This is a very brief post about the Australian study you'll be hearing a lot about this week, ADVANCE. That's the one that found that lowering blood sugar to "normal" did not prevent heart disease in people with diabetes. I've gotten some mail asking me to comment on it, so here goes:
1. Normal blood sugar in this study was defined as an A1c of 6.5%. This represents an average blood sugar of 140 mg/dl (7.7 mmol/L). With the technique used to lower blood sugar in the Australian study that average was most likely achieved by having the blood sugar seesaw between 85 and 200 mg/dl.
Looking at the graphs relating heart disease to blood sugar you can easily see that the 6.5 A1c is far from normal. Studies show that with ever 1% rise over 4.7% heart disease risk increases greatly. You can check out some studies linking A1c to heart disease in people with and without diabetes HERE.
2. The Australian study lowered blood sugar using sulfonylurea drugs. These drugs have long been known to be associated with an increased risk of heart attack. In the U.S. every sulfonylurea drug (Amayrl, Glipizide, etc) carries a black box warning that specifically cites the increased risk of heart disease found with some members of this class of drugs.
3. The people in this study, like people with diabetes all over the world had undiagnosed prediabetes and even undiagnosed Type 2 diabetes for decades before diagnosis. The studies I cited above show that even prediabetic blood sugars are linked to heart disease.
So heart disease in people with diabetes may be very well established in their bodies at the time of diagnosis. Unfortunately, in both the large studies of lowering blood sugar in the news this week (ADVANCE and ACCORD, the study that used Avandia and Byetta along with the high carb diet) the technique used to lower the blood sugar was a high carbohydrate/low fat diet combined with high doses of drugs that are not good for the heart. It is well known that the high carb/low fat diet pushes all the cardiovascular markers in the wrong direction.
4. There is no large scale study of what happens to people with diabetes who lower their carbohydrate intake dramatically and use the smallest doses needed of only metformin (which appears cardio-protective) and insulin to regain control.
If you follow the advice found at http://alt-support-diabetes.org/newlydiagnosed.htm
you will flatten your blood sugar and avoid ever going over 140 mg/dl, rather than having a blood sugar that averages 140 mg/dl and goes much higher for hours ever day. This approach has helped many of us online who share our diabetes experiences avoid heart disease if we did not have it already and heart attack if we do.
5. The Australian study did show a very significant drop in kidney disease occurring when the A1c dropped to 6.5%. We will have to wait for the publication of the results to see the actual details of this study and what else it might have found that wasn't reported in the Newsbytes for Dummies health reports.
P.S.: I'm going to he having some fairly major surgery this next week (nothing scary, just something badly needed) so the blog will be on hiatus for the next week or two. When I'm back I'll comment at length on the research and drug company puffery presented at the ADA annual meeting.
See you then!
Saturday, June 7, 2008
Thursday, June 5, 2008
How Long Does It Take to Develop Complications?
If you've been diagnosed with diabetes you may well be terrified that you will develop the horrible diabetic complications you have seen ruin the lives of relatives who also had diabetes. You've seen your loved ones' feet literally rot off, their kidneys fail, their eyes grow dim. Now, you fear, it will be your turn.
But it doesn't have to be!
To understand why the horrors of complications devastate people with diabetes and why they don't have to ruin your life you have to understand something about the natural history of these complications: how long they take to develop and what research has found about what can slow them down or stop them.
You won't develop any diabetic complication immediately after the onset of diabetes--though because so many people with Type 2 diabetes have had undiagnosed diabetes for 5 years or more, many people with Type 2 diabetes do already have complications on the day of their diagnosis.
The most common diabetic complication found in these "newly diagnosed" Type 2s is neuropathy--pain or numbness in the nerves, usually of the feet, followed by protein in the urine--a sign that the kidney filtration units are getting clogged, and early retinal changes.
But if you get an early diagnosis, it is almost certain you will have none of these complications at diagnosis, because studies of people with both Type 1 and Type 2 diabetes suggest that it takes about 5 years of exposure to high blood sugars for any of these complications to develop. For example, one study of Type 2s who had no retinopathy at diagnosis found that at 6 years after diagnosis 22% (1 in 5) had developed some retinopathy. The study states, "Development of retinopathy (incidence) was strongly associated with baseline glycaemia [high blood sugar], glycaemic exposure over 6 years, higher blood pressure and with not smoking."
A Japanese Study tracked the development of retinopathy and kidney dysfunction and found that at 6 years between 32 and 44% of those using an old-fashioned, inadequate twice a day insulin dosing schedule and only about 8% in those using the more modern basal/bolus insulin regimen had developed retinopathy (or seen it get worse). A very similar pattern was found in the progression of kidney dysfunction.
Surprisingly, there is very little research on the development of neuropathy. What little there is (discussed in detail here: Research Connecting Organ Damage with Blood Sugar Level suggests that neuropathic damage starts out when blood sugars are in the poorly named "pre-diabetic" range when small nerve fibers are affected and moves to larger fibers as blood sugars are allowed to rise over 200 mg/dl as they do in the people with Type 2 diabetes who attempt to control their blood sugar with nothing more than pills and hence have an average A1c according to the NHANES III data near 10%.
