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.
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.
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.
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.
May 20, 2008
How the Blood Sugar 101 Book is Doing
Well, it's been about two months since my book came out, and I've been really happy with the reception. I have gotten a lot of email from buyers who found it very helpful, and their words have been really heartening. A few have told me they went on to buy copies for friends and relatives and some bought copies for their local libraries. Thanks so much to all of you!
Just last week I got a letter from my hero, Dr. Richard K. Bernstein. I'd sent him a copy at the suggestion of Steve Freed of Diabetes in Control after he published a very positive review of the book. But I didn't expect to hear back from Dr. Bernstein since I take a very different approach to diet than he does and because I knew he was still enthusiastic about TZD drugs which I write are dangerous for people with diabetes.
So imagine my surprise when I opened his letter and read that the enjoyed Blood Sugar 101 and believed it contained information available nowhere else and that people with diabetes should read it! I've written to ask him if I can quote what he wrote and until I hear from him, I won't cite his exact words, but you better believe I was walking on air for a few days after I got that letter!
The challenge with marketing this kind of book is that because I'm not a doctor and because the book is published by a small press, I can't go on the radio or TV to promote it, and the book chains won't stock it on their shelves. So that means I pretty much have to rely on whatever word of mouth recommendations I can stimulate to get people to buy it from the online bookstores where it is available.
So that leads to this blatant plea for your help. If you have read Blood Sugar 101 and have found it helpful, let people know. Also, ask your local public library to stock it. It is available from Baker & Taylor, the company that sells to libraries, and most libraries will order books that patrons ask for.
If you have any other ideas for how we can get more people reading this book, let me know. Sales have been very good for a small press book, but in absolute numbers that is still not a lot of books. Now that I have gotten the kind of enthusiastic feedback I have, it seems even more important to get the word out about this book. It seems there are still a lot of people who don't read the web sites and blogs and who really benefit from access to the "Dead Tree" version.
Here's a page that links to some of the excellent reviews and blog discussions that have been published online and the sites where you can buy Blood Sugar 101:
Blood Sugar 101, The Book.
Just last week I got a letter from my hero, Dr. Richard K. Bernstein. I'd sent him a copy at the suggestion of Steve Freed of Diabetes in Control after he published a very positive review of the book. But I didn't expect to hear back from Dr. Bernstein since I take a very different approach to diet than he does and because I knew he was still enthusiastic about TZD drugs which I write are dangerous for people with diabetes.
So imagine my surprise when I opened his letter and read that the enjoyed Blood Sugar 101 and believed it contained information available nowhere else and that people with diabetes should read it! I've written to ask him if I can quote what he wrote and until I hear from him, I won't cite his exact words, but you better believe I was walking on air for a few days after I got that letter!
The challenge with marketing this kind of book is that because I'm not a doctor and because the book is published by a small press, I can't go on the radio or TV to promote it, and the book chains won't stock it on their shelves. So that means I pretty much have to rely on whatever word of mouth recommendations I can stimulate to get people to buy it from the online bookstores where it is available.
So that leads to this blatant plea for your help. If you have read Blood Sugar 101 and have found it helpful, let people know. Also, ask your local public library to stock it. It is available from Baker & Taylor, the company that sells to libraries, and most libraries will order books that patrons ask for.
If you have any other ideas for how we can get more people reading this book, let me know. Sales have been very good for a small press book, but in absolute numbers that is still not a lot of books. Now that I have gotten the kind of enthusiastic feedback I have, it seems even more important to get the word out about this book. It seems there are still a lot of people who don't read the web sites and blogs and who really benefit from access to the "Dead Tree" version.
Here's a page that links to some of the excellent reviews and blog discussions that have been published online and the sites where you can buy Blood Sugar 101:
Blood Sugar 101, The Book.
May 15, 2008
When Going Low Makes You Go High: Mysteries of Counterregulation
If you use insulin, one of the weirder phenomena you're likely encounter as you work on normalizing your blood sugar is the way that when you use a bit too much insulin you'll see your blood sugar go up, not down.
This can be very confusing, and it is all the more confusing when you have to rely for help on doctors who aren't familiar with this phenomenon.
Counter-regulation is the official term for what is going on here. It refers to the built-in protective system most of us have that monitors our blood sugar level and, if it drops too low, causes the release of hormones that will cause our livers to dump some glucose into our blood streams to raise it back up again.
The hormones that do this are our old friends, the stress hormones. So often the only signal you get that you have experienced a bust of counter-regulation is that your heart speeds up, your pulse pounds and your blood pressure goes up.
By the time you feel any of those symptoms, your blood sugar will have risen, so testing it will often reveal a normal blood sugar. It's too late to catch the low that triggered the release of hormones.
A common time to experience a burst of counter-regulation is at 4AM, a time when blood sugar may naturally drop to its lowest level. If you wake up out of a deep sleep with your heart pounding this may have happened. Check your blood sugar and it will be higher than usual.
Even worse, after you've experienced counter-regulation you may be more insulin resistant than usual for a few hours.
All this sounds very simple, but several things complicate the issue.
1. The level your body believes to be "too low" may actually be a normal blood sugar.. This happens if you have been running high for a while, because your body defines "normal" as being whatever blood sugar level you've been living at and if that level has been high it may react with a burst of hormones to raise your blood sugar when it is at a perfectly healthy level.
Ignorant nutritionists often advise people with diabetes to eat carbs (and thus raise their blood sugars) to avoid these "liver dumps." In fact, that's the worst thing you can do. You want to keep working on lowering your blood sugar so that your body resets the "normal" thermostat to--duh--normal.
Though you might experience counter-regulatory bursts at first when you lower your blood sugar to normal levels, the more often you get your blood sugar down to normal--even if your body pushes your blood sugar back up--the lower that thermostat will be set. You just have to wait it out, keep lowering your blood sugar, and eventually you won't get those bursts when you "drop" to normal levels any more.
The strength of the counter-regulatory response varies from person to person. Mine is extremely strong and it took me literally months for my body to get used to the low 90s. And more months to get used to the 80s. But now I do not get counter-regulatory bursts until I'm in the low 70s, and that works for me.
2. If your blood sugar thermostat is set correctly, getting your basal insulin doses wrong can make your morning fasting blood sugar high, tempting you to add more basal insulin and resulting in more counter-regulation.
This one can be VERY hard to debug. Because my natural fasting blood sugar was around 108 for many years, I've learned, after a lot of observation, that if I use even so much as 1/4 unit too much basal insulin, I'll wake up with a pounding pulse and a blood sugar of 108. If I drop that 1/4 unit, I'll wake up at 86. I'm extremely sensitive to basal insulin. So most people will see that kind of difference in response to changes of 3-5 units.
