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Old 08-29-2009, 10:46 PM #1
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Default 12 y.o nephew dx w/ diabetes yesterday - Auto-immune diseases hitting our family hard

We are a group of 3 siblings -- 5 kids between our 3 families.
Me -- MS
DD - nothing
DS - nothing

Sister -- diabetes
Niece -- thyroid
Nephew -- diabetes

Brother -- diabetes, thyroid
Niece -- nothing
8 people, 5 with auto-immune diseases, 6 dx.

Very little auto-immune stuff going on, though, in our larger extended family. (Parents, grandparents, aunts, uncles, cousins)

~ Faith
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Old 08-30-2009, 12:33 AM #2
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Hi Faith,

I'm sorry to hear about your nephew's dx.
It must be devastating for the whole family.

Auto-immune diseases do run in families. I don't know about the pattern of generations though.
At least your brother and sister can support your nephew.

It's a great comfort when someone else can understand what you're going through, and even better when they're close to you.

Sending you hugs at this difficult time.
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Old 08-30-2009, 07:34 AM #3
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no advice just hugs I know its a hard time for your family.
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Old 08-30-2009, 06:51 PM #4
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Awwwww, bless his heart. That stinks..
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Old 08-30-2009, 07:40 PM #5
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I'm sorry your nephew was dx'd with diabetes.
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Old 09-09-2009, 03:22 PM #6
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Sorry to hear about your nephew. Autoimmune issues run heavy in my family also.
However: talk to everyone about getting their vitamin D3 checked. It won't cure anything....but it won't hurt either. Seems like these diseases show low levels of D3
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Old 09-10-2009, 11:23 PM #7
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Sorry to hear that news. I just got the same news about my mom. She got the dx about 1 month ago. She was dxed with fribromyaligia last year. They are in the process of doing more specific blood work for lupus. She also has IBS...is that autoimmune? I don't know. Her mom also has fibro (and schizophrenia , but we're just doing to put that out of our mind!)

I have MS and some autoimmune thing that causes keratin spots to pop up on your skin. Hopefully, that's it for me! We'll have to really keep an eye on DD b/c my mom is diabetic, as well as my DH's dad.

Well, good luck to your nephew.
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Old 09-11-2009, 09:45 AM #8
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Hi Faith,

I'm sorry to hear that your nephew was just diagnosed with T1DM.

You may already be aware, but if not..... there is continually increasing evidence that gluten (wheat, barley, rye) sensitivity may also be associated with other autoimmune disease, particularly T1DM. The subject is huge, and still in early stages of research, but given all those autoimmune diseases within your family... it may be worth taking a closer look at. At a minimum, family members should probably consider being screened for celiac disease/gluten sensitivity.

Wheat Consumption May Contribute to Diabetes
Wednesday, August 26, 2009
Overreaction in gut noted in study of people with type 1 version of disease
http://www.nlm.nih.gov/medlineplus/n...ory_88621.html

The newer research on zonulin, a protein that regulates the tight junctions of the intestinal wall and the blood brain barrier, is key. The Gluten File is chock full of references... with pages for diabetes, thyroid disease, MS, other autoimmune diseases. Casein sensitivity has been implicated in TIDM as well.

Here are a few studies that are filed in TGF:

Quote:

Earlier research by Fasano and colleagues led to the discovery of the human protein zonulin. They observed that zonulin regulates the permeability of the intestines by controlling the opening and closing of specialized structures that act like gates between cells. When the body produces too much zonulin, these gates remain open for too long, allowing undigested foodstuff, toxins and other bacterial and viral particles access to the immune system. That contact, in turn, leads to the production of antibodies that can destroy the insulin-producing islet cells in the pancreas among people genetically predisposed to develop Type 1 diabetes. The final result is the appearance of Type 1, or insulin-dependent, diabetes.

Fasano's group also discovered that zonulin is produced in very large amounts in people who have autoimmune disorders such as diabetes, celiac disease, multiple sclerosis, and rheumatoid arthritis. The researchers performed their latest study on rats genetically prone to develop Type 1 diabetes.

"With autoimmune diseases, the body mistakes its own tissues as foreign, resulting in an attack and destruction by the body's own immune system. These diseases are all characterized by an extremely permeable intestinal wall," says Fasano. "We already knew that there was a distinct connection between an increase in zonulin levels and an increased permeability of the intestines. With this study, we've been able to identify a way to prevent zonulin from causing leakage from the intestines as it does in people with these autoimmune diseases."
This paper presents a hypothesis of the aetiology of the increasing incidence of type 1 diabetes (T1D). This together with the global increased incidence of celiac disease (CD) and that these increases cannot be explained by genetic factors suggest a common environmental factor for these two diseases. Even though enterovirus (EV) infections are believed to trigger T1D and gluten is the trigger of CD, the increasing intake of gluten containing products all over the world could be the trigger for both diseases directly and indirectly. It has been shown that the duration of exposure to gluten is related to the prevalence of T1D. It has also been shown that T1D patients at onset have an inflammatory reaction in the gut. Hence, early diagnose of CD followed by elimination of dietary gluten will lead to a decreased incidence of T1D.
A unifying hypothesis on the development of type 1 diabetes and celiac disease: Gluten consumption may be a shared causative factor.
PMID: 18249499 Feb 2008

The most frequent reported CD associated conditions are type 1 diabetes mellitus and autoimmune thyroiditis. Associated autoimmune antibodies are frequent in CD and their first-degree relatives, spanning anti-endocrine, anti-gastrointestinal, anti-nuclear, anti-cytoskeleton and anti-neurological antibodies. More specifically, antibodies against thyroid and the endocrine pancreas, anti-gastric and liver, anti-nuclear constituents, anti-reticulin, actin, smooth muscle, calreticulin, desmin, collagens and bone, anti-brain, ganglioside, neuronal and blood vessel were described in sera of the patients in numerous studies.
Associated autoantibodies in celiac disease.
PMID: 17854749 Sept 2007

