Aluminum Adjuvants in Vaccines

Aluminum Adjuvants in Vaccines

October 21, 2020

Aluminum Adjuvants in Vaccines

by James Odell, ND, OMD, L.Ac.

Aluminum is used as a vaccine adjuvant—a substance that when mixed with an antigen from a virus or bacteria, elicits a greater inflammatory immune response and theoretically a higher response of protective antibodies. Aluminum-containing adjuvants are often simply referred to as “alum.” This term should be avoided for two reasons. First, alum is the name of a specific chemical compound, hydrated potassium aluminum sulfate, KAl(SO4)2·12 H2O. Precipitation of a solution of alum and antigen was originally used for the preparation of aluminum-adjuvanted vaccines. The chemical composition of the aluminum precipitate depends on the type of ions present in the antigen solution. The precipitation method is difficult to reproduce in a consistent manner and has largely been replaced by adsorption of antigens to aluminum-containing gels. The second reason to avoid the term alum is that it fails to specify which type of aluminum-containing adjuvant was used for the vaccine preparation. The two main types of aluminum adjuvants that are commercially available are aluminum hydroxide adjuvant (AH) and aluminum phosphate adjuvant (AP). The physical and chemical composition of AH and AP are quite different and this has important implications for the formulation with antigens.


Thus, there are two aluminium based adjuvants (ABAs) commonly used in vaccines. Alhydrogel® is a semi-crystalline form of aluminium oxyhydroxide and AdjuPhos® is an amorphous salt of aluminium hydroxyphosphate. A sulphate salt of the latter (AAHS) is also listed as being one component of an adjuvant system used in HPV vaccinations. Alhydrogel® and AdjuPhos® are commonly referred to as ‘clinically approved ABAs’, however, this is not the case. There are no ABAs which have been approved for intramuscular or subcutaneous injection into humans. Aluminium salts are the most common type of vaccine adjuvant in use, despite abundant science establishing aluminium as a neurotoxin. Generally, live vaccines will not contain aluminum. Only vaccines made with killed/inactivated viruses and so-called “toxoid” vaccines may contain it, and this goes for both childhood and adult vaccines. In 2002, only two childhood vaccines contained aluminum adjuvants, but the aluminium picture had changed dramatically by 2016, when children received five aluminium-containing vaccines from birth to age three and at least two more in the teenage years. Thus, in the United States, Canada, Europe, Australia, and many other parts of the world, infants and young children receive high quantities of aluminium from multiple inoculations.


Adjuvants are classed as a vaccine excipient. The following link summarizes most other vaccine excipients:


Excipient List:

  • Preservatives used to prevent contamination. For example, thimerosal.

  • Adjuvants used to stimulate a stronger immune response. For example, aluminum salts.

  • Stabilizers used to keep the vaccine potent during transportation and storage. For example, sugars or gelatin.

  • Inactivating ingredients used to kill viruses or inactivate toxins. For example, formaldehyde.

  • Antibiotics used to prevent contamination by bacteria. For example, neomycin.

  • Others are residual trace amounts of materials that were used during the manufacturing process and removed. These can include: Cell culture materials, used to grow the vaccine antigens. For example, egg protein, various culture media.

Despite almost 90 years of widespread use of aluminium 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. Despite this, the false notion that aluminium in vaccines is safe appears to be widely accepted. Experimental research clearly shows that aluminium adjuvants have a potential to induce serious immunological disorders in humans. Aluminium 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.


When you orally ingest aluminium, your body will absorb between 0.2 to 1.5% of it. When aluminum is injected into muscle, your body absorbs 100%, which is why aluminum-containing vaccines are likely far more dangerous than eating aluminium. Numerous studies provide compelling evidence that injected aluminium is detrimental to health. In a paper by Lyons-Weiler and colleagues published in the Journal of Trace Elements in Medicine and Biology, the researchers methodically show that current levels of aluminum in vaccines are wrongly termed “safe” by the Food and Drug Administration and derive from “outdated information, unwarranted assumptions and errors.” They further state that “the levels of aluminium currently present in individual vaccines and in the modern vaccine schedule as a whole are “problematically high.


Another paper by Tomljenovic and Shaw affirmed that aluminium is a neurotoxin and may be a co-factor in several neurodegenerative disorders and diseases, including Alzheimer’s, Parkinson’s, multiple sclerosis, amyotrophic lateral sclerosis (ALS), autism, and epilepsy. According to the authors, “The continued use of aluminium adjuvants in various vaccines for children as well as the general public may be of significant concern. In particular, aluminium presented in this form carries a risk for autoimmunity, long-term brain inflammation and associated neurological complications and may thus have profound and widespread adverse health consequences.”


Recent data by Perricone et al. showed that aluminium adjuvants in vaccines have been linked to multiple sclerosis, systemic lupus erythematosus, chronic fatigue syndrome, Gulf War syndrome, macrophagic myofasciitis, arthritis, and autoimmune/inflammatory syndrome induced by adjuvants (ASIA syndrome), an autoimmune disease with neurological and cognitive manifestations. Clinical symptoms associated with vaccine-induced autoimmunity can take months or years to manifest, much longer than the time intervals utilized in most vaccine safety studies


In another study by Morris et al. published in Metabolic Brain Disease, the authors concluded, “Accordingly, it is recommended that the use of aluminium salts in immunizations should be discontinued and that adults should take steps to minimize their exposure to environmental aluminium.”

There is now abundant scientific data that clearly confirms aluminium as used as an vaccine adjuvant is a dangerous neurotoxin and should be immediately removed form vaccines. The following are selected articles on the health dangers and toxicity of aluminium adjuvants in vaccines.




Cerpa-Cruz, S., P. Paredes-Casillas, E. Landeros Navarro, A. G. Bernard-Medina, G. Martinez-Bonilla, and S. Gutierrez-Urena. Adverse events following immunization with vaccines containing adjuvants.” Immunologic research 56, no. 2-3 (2013): 299-303. 

A traditional infectious disease vaccine is a preparation of live attenuated, inactivated or killed pathogen that stimulates immunity. Vaccine immunologic adjuvants are compounds incorporated into vaccines to enhance immunogenicity. Adjuvants have recently been implicated in the new syndrome named ASIA autoimmune/inflammatory syndrome induced by adjuvants. The objective describes the frequencies of post-vaccination clinical syndrome induced by adjuvants. We performed a cross-sectional study; adverse event following immunization was defined as any untoward medical occurrence that follows immunization 54 days prior to the event. Data on vaccinations and other risk factors were obtained from daily epidemiologic surveillance. Descriptive statistics were done using means and standard deviation, and odds ratio adjusted for potential confounding variables was calculated with SPSS 17 software. Forty-three out of 120 patients with moderate or severe manifestations following immunization were hospitalized from 2008 to 2011. All patients fulfilled at least 2 major and 1 minor criteria suggested by Shoenfeld and Agmon–Levin for ASIA diagnosis. The most frequent clinical findings were pyrexia 68 %, arthralgias 47 %, cutaneous disorders 33 %, muscle weakness 16 % and myalgias 14 %. Three patients had diagnosis of Guillain–Barre syndrome, one patient had Adult-Still’s disease 3 days after vaccination. A total of 76 % of the events occurred in the first 3 days post-vaccination. Two patients with previous autoimmune disease showed severe adverse reactions with the reactivation of their illness. Minor local reactions were present in 49 % of patients. Vaccines containing adjuvants may be associated with an increased risk of autoimmune/inflammatory adverse events following immunization.