But if you start increasing your basal insulin and see your blood sugar going up in the morning rather than down, it's worth testing the idea that you are using too much and lowering the dose, night by night, until you see it going down again.
3. Counter-regulation also occurs if your blood pressure drops. This can make it really tough to debug blood sugar highs. At the same time of night when you are prone to lows, your blood pressure drops, and if it is too low, your body will secrete stress hormones to push that blood pressure back into the safe zone. That also pushes up your blood sugar and figuring out what is causing that 4AM pulse pounding can be very tough indeed if you are also taking blood pressure medication.
To make it even more complex, lowering your blood sugar may cause your blood pressure to improve--as may cutting the carbs out of your diet. So just as you get your blood sugar near where it belongs, your blood pressure may drop and you may start having those bouts of early morning counter-regulation and wake up with your blood pressure--and sugar--higher.
Family doctors are very unlikely to understand this phenomenon at all and may make things worse by telling you to raise your blood pressure medication or insulin rather than lower it since both may be quite high after a burst of counter-regulation. Mine sent me off to a cardiologist when I developed a pounding pulse in response to what I only much later realized was a serious overdose of basal insulin. (About 3 times more than my body can handle.) The cardiologist never suggested that the problem might be counter-regulatory in nature, but instead wanted me to take a beta-blocker to lower my pulse. A beta blocker would have damped down the counter-regulation--and set me up to experience really dangerous lows since my body would no longer be correcting the response to too much insulin!
Counter-regulation is there for a reason. People with diabetes who experience a lot of lows eventually reset their blood sugar thermostats extremely low and can have extremely dangerous hypos.
How To Handle Counter-Regulatory Problems
If you take insulin and are experiencing counter-regulatory bursts do the following:
1. Check your blood sugar before you go to sleep. If it is near your morning target take a few grams of glucose before you go to bed and see if that solves the problem. That helps a lot for me. You can also try eating a protein snack before bed to provide some glucose for those early morning hours.
2. If the snack doesn't work try lowering your nighttime basal insulin dose by a small increment and see if your blood sugar goes higher, stays the same, or drops. If it stays the same, you can drop it a bit more. If it goes up, counter-regulation is probably not the problem. If it drops you might be on the right track.
3. Test your blood pressure with a meter at various times of day. If you see values in the low end of normal--90/60 for example, it is very likely you are dropping even lower at night. If so, talk with your doctor about lowering your blood pressure medicine.
4. If you are using Lantus and can't eliminate counter-regulation (I couldn't) ask your doctor if you can try switching to Levemir because it is shorter in action especially when used in smaller doses. With Levemir you can use a larger morning dose and a smaller night time dose, and that may avoid those 4AM lows.
5. If you have access to a CGMS you may be able to see late night lows you are otherwise missing. This is described in detail with several sample CGMS logs in the book, Type 1 Diabetes: A Guide for Children, Adolescents, Young Adults--and Their Caregivers. by Ragnar Hanas. It was only after reading this book a few years ago that I was finally able to figure out what was going on with my blood sugars since they so often went up, not down, when I used basal insulin.
6. Aim for a basal Level in the mid-80s. Setting your basal too low may eliminate counter-regulation problems, but it sets you up for dangerous hypos. If you are waking up in the low 70s every day you might be resetting your blood sugar thermostat at a level that keeps you from getting a helpful counter-regulatory response when you drop into the low 60s or lower.
This can be very confusing, and it is all the more confusing when you have to rely for help on doctors who aren't familiar with this phenomenon.
Counter-regulation is the official term for what is going on here. It refers to the built-in protective system most of us have that monitors our blood sugar level and, if it drops too low, causes the release of hormones that will cause our livers to dump some glucose into our blood streams to raise it back up again.
The hormones that do this are our old friends, the stress hormones. So often the only signal you get that you have experienced a bust of counter-regulation is that your heart speeds up, your pulse pounds and your blood pressure goes up.
By the time you feel any of those symptoms, your blood sugar will have risen, so testing it will often reveal a normal blood sugar. It's too late to catch the low that triggered the release of hormones.
A common time to experience a burst of counter-regulation is at 4AM, a time when blood sugar may naturally drop to its lowest level. If you wake up out of a deep sleep with your heart pounding this may have happened. Check your blood sugar and it will be higher than usual.
Even worse, after you've experienced counter-regulation you may be more insulin resistant than usual for a few hours.
All this sounds very simple, but several things complicate the issue.
1. The level your body believes to be "too low" may actually be a normal blood sugar.. This happens if you have been running high for a while, because your body defines "normal" as being whatever blood sugar level you've been living at and if that level has been high it may react with a burst of hormones to raise your blood sugar when it is at a perfectly healthy level.
Ignorant nutritionists often advise people with diabetes to eat carbs (and thus raise their blood sugars) to avoid these "liver dumps." In fact, that's the worst thing you can do. You want to keep working on lowering your blood sugar so that your body resets the "normal" thermostat to--duh--normal.
Though you might experience counter-regulatory bursts at first when you lower your blood sugar to normal levels, the more often you get your blood sugar down to normal--even if your body pushes your blood sugar back up--the lower that thermostat will be set. You just have to wait it out, keep lowering your blood sugar, and eventually you won't get those bursts when you "drop" to normal levels any more.
The strength of the counter-regulatory response varies from person to person. Mine is extremely strong and it took me literally months for my body to get used to the low 90s. And more months to get used to the 80s. But now I do not get counter-regulatory bursts until I'm in the low 70s, and that works for me.
2. If your blood sugar thermostat is set correctly, getting your basal insulin doses wrong can make your morning fasting blood sugar high, tempting you to add more basal insulin and resulting in more counter-regulation.
This one can be VERY hard to debug. Because my natural fasting blood sugar was around 108 for many years, I've learned, after a lot of observation, that if I use even so much as 1/4 unit too much basal insulin, I'll wake up with a pounding pulse and a blood sugar of 108. If I drop that 1/4 unit, I'll wake up at 86. I'm extremely sensitive to basal insulin. So most people will see that kind of difference in response to changes of 3-5 units.
But if you start increasing your basal insulin and see your blood sugar going up in the morning rather than down, it's worth testing the idea that you are using too much and lowering the dose, night by night, until you see it going down again.
3. Counter-regulation also occurs if your blood pressure drops. This can make it really tough to debug blood sugar highs. At the same time of night when you are prone to lows, your blood pressure drops, and if it is too low, your body will secrete stress hormones to push that blood pressure back into the safe zone. That also pushes up your blood sugar and figuring out what is causing that 4AM pulse pounding can be very tough indeed if you are also taking blood pressure medication.
