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Vaccines, Aluminium and Autism

Aluminium Causes Cell Death

Aluminum-based adjuvants (aluminum salts or alum) are widely used in human vaccination, although their mechanisms of action are poorly understood. Here we report that, in mice, alum causes cell death and the subsequent release of host cell DNA, which acts as a potent endogenous immunostimulatory signal mediating alum adjuvant activity. Furthermore, we propose that host DNA signaling differentially regulates IgE and IgG1 production after alum-adjuvanted immunization. We suggest that, on the one hand, host DNA induces primary B cell responses, including IgG1 production, through interferon response factor 3 (Irf3)-independent mechanisms. On the other hand, we suggest that host DNA also stimulates ‘canonical’ T helper type 2 (TH2) responses, associated with IgE isotype switching and peripheral effector responses, through Irf3-dependent mechanisms. The finding that host DNA released from dying cells acts as a damage-associated molecular pattern that mediates alum adjuvant activity may increase our understanding of the mechanisms of action of current vaccines and help in the design of new adjuvants.

Source: http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.2403.html

Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?

Autism spectrum disorders (ASD) are serious multisystem developmental disorders and an urgent global public health concern. Dysfunctional immunity and impaired brain function are core deficits in ASD. Aluminum (Al), the most commonly used vaccine adjuvant, is a demonstrated neurotoxin and a strong immune stimulator. Hence, adjuvant Al has the potential to induce neuroimmune disorders. When assessing adjuvant toxicity in children, two key points ought to be considered: (i) children should not be viewed as “small adults” as their unique physiology makes them much more vulnerable to toxic insults; and (ii) if exposure to Al from only few vaccines can lead to cognitive impairment and autoimmunity in adults, is it unreasonable to question whether the current pediatric schedules, often containing 18 Al adjuvanted vaccines, are safe for children? By applying Hill’s criteria for establishing causality between exposure and outcome we investigated whether exposure to Al from vaccines could be contributing to the rise in ASD prevalence in the Western world. Our results show that: (i) children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines; (ii) the increase in exposure to Al adjuvants significantly correlates with the increase in ASD prevalence in the United States observed over the last two decades (Pearson r = 0.92, p < 0.0001); and (iii) a significant correlation exists between the amounts of Al administered to preschool children and the current prevalence of ASD in seven Western countries, particularly at 3–4 months of age (Pearson r = 0.89–0.94, p = 0.0018–0.0248). The application of the Hill’s criteria to these data indicates that the correlation between Al in vaccines and ASD may be causal. Because children represent a fraction of the population most at risk for complications following exposure to Al, a more rigorous evaluation of Al adjuvant safety seems warranted.

Source: Journal of Inorganic Biochemistry, doi:10.1016/j.jinorgbio.2011.08.008 http://www.sciencedirect.com/science/article/pii/S0162013411002212

The health effects of aluminium–a review

This review covers the occurrence of aluminium in soil, air, water and food. In addition, aluminium levels in body tissues and its movement within the body have been considered. The adverse effects of aluminium that have been reported in recent years include Alzheimer’s disease, dementia and hyperactivity and learning disorders in children.

Source: J R Soc Health. 1991 Oct;111(5):163-8

Mechanisms of aluminum adjuvant toxicity and autoimmunity in pediatric populations

