Talk:Insulin resistance
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[edit] I
I added back the reference to the presentation of Dr. Andrew P. Selwyn on CME on Diabetes that has been deleted during (I suppose) a spamming done a few days ago. This source has been used for the Pathophysiology section. -Eridanis
Why is there an IP number on top of this article? 205.174.22.25 03:36, 6 February 2007 (UTC)
[edit] Spam
An anon keeps on inserting an animal study linking bisphenol A with insulin resistance[1]. We have to be very very selective with animal studies. Only if they display a major trend in research, a very useful animal model, or somesuch, are they worthy of inclusion. I agree with Wouterstomp (talk ยท contribs) this link should stay out until its relevance in humans becomes known. JFW | T@lk 23:35, 18 December 2005 (UTC)
This article is a little heavy for the lay person like myself. Could someone maybe make it a bit more readable for the non medically trained? Pipedreambomb 23:37, 3 March 2006 (UTC)
[edit] Intelligibility
Someone should really re-write that opening sentence in English, no? I think I understand what it's saying, but I'm not confident enough to re-explain it.
...in fact, that goes for much of this article. At the minimum, medical jargon which is likely to be unfamiliar to the educated lay reader should be linked. --Oolong 21:12, 5 June 2006 (UTC)
- I have rewritten the introduction in what I believe is simpler terms and more detail, making wikilinks to all of the medical terms. I hope that this satisfies you. It looks better to me. --Ben Best 14:39, 6 June 2006 (UTC)
[edit] identical to "metabolic syndrome" ?
Since I'm being flamed for edits, I'll just leave the reference, so an approved editor can deal with it:
http://www.ajcn.org/cgi/content/abstract/83/6/1237
The article is heavy. It should also note that there are many causes of insulin resistance including atrophy and cells already being plump with glycogen, autoimmunity is just one, and that both cells and people can be so referred to, since some cells in an individual can be insulin resistant while others aren't.
The essential point is that insulin is a hormone - just the messenger. It requests cells that "excess" glucose be stored as glycogen. If the message isn't acted on, for whatever reason (including not getting to the cell as in autoimmunity), that's "insulin resistance" or at most what parents refer to as "selective hearing." (to be much too flip)
Again, I'm being flamed for contributions, so I will leave this editing task to someone in the inner circle, or much closer to it.
[edit] Monounsaturated Fat-Olive Oil leads to Insulin Resistance? Polyunsaturated Fats All Good?
The one study that I've seen that promotes this hypothesis concerning olive oil is the one this article refers to. There are many more studies that cite olive oil (and other monounsaturated fats)as neutral to good. Additionally, the blanket statement that polyunsaturates (which include omega-6 and omega-3 oils) lessen/mitigate insulin resistance sidesteps the extreme difference in effects of the two on hormone production and inflammation. In essence, the information on fats and insulin resistance appears both biased toward a limited amount of evidence for one hypothesis about monounsaturates(to the exclusion of the greater body of evidence), and a gross generalization that could lead people to believe that all polyunsaturated fats are equal (omega-3's are known to lessen inflammation, while most omega-6's are known for inflammatory properties). I've read that a quarter of the adult population has developed, or is at risk for developing some form of insulin resistance. That's a lot of people who could be coming here for guidance after the doctor has told them they are pre-diabetic, and they deserve better.
-Believe it or not, there are interesting individuals out there (Perricone fans?) who think that fish-based omega-3s reduce inflammation while plant-based omega-3s increase it. I wish I knew where they were getting this.--Dseilhan 21:38, 20 March 2007 (UTC)
[edit] Connecting the Dots
The National Insulin Resistance Council (NIRC) appreciates both the technical complexity and the mystery of how insulin resistance starts and works. While scientific research goes on, NIRC believes that there are enough dots to be connected into a pretty clear picture. And the picture leads us to believe that there are specific things that can be done to improve it by a wide margin.
Consider this logic: No one doubts the links between insulin resistance (IR), diabetes and IR and CVD. Nor are the links between IR and PCOS and metabolic syndrome in question. Intervention with IR patients even when they have become symptomatic prolongs healthy life, and defers disease. The villian in IR is hyperinsulinemia, having too much insulin too much of the time. Insulin is suspect in liver signaling related to glycogen creation. Insulin is caustic and erodes the inner linings of vascular tissue and the outer sheathing of certain nerve tissue. These effects occur whether a patient is symptomatic or not. IR appears to be genetically programmed, evidenced by the epidemiological data relating family diabetes and CVD histories. IR certainly is aggravated by excess weight, and may be triggered by it. If IR is the staging for consequential illness, and its effects occur unseen until symptoms like high blood pressure, elevated blood sugar or menstrual disruption show up, then why don't we seek to identify its presence early, before it does so much of its slow, relentless damage? More logic, this part social: There are 21+ million active diabetics in the US today and over 400 thousand fatal heart attacks not attributable to cholesterol. Related sick care costs all taxpayers nearly 30% of Medicare expenses, all linked to IR. PCOS, caused by IR, is a significant cause of fertility issues, but the proportion is not known for lack of tracking. In addition to the costs of active non-infectious disease care, who would guess at the cost of all the avoidable cases of PCOS, hypertension, gestational diabetes, diabetes, and CVD? The children and young adults of today with undetected IR are tomorrow's diabetics and CVD victims, yet they don't have to be. Why aren't we scrambling to find ways to prevent non-infectious disease as hard as we scramble to deal with it?
NIRC proposes specific actions: 1. Immediate efforts to find the easist, least costly, least intrusive, and most effective means to screen children and young adults for IR should be started and the best ones rolled out. 2. The CDC should track and report the incidence of IR. Today, it does not even include IR in its index of conditions. 3. The CDC should track and report the incidence of PCOS and especially the fertility complications from it. 4. The CDC should track and report the incidence of metabolic syndrome.
Decades before the tobacco industry conceded that smoking caused cancer, warnings were put on their products. Shouldn't people who have IR know it, so they can take action to blunt its effects before their lives have been shortened by it?
The National Insulin Resistance Council's purpose is to educate health care professionals and the public about IR, its effects and to propogate workable interventions.
151.200.237.196 00:59, 17 May 2007 (UTC)fs@insulinresistancecouncil.org
[edit] NIRC, source your edits
First, Wikipedia is not the place for starting social change, or making social commentary. Wikipedia is a place for facts, and NIRC's comments above in "Connecting the Dots" are inappropriate. Secondly, NIRC makes a verifiable claim, to wit: "Nevertheless, metformin, the 8th most often prescribed drug in the US, is often prescribed for pre-diabetes and insulin resistance, despite FDA instructions". I am deleting this phrase, but anyone may feel free to re-add it should they be able to properly cite a reference for it. Finally, the use of "NIRC ED" to distinguish edits made by NIRC is inappropriate. The proper place to note the source of a fact is in a footnote to that effect, and anything that is not a fact, if it deserves to be in the article (e.g. connecting text), does not deserve to be especially distinguished from the rest of the article.
--Popefelix 18:54, 8 October 2007 (UTC)