To make it even more complex, lowering your blood sugar may cause your blood pressure to improve--as may cutting the carbs out of your diet. So just as you get your blood sugar near where it belongs, your blood pressure may drop and you may start having those bouts of early morning counter-regulation and wake up with your blood pressure--and sugar--higher.
Family doctors are very unlikely to understand this phenomenon at all and may make things worse by telling you to raise your blood pressure medication or insulin rather than lower it since both may be quite high after a burst of counter-regulation. Mine sent me off to a cardiologist when I developed a pounding pulse in response to what I only much later realized was a serious overdose of basal insulin. (About 3 times more than my body can handle.) The cardiologist never suggested that the problem might be counter-regulatory in nature, but instead wanted me to take a beta-blocker to lower my pulse. A beta blocker would have damped down the counter-regulation--and set me up to experience really dangerous lows since my body would no longer be correcting the response to too much insulin!
Counter-regulation is there for a reason. People with diabetes who experience a lot of lows eventually reset their blood sugar thermostats extremely low and can have extremely dangerous hypos.
How To Handle Counter-Regulatory Problems
If you take insulin and are experiencing counter-regulatory bursts do the following:
1. Check your blood sugar before you go to sleep. If it is near your morning target take a few grams of glucose before you go to bed and see if that solves the problem. That helps a lot for me. You can also try eating a protein snack before bed to provide some glucose for those early morning hours.
2. If the snack doesn't work try lowering your nighttime basal insulin dose by a small increment and see if your blood sugar goes higher, stays the same, or drops. If it stays the same, you can drop it a bit more. If it goes up, counter-regulation is probably not the problem. If it drops you might be on the right track.
3. Test your blood pressure with a meter at various times of day. If you see values in the low end of normal--90/60 for example, it is very likely you are dropping even lower at night. If so, talk with your doctor about lowering your blood pressure medicine.
4. If you are using Lantus and can't eliminate counter-regulation (I couldn't) ask your doctor if you can try switching to Levemir because it is shorter in action especially when used in smaller doses. With Levemir you can use a larger morning dose and a smaller night time dose, and that may avoid those 4AM lows.
5. If you have access to a CGMS you may be able to see late night lows you are otherwise missing. This is described in detail with several sample CGMS logs in the book, Type 1 Diabetes: A Guide for Children, Adolescents, Young Adults--and Their Caregivers. by Ragnar Hanas. It was only after reading this book a few years ago that I was finally able to figure out what was going on with my blood sugars since they so often went up, not down, when I used basal insulin.
6. Aim for a basal Level in the mid-80s. Setting your basal too low may eliminate counter-regulation problems, but it sets you up for dangerous hypos. If you are waking up in the low 70s every day you might be resetting your blood sugar thermostat at a level that keeps you from getting a helpful counter-regulatory response when you drop into the low 60s or lower.
May 12, 2008
The LADA Epidemic. What's Going on Here?
A surprising number of people who are joining the online diabetes community after recent diagnoses are people who have been diagnosed with a new form of diabetes which is called LADA, which stands for Latent Autoimmune Diabetes of Adults. It is neither Type 1 or Type 2, but is often called "Type 1.5."
Typically, a person with LADA goes to the doctor sometime after the age of 35 and is told they have type 2 diabetes. They are put on oral drugs like metformin or Avandia and almost nothing happens. If they read up online and cut their carbs their blood sugars do improve, but even so, over time they continue to rise.
Within an average of four years, they have no insulin production left at all. At this point they must go on insulin. But the Lantus-only regimens most doctors prescribe--the ones that work well for many people with Type 2 diabetes--do not stop the inexorable rise in their blood sugars, and eventually they end up needing the full basal/bolus treatment that Type 1s use.
That's because LADA is really a slow-developing form of Type 1. The body mounts an immune attack on the pancreas and wipes out the insulin producing cells. The difference between LADA and classic Type 1 is the speed with which this happens. In young Type 1s a person can go from normal to completely whacked in a week. People with LADA may take up to a decade to lose all their insulin-secreting capacity.
People with LADA are often thin, so if you are thin and are told you have Type 2 diabetes, you should demand the antibody tests that are used to diagnose LADA. The antibodies tested for are: GAD antibodies, Islet cell antibodies, and more rarely, tyrosine phosphatase antibodies.
But not all people with LADA are slim. People with defective autoimmune genes are also prone to get thyroid disease and rheumatoid arthritis both of which can promote obesity, the first because incorrectly treated thyroid disease will make you fat and the latter because it limits mobility and hence the ability to exercise and because it is often treated with steroids that promote weight gain.
People with LADA benefit from being put onto full basal/bolus insulin regimens as soon as possible. There's some evidence that injecting insulin may turn off the immune attack on the beta cells and preserve them.
But because overweight people with LADA are universally diagnosed as having Type 2 they are almost always denied insulin treatment until they have spent years with extremely high blood sugars. This isn't because they are overweight, it's because that's the treatment given to ALL people diagnosed with Type 2 whose doctors allow them to maintain criminally high blood sugars for years out of a misguided belief that insulin will worsen, not better, their insulin resistance.
Genetic testing recently revealed that people with LADA have similar immunity-related genetic errors to people with juvenile onset Type 1 diabetes but that they also have defects in a gene, TCF7L2, that are frequently found in people with Type 2. Since just about every LADA I've ever met is thin, this suggests to me that there are probably a lot more people out there who are carrying Type 2 diagnoses who have LADA than we realize who are not getting diagnosed correctly because of their weight and because that TCF7L2 gene may cause enough insulin resistance to make them look like a classic Type 2.
I have to wonder though, WHY we are seeing so many people developing what was an extremely rare syndrome just a few decades ago. Is it better diagnosis, or is it the same thing that is driving the huge increase in the number of kids getting autoimmune diabetes? My guess is the latter, and though there is officially no explanation for this, my guess is that it has a lot to do with the environmental pollutants that saturate our bodies. Plastics, industrial chemical residues, pesticides, PCBs, etc.
Many genetic flaw--for instance those that lead to cancer--do not manifest in overt disease until the borderline-defective gene takes a hit from some environmental exposure. Chemicals, radiation, and viruses can all cause cancer in people with defective genes, and probably they cause autoimmune diabetes in people with defects in their autoimmune genes.
This is likely because even among identical twins who share genes, it is possible for one twin to develop autoimmune diabetes while the other remains normal. So my guess is that many of us have carried slight abnormalities in our autoimmune genes that did not get those extra hits until we started filling our world with plastics and the other toxic chemicals that are now found in our blood, tissues and even, as I blogged earlier, in mothers' milk.
The Warning Signs YOU May Have LADA
1. You are diagnosed with Type 2 diabetes while at a normal weight.
2. Whatever your weight, either you or a member of your family has some other autoimmune disease such as thyroid disease, rheumatoid arthritis, lupus, or multiple sclerosis.