Immune challenges during early development, including those vaccine-induced, can lead to permanent detrimental alterations of the brain and immune function. Experimental evidence also shows that simultaneous administration of as little as two to three immune adjuvants can overcome genetic resistance to autoimmunity. In some developed countries, by the time children are 4 to 6 years old, they will have received a total of 126 antigenic compounds along with high amounts of aluminum (Al) adjuvants through routine vaccinations. According to the US Food and Drug Administration, safety assessments for vaccines have often not included appropriate toxicity studies because vaccines have not been viewed as inherently toxic. Taken together, these observations raise plausible concerns about the overall safety of current childhood vaccination programs. When assessing adjuvant toxicity in children, several key points ought to be considered: (i) infants and children should not be viewed as “small adults” with regard to toxicological risk as their unique physiology makes them much more vulnerable to toxic insults; (ii) in adult humans Al vaccine adjuvants have been linked to a variety of serious autoimmune and inflammatory conditions (i.e., “ASIA”), yet children are regularly exposed to much higher amounts of Al from vaccines than adults; (iii) it is often assumed that peripheral immune responses do not affect brain function. However, it is now clearly established that there is a bidirectional neuro-immune cross-talk that plays crucial roles in immunoregulation as well as brain function. In turn, perturbations of the neuro-immune axis have been demonstrated in many autoimmune diseases encompassed in “ASIA” and are thought to be driven by a hyperactive immune response; and (iv) the same components of the neuro-immune axis that play key roles in brain development and immune function are heavily targeted by Al adjuvants. In summary, research evidence shows that increasing concerns about current vaccination practices may indeed be warranted. Because children may be most at risk of vaccine-induced complications, a rigorous evaluation of the vaccine-related adverse health impacts in the pediatric population is urgently needed.

Source: Lupus. 2012;21(2):223-30. http://www.ncbi.nlm.nih.gov/pubmed/22235057

Hypothesis: conjugate vaccines may predispose children to autism spectrum disorders.

The first conjugate vaccine was approved for use in the US in 1988 to protect infants and young children against the capsular bacteria Haemophilus influenzae type b (Hib). Since its introduction in the US, this vaccine has been approved in most developed countries, including Denmark and Israel where the vaccine was added to their national vaccine programs in 1993 and 1994, respectively. There have been marked increases in the reported prevalence of autism spectrum disorders (ASDs) among children in the US beginning with birth cohorts in the late 1980s and in Denmark and Israel starting approximately 4-5 years later. Although these increases may partly reflect ascertainment biases, an exogenous trigger could explain a significant portion of the reported increases in ASDs. It is hypothesized here that the introduction of the Hib conjugate vaccine in the US in 1988 and its subsequent introduction in Denmark and Israel could explain a substantial portion of the initial increases in ASDs in those countries. The continuation of the trend toward increased rates of ASDs could be further explained by increased usage of the vaccine, a change in 1990 in the recommended age of vaccination in the US from 15 to 2 months, increased immunogenicity of the vaccine through changes in its carrier protein, and the subsequent introduction of the conjugate vaccine for Streptococcus pneumoniae. Although conjugate vaccines have been highly effective in protecting infants and young children from the significant morbidity and mortality caused by Hib and S. pneumoniae, the potential effects of conjugate vaccines on neural development merit close examination. Conjugate vaccines fundamentally change the manner in which the immune systems of infants and young children function by deviating their immune responses to the targeted carbohydrate antigens from a state of hypo-responsiveness to a robust B2 B cell mediated response. This period of hypo-responsiveness to carbohydrate antigens coincides with the intense myelination process in infants and young children, and conjugate vaccines may have disrupted evolutionary forces that favored early brain development over the need to protect infants and young children from capsular bacteria.

Source: Med Hypotheses. 2011 Dec;77(6):940-7. http://www.ncbi.nlm.nih.gov/pubmed/21993250#

Aluminum vaccine adjuvants: are they safe?

Aluminum is an experimentally demonstrated neurotoxin and the most commonly used vaccine adjuvant. Despite almost 90 years of widespread use of aluminum adjuvants, medical science’s understanding about their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds. In spite of this, the notion that aluminum in vaccines is safe appears to be widely accepted. Experimental research, however, clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans. In particular, aluminum in adjuvant form carries a risk for autoimmunity, long-term brain inflammation and associated neurological complications and may thus have profound and widespread adverse health consequences. In our opinion, the possibility that vaccine benefits may have been overrated and the risk of potential adverse effects underestimated, has not been rigorously evaluated in the medical and scientific community. We hope that the present paper will provide a framework for a much needed and long overdue assessment of this highly contentious medical issue.

