Archive for the ‘vaccines’ Category

Mechanisms of Vaccine Injury – Part 2 Nov, 2017 by James Lyons Weiler

THIS IS THE SECOND PART OF A SERIES OF ARTICLES ON THE BIOLOGICAL MECHANISMS OF VACCINE INJURY. The first of the series focused on the scientific evidence for (1) vaccine-induced mitopathy, (2) vaccine-induced persistent gliosis, (3) vaccine-induced endoplasmic reticulum failures (with both damage to detoxification pathways and to compromised immune systems via downregulation of ERAP1).  Part 1:

This article presents the scientific basis of autoimmunity from vaccines.

WHEN MOST OF THE KNOWLEDGE from basic science (cell culture and animal studies) seemingly falls apart in clinical trials, something is terribly wrong. Translational research falls apart when the basic science has it wrong, or when the clinical studies are flawed, fraudulent, or non-existent. Our governments have, in the past, relied heavily on the absence of evidence to assure the public on vaccine safety. “There are no studies” does not mean that the studies have been conducted… sometimes, it simply means “We don’t yet know”. They also rely on consistently over-cooked results that would raise the ire of any bona fide and ethical statistician.

Which is why it was most unscientific of the IOM to call for an end to science – after they ignored all of the basic studies on the question of a link between vaccines and autism – even though not all vaccines had been studied.

First, Immunology 101.

The mammalian adaptive immune system is a marvel of natural selection. Foreign proteins, or part of proteins (antigens) are taken up by antigen-presenting cells (APCs) including dendritic cells (DCs), where they processed into peptides and then loaded onto major histocompatibility complex (MHC) molecules for presentation to CD8 T cells via clonotypic T cell receptors (TCRs). (Stick with me, all of this is relevant, I assure you).

One type of T cell, the cytolytic T cells (Tc) can directly lyse a target pathogen cell. Tc’s are activated by MHC Class I on APCs. Another type of T cell, T helper cells (Th’s) are activated by MHC class II and release cytokines that have direct cellular effects themselves. Cytokines also activate macrophages, monocytes and B cells. B cells in particular express surface receptors that bind to surface antigens. When Th cells signal B cells, the B cells secrete antibodies that are supposed to be uniquely specific for the antigen responsible for the Th signal. Those antibodies can bind their specific targets alone, or they can also bind to and activate macrophages simultaneously, via the Fc receptor.

‘Priming’ of the immune system toward autoimmunity has been postulated. Vaccination, of course, often involves multiple exposures due to boosters. There are four mechanisms by which host infection by a pathogen can lead to autoimmunity. These are:

Molecular Mimicry. The pathogen carries elements that are similar enough in amino acid sequence or structure to self-antigen that the pathogen acts as a self-‘mimic’. In molecular mimicry, T or B cells activated in response to the pathogen also happen to be cross-reactive to self proteins. This can lead to direct autoimmune damage and false-positive “friendly-fire” activation of the immune system (via, for example, cytokine signalling due to the release of cytokines as result of autoimmune attacks on self proteins, cells, and tissues).

Epitope Spreading. A pathogen can also cause autoimmune disease via epitope spreading. In epitope spreading, damage to self-tissue occurs due either to the immune response to tissue infected by a persisting pathogen, or direct lysis of healthy cells by the pathogen. APCs take up antigens released from damaged tissue, initiating a self-specific immune response.

Bystander Activation. In this model, an indirect or non-specific activation of autoimmune cells is caused by the generally inflammatory environment that results from infection. The non-specific activation of one part of the immune system leads to the activation of other parts.

Cryptic Antigens. Foreign antigens can lead to autoimmunity via the activation of immunity to antigens that are not usually dominant – they are instead normally invisible to the immune system. It is generally described as an increase in “subdominant” antigens, and is usually attributed, like bystander activation, to the inflammatory environment that arises after infection. The involvement of cryptic antigens is considered likely when one observes increased protease production, and differential processing of released self-epitopes by APCs.

In the first article of this series, I reviewed the role of thimerosal as a specific inhibitor of ERAP1, a critically important protein for healthy immune systems. Read this description of the role of ERAP1 in APCs (Rock et al. 2010):

“ERAP1-deficient cells have reduced surface levels of MHC class I molecules and the peptide-MHC complexes that are made are less stable than on wild type cells… These results suggest that ERAP1 makes an important contribution both to the quantity and quality of peptides available for antigen presentation.”

Peptides presented by healthy cells come from normal autologous (self-generated) genes and are ignored because the immune system is tolerant to them. Aberrant peptide presentation due to low ERAP1 will lead to confusion of the immune system. When CD8 T-cells detect what appear to be foreign proteins because they are mis-processed, any tissue expressing the incorrectly trimmed peptides, either on their surface of during cell death is at risk of autoimmune attack.

The process of thimerosal-compromised ERAP1 failure will match the cryptic peptide model because peptides that do not normally initiate an immune response will appear to be highly immunogenic.


When a total breakdown of normal controls against attacks against the self occurs, widespread autoimmune attacks lead to recurrent cycles of cytokine release and cell death – and any, or all of the processes described can be unleashed simultaneously. Organ damage, damage to blood vessels, and high fever can result in death.

A study of the rates of anaphylaxis reported to the Vaccine Safety Datalink (VSD) by McNeil et al. (2016) resulted in a finding of 33 confirmed cases of anaphylaxis from January 2009 through December 2011. Using the rate of 33 confirmed cases after 25,173,965 doses, they estimated the risk of anaphylaxis to be 1.31/million doses. It is interesting to note that 85% of the case of anaphylaxis had prior evidence of atopy (3 with prior anaphylaxis, 16 with asthma, and 9 with specific prior allergies).

The rate of 1.31 per million doses may seem small. However, a search of the VAERS (Vaccine Adverse Event Reporting System) database over the same time period (January 2009 through December 2011) reveals that 550 cases of anaphylaxis were reported to VAERS. VAERS is a passive reporting system, and users must acknowledge that the data cannot be used to attribute causality. Individuals who like to claim that VAERS is a sufficient and adequate system point to the positive finding of problems with a rotavirus vaccine. But unless causality can be established using data from VAERS, negative association results of no increase in risk of adverse events are suspect due to under-reporting.

Under-reporting of vaccine injuries is a serious issue for VAERS; estimates range from only 1% to 10% of adverse events captured. Using that range, the actual number of cases of anaphylaxis nationwide would be anywhere from 550 (20.1 per 1,000,000 doses), to 55,000 (2,000 per 1,000,000 doses). Although they are required to report all vaccine adverse events, there is no penalty to doctors who fail to report. Clearly, the post-market surveillance systems that are supposed to allow our scientists to detect upticks in vaccine injury (pharmacovigilence) do not work.

Guillan-Barré Syndrome (GBS)

The National Vaccine Compensation Program recently added GBS as a vaccine injury for which plaintiffs can be awarded compensation. GBS occurs when vaccines (or viruses) cause an autoimmune reaction against myelin proteins. These proteins act as insulation around nerves, and are essential for proper transmission of nerve impulses. GBS is not the only demyelination disease; in fact, most of the conditions that involve demyelination mostly differ in which tissue the syndrome represents (e.g., transverse myelitis (TM), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and neuromyelitis optica (NMO).

Molecular mimicry was seen as a likely culprit way back in 1989:

“Thus, it is biologically plausible that injection of an inactivated virus, bacterium, or live attenuated virus might induce in the susceptible host an autoimmune response by deregulation of the immune response, by nonspecific activation of the T cells directed against myelin proteins, or by autoimmunity triggered by sequence similarities of proteins in the vaccine to host proteins such as those of myelin. The latter mechanism might evoke a response to a self-antigen, so-called molecular mimicry (Fujinami and Oldstone, 1989).”

Molecular mimicry due to exposure of individuals to proteins via infection by pathogens is non-controversial and widely accepted. Some examples of sequence-level similarity include the measles P3 protein and the human mylein basic protein (MBP), which shares at least 78% sequence identity:



The likely effect of this level of sequence similarity is autoimmunity against the MBP, leading to change in the behavior of a host from mobile, and upright, to supine and sedentary – behaviors sure to elicit a social response by the host’s conspecifics, perhaps increasing the likelihood of transmission of the virus.

Some individuals are likely to more susceptible to autoimmunity due to exposure to proteins from pathogens owing to genetic variation that changes one or two amino acids in their self antigen sequence, making it more similar in sequence or in structure to the pathogen antigen.

The principles of autoimmunity from both viral infection and from vaccination have been absolutely demonstrated both in animals and in humans. McCoy et al. (2006) found that mice that were first exposed to a vaccinia virus encoding mylein protein, and then vaccinated against murine cytomegalovirus developed multiple sclerosis. In humans, cross-reactivity between MBP and a herpesvirus-6 protein has been reported (Tejada-Simon, et al. 2003). At the population level, a small increase in risk of MS and other demyelinating disorders due to vaccination (any vaccine) has been detected (Langer-Gould et al., 2014), but the authors concluded that the increased risk was real, but small.

A natural experiment in France occurred when the government brought Hepatitis B vaccination to the population. The uptake in HepB vaccine was followed by an increase in reported cases of MS to insurers (Figure 1). The government stopped purchasing the HepB vaccine, and as the remaining lots worked their way through the healthcare systems, HepB vaccine uptake declined, followed by a decline in the reported cases of MS (Figure 1). Other than a large randomized clinical trial that did not “correct for” or exclude individuals at risk of MS, this is the closest demonstration of causality between MS and vaccination that we can expect to see.

francemsFigure 1. See Le Houézec, D. 2014. Evolution of multiple sclerosis in France since the beginning of hepatitis B vaccination. Immunol Res. 2014; 60(2-3): 219–225.

This outcome is not surprising, given the large amount of similarity shared by proteins in the HepB proteome and human neurological proteins (Ricco and Kanduc, 2010). Ample evidence exists in the form of cross-reactivity between antibodies against HepB myelin mimics and human myelin-related proteins (Bogdanos et al., 2005).

Individuals might experience varying degrees of severity of demyelination after vaccination due to genetic variation. Half of their myelin proteins and myelin oligodendrocyte glycoproteins might show low cross-reactivity because one of their parents had the canonical amino acid sequence, while the other half of their proteins might be more reactive due to genetic variation that alters the amino acid sequence in a way that increases the similarity to the pathogen’s matching peptide sequences. Further, over time, the progression and severity of demyelination could occur due to increased autoimmunity to the other version of the protein due to a process similar to bystander activation.

Aluminum Hydroxide and Autoimmunity

Vaccine risk denialists would have the public believe that the amount of aluminum in vaccines is not a threat to public health. With the exclusion of thimerosal in most pediatric vaccines came an expansion of the pediatric schedule, adding many vaccines that include aluminum hydroxide – with numerous doses.

