It's easy to get frustrated about the current state of diabetes treatment. As my daily email inbox will show, doctors still fail to diagnose diabetes until it has been given years to damage patients' bodies and when they do diagnose it, they all too often treat it with dangerous drugs and toxic low fat dietary advice.
But as infuriated as we may feel that so many people are suffering tragically unnecessary complications because their doctors don't have the time or inclination to learn more about diabetes than the "education" they receive from perky ex-cheerleader drug reps, there are some grounds for optimism.
The greatest of these is the increasingly powerful role of online patient-provided diabetes education.
It's been a decade since my own diabetes diagnosis. When I first checked into an online diabetes support group in 1998 people who would suggest using a low carb diet to lower blood sugars would be greeted with accusations that they were trying to murder diabetics because everyone knew that the low carb diet destroyed kidneys and gave people heart attacks. (You can read the research that found these beliefs to be wrong HERE.)
The diagnostic criteria for diagnosing Diabetes based on fasting glucose had just been changed in 1997 to 126 mg/dl, but the news of this change was slow to get out and many family doctors were still diagnosing diabetes only when fasting blood sugar rose over 140 mg/dl. This meant that most people who were newly diagnosed already had significant neuropathy.
Many people with Type 2 diabetes were taking Rezulin. A few months later we learned that Rezulin had caused many completely unnecessary deaths due to liver failure, mostly because doctors ignored the warning not to prescribe it to people with elevated liver enzymes --which are very common among people with Type 2. Only after many people died was it was finally taken off the market.
There were also discussions going on in 1998 about whether Metformin, approved three years earlier, was safe. Some people posting online interpreted the transient early side effects of metformin as signs they were developing lactic acidosis and stopped taking it, though subsequent studies have shown this side effect to be extremely rare and to occur at the same incidence in people taking Metformin as it does in those who do not take it.
A friend diagnosed a year before I was was taking part in a pre-approval study of a new "miracle" diabetes drug. That drug was Avandia which was only approved by the FDA the next year.
Back then, people whose A1cs were near 7% were convinced they were in excellent control even when they were experiencing blood sugars above 200 mg/dl at every meal--though few people back then knew what their blood sugars were after eating, because doctors rarely told people with Type 2 to test their blood sugar at all, and if they did tell them to test, they told them to test once or twice a week first thing in the morning, fasting.
There was no understanding within the medical community a decade ago that blood sugar spikes were to blame for the damage caused by diabetes. My own doctor said my blood sugars in the mid 200s were "nothing to worry about" because my A1c was in the 6% range and would not prescribe test strips to me because my fasting blood sugar was normal (i.e. under 110 mg/dl) thanks largely to my low carbohydrate diet.
I had to pay for my own test strips myself, at $.60 a piece which was a lot more money than it is now thanks to inflation. There were no cheap brands available. These test strips were even less consistent in their readings than the ones we have now and tended to go bad by the end of the container.
There was little to no understanding even among specialists of the "Type 1.5" forms of diabetes. The expensive endocrinologist I saw offered me no treatment or explanation for why I had diabetes despite maintaining a normal weight or why I had had abnormal GTTs and Gestational Diabetes in my 20s and 30s when I weighed under 120 lbs. All he did was suggest I switch from my Bernstein diet to a "Meditteranean" diet. I did that for several weeks, gained ten pounds, got back on the blood sugar rollercoaster and spent the next year badly out of control.
Other adults I met online reported that they had been treated as "Type 2s" even though their blood sugars went higher and higher until they ended up in the hospital with DKA and were told they were Type 1s.
When I visit an online diabetes support community today, the picture is very different. Though most doctors aren't giving people much better dietary advice than they were getting a decade ago, they are diagnosing people earlier and they are taking pre-diabetes much more seriously. This is important, because the evidence is very strong that the most significant "diabetic" complications, neuropathy, retinopathy, and heart disease begin at blood sugar levels that are defined as "pre-diabetic."
Every online community now has its "greeters" who orient new visitors and explain to them the importance of testing their blood sugar and keeping their post-meal blood sugars as low as possible.