Source: Curr Med Chem. 2011;18(17):2630-7.  http://www.ncbi.nlm.nih.gov/pubmed/21568886

Toxic Metals and Essential Elements in Hair and Severity of Symptoms among Children with Autism

Abstract

OBJECTIVE:

The objective of this study was to assess the levels of ten toxic metals and essential elements in hair samples of children with autism, and to correlate the level of these elements with the severity of autism.

METHOD:

The participants were 44 children, age 3 to 9 years, with Autistic Spectrum Disorder (ASD) according to Diagnostic and Statistical Manual of Mental Disorders 4th Edition, (DSM-IV). The severity of autistic symptomatology was measured by the Childhood Autism Rating Scale (CARS). Hair analysis was performed to evaluate the long term metal exposure and mineral level.

RESULTS:

By comparing hair concentration of autistic vs nonautistic children, elevated hair concentrations were noted for aluminum, arsenic, cadmium, mercury, antimony, nickel, lead, and vanadium. Hair levels of calcium, iron, iodine, magnesium, manganese, molybdenum, zinc, and selenium were considered deficient. There was a significant positive correlation between lead & verbal communication (p = 0.020) and general impression (p = 0.008). In addition, there was a significant negative correlation between zinc & fear and nervousness (p = 0.022).

CONCLUSION:

Our data supports the historic evidence that heavy metals play a role in the development of ASD. In combination with an inadequate nutritional status the toxic effect of metals increase along with the severity of symptoms.

Source: Maedica (Buchar). 2012 Jan;7(1):38-48.  http://www.ncbi.nlm.nih.gov/pubmed/23118818

Heavy metals and trace elements in hair and urine of a sample of arab children with autistic spectrum disorder.

Abstract

General information: Autism is a severe developmental disorder which involves social withdrawal, communication deficits, and stereotypic/repetitive behavior. The pathophysiological etiologies which precipitate autism symptoms remain elusive and controversial in many cases, but both genetic and environmental factors (and their interactions) have been implicated. While autism is considered multicausal, environmental factors have received significant attention. International discussion has ocused on neurotoxins such as mercury and lead, suggesting that these and other toxic metals contribute to the development of the disorder. An epidemiological study released in 2006 (Palmer et al.) linking Toxic Release Inventory (TRI) data on mercury to special education data in Texas reported a 61% increase in autism prevalence rates (or 17% adjusted) per 1000 pounds of mercury released into the environment (1). We attempted to further evaluate whether exposure to variable environmental contributes to the genesis of autistic spectrum disorder, and thus is a factor increasing the risk for developing autism symptoms in utero or in early childhood.

PURPOSE:

The purpose of this study is to examine possible environmental risk factors and sources of exposure to mercury and other heavy metals in children with autism spectrum disorder versus controls. Through laboratory diagnostics we are able to distinguish between present and past exposure (i.e. hair analysis measurements reflect past exposure), urinary excretion levels of unprovoked urine represent immediate exposure. By assessing a spectrum of trace elements and heavy metals in hair and urine of both autistic and control groups, we focused on the participants≈ past and present exposure.

METHODOLOGY:

The participants were 25 Autistic Spectrum Disorder (ASD) children (22 boys and 3 girls) between the age of 3 and 9 years. They were either diagnosed previously by other psychiatrist, psychologist, and developmental pediatrician or suspected by their parents as being autistic. All children were attendants to the Child Psychiatric Clinic in Erfan Psychiatric Hospital in Jeddah, KSA. Samples were collected during the period of June 2006 to March 2008. A control group of 25 children without any psychiatric or medical disorders was age-matched and sex-matched. All parents signed informed consent forms. All autistic children were subjected to a full clinical child psychiatric sheet for the diagnosis of autism spectrum disorder and exclusion of other psychiatric disorders according to the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM IV). The severity of autistic symptomatology was measured by the Childhood Autism Rating Scale (CARS) and Autism Behavior Checklist (ABC) using the Arabic versions. Both groups were subjected to the Questionnaire on Exposure to Heavy Metals, Physical Symptoms, and Child Development. Hair and baseline urine samples (i.e. unprovoked urine) were taken from both groups and sent to the German clinical and environmental laboratory Micro Trace Minerals Gmbh, for the detection of heavy metals and trace elements levels where metal testing was performed via ICP-MS spectroscopy utilizing cell technique.

