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    ― Dr. Tom Cowan

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Vaccine Syndrome

The politics of terror has no place in your Doctor’s Office: This is the story of the Anthrax Vaccine

To protect troops against the use of anthrax as a biological weapon, the US Department of Defense began an anthrax vaccination program in 1998. 14 years after the inception of the vaccination program, there is no evidence suggesting vaccination against anthrax carries long-term health risks for Active Duty Soldiers. (so says the NIH)

NIH Disability among US Army Veterans vaccinated against anthrax

 Defense Secretary William Cohen announced the implementation of an Anthrax Vaccine Immunization Program for all active duty military personnel which was distributed to some 455,000 active duty personnel .A shortage in 2000 caused the program to be placed in limbo after a court ruled that the vaccines were not properly approved for use. (sound familiar?) Many have questioned the safety and efficacy of the vaccine. Criticizing any vaccine brings with it the wrath of the mafia protection racket for big pharma to discredit the claims, defame and ostracize anyone who attempts to cast doubt on the sacred cash cow of the pharmaceutical industry.

In the field of post-vaccination adverse reactions (AEs or AEFI), there are two major problems:

  • The WHO.
  • The unbundled report system that is present in the vaccines data sheets.

2.1 The first problem: WHO

In January 2018, the WHO produces a document on how to catalog the adverse reactions that are indicated by the acronym AEFI. The WHO states: “Causality assessment is the systematic review of data about an AEFI case; it aims to determine the likelihood of a causal association between the event and the vaccine(s) received” [50]. It also specifies: “At the individual level it is usually not possible to establish a definite causal relationship between a particular AEFI and a particular vaccine on the basis of a single AEFI case report” [50]. Since all adverse reactions are case reports (because they occur in a single vaccinated individual), excluding them results in the consequent elimination of all post-vaccine AEs. Furthermore, the report cases form the series of reports that will never exist with this evaluation system that excludes the individual case reports.

A practical example shows that the reports of AEs do not end up on the reports of the regulatory agencies. These are two cases of transient neutropenia from MMRV vaccines (Measles, Mumps, Rubeola and Varicella) that have been published [51] after reporting to the Italian Medicines Agency [52], but it do not appear in the Agency Report [53].

2.2 The second problem: Vaccines Data Sheets

Taking as an example a vaccine widely used in Europe [54], we immediately notice that the adverse reactions are cataloged reporting the frequency of the single symptom, but there are no data on the combination of reactions in the same subject (GSK, 2018). Infanrix Hexa is indicated for primary and booster vaccination of infants and toddlers against diphtheria, tetanus, pertussis, hepatitis B, poliomyelitis and disease caused by Haemophilus influenzae type b. The following drug-related reported adverse reactions in clinical studies (data from more than 16,000 subjects) and during post-marketing surveillance (GSK, 2018).

Very Common Adverse Events (≥ 1/10 doses)

  1. Appetite lost.
  2. Crying abnormal and pain.
  3. Irritability.
  4. Fever ≥ 38°C.

The presence of all these symptoms in the same subject suggests a post-vaccination reactive brain inflammation produced by proinflammatory cytokines, secreted after vaccine injection.

2.3 Post-Vaccination Reactive Brain Inflammation

During the first two years of life, particularly in the winter months, the immune system is often engaged with several infectious challenges. These are immune stimulations added to the immune challenges, linked to the adoption of the vaccination schedule.

After vaccine injection, especially if multiple doses are given to a young child during a single office visit, significant systemic immune activation may occur with signs suggesting reactive brain inflammation, such as acute crying, fever, restlessness and failure to eat [32,36]. When this reaction takes place, it is necessary to suspend the vaccination schedule for at least 6 months to allow the innate immune system to “forget that it has become so little tolerant in the brain”. Otherwise, the neuroinflammation may produce serious damages especially if the microglia continues to be stressed by peripheral cytokines produced after each vaccination. It is a warning of danger to the brain and you can choose to continue the vaccination schedule (putting at risk the health of the small child) or, vice versa, stop with vaccinations to respect the principle of “primum non nocere”.