It may surprise some, therefore, that aluminum hydroxide is routinely used in animal studies designed to model allergic rhinitis, (seasonal allergies), asthma (Elsakkar et al, 2016), food allergies (Ahren et al., 2014), autoimmunity, demyelination syndromes, and many other conditions (e.g., chronic prostatitis/chronic pelvic pain syndrome). Many of these studies use aluminum hydroxide to induce conditions identical to mysterious diseases in humans to show the efficacy of novel treatments.

Vaccine-Induced Asthma. Some of these studies take the additional step and use (all but in name) vaccine mimics – aluminum hydroxide combined with ovalbumin. Elsakkar et al. (2016), for example, used both aluminum hydroxide and ovalalbumin to induce asthma in mice to study the effect of adalimumab (aka Humira(R)). Other studies (e.g., Brandt et al., 2006) had previously demonstrated non-specific airway allergic reactions after dietary exposures to ovalbumin following exposure to aluminum hydroxide.

Vaccine-Induce Food Allergies. Up to 200 children die from anaphylaxis due to peanut allergies each year in the US, and the cost of caring for children with food allergies is estimated to be between $25 and $31 Billion – annually. In spite of this cost, no standard medical procedures exist advising parents against feeding their children peanuts or peanut butter after vaccinations.

In fact, the opposite approach is being tried. With limited scientific studies backing, the National Institutes of Health’s has, in 2017, recommended that parents feed infants as young as 4 to 6 months peanut puree to reduce the risk of the development of peanut allergies. This is based on one clinical study – with questionable results. While the study cites a marked reduction in the rate of evidence of peanut allergy in children with other allergies, only 82.9% of the SPT-positive group who were fed peanuts made it to the outcome determination, compared to 98% of the SPT positive arm who were not fed peanuts. The difference in patient attrition (98%-82.9%) in the SPT-positive group is a whopping 15% – much, much higher than the incidence of peanut allergy in the population (estimates range from 0.4%-1.4%). The drop-out rate difference would easily swamp the actual risk due to genotype.

Studies of treatments to reduce anaphylatic reaction (e.g., Shishehbor et al., 2010) use aluminum hydroxide. It known that that the simultaneous exposure of rats and mice to aluminum hydroxide and to foods such as egg. wheat, dairy, and nuts will likely cause the development of vaccine-induced food allergies. It would be remarkable if somehow humans did not also develop autoimmunity due to the combined effects of thimerosal ERAP1 suppression and the adjuvantive effects of aluminum hydroxide.

Rheumatoid Arthritis

A case report of three cases of RA after HepB vaccination (Gross et al., 1995) provides a clue that it is likely to be caused by vaccines in some people. Other similar reports exist, but population-level studies have failed to detect an association. Mouse models of arthritis exist that employ – you guessed it – injected aluminum hydroxide. So why would epidemiologic studies of samples of patients from the general population fail to detect association of RA and vaccines?

In humans, RA risk due to variation in the HLA genotypes should be a factor considered when designing studies of risk of RA due to vaccination. No study of the effect of vaccination on RA risk on individuals with HLA genotypes of known risk to RA has been conducted. These individuals are at highest risk. Like autism, RA risk has a genetic component, but certainly involves environmental factors. Karlson et al. (2013) found that the best model that could predict risk of RA includes both genes and environment. Unfortunately, vaccination status was not studied. If RA risk is enhanced via HLA genotype, only studies of that consider HLA RA risk (high and low) and vaccination status (vaccinated vs. unvaccinated) could answer the question of association whether HLA x vaccine interaction exists.

Molecular mimicry to pathogen proteins is suspected in RA (Singh and Karrar, 2014). Cross-reactivity is observed against mycobacteria protein and human cartilage (Holoshitz et al., 1986). Antibodies reactive to bacterial enolase have also been found in patients with RA (Lundberg et al., 2008). The specific human protein to which cross-reactivity was found is the human enolase protein (aka. CEP1, Enolase 1 (ENO1) alpha enolase 5-21). Rashid et al., (2007) found elevated antibodies that are cross-reactive to Proteus microbes – as well as to antigens that are not cross-reactive – in patients with RA.

Many patients with RA show cross-reactivity with citrullinated proteins. High among the likely candidates of self-antigen sources is the human protein vimentin. It is highly plausible that prior, or simultaneous exposure to vaccines and to non-pathogenic, or mildly pathogenic bacteria would be sufficient to induce (trigger) RA in genetically susceptible individuals. Studies focused on thorough searches for cross-reactive antibodies matching both human targets in tissues – and in pathways – are required.

It is worth noting that HLA genotypes confer risk of a diversity of autoimmune conditions, and thus studies of familial risk and environmental risk would be made more powerful by combining conditions influenced by similar HLA genotypes. It is plausible that the reason why whole population studies fail to detect association may well be that the association exists for an genetically identifiable minority of individuals.

It is also worth noting that some genetic variants in the ERAP1 gene, which is down-regulated by thimerosal, are associated with ankylosing spondylitis (AS) – an autoimmune form of arthritis in which the vertebrae of the spine can become fused. Individuals with RA are removed from studies of AS (e.g., Wang et al. 2012). Variants in ERAP1 are also associated with juvenile idiopathic arthritis (Hinks e al., 2011) and psoriasis (Strange et al., 2010).


One of the best examples of vaccine-induced autoimmunity is the sporadic occurrence of narcolepsy among families in Europe following H1N1 swine flu vaccination. Narcolepsy is a debilitating disorder in which sufferers suddenly fall asleep without warning. Researchers at Stanford University suspected the target protein was orexin (aka hypocretin), a protein secreted by cells in the brain that regulate the sleep/wake cycles. Their initial successful attempts to identify cross-reactive antibodies could not be reproduced, but then a study found strong cross-reactivity to influenza nucleoprotein and a receptor of hypocretin, hypocretin receptor 2 (Ahmed et al., 2015).

The vaccine that caused narcolepsy across Europe was Pandemrix, manufactured by GlaxoSmithKline. Other H1N1 flu vaccines with lower amounts of influenza nucleoprotein did not lead to narcolepsy. Incredibly, ministers in DPW in Britain fought to prevent a dozen children who developed narcolepsy due to vaccination with Pandemrix from being compensated for injury from the Vaccine Damage Payment Act. Fortunately for those individuals injured by Pandremix vaccination, the courts sided with the families.


Anti-brain protein antibodies are known to be found in children with autism (e.g., Zimmerman et al., 2007; Singer et al., 2008; Heuer et al., 2011). In 1988, a major report on pertussis and pertussis immunization (Cherry et al., 1988) reported:

“For more than 25 years, it has been known that pertussis vaccine is a reliable adjuvant for the production of experimental allergic encephalitis… This experimental allergic encephalomyelitis is mediated by sensitized lymphocytes rather than serum antibody mechanisms. Pertussis vaccine has also been used as an adjuvant in the following experimental autoimmune diseases: thyroiditis, myocarditis, glomerulonephritis, uveoretinitis, and hemolytic anemia.”

They then cited a lack of population-level association studies (i.e., no evidence) that pertussis vaccination results in these conditions in children. Gallup (2004) reminded the research community of this long-standing knowledge of the autoimmune-induced powers of DPT, citing his son’s case as an example. His son has “regressive autism and tested positive for myelin basic protein antibodies, has elevated measles antibody titers, T-cell abnormalities and colitis“.

Unless and until we study either “vaccine injured” vs. “not injured” to find biomarker signatures of moderate and serious adverse events, as was conducted with success for mild adverse events by Christian et al. (2015), or “likely susceptible” vs. “not likely susceptible” based on genetics, the study of the role of vaccines in inducing autoimmunity in humans will remain forever broken.

For now, the evidence that exists is simply overwhelming: vaccines can cause autoimmunity in some people, and we need (a) genetic screens to keep people out of harm’s way; (b) state bans on the use of unsafe peptides and epitopes in vaccines; (c) a test of Th1/Th2/Th17 balance prior to vaccination; (d) aluminum patch testing for aluminum sensitivity prior to vaccination. Consideration of HLA genotype for RA risk, or at least family history of autoimmune disorder, should be a matter of routine to reduce the likelihood of any vaccine-induced autoimmunity. The HLA-DR4 genotype is higher in frequency in autism (Lee et al., 2006).

We also need to start holding pediatricians accountable to treat all moderate and serious adverse events due to vaccination with appropriate follow-up testing, and emergent medical intervention. Failure to attend to their vaccine-injured patients should be reported as malpractice. The public does not need CDC, nor NIH, nor the AMA or AAP to acknowledge that vaccines induce autoimmunity in humans occurs to file complaints to the medical board or to their State Legislature.

NB: While completing this article, news of the publication of findings of record measurements of aluminum in the post-mortem autopsied brains of children with autism by Dr. Chris Exley’s team make a rather stunning bookend. The time has arrived for every person to let every member of the medical community know that aluminum is making us sick, and that one way or the other, they will be held responsible if they persist in their silence on the use of aluminum in vaccines. With all due respect, pediatricians, please join the Vaccine Risk Aware community in our calls for a reduction in the amount of aluminum in vaccines, a ban on thimerosal, and a ban on the use of unsafe peptides that match human proteins in vaccines.


Ahmed SS et al., 2015. Antibodies to influenza nucleoprotein cross-react with human hypocretin receptor 2. Sci Transl Med;7294):294ra105. doi: 10.1126/scitranslmed.aab2354.

Bogdanos et al., 2005. A study of molecular mimicry and immunological cross-reactivity between hepatitis B surface antigen and myelin mimics. Clinical and Developmental Immunology 12:217-224.

Cherry, J.D. 1988. Report of the task force on pertussis and pertussis immunization, Pediatrics 81:6 Part 11 (June 1988) Supplement pp 936-984.

Christian, LM et al. 2015. Proinflammatory cytokine responses correspond with subjective side effects after influenza virus vaccination. Vaccine. 33(29): 3360–3366.

Gallup, R. 2004. The new MMR? No! The Old DPT

Gross et al., 1995. Arthritis after hepatitis B vaccination. Report of three cases. Scand J Rheumatol. 24(1):50-2.

Heuer L et al., 2011. Association of a MET genetic variant with autism-associated maternal autoantibodies to fetal brain proteins and cytokine expression.Transl Psychiatry. 1:e48. doi: 10.1038/tp.2011.48.

Hinks A, Martin P, Flynn E, et al. 2011. Subtype specific genetic associations for juvenile idiopathic arthritis: ERAP1 with the enthesitis related arthritis subtype and IL23R with juvenile psoriatic arthritis. Arthritis Res Ther 13:R12.

Holoshitz J, 1986. T lymphocytes of rheumatoid arthritis patients show augmented reactivity to a fraction of mycobacteria cross-reactive with cartilage. Lancet. 2(8502):305-9.

Karlson, E et al., 2013. Association of Environmental and Genetic Factors and Gene-Environment Interactions with Risk of Developing Rheumatoid Arthritis. Arthritis Care Res (Hoboken). 65(7): 1147–1156.

Langer-Gould A 2014. Vaccines and the risk of multiple sclerosis and other central nervous system demyelinating diseases. JAMA Neurol. 71(12):1506-13. doi: 10.1001/jamaneurol.2014.2633.