RESULTS:

By comparing the ASD Group to the Control Group, we found a statistically significant difference in the mean hair levels of arsenic, cadmium, barium, cerium and lead (p=0.01, 0.03, 0.003, 0.003, and 0.03 respectively), and in the mean hair levels of magnesium and zinc (p=0.001 and 0.003 respectively). There were also statistically significant differences in the mean urine levels of aluminum, barium, cerium, mercury, and lead (p=0.004, 002, 0.014, 0.006 and 0.004 respectively), and in the mean urine levels of copper and germanium (p=0.049 and 0.02 respectively). An agreement was found in both specimen (hair and urine) for barium and lead. The statistically significant differences in mean hair levels of arsenic, cadmium, and cerium were not supported by urine baseline levels. Also, the statistically significant magnesium and zinc levels of hair were not supported by urine levels. A disagreement was also found with copper and germanium concentrations.

Source: Maedica (Buchar). 2011 Oct;6(4):247-57.  http://www.ncbi.nlm.nih.gov/pubmed/22879836

Environmental factors in the development of autism spectrum disorders.

Abstract

Autism spectrum disorders (ASD) are highly heterogeneous developmental conditions characterized by deficits in social interaction, verbal and nonverbal communication, and obsessive/stereotyped patterns of behavior and repetitive movements. Social interaction impairments are the most characteristic deficits in ASD. There is also evidence of impoverished language and empathy, a profound inability to use standard nonverbal behaviors (eye contact, affective expression) to regulate social interactions with others, difficulties in showing empathy, failure to share enjoyment, interests and achievements with others, and a lack of social and emotional reciprocity. In developed countries, it is now reported that 1%-1.5% of children have ASD, and in the US 2015 CDC reports that approximately one in 45 children suffer from ASD. Despite the intense research focus on ASD in the last decade, the underlying etiology remains unknown. Genetic research involving twins and family studies strongly supports a significant contribution of environmental factors in addition to genetic factors in ASD etiology. A comprehensive literature search has implicated several environmental factors associated with the development of ASD. These include pesticides, phthalates, polychlorinated biphenyls, solvents, air pollutants, fragrances, glyphosate and heavy metals, especially aluminum used in vaccines as adjuvant. Importantly, the majority of these toxicants are some of the most common ingredients in cosmetics and herbicides to which almost all of us are regularly exposed to in the form of fragrances, face makeup, cologne, air fresheners, food flavors, detergents, insecticides and herbicides. In this review we describe various scientific data to show the role of environmental factors in ASD.

Source: Environ Int. 2016 Mar;88:288-98. doi: 10.1016/j.envint.2015.12.021. Epub 2016 Jan 28.

http://www.ncbi.nlm.nih.gov/pubmed/26826339

The toxicity of aluminium in humans.

Abstract

We are living in the ‘aluminium age’. Human exposure to aluminium is inevitable and, perhaps, inestimable. Aluminium‘s free metal cation, Alaq(3+), is highly biologically reactive and biologically available aluminium is non-essential and essentially toxic. Biologically reactive aluminium is present throughout the human body and while, rarely, it can be acutely toxic, much less is understood about chronic aluminium intoxication. Herein the question is asked as to how to diagnose aluminium toxicity in an individual. While there are as yet, no unequivocal answers to this problem, there are procedures to follow to ascertain the nature of human exposure to aluminium. It is also important to recognise critical factors in exposure regimes and specifically that not all forms of aluminium are toxicologically equivalent and not all routes of exposure are equivalent in their delivery of aluminium to target sites. To ascertain if Alzheimer’s disease is a symptom of chronic aluminium intoxication over decades or breast cancer is aggravated by the topical application of an aluminium salt or if autism could result from an immune cascade initiated by an aluminium adjuvant requires that each of these is considered independently and in the light of the most up to date scientific evidence. The aluminium age has taught us that there are no inevitabilities where chronic aluminium toxicity is concerned though there are clear possibilities and these require proving or discounting but not simply ignored.

