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diabetes FAQ: research (part 5 of 5)

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Archive-name: diabetes/faq/part5
Posting-Frequency: biweekly
Last-modified: 14 July 2005

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Changes: see part 1 of the FAQ for a list of changes to all parts.


Subject: READ THIS FIRST Copyright 1993-2005 by Edward Reid. Re-use beyond the fair use provisions of copyright law and convention requires the author's permission. Advice given in m.h.d is *never* medical advice. That includes this FAQ. Never substitute advice from the net for a physician's care. Diabetes is a critical health topic and you should always consult your physician or personally understand the ramifications before taking any therapeutic action based on advice found here or elsewhere on the net.
Subject: Table of Contents INTRODUCTION (found in all parts) READ THIS FIRST Table of Contents GENERAL (found in part 1) Where's the FAQ? What's this newsgroup like? Abuse of the newsgroup The newsgroup charter Newsgroup posting guidelines What is glucose? What does "bG" mean? What are mmol/L? How do I convert between mmol/L and mg/dl? What is c-peptide? What do c-peptide levels mean? What's type 1 and type 2 diabetes? Is it OK to discuss diabetes insipidus here? What is it? How about discussing hypoglycemia? Helping with the diagnosis (DM or hypoglycemia) and waiting Exercise and insulin BLOOD GLUCOSE MONITORING (found in part 2) How accurate is my meter? Ouch! The cost of blood glucose measurement strips hurts my wallet! What do meters cost? Comparing blood glucose meters How can I download data from my meter? I've heard of a non-invasive bG meter -- the Dream Beam? What's HbA1c and what's it mean? Why is interpreting HbA1c values tricky? Who determined the HbA1c reaction rates and the consequences? HbA1c by mail Why is my morning bg high? What are dawn phenomenon, rebound, and Somogyi effect? TREATMENT (found in part 3) My diabetic father isn't taking care of himself. What can I do? Managing adolescence, including the adult forms So-and-so eats sugar! Isn't that poison for diabetics? Insulin nomenclature What is Humalog / LysPro / lispro / ultrafast insulin? Travelling with insulin Injectors: Syringe and lancet reuse and disposal Injectors: Pens Injectors: Jets Insulin pumps Type 1 cures -- beta cell implants Type 1 cures -- pancreas transplants Type 2 cures -- barely a dream What's a glycemic index? How can I get a GI table for foods? Should I take a chromium supplement? I beat my wife! (and other aspects of hypoglycemia) (not yet written) Does falling blood glucose feel like hypoglycemia? Alcohol and diabetes Necrobiosis lipoidica diabeticorum Has anybody heard of frozen shoulder (adhesive capsulitis)? Gastroparesis Extreme insulin resistance What is pycnogenol? Where and how is it sold? What claims do the sales pitches make for pycnogenol? What's the real published scientific knowledge about pycnogenol? How reliable is the literature cited by the pycnogenol ads? What's the bottom line on pycnogenol? Pycnogenol references SOURCES (found in part 4) Online resources: diabetes-related newsgroups Online resources: diabetes-related mailing lists Online resources: commercial services Online resources: FTP Online resources: World Wide Web Online resources: other Where can I mail order XYZ? How can I contact the American Diabetes Association (ADA) ? How can I contact the Juvenile Diabetes Foundation (JDF) ? How can I contact the British Diabetic Association (BDA) ? How can I contact the Canadian Diabetes Association (CDA) ? What about diabetes organizations outside North America? How can I contact the United Network for Organ Sharing (UNOS)? Could you recommend some good reading? Could you recommend some good magazines? RESEARCH (found in part 5) What is the DCCT? What are the results? More details about the DCCT DCCT philosophy: what did it really show? Is aspartame dangerous? IN CLOSING (found in all parts) Who did this?
Subject: What is the DCCT? What are the results? The Diabetes Control and Complications Trial was a large multi-center trial involving over 1400 volunteer patients with type 1 diabetes. It began in 1983, ramped up to full speed by 1989, and ended early in 1993 when the investigators felt the results were clear. The volunteers were all undergoing "standard" treatment when they were recruited, meaning one or two injections per day. They were randomly assigned to two groups. One group continued as before. The other group received intensive treatment aimed at achieving blood glucose (bG) profiles as close as possible to normal. The intensive treatment involved multiple bG checks per day, multiple injections and/or an insulin pump, and access to and regular consultation with a team of treatment experts. It is particularly important to note that intensive treatment was defined as a collaborative effort involving the patient and a skilled team of health care professionals. It was not defined by particular techniques, although certain techniques were typically used. The