It's already happening. My email box is starting to fill with letters that say things like this: "My [Mother, Brother, Friend--choose one] told me they heard on NPR that lowering blood sugar kills people."
The story they are referring to is the one that reported "excess mortality" in the ACCORD study. This was the study where they took a group of older people with Type 2 diabetes who had already had heart attacks and lowered their average A1c to 6.5% by pumping them full of every diabetes drug known to man. They hired dietitians to phone the study subjects on a regular schedule and nag them to eat a low fat/very high carbohydrate diet full of "healthy whole grains." To counteract the effects of all those "healthy" grains they added the high doses of insulin.
Unfortunately, the people who report on medicine in the media rarely do more than repeat what they read in press releases. They don't ask the hard questions they should ask--like, in this case, "What exactly were the researchers doing to lower blood sugar?"
And because most of their audience is scientifically illiterate, reporters have to dumb down everything they say until someone who has no understanding of physiology or medicine can grasp it. Hence a complex story about a group of seriously ill people who were attempting to lower one of the more complicated measures of blood sugar function, who were given a toxic mixture of drugs whose interactions are not well understood, and who ended up experiencing very slightly more deaths per thousand than expected turns into this: lowering your blood sugar will kill you.
A second large study, ADVANCE, found no excess deaths associated with lowering average A1c to 6.5%. Sometime this summer when that study's results start to be published we will find out if their subjects' health actually improved. I've blogged about the differences in these two studies HERE.
But the media, having come up with the Man Bite's Dog story--lower blood sugars kill--did not spend much time on the ADVANCE story. Too Dog Bites Man.
But if my mail is anything to go by, it is likely that all over America people with diabetes have taken the dumbed down message they heard on the news and translated it into more carbs on the plate and less blood sugar testing. Mothers are calling their grown up kids and warning them not to keep their A1cs too low. And toes are dying, eyes are dimming and kidneys are clogging up. All because journalists translated a complex story into something the dumbest third grader could grasp.
I call it the "Brody Effect" in honor of The New York Times' Jane Brody, who built her career promoting another over-simplication that has had a toxic effect on people who get their health education from the media, the mantra: "Eating fat makes you fat."
Real science is complicated. Be very skeptical about any single sentence that purports to give you all you need to stay healthy. Be even more skeptical of health stories that get a lot of play in the media. The really interesting stuff rarely does. Especially if it takes more than thirty seconds to explain.
Thank goodness for the many folks online--most of them unpaid--who DO do the research, do report it accurately, and make it possible to find out the truth about what is really going on in the world of medical research!
Wednesday, March 26, 2008
Monday, March 24, 2008
Why Me?
This isn't another rant about how come I got dealt a crappy pancreas. It's about something else.
Last year I went to the skin doctor who did my melanoma surgeries. He found another "precancerous" lesion and removed it. So I asked him whether the Januvia I'd been taking might be harmful to me because of the way it suppressed DPP-4 which is known to be implicated in the process that keeps melanocytes from going metatastic.
This guy is an MD/PhD and pretty sharp, and, incidentally, he saved my life after the other local skin doctor told me the big brown patch on my chest was nothing to worry about. So I figured maybe he'd have some ideas.
Instead he said, "Wait a moment," and left me in the cubicle in the skimpy johnnie for about fifteen minutes. Then he came back and told me that all he could find online that had any information on the subject was on one web site. With a sinking feeling, I asked him if it was on phlaunt.com and sure enough, it turned out to be mine.
I had something similar happen last week. I read an article in a newsletter published for practicing endocrinologists written by some endos who have been diagnosing patients with MODY here in the U.S.
Since the only doctors I'd previous found who had even heard of MODY were treating it in the UK, I quickly fired off a letter in which I mentioned my site and added that I hear from quite a few people diagnosed with MODY who are frustrated that their doctors only give them a diagnosis and no other information about what to expect. I also asked a couple questions that grew out of both my own experience and that of the people around the world who email me.
The author wrote back that he had checked out my web site and loved it and was going to refer his MODY patients to it. But no, he didn't know anything more about any of the questions I'd asked. He hoped that the information exchange my site makes possible would add to our knowledge about MODY.
Tag. I'm it.
The media are full of articles extolling how web-based patient information is transforming the treatment of chronic diseases. The New York Times had a big article on this topic just yesterday. But what none of these articles points out is that the patient movement is fueled by dozens if not hundreds of people like me who put in literally thousands of hours answering emails, posting on bulletin boards, and participating in the blogsphere for free. Doctors, last time I checked, bill $500 an hour to give their advice, even though, as may people with diabetes have learned, that advice is often dead wrong.
Don't get me wrong. I'm happy I can help people. And I'm happy that I'm hearing from an increasing number of MDs who tell me that the information on my site is extremely helpful to their patients. But I'm not happy about the system where doctors can answer any request for information about a serious condition with a shrug, a referral to my web site and leave it at that. And when I have to pay them to find out that I know more than they do about something very important to my health.
Last year I went to the skin doctor who did my melanoma surgeries. He found another "precancerous" lesion and removed it. So I asked him whether the Januvia I'd been taking might be harmful to me because of the way it suppressed DPP-4 which is known to be implicated in the process that keeps melanocytes from going metatastic.
This guy is an MD/PhD and pretty sharp, and, incidentally, he saved my life after the other local skin doctor told me the big brown patch on my chest was nothing to worry about. So I figured maybe he'd have some ideas.