This paper presents a series of 10 hypotheses on the etiology of type 1 diabetes. We begin with the hypothesis that wheat gluten is one of the elusive environmental triggers in type 1 diabetes. Habitual consumption of wheat gluten increases the intestinal synthesis of dipeptidyl peptidase IV. This enzyme helps to shape the repertoire of peptides released into the small intestine following the ingestion of wheat gluten by catalyzing the release of X-Pro dipeptides from the N-terminus of the proline-rich glutenins and gliadins in wheat gluten. The release of gluten-derived peptides causes the tight junctions of the small intestine to open through a zonulin-dependent mechanism, which allows these peptides to enter the lamina propria where they get presented as antigens by HLA-DQ, -DR and CD1d molecules. Binding of one or more gluten peptides by CD1d leads to abrogation of oral tolerance, and a marked increase in peripheral immune responses to wheat proteins. Furthermore, it is our contention, that in response to beta cell apoptosis during normal remodeling of the pancreas and CCL19/CCL21 expression within the pancreatic lymph nodes (PLNs), gluten-loaded dendritic cells migrate from the small intestine to the PLNs. These dendritic cells present gluten-derived antigens on the surface of the PLNs, which leads to migration of CD4(-)CD8(-) gammadelta and CD4(-)CD8(+) alphabeta T cells to the pancreas where they mediate Fas and perforin dependent cytotoxicity. We also hypothesize that at least one of the type 1 diabetes associated HLA-DR molecules that bind and present wheat-derived peptide(s) also bind and present an islet cell antigen(s), activating plasma cell synthesis of islet cell autoantibodies and irrevocable, complement-dependent destruction of islet cells. Our final two hypotheses state that type 1 diabetes morbidity is reduced in those areas of globe where genetically susceptible individuals get adequate amounts of vitamin D, in the diet and/or through exposure to sunlight, and in areas where people are exposed to bacterial, viral, or parasitic infections in early childhood.
PMID: 17045415
Putting the pieces of the puzzle together - a series of hypotheses on the etiology and pathogenesis of type 1 diabetes. PMID: 17045415 Oct 2006

There is, however, growing evidence that the loss of the intestinal barrier function typical of celiac disease could be responsible of the onset of other autoimmune disease. This concept implies that the autoimmune response can be theoretically stopped and perhaps reversed if the interplay between autoimmune predisposing genes and trigger(s) is prevented or eliminated by a prompt diagnosis and treatment.
Systemic autoimmune disorders in celiac disease.
PMID: 17053448 Nov 2006 Full text on Medscape

Thus, screening program for coeliac disease are recommended in individuals with type 1A diabetes and/or auto-immune thyroid conditions, as well as in their first-degree relatives.
Coeliac disease in patients with type 1 diabetes mellitus and auto-immune thyroid disorders PMID: 14618956


From:
Emerging concepts in celiac disease by William Treem, MD
"The association of CD with autoimmune diseases, particularly Type 1 diabetes and autoimmune thyroid disease, has been widely reported with some investigators finding a ten-fold increase in patients with CD compared with the general population [68,69].Less clear is the link between CD and Sjögren syndrome, primary biliary cirrhosis, Addison disease, autoimmune chronic active hepatitis, cardiomyopathy, and peripheral neuropathy (not due to B-12 or vitamin E deficiency) [70–73•,74•].
When both CD and autoimmune disease occur in a patient, CD is most often silent.The autoimmune disease is diagnosed first with the diagnosis of CD the result of serologic screening in this high-risk population.
The question whether the early diagnosis and treatment of CD reduces the risk of developing other autoimmune diseases is still open to debate.There are several lines of evidence that support the notion that CD is a causative factor in the development of other autoimmune diseases. A recent study suggests that the prevalence of autoimmune diseases is closely related to the duration of gluten exposure and the age of initiation of a GFD with children diagnosed and treated before 2 years of age having little subsequent increased risk [75].Older children diagnosed with CD have a higher than expected frequency of organ-specific autoantibodies that tend to disappear after starting a GFD.Anecdotal reports suggest that socalled "celiac neuropathy", IgA nephropathy, juvenile rheumatoid arthritis, and autoimmune myocarditis will all improve when patients who have underlying CD are maintained on a strict GFD [73•,74•,76,77]. "



Also... everyone in the family should have awareness of B12 deficiency symptoms (that can mimic MS, Lupus, Lyme Disease). B12 deficiency often occurs within in this "autoimmune group" due to pernicious anemia (yet another autoimmune disease) or through malabsorption as a result of celiac disease/ gluten sensitivity.
AAFP on Vitamin B12 Deficiency
Emedicine on Pernicious Anemia
eMedicine link on vitamin B12 associated neurological diseases:


These things occur together so frequently, they have named it a "syndrome".




Autoimmune Polyglandular Syndrome 3


Gluten Ataxia can mimic MS as well.

Neurological manifestations of gastrointestinal disorders are described, with particular reference to those resembling multiple sclerosis (MS) on clinical or MRI grounds. Patients with celiac disease can present cerebellar ataxia, progressive myoclonic ataxia, myelopathy, or cerebral, brainstem and peripheral nerve involvement. Antigliadin antibodies can be found in subjects with neurological dysfunction of unknown cause, particularly in sporadic cerebellar ataxia ("gluten ataxia").
Neurological manifestations of gastrointestinal disorders, with particular reference to the differential diagnosis of multiple sclerosis.
PMID: 11794474 Nov 2001
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