frequent consultations and availability of a professional team were critical components of intensive therapy. The results show that the intensive treatment group did indeed achieve bG levels closer to normal, and that they experienced far fewer diabetic complications though also more hypoglycemia. In particular, patients who maintained HbA1c levels around 7% appear to be much better off than those whose HbA1c hovers around 9%. (See caveats in the section on HbA1c.) Though it is not possible to separate the effects of all the aspects of the intensive treatment, it is reasonable to believe that lowering average bG may be effective even in isolation from the other aspects of the intensive treatment. In its position statement, the ADA says Patients should aim for the best level of glucose control they can achieve without placing themselves at undue risk for hypoglycemia or other hazards associated with tight control. Though type 2 patients were not included in the study, it is generally believed that the results showing the benefits of tight control apply to type 2 patients as well. The entire position statement was published in most of the ADA's publications (see "could you recommend some good reading") in the summer and fall of 1993. The formal report detailing the results was published in The New England Journal of Medicine, aka NEJM, of September 30,1993 (v 329 pp 977-986). The following discussion is based on that article. Several DCCT subjects participate in m.h.d and are willing to answer questions related to the personal aspects of DCCT participation.
Subject: More details about the DCCT The study placed subjects into two cohorts, primary prevention or secondary intervention, depending on duration of diabetes and existing complications -- the primary prevention cohort were those with essentially no complications. Specifically: all subjects met these criteria: Insulin dependent as evidenced by deficient C-peptide secretion Age 13 to 39 years at entry to the study No hypertension, hypercholesterolemia, severe diabetic complications, or other severe medical conditions Meet the criteria for one of the cohorts and were separated into the two cohorts by these criteria: Primary Secondary Prevention Intervention Cohort Cohort Duration of IDDM 1-5 yrs 1-15 yrs Retinopathy none detectable very mild to moderate nonproliferative Urinary albumin < 40 mg / 24 hr < 200 mg / 24 hr Within each cohort, the subjects were randomly assigned to either conventional therapy or intensive therapy. Thus the study compared intensive to conventional therapy in two different cohorts. The two questions the study was mainly designed to answer were 1) Will intensive therapy prevent the development of diabetic retinopathy in patients with no retinopathy (primary prevention), and 2) Will intensive therapy affect the progression of early retinopathy (secondary intervention)? Conventional therapy included one or two injections per day, daily self monitoring of blood or urine glucose, education, quarterly consultations, and intensive therapy during pregnancy. Intensive therapy included three or more daily injections or an insulin pump, bG monitoring at least 4x/day, adjustment of insulin dosage for bG level and food and exercise, monthly personal consultations and more frequent phone consultations. To simplify a lot, the DCCT showed the following changes in the intensive therapy groups compared to the conventional therapy groups. Note that '-' shows a decrease, '+' shows an increase, in the number of patients affected. Patients were judged as affected or not based on binary criteria, so the results only say how many subjects were affected, not how severely those subjects were affected. Intensive therapy compared to conventional therapy: Primary Secondary Complication Prevention Combined Intervention ------------ ---------- -------- ------------ Retinopathy(*) - 75% - 55% Nephropathy(*) - 35% - 45% Neuropathy(*) - 70% - 55% Hypoglycemia(*) +200% Weight gain(*) + 33% Hypercholesterolemia(*) - 35% (*) This brief table begs many questions about what exactly was measured and how. For more details, read the paper. There were no detectable differences on several measures: Macrovascular disease Mortality Changes in neuropsychological function (a feared result of severe hypoglycemia) Quality of life (based on a questionnaire) Some limitations of the study: type 1 only, patients young and with short duration (under 15 years) of diabetes, and short duration of the study (5-9 years). Measured only number of subjects affected according to binary criteria, not by measurement of severity of complications. Excluded patients who already had severe complications and who thus might benefit the most. The difference between the groups increased during the study, but there is no proof that the difference would continue to increase with time. It is tempting to extrapolate the results to all diabetic patients -- all types, ages, and durations -- and there is at least some support for doing so. However, the DCCT by itself does not show results for type 2 patients, older patients, patients who have had diabetes for many years, or those who already have severe complications. On the other hand, a different group of subjects might shows differences in areas such as mortality and macrovascular disease, where the young DCCT cohorts simply did not have significantly measurable incidence. The DCCT subjects are being tracked in a followup study which may shed light on some of the unanswered questions. Secondary analysis of the data indicates that retinopathy decreases with decreasing HbA1c. This measure was not part of the study design and is more difficult to interpret, but still shows clearly a correlation between HbA1c and retinopathy.
