Talk:Type 1 diabetes/Archive 1

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)

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):

• Absence of breast-feeding is associated with the risk of type 1 diabetes: a case-control study in a population with rapidly increasing incidence

Recent (2005) review article:

• Is type 1 diabetes a disease of the gut immune system triggered by cow's milk insulin?

2004 review article:

• Bovine serum albumin and insulin-dependent diabetes mellitus; is cow's milk still a possible toxicological causative agent of diabetes?

Older work:

• Nutritional risk predictors of beta cell autoimmunity and type 1 diabetes at a young age
• Cow's milk and type 1 diabetes: the real debate is about mucosal immune function
• Lack of association between duration of breast-feeding or introduction of cow's milk and development of islet autoimmunity
• Nutritional factors and worldwide incidence of childhood type 1 diabetes
  

--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)

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)

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)

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)

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)

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)

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 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)

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]". Klinicheskaia meditsina (in Russian). 61 (4): 73–5. PMID 6865295.{{cite journal}}: CS1 maint: multiple names: authors list (link)

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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
• 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)

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.{{cite journal}}: CS1 maint: multiple names: authors list (link) - 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)

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)

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)

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 (talk • contribs) 19:15, 31 July 2008 (UTC)

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)

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)

??

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

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)

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)

&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   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 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)

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)

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)

Have moved much of it to the management page. Doc James (talk · contribs · email) 11:34, 9 December 2009 (UTC)

Preventive measures / dietary influences

The article currently reads: "There is no preventive measure against developing type 1 diabetes." but this is not strictly true. There is no firmly established preventive measure against developing type 1 diabetes but there is some evidence from animal studies that omitting wheat from the diet could possibly prevent it. There's a difference between something not being known and not existing--the sentence as-is implies that it is known that none exists. Rather, it is not firmly known that any exists but there is some evidence that it may be possible to prevent diabetes through change in diet (though again, it's mostly unknown territory).

See: [4]. This article references "growing evidence that dietary components may be involved in the disease process resulting in clinical type 1 diabetes by intestinal pathways". I'm removing the sentence and adding material about the dietary connection. Cazort (talk) 23:23, 25 March 2010 (UTC)

There are many possible factors that might contribute to the development of diabetes. As long as there is only some evidence these should be mentioned briefly, but not as prevention. Also, it is WP:UNDUE to single out wheat, at least until more research has been done that establishes a firm connection. The statement that there is no prevention (today) is in my opinion an important fact that should remain in the article.Sjö (talk) 07:37, 26 March 2010 (UTC)

I think debate here is healthy, but I'm not satisfied with your straight reversion of my edit. The sentence I wrote was directly sourced with a recent article published in a reputable peer-reviewed journal. This article not only describes research supporting the dietary connection, but it also cites other articles and references a growing body of evidence supporting the dietary connection. This article and the articles it cites thus directly conflicts with the old, unsourced sentence. If you think the old sentence should stand as-is, at the very least I think it's necessary to find multiple reliable sources that justify it as scientific consensus and establish the article/source I cited and its perspective as a fringe view. If you think the wheat connection is being given undue weight, let's discuss that and working on making the article more accurate given the existence of the source I have pointed to...not just reverting back to something which is unsourced and in conflict with recent research. Cazort (talk) 16:50, 4 April 2010 (UTC)

Latent autoimmune diabetes on Simple English Wikipedia

That article will require proper editings and will need additional sources. Can someone please help out in editing on the page on Simple English about Latent autoimmune diabetes? The article needs proper editing, no original research and additional proper sources.

63.230.156.31 (talk) 18:38, 24 April 2010 (UTC)

Great review

• Daneman, D (2006 Mar 11). "Type 1 diabetes". Lancet. 367 (9513): 847–58. PMID 16530579. {{cite journal}}: Check date values in: |date= (help)

Doc James (talk · contribs · email) 23:50, 24 January 2011 (UTC)

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)

In some cases, the cause of Diabetes I, comes from the pancreas failing to produce the insulin. Not only does it come from genetics, health and environment but it also comes from the own body failing top produce its own insulin. Therefore, that leads to the injection of insulin made already for you. ARod122491 (talk) 05:58, 17 March 2011 (UTC)

first paragraph of subsection Driving misplaced

The information on this paragraph does not belong to the Diabetes managament section, as it talks more about the effects of the disease without really relating them to driving. Fmreina (talk) 10:32, 21 March 2011 (UTC)

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)

Not necessarily. Type 2 is characterised by consistently high blood sugar levels causing the body to produce more and more insulin, to a point that the body's cells become insensitive to the insulin. You can stimulate the pancreas to produce more insulin while at the same time resensitising the body cells to actually utilise the insulin. But this can wear out the pancreatic cells and eventually they will stop producing insulin. At this point type 2 diabetics can become insulin dependent (they need to inject insulin). Contrast this to type 1 where the entire problem is the auto-immune destruction of the insulin-producing cells. — Preceding unsigned comment added by 139.80.123.42 (talk) 12:38, 22 July 2012 (UTC)

Autoimmune versus immune

This article says that although the cause of Type One diabetes mellitus is not understood, it is believed to be of immunological origin. Shouldn't that really read "auto-immunological"? ACEOREVIVED (talk) 15:56, 11 September 2012 (UTC)