Couette, Maryline, Marie-Françoise Boisse, Patrick Maison, Pierre Brugieres, Pierre Cesaro, Xavier Chevalier, Romain K. Gherardi, Anne-Catherine Bachoud-Levi, and François-Jérôme Authier. “Long-term persistence of vaccine-derived aluminum hydroxide is associated with chronic cognitive dysfunction.” Journal of inorganic biochemistry 103, no. 11 (2009): 1571-1578.

Macrophagic myofasciitis (MMF) is an emerging condition, characterized by specific muscle lesions assessing long-term persistence of aluminum hydroxide within macrophages at the site of previous immunization. Affected patients mainly complain of arthromyalgias, chronic fatigue, and cognitive difficulties. We designed a comprehensive battery of neuropsychological tests to prospectively delineate MMF-associated cognitive dysfunction (MACD). Compared to control patients with arthritis and chronic pain, MMF patients had pronounced and specific cognitive impairment. MACD mainly affected (i) both visual and verbal memory; (ii) executive functions, including attention, working memory, and planning; and (iii) left ear extinction at dichotic listening test. Cognitive deficits did not correlate with pain, fatigue, depression, or disease duration. Pathophysiological mechanisms underlying MACD remain to be determined. In conclusion, long-term persistence of vaccine-derived aluminum hydroxide within the body assessed by MMF is associated with cognitive dysfunction, not solely due to chronic pain, fatigue and depression.

Dórea, José G. “Exposure to mercury and aluminum in early life: developmental vulnerability as a modifying factor in neurologic and immunologic effects.” International Journal of Environmental Research and Public Health 12, no. 2 (2015): 1295-1313.

Currently, ethyl mercury (EtHg) and adjuvant-Al are the dominating interventional exposures encountered by fetuses, newborns, and infants due to immunization with Thimerosal-containing vaccines (TCVs). Despite their long use as active agents of medicines and fungicides, the safety levels of these substances have never been determined, either for animals or for adult humans—much less for fetuses, newborns, infants, and children. I reviewed the literature for papers reporting on outcomes associated with (a) multiple exposures and metabolism of EtHg and Al during early life; (b) physiological and metabolic characteristics of newborns, neonates, and infants relevant to xenobiotic exposure and effects; (c) neurobehavioral, immunological, and inflammatory reactions to Thimerosal and Al-adjuvants resulting from TCV exposure in infancy. Immunological and neurobehavioral effects of Thimerosal-EtHg and Al-adjuvants are not extraordinary; rather, these effects are easily detected in high- and low-income countries, with co-exposure to methylmercury (MeHg) or other neurotoxicants. Rigorous and replicable studies (in different animal species) have shown evidence of EtHg and Al toxicities. More research attention has been given to EtHg and findings have showed a solid link with neurotoxic effects in humans; however, the potential synergic effect of both toxic agents has not been properly studied. Therefore, early life exposure to both EtHg and Al deserves due consideration.

Dórea, José G., and Rejane C. Marques. “Infants’ exposure to aluminum from vaccines and breast milk during the first 6 months.” Journal of Exposure Science & Environmental Epidemiology 20, no. 7 (2010): 598-601.

The success of vaccination programs in reducing and eliminating infectious diseases has contributed to an ever-increasing number of vaccines given at earlier ages (newborns and infants). Exposure to low levels of environmental toxic substances (including metals) at an early age raises plausible concerns over increasingly lower neuro-cognitive rates. Current immunization schedules with vaccines containing aluminum (as adjuvant) are given to infants, but thimerosal (as preservative) is found mostly in vaccines used in non-industrialized countries. Exclusively, breastfed infants (in Brazil) receiving a full recommended schedule of immunizations showed an exceedingly high exposure of Al (225 to 1750 μg per dose) when compared with estimated levels absorbed from breast milk (2.0 μg). This study does not dispute the safety of vaccines but reinforces the need to study long-term effects of early exposure to neuro-toxic substances on the developing brain. Pragmatic vaccine safety needs to embrace conventional toxicology, addressing especial characteristics of unborn fetuses, neonates and infants exposed to low levels of aluminum, and ethyl mercury traditionally considered innocuous to the central nervous system.

Exley, Christopher, Louise Swarbrick, Rhomain K. Gherardi, and Francois-Jérôme Authier. A role for the body burden of aluminium in vaccine-associated macrophagic myofasciitis and chronic fatigue syndrome.” Medical hypotheses 72, no. 2 (2009): 135-139.

Macrophagic myofasciitis and chronic fatigue syndrome are severely disabling conditions which may be caused by adverse reactions to aluminium-containing adjuvants in vaccines. While a little is known of disease aetiology both conditions are characterised by an aberrant immune response, have a number of prominent symptoms in common and are coincident in many individuals. Herein, we have described a case of vaccine-associated chronic fatigue syndrome and macrophagic myofasciitis in an individual demonstrating aluminium overload. 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.

Fanni, Daniela, Rossano Ambu, Clara Gerosa, Sonia Nemolato, Nicoletta Iacovidou, Peter Van Eyken, Vassilios Fanos, Marco Zaffanello, and Gavino Faa. “Aluminum exposure and toxicity in neonates: a practical guide to halt aluminum overload in the prenatal and perinatal periods.” World Journal of Pediatrics 10, no. 2 (2014): 101-107.

Pediatricians and neonatologists must be more concerned about aluminum content in all products our newborns are exposed to, starting from monitoring aluminum concentrations in milk- and soybased formulas in which, on the on the basis of recent studies, there is still too much aluminum.

Fanni, Daniela, Rossano Ambu, Clara Gerosa, Sonia Nemolato, Nicoletta Iacovidou, Peter Van Eyken, Vassilios Fanos, Marco Zaffanello, and Gavino Faa. “Aluminum exposure and toxicity in neonates: a practical guide to halt aluminum overload in the prenatal and perinatal periods.” World Journal of Pediatrics 10, no. 2 (2014): 101-107.

Background: During the last years, human newborns have been overexposed to biologically reactive aluminum, with possible relevant consequences on their future health and on their susceptibility to a variety of diseases. Children, newborns and particularly preterm neonates are at an increased risk of aluminum toxicity because of their relative immaturity.

Data sources: Based on recent original publications and classical data of the literatures, we reviewed the aluminum content in mother’s food during the intrauterine life as well as in breast milk and infant formula during lactation. We also determined the possible role of aluminum in parenteral nutrition solutions, in adjuvants of vaccines and in pharmaceutical products. A special focus is placed on the relationship between aluminum overexposure and the insurgence of bone diseases. 

Results: Practical points of management and prevention are suggested. Aluminum sources that infants may receive during the first 6 months of life are presented. In the context of prevention of possible adverse effects of aluminum overload in fetal tissues during development, simple suggestions to pregnant women are described. Finally, practical points of management and prevention are suggested. 