But it is the slowness with which diabetic complications develop, ironically, that has a lot to do with WHY they occur at all. Because it takes so long for them to develop, people with diabetes may go for years with blood sugars surging into the 200s--which they may not even know about, since their doctors tell them to test only their fasting blood sugars once a week, without experiencing any complications. Because they don't develop detectable complications during these early years they assume that they are somehow magically protected and that their mediocre blood sugar control is not harming them.
Then, one day, six or even ten years later, the doctor gives them the bad news. There are abnormal blood vessels in their retina. There's protein in their urine. That infection on their foot is not going to heal.
Sadly, many of these patients have been under a doctor's care and many have been achieving the 7% A1cs their doctors have told them is "excellent control" though of course it is far from that.
That's because almost all the major research studies that attempt to connect the progression of complications with blood sugar level accept 7% A1cs as the lowest possible blood sugar level you could attain. They show that the development of complications is slowed when you maintain a 7% A1c as opposed, say to a 10% A1c. But they also come up with something else: if you have Type 2 diabetes as opposed to Type 1, your chance of developing complications when you maintain that 7% A1c is still very, very high.
Type 1s have far fewer complications at the 7% A1c level, possibly because they achieve that A1c by seesawing swiftly between 60 and 400 while Type 2s are more likely to get the same 7% A1c by spending all their time between 180 and 250. It appears that it is the hours spent at high blood sugar levels that don't swiftly drop low that bind the glucose to your nerves, blood vessels and kidney filtration units.
There is no major research that looks at the progression of complications in people diagnosed with diabetes whose A1cs is in the 4.5-6% range and whose blood sugar is kept under 140 mg/dl. But we know from multiple studies by neurologists that people NOT diagnosed with diabetes whose blood sugar stays under 140 mg/dl on glucose tolerance tests almost never have neuropathy while those whose blood sugar is routinely going over that level, whether diagnosed or not do have more neuropathy. And we also know that people whose blood sugar stays under 140 mg/dl have a much lower incidence of heart attack than those with or without a diabetes diagnosis whose blood sugar after a glucose challenge is higher.
So what is the take home message from all this?
It's simple. Keeping your blood sugar in the normal range and controlling your blood pressure probably will prevent you from experiencing the horrors of diabetic complications. Your relative who lost his or her leg did so because their doctor allowed them to walk around with blood sugars well over 200 mg/dl after every meal for decades. Those bad kidneys likewise result from many years of exposure to very high blood sugars, along with some other factors including poorly controlled blood pressure and, possibly, overuse of painkillers like Tylenol and Advil and drinking too much Coke and Pepsi, even the diet kind.
But for those of you who are conscientious, it cuts the other way too: three days or even three months of high blood sugars aren't going to make you go blind. Three years, is a different story. But if you have been doing really well for a year or two and get off track for a few months, you aren't doomed. And if you have been the victim of poor medical advice and have been running those 7% A1cs and over 140 mg/dl blood sugars for years because you were told that was all you needed to do and are starting to see complications, there is still plenty of time to prevent them from getting worse and possibly--if you are willing to really work at it--to reverse them.
Normal blood sugars are possible, and over the almost ten years I've been observing the diabetes scene things have improved immensely. A recent poll on Tudiabetes.com revealed that 20% of the members of that community--many of them people with Type 1 diabetes, had A1cs in the normal 5% range. If that poll had been run a decade ago, the number with that kind of A1c might have been only 2%!
So if you're terrified of complications, use that fear to motivate you to make sure you never have to experience them. Keep your A1c in the 5% range using whatever it takes. Cut the carbs, demand a modern insulin regimen. If you can afford it, get a continuous glucose monitor. All these techniques work. In another 30 years it is my belief we will have a generation of people who have lived with diabetes for decades, both Type 1 and Type 2, who will look at the incidence of horrifying diabetic complications common in the 1990s and even now as being as unnecessary as the hundreds of thousands of deaths from cholera that occurred throughout the 19th century when people did not understand the dangers of drinking from wells contaminated with human sewage.
But it doesn't have to be!
To understand why the horrors of complications devastate people with diabetes and why they don't have to ruin your life you have to understand something about the natural history of these complications: how long they take to develop and what research has found about what can slow them down or stop them.
You won't develop any diabetic complication immediately after the onset of diabetes--though because so many people with Type 2 diabetes have had undiagnosed diabetes for 5 years or more, many people with Type 2 diabetes do already have complications on the day of their diagnosis.
The most common diabetic complication found in these "newly diagnosed" Type 2s is neuropathy--pain or numbness in the nerves, usually of the feet, followed by protein in the urine--a sign that the kidney filtration units are getting clogged, and early retinal changes.