Insulitis and imaging beta cell mass

Something for a "research directions" or "pathophysiology" section: doi:10.1210/er.2011-1041 11:29, 9 December 2012 (UTC)

confirmed viral

http://yle.fi/uutiset/finnish_team_makes_diabetes_vaccine_breakthrough/6893356

Dropping this there instead of editing myself as this looks to require a bit of verification and some significant rewriting if it is indeed true. — Preceding unsigned comment added by Draeath (talk • contribs) 15:12, 22 October 2013 (UTC)

Proposed merge

I have proposed a merge between Honeymoon period (diabetes) and this article, as I believe the majority of the content covered in the merged article is covered here, and any remaining reliably-sourced information would be better included in the body of this article rather than as a standalone article. This would have the additional effect of increasing the overall quality of this article, and by marginally increasing the readership more attention will be given to any merged information. --LT910001 (talk) 02:10, 6 December 2013 (UTC)

• Support merge. There is scope for shortening the "honeymoon period" article and to incorporate it into the DM1 article with more context. JFW | T@lk 11:05, 5 January 2014 (UTC)

Verapamil as a possible medication - first human trials soon

I'm unable to verify the veracity of this myself (not my field) but thought I should at least mention it here on the talk page in hopes that someone else knows what to do with it:

http://www.iflscience.com/health-and-medicine/trial-announced-diabetes-drug-following-success-mice (plenty of refs linked from there)

"Verapamil is a calcium channel blocker used to treat hypertension, irregular heartbeats and some sorts of headaches. It has been approved for some of these purposes for over 30 years. [...] The potential application to diabetes arises from the discovery by Dr. Anath Shalev of the University of Alabama, Birmingham (UAB) that verapamil lowers the level of the protein TXNIP in pancreatic beta cells. [...] high levels of thioredoxin have been shown to keep the pancreas' insulin-producing islet beta cells alive"

-- Mikeclueby4 (talk) 02:43, 11 November 2014 (UTC)

Lancet again

Seminar doi:10.1016/S0140-6736(13)60591-7 JFW | T@lk 21:23, 22 November 2014 (UTC)

Removed to talk for sourcing

I started in to this new content, and was consistently finding very outdated, US-specific (where healthcare laws have changed) and primary sources, so have removed this to talk for review. SandyGeorgia (Talk) 15:35, 9 December 2014 (UTC)

Yes needs some work. Lets see if the student is still around. User:Bnard1234 They have however now "handed" in their assignment. US perspective is provided with explaining it as such. Doc James (talk · contribs · email) 18:06, 9 December 2014 (UTC)