Instead he said, "Wait a moment," and left me in the cubicle in the skimpy johnnie for about fifteen minutes. Then he came back and told me that all he could find online that had any information on the subject was on one web site. With a sinking feeling, I asked him if it was on phlaunt.com and sure enough, it turned out to be mine.
I had something similar happen last week. I read an article in a newsletter published for practicing endocrinologists written by some endos who have been diagnosing patients with MODY here in the U.S.
Since the only doctors I'd previous found who had even heard of MODY were treating it in the UK, I quickly fired off a letter in which I mentioned my site and added that I hear from quite a few people diagnosed with MODY who are frustrated that their doctors only give them a diagnosis and no other information about what to expect. I also asked a couple questions that grew out of both my own experience and that of the people around the world who email me.
The author wrote back that he had checked out my web site and loved it and was going to refer his MODY patients to it. But no, he didn't know anything more about any of the questions I'd asked. He hoped that the information exchange my site makes possible would add to our knowledge about MODY.
Tag. I'm it.
The media are full of articles extolling how web-based patient information is transforming the treatment of chronic diseases. The New York Times had a big article on this topic just yesterday. But what none of these articles points out is that the patient movement is fueled by dozens if not hundreds of people like me who put in literally thousands of hours answering emails, posting on bulletin boards, and participating in the blogsphere for free. Doctors, last time I checked, bill $500 an hour to give their advice, even though, as may people with diabetes have learned, that advice is often dead wrong.
Don't get me wrong. I'm happy I can help people. And I'm happy that I'm hearing from an increasing number of MDs who tell me that the information on my site is extremely helpful to their patients. But I'm not happy about the system where doctors can answer any request for information about a serious condition with a shrug, a referral to my web site and leave it at that. And when I have to pay them to find out that I know more than they do about something very important to my health.
Friday, March 21, 2008
A Lesson from the Worms
Two related findings have come out recently that point to the role of insulin and insulin-like growth factor (IGF) in longevity.
One was the finding from the Albert Einstein School of Medicine's Longevity Study that longevity was associated, at least in females, with the presence of a gene that decreased the secretion of IGF. They discovered this after noting that female offspring of female centenarians tended to be about an inch shorter than normal.
Functionally significant insulin-like growth factor I receptor mutations in centenarians. Yousin Suh et al.
The other was the finding in the worm, c. elegans, that, as Science Daily reports, "insulin inhibits a master gene regulator protein known as SKN-1, and that increased SKN-1 activity increases lifespan. SKN-1 controls what is called the Phase 2 detoxification pathway, a network of genes that defends cells and tissue against oxidative stress -- damage caused by elevated levels of free radicals (byproducts of metabolism) -- and various environmental toxins."
Science Daily: Insulin Has Previously Unknown Effect that has Role in Aging and Lifespan
I was a subject in the centenarian study since my dad was a centenarian, but because they only looked at the genes of the children of female centenarians I don't have any data about whether I carry this gene. Still, this is the first time I've ever heard anything suggesting that all those years of being called "shrimp" on the playground and of always being the shortest kid in my class might pay off, big time.
Scientists have long known that you can extend the lifespan of most organisms by cutting way back on their food. But perhaps these findings mean the eat-less longevity approach it isn't about cutting down on food so much as it is about cutting back on foods that stimulate insulin secretion. Those foods are, of course, carbohydrates and to a much lesser extent proteins.
So once again, we get a very good reason to embrace eating fat and back off those "healthy grains and fruit" nutritionists insist are "good for us."
But what about those of us, self-included, who inject insulin or take drugs that increase insulin production? Well, it's a matter of trade offs. We know that high blood sugars damage our bodies, so whatever longevity benefits there might be in cutting back on insulin are going to be balanced by the life-shortening effects of clogging our capillaries and killing our nerves when our blood has become glucose-laden sludge.
We should also be very careful about taking drugs that increase our insulin resistance, most notably the SSRI antidepressants. These drugst raise insulin resistance and hence raise insulin levels in people who take them, no matter what their blood sugar level might be.
What lowers insulin resistance?
1. Keeping blood sugars at normal levels. When your blood sugar goes up to 200 mg/dl you get a lot more insulin resistant no matter what your fundamental level of insulin resistance might be.
2. Exercise--for many people. (Not all, but that's another blog post!) But be careful about what kind of exercise you pursue. If you work up a huge appetite when you exercise and end up eating more than you otherwise would have, you'll undo any benefit of that exercise because more food will mean more insulin. This may be one reason that brisk walking or modest amounts of biking, which aren't likely to cause dramatic blood sugar swings and the resulting hunger might be more healthy, long term, than more heroic exercise routines.
3. Weight loss in people who are seriously overweight. And if you are insulin resistant, the research suggests that you are much more likely to lose weight on a low carb diet, though the same research suggests that people who are NOT insulin resistant can lose equally well on any diet that reduces calories.
4. Metformin.
5. Avandia and Actos, though they appear to cause so many undesirable side effects long term, including osteoporosis, that they are probably not going to increase your longevity.
If you are doing all you can and are, like many people with diabetes still insulin resistant and still dependent on large amounts of insulin to control your blood sugar, should this data ruin your day?
