[acb-diabetics] many articles

Sat Dec 29 18:44:33 EST 2012

Thanks so much always very informative.

Nancy Matulis
ACB Maine member
Sent from my iPad

On Dec 29, 2012, at 5:35 PM, "Patricia LaFrance-Wolf" <plawolf at earthlink.net> wrote:

> 1.%% M 11/2 How Does DM Affect the Brain?  EASD  Leszek Czupryniak, MD, PhD: Dr. Boris Mankovsky,  Kiev U/  Boris, you're an expert in diabetic neuropathy [DMN ]..what can you tell us about the latest research on DMN Dr. M: one interesting discussions was re the failures in recent clinical trials; we had many promising new drugs to treat pts with DMN, but most of those failed.. In treating DMN, we usually have to distinguish between  disease- modifying meds, &  symp tom [pain] -modifying meds. Of course, it would be great to have meds that could [do both] new trials,COMBO-DN ,com pared the efficacy of 2 pain-relieving drugs,,duloxetine & pregabalin, in painful DMN...only one third of the pts got a reduc tion of pain of more than 50%. ..in many cases, painful DMN is very difficult to treat.
> %% Dr. M- this was probably the first time in the long history of EASD that we had a special session devoted to hyperglycemia & the brain. It's really very exciting because for many years, we believed that the brain was not affected by DM. Now, the brain is probably considered another target for DM  complications.
> Brain damage can occur in 3 ways. By cere- brovascular disorders - DM is an indepen dent risk factor for stroke. Also, DM could lead to cognitive impairments & even dementia - many trials have confirmed that DM is assoc with a 2-3 times higher risk for Alzheimers. Finally, DM is also assoc with a higher risk for depression.  Researchers in Poland did a 10yr study of pts with DM  identifying risk factors for stroke:age,fasting glycemia level,  albuminuria, atrial fibrillation & smoking. Another discussion  noted once again that DM  is assoc with memory & executive function impairments, so we should keep this in mind when treating our pts with DM.  Dr C:Yes  my feeling is that brain problems in DM  are under recognized by the general medical community. We remember to think about the kidneys, heart, eyes, & feet, but the brain often is omitted in this long list of potential DM complications.
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> 2.%% MP 11/26  Caffeine-diabetes link still unresolved: Sugary drinks are linked to a heightened risk of developing T2DM. In recent studies it has been confirmed that there is little knowledge on whether caffeine, as suggested in past studies, has a link to sugar processing. Among more than 100,000 men & women followed for 22 years, those who drank sugar-sweetened drinks were as much as 23% more likely to develop DM than those who didn't. According to a study that appeared in The AmerJ of Clinical Nutrition it has been said that coffee can be beneficial & the caffeine doesn't appear to have a positive or negative effect on DM risk. Numerous past studies have linked regular consumption of soft drinks, both sugar & artificially-sweetened, to increased risk of DM. Research over the past decade has also suggested that caffeine temporarily prevents the body from processing sugar efficiently. Recent studies have examined the health habits of 75,000 women & 39,000 men involved in long-term health studies that began in the mid-1980s. Compared to people who didn't consume sugary drinks, the likelihood of developing DM over the years for those who did was higher by 13% for caffeinated sugary drinks. Caffeine-free artificially sweetened drinks were also linked to a 6% increase in risk among women. However, coffee drinkers showed slightly lower risks vs non-drinkers. The chances of developing DM were 8% lower among women, whether they drank decaf or regular coffee, & for men, 4% lower with regular coffee & 7% lower with decaf. The same dataset, which contains the health habits of mostly white health professional, suggest that regular coffee drinking, in general, is tied to a lower risk of DM. But past studies have also found that the risk falls even lower if adults drink decaffeinated coffee. There are studies that link caffeine to a disruption of the body's ability to process glucose. The latest study suggests that pts  who currently drink sugary beverages could substitute coffee or tea, instead. But other researchers said that more work is necessary to untangle caffeinated coffee's complicated relationship with DM risk, & that it is still too early to advise people to drink coffee if they don't do so already. Reuters Health   ca
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> 3.%% ADA 11/30 Genetic variant associated with T1 & other autoimmune diseases  influences susceptibility to autoimmunity.  Scientists (Joslin) have shown that a mutation in  PTPN22 which has a role in lymphocyte function can lead to T1DM . The gene is involved in the formation of a key protein (lymphoid tyrosine phosphatase (LYP), which helps control the activity of T & B cells in the immune system. The mutation  generates a variation of LYP with a different molecular structure.. Using a mouse model, the team was able to turn off & on the PTPN22 gene in the  mouse. When this gene was turned off they saw a  increase in regulatory T cells & decreased risk of autoimmune DM. Thus, the PTPN22 knockdown actually conferred protection from disease. The study may further the development of new therapeutic options that inhibit LYP to reduce or prevent autoimmunity.