Conclusions: Pediatricians and neonatologists must be more concerned about aluminum content in all products our newborns are exposed to, starting from monitoring aluminum concentrations in milk- and soy based formulas in which, on the basis of recent studies, there is still too much aluminum.

Gherardi, Romain K., Guillemette Crépeaux, François-Jerome Authier, and Lluis Lujan. “Animal studies are mandatory to investigate the poorly understood fate and effects of aluminum adjuvants administered to billions of humans and animals worldwide.” Autoimmunity reviews 17, no. 7 (2018): 735-737.

Gherardi, Romain K., Guillemette Crépeaux, and François-Jérome Authier. “Myalgia and chronic fatigue syndrome following immunization: macrophagic myofasciitis and animal studies support linkage to aluminum adjuvant persistency and diffusion in the immune system.” Autoimmunity reviews 18, no. 7 (2019): 691-705.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a multifactorial and poorly undersood disabling disease. We present epidemiological, clinical and experimental evidence that ME/CFS constitutes a major type of adverse effect of vaccines, especially those containing poorly degradable particulate aluminum adjuvants. Evidence has emerged very slowly due to the multiplicity, lack of specificity, delayed onset, and frequent medical underestimation of ME/CFS symptoms. It was supported by an epidemiological study comparing vaccinated vs unvaccinated militaries that remained undeployed during Gulf War II. Affected patients suffer from cognitive dysfunction affecting attention, memory and inter-hemispheric connections, well correlated to brain perfusion defects and associated with a stereotyped and distinctive pattern of cerebral glucose hypometabolism. Deltoid muscle biopsy performed to investigate myalgia typically yields macrophagic myofasciitis (MMF), a histological biomarker assessing longstanding persistency of aluminum agglomerates within innate immune cells at site of previous immunization. MMF is seemingly linked to altered mineral particle detoxification by the xeno/ autophagy machinery. Comparing toxicology of different forms of aluminum and different types of exposure is misleading and inadequate and small animal experiments have turned old dogma upside down. Instead of being rapidly solubilized in the extracellular space, injected aluminum particles are quickly captured by immune cells and transported to distant organs and the brain where they elicit an inflammatory response and exert selective low dose long-term neurotoxicity. Clinical observations and experiments in sheep, a large animal like humans, confirmed both systemic diffusion and neurotoxic effects of aluminum adjuvants. Post-immunization ME/CFS represents the core manifestation of “autoimmune/inflammatory syndrome induced by adjuvants”


Igbokwe, Ikechukwu Onyebuchi, Ephraim Igwenagu, and Nanacha Afifi Igbokwe. “Aluminium toxicosis: a review of toxic actions and effects.” Interdisciplinary Toxicology 12, no. 2 (2019): 45-70.

Aluminium (Al) is frequently accessible to animal and human populations to the extent that intoxications may occur. Intake of Al is by inhalation of aerosols or particles, ingestion of food, water and medicaments, skin contact, vaccination, dialysis and infusions. Toxic actions of Al induce oxidative stress, immunologic alterations, genotoxicity, pro-inflammatory effect, peptide denaturation or transformation, enzymatic dysfunction, metabolic derangement, amyloidogenesis, membrane perturbation, iron dyshomeostasis, apoptosis, necrosis and dysplasia. The pathological conditions associated with Al toxicosis are desquamative interstitial pneumonia, pulmonary alveolar proteinosis, granulomas, granulomatosis and fibrosis, toxic myocarditis, thrombosis and ischemic stroke, granulomatous enteritis, Crohn’s disease, inflammatory bowel diseases, anemia, Alzheimer’s disease, dementia, sclerosis, autism, macrophagic myofasciitis, osteomalacia, oligospermia and infertility, hepatorenal disease, breast cancer and cyst, pancreatitis, pancreatic necrosis and diabetes mellitus. The review provides a broad overview of Al toxicosis as a background for sustained investigations of the toxicology of Al compounds of public health importance.

Katzav, A., S. Kivity, M. Blank, Y. Shoenfeld, and J. Chapman. “Adjuvant immunization induces high levels of pathogenic antiphospholipid antibodies in genetically prone mice: another facet of the ASIA syndrome.” Lupus 21, no. 2 (2012): 210-216.

Adjuvants may induce autoimmune diseases in susceptible individuals, a phenomenon recently defined as autoimmune/inflammatory syndrome induced by adjuvants (ASIA). Patients with both antiphospholipid antibodies (aPL) and the genetic coagulopathy factor V Leiden (FVL) are frequently found. We therefore evaluated whether adjuvant can induce aPL in heterozygous FVL mice. aPL were measured in naı¨ve mice and at 1 and 5 months after immunization with either complete or incomplete Freund’s adjuvant (CFA, IFA) in FVL and control C57/ B6 background mice. We defined antibody levels 3 SD above the mean of C57/B6 mice immunized with adjuvant as positive (specificity of 99%). For b2GPI-dependent aPL, 28.6% (6/21) of FVL mice 5 months after immunization with adjuvant (both IFA and CFA) were positive compared with 4.8% (1/22) of FVL mice 1 month after adjuvant and 0% of naı¨ve FVL and C57/B6 mice (0/16, p < 0.001). aPL levels correlated with behavioral hyperactivity in the staircase test. FVL mice immunized with adjuvant did not develop b2GPIindependent aPL. We hypothesize that the FVL aPL association is not a coincidence, but that chronic coagulation defects combined with external inflammatory stimuli analogous to adjuvant may induce aPL and also antiphospholipid syndrome, thus supporting the notion of ASIA. 

Lyons-Weiler, James, and Robert Ricketson. “Reconsideration of the immunotherapeutic pediatric safe dose levels of aluminum.” Journal of Trace Elements in Medicine and Biology 48 (2018): 67-73.

FDA regulations require safety testing of constituent ingredients in drugs (21 CFR 610.15). With the exception of extraneous proteins, no component safety testing is required for vaccines or vaccine schedules. The dosing of aluminum in vaccines is based on the production of antibody titers, not safety science. Here we estimate a Pediatric Dose Limit that considers body weight. We identify several serious historical missteps in past analyses of provisional safe levels of aluminum in vaccines, and provide updates relevant to infant aluminum exposure in the pediatric schedule considering pediatric body weight. When aluminum doses are estimated from Federal Regulatory Code given body weight, exposure from the current vaccine schedule are found to exceed our estimate of a weight-corrected Pediatric Dose Limit. Our calculations show that the levels of aluminum suggested by the currently used limits place infants at risk of acute, repeated, and possibly chronic exposures of toxic levels of aluminum in modern vaccine schedules. Individual adult exposures are on par with Provisional Tolerable Weekly Intake “limits”, but some individuals may be aluminum intolerant due to genetics or previous exposures. Vaccination in neonates and low birth-weight infants must be re-assessed; other implications for the use of aluminum-containing vaccines, and additional limitations in our understanding of neurotoxicity and safety levels of aluminum in biologics are discussed.

Masson, Jean-Daniel, Guillemette Crépeaux, François-Jérôme Authier, Christopher Exley, and Romain K. Gherardi. “Critical analysis of reference studies on the toxicokinetics of aluminum-based adjuvants.” Journal of Inorganic Biochemistry 181 (2018): 87-95.