Post-Vaccination Inflammatory Syndrome: A new Syndrome.

Human papillomavirus vaccines (HPV Vaccines) are neither safe nor effective as claimed by so much scientific literature. These vaccines are anti-virus vaccines, but they are not anti-tumor vaccines [2], In our previous publication, we addressed the issues of the alleged safety and efficacy of these vaccines [2]. In this paper we will discuss the molecular biology that supports our hypothesis of a new post-vaccination inflammatory syndrome triggered by HPV vaccines.

Let us just remember that it was shown that vaccinated young women have had a higher prevalence of any HPV type infection (type with high and low risk for cancer), and a higher prevalence of virus infection with high risk of non-vaccine types, despite having a lower prevalence of vaccination types [55].

3.1 History of adverse reactions

In Japan, the period of HPV vaccination overlapped with the development of HPV vaccine-related symptoms in the vaccinated patients, including chronic regional pain syndrome (CRPS) and autonomic and cognitive dysfunctions [56]. Brinth [57] reported the characteristics of a number of patients with a syndrome of orthostatic intolerance, headache, fatigue, cognitive dysfunction, and neuropathic pain starting in close relation to HPV vaccination. The Lareb in the Netherlands, has received a substantial number of reports concerning long-lasting AEs after vaccination with Cervarix® [58,59].

3.2 HPV vaccines and pain

In the Cervarix Package insert [54] it is reported that: 20% of subjects were in pain, 20% of subjects had a sense of fatigue. In the Gardasil 4 Package insert [60] it is reported that: headache, fever, nausea, and dizziness; and local injection site reactions (pain, swelling, erythema, pruritus, and bruising) occurred after the administration of Gardasil. In the Gardasil 9 Package insert [61], pain is reported to be present in almost 90% of vaccinated girls.

3.3 HPV vaccines and pain: the molecular bases

Vaccination produces always inflammation. During inflammation, tissue resident and recruited immune cells secrete molecular mediators that act on the peripheral nerve terminals of nociceptor neurons to produce pain sensitization . Nociceptor peripheral nerve terminals possess receptors and ion channels that detect molecular mediators released during inflammation. Nociceptor neurons express receptors for immune cell-derived cytokines, lipids, proteases, and growth factors . High circulating plasma cytokine/chemokine levels were observed after the first dose of Gardasil 4® vaccine and the proinflammatory cytokines were elevated after the 1st and 3rd injection of the Cervarix® vaccine [62,63,64].

In summary, proinflammatory cytokines produced after vaccine injection are able to stimulate specific receptors that are present on nociceptor neurons. Indeed, Nociceptor neurons are also sensitized by TNF-α, IL-1β and IL-6 produced by mast cells, macrophages, and neutrophils [63]. All these proinflammatory cytokines are produced after vaccine injection.

3.4 Pain processing

Understanding pain processing is fundamental to identify the roots of post-vaccination inflammatory syndrome caused by HPV vaccines . This is a complicated path that begins with the expression of proinflammatory cytokines on the vaccine injection site, and then arrives at the somatosensory cortex.

3.5 Nociceptors

Physiological pain is initiated by specialized sensory nociceptor fibers which innervate peripheral tissues and are only activated by noxious stimuli [61]. The stimulation of nociceptors determines the onset of an action potential that is propagated along the axons of nociceptive Aδ and C fibres, through the dorsal root ganglion (DRG) to the axon terminals in the spinal cord dorsal horn [63]. A brief period of low frequency C-fibre stimulation, in the absence of nerve damage, is sufficient to activate microglia resulting in behavioural hyperalgesia [64].