But if you get an early diagnosis, it is almost certain you will have none of these complications at diagnosis, because studies of people with both Type 1 and Type 2 diabetes suggest that it takes about 5 years of exposure to high blood sugars for any of these complications to develop. For example, one study of Type 2s who had no retinopathy at diagnosis found that at 6 years after diagnosis 22% (1 in 5) had developed some retinopathy. The study states, "Development of retinopathy (incidence) was strongly associated with baseline glycaemia [high blood sugar], glycaemic exposure over 6 years, higher blood pressure and with not smoking."
A Japanese Study tracked the development of retinopathy and kidney dysfunction and found that at 6 years between 32 and 44% of those using an old-fashioned, inadequate twice a day insulin dosing schedule and only about 8% in those using the more modern basal/bolus insulin regimen had developed retinopathy (or seen it get worse). A very similar pattern was found in the progression of kidney dysfunction.
Surprisingly, there is very little research on the development of neuropathy. What little there is (discussed in detail here: Research Connecting Organ Damage with Blood Sugar Level suggests that neuropathic damage starts out when blood sugars are in the poorly named "pre-diabetic" range when small nerve fibers are affected and moves to larger fibers as blood sugars are allowed to rise over 200 mg/dl as they do in the people with Type 2 diabetes who attempt to control their blood sugar with nothing more than pills and hence have an average A1c according to the NHANES III data near 10%.
But it is the slowness with which diabetic complications develop, ironically, that has a lot to do with WHY they occur at all. Because it takes so long for them to develop, people with diabetes may go for years with blood sugars surging into the 200s--which they may not even know about, since their doctors tell them to test only their fasting blood sugars once a week, without experiencing any complications. Because they don't develop detectable complications during these early years they assume that they are somehow magically protected and that their mediocre blood sugar control is not harming them.
Then, one day, six or even ten years later, the doctor gives them the bad news. There are abnormal blood vessels in their retina. There's protein in their urine. That infection on their foot is not going to heal.
Sadly, many of these patients have been under a doctor's care and many have been achieving the 7% A1cs their doctors have told them is "excellent control" though of course it is far from that.
That's because almost all the major research studies that attempt to connect the progression of complications with blood sugar level accept 7% A1cs as the lowest possible blood sugar level you could attain. They show that the development of complications is slowed when you maintain a 7% A1c as opposed, say to a 10% A1c. But they also come up with something else: if you have Type 2 diabetes as opposed to Type 1, your chance of developing complications when you maintain that 7% A1c is still very, very high.
Type 1s have far fewer complications at the 7% A1c level, possibly because they achieve that A1c by seesawing swiftly between 60 and 400 while Type 2s are more likely to get the same 7% A1c by spending all their time between 180 and 250. It appears that it is the hours spent at high blood sugar levels that don't swiftly drop low that bind the glucose to your nerves, blood vessels and kidney filtration units.
There is no major research that looks at the progression of complications in people diagnosed with diabetes whose A1cs is in the 4.5-6% range and whose blood sugar is kept under 140 mg/dl. But we know from multiple studies by neurologists that people NOT diagnosed with diabetes whose blood sugar stays under 140 mg/dl on glucose tolerance tests almost never have neuropathy while those whose blood sugar is routinely going over that level, whether diagnosed or not do have more neuropathy. And we also know that people whose blood sugar stays under 140 mg/dl have a much lower incidence of heart attack than those with or without a diabetes diagnosis whose blood sugar after a glucose challenge is higher.
So what is the take home message from all this?
It's simple. Keeping your blood sugar in the normal range and controlling your blood pressure probably will prevent you from experiencing the horrors of diabetic complications. Your relative who lost his or her leg did so because their doctor allowed them to walk around with blood sugars well over 200 mg/dl after every meal for decades. Those bad kidneys likewise result from many years of exposure to very high blood sugars, along with some other factors including poorly controlled blood pressure and, possibly, overuse of painkillers like Tylenol and Advil and drinking too much Coke and Pepsi, even the diet kind.
But for those of you who are conscientious, it cuts the other way too: three days or even three months of high blood sugars aren't going to make you go blind. Three years, is a different story. But if you have been doing really well for a year or two and get off track for a few months, you aren't doomed. And if you have been the victim of poor medical advice and have been running those 7% A1cs and over 140 mg/dl blood sugars for years because you were told that was all you needed to do and are starting to see complications, there is still plenty of time to prevent them from getting worse and possibly--if you are willing to really work at it--to reverse them.
Normal blood sugars are possible, and over the almost ten years I've been observing the diabetes scene things have improved immensely. A recent poll on Tudiabetes.com revealed that 20% of the members of that community--many of them people with Type 1 diabetes, had A1cs in the normal 5% range. If that poll had been run a decade ago, the number with that kind of A1c might have been only 2%!
