Why?


(mamacolby) #1

Do you know why your son or daughter has type one?  I know they really do not know why it happens, but what are your feelings on the subject?  Any crazy rumors out there that you want to share too? 

A great, great aunt on my side had type one.  She died at the age of 11 from what I cannot even imagine to be a pretty horrible death.  This was in the late 1890's, so before the advent of insulin.  Thank you insulin!  I think that this family history may have contributed to my son's diagnosis, but it could be anything really.


(rmeadowsaprn) #2

Out of my 6 children, Carol Ann was the only one to have the meningococcal vaccine. And she got it late. Also, she was my only child to ever have lice and be treated with those "pesticides". I know the former sounds crazy but she had to be treated 2-3 times and I've always felt guilty "poisoning" her like that. I know. Crazy. No genetic link. (She's one of the 80%) My cousin's daughter was recently diagnosed at 5 years old also.


(mismidge) #3

I myself really think vaccines play some kind of role. I find it odd that a lot of d-days are near a birthdate. A lot of children at 5. I know not all cases are that, but I believe that it plays a role in the increase of dx. Do you know the first vaccine a baby recieves ,you need to weigh over 200lbs. to safely absorb the amount of mercury in it! They do not tell you that when you sign the paper. I don't know just one theory. I know not all cases have heriditary links. So thats my thoughts.


(rmeadowsaprn) #4

Most research is case study research which is not generalizable but there has been a recent increase in research linking autoimmune diseases with vaccines.

Here's an interesting one:

 

