxide has previously been shown to stimulate a Th2-cytokine response [9, 58].’

Smoking gun Study liking Macrophalgic Myofascitis to Aluminum adjuvant toxicity from vaccines: “This is the first report linking the latter with either of these two conditions and the possibility is considered that the coincident aluminium overload contributed significantly to the severity of these conditions in this individual. This case has highlighted potential dangers associated with aluminium-containing adjuvants and we have elucidated a possible mechanism whereby vaccination involving aluminium-containing adjuvants could trigger the cascade of immunological events which are associated with autoimmune conditions including chronic fatigue syndrome and macrophagic myofasciitis.”

NOTE: ‘…

Aluminum, combined with other ingredients commonly added to vaccines, will trigger more rapid & profound cell toxicity. Mercury, another devastating neurotoxin & one of the few liquid elements, actually binds with hemoglobin, which is responsible for oxygen transport to the tissues. In addition it “inhibits the regulation of brain glutamate levels, triggers excitotoxicity, increases brain free radicals and lipid peroxidation products, inhibits critical brain enzymes, inhibits antioxidant enzymes and impairs DNA repair ability”.

Dr. Boyd E. Hayley performed a synergy experiment using aluminum hydroxide, mercury & neomycin (antibiotic associated with Kidney Failure, hazardous to a fetus):

A set of 100 healthy cells were exposed to Aluminum. All the cells died at a certain rate. Another batch of healthy cells were then exposed to Thimerosal Mercury. All the cells died at a comparable rate. A third test of this kind was conducted using Neomycin. All the cells died at a similar rate. Then Haley exposed a healthy set of cells to Aluminum & Thimerosal together. The cells died at twice the previous rate. Finally he combined Aluminum, Thimerosal & Neomycin under the same conditions.

Note: The results indicated a 75% acceleration in cell deaths when all 3 ingredients were combined.

Thimerosal Mercury in vaccines permanently damages tissue sensitivity – ‘Neonatal administration of a vaccine preservative, thimerosal, produces lasting impairment of nociception (awareness of tissue injury) and apparent activation of opioid system in rats. Present findings show that THIM (Thimerosal) administration to suckling or adult rats impairs sensitivity to pain, apparently due to activation the endogenous opioid system.’

Aluminum + Thimerosal = twice the toxic overload – ‘Mercury readily combines with aluminium to form a mercury-aluminium amalgam when the two pure metals come into contact. A small amount of mercury can “eat through” a large amount of aluminium over time, by progressively forming amalgam and relinquishing the aluminium as oxide.‘

Whereas Aluminum is the more dominant metal as a coagulant & in terms of its net charge on the body, Mercury is clearly the more corrosive element.

“A small dose of mercury that kills 1 in 100 rats and a dose of aluminum that will kill 1 in 100 rats, when combined have a striking effect: all the rats die. Doses of mercury that have a 1 percent mortality will have a 100 percent mortality rate if some aluminum is there.” Donald Miller, M.D. Professor of Surgery, University of Washington

Formaldehyde, yet another common additive in vaccines ( used as “a preservative & disinfectant”, linked to cancer & chronic bronchitis) can cause proteins to irreversibly bind to DNA.

3 separate ingredients, each with the properties of a binding agent or coagulant.

a) Aluminum is a coagulant which inherently binds to any toxin

b) Ethyl Mercury (Thimerosal) binds with hemoglobin

c) Formaldehyde causes proteins to irreversibly bind to DNA

How is it possible scientists have overlooked these obvious hazards to neurological & physiological functioning? The overwhelming body of evidence suggests a much darker agenda afoot behind the veil of public policy-making.

Remember, aluminum saturates/coagulates with any toxin in its path, upon entry to the bloodstream via deep muscle tissue. Ethyl Mercury traps hemoglobin, which triggers Ischemia, (a singeing of the neural pathways from toxic overload which prevents vital oxygen from reaching the brain, literally inhibiting normal development; a form of suffocation); while Formaldehyde, a known carcinogen, causes proteins to irreversibly bind to DNA. In essence live/attenuated viruses and other powerful toxins literally piggy back in to these centers without any resistance (disabling most kidney & liver functionality along the way) via the “bully” catalyst, aluminum, coupled with the back door point of entry into the body – past the primary line of natural defences.

Given the vulnerability of babies & young children, with an under-developed blood barrier on the brain & Myelin Sheath (to which aluminum binds due to its composition of electrical tissues), the paths leading to autism, schizophrenia, chronic allergies & a myriad of other disorders & viral infections become increasingly apparent.

