After I posted that my fasting bgs had gone back up on the R-only regimen, they came back down. Ninety-two on Tuesday, 88 mg/dl (4.9 mmol/l) today.
This is one of the most annoying things about using insulin, for me, at least. No matter what I get figured out, a week later it is different. But at least this particular "different" in the right direction. If I can keep things at this level, the R-only regimen will work for me.
Strangely, the near normal fasting bg this morning followed a massive overindulgence at dinner last night wherein I managed to figure the insulin right for the most obscene carb overdose possible--to wit, Pad Thai. I get it made with mostly sprouts and very few noodles, as otherwise it is well over 100 grams per serving, but just the sauce can clock in at 40 grams per serving. I did my 3 units of R, waited about 90 minutes before eating and I tested a couple times and didn't see anything over 110 at 90 minutes or 3 hours though the two readings were so close it's possible I peaked in the middle. (I only have so many test strips and I'm going through them far too fast with all this insulin testing.) Still, that beats the 180 I've seen when testing Pad Thai before.
The downside was that I was hungry after eating it and for me, hunger is always a symptom of blood sugars out of whack. Well, I'm not planning to do this again any time soon. But it validated I'm starting to get a handle on how to use the R.
Note to anyone reading who knows anything about insulin: the R-only regimen works for me because the kind of diabetes I have is characterized by rotten post-prandials and only impaired fasting bgs. This regimen would NOT work for someone with Type 1 diabetes. It might work for someone with mild type 2 if their fasting did not rise at night as mine doesn't. I have to eat an all protein breakfast to make it work as I don't have any insulin in my system when I eat breakfast.
June 28, 2006
June 27, 2006
Deluding yourself about the A1c
I went to the lab this morning in preparation for my visit to the endo in two weeks. As usual, she wanted an A1c and cholesterol test, though this time she also did a microalbumin and the cheap thyroid check (TSH).
That got me thinking about what a worthless test the A1c is and how it sucks that the A1c is the only test a lot of docs pay attention to.
The A1c is a very rough, indirect measure of average blood sugar over the recent months. What's actually being measured is how much glucose is stuck to your hemoglobin molecules. If you are anemic and have few of these hemoglobin molecules, your A1c may be deceptively low while high blood sugars are devastating your body. Many general practitioners don't know this. If your hemoglobin cells for some reason live longer or shorter lives than most people, you'll also end up with an A1c value that is misleading.
But even if the A1c is an accurate reflection of your blood sugar control, it isn't average blood sugars that cause complications--unless your control is so bad that your very lowest blood sugar level is well into the damage danger zone (over 140 mg/dl or 7.7 mmol/l). If your average is attained by going high for a few hours and then going low, you may easily end up with an A1c in the range that the lab flags as "excellent control", while elevated blood sugars during each of your spikes isflooding into your nerves, capillaries and retinas, setting you up for the classic, and very ugly, diabetic complications.
Relying on the A1c might have made sense 20 years ago when people with diabetes didn't own blood sugar meters, but now, when home testing is accurate and easy, it's another of the old fashioned medical practices that keeps people with diabetes getting old fashioned complications.
That got me thinking about what a worthless test the A1c is and how it sucks that the A1c is the only test a lot of docs pay attention to.
The A1c is a very rough, indirect measure of average blood sugar over the recent months. What's actually being measured is how much glucose is stuck to your hemoglobin molecules. If you are anemic and have few of these hemoglobin molecules, your A1c may be deceptively low while high blood sugars are devastating your body. Many general practitioners don't know this. If your hemoglobin cells for some reason live longer or shorter lives than most people, you'll also end up with an A1c value that is misleading.
But even if the A1c is an accurate reflection of your blood sugar control, it isn't average blood sugars that cause complications--unless your control is so bad that your very lowest blood sugar level is well into the damage danger zone (over 140 mg/dl or 7.7 mmol/l). If your average is attained by going high for a few hours and then going low, you may easily end up with an A1c in the range that the lab flags as "excellent control", while elevated blood sugars during each of your spikes isflooding into your nerves, capillaries and retinas, setting you up for the classic, and very ugly, diabetic complications.