Nociceptors by responding directly to cytokines can directly “sense” the immune response in inflamed tissue; essentially they are, therefore, not only noxious stimulus detectors, but also inflammation sensors [65]. Moreover, TNF-α is a key regulator of the inflammatory response and is involved in the increased production of proalgesic agents [64].

3.6 The second order neurons

The second order dorsal horn neurons, involved in pain circuitry, exist in two broadly characterised populations. After synapsing at the spinal cord, the second neuron travels in the spinal tracts, crosses the midline and runs up the spinothalamic tract to the thalamus where they synapse again and the next neuron travels to the somatosensory cortex. Here the impulses are processed in distinct areas, known collectively as the “pain matrix” so the nature of the pain can be perceived.

3.7 Neurophatic and inflammatory pain

Peripheral nerve injury activates spinal microglia. This leads to lasting changes in the properties of dorsal horn neurons that initiate central sensitization and the onset of neuropathic pain [66]. Vice versa, inflammatory pain is initiated by tissue damage/inflammation. Both are characterized by hypersensitivity at the site of damage and in adjacent normal tissue [67].

3.8 Chronic pain

It is now well established that chronic pain, such as inflammatory pain, neuropathic pain, and cancer pain, is an expression of neural plasticity, both in the peripheral nervous system as peripheral sensitization [68,69], and in the central nervous system (CNS) as central sensitization [69,70].

The rules of perception and pain management change in chronic pain. In fact, at peripheral level, nociceptors undergo sensitization and hyper-excitability (peripheral sensitization); while at the central level, excitatory synaptic transmission is increased in spinal cord, brainstem, and cortical neurons (central sensitization), caused by transcriptional, translational, and post-translational regulation [71].

3.9 Peripheral sensitisation

The International Association for the Study of Pain (IASP) definition of peripheral sensitisation is: “Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields” [72]. Then, Peripheral sensitisation induces a hyperexcitability of afferent nociceptive neurons [63].

3.10 Central Sensitization

The IASP definition of central sensitisation is: “Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input” [73]. Then, central sensitization refers to the amplification of pain by central nervous system mechanisms. On a cellular level, central sensitization results from multiple processes altering the functional status of nociceptive neurons [74]. Central sensitization increases response to pain sensation. Heightened sensitivity results in the perception of pain from non painful stimuli (allodynia) and greater pain than what one would be expected to get from normal painful stimuli (hyperalgesia).

3.11 Effects of Peripheral and central sensitization

While peripheral sensitization in nociceptors is essential for the development of chronic pain [75], and transition from acute pain to chronic pain [74], central sensitization regulates the chronicity of pain, causes the spread of pain beyond the site of injury, and influences the emotional and affective aspects of pain [62].

3.12 Spinal cord microglia

The spinal cord microglia, can respond to peripheral injuries that are distant from the spinal cord to produce neuroinflammation in the central nervous system [70]. Spinal glia activation is necessary and sufficient to induce neuropathic pain [74]. Astrocytes perform numerous critical functions such as neurotransmitter recycling, formation of the blood-brain barrier, regulation of extracellular ion concentration, and modulation of synaptic transmission, among many others [75].

3.13 Nociceptors activates microglia and astrocytes

In the case of strong and repetitive noxious stimuli, larger quantities and additional signaling molecules are released from the spinal terminals of nociceptive nerve fibers leading to the activation of microglia and astrocytes [76], and in some cases, to the degranulation of dural mast cells, to vasodilation, impairment of the blood–spinal cord barrier, and to the recruitment of T-cells to the spinal parenchyma [77]. This in turn causes the release of inflammatory mediators in the spinal cord, including chemokines and cytokines [76]. Hathway [63] had shown that a brief period of low frequency C-fibre stimulation, in the absence of nerve damage, is sufficient to activate microglia resulting in behavioural hyperalgesia.

3.14 Neuroinflammation in chronic pain

Neuroinflammation (in the peripheral and central nervous system) drives and manteined widespread chronic pain via central sensitization, which is a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults [78]. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines [78]. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites [78].