We reviewed the three toxicokinetic reference studies commonly used to suggest that aluminum (Al)-based adjuvants are innocuous. A single experimental study was carried out using isotopic 26Al (Flarend et al., Vaccine, 1997). This study used aluminum salts resembling those used in vaccines but ignored adjuvant uptake by cells that was not fully documented at the time. It was conducted over a short period of time (28 days) and used only two rabbits per adjuvant. At the endpoint, Al elimination in the urine accounted for 6% for Al hydroxide and 22% for Al phosphate, both results being incompatible with rapid elimination of vaccine-derived Al in urine. Two theoretical studies have evaluated the potential risk of vaccine Al in infants, by reference to an oral “minimal risk level” (MRL) extrapolated from animal studies. Keith et al. (Vaccine, 2002) used a high MRL (2 mg/kg/d), an erroneous model of 100% immediate absorption of vaccine Al and did not consider renal and blood-brain barrier immaturity. Mitkus et al. (Vaccine, 2011) only considered solubilized Al, with erroneous calculations of absorption duration. Systemic Al particle diffusion and neuro-inflammatory potential were omitted. The MRL they used was both inappropriate (oral Al vs. injected adjuvant) and still too high (1 mg/kg/d) regarding recent animal studies. Both paucity and serious weaknesses of reference studies strongly suggest that novel experimental studies of Al adjuvants toxicokinetics should be performed on the long-term, including both neonatal and adult exposures, to ensure their safety and restore population confidence in Al-containing vaccines.

McFarland, G., La Joie, E., Thomas, P., & Lyons-Weiler, J. (2020). “Acute exposure and chronic retention of aluminum in three vaccine schedules and effects of genetic and environmental variation.” Journal of Trace Elements in Medicine and Biology, 58, 126444.

Like the mechanisms of action as adjuvants, the pharmacodynamics of injected forms of aluminum commonly used in vaccines are not well-characterized, particularly with respect to how differences in schedules impact accumulation and how factors such as genetics and environmental influences on detoxification influence clearance. Previous modeling efforts are based on very little empirical data, with the model by Priest based on whole-body clearance rates estimated from a study involving a single human subject. In this analysis, we explore the expected acute exposures and longer-term whole-body accumulation/clearance across three vaccination schedules: the current US Centers for Disease Control and Prevention (CDC) schedule, the current CDC schedule using low aluminum or no aluminum vaccines, and Dr. Paul Thomas’ “Vaccine Friendly Plan” schedule. We then study the effects of an implicit assumption of the Priest model on whether clearance dynamics from successive doses are influenced by the current level of aluminum or modeled by the assumption that a new dose has its own whole-body dynamics “reset” on the day of injection. We model two additional factors: variation (deficiency) in aluminum detoxification, and a factor added to the Priest equation to model the potential impact of aluminum itself on cellular and whole-body detoxification. These explorations are compared to a previously estimated pediatric dose limit (PDL) of whole-body aluminum exposure and provide a new statistic: %alumTox, the (expected) percentage of days (or weeks) an infant is in aluminum toxicity, reflecting chronic toxicity. We show that among three schedules, the CDC schedule results in the highest %alumTox regardless of model assumptions, and the Vaccine Friendly Plan schedule, which avoids >1 ACV per office visit results in the lowest (expected) %alumTox. These results are conservative, as the MSL is derived from data used by FDA to estimate safety of aluminum in adult humans. These results demonstrate high potential utility of modeling variation in patient responses to aluminum. More empirical data from individuals who are suspected of being intolerant of aluminum from vaccines, evidenced by high aluminum retention, neurodevelopmental disorders and/or a myriad of chronic illnesses would help answer questions on whether the model predictions can be used to estimate parameter values tied to genetic factors including genomic sequence variation and family history of chronic illnesses tied to aluminum exposure.

Miller, Neil Z. “Aluminum in childhood vaccines is unsafe.” Journal of American Physicians and Surgeons 21, no. 4 (2016): 109-117.

Aluminum is a neurotoxin, yet infants and young children are repeatedly injected with aluminum adjuvants from multiple vaccines during critical periods of brain development. Numerous studies provide credible evidence that aluminum adversely affects important biological functions and may contribute to neurodegenerative and autoimmune disorders. It is impossible to predetermine which vaccinated babies will succumb to aluminum poisoning. Aluminum-free health options are needed.

Mold, Matthew, Dorcas Umar, Andrew King, and Christopher Exley. “Aluminum in brain tissue in autism.” Journal of Trace Elements in Medicine and Biology 46 (2018): 76-82.

Autism spectrum disorder is a neurodevelopmental disorder of unknown aetiology. It is suggested to involve both genetic susceptibility and environmental factors including in the latter environmental toxins. Human exposure to the environmental toxin aluminum has been linked, if tentatively, to autism spectrum disorder. Herein we have used transversely heated graphite furnace atomic absorption spectrometry to measure, for the first time, the aluminum content of brain tissue from donors with a diagnosis of autism. We have also used an aluminum-selective fluor to identify aluminum in brain tissue using fluorescence microscopy. The aluminum content of brain tissue in autism was consistently high. The mean (standard deviation) aluminum content across all 5 individuals for each lobe were 3.82(5.42), 2.30(2.00), 2.79(4.05) and 3.82(5.17) μg/g dry wt. for the occipital, frontal, temporal and parietal lobes respectively. These are some of the highest values for aluminum in human brain tissue yet recorded and one has to question why, for example, the aluminum content of the occipital lobe of a 15 year old boy would be 8.74 (11.59) μg/g dry wt.? Aluminum-selective fluorescence microscopy was used to identify aluminum in brain tissue in 10 donors. While aluminum was imaged associated with neurones it appeared to be present intracellularly in microglia-like cells and other inflammatory non-neuronal cells in the meninges, vasculature, grey and white matter. The pre-eminence of intracellular aluminum associated with non-neuronal cells was a standout observation in autism brain tissue and may offer clues as to both the origin of the brain aluminum as well as a putative role in autism spectrum disorder.

Morris, Gerwyn, Basant K. Puri, and Richard E. Frye. “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?.” Metabolic brain disease 32, no. 5 (2017): 1335-1355.

The conceptualization 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 aluminum, 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 aluminum 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 aluminum introduced via immunization could produce chronic neuropathology in genetically susceptible children. Accordingly, it is recommended that the use of aluminum salts in immunizations should be discontinued and that adults should take steps to minimize their exposure to environmental aluminum.

Parker, Albert. “Testing new hypotheses of neurological and immunological outcomes with aluminum-containing vaccines is warranted.” Journal of trace elements in medicine and biology: organ of the Society for Minerals and Trace Elements (GMS) 51 (2019): 28.

Petrik, Michael S., Margaret C. Wong, Rena C. Tabata, Robert F. Garry, and Christopher A. Shaw. “Aluminum adjuvant linked to Gulf War illness induces motor neuron death in mice.” NeuroMolecular Medicine 9, no. 1 (2007): 83-100.

