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[edit] newly refactored; requires major work

This article was just recently extracted from the general diabetes article (see the talk page and history there) and is currently inadequate as a standalone article. Missing are discussions of potential cures, vaccines, other possible causes of auto-immune reaction (eg, German measles), etc.

As it now stands this article needs much work. I'll try to remember to figure out how to install a "stub" notice. ww 17:46, 14 December 2005 (UTC)

[edit] Type 1 incidence in adults

This entry states "the adult incidence of Type 1 is similar to that for children[1], which is why 'Type I' is the preferred term." While this goes against my understanding, I was open to reading the reference. However, the reference does not substantiate this sentence at all. The linked abstract tells us that the study was conducted of a Mediterranean population--yet, I know the incidence of type 1 diabetes is much higher in northern European populations. Further, the abstract states only that the incidence of the onset of type 1 in 15 to 29 year-olds is similar (albeit slightly greater) to the incidence among adults in their thirties. The highest incidence is in the 0 to 15 year grouping. In sum, I have not removed the line, but I think it should be. I might add, the studies methodology of defining who is afflicted with type 1 is, in my view, questionable. While c-peptide levels indicate insulin production as oppposed to insulin resistance, the article somehow seems to ignore the commonly accepted notion that insulin production will often cease in longterm cases of type 2. This does not, however, mean that there is an auto-immune attack of the beta cells that wipes out insulin production in a relatively short span of time as is the case in type 1. But anyway...

In fact, the adult incidence of Type 1 diabetes is far greater than the childhood incidence of Type 1 diabetes. It has been documented for at least 70 years that new-onset Type 1 diabetes is more commonly seen in adults, not children. In 1934 Dr. Elliot Joslin noted that the incidence of diabetes in lean individuals was relatively constant in each decade of life, but that diabetes in the obese was related to older age. A book published in 1958 (“How to Live With Diabetes” by Henry Dolger, M.D. and Bernard Seeman) that states that “[Type 1] diabetes is almost three times more frequent among young adults than among youngsters.” Today, with antibody testing (glutamic acid decarboxylase antibodies (GADA), islet cell antibodies (ICA), and insulinoma-associated (IA-2) autoantibodies), the same statement is proven true. A new book, “Type 1 Diabetes in Adults: Principles and Practice” (Informa Healthcare, 2008) says that adult-onset autoimmune diabetes is two to three times more common than classic childhood onset autoimmune diabetes (p. 27).

The CDC’s most current information on the prevalence and incidence of Type 1 diabetes comes from Diabetes in America, Chapter 3, “Prevalence and Incidence of Insulin-Dependent Diabetes” (Diabetes in America, Second Edition, 1995). Often people who use that reference as a source of incidence statistics state that there are about 30,000 new cases of Type 1 diabetes each year and that half of those cases are children. In fact, that source states that children (<20 years of age) account for 13,171 cases and adults (>20 years of age) account for 16,542 cases, for a total of 29,713 new cases of Type 1 diabetes per year, 56% seen in adults. Furthermore, that source states that there is an “unknown number of adults identified as NIDDM (non-insulin dependent diabetes mellitus, now called Type 2 diabetes) who have slowly progressive IDDM (insulin dependent diabetes mellitus, now called Type 1 diabetes). In summary, according to the CDC, of those new onset Type 1 diabetics who are correctly diagnosed, 56% are adults, and an unknown number of new onset Type 1 diabetics have been misdiagnosed as having Type 2 diabetes and thus the majority of new onset Type 1 diabetes is seen in adults. Redyoga (talk) 22:16, 6 October 2009 (UTC)

[edit] milk

moved here from Talk:Diabetes mellitus

I'm not sure why the cow's milk issue is back, it seems to be part of a larger debate over diet in general. Recent study (2006):

Recent (2005) review article:

2004 review article:

Older work:

--JWSchmidt 14:02, 22 January 2006 (UTC)


This is only a controversial hypothesis and should be presented as such. Here are some sources:

  • Vaarala O. Is type 1 diabetes a disease of the gut immune system triggered by cow's milk insulin? Adv Exp Med Biol. 2005;569:151-6. Review.
  • Truswell AS. The A2 milk case: a critical review. Eur J Clin Nutr. 2005 May;59(5):623-31. Review.
  • Persaud DR, Barranco-Mendoza A. Bovine serum albumin and insulin-dependent diabetes mellitus; is cow's milk still a possible toxicological causative agent of diabetes? Food Chem Toxicol. 2004 May;42(5):707-14. Review.
  • Wasmuth HE, Kolb H. Cow's milk and immune-mediated diabetes. Proc Nutr Soc 2000 Nov;59(4):573-9. Review.
  • Truswell AS. The A2 milk case: a critical review. Eur J Clin Nutr. 2005 May;59(5):623-31. Review. Andreas 14:25, 22 January 2006 (UTC)

I'm not an expert on this; however, from experience with diabetics I have found that cow's milk is regarded as to be avoided. It is not cow's milk that directly causes the diabetes, but it changes the environment inside the human body to allow for such symptoms as diabetes (and other non-related cases). This is more common(?) in those that only show diabetic symptoms but do not have a case of diabetes. Some of the sources above seem to hint at that. Instead of a view directed at cow's milk, I suggest a view directed at diabetic symptoms with those that are lactose intollerant and if there is any equality with those that are not lactose intollerant. — Dzonatas 15:46, 28 January 2006 (UTC)

  • I looked into the issue based on the RFC, the evidence is more on the side of not than is. Thatcher131 21:13, 14 February 2006 (UTC)
  • I added some comments to the main page describing the theory and recent findings, all with citations from the medical literature. The hypothesis relates to causation--the theory is that either the mother's consumption of cow's milk proteins leads to antibodies that are passed to the infant in breast milk; or that early introduction of cows' milk proteins to the infant's diet leads to the production of damagin antibodies. It is an interesting theory, and the fact that longer breastfeeding reduces the risk of diabetes is intriguing, but there are many possibilities and the antibody theory isn't holding up too well. Thatcher131 01:27, 19 February 2006 (UTC)
  • Regarding cow's milk consumption in people with diabetes (i.e. avoid as part of disease management) I don't know anything about that, though I could investigate; but any discussion in the article needs to separate issue of disease management from issue of possible causes. Thatcher131 01:27, 19 February 2006 (UTC)

[edit] Immunosuppression?

The section of Immunosuppression that has a brief description of Faustman's work, in my opinion is not correct.. Immunosuppression refers to supressing the entire immune system, whereas Denise Faustman's work was directed at stopping the specific attack on the beta cells, while not suppressing or changing any other function of the immune system --Nirvana- 12:09, 11 March 2006 (UTC)

  • Dr. Faustman's hypothesis is that autoimmune T cells are more susceptible to induction of apoptosis by TNF-alpha than hetero-immune T cells. I know that's a little too techie for many readers, I tried to do better job of explaining it in her personal article, the first version of which seemed to have been written by someone lacking a research background. So what she is doing is not immunosuppression in the same way that you would suppress the immune system in a transplant patient, for example. I have tried to clarify a bit.Thatcher131 13:27, 11 March 2006 (UTC)

[edit] Immune Tolerance Network

The ITN link seems to be getting ping-ponged in and out of the article. Proposal for consideration: while ITN does feature information on current clinical trials on IDDM, its scope goes well beyond just the one autoimmune disease. We can try to keep it out of articles on individual diseases and direct it to more general articles. Rather than add it here, I'll add it to the Autoimmunity article. Agreed? Jbarin 03:08, 12 December 2006 (UTC)

[edit] Odd content -- should it stay?

Large content devoted to a cow's milk hypothesis which ends up susggesting there may be no there, there. Should this much space be devoted here to what seems to be speculation?

Additionally, there is a paragraph -- perhaps related -- about vitamin D and Type 1. Again, should there be this much mention?