Content removed
The following discussion has been closed. Please do not modify it.
Updated source needed for any reinsertion of BCG The BCG Human Clinical Trial Program  This program is investigating whether bacillus Calmette-Guérin(BCG) vaccination will eliminate the pancreas-destroying T cells in humans with advanced type 1 diabetes.  BCG is a generic drug that has been used for over 80 years in different capacities, including vaccination against tuberculosis. We are testing BCG at different doses and schedules than those currently used.  In humans, BCG temporarily elevates levels of a substance called tumor necrosis factor, or TNF. We have shown in lab experiments3 and in a Phase I human clinical trial4 that elevating TNF can eliminate the bad T cells in the blood of individuals with type 1 diabetes, which may have clinical benefits.  Our goal is to bring forward a new, inexpensive, non-toxic treatment for advanced type 1 diabetes. — Preceding unsigned comment added by 2001:558:6014:36:DA9:ED77:DEFA:20FF (talk) 04:13, 4 January 2015 (UTC) I think an updated reference is needed before reinsertion of the text on BCG (in box below) as a potential preventive method. Even originally, in 2001, it appears only theoretical [5], and in the recent review from 2010 of preventive measures [6], it is not mentioned at all. Mikael Häggström (talk) 06:36, 29 January 2011 (UTC) Tumor necrosis factor-alpha, or TNF-α, is part of the immune system. It helps the immune system distinguish self from non-self tissue. People with type 1 diabetes are deficient in this substance. Dr. Denise Faustman theorizes that giving Bacillus Calmette-Guérin (BCG), an inexpensive generic drug used to immunize against Mycobacterium tuberculosis, would have the same impact as injecting diabetic mice with Freund's Adjuvant, which stimulates TNF-α production. TNF-α kills the white blood cells responsible for destroying beta cells, and thus prevents, or reverses diabetes. She has reversed diabetes in laboratory mice with this technique, but was only able to receive funding for subsequent research from The Iaccoca Foundation, founded by Lee Iacocca in honor of his late wife, who died from diabetes complications. Human trials are set to begin in 2008. Type 1 produces much more insulin than previously expected See this revert. I think that this edit (or a modified one) should be included. WP:MEDREV states "If the conclusions of the research are worth mentioning (for instance, publication of a large, randomized clinical trial with surprising results), they should be described as being from a single study, for example:", I think this is worth mentioning (since it kind-of goes against the type definition of type 1 diabetes, or at least redefines it a bit) and the study also references a few other study's that also have detected this, so it is not like it is total new and never reproduced anywhere else. Comments? --Stefan talk 00:13, 17 March 2015 (UTC) thanks for bringing this to talk. Very few individuals clinical trials are That Important. As you say this incrementally advances the field. This is a well-studied and often reviewed field, and there will soon be a review that discusses these results. There is WP:NODEADLINE here and i see no reason (and you give no reason) not to wait.... Jytdog (talk) 00:18, 17 March 2015 (UTC) (amended Jytdog (talk) 08:32, 17 March 2015 (UTC)) If it is not totally new and other have commented that there should be secondary sources. Doc James (talk · contribs · email) 02:54, 17 March 2015 (UTC) Sorry my wikiknowledge is way out of date, I do not know what you mean by a acceptable secondary source. I assume that this and this is not? You want publications like science and nature? or? Please give me a direction so that I know what to look for. I also wonder how you define a single study, what do we do with meta studies, i.e. is that a primary or secondary source? this study actually refers to 4-5 others plus adds their own research. So it is not really a single study? Jytdog I don't understand what you mean with individuals being that important? --Stefan talk 04:58, 17 March 2015 (UTC) Hi sorry about that - I meant "individual clinical trials" - left out those words and wrote nonsense. My apologies. The relevant guideline here is WP:MEDRS, particularly the section, WP:MEDREV. The two news sources there are the kind of popular media sources mentioned in MEDREV. And yes, secondary sources are reviews (including meta-analyses) and statements by major scientific or medical bodies. Jytdog (talk) 08:32, 17 March 2015 (UTC) If you use pubmed you can limit your search to secondary sources on the left. Click review articles Doc James (talk · contribs · email) 18:46, 17 March 2015 (UTC) Vaccine trials faild See this revert Sources 59 and 60 state that trials have been terminated, why not to say about negative reasult? Rafis v (talk) 19:39, 22 May 2015 (UTC) per WP:MEDRS we use review articles. i just updated the section. Jytdog (talk) 23:00, 22 May 2015 (UTC) Behaviour programmes Work at least in the short term. doi:10.7326/M15-1399 JFW | T@lk 21:30, 7 October 2015 (UTC) Comorbidities with other autoimmune disease It's a bit funny that on T2DM there's list of comorbidities to things like hypothyroidism, but for some reaosn it's missing on the T1DM one that actually is autoimune... 1.129.97.52 (talk) 23:52, 10 May 2016 (UTC) Yes agree this article would benefit from that. Doc James (talk · contribs · email) 00:07, 11 May 2016 (UTC) I also agree. We must work on it. Best regards. --BallenaBlanca (talk) 07:19, 11 May 2016 (UTC) Risk factors Lancet: doi:10.1016/S0140-6736(16)30582-7 - Genetic doi:10.1016/S0140-6736(16)30507-4 - Environmental JFW | T@lk 12:10, 3 June 2016 (UTC) Primary source highly heritable (88% in a large study of Finnish twins) This is a primary source. Let me check the secondary one above. References Doc James (talk · contribs · email) 00:14, 21 August 2016 (UTC) Okay updated with more recent sources and more details. Doc James (talk · contribs · email) 00:36, 21 August 2016 (UTC) Any particular reason this was singled out as suspicious? High heritabilities of highly polygenic disease traits is a common finding as are high heritabilities for adults in developed in general. I think it is better to source to papers instead of books because papers are more easily available. Your edit removed the paper I cited (not my own paper, picked a recent one at random with a large sample), and added two books that people probably cannot access. You should at least re-add the paper. --Deleet (talk) 13:08, 1 October 2016 (UTC) Please read [WP:MEDRS]] - we use literature reveiws not primary sources like the one you used - reviews provide accepted knowledge, which is what we want; a primary source picked "at random" is exactly that; random and not a good conduit to finding what a given field defines as accepted knowledge. Jytdog (talk) 17:39, 1 October 2016 (UTC) External links modified Hello fellow Wikipedians, I have just modified 2 external links on Diabetes mellitus type 1. Please take a moment to review my edit. If you have any questions, or need the bot to ignore the links, or the page altogether, please visit this simple FaQ for additional information. I made the following changes: Added archive https://web.archive.org/web/20130826174444/http://www.who.int/mediacentre/factsheets/fs312/en/ to http://www.who.int/mediacentre/factsheets/fs312/en/ Added archive https://web.archive.org/web/20151117024828/http://journals.plos.org/plosone/article?id=10.1371%252Fjournal.pone.0137950 to http://journals.plos.org/plosone/article?id=10.1371%252Fjournal.pone.0137950 When you have finished reviewing my changes, please set the checked parameter below to true or failed to let others know (documentation at {{Sourcecheck}}). This message was posted before February 2018. After February 2018, "External links modified" talk page sections are no longer generated or monitored by InternetArchiveBot. No special action is required regarding these talk page notices, other than regular verification using the archive tool instructions below. Editors have permission to delete these "External links modified" talk page sections if they want to de-clutter talk pages, but see the RfC before doing mass systematic removals. This message is updated dynamically through the template {{source check}} (last update: 18 January 2022). If you have discovered URLs which were erroneously considered dead by the bot, you can report them with this tool. If you found an error with any archives or the URLs themselves, you can fix them with this tool. Cheers.