Aluminum and more - Adverse Effects of Adjuvants in Vaccines by Viera Scheibner (Part 2 of 2)

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Adverse Effects of Adjuvants in Vaccines by Viera Scheibner (Part 2 of 2)

ADVERSE EFFECTS OF ADJUVANTS IN VACCINES by Viera Scheibner (Part 2 of 2}

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ADVERSE EFFECTS OF ADJUVANTS IN VACCINES

by Viera Scheibner, Ph.D. Ó 2000

Nexus Dec 2000 (Vol 8, No1) & Feb 2001 (Vol 8, Number 2)

ADJUVANTS, PRESERVATIVES AND TISSUE FIXATIVES IN VACCINES

Part 2 of 2

Other Adjuvants: Squalene

Squalene is an organic polymer with some

antigenic epitopes which might be shared with

other organic polymers acting as

immunostimulators. It has been used in

experimental vaccines since 1987 (Asa et aL,

2000) and it was used in the experiments vaccines

given to a great number of the participants in

the Gulf War. These included those who were not

deployed but received the same vaccines as those who were deployed.

The adjuvant activity of non-ionic block

copolymer surfactants was demonstrated when given

with 2% squalene-in-water emulsion. However, this

adjuvant contributed to the cascade of reactions

called " Gulf War syndrome " , documented in the

soldiers involved in the Gulf War. The symptoms

they developed included arthritis, fibromyalgia,

lymphadenopathy, rashes, photosensitive rashes,

malar rashes, chronic fatigue, chronic headaches,

abnormal body hair loss, non-healing skin

lesions, aphthous ulcers, dizziness, weakness,

memory loss, seizures, mood changes,

neuropsychiatric problems, anti-thyroid effects,

anaemia, elevated ESR (erythrocyte sedimentation

rate), systemic lupus erythematosus, multiple

sclerosis, ALS (amyotrophic lateral sclerosis),

Raynaud's phenomenon, Sjorgren's syndrome,

chronic diarrhoea, night sweats and low-grade fevers.

This long list of reactions shows just how much

damage is done by vaccines, particularly when

potentiated by powerful " immunoenhancers " such as

squalene and other adjuvants. Interestingly,

vaccinators as a rule consider such problems as

mysterious and/or coincidental with vaccines.

Since the administration of a multitude of

vaccines to the participants (and prospective

participants) in the Gulf War is well-documented

(in fact, veterans claim they were given many

more than were even recorded), this list of

observed reactions further incriminates the vaccines as causing such problems.

IMMUNOLOGY PRINCIPLES: ANTIBODY RESPONSE

To explain the action of adjuvants, we should

look into immunology. The theory of vaccine

efficacy is based on the ability of vaccines to

evoke the formation of antibodies. This is of

varying efficacy, depending on the nature of the

antigen(s) and the amount of antigenic substance administered.

However, the mechanisms for the diversity of

immune reactions are complex, and to this day are

not quite known and understood. There are

numerous theories, the favoured one being

antibody response as the sign of immunisation (acquiring immunity).

Specific immunity to a particular disease is

generally considered to be the result of two

kinds of activity: the humoral antibody and the cellular sensitivity.

The ability to form antibodies develops partly in

utero and partly after birth in the neonatal

period. In either case, immunological

competence—the ability to respond immunologically

to an antigenic stimulus—appears to originate with the thymic activity.

The thymus initially consists largely of

primitive cellular elements which become

peripheralised to the lymph nodes and spleen.

These cells give rise to lymphoid cells,

resulting in the development of immunological

competence. The thymus may also exert a second

activity in producing a hormqne-lilce substance

which is essential for the maturation of

immunological competence in lymphoid cells. Such

maturation also takes place by contact with thymus cells in the thymus.

Stimulation of the organism by antigen results in

proliferation of cells of the lymphoid series

accompanied by the formation of immunocytes, and

this leads to the antibody production. Certain

lymphocytes and possibly reticulum cells may be

transformed into immunoblasts, which develop into

immunologically active ( " sensitised " ) lymphocytes

and plasmocytes (plasma cells). Antibody

formation is connected with plasma cells, while

cellular immunity reactions are mainly lymphocytic.