No. One other thing that the Albert Einstein Med School longevity research has proven is that longevity is mostly a matter of getting lucky genes. In a CNN interview, Dr Barzilai, the chief researcher on the longevity project said in regards to the population of centenarians he's following, "We don't have yoga teachers. We don't have vegetarians. Thirty percent of them were overweight or obese in the 1950s. We don't have anybody that's exercising. There are several people who smoked. So for those people, the environment didn't matter. They had something else that we think is genetic."
So taking heroic efforts to extend your own life is usually futile. Don't forget the fate of Dr. Roy Walford, the most famous proponent of the Life Extension diet, dead at 79 of ALS. Or my mom, whose fasting blood sugar at age 92 is 81 but who got dementia from cancer chemotherapy a decade ago. It isn't all about blood sugar. . .
One was the finding from the Albert Einstein School of Medicine's Longevity Study that longevity was associated, at least in females, with the presence of a gene that decreased the secretion of IGF. They discovered this after noting that female offspring of female centenarians tended to be about an inch shorter than normal.
Functionally significant insulin-like growth factor I receptor mutations in centenarians. Yousin Suh et al.
The other was the finding in the worm, c. elegans, that, as Science Daily reports, "insulin inhibits a master gene regulator protein known as SKN-1, and that increased SKN-1 activity increases lifespan. SKN-1 controls what is called the Phase 2 detoxification pathway, a network of genes that defends cells and tissue against oxidative stress -- damage caused by elevated levels of free radicals (byproducts of metabolism) -- and various environmental toxins."
Science Daily: Insulin Has Previously Unknown Effect that has Role in Aging and Lifespan
I was a subject in the centenarian study since my dad was a centenarian, but because they only looked at the genes of the children of female centenarians I don't have any data about whether I carry this gene. Still, this is the first time I've ever heard anything suggesting that all those years of being called "shrimp" on the playground and of always being the shortest kid in my class might pay off, big time.
Scientists have long known that you can extend the lifespan of most organisms by cutting way back on their food. But perhaps these findings mean the eat-less longevity approach it isn't about cutting down on food so much as it is about cutting back on foods that stimulate insulin secretion. Those foods are, of course, carbohydrates and to a much lesser extent proteins.
So once again, we get a very good reason to embrace eating fat and back off those "healthy grains and fruit" nutritionists insist are "good for us."
But what about those of us, self-included, who inject insulin or take drugs that increase insulin production? Well, it's a matter of trade offs. We know that high blood sugars damage our bodies, so whatever longevity benefits there might be in cutting back on insulin are going to be balanced by the life-shortening effects of clogging our capillaries and killing our nerves when our blood has become glucose-laden sludge.
We should also be very careful about taking drugs that increase our insulin resistance, most notably the SSRI antidepressants. These drugst raise insulin resistance and hence raise insulin levels in people who take them, no matter what their blood sugar level might be.
What lowers insulin resistance?
1. Keeping blood sugars at normal levels. When your blood sugar goes up to 200 mg/dl you get a lot more insulin resistant no matter what your fundamental level of insulin resistance might be.
2. Exercise--for many people. (Not all, but that's another blog post!) But be careful about what kind of exercise you pursue. If you work up a huge appetite when you exercise and end up eating more than you otherwise would have, you'll undo any benefit of that exercise because more food will mean more insulin. This may be one reason that brisk walking or modest amounts of biking, which aren't likely to cause dramatic blood sugar swings and the resulting hunger might be more healthy, long term, than more heroic exercise routines.
3. Weight loss in people who are seriously overweight. And if you are insulin resistant, the research suggests that you are much more likely to lose weight on a low carb diet, though the same research suggests that people who are NOT insulin resistant can lose equally well on any diet that reduces calories.
4. Metformin.
5. Avandia and Actos, though they appear to cause so many undesirable side effects long term, including osteoporosis, that they are probably not going to increase your longevity.
If you are doing all you can and are, like many people with diabetes still insulin resistant and still dependent on large amounts of insulin to control your blood sugar, should this data ruin your day?
No. One other thing that the Albert Einstein Med School longevity research has proven is that longevity is mostly a matter of getting lucky genes. In a CNN interview, Dr Barzilai, the chief researcher on the longevity project said in regards to the population of centenarians he's following, "We don't have yoga teachers. We don't have vegetarians. Thirty percent of them were overweight or obese in the 1950s. We don't have anybody that's exercising. There are several people who smoked. So for those people, the environment didn't matter. They had something else that we think is genetic."
So taking heroic efforts to extend your own life is usually futile. Don't forget the fate of Dr. Roy Walford, the most famous proponent of the Life Extension diet, dead at 79 of ALS. Or my mom, whose fasting blood sugar at age 92 is 81 but who got dementia from cancer chemotherapy a decade ago. It isn't all about blood sugar. . .
Tuesday, March 18, 2008
The Media Get It Right!!!!!!
The tide is turning folks! It has taken decades, but very slowly the message is starting to get through that diabetes is NOT caused by obesity and that the best way to determine if you are heading towards diabetes is to test your blood sugar with a meter.
Check out this spectacularly brilliant health feature from The Daily Mail (UK):
Tired? Don't Assume It's Your Lifestyle.
The writers quote a doctor as saying re diabetes, ""Even someone who looks perfectly well, not overweight at all, can be affected." Then they take a blood sugar meter and test a bunch of people. They present the people's photos, data about their age, weight, and lifestyle and what their blood sugar turned out to be. If it wasn't normal they sent them to a doctor. The cutoff they used for normal was 160 mg/dl after eating and 106 mg/dl fasting.