Perhaps a section on cause speculation instead? ww 23:17, 24 February 2007 (UTC)

No small part of the problem is that the general etiology of autoimmune diseases are largely speculative. Specific exemplars throughout these pathologies are largely circumstantial. To put it another way, it's hard to sort out the fringe, when even the more "mainstream" theories are a little fringe themselves. Novel (and often marginally evidenced) theories as to the underlying causes of autoimmune disease are frequent, cyclical and given to scientific fashion. I do agree that the studies listed do not represent anything resembling scientific consensus, and are definitely given more verbiage than they merit for Wiki purposes. Jbarin 09:38, 30 April 2007 (UTC)

I agree completely. These are ongoing theories under investigation which detract from the credibality of the overall article. I would call it non-enclyclopedic. The fact that they are being studied is not nearly as interesting as when a conclusion from a peer reviewed medical journal might become available. So go ahead and change it. Beware however, that the "owners' of this article (who are admins) are likely to resist. mbbradford 20:07, 3 May 2007 (UTC)

For what consolation it's worth, it seems to be a unifying commonality among all the autoimmune disease topics -- that poorly conclusive theories, well-outside of scientific consensus are what's being offered. Consensus throughout many of these diseases, is that there's no consensus. A lot of these disease systems a great deal of pathophysiologic speculation in the scientific literature -- my point is that what we do get to see around here is exceptionally unrepresentative. Jbarin 07:46, 8 May 2007 (UTC)

[edit] Potential Cure?

http://www.timesonline.co.uk/tol/life_and_style/health/article1637528.ece

According to the above article, some fifteen people were able to produce insulin naturally when their immune systems were temporarily weakened via chemotherapy to halt beta cell death, and then injected with their own stem cells.

added original reference  Andreas  (T) 12:36, 11 April 2007 (UTC)


"Cure" is pretty loaded. But that's a more general, tangential problem with disease articles. Similar autologous hematopoietic stem cell transplantation strategies have undergone trials in other autoimmune diseases, perhaps most notably, multiple sclerosis. Data from Roland Martin's group[1] at NIH in MS patients suggests that while autologous HSC largely "resets" the immune system, as intended, some patients appear to retain T cell clonalities overrepresented prior to the "reboot". In essence, the underlying etiology of T1D (particularly genetic components) may not be reliably therapeutically altered. Jbarin 09:31, 30 April 2007 (UTC)

What about Chili Peppers? —Preceding unsigned comment added by 69.22.71.123 (talk) 17:16, 30 October 2007 (UTC)

[edit] References Needed

A lot of statements need valid references. I standardized the ones that were already there. When you add more,use this tool http://diberri.dyndns.org/wikipedia/templates Be sure to check the add ref tag box. Demantos 19:48, 4 June 2007 (UTC)

[edit] Aspirin therapy

Single reports of a finding rarely make for medical consensus (i.e. the majority viewpoint), indeed if no subsequent research publised in reliable sources then not only a minority opinion, but a trivial minority. Under WP:NPOV, trivial opinions should not be included at all. I leave below the original paragraph from the article:

In about 1988 a russian doctor named B. I. Bleskin experimented aspirin on young diabetics, whose diabetes had just come. He gave the patients aspirin and treated them with electrophoresis. With the elektrophoresis he guided the aspirin to the patient´s pancreas. After 15-20 treatments of 10 minutes each the patients´ insulin producement came back and their blood sugar dropped. The condition of this treatment is that the patient is young.Suomen Kuvalehti, september 1988, page 62

The citation provided can not easily be quickly verified online, but a search of PubMed for the mentioned researcher does give just one original paper:

  • Bleskin BI, Asauliuk IK, Fominov AT (1983). "[Use of anti-inflammatory therapy in diabetes mellitus]" (in Russian). Klinicheskaia meditsina 61 (4): 73-5. PMID 6865295. 