Relying on the A1c might have made sense 20 years ago when people with diabetes didn't own blood sugar meters, but now, when home testing is accurate and easy, it's another of the old fashioned medical practices that keeps people with diabetes getting old fashioned complications.
June 26, 2006
It's Always Something
Back in January after a lot of experimentation I learned that I could achieve near normal blood sugars using Ultralente insulin. There was only one catch. They've stopped making it. I found a couple pharmacies that still had a supply in their fridges and stocked up, figuring that since I only used a couple units a day, I could make the stash last for years.
Boy, was I wrong!
It turned out each vial lasted me about 6 weeks before it stopped working--usually because the stuff started to clump, but not always. I tried everything to keep the stuff alive. I kept the insulin in the butter compartment of the fridge with a thermometer making sure the temperature was right. I shook the vials very gently. I never reused a needle.
It made no difference.
So when it became clear that UL was not going to be a solution for me for much longer, I started checking out alternatives.
Lantus, alas, while it brought my fasting level down, caused my post-meal numbers to shoot up even higher than normal. Since I'd had problems with Lantus before (which is why I tried UL) I figure this is because of some kind of antibody problem. Since I am not ready for a 5 shot a day regimen, I bagged that.
Levemir caused my blood pressure to rise into the stroke zone. When I called the company, they claimed they'd never heard of such a thing but someone on an online diabetes board told me they had heard of someone else who experienced the same thing. I reported this to the FDA and moved on.
The endo suggested that since my main problem is with my post-meal blood sugars, I try using a fast acting insulin. Unfortunately, here again, when I tried an analog insulin, Humalog, I ran into a similar problem as with lantus. My numbers one hour after injecting were much higher than they were if I ate the same food without insulin and then I dropped low at three hours. After a couple days of testing Humalog my numbers in general started rising. Hmmm. Looks like antibodies for sure.
Since it looks like analogs aren't for me, I went back to Regular R insulin which is what I'd started with back in December. I found I could get it to work pretty well for meals if I raised the dose higher than what I'd been using before and timed it so that the insulin was injected 2 hours before the food would peak and then ate a little bit more carb at 3 hours after injection to mop up the last bit of activity.
I was just cheering up after 4 days of the new regimen--2.75 units of R at 10:30 and 4:30 with no basal, because I had not gone over 120 at all eating almost like a normal person, when I noticed that my fasting bg had gone up from the 89-91 mg/dl where it had been for months on UL to 103 the past two days.
I'd been hoping the first reading was a fluke. But it looks like the UL washed out of my body and fasting control will start to tank.
So on to the next option. I've avoided sulf drugs all these years because Dr. Bernstein warns they burn out beta cells and because research has shown that some of them increase the incidence of heart attack. However, it turns out that for some people with MODY very low doses (1/4 of the usual starting dose) work like magic. This is the case when the genetic defect is one that keeps the cells from secreting, rather than a defect in the insulin which I may or may not have.
Amaryl is one sulf that turns out not to affect the receptor on the heart that the older drugs did. So I figure it's time to see if a tiny dose of Amaryl will work better than the insulin. The big plus of that approach is that the insulin goes into the portal vein of the liver rather than into fat which may do more to keep blood sugars from rising. Plus, there isn't the problem of antibodies. My insulin dose kept rising all these past months which suggests antibodies are a factor.
The challenge will be to get a small enough dose. I'll start out with the smallest amount it is possible to divide the pill into and take it from there.
If that doesn't work, on to Byetta. If that doesn't work, well, back to the bolus R and accept that I can't normalize my fasting blood sugars.
Damn Lilly for discontinuing UltraLente!
Boy, was I wrong!
It turned out each vial lasted me about 6 weeks before it stopped working--usually because the stuff started to clump, but not always. I tried everything to keep the stuff alive. I kept the insulin in the butter compartment of the fridge with a thermometer making sure the temperature was right. I shook the vials very gently. I never reused a needle.
It made no difference.
