Several of the online bookstores are listing my book, Blood Sugar 101, as being "out of stock." This is very temporary. Our distributor is adding UK distribution to their system, which required changing the listing in their database. This caused the book to be listed as "temporarily out of stock" while the update was applied
I'm assured that it will be back in stock within a few days, and when it is, UK buyers should be able to buy Blood Sugar 101 from online bookstores in the UK.
Thanks to everyone who has purchased the book until now. Sales are going really well. The Amazon ranking has been consistently high on the list of Type 2 books, which means people who aren't aware of this blog can find it on a search.
I'm so happy this is happening, as it means more people are getting the benefit of the information Blood Sugar 101 contains.
June 30, 2008
June 25, 2008
Details: The "Big Breakfast Diet" was Low Carb & Very Low Cal
There's been a lot of ignorant coverage of the supposed benefits of a high carb big breakfast for dieters.
Now Diabetes in Control has published the details of this study and they are quite different than what the media coverage would suggest.
Here are the pertinent facts:
1. The specific of the diets (emphasis mine):
The low-carb diet allowed 1,085 calories a day with 17 grams of carbohydrates, 51 grams of protein, and 78 grams of fat. Breakfast for members of this group was to be 290 calories with 7 grams of carbohydrates and 12 grams of protein.
The modified form of this diet allowed 1,240 calories a day with less total fat (46 grams) but more carbs (97 grams) and protein (93 grams). The main feature was a 610-calorie "big breakfast" accounting for about half of the daily carbohydrates (58 grams), protein (47 grams), and fat (22 grams).
2. So as you can see, both diets were both technically low carb. But the first version is TOO low carb. The carb intake on that diet is so low that it is not possible for dieters eating it to eat the healthy low carb greens and vegetables which are essential to eating a healthy low carb diet.
That "low carb" diet does not match the description of any of the low carb diets that long term low carbers eat. Even Dr. Bernstein--the most stringent of all the low carb diet gurus--allows his dieters 30 grams a day of carbohydrate with possibly another 6 gram snack and recommends eating those carbs in the form of low carb vegetables.
3. These diets were also very unhealthy because they were extremely low calorie. The dieters were eating at a level so low that they were likely to depress their metabolisms. This guarantees weight regain.
Moreover, the "low carb" diet had 14% less calories than the other diet, a significant difference quite capable of explaining the result independent of the meal composition.
The beauty of the low carb diet is that it makes it possible for obese people to lose weight while eating a lot more calories than is possible on other diets.
The weight regain suffered by the so-called low carb dieters may have been the usual rebound suffered by any dieter eating under 1200 calories a day. That the two diets had different calorie intake levels should make any result attributed to dietary composition suspect.
3. This study was done in normal people and the carb loading technique it explored is not suitable for people with diabetes. This is because people with diabetes are most resistant to insulin in he morning thanks to dawn effect. That means they would end up with very high blood sugars after such a high carb meal which would result in a blood sugar swing that would make them very hungry by lunch time, tempting them to eat more.
4. This was not a peer reviewed study. It was a "poster session" at a conference where the researchers briefly described their research. This means that the quality of the research still has to be assessed.
If there is any value to the finding here--which is questionable, it might be that eating more early in the day can help prevent the after dinner snacking that derails so many dieters. Unfortunately the poor design of this study makes it hard to know if it really proved that.
You can test the idea in your own diet by moving some calories to breakfast from lunch or dinner and seeing if it makes you less hungry. Make them fat or protein calories, though, as a high carb breakfast is guaranteed to make you hungry unless you have rock solid normal blood sugar!
Now Diabetes in Control has published the details of this study and they are quite different than what the media coverage would suggest.
Here are the pertinent facts:
1. The specific of the diets (emphasis mine):
The low-carb diet allowed 1,085 calories a day with 17 grams of carbohydrates, 51 grams of protein, and 78 grams of fat. Breakfast for members of this group was to be 290 calories with 7 grams of carbohydrates and 12 grams of protein.