Unfortunately no abstract and the original was in Russian anyway ! A search for anti-inflammatory and diabetes gave some intriguing papers to look at:

  • Tornvall G, Allgén LG (1980). "Acute effects of acetylsalicylic acid on blood glucose and insulin in non-insulin dependent diabetes". Acta endocrinologica. Supplementum 239: 6-8. PMID 7001843. 
  • Seino Y, Usami M, Nakahara H, et al (1982). "Effect of acetylsalicylic acid on blood glucose and glucose regulatory hormones in mild diabetes". Prostaglandins, leukotrienes, and medicine 8 (1): 49-53. PMID 7043491. 
  • Moloney F, Toomey S, Noone E, et al (2007). "Antidiabetic effects of cis-9, trans-11-conjugated linoleic acid may be mediated via anti-inflammatory effects in white adipose tissue". Diabetes 56 (3): 574-82. doi:10.2337/db06-0384. PMID 17327424. 

However these effects on glucose tolerance are temporary effects - the aspirin needs to be continued and no suggestion is made for permenant cure. Indeed one study found no effect:

  • Giugliano D, Luyckx AS, Lefebvre PJ (1980). "Effects of acetylsalicylic acid on blood glucose, plasma FFA, glycerol, 3-hydroxybutyrate, alanine, C-peptide, glucagon and growth hormone responses to arginine in insulin-dependent diabetics". Diabète & métabolisme 6 (1): 39-46. PMID 6989660.  - concludes "ASA treatment resulted in no significant changes in either basal or arginine-stimulated blood glucose"

As for claim Bleskin used electrophoresis to guide aspirin into a live patient's pancreas, sounds utter nonsense to me (electrophoresis used to separate out proteins on test media, not to electrocute real patients).

There are separate papers looking at anti-inflammatory effects at reducing complication of diabetes such as retinopathy (eg PMID 17259377) or reducing cardiovascular risks (eg PMID 17488145), but these are separate from curing/treating the diabetes itself. David Ruben Talk 18:53, 6 July 2007 (UTC)


Skele,
I edited the aspirin/diabetes paragraph, but only for historical reasons. Please consider that diabetes is one of the best researched diseases and that it is very improbable that an effective treatment has been fond that is not well-known to main stream medicine. I would strongly suggest to you that you follow the instructions given to you by your health care provider and do not experiment with treatments that have not been verified by the scientific community. That said, I would be curious to see what is written in the Russian article that I cited in the article, if you could get hold of it.  Andreas  (T) 19:22, 27 July 2007 (UTC)


I've removed the section on Aspirin. It's not a possible treatment that's recognised by the medical community as a whole, it seems to be restricted to a single paper published nearly 2 decades ago and it has been reposted several times, presumably by someone with a personal axe to grind. I don't see that it's in any way useful to a reader of this article, and only serves to create confusion. David-i98 (talk) 21:34, 24 December 2007 (UTC)

[edit] Islet Transplantation: Encapsulation?

Maybe I should call it plasticization. I've been looking online for a reference that could at least give me the researcher's name for the process, but have yet to find any success. Specifically, I read an article a decade ago about a researcher at University of Alberta who had developed an encapsulation process that would protect islet cells from immune system attack but would allow insulin response to glucose. The problem, as I recall, was the difficulty of producing enough encapsulated cells to make it an effective treatment. The cells would eventually be destroyed as the plastic coating would wear away, but at the time it seemed very promising as an alternative to immunosuppression. Since that time, I've seen things that would seem to be greater improvements on the technology like AmCyte[1], but I was hoping somebody could contribute a more knowledgeable summary of this as a subtopic of Islet Transplantation. AnthroGael 17:03, 30 October 2007 (UTC)

[edit] Vitamin D3

The article says: "Some suggest that Vitamin D3 (one of several related chemicals with Vitamin D activity) may be an important pathogenic factor in Type 1 diabetes independent of geographical latitude." Could a reference be supplied for this? If this is the source of the article sentence, then the suggestion that D3 may be harmful is misleading. robert2957 (talk) 13:00, 29 December 2007 (UTC)

[edit] Residual Beta Cell Mass at Onset

It is common wisdom that precipitation of clinical symptoms of Type 1 diabetes occurs when 80-95% of an individual's beta cells are destroyed. However, a recent paper suggests that the original data does not support this common wisdom [2]. A meta-analysis was applied to the data presented in these landmark studies of pancreata obtained from recent onset patients. The results of the meta-analysis suggest that the extent of reduction in beta cell mass at the onset of clinical symptoms is the result of a dynamic balance between insulin production capacity, which is proportional to beta cell mass, and insulin demand, which is proportional to body weight. This analysis revealed that in infants an 85% reduction, on average, corresponds to the onset of clinical symptoms of the disease. In contrast, as little as a 40% reduction in beta cell mass is sufficient to precipitate clinical symptoms in a 20-year old individual. D-klinke (talk) 21:34, 5 January 2008 (UTC)

[edit] Cause

In the article's introductory paragraph, it states Type 1 diabetes is an autoimmune disease that results in the permanent destruction of insulin producing beta cells of the pancreas.