The Open Endocrinology Journal, 2008, 2, 9-15 9
1874-2165/08 2008 Bentham Open
Open Access
Type 1 Diabetes Versus Type 2 Diabetes/Metabolic Syndrome, Opposite
Extremes of an Immune Spectrum Disorder Induced by Vaccines
John Barthelow Classen*
Classen Immunotherapies Inc., 6517 Montrose Avenue, Baltimore, MD 21212, USA
Abstract: There is an epidemic in children of type 2 diabetes and metabolic syndrome including individual diseases that
form the components of metabolic syndrome. The epidemic resembles the epidemic of type 1 diabetes in children which
has been linked to immunization. The epidemic of obesity in US children has a statistically significant positive correlation
with the number of vaccine doses recommended. There is a similar trend with both hypertension and metabolic syndrome.
The incidence of type 2 diabetes in Japanese children decreased significantly following the discontinuation of the BCG
vaccine, a vaccine which is associated with an increased risk of type 1 diabetes. This paper describes two aberrant responses
to immunization. At one extreme immunization leads to progressive autoimmune diseases including type 1 diabetes.
A second response to immunization, and an opposite extreme to autoimmunity, is for the body to suppress the immune
system through increased cortisol activity and other counter measures leading to type 2 diabetes and metabolic syndrome.
Some vaccine recipients may have a mixed response, falling between the extremes, such as an incomplete autoimmune
disorder or an intermittent autoimmune disorder. The propensity to develop a particular response relates to race.
Japanese children produce large amounts of cortisol following immunization and have lower risk of type 1 diabetes but
higher risk of type 2 diabetes than White children. Analysis using Austin Bradford-Hill criteria for causation support a
causal relation between immunization and metabolic syndrome. Additional studies are needed to further characterize this
risk.
Keywords: Vaccines, type 1 diabetes, type 2 diabetes, metabolic syndrome.
I. BACKGROUND
There is an epidemic of several diseases in human children
and adults including hypertension, obesity, hyperlipidemia,
low high density lipoprotein [HDL] cholesterol, microalbuminurea,
and insulin resistance [1, 2]. This syndrome
has been collectively classified as metabolic syndrome [3]
and is closely associated with type 2 diabetes [4] and other
health problems including death [5]. Many have blamed poor
diet [6] and lack of exercise for the epidemics of type 2 diabetes
and metabolic syndrome. Diet and exercise have been
touted as the cure for metabolic syndrome but have not been
very effective [7] and have not stopped the epidemic to date.
The poor diet and exercise theory does not explain the obesity
epidemic in children under 6 month of age who don't
drink many sodas, don't eat a lot of fried potatoes and have
never been very active. Recent data from a Massachusetts
health maintance organization [HMO] shows a 73% increase
in overweight infants under 6 months of age from 1980 to
2001 [8].
Several investigators have proposed that metabolic syndrome
is an inflammatory condition or the result of increased
cortisol production, a hormone that suppresses inflammatory
conditions. The epidemic of metabolic syndrome in children
mirrors an epidemic of type 1 diabetes in children, which has
*Address correspondence to this author at the Classen Immunotherapies
Inc., 6517 Montrose Avenue, Baltimore, MD 21212, USA; Tel: (410) 377-
8526; E-mail: Classen@vaccines.net
been linked to a class of immune stimulants, vaccines [9-12].
A proposed mechanism of vaccine induced metabolic syndrome
is presented. Epidemiological evidence supporting an
association between immunization and metabolic syndrome
is presented. Epidemiological and experimental data are reviewed
supporting a racial basis for determining whether an
individual is more likely to develop an autoimmune disease
like type 1 diabetes or metabolic disease as a complication of
immunization.
II. PROPOSED MECHANISM OF VACCINE INDUCED
METABOLIC SYNDROME
A. Autoimmunity and Metabolic Syndrome are Opposing
Ends of an Immune Spectrum Disorder
The proposed mechanism of immunization induced
metabolic syndrome is by an intrinsic neuroendrocrine feedback
loop to suppress an immune system chronically activated
by immunization. It is well accepted that in all organ
systems there are homeostatic mechanisms to regulate their
activity. Autoimmune diseases are conditions that result
from an over active immune system. Likewise one would
expect that there would be one or more diseases that arise
when the body attempts to suppress what it interprets as an
over active immune system. Cortisol is a hormone that suppresses
the immune system and can prevent autoimmunity.
Hypersecretion of cortisol however can lead to Cushingoid
Syndrome which closely resembles metabolic syndrome.
Vaccines have been shown to cause autoimmune diseases
including type 1 diabetes [9-12] and other chronic inflamma10
The Open Endocrinology Journal, 2008, Volume 2 John Barthelow Classen
tory conditions [13]. Vaccines are also known to cause cortisol
secretion [14-21].
B. Inflammation as the Cause of Metabolic Syndrome
It has been proposed that metabolic syndrome is an inflammatory
condition [22]. This belief is supported by studies
have shown that inflammation predates metabolic syndrome
[23, 24]. A study on Finnish middle age men [23]
found men with elevated C-reactive protein [CRP] concentrations
had higher age-adjusted risk of developing metabolic
syndrome. A study of men and women in Mexico [24] found
women with elevated CRP in the highest tertile had an increased
relative risk of developing metabolic syndrome.
Some have suggested that metabolic syndrome causes
inflammation [25]. While metabolic syndrome may cause
inflammation it is more likely that inflammation initially
causes metabolic syndrome. Inflammation has been associated
with the development of components of metabolic syndrome,
independent of the presence of characteristics of
metabolic syndrome [23, 24]. Glucose intolerance/type 2
diabetes [26] and hypertension [27, 28] are both independently
associated with inflammation. There is additional evidence
that once metabolic syndrome begins it causes more
inflammation [25] which in turn makes the disease worse.
Adiposites and the accompanying macrophages appear to