Lee et al., 2006. HLA-DR4 in families with autism. Pediatr Neurol. 35(5):303-7.

Lundberg, K et al., 2008. Antibodies to Citrullinated a-Enolase Peptide 1 Are Specific for Rheumatoid Arthritis and Cross-React With Bacterial Enolase. Arthritis & Rheumatism 58:3009–3019

McCoy L et al., 2006. Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Autoimmunity. 39(1):9-19.

Rashid et al, 2007. Rheumatoid arthritis patients have elevated antibodies to cross-reactive and non cross-reactive antigens from Proteus microbes. Clin Exp Rheumatol. 25(2):259-67.

Ricco, R and D. Kanduc. 2010. Hepatitis B virus and Homo sapiens proteome-wide analysis: A profusion of viral peptide overlaps in neuron-specific human proteins. Biologics. 4: 75–81.

Rock KL et al., 2010. Proteases in MHC class I presentation and cross-presentation. J Immunol. 184(1):9-15. doi: 10.4049/jimmunol.0903399.

Singer HS et al., 2008. Antibodies against fetal brain in sera of mothers with autistic children. J Neuroimmunol. 194:165–172.

Singh A, Karrar S. 2014. The role of intracellular organisms in the pathogenesis of inflammatory arthritis. Int J Inflam. 2014:158793. doi: 10.1155/2014/158793.

Strange A, Capon F, Spencer CC, et al. 2010. A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1. Nat Genet 2010;42:985–90.

Tejada-Simon MV et al., 2003. Cross-reactivity with myelin basic protein and human herpesvirus-6 in multiple sclerosis. Ann Neurol. 53(2):189-97.

Wang, C-M et al., 2012. ERAP1 genetic variations associated with HLA-B27 interaction and disease severity of syndesmophytes formation in Taiwanese ankylosing spondylitis Arthritis Research & Therapy 201214:R125

Zimmerman AW et al., 2007. Maternal antibrain antibodies in autism. Brain Behav Immun. 21(3):351-7. Epub 2006 Oct 6.

Dr. Lyons-Weiler is a research scientist and author of three books, the latest of which is “The Environmental and Genetic Causes of Autism”. He is available for speaking engagements and book signing events at your location. To contact, follow on twitter @lifebiomedguru, email ebolapromo[at], and connect via LinkedIn

Bought – Documentary on Pharma, Vaccines, & GMOs

The truth about vaccines and Big Pharma, and info on GMO foods

Bought, according to Dr. Mercola, reveals: Forced vaccinations are part and parcel of this larger scheme where industries write the rules and profit from public health policies, such as recommendations for universal use of all federally recommended vaccines and state mandatory vaccination laws that restrict or eliminate vaccine exemptions.”

People opting out of the flu vaccine are losing their jobs.  What’s behind this draconian measure?  Why, it’s Money of course.

“The goal of officials at the U.S. Centers for Disease Control and Prevention (CDC) is to achieve a 90 percent health care worker vaccination rate by 2020,22 and a key strategy for meeting this goal is to tie a health care facility’s employee flu vaccination rate to the facility’s Medicare and Medicaid reimbursements from the federal government.23

In other words, health care facilities participating in the Centers for Medicare and Medicaid Services Inpatient Prospective Payment System Hospital Inpatient Quality Reporting Program that fail to meet a 90 percent employee flu vaccination rate now get reimbursed 2 percent LESS from Medicare and Medicaid.

This is a drop in funding that can translate into hundreds of thousands of dollars each year.24 This loss of federal funding, far more so than any concern for patient welfare, is a more likely explanation for why hospitals are now choosing to fire essential medical personnel refusing a flu shot rather than allow them to simply wear a mask during flu season, as was done in the past.

So, who came up with this strategy? A key ‘mastermind’ behind the Patient Protection and Affordable Care Act, abbreviated as ACA, but colloquially known as Obamacare, was Elizabeth Fowler, chief health policy counsel to the Democratic chairman of the Senate Finance Committee, Max Baucus. Evidence suggests Fowler drafted the entire legislation.25,26

As reported by The Guardian in 2012, before joining Baucus’ office, Fowler was vice president for public policy and external affairs at WellPoint, the largest health insurance provider in the U.S. ‘Watch the five-minute Bill Moyers report from 2009 …  on the key role played in all of this by Liz Fowler and the ‘revolving door’ between the health insurance/lobbying industry and government officials at the time this bill was written and passed,’ The Guardian wrote.27”


Being informed about vaccines is everyone’s right; however, those infected with Lyme/MSIDS need to be even more vigilant, informed, and proactive as their bodies are in a war of epic proportions which translates to a messed up immune system.  Since the mechanism of vaccines is to illicit an immune response, this helps explain how in an infected person, vaccines themselves can trigger latent infections as discussed by this Scottish doctor: and here as well:  Asymptomatic girls after receiving Gardasil activated dormant Bartonella which was confirmed by testing.

Microbiologist Judy Mikovitz also blew the whistle on retroviruses contaminating vaccines:

For the basics on how vaccines work:

How vaccines are made:

For highlighted notes on a 9-part documentary on vaccines which includes many types of vaccines:

Don’t be fooled.  The push for vaccines has far more to do with money than science.

Ingredients in Kinrix a DTap-IPV Vaccine

Ingredients in DTaP-IPV Vaccine Kinrix

medical researcher mixing vial contentsSTORY HIGHLIGHTS
  • Manufacturer package inserts for each vaccine contain important information on ingredients, contraindications, reported adverse reactions, pre-licensure clinical studies and more.
  • The package insert for Kinrix (DTaP-IPV) lists the following ingredients: bovine extract, bovine casein, formaldehyde, glutaraldehyde, aluminum hydroxide, VERO cells, sodium chloride, polysorbate 80, neomycin and polymyxin B.
  • There is a glaring lack of basic science research and safety testing of vaccine ingredients.

Vaccine ingredients, their side effects and impact on human health have been a topic of debate and discussion for many years. While there has been a lot of publicity about the potential adverse effects of individual ingredients in vaccines, such as mercury and aluminum, it is also important to be aware of the potential synergistic effects of all the combined ingredients contained in each vaccine.

By federal law, vaccine manufacturers must publish a list of vaccine ingredient information in the package insert approved by the U.S. Food and Drug Administration (FDA) that accompanies vials of vaccine sold and provided to doctors’ offices, public health clinics, pharmacies and other places where vaccines are administered. Package inserts are available for all vaccines licensed for distribution in the United States on the FDA website.1 As an example, let’s look at the childhood vaccine Kinrix that is  manufactured by GlaxoSmithKline (GSK).

What is Kinrix?

In 2008, the FDA licensed GSK’s diphtheria and tetanus toxoids and acellular pertussis adsorbed (DTaP) vaccine combined with an inactivated poliovirus (IPV) vaccine known as Kinrix (DTaP-IPV).2 Kinrix is licensed for use in the U.S as the fifth dose of the DTaP vaccine series and the fourth dose of the IPV series in children between the ages of four to six years old whose previous DTaP vaccine doses were Infanrix (DTaP) and/or Pediarix (DTaP-Hepatitis B-IPV) for the first three doses, and Infanrix for the fourth dose.2

Both DTaP and IPV vaccines are recommended in the 2017 Centers for Disease Control and Prevention’s (CDC) childhood vaccine schedule.3

Ingredients in Kinrix

According to the vaccine insert for Kinrix, it is a non-infectious, sterile vaccine to be administered intramuscularly. Each dose includes diphtheria toxoid, tetanus toxoid, inactivated pertussis toxin, pertactin, filamentous hemagglutinin and antigen units of Type 1, Type 2 and Type 3 poliovirus.4

The insert describes how the diphtheria and tetanus toxin is produced:

The diphtheria toxin is produced by growing Corynebacterium diphtheriae in Fenton medium containing a bovine extract. Tetanus toxin is produced by growing Clostridium tetani in a modified Latham medium derived from bovine casein. The bovine materials used in these extracts are sourced from countries which the United States Department of Agriculture (USDA) has determined neither have nor are at risk of bovine spongiform encephalopathy (BSE). Both toxins are detoxified with formaldehyde, concentrated by ultrafiltration, and purified by precipitation, dialysis, and sterile filtration.”4

Some ingredients mentioned above are bovine extract, bovine casein, and formaldehyde. What exactly are these ingredients and what role do they play in the Kinrix vaccine?

In brief, bovine extract is a water-based extract of pituitary glands from cattle used as a stabilizer in the vaccine.5 Bovine casein is milk protein from cattle used as a medium nutrient.5 Formaldehyde is a known carcinogen,6 and is used as an inactivating agent.5

The insert goes on to state:

The acellular pertussis antigens (PT, FHA, and pertactin) are isolated from Bordetella pertussis culture grown in modified Stainer-Scholte liquid medium. PT and FHA are isolated from the fermentation broth; pertactin is extracted from the cells by heat treatment and flocculation. The antigens are purified in successive chromatographic and precipitation steps. PT is detoxified using glutaraldehyde and formaldehyde. FHA and pertactin are treated with formaldehyde. Diphtheria and tetanus toxoids and pertussis antigens (inactivated PT, FHA, and pertactin) are individually adsorbed onto aluminum hydroxide.4

Additional ingredients include glutaraldehyde, a disinfectant used as an inactivating agent, and aluminum hydroxide, which is a known neurotoxin used as an adjuvant to hyperstimulate inflammatory immune responses in an effort to make the vaccine effective.7

The Kinrix package insert further describes the production process:

The inactivated poliovirus component of KINRIX is an enhanced potency component. Each of the 3 strains of poliovirus is individually grown in VERO cells, a continuous line of monkey kidney cells, cultivated on microcarriers. Calf serum and lactalbumin hydrolysate are used during VERO cell culture and/or virus culture. Calf serum is sourced from countries the USDA has determined neither have nor are at risk of BSE. After clarification, each viral suspension is purified by ultrafiltration, diafiltration, and successive chromatographic steps, and inactivated with formaldehyde.4

VERO cells are a lineage of kidney epithelial cells extracted from an African green monkey in 1962 and used as a growth medium for polioviruses in the vaccine.5 8

The description of the production process ends with:

Each 0.5-mL dose contains aluminum hydroxide as adjuvant (not more than 0.6 mg aluminum by assay) and 4.5 mg of sodium chloride. Each dose also contains ≤100 mcg of residual formaldehyde and ≤100 mcg of polysorbate 80 (Tween 80). Neomycin sulfate and polymyxin B are used in the poliovirus vaccine manufacturing process and may be present in the final vaccine at ≤0.05 ng neomycin and ≤0.01 ng polymyxin B per dose.4

Sodium chloride is commonly known as salt used to adjust tonicity in the vaccine.5Polysorbate 80 is a surfactant used as an emulsifier.5 9 Neomycin and Polymyxin B are antibiotics used as antimicrobials in the vaccine.5

As Americans, we expect and want to believe that the vaccine recommendations being made by public health officials are evidence-based and thoroughly tested for safety; however this is not the case. The Kinrix package insert barely provides any evidence of safety testing of ingredients.