Neomycin & Polymixin B are antibiotics associated with Kidney failure; both hazardous to a fetus. They carry serious side effects, predominantly kidney failure. Neomycin is in the FDA pregnancy category D. This means that it is known to be harmful to an unborn baby. In the “first tier” of candidates to receive this unregistered, unapproved vaccine, pregnant women are on top of the list. Once again a case of gross negligence, endorsing the use of a toxic product in influenza vaccines recommended for Pregnant women, in light of this stern FDA warning,

Additionally, Polysorbate 80 or ‘Tween 80‘ is a type of detergent stabilizer commonly found in vaccines; which is linked to infertility & severe allergic reactions (ie. Anaphylaxis). ‘Neonatal female rats were injected with Tween 80 after birth. Treatment accelerated maturation, prolonged the oestrus cycle & induced persistent vaginal oestrus. Ovaries were without corpora lutea & had degenerative follicies.‘

Based on this verifiable clinical data no such toxin should ever, under any circumstances, be injected into a pregnant woman. Despite such conclusive evidence of its implications on female fertility, Polysorbate 80 is, in fact, added to many current vaccines including: HPV (Gardasil/Cervavix), DTaP (Infanrix, Tripedia), DTaP-IPV (Kinrix), DTaP/Hib (TriHIBit), DTaP-HepB-IPV (Pediarix), DtaP-IPV/Hib (Pentacel), Hep A (Havrix). 2009’s H1N1 ‘Swine Flu’ vaccine (produced by GlaxoSmithKline (Pandemrix/Arepanrix), Novartis (Focetria) & Baxter Pharmaceuticals (Celvapan), widely promoted as a mandatory safety precaution for ALL pregnant women, contained this ingredient; yet another glaring red flag to be considered.

“Polysorbate 80 was identified as the causative agent for the anaphylactoid reaction of nonimmunologic origin in the patient. Polysorbate 80 is a ubiquitously used solubilizing agent that can cause severe nonimmunologic anaphylactoid reactions.” Department of Dermatology, University of Aachen, Aachen, Germany

Specific role of polysorbate 80 coating on the targeting of nanoparticles to the brain (causes a blood/brain barrier breach) “Partial coverage was enough for Tween-80 coating to play a specific role in brain targeting of nanoparticles; concerned with the interaction between T-80 coating and brain micro-vessel endothelial cells. Therefore, the specific role of T-80 coating on nanoparticles in brain targeting was confirmed.” Department of Material Science and Engineering, Huazhong University of Science and Technology, China Study, 2003

To reiterate: 2 separate ingredients, either which contribute to an increased likelihood of infertility.

a) Neomycin/Polymixin B – antibiotics associated with Kidney failure; both hazardous to a fetus. “There is evidence to indicate that exposure to Neomycin during pregnancy may have a teratogenic effect on the fetus. A teratogen is a substance that can cause birth defects.’

b) Polysorbate 80/Tween 80 – detergent stabilizer commonly found in vaccines; which is linked to infertility & severe allergic reactions (ie. Anaphylaxis). “Delayed effects of neonatal exposure to Tween 80 on female reproductive organs in rats.

The mother’s placenta, & breast milk (Colostrum) are inextricably linked, providing a baby’s primary initial source of nourishment through the long journey of formation in utero; while supplying the basic building blocks of life necessary to guarantee a safe transition into early childhood development. It seems almost inconceivable given the scientific literature in circulation, but somehow the CDC, WHO & local health authorities in countries around the world have begun vehemently recommending all pregnant women & babies as young as 6 months receive the seasonal flu vaccine during first trimester. It is common knowledge in medical circles that Thimerosal crosses not only the blood barrier into the brain, but also gets absorbed into the placenta when introduced to the bloodstream. Their justification borders on attempted infanticide.
Long-term implications of mercury exposure at this stage include Down’s Syndrome, early onset Autism, Lupus, Schizophrenia & a host of other chronic disorders & allergies (ie. Hyperbetacarotenemia, a form of intestinal disfunction linked to Measles marked by excessive beta-carotene in the blood & Vitamin A depletion).

‘The Advisory Committee on Immunization Practices (ACIP) recommends that pregnant and postpartum women receive the seasonal influenza vaccine this year, even if they received 2009 H1N1 or seasonal influenza vaccine last year. Influenza vaccine can be given to pregnant women in any trimester. Postpartum women, even if they are breastfeeding, can receive either type of vaccine. Administer annually to children aged 6 months through 18 years.’ CDC

It should come as no surprise that many pregnant women reported miscarriages during 2009’s H1N1 vaccination campaign. Of those who received the shot upwards of 3,600 cases of miscarriages and stillbirths have been reported, based on current estimates. Bare in mind that figure represents only approximately 10% of the overall numbers. Meaning only 10% of cases are ever reported officially. That translates to upwards of 30,000 possible vaccine induced miscarriages having actually occurred in the US alone.