3. You lower your carbohydrate intake shortly after diagnosis to no more than 15 grams a meal and still have a fasting blood sugar over 110 mg/dl and blood sugars that rise 40 mg/dl or more after each meal.
4. No matter what your weight, you do not see a dramatic drop in your blood sugar when you take metformin, Avandia, Actos, Januvia or Byetta in combination with a lowered carbohydrate intake.
5. Your blood sugar deteriorates significantly over the period of a year despite treatment with oral drugs and carbohydrate restriction.
What To Do To Get A LADA Diagnosis
If you think you have LADA ask your doctor for:
1. A fasting C-peptide test. If the value is low, it is suggestive of LADA.
2. GAD and Islets antibody tests. High levels of these antibodies are diagnostic of LADA especially in combination with lowered C-peptide.
The Next Step
Many doctors assume patients will do anything to avoid shots and delay giving people insulin. If you have LADA you want to go on a full-fledged Type 1 insulin regimen as fast as possible.
The sooner you start insulin the easier it will be to control your blood sugar with insulin for many years to come. And by injecting insulin you may be able to stop the attack on your beta cells completely. This is essential because technologies are emerging that might be able to stop the immune attack permanently and even regrow your beta cells. But for these treatments to work you need to have living beta cells. The longer you delay insulin, the fewer beta cells you will have left.
Insulin shots are painless and if you have been running high blood sugars for a while, you will feel much, much better once you start using insulin to get normal blood sugars.
Get Support From Others with LADA
There are lots of people with LADA active on all the online discussion boards that provide diabetes support. If you have LADA be sure to seek out others because their personal experiences will be extremely helpful to you once you start working on adjusting your insulin doses and diet.
You can find people with LADA at Tudiabetes.com, Diabetes Daily Forums, and Diabetesforums.com. LADA is usually discussed in the "Type 1.5" area.
Typically, a person with LADA goes to the doctor sometime after the age of 35 and is told they have type 2 diabetes. They are put on oral drugs like metformin or Avandia and almost nothing happens. If they read up online and cut their carbs their blood sugars do improve, but even so, over time they continue to rise.
Within an average of four years, they have no insulin production left at all. At this point they must go on insulin. But the Lantus-only regimens most doctors prescribe--the ones that work well for many people with Type 2 diabetes--do not stop the inexorable rise in their blood sugars, and eventually they end up needing the full basal/bolus treatment that Type 1s use.
That's because LADA is really a slow-developing form of Type 1. The body mounts an immune attack on the pancreas and wipes out the insulin producing cells. The difference between LADA and classic Type 1 is the speed with which this happens. In young Type 1s a person can go from normal to completely whacked in a week. People with LADA may take up to a decade to lose all their insulin-secreting capacity.
People with LADA are often thin, so if you are thin and are told you have Type 2 diabetes, you should demand the antibody tests that are used to diagnose LADA. The antibodies tested for are: GAD antibodies, Islet cell antibodies, and more rarely, tyrosine phosphatase antibodies.
But not all people with LADA are slim. People with defective autoimmune genes are also prone to get thyroid disease and rheumatoid arthritis both of which can promote obesity, the first because incorrectly treated thyroid disease will make you fat and the latter because it limits mobility and hence the ability to exercise and because it is often treated with steroids that promote weight gain.
People with LADA benefit from being put onto full basal/bolus insulin regimens as soon as possible. There's some evidence that injecting insulin may turn off the immune attack on the beta cells and preserve them.
But because overweight people with LADA are universally diagnosed as having Type 2 they are almost always denied insulin treatment until they have spent years with extremely high blood sugars. This isn't because they are overweight, it's because that's the treatment given to ALL people diagnosed with Type 2 whose doctors allow them to maintain criminally high blood sugars for years out of a misguided belief that insulin will worsen, not better, their insulin resistance.
Genetic testing recently revealed that people with LADA have similar immunity-related genetic errors to people with juvenile onset Type 1 diabetes but that they also have defects in a gene, TCF7L2, that are frequently found in people with Type 2. Since just about every LADA I've ever met is thin, this suggests to me that there are probably a lot more people out there who are carrying Type 2 diagnoses who have LADA than we realize who are not getting diagnosed correctly because of their weight and because that TCF7L2 gene may cause enough insulin resistance to make them look like a classic Type 2.
I have to wonder though, WHY we are seeing so many people developing what was an extremely rare syndrome just a few decades ago. Is it better diagnosis, or is it the same thing that is driving the huge increase in the number of kids getting autoimmune diabetes? My guess is the latter, and though there is officially no explanation for this, my guess is that it has a lot to do with the environmental pollutants that saturate our bodies. Plastics, industrial chemical residues, pesticides, PCBs, etc.
Many genetic flaw--for instance those that lead to cancer--do not manifest in overt disease until the borderline-defective gene takes a hit from some environmental exposure. Chemicals, radiation, and viruses can all cause cancer in people with defective genes, and probably they cause autoimmune diabetes in people with defects in their autoimmune genes.
This is likely because even among identical twins who share genes, it is possible for one twin to develop autoimmune diabetes while the other remains normal. So my guess is that many of us have carried slight abnormalities in our autoimmune genes that did not get those extra hits until we started filling our world with plastics and the other toxic chemicals that are now found in our blood, tissues and even, as I blogged earlier, in mothers' milk.
The Warning Signs YOU May Have LADA
1. You are diagnosed with Type 2 diabetes while at a normal weight.
2. Whatever your weight, either you or a member of your family has some other autoimmune disease such as thyroid disease, rheumatoid arthritis, lupus, or multiple sclerosis.
3. You lower your carbohydrate intake shortly after diagnosis to no more than 15 grams a meal and still have a fasting blood sugar over 110 mg/dl and blood sugars that rise 40 mg/dl or more after each meal.
4. No matter what your weight, you do not see a dramatic drop in your blood sugar when you take metformin, Avandia, Actos, Januvia or Byetta in combination with a lowered carbohydrate intake.
5. Your blood sugar deteriorates significantly over the period of a year despite treatment with oral drugs and carbohydrate restriction.
What To Do To Get A LADA Diagnosis
If you think you have LADA ask your doctor for:
1. A fasting C-peptide test. If the value is low, it is suggestive of LADA.
2. GAD and Islets antibody tests. High levels of these antibodies are diagnostic of LADA especially in combination with lowered C-peptide.
The Next Step
Many doctors assume patients will do anything to avoid shots and delay giving people insulin. If you have LADA you want to go on a full-fledged Type 1 insulin regimen as fast as possible.
