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Thread: -- Breanne -- Trialnet questions..

  1. #1
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    Default -- Breanne -- Trialnet questions..

    Breanne, in thread 'Trialnet free screening for first cousins....recommend it?' you posted ----------T1D is not mendelian. Oh, and one more thing: Diabetes is not a mendelian inherited gene! Recessive vs dominant has nothing do to with it!!! T1D is a VERY complex disease that comes from both sides of the family, and most importantly, the TRIGGER.----------

    Will you help me, us, to understand a little better how a person develops T1? My side of the family is D-free. DH side, 4 gens back, had 1 person T1. There are a few T2s but they are either chemical, obesity or diet related and they are not direct blood kin.

    TrialNet told us they are studying what may trigger T1. Environment, genetic, inherited.. whatever. Ive heard and read that none or all can trigger it. Sooo... What in the enviroment? How genetic? You already said not inherited. What about childhood immunizations including Flu shots could they trigger this? I was also told that a simple cold could trigger?

    What are the names of the 4 different antibodies? Are IA2 and ICA-512 the same? (Our endo said he thinks they are the same but not sure to ask a Trialnet person)

    Presuming IA2 and ICA-512 are the same, since each of my sons share 2 of the antibodies, in your expert, granted statistical (I understand all the ifs and butts) opinion, does this put my non-D son at even a higher risk?

    Thanks!
    T


    Samuel
    b.06/23/06, VSD, clear by 1 y.o.,
    01/28/08 DX @ 19 mths old, antibodies; mIAA, IA2, ICA512 and GAD65,
    09/15/08 Animas *Ping* :, Insets
    04/10/09 Dexcom
    03/29/10 Celiac

    James
    b.11/18/04 non-d
    05/20/08, Positive antibodies; mIAA, IA2, and ICA512



    Got Facebook? FR me @ https://www.facebook.com/enragedbliss
    or Tracie Fenske McClelland
    Be sure to mention you are from CWD so I can put you on my CWD friends list!

    *May the God of your choice bless you*

  2. #2
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    Quote Originally Posted by TracieandJim View Post

    What are the names of the 4 different antibodies? Are IA2 and ICA-512 the same? (Our endo said he thinks they are the same but not sure to ask a Trialnet person)

    Thanks!
    T
    I just found the answer to this question here. http://jcem.endojournals.org/cgi/content/full/82/2/375 Under 'Abstract' it says 'Islet cell antigen (ICA) 512 also termed IA-2 is a novel autoantigen of type 1 diabetes, which has a tyrosine phosphatase-like domain. ' SO they are the same. So far I have seen only 3 antibodies. What is the fourth?

    And something else here.. a 5th antibody ? http://findarticles.com/p/articles/m...133/ai_6818733

    So.. so far Ive found IAA, GAD65, IA2/ICA-512 and ZnT8 autoantibodies. ZnT8 was only discovered last October. SO.. A 5th antibody called 64K ??
    Last edited by TracieandJim; 06-07-2008 at 08:43 AM.


    Samuel
    b.06/23/06, VSD, clear by 1 y.o.,
    01/28/08 DX @ 19 mths old, antibodies; mIAA, IA2, ICA512 and GAD65,
    09/15/08 Animas *Ping* :, Insets
    04/10/09 Dexcom
    03/29/10 Celiac

    James
    b.11/18/04 non-d
    05/20/08, Positive antibodies; mIAA, IA2, and ICA512



    Got Facebook? FR me @ https://www.facebook.com/enragedbliss
    or Tracie Fenske McClelland
    Be sure to mention you are from CWD so I can put you on my CWD friends list!

    *May the God of your choice bless you*

  3. #3
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    I can't answer all of those questions, but I do recall reading in the Pink Panther Book that a gene from each parent is responsible for the genetic tendency for T1D. IIRC, they're called DR3 and DR4.
    ~Andie~

    Wife to Bryan (BadgerMan) for 14 years

    Mom to Elizabeth (7.5), non-D

    And Emily (11.5) diagnosed 5/06;
    Pumping Cozmore 1800; Cleo 90 and Cozmonitor
    and using Navigator CGMS

    Emily with the Jonas Brothers 7.15.08! <3

  4. #4

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    I have to be quick here, Im in the middle of finals week here at UC Davis, but I'll give you the "quick and dirty" version of what I know.

    Autoimmune diseases like diabetes run in families: If you have an autoimmune disease in your family, you are more likely to have relatives that develop t1d. However, its not like diseases like hemophilia or huntington's disease where its one gene, and if you have the gene you will develop it. There is a whole host of areas in the genome that could be a factor in developing an autoimmune disease: mutant T cells, specific antigens on specific types of proteins etc. So, the genetics here are that you would inherit the likelihood of autoimmune disease by inheriting the specific mutations that make you more likely to develop an autoimmune disease.