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> 4.%% ADA 11/30 When You're Sick    Being sick can make your blood glucose (sugar) go up & possibly put you in a coma. To prevent illness from being a problem, work out a sick-day action plan.  When you are sick, you're under stress. Your body releases hormones that help it fight disease. But these  hormones have side effects. They raise blood sugar levels & interfere with the BS-lowering effects of insulin. As a result, when you are sick, it is harder to keep your BS in your target range.    Ketoacidosis can lead to a diabetic coma a dangerous condition. It is key to measure BS & urine ketones. Work with your doctor, or a DM educator. Contact either/both when: 1)you have had a fever for a couple of days & aren't getting better, 2) when you've been vomiting/having diarrhea for more than 6 hours, 3) when you have large amounts of ketones in your urine & your glucose levels are higher than 240, 4) when you have symptoms that might signal ketoacidosis or dehydration, also if you are having trouble breathing or your breath smells fruity/your lips or tongue is dry & cracked). Then: be ready to tell what medicines you've taken & how long you've been sick, whether you can eat & keep food down, whether you've lost weight. Keep written records as you become sick. No matter what kind of DM you have, measure your BS & urine ketones more often than usual. If you have T1DM, you may need to measure BS & urine ketones every 4 hours. Measuring ketones is very important because these waste products build up when you are sick & lead to ketoacidosis. If you have T2DM, you only need to measure ketones if your BS is higher than 300. If you have T1, you may have to take extra insulin to bring down the higher blood sugar levels. If you have T2, you may be able to take your pills, or use insulin for a short time. In either case, work with your DM team to develop your sick-day plan. For eating & drinking, stick to your normal meal plan. Drink lots of non-caloric liquids to keep from getting dehydrated. Using extra fluids will help get rid of the extra sugar & ketones in your blood. Take in your normal number of calories eating easy-foods like regular gelatin, soups, crackers, & applesauce. Aim for 50 grams of carbo hydrate every 3-4 hours. Have on hand at home a small stock of non-diet soft drinks, broth, applesauce, & regular gelatin.  ca
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> 6.%% ADA 12/1 Treat T1 to Treat Hardened Arteries    Pancreatic islet transplantation [ITr] may improve atherosclerosis related to DM. Atherosclerosis occurs when fat, & cholesterol build up to form plaque.Trans- planting pancreatic islet cells may improve arteries in pts with T1DM. Islet cells are made of beta cells,which produce insulin. When these cells become damaged the body does not get the insulin needed to control levels of sugar in the blood. One marker of  athero sclerosis is the thickness of the carotid arteries, that carry blood to the head, neck & brain. Pancreatic ITr involves taking islets from the pancreas of a deceased organ donor & implanting them in another person. From their study, Dr. Danielson & team found carotid intima-media thickness decreased by about 0.058 mm 12 months after pts underwent ITr. The decrease continued from 12-50 m. Pts who underwent the procedure had improved HbA1c & better DM control. More research on larger groups is needed to see if islet transplantation actually relieves atherosclerosis in pts with T1. pub Nov 19 in Diabetes Care, a journal of the ADA  By: Travis Hill   ca
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> 7.%% MPD 12/5 Diabetes-Statin Link Hinges on Risk Factors   Compared with lower-dose statin therapy, atorvastatin (Lipitor) [ator] 80 mg/d did not increase the incidence of new onset DM in pts with only one risk factor for [it] Among those with 2-4 risk factors, however, the higher dose increased the rate of new- onset DM. However compared with low- dose statins, ator 80 mg reduced the number of CV events in pts at both low & high risk for DM. [15,056pts] w coronary disease but not DM at baseline; analysis of 2 random ized trials.  TNT & IDEAL trials funded by Pfizer.
