let's get this settled! please? edit

On rereading the article I have again found comments (at section ketoacidosis) implying that lipids can be so processed as to generate glucose. As I have been told in authoritative terms that this is possible only for the glycerol triglyceride backbone and not for the fatty acid chains themselves, this would appear to be a limited issue. Can someone who knows the relevant biochemistry in vivo please settle this? (Alterprise, Alextan, jdwolff, ...; hint hint).

In addition, both that section and the ketoacidosis article are at minimum confusing. It is my understanding that ketone body production is normal during fat metabolism, and that they are normally dealt with without causing trouble. Only when glucose is being produced from degraded protein is there a competitive inhibition with a step in the ketone metabolism chain which allows dangerous buildup of ketone bodies, leading perhaps to acidosis. At present, ketoacidosis talks about the ratio of glucagon to insulin as being the cause ??? . Again, can we have some clarification from someone who actually knows the biochemical pathways?

Neither of these two claims should be permitted to remain if they are wrong. Given the prominence of Atkins diet folk, WP ought to have its factual ducks in a row on such questions. In my view anyway. ww 18:04, 14 Feb 2005 (UTC)


You are correct, the article is a mess, with lots of minor errors or least confusing assertions. I am removing the section you criticized and replacing it with something simpler and more accurate. Unfortunately many other sections need the same treatment. I hope to get a "round tuit" some day. This is the old section:

In situations where there is a severe deficiency in insulin levels, the body switches to fat metabolism, a mechanism which actually exists to protect the organs during periods of starvation, as glucose is not available to be taken up due to the lack of insulin even though blood levels of glucose are high. Ketones are produced from fats, partly because the brain can utilize ketones for energy as they can pass the blood-brain barrier. As the level of available glucose for the brain (and other organs) runs low due to the persistent low levels of insulin - despite the rising levels of serum glucose as a byproduct of the fat metabolism - more and more fats are metabolized releasing more and more ketones (acetone, acetoacetate and beta-hydroxybutyrate).

Runaway accumulation of these ketone bodies results in metabolic acidosis as pH buffers in the serum are used up. At the same time, as rising levels of glucose and ketones increase the osmolality of the serum, the hyperglycemic state initially encourages the patient's kidneys to produce more urine, causing the body to lose water and electrolytes such as potassium and phosphate, leading to dehydration and hypokalemia.

On presentation to hospital, the patient in DKA is typically dehydrated and hypokalemic (deficient in potassium). Urgent intravenous fluid resuscitation, potassium replacement and insulin replacement should be instituted.

Reasons for removal: first sentence is confusing because it seems to switch from describing starvation to describing insulin deficiency (glu is not high in starvation). Avoid teleological descriptions when gracefully possible ("because the brain can utilize ketones..."). The level of glucose available to the brain does not "run low" because the brain does not depend on insulin to use glucose-- which is why unconsciousness is so rare even in moderately severe dka. More Na is lost than K or PO4. At presentation most patients are NOT hypokalemic; they are K depleted. A classic managment error of the inexperienced physician is to discount the degree of K depletion because the serum levels are initially high.

Anyway, I hope no one's feelings are hurt. Discussion here please if anyone has a problem with the change.alteripse 19:01, 14 Feb 2005 (UTC)

Is WP great or what?! Here I gripe and within minutes an expert steps in, fixes much (A is right about more needing to be done) and leaves a long comment. Thanks and may your karma be blessed! ww 21:23, 14 Feb 2005 (UTC)

revert and rerevert edit

Astanhope added a pointer to a site called goldbamboo and jfdwolff removed it by reverting to the previous version. Astanhope than reverted jfdwolff's reversion. As this is back and forth has led nowhere, I investigated the site. Gold bamboo provides some not very distinguished background information, and appears to be primarily a commercial operation, with a prominent orientation toward 'alternative therapies' for various things, including diabetics. The question is thus, is this an appropriate pointer for WP. I think I would agree with jfdwolff as it adds little to the existing references and WP ought not to be pointing to commercial sites. As for the question of the value of alternative therapy approaches, that is controversial. Because it is, I think that I would suggest that Astanhope create an article on alternative therapies for diabetes in encyclopedic NPOV form and point to it from this one. The indirect endorsement is troubling as diabetes is dangerous if not effectively treated (whatever treatment that might be) and ineffective treatments (whatever they might be) ought not to survive here. Even by indirect implication.