    The trigger is the important part: If you have the genetic predisposition (the array of genes and proteins that you have inherited that make you more likely to develop autoimmune disease), and you are exposed to the right trigger at the right time, then you develop it.
    Researchers have theorized tons of factors being triggers: infections may overstimulate your immune system and you are no longer able to distingish "self" from "non-self". So, colds, the flu, mono, chicken pox, you name it, could be a trigger.
    Other potential triggers that are being investigated include casein (protein in milk), decreased levels of vitamin D, not enough time spent breast feeding as a baby and leaky gut syndrome (where bits of food leaks through your gut wall and trigger your immune system to attack the food pieces, which may look like proteins similar to "self"proteins).

    Apart from my work with TrialNet, I have always been a supporter of research, and I would recommend getting involved if you can. Of course, it is up to you to decide whether the information will be valuable or harmful to your relatives. I personally recommend doing it, especially because a positive test does not mean a difinitive T1D diagnosis.
    Ok, back to studying!

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    Ok.. soo.. how many antibodies are there? I found 5 but the 64k antibody seemed to be mentioned only along with GAD in lot of study reports. I haven't seen yet where its clear they are the same like I did with the IA2/ICA-512.

    I've read and been told many times that a flu shot couldn't be a reason but isn't it feasible it could be a trigger? It is a killed virus so..? One main thing that bugs me so much about this is right after he got the flu shot he began developing symptoms. My DS rarely got ill and if he did he would be over it in a day or two unlike my oldest who would take a week or more.

    Now I'm no scientist here but it just seems to me that a T1 child popping up in a family who has never had T1 is quite off-base. I just dont understand how suddenly its there. I know.. triggers.. So why not triggers in the ancestors? Why now? My DH 4th great relative had T1 on his fathers side and nothing on his mothers side. So I suppose thats it. Geez though.. with those odds wheres my freaking lottery ticket. Ya know!?

    It just wont ever make sense to me. Thanks for answering my questions. Feel free anytime to pop in with some sort of straw that I.. we.. can grasp.

    T


    Samuel
    b.06/23/06, VSD, clear by 1 y.o.,
    01/28/08 DX @ 19 mths old, antibodies; mIAA, IA2, ICA512 and GAD65,
    09/15/08 Animas *Ping* :, Insets
    04/10/09 Dexcom
    03/29/10 Celiac

    James
    b.11/18/04 non-d
    05/20/08, Positive antibodies; mIAA, IA2, and ICA512



    Got Facebook? FR me @ https://www.facebook.com/enragedbliss
    or Tracie Fenske McClelland
    Be sure to mention you are from CWD so I can put you on my CWD friends list!

    *May the God of your choice bless you*

  6. #6

    Default Sorry for the scientific jargon...

    I've been doing some research on pubmed, it looks like specific infections have been associated with developing T1D.
    THis is from an article called "autoimmune disease and vaccinations" in the European journal of Dermatology (I know, weird source, but lots of skin conditions are autoimmune) THis section specifically deals with T1D:

    "Several experimental data have suggested that vaccination might exert a protecting or aggravating effect on the occurrence of diabetes, depending on the timing of vaccination. Classen [22] hypothesized that several vaccines administered at birth can decrease the risk of developing diabetes mellitus whereas primary vaccination after 2 months of age increased the risk of diabetes " " there was no increased risk of type 1 diabetes with any of the routinely administered childhood vaccines. The risk of diabetes was not different between children vaccinated at birth with the hepatitis B vaccine and those who received their first dose at 2 months of age or later, suggesting that the timing of vaccination did not influence the likelihood of developing diabetes. Finally, a case control study of 317 children who had a first-degree family member with type 1 diabetes found no significant association between the development of β-cell autoimmunity and exposure to a number of vaccines, and no effect of the timing of exposure [30].
    Most of the debate focused on a possibly increased risk in the incidence of type 1 diabetes mellitus that was temporally associated with the nationwide introduction of haemophilus influenzae type b (Hib) vaccine in Finland. However, a large 10-year follow-up study of over 110,000 Finnish children who participated in a clinical trial of Hib vaccine did not evidence any increased risk of diabetes in children first vaccinated at the age of 24 months as compared to a cohort of children born in the preceding 24 months before the vaccination period [31]. Classen and Classen [32] subsequently questioned the way the data had been analyzed. Their own analysis suggested an increase in the cumulative incidence of diabetes in children first vaccinated at 3 months of age who received four doses of the vaccine as compared to unvaccinated children. They also found that cases clustered between 36 and 48 months after immunization. Another 10-year follow-up study performed in children from the United States failed to identify an increased risk of diabetes after Hib vaccination [33]. A recent study still suggests that Hib vaccine might be a risk factor in the induction of islet cell and glutamic acid decarboxylase autoantibodies measured at one year of age [34]. The authors proposed that this vaccine produced an unspecific stimulatory polyclonal effect, which might be of clinical importance in the presence of other factors stimulating β-cell autoimmunity.
    Although additional data regarding the effects of Hib vaccine are required to clarify this issue, there is no clear evidence that vaccines are associated with an increased risk of diabetes, whatever the timing of vaccination and including children with a familial history of diabetes."