So if you're terrified of complications, use that fear to motivate you to make sure you never have to experience them. Keep your A1c in the 5% range using whatever it takes. Cut the carbs, demand a modern insulin regimen. If you can afford it, get a continuous glucose monitor. All these techniques work. In another 30 years it is my belief we will have a generation of people who have lived with diabetes for decades, both Type 1 and Type 2, who will look at the incidence of horrifying diabetic complications common in the 1990s and even now as being as unnecessary as the hundreds of thousands of deaths from cholera that occurred throughout the 19th century when people did not understand the dangers of drinking from wells contaminated with human sewage.
Tuesday, June 3, 2008
HOMA Wrong on IR and Insulin Deficiency. Early Type 2s have Insulin Deficiency NOT Just IR.
Buried in this month's issue of the journal Diabetes is a study that, properly understood, suggests that most of what doctors "know" about Type 2 diabetes is wrong.
The study is titled β-Cell Dysfunction in Subjects With Impaired Glucose Tolerance and Early Type 2 Diabetes: Comparison of Surrogate Markers With First-Phase Insulin Secretion From an Intravenous Glucose Tolerance Test.
To understand why this study is important, you have to know that for decades scientists have evaluated insulin resistance using something called HOMA or homeostasis model assessment. HOMA is nothing more than a formula that computes insulin resistance from fasting C-peptide, fasting insulin and blood sugar. If you have had a fasting insulin or C-peptide test, you can compute your own HOMA using the Oxford University HOMA calculator.
What the scientists did in this latest study was something blindingly simple. They hooked up people who had been recently diagnosed with pre-diabetes or diabetes to an intravenous glucose tolerance test and measured their insulin and preinsulin levels. Then then compared what they found with the HOMA calculations.
What they found was "HOMA-B markedly underestimated the magnitude of the β-cell defect across declining glucose tolerance." They went on to conclude, "Subjects with IGT and early-stage, asymptomatic type 2 diabetic patients have more pronounced β-cell defects than previously estimated from epidemiological studies using homeostasis model assessment."
What this means in plain English is that contrary to what you have been reading for decades, prediabetes and early Type 2 diabetes are NOT primarily caused by insulin resistance. Instead, this study found these people had an unexpectedly high deree of insulin deficiency which was NOT apparent when they calculated HOMA using the cheap fasting tests.
This should be a shocker, but like most of the truly important research about Type 2 diabetes it probably won't even get noticed because no drug company is going to talk it up at the big ADA dog and pony show this week. Instead the medical news will be full of reports of how wonderful Drug A is and how all people with Type 2 should be taking Drug B--even if Drug B only lowers A1c from 7.5% to 7.0% and costs $200 a month.
The finding that people with pre-diabetes already show insulin secretion defects points to several things.
1. It emphasizes that there are genetic defects involved in blood sugar deterioration that have nothing to do with overeating or obesity. No one has ever found anything that connected overeating with the failure of beta cells to secrete properly.
2. It calls into question huge amounts of diabetes research done over the past decades because the HOMA formula has been used almost universally to determine if people had IR or beta cell deficiency. This study suggests that the HOMA result is wrong and so any research about insulin resistance based on HOMA is wrong. That's almost ALL large group research.
3. It makes it all the more clear why people with early diabetes diagnoses should consider a trial of insulin when lowering insulin resistance with diet or drugs like metformin does not give normal blood sugars. If your beta cells can't produce insulin, you need insulin. End of story.
4. It makes me wonder how much of the IR that doctors believe to be the sole cause of Type 2 diabetes is actually being caused by abnormally high blood sugars. it is possible that IR increases dramatically when blood sugars go over a much lower threshold than previously believed. Possibly as low as 130 mg/dl. If so, much of the IR found in Type 2 diabetes may be caused by high blood sugars caused by insulin deficiency. If that isn't a mind blower, what is?
Now mind you many people with Type 2 diabetes do have insulin resistance that is independent of their blood sugars. But they also may have decades of functioning with higher than normal blood sugars due to insulin deficiency. What the impact of that on their metabolisms may have been is unknown.
But one thing is for sure, this is a major blow to the idea that type 2 is caused by insulin resistance caused by obesity and that people with Type 2 secrete higher than normal levels of insulin which their body can't use. That belief came from studies based on HOMA calculations, but this study that measured the actual insulin secreted found that simply wasn't true.
P.S. My own HOMA calculation showed that I was twice as insulin resistant as normal. However, when I started to inject insulin I learned that I have normal insulin sensitivity in that one unit of insulin lowers my blood sugar the same amount that it would for a normal person. I use about 1/10 the total daily dose of insulin that an insulin resistant person my size would use. I thought that this discrepancy was because I have an oddball form of diabetes. But it is more likely that it is an example of just how badly this HOMA formula works for people whose fasting blood sugar has not yet reached the 200 mg/dl level which was typical of the population in which the formula was first computed.
The study is titled β-Cell Dysfunction in Subjects With Impaired Glucose Tolerance and Early Type 2 Diabetes: Comparison of Surrogate Markers With First-Phase Insulin Secretion From an Intravenous Glucose Tolerance Test.