Loop Holes in Safety Testing of Vaccine Ingredients

There is a glaring lack of basic science research into the toxic effects of all the ingredients present in Kinrix and other vaccines, including evidence that ingredients have been tested for (1) entry into the body through injection; (2) synergistic toxicity of combined ingredients; and (3) long-term cumulative adverse effects on health.

The argument that such ingredients are harmless simply because they are present in miniscule amounts is not adequate.  The route of entry into the body for these ingredients is never considered during safety testing. The effect of toxins on brain and immune function through ingestion and inhalation is different from injection into a muscle in terms of how it is metabolized through biological processes in the body.10 Yet arguments made to justify the use of many vaccine ingredients focus on how the body processes toxins through ingestion and inhalation rather than injection.11 

Secondly, safety testing ignores the synergistic toxicity of all the ingredients combined in the vaccine. Synergism in toxicology refers to the effects of exposure to two of more toxins at the same time that leads to harmful health effects much more severe than the sum of individual ingredients given separately. Since children are usually given more than one vaccine at a time, safety testing of individual ingredients separately is hardly adequate to label a vaccine as safe.12 

Lastly, the long-term cumulative effects of the vaccine given in combination with other vaccines in the CDC’s recommended childhood vaccine schedule is overlooked. While small concentrations of particular chemicals used in vaccines may not necessarily lead to acute short-term health effects, chronic long-term effects of repeated exposure to small amounts of various ingredients in all vaccines administered to children have not been thoroughly studied.12

Looking back at the vaccine insert, it states, KINRIX has not been evaluated for carcinogenic or mutagenic potential, or for impairment of fertility.”4 This statement alone implies that this childhood vaccine has not undergone thorough safety testing.



More on DTap:

More on aluminum:

Vaccines have been found to activate latent Lyme/MSIDS infections:  (Please read comment section after article for more links)

Dengue Vaccine Causing Severe Dengue

Vaccinated Filipino youth now at risk of getting severe dengue

Published November 30, 2017

After Sanofi Pasteur’s advisory on Dengvaxia, Dr Anthony Leachon says students who already got their dengue shots from DOH will live with the possibility of getting severe dengue ‘for the rest of their lives’.

SCHOOL-BASED IMMUNIZATION. A student from Parang Elementary School gets a shot of Dengvaxia, the world's first-ever dengue vaccine. File photo by Ben Nabong/Rappler

SCHOOL-BASED IMMUNIZATION. A student from Parang Elementary School gets a shot of Dengvaxia, the world’s first-ever dengue vaccine. File photo by Ben Nabong/Rappler

MANILA, Philippines – Health advocates once again slammed the Department of Health’s (DOH) school-based immunization program after Sanofi Pasteur said its dengue vaccine poses more risk for people who have no prior infection.

Dr Anthony Leachon, former president of the Philippine College of Physicians Foundation, said on Thursday, November 30, that Sanofi’s advisory against its own vaccine is alarming for thousands of Filipino schoolchildren who already received their Dengvaxia shots.

“We don’t know the status of 700,000 kids vaccinated in NCR (National Capital Region), Region 4-A (Calabarzon), [and Region] 3 (Central Luzon) since they were not tested [for] previous exposure to dengue virus. We advised Congress and Senate that mass vaccination is not advisable without a rigid selection process,” he said.

“It means some of them will develop severe dengue; we don’t know who. All of them will have to live with this possibility for the rest of their lives,” added Leachon, who has 20 years of experience in pharmaceutical medicine.

On Thursday, Sanofi said new analysis of 6 years’ worth of clinical data revealed Dengvaxia could lead to “more cases of severe disease” when administered on a person who had never been infected by dengue prior the vaccination.

Former health chief Janette Garin launched the dengue school-based immunization program for Grade 4 students in 3 regions in April 2016, just 4 months after the Philippines approved the sale of the world’s first dengue vaccine.

A whopping P3.5 billion was allocated for it by the administration of then President Benigno Aquino III.

But this was met by strong criticism from various health advocates, who questioned the DOH’s decision for mass vaccination when studies on Dengvaxia was still being conducted at the time. (READ: DOH denies dengue vaccine to blame for 11-year-old’s death)

Garin had dispelled the public’s fears over the dengue vaccine. But a year later, Sanofi issued its announcement that confirmed the apprehensions of health advocates.

Current DOH Secretary Francisco Duque III said their technical assistance office is now meeting with individual experts to determine how to proceed following Sanofi’s advisory.

But he assured the public that children’s safety is “paramount” and will be the main consideration in their decision.

Prior to Sanofi’s announcement, DOH officials under President Rodrigo Duterte’s term said they plan to expand the dengue immunization program in Central Visayas.

‘Scam of an experimental drug’

Former health undersecretary Susan Pineda Mercado took to Facebook to express her frustration over the “biggest government funded clinical-trial-masked-as-a-public-health-program scam of an experimental drug in the history of the DOH.”

“This was reckless and irresponsible from the start and the public was deceived into thinking this vaccine would protect children from dengue. The public health community has been outraged for over a year. Legal action is now necessary,” said Mercado.

House probe into the dengue vaccination program was conducted late last year, led by Quezon 4th District Representative Angelina Tan, health committee chairperson.

“We asked that there should be proper social preparation and precautionary/screening test should be done prior to vaccination,” said Tan.

Her committee’s recommendations were already submitted in December 2016 to the good government and public accountability panel, which has the power to investigate alleged wrongdoings of government agencies and officials.

Tan said she plans to speak to the House leadership on Monday, December 4, to follow up on action on her committee’s recommendations in view of Sanofi’s advisory. –


The Lyme vaccine also caused the exact same symptoms as Lyme disease.  For more:  New Lyme Vaccine Coming Soon. Caveat Empter – Buyer Beware!

Scottish Doctor Gives Insight on Lyme/MSIDS

We don’t have perfect tests for diagnosis of Lyme

Written by Huib Kraaijeveld (On Lyme Foundation)

Dr. Jack Lambert is a Scottish doctor who is currently working as an Infectious Diseases consultant in a public hospital in Dublin, Ireland. He has started treating Lyme Borreliosis patients 20 years ago in the USA and during the last 5 years in Ireland. He has also successfully treated a number of young women who fell ill after their HPV vaccination, which seems to have stimulated a latent Lyme infection to reactivate. In this exclusive interview in two parts, Dr. Lambert shares his experience with different emerging serious conditions caused by complex infections and looks at similarities and differences as to how they present clinically and are treated.

Dr. Lambert: I am a Infectious Diseases (ID) specialist that is managing a wide range of different infectious diseases, in parallel with being an academic doctor, research and teaching at the Medical School. In my 25 years career I have seen many different infections in immuno-compromised hosts, like HIV Hepatitis C and those immunocompromised by cancer treatment and transplant recipients. Many of the textbooks describing these infections were written by my former mentors and bosses; some of whom were nominees for the Nobel prize in Medicine.

In the last couple of years, it has become very clear to me that there are many similarities between HIV, Hepatitis C, transplant medicine and the many complications that patients with Lyme and co-infections live with.

Billions are invested annually into HIV research, billions are put into transplant medicine, but for some reason little money is spent on researching Lyme and co-infections for example Anaplasma, Babesia and Bartonella. Yet these infections can be just as damaging and debilitating as HIV and Hepatitis used to be, before we found medicines to treat these conditions.

Seronegative infections

My early experience with difficult diagnoses with imperfect techniques was when I was training in Rochester, New York, in adult and paediatric medicine training programme. By default I ended up taking care of the HIV infected pregnant women as well, as few were willing to take care of them in this time period. So I also took care of a lot of seropositive mothers, who had delivered their babies prematurely.

My first presentation on this subject was about seronegative babies who were born to HIV seropositive Afro-American mothers, which were initially put in the premature nursery but died at home after being released from the hospital. They were dying from what was believed to be SIDS or cot death. When I saw the pathology reports on these children and cultivated the HIV virus from their blood in my laboratory from post mortem blood samples, I discovered that they had died of HIV and their blood cultivated positive for the HIV virus. Yet in none of these children had the ‘standard’ HIV antibody tests showed up positive. If one looked at the clinical signs however, they were all the same as of the ones of children who were HIV seropositive.

The main question of my paper was that HIV and AIDS was masquerading as SIDS. We thought it was SIDS, because it looked like it and nobody had another diagnosis. But looking back, these children were premature, they had had blood and exchange transfusions, they were severely so immuno-compromised that they had no antibodies, and we did not have the technology that we have now to culture the HIV virus.

So I learned the lesson very quickly: a positive test is helpful, but if you have a child coming from a high-risk group, who has all the signs and clinical manifestations of HIV and AIDS, while the antibody test is negative, the conclusion is not ‘oh, they don’t have HIV and AIDS”. The proper conclusion is “we don’t have the optimal test”.

With Lyme and co-infections I see the same thing. If you have a positive test and you have consistent clinical manifestations of the disease, that combination gives you an answer – but basically it is just using common sense. It is the work of a clinician to put the pieces of the puzzle together.

Did somebody have a tick-bite, who is sick with a Lyme-like illness – either acutely or chronically – and the test is negative? Then you should pursue the clinical manifestations and look for alternative testing. Or treat them; even if the testing is negative. We do this for most other infectious diseases, use clinical diagnosis, when testing is ‘imperfect’ or when not available. And when patients get better with our treatment, we say we have had a ‘therapeutic success’.

Current situation

I work fulltime in a public hospital clinic in Dublin, but I also have the opportunity to see patients privately, often those who don’t want to go into public care for privacy reasons, or for convenience and flexibility. I treat many highly functioning people, both from Ireland and abroad, who want confidential treatment or who want an alternative opinion as they are unhappy with the current opinion give by other doctors.

These patients come in for different reasons, travel medicine, HIV, other STI infections, but over the last several years I have seen a sharp rise of the number of Lyme patients, especially those with ‘chronic Lyme’. Because of my experience in America, I have been identified as probably the only Infectious Disease doctor in Ireland who was willing to see patients with symptoms that were suspicious for Lyme – despite the fact that many of the antibody tests were negative. These patients had not been willing to accept the ‘atypical’ and unknown diagnoses being given to them by other specialists.


So I went through the same awakening with these patients as I did early on with these children who were dying of HIV AIDS. If you see all these patients who have a negative test, who had an obvious tick bite, who were previously well, or went off travelling, developed a fever, came back sick and were still sick 12 months later with disseminated clinical manifestations in the joints, neurology, etc, etc – then you need to take their history seriously, and investigate and treat them properly.

Many of my patients had looked for other Lyme tests, which they had to pay for themselves. Often when their standard (serological) Lyme test was read as ‘false positive’, still the pieces of the puzzle were easily put together, when I took their history. They were previously healthy, went traveling to Lyme endemic areas, came back and fell ill with consistent clinical manifestations of Lyme. Many had short term treatment and had gotten temporarily better and then their symptoms had returned.