The sooner you start insulin the easier it will be to control your blood sugar with insulin for many years to come. And by injecting insulin you may be able to stop the attack on your beta cells completely. This is essential because technologies are emerging that might be able to stop the immune attack permanently and even regrow your beta cells. But for these treatments to work you need to have living beta cells. The longer you delay insulin, the fewer beta cells you will have left.
Insulin shots are painless and if you have been running high blood sugars for a while, you will feel much, much better once you start using insulin to get normal blood sugars.
Get Support From Others with LADA
There are lots of people with LADA active on all the online discussion boards that provide diabetes support. If you have LADA be sure to seek out others because their personal experiences will be extremely helpful to you once you start working on adjusting your insulin doses and diet.
You can find people with LADA at Tudiabetes.com, Diabetes Daily Forums, and Diabetesforums.com. LADA is usually discussed in the "Type 1.5" area.
May 7, 2008
Yet Another Drug Study Shows Lowering LDL Does Not Affect Clogging of Arteries
The proposition that lowering LDL with drugs will protect you against developing clogged arteries just took another body blow.
We already saw that lowering LDL with Zetia and Vytorin did not lead to any improvement in the thickening in artery walls, and may, in fact, have actually worsened it in the case of Vytorin.
Now a 5 year study of fenofibrate, another drug that lowers LDL dramatically, has found the same thing. People who took it saw their LDL decline, but their arterial walls continued to thicken.
You can read about the presentation that described this finding in a report on HERE It was published in Diabetes in Control.
It's time to face the fact that the only reason doctors believe that lowering LDL is protective against heart disease is that the statin manufacturers sold their drugs for years on that premise.
But subsequent research is showing that the only reason that the statins seem to slightly lower the incidence of heart attack in middle aged men with pre-existing heart disease is because they fight inflammation. Studies reveal that statins do not prevent heart disease in women nor in men not already diagnosed with heart disease.
So as study after study finds that lowering LDL has no effect on how clogged arteries get, it is starting to look very clear that lowering your LDL is not going to prevent arterial thickening.
This is an issue of major concern to people with abnormal blood sugar now that we have learned that statins increase insulin resistance. There is also accumulating evidence that statins may promote cancer in older people. You can find the research cites that back up those findings that by visiting my web page about Dangerous Drugs for People with Diabetes.
So if these drugs won't prevent artery clogging, what will? Well, if you have been reading this blog for a while, you probably know my answer:
1. Maintain normal blood sugar levels.
2. Achieve normal blood sugars using the strategies that minimize the amount of insulin in your system. Insulin is a growth hormone and too much of it may grow the lining of your arteries.
3. The best way to do this is to cut back on your carb intake until you are getting normal blood sugars after meals. Avoid drugs like glyburide, amaryl, Prandin, and Starlix that lower blood sugar stimulating insulin production and use instead metformin which lowers blood sugar by decreasing insulin resistance.
Another study published in this week's Diabetes in Control newsletter found that metformin had a much more positive effect on the cardiovascular system than did Prandin even when blood sugars achieved were the same.
We already saw that lowering LDL with Zetia and Vytorin did not lead to any improvement in the thickening in artery walls, and may, in fact, have actually worsened it in the case of Vytorin.
Now a 5 year study of fenofibrate, another drug that lowers LDL dramatically, has found the same thing. People who took it saw their LDL decline, but their arterial walls continued to thicken.
You can read about the presentation that described this finding in a report on HERE It was published in Diabetes in Control.
It's time to face the fact that the only reason doctors believe that lowering LDL is protective against heart disease is that the statin manufacturers sold their drugs for years on that premise.
But subsequent research is showing that the only reason that the statins seem to slightly lower the incidence of heart attack in middle aged men with pre-existing heart disease is because they fight inflammation. Studies reveal that statins do not prevent heart disease in women nor in men not already diagnosed with heart disease.
So as study after study finds that lowering LDL has no effect on how clogged arteries get, it is starting to look very clear that lowering your LDL is not going to prevent arterial thickening.
This is an issue of major concern to people with abnormal blood sugar now that we have learned that statins increase insulin resistance. There is also accumulating evidence that statins may promote cancer in older people. You can find the research cites that back up those findings that by visiting my web page about Dangerous Drugs for People with Diabetes.
So if these drugs won't prevent artery clogging, what will? Well, if you have been reading this blog for a while, you probably know my answer:
1. Maintain normal blood sugar levels.
2. Achieve normal blood sugars using the strategies that minimize the amount of insulin in your system. Insulin is a growth hormone and too much of it may grow the lining of your arteries.
3. The best way to do this is to cut back on your carb intake until you are getting normal blood sugars after meals. Avoid drugs like glyburide, amaryl, Prandin, and Starlix that lower blood sugar stimulating insulin production and use instead metformin which lowers blood sugar by decreasing insulin resistance.
Another study published in this week's Diabetes in Control newsletter found that metformin had a much more positive effect on the cardiovascular system than did Prandin even when blood sugars achieved were the same.
May 5, 2008
A Lesson from People with Lyme Disease
There was an interesting story in the news last week about how people with Lyme Disease organized and brought so much legal pressure on the Infections Disease Society--the organization that provides treatment guidelines for infectious disease--that the IDS was forced to agree to reconsider the recommendations it puts out for the diagnosis and treatment of Lyme Disease.
You can read about it here: Doctors to Reassess Antibiotics for 'Chronic Lyme Disease'.
The background on this story is that the doctors who make up the IDS have continued to deny that there is such a thing as Chronic Lyme Disease or that it should be treated with aggressive antibiotic campaigns despite the experience of many sufferers from Lyme Disease who have developed long term disease syndromes that responded dramatically to the antibiotic treatment.
Because the official treatment guidelines claim that chronic Lyme Disease does not exist and discourage antibiotic treatment for it, people with Lyme Disease cannot get insurance coverage for their treatments, to say nothing of being unable to get their doctors to prescribe the drugs that other people with Lyme Disease have found so helpful.
Does this remind you of anything we people with diabetes go through? Like, perhaps, the way that the American Diabetes Association--a wholly owned subsidiary of Big Pharma and the large junk food companies--has taken to itself the role of defining not only the diagnostic criteria for diabetes but also the blood sugar targets doctors are told to recommend as well as what the drugs and dietary approaches those doctors should prescribe?
The ADA's criteria and treatment recommendations hurt every single person with diabetes, but because they are the official treatment standards, no doctor can be sued for following them.
Let's review exactly what is wrong with the ADA's many positions on Diabetes:
1. The ADA's Diagnostic Criteria were set intentionally high so that people with Type 2 diabetes are not diagnosed until very late in the disease process, right before they are likely to develop retinopathy. That is why more than 1/2 of all people with Type 2 diabetes have a serious diabetic complication--usually neuropathy (nerve pain)--on the day of diagnosis, despite the fact that we know it takes about ten years of exposure to high blood sugars for neuropathy to develop.