In the Cure section, it states, Diabetes type 1 is caused by the non-existence of a sufficient number of beta cells in the body.

My understanding of the above two statements is that the first statement says that the non-existence of beta cells is a result of the disease, whereas the second statement says that the non-existence of beta cells is a cause of the disease. This is a contradiction. I am not a medical expert, but surely the first statement is correct and the second statement is incorrect. If that is true, a cure for diabetes mellitus type 1 should be treating the immune system and not only "causing a maintenance or restoration of the endogenous ability of the body to produce insulin in response to the level of blood glucose". If this is also true, most of the Cure section should be moved to the Treatment section. Coyets (talk) 18:00, 13 January 2008 (UTC)

Type 1 is a serious (and formerly universally fatal) problem because patients metabolisms are deranged. The derangement is the result of no (or almost none) insulin. So in some sense this is the cause. But in another context, the cause of the lost insulin is the death of beta cells, and that is caused by an auto-immune reaction. So the cause is any of these, depending on your desired context. Of course, what may be the most interesting issue is the cause of the tendency toward vulnerability to the auto-immune reaction. Most people don't have it, so it's probably genetic and some genes (having to do with HLA types) have been associated with the vulnerability. Just how that works is not so clear. So the ultimate cause is still unknown.
This may clarify some of the confusion. ww (talk) 06:45, 14 January 2008 (UTC)
As I have been told; one of the causes is that a viral infection at the pancreas stops the insulin production and well after a while the pancreas stops. Skele (talk) 17:26, 29 January 2008 (UTC)
Ought to read things more frequently. This is actually not so. The pancreas (taken as whole) has several functions. The bulk of it is a ducted gland providing digestive chemicals to the intestines. Some blobs of cells throughout the pancreas (why are they there and not, say in the liver? Who knows?) are responsible for several other functions. They are jointly a complex ductless gland (ie, endocrine). One type of cells in these clumps (the alpha cells) produce glucagon, another type produces a hormone involved indigestion somehow, and the best known type (beta cells) produces insulin. The auto-immune attack mounted by the body in Type 1 diabetes is characteristically aimed at the beta cells. Ducted gland function continues, as does glucagon production (though in many Type 1s it fails after several years for reasons that remain unclear), etc. The problem of what you've been told is the implicit unstated assumption that the pancreas does only one thing. It doesn't. It's more flexible than that. ww (talk) 16:09, 29 March 2009 (UTC)

[edit] CURE

I have once already written about a cure that a russian doctor B. I. Bleskin in 1988 developed, BUT then someone deleted it. The cure involved electrophoresis and aspirin. Why was it deleted?Skele (talk) 19:22, 16 January 2008 (UTC)

No credible references. ww (talk) 22:10, 16 January 2008 (UTC)
I have/had a perfect reference but why was it deleted. Skele (talk) 21:21, 23 January 2008 (UTC)


I think it would be well worthwhile to get in on that test subject thing.. if it will Cure me Then I think it would be well worth it.. Diabetes has no discression, it picks on the rich and the poor.. I happen to be poor, Can't afford insulin. It will kill me if I can't get it cured. I am on Humalog and Lantus at this current time, and I can barely afford them. Please Someone come up with a cure.. I am literally dying here! —Preceding unsigned comment added by 75.27.227.131 (talk) 13:18, 22 September 2008 (UTC)

[edit] Dentistry and Diabetes: The Oral Systemic Connection

Scientific data has now proven that there is a direct link between oral health (how healthy your teeth and gums are) and total body health.