Gulf War illness (GWI) affects a significant percentage of veterans of the 1991 conflict, but its origin remains unknown. Associated with some cases of GWI are increased incidences of amyotrophic lateral sclerosis and other neurological disorders. Whereas many environmental factors have been linked to GWI, the role of the anthrax vaccine has come under increasing scrutiny. Among the vaccine’s potentially toxic components are the adjuvants aluminum hydroxide and squalene. To examine whether these compounds might contribute to neuronal deficits associated with GWI, an animal model for examining the potential neurological impact of aluminum hydroxide, squalene, or aluminum hydroxide combined with squalene was developed. Young, male colony CD-1 mice were injected with the adjuvants at doses equivalent to those given to US military service personnel. All mice were subjected to a battery of motor and cognitive-behavioral tests over a 6-mo period postinjections. Following sacrifice, central nervous system tissues were examined using immunohistochemistry for evidence of inflammation and cell death. Behavioral testing showed motor deficits in the aluminum treatment group that expressed as a progressive decrease in strength measured by the wire-mesh hang test (final deficit at 24 wk; about 50%). Significant cognitive deficits in water-maze learning were observed in the combined aluminum and squalene group (4.3 errors per trial) compared with the controls (0.2 errors per trial) after 20 wk. Apoptotic neurons were identified in aluminum-injected animals that showed significantly increased activated caspase-3 labeling in lumbar spinal cord (255%) and primary motor cortex (192%) compared with the controls. Aluminum-treated groups also showed significant motor neuron loss (35%) and increased numbers of astrocytes (350%) in the lumbar spinal cord. The findings suggest a possible role for the aluminum adjuvant in some neurological features associated with GWI and possibly an additional role for the combination of adjuvants.

Perricone C, Colafrancesco S, Mazor RD, et al. “Autoimmune/inflammatory syndrome induced by adjuvants.” (ASIA) 2013: Unveiling the pathogenic, clinical and diagnostic aspects. J Autoimmun 2013;47(Dec):1-16

In 2011 a new syndrome termed ‘ASIA Autoimmune/Inflammatory Syndrome Induced by Adjuvants’ was defined pointing to summarize for the first time the spectrum of immune-mediated diseases triggered by an adjuvant stimulus such as chronic exposure to silicone, tetramethylpentadecane, pristane, aluminum and other adjuvants, as well as infectious components, that also may have an adjuvant effect. All these environmental factors have been found to induce autoimmunity by themselves both in animal models and in humans: for instance, silicone was associated with siliconosis, aluminum hydroxide with postvaccination phenomena and macrophagic myofasciitis syndrome. Several mechanisms have been hypothesized to be involved in the onset of adjuvant-induced autoimmunity; a genetic favorable background plays a key role in the appearance on such vaccine-related diseases and also justifies the rarity of these phenomena. This paper will focus on protean facets which are part of ASIA, focusing on the roles and mechanisms of action of different adjuvants which lead to the autoimmune/inflammatory response. The data herein illustrate the critical role of environmental factors in the induction of autoimmunity. Indeed, it is the interplay of genetic susceptibility and environment that is the major player for the initiation of breach of tolerance.

Shaw, Christopher A., Dan Li, and Lucija Tomljenovic. “Are there negative CNS impacts of aluminum adjuvants used in vaccines and immunotherapy?.” Immunotherapy 6, no. 10 (2014): 1055-1071.

In spite of a common view that aluminum (Al) salts are inert and therefore harmless as vaccine adjuvants or in immunotherapy, the reality is quite different. In the following article we briefly review the literature on Al neurotoxicity and the use of Al salts as vaccine adjuvants and consider not only direct toxic actions on the nervous system, but also the potential impact for triggering autoimmunity. Autoimmune and inflammatory responses affecting the CNS appear to underlie some forms of neurological disease, including developmental disorders. Al has been demonstrated to impact the CNS at every level, including by changing gene expression. These outcomes should raise concerns about the increasing use of Al salts as vaccine adjuvants and for the application as more general immune stimulants.

Shaw, Christopher A., and Michael S. Petrik. “Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration.” Journal of inorganic biochemistry 103, no. 11 (2009): 1555-1562.

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.

Sheth, Sneha KS, Yongling Li, and Christopher A. Shaw. “Is exposure to aluminium adjuvants associated with social impairments in mice? A pilot study.” Journal of inorganic biochemistry 181 (2018): 96-103.

This is the first experimental study, to our knowledge, to demonstrate that aluminum adjuvants can impair social behaviour if applied in the early period of postnatal development. The study, however, is insufficient to make any assertive claims about the link between aluminium adjuvants and ASD in humans.

Strunecka, Anna, Russell L. Blaylock, Jiri Patocka, and Otakar Strunecky. “Immunoexcitotoxicity as the central mechanism of etiopathology and treatment of autism spectrum disorders: A possible role of fluoride and aluminum.” Surgical Neurology International 9 (2018).

Our review suggests that most autism spectrum disorder (ASD) risk factors are connected, either directly or indirectly, to immunoexcitotoxicity. Chronic brain inflammation is known to enhance the sensitivity of glutamate receptors and interfere with glutamate removal from the extraneuronal space, where it can trigger excitotoxicity over a prolonged period. Neuroscience studies have clearly shown that sequential systemic immune stimulation can activate the brain’s immune system, microglia, and astrocytes, and that with initial immune stimulation, there occurs CNS microglial priming. Children are exposed to such sequential immune stimulation via a growing number of environmental excitotoxins, vaccines, and persistent viral infections. We demonstrate that fluoride and aluminum (Al3+) can exacerbate the pathological problems by worsening excitotoxicity and inflammation. While Al3+ appears among the key suspicious factors of ASD, fluoride is rarely recognized as a causative culprit. A long-term burden of these ubiquitous toxins has several health effects with a striking resemblance to the symptoms of ASD. In addition, their synergistic action in molecules of aluminofluoride complexes can affect cell signaling, neurodevelopment, and CNS functions at several times lower concentrations than either Al3+ or fluoride acting alone. Our review opens the door to a number of new treatment modes that naturally reduce excitotoxicity and microglial priming.

Tomljenovic, Lucija, and C. A. Shaw. “Mechanisms of aluminum adjuvant toxicity and autoimmunity in pediatric populations.” Lupus 21, no. 2 (2012): 223-230.

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 crosstalk 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.

Tomljenovic, Lucija, and Christopher A. Shaw. “Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?.” Journal of inorganic biochemistry 105, no. 11 (2011): 1489-1499.

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: 

1. children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines.


2. 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


3. 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.

Recent Posts

COVID 19 Vaccine Safety Concerns

COVID 19 Vaccine Safety Concerns

Jun 30

COVID 19 Vaccine Safety Concerns

James Odell, OMD, ND, L.Ac.

The development of antibodies has long been the basis or rationale for vaccine efficacy against a large range of infective agents such as viruses and bacteria. However, it is well known that antibodies, which the immune system develops from natural infections, differ from those that are created from vaccines. (Bear this important difference in mind when reading this article.) Additionally, when vaccines do elicit antibodies, most are only temporary and thus require boosters, unlike lifelong immunity gained from an infectious disease, such as childhood measles. Anthony Fauci and others developing or promoting COVID-19 vaccination are talking about the likelihood that the new coronavirus vaccine will have to be administered in multiple doses, perhaps even annually like the influenza vaccine. This article explores COVID-19 vaccine development and safety concerns around “fast tracking” the manufacturing and testing process.