Though the ADA continues to promote the ineffectual, low fat diet that raises blood sugar and provides a steady stream of customers for the junk food companies and drug companies that are its largest sponsors, the diabetes patient community as a whole has accepted that the low carb diet is safe and effective.
It is impossible now to spend more than a few minutes reading any online diabetes discussion board without reading of the benefits of cutting back on carbohydrates. My inbox is filled with letters from people with Type 2 who have done just that and achieved the 5%-range A1cs that almost always result from cutting back on carbohydrates. The online community is also helping people become more aware of the impact of the drugs they take and alerting people who are misdiagnosed with Type 2 about the possiblity that they might have one of the Type 1.5 forms of diabetes.
The situation for Type 1s is even more dramatically improved. Pumps and CGMSs are helping people with Type 1 achieve blood sugars in the truly normal range. Newer, faster meal-time insulins like Apidra also help make this possible. I am heartened by how many young Type 1s report that they have A1cs in the mid 5% to low 6% range. Ten years ago, this simply did not happen and long term it means that these people are likely to be much more healthy and complication free.
It stinks that much of this improvement has been going on despite rather than because of the current standard of medical care. But I have hopes that the new administration in Washington will make changes to the FDA that might rein in the drug companies, limit drug advertising, and even, one allows oneself to dream, encourage doctors to recieve their continuing medical education from sources other than drug company representatives.
But even if that doesn't happen, the power the internet has given people with diabetes to reach out to others and give them the education they need to remain healthy is such that it is transforming diabetes management no matter how far doctors lag behind.
And not all doctors are lagging. Some who see patients making dramatic changes in their health with non-drug solutions are recommending low carb diets to their patients. Some doctors who themselves have developed diabetes in middle age are discovering the limits of the treatments they have been prescribing. Eventually we will reach critical mass and even the ADA will not be able to keep everyone from understanding the impact of dietary carbohydrate on our blood sugars or the importance of achieving normal blood sugar levels.
Looking forward, the most interesting development I see is this: Over the past year or two, the drop in price of the arrays used to do genetic testing is making it possible for researchers, finally, to investigate the genetic underpinnings of diabetes by testing large populations and statistically analyzing hundreds of thousands of SNPs (single nucleotide polymorphisms) looking for the subtle genetic flaws that until now were impossible to detect.
What they are discovering is laying to rest the idea that Type 2 diabetes is caused by gluttony and sloth. Almost every week a new genetic flaw is discovered to be prevalent in people with Type 2, many of them, to the surprise of investigators, flaws that limit insulin secretion, though a few common SNPs found in people with Type 2, are alsoo being linked with increases insulin resistance or, more interestingly, defects in the way that the liver releases glucose.
Though doctors are not aware of this research and many still blame patients for their diabetes, the genetic advances we are starting to see are beginning to change this. Only this year the media have started to describe Type 2 as being genetic in origin rather than, as was the case in the past, describing it as being caused by an indulgent lifestyle.
Over time, these genetic discoveries will lead to improvements both in early diagnosis and to the development of carefully targeted and more effective treatments. We will start to understand the impact of specific genes and see that Type 2 diabetes is not one uniform disease but a constellation of genetic flaws which impact different parts of glucose metabolism and hence require slightly different treatments.
It is even possible that with the political changes we are seeing, society will finally be informed that the main reason for the so-called "obesity epidemic" and spread of diabetes is factors that are causing genetic damage: Exposure of infants to environment toxins like BPA, pesticides, PCBS etc, and to the overuse of food science disasters like immunotoxic soy in our food supply. There is already a lot of research that backs this up. It has only been because our EPA was hijacked and set to serve the interests of huge industrial polluters that this information has not been acted on.
We still have a long, hard battle. Industry profits when they pollute or use cheap chemicals in food instead of expensive natural ingredients. They profit again when we get sick and require expensive drugs.
Doctors have no incentive to make us so healthy we don't need to pay them for $30,000 operations, so you will always see more press about how diabetes can be cured by expensive surgeries or controlled with $200/month drugs than you will about how cutting back on junk carbs could do the same thing.