They may have had neurological or rheumatoid symptoms, and often had been seen by neurology or rheumatology specialists and were given what I call ‘garbage bag’ diagnoses: Fibromyalgia, chronic fatigue (ME), chronic pain syndrome (CRPS) or atypical neurological diagnoses such as “a-typical MS”, “a-typical Parkinson”, “a-typical ALS”. So it was very clear that these neurologists and rheumatologists didn’t know what caused their symptoms, and indeed most of the treatments given to them had not helped them, and in many cases made them worse.

Immunologists and hematologists saw many of these patients who also had low white cell counts and were working them up for cancers, lymphomas or similar disorders. But it simply took a look at the history: these patients were previously well, had a sudden onset of illness, were coming from a Lyme endemic area, they had low white cell counts and they had fevers and sweats. It wasn’t only low white cell counts; they had manifestations of multisystem disease. Some of the more forward thinking hematology specialists then referred these patients onwards, as up until then no one had entertained an infectious etiology.

Lyme and co-infections are not on the ‘radar screen’ of most specialists in Ireland, and they are not aware of the complexities of the diagnostic issues. They follow the IDSA mantra that a negative test means you don’t have it. So on top of my standard clinical public hospital practice, this is what I have started doing over the last five years with some 500 patients who have been treated. Unfortunately I have become too busy to keep accurate statistics on these patients, but in about 70 percent of the people, who follow my treatment regime, there is recovery. Either fully or they improve so much that they can get their lives back.

The Irish governments only reports a few dozen cases over the last years. On their surveillance website, they only keep track of ‘neuroborreliosis’, so you have to end up in the hospital with a lumbar puncture to be counted. So what about all those with a bite or a non specific manifestation, who does not end up in the hospital? They don’t count? I would say that many additional cases are been missed. We have imperfect surveillance of the incidence of Lyme in Ireland. We don’t keep records of patients with these conditions, so it is easy to say there is no Lyme in Ireland. And its not all about Lyme; there are other infections you can get from a tick, the co-infections; not on anyone’s radar screen it seems.

This may be a reason why my colleagues don’t know about Lyme, but it’s quite surprising to me. I don’t really know why my colleagues quote the national government statistics, when they know they are not accurate. In contrast there are the Sexually Transmitted Infections (STI’s). Everybody is aware that the statistics about STI’s are also not well documented and recorded in Ireland, but we all know there is sex in Ireland and people get STI’s. And we know there are a lot more cases of herpes and genital warts, as the under reporting of these conditions is well accepted. My colleagues accept these statistics, those of STI’s , but do not use the same thought process when it comes to Lyme.

We have Lyme endemic areas in Ireland, where ticks are found in large numbers and people pick the ticks off their bodies and their pets bodies in the summertime. But still, the government and our doctors don’t believe these conditions exists in any significant fashion. Vets seem more aware and keyed into this issue in Ireland than the medical doctors. There seems to be a “Lyme denial” in this country, as there is in many other countries, including those within the EU.


After my qualification as an Infectious Diseases specialist in America in 1991, I became a member of the IDSA. Although I’ve never been active politically, I personally know many of the doctors in IDSA leadership positions. Many of my old bosses are past presidents and committee members of the IDSA.

Before moving to Ireland I never paid much attention to ILADS, because I never found the need to look for more information on this disease. There is a huge body of knowledge on these other infectious diseases that is coming out of the IDSA and I found it very helpful. The IDSA had provided me with the accurate and up-to-date knowledge on other severe infectious diseases, such as HIV, Hepatitis and Tuberculosis, so I assumed they would also provide that same quality of information about Lyme and co-infections. However, further inspection of their documents on Lyme and co-infections find a very selective choice of studies, and not a comprehensive view of the subject.

I would even say that when it comes to Lyme and co-infections, there is just a very limited – I would say “censored” – kind of opinion. I don’t even think there is a broad understanding of Infectious Diseases doctors on the literature about Lyme and co-infections. So I found out I actually had to also become member of ILADS, because they have made an effort to really study these tick borne diseases more intensively and look at the scientific literature on the subject to support their claims that a. antibody testing is imperfect (which we all know is the case) and that b. the current recommended treatments by the IDSA are too limited and fail many patients.

Very few IDSA members have the experience of treating Lyme patients in the same numbers and often with the same complexity when compared to ILADS members. So I’ve found it very helpful to learn from the ILADS doctors and to bring my knowledge up to speed and also learn about chronic Lyme. As a regular ID specialist in a public hospital you might see a few chronic Lyme patients a year. But if you are specialised in chronic Lyme, you may see hundreds or thousands of patients. You do learn from your patients, and the more you see of a certain patient group, the more you can understanding the commonalities that these patients present with.

Officially almost everybody follows the IDSA Guidelines, but increasingly many of my ID colleagues have started referring their patients, often at the insistence of the patients, when they see the treatment fails them or when they want a second opinion or another type of test. They are starting to understand that they may be missing a lot of infected patients, because of the rigidity in testing policies; and sometimes they reconsider their opinion when they see that patients are getting better because of longer antibiotic treatments and combination antibiotic treatments.

With an infection such as Lyme that one cannot culture in most clinical settings, meaning there is no ‘before and after’ measurement, clinical treatment results are the best indication of the infection being cured. If the symptoms return when you stop treatment, you probably need to treat a bit longer. However doctors are afraid to treat for longer for Lyme. If it is a prostatitis, there is no issue with treating longer, but if it is a life affecting condition. Doctors are afraid to treat longer, as the IDSA guidelines say 2 to 3 weeks.

And after that, it must be post infectious, even if the patient is not better. And does not get better until antibiotics are restarted and continued for a longer period of time. So who made this law that forbids doctors to treat for longer, especially when patients are getting better with the recommended treatment? Guidelines are suggestions for protocols to follow, and patients must be individually treated, as patient centred medicine is critical to all infectious diseases.


This paradox with Lyme is puzzling to me. Back in the days when we had HIV AIDS, in 1981 before we knew it was HIV AIDS as we didn’t have an antibody test until 1984 and we couldn’t culture the virus until 1987, when we saw that something was wrong with a patient, we stood up for them. We performed evaluations of gay men in New York and we knew they were immuno-compromised and that they were infected with all these opportunistic infections. We knew there had to be something we missed and we kept looking until we found it. It took a lot of hard work, science, resources and thinking ‘outside of the box’ to come up with the right diagnostics tests and later with medication which has changed the course of history with regards to HIV and AIDS.

We have done the same, put energy and initiative into the evaluation, understanding and ultimately optimal treatment for Syphilis, Tuberculosis, HIV AIDS and Hepatitis, among other diseases. Why we don’t do it for Lyme and co-infections, which are affecting an awful lot of people in a tragic way, is a mystery to me. The notion that many governments (e.g. Australia, Norway, France and many other European countries including the Netherlands) are suddenly repeating the 2016 publications by some IDSA doctors and CDC authors, is ridiculous. These guidelines are outdated and not evidence based in my opinion. We are sticking to the old traditional view even when the data and the patients in front of us do not fit into the ‘guidelines’.

Following the analogy of other spirochetal infections such as Syphilis, everybody knows that in the acute stage the blood tests are relatively reliable, but may be negative during the ‘window period. But in later stages the syphilis antibody titres go down and may often go negative. Why we don’t use such same wisdom with Lyme – another spirochete – puzzles me.

So how are these antibody tests supposed to perform optimally, when used in chronic patients who are immuno-compromised? We all know these infections go into the immune cells of the human body. They cause inflammatory and auto-immune responses, so there should be no surprise that these patients don’t have an optimal antibody response. We have imperfect technology, and to use a test that is not 100% sensitive in early infection, when the bacteria is circulating in the blood stream and in highest quantities. And then to say for chronic Lyme the same test must be used makes no sense. Just like with Syphilis and other infections, antibody titres decrease with treatment and also just decrease without treatment, so chronic Lyme sufferers suffer even further when standard antibody tests, never really validated in this population, are used.

Chronic Lyme?

If you look at major medical microbiology and infectious disease textbooks, they state that after 4 weeks you can’t find the Lyme bacteria anymore. Therefore Lyme is then categorised as ‘post infectious’. But I get back to the point I’ve made before: if you can’t culture it, you cannot know anything about its viability. You do not have a organism specific test (culture or PCR), that guides your ‘test of cure’. How do you say that a bacteria is killed, when you couldn’t grow and measure it in the first place?

All you have as a doctor managing the patient in the treatment partnership, is your patient’s response to treatment. If they say they are better on the treatment, you believe them. And make decisions accordingly. If they are not better, you have an option as a doctor: you can say to your patient, that their symptoms are post-infectious, to just ‘bite the bullet’ and give it time………

Or you can treat them for longer and see if they then improve.Many of such patients get better and get cured. To withhold treatment is this clinical scenario is fraught with significant problems, breaching a doctor’s responsibility to his patient and also basic human rights legislation.

We operate, as clinicians, in such a manner in all of our clinical career for other clinical conditions. I treat people with diabetic foot infections of the bone and I keep them on treatment for months – until their clinical symptoms are gone and their inflammatory markers go down. The textbooks don’t say how long to treat, or say treat for six weeks, at which time the infection should be eradicated. Then you wouldn’t say it’s ‘post-infectious’ after a few weeks, when the patient is still not better.

So why cant we manage with the same algorithm of ‘cure of infection’ with Lyme in parallel to the way we operate with other infectious diseases, is beyond me. Especially when we see patients getting better after treating longer than the guidelines say’ and that they relapse when the treatment is stopped too soon. Relapse with a diabetic foot infection is a treatment failure, not a post-infection or a “Post Treatment Syndrome”.

The guideline for Infectious Disease specialist is “continue treatment and make clinical assessment”. Of course we don’t want to treat people unnecessary, following antimicrobial stewardship guidelines. Yet we can treat acne with six months of antibiotics, but we cannot treat a severe infection like Lyme? Acne is just a cosmetic issue, while Lyme is a debilitating, life-changing disease.

In the absence of ideal diagnostic tools, when you think your patients may have the disease, treat them for a reasonable duration of time and assess and reassess the treatment response. One of the rules of infectious diseases medicine is that once you stop treatment and the patient stays better, they are cured. When they get worse, the infection has returned and they have relapse of infection and need repeat treatment. My ID colleagues live by that rule with most other infections, but not with Lyme.

Most of the Lyme patients I see have chronic Lyme, but I also try to see people with acute infections, which are often misdiagnosed as ringworm, a non-specific rash or as cellulitis.. I find that in cases of acute infection mostly a short course of antibiotics works well. For people who have been sick for 5, 10 or 20 years this short course treatment is not enough.

If their “a-typical” MS, Parkinson or ALS would have really been MS, Parkinson or ALS, they would not improve after treatment for a bacterial infection. Often these are young people, who are given diagnoses that rarely occur at a young age and who also responded negatively to their neurological medication. That is a red flag to me that someone is ‘missing the boat’.

Not every case of these diseases will be Lyme, but I am sure it is being missed a lot of the time. That is wrong to miss a treatable disease: MS is a life-long disease, ALS is a death sentence, while Lyme disease is a potentially curable disease that will never relapse again, when it’s appropriately treated. And patients can go back to a normal life with full function.