The guy diagnosed as fully diabetic was surprised because he was a vegetarian (No surprise to me. A vegetarian diet is almost always an extremely high carb diet.)
Lots of overweight people they tested came out completely normal. In fact the second lowest reading, 82 mg/dl was that of an obese woman. The only reading lower was 55 mg/dl which looks like reactive hypogycemia. The woman with that reading had a family history of diabetes.
A few young people of normal weight they tested turned out to have abnormal blood sugars. One, only slightly overweight, was told by a doctor she had prediabetes and the other who was completely normal weight-wise but tested at 165 mg/dl and then 130 an hour later and was told she needs more follow up. Those readings suggest very early deterioration.
But isn't this exciting! Just imagine if people started bringing meters to work and having parties to see what everyone's random blood sugar was and sending everyone with abnormal readings to get checked out.
Of course, this happened in the UK where doctors do the oral glucose tolerance test to check for diabetes, NOT the fasting blood sugar test used in the U.S. which is almost worthless at identifying anything but fully-progressed diabetes of several years duration. Still, what a concept. How different my life might have been if someone had taken my abnormal glucose tolerance results seriously when I was a very thin 28 year old!
Coincidentally, yesterday's AP newswire ran a story about MODY and other forms of genetic diabetes.
Genes Point to Varied Diabetic Subtypes
My top fave diabetes researcher, Dr. Hattersley was quoted. He's the doctor who was so helpful to me when I was trying to figure out what was going on with my own diabetes.
Most interestingly, the article had this to say about genes so far identified as being involved with Type 2 diabetes: "Surprisingly, the Type 2 genes don't affect how the body uses insulin, thought to be the trigger. Instead, they alter how the pancreas makes insulin in the first place, explains Dr. David Altshuler of Harvard and the Massachusetts Institute of Technology."
In short, these Type 2 genes don't cause IR, they cause secretory defects which the article goes on to suggest become critical when environmental factors like weight gain stress the glucose control system.
What the article doesn't say, but what research has shown is that weight gain often RESULTS from the marginal blood sugar control caused by the original secretory defect.
But oh my stars! What a nice change from all that media bleating about how "diabetes is caused by lazy people eating too much."
All that remains to make me a very happy lady is for another mass media organ to highlight the fact that cutting way down on carbs is far more effective at normalizing diabetic blood sugar than either oral drugs or WLS. But to see that I'll probably have to live to be very, very old.
I'm working on it!
Check out this spectacularly brilliant health feature from The Daily Mail (UK):
Tired? Don't Assume It's Your Lifestyle.
The writers quote a doctor as saying re diabetes, ""Even someone who looks perfectly well, not overweight at all, can be affected." Then they take a blood sugar meter and test a bunch of people. They present the people's photos, data about their age, weight, and lifestyle and what their blood sugar turned out to be. If it wasn't normal they sent them to a doctor. The cutoff they used for normal was 160 mg/dl after eating and 106 mg/dl fasting.
The guy diagnosed as fully diabetic was surprised because he was a vegetarian (No surprise to me. A vegetarian diet is almost always an extremely high carb diet.)
Lots of overweight people they tested came out completely normal. In fact the second lowest reading, 82 mg/dl was that of an obese woman. The only reading lower was 55 mg/dl which looks like reactive hypogycemia. The woman with that reading had a family history of diabetes.
A few young people of normal weight they tested turned out to have abnormal blood sugars. One, only slightly overweight, was told by a doctor she had prediabetes and the other who was completely normal weight-wise but tested at 165 mg/dl and then 130 an hour later and was told she needs more follow up. Those readings suggest very early deterioration.
But isn't this exciting! Just imagine if people started bringing meters to work and having parties to see what everyone's random blood sugar was and sending everyone with abnormal readings to get checked out.
Of course, this happened in the UK where doctors do the oral glucose tolerance test to check for diabetes, NOT the fasting blood sugar test used in the U.S. which is almost worthless at identifying anything but fully-progressed diabetes of several years duration. Still, what a concept. How different my life might have been if someone had taken my abnormal glucose tolerance results seriously when I was a very thin 28 year old!
Coincidentally, yesterday's AP newswire ran a story about MODY and other forms of genetic diabetes.
Genes Point to Varied Diabetic Subtypes
My top fave diabetes researcher, Dr. Hattersley was quoted. He's the doctor who was so helpful to me when I was trying to figure out what was going on with my own diabetes.
Most interestingly, the article had this to say about genes so far identified as being involved with Type 2 diabetes: "Surprisingly, the Type 2 genes don't affect how the body uses insulin, thought to be the trigger. Instead, they alter how the pancreas makes insulin in the first place, explains Dr. David Altshuler of Harvard and the Massachusetts Institute of Technology."
In short, these Type 2 genes don't cause IR, they cause secretory defects which the article goes on to suggest become critical when environmental factors like weight gain stress the glucose control system.
What the article doesn't say, but what research has shown is that weight gain often RESULTS from the marginal blood sugar control caused by the original secretory defect.
But oh my stars! What a nice change from all that media bleating about how "diabetes is caused by lazy people eating too much."
All that remains to make me a very happy lady is for another mass media organ to highlight the fact that cutting way down on carbs is far more effective at normalizing diabetic blood sugar than either oral drugs or WLS. But to see that I'll probably have to live to be very, very old.
I'm working on it!
