Archive for the ‘vaccines’ Category

A Strange Itch, Trouble Breathing, Then Anaphylactic Shock

https://www.nytimes.com/2018/01/04/magazine/a-strange-itch-trouble-breathing-then-anaphylactic-shock.html?_r=1

A Strange Itch, Trouble Breathing, Then Anaphylactic Shock

By LISA SANDERS, M.D. JAN. 4, 2018

“I can’t breathe,” the woman panted, her voice a husky monotone. Her sister looked anxiously at the clerk at the triage desk at the University of Iowa hospital emergency room. The woman’s breath was rapid and coarse. Her chest heaved with the work of simply breathing. She pulled at the neck of her sweatshirt — suddenly it was too tight. She pulled it over her head and dropped it to the floor. She was naked beneath the top; she had been in bed when this attack came on.

The 54-year-old woman was helped into a wheelchair and whisked into the inner sanctum of the E.R. What followed was a blur of concerned faces, needles and medical data. Her blood pressure was dangerously low; her heart was racing. She was given epinephrine and steroids, but it was hours before she could explain what had happened that night.

She was staying at her mother’s house in rural Iowa, she told the doctors. Just as she was going to bed, she felt a sudden tingling in the palms of her hands. She recognized the sensation immediately: Twice in the past eight years, she had felt the same strange itch on her hands and sometimes her feet. Each time it was quickly followed by a terrifying sense of her throat closing.

Anaphylactic Shock

She had driven herself to her sister’s house, several miles away, and her sister drove her the rest of the way to the hospital. She opened the car window to let in the frigid winter night air. She struggled to breathe. Black spots swam before her eyes, but she willed herself not to pass out.

She had had this kind of allergic reaction twice before but never as severely. She knew from her own research that this was anaphylactic shock — a potentially deadly allergic reaction. After she got the medications, the woman’s symptoms resolved. She stayed in the hospital overnight, and when it was clear that the episode was over, she went back to her mother’s house. She made an appointment to see a local allergy specialist right away.

A Mystified Allergist

The specialist spent nearly two hours going over everything the woman had been exposed to — food, plants, toxins, anything that might have triggered this nearly fatal allergic reaction. There were no new exposures that day, nothing she hadn’t eaten or touched many times before and after this latest attack. The most common cause of severe allergic reactions in adults is food, but the allergist couldn’t identify any likely suspects. He was mystified. He asked her to share her diagnosis when she got one.

For months after returning to her home on Long Island, the woman was anxious about everything she ate, and she worried every night when she went to bed. She always kept a bottle of Benadryl and an EpiPen with her, but still she was terrified about what might happen if she was too far from a hospital the next time.

‘I Need a Nurse!’

When her next attack happened — just 10 months later — she was already in Brookhaven Memorial Hospital in East Patchogue, N.Y. She was being treated with antibiotics for a devastating case of gastroenteritis due to salmonella. Her first meal, after days of nothing but clear liquids, was beef brisket with potatoes and carrots. It smelled good, but she had no appetite. She made herself eat a few bites anyway, knowing it was her first step toward going home.

A couple of hours later, she felt a strange itch on the top of her head. She scratched reflexively. Then the recognition hit her like a slap: Not now, she thought. She grabbed the IV pole, still dripping fluids into her system, and ran out into the hallway. “I need a nurse,” she shouted. Her heart was pounding, and she knew what was coming next. Hospital staffers in scrubs descended on her. Was she having a panic attack? No, an allergy attack, she told them.

They helped her back into bed and gave her oxygen, Benadryl and steroids. “What happened?” someone asked. She told the whole story, plus something she now realized — every one of her attacks seemed to come a few hours after she ate beef. She didn’t go through this every time she had a hamburger or steak; meat was a regular and much-loved part of her diet. But she was pretty sure that she had steak — or beef brisket, this time — before each episode.

Her doctors were dubious. New food allergies — especially severe ones like hers — are uncommon in adults. This was much more likely to be an allergic response to one of the antibiotics they were giving her. The patient, though, found that theory hard to swallow. It might explain this episode, but what about the earlier ones? She hadn’t been on antibiotics then. The doctors had no answer.