The modified form of this diet allowed 1,240 calories a day with less total fat (46 grams) but more carbs (97 grams) and protein (93 grams). The main feature was a 610-calorie "big breakfast" accounting for about half of the daily carbohydrates (58 grams), protein (47 grams), and fat (22 grams).
2. So as you can see, both diets were both technically low carb. But the first version is TOO low carb. The carb intake on that diet is so low that it is not possible for dieters eating it to eat the healthy low carb greens and vegetables which are essential to eating a healthy low carb diet.
That "low carb" diet does not match the description of any of the low carb diets that long term low carbers eat. Even Dr. Bernstein--the most stringent of all the low carb diet gurus--allows his dieters 30 grams a day of carbohydrate with possibly another 6 gram snack and recommends eating those carbs in the form of low carb vegetables.
3. These diets were also very unhealthy because they were extremely low calorie. The dieters were eating at a level so low that they were likely to depress their metabolisms. This guarantees weight regain.
Moreover, the "low carb" diet had 14% less calories than the other diet, a significant difference quite capable of explaining the result independent of the meal composition.
The beauty of the low carb diet is that it makes it possible for obese people to lose weight while eating a lot more calories than is possible on other diets.
The weight regain suffered by the so-called low carb dieters may have been the usual rebound suffered by any dieter eating under 1200 calories a day. That the two diets had different calorie intake levels should make any result attributed to dietary composition suspect.
3. This study was done in normal people and the carb loading technique it explored is not suitable for people with diabetes. This is because people with diabetes are most resistant to insulin in he morning thanks to dawn effect. That means they would end up with very high blood sugars after such a high carb meal which would result in a blood sugar swing that would make them very hungry by lunch time, tempting them to eat more.
4. This was not a peer reviewed study. It was a "poster session" at a conference where the researchers briefly described their research. This means that the quality of the research still has to be assessed.
If there is any value to the finding here--which is questionable, it might be that eating more early in the day can help prevent the after dinner snacking that derails so many dieters. Unfortunately the poor design of this study makes it hard to know if it really proved that.
You can test the idea in your own diet by moving some calories to breakfast from lunch or dinner and seeing if it makes you less hungry. Make them fat or protein calories, though, as a high carb breakfast is guaranteed to make you hungry unless you have rock solid normal blood sugar!
June 24, 2008
A Giant Step Backwards: Misinterpreting ACCORD Harms People with Diabetes
The fallout from the ACCORD study continues, and it is going to cause a lot of unnecessary kidney failure and neuropathy.
If you'll remember, ACCORD was the study where they took people who had diabetes and preexisting heart disease , put them on every drug possible, including Avandia, Actos, Byetta and Insulin, encouraged them to eat a high carb/low fat diet and discovered that there were a very small number of so-called "excess deaths" in the group who achieved blood sugars nearer 6.5% compared to those who aimed for the old 7.0% ADA target.
The take home message from this for doctors was that lowering the A1c kills people with diabetes.
A second study, ADVANCE, which involved a lot more people with diabetes and lasted longer--a study which did NOT use Avandia, Actos, or Byetta found NO such excess deaths in the group that lowered their A1c. Not only that, but the group in the ADVANCE study that achieved the 6.5% A1cs had 21% less kidney disease--a major finding given how many type 2s end up on dialysis.
Clearly the problem illuminated in ACCORD was not that lowering A1c kills people with diabetes but that the combination of drugs given to people with diabetes to lower their blood sugar along with the high carbohydrate diet was not safe for people with preexisting heart disease.
The lack of excess deaths and the decrease in kidney disease found in the ADVANCE study should have in itself been reason to advise lowering the blood sugar targets for all people with diabetes using a protocol similar to that used in ADVANCE--which was one that did not use the newer, possibly more dangerous diabetes drugs. Ideally more scientific effort would now be put into analyzing the differences between the two studies to determine why ACCORD showed those excess cardiac deaths and the larger, longer ADVANCE study did not.
My guess is that the ACCORD population was sicker to start with--i.e. their diabetes was of much longer standing at the time the study began, that their diets were probably higher in carbs, trans fat, and junk food (ACCORD was an American study while ADVANCE was not), and that the addition of Avandia and Actos to their protocols--both known to be cardiotoxic--was probably more significant than the drug company funded researchers revealed.