Monday, March 17, 2008
More Insight into Why A1c Doesn't Match Your Meter Measurements
My book is at the printer and the house is finally clean. I am not constitutionally capable of writing books and cleaning bathrooms at the same time, so when a book is finally done, the next thing I have to do is get scrubbing. Now back to blogging!
I found an interesting editorial in an issue of Diabetes Care published last year that pointed me to a couple research studies that have a lot more to contribute to our understanding of how well the A1c test result correlates to measurements of blood glucose.
Here's the article. A1c Does One Size Fit All? By Robert M. Cohen, MD.
Cohen states that his own work found that, in a small group of Type 1s, when they compared a simultaneously drawn fructosamine (FA) test and an A1c test "23% of subjects had A1C >1 percentage point higher and 17% had A1C >1 percentage point lower than the value predicted from simultaneously drawn glycated serum proteins." [i.e. a Fructosamine test]
Cohen explains that the FA is more closely correlated to blood glucose levels than the A1c.
More interestingly, for individuals, the gap between the two measures stayed constant over time when the test was repeated. So if the A1c was lower than expected once, it would be lower by a similar amount on subsequent testing.
Cohen then cites another study from his lab saying, "Our laboratory showed data demonstrating, with a new highly precise technique for red cell survival determination, that much more variation in A1C in hematologically normal people can be explained by differences in the mean age of circulating red cells than is currently appreciated."
He adds, "We have also shown data suggesting interindividual differences in how the steady-state concentration of sugar in the red cell relative to that outside the red cell relates to differences in the level of hemoglobin glycation". Which means that different people have red blood cells that will glycosylate at different blood sugar concentrations.
So these findings confirm that no, you are not alone when your A1c doesn't match your measured glucose, test after test. Forty percent of people will read 1% higher or lower than expected according to Cohen's data. He estimates that there are Three Million people in the U.S. whose A1cs don't match their measured blood glucose.
Cohen then cites a new study that found that when non-white populations were studied, the A1c was found to be even more likely not to match predictions based on measuring blood glucose.
Quoting Cohen again, "A1C was consistently lower in whites than in any of the other groups."
The difference was greatest in Black people whose average A1c was almost .5% higher than that of whites. Cohen points out that the DCCT and UKPDS both studied almost entirely white populations, making this a very significant finding.
The zillion dollar question is: which matters most, A1c or measured blood sugar?
We have seen that with neuropathy, in people with prediabetes there is no relationship between a person's A1c and the incidence of neuropathy but there IS a relationship between their 2 hour Glucose Tolerance Test result and the likelihood of neuropathy. This points pretty clearly to the conclusion that it is the post-meal spikes, rather than average blood sugar of any type that causes complications.
Cohen's study of Type 1s found that when A1c was higher than the value predicted by the Fructosamine test there was a tendency to have more kidney problems, though he states that it is possible that poor kidney function might be responsible for the gap, not the other way around.
But the fact remains that because researchers rarely measure post-meal blood sugars in the free range person with diabetes, we don't know where to point the finger: A1c or post-meal spikes?
The Glucose Tolerance Test (GTT) doesn't really duplicate the kind of blood sugar you will see day in and day out your after meals. If you have any insulin production capability left, when you take an Glucose Tolerance Test you are likely to see higher one hour highs and lower two hour values on the GTT than you see when you eat real food.
Wen you eat real food, your blood sugar is likely to climb more slowly and stay high longer, because of the speed of digestion and the impact of simultaneously eaten fat and protein on that speed. If it is a couple hours of exposure to a blood sugar of, say 150 mg/dl, a person with marginal blood sugar control might get that damaging exposure eating a bagel with cream cheese, but not see that 150 mg/dl as the 2 hour value on a glucose tolerance test.
Another thing that sheds light on the question, "Which matters, the A1c or the post-meal blood sugar?" is one large study, the Kumamoto Study, which found that a group of Japanese people who get an average 7% A1c by limiting their post-meal blood sugar spikes got far fewer complications than did the group of people in the UKDPS study who got the same average 7% A1c but made no attempt to limit post meal spikes.
The study Cohen cited suggests that Asian people's average A1cs were .16% higher than Whites (meaning that that if the White Average was 5% the Asian would be 5.16%) , which may suggest that the Japanese group's 7% A1c reflected a slightly lower blood glucose level than the White group's 7%. But even so, the difference probably isn't enough to explain the far more significant decrease in complications seen in the Japanese study compared to the UK study.
For now, I'm betting that it is those post-meal spikes causing the mischief. But because of the cost of testing, we aren't likely to see any large-scale studies where the complication profiles of people adhering to stringent post-meal blood sugar goals like the 140 mg/dl AACE 2 hour goal are compared to those with looser goals--like the ADA's anemic 180 mg/dl 2 hour goal.
What I do know is that, since the complications that matter to me are the ones I get, I'm going to be a lot better off if I go for the most stringent goal. Beyond that, if the A1c is the problem, past a certain point, there isn't a darn thing I can do. I can lower my post meal blood sugars but no matter how much they drop, since I started cutting back on carbohydrates, my A1c is always about .5% higher than predicted. Oddly, in the past when I was eating a lot of carbs,it was always lower than predicted from blood sugar measurements. This might point to yet another factor that isn't ever going to be researched.
What a complicated mess all this blood sugar stuff is, eh?