But we people with diabetes are uniquely fortunate among those who have chronic diseases that we can reach out to each other and improve our own condition simply by sharing common sense proven techniques with each other.
So with that in mind I wish you all a Happy New Year, one filled with health, hope, and prosperity. If you are out of control thanks to the holidays, check back on Friday and we'll start our New Years Diabetes Detox together.
December 31, 2008
December 29, 2008
Holiday Excess is Nearly Over and Diet Season is Coming
I am seeing people all over the web posting messages blaming themselves for being weak, sinful and worthless because they have been eating all the same holiday fare everyone else eats and seeing their blood sugars soar.
In fact, they are doing exactly what everyone else does this time of year. All that is different is that they have diabetes and blood sugar meters so they KNOW what the impact is on their bodies of this season of "holiday joy."
There are a lot of factors that have nothing to do with personal worthlessness which have been driving us all to eat: It's dark. It's cold. Millions of years of evolutionary pressures have taught our bodies to store every bit of nourishment we can get this time of year because it is going to be four long months until the first green shoots appear, and unless we've packed away a good store of body fat we may not live to see that distant Spring.
And, of course, this is also the time of year when zillions of advertising dollars are put into convincing us that everyone else has a much more wonderful family and far more thoughtful friends than we do. Merchants give us the message that we can only demonstrate our love for others by showering them with perfectly chosen, extremely expensive gifts. To make it even worse, to mention our less than positive feelings this time of year risks being labeled a "Scrooge." Is it any wonder that comfort eating can quickly escalate into obsessional drownings in food and drink?
The good news is that the Season of Excess is almost over. On Friday the supermarkets will put diet food on the "Seasonal Aisle" and for a few brief weeks everyone --with or without diabetes--will struggle to undo the dietary damage they've done to themselves through the holiday season.
Most will fail. By Superbowl Sunday, the supermarkets will replace the diet food in the "seasonal" aisle with chips and dip and cheese whiz. But if you are sick of being out of control, January 2 is a great time to use the momentum of the brief Diet Season to achieve some small but useful goal.
Keep your chosen goal simple. Do not resolve to lose 100 lbs, go to the gym five times a week, get control of your spending and achieve a 4.7% A1c. Indulging in fantasy is fun, but unless you chose a goal you have a good chance of achieving in three weeks, your "goals" will remain fantasies.
My goal this January is to lose the weight I put on this holiday season--3 to 5 lbs. I was able to keep my blood sugar in range the whole time, which I'm proud of, but only by using more insulin than usual, which invariably leads to weight gain.
So I'll be cutting carbs so that I can cut my insulin dose. I'll also have to cut back dramatically on calories because that is the only way I can lose weight. I do this every January and I know that by Super Bowl Sunday I will be sick of it, but hopefully by then I will have knocked off a few pounds and gotten back into better eating habits.
Are you setting yourself any special goals for January?
In fact, they are doing exactly what everyone else does this time of year. All that is different is that they have diabetes and blood sugar meters so they KNOW what the impact is on their bodies of this season of "holiday joy."
There are a lot of factors that have nothing to do with personal worthlessness which have been driving us all to eat: It's dark. It's cold. Millions of years of evolutionary pressures have taught our bodies to store every bit of nourishment we can get this time of year because it is going to be four long months until the first green shoots appear, and unless we've packed away a good store of body fat we may not live to see that distant Spring.
And, of course, this is also the time of year when zillions of advertising dollars are put into convincing us that everyone else has a much more wonderful family and far more thoughtful friends than we do. Merchants give us the message that we can only demonstrate our love for others by showering them with perfectly chosen, extremely expensive gifts. To make it even worse, to mention our less than positive feelings this time of year risks being labeled a "Scrooge." Is it any wonder that comfort eating can quickly escalate into obsessional drownings in food and drink?
The good news is that the Season of Excess is almost over. On Friday the supermarkets will put diet food on the "Seasonal Aisle" and for a few brief weeks everyone --with or without diabetes--will struggle to undo the dietary damage they've done to themselves through the holiday season.