3.15 CRPS type I

Individuals without a confirmed nerve injury are classified as having CRPS type I, while in CRPS type II there is an associated and confirmed nerve injury. When pain arises in the absence of a nerve injury it is nociceptive pain. The term nociceptive pain is used to describe pain occurring with a normally functioning somatosensory nervous system to contrast with the abnormal function seen in neuropathic pain [71]. CRPS describes an array of painful conditions (nociceptive pain in CRPS type I) that are characterized by a continuing (spontaneous and/or evoked) limb pain that is seemingly disproportionate in time or degree to the usual course of any known trauma or other lesion. The pain is regional (not in a specific nerve territory or dermatome) and usually has a distal predominante [79]. Symptoms of CRPS-I include spontaneous pain (“burning” pain referred to the skin, and “aching” pain referred to deep tissues), and a variety of stimulus-evoked abnormal pain sensations, including mechano-hyperalgesia, mechano-allodynia, cold-allodynia and sometimes heat-hyperalgesia. Other symptoms include disorders of vasomotor and sudomotor regulation; trophic changes in skin, hair, nails, and bone, and dystonia and other motor abnormalities [80].

Thus, the most prominent mechanism appears to be the inflammatory process because all the classic signs of inflammation (oedema, redness, hyperthermia, and impaired function) are conspicuous in the early stages of CRPS [81]. High levels of the proinflammatory cytokines (TNF-α and IL-6) have been found in skin blister fluid of the affected limbs versus the unaffected limbs of CRPS patients [82]. In patients with CRPS, the levels of IL-1β and IL-6 were significantly increased in cerebrospinal fluid (CSF), compared to other subjects [83,84]. In the blood of subjects with painful neuropathy, TNF-α levels were doubled, compared to healthy subjects and those with non-painful neuropathy [85]. IL-1β can modulate the transmission of sensory neurons because it increases the release of substance P [86,87]. Thus, CRPS type I is associated with high levels of IL-1β and IL-6 in CSF, and high levels of TNF-α in the blood. Furthermore, these proinflammatory cytokines are strongly expressed after the injection of HPV vaccines.

Conclusion

The existence of extensive lines of communication between the nervous system and immune system represents a fundamental principle underlying neuroinflammation. Immune memory in the brain is an important modifier of neuropathology. Systemic inflammation generates signals that communicate with the brain and lead to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Two types of immunological imprinting can be distinguished: Training and tolerance. These are epigenetically mediated and enhance or suppress subsequent inflammation respectively.

The molecular mechanisms presented here demonstrate how peripheral cytokines, expressed after vaccination, can cause neuroinflammation in some subjects, after microglia activation, depending on the immunogenetic background and the innate immune memory. The effects produced by the activation of the microglia, and the subsequent neuroinflammation, are diversified according to age: before the first two years of life they can contribute to producing ASD (in some subjects with ASD there is neuroinflammation and aluminum accumulation in the brain); while a different neurological symptomatology can arise in girls vaccinated with HPV vaccines. Indeed, the proinflammatory cytokines expressed after HPV vaccine injections can cause neuroinflammation and chronic pain, and we hypothesize that the aforementioned cytokines are capable of producing a post-vaccination inflammatory syndrome in which chronic pain and neuroinflammation are practically always present.

In all girls mentioned in the book “The HPV vaccine on trail” [98], the chronic pain is always present and highly debilitating. Furthermore, many girls present the signs and symptoms of central sensitization with the associated psychic and motor symptoms (Table 1). Finally, in Japanese girls, the period of human papillomavirus vaccination considerably overlapped with that of unique post-vaccination symptom development (symptoms including chronic regional pain syndrome and autonomic and cognitive dysfunctions in the vaccinated patients).

source: Post-Vaccination Inflammatory Syndrome: a new syndrome

Report A COVID-19 Vaccine Injury

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