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> 8.%% MP 12/6 Mouse Study Offers Clues to Obesity- Diabetes Link   Researchers say they've found a way to weaken the connection between the two -- at least in mice. The key, they say, is blocking the body's inflammation response to high-fat foods. The team
> turned off the JNK (pronounced "junk") genetic  pathway in mice, & fed them high-fat diets. Even though the mice became obese, they didn't develop insulin resistance, a forerunner to DM. Other similarly stuffed mice with intact JNK pathways, did become insulin resistant... it's too early to say whether the findings might apply to humans. "Everybody has these genes -they're in all cells of your body all the time," said author R Davis. "What they do is respond to the diet that you're eating. So if you eat a high-fat, cafeteria diet, it leads to activation of the protein products (enzymes) of these genes...we  discovered that JNK genes in the macrophages [Mp] are critical for the ability of Mps to cause inflammation, specific ally in response to eating a high-fat diet. Macrophages (white blood cells) attack foreign invaders of the body They fight infection but their inflamm response can be harmful too. Inflammation has been linked to condi tions such as arthritis, heart disease & cancer.  In the study..not having JNK genes in [mice Mps] prevented the inflamm that takes place in the body in response to feeding & that in turn prevented the development of symptoms of pre-DM, like insulin resistance,"  Dr J Zonszein, Montefiore) who was not assoc with the study, said science in this area has gone beyond realizing that having more body fat is a risk factor for DM. "We have the so-called healthy obese who have less fatty tissue, they have less inflamm, they have less Mps..And we have some pts  who don't look obese but their [fat] tissue is loaded with Mps particu larly bad macrophages."  He added, however, that what goes on in the human body is much more complex.[than in mice].. this is science - something that we need to learn from. But from this to drug- development in humans, there is a big, big stretch,". One take-away message, he said, is that eating unhealthy foods immediately affects your body. "Sometimes people think that you eat a poor diet & at some later time there are some bad effects...But some of these things can be much more direct." Source Roger Davis, PhD,molecular med, U Mass Med School
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> 9.%% NIH 12/2012 Review supports use of metformin as first-line therapy for pts with T2   New research from the Effective Health Care Program of the Agency for Healthcare Research & Quality, studied metformin & sulfonylureas use among pts beginning to take oral meds to treat T2. The use of sulfos was assoc with an increased risk of CVD events including death- among study pts compared with metformin use. More studies are needed to clarify whether the difference in risk is due to harm from sulfos, benefits from met, or both. [250,000pts] from VA. The findings support the use of metformin for first-line T2 Rx for pts without other contraindications "Comparative Effectiveness of Sulfo...& Met...Monotherapy on CV Events in T2DM CL Roumie et al; Nov 2012 Annals Internal Med 157(9)
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> 10.%% Ahrq Dec 2012 Delaying the control of BP among middle-aged adults with DM lowers quality of life.  [10,000 hypothetical pts]The team estimated the harm levels of different delays in controlling BP in adults age 50-59 w T2. With a lifetime of uncontrolled systolic BP, complications increased by 1855 events per 10000 pts, av life expectancy decreased by 209 days, & av quality-adjusted life expectancy (QALE) decreased by 332days, compared to a group w T2 who had a lifetime of controlled systolic BP (130 mmHg).  A 1year delay in Rx increased lifetime complications by 14 events/10,000 pts  A 10year delay increased lifetime complications by 428 ev/10,000 pts & decreased QALE by 145 days- the same extent as smoking in pts with CVD. study supported in part by the Agency for Healthcare Research and Quality (HS16967).