—InternetArchiveBot (Report bug) 08:39, 12 December 2016 (UTC) ADA doi:10.7326/M17-1259 JFW | T@lk 12:30, 12 September 2017 (UTC) Research on cause In my view the medical sections of articles about health should express what is actually known. Accepted knowledge. If things are unknown, we should state that, simply. Research to acquire accepted knowledge should be located in the Research section. So I moved research on cause to the Research section. User:Doc James, you disagree and moved it back. How about what I said above? Thx Jytdog (talk) 18:48, 27 August 2016 (UTC) User:Jytdog My position is slightly different. With respect to treatment I think we agree, the treatment section should contain what is actually used with the level of support supporting its us. So if something is used and not supported that goes in the treatment section. But if something is simply in early research and not used it goes in the research section. With respect to causes, we usually state that the cause is unknown first followed by the potential theories around causes within the cause section. This is followed in hundreds if not thousands of articles in which the cause is not known including many FA such as Autism#Causes. What you are suggesting is a major change in current practice. From the perspective of our readers, I do not see the same degree of need to separate established treatments from treatments in research (a high need) as to separate likely from possible from proposed causes. When I write about causes I simply put those with the greatest support first. Doc James (talk · contribs · email) 21:27, 27 August 2016 (UTC) OK, that makes sense. Thanks. Jytdog (talk) 00:44, 28 August 2016 (UTC) I undid this edit. This topic was discussed here and Doc James restored the content [7]. And I also agree with him. --BallenaBlanca (Talk) 23:21, 15 October 2017 (UTC) It continues here #Gliadin/gluten as cause --BallenaBlanca (Talk) 00:06, 16 October 2017 (UTC) Gliadin/gluten as cause This is research, not actual, well-accepted cause. Current reviews about diabetes per se do not discuss this as a cause. Happy to have it as a line of research, which is what it is. Jytdog (talk) 23:36, 15 October 2017 (UTC) Why do you open a new section? This was already talked here #Research on cause and where I explained my last edit. To keep your claims, you have to provide sources that explicitly contradict what the reviews we already have on the page conclude. The version before the reverted changes should be kept until a consensus is reached per WP:BRD, so I will restore it again. --BallenaBlanca (Talk) 00:04, 16 October 2017 (UTC) Just look at the refs in the article. NDDK (ref #1), no mention of this WHO ref #4, no mention of this. PMID 24935775 mentions that celiac occurs more often in people with diabetes than people without. Does not discuss gliadin as a cause. ADA fact sheet, not mentioned etc etc. yes it is a line of investigation but it is far from a mainstream consideration of cause. Belongs in research. (I am not trying to delete it! Just put it where it belongs) Jytdog (talk) 00:53, 16 October 2017 (UTC) This does not justify you moving it to research section. In Wikipedia we do not limit ourselves to what this organisations say. Per WP:NPOV we must include all of the significant views that have been published by reliable sources on a topic. The sources you provide, except one, are not specific to type 1 diabetes and therefore address the issue in less depth. In addition, none of them says that gliadin has been ruled out as a possible cause, which is what you have to prove. Is as valid talking about gluten as a possible cause as other possible causes, like viruses, which are also just hypotheses (remember again what Doc James explained to you here). NDDK talks about environmental factors "such as", is an open list and mentions an example (virus). WHO does not mention any example (that does not prevent the NDDK does...). PMID 24935775 is the only one that focus on diabetes type 1; is older (2014) than this review already present in the page PMID 26343710 (2015) and also, it does not talk about causes because it is not its purpose (I have the full paper). ADA fact sheet, not mentioned... because not discuss causes (is a very summary and not limited to type 1 diabetes). --BallenaBlanca (Talk) 01:55, 16 October 2017 (UTC) I have asked others to give input via WT:MED. Though we are aligned in so many ways you and I don't live in the same universe when it comes to this gluten stuff and we are going to need other input. Jytdog (talk) 02:26, 16 October 2017 (UTC) I invite you to review the history of edits, from this one. This topic was already discussed and it was agreed to maintain in Causes, not in Research. Jytdog why do you question it again? Please apply to you what you apply to other users and do not make unilateral editions on heavily edited topics. Restore the previous version and wait for the conversation. --BallenaBlanca (Talk) 08:05, 16 October 2017 (UTC) The association between celiac and DM Type I is well accepted. Whether one causes the other is less clear. I think discussion in the research section is reasonable. I base this on "However; an analogous causative agent has not yet been identified for T1D. Nevertheless; the role of dietary gluten in development of T1D and the potentially beneficial effect of removing gluten from the diet of patients with T1D are still debated."[8] We mention that celiac disease is associated under "signs and symptoms" which we should. Doc James (talk · contribs · email) 08:17, 16 October 2017 (UTC) And then, we come back to this same point, again...: (Moved. Better here, evidence is strong. If we follow the same criteria, we should move the entire section to research.) Doc James you did this edit (→‎Cause: moved back) which, after several intermediate edits and exchange of messages, put an end to the controversy. Nothing has changed since then, there have been no papers that downplay the theory about gluten. I do not understand why do you change your criteria now. Remember your reasoning "With respect to causes, we usually state that the cause is unknown first followed by the potential theories around causes within the cause section. This is followed in hundreds if not thousands of articles in which the cause is not known including many FA such as Autism#Causes. What you are suggesting is a major change in current practice. " This apply to the whole section, not only gluten. See for example the virus theory Diabetes mellitus type 1#Virus: we are in the same scenario. Both diseases (CD and DT1) share the same risk genetics. This is another fact that reinforces the theory. --BallenaBlanca (Talk) 11:35, 16 October 2017 (UTC) You extracted this from the abstract: However; an analogous causative agent has not yet been identified for T1D. Nevertheless; the role of dietary gluten in development of T1D and the potentially beneficial effect of removing gluten from the diet of patients with T1D are still debated." [9] and if we go to the full text, we can see "Conclusions. In this review, we focused on the role of gluten as an important player in the pathogenesis of CD and T1D. --BallenaBlanca (Talk) 11:40, 16 October 2017 (UTC) This edit[10] was moving the discussion of causes back to were it was before. We give a lot of weight right now to gluten / celiac in this article. Gluten is mentioned 5 times and celiac 6 times. I think discussion of dietary gluten with the discussion of removing gluten from the diet as a treatment works well together in the research section. Doc James (talk · contribs · email) 12:22, 16 October 2017 (UTC) Yes celiac disease and T1D are associated and share many genetic loci, but the risk alleles are not always the same. See