To understand why this study is important, you have to know that for decades scientists have evaluated insulin resistance using something called HOMA or homeostasis model assessment. HOMA is nothing more than a formula that computes insulin resistance from fasting C-peptide, fasting insulin and blood sugar. If you have had a fasting insulin or C-peptide test, you can compute your own HOMA using the Oxford University HOMA calculator.
What the scientists did in this latest study was something blindingly simple. They hooked up people who had been recently diagnosed with pre-diabetes or diabetes to an intravenous glucose tolerance test and measured their insulin and preinsulin levels. Then then compared what they found with the HOMA calculations.
What they found was "HOMA-B markedly underestimated the magnitude of the β-cell defect across declining glucose tolerance." They went on to conclude, "Subjects with IGT and early-stage, asymptomatic type 2 diabetic patients have more pronounced β-cell defects than previously estimated from epidemiological studies using homeostasis model assessment."
What this means in plain English is that contrary to what you have been reading for decades, prediabetes and early Type 2 diabetes are NOT primarily caused by insulin resistance. Instead, this study found these people had an unexpectedly high deree of insulin deficiency which was NOT apparent when they calculated HOMA using the cheap fasting tests.
This should be a shocker, but like most of the truly important research about Type 2 diabetes it probably won't even get noticed because no drug company is going to talk it up at the big ADA dog and pony show this week. Instead the medical news will be full of reports of how wonderful Drug A is and how all people with Type 2 should be taking Drug B--even if Drug B only lowers A1c from 7.5% to 7.0% and costs $200 a month.
The finding that people with pre-diabetes already show insulin secretion defects points to several things.
1. It emphasizes that there are genetic defects involved in blood sugar deterioration that have nothing to do with overeating or obesity. No one has ever found anything that connected overeating with the failure of beta cells to secrete properly.
2. It calls into question huge amounts of diabetes research done over the past decades because the HOMA formula has been used almost universally to determine if people had IR or beta cell deficiency. This study suggests that the HOMA result is wrong and so any research about insulin resistance based on HOMA is wrong. That's almost ALL large group research.
3. It makes it all the more clear why people with early diabetes diagnoses should consider a trial of insulin when lowering insulin resistance with diet or drugs like metformin does not give normal blood sugars. If your beta cells can't produce insulin, you need insulin. End of story.
4. It makes me wonder how much of the IR that doctors believe to be the sole cause of Type 2 diabetes is actually being caused by abnormally high blood sugars. it is possible that IR increases dramatically when blood sugars go over a much lower threshold than previously believed. Possibly as low as 130 mg/dl. If so, much of the IR found in Type 2 diabetes may be caused by high blood sugars caused by insulin deficiency. If that isn't a mind blower, what is?
Now mind you many people with Type 2 diabetes do have insulin resistance that is independent of their blood sugars. But they also may have decades of functioning with higher than normal blood sugars due to insulin deficiency. What the impact of that on their metabolisms may have been is unknown.
But one thing is for sure, this is a major blow to the idea that type 2 is caused by insulin resistance caused by obesity and that people with Type 2 secrete higher than normal levels of insulin which their body can't use. That belief came from studies based on HOMA calculations, but this study that measured the actual insulin secreted found that simply wasn't true.
P.S. My own HOMA calculation showed that I was twice as insulin resistant as normal. However, when I started to inject insulin I learned that I have normal insulin sensitivity in that one unit of insulin lowers my blood sugar the same amount that it would for a normal person. I use about 1/10 the total daily dose of insulin that an insulin resistant person my size would use. I thought that this discrepancy was because I have an oddball form of diabetes. But it is more likely that it is an example of just how badly this HOMA formula works for people whose fasting blood sugar has not yet reached the 200 mg/dl level which was typical of the population in which the formula was first computed.
Saturday, May 31, 2008
Great Vial Experiment Appears to be a Bust
Levermir placed in the purchased sterile vial appears to get cloudly and lose potency after 3 days. So perhaps what the pharmacist told me, that they coat the vials with something special, is true.
Wednesday, May 28, 2008
Insulin Right After Diagnosis Dramatically Improves Type 2 Outcome
Two studies just published in the journal Lancet show you just how mistaken is the current practice of starting Type 2s on oral drugs and withholding insulin until their A1c with a full load of oral drugs is 10% or higher.
These are the studies:
Effect of intensive insulin therapy on β-cell function and glycaemic control in patients with newly diagnosed type 2 diabetes: a multicentre randomised parallel-group trial. Jianping Weng et al. The Lancet 2008; 371:1753-1760
and
Intensive insulin therapy in newly diagnosed type 2 diabetes. Ravi Retnakaran and Daniel J Drucker. Lancet 2008; 371:1725-1726. (Subscription required)
In the first study, "The patients, with fasting plasma glucose of 7·0–16·7 mmol/L [126 - 300] , were randomly assigned to therapy with insulin (CSII [pump] or MDI [basal/bolus shots]) or oral hypoglycaemic agents [oral drugs] for initial rapid correction of hyperglycaemia. Treatment was stopped after normoglycaemia [normal blood sugar] was maintained for 2 weeks. Patients were then followed-up on diet and exercise alone."