make inflammatory mediators. While there is an association
between obesity and inflammation [29], obesity can exist
without inflammation as demonstrated by obese individuals
with a healthy metabolic profile [30]. The later evidence
supports the view that in many inflammation precedes the
development of metabolic syndrome.
Metabolic syndrome has a remarkable similarity to mild
Cushingoid Syndrome [31, 32] and several have suggested
that metabolic syndrome is caused by increased cortisol activity
[33-35]. There is data showing increased cortisol levels
associated with metabolic syndrome [36]. There is evidence
that increased peripheral activation of cortisol secondary to
increased enzymatic activity of 11-beta hydroxysteroid dehydrogenase
type 1 contributes to the development of metabolic
syndrome [37, 38]. Some have also suggested that
metabolic syndrome is in part due to increased cellular uptake
of cortisol [39]. Excessive amounts of exogenous glucocorticoids
are known to cause hypertension, obesity, hyperlipidemia,
and glucose intolerance. The effect is dose
dependent. There are many similarities between excessive
cortisol activity and metabolic syndrome. Excessive cortisol
activity is associated with metabolic disturbances including
increased glucose levels, obesity and hyperlipidemia [40]
just like in metabolic syndrome. Excessive cortisol activity is
also associated with increased cardiovascular events [41, 42]
just like metabolic syndrome.
There is biological evidence that specific lymphokines
released during inflammation can cause the release of cortisol
and cause the biological changes that occur in metabolic
syndrome. It has been hypothesized [43] that the metabolic
syndrome like responses to lymphokines provide a short
term survival advantage helping the host survive noxious
events. Hyperlipidemia for example may help the body clear
fat soluble toxins. A problem arises in certain individuals
when inflammation becomes chronic and the changes lead to
metabolic syndrome. In these cases changes that are a survival
advantage acutely are chronically an hazard.
C. Vaccines as an Inducer of Metabolic Syndrome
Vaccines have been shown to stimulate the immune system
in the short term causing the release of cytokines that
can increase cortisol activity. The acellular diphtheria tetanus
pertussis vaccine has been reported to cause the release of
IL-6 [44]. The Diptheria-Tetanus-Polio-Typhim vaccine
stimulated IL-6 production [45]. The Diptheria-Tetanuswhole
cell Pertussis but not the Diptheria-Tetanus- acellular
Pertussis vaccine elicited increased IL-6 at 2 days post immunization
[46]. The influenza vaccine stimulated release of
IL-6 and IL-10 [47]. The influenza and pneumococcal vaccine
caused rises in CRP [48]. Researchers in France have
linked aluminum adjuvants in vaccines to an inflammatory
condition called myofascititis [13, 49]. Several papers have
shown that immunization of children can increase cortisol
levels at least in the short term [14-21].
Cytokine production, particularly IL-6, increases with
age [50-52] and this can explain the increase in metabolic
syndrome with age. Both IL-1 [53, 54] and IL-6 [55-57] enhance
cortisol release and thus have the potential to cause
metabolic syndrome. IL-6 has been associated with the development
of metabolic syndrome [58, 59]. In addition IL-6
has been directly associated with the development of diabetes
[26], insulin resistance [60] and altered lipid levels [61-
63].
D. Resetting the Hypothalamus
A second mechanism by which immunization may lead
to the induction of metabolic syndrome is through the resetting
of the hypothalamus. Immunization in the first year of
life may affect the onset of metabolic syndrome by resetting
of the hypothalamus, creating more cortisol release. Two
well characterized examples support this hypothesis. It has
been shown that the hypothalamus is reset in children who
undergo stress in utero. These children produce higher cortisol
release and hence have increased symptoms resembling
metabolic syndrome [64-66]. A second example of reseting
the hypopthalamus is in children which are born with low
birth weight and are at increased risk of developing metabolic
syndrome [67].
III. EPIDEMIOLOGY OF VACCINE INDUCED TYPE
2 DIABETES AND METABOLIC SYNDROME
Epidemiological data support the proposed mechanism of
vaccine induced type 2 diabetes and metabolic syndrome.
A. Epidemic of Type 2 Diabetes and Metabolic Syndrome
Resembles the Epidemic of Type 1 Diabetes
One line of support for the proposed mechanism of vaccine
induced metabolic syndrome is that the epidemic of
metabolic syndrome and type 2 diabetes resembles the epidemic
of type 1 diabetes. The role of vaccines in causing the
epidemic of type 1 diabetes is supported by data from a prospective
clinical trial, animal toxicity data as well as epidemiological
data [9-12]. There is an epidemic of metabolic
syndrome and its components in children living in the US [1,
2] and other countries including the UK and Australia [68,
Type 1 Diabetes Versus Type 2 Diabetes/Metabolic Syndrome The Open Endocrinology Journal, 2008, Volume 2 11
69]. Data on the prevalence of metabolic syndrome, obesity,
and hypertension in US children has been published covering
a period of at least 10 years. Obesity in US children aged 4
to 12 years old increased on average of 3.23-5.85% per year,
depending on race, from 1986 to 1998 in the National Longitudinal
Survey of Youths [70]. The prevalence of overweight
children increased on average of 1.41% to 3.60% per year,
depending on race, in the same age group. Similar rises were
seen in children age 0-19 years old in the NHANES study
[71, 72]. Between 1988 and 2000 the prevalence of obesity
rose 4.4% per year in children age 12-19 years old, 3.4%
year in children age 6-11 years old, and 4.2% per year in
children age 2-5 years old. Blood pressure also rose in children
and adolescents between 1988 to 2000 [73] [p<0.001].
Metabolic syndrome increased on average of 4% a year in
adolescents aged 12-19 years old according to US NHANES
data from 1988-1992 to 1999-2000 [2] [p<0.001]. In comparison
Type 1 diabetes in children increased 2.3% per year
in the US from 1978-2004 [74].
The findings do not appear to be limited to the US. Data
from Finnish children [75] shows the prevalence of obesity
in children age 12-18 in the years 1977 to 1999 increased
from 1.1% to 2.7% in boys [relative risk 2.45] and from 0.4