Source: Morphologie. 2016 Jun;100(329):51-5. doi: 10.1016/j.morpho.2015.12.003. Epub 2016 Feb 28.

http://www.ncbi.nlm.nih.gov/pubmed/26922890

What is the risk of aluminium as a neurotoxin?

Abstract

Aluminium is neurotoxic. Its free ion, Al(3+) (aq), is highly biologically reactive and uniquely equipped to do damage to essential cellular (neuronal) biochemistry. This unequivocal fact must be the starting point in examining the risk posed by aluminium as a neurotoxin in humans. Aluminium is present in the human brain and it accumulates with age. The most recent research demonstrates that a significant proportion of individuals older than 70 years of age have a potentially pathological accumulation of aluminium somewhere in their brain. What are the symptoms of chronic aluminium intoxication in humans? What if neurodegenerative diseases such as Alzheimer’s disease are the manifestation of the risk of aluminium as a neurotoxin? How might such an (outrageous) hypothesis be tested?

Source: Expert Rev Neurother. 2014 Jun;14(6):589-91. doi: 10.1586/14737175.2014.915745. Epub 2014 Apr 30.

http://www.ncbi.nlm.nih.gov/pubmed/24779346

Assessment of Hair Aluminum, Lead, and Mercury in a Sample of Autistic Egyptian Children: Environmental Risk Factors of Heavy Metals in Autism.

Abstract

BACKGROUND AND AIMS:

The etiological factors involved in the etiology of autism remain elusive and controversial, but both genetic and environmental factors have been implicated. The aim of this study was to assess the levels and possible environmental risk factors and sources of exposure to mercury, lead, and aluminum in children with autism spectrum disorder (ASD) as compared to their matched controls.

METHODS:

One hundred ASD children were studied in comparison to 100 controls. All participants were subjected to clinical evaluation and measurement of mercury, lead, and aluminum through hair analysis which reflects past exposure.

RESULTS:

The mean Levels of mercury, lead, and aluminum in hair of the autistic patients were significantly higher than controls. Mercury, lead, and aluminum levels were positively correlated with maternal fish consumptions, living nearby gasoline stations, and the usage of aluminum pans, respectively.

CONCLUSION:

Levels of mercury, lead, and aluminum in the hair of autistic children are higher than controls. Environmental exposure to these toxic heavy metals, at key times in development, may play a causal role in autism.

Source: Behav Neurol. 2015;2015:545674. doi: 10.1155/2015/545674. Epub 2015 Oct 5.

http://www.ncbi.nlm.nih.gov/pubmed/26508811

Administration of aluminium to neonatal mice in vaccine-relevant amounts is associated with adverse long term neurological outcomes.

Abstract

Our previous ecological studies of autism spectrum disorder (ASD) has demonstrated a correlation between increasing ASD rates and aluminium (Al) adjuvants in common use in paediatric vaccines in several Western countries. The correlation between ASD rate and Al adjuvant amounts appears to be dose-dependent and satisfies 8 of 9 Hill criteria for causality. We have now sought to provide an animal model to explore potential behavioural phenotypes and central nervous system (CNS) alterations using s.c. injections of Al hydroxide in early postnatal CD-1 mice of both sexes. Injections of a “high” and “low” Al adjuvant levels were designed to correlate to either the U.S. or Scandinavian paediatric vaccine schedules vs. control saline-injected mice. Both male and female mice in the “high Al” group showed significant weight gains following treatment up to sacrifice at 6 months of age. Male mice in the “high Al” group showed significant changes in light-dark box tests and in various measures of behaviour in an open field. Female mice showed significant changes in the light-dark box at both doses, but no significant changes in open field behaviours. These current data implicate Al injected in early postnatal life in some CNS alterations that may be relevant for a better understanding of the aetiology of ASD.

