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<\/p>\nThe ACCORD study continues to generate controversy. \u00a0This study, with eight study groups and over 10,000 patients (at 77 centers), essentially asked whether taking type 2 diabetics from normal to intensive therapy in combination with enhanced lipid reduction therapy or enhanced hypertension therapy would reduce vascular events. \u00a0The good news is that strokes were reduced significantly, so work on your blood sugars, type 2\u2019s.\u00a0 But that is pretty much the end of the good news. \u00a0Although the enhanced therapies reduced the number of heart attacks, death by heart attack actually went up. \u00a0In short, you were less likely to have a heart attack,\u00a0 but if you did more likely to die.\u00a0 Last year the safety committee\u2019s decision to suspend intensive control because of the excess death made waves. \u00a0The controversy continues, apparently on two issues. \u00a0Why did the safety committee suspend intensive controls when the excess deaths were not statistically significant? \u00a0Some argued that if the study had continued to the end the question would be answered. \u00a0But the safety committee has not made public its reasons and is not required to. \u00a0The other question is: did tight control cause death by heart attack?<\/p>\n
Dr. Gerstein, a main author of the study, says that tight control did not do it. \u00a0He said that it is impossible to find any reason for the excess death in the study data. \u00a0In particular, on the question of tight control, the correlation of glycated hemoglobin with death was too weak for blood sugars to explain the excess deaths. \u00a0But he did offer an interesting clue. \u00a0It appears that, within the intensive control group, the patients whose\u00a0glycated hemoglobin<\/a> responded least to the intensive therapy were the most likely to die. \u00a0To put it simply, if your Lantus<\/a> dose went \u00a0up and your\u00a0glycated hemoglobin did not change, you were susceptible to death by heart attack. \u00a0As a man managing type 1 diabetes I suggest that more insulin and the same average means more blood glucose oscillations. \u00a0Most of the patients were using Lantus, and a bigger dose might well cause a lot of overnight hypoglycemia. \u00a0So the excursions from normal could be bigger but the average (measured by\u00a0glycated hemoglobin) is the same. \u00a0In plain language, maybe overnight low blood sugar makes heart attacks more likely to be fatal.<\/em><\/p>\n This hypothesis would be answered by examining the blood sugars of the intensively treated diabetics along side their\u00a0glycated hemoglobin. \u00a0But imagine this: there was no systematic measurement of blood sugars in the ACCORD study.\u00a0 So in a major diabetes study they did not measure blood sugar, only\u00a0glycated hemoglobin<\/a>. I find that an astonishing oversight in the design. \u00a0We now know that stability of blood glucose\u2019s is as important as the average level. \u00a0I hereby prohibit the use of\u00a0glycated hemoglobin in future diabetes clinical trials!\u00a0So because of a badly designed trial the important clinical question of intensive control for type 2 diabetics has been muddied. \u00a0Your tax dollars at work.<\/em><\/p>\n I went over to the Dexcom booth to meet Dr. Price, their medical director. \u00a0As a new and happy user of the Dexcom device for Continuous Glucose Monitoring, I wanted to discuss using Dexcom as part of our large animal studies of the Islet Sheet. \u00a0We had a nice chat and he promised to look into the feasibility. \u00a0As a bonus, I met Apurv Kamath who actually manages the algorithm that estimates blood sugar from the sensor and calibration data. \u00a0I asked him some pretty geeky questions about how the\u00a0algorithm\u00a0works.<\/p>\n The old insulin pump versus multiple daily injections controversy rolls along. \u00a0This is an issue I think of as, The Engineers<\/strong> versus The Medical Practitioners<\/strong>.\u00a0 Engineers think of diabetics<\/em> as machines with faulty parts.\u00a0 Medical Practitioners think of us as fallible humans who need\u00a0 help. \u00a0(When said to a member of the Engineer Tribe<\/em> that people won\u2019t actually do something he was proposing, he responded, \u201cThat\u2019s not my problem.