Whatever the explanation, if your doctor tells you to RAISE your A1c to "be safe"--which I am hearing from my correspondents is becoming horrifyingly common-- remind him or her that:
1. There is NO study about the safety of lowering A1c using a low carb diet rather than using dangerous drugs like Actos and Avandia with the high carb/low fat diet that was used in ACCORD. All early indications from small studies are that lowering blood sugar by lowering carb intake improves all cardiovascular markers and does not worsen heart disease.
2. ADVANCE showed decisively that lowering A1c prevents kidney disease.
3. ADVANCE lasted longer and involved more people with diabetes than ACCORD and found NO increase in cardiac deaths.
There's a petition you can fill out addressing the NIH's dangerous issuing of a warning about the dangers of lowering A1c based on the ACCORD findings. You will find it here:
Petition: NIH must acknowledge existing science
Don't hold your breath expecting this to change anything.
If you'll remember, ACCORD was the study where they took people who had diabetes and preexisting heart disease , put them on every drug possible, including Avandia, Actos, Byetta and Insulin, encouraged them to eat a high carb/low fat diet and discovered that there were a very small number of so-called "excess deaths" in the group who achieved blood sugars nearer 6.5% compared to those who aimed for the old 7.0% ADA target.
The take home message from this for doctors was that lowering the A1c kills people with diabetes.
A second study, ADVANCE, which involved a lot more people with diabetes and lasted longer--a study which did NOT use Avandia, Actos, or Byetta found NO such excess deaths in the group that lowered their A1c. Not only that, but the group in the ADVANCE study that achieved the 6.5% A1cs had 21% less kidney disease--a major finding given how many type 2s end up on dialysis.
Clearly the problem illuminated in ACCORD was not that lowering A1c kills people with diabetes but that the combination of drugs given to people with diabetes to lower their blood sugar along with the high carbohydrate diet was not safe for people with preexisting heart disease.
The lack of excess deaths and the decrease in kidney disease found in the ADVANCE study should have in itself been reason to advise lowering the blood sugar targets for all people with diabetes using a protocol similar to that used in ADVANCE--which was one that did not use the newer, possibly more dangerous diabetes drugs. Ideally more scientific effort would now be put into analyzing the differences between the two studies to determine why ACCORD showed those excess cardiac deaths and the larger, longer ADVANCE study did not.
My guess is that the ACCORD population was sicker to start with--i.e. their diabetes was of much longer standing at the time the study began, that their diets were probably higher in carbs, trans fat, and junk food (ACCORD was an American study while ADVANCE was not), and that the addition of Avandia and Actos to their protocols--both known to be cardiotoxic--was probably more significant than the drug company funded researchers revealed.
Whatever the explanation, if your doctor tells you to RAISE your A1c to "be safe"--which I am hearing from my correspondents is becoming horrifyingly common-- remind him or her that:
1. There is NO study about the safety of lowering A1c using a low carb diet rather than using dangerous drugs like Actos and Avandia with the high carb/low fat diet that was used in ACCORD. All early indications from small studies are that lowering blood sugar by lowering carb intake improves all cardiovascular markers and does not worsen heart disease.
2. ADVANCE showed decisively that lowering A1c prevents kidney disease.
3. ADVANCE lasted longer and involved more people with diabetes than ACCORD and found NO increase in cardiac deaths.
There's a petition you can fill out addressing the NIH's dangerous issuing of a warning about the dangers of lowering A1c based on the ACCORD findings. You will find it here:
Petition: NIH must acknowledge existing science
Don't hold your breath expecting this to change anything.
June 18, 2008
Dr. Bernstein's Letter Recommending Blood Sugar 101
I posted earlier that Dr. Bernstein had written me a very nice letter praising my book, Blood Sugar 101. I wrote back and asked his permission to quote what he'd written and received that permission from him last week.
So here's what Dr. Bernstein had to say about my book:
"Thanks for sending me a copy of BLOOD SUGAR 101. I enjoyed it very much and actually learned a lot of important facts.