None of the theories for antibody formation

comprehends all the biological and chemical data

now available. However, several principal

theories have been considered at length.

The so-called instructive theory holds that the

antigen is brought to the locus of antibody

synthesis and there imposes in some way the

synthesis of the specific antibody with reactive

sites which are complementary to the antigen.

The clonal selection theory, evolved by Burnett

(1960), presupposes that the information

requisite to the synthesis of the antibody is

part of the genetics. While the body develops a

wide range of clones of cells necessary to cover

all antigenic determinants by random mutation

during early embryonic life, those clones which

are capable of reacting with antigens of the body

( " self') are destroyed, leaving only those cells

which are not oriented to self ( " non-self'). Upon

stimulation by a foreign antigen, the clones of

the cells corresponding to the particular foreign

antigen are stimulated to proliferate and to produce the antibody.

Other researchers demonstrated that there are at

least four different antigens formed by

descendants of a single cloned cell. By this

mechanism, the information for antibody synthesis

is contained in the genetic material of each cell

(DNA) but is normally repressed. The antigen then

assumes the role of a de-repressor and initiates

(provokes) the RNA synthesis for a particular

messenger, resulting in the corresponding

antibody production. The antigen would instruct

the genetically predisposed capability of

multipotential cells as to which antibody to

produce and might also command the cells to

proliferate, resulting in clones of properly instructed cells.

There are two possible mechanisms for the

elimination of antibodies against self:

immunological nonresponsiveness and immunological

paralysis. There are several states of

immunological nonresponsiveness; one is

illustrated by the exposure of a foetus or

newborn to an antigen prior to the development of

its ability to recognise the antigen as non-self

(immunological incompetence). Immunological

paralysis results from the injection of a very

large amount of antigen into immunologically

competent individuals. Nonspecific immunological

suppression by cortisone, ACTH, nitrogen mustards

and irradiation is also well known.

Cellular sensitivity, also known as delayed or

cellular hypersensitivity, depends on the

development of immunologically reactive or

" sensitive " lymphocytes and possibly other cells

which react with the corresponding antigen to

give a typical delayed-type reaction after a

period of several hours, days or even weeks.

Cellular hypersensitivity depends on the original

antigenic stimulation and a latent period, and is

specific in its response. Delayed-type

hypersensitivity is characteristic of the body's

response to various infectious agents such as

viruses, bacteria, fungi, spirochetes and

parasites. It is also characteristic of the

body's response to various chemicals, such as

mercury, endotoxins, antibiotics, various drugs

and many other substances foreign to the body.

The induction of a hypersensitivity reaction

requires the presence in the tissues of the whole

organism or certain derivatives of it, in

addition to the specific antigen such as a lipid

in addition to tubercle bacillus protein.

Sensitisation to a non-infectious substance must

be mediated through the skin or mucuous membranes

which probably provide further necessary co-factors.

A delayed hypersensitivity reaction may be

enhanced experimentally by the employment of the

antigen in a mineral oil adjuvant with added

Mycobacterium tuberculosis or by injection of the

antigen directly into the lymphatics. The delayed

hypersensitivity response is accompanied by mild

to severe inflammation which may cause cell

injury and necrosis. The inflammatory response

which occurs in delayed-type hypersensitivity may

not be protective, and in many instances may even

be harmful (e.g., rejection of grafts is directly

linked to delayed hypersensitivity).

IMMUNOPATHOLOGY OF HYPERSENSITIVITY REACTIONS:

Immediate Hypersensitivity

This is the antibody-type reaction that is a

secondary consequence to the beneficial effect of

the combination of an antibody with its antigen.

Arthus-type Reaction

This reaction results from the precipitative

union of a large amount of antigen with a highly

reactive antibody in the blood vessels, and leads

to vascular damage. The cascade of events

includes spastic contraction of the arterioles,

endothelial damage, formation of leukocyte

thrombi, exudation of fluid and blood cells into

the tissues, and sometimes ischemic necrosis.