So when it became clear that UL was not going to be a solution for me for much longer, I started checking out alternatives.
Lantus, alas, while it brought my fasting level down, caused my post-meal numbers to shoot up even higher than normal. Since I'd had problems with Lantus before (which is why I tried UL) I figure this is because of some kind of antibody problem. Since I am not ready for a 5 shot a day regimen, I bagged that.
Levemir caused my blood pressure to rise into the stroke zone. When I called the company, they claimed they'd never heard of such a thing but someone on an online diabetes board told me they had heard of someone else who experienced the same thing. I reported this to the FDA and moved on.
The endo suggested that since my main problem is with my post-meal blood sugars, I try using a fast acting insulin. Unfortunately, here again, when I tried an analog insulin, Humalog, I ran into a similar problem as with lantus. My numbers one hour after injecting were much higher than they were if I ate the same food without insulin and then I dropped low at three hours. After a couple days of testing Humalog my numbers in general started rising. Hmmm. Looks like antibodies for sure.
Since it looks like analogs aren't for me, I went back to Regular R insulin which is what I'd started with back in December. I found I could get it to work pretty well for meals if I raised the dose higher than what I'd been using before and timed it so that the insulin was injected 2 hours before the food would peak and then ate a little bit more carb at 3 hours after injection to mop up the last bit of activity.
I was just cheering up after 4 days of the new regimen--2.75 units of R at 10:30 and 4:30 with no basal, because I had not gone over 120 at all eating almost like a normal person, when I noticed that my fasting bg had gone up from the 89-91 mg/dl where it had been for months on UL to 103 the past two days.
I'd been hoping the first reading was a fluke. But it looks like the UL washed out of my body and fasting control will start to tank.
So on to the next option. I've avoided sulf drugs all these years because Dr. Bernstein warns they burn out beta cells and because research has shown that some of them increase the incidence of heart attack. However, it turns out that for some people with MODY very low doses (1/4 of the usual starting dose) work like magic. This is the case when the genetic defect is one that keeps the cells from secreting, rather than a defect in the insulin which I may or may not have.
Amaryl is one sulf that turns out not to affect the receptor on the heart that the older drugs did. So I figure it's time to see if a tiny dose of Amaryl will work better than the insulin. The big plus of that approach is that the insulin goes into the portal vein of the liver rather than into fat which may do more to keep blood sugars from rising. Plus, there isn't the problem of antibodies. My insulin dose kept rising all these past months which suggests antibodies are a factor.
The challenge will be to get a small enough dose. I'll start out with the smallest amount it is possible to divide the pill into and take it from there.
If that doesn't work, on to Byetta. If that doesn't work, well, back to the bolus R and accept that I can't normalize my fasting blood sugars.
Damn Lilly for discontinuing UltraLente!
June 25, 2006
Big Pharma's Guinea Pigs & Nazi Doctor-Type Ethics
Read any drug study involving a new diabetes drug and you'll notice that the subjects invariably start out with A1cs between 8 and 10%.
For anyone reading this who isn't diabetic, the A1c is a blood test that is used to assess long-term blood sugar control. Normal values are under 5%. The American Association of Clinical Endocrinologists' guidelines recommends that A1cs be kept under 6.5%, the leve at which dangerous complications become more likely.)
Drug companies trying to prove the efficacy of new drugs love the patient with a 10% A1c because those are the ones likely to show the most response to a drug. It's much better to be able to say, "Our drug dropped the average patient's A1c by a full 1%" than to say, "Our drug dropped the average a1c by .1%," which is what happens when you give a diabetes oral drug to a patient whose blood sugar is already under the level associated with diabetic retinopathy.
Even worse, when you look at the results of these drug tests, you also will see, just as invariably, that the drug only dropped the person with that 8-10% a1c by an average of 1%. So while the drop looks good, percentage wise, at the end of the year of study, the subjects were still running blood sugars well over the level where they are almost guaranteed to experience nerve damage, amputation, blindness and/or heart attack death.
And this is where the ethical problem arises that has me fuming.