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> 11.%% M12/12  Visual Impairment Rise Tied to Increased Diabetes Prevalence  Troy Brown     The prevalence of non-refractive visual impairment [VI] in the US has increased 21% overall & 40% among non-Hispanic whites aged 20-39 years, according to a study published in the December 12 issue of JAMA.   A sample of the US population of non-refractive visual impairment & its relationship risk factors including diagnosed DM was used. A key finding is that longer- duration DM which is likely leading to visual outcomes that are going to affect not only older people who frequently have longer-term DM but more young people as well.  DM prevalence increased from 6.5% in 1999-2002 to 8.2% in 2005-2008.When considering age & ethnicity together, prevalence of non-refractive VI increased in most groups. The passage of 10 or more yrs. from the time of DM diagnosis was associated with an increased risk for non-refractive VI. The most harmful factors were lack of health insurance, lower education level, & poverty.  "The visual acuity that we used for this study is worse than 20/40 in both eyes, which cannot be corrected with glasses. It's not blindness, but it is meaningful vision loss..... That kind of vision loss doubled among those 20-40 yrs of age. The study stated that all permanent blindness from DM can be prevented with proper vision screening. A biological chain of events is activated in a person who is obese, & non-refractive VI is one potential outcome. Improvement in nutrition & exercise, are important risk factors for DM.  Ca study support by [includes] Centers for Disease Control and Prevention. JAMA. 2012;308(22)
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> 12.%% NrevEndo Jan 2013  Diabetes:O-GlcNAcylation a new diagnostic tool for T2DM?  The extent of protein modification by O-linked ß-N-acetylglucosamine (O-GlcNAcylation) shows potential as a tool for the diagnosis of T2 suggest South African researchers. To read this article in full..
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> 13.%%NREndo Jan 2013 Consumption of legumes might be beneficial in T2   Abstract  A low glycaemic index diet that included high consumption of legumes reduced HbA1c levels & systolic blood pressure in patients with T2 reveal the results of a randomized controlled trial. To read this article in full ...
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> 14.%% NREndo Jan 2013 Effect of vitamin D on diabetic kidney disease [DKD]  in T1DM  Abstract DKDis a leading cause of end-stage renal disease across the world, & in addition, pts with DKD have an increased risk of CV morbidity [sickness] & mortality. Although improved glycaemic control  & aggressive treatment of hypertension with agents that block the renin– angiotensin–aldosterone system (RAAS) have improved the prognosis, diabetic kidney disease remains a considerable problem. ....  © 2012 Nature PubGroup, a division of Macmillan Publishers Limited. All Rights Reserved  partner of AGORA, HINARI, OARE, INASP, ORCID, CrossRef & COUNTER
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> 15.%% M 12/7 Microaneurysm Turnover May Predict Retinopathy Progression  Automated analysis of microaneurysm (MA) turnover predicted the development of clinically significant macular edema (CSME) among patients with mild nonproliferative diabetic retinopathy (MNDR)  "The most important message is that [MA] turnover, obtained in an automated fashion from fundus digital photographs, which is a simple noninvasive test, can identify the eyes/patients at risk of developing [CSME], the most frequent cause of vision loss due to diabetes," author J Cunha-Vaz told Medscape Med News "Eyes/patients with nonproliferative retinopathy & repeatedly showing little disease activity (low [MA] turnover) may need less frequent eye care,"
> In this prospective observational study, the team used  RetmarkerDR diagnostic system to measure the rates of MA appearances/ disappearances from color fundus photographs. This dynamic measure, which reflects both the closing down of MA because of thrombosis & the appearance of new aneurysms in different places   in the vascular tree, was previously shown to predict worsening of retinopathy to CSME. [410pts w T2 + MNDR;2yrs] The eyes that developed CSME had an average of 6.2 MA vs just 3.3 among eyes that did not develop CSME. multivariate analysis accounting for baseline parameters including age, sex, DM duration, BP, BCVA & central retinal thickness, the rate of MA turnover in the first 6 months independently predicted development of CSME. Eyes with an MA turnover greater than 9 during the initial 6 months had nearly a 6-fold higher risk of developing CSME vs eyes that had a lower turnover   A higher hemoglobin A1c value was the only other significant predictor of progression to CSME among the other parameters analyzed Dr. Cunha-Vaz said that the RetmarkerDR could be used to annually screen pts to identify those at higher risk who might need closer monitoring. "By promptly identifying the eyes/pts at risk for vision-threatening complications, it is possible to treat earlier. These cases will respond better to therapy, thus avoiding late treatment associated with more complex and expensive therapies."  According to P Silva, Harvard Med  "This is an interesting study and potentially may support the use of predictive algorithms & retinal imaging to identify progressive retinal disease in both clinical and research settings." However, he cautioned that 2 years is not sufficient follow-up. "longer and more definitive follow-up studies will be needed to establish broad clinical acceptance of this observation
