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[IP] vaccine info-long



FYI, this came from the website: 
http://www.vaccines.net/  check it out.

 Both animal data and human data indicates that
vaccines alter the risk of developing diabetes.
      Immunization starting at birth is associated
with a decreased risk of diabetes while immunization
starting
      after 2 months is associated with an increased
risk of diabetes. Vaccines probably affect the risk of
diabetes
      by modulating the immune system. The data in
humans shows a strong association between immunization
      and the risk of insulin dependent diabetes
(IDDM) Type I diabetes, an autoimmune disease. At this
time
      studies have not been performed to determine if
Type II diabetes is also associated with vaccination.
Based
      on the fact that many people diagnosed with Type
II diabetes also have autoimmune destruction of there
      insulin secreting cells of the pancrease, it is
reasonable to assume that immunization may be altering
the risk
      of Type II diabetes as well. A review of Type I
and Type II diabetes are included below. Data
supporting a link
      between immunization and diabetes in humans and
animals can be viewed on the corresponding linked
      pages. 

       

      Type I diabetes mellitus (IDDM)

              Type I diabetes mellitus, insulin
dependent diabetes, is a chronic disease of humans
with a primary onset
      occurring mainly in childhood and adolescence.
The risk of developing type I diabetes varies
significantly by
      country and race but not by sex. It is estimated
that up to one in every 100 Caucasians may develop
type I
      diabetes and that more than one million
Americans are afflicted with the disease. The disease
is a significant
      social and financial burden to most western
nations. Its onset is often associate with an abrupt
occurrence of
      polydipsia, polyuria, weight loss, fatigue,
irritability and typically results in death if insulin
therapy is not
      initiated. Serious chronic complications
frequently afflict insulin treated diabetics later in
life resulting in
      expensive hospitalization, loss of employment,
and a decline in quality of life. 

              Substantial evidence has existed for a
while suggesting that type I diabetes is an autoimmune
disease.
      This data has been extensively reviewed in
several papers (Flier & Underhill, 1986; Barbosa &
Bach, 1987;
      Zielasek, Jackson & Eisenbarth, 1989; Maclaren,
1992) so only some of the essential points will be
discussed
      here. Findings suggesting an autoimmune etiology
include the presence of insulitis in the pancreas of
recently
      diagnosed type I diabetics along with the
presence of islet cell antibodies in early diabetics
and prediabetics.
      Glutamic acid decarboxylase reacts with sera
from prediabetics and early diabetics in 70% or more
of cases
      leading some believe that it may trigger the
development of an anti-islet cell autoimmune response.


              Clinical trials and epidemiological
studies have supported an immunological link to type I
diabetes.
      Treatment of newly diagnosed type I diabetics
with cyclosporine can reverse diabetes temporarily
(Marks &
      Skyler, 1991; Martin, Schernthaner, Nerupet
al.1991). Epidemiology has shown strong linkage of
type I
      diabetes with the major histocompatability genes
that control the development of immune responses.
      Approximately 95% of Caucasian type I diabetics
express MHC class II alleles DR3 or DR4 while these
alleles
      are expressed in only about 40% of the Caucasian
population (Trucco & Dorman, 1989). Other studies
      suggest a protective effect of certain MHC
alleles as demonstrated by an inverse correlation
between the
      expression of the DR2 allele and the development
of diabetes. Studies of type I diabetes in identical
twins
      show that the concordance rate is only about
50%. This finding suggests that genes do not have
absolute
      control on the development of diabetes and that
environmental factors have a strong effect also.

              An extensive search has been underway to
try to determine immunologic defects that could
predispose
      individuals to develop type I diabetes but the
findings are inconclusive. The difficulty in this
endeavor is that it
      is hard to differentiate immunologic
abnormalities that may cause diabetes from immunologic
abnormalities
      caused by diabetes. This problem along with
genetic heterogeneity and various environmental
factors has led
      to often conflicting reports of immune disorders
in diabetics. Autologous mixed lymphocyte reactions as
well as
      responses to Concanavalin A and
Phytohemagglutinin have been found to be decreased in
newly diagnosed
      type I diabetics (Al-Kassab & Raziuddin, 1990;
Knospe, Kohler, Rjasanowskiet al.1990) however studies
      focusing on long standing diabetics have failed
to find any permanent defects (Pozzilli, Pagani,
Arduiniet
      al.1987; Surcel, Karttunen, Ilonenet al.1987;
Lorini, De Amici & Cortona, 1989). Some of the best
evidence
      suggesting diabetics may have an immune disorder
include papers showing an increased incidence of
classic
      autoimmune diseases like thyroiditis in type I
diabetics (Landin-Olsson, Karlsson, Dahlquistet
al.1989a). That
      antithyroid antibodies are more common in
females but islet cell antibodies and diabetes are
equally common
      in males and females has raised questions on
whether the disorders are casually related or are
derived from
      common immunologic defects. 

       

      Type II diabetes mellitus

              Type II diabetes is a second and more
common form of diabetes mellitus. The diseases
typically occurs in
      patients over 35 years of age and affects 5% of
the population in the U.S.A. Some of these patients
suffer
      from low insulin sensitivity, while others have
reduced insulin secretion. Diabetics have
traditionally been
      classified as type II if their diabetes is
controlled without insulin and if they failed to
develop ketosis. Several
      recent studies have shown that many people
classified as type II diabetics may actually suffer
from a slowly
      progressing autoimmune destruction of the
insulin secreting islet cells. These individuals may
be better
      classified as having type I diabetes or both
type I and type II diabetes (Groop, Bottazzo &
Doniach, 1986;
      Landin-Olsson, Karlsson, Dahlquistet al.1989b;
Niskanen, Karjalainen, Sarlundet al.1991; American
Diabetes
      Association, 1993; Arnqvist, Littorin, Nystromet
al.1993); (Temple, Luzio, Schneideret al.1989; King &
Rewers,
      1993) . 

             Data suggests that 10% or more of
patients diagnosed with type II diabetes suffer from
low insulin
      production due to an autoimmune response against
the pancreatic islet cells, as occurs in type I
diabetes.
      Studies of Caucasians diagnosed with type II
diabetes have revealed that between 14% and 32%
develop
      autoantibodies to islet cell antigens within the
first 5 years of diagnosis. These individuals
represent a special
      subset of type II diabetics as seen by their
deficiency of insulin secretion, elevated frequency of
certain HLA
      genes, elevated frequency of thyroid or gastric
autoantibodies and high risk for requiring insulin
treatment.
      Twenty-nine percent of all diabetics in the USA
use insulin. Assuming 10% of all diabetics are
actually
      diagnosed as type I, insulin dependent
diabetics, the remaining 19% of diabetics taking
insulin are diagnosed
      as type II, non insulin dependent diabetics.
Many of these 19% could be type I diabetics that were
incorrectly
      diagnosed due to a slow progression of disease
and inadequate laboratory testing (Turner, Stratton,
      Hortonet al.1997).

PS:

I got a silver 'ribbon' pin from JDFI, contact the
Wash, DC office and see if they will supply for free.

       

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