If there were no way of lowering the typical diabetic's blood sugar below that damaging level, one could say, well, that is how it is. But this is far from the case. We have a drug that can lower the A1c to the safe levels in almost any diabetic--one that has been thoroughly tested and used in one form or another for almost 90 years: Insulin. But in these drug approval studies, NONE of the people with type 2 diabetes who are running those dangerous blood sugar levels are taking insulin.
So it seems to me that the patients in these drug studies who start out with that 8- 10%a1c should not be screwing around with experimental drugs. They should be put on carefully tailored insulin regimens until they have brought their A1cs down to the safe level below 6.5%. Then, once they are no longer walking time bombs, doctors can sign them up for new and experimental drugs that might lower their A1cs a tiny bit more.
You may hear doctors say that they can't get their Type 2 patients on insulin down to those levels, but if you probe further, you'll always find that the reason is that these same doctors are instructing their patients to eat a "healthy low fat diet" where each meal contains enough carbohydrates to overwhelm the generic insulin doses they've prescribed. Or you may find that they are only prescribing a basal insulin, like Lantus, which has no effect on the carbohydrates eaten at meals.
When doctors (or diabetes educators) take the time to learn how each individual's body responds to a set dose of insulin and design meal plans that work with sliding insulin doses, insulin, will bring blood sugar into the safe range of 6.5% or less. When doctors and nutritionists combine insulin used with moderate carb restriction (less than 25 grams per meal, for example) insulin can often bring blood sugar into the NORMAL range.
So if doctors were being ethical, i.e. working in the best interests of the patients, no study of any new and possibly ineffective drug should ever start with a population of diabetics whose blood sugar is at a level that even the ultra-conservative American Diabetes Association agrees causes severe complications. And those with responsibility for managing health care should make it clear that drug company operatives who draft patients into drug studies where their blood sugar from start to finish is allowed to remain in the danger zone are operating in an ethical zone only one step removed from Nazi doctors.
As Hippocrates said, "First Do No Harm!"
For anyone reading this who isn't diabetic, the A1c is a blood test that is used to assess long-term blood sugar control. Normal values are under 5%. The American Association of Clinical Endocrinologists' guidelines recommends that A1cs be kept under 6.5%, the leve at which dangerous complications become more likely.)
Drug companies trying to prove the efficacy of new drugs love the patient with a 10% A1c because those are the ones likely to show the most response to a drug. It's much better to be able to say, "Our drug dropped the average patient's A1c by a full 1%" than to say, "Our drug dropped the average a1c by .1%," which is what happens when you give a diabetes oral drug to a patient whose blood sugar is already under the level associated with diabetic retinopathy.
Even worse, when you look at the results of these drug tests, you also will see, just as invariably, that the drug only dropped the person with that 8-10% a1c by an average of 1%. So while the drop looks good, percentage wise, at the end of the year of study, the subjects were still running blood sugars well over the level where they are almost guaranteed to experience nerve damage, amputation, blindness and/or heart attack death.
And this is where the ethical problem arises that has me fuming.
If there were no way of lowering the typical diabetic's blood sugar below that damaging level, one could say, well, that is how it is. But this is far from the case. We have a drug that can lower the A1c to the safe levels in almost any diabetic--one that has been thoroughly tested and used in one form or another for almost 90 years: Insulin. But in these drug approval studies, NONE of the people with type 2 diabetes who are running those dangerous blood sugar levels are taking insulin.
So it seems to me that the patients in these drug studies who start out with that 8- 10%a1c should not be screwing around with experimental drugs. They should be put on carefully tailored insulin regimens until they have brought their A1cs down to the safe level below 6.5%. Then, once they are no longer walking time bombs, doctors can sign them up for new and experimental drugs that might lower their A1cs a tiny bit more.
You may hear doctors say that they can't get their Type 2 patients on insulin down to those levels, but if you probe further, you'll always find that the reason is that these same doctors are instructing their patients to eat a "healthy low fat diet" where each meal contains enough carbohydrates to overwhelm the generic insulin doses they've prescribed. Or you may find that they are only prescribing a basal insulin, like Lantus, which has no effect on the carbohydrates eaten at meals.