"I was impressed by your ability to scour the scientific literature and document your findings.
"I think this book should be read by all diabetics because of the valuable material that cannot be found elsewhere."
I am thrilled beyond words. Simply stated, there is no one in the world whose praise could mean more to me, because there is no one else whose own work has had such a huge impact on my life and health as Dr. Bernstein's has.
I had a terrible time getting a diagnosis because of the peculiar nature of my diabetes--very high blood sugars after meals, normal fasting blood sugar. Without Dr. Bernstein's book I might have gone for years more with the continual UTIs and yeast infections and have developed the heart disease that is endemic in the side of my family that carries this oddball diabetes gene.
But the tools he gave me in his books helped me get to near normal blood sugars, and also helped me understand enough about diabetes and its treatment to be able to evaluate the quality of the medical treatment I was getting.
He broke the way for a generation of people with diabetes--both Type 1 and Type 2--by championing the idea that lowering blood sugars will prevent complications years before that concept was proven by the DCCT, as this 1993 New York Times article makes that very clear: Vindication for a Diabetes Expert
For decades his was the sole voice calling for people with diabetes to cut the carbs, throughout the period when all people with diabetes were told that fat would kill them and the only safe diet for them was one that contained 300 g a day of "healthy carbs"--a diet that raised their blood sugar dramatically after every meal they ate.
Because many people with diabetes find the austerity of the diet that Dr. Bernstein recommends hard to accept, one of the things I set out to do when I did the research that led to Blood Sugar 101 was to learn what the academic research had found about the connection between blood sugar level and complications. This seemed to me the best way to determine if the blood sugar targets that Dr. Bernstein insists on are what is required for health.
My conclusion, based on the data, is that achieving Dr. Bernstein's blood sugar targets probably is ideal--especially if it can be done without using questionable drugs like the TZDs and sulfonylureas, but that true normal probably is a bit higher than what he prescribes. So it is likely that a slightly higher set of blood sugar targets probably confers the same health benefits as his do with the advantage of being easier to achieve for people who do not have personalities that incline them to iron discipline.
Dr. Bernstein addressed this difference between us, too, in his letter, which made his praise all the more valuable to me.
He wrote, "I wish that our guidelines for blood sugar targets and carbohydrate intake were closer together but this is a battle that I have been losing for many years."
But that said, I don't think he's losing that battle at all. I think his shadow lies over a whole generation of us who have learned how our blood sugar rises when we eat carbs, who use basal/bolus regimens (which he appears to have pioneered), and who are ten years or more past a diabetes diagnosis without having developed the horrible complications that even a decade ago most doctors assumed that we would get.
My book grows out of the revelations that his work provided and without his work, none of mine would have happened.
Thank you Dr. Bernstein.
So here's what Dr. Bernstein had to say about my book:
"Thanks for sending me a copy of BLOOD SUGAR 101. I enjoyed it very much and actually learned a lot of important facts.
"I was impressed by your ability to scour the scientific literature and document your findings.
"I think this book should be read by all diabetics because of the valuable material that cannot be found elsewhere."
I am thrilled beyond words. Simply stated, there is no one in the world whose praise could mean more to me, because there is no one else whose own work has had such a huge impact on my life and health as Dr. Bernstein's has.
I had a terrible time getting a diagnosis because of the peculiar nature of my diabetes--very high blood sugars after meals, normal fasting blood sugar. Without Dr. Bernstein's book I might have gone for years more with the continual UTIs and yeast infections and have developed the heart disease that is endemic in the side of my family that carries this oddball diabetes gene.
But the tools he gave me in his books helped me get to near normal blood sugars, and also helped me understand enough about diabetes and its treatment to be able to evaluate the quality of the medical treatment I was getting.
He broke the way for a generation of people with diabetes--both Type 1 and Type 2--by championing the idea that lowering blood sugars will prevent complications years before that concept was proven by the DCCT, as this 1993 New York Times article makes that very clear: Vindication for a Diabetes Expert
For decades his was the sole voice calling for people with diabetes to cut the carbs, throughout the period when all people with diabetes were told that fat would kill them and the only safe diet for them was one that contained 300 g a day of "healthy carbs"--a diet that raised their blood sugar dramatically after every meal they ate.