> and technology." RetmarkerDR is not currently available in the US   Cunha-Vaz is a consultant at Allergan, Alimera Sciences, Bayer, +. Pub online Nov 30, 2012. Diabetes Care
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> 16.%% M The Impact of Serum Lipids on Risk for Microangiopathy [diseased tiny blood vessels] in pts with T2DM   Large-scale study [72,267pts;10yrs) assessed the relative associations of lipid fractions with DM microvascular events. The tested lipid profile components were high density lipoprotein cholesterol (HDL-C), low density lipoprotein chol  (LDL-C), triglycerides (TG), & non-high density lipoprotein chol (non-HDL-C) ..Conclusion: This study demonstrates significant independent assoc among lipid fractions &  risk for microangiopathy. These findings suggest that reaching ADA goals for HDL-C, TG, & non-HDL-C may reduce risk for microvascular events among pts with DM. Cardiovasc Diabetol 2012;11© 2012  BioMedCent,
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> 17.%% M 12/7 FDA Clears Sensus for Painful Diabetic Neuropathy
> The Sensus  Pain Management System, (NeuroMetrix,) has been granted clearance by the FDA   The device is intended to relieve and manage symptoms of chronic intractable pain in the lower leg and foot that can occur with diabetic neuropathy. The device is a transcutaneous electrical nerve stimulator and is worn on the upper calf under clothing. "We believe that physicians treating patients with painful diabetic neuropathy, a severe and debilitating form of chronic pain, will find Sensus to be a useful therapeutic option." The company states that they will be launching the device commercially before the end of the year.
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> 18.%% M 12/16 Estimation of the Glycation Gap in Diabetic Patients With Stable Glycemic Control  The glycation gap (the difference between measured A1C and the value predicted by regression on fructosamine) is stable and is associated with microvascular complications of DM but has not hitherto been estimated within a clinically useful time frame. [311pts-T1&2] Conclusions —The glycation gap can be calculated reliably from pairs of A1C and fructosamine measurements taken 1 month apart   Introduction It is now well established that among pts T1, T2 nondiabetic patients,  there are considerable interindividual differences in A1C that are not accounted for by corresponding differences in glycemia but instead seem to reflect the different glycabilities of hemoglobin in different individuals. McCarter et al.  quantified these tendencies as the hemoglobin glycation index, the difference between measured A1C & the value predicted by regression of A1C on mean blood glucose in the study sample, and found that the hemoglobin glycation index was a statistically significant predictor of retinopathy and nephropathy in the Diabetes Control and Complications Trial (DCCT)...
> Diabetes Care. 2012;35(12):© 2012 American Diabetes Association Inc
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> AhrQ - Agency for Healthcare Research and Quality
> AAO- Amer Academy Ophthalmology
>  Abbreviations-acronyms fup-follow up; pt - patient/participant ; CGM - continuous blood-glucose monitoring ; DM - diabetes Mellitus; T1- type 1 DM;T1A -autoimmune T1; T2 - type 2; DME - diabetic macular edema;DR - DM retinopathy; BS/BG- blood sugar/glucose;  HA1C, glycated hemoglobin A1C; BP -blood pressure; CVD - cardio-vasc disease; IR- insulin resistance; OCT-optical coherence tomography;Pb -placebo; BCVA - best corrected visual acuity; RYGB- Roux- en-Y gastric bypass;  RCT -Randomized controlled trial; ADA - Am Diab Ass;IMN -Internat Med News; M- Medscape Web MD; MA- Medline Abstract, MP- Medline Plus; MPD - Med Page Today; NEI - Nat Eye Institute; SciA-Scientific Amer.   Definitions via online Medical dictionaries.  Disclaimer, I am a BSN RN but not a diabetic or diabetic educator. Assistant Editor: Cam Acker, 50yr DM survivor.  Reports  excerpted unless otherwise noted. [translations/explanations by thl] This project is done as a courtesy to the blind/visually impaired & diabetic com munities. Dawn Wilcox RN BSN Coordinator The Health Library at Vista Center; an affiliate of the Stanford Hospital Health Library.   contact above e-mail or thl at vistacenter.org    
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