Source: J Inorg Biochem. 2013 Nov;128:237-44. doi: 10.1016/j.jinorgbio.2013.07.022. Epub 2013 Jul 19.

http://www.ncbi.nlm.nih.gov/pubmed/23932735

 Insight into the cellular fate and toxicity of aluminium adjuvants used in clinically approved human vaccinations

Aluminium adjuvants remain the most widely used and effective adjuvants in vaccination and immunotherapy. Herein, the particle size distribution (PSD) of aluminium oxyhydroxide and aluminium hydroxyphosphate adjuvants was elucidated in attempt to correlate these properties with the biological responses observed post vaccination. Heightened solubility and potentially the generation of Al3+ in the lysosomal environment were positively correlated with an increase in cell mortality in vitro, potentially generating a greater inflammatory response at the site of simulated injection. The cellular uptake of aluminium based adjuvants (ABAs) used in clinically approved vaccinations are compared to a commonly used experimental ABA, in an in vitro THP-1 cell model. Using lumogallion as a direct-fluorescent molecular probe for aluminium, complemented with transmission electron microscopy provides further insight into the morphology of internalised particulates, driven by the physicochemical variations of the ABAs investigated. We demonstrate that not all aluminium adjuvants are equal neither in terms of their physical properties nor their biological reactivity and potential toxicities both at the injection site and beyond. High loading of aluminium oxyhydroxide in the cytoplasm of THP-1 cells without immediate cytotoxicity might predispose this form of aluminium adjuvant to its subsequent transport throughout the body including access to the brain.

Source: Scientific Reports 6, Article number: 31578 (2016).

http://www.nature.com/articles/srep31578

Multifaceted effects of aluminium in neurodegenerative diseases: A review.

Aluminium (Al) is the most common metal and widely distributed in our environment. Al was first isolated as an element in 1827, and its use began only after 1886. Al is widely used for industrial applications and consumer products. Apart from these it is also used in cooking utensils and in pharmacological agents, including antacids and antiperspirants from which the element usually enters into the human body. Evidence for the neurotoxicity of Al is described in various studies, but still the exact mechanism of Al toxicity is not known. However, the evidence suggests that the Al can potentiate oxidative stress and inflammatory events and finally leads to cell death. Al is considered as a well-established neurotoxin and have a link between the exposure and development of neurodegenerative diseases, including Amyotrophic Lateral Sclerosis (ALS), Alzheimer’s disease (AD), dementia, Gulf war syndrome and Parkinsonism. Here, we review the detailed possible pathogenesis of Al neurotoxicity. This review summarizes Al induced events likewise oxidative stress, cell mediated toxicity, apoptosis, inflammatory events in the brain, glutamate toxicity, effects on calcium homeostasis, gene expression and Al induced Neurofibrillary tangle (NFT) formation. Apart from these we also discussed animal models that are commonly used for Al induced neurotoxicity and neurodegeneration studies. These models help to find out a better way to treat and prevent the progression in Al induced neurodegenerative diseases.

Source: Biomed Pharmacother. 2016 Jul 29;83:746-754. doi: 10.1016/j.biopha.2016.07.035.

http://www.ncbi.nlm.nih.gov/pubmed/27479193?log$=activity

Potential for early-life immune insult including developmental immunotoxicity in autism and autism spectrum disorders: focus on critical windows of immune vulnerability.