Antibody-Dependent Enhancement (ADE)

In the 1960s, immunologists discovered the phenomenon of what is now commonly referred to as antibody-dependent enhancement (ADE). Virus ADE is a mechanism in which virus specific antibodies (from an infection or from a vaccine) promote the entry and/or the replication of another virus into white cells such as monocytes/macrophages and granulocytic cells. ADE modulates the immune response and may induce chronic inflammation, lymphopenia, and/or a ‘cytokine storm’, one or more of which have been reported to cause severe illness and even death. Essentially, ADE is a disease dissemination cycle causing individuals with secondary infection to be more immunologically upregulated than during their first infection (or prior vaccination) by a different strain.

A more technical explanation of ADE is that when patients are infected by one stereotype of a virus (whether due to a vaccine or by nature) they produce neutralizing antibodies targeting that particular viral serotype (or distinct variation within a virus species). However, if they are later infected with another viral serotype (i.e., from a secondary infection or vaccine), the preexisting antibodies cannot completely neutralize the virus. Instead, the antibodies first bind to the virus and then bind to the immune cell IgG Fc receptors and mediate viral entry into these cells. For certain cases, however, the ADE of these viruses is responsible for non-neutralizing or binding antibodies.

Early stages of the viral infection cycle requires attachment and entry of viruses into the host cell. Virus attachment is typically mediated by the specific binding of viral surface proteins to host cell receptor molecules, concentrating the virus at the cell plasma membrane. Viruses are often studded with one or more surface proteins, each potentially containing multiple subdomains, to facilitate interaction with cellular receptors and induce the entry of the virus into the cell. However, the surface of the virus is also a highly antigenic structure that can trigger cellular and humoral immune responses that eradicate or neutralize the virus in the host. Antibodies contribute to several levels of antiviral defense to efficiently neutralize the virus and reduce its infectivity. In simple terms, antibody neutralization is good, whereas antibody binding is bad.

After the 1960s, studies on vaccine candidates for diseases such as dengue, respiratory syncytial virus and severe acute respiratory syndrome (SARS) have demonstrated a paradoxical trend. Many animals and humans who received the vaccine and were subsequently exposed to the virus developed a more serious disease than those who had not been vaccinated.1, 2, 3 ADE’s have been observed for a variety of viruses, such as dengue virus, Ross River virus, other alpha and flaviviruses, HIV and influenza viruses.4, 5, 6, 7, 8, 9

Developing the COVID 19 Vaccine

Importantly, during the production of new vaccines for a variety of infectious agents, the ADE effects must be carefully examined to ensure that the vaccines do not harm the recipients. ADE is a clear concern about coronavirus vaccines that are soon to be tested on millions – if not billions – from the healthy to the ill and young to old. As a result of ‘fast-tracking,’dozens of coronavirus manufacturers have been given the green light by the FDA to bypass critical manufacturing safety rules, such as pre-human animal trials and the use of ‘inert’ placebo controls. Most significantly the concept of ‘fast track’ means that the length of the trials will be short; not more than 6 weeks. It can take two to three years to learn if there are negative health effects resulting from a vaccine. Many autoimmune and neurological side effects will not manifest within a few short weeks. Several companies are now cutting corners by conducting phase 1, 2 and 3 human trials simultaneously. Global pharmaceutical and biotech companies are now developing over 100 experimental COVID-19 vaccines, with a few leading the race after securing billions of dollars in funding from the U.S. government, the Gates Foundation, and other organizations.10, 11

At the time of this writing, at least 10 of these vaccine-development programs have reached the clinical stage of evaluation, either phase 1 or phase 2. These include programs led by Western pharmaceutical companies such as AstraZeneca plc (in partnership with the University of Oxford); BioNTech SE partnered with Pfizer, Inc.; Inovio Pharmaceuticals, Inc.; Moderna, Inc. (in partnership with NIAID) and Novavax, Inc. 123 other programs to develop a COVID-19 vaccine remain in preclinical evaluation.

Astonishingly, the University of Oxford’s Jenner Institute and Oxford Vaccine Group in the United Kingdom have announced that their researchers are beginning to recruit children aged 5 to 12 years for phase II and phase III clinical trials of the experimental COVID-19 vaccine developed by the university in collaboration with AstraZeneca plc. Researchers at The University of Oxford and AstraZeneca researchers are proceeding with testing the experimental ChAdOx1 nCov-19 vaccine in children, although a report published on May 13, 2020 indicated that small vaccine trials in mice and monkeys were not successful in proving effectiveness against infection. While the animal studies presented evidence that the experimental vaccine induced a “robust humoral and cell-mediated response” in mice and appeared to protect against development of viral pneumonia in monkeys, it did not prevent infection with COVID-19.12, 13 In other words, the animal studies failed, but the developers intend to continue with human trials.

Some of these coronavirus vaccines being developed will use unlicensed DNA, messenger RNA and nanoparticle technology, oil-based adjuvants and even electricity, to genetically manipulate and hyper-stimulate strong inflammatory immune responses in the body.14 Messenger RNA vaccines, which have never been licensed for use in humans, inject cells with mRNA, usually within lipid nanoparticles, to stimulate cells in the body to become manufacturers of viral proteins. mRNA vaccines like all vaccines stimulate cells in the body to become manufacturers of viral proteins. mRNA vaccines have potential safety issues, including local and systemic inflammation and stimulation of auto-reactive antibodies and autoimmunity, as well as the development of edema (swelling) and blood clots.

Conventional vaccines usually contain inactivated disease-causing organisms or proteins made by the pathogen (antigens) that mimic the infectious agent. These activate the body’s immune response, so it is primed to respond more quickly and efficiently if exposed to the infectious agent in the future. RNA vaccines use a different approach that takes advantage of the process that cells use to make proteins: cells use DNA as the template to make messenger RNA (mRNA) molecules, which are then translated to build proteins. An RNA vaccine consists of an mRNA strand that codes for a disease-specific antigen. Once the mRNA strand in the vaccine is inside the cells of the body, the cells use the genetic information to produce the antigen. This antigen is then displayed on the cell surface, where it is recognized by the immune system.

Safety Issues Bypassed

Vaccine safety experts generally agree that animal studies should always be conducted prior to any human clinical trial with any vaccine; COVID-19 (SARS-CoV-2) vaccines are no exception. Clinical trials should always be double-blind placebo-controlled (with an inert placebo and not with another vaccine or adjuvant as a placebo).Careful assessment of possible immune complications should then be made prior to release of the vaccine to the public. In the case of vaccines, this ‘careful assessment’ is a time of waiting and should be no less than two to three years. Importantly, over the last two decades vaccines manufactures have never been able to develop an effective and safe coronavirus vaccine. Previous coronavirus vaccine animal studies with ferrets and mice have demonstrated significant and serious side-effects. After two decades of failed trials, the question is posed as to why a fast-tracking coronavirus vaccine will now result in a different outcome? Given that many of these fast-track trials have bypassed animal studies, are only performed on healthy volunteers and children (not the elderly or those with pre-morbidities), and that trials are conducted without an inert double-blind placebo-controlled environment, and are not given sufficient time to observe effects on the human trials, there is serious safety concern. Many epidemiologists feel this fast track policy is a recipe for mass disaster. According to Marc Lipsitch, an epidemiologist at the Harvard Chan School of Public Health in Boston, MA, “You really have to test a vaccine carefully and not just roll it out because people are clamoring for it with an epidemic underway.”