    So basically: some studies indicate that yes, vaccines do, others indicate that no, vaccines don't, but the consensus is that more research needs to be done. The vaccines involved here are: "normal childhood vaccines", HepB, and Hib (influenza).

    So if your doc says "no way the flu vaccine could have cause it" he or she ist trusting the results that indicate that it doesn't, without acknowledging that more research needs to be done.

  7. #7

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    So the people that are identified as having the antibodies in the TrialNet studies and go on to the next phases of testing, they have the predisposition for diabetes, right? Could it be said that those people just havent experienced the trigger yet?
    Jill

    Wife to Steve
    Mom to
    Dakota-16
    Hunter-14
    and
    Kylee-12~diagnosed 11/5/07 using Novolog and Lantus and CGMing with Dexcom

  8. #8
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    Quote Originally Posted by kyleesmom View Post
    So the people that are identified as having the antibodies in the TrialNet studies and go on to the next phases of testing, they have the predisposition for diabetes, right? Could it be said that those people just havent experienced the trigger yet?
    That is exactly the way I think of it!
    ~Rachael~
    I was dxd October 8,1998 @ 7 years old
    pumping since 2003 with minimed 511,712, 722
    Tslim pump 6/5/2013
    Dexcom G4 10/4/2013

  9. #9
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    Here is a list of auto immune and poss auto immune diseases...Are you sure no one inNote: Because the specific causes of many diseases are unknown, there is debate among scientists about whether some of these are truly autoimmune diseases. Your own doctor may classify some of these diseases differently.

    Alopecia areata--A disorder in which the immune system attacks the hair follicles, causing loss of hair on the scalp, face, and other parts of the body.

    Ankylosing spondylitis--A rheumatic disease that causes inflamed joints in the spine and sacroiliac (the joints that connect the spine and the pelvis) and, in some people, inflamed eyes and heart valves.

    Arthritis--A general term for more than 100 different diseases that affect the joints. Many forms of arthritis and related conditions are believed to have an autoimmune component.

    Autoimmune hemolytic anemia--A condition in which immune system proteins attack the red blood cells, resulting in fewer of these oxygen-transporting cells.

    Autoimmune hepatitis--A disease in which the body's immune system attacks liver cells, causing inflammation. If not stopped, inflammation can lead to cirrhosis (scarring and hardening) of the liver and eventually liver failure.

    Behçet's disease--A condition characterized by sores in the mouth and on the genitals and by inflammation in parts of the eye. In some people, the disease also results in inflammation of the joints, digestive tract, brain, and spinal cord.

    Crohn's disease--An inflammatory disease of the small intestine or colon that causes diarrhea, cramps, and excessive weight loss.

    Dermatomyositis--A rare autoimmune disease that causes patchy red rashes around the knuckles, eyes, and other parts of the body along with chronic inflammation of the muscles. It may occur along with other autoimmune diseases such as rheumatoid arthritis or systemic lupus erythematosus.

    Diabetes mellitus, type 1--A condition in which the immune system destroys insulin-producing cells of the pancreas, making it impossible for the body to use glucose (blood sugar) for energy. Type 1 diabetes usually occurs in children and young adults.

    Glomerulonephritis--Inflammation of the kidney's tiny filtering units, which in severe cases can lead to kidney failure.

    Graves' disease--An autoimmune disease of the thyroid gland that results in the overproduction of thyroid hormone. This causes such symptoms as nervousness, heat intolerance, heart palpitations, and unexplained weight loss.

    Guillain-Barré syndrome--A disorder in which the body's immune system attacks part of the nervous system, leading to numb, weak limbs and, in severe cases, paralysis.

    Inflammatory bowel disease--The general name for diseases that cause inflammation in the intestine, the most common of which are ulcerative colitis and Crohn's disease.

    Lupus nephritis--Damaging inflammation of the kidneys that can occur in people with lupus. If not controlled, it may lead to total kidney failure.

    Multiple sclerosis--A disease in which the immune system attacks the protective coating called myelin around the nerves. The damage affects the brain and/or spinal cord and interferes with the nerve pathways, causing muscular weakness, loss of coordination, and visual and speech problems.