‘A shocking report from the National Coalition of Organized Women (NCOW) presented data from two different sources demonstrating that the 2009/10 H1N1 vaccines contributed to an estimated 1,588 miscarriages and stillbirths – as high as 3,587 cases. Studies conducted by the CDC have been shown to miss from 10% to 90% of the actual cases because of under-reporting.’

‘Studies of the organs and tissues of the first generation progeny revealed mercury in the stomach and intestine at birth and in the first week of life, apparently on account of the entry of mercury through the placental barrier and by way of their mother’s milk. Subsequently, it was noted that the first-generation progeny of mothers that had been previously exposed to the ethyl mercury compound had significantly reduced fertility in comparison to controls. The second generation progeny had low viability, lagged in their weight growth, and were retarded with respect to ossification in several cases. Finally, it was then observed when mating the second generation progeny that there was a significant decrease in fertility in comparison to the control group.’

Note: Soy formula (typically GMO) is never a viable alternative to colostrum; as it is found to be ‘nutritionally inadequate and contain Manganese (Mn) at levels which may present an increased risk of adverse neurological effects if used as a sole source of nutrition‘.

Methylation assists in a critical stage of early development involving the viability of cells. ‘an on/off switch that allows the body to learn how to respond to environmental change. It represents the only cellular pathway that effects both adaptability and structural integrity of the body. Like the simple water molecule, methyl groups are necessary for life. This pathway is directly related to most major chronic conditions.’ Heavy metal toxicity breaks down this vital operation; yet another primary culprit in the eventuality of autism.

‘Methylation events play a critical role in the ability of growth factors to promote normal development. Neurodevelopmental toxins, such as ethanol and heavy metals, interrupt growth factor signaling, raising the possibility that they might exert adverse effects on methylation. We found that insulin-like growth factor-1 (IGF-1)- and dopamine-stimulated methionine synthase (MS) activity and folate-dependent methylation of phospholipids in SH-SY5Y human neuroblastoma cells, via a PI3-kinase- and MAP-kinase-dependent mechanism.

The stimulation of this pathway increased DNA methylation, while its inhibition increased methylation-sensitive gene expression. The ethylmercury-containing preservative thimerosal inhibited both IGF-1- and dopamine-stimulated methylation with an IC50 of 1 nM and eliminated MS activity. Our findings outline a novel growth factor signaling pathway that regulates MS activity and thereby modulates methylation reactions, including DNA methylation. The potent inhibition of this pathway by ethanol, lead, mercury, aluminum and thimerosal suggests that it may be an important target of neurodevelopmental toxins.’ Molecular Psychiatry (2004)

Vaccines, by their very nature, play off each other – a synergistic reaction; triggering further infections & disorders. In many cases the very signature disease/disorder they claim to protect you against is PRECISELY that which they inadvertently spread.

Prevnor, for example, a childhood vaccine designed to “prevent” invasive pneumococcal disease (administered in 3 doses to 7-11 year olds not only doesn’t work, but also opens the reactive door to other crossover infections & diseases from vaccines given simultaneously during this age phase. Resulting cross reactions include Polio, Whooping cough, Diphtheria, Measles, Meningitis, Pneumonia, Chicken Pox & all varieties of chronic allergies ie. ear infections etc.

‘The vaccine schedule for infants(‘Prevnor’) is three doses at least one month apart, followed by a fourth dose at 12 to 15 months. It can be given at the same time as other vaccines but in a different site. For children 7 to 11 months of age, 3 doses are recommended, with the first 2 at least 1 month apart, followed by a third dose after the one-year birthday. For children 12 to 23 months of age, 2 doses are required at least 2 months apart, and 1 dose is required for children from 2 to 5 years of age.’

‘The efficacy of Prevnar appears to be very limited – 7% fewer new earaches, and 0.1% fewer instances of invasive pneumococcal disease (compared to an experimental vaccine used as a control). Prevnar Interferes With Other Childhood Vaccines The studies done on Prevnar suggest that it may interfere with the efficacy of two other vaccines (pertussis and IPV ‘Inactivated Polio Vaccine’) and could interfere with two more vaccines (MMR and Varicella).

According to the American Academy of Pediatrics: “Available data suggest that PCV7 (i.e. Prevnar) may prove to be among the most reactogenic (e.g., local reactions and incidence of fever) vaccine of those currently used, including the DTaP and Haemophilus conjugate vaccines.”36′

‘The pneumococcus bacteria cause infections that lead to the following diseases – meningitis, bacteraemia, pneumonia and otitis media.’