Here's what happened:
"A year after stopping therapy, the remission rate was 42% among those who reached normal blood glucose levels during the treatment period, the researchers said.
But the rates were 51.1% among those who were treated with insulin infusion, 44.9% among those given insulin injections, and only 26.7% in the oral hypoglycemic agents group."
What this means is that almost twice as many newly diagnosed people with Type 2 diabetes who received intensive insulin treatment right after diagnosis were able to achieve normal blood sugars using only diet and exercise than did the people treated only with oral drugs. Even though the patients given insulin were taken off insulin after experiencing only two weeks of normal blood sugars!
This is a monumental finding and one that should make you insist that your doctor give you a basal/bolus insulin regimen as soon as you are unable to maintain normal blood sugars with diet and exercise alone. If you can't get truly normal blood sugars by cutting the carbs and increasing your physical activity, skip the expensive and ineffective oral drugs and go to the drug that always lowers blood sugar: insulin.
Why does insulin work so much better than other drugs?
The answer is probably because it is the only drug that reliably drops blood sugars below the level that cause secondary insulin resistance. Many doctors do not seem to understand that if your blood sugar is high the high blood sugar itself causes insulin resistance no matter what your underlying physiology might be. And this additional blood-sugar related insulin resistance starts at relatively low levels--much lower than doctors understand. I personally see a huge difference in my insulin resistance after meals--measured by how much insulin I need to cover a given number of carbs--when my fasting blood sugar is 108 mg/dl and when it is 85 mg/dl.
But when you take an oral drug that does a feeble job of lowering your blood sugar, you have to contend not only with the damage caused by the too-high blood sugar, but also with the additional insulin resistance caused by your too-high blood sugars. This IR packs on additional pounds and hastens the burnout of your insulin producing beta cells because they must make much more insulin to cover the meals you eat.
A telling fact that came out at the recent AACE conference that got no play in the media at all is that in the last decades the average A1c of people with diabetes in America has risen dramatically.
As reported in the Endocrinology Today newsletter: "Between 1988 and 1994, NHANES data reported 44.5% of patients reaching a target HbA1c of 7.0% or less. Between 1999 and 2000, that percentage dropped to 35.8%."
The reason fort this? The endocrinologists scratch their head but admit that with the greater choice of oral drugs, fewer patients are using diet to control blood sugar. And though the article doesn't spell this out, it is also likely that because there are so many new, expensive, highly promoted oral drugs, doctors are delaying the move to insulin for much longer than they did in the late 80s when they had few oral drugs to try and moved to insulin faster. The article does report, "Insulin use in the United States remains low."
Doctors like oral drugs because they don't have to follow up with patients, educate them, or worry about hypos. Drug company reps make it sound like their drugs can provide healthy blood sugars, even though the prescribing information (that doctors rarely read) shows that most lower A1c by no more than 1% and many by only .5%--in patients whose blood sugar starts at levels of 8% or higher.
Until now we had vague information suggesting that using insulin immediately after diagnosis could preserve the beta cell function of people with LADA. Now, with this new data, we see that using insulin right after diagnosis benefits Type 2s, too.
So don't let your doctor tell you that it's better to try all of the many oral drugs before you start insulin. It isn't true, and waiting three or four years while taking drugs that can't normalize your blood sugar may mean that by the time you start insulin you have few beta cells left to save.
These are the studies:
Effect of intensive insulin therapy on β-cell function and glycaemic control in patients with newly diagnosed type 2 diabetes: a multicentre randomised parallel-group trial. Jianping Weng et al. The Lancet 2008; 371:1753-1760
and
Intensive insulin therapy in newly diagnosed type 2 diabetes. Ravi Retnakaran and Daniel J Drucker. Lancet 2008; 371:1725-1726. (Subscription required)
In the first study, "The patients, with fasting plasma glucose of 7·0–16·7 mmol/L [126 - 300] , were randomly assigned to therapy with insulin (CSII [pump] or MDI [basal/bolus shots]) or oral hypoglycaemic agents [oral drugs] for initial rapid correction of hyperglycaemia. Treatment was stopped after normoglycaemia [normal blood sugar] was maintained for 2 weeks. Patients were then followed-up on diet and exercise alone."
Here's what happened:
"A year after stopping therapy, the remission rate was 42% among those who reached normal blood glucose levels during the treatment period, the researchers said.
But the rates were 51.1% among those who were treated with insulin infusion, 44.9% among those given insulin injections, and only 26.7% in the oral hypoglycemic agents group."
What this means is that almost twice as many newly diagnosed people with Type 2 diabetes who received intensive insulin treatment right after diagnosis were able to achieve normal blood sugars using only diet and exercise than did the people treated only with oral drugs. Even though the patients given insulin were taken off insulin after experiencing only two weeks of normal blood sugars!