If there is not some discussion here in the next few days, I'll (try to remember to come back and) rerevert the readdition of the pointer.

Comments on this? ww 18:55, 28 Feb 2005 (UTC)

I thought that the juxtaposition of "Eastern" vs. "Western" on that site was valuable. I was also annoyed that JFDWOLFF simply nixed without discussion. We must choose our battles in life and in WP. Removing a link sans commentaire that was placed with forethought struck me as a poor choice of a battle.
As for your suggestion regarding creating an article on alternative diabetes therapy, I think this is an excellent idea to add to my "list." I appreciate the feedback. --AStanhope 19:28, 28 Feb 2005 (UTC)
ww said "...WP ought not to be pointing to commercial sites." I'm curious what you consider WebMD to be all about? --AStanhope 20:27, 28 Feb 2005 (UTC)
Good point. The unvoiced (to me at least) consensus on WebMD appears to be that it is (at base) a general information site. That is long ago became commercial what with mergers and re-purposing and all, makes your question quite to the point. I don't know what to do about pointers to it. But now that it's been brought to the foreground of my attention, I suppose I would think removing those links would be well. But I suspect others will have thoughts on this. Comment? From anyone? ww 21:26, 2 Mar 2005 (UTC)
Astanhope: by adding that link you joined a large horde of editors who frequently add external links to Wikipedia. Some of these are harmless, some are hopeless. As I try to do a lot of Wikipedia maintenance, I use the revert facility open to administrators, which is almost automatic and does indeed work sans commentaire. Before taking offense, perhaps you should have realised that external links is about the last thing Wikipedia needs to be informative. Google works better for web-wide resources.
Please contribute to articles by working on the text, not by fighting turf wars over mediocre outlinked resources. JFW | T@lk 23:05, 28 Feb 2005 (UTC)
I can accept that. Thanks for the honesty and feedback. --AStanhope 23:43, 28 Feb 2005 (UTC)

on type 2 causing obesity edit

User Bollar, I am not sure your sentence belongs in the cause section. Were you implying that the this fact contradicted the previous sentence on ob causing type 2 (which is a misunderstanding of your reference), or is your sentence erroneously placed and should have been put in the complications of diabetes section? Many people with both kinds of diabetes gain wt with treatment; it is a long-recognized treatment complication that can often but not always be avoided with the usual measures (exercise and eating better). This reference looks like a pretty obscure and not very important one, but if you can provide PMID link, I will look at it. I infer from your sentence and the title that they demonstrate thermogenesis is reduced in some circumstances in type 2 and that therefore it is easier to gain wt? If so, other factors such as treatment effects are quantitatively more important and this could be explained in the complications section.

I haven't removed the sentence because much of the article needs a rewrite for balance, completeness, accuracy and style, but could you clarify your sentence please or move it? thanks alteripse 14:14, 15 Mar 2005 (UTC)

Hi Alteripse - no problem PMID 10643689 - I'm willing to discuss where this research is placed in the article, and I'm reluctant to add lots of text to an already long article, but let me be clear that I do believe that T2 predisposes an individual to obesity. The NIDDK has done much research on the topic with the Pima Indians and I think this article, which discusses the "thrifty gene" theory is a good synopsis: Obesity Associated with High Rates of Diabetes in the Pima Indians. I think this could easily become a "chicken and egg" discussion, couldn't it? Do the Pima have diabetes because they're fat, or are they fat because they have diabetes? Bollar 14:53, Mar 15, 2005 (UTC)
I'm with Alteripse, you got the chicken and egg mixed up. Obesity leads to type 2 DM, not the other way around. You may or may not be predisposed to obesity or DM genetically but the relationship between obesity and DM seems clear enough. Alex.tan 05:10, 20 Mar 2005 (UTC)

It's an interesting topic. I agree that in some circumcstances it might be difficult to determine which comes first and the research article suggests that there is an association between poorer insulin sensitivity and reduced glucose thermogenesis. We think that poorer insulin sens is a precursor to type 2 diabetes. In children and adolescents we see the obesity precede the type 2 diabetes almost always, and it can often be reversed by wt loss. It's hard to be persuaded that the main relationship isn't the conventional wisdom of ob leads to ins resistance, insulin resistance plus genetic risk for inadequate beta cell insulin response leads to hyperglycemia, chronic hyperglycemia kills off remaining beta cells. Nothing in the Pima link contradicts this paradigm. Let's leave it and elaborate the issue when we break this into a separate type 2 article. alteripse 00:06, 16 Mar 2005 (UTC)