After we discovered the right test for HIV and proper treatment was developed, many scientists and doctors jumped on that bandwagon to move forward with the successes of the new treatments. But my interest started waning, as my interest is really in the early discovery and understanding of infectious diseases. So the first part of my career I focused on HIV as it was poorly understood and very few people were working in this arena. Around 2000 I moved into the field of Hepatitis C, because there was a huge portion in the world population suffering from it, while we did not have good drugs at that time and it affected a very vulnerable population. The severity and impact on a large population of the world was similar to HIV.

That is why, when I realised there was a very small burden of HIV in Ireland and a large burden of HCV disease, I focused on doing studies on Hepatitis C, and between 2008, where we conducted the first clinical trials with the new drugs for HCV, we now have easy cures, and the job is done. There are lots of people who want to jump on the bandwagon when the work is done, to get involved in the implementation science, and that is also very important.

But I think it was time for me to jump ‘off this bandwagon’ and look for a new poorly understood and challenging infectious disease area. What more challenging than Lyme? I initially became involved in HIV when nobody seemed to care about it, especially HIV in pregnant women. I was involved in Hepatitis C when there wasn’t a huge interest in it. So I saw Lyme as an opportunity or as a challenge. Because there are lots of unknowns, many people are severely disabled by it and I am in the position to contribute.

I work at a university, I publish, I teach at a medical school. In five years from now, when we have much better diagnostics tests for Lyme, better knowledge and treatments, there will be hundreds of doctors and scientists willing to take over the work, I hope. To me this is a really exciting time to get involved in this field, as so much good can occur if we just come together and quit the Lyme Wars. The side effect of such war is the patient suffering and being denied recognition of their disease and their symptoms.

The most exciting part is to see your patients get better! And to see them being validated that there is really something wrong with them, as they have so many rejections from the medical community. It’s just amazing; you have these patients who have seen multiple specialists with their very complex conditions. They have previously run marathons, and now can barely walk because of chronic pain and they are told that they are “seeking pain killers”. But actually they are in pain because they have an inflammation in their brain and inflammation in their joints, which is not being picked up on ‘standard testing’.

So all of a sudden these high performing people are considered to be crazy. Most are frustrated because their previously successful life in society is over and it’s hard for them to lie down and just give up, because nobody can figure out their problem. I say that if all the tests are negative and the patient is sick, the answer is not “there is nothing wrong with them”. The problem is we are not doing the right test or we have not yet developed the right test.

They get labeled wrongly, because the specialists and GP’s get tired of them. I love to see these patients, who weren’t willing to lay down and roll over. And to accept the opinion of their consultations. They are the ones who are thinking out of the box; and not the doctors that are supposed to take care of them. These patients come up with ideas and answers, seeking out people that would help them and many of them get better. As a result of this persistence and refusal to ‘throw in the towel’.

For me as a physician, most of these patients are very satisfying to work with. I have never seen such pro-activeness by such patients in any other disease area and it amazes me. They are stubbornly pursuing wellness against the negative opinions of the medical profession, who should really be accepting their condition and not writing them off.

That is the current paradox: we, the medical profession, often treat patients with suspected Lyme and Co-infections without dignity and respect, and discount their symptoms when they do not fit into our traditional ‘medical tick box’.




Please notice Lambert’s acknowledgement that the HPV vaccination has served to activate latent Lyme/MSIDS infections.  This is why I keep pounding the vaccine issue.

Please know that vaccines are filled with ingredients that your body considers toxic.

Vaccines are contaminated with other pathogens:

Vaccines have adjuvants which your body considers neurotoxic:

Mercury (thimerosol) is another neurotoxin proving to cause severe side-effects:

Mechanisms of vaccine injury:

The Lyme vaccine is deadly:

There are moral & ethical issues to consider with vaccines:

For a review of numerous vaccines, go here and read my highlighted notes on Dr. Gentempo’s 9-part vaccine series:

The HPV vaccine is also deadly:  (Other links at end of article on the deadly HPV vaccine)  Dr. Lapenta weighs in on the HPV vaccine:  they protect against less than 50% of the cancerous types of HPV, they are made by mixing antigens of each type of HPV in a single solution, i.e., a biological bomb provoking death and irreparable health conditions, contains aluminum (a neurotoxin) is an adjuvant, and has caused severe side-effects such as CFS, POTS, and sudden death.

A link has also been connected between the HPV vaccine and Bartonella:

The first peer-reviewed study using vaccinated vs unvaccinated kids  The study suggests that fully vaccinated children may be trading the prevention of certain acute illnesses (chicken pox, pertussis) for more chronic illnesses and neurodevelopmental disorders like ADHD and Autism. The scientists also found that children born prematurely, who were vaccinated, were 6.6 times more likely to have a neurodevelopmental disorder.

A short quiz to determine if you know facts about vaccines:


Biological Mechanisms of Vaccine Injury

Biological Mechanisms of Vaccine Injury

by jameslyonsweiler, Nov, 2017

When Dr. Chris Exley and his research team discovered aluminum co-localized with amyloid plaques in the brains of patients who died from Alzheimer’s, it made big news, even though a study in 1985 discussed the aluminum silicate portion of amyloid. That’s right. We’ve known since 1985 at least that amyloid plaque in the brain is partly aluminum silicate. Now, Exley’s findings completely destroy any hope that aluminum somehow stayed out of the brain,  unnamed
Aluminum, it turns out, plays a critical role in our understanding of the biological mechanisms of vaccine injury. In this article, I will review the scientific evidence of four major ways that vaccines can cause harm. These are (1) Vaccine-Induced Mitopathy; (2) Vaccine-Induced Persistent Gliosis; (3) Vaccine-Induced Endoplasmic Reticulum Damage, and (4) Vaccine-Induced Autoimmunity (to appear as a separate article). My intent and purpose is not and has never been to discourage anyone from accepting vaccines, nor to provide medical advice of any kind; rather, my intent is to make a clear path toward safer routes to artificial immunization and communicate the state of scientific knowledge about mechanisms of the pathophysiology of disease caused by vaccines, and how such human pain and suffering can be mitigated.


(1) Vaccine-Induced Mitopathy
Individuals born with mitochondrial disorders have partially disable cellular energetics. Mutations that alter proteins in the various specific mitochondrial pathways lead to a variety of congenital conditions, including encephalomyopathy and seizures. We need mitochondria to work in all of our tissues. However, our brains consume so much energy, any weakening of mitochondrial ATP flux will almost certainly lead to neurological disorders.

Environmental damage to mitochondria is known to occur from exposure to lead and includes depletion of mitochondrial membrane potential (ΔΨ) and intracellular glutathione (GSH), elevation of caspase-3 activity, intracellular reactive oxygen species, and malondialdehyde levels, and inhibition of GSH peroxidase (GSH-Px) activity (Liu et al., 2014).

Why discuss lead-induced mitochondrial toxicity in an article on vaccine injury? In part because many individuals familiar with brain injuries and conditions that lead to brain injuries will recognize the critical role of GSH, the importance of shutting down ROS, and the potential use of malondialdehyde as a screen for brain injury following vaccination. Another reason is that 25% of the homes in Pittsburgh have higher lead levels in the water coming into the homes than the levels found in the water in Flint, MI, and individuals with mitochondrial damage due to lead are likely to be a higher risk of the toxic effects from vaccines.

The science of the specific actions and mechanisms of mitochondrial injury from vaccines include some of these events, including recognition of aluminum as an intracellular ROS generator (Han et al., 2013). Aluminum is present in vaccines as an adjuvant in a variety of forms, most commonly aluminum hydroxide (a well-known neurotoxin Vaccine risk denialists spend a lot of time denying the massive literature on the neurotoxicity of aluminum. Nevertheless, studies show that aluminum also disrupts cytoskeletal dynamics (Lemire et al., 2009).

Thimerosal also has damaging influences on mitochondria, including direct damage to the mitochondrial genome. Sharpe et al. (2012) found that thimerosal induced a five-fold increase in the levels of oxidant damaged mitochondrial DNA bases and increases in the levels of mtDNA nicks and blunt-ended breaks.

Increases in DNA damage to mitochondrial DNA can only increase the likelihood of heteroplasmy (the occurrence of >1 mitotype in a tissue or a person) – and low-energy regions of the brain can result because mitochondria are inherited in soma via cellular division.

Repeated exposures to mercury can have myriad ill effects as well. Exposure to Methyl mercury (not the type found in vaccines) shows an increase in total reactive oxygen species (ROS) over time in the brain in autoimmune encephalomyelitis (Kharizi et al., 2016). The same ROS-generating effects, along with mitochondrial DNA damage, are seen due to the exposure of ethyl mercury in thimerosal, found in vaccines (Sharpe et al., 2012).

(2) Vaccine-Induced Persistent Gliosis
Mice injected with aluminum adjuvant doses equivalent to those given to US military service personnel showed both neuroinflammation and cell loss in the spinal cord and motor cortex, with consequent memory deficits (Petrik et al., 2007).

The cause of macrophagic myofascitis (MMF) has since been identified asaluminum hydroxide from vaccines lesions (Gherardi et al., 2001; Authier et al., 2006; Gherardi et al., 2012; Rigolet M et al., 2014). Patients with MMF have an unusually long reaction at the site of injection of aluminum-containing vaccines in their muscle, and biospies show infiltration of muscle tissue by macrophages. (See:

Here is chilling description of the effect of aluminum when used as an adjuvant:

“…poorly biodegradable aluminum-coated particles injected into muscle are promptly phagocytosed in muscle and the draining lymph nodes, and can disseminate within phagocytic cells throughout the body and slowly accumulate in the brain” (Gherardi et al., 2015).

While reading thousands of studies for “The Environmental and Genetic Causes of Autism”, I was amazed by the number and the high diversity of types of studies that showed that microglia are chronically activated in autism. Microglia are cells in the brain that normally work to help form complex many:many synapses, leaving behind an abundance of 1:1 synapses. This is reflected in the altered Inhibitory/Excitatory ratio found in ASD and other neurodevelopmental disorders. Microglia also play the role of pruners. When there is a physical injury or an infection that damages nerve cells, glutamate is released. This amino acid is a neurotransmitter, and in high concentrations, glutamate is also a signal to microglia that cellular damage exists in the brain. Local microglia respond by changing shape, becoming macrophagic, and they go to work cleaning up cellular debris. They can induce apoptosis (cell death) and destroy both dendrites and neural precursor cells.

When metals such as aluminum and mercury enter the body, they are taken up by macrophages, and they slowly accumulate in the brain. Harm to astrocytes can occur, as we have seen, via direct mutagenesis, ROS species generation, endoplasmic dysfunction, and other mechanisms (including blockage of normal functioning of cytoskeletal dynamics (coordinated actions of actin and microtubule filaments, nucleolar membrane pores). The individual or cumulative effects of these insults reduce astrocytic uptake of glutamate, causing a rise in the brain-wide concentration of glutamate, leading to excitoxicity – the activation of microglia leading to specific types of deficits and surpluses of pruning activity, and unwarranted, unhealthy microglia-mediated apoptosis (cell death). (See the Companion site “Causes”: The Environmental and Genetic Causes of Autism Reference Resource: for relevant references).