I found an interesting editorial in an issue of Diabetes Care published last year that pointed me to a couple research studies that have a lot more to contribute to our understanding of how well the A1c test result correlates to measurements of blood glucose.
Here's the article. A1c Does One Size Fit All? By Robert M. Cohen, MD.
Cohen states that his own work found that, in a small group of Type 1s, when they compared a simultaneously drawn fructosamine (FA) test and an A1c test "23% of subjects had A1C >1 percentage point higher and 17% had A1C >1 percentage point lower than the value predicted from simultaneously drawn glycated serum proteins." [i.e. a Fructosamine test]
Cohen explains that the FA is more closely correlated to blood glucose levels than the A1c.
More interestingly, for individuals, the gap between the two measures stayed constant over time when the test was repeated. So if the A1c was lower than expected once, it would be lower by a similar amount on subsequent testing.
Cohen then cites another study from his lab saying, "Our laboratory showed data demonstrating, with a new highly precise technique for red cell survival determination, that much more variation in A1C in hematologically normal people can be explained by differences in the mean age of circulating red cells than is currently appreciated."
He adds, "We have also shown data suggesting interindividual differences in how the steady-state concentration of sugar in the red cell relative to that outside the red cell relates to differences in the level of hemoglobin glycation". Which means that different people have red blood cells that will glycosylate at different blood sugar concentrations.
So these findings confirm that no, you are not alone when your A1c doesn't match your measured glucose, test after test. Forty percent of people will read 1% higher or lower than expected according to Cohen's data. He estimates that there are Three Million people in the U.S. whose A1cs don't match their measured blood glucose.
Cohen then cites a new study that found that when non-white populations were studied, the A1c was found to be even more likely not to match predictions based on measuring blood glucose.
Quoting Cohen again, "A1C was consistently lower in whites than in any of the other groups."
The difference was greatest in Black people whose average A1c was almost .5% higher than that of whites. Cohen points out that the DCCT and UKPDS both studied almost entirely white populations, making this a very significant finding.
The zillion dollar question is: which matters most, A1c or measured blood sugar?
We have seen that with neuropathy, in people with prediabetes there is no relationship between a person's A1c and the incidence of neuropathy but there IS a relationship between their 2 hour Glucose Tolerance Test result and the likelihood of neuropathy. This points pretty clearly to the conclusion that it is the post-meal spikes, rather than average blood sugar of any type that causes complications.
Cohen's study of Type 1s found that when A1c was higher than the value predicted by the Fructosamine test there was a tendency to have more kidney problems, though he states that it is possible that poor kidney function might be responsible for the gap, not the other way around.
But the fact remains that because researchers rarely measure post-meal blood sugars in the free range person with diabetes, we don't know where to point the finger: A1c or post-meal spikes?
The Glucose Tolerance Test (GTT) doesn't really duplicate the kind of blood sugar you will see day in and day out your after meals. If you have any insulin production capability left, when you take an Glucose Tolerance Test you are likely to see higher one hour highs and lower two hour values on the GTT than you see when you eat real food.
Wen you eat real food, your blood sugar is likely to climb more slowly and stay high longer, because of the speed of digestion and the impact of simultaneously eaten fat and protein on that speed. If it is a couple hours of exposure to a blood sugar of, say 150 mg/dl, a person with marginal blood sugar control might get that damaging exposure eating a bagel with cream cheese, but not see that 150 mg/dl as the 2 hour value on a glucose tolerance test.
Another thing that sheds light on the question, "Which matters, the A1c or the post-meal blood sugar?" is one large study, the Kumamoto Study, which found that a group of Japanese people who get an average 7% A1c by limiting their post-meal blood sugar spikes got far fewer complications than did the group of people in the UKDPS study who got the same average 7% A1c but made no attempt to limit post meal spikes.
The study Cohen cited suggests that Asian people's average A1cs were .16% higher than Whites (meaning that that if the White Average was 5% the Asian would be 5.16%) , which may suggest that the Japanese group's 7% A1c reflected a slightly lower blood glucose level than the White group's 7%. But even so, the difference probably isn't enough to explain the far more significant decrease in complications seen in the Japanese study compared to the UK study.
For now, I'm betting that it is those post-meal spikes causing the mischief. But because of the cost of testing, we aren't likely to see any large-scale studies where the complication profiles of people adhering to stringent post-meal blood sugar goals like the 140 mg/dl AACE 2 hour goal are compared to those with looser goals--like the ADA's anemic 180 mg/dl 2 hour goal.
What I do know is that, since the complications that matter to me are the ones I get, I'm going to be a lot better off if I go for the most stringent goal. Beyond that, if the A1c is the problem, past a certain point, there isn't a darn thing I can do. I can lower my post meal blood sugars but no matter how much they drop, since I started cutting back on carbohydrates, my A1c is always about .5% higher than predicted. Oddly, in the past when I was eating a lot of carbs,it was always lower than predicted from blood sugar measurements. This might point to yet another factor that isn't ever going to be researched.
What a complicated mess all this blood sugar stuff is, eh?
Wednesday, March 5, 2008
Blood Sugar 101: The Book!
I finally figured out how to turn the information on my Bloodsugar101.com web site into a book that would provide real value for readers. I'm polishing up the text now and the book should be coming out in April. You can see the cover mock up above.