Most will fail. By Superbowl Sunday, the supermarkets will replace the diet food in the "seasonal" aisle with chips and dip and cheese whiz. But if you are sick of being out of control, January 2 is a great time to use the momentum of the brief Diet Season to achieve some small but useful goal.
Keep your chosen goal simple. Do not resolve to lose 100 lbs, go to the gym five times a week, get control of your spending and achieve a 4.7% A1c. Indulging in fantasy is fun, but unless you chose a goal you have a good chance of achieving in three weeks, your "goals" will remain fantasies.
My goal this January is to lose the weight I put on this holiday season--3 to 5 lbs. I was able to keep my blood sugar in range the whole time, which I'm proud of, but only by using more insulin than usual, which invariably leads to weight gain.
So I'll be cutting carbs so that I can cut my insulin dose. I'll also have to cut back dramatically on calories because that is the only way I can lose weight. I do this every January and I know that by Super Bowl Sunday I will be sick of it, but hopefully by then I will have knocked off a few pounds and gotten back into better eating habits.
Are you setting yourself any special goals for January?
December 19, 2008
What I'd Like to See Change at the FDA
The FDA announced some changes in how it will approve drugs for Type 2 diabetes which have sparked controversy in the diabetes community. Unlike many, I believe this is good news, not bad. A fellow diabetes activist asked me what I would like to see changed in the FDA and I wrote him a reply which I am sharing with you here.
The most important thing I'd like to see change at the FDA is going to happen without our needing to submit petitions: restoring science as a criteria for drug approval. The Bush FDA was notorious for the way that decisions were made based on financial connections of FDA staff to drug makers and their religious beliefs. But beyond that I think the following are most important:
1. End "direct to consumer" drug advertisements. These are well-known to be full of lies, but it takes so many months until an ad is shut down for false claims that these lies cando their work.
2. Make drug testing compare a new drug with the safe, cheap existing drugs. If there is no significant benefit compared to safe, cheap drugs, do not approve the drug. Right now, most drugs are only compared to placebo. So a new drug that is no more effective than a safe, cheap proven drug but costs 20 times more per pill gets approved with huge fanfare and becomes the subject of a billion dollar advertising campaign that gets doctors switching patients to it from the safe cheap drug.
3. Do not let drug companies claim a drug "rejuvenates beta cells" until this has been proven by direct measurement in humans. Every single such claim for a drug in the past, which included the major claim used to market Avandia, has been based on surrogates like HOMA measurements which turn out to be a false guide or on findings in rodents which did not extend to humans.
After a decade we finally saw research that showed conclusive evidence that Avandia did NOT rejuvenate beta cells. But for a decade doctors prescribed it on that premise.
Currently Januvia and Byetta are being sold with the same claim, based only on test tube and rodent studies. This motivates doctors to keep people on these drugs EVEN when their blood sugars are deteriorating and they are experiencing severe side effects. The long term deterioration in blood sugars experienced by people who are taking Byetta long-term suggests that just like Avandia, it does not rejuvenate beta cells. But doctors continue to tell patients it does.
4. When a new designer drug is targeting a gene or specific receptor, the approval process MUST included investigation of the other uses of that gene or receptor and the impact of the drug on those other functions must be explored.
The dangerous side effects of ALL drugs from sulfonylureas to Avandia to Januvia turned out to be caused by the OTHER functions of the genes or receptors they target. There is currently NO requirement in the testing process that the drug company do this. The technology for exploring gene expression has advanced greatly and the cost of this kind of research has dropped dramatically. It is now very possible to see which genes are expressing in response to different stimuli. It is possible to see which receptors are accepting a drug.
We can no longer approve 21st century drugs only with techniques developed in the first half of the 20th century.
People who have not been prescribed the drugs given to people with Type 2 diabetes can have little idea how dreadful the many side effects of Type 2 drugs really are.
But many patients trust their doctors completely, and if the doctor gives them a drug, no matter how awful it makes them feel, they take it, especially if they have been told, as many have, that the drug is "regrowing their beta cells."
