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Hi all,

I recently came across a paper from (sent to me by a doctor who prescribes to this service for medical professionals). Excerpt below. I was really surprised about one thing in particular: that getting type 1 is not a sudden process, but in fact "usually progresses over many months or years". In other words, your symptoms may not manifest until *years* after it was triggered in your body. I had previously thought, perhaps out of my own ignorance, that the symptoms would manifest a matter of weeks after whatever triggered the disease - be it a virus or something else in the environment, which probably triggered a genetic predisposition.

Is this long latent period news to anyone else?


Pathogenesis of type 1 diabetes mellitus
David K McCulloch, MD
Section Editor
Irl B Hirsch, MD
Deputy Editor
Jean E Mulder, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2012. | This topic last updated: Aug 09, 2012.
INTRODUCTION — Type 1A diabetes mellitus results from autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans [1]. This process occurs in genetically susceptible subjects, is probably triggered by one or more environmental agents, and usually progresses over many months or years during which the subject is asymptomatic and euglycemic. Thus, genetic markers for type 1A diabetes are present from birth, immune markers are detectable after the onset of the autoimmune process, and metabolic markers can be detected with sensitive tests once enough ß-cell damage has occurred, but before the onset of symptomatic hyperglycemia [2]. This long latent period is a reflection of the large number of functioning beta cells that must be lost before hyperglycemia occurs (figure 1). Type 1B diabetes mellitus refers to non-autoimmune islet destruction (Type 1B diabetes). (See "Classification of diabetes mellitus and genetic diabetic syndromes".)

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Would you email me this whole article? abellsam at hotmail ( you'd have to properly format that into a proper email address)

This is not new news.... it is fairly well accepted in the scientific literature.

The pancreas has a large number beta cells -more than you need - and an extremely large fraction have to be destroyed before metabolic control fails and BG starts to become abnormal. The estimate is more than 80% have to be destroyed before control fails. The autoimmune process can "simmer" for some time before this happens. Auto-antibodies can be detected in people developing type 1 while their BG is still normal and in control.... no one ever thinks to screen though, except in the case where there are a number of T1s in a family.

When it does fail, though ,the results are dramatic and fast.

The latency period can be as short as a few months or as long as a decade. That is also why there is some hope of arresting the process and/or restoring function.

Another reference is the New England Journal of Medicine, June 23, 2005.Insulin Needs after CD3-Antibody Therapy in New-Onset Type 1 Diabetes

THe authors say in an interview :

The new therapy relies on the fact that people with type 1 diabetes do not lose their ability to make insulin all at once. "Diabetes is preceded by an incubation period that can be as short as months or as long as over a decade," Insel explained. "Overt diabetes does not occur until the beta cell reserves fall by about 80 percent."

The researchers sought to intervene before reserves hit that 80 percent mark. Eighty patients with new-onset type 1 diabetes were randomly assigned to receive either a new antibody or a placebo for six consecutive days.

The antibody was directed against CD3 (ChAglyCD3), a molecule on the surface of T-cells. The antibody does not actually kill the T-cells, Insel explained, but rather "resets" them.

People who received the antibody had higher residual beta-cell function than people who received the placebo. Although no participants were able to give up insulin altogether, people in the antibody group needed less insulin, while people in the placebo group needed increasing amounts of the hormone as time wore on.

The antibody also worked better on people who started with a higher level of beta-cell function (50 percent or more).

There was one notable side effect: the antibody produced flu-like symptoms and symptoms of Epstein-Barr viral mononucleosis.

And, the study's lead author pointed out, the research only involved adults.

Thanks, good to know. Obviously I hadn't quite groked the latency period before.

The idea of a long latent period was the belief at least 20-30 years ago, and in fact was stated to me when I went to the internist and said, "I have diabetes." It was believed that neuropathies and retinopathies had gotten a head start because of the long genesis.
We believed that within 5 years a new diabetic would (not might) start having complications!
We did not have Type 1A and 1B back then, however.
The ability to be certain by genetic and immune markers is what is new.

I found a graph that I think explains this theory pretty well. It is part of "Diabetes Melitus: A fundamental and Clinical Text, 3rd Edition" (2004)(chapter 31):

The graph I was citing is here: The graph is vauge in terms of length of time, but this is the general premise of the Type 1 Diabetes Trialnet research where researchers test close relative of a Type 1 for specific auto-antibodies.

Further, this graph ( shows how long individuals took to progress onto actually T1D. 2 auto-antibodies took 7-10 years for half the participants to be diagnosed while the other autoantibody was only losely directly related to T1D.

Thanks for the info.




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