Periarteritis nodosa results from a similar

antigen-antibody reaction and is characterised by

inflammation of the smaller arteries and

periarterial structures. it is accompanied by

proliferation of the intima and two types of

occlusion: (a) by proliferation or thrombosis; or

( by the formation of nodules containing neutrophils and eosinophils.

Anaphylaxis

Injection of antigen and its combination with

antibody may cause release from the cells

(especially mast-cell fixed basophils) of

physiologically active substances such as

histamine, serotonin, acetyicholine,

slow-reacting substances (SRS) and heparin. They

act on smooth muscle and blood vessels and cause

anaphylactic (hypersensitivity) shock, asthma

attack, allergic oedema, rhinitis or hay fever,

and accumulation of fluid in the joints.

Atopy

Atopy is caused by the union of antigen—usually

pollens, dust, milk, wheat and animal

danders—with a peculiar type of antibody

(reagin). This reaction is relatively heat-labile

and cannot be demonstrated by in vitro procedure.

It has a special affinity for the skin and for

familial predisposition to the disease. The

reaction is nevertheless similar to other

immediate-type sensitivities, with the release of

histamine and its manifestation principally as

asthma (breathing paralysis), hay fever,

urticaria, angioedema and infantile eczema.

Delayed Hypersensitivity

The typical pathology of delayed hypersensitivity

due to infectious agents involves perivascular

infiltration of lymphocytes and histiocytes with

the destruction of the antigen-containing

parenchyma in the infiltrated area. The visual

manifestations may vary from slight erythema and

oedema to a violent reaction with progressive

tissue destruction and necrosis. Local reactions

include papular rose spots of typhoid fever,

meningitis and a variety of infectious diseases,

and contact sensitivities to plant and chemical

substances manifesting as erythema, followed by

papule and vesicle formation with resultant

tissue damage and desquamation. Systemic

reactions may accompany severe local reactions or

may result from inhalation of the allergenic substances.

Humoral antibodies do not seem to play a role in

delayed hypersensitivity reaction. The reactivity

is transferred only by cells, presumably

sensitised lymphocytes, and it is unlikely that

histamine or other physiologically active

substances play a role in the reaction. The

reaction extends to any or all tissues where the offending antigen may occur.

Isoimmunological Disease

This is the result of an immunological reaction

of a member of the same species to the tissue of

another member of the same species. A blood

transfusion reaction in a person given an

incompatible blood type is a typical example.

Another example is erythroblastosis fetalis,

which results from the transfer of antibodies

against the red blood cells of the foetus to the

foetal circulation. Homograft rejection of

tissues or organs between nonisologous members of

a species is also immunologically based.

Immunological Disease Resulting from Adsorption of Foreign Substances

Under certain circumstances, foreign substances

such as medications may combine with cells to

render them antigenic. Subsequent exposure to

such a foreign substance results in lytic,

agglutinative or other types of cell-destructive

activity. Such a reaction may involve red blood

cells (drug-induced anaemias), platelets

(drug-induced thrombocytopemc purpura), and

leukocytosis (drug-induced agranulocytosis).

Bacteria or viruses may also alter cell surfaces

by coating or by unmasking antigens through

enzymatic activity which may render them

vulnerable to immunological destruction.

Autoimmune Disease

Under certain circumstances, the body may respond

immunologically to its own components or to

intrinsic substances which are related

antigenically to the host's own tissues. The

circulating antibody or sensitised cells which

are produced are then active in causing cellular

injury to the tissues or organs of the body which

bear the corresponding antigen.

Waksman (1962) proposed several mecnamsms of autoimmunisation, such as:

1.Vaccination with organ-specific antigens which

are isolated from the lymphatic channels and

bloodstream and are not recognised as self when

brought into contact with the immunologic

process. They are represented in the central and

peripheral nervous systems, lens, uvea, testes,

thyroid (thyroglobulin), kidneys and other organs.

2.Vaccination against constituents of tissues

which have been altered antigenetically by

various factors. These include myocardial

infarction, X-irradiation, enzymatic or other

chemical alteration, and changes induced by

infectious disease agents or by drugs.