Their reward for this may be enormous weight gain, osteoporosis, and even blindness (Actos and Avandia), heart attack (Avandia, Glipizide), pancreatitis (Byetta), irreversible inflammation syndromes or cancer (Januvia.)
I get heartbreaking emails from people who have suffered these permanent side effects. They are very real. I myself live every day with a miserable permanent side effect of a prescription drug. So I would far rather that a drug not be approved, than that it be "fast-tracked", sold to hundreds of thousands of people, and worsen their lives. Especially when there are already other drugs that work just as well.
To the argument that making drug approval harder will stifle drug development, I say only, look at the profits on a single successful drug. As long as a company can earn $200 a month from a vial of 30 pills or 60 units of an injectable drug, drug development will continue.
As it is, the drug companies are not doing new research. They are putting most of their efforts into making tiny changes to existing drugs to keep them under patent or into developing copycat versions of drugs sold by other companies. If the incentive to copy other drugs were lost, we might actually see new drugs coming in the pipeline, which is far from the case now.
The most important thing I'd like to see change at the FDA is going to happen without our needing to submit petitions: restoring science as a criteria for drug approval. The Bush FDA was notorious for the way that decisions were made based on financial connections of FDA staff to drug makers and their religious beliefs. But beyond that I think the following are most important:
1. End "direct to consumer" drug advertisements. These are well-known to be full of lies, but it takes so many months until an ad is shut down for false claims that these lies cando their work.
2. Make drug testing compare a new drug with the safe, cheap existing drugs. If there is no significant benefit compared to safe, cheap drugs, do not approve the drug. Right now, most drugs are only compared to placebo. So a new drug that is no more effective than a safe, cheap proven drug but costs 20 times more per pill gets approved with huge fanfare and becomes the subject of a billion dollar advertising campaign that gets doctors switching patients to it from the safe cheap drug.
3. Do not let drug companies claim a drug "rejuvenates beta cells" until this has been proven by direct measurement in humans. Every single such claim for a drug in the past, which included the major claim used to market Avandia, has been based on surrogates like HOMA measurements which turn out to be a false guide or on findings in rodents which did not extend to humans.
After a decade we finally saw research that showed conclusive evidence that Avandia did NOT rejuvenate beta cells. But for a decade doctors prescribed it on that premise.
Currently Januvia and Byetta are being sold with the same claim, based only on test tube and rodent studies. This motivates doctors to keep people on these drugs EVEN when their blood sugars are deteriorating and they are experiencing severe side effects. The long term deterioration in blood sugars experienced by people who are taking Byetta long-term suggests that just like Avandia, it does not rejuvenate beta cells. But doctors continue to tell patients it does.
4. When a new designer drug is targeting a gene or specific receptor, the approval process MUST included investigation of the other uses of that gene or receptor and the impact of the drug on those other functions must be explored.
The dangerous side effects of ALL drugs from sulfonylureas to Avandia to Januvia turned out to be caused by the OTHER functions of the genes or receptors they target. There is currently NO requirement in the testing process that the drug company do this. The technology for exploring gene expression has advanced greatly and the cost of this kind of research has dropped dramatically. It is now very possible to see which genes are expressing in response to different stimuli. It is possible to see which receptors are accepting a drug.
We can no longer approve 21st century drugs only with techniques developed in the first half of the 20th century.
People who have not been prescribed the drugs given to people with Type 2 diabetes can have little idea how dreadful the many side effects of Type 2 drugs really are.
But many patients trust their doctors completely, and if the doctor gives them a drug, no matter how awful it makes them feel, they take it, especially if they have been told, as many have, that the drug is "regrowing their beta cells."
Their reward for this may be enormous weight gain, osteoporosis, and even blindness (Actos and Avandia), heart attack (Avandia, Glipizide), pancreatitis (Byetta), irreversible inflammation syndromes or cancer (Januvia.)