The number of doses of vaccines recommended for children in the US increased from 24 to 45 in the years 1978 to 2006. The rise in the number of doses is statistically associated
with the increase in obesity in US children age 2-19. A similar but not statistically significant association is also seen in the US with metabolic syndrome and diastolic blood pressure
in children.
12 The Open Endocrinology Journal, 2008, Volume 2 John Barthelow Classen
to 1.4% in girls [relative risk 3.5]; on average a 5% rise per
year. The prevalence of overweight increased from 7.2% to
16.7% in boys and 4.0% to 9.8% in girls, on average a 4%
rise per year. During this time the combined measles mumps
rubella and hemophilus vaccines were added to the immunization
schedule as well as an more potent pertussis vaccine
[10]. This increase in obesity is very similar to the 3.4% per
year increase in type 1 diabetes from 1965 to 1996 [76]
which has been attributed to an increase in number of vaccines
[10, 11].
B. Positive Correlation Between the Number of Doses of
Vaccine Administered and the Prevalence of Obesity
There is an association between the number of vaccine
doses recommended for US children and rises in obesity and
metabolic syndrome. The number of pediatric vaccines universally
recommended in the US by the Centers for Disease
Control and Prevention [CDC] has increased from seven to
thirteen and the number of recommended doses from 24 to
45. There was a statistically significant correlation between
the number of doses of vaccine given and obesity in children
age 2-5, 6-11 and 12-19 (Table 1). Statistics were performed
using the program Statistica, Stat Soft, 1993. The Pearson
Product-Moment Correlation module was used to determine
the statistical association between number of vaccines doses
recommended with obesity. Data on US rates of metabolic
syndrome and hypertension in children exists for only two
periods of time, two data points, so statistical correlations
can not be calculated. However there was a similar trend
with both of these outcomes and both outcomes showed a
statistically significant rises during the study period. There
was a similar trend in Finland with a positive correlation
between the number of vaccine doses given and an increased
prevalence of obesity, just like in the US [10, 11].
C. Decline in Type 2 Diabetes Occurred Following Discontinuation
of the Tuberculosis Vaccine [BCG]
The rates of Type 2 diabetes and metabolic syndrome is
increasing throughout the world [77]. However, there was a
statistically significant drop in the incidence of Type 2 diabetes
in Tokyo Japan in elementary and junior high school
students [78, 79]. The drop occurred in 2003 after the discontinuation
of routine BCG vaccination of elementary and
junior high school students in Japan [80]. BCG vaccination
has previously been associated with an increased risk of type
1 diabetes [9].
D. Racial Predisposition for Development of Type 1 or
Type 2 Diabetes and the Association with Cortisol Secretion
Following Immunization
The proposed mechanism that some respond to immunization
by developing autoimmune disease while others respond
to immunization by developing metabolic syndrome is
supported by racial differences in the rates of type 1 and type
2 diabetes and cortisol secretion following immunization.
Type 1 diabetes is an autoimmune disease while type 2 diabetes
is related to insulin resistance, a component of metabolic
syndrome. Type 2 diabetes is associated with obesity,
another component of metabolic syndrome, while type 1
diabetes is not. White children including adolescents tend to
have an high absolute incidence of type 1 diabetes and a high
ratios of the incidence of type 1/type 2 diabetes compared
children of Japanese or Chinese decent. The later children
have higher incidences of type 2 diabetes and, consequently,
a lower ratio of the incidence of type 1 to type 2 diabetes
[78, 81-83].
The racial differences in the incidence of type 1 and type
2 diabetes can be explained by cortisol release following
immunization. Japanese children have a higher cortisol responses
to immunization than White children [84]. The differences
in cortisol responses of Whites and Japanese appears
to extend into adulthood as well [85]. Because they
release more cortisol following immunization, Japanese
children would be expected to have a lower rate of autoimmune
diseases including type 1 diabetes as well as a lower
ratio of type 1/type 2 diabetes compared to Caucasians. Elevated
cortisol secretion can cause metabolic syndrome, as
described above, but cortisol is an immune suppressant and
prevents autoimmune disease. Decreases in cortisol following
adrenalectomy leads to increased rates of type 1 diabetes
in mice [86] and experimental autoimmune diseases [87, 88].
IV. AUSTIN BRADFORD-HILL CRITERIA FOR ESTABLISHING
CAUSATION
Austin Bradford-Hill’s criteria [89] are used to show
whether an association is likely to be an causative relationship.
He listed nine factors and all nine are met in the association
between immunization and metabolic syndrome (Table
2). Austin Bradford-Hill analysis in part relies on
bioplausibility. Based on the existing knowledge it is proposed
that vaccines induce inflammation which increases
cortisol or cortisol like activity leading to a Cushingoid like
state which is metabolic syndrome.
V. CLINICAL IMPLICATIONS FOR REVERSIBILITY
OF THE METABOLIC SYNDROME
Current studies are being performed to try to reverse or