Erythrocytes, platelets and leucocytes are the

most affected cells. Various organs may also be affected.

3.Vaccination with heterologous antigens which

are sufficiently different to permit an

immunological response but sufficiently alike to

react with autologous antigens.

4.Alteration of the immunological apparatus so as

to result in the failure of recognition of self.

This occurs in neoplasia of the lymphatic system

and in experimental grafting of immunologically

competent heterologous lymphatic tissues under

conditions which suppress the host's response to

the graft and give rise to the wasting " runt disease " or " homologous disease " .

5.Possible hereditary or other immunological

abnormality. This is represented by a

hyper-reactivity to antigens or other aberrations

without apparent antigenic stimulation. Such

mechanisms might be related to certain forms of

the " collagen diseases " , such as systemic lupus

erythematosus in which there is an antibody against a diversity of antigens.

6.Experimentally, Freund's mineral oil adjuvant

(usually with added mycobacteria) and certain

bacteria or bacterial toxins may so alter the

host as to bring about a ready response to

unaltered normal homologous tissue. These

" experimental autoallergies " include a wide

variety of organs and tissues, and are now being

employed as model systems for investigation of autoimmune phenomena.

Both humoral antibody and sensitised cells may

function in autoimmune disease. Auto-antibodies

seem to be involved in reactions with cells which

are easily accessible, such as the formed

elements of the blood (in haemolytic anaemia,

leucopeni thrombocytopenia), vascular

endothelium, vascular basement membrane including

the glomerulus (in acute glomerulonephritis and

ascites cells (neoplastic immunity).

Production of lesions in the solid vascularised

tissues appears to depend on delayed

hypersensitivity reactions with sensitised

lymphoid cells (such as in allergic

encephalomyeitis, thyroiditis, subacute and

chronic glomerulonephritis, orchitis, adrenalitis and many other diseases).

It is quite obvious now that the same autoimmune

mechanisms are responsible for the same diseases

in human beings and that the extent of such

damage is enormous and keeps increasing with more

and more vaccines added to to " recommended " schedule.

Indeed, vaccines such as the pertussis vaccine

are actually used to induce autoimmune diseases

in laboratory animals, the best and most

publicised example being the so-called

experimental allergic encephalomyelitis (EAE).

When, as expected, these unfortunate animals

develop EAE from the pertussis vaccine, the

causal link is never disputed; yet when babies

after vaccination with the same vaccines develop

the same symptoms of EAE as the laboratory

animals, the causal link to the administered

vaccine is always disputed and usually considered

" coincidental " . Lately, innocent parents and

other carers have been accused of causing the

symptoms of vaccine darn age by allegedly shaking their babies.

Systemic lupus erythematosus is one of the

innumerable recognised side effects of a number

of vaccinations. One of the best papers (if not

the best on this is by Ayvazian and Badger

(1948), and it has not lost any of its punch and

relevance since it was published. They describe

three cases of nurses who were literally

vaccinated to death. The authors surveyed a group

of 750 nurses who trained at a large municipal

hospital between 1932 and 1946, and detailed the

cases of three nurses who were vaccinated with a

multitude of vaccines over a period of time and

developed and succumbed to disseminated lupus erythematosus.

Typically, these nurses were given the following

tests and vaccines in short succession: the

Schick test; three days later, the Dick test;

seven days later, typhoid-paratyphoid vaccine;

seven days later, another typhoid-paratyphoid

vaccine (a double dose); seven days later, the

third typhoid-paratyphoid vaccine; and seven days

later, the fourth typhoid-paratyphoid vaccine.

Every time, the recipient developed local

erythema and/or fever and malaise, but it did not

deter the doctor from administering yet another

series of vaccines, starting only 14 days after

the first lot of tests and typhoid-paratyphoid vaccines.

This time, after all these injections, one of the

trainee nurses was given her first injection of

scarlet fever streptococcus toxin with " no ill

results " . One week later, she was given the

second injection of streptococcus toxin, after

which she developed joint pains and fever. She

did not report these reactions to the health

office. Nine days later, she returned and

received the third injection of a fourfold dose

of streptococcus, after which she developed

severe arthralgia in the fingers and knees and a sore throat.