Abstract

Early-life immune insults (ELII) including xenobiotic-induced developmental immunotoxicity (DIT) are important factors in childhood and adult chronic diseases. However, prenatal and perinatal environmentally induced immune alterations have yet to be considered in depth in the context of autism and autism spectrum disorders (ASDs). Numerous factors produce early-life-induced immune dysfunction in offspring, including exposure to xenobiotics, maternal infections, and other prenatal-neonatal stressors. Early life sensitivity to ELII, including DIT, results from the heightened vulnerability of the developing immune system to disruption and the serious nature of the adverse outcomes arising after disruption of one-time immune maturational events. The resulting health risks extend beyond infectious diseases, cancer, allergy, and autoimmunity to include pathologies of the neurological, reproductive, and endocrine systems. Because these changes may include misregulation of resident inflammatory myelomonocytic cells in tissues such as the brain, they are a potential concern in cases of prenatal-neonatal brain pathologies and neurobehavioral deficits. Autism and ASDs are chronic developmental neurobehavioral disorders that are on the rise in the United States with prenatal and perinatal environmental factors suspected as contributors to this increase. Evidence for an association between environmentally associated childhood immune dysfunction and ASDs suggests that ELII and DIT may contribute to these conditions. However, it is not known if this linkage is directly associated with the brain pathologies or represents a separate (or secondary) outcome. This review considers the known features of ELII and DIT and how they may provide important clues to prenatal brain inflammation and the risk of autism and ASDs.

Source: J Toxicol Environ Health B Crit Rev. 2008 Oct;11(8):660-80. doi: 10.1080/10937400802370923.

Administration of aluminium to neonatal mice in vaccine-relevant amounts is associated with adverse long term neurological outcomes.

Abstract

Our previous ecological studies of autism spectrum disorder (ASD) has demonstrated a correlation between increasing ASD rates and aluminium (Al) adjuvants in common use in paediatric vaccines in several Western countries. The correlation between ASD rate and Al adjuvant amounts appears to be dose-dependent and satisfies 8 of 9 Hill criteria for causality. We have now sought to provide an animal model to explore potential behavioural phenotypes and central nervous system (CNS) alterations using s.c. injections of Al hydroxide in early postnatal CD-1 mice of both sexes. Injections of a “high” and “low” Al adjuvant levels were designed to correlate to either the U.S. or Scandinavian paediatric vaccine schedules vs. control saline-injected mice. Both male and female mice in the “high Al” group showed significant weight gains following treatment up to sacrifice at 6 months of age. Male mice in the “high Al” group showed significant changes in light-dark box tests and in various measures of behaviour in an open field. Female mice showed significant changes in the light-dark box at both doses, but no significant changes in open field behaviours. These current data implicate Al injected in early postnatal life in some CNS alterations that may be relevant for a better understanding of the aetiology of ASD.

Source: J Inorg Biochem. 2013 Nov;128:237-44. doi: 10.1016/j.jinorgbio.2013.07.022. Epub 2013 Jul 19.

Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration

Gulf War Syndrome is a multi-system disorder afflicting many veterans of Western armies in the 1990–1991 Gulf War. A number of those afflicted may show neurological deficits including various cognitive dysfunctions and motor neuron disease, the latter expression virtually indistinguishable from classical amyotrophic lateral sclerosis (ALS) except for the age of onset. This ALS “cluster” represents the second such ALS cluster described in the literature to date. Possible causes of GWS include several of the adjuvants in the anthrax vaccine and others. The most likely culprit appears to be aluminum hydroxide. In an initial series of experiments, we examined the potential toxicity of aluminum hydroxide in male, outbred CD-1 mice injected subcutaneously in two equivalent-to-human doses. After sacrifice, spinal cord and motor cortex samples were examined by immunohistochemistry. Aluminum-treated mice showed significantly increased apoptosis of motor neurons and increases in reactive astrocytes and microglial proliferation within the spinal cord and cortex. Morin stain detected the presence of aluminum in the cytoplasm of motor neurons with some neurons also testing positive for the presence of hyper-phosphorylated tau protein, a pathological hallmark of various neurological diseases, including Alzheimer’s disease and frontotemporal dementia. A second series of experiments was conducted on mice injected with six doses of aluminum hydroxide. Behavioural analyses in these mice revealed significant impairments in a number of motor functions as well as diminished spatial memory capacity. The demonstrated neurotoxicity of aluminum hydroxide and its relative ubiquity as an adjuvant suggest that greater scrutiny by the scientific community is warranted.

Source: J Inorg Biochem. 2009 Nov; 103(11): 1555.

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