prevent metabolic syndrome by decreasing cortisol activity.
One approach is to inhibit the enzyme 11-beta hydroxysteroid
dehydrogenase type 1, an enzyme which increases the activity
of cortisol in the peripheral tissue. Evidence from animal
models of autoimmune disease suggests that suppression of
cortisol, while likely to suppress metabolic syndrome, will
increase the risk of autoimmune diseases. Decreasing cortisol
production in rodents by adrenalectomy, for example, greatly
increases the risk of diabetes in [86]. A safe and effective
method of suppressing metabolic syndrome will require the
reduction of inflammation, the precursor to both autoimmune
disease and metabolic syndrome. Ideally one will want to reduce
exposure to vaccines that lead to chronic inflammation.
Once exposure to inflammatory mediators have been initiated,
one can attempt to suppress the inflammation. There is evidence
that certain anti-inflammatory agents will prevent development
of metabolic syndrome. An anti-inflammatory drug
AGI-1067 in its Phase III study called ARISE, showed a 64
percent reduction in patients developing diabetes in the group
reviving AGI-1067 as compared to prospective controls.
VI. FUTURE STUDIES
Vaccines continue to be approved based on small studies
with only short term follow up. Theses studies are inadeType
1 Diabetes Versus Type 2 Diabetes/Metabolic Syndrome The Open Endocrinology Journal, 2008, Volume 2 13
quate to address safety issues such as metabolic syndrome
[90]. Large prospective randomized clinical studies need to
be performed to study the long term effects of specific vaccines
on the risk of metabolic syndrome and its component
diseases.
Table 2. Austin Bradford-Hill Criteria For Establishing Causation
The nine criteria set by Austin Bradford-Hill for establishing causation
are met with the association between vaccination and metabolic syndrome,
supporting an causal relationship between vaccination and metabolic
syndrome. The nine criteria are:
1. Strength
Answer: Yes. The association is strong and in children under 6 months
of age the rise of obesity can not be explained by competing theories of
poor diets and lack of exercise. The drop in type 2 diabetes in Japan
following the discontinuation of BCG immunization is unprecedented.
Only immunization has been published to cause such an effect on diabetes.
2. Consistency
Answer: Yes. The effect is consistent in different areas of the world
including the US and Finland.
3. Specificity
Answer: Yes. Exposure to vaccines has been linked to immunological
disorders and not to unrelated disorders.
4. Temporality
Answer: Yes. Children are immunized at 2 months of age and metabolic
syndrome occurs later. The incidence of type 2 diabetes decreased after
discontinuation of BCG vaccine in Japan.
5. Biological Gradient
Answer: Yes. There is a statistically significant correlation linking the
number of vaccine doses to the prevalence of obesity.
6. Plausibility
Answer: Yes. The proposed mechanism has been described.
7. Coherence
Answer: Yes. There is an epidemic of obesity, hypertension, metabolic
syndrome, type 2 diabetes and type 1 diabetes which increased with the
increased number of vaccine doses recommended.
8. Experimental Evidence
Answer: Yes. Studies show increased inflammation and cortisol levels
after immunization. An anti-inflammatory drug reduced the incidence of
new cases of diabetes.
9. Analogy
Answer: Yes. The findings are analogous to vaccine induced type 1
diabetes.
VII. CONCLUSION
There is an epidemic of metabolic syndrome and its
components in children in the US. The epidemic of metabolic
syndrome resembles the epidemic of type 1 diabetes in
children which has been linked to vaccines. There is a statistically
significant correlation between the prevalence of obesity
and the number of vaccine doses recommended. A similar
trend exists for hypertension, type 2 diabetes and metabolic
syndrome. The data presented and prior publications
indicates vaccine induce an immune spectrum disorder. One
extreme of the disorder is the development of progressive
autoimmune diseases such as type 1 diabetes. A second response
to immunization, and an opposite extreme to autoimmunity,
is for the body to suppress the immune system
through increased cortisol activity and other counter measures
leading to type 2 diabetes and metabolic syndrome.
Some vaccine recipients may have a mixed response, falling
between the extremes, such as an incomplete autoimmune
disorder or an intermittent autoimmune disorder. The propensity
to develop a particular response relates to race. The
propensity to develop a particular response with racial differences.
Japanese children produce larger amounts of cortisol
following immunization and have a lower risk of type 1
diabetes but higher risk of type 2 diabetes than white children.
Additional studies are needed to further characterize
this risk.
ACKNOWLEDGEMENT
The author is president and share holder of Classen Immunotherapies.
Classen Immunotherapies holds many patents
and patent applications related to testing vaccines for
their risk of chronic diseases including type 1 and type 2
diabetes.
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Received: May 14, 2008 Revised: July 22, 2008 Accepted: August 6, 2008
© John Barthelow Classen; Licensee Bentham Open.
This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/bync/
3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited


(avonlady94) #5

My daughter was almost 20 yrs. old when she was diagnosed.  Neither her father, I or any of her grandparents have any diabetes.  My husband has 2 cousins (on both sides) and an uncle (on his dad's side) that had Type 1.  My grandfather on my dad's side had it but I don't know if it was 1 or 2.  The doctors said that they don't consider Meg's "hereditary".  However, they did say the gene was there and when she came down with a high fever (2 months before her diagnosis) that "flipped the switch" on the gene.

Oh, and she'd had all of the childhood vaccines + (as did her 2 brothers).  They also had a bought with lice at the same time.  The boys do not have diabetes.


(Jana) #6

I agree, my daughter Lea was diagnosed 3 months after her immunization shots . She was 4 at the time and i thought it was to early to get them. She wasn't starting kindergarten till the following year. Her pediatrition said it was fine to do them(all four). She is 5 now and in kindergarten. Being injected with 4 different viruses must do something to the immune system.

Jana


(system) #7

My Son was 11 when he was diagnosed (July of 08).  He wasn't due for his next round of immunization shots until September of 08 when school started.  His last round of immunizations was when he was almost 6 years old (so that was in 2003).  We do not have members on either side of our families with Diabetes.  Our diagnoses did not follow any type of pattern around immunizations or family history. He was healthy kid and only missed 1 day of school last year. There were no major illnesses leading up to his diagnoses.  Of course he’s had his bouts of illnesses over the years but nothing recently. So we are baffled as we do not fall into any of the suggested potential scenarios’.   When he was 15 months old he had some seriously high fevers and experienced convulsions and was in the hospital.  His fevers were anywhere from 104-106.  It was very scary.  But that was so long ago.


(rs14hubbard) #8

Our daughter was diagnosed when she was 5 right before her 6th birthday. It was January and she had not been ill all winter. The only thing that was out of the ordinary was that we had her get a flu shot in the October prior to her diagnosis. There is no one on either side of our family that has Type I or Type II. We have always thought it was that flu shot...