When doctors (or diabetes educators) take the time to learn how each individual's body responds to a set dose of insulin and design meal plans that work with sliding insulin doses, insulin, will bring blood sugar into the safe range of 6.5% or less. When doctors and nutritionists combine insulin used with moderate carb restriction (less than 25 grams per meal, for example) insulin can often bring blood sugar into the NORMAL range.
So if doctors were being ethical, i.e. working in the best interests of the patients, no study of any new and possibly ineffective drug should ever start with a population of diabetics whose blood sugar is at a level that even the ultra-conservative American Diabetes Association agrees causes severe complications. And those with responsibility for managing health care should make it clear that drug company operatives who draft patients into drug studies where their blood sugar from start to finish is allowed to remain in the danger zone are operating in an ethical zone only one step removed from Nazi doctors.
As Hippocrates said, "First Do No Harm!"
June 24, 2006
Launching into the blogsphere
Yeah, I like newsgroups a lot better, because they're interactive. I'm too old to think talking to yourself in public is normal. But "young folks nowadays" aren't hanging in newsgroups any more and even I can see that the blog thing isn't going to go away. So here goes . . .
I've already put most of what I've learned over 8 years of contending with medical imbecility relative to Diabetes on my web site, "What they Don't Tell You about Diabetes". What I'm going to do here is comment from time to time on the latest media blither about diabetes and, where possible, shed some light on what the press releases might have left out. Some of it could save your life.
Beside that, well, it's a blog. So there needs to be some self-indugent ruminations. Right? So I'll post about about my own battle to keep control, which by now involves depressing amounts of dietary regulation, insulin, and do-it-yourself doctoring, since the kind of Diabetes I have turns out to be something that only a small group of specialists in the UK seem to know anything about: MODY.
Brief explanation : MODY have genetic bizarrities that mean they go completely out of control unless they use tiny doses of insulin or sulfonylurea drugs--doses the size of what you'd give the average diabetic house cat. MODYs are also rare, so you can run into endos (as I have) who have never had a patient with one before and think you are simply a nutter when you tell them that you hypoed on 6 units of Lantus--until they see the nonfasting glucose test where you went over 200 mg/dl with a full load of metformin and show normal C-peptide levels. Then show them how 4 units of basal dropped your fasting glucose 20 mg/dl and they move you from the "nuts" to "wierd" category, which, believe it or not, is an improvement.
So I'll post a bit about what it takes to keep my blood sugar in control and how MODY works. Every couple weeks I seem to learn something new about it, and if I can pass it on, well that seems worth doing!
I've already put most of what I've learned over 8 years of contending with medical imbecility relative to Diabetes on my web site, "What they Don't Tell You about Diabetes". What I'm going to do here is comment from time to time on the latest media blither about diabetes and, where possible, shed some light on what the press releases might have left out. Some of it could save your life.
Beside that, well, it's a blog. So there needs to be some self-indugent ruminations. Right? So I'll post about about my own battle to keep control, which by now involves depressing amounts of dietary regulation, insulin, and do-it-yourself doctoring, since the kind of Diabetes I have turns out to be something that only a small group of specialists in the UK seem to know anything about: MODY.
Brief explanation : MODY have genetic bizarrities that mean they go completely out of control unless they use tiny doses of insulin or sulfonylurea drugs--doses the size of what you'd give the average diabetic house cat. MODYs are also rare, so you can run into endos (as I have) who have never had a patient with one before and think you are simply a nutter when you tell them that you hypoed on 6 units of Lantus--until they see the nonfasting glucose test where you went over 200 mg/dl with a full load of metformin and show normal C-peptide levels. Then show them how 4 units of basal dropped your fasting glucose 20 mg/dl and they move you from the "nuts" to "wierd" category, which, believe it or not, is an improvement.
So I'll post a bit about what it takes to keep my blood sugar in control and how MODY works. Every couple weeks I seem to learn something new about it, and if I can pass it on, well that seems worth doing!
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