I get heartbreaking emails from people who have suffered these permanent side effects. They are very real. I myself live every day with a miserable permanent side effect of a prescription drug. So I would far rather that a drug not be approved, than that it be "fast-tracked", sold to hundreds of thousands of people, and worsen their lives. Especially when there are already other drugs that work just as well.
To the argument that making drug approval harder will stifle drug development, I say only, look at the profits on a single successful drug. As long as a company can earn $200 a month from a vial of 30 pills or 60 units of an injectable drug, drug development will continue.
As it is, the drug companies are not doing new research. They are putting most of their efforts into making tiny changes to existing drugs to keep them under patent or into developing copycat versions of drugs sold by other companies. If the incentive to copy other drugs were lost, we might actually see new drugs coming in the pipeline, which is far from the case now.
December 17, 2008
More Bad Science: The "Low Glycemic" Diet in the JAMA Study is the ADA Low Fat Diet
The media are abuzz with the results of a diet study published in JAMA which supposedly "proves" that the Low Glycemic diet has benefits for people with diabetes.
It doesn't, but to see why, you have to download the entire, free, PDF, which includes the damning details that make it clear that the diet used in this study was not by any but the most twisted logic a "low glycemic diet."
To see these details and read what the participants ate in this diet study, click on the link below and then click on the PDF link to the right.
Effect of a Low–Glycemic Index or a High–Cereal Fiber Diet on Type 2 Diabetes: A Randomized Trial JAMA. 2008;300(23):2742-2753.
Despite the media spin, what this study actually did was attempt to answer a stupid question: Is a high carb diet/low fat made up predominantly of pasta, beans, carrots, pears, oranges and skim milk better for people with diabetes than a high carb/low fat diet made up of Wheetabix, potatoes, mangoes, skim milk and toast.
The answer turns out to be "yes," very slightly. This is one step away from asking if a diet made up of pasta and fruit is better than one made of hot fudge sundaes and soda. It is, but neither is a diet you would feed to someone with diabetes if you cared about their long term health.
Neither diet in the JAMA study lowered the blood sugar of the study subjects to the range that avoids complications. The average fasting glucose in the group eating the supposedly "low glycemic" diet ended up well over 130 mg/dl, and this was in a group of people taking Avandia, Actos, Metformin and sulfonylurea drugs.
With fasting blood sugars that high, the post-meal blood sugars of those eating either diet had to be spiking well over the 140 mg/dl level at which complications begin to occur and spending lots of time over the 200 mg/dl level where they become dangerous.
That the high carb/low fat diet raises blood sugars is not news. Nor is it news that it makes very little improvement in lipids compared to a lower carbohydrate diet. But what had me really scratching my head after reading this study was the definition of "low glycemic" used to craft the supposedly "low glycemic" diet used in this study. Because that diet was filled with stuff like skim milk, Carrot coins, Oranges, and tomato sauce, which even the most dedicated follower of the Glycemic Index would find baffling.
After all, doctors suggest people use orange juice to treat hypos because orange juice is one of the fastest carbs available and though oranges have fiber, any time I eat one, I see it hit my bloodstream within an hour and when it does, all 20 grams of carbohydrate make themselves known.
More "low glycemic" diet foods fed people on the low glycemic diet here were "low fat yogurt" and pears. Also jam. Also Balsamic vinaigrette salad dressing. I have eaten all these foods and tested afterwards I can tell you they will all hit my blood sugar with full force within one hour after eating.
Add to these super fast carbs the slower to digest but very high carb foods that fill out the diet, the rye pita, lentils and the full cup of spaghetti, and you have a diet that should keep blood sugars elevated for all day long without a break. No wonder that fasting blood sugars were well over 130 mg/dl despite a full load of meds. You can only imagine what blood sugars would have looked like without meds, too!
This is just plain nuts, people. This isn't a low glycemic index diet. This is the classic ADA low fat diet hiding behind a new name.
But it isn't 1998 anymore and the health claims for the low fat diet have been completely discredited. We now have a lot of high quality research showing that low carbohydrate diets with adequate protein and lots of healthy fat lower blood sugars much better than this tired old, hunger