Government data admits to a probable causal link between vaccines & the presence of Measles in the bowels of young children (related to Inflammatory Bowel Disease); while promoting a deliberate cover-up of these inherent risks to the general public,

‘That Crohn’s disease and other chronic inflammatory illnesses of the intestine might be caused by a virus such as measles is an interesting hypothesis. Until the present time, microbiologic and epidemiologic arguments either for or against this hypothesis have not been very convincing. It is not very likely that other epidemiologic studies will provide conclusive evidence. In fact, it would be difficult to find a population that includes both individuals who have been exposed to the virus or to the vaccine and individuals who have not been exposed. However, new microbiologic studies might prove conclusive.

First, it would be necessary to demonstrate that the measles virus is indeed present in the lesions, that it is active, and that it contributes to inflammatory responses. Also, it would be necessary to prove that the pathogenic reaction can be induced by the wild virus and by the attenuated viruses present in vaccines. Strains and attenuation procedures vary from one manufacturer to another, and it is far from certain that all strains have the same ability to persist in tissues and to subsequently produce chronic inflammations.

As was stated above, measles vaccine does not seem to be associated with SSPE, although the wild virus may be isolated (with difficulty) in patients with SSPE. The measles virus was isolated neither in patients with Crohn’s disease or other chronic inflammatory diseases (Paget’s disease, active chronic hepatitis, multiple sclerosis) in which a role for it has been claimed on morphologic, histologic or serologic grounds.

Current scientific data do not permit a causal link to be drawn between the measles virus and chronic inflammatory bowel diseases. While awaiting production and publication of other research, it would not be appropriate to alarm recipients of the vaccine by notifying them of this hypothetical risk, thus jeopardizing an immunization program of proven benefit.’

Scandalous cover-up: “…it would not be appropriate to alarm recipients of the vaccine by notifying them of this hypothetical risk, thus jeopardizing an immunization program of proven (cost) benefit.”

“We know in the world of infectious disease, that when women develop certain infections during mid term & later term of pregnancy (second & third trimester) they have a higher instance of having a child born with & developing autism or later in life, schizophrenia. that’s been known & shown in animal & in human studies. If you vaccinate pregnant women you’re significantly elevating their immune reaction. and the studies, as I began to look at this phenomenon, first they thought the mother was infecting the baby while the baby was in the uterus.

Then they found out actually the virus never gets through the placenta so the baby’s not effected at all. It’s the immune reaction in the mother and these immune cytokines, these immune chemicals, that pass through the placenta into the baby that’s causing the baby’s brain to develop abnormally. So any immune stimulation of the mother can produce abnormalities in the baby with no virus whatsoever. And that’s what they proved experimentally. You could just stimulate the immunity with no infectious agent and still get high autism & schizophrenia.

If you run the risk of getting the flu during this season your risk is about 300’s of 1/1000th of 1% for a pregnant woman. In other words you have a 99.97 – 99.99% chance that you’re not going to end up in the hospital sick from the flu. And that’s by their own statistics. If you get the vaccine, and they give it to all pregnant women, then that means 100% of women have had a powerful immune stimulation during this critical period of brain formation of their baby.

So that puts every woman at risk of having a baby born with high risk of autism or schizophrenia. And we’re talking about, according to the data we have, an increased risk of about 7 fold to as much as 14 fold (incidence of autism & schizophrenia in babies), a tremendous increase, depending on how much you stimulate the immune system. Other studies have shown it increases the baby’s risk of being susceptible to seizures early in life or even later in life, neuro-developmental problems, behavioral problems, all these subtle things.” Dr. Russell Blaylock

“The mechanism by which the immune system is corrupted can best be realized when you understand that the two poles of the immune system (the cellular and humoral mechanisms) have a reciprocal relationship. Thus, when one is stimulated, the other is inhibited. Since vaccines activate the B cells to secrete antibody, the T cells are subsequently suppressed. This suppression of the cell-mediated response is a key factor in the development of cancer and life threatening infections. In fact, the “prevention” of a disease via vaccination is, in reality, an inability to expel organisms due to the suppression of the cell-mediated response.

Thus, rather than preventing disease, the disease is actually prevented from ever being resolved. The organisms continue circulating through the body, adapting to the hostile environment by transforming into other organisms depending on acidity, toxicity and other changes to the internal terrain of the body. Thus, treatment of infection with antibiotics as well as “prevention” of disease with vaccines are both just corrupted attempts at cutting off the branches of dis-ease, when the root of the cause is a toxic internal environment combined with nutritional deficiency.” Dr. Rebecca Carley, M.D.