The ADA has fought very hard against any revision of its diagnostic criteria, though study after study shows that truly normal blood sugars are much lower than the range that the ADA defines as "prediabetic." The fasting blood sugar test that the ADA tells doctors to use for screening for diabetes also is known to miss full fledged diabetes in women and people of color who usually develop extremely high blood sugars after meals long before their fasting blood sugar deteriorates. This is documented in great detail here: Misdiagnosis by Design the Story Behind the ADA Diagnostic Criteria.
2. The ADA's Blood Sugar Targets for People with Diabetes which are the one most family doctors still follow are set so high that a person with Type 2 who follows them almost guarantees that they will develop complications. Despite a load of peer-reviewed evidence that blood sugars over 140 mg/dl (7.7 mmol/L) are associated with the development of retinopathy and neuropathy, the ADA still tells doctors that a blood sugar of 180 mg/dl (10 mmol/L) two hours after a meal is "tight control" and that an A1c of 7% which represents an average blood sugar well over 140 at all times is "Excellent."
It isn't, but the ADA has refused to lower its blood sugar targets, possibly because the drugs that its financial sponsors sell are not capable of lowering the blood sugar of the typical Type 2 below those very high levels. To do that, a person with Type 2 Diabetes must also cut carbohydrates. If they do that, they can usually achieve normal blood sugars. Which brings us to the third and most damning failure of the ADA:
3. The ADA Actively Promotes the Consumption of Very High Carbohydrate Diets despite decades of evidence that these diets harm people with diabetes. You need only look at the recipes in an ADA magazine for people with Diabetes to see that the ADA is still promoting the idea that people with diabetes need to eat high carbohydrate fruits like bananas and apples along with high carbohydrate pastas and grains. The ADA partnered with Campbell Soups--a company whose high carbohydrate foods are notorious for their unnecessarily high levels of sodium and high fructose corn syrup. The ADA tells people with diabetes that they should eat sugar--possibly as a sop to their other huge contributor, Cadbury Scweppes, the candy maker.
And though it's main mission is "education" the ADA does not mention anywhere in its educational materials that it is carbohydrates that raise blood sugar and that by lowering carbohydrate intake, people with diabetes can restore their blood sugar control. Instead, the ADA tells people with diabetes to eat high carb diets and then take every single one of the drugs its Big Pharma sponsors sell, including Avandia, which the ADA went out of its way to urge patients to continue to take after the data came out showing it increased the likelihood of heart attack.
4. The millions of dollars that pour into ADA coffers thanks to its aggressive fundraising do not fund diabetes research. The ADA's primary mission is solely "education." The one thing that the ADA does re research is to publish two medical journals, Diabetes and Diabetes Care, which publish research--much of it funded by its drug company sponsors. However, if you price a subscription to either of these magazines, you will see that these journals are a profit center for the ADA. They are expensive! And the ADA's leadership usually ignores the results of the research published in those journals when setting treatment guidelines.
Much of the money you hard working people with diabetes raise with bake sales and other community activities funds the enormous salaries of the ADA's top executives, who are people who come from backgrounds as health industry lobbyists or from heading other disease charities completely unrelated to diabetes. The ADA's leadership do not have diabetes themselves, and have been known to refer to us folks who do as "poor victims."
Well, we are poor victims as long as we let these health industry profiteers earn huge salaries for fighting AGAINST us people with diabetes getting timely diagnoses, while refusing to teach physicians the safe blood sugar target recommendations that could keep us from developing complications, and actively campaigning against giving people with diabetes accurate dietary advice.
It is time we looked into how the people with Lyme Disease got some action from the organization that has a stranglehold on the treatment for their health condition and got into doing some organizing of our own.
The damage being done by the ADA to people with diabetes is far, far worse than anything the Lyme Disease people have to contend with!
You can read about it here: Doctors to Reassess Antibiotics for 'Chronic Lyme Disease'.
The background on this story is that the doctors who make up the IDS have continued to deny that there is such a thing as Chronic Lyme Disease or that it should be treated with aggressive antibiotic campaigns despite the experience of many sufferers from Lyme Disease who have developed long term disease syndromes that responded dramatically to the antibiotic treatment.
Because the official treatment guidelines claim that chronic Lyme Disease does not exist and discourage antibiotic treatment for it, people with Lyme Disease cannot get insurance coverage for their treatments, to say nothing of being unable to get their doctors to prescribe the drugs that other people with Lyme Disease have found so helpful.
Does this remind you of anything we people with diabetes go through? Like, perhaps, the way that the American Diabetes Association--a wholly owned subsidiary of Big Pharma and the large junk food companies--has taken to itself the role of defining not only the diagnostic criteria for diabetes but also the blood sugar targets doctors are told to recommend as well as what the drugs and dietary approaches those doctors should prescribe?
The ADA's criteria and treatment recommendations hurt every single person with diabetes, but because they are the official treatment standards, no doctor can be sued for following them.
Let's review exactly what is wrong with the ADA's many positions on Diabetes:
1. The ADA's Diagnostic Criteria were set intentionally high so that people with Type 2 diabetes are not diagnosed until very late in the disease process, right before they are likely to develop retinopathy. That is why more than 1/2 of all people with Type 2 diabetes have a serious diabetic complication--usually neuropathy (nerve pain)--on the day of diagnosis, despite the fact that we know it takes about ten years of exposure to high blood sugars for neuropathy to develop.
The ADA has fought very hard against any revision of its diagnostic criteria, though study after study shows that truly normal blood sugars are much lower than the range that the ADA defines as "prediabetic." The fasting blood sugar test that the ADA tells doctors to use for screening for diabetes also is known to miss full fledged diabetes in women and people of color who usually develop extremely high blood sugars after meals long before their fasting blood sugar deteriorates. This is documented in great detail here: Misdiagnosis by Design the Story Behind the ADA Diagnostic Criteria.
2. The ADA's Blood Sugar Targets for People with Diabetes which are the one most family doctors still follow are set so high that a person with Type 2 who follows them almost guarantees that they will develop complications. Despite a load of peer-reviewed evidence that blood sugars over 140 mg/dl (7.7 mmol/L) are associated with the development of retinopathy and neuropathy, the ADA still tells doctors that a blood sugar of 180 mg/dl (10 mmol/L) two hours after a meal is "tight control" and that an A1c of 7% which represents an average blood sugar well over 140 at all times is "Excellent."