Some interesting research is published in this month's Diabetes. In short, it indicates that a variant of the ENPP1 gene is much more common in people with diabetes and helps to explain why all obese people don't develop T2 and some thin people do develop T2. It also confirms why ethnic groups develop T2 at differing rates. Abate, N. Diabetes, April 2005; vol 54: pp 1207-1213. Bollar 21:31, Mar 28, 2005 (UTC)

Articles of this type are published at rates of 20 a month. If it's truly a breakthrough. we'll hear about it. JFW | T@lk 19:34, 10 Apr 2005 (UTC)

Declaration of St Vincent edit

That is a red link. Who knows more about it? Was it composed by doctors, patients, busybodies or all of the above? JFW | T@lk 20:03, 13 Apr 2005 (UTC)

It is really unobjectionable. As I recall it dates to the late 1980s and was primarily a result of an international congress that was mainly European if I recall correctly. It outlines basic health care "rights" or least minimal desires for diabetes care (like access to blood testing supplies and insulin) in a very vague and general way. I think it was mainly diabetes doctors but couldn't swear to the absence of busybodies. I will see if I can find a live link. alteripse 00:31, 14 Apr 2005 (UTC) My memory is pretty good. Here: [1]

too many external links edit

Wikipedia is not a collection of links. Would someone like to go through the external links and prune them down to relevant links? Perhaps best link in each category? Thanks. Alex.tan 17:06, 27 Apr 2005 (UTC)

The reasoning behind including Pancreatic cancer link and a hundred others edit

I noticed that the link for Pancreatic cancer in the diabetics article under the See Also section is removed. The reason why i included it was that a distant relative of mine was infected with pancreatic cancer and it seems he later had diabetes. I was initially confused and the doctors later told me that pancreatic cancer generally leads to diabetes and occasionally vice versa, since both diseases affect the pancreas. So I decided to add a link to a disease closely related to the organ that it affects to the article. Here are some reports and links on the matter. [2] [3] Hope this clarifies. --Idleguy 08:30, Jun 23, 2005 (UTC)

Your first link states quite unequivocally that diabetes is not a recognised risk factor. The second one (a very good find!) also surmises that the evidence is conflicting and far from conclusive. As most diabetics do not get pancreatic cancer, and most pancreatic cancer patients do not have diabetes, I would really prefer this article to focus on the basics. PS one is not "infected" with cancer :-) JFW | T@lk 23:32, 23 Jun 2005 (UTC)

We should be reluctant to discourage a new contributor. Let's at least give him more of an explanation. First, the pancreatic cancer/diabetes link is a relatively trivial, one way association. There is not much of a risk of having pancreatic cancer from diabetes. Since most patients with the misfortune to get pancreatic cancer end up with all or most of their pancreas removed (assuming they are even operable) and getting marinated in chemotherapy, the diabetes is a result of the pancreas removal rather than the cancer itself. Second, at some point when the article is better organized, balanced, and pruned, there should be a list of conditions which predispose or are causally or statistically associated with diabetes. In addition to pancreatic cancer, it would include everything from MELAS mitochondrial disease to PGA1 to long-term evolution of congenital hyperinsulinism to several forms of polycystic kidney disease to organ transplants to pancreatectomy to bone marrow transplants to cystic fibrosis to myotonic dystrophy to celiac disease to Friedreichs ataxia to pancreatitis to diabetes insipidus/optic atrophy to acromegaly to Berardinelli-Seip Lipodystrophy syndrome to Cushing syndrome to... you get the picture: there are literally hundreds of diseases we could link to. Rather than put them all in the See also section, I would propose a table/list somewhere in the article. alteripse 01:07, 24 Jun 2005 (UTC)

I would have to agree with Alteripse's suggestion. I'm just a layman with an interest in bio-sciences, but diabetes has been one area I happened to know a lot more since many of my relatives seem to have it and so I stumbled upon pancreatic cancer patients too. Some doctors here swear that one is doomed to get diabetes once pancreatic cancer "sets in" or "attacks" (since I don't know the right medical term). Others are not convinced, so maybe a list of other closely linked diseases could be put up in a list that affect pancreas. Tx for the info. --Idleguy 04:59, Jun 24, 2005 (UTC)
Perhaps it was the use of "see also". Articles in "see also" should really have a fairly close relationship with the linking article to qualify. JFW | T@lk 07:19, 24 Jun 2005 (UTC)