The destruction of dendrites, neural precursor cells and otherwise healthy nerve cells leads to the further release of glutamate – and cytokines – signaling the brain inflammasome. Astrocytic cell death leads to the re-distribution of accumulated metals to new brain cells.

The reactive microglia are induced on a repeated basis – 33 times – over the course of the first 18 months of life (See CDC schedule to 18 mos: If any child has a mutation in any number of genes encoding proteins involved in cellular detoxification, downregulation of microglial activation, mitochondrial function or even synaptic transmission, these environmental exposures can lead to devastating encephalopathy. Clearly, vaccine safety science at the population level will be uninformative on the reality of specific risk in certain families.

(3) Vaccine-Induced Endoplasmic Reticulum Damage
Like mutations that reduce a person’s ability to detoxify their brains (and other tissues)

normally, both aluminum and mercury have toxic effects on the cell’s garbage removal system – the endoplasmic reticulum. The effects of aluminum are rather dramatic – it causes the ER to “glom-up” against the nuclear membrane. This is due in part to the failure of microtubule functions, which aids in the “unfolding” and movement and function of the ER. This mechanism is independent of the P53 apoptosis pathway (Rizvi et al., 2014) – but neuronal death occurs nevertheless.

A very important study by Stamogiannos et al. (2016) showed that thimerosal specifically inhibits the protein Endoplasmic Reticulum Aminopeptidase 1 protein (ERAP1). ERAP1 is is responsible for the proper shortening of proteins on their way to functioning in the adaptive immune system. From the UNIPROT database entry for ERAP1:

“Aminopeptidase … plays a central role in peptide trimming, a step required for the generation of most HLA class I-binding peptides. Peptide trimming is essential to customize longer precursor peptides to fit them to the correct length required for presentation on MHC class I molecules”. ml6b00084  (article here)

The significance of disabling ERAP1 to immunity to pathogens cannot be underestimated. The very proteins that patients are attempting to use to protect themselves against infectious agents that cause disease are prevented from being properly trimmed – thus disrupting proper everyday immunological signaling. This may explain why patients who have received a vaccine against influenza have higher rates of non-influenza respiratory infections (Cowling et al., 2012).

The vaccine studied (Vaxigrip) from Sanofi Pasteur includes thimerosal:

Widespread “anecdotal” experiences by patients reporting “getting the flu” after receiving the flu vaccine are likely due to them becoming immunologically compromised by thimerosal-containing flu vaccine, allowing viruses to which they were immune prior to the vaccine to exert a pathogenic effect.

A study in 2011 found that annual vaccination of children against influenza indeed hampers the development of virus-specific CD8+ T cell immunity (Bodewes et al., 2011). Clearly, vaccination using thimerosal is not benign to human health. Patients who choose to receive vaccination as an attempt to achieve immunity against influenza can opt for the flu vaccine without thimerosal. Quite problematically, however, many doctors are not even aware that they are injecting thimerosal into patients. It is important, therefore, for patients to share all of these findings with their health care providers and their county and state health departments.

An exciting new realization is the finding that amyloid plaques may play a direct role in severe autism with self-injury and aggression. Amyloid is made partly of aluminum. The notion that aluminum cannot cross the blood-brain barrier has been known to be false since at least 1985 (Colin et al., 1985).

Dr. Exley’s most recent findings of record measurements of aluminum in the brains of people who died from Alzheimer’s confirms the truth: aluminum is at the very core of Alzheimer pathophysiology. The most significant source of aluminum in children from birth to three years of age is vaccination. This is reversed in adults due to increased body weights and higher amounts of aluminum in the diet. Generally speaking, humans absorb 0.2-0.3% of the aluminum present in their water and food. In contrast, every microgram of aluminum injected must be dealt with metabolically. Around 10% aluminum introduced to the body (past an epithelial layer, either by diet or by injection) makes it to the brain and stays there for decades.

Children with severe autistic behavior and aggression have increased levels of beta-amyloid precursor protein (Sokol et al., 2006). Aluminum from all sources in their brains (water, food, vaccines) would foster the development of amyloid plaques, and should be avoided.

This knowledge is also exciting for families with loved ones with ASD who are suffering from self-injurious behavior and aggressive behavior because intranasal insulin is known to activate the enzymatic pathway that clears amyloid plaques: Research studies on the efficacy – and safety – of intranasal insulin in ASD are needed.

It is very important to reduce the total aluminum and toxin exposures to children being vaccinated. Some water filters such as Zero Water reduce aluminum absorption from the diet; silica drops and high-silica mineral water both cause aluminum in the diet to become bound as aluminum silicate and thus pass through the digestive tract unabsorbed.

Part (4) Vaccine-Induced Autoimmunity
This section will be published in a separate article.

Allegheny County Health Department dropped the ball on lead in the drinking water:, calling on a vaccine risk apologist to distract from the lead in the water coming into their homes. In a press conference, the individual pointed out that there was more lead in the soil and paint in these homes than in the water the occupants consume: This was a move to try to (but failed to) deflect responsibility away from the Allegheny County Board of Health’s (ACBH) failure to address the issue of lead in the water in homes in and around Pittsburgh. However, as discussed elsewhere, ACBH should have been more, not less concerned about lead exposure from the water due to the presence of lead in the soil and paint, because toxicity is dose-related. Risk of neurodevelopmental disorder cannot be siloized by mere mention of sources of toxins that have accumulative effects and that interact with other toxins.

The ill effects of lead on the mitochondria should therefore also cause ACBH and health care workers everywhere to pause when recommending vaccination for children known to have high lead levels. Children in urban areas should be tested for lead prior to vaccinations – and those with high lead levels should be recommended to avoid vaccines with thimerosal and aluminum. The ACBH knows where these children live, and who they are. Will they alert the parents of these children to the potential for increased risk of vaccine injury due to their lead exposures?

My most ardent supporters, many of who are completely against vaccines because, in part, they see the future of immunity as stemming from healthy societies instead of artificial immunization, understand that I will never call for an end to improving means of artificial vaccination, for to do so would to be lock into place the specific vaccines that currently are causing millions to suffer from autoimmune and neurological disorders across the globe. Many of them disagree with me on this point, some quite vigorously. Vaccine industrialists take note: the flaws in your products are putting the entire immunization paradigm at risk. Those who develop the next-generation of infection-protection products should be aware that as long as you shield yourselves from liability, they will remain unacceptable to a growing segment of the general population. The public correctly believes that it is immoral to indemnify anyone against liability for flawed products, medical or otherwise. Removing the protections of yourselves and products from liability will be one gesture that could possibly restore some confidence. Conducting randomized double-blinded clinical trials large enough to detect rare adverse events, designed to include and report on those likely to suffer adverse events (at least in the math, preferably in the study design), avoiding the use of confidence intervals, not over-correcting your analyses, defining, publishing and sticking to a data analysis plan prior to conducting any analyses, reporting NNT (numbers needed to treat) and related measures (numbers needed to invite) and providing a fully transparent report of the fate all patients enrolled in the study will help restore confidence.

I join many voices from around the globe calling for the ban on the use of thimerosal at any stage of vaccine development. We have forthcoming results that show that aluminum dosing in pediatric vaccines is too high, and was not determined by dosage escalation trials in which aluminum was injected into animals. I also strongly recommend that unsafe epitopes should be identified, and excluded from all vaccines. Legislation from the people at the state level banning the sale or distribution of vaccines with mercury, aluminum and unsafe epitopes could prove to be an effective means for the people to gain control of what goes into their bodies.

The NVCIA (42 U.S.C. §§ 300aa-1 to 300aa-34) mandated safer vaccines. I am grateful to Informed Choice Washington for this info, esp. Bernadette Pajer)

I’ve also called for biomarkers to screen people away from vaccines due to increased risk. This is consistent with the legislation that mandated the identification of individuals most susceptible to risks from vaccines.

Doubly grateful for Informed Choice Washington for sending this information (esp. Bernadette Pajer)

Specifically, the Act mandated the identification of “the groups, categories, or characteristics of potential recipients of such vaccine who may be at significantly higher risk of major adverse reactions to such vaccine than the general population“.

Not only has that not happened, the CDC has actually taken action to weaken the available information – and for that, last December (2016), Bernadette Pajer and my joint public comments were censored:, along with hundreds of other public comments. Our redacted comments and hundreds of others were made public after a brief consultation with my lawyer.

In my view, and in the view of thousands of parents, the National Childhood Vaccine Injury Act has been abrogated due to the failure of our government, vaccine manufacturers, and the medical community to do their part. They are now pushing mandates at the State level at frenzied pace with legislation designed to strip citizens of their existing liberties to opt out of vaccination. Exemptions exist in 48/50 states, and they must be defended so people who have reason to believe they, or their children are at risk of vaccine injury, can opt out.

Under any other area of biomedical inquiry, these rational moves would come as recommendations. Under the current likely rates of vaccine injury, these steps are not mere recommendations. Under the National Childhood Vaccine Injury Act (NCVIA) of 1986 (42 U.S.C. §§ 300aa-1 to 300aa-34), they are mandated by Congress.

Religious exemptions must also be respected, in part due to the use of aborted fetal cells in the production of vaccines:

The rate of death on the first day of life in the US is highest among all rich nations. Maternal deaths during pregnancy are at an all-time high, and yet CDC is still recommending Tdap vaccination, against FDA label, every pregnancy, every time. This recommendation was made with no safety studies – and the safety studies conducted since left out mothers who were at risk of complicated pregnancies, or simply excluded fetal deaths due to a lack of scientific ability to know the date of a spontaneous abortion. See the first #braintrust episode on this topic here:

The not-for-profit I founded, IPAK, has called for a ban on vaccination in the NICU (see #nicuchallenge on social media) until studies are produced that demonstrate that vaccination in the NICU is safe. Many people don’t know that NICU’s vaccinate all of their patients at once, and have crash teams that stand by for respiratory distress, seizures, and other serious adverse events that occur due to the vaccination of low birthweight infants with 250 mcg of aluminum in the HepB vaccine. IPAK has also published a major report: on the potential role that vaccination against HepB on the first day of life has played in preventing the bankruptcy of the medical industry in the US, Canada and the UK. It includes a call for screening programs to keep those most at risk out of harm’s way.

Reform Must Happen
I join many other voices in calls to mandate reporting of vaccine adverse events with fines for failing to report. VAERS is a failed system, capturing only between 1% and 10% of adverse events from vaccination, and users are required to acknowledge that the data are so poor they cannot be used to determine causality. The legendary VSD of CDC folklore is not available for public review and use. Professional obfuscationists currently inhabit high-ranking offices at the CDC, the NIAID, and the NIH. Their continued involvement in the areas of infectious disease, and public health insures that no reform can take place, in spite of the overwhelming evidence that vaccines are making many – if not most – recipients sick. They need to resign, accept early retirement, or get behind the movement sweeping the nation to protect our children – and ourselves – from serious adverse events and injuries. The misinformation campaign based on fear that people will stop vaccinating must be replaced by science.