The reason I felt it was time for a book was two-fold. One was that the message I was getting from the many people who email me is that while they found the information on the site extremely valuable, they didn't have time to read it all online. They often write to ask me questions that are answered on the site, so it was becoming clear to me that the sheer size of the site was making it harder to find important relevant information stored on it.
The other reason for putting this information into book form is that the linear structure of a book makes it possible to control the sequence in which readers encounter information. This makes it possible to explain things in a way where one idea builds on the previous one. Because you can't control the order in which visitors encounter information on a Web site, you often can't rely on their having the concepts needed to grasp the importance of a particular fact. The information on the Bloodsugar101.com site assumes a certain level of understanding about our bodies and our health that many people, even educated people, do not have. The book form is perfect for addressing this problem.
What I am loving about this book is the way that it takes readers step by step through the concepts they need to understand to control their blood sugar and prevent complications. The process of writing it has been valuable for me, too. I've had to to go back and revisit the content of the site, check my references, and sharpen my own understanding of the information presented there. The site has certainly grown beyond my ability to keep it all in my head!
This isn't my first venture into publishing. As some of you know, I'm the author of seven published business books including one that was a bestseller for John Wiley & Sons. After the success of the bestseller, I started my own small press and sold almost 20,000 books on my own. Unlike most self-published books, my books made it to the shelves in Borders, Barnes & Noble and other chains. I learned a great deal about publishing with those books, and I'm hoping to put that knowledge to use with this one.
The Blood Sugar 101 book will be available through Amazon and the other online bookstores. I'll also be offering it through the Bloodsugar101.com web site where you will be able to buy it using PayPal.
I'm going to be running a pre-publication offer where book rate shipping to addresses in the United States will be free. More about that when I get the web site set up to handle it.
Wednesday, February 27, 2008
Big Pharma Lives to Cheat Again
Two stories in the news this week reflect increased scrutiny of Big Pharma malfeasance coupled with evidence that this scrutiny isn't going to change anything soon.
1. After many months of running the ad campaign where Robert "I am not a licensed doctor, but I play one on Television" Jarvik promoted Lipitor, Pfizer announced it was ending the campaign.
Pfizer to End Lipitor Campaign by Jarvik (NY Times)
This might look like a triumph for those who pointed out that "Dr. " Jarvik was never licensed to practice medicine, that he didn't actually invent the artificial heart, and that the footage of a man looking exactly like him indulging in energetic rowing was actually shot using a body double, since Jarvik doesn't row.
But it isn't that significant because this ad campaign has been running for so many months already that it was due to be replaced. Pfizer is hard at work on yet another campaign whose message is that the you shouldn't use a cheap generic statin. If you do, Pfizer's profits will tumble.
This deceptive ad campaign was very suited for Lipitor. This is, after all, the most misrepresented drug in history. Research studies have shown that statins do not prevent heart attacks in anyone except males under 56 years old who have already had heart attacks.
Statins do cause significant cognitive symptoms--including what can be permanent memory loss. They can compromise your liver. They can even weaken your heart muscle. But such is the power of the saturation advertising pursued by Pfizer and other statin manufacturers that few doctors are informed about the actual data supporting the claims that statins prevent heart attack.
2. Our second story is about the second most oversold family of drugs, SSRI antidepressants. Scientists invoked the Freedom of Information Act to get access to the many studies submitted to the FDA as part of the drug approval process for a long list SSRI antidepressants. In many cases, the publication of these studies had been suppressed by the drug manufacturers. In others they had been published with critical information left out so that misleading conclusions could be drawn.
The latter is a common practice. If, say, a placebo cures 30% of those who take it and the drug under study cures 30% of those who take it--which shows it is no more effective than a sugar pill--a misleading way of publishing the study would be to leave out any mention of placebo and headline the study, "New Drug cures 30% of those who take it." This, it turns out is exactly the way that the SSRI manufacturers spun a bunch of studies.
The meta-analysis of this suppressed and misrepresented data showed conclusively that SSRI antidepressants don't work any better than sugar pills except in the case of people with severe depression where they are only slightly more effective. Severe depression is the kind of depression that renders a person completely unable to function. Untreated people who have it end up institutionalized. It is not the mild depression that characterizes 98% of those prescribed Prozac, Zoloft, Paxil, etc.
You can read the published research paper about the actual effectiveness of SSRIs here in the metastudy published in Public Library of Science (PLoS) Medicine :
Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration
You would think this would have been front page news, given how these drugs have been prescribed to over 40 million people. But since drug company advertising heavily funds most media outlets in the U.S. the story went almost unreported. Fortunately, the British press which is not allowed to advertise drugs picked it up and that brought it to my attention.
What many people don't know about depression is this: studies conducted decades ago found that if you give psychotherapy to a group of people with mild depression one third will get better. But if you give no treatment at all to another group of people with mild depression one third will also get better. So with that in mind, you can reinterpret the way that drug companies promote these drugs with statistics showing, you guessed it, that one third of those given the drugs get better.
Unfortunately, getting better using an SSRI also means getting fatter, increasing your insulin resistance, decreasing your sexual function, and developing a dependency on the drug that will cause you to suffer serious neurological symptoms if you try to stop taking it.
And as I reported a few blog postings ago, taking an SSRI also seems to remodel the neuron distribution in your hippocampus, an effect whose long-term impact is unknown but should be troubling. Changes to the hippocampus as we age cause dementia.