She was hospitalised for five days and discharged

with the diagnosis " Dick-toxin reaction " . Only

five days later her inoculations were continued,

first in lower and then in gradually increasing

doses so that the series included a total of 10

instead of the usual seven injections.

Epinephrine was administered with each of these

injections of streptococcus toxin and toxin-antitoxin.

Two months after the last lot, the trainee nurse

was re-admitted to the hospital with swelling and

pain of the ankles and toes and tenderness of the

joints of both hands, which had been constant

since the first Dick test five months earlier.

The diagnosis was " rheumatic arthritis " . She was

given aspirin, but two weeks later the pain came

back and she developed chills and fever, sore

throat and cough. One month later, the trainee

nurse was re-admitted to hospital for two weeks,

and during this admission a streptococcus vaccine

was started in small doses, but because of her

severe reaction " further vaccines were refused " .

The diagnosis after this admission was

" rheumatoid arthritis and infectious

mononucleosis " . Four months later, the trainee

nurse noticed skin eruptions over her nose and

both cheeks, and her saliva became foul. The skin

and cheeks, upper lips and the bridge of the nose

were covered with purplish red, mottled and

indurated rash eruptions. Two months later, the

eruptions spread over much of the body. A year

later, the trainee nurse died, but not before

developing severe symptoms of high fever,

tachycardia, diarrhoea and showing abnormal blood tests.

It was not enough that this unfortunate trainee

nurse died; there were another two cases

reported, almost identical to the first case. We

shall never know bow many of the remaining 747

trainee nurses developed less lethal, but still

health-incanacitating. reactions.

If someone said that this type of " medical

treatment' had been given to the inmates of the

Nazi concentration camps, I would not be

surprised. However, this type of " medical

treatment " was and is being given with impunity

to millions of babies, children, teenagers and

adults in so-called free and democratic countries

as well as in the Third World. Meanwhile, the

health authorities refuse to accept that vaccines

cause such reactions and even deaths.

VACCINATION: A SAFETY WARNING

The conclusions which follow the study of

relevant medical and immunological literature

dealing with vaccines and the adjuvants used in

vaccines is that the absolute safety of these

substances can never be guaranteed. According to

Gupta et al. (1993), the toxicity of adjuvants

can be ascribed in part to the unintended

stimulation of various mechanisms of the immune

response. That's why the safety and adjuvancy

must be balanced to get the maximum immune

stimulation with minimum side effects.

My conclusion is that such balance is impossible

to achieve, even if we fully understood the

immune system and the full spectrum of

deleterious effects of foreign antigens and other

toxic substances such as vaccine and drug

adjuvants and medications on the immune system of

humans, and particularly on the immature immune

system of babies and small children. Injecting

any foreign substance straight into the

bloodstream will only cause anaphylactic

(sensitisation) reactions. Nature, over thousands

and thousands of years, has developed effective

immune responses; yet man, without respect for

nature, demonstrably causes more harm than good.

Vaccination procedures are a highly politically

motivated non-science, whose practitioners are

only interested in injecting multitudes of

vaccines without much interest or care as to

their effects. Data collection on reactions to

vaccines is only paid lip service, and the

obvious ineffectiveness of vaccines to prevent diseases is glossed over.

The fact that natural infectious diseases have

beneficial effect on the maturation and

development of the immune system is ignored or deliberately suppressed.

Consequently, parents of small children and any

potential recipients of vaccines and any orthodox

medications should be wary of any member of the

medical establishment (which is little more than

a highly politicised business system) extolling

the non-existent virtues of vaccination. Even

though Australian law requires doctors to warn

patients about all side-effects of all

medications and procedures of a material nature,

whether the patient asks or not, doctors as a

rule do not uphold this important law.

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Antibodies to Squalene in Gulf War Syndrome.

Experimental Molecular Pathology 68:55—64.

• Ayvazian, L.F. and Badger, TL, 1948.

Disseminated lupus erythematosus occurring among

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