PMID 19073967 for data. Association is not causation. Interventional studies are limited. Gliadin as a cause is OK in Research, or as a small subsection in Environmental factors, but doesn't merit more weight. The Nutrients 2015 review is the best source. Jrfw51 (talk) 20:58, 16 October 2017 (UTC) would agree w/ Jrfw51(on this topic)--Ozzie10aaaa (talk) 11:18, 17 October 2017 (UTC) Thanks for your comment, Jrfw51. Yes, of course the risk alleles are not always the same but share many genetic loci. Gliadin as a small subsection in Environmental factors is how the page was before the Jytdog edit, since August 2016 and is what I am asking to restore. So I understand that you agree with this version [11]? --BallenaBlanca (Talk) 22:24, 16 October 2017 (UTC) Therefore, if I am understanding well, Jrfw51, Ozzie10aaaa and I think that it is appropriate that it be a small subsection in Environmental factors. Doc James, we are talking on two scenarios: On one hand the association of CD and type 1 diabetes, which in fact is one of the clearest and most studied associations. On the other hand, gluten as a possible cause not necessarily associated with celiac disease, which is a theory at least at the same level as that of viruses and therefore deserves to be in the same level / section. --BallenaBlanca (Talk) 23:55, 17 October 2017 (UTC) Good point on viruses. Moved to research. Jytdog (talk) 07:14, 18 October 2017 (UTC) We could also mention it in a sentence in the causes section under environmental factors. Does not need its own section there. Ah, that is what just occured in these edits thanks to Jrfw51 and Jyt[12] Doc James (talk · contribs · email) 07:57, 18 October 2017 (UTC) Yep, just done. Jrfw51 (talk) 09:35, 18 October 2017 (UTC) {{dashboard.wikiedu.org assignment}} Society and culture See also: List of people with diabetes mellitus type 1 The disease was estimated to cause $10.5 billion in annual medical costs ($875 per month per diabetic) and an additional $4.4 billion in indirect costs ($366 per month per person with diabetes) in the U.S. Socioeconomic status Numerous studies show a proven link between higher socioeconomic status and better glycemic control in people with Type 1 (T1) diabetes. Financial and social causes have been cited to explain this correlation. The 2014 National Diabetic Statistics Report found that “the average medical expenditure among people with diagnosed diabetes was 2.3 times higher than people without diabetes.” These costs are largely attributed to hospital inpatient care (50% of total cost) and diabetic medication and supplies (12%). Most states (with the exception of Alabama, Idaho, North Dakota, and Ohio) require partial coverage for equipment. Thus, although diabetic costs are partially subsidized by state governments, T1 diabetics are, to some degree, financially responsible for their medical costs. The 2014 Report strongly suggests that those unable to afford proper diabetes care are at higher risk of developing diabetic complications. The financial burden of diabetes can have damaging biologic ramifications, particularly on individuals of low socioeconomic status (SES). For instance, it is more difficult for patients of lower SES to stay technologically up to date with medical changes and innovations. In a study done on 1500 patients with TID, researchers found that insulin pump therapy, which supports tight control of blood sugars, is much more likely to be used by patients of higher SES. Because insulin pumps cost upwards of $4,000, many government insurance plans do not provide them. This lack of access to supplies and expensive treatments have been cited as a potential reason for poorer glycemic control in patients of lower SES. Social reasons may also account for the correlation between socioeconomic status and glycemic control. Wealthy people not only have greater means with which to purchase necessary supplies and devices, but can also more ably provide additional forms of support. A study done on glycemic control and socioeconomic status concluded that, for financially stressed families, “providing adequate food, housing and clothing may have to come before devoting time to diabetes-related care.” Furthermore, financially secure parents can more easily “look at blood sugar patterns and adjust insulin doses, food intake and exercise level accordingly.” This is of particular importance as the affected individual often continues childhood management patterns when transitioning from adolescence to adulthood. Other SES linked behaviors, such as the increased rate of alcohol and cigarette consumption amongst individuals of lower SES, have also been cited as reasons for the disparity in glycemic control between diabetics of varying SES. Ethnicity In a 2011 study comparing glycemic control amongst Hispanics, African Americans, and Caucasians, Hispanics had the highest baseline A1C levels (average blood sugar levels for past two to three months), Caucasians had the lowest, and African American's fell in between the two ethnic groups. It is important to note, however, that African American's and Hispanics had significantly fewer glucose uploads than Caucasians, making their data less accurate than that pertaining to Caucasian's. In addition, Hispanics had the lowest level of education, income, BMI, and suffered most from depression. The disparity in glycemic control between varying ethnic groups has been attributed to multiple social factors. Researchers have credited poor glycemic control in Hispanics to a potential distrust of medication and difficulty with numeracy. In addition, compliance differences could be explained by annual household income. Hispanic participants made, on average, $5,000-$10,000, whereas the majority of Caucasians made between $10,000-$30,000 a year. Factors associated with low SES, like less available free time and more pressing baseline issues, may account for differences in glucose uploads. The established correlation between health and education can help explain disparities in glycemic control between ethnic groups. Due to “multiple different mechanisms that operate at different levels of society,” individuals who have completed more years of schooling tend to be in better health and exhibit healthier behaviors than high-school and college dropouts. In fact, a 2002 study done by Goldman and Smith found that diabetics who are less educated tend to frequently switch treatment, leading to poorer glycemic stability. This study is reinforced by a 2014 report which found that the rate of 18-24 year old Hispanic students dropping out of high school was 14%, compared to 8% of African American's students and 4% of Caucasian students. Thus, ethnicity interacts with external factors, like education (which is inherently related to socioeconomic class), to affect metabolic processes. Blood glucose levels, in essence, do not operate alone. Rather, evidence suggests that they are a biological function heavily influenced by the social world. Age Studies have consistently found that glycemic control worsens with age. Puberty, a period characterized by rapid growth and hormonal change, causes greater insulin insensitivity. During this transitional stage, diabetic's, whose pancreas cannot appropriately adjust to metabolic changes, frequently suffer from high blood sugars. Because insulin requirements increase between 30% and 50% during puberty, pediatric endocrinologists should adjust patient insulin dosage accordingly. Behavioral and psychological changes inherent in puberty can also affect blood glucose levels. Puberty is a time when young people seek independence from their parents and caregivers. However, due to the nature and severity of diabetes, this transition can be difficult for adolescents and their caregivers. It is not uncommon for young teens to assert their freedom and independence by refusing to monitor blood sugars. Additionally, teens start to establish their sexual identity during puberty, which can pose psychological problems for those that feel detached and betrayed by their bodies. This cognitive volatility can result in liberal self-care. Thus, as stated in the “Diagnosis and Management of Type 1 Diabetes in Children and Young People,” produced by the National Collaborating Centre for Women’s and Children’s Health, “there is a need to assist young people with type 1 diabetes in maintaining a sense of competence and self-esteem and to provide reassurance that they have not lost control of their life or body during this critical period of change.” Psychological support can help diabetic’s combat the worsening of metabolic control during puberty. Due to the age-related transition from parental to independent insurance coverage, 23%-33% of U.S. youth and young adults are uninsured. As a result, glycemic control declines in diabetic individuals aged 18-39. Typically older adult type 1 Diabetics have better glycemic control. In a study done by the Centers for Disease Control and Prevention, researchers found that diabetic patients aged 50-64 were more than twice as likely as patients aged 45-49 to have “good” glycemic control. Greater financial and emotional stability, as well as improved access to healthcare have been cited as potential reasons for this difference.