What is even more troubling is that it took more than 20 years for the suppressed studies to see the light of day. This is long enough for many of the drugs involved in those studies to go off patent, after earning billions for the companies that suppressed the evidence that they were selling expensive, addictive placebos that have frightening side effects and most definitely increase insulin resistance.
If you care about your health, demand that your elected representatives change the laws that allow drug companies to sell their drugs to the public via television advertising. These ads are alway full of misrepresentations, but the drug companies know that by the time they get nailed for them, the ad will have already been seen hundreds of times by hundreds of millions of medically naive consumers.
And if you care about health, you should also demand that your elected representatives demand that the FDA make public all studies submitted as part of the drug approval process. Before the drug is approved.
Our ability to trust the safety of FDA-approved medications is lower now than it has been at any time since the FDA was first chartered to protect the public from drugs that were maiming and killing people. If the system isn't cleaned up, it is only a matter of time until we have a drug-induced disaster that will make the effects Thalidomide look trivial.
For that matter, we may already have had it. It may just take another decade for people to realize it.
1. After many months of running the ad campaign where Robert "I am not a licensed doctor, but I play one on Television" Jarvik promoted Lipitor, Pfizer announced it was ending the campaign.
Pfizer to End Lipitor Campaign by Jarvik (NY Times)
This might look like a triumph for those who pointed out that "Dr. " Jarvik was never licensed to practice medicine, that he didn't actually invent the artificial heart, and that the footage of a man looking exactly like him indulging in energetic rowing was actually shot using a body double, since Jarvik doesn't row.
But it isn't that significant because this ad campaign has been running for so many months already that it was due to be replaced. Pfizer is hard at work on yet another campaign whose message is that the you shouldn't use a cheap generic statin. If you do, Pfizer's profits will tumble.
This deceptive ad campaign was very suited for Lipitor. This is, after all, the most misrepresented drug in history. Research studies have shown that statins do not prevent heart attacks in anyone except males under 56 years old who have already had heart attacks.
Statins do cause significant cognitive symptoms--including what can be permanent memory loss. They can compromise your liver. They can even weaken your heart muscle. But such is the power of the saturation advertising pursued by Pfizer and other statin manufacturers that few doctors are informed about the actual data supporting the claims that statins prevent heart attack.
2. Our second story is about the second most oversold family of drugs, SSRI antidepressants. Scientists invoked the Freedom of Information Act to get access to the many studies submitted to the FDA as part of the drug approval process for a long list SSRI antidepressants. In many cases, the publication of these studies had been suppressed by the drug manufacturers. In others they had been published with critical information left out so that misleading conclusions could be drawn.
The latter is a common practice. If, say, a placebo cures 30% of those who take it and the drug under study cures 30% of those who take it--which shows it is no more effective than a sugar pill--a misleading way of publishing the study would be to leave out any mention of placebo and headline the study, "New Drug cures 30% of those who take it." This, it turns out is exactly the way that the SSRI manufacturers spun a bunch of studies.
The meta-analysis of this suppressed and misrepresented data showed conclusively that SSRI antidepressants don't work any better than sugar pills except in the case of people with severe depression where they are only slightly more effective. Severe depression is the kind of depression that renders a person completely unable to function. Untreated people who have it end up institutionalized. It is not the mild depression that characterizes 98% of those prescribed Prozac, Zoloft, Paxil, etc.
You can read the published research paper about the actual effectiveness of SSRIs here in the metastudy published in Public Library of Science (PLoS) Medicine :
Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration
You would think this would have been front page news, given how these drugs have been prescribed to over 40 million people. But since drug company advertising heavily funds most media outlets in the U.S. the story went almost unreported. Fortunately, the British press which is not allowed to advertise drugs picked it up and that brought it to my attention.
What many people don't know about depression is this: studies conducted decades ago found that if you give psychotherapy to a group of people with mild depression one third will get better. But if you give no treatment at all to another group of people with mild depression one third will also get better. So with that in mind, you can reinterpret the way that drug companies promote these drugs with statistics showing, you guessed it, that one third of those given the drugs get better.
Unfortunately, getting better using an SSRI also means getting fatter, increasing your insulin resistance, decreasing your sexual function, and developing a dependency on the drug that will cause you to suffer serious neurological symptoms if you try to stop taking it.
And as I reported a few blog postings ago, taking an SSRI also seems to remodel the neuron distribution in your hippocampus, an effect whose long-term impact is unknown but should be troubling. Changes to the hippocampus as we age cause dementia.
What is even more troubling is that it took more than 20 years for the suppressed studies to see the light of day. This is long enough for many of the drugs involved in those studies to go off patent, after earning billions for the companies that suppressed the evidence that they were selling expensive, addictive placebos that have frightening side effects and most definitely increase insulin resistance.
If you care about your health, demand that your elected representatives change the laws that allow drug companies to sell their drugs to the public via television advertising. These ads are alway full of misrepresentations, but the drug companies know that by the time they get nailed for them, the ad will have already been seen hundreds of times by hundreds of millions of medically naive consumers.
And if you care about health, you should also demand that your elected representatives demand that the FDA make public all studies submitted as part of the drug approval process. Before the drug is approved.
Our ability to trust the safety of FDA-approved medications is lower now than it has been at any time since the FDA was first chartered to protect the public from drugs that were maiming and killing people. If the system isn't cleaned up, it is only a matter of time until we have a drug-induced disaster that will make the effects Thalidomide look trivial.
For that matter, we may already have had it. It may just take another decade for people to realize it.
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