Was a Tick to Blame?

A nurse had a different theory about what happened, one the patient had heard before but never believed. There was some kind of tick, the nurse told her, whose bite could make you allergic to meat. She didn’t know much about it. But, the nurse suggested, she should check it out.

The woman had been bitten by ticks before — who on Long Island hasn’t? But was it really possible for a bite to produce this crazy reaction? Indeed it was, she discovered, when she got home and began doing some research. The bite of the lone star tick — named for a white spot shaped like Texas on the arachnid’s back — could cause an allergic reaction to mammalian meat. The trigger was a sugar, identified as galactose-α-1,3-galactose and more casually known as alpha-gal, a carbohydrate found in the flesh of all nonprimate mammals.

How the tick bite triggers this allergy is not yet known. The link between the tick — whose range extends from southern Florida to Maine and as far west as Iowa — and the resulting alpha-gal allergy was first described in 2009 by Thomas Platts-Mills, a professor at the University of Virginia, who himself developed the disorder. Unlike most food allergies, in which symptoms occur within minutes of consuming the allergen, the alpha-gal reaction is delayed. The symptoms — ranging from a rash to nausea to shortness of breath and even anaphylaxis — can appear four to six hours after a meal containing meat. Stranger still, the reaction doesn’t occur after every exposure.

A Diet Changed Forever

The diagnosis of mammalian meat allergy (M.M.A.) can be confirmed with a blood test that identifies antibodies to alpha-gal. The patient contacted Diane Cymerman, an allergist she had seen years earlier for seasonal allergies. Cymerman asked her to list all the foods she consumed before her last episode in the hospital and had her blood tested for antibodies to everything on the list, down to the black pepper and parsley seasoning. And to alpha-gal.

The first results came back the following week: She had a moderate allergy to beef, but everything else was normal. The following month, the test results for alpha-gal antibodies came back. She was wildly allergic to galactose-α-1,3-galactose. Cymerman called the patient with the news. She had to avoid eating meat from mammals — and everything derived from them, including Jell-O and other foods and medications made from gelatin. Even safe foods cooked on a grill that has also been used for meat can be contaminated with enough alpha-gal to trigger a reaction.

The patient contacted the allergist back in Iowa and told him what she had. He was amazed. He had only recently heard a lecture on this phenomenon. He had never seen it before her case.

It hasn’t been easy for this Iowa transplant to give up beef and other meat that comes from mammals. Some days, she tells me, just thinking about a juicy hamburger or steak makes her stomach growl. But she remembers her terror and that long drive to the Iowa hospital and sticks to chicken, fish and vegetables.

Lisa Sanders, M.D., is a contributing writer for the magazine and the author of “Every Patient Tells a Story: Medical Mysteries and the Art of Diagnosis.” If you have a solved case to share with Dr. Sanders, write her at Lisa.Sandersmd@gmail.com.

________________

**Comment**

For more on Alpha-Gal:  http://alpha-gal.org

https://madisonarealymesupportgroup.com/2017/01/12/tick-related-red-meat-allergy-found-in-minnesota-wisconsin/

Approx. 5 Min.

Great video by Dr. Greger at nutritionfacts.org on tick bites, meat allergies, and chronic urticaria

https://madisonarealymesupportgroup.com/2016/02/05/paralysis-tick-the-immune-system/  Australian allergy specialist Sheryl van Nunen got her red meat allergy mystery solved when there was a surge in allergic reactions in the U.S. to a drug, Cetuximab, used to treat colorectal cancer developed using a mouse cell line, also containing alpha-gal.

Pause

If you haven’t read the articles on vaccines, please do.
https://madisonarealymesupportgroup.wordpress.com/2015/06/19/a-word-on-vaccines/ and https://madisonarealymesupportgroup.wordpress.com/2015/07/15/vaccines-continued/
Some vaccines used to be run through mouse brains. This is important to know as mice are one of the biggest reservoirs for borrelia, the causative agent known to cause Lyme Disease.