It isn't, but the ADA has refused to lower its blood sugar targets, possibly because the drugs that its financial sponsors sell are not capable of lowering the blood sugar of the typical Type 2 below those very high levels. To do that, a person with Type 2 Diabetes must also cut carbohydrates. If they do that, they can usually achieve normal blood sugars. Which brings us to the third and most damning failure of the ADA:
3. The ADA Actively Promotes the Consumption of Very High Carbohydrate Diets despite decades of evidence that these diets harm people with diabetes. You need only look at the recipes in an ADA magazine for people with Diabetes to see that the ADA is still promoting the idea that people with diabetes need to eat high carbohydrate fruits like bananas and apples along with high carbohydrate pastas and grains. The ADA partnered with Campbell Soups--a company whose high carbohydrate foods are notorious for their unnecessarily high levels of sodium and high fructose corn syrup. The ADA tells people with diabetes that they should eat sugar--possibly as a sop to their other huge contributor, Cadbury Scweppes, the candy maker.
And though it's main mission is "education" the ADA does not mention anywhere in its educational materials that it is carbohydrates that raise blood sugar and that by lowering carbohydrate intake, people with diabetes can restore their blood sugar control. Instead, the ADA tells people with diabetes to eat high carb diets and then take every single one of the drugs its Big Pharma sponsors sell, including Avandia, which the ADA went out of its way to urge patients to continue to take after the data came out showing it increased the likelihood of heart attack.
4. The millions of dollars that pour into ADA coffers thanks to its aggressive fundraising do not fund diabetes research. The ADA's primary mission is solely "education." The one thing that the ADA does re research is to publish two medical journals, Diabetes and Diabetes Care, which publish research--much of it funded by its drug company sponsors. However, if you price a subscription to either of these magazines, you will see that these journals are a profit center for the ADA. They are expensive! And the ADA's leadership usually ignores the results of the research published in those journals when setting treatment guidelines.
Much of the money you hard working people with diabetes raise with bake sales and other community activities funds the enormous salaries of the ADA's top executives, who are people who come from backgrounds as health industry lobbyists or from heading other disease charities completely unrelated to diabetes. The ADA's leadership do not have diabetes themselves, and have been known to refer to us folks who do as "poor victims."
Well, we are poor victims as long as we let these health industry profiteers earn huge salaries for fighting AGAINST us people with diabetes getting timely diagnoses, while refusing to teach physicians the safe blood sugar target recommendations that could keep us from developing complications, and actively campaigning against giving people with diabetes accurate dietary advice.
It is time we looked into how the people with Lyme Disease got some action from the organization that has a stranglehold on the treatment for their health condition and got into doing some organizing of our own.
The damage being done by the ADA to people with diabetes is far, far worse than anything the Lyme Disease people have to contend with!
May 2, 2008
Type What?
A study published in the most recent edition of the journal Diabetes makes it even more clear that the usual division of diabetes into "Type 1" and "Type 2" is an oversimplification.
The usual mythology has it that Type 1 is an autoimmune disease and people who get it are innocent bystanders while Type 2 is caused by overindulgence and people who get it should be ashamed of themselves.
I've written at length about why the second part of this formula is bull crud. You can read the many reasons HERE.
But there is no question that framing the diagnosis of diabetes this way has made many people with autoimmune forms of diabetes hostile to those with Type 2, because they feel that an ignorant public unfairly blames them for causing their condition and believe, with the rest of that ignorant public that those gluttonous lazy type 2s do deserve such blame.
But the latest research on LADA, the adult onset form of autoimmune diabetes, has come up with a finding that makes it clear how wrong this kind of thinking is. The researchers in this study, which you can find at the Diabetes web site:
Autoimmune Diabetes in Adults, Type 1 Diabetes, and Type 2 Diabetes
examined the genes of 361 peole with LADA, 718 people with type 1 diabetes, and 1,676 type 2 diabetic patients, as well as 1,704 healthy control subjects from Sweden and Finland.
They found that "LADA subjects showed, compared with type 2 diabetic patients, increased frequency of risk for the HLA-DQB1 *0201/*0302 genotype with similar frequency as with type 1 diabetes (36%)." There were some other similarites with Type 1, genetically, but then they also found that "the frequency of the type 2 diabetes–associated CT/TT genotypes of rs7903146 in the TCF7L2 were increased in LADA subjects (52.8%; P = 0.03), to the same extent as in type 2 diabetic subjects (54.1%, P = 3 x 10–7), compared with control subjects (44.8%) and type 1 diabetic subjects (43.3%).
In short, these LADAs had both type 1 genes--autoimmune genes--AND type 2 genes.
This finding is particularly interesting in light of an earlier finding that slightly under 10% of people diagnosed with Type 2 also have autoimmune markers like elevated GAD antibodies.
TCF7L2 is one of the more common defective genes found in Type 2 diabetes but by no means the only one. HNF4-a is another gene that has been found in association with both a form of MODY and with a Type 2 diabetes in both Ashkenazi Jewish and Danish populations.
In addition, as they get older, many Type 1s find their insulin needs rise, as they become insulin resistant and probably start expressing the Type 2 genes they inherited. Doctors do not give Type 1s who are using larger doses of insulin metformin, but my guess is that they probably should. I'm not very insulin resistant at all--two or three units is all it takes to drop my blood sugar dramatically, but even so, I can drop my insulin needs by about 1/3 by taking metformin. But here again, the division of diabetes into these two artificial types is hurting people because doctors do not think that a "Type 1" might also have the genes that in middle age would have expressed as "Type 2" had they not also suffered an autoimmune attack.
So it is time we dispensed with the artificial division of diabetes into Type 1 and Type 2. Let's admit that "Diabetes" is really nothing more than a symptom--high blood sugar--and that the causes of that symptom are many and not mutually exclusive.
When the damage is to the immune system, we get autoimmune attack on the beta cells. When the damage is to the genes that regulate insulin resistance in the muscles--and possibly mitochondrial function, we get another form of diabetes, when the damage is to the genes that regulate the beta cell's response to rising glucose levels in the blood we get secretory defects, when the body suffers genetic damage thanks to exposure to chemicals in the environment we get yet more blood sugar abnormalities, and like the unlucky LADAs, some of us get more than one of these problems going on at once.
And those of us who do have abnormal glucose metabolism should resist the temptation to divide people with diabetes into types and to use this typology to define some of us as blameless and others as blamable diabetics.
That kind of division helps no one. All of us should be putting our efforts into ensuring that EVERY person with diabetes gets the kind of excellent, health-preserving treatment that so few of us currently get from the doctors, nutritionists, and drug companies who see us as little more than a huge profit center.
The usual mythology has it that Type 1 is an autoimmune disease and people who get it are innocent bystanders while Type 2 is caused by overindulgence and people who get it should be ashamed of themselves.
I've written at length about why the second part of this formula is bull crud. You can read the many reasons HERE.