This is a monumental finding and one that should make you insist that your doctor give you a basal/bolus insulin regimen as soon as you are unable to maintain normal blood sugars with diet and exercise alone. If you can't get truly normal blood sugars by cutting the carbs and increasing your physical activity, skip the expensive and ineffective oral drugs and go to the drug that always lowers blood sugar: insulin.
Why does insulin work so much better than other drugs?
The answer is probably because it is the only drug that reliably drops blood sugars below the level that cause secondary insulin resistance. Many doctors do not seem to understand that if your blood sugar is high the high blood sugar itself causes insulin resistance no matter what your underlying physiology might be. And this additional blood-sugar related insulin resistance starts at relatively low levels--much lower than doctors understand. I personally see a huge difference in my insulin resistance after meals--measured by how much insulin I need to cover a given number of carbs--when my fasting blood sugar is 108 mg/dl and when it is 85 mg/dl.
But when you take an oral drug that does a feeble job of lowering your blood sugar, you have to contend not only with the damage caused by the too-high blood sugar, but also with the additional insulin resistance caused by your too-high blood sugars. This IR packs on additional pounds and hastens the burnout of your insulin producing beta cells because they must make much more insulin to cover the meals you eat.
A telling fact that came out at the recent AACE conference that got no play in the media at all is that in the last decades the average A1c of people with diabetes in America has risen dramatically.
As reported in the Endocrinology Today newsletter: "Between 1988 and 1994, NHANES data reported 44.5% of patients reaching a target HbA1c of 7.0% or less. Between 1999 and 2000, that percentage dropped to 35.8%."
The reason fort this? The endocrinologists scratch their head but admit that with the greater choice of oral drugs, fewer patients are using diet to control blood sugar. And though the article doesn't spell this out, it is also likely that because there are so many new, expensive, highly promoted oral drugs, doctors are delaying the move to insulin for much longer than they did in the late 80s when they had few oral drugs to try and moved to insulin faster. The article does report, "Insulin use in the United States remains low."
Doctors like oral drugs because they don't have to follow up with patients, educate them, or worry about hypos. Drug company reps make it sound like their drugs can provide healthy blood sugars, even though the prescribing information (that doctors rarely read) shows that most lower A1c by no more than 1% and many by only .5%--in patients whose blood sugar starts at levels of 8% or higher.
Until now we had vague information suggesting that using insulin immediately after diagnosis could preserve the beta cell function of people with LADA. Now, with this new data, we see that using insulin right after diagnosis benefits Type 2s, too.
So don't let your doctor tell you that it's better to try all of the many oral drugs before you start insulin. It isn't true, and waiting three or four years while taking drugs that can't normalize your blood sugar may mean that by the time you start insulin you have few beta cells left to save.
Sunday, May 25, 2008
New Widget Converts A1c/Glucose/mg/dl/mmol/L
I had some spare time this morning and turned my A1c/Avg converter into a widget you can put on your own blog or web pages. It will convert A1c to average blood sugar and vice versa using either mg/dl or mmol/L. You can also use it to convert mmol/L and mg/dl back and forth. Enter one measurement, and the converter will fill in the others.
This converter uses the most recent ADAG formula which was just published this past fall. It is based on a large number of CGMS measurements and is supposed to be more accurate than the old DCCT formula which is the one most commonly used. That's because the DCCT formula was derived from infrequent meter testing. I find this formula gives a lower equivalent than the DCCT formula. And to me it appears more accurate.
You will find the new widget at Widgetbox.com HERE
Give it a try and let me know what you think. Also let me know if you have a problem displaying it on your screen. I've tested it on our computers but there may be problems with some screen sizes and fonts.
If you want to install it on a page of your own, click the "get widget" link and past the code into your own page. In blogger, use the "Layout" feature and create a new "HTML/Javascript" item.
I've also added a "Recent Posts" widget which shows more posts by title than the Blogger Archive does. The archive is now at the bottom of the page.
This converter uses the most recent ADAG formula which was just published this past fall. It is based on a large number of CGMS measurements and is supposed to be more accurate than the old DCCT formula which is the one most commonly used. That's because the DCCT formula was derived from infrequent meter testing. I find this formula gives a lower equivalent than the DCCT formula. And to me it appears more accurate.
You will find the new widget at Widgetbox.com HERE
Give it a try and let me know what you think. Also let me know if you have a problem displaying it on your screen. I've tested it on our computers but there may be problems with some screen sizes and fonts.
If you want to install it on a page of your own, click the "get widget" link and past the code into your own page. In blogger, use the "Layout" feature and create a new "HTML/Javascript" item.
I've also added a "Recent Posts" widget which shows more posts by title than the Blogger Archive does. The archive is now at the bottom of the page.
Thursday, May 22, 2008
The Great Vial Experiment
I use very small doses of basal insulin. No more than 2.5 units a day.
But though I've been able to make an insulin pen last long enough to use up every drop of insulin in it, my experience with vials over the past several years has been that the insulin in them always goes bad, no matter what I do to try to keep them alive.