Because many people with diabetes find the austerity of the diet that Dr. Bernstein recommends hard to accept, one of the things I set out to do when I did the research that led to Blood Sugar 101 was to learn what the academic research had found about the connection between blood sugar level and complications. This seemed to me the best way to determine if the blood sugar targets that Dr. Bernstein insists on are what is required for health.
My conclusion, based on the data, is that achieving Dr. Bernstein's blood sugar targets probably is ideal--especially if it can be done without using questionable drugs like the TZDs and sulfonylureas, but that true normal probably is a bit higher than what he prescribes. So it is likely that a slightly higher set of blood sugar targets probably confers the same health benefits as his do with the advantage of being easier to achieve for people who do not have personalities that incline them to iron discipline.
Dr. Bernstein addressed this difference between us, too, in his letter, which made his praise all the more valuable to me.
He wrote, "I wish that our guidelines for blood sugar targets and carbohydrate intake were closer together but this is a battle that I have been losing for many years."
But that said, I don't think he's losing that battle at all. I think his shadow lies over a whole generation of us who have learned how our blood sugar rises when we eat carbs, who use basal/bolus regimens (which he appears to have pioneered), and who are ten years or more past a diabetes diagnosis without having developed the horrible complications that even a decade ago most doctors assumed that we would get.
My book grows out of the revelations that his work provided and without his work, none of mine would have happened.
Thank you Dr. Bernstein.
June 16, 2008
Post Surgery: I'm Doing Great!
I had my surgery last Tuesday and I'm doing very well, but I'm supposed to rest and not use my arms much, so I'll keep this brief.
I asked my surgeon what blood sugar they prefer in someone with diabetes and she said "Under 200" which is pretty appalling. I explained my outlook and she was very supportive of my low carb diet and blood sugar targets. I asked her if I needed to eat more carbs during the healing phase, and she said, "No. The low carb diet is an excellent diet for healing."
I'd been eating very low carb with lots of colorful veggies and greens for the three weeks before surgery and have continued with that diet for the past week.
At the hospital I tested at 88 mg/dl on their meter at 7 AM which the nurse thought was dangerously low. I explained it wasn't and that I had not used any basal insulin that morning. They promptly hooked me up to a lactate drip so they could raise my blood sugar.
I made a huge point to the anesthesiologist about my insulin sensitivity and made it clear that if they had to lower my blood sugar, using a typical Type 2 insulin dose could literally kill me. (Which it could.) I'm still alive, so she must have listened.
The surgery lasted three hours. They told me after the surgery that my blood sugar had gone up to 139. It dropped back into the 90s by the time I went home.
I'm currently using my usual basal insulin but almost no meal time insulin as I am eating only meat, cheese, greens, LC veggies and lots of berries, and that keeps my blood sugar between 95 and 115 most of the time. I'm trying to get about 100 g of protein a day, which is about right for my weight. I don't want to screw around with insulin shots at meals if I don't have to because the pain drug slows digestion and it is hard to know when the food will digest.
But I'm on the mend, everything is going really well, and I'm really enjoying taking time off from doing all the stuff I usually do.
I'll leave you with this fascinating piece of diabetes research published in this past months edition of the journal, Diabetes Research and Clinical Practice:
Dietary Breads: Myth or Reality
Someone finally decided to see if the so called glycemic index works for people with diabetes. Here's what they did:
"One hundred twenty one type 2 diabetic patients were randomized into three groups as whole wheat, wheat bran and rye bread groups. Each group ate 100 g of bread with water with in 10 min. Blood glucose measurements were made at every 30 min in 2 h. Insulin was measured at fasting and at the second hour in the patients who do not use insulin. The same processes were repeated on the following day, with white wheat bread for each group."
Here's what they found:
"No significant difference was found in either glycemic or insulinemic effects between four types of breads when compared to each other. (p = 0.093 for glycemic effect and p = 0.297 for insulinemic effect)."
In short, "healthy" whole grains raised blood sugar as much as white bread.
Show this article to your doctor!