National Childhood Vaccine Injury Act and Immunity from Liability for Vaccine Harms

By the early 1980s, pharmaceutical companies faced crippling liability for injuries to children caused by their vaccines. Instead of allowing such market forces to push them to develop safer vaccines, Congress passed the National Childhood Vaccine Injury Act (the 1986 Act) which eliminated the liability of pharmaceutical companies for injuries caused by their vaccine products. After eliminating liability for pharmaceutical companies, the 1986 Act established the Vaccine Injury Compensation Program (Vaccine Court), part of the U.S. Court of Federal Claims, to compensate people injured by vaccines. Under the 1986 Act, the U.S. Department of Health and Human Services (HHS) is the defendant in Vaccine Court and is legally obligated to defend against any claim that a vaccine causes injury. HHS is represented by the formidable resources of the U.S. Department of Justice (DOJ). In nearly every case the injured person must prove the vaccine caused the injury. Notwithstanding these hurdles, since 1986, HHS has paid over $4 billion for vaccine injuries with taxpayers’ money, not with pharmaceutical manufacturers’ dollars. Safety is regulated, not only by comprehensive and thorough manufacturing and testing procedures, but also with liability laws. Without any liability consequences, pharmaceutical vaccine manufacturers are less likely to pay due diligence regarding the safety of the vaccine.

Upon removing the market mechanisms that assured vaccine safety, Congress made HHS exclusively responsible for vaccine safety under the ‘Mandate for Safer Childhood Vaccine’ provision of the 1986 Act. HHS recently conceded in federal court, that it did not comply with the essential provisions of this act, such as submitting reports to Congress on how HHS has improved vaccine safety. Such government neglect of vaccine safety also casts a doubt on the future development of coronavirus vaccines.  

Vaccine-Associated Enhanced Respiratory Disease (VAERD)

Similar to ADE, another immune enhancement phenomena came to the foreground in the 1960s during clinical trials in which young children were immunized with whole-inactivated respiratory syncytial virus (RSV) vaccines.15 When the children contracted RSV naturally a few months after the vaccinations, those who were immunized became significantly sicker than those who had not been vaccinated. In fact, in one trial, 80 percent of children in the youngest cohort had to be hospitalized, and two died.16 The syndrome the hospitalized children developed is sometimes called vaccine-associated enhanced respiratory disease (VAERD). VAERD is like ADE in that a high concentration of binding antibodies do not fully neutralize the virus and results in the formation of binding antibody-virus complexes that elicit a cytokine storm. As a consequence, elevated pro-inflammatory cytokines associated with the innate immune system have been associated with the VAERD phenomenon.17 In these children, the binding-antibody complexes affected the small airways of the lungs, obstructing these spaces and increasing inflammation. 

In another noteworthy study, “Abstract: a formalin-inactivated monkey kidney culture propagated 100-fold concentrated respiratory syncytial (RS) virus vaccine was administered intramuscularly to residents of Harrison and Arthur Cottages in Junior Village, a District of Columbia Welfare Institution for homeless infants and children. No significant local or systemic vaccine reactions were (initially) observed. A sharp outbreak of RS virus infection occurred approximately 9 months after the vaccine study was initiated. Recovery of RS virus was found to be significantly associated not only with the onset of febrile illness but also with the onset of febrile pneumonia illness. The vaccine not only failed to offer protection, but also induced an exaggerated altered clinical response to naturally occurring RS virus infection in the younger vaccines as 9 (69%) of 13 vaccinated and only 4 (9%) of 47 nonvaccinated Harrison Cottage residents, 6–23 months of age developed pneumonia.” The authors concluded, “The paradoxical effect of vaccination suggests that serum antibody may play an active role in the pathogenesis of RS virus disease.”18

Institutions for the homeless and ‘wards of the state’, orphanages, prisons, and developing countries (Uganda, Kenya, Latin America, Caribbean, Thailand) have historically been targeted for experimental vaccine trials. Some larger trials (rarely reported by the media) in Africa have resulted in mass sterility and even death.

The ever-changing mutation terrain of viruses results in ‘vaccine mismatch’ due to the lack of relatedness between the vaccine and the numerous circulating strains. This can potentially create vaccine reactions such as VAERD. Influenza vaccines contain inactivated virus formulated with adjuvants (aluminum, squalene, and several immunological toxins), and this formulation could certainly contribute to the pathology observed in VAERD.19

Another example of VAERD occurred with “Abstract: Field evaluation of two formalin-inactivated respiratory virus vaccines in a selected pediatric population in California during the 1966—1967 respiratory disease season. A total of 441 children ranging in age from four months to nine years were vaccinated: 219 with a respiratory syncytial (RS) virus vaccine and 222 with a trivalent parainfluenza virus (types 1, 2, and 3) vaccine. Very high attack rates of parainfluenza virus types 1 and 3 and RS virus was observed during the study period in infants and children in both vaccine groups. A protective effect was not demonstrable for either vaccine. Infants who received the RS virus vaccine and who subsequently became infected with RS virus tended to have a more severe clinical illness than infants who did not receive this vaccine.”20

There have been numerous studies on VAERD, particularly in children. Unfortunately, mainstream media report little information on this important issue.

COVID-19 Occurrence and Prior Vaccination

One of the more perplexing concerns regarding the current COVID-19 epidemic is the discrepancy between the severity of cases observed in Wuhan, Northern Italy, New York, and those occurring elsewhere in the world. Among the several reasons, such as air pollution, age, and pre-morbidities, another plausible justification is the antibody-dependent enhancement of SARS-CoV-2 due to previous exposure to coronaviruses and widespread influenza vaccine campaigns. Prior to the COVID-19 outbreak, both China and Italy implemented mass influenza vaccination campaigns.21, 22, 23 In one study, ADE was suggested to account for the severity of COVID-19 cases initially observed in China (and elsewhere) relative to other regions of the world.24 The previous infection with other coronaviruses, and/or influenza vaccines may have primed COVID 19 patients, predisposing them to the development of severe disease once infected with SARS-CoV-2.  

ADE and VAERD require prior exposure to viral antigenic epitopes, such as those contained in flu and pneumonia vaccines, making it a possible explanation for the observed geographic limitation of severe cases and deaths, as well as the age discrepancy – affecting primarily the elderly people who have received mandated flu and pneumonia vaccines, particularly in nursing homes. 