\u201d<\/em>)\u00a0 Both groups have a point. \u00a0There are a lot of people who will benefit from the pump compared with MDI. \u00a0I may not be one \u2014 it seems that my overnight needs perfectly match what Levemir<\/a> delivers. \u00a0Choice of insulin delivery method continues to be based on many factors, including individual preference and efficacy.<\/p>\n The genetics of type 1 diabetes has made progress, although nothing of therapeutic relevance has been discovered.\u00a0 Researchers are beginning to sort out different subtypes of type 1 seemingly differentiated by the pattern of beta cell destruction. \u00a0The most common form is lobular destruction, where large zones of beta cells are completely destroyed, but a few remain in edge areas.<\/p>\n Islet transplantation with immunosuppressant drugs continues its snail-like advance. \u00a0Drug therapies are getting a bit better, especially the addition of exenatide-like hormones that stimulate islet function. \u00a0And it is clear that the residual transplanted islet functions even when insulin injections are required. The residual function is good for the islet recipients. \u00a0But the trade-off between improved glycemia and side effects of immune suppression drugs leaves conventional islet transplantation clinically marginal.<\/p>\n A controversy as old as my diabetes (30 years) is the cause of type 2 diabetes. Every ADA meeting produces more proposals supported by muddy data. \u00a0It is beginning to look like real progress is being made, at least for the most common cause of type 2 diabetes in the US. \u00a0Experimental animals can be made diabetic with high fat diets, and high fat diets are probably the biggest single problem in the US population. \u00a0Several researchers led by Professor Bergman of USC are finding that, in essence, fat cells are as important as islets in regulating metabolism. \u00a0Who knew? \u00a0I was taught that adipocytes<\/a> were completely passive, taking up and releasing fat under hormonal orders. \u00a0It turns out that the release of Free Fatty Acids by adipocytes<\/a> controls how much glucose the liver releases, and glucose output by the liver is the most important component in fasting blood sugar in type 2 \u00a0diabetics. \u00a0A lot of the evidence presented was new to me. \u00a0Look for this line of inquiry to produce new therapeutic approaches in the coming years.<\/p>\n Advocates of the artificial pancreas<\/a> continue their hard work. Using Continous Glucose Monitoring (CGM) to help the people control the pump is the first step. \u00a0The next is sensor assisted pump therapy and finally \u2026 the fully closed loop. \u00a0The big study to date showed the CGM helps, but only<\/strong> adult diabetics, not adolescents. \u00a0An interesting study atom at Joslin showed that CGM works best in diabetics who (1)<\/strong> react to CGM data with problem solving, not emotion; (2)<\/strong> use patterns as well s recent data to improve insulin therapy and (3)<\/strong> have spousal support. \u00a0Some diabetics discontinue the sensor when their spouse made cyborg jokes. \u00a0The STAR 3 study showed the CGM sensor augmentation shows insulin pump therapy is better then multiply injection therapy without sensor augmentation. \u00a0However, I remain unconvinced that the fully closed look system will ever be safe and effective.<\/p>\n I attended all the sessions devoted to new sources of islet tissue, nanotechnology, and encapsulation. \u00a0Not much has changed since the International Pancreas and Islet Transplant Association<\/a> meeting last October. I learned a lot I did not know about Colin Weber\u2019s encapsulation work ar Emory and Cherie Stabler\u2019s matrix and nanoencapslation work at Miami. \u00a0Colin showed some advanced work with his microencapsulated islets in Miami. \u00a0For reasons he could not identify. the fasting blood sugars were low and postprandial high.<\/p>\n Scott King, a type 1 diabetic for 30 years, is President of Cerco Medical<\/a>, and one of the founding partners of the Solving Diabetes Project<\/a>.<\/em><\/p>\n Originally posted at Diabetes24-7.com<\/a>.<\/p>\n