    Myasthenia gravis--A disease in which the immune system attacks the nerves and muscles in the neck, causing weakness and problems with seeing, chewing, and/or talking.

    Myocarditis--Inflamed and degenerating muscle tissue of the heart that can cause chest pain and shortness of breath. This can lead to congestive heart failure.

    Pemphigus/pemphigoid--An autoimmune disease of the skin characterized by itching and blisters.

    Pernicious anemia--A deficiency of the oxygen-carrying red blood cells that often occurs in people with autoimmune diseases of the thyroid gland.

    Polyarteritis nodosa--An autoimmune disease that causes inflammation of the small and medium-sized arteries. This leads to problems in the muscles, joints, intestines, nerves, kidney, and skin.

    Polymyositis--A rare autoimmune disease characterized by inflamed and tender muscles throughout the body, particularly those of the shoulder and hip girdles.

    Primary biliary cirrhosis--A disease that slowly destroys the bile ducts in the liver. When the ducts are damaged, bile (a substance that helps digest fat) builds up in the liver and damages liver tissue.

    Psoriasis--A chronic skin disease that occurs when cells in the outer layer of the skin reproduce faster than normal and pile up on the skin's surface. This results in scaling and inflammation. An estimated 10 to 30 percent of people with psoriasis develop an associated arthritis called psoriatic arthritis.

    Rheumatic fever--A disease that can occur following untreated streptococcus (strep) infection. It most often affects children, causing painful, inflamed joints and, in some cases, permanent damage to heart valves.

    Rheumatoid arthritis--A disease in which the immune system is believed to attack the linings of the joints. This results in joint pain, stiffness, swelling, and destruction.

    Sarcoidosis--A disease characterized by granulomas (small growths of blood vessels, cells, and connective tissue) that can lead to problems in the skin, lungs, eyes, joints, and muscles.

    Scleroderma--An autoimmune disease characterized by abnormal growth of connective tissue in the skin and blood vessels. In more severe forms, connective tissue can build up in the kidneys, lungs, heart, and gastrointestinal tract, leading in some cases to organ failure.

    Sjögren's syndrome--A condition in which the immune system targets the body's moisture-producing glands, leading to dryness of the eyes, mouth, and other body tissues.

    Systemic lupus erythematosus--An autoimmune disease, primarily of young women, that can affect many parts of the body, including the joints, skin, kidneys, heart, lungs, blood vessels, and brain.

    Thyroiditis--An inflammation of the thyroid gland that causes the gland to become underactive. This results in symptoms such as fatigue, weakness, weight gain, cold intolerance, and muscle aches.

    Ulcerative colitis--A disease that causes ulcers in the top layers of the lining of the large intestine. This leads to abdominal pain and diarrhea.

    Uveitis--The inflammation of structures of the inner eye, including the iris (the colored tissue that holds the lens of the eye) and the choroid plexus (a network of blood vessels around the eyeball). Uveitis occurs with some rheumatic diseases, including ankylosing spondylitis and juvenile rheumatoid arthritis.

    Vitiligo--A disorder in which the immune system destroys pigment-making cells called melanocytes. This results in white patches of skin on different parts of the body.

    Wegener's granulomatosis--An autoimmune disease that damages the small and medium-sized blood vessels throughout the body, resulting in disease in the lungs, upper respiratory tract, and kidneys
    your family history had any of these? It doesn't have to be type 1 to make it a risk factor...For example, my brother had thyroid issues as a kid...


    Seth 17, dx'd at 7 (shots for most of 9+ years, has been on the Omnipod/Apidra for 1 year)

    Always always always....Trust your gut!:

  10. #10
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    None of those listed are in either side of our family. We have your basic heart and various cancer issues, glaucoma.. What I find interesting is that Trialnet is doing this research and including only parents, siblings and 1st cousins. Why not more family members? Why don't they build a family 'disease' profile going back to grandparents or further and include that on their research. I think that if we are waiting for the 'trigger' then that trigger can stay well out of sight for many generations and then pop up like now. By going back as far as possible and building that profile might help their quest in finding this trigger quicker.

    Breanne, do you know the names and how many antibodies there are?


    Samuel
    b.06/23/06, VSD, clear by 1 y.o.,
    01/28/08 DX @ 19 mths old, antibodies; mIAA, IA2, ICA512 and GAD65,
    09/15/08 Animas *Ping* :, Insets
    04/10/09 Dexcom
    03/29/10 Celiac

    James
    b.11/18/04 non-d
    05/20/08, Positive antibodies; mIAA, IA2, and ICA512



    Got Facebook? FR me @ https://www.facebook.com/enragedbliss
    or Tracie Fenske McClelland
    Be sure to mention you are from CWD so I can put you on my CWD friends list!

    *May the God of your choice bless you*

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