 This is vitally important for the diabetic, who is TWICE as likely to have gum and bone disease as non-diabetics.   In fact, a recent report from the U.S. Surgeon General outlines the direct connection between gum and bone disease and dental care for diabetics.  
 The worst part is, diabetes can aggravate, worsen and even accelerate gum and bone disease….which in turn, makes it more difficult to control blood sugar levels. If you teeth and gums are in bad shape, they can make your diabetes worse, and if you diabetes is out of control, it can accelerate bone and gum disease, leaving your mouth a wreck. 

To top it all off, gum disease or Gingivitis, if left untreated and uncontrolled, progresses to ‘periodontitis’ which can involve chronic infection, tooth loss, bone loss as well as make it almost impossible to control your blood sugar levels.

Anyone with diabetes interested in learning more can request information at [3] —Preceding unsigned comment added by Cm3208708 (talkcontribs) 19:15, 31 July 2008 (UTC)

[edit] Lancet

Seminar specifically about the effects by DM1 on the heart: doi:10.1016/S0140-6736(08)60767-9 JFW | T@lk 21:45, 27 August 2008 (UTC)

[edit] ??

hey —Preceding unsigned comment added by 24.185.203.201 (talk) 05:54, 9 January 2009 (UTC)

[edit] Living Cell company in NZ

An editor has made two edits mentioning this company by name as the exemplar of the encapsulated beta cell approach to evading immune system attack. I seem to recall at least two other approaches have been (being?) investigated experimentally, so I'm not sure this is actually a good exemplar. In any case, the edits together seem somewhat POV and commercially favoring, so I'm somewhat dubious. Comments? ww (talk) 16:23, 9 March 2009 (UTC)

[edit] Richard Lane - the hope for a cure

Who remembers how, by 2005, a diabetic named Richard Lane was treated with cell transplantation and this formed a cure for his diabetes? All right,I know that most diabetics have to take insulin, at least if they are Type One, but maybe this story would at least add some touches of hope to this article. ACEOREVIVED (talk) 20:29, 24 June 2009 (UTC)

[edit] &nbsp

Re: User Terrillja's (Reverted good faith edits by Afaprof01; Adding &nbsp for every space maes the article unreadble to the point of being uneditable. If you have a reason to do this, explain it on the talkpage.

&nbsp stands for "non-breaking space." The concept appears in MS Word and all other major word/text processors. It does not appear for "every space." It connects the word "type" with the numerals "1" and "2" so that the 1 or 2 cannot be separated from the word "type" by the software, especially at a line break. Without it, there will be occasions where the "1" or "2" starts a new line.

It is used in other diabetes articles on Wiki. It does not make the articles unreadable or uneditable. If it did, it would not be included as a Wikipedia command. Please undo your RV. Thank you. Afaprof01 (talk) 04:07, 6 July 2009 (UTC)

For what it's worth, I agree that it should be a non-breaking space, but putting the &nbsp; code in there does make it awkward to edit. (Personally, I usually hyphenate it, but that's probably grammatically incorrect).
Would it make sense to create a template, so {{Type1}} would be interpreted as Type&nbsp;1?. I've seen this done on other articles, particularly ones on the New York Subway (see this one, where a template replaces a long, cumbersome piped link). It would be a change in how we edit diabetes articles, but readability/editibility wouldn't be compromised. I'm not so skilled in templates, so if we decided to do this, I'd ask someone's assistance. -Sme3 (talk) 12:57, 6 July 2009 (UTC)

[edit] Many type 2 diabetics continue to produce insulin internally...

Surely if you no longer make insulin, you have Type 1 diabetes? So all Type 2 diabetics still make insulin, surely?80.47.181.212 (talk) 22:09, 16 September 2009 (UTC)

[edit] Needs to be split

Most of this page pertains to current / ongoing research and not DM type 1.Doc James (talk · contribs · email) 21:07, 3 November 2009 (UTC)

I agree. The sections about cure and prevention could be split to another article and only summarized in this one. See also the discussion above.Sjö (talk) 09:49, 14 November 2009 (UTC)



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