<ref>{{cite journal|last1=Kaur|first1=Jaspinder|last2=Singh|first2=Sargun|last3=Kaur|first3=Kawaljit|title=Determinants of the glycemic status and its relationship with cardiovascular risk factors|journal=Journal of Biochemical and Pharmacological Research|date=September 2014|volume=2|issue=3|pages=159-166|url=http://researchpub.org/journal/jbpr/number/vol2-no3/vol2-no3-4.pdf|accessdate=5 December 2014}}</ref> - predatory open access It is important to note, however, that due to the numerous long-term health implications of T1 diabetes, glycemic control declines again from age 65-79. Understanding the cause of glycemic fluctuations has begun to shape the way diabetes is managed and treated. For instance, juvenile endocrinologist Hala Tfayli used empirically backed evidence to link puberty with poor glycemic control, and has since proposed reasonable medical responses that would help alleviate these age-related health issues. Mental Health Research finds that diabetic patients with severe mental illness are at “significantly increased risk of not receiving appropriate elements of care such as eye examinations, plasma lipid testing, and glycated hemoglobin monitoring.” As a result, psychological instability in diabetic patients is shown to cause a markedly reduced life expectancy. Stress and depression Due to the labor intensive and persistent nature of the disease, diabetics often suffer from chronic stress. The effects of chronic stress are serious, as it strongly correlates to anxiety and depression. Stress can affect blood glucose levels in varying ways. Depending on the type of stress, blood sugars either rise or fall. For instance, in a fight or flight situation, when the body responds to a perceived harmful event or attack, breathing, heart rate, blood pressure and blood sugar all rise. On the other hand, a long term-fight against stress (chronic stress) reduces the body’s energy and makes an individual more susceptible to depression, sleeplessness, poor appetite, and volatile blood sugars. This established understanding of chronic stress supports a study published in The Journal of Health and Behavior, which states that people with type 1 Diabetes are more susceptible to physical harm from stress. It is important to note, however, that of these studied individuals, those who felt in control of their life had more stable blood glucose levels and less indication of physical harm from stress than the more emotional, reactive type who suffered from fluctuating, unstable blood sugars. Individuals with chronic conditions are three times more likely to suffer from depression than the general population. Depression can have negative biological ramifications, especially on diabetics, as it has been shown to make patients less likely to take medication, eat properly, and function well on a physical and mental level. In fact, depression, in conjunction with diabetes, has been said to have “the greatest negative effect on the quality of life compared to diabetes or depression alone.” Patients with diabetes are at an increased risk for suicide. A British Study found that individuals with type 1 diabetes had 11 times the suicide rate as the general population. Of these, a large number were insulin induced overdoses. Interestingly, numerous studies and researchers have found a strong association between medical noncompliance and suicidal thoughts. There are numerous empirically backed studies that indicate a relationship between anxiety, depression and glycemic control. As such, the first step to combating these forms of mental illness in diabetic patients is proper diagnosis. Three quarters of depression cases in diabetics go undiagnosed. Due to poor detection techniques, a lack of patient reporting, and difficulty distinguishing one disease from another, symptoms of depression, such as fatigue, change in appetite, and loss of energy might be misinterpreted as signs of hyperglycemia. Having said that, the need to screen diabetics for depression has been magnified over the past few years, however there is still no unanimous agreement or established rubric on how to best do so. Once diagnosed with depression, an individual should receive proper treatment. Cognitive-behavioral therapy, support groups, electroconvulsive therapy and anti-depressants are all effective methods of alleviating depression. Moreover, a study found that these approaches can also improve glycemic control, mood, weight, and overall quality of life. Educating patients about the importance of exercise and sleep have also been cited as additional methods to combating mental illness. Optimal diabetic care, in essence, incorporates much more than daily insulin injections, routine check ups, and dietary monitoring. Psychological support is also important, as factors like stress and depression affect the mental, physical and metabolic health of diabetic individuals. Eating disorders Both eating disorders and diabetes involve consciously and systematically controlling food (specifically carbohydrate) intake. As a result, the two diseases often run hand-in-hand, especially in adolescent females. Females with type 1 diabetes are at twice the risk of developing eating disorders than those without diabetes. Issues relating to the self-management of the disease, such as stringent monitoring of diet, exercise, and frequent blood glucose monitoring have been cited to explain this relationship. In addition, insulin therapy is associated with weight gain (especially after initial diagnosis), which can cause diabetics to be heavier on average than their non-diabetic counterparts, and, in turn, more dissatisfied with their bodies. Poor self-perception can have biologic consequences, as there is a proven correlation between self-esteem and blood glucose levels. Diabetic patients with low self-esteem are more emotionally unstable, less agreeable and suffer more from diabetes-related health problems than patients with high self-esteem. Furthermore, children in better control of blood sugars have significantly higher-self esteem than their counterparts. As such, type-1 diabetes, low-self esteem and anorexia are all distinct entities, but, at the same time, entangled. Eating disorders cause adverse health consequences, especially on diabetic individuals. Anorexia nervosa and Bulimia nervosa can lead to severe hypoglycemia (below 70mg/dL), which, left untreated, can result in unconsciousness, seizures, and/or diabetic coma’s. On the other hand, diabulimia, a condition in which diabetic’s deliberately restrict insulin to lose weight, results in hyperglycemia (above 250mg/dL). High-blood sugars lead to an increased risk of microvascular complications, diabetic retinopathy, diabetic ketoacidosis, and potential death. Diabulimia is becoming increasingly common, and is said to affect 30% to 40% of young females. However, because this form of insulin misuse is a relatively new phenomenon, and has yet to be recognized as a mental health disorder in many countries, healthcare professionals are having difficulty recognizing the condition and responding appropriately to it.