Subject: DCCT philosophy: what did it really show? It is often stated that the DCCT proved that tight control or lowered HbA1c reduces complications. This is not the case. The controlled variable in the DCCT was intensive vs conventional therapy, and intensive therapy was defined by several factors including a team of skilled health care professionals acting in partnership with the patient. The results show that intensive therapy results in both lowered HbA1c and fewer complications, but do not show that one causes the other. The lead authors provide a good summary of this point in a followup (NEJM 330:642, March 3, 1994): We want to stress that the most valid interpretation of the trial is that intensive therapy, with the **goal** of achieving blood glucose concentrations as close to the nondiabetic range as possible, delays the onset and slows the progression of long-term diabetic complications. The secondary analyses support the notion that lower glycosylated hemoglobin values are associated with a lower risk of progression of retinopathy, but they do not prove that hyperglycemia in itself causes retinopathy. [emphasis added] Many of us believe, and believed before the DCCT, that actually achieving good control aids our health. The DCCT adds weight to this case but does not prove the point.
Subject: Is aspartame dangerous? In short, no, except for phenylketonurics. Aspartame is one of the most intensively studied food additives ever, and the overwhelming scientific evidence is that it poses no danger. The many claims of harm are all either anecdotal and not supported by adequate observation, or are based on serious lack of understanding of how to demonstrate facts scientifically. One of the most egregious is the claim that studies with aspartame in capsules are invalid and that it's only dangerous in solution. But d'oh -- if you administer aspartame in solution, the patient will know whether he/she is getting aspartame or not. This unblinds the experiment. Refer to Reid's Third Law: Never Underestimate the Power of Suggestion. An good set of links to web pages on aspartame is at http://urbanlegends.about.com/library/blasp3.htm. (Unfortunately the links open framed by about.com's heading, an unfair practice eschewed by the vast majority of web sites. Ten demerits for about.com.) The well known low-calorie sweeteners are pretty much all safe: cyclamates, saccharin, aspartame, acesulfame, sucralose. Yes, even cyclamates and saccharin -- the studies which resulted in their banning turned out to be non-reproducible. I don't list stevia because it has not been adequately studied, but I know of no significant indications of danger. If you don't like a given sweetener, try another. If you think you respond badly in some way to a sweetener, try another. But unless you have at least a heterozygous gene for phenylketonuria, it's unlikely that you'll have a verifiable response to aspartame.
Subject: Who did this? -- Edward Reid <edward@paleo.org> Tallahassee FL -- Art works by Melynda Reid: http://paleo.org eid: http://paleo.org y Melynda Reid: http://paleo.org

User Contributions:

Raqiba Shihab
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May 10, 2012 @ 2:14 pm
Many thanks. My husband has Type 2 diabetes and we were a bit concerned about his blood sugar/glucose levels because he was experiencing symptoms of hyperglyceamia. We used a glucometer which displays the reading mg/dl so in my need to know what the difference
between and mg/dl and mmol/l is, i came across your article and was so pleased to aquire a lot more info regarding blood glucose, how to read and convert it.
Bhavani
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Aug 11, 2012 @ 9:09 am
It was really informative and useful for people who don't know conversion. Thanks to you
tamilarasan
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Oct 15, 2014 @ 1:01 am
The aqueous solution was prepared by mixing the calculated amount of KOH (5.61&#8201;g, 100&#8201;mmol) and Cobalt acetate (7.08&#8201;g, 40&#8201;mmol) and then stirred for 2 hours followed by refluxing for 4 hours as shown in Scheme 1. After filtration, the residue was washed with distilled water until the eluent shows pH 7. The residue was calcinated at 450C for 4 hours in dry nitrogen. Black powder was obtained with 85% yield

how much di water used for cobal oxide preparation sir please tell me sir

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