Studies have shown that vaccines developed against another coronavirus, feline infectious peritonitis virus, increased the risk for cats to develop disease caused by the virus.25 Similar effects have been seen in animal studies for other viruses, including the coronavirus, which causes SARS.26, 27

Research suggests that prior infection with other coronaviruses, from the agents of the common cold, as well as certain vaccines may have ‘primed’ COVID-19 patients, predisposing them to the development of severe disease once they have been infected with SARS-CoV-2. While severe cases of COVID-19 were reported later from all over the world, this has occurred mainly in the elderly population with pre-morbidities. Thus, the above hypothesis cannot be completey dismissed. Cross-reactivity of antibodies against to SARS-CoV-2 and SARS-CoV spike proteins is common and some preliminary data claim that they seem to be rarely cross-neutralising.28.

Safety Conclusion

Normally, vaccine development is a lengthy and complicated process, often lasting 10-15 years and involving a combination of public and private involvement. Unfortunately, the rapid worldwide competition between pharmaceutical companies to develop a COVID-19 vaccine has bypassed multiple safety controls, rendering the result both dubious and potentially dangerous for the public. Financial interests have taken precedence over the health and safety of the public. Hasty development of vaccines is always risky, and only thorough research employing all the safety precautions will lead to a safe and effective vaccine.

There are other concerns related to the safety of vaccines not discussed here due to space limitations, in particular adjuvants. Adjuvants are used to induce a stronger immune response from vaccines. These chemicals can have a wide range of compositions, including lipids, proteins, nucleic acids, and even inorganic material, such as aluminum salts. What they all have in common is that they hyper stimulate receptors in immune cells and most do this through their cellular toxicity. Animal studies reveal that aluminum adjuvant particles in vaccines deposit in the brain and bones and are neurologically (brain) toxic. Aluminum ingested in the diet has low oral absorption (about 0.3%), is rapidly excreted by the kidneys, is (mostly) excluded from the brain by the blood-brain barrier, and is in a solubilized, ionic (not particulate)Al3+ form. These defenses are adequate for protecting the brain from natural levels of aluminum exposure. These protective mechanisms are unable to protect the brain from injected aluminum adjuvant particles. Aluminum adjuvant particles are too large to be removed by the kidneys and are transmitted across the blood-brain barrier by macrophages.

Regulators (the Center for Biologics Evaluation and Testing of the U.S. Food and Drug Administration are reckless and unethical not to require that vaccine developers check for potentially adverse reactions in animal studies first, and should insist on double-blind, inert placebo controls with human trials that extend at least two to three years, if not longer. The National Institute of Allergy and Infectious Diseases (NIAID), led by Anthony Fauci argue that the risk of delaying vaccine advancement is far greater than the risk of causing illness in healthy volunteers (children remember). Testing vaccines without proper safety precautions or taking the time required to thoroughly analyze the effects of research volunteers could bring untold disastrous consequences on millions of lives well into the future.


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Vaccine Viral Interference

Vaccine Viral Interference

May 8, 2020

Vaccine Viral Interference

Here is an excellent and thought-provoking article by Dr. Allan S. Cunningham, retired pediatrician dated 02/23/2020 entitled “TAMIFLU & INFLUENZA VACCINES: MORE HARM THAN GOOD?”

Dr. Cunningham discusses how flu vaccines increase the risk of illness from noninfluenza virus infections such as rhinoviruses, coronaviruses, RS viruses, parainfluenza viruses, adenoviruses, HMP viruses and enteroviruses. After reading this think of the tri-and particularly quadrivalent flu vaccines administered in Italy in 2019 to thousands of elderlies. According to data most of the people who received flu vaccination were over 65 years old. Particularly, implicated as potentially causing was this newly concocted quadivalent flu vaccine that contained influenza A-(H1N1)pdm09; influenza A(H3N2); influenza B/Yamagata and influenza B/Victoria together with proprietary adjuvants. Adjuvants are substances, like aluminum, added to vaccines to boost immune response Did this flu (influenza) vaccine campaign cause Vaccine Interference and increase the coronavirus pandemic numbers across Italy recently?

More References of Vaccination Viral Interference:

Cowling, Benjamin J., and Hiroshi Nishiura. “Virus interference and estimates of influenza vaccine effectiveness from test-negative studies.” Epidemiology 23, no. 6 (2012): 930-931.

Authors concluded, “In a separate placebo-controlled trial of influenza vaccination, we reported that recipients of influenza vaccine had significantly higher risk of non-influenza respiratory virus infections.”

Viboud, Cecile, and Lone Simonsen. “Does seasonal influenza vaccination increase the risk of illness with the 2009 A/H1N1 pandemic virus?.” Plos medicine 7, no. 4 (2010).

Authors concluded, “In summary, we report findings from four epidemiologic studies in Canada showing that prior receipt of 2008–09 TIV was associated with increased risk of medically attended pH1N1 illness during the spring–summer 2009.”

Janjua, Naveed Z., Danuta M. Skowronski, Travis S. Hottes, William Osei, Evan Adams, Martin Petric, Suzana Sabaiduc et al. “Seasonal influenza vaccine and increased risk of pandemic A/H1N1-related illness: first detection of the association in British Columbia, Canada.” Clinical Infectious Diseases 51, no. 9 (2010): 1017-1027.

Authors concluded, “In this article, we present the first observation of an unexpected association between prior seasonal influenza vaccination and pH1N1 illness during the spring and summer of 2009 in Canada. Specifically, outbreak investigation conducted during the early stages of the pandemic in a northern BC community identified that participants reporting pH1N1-related ILI during the period 1 April through 5 June 2009 were more than twice as likely to report having previously received seasonal influenza vaccine.”

Rikin, Sharon, Haomiao Jia, Celibell Y. Vargas, Yaritza Castellanos de Belliard, Carrie Reed, Philip LaRussa, Elaine L. Larson, Lisa Saiman, and Melissa S. Stockwell. “Assessment of temporally-related acute respiratory illness following influenza vaccination.” Vaccine 36, no. 15 (2018): 1958-1964.

Authors concluded, “Vaccinated individuals were no more likely to get influenza after influenza vaccination; however, patients’ experiences of illness after vaccination may be validated by these results which suggest increased risk of ARI caused by non-influenza respiratory pathogens following influenza vaccination among children <18 years.”

Skowronski, Danuta M., Gaston De Serres, Natasha S. Crowcroft, Naveed Z. Janjua, Nicole Boulianne, Travis S. Hottes, Laura C. Rosella et al. “Association between the 2008–09 seasonal influenza vaccine and pandemic H1N1 illness during spring–summer 2009: four observational studies from Canada.” PLoS medicine 7, no. 4 (2010).

Authors concluded, “we report findings from four epidemiologic studies in Canada showing that prior receipt of 2008–09 Trivalent Inactivated Influenza Vaccine (TIV) was associated with increased risk of medically attended pandemic-H1N1 illness during the spring–summer 2009.

Wolff, Greg G. “Influenza vaccination and respiratory virus interference among Department of Defense personnel during the 2017–2018 influenza season.” Vaccine 38, no. 2 (2020): 350-354.

Authors concluded, “Examining virus interference by specific respiratory viruses showed mixed results. Vaccine derived virus interference was significantly associated with coronavirus and human metapneumovirus; however, significant protection with vaccination was associated not only with most influenza viruses, but also parainfluenza, RSV, and non-influenza virus coinfections.”

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