Lancet

Seminar doi:10.1016/S0140-6736(18)31320-5 JFW | T@lk 11:11, 17 June 2018 (UTC)

Glucagon dysregulation as a major complication

I will be adding glucagon dysregulation as a complication of type 1 diabetes. It has been thoroughly shown to be a characteristic of type 1, and though not all the implications of it are fully understood as to their mechanisms, just citing that it is in dysregulation should be important, being that it is a major metabolic hormone, and specifically the counter-regulator of insulin. I will also be adding this to the complications portion of the page "Complications of Diabetes Melitus. feedback in balancing the information into the most appropriate places would be appreciated.

Basics of this add are:

Glucagon is dysregulated. Hyperglucagonemia under euglycemia and hypoglucagonemia under hypoglycemia. Too much glucagon can bring on ketosis. lack of sufficient glucagon under insulin induced hypoglycemia means inability for body to recuse blood sugar via glycogen dump and gluconeogenesis.

Mechanisms of dysregulation still to be elicudated, but there is known loss of islet alpha cell controls. Islet-produced insulin helps regulate glucagon via paracrine signaling. loss of islet produced insulin changes how alpha cells experience insulin regulation All type 1 diabetics experience rapid early islet sympathetic nerve pruning during the autoimmune destruction of beta cell mass. sympathetic stimulation is a main form of glucagon secretion when bloodsugar falls to dangerous levels. Pruning is due to p75 ntr, though the mechanism by which it is activated is still being researched.