I asked my surgeon what blood sugar they prefer in someone with diabetes and she said "Under 200" which is pretty appalling. I explained my outlook and she was very supportive of my low carb diet and blood sugar targets. I asked her if I needed to eat more carbs during the healing phase, and she said, "No. The low carb diet is an excellent diet for healing."
I'd been eating very low carb with lots of colorful veggies and greens for the three weeks before surgery and have continued with that diet for the past week.
At the hospital I tested at 88 mg/dl on their meter at 7 AM which the nurse thought was dangerously low. I explained it wasn't and that I had not used any basal insulin that morning. They promptly hooked me up to a lactate drip so they could raise my blood sugar.
I made a huge point to the anesthesiologist about my insulin sensitivity and made it clear that if they had to lower my blood sugar, using a typical Type 2 insulin dose could literally kill me. (Which it could.) I'm still alive, so she must have listened.
The surgery lasted three hours. They told me after the surgery that my blood sugar had gone up to 139. It dropped back into the 90s by the time I went home.
I'm currently using my usual basal insulin but almost no meal time insulin as I am eating only meat, cheese, greens, LC veggies and lots of berries, and that keeps my blood sugar between 95 and 115 most of the time. I'm trying to get about 100 g of protein a day, which is about right for my weight. I don't want to screw around with insulin shots at meals if I don't have to because the pain drug slows digestion and it is hard to know when the food will digest.
But I'm on the mend, everything is going really well, and I'm really enjoying taking time off from doing all the stuff I usually do.
I'll leave you with this fascinating piece of diabetes research published in this past months edition of the journal, Diabetes Research and Clinical Practice:
Dietary Breads: Myth or Reality
Someone finally decided to see if the so called glycemic index works for people with diabetes. Here's what they did:
"One hundred twenty one type 2 diabetic patients were randomized into three groups as whole wheat, wheat bran and rye bread groups. Each group ate 100 g of bread with water with in 10 min. Blood glucose measurements were made at every 30 min in 2 h. Insulin was measured at fasting and at the second hour in the patients who do not use insulin. The same processes were repeated on the following day, with white wheat bread for each group."
Here's what they found:
"No significant difference was found in either glycemic or insulinemic effects between four types of breads when compared to each other. (p = 0.093 for glycemic effect and p = 0.297 for insulinemic effect)."
In short, "healthy" whole grains raised blood sugar as much as white bread.
Show this article to your doctor!
June 9, 2008
Here is the NEJM Publication About ADVANCE
http://content.nejm.org/cgi/reprint/NEJMoa0802987v1.pdf
Download it and check out the graphs yourself. They appear to me to demonstrate clear cut improvement in the group that lowered their blood sugar more aggressively. Also check out the description of the drugs they used. All were put on Gliclazide (Diamicron), which is the sulfonylurea drug that is not approved for use in the U.S.. Most were also given Metformin and many were given insulin too. And of course, the high carb diet.
I don't, alas, have the time to go into this further now. I'll discuss it in 2 weeks when I'm back. It's a shame there isn't a Metformin ONLY study where people were encouraged to drop their carbs rather than follow the toxic "Eat your carbs! Cut out Fat!" advice that these people were given.
Download it and check out the graphs yourself. They appear to me to demonstrate clear cut improvement in the group that lowered their blood sugar more aggressively. Also check out the description of the drugs they used. All were put on Gliclazide (Diamicron), which is the sulfonylurea drug that is not approved for use in the U.S.. Most were also given Metformin and many were given insulin too. And of course, the high carb diet.
I don't, alas, have the time to go into this further now. I'll discuss it in 2 weeks when I'm back. It's a shame there isn't a Metformin ONLY study where people were encouraged to drop their carbs rather than follow the toxic "Eat your carbs! Cut out Fat!" advice that these people were given.
June 7, 2008
Australian Study: 6.5% is NOT Normal and Sulfs aren't Great for Your Heart
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!
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!
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 2008 poll on tudiabetes.org, a social media site for people with diabetes, 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 2008 poll on tudiabetes.org, a social media site for people with diabetes, 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.
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.
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