But there is no question that framing the diagnosis of diabetes this way has made many people with autoimmune forms of diabetes hostile to those with Type 2, because they feel that an ignorant public unfairly blames them for causing their condition and believe, with the rest of that ignorant public that those gluttonous lazy type 2s do deserve such blame.
But the latest research on LADA, the adult onset form of autoimmune diabetes, has come up with a finding that makes it clear how wrong this kind of thinking is. The researchers in this study, which you can find at the Diabetes web site:
Autoimmune Diabetes in Adults, Type 1 Diabetes, and Type 2 Diabetes
examined the genes of 361 peole with LADA, 718 people with type 1 diabetes, and 1,676 type 2 diabetic patients, as well as 1,704 healthy control subjects from Sweden and Finland.
They found that "LADA subjects showed, compared with type 2 diabetic patients, increased frequency of risk for the HLA-DQB1 *0201/*0302 genotype with similar frequency as with type 1 diabetes (36%)." There were some other similarites with Type 1, genetically, but then they also found that "the frequency of the type 2 diabetes–associated CT/TT genotypes of rs7903146 in the TCF7L2 were increased in LADA subjects (52.8%; P = 0.03), to the same extent as in type 2 diabetic subjects (54.1%, P = 3 x 10–7), compared with control subjects (44.8%) and type 1 diabetic subjects (43.3%).
In short, these LADAs had both type 1 genes--autoimmune genes--AND type 2 genes.
This finding is particularly interesting in light of an earlier finding that slightly under 10% of people diagnosed with Type 2 also have autoimmune markers like elevated GAD antibodies.
TCF7L2 is one of the more common defective genes found in Type 2 diabetes but by no means the only one. HNF4-a is another gene that has been found in association with both a form of MODY and with a Type 2 diabetes in both Ashkenazi Jewish and Danish populations.
In addition, as they get older, many Type 1s find their insulin needs rise, as they become insulin resistant and probably start expressing the Type 2 genes they inherited. Doctors do not give Type 1s who are using larger doses of insulin metformin, but my guess is that they probably should. I'm not very insulin resistant at all--two or three units is all it takes to drop my blood sugar dramatically, but even so, I can drop my insulin needs by about 1/3 by taking metformin. But here again, the division of diabetes into these two artificial types is hurting people because doctors do not think that a "Type 1" might also have the genes that in middle age would have expressed as "Type 2" had they not also suffered an autoimmune attack.
So it is time we dispensed with the artificial division of diabetes into Type 1 and Type 2. Let's admit that "Diabetes" is really nothing more than a symptom--high blood sugar--and that the causes of that symptom are many and not mutually exclusive.
When the damage is to the immune system, we get autoimmune attack on the beta cells. When the damage is to the genes that regulate insulin resistance in the muscles--and possibly mitochondrial function, we get another form of diabetes, when the damage is to the genes that regulate the beta cell's response to rising glucose levels in the blood we get secretory defects, when the body suffers genetic damage thanks to exposure to chemicals in the environment we get yet more blood sugar abnormalities, and like the unlucky LADAs, some of us get more than one of these problems going on at once.
And those of us who do have abnormal glucose metabolism should resist the temptation to divide people with diabetes into types and to use this typology to define some of us as blameless and others as blamable diabetics.
That kind of division helps no one. All of us should be putting our efforts into ensuring that EVERY person with diabetes gets the kind of excellent, health-preserving treatment that so few of us currently get from the doctors, nutritionists, and drug companies who see us as little more than a huge profit center.
May 1, 2008
More Evidence Scary Chemicals are In our Bodies
Science Daily today reported on a recent study that found both Teflon and Scotchgard in the milk of nursing mothers. The study turned out to have been done by a wonderful woman scientist I have the privilege of knowing personally, but that wasn't why I clicked through on the headline. It looked like yet another study, like those on plastics and pesticides, which point to hidden causes of the so-called "diabetes epidemic."
Suspected Carcinogenic Chemicals Used To Make Teflon, Scotchgard, Found In Human Milk
If this doesn't scare you, you don't understand much about physiology.
It scares me plenty, not just because these are carcinogens, but because this is yet more proof of the extent to which bizarre, not-found-in-nature, chemicals that are added to food packaging get into our bodies where no one really has much idea of what they do.
The other scary thing about this particular bunch of chemicals is that they don't break down once they are in the body. So whatever the "safe" level might be over time, you are getting more and more of them over time and they are probably being deposited in random places throughout your organs.
These ubiquitous chemicals like bisphenol-A and pesticides may also raise the incidence of diabetes and increase insulin resistance. Things that cause cancer often do.
Many people attribute the diabetes "epidemic" to the huge surge in obesity. There is no doubt that the incidence of obesity has greatly increased, but what people don't understand is that obesity is often the result of genetic damage caused by environmental toxins. In fact, lab scientists usually interpret obesity in animals as a sign that they have experienced genetic damage. A healthy animal won't overeat, but those with genetic damage do.
Note that the article mentions that "Food sources of PFCs [Perfluorinated compounds] include grease-resistant packaging such as microwave popcorn bags and pizza boxes, as well as fish and other animals that contain these chemicals. Exposure can also come from personal care products including dental floss and shampoo." And of course, your nonstick cookware is coated with Teflon and it leaches into food, especially when you heat it a bit too much.
Suspected Carcinogenic Chemicals Used To Make Teflon, Scotchgard, Found In Human Milk
If this doesn't scare you, you don't understand much about physiology.
It scares me plenty, not just because these are carcinogens, but because this is yet more proof of the extent to which bizarre, not-found-in-nature, chemicals that are added to food packaging get into our bodies where no one really has much idea of what they do.
The other scary thing about this particular bunch of chemicals is that they don't break down once they are in the body. So whatever the "safe" level might be over time, you are getting more and more of them over time and they are probably being deposited in random places throughout your organs.
These ubiquitous chemicals like bisphenol-A and pesticides may also raise the incidence of diabetes and increase insulin resistance. Things that cause cancer often do.
Many people attribute the diabetes "epidemic" to the huge surge in obesity. There is no doubt that the incidence of obesity has greatly increased, but what people don't understand is that obesity is often the result of genetic damage caused by environmental toxins. In fact, lab scientists usually interpret obesity in animals as a sign that they have experienced genetic damage. A healthy animal won't overeat, but those with genetic damage do.
Note that the article mentions that "Food sources of PFCs [Perfluorinated compounds] include grease-resistant packaging such as microwave popcorn bags and pizza boxes, as well as fish and other animals that contain these chemicals. Exposure can also come from personal care products including dental floss and shampoo." And of course, your nonstick cookware is coated with Teflon and it leaches into food, especially when you heat it a bit too much.
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