(amyb856) #9

Our daughter had an MMR shot on the Friday before she got dx on Tuesday. (2 days after her 4th birthday). We always thought it was the live virus attacking her pancreas. That was 9 years ago. As with you, no other history on either side of type 1 or 2.

Amy


(ShannonSamples) #10

My son Christopher was diagnosed on June 30, 2008.  I took him to the doctor because he had strep. His blood sugar was 399 even though he hadn't eaten anything in a day and had been throwing up during that time.  He has always been prone to strep.  His doctor said his immune system just rebelled. He thought that may have caused type 1 diabetes.


(Tracey B.) #11

My husband was diagnosed with type one when he was 13.  His younger sister was diagnosed at 17 and to our knowledge they can't find any other diabetes in their family.  Our daughter was diagnosed at 10.  She was diagnosed 2 weeks after her school vaccinations.  Whenever I ask about the timing of the vaccinations and the dx our endo and pediatrician don't think they are related.  In some of my reading it has been mentioned that if your father is type one you have a 1 in 20 chance of a child developing the disease.  Some seem to think that a person may carry a tendency towards diabetes and that something triggers it (virus, stress, exposure to chemicals) and some of the research is looking at trying to find and block triggers. 

I guess there is no such thing as a simple explanation - darn!  :)  I hadn't heard the lice one!


(IndyDon) #12

Why?  That's a great question.  Personally, my wife and I think our son's allergic reaction to penicillin was a trigger for the diabetes.  He developed a very severe rash in his abdomen area after taking penicillin at age 2 (it appeared he was beaten in his abdomen since he had a "black and blue" rash with the blue actually being purplish .  One endo did not see the link between an allergic reaction and an autoimmune disease like diabetes.  But, I know of a few others that have had kids diagnosed with diabetes after an allergic reaction to penicillin. 

There may be a host of triggering mechanisms.  But, from what I have read (admittedly, not a lot) there is little evidence, if any, that vaccines trigger diabetes.  Who knows (I don't!).  It could be a trigger for some.  However, even if a vaccine were a trigger, it seems implausible that it would lead to diabetes in a matter of days or a few weeks.  An easy way of fact-checking that would be to know the child's A1C at diagnosis.  If it is high then the diabetes had been present for a number of weeks or even a few months.  I have not heard of any cases where the A1C at diagnosis was low.  I'm sure sometimes diabetes is diagnosed early but most of us can attest that our child's A1C was in the double digits at diagnosis. 

Another aspect is which vaccine would trigger it.  From what I recall it was thought by many (the majority?) of those who thought a vaccine could trigger diabetes, that the culprit was the pneumococcal vaccine.  Ironically, my wife and I did not have our son receive two vaccines, one being the pneumococcal shot.  However, after he was diagnosed we knew it was important for him to have the vaccine so he was immunized.

It's interesting to look at diabetes incident rates across the globe.  Why does Finland have such a high incident rate while Shanghai, China is so low?  Why are there fewer cases of diabetes diagnosed in the summer than other times of the year?  Why are there peaks at other times of the year?  There seems to be lots and lots of studies available.  But, I think it's hard to make conclusions without diabetes registries and long-term study.  Again from some studies I have read, there are spikes in diabetes cases after the presence of certain viruses in an area.  That is probably one reason so many think that a virus is a triggering mechanism to someone who is already predisposed to developing diabetes. 

And, I don't want to open a can of worms...but, a number of studies link the introduction of cow's milk at an early age to higher incident rates of diabetes.  Early consumption of cow's milk and/or diminished breast feeding may create a predisposition to diabetes later in life. 

Again, great question even if there are no great answers.


(rs14hubbard) #13

It is very interesting that you mention the allergic reaction to penicillin. My daughter had an allergic reaction to amoxicillin when she was 18 months...so severe it caused the same bruising you mentioned. She truly looked like someone had beaten her. Two years later she got Henoch Scholein Purpura (HSP) which caused the same bruising. HSP is also an allergic reaction to either a medication or a virus. She had HSP for almost a year which is relatively long.