More damning evidence of the mouse/vaccine connection:  https://madisonarealymesupportgroup.com/2017/10/15/vaccines-and-retroviruses-a-whistleblower-reveals-what-the-government-is-hiding/

 

 

 

 

 

 

Category:

Activism, Ticks, vaccines, Viruses

Mechanisms of Vaccine Injury – Part 2

https://jameslyonsweiler.com/2017/11/28/biological-mechanisms-of-vaccine-injury-2-autoimmunity/ 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:  https://madisonarealymesupportgroup.com/2017/11/28/biological-mechanisms-of-vaccine-injury/

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.

Anaphylaxis

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:

MEASLES P3 …………………………….….EISDNLGQEGRASTSGTP….

HUM. MYLEIN BASIC PROTEIN ….EISFKLGQEGRDSRSGTP….

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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266455/

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).

Narcolepsy

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.

Autism

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.

References

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 http://www.bmj.com/rapid-response/2011/10/30/re-no-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]gmail.com, and connect via LinkedIn https://www.linkedin.com/in/jameslyonsweiler

Category:

Activism, vaccines

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”  

https://articles.mercola.com/sites/articles/archive/2017/12/05/mandatory-influenza-vaccinations.aspx?utm_source=dnl&utm_medium=email&utm_content=art1&utm_campaign=20171205Z1_UCM&et_cid=DM175374&et_rid=142884544

______________

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:  https://madisonarealymesupportgroup.com/2017/12/02/scottish-doctor-gives-insight-on-lyme-msids/ and here as well:  https://madisonarealymesupportgroup.com/2016/04/24/gardasil-and-bartonella/  Asymptomatic girls after receiving Gardasil activated dormant Bartonella which was confirmed by testing.

Microbiologist Judy Mikovitz also blew the whistle on retroviruses contaminating vaccines:  https://madisonarealymesupportgroup.com/2017/10/15/vaccines-and-retroviruses-a-whistleblower-reveals-what-the-government-is-hiding/

For the basics on how vaccines work:  http://pathwaystofamilywellness.org/Informed-Choice/how-do-vaccines-work-immune-mechanisms-and-consequences.html

https://madisonarealymesupportgroup.com/2015/06/19/a-word-on-vaccines/

How vaccines are made:  https://madisonarealymesupportgroup.com/2017/04/06/video-how-vaccines-are-made/

For highlighted notes on a 9-part documentary on vaccines which includes many types of vaccines:  https://madisonarealymesupportgroup.com/2017/03/30/ty-bollinger-the-truth-about-vaccines-series/

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

Category:

Activism, Lyme, vaccines

Ingredients in Kinrix a DTap-IPV Vaccine

http://www.thevaccinereaction.org/2017/10/ingredients-in-dtap-ipv-vaccine-kinrix/

Ingredients in DTaP-IPV Vaccine Kinrix

by Rishma Parpia
Published October 20, 2017 | Vaccination, Ingredients
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.

________________

**Comment**

More on DTap:  https://madisonarealymesupportgroup.com/2017/10/04/pharma-using-scare-tactics-over-pertussis-vaccine-failure/

More on aluminum:  https://madisonarealymesupportgroup.com/2017/09/21/aluminum-flawed-assumptions-fueling-autoimmune-disease-and-lyme/

Vaccines have been found to activate latent Lyme/MSIDS infections:  https://madisonarealymesupportgroup.com/2017/12/02/scottish-doctor-gives-insight-on-lyme-msids/  (Please read comment section after article for more links)

Category:

Activism, Lyme, vaccines

Dengue Vaccine Causing Severe Dengue

https://www.rappler.com/science-nature/life-health/190008-dengvaxia-dengue-vaccine-filipino-youth-risks

Vaccinated Filipino youth now at risk of getting severe dengue

BY Mara Cepeda  @maracepeda

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.

A 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. – Rappler.com

_____________

The Lyme vaccine also caused the exact same symptoms as Lyme disease.  For more:

https://madisonarealymesupportgroup.com/2017/07/01/pbs-lyme-vaccine/

https://madisonarealymesupportgroup.com/2017/01/26/lyme-vaccine-to-be-tested-on-humans/

https://madisonarealymesupportgroup.com/2017/09/07/20268/  New Lyme Vaccine Coming Soon. Caveat Empter – Buyer Beware!

Category:

Activism, Lyme Vaccine, vaccines