Glucagon is being included as part of closed loop artificial pancreas systems, in attempt to improve the metabolic balance of insulin and glucagon.

Jthibaudeau (talk) 16:35, 7 December 2018 (UTC)

References

New research on possible causes

Can someone update the article to reflect the following research:

• https://www.independent.co.uk/news/health/diabetes-type-1-drug-treatment-insulin-cancer-university-california-study-a8790431.html
• https://medicalxpress.com/news/2019-02-cellular-sickness-linked-diabetes-onset.html

172.219.53.146 (talk) 02:36, 26 February 2019 (UTC)

Only specialized medical literature may be used in the article. Please, do not cite popular magazines written by incompetent people. Ruslik_Zero 21:00, 26 February 2019 (UTC)

Issues being discussed on my talk page

User_talk:Doc_James#unreliable_sources?

Basically we have an IP adding a bunch of poor sources. Doc James (talk · contribs · email) 06:42, 28 February 2019 (UTC)

Specifically this needs a much better reference.

"Researcher Dr. Denise Faustman of Harvard and MGH has successfully reversed type 1 diabetes in humans.[13]"

But so does the rest of it. Doc James (talk · contribs · email) 06:48, 28 February 2019 (UTC)

BCG vaccine associated with lower rates

Ref says "Participants who received greater than 2 childhood vaccines of BCG had diminished lifelong risk for developing T1D".[14]

Doc James (talk · contribs · email) 07:14, 28 February 2019 (UTC)

Thanks for restoring. Doc James (talk · contribs · email) 07:30, 28 February 2019 (UTC)

Press releases

Are not appropriate sources for medical content.[15]

Doc James (talk · contribs · email) 06:59, 2 March 2019 (UTC)

No mention of hygiene hypothosis / possibly reduced incidence in "Helminth" (ie parasitic worm) infected populations ???

Hi, I was just reading some articles on Pubmed about links between infections by parasitic worm and modulated immune responses (linked to lower rates of autoimmune and allergenic responses). I checked by here because I wasn't sure if "insulin dependant diabetes" is type I Diabetes (which I was familiar with). While I was here I browsed through, curious whether there was any mention of the Hygiene hypothesis, or the (possible?) increased prevalence of Type I Diabetes in "uninfected" population, and was a bit surprised to see nothing. I've been reading up more with regard to the link to allergies, so I've not got anything specific, but here is an (old) article that talks about reduced prevalence of Type I diabetes in mouse models infected by parasitic worms : https://www.ncbi.nlm.nih.gov/pubmed/10320614/ (its the one I just happened to be reading).

Adding info to the article would obviously require a lot more digging and sourcing references, but I just wanted to ask what thoughts people had on the subject? Regards 37.49.76.172 (talk) 13:23, 7 March 2019 (UTC)

Ref is too old

User:The RedBurn this is an extraordinary statement and as such would require an exceedingly good reference. The ref in question is from 2004 so too old.

This ref is too old "Vitamin D deficiency as a child may be an important factor, causing as much as 80% of cases."

References

Doc James (talk · contribs · email) 04:12, 11 March 2019 (UTC)

Requested move 19 May 2019

The following is a closed discussion of a requested move. Please do not modify it. Subsequent comments should be made in a new section on the talk page. Editors desiring to contest the closing decision should consider a move review after discussing it on the closer's talk page. No further edits should be made to this discussion.

The result of the move request was: Moved. (closed by non-admin page mover) SITH (talk) 11:06, 27 May 2019 (UTC)

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• Diabetes mellitus type 1 → Type 1 diabetes
• Diabetes mellitus type 2 → Type 2 diabetes
• Neonatal diabetes mellitus → Neonatal diabetes
• Complications of diabetes mellitus → Complications of diabetes

– For WP:CONSISTENCY with the recent move of the main article from Diabetes mellitus to Diabetes and with Type 3 diabetes, and in accordance with WP:COMMONNAME and WP:CONCISE, I propose moving these pages to their common names. Rreagan007 (talk) 20:39, 19 May 2019 (UTC)

• Support for 1, 2, and 4, being the common names. Leaning support for neonatal diabetes, the disease isn't as common, so the full term is maybe more often seen. (Type 3 diabetes is sort of a fringe term so we don't really need to aim for consistency with it, but it's good to have consistency with diabetes!) – Þjarkur (talk) 21:22, 19 May 2019 (UTC)
• Support all per nom. -- King of ♥ ♦ ♣ ♠ 01:51, 21 May 2019 (UTC)

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The above discussion is preserved as an archive of a requested move. Please do not modify it. Subsequent comments should be made in a new section on this talk page or in a move review. No further edits should be made to this section.

Question about pancreatic transplants/ islets transplant- If a transplant was to be done, what would stop the autoantibodies from attacking the beta cells again? Does this also apply to the generation of new beta cells from stem cells? Lbenegas4 (talk) 18:22, 1 February 2020 (UTC)

NAFLD

Not precisely uncommon in DM1 doi:10.1210/clinem/dgaa575 JFW | T@lk 17:15, 2 November 2020 (UTC)