All of that being said, we were convinced it was the flu shot that caused our daughter to become diabetic...based on exactly what you mentioned above...her A1c at diagnosis. She had not been ill for almost a year at diagnosis. The only thing we could link it back to during the time period the doctor's mentioned was the flu shot.

Of course, it is very likely that the combination of these factors caused her to get diabetes. As I mentioned before, no one on either side of my husband or my family has a history of diabetes (type I or II).

I agree...great question even if there are no great answers

 


(BrookeAH) #14

Casey was diagnosed on 1/27/09.  Both my husband and I have people on both sides with type 2, I have a cousin with type 1 but onset at 25.  We don't know yet if she has the gene, but she had a fever in August that lasted for a week with no other symptoms - I think that was her trigger and for some reason symptoms didn't show until recently.  My husband and several members of his family have thyroid issues and we're thinking that she may have that to deal with too. 


(denisem5823) #15

Madison was dx october 2, 2008 right before her dx she had the flew shot in sept so she could enter preschool. No one on either side my husband and mine have had type 1 diabetes but his mom and grandma had gotten type 2 as they got older. During the summer she had a the virus coc saci (spelling) which they said may have triggered type 1.  That was in July/ august sometime. Makes u think flue shot or coc saci????


(peteandjulesmom) #16

My son Peter was dx in May of 08 at 4.5 years old.  He had coxsackie virus in August of 08--and got it pretty much every summer since he was 9 months old. My doctor told me that coxsackie virus is one of the viruses suspected of being a trigger for Type 1 diabetes.

 

Any thoughts??

 

Pete and Jules mom


(peteandjulesmom) #17

I meant August of 07

 

Pete and Jules mom


(pjay) #18

Wow, that's the question of my life!

I had a cousin that was diagnosed with Type 1 when she was a young child, not sure what age.  My parents and three of my grandparents had Type 2.  I don't believe there is a link between Type 1 and Type 2.

I now have two sons who were diagnosed.  My oldest was diagnosed 8 years ago when he was 9.  My youngest was diagnosed this summer when he was 10.  One in the winter one in the summer, neither around a birthday.  We plan to have my middle son tested for the antibody that is present in both of my other two.  When my oldest was diagnosed, I did a lot of research and thought it was extremely rare for siblings to be diagnosed.  Since my youngest, I have found that it isn't as uncommon as I first thought.

Honestly with my oldest, I don't remember any "trigger" event.  He had been very tired, not thriving, and bedwetting for months.  I finally decided to make the pediatrician test him for an infection.  I suspected a bladder or kidney infection. 

With my youngest, he was given Prednisone one week prior to being diagnosed.  The Endo team believe that the prednisone didn't cause the Diabetese, just made it more prominent.  We were able to catch his very early and his sugar levels have been pretty level. 

It has been explained to us that some people are born with this antibody and a virus may trigger it.  The antibodies then attack the pancreas and kill the beta cells.  All three of my boys had their immunizations.  Some were late, others were on time.  We homeschooled for a long time, so we weren't concerned about keeping them as up to date.  I would love to see a study done on the antibody's reaction to immunizations.  It could be that in some cases, they trigger the antibody to attack.

 


(Dave) #19

My son was diagnosed at 2 1/2yrs old and it was not after receiving any immunization shots.  Prior to this our son has had a number of ear infections and a bladder infection.  It was mentioned that one of those may have triggered his diabetes.  THere is also a history of Type 1 and Type 2 on both sides of our family so I'm sure genetics played a large part in him having diabetes.  I myself am not diabetic but have had a few lows in the past 6 months, so I now consider myself pre-diabetic.  Nothing has shown up after being tested yet so it's up to me to take care of myself.  Let me tell ya I now know how my son feels when he is low, I was as low as 2.1 and it's not a nice feeling at all, but at 4yrs old my little guy knew how to look after me by running to get me one of his juiceboxes. Until it is proven what causes diabetes we can only guess but it makes you wonder just what it is that does cause it.


(melbaugher) #20

There is only one very distant cousin who is a type 1 in my family.

I have wondered, however about vaccines. My daugher was 9 and had the varivax (Chicken Pox) booster shot at her 9 year check up in April. I don't know if there is a connection, but she started showing symptoms 2.5 months later, and was diagnosed 4 months later.