As a scientist and a citizen, I am calling on every citizen, vaccine manufacturer, ACIP, the CDC and independent researchers to request funding from Congress for $1Billion in funding to be distributed to Universities to conduct immediate prospective RCTs on the safety of all vaccines currently on the market to determine if we can predict who will experience immediate, short-term and long-term adverse events and injuries from vaccines. CDC cannot be trusted, and won’t be trusted. Vaccine manufacturers have lost all credibility to a fast-growing portion of the American public, and other than joining their fellow citizens in a call for science, they should step aside and let vaccine safety science occur. Only a bought press and captured regulatory agencies are keeping the vaccine house of cards from falling apart. Moves to make the vaccination a police action are happening around the world. Dishonest moves by the likes of State Senator Richard Pan leading to the persecution of his former colleagues – medical doctors who honor requests for exemptions – show a true lack of personal character. The entire medical industry ignores the right of patients to refuse to participate in clinical trials – fully aware that the vaccines they are administering are subject to ongoing clinical safety trials.

A clause in the 21st Century Cures Act: allows doctors to enroll their patients in clinical trials as long as the IRB overseeing the trial has determined that the risk to those enrolled is minimal. Clearly this act cannot possibly be relevant for vaccines, for which post-market surveillance studies are needed to determine long-term risk – the very information needed to allow this clause to be invoked. Citizens can opt out of vaccination on the basis of their refusal to be enrolled in the ongoing post-market safety studies. Citizen groups can also consider challenging and educating individual medical doctors who enroll patients in the ongoing clinical safety trials without securing informed consent.

We need outcome studies of injured vs. non-injured, and studies of rates of vaccine adverse events in genetic groups defined by the basic and translational science conducted that points to increased genetic risk of mysterious diseases with no known cause but many suspected environmental triggers. It is morally wrong to hide specific risk to identifiable subgroups in whole-population comparisons. Where is the study to determine if people with HLA genotypes with high risk of RA are at higher risk of RA due to vaccines than people with HLA genotypes with low risk of RA?

In part two of this article, I will review the evidence of autoimmunity from vaccines as the fourth mechanism of vaccine injury.


Bodewes et al., 2011. Annual Vaccination against Influenza Virus Hampers Development of Virus-Specific CD8+ T Cell Immunity in Children J Virol 85:11995-12000.

Cowling, BJ et al., 2012. Increased risk of noninfluenza respiratory virus infections associated with receipt of inactivated influenza vaccine. Clin Infect Dis. 54(12):1778-83. doi: 10.1093/cid/cis307.

Gherardi RK et al., 2015. Biopersistence and brain translocation of aluminum adjuvants of vaccines. Front Neurol. 2015 Feb 5;6:4. doi: 10.3389/fneur.2015.00004. eCollection 2015.

Han, S. 2013. How aluminum, an intracellular ROS generator promotes hepatic and neurological diseases: the metabolic tale. Cell Biol Toxicol. 29:75-84.

Kahrizi F 2016. Repeated Administration of Mercury Intensifies Brain Damage in Multiple Sclerosis through Mitochondrial Dysfunction. Iran J Pharm Res. 15:834-841.

Lemire et al., 2009. Aluminum-induced defective mitochondrial metabolism perturbs cytoskeletal dynamics in human astrocytoma cells. J. Neurosci Res 87:1474-83

Liu G et al., 2014. Puerarin protects against lead-induced cytotoxicity in cultured primary rat proximal tubular cells. Hum Exp Toxicol. 33(10):1071-80. doi: 10.1177/0960327114521048.

Mizra et al., 2017. Aluminium in brain tissue in familial Alzheimer’s disease. Journal of Trace Elements in Medicine and Biology 40:30 – 36.

Petrik MS et al., 2007. Aluminum adjuvant linked to Gulf War illness induces motor neuron death in mice. Neuromolecular Med 9:83–100.

Sharpe, MA et al., 2012. Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes: Possible Role of Fenton Chemistry in the Oxidation and Breakage of mtDNA Journal of Toxicology Volume 2012 Article ID 373678, 12 pages

Stamogiannos, A et al., 2016. Screening Identifies Thimerosal as a Selective Inhibitor of Endoplasmic Reticulum Aminopeptidase 1 ACS Med. Chem. Lett. 7:681–685.


For more on vaccines: (I highlight Dr. Gentempo’s 9 part vaccine series)

Lyme Vaccine:


Vaccine Awareness Week

Everyone needs to consider what they put into their body; however, those with Lyme/MSIDS need to be especially informed and cautious as our bodies are in a war of epic proportions.

This week from November 5-11, 2017 and the National Vaccine Information Center (NVIC) are co-sponsoring the Eighth Annual Vaccine Awareness Week (VAW), a week dedicated to raising awareness about vaccines and informed consent rights. With all the uncertainty surrounding the risks and failures of vaccines, it’s critical to protect your legal right to make independent health choices and exercise voluntary informed consent to vaccination. It is urgent that everyone stand up and fight to protect flexible medical, religious and conscientious belief vaccine exemptions and expand informed consent protections in state public health and employment laws.

In that effort, please take the quiz to see how much you know.

True or False? How Much Do You Know about Vaccine Risk?
by jameslyonsweiler

  • The TdaP vaccine prevents pertussis infection. A: FALSE
  • The majority of vaccine adverse reactions which occur are reported. A: FALSE
  • 40 healthy screened girls died in Gardasil clinical trials. A: TRUE
  • Vaccines are required for school attendance in the United States? A: FALSE Exemptions are available in all States.
  • The National Vaccine Injury Compensation has paid out over $3.7 billion dollars to the vaccine injured and their families’ (proven cases only). A: TRUE
  • FLULAVAL was tested against Hep A vaccine, not against placebo. A: TRUE
  • Merck used Aluminum (a known neurotoxin) as a placebo in Gardasil clinical trials. A: True!
  • The Salk Polio vaccine was scrapped after it became evident it contained live polio virus. A:TRUE
  • The American Academy of Pediatrics advocates for legislation in states to do away with nonmedical exemptions. A: TRUE
  • Vaccines are rigorously tested for safety prior to release on the market. A: FALSE
  • The National Childhood Vaccine Injury Act (NCVIA) of 1986 mandated that vaccines be made safer. A: TRUE
  • The US Supreme Court ruled that vaccines are “unavoidably unsafe“. A: TRUE
  • You can’t sue your doctor, or a vaccine manufacturer, for vaccine injuries. A: TRUE
  • If you’re injured by a vaccine, you have to sue the US Govt  A: TRUE
  • Vaccine injury risk rates are 1:1,000,000. A: WE DON’T KNOW THE ACTUAL RATES.
  • HPV Vaccines were thoroughly tested with saline placebo. A: FALSE. Most studies used aluminum hydroxide Amorphous Aluminum Hydroxyphosphate Sulfate, a potent neurotoxin.
  • CDC Vaccine Information Sheets contain all the information on vaccine risk. A: FALSE
  • Pediatric practices don’t make money from vaccines. A: FALSE, in a big way.
  • Anyone who speaks about vaccine risk is “anti-vax”. A: FALSE
  • You get more aluminum from food than from vaccines. A: FALSE, 0-6 years, considering body weight.
  • Ethyl mercury (in thimerosal) is cleared from the body faster than methyl mercury: FALSE
  • Aluminum is a neurotoxin. A: TRUE
  • Aluminum is a nutrient. A: FALSE. Dr. Offit made that up.
  • Vaccines can cause febrile seizures. A: TRUE
  • Vaccines can cause autoimmunity. A: TRUE
  • Vaccines can cause food allergies: A: TRUE
  • VAERS is a reliable and accurate source of rates of vaccine injury. A: FALSE >1% of injuries are reported.
  • Vaccines given in pregnancy are tested for miscarriage rates before being used. A: FALSE.
  • Merck is currently being sued for allegedly tampering with mumps vaccine data. A: TRUE. Rabbit Antibodies
  • The committee that adds vaccines to the schedule clear of financial conflicts of interest. A: FALSE. COIs are ALLOWED.
  • Aluminum in vaccines does not cross the blood-brain barrier. A: FALSE. See Chris Exley’s research.
  • Unvaccinated Kids Have less Pneumonia, Ear Infections, Allergies and Neurodevelopmental Disorders : TRUE #mawsonstudy
  • CDC had, before 2003, and still has data supporting the link b/t vax + neurodevelopmental disorders, secretively kept from the public. TRUE #cdctruth
  • HPV Vaccine reduces the prevalance of HPV Infection A: FALSE. Only vaccine-targeted types are reduced. #vaxwithme
  • Doctors do not vaccinate patients from subgroups excluded from vaccine studies because safety is known for them. A: FALSE
  • Dr Wakefield’s retracted paper claimed MMR vaccine causes autism. A: FALSE They PROPOSED the idea+said more data was needed.
  • The National Childhood Vaccine Injury Act (NCVIA) of 1986 mandated that groups susceptible to injury be identified. A: TRUE
  • The safety of using more than one vaccine per day has been tested, and found to be safe. A: FALSE, see
  • CDC and Pharma met in an illegal meeting in Simpsonwood, GA to hide risks of developmental disorders from vaccines. A: TRUE
  • CDC omitted key results from linking MMR to autism from a 2004 study. A: TRUE (watch Vaxxed)
  • No One Knows What Causes Autism. A: FALSE
  • No Study Has Ever Found an Association Between Vaccines and Autism. A: FALSE
  • All vaccines have been tested for asssociation w/autism: A: FALSE
  • Aluminum hydroxide is used to routinely cause autoimmune disorders in animal models. A: TRUE
  • Aluminum hydroxide is used to routinely cause food allergies in animal models. A: TRUE
  • Aluminum hydroxide is used to routinely cause allergic rhinitis in animal models. A: TRUE
  • No one knows how to reduce the risk of vaccine injury. A: FALSE
  • Pediatricians are well-trained in vaccine risk. A: FALSE
  • CDC has publicized advice on how to make the public believe that childhood infections are more dangerous than they are. A: TRUE
  • CDC has repeatedly and consistently worked to minimize the public’s perception of vaccine risk: A: TRUE
  • ACIP, the committee that makes recommendations on vaccines in the pediatric schedule, is free from conflicts of interest. A: FALSE

For a quick read on CDC interagency corruption – vaccine division included, please read:

More on vaccines:


During this week, Dr. Joseph Mercola will double match your donations up to $100,000 to the National Vaccine Information Center (NVIC), a non-profit charity advocating for vaccine safety and protection of the ethical principle of informed consent to medical risk taking, including vaccine risk taking.

NVIC’s mission since 1982 has been to prevent vaccine injuries and deaths through public education and to defend your legal right to exercise informed consent to vaccination. You can also donate directly to NVIC here: