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Vaccinations Increase Risk of Epilepsy

Reference #: 1,359
Submit Date: 05 Nov 2007
Browse Category: epilepsy
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Email Address: wsotr@hotmail.com
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Browse: epilepsy

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For a consultation and research contact Waters-singing-on-the-rocks at wsotr@hotmail.com

Vaccinations Increase Risk of Epilepsy

This post is very similar to a prior post about vaccinations and the risk

of Alzheimer's related to infection with herpes simplex virus. In this

post and its citations, a link among epilepsy, herpes simplex, and

vaccinations is delineated.


The work of Diane E Griffin and colleagues of Johns Hopkins establishes

that measles virus and measles-vaccinations impair cell-mediated immunity

(CMI) and increase the likelihood of other viral infections (eg, 1-3).

These findings are supported by the work of Martinez et al (i) who

admit and are trying to solve vaccination-induced, *long-term* impairment

of CMI, and (ii) who mention herpes simplex virus (HSV) as an example of

the kind of infection exacerbated by vaccination-induced, long-term

impairments of CMI (4). In fact, Martinez et al describe impaired-CMI as a

general and long-term effect of traditional vaccinations, not just measles

vaccinations (4).

Fisher and colleagues have identified HSV as an important component

in a high percentage of persons with epileptic seizures (5), a finding

supported by a fascinating case history (6).


1. These data suggest that a person's risk of developing HSV-related

epileptiform patterns or epilepsy is increased by having had vaccinations

and the resulting long-term impairment of cell-mediated immunity.

2. These data also suggest that, if vaccinated, an older person who has a

latent infection with one of the herpes-class viruses (i) would be

likelier to experience a significant re-activation of the virus, and/or

(ii) would be at increased risk for other viral infections -- due to

vaccination-induced impairments of cell-mediated immunity.

Teresa who believes newer research-findings (eg, 1-4) are helping us

understand heretofore unappreciated side-effects of vaccinations.

1) Karp CL et al. Mechanism of suppression of cell-mediated immunity by

measles virus. Science. 273(5272):228-31, 1996 Jul 12.

The mechanisms underlying the profound suppression of cell-mediated

immunity (CMI) accompanying measles are unclear. Interleukin-12 (IL-12),

derived principally from monocytes and macrophages, is critical for the

generation of CMI. Measles virus (MV) infection of primary human monocytes

specifically down-regulated IL-12 production.

<2 Hussey GD... Griffin DE.

The effect of Edmonston-Zagreb and Schwarz measles vaccines on immune

response in infants.

Journal of Infectious Diseases. 173(6):1320-6, 1996 Jun.

...Eighty-eight children were immunized at 6 or 9 months of age with the

Edmonston-Zagreb (EZ) or Schwarz (SW6, SW9) strain of measles vaccine.

Children were studied before and 2 weeks and 3 months after immunization.

...Mitogen-induced lymphoproliferation was decreased at 2 weeks

in the SW9 group and at 3 months in all groups and was negatively

correlated with measles antibody level at 3 months (r = -.387, P = .003).

CD8 T cells, soluble CD8, neopterin, and beta2-microglobulin were

increased at 2 weeks in the SW9 group, and soluble CD8 and

beta2-microglobulin remained elevated at 3 months. Therefore, measles

immunization resulted in suppression of lymphoproliferation, which was

most evident in infants with the highest antibody responses and most

immune activation.

3) Auwaerter PG... Griffin DE.

Changes within T cell receptor V beta subsets in infants following measles


Clinical Immunology & Immunopathology. 79(2):163-70, 1996 May.

Measles produces immune suppression which contributes to an increased

susceptibility to other infections. Recently, high titered measles

vaccines have been linked to increased long-term mortality among some

female recipients....

[The following citation reiterates that vaccinations can impair

cell-mediated immunity by shifting cytokines release into a Th2 pattern,

thereby allowing intracellular pathogens (eg, many viruses) to be more

successful. We note that the authors of this 1997 study are trying to

devise a way around the general immune-impairing effect of conventional


4. Martinez X et al. DNA immunization circumvents deficient induction of T

helper type 1 and cytotoxic T lymphocyte responses in neonates and during

early life. Proc of the National Academy of Sciences 94.8726-31 1997.

ab: The relative deficiency of T helper type 1 (Th1) and cytotoxic T

lymphocyte (CTL) responses in early life is associated with an increased

susceptibility to infections by intracellular microorganisms. This is

likely to reflect a preferential polarization of immature CD4 T cells

toward a Th2 rather than a Th1 pattern upon immunization with conventional




REACTION -PRELIMINARY STUDY. Archives of Neurology. 54(8):954-960,

1997 Aug.

Objectives: To determine whether herpes simplex virus causes monofocal

epilepsy and to assess the presence of herpes simplex virus 1 (HSV-1) and

HSV-2 in surgical specimens from patients with epilepsy by using

polymerase chain reaction and Southern blot analysis.

Background: Herpes simplex virus is a common neurotropic virus capable of

latency within the central nervous system; it has a predilection for the

temporal lobe. Central nervous system infection with HSV has been

associated with seizure activity.

Design and Methods: Surgical specimens were removed from 50 patients as

part of a treatment protocol for monofocal epilepsy. Neuropathological

classification was done, and adjacent sections were screened for HSV by

using polymerase chain reaction. Tissues obtained post mortem from the

temporal lobe cortex of persons with Alzheimer disease (n = 17), Parkinson

disease (n = 14), or nonneurological disease (n = 17) served as controls.

Results: Twenty (40%) of the 50 epilepsy cases and 2 (4%) of the 48

control cases had at least one sample that tested positive for HSV (P <

.001). Sixty-seven percent (8/12) of the epilepsy cases with heterotopia

were positive for HSV.

Conclusions: There was a statistically significant difference in the

frequency of HSV-positive surgical specimens from monofocal seizure

epicenters compared with nonepilepsy control specimens. These data suggest

an association of the virus with seizure activity. All specimens positive

for HSV (surgical specimens and control specimens) should be examined to

determine the activity or latency state of the virus and cellular


6. Cornford ME, McCormick GF. Adult-onset temporal lobe epilepsy

associated with smoldering herpes simplex 2 infection. Neurology 48.425-30


A 40-year-old man with chronic genital herpes simplex infection developed

partial complex temporal lobe seizures of insidious onset, with EEG and

MRI evidence of a unilateral temporal lobe destructive, atrophic process.

Extensive workup did not reveal an infectious etiology. Three years of

escalating number and severity of daily seizures with memory loss led to

temporal lobectomy. Histologic study revealed active, low-level viral

infection in the resected hippocampus and temporal lobe cortex, with

immunohistochemical evidence for infection by herpes simplex 2,

principally in neurons. In situ hybridization confirmed the presence of

herpes simplex virus in neurons. Anticonvulsant-resistant seizure episodes

began to recur several times daily soon after surgery, but the addition of

acyclovir to the treatment regimen resulted in a substantial reduction in

seizure occurrence, maintained for the subsequent 2.5 years.

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