I've tried all of the following: Alway using a new syringe, wiping the top with alcohol, and refrigerating the vial with a thermometer near it to make sure it isn't getting too cold. It doesn't matter. Insulin from the vial always starts to weaken after about six weeks and my blood sugars start creeping up. If I get a new vial, it's immediately very clear how weak my old vial was and if my doses have been creeping up I can have an interesting day the first time I use the new vial.
Pens don't do this even when I reuse pen needles, and my guess is it has something to do with the pressure inside the pen which pushes anything in the needle out before it can enter the insulin container and contaminate it.
Whatever the explanation, my current insurer charges the top copay--$50--for a vial of the kinds of insulin I'm using and won't cover pens without a long and complicated appeal put in by my endocrinologist. I don't like to use pens for the basal anyway, as I use fractional doses and I don't trust the pen to dispense 1 unit accurately. So when I bought my latest expensive vial of Levemir, I decided to try an experiment to see if I could keep the insulin in the vial alive for a longer time.
What I did was mail order some sterile 10 ml vials and transfer 100 units of insulin into the new sterile vial. I'm going to draw the insulin from that sterile vial, not the manufacturer's vial and thus cut way down on the number of times I introduce a needle into the main vial. Hopefully this means I'll be able to use all of those 1,0000 units instead of only 150 or so.
Another benefit of this approach compared to pens is that I won't be wasting the many air shots I have to waste when I use pens. The air shots can use up even more insulin than my basal shots. The convenience of the pen is a huge issue with post-meal insulin, but not for basal.
I'll be reporting back in a few months about whether this strategy is effective. If any of you who use tiny doses have any other suggestions about how to keep insulin in vials alive. Let me know.
UPDATE: 5/24/08
The insulin in the mail order vial is still working as it should. The only problem I've run into is that my syringes are dulling out much faster than they do I've been reusing them with a manufacturer's pen. This is probably because the rubber seal on the mail order vial is made out of a cheaper material.
The result is that the shots will hurt and bruise if I don't change the needle after no more than 2 shots.
NOTE: I have tried not reusing needles and reusing needles and have not seen any difference in how well my insulin holds up. When I reuse a syringe I do not inject air into the vial and I carefully expel any insulin left in the needle squirt-gun style after each use. Periodically I bleed the air out of the syringe by inserting a new needle with the plunger removed. This is the procedure described in the book, Dr. Bernstein's Diabetes Solution.
But though I've been able to make an insulin pen last long enough to use up every drop of insulin in it, my experience with vials over the past several years has been that the insulin in them always goes bad, no matter what I do to try to keep them alive.
I've tried all of the following: Alway using a new syringe, wiping the top with alcohol, and refrigerating the vial with a thermometer near it to make sure it isn't getting too cold. It doesn't matter. Insulin from the vial always starts to weaken after about six weeks and my blood sugars start creeping up. If I get a new vial, it's immediately very clear how weak my old vial was and if my doses have been creeping up I can have an interesting day the first time I use the new vial.
Pens don't do this even when I reuse pen needles, and my guess is it has something to do with the pressure inside the pen which pushes anything in the needle out before it can enter the insulin container and contaminate it.
Whatever the explanation, my current insurer charges the top copay--$50--for a vial of the kinds of insulin I'm using and won't cover pens without a long and complicated appeal put in by my endocrinologist. I don't like to use pens for the basal anyway, as I use fractional doses and I don't trust the pen to dispense 1 unit accurately. So when I bought my latest expensive vial of Levemir, I decided to try an experiment to see if I could keep the insulin in the vial alive for a longer time.
What I did was mail order some sterile 10 ml vials and transfer 100 units of insulin into the new sterile vial. I'm going to draw the insulin from that sterile vial, not the manufacturer's vial and thus cut way down on the number of times I introduce a needle into the main vial. Hopefully this means I'll be able to use all of those 1,0000 units instead of only 150 or so.
Another benefit of this approach compared to pens is that I won't be wasting the many air shots I have to waste when I use pens. The air shots can use up even more insulin than my basal shots. The convenience of the pen is a huge issue with post-meal insulin, but not for basal.
I'll be reporting back in a few months about whether this strategy is effective. If any of you who use tiny doses have any other suggestions about how to keep insulin in vials alive. Let me know.
UPDATE: 5/24/08
The insulin in the mail order vial is still working as it should. The only problem I've run into is that my syringes are dulling out much faster than they do I've been reusing them with a manufacturer's pen. This is probably because the rubber seal on the mail order vial is made out of a cheaper material.
The result is that the shots will hurt and bruise if I don't change the needle after no more than 2 shots.
NOTE: I have tried not reusing needles and reusing needles and have not seen any difference in how well my insulin holds up. When I reuse a syringe I do not inject air into the vial and I carefully expel any insulin left in the needle squirt-gun style after each use. Periodically I bleed the air out of the syringe by inserting a new needle with the plunger removed. This is the procedure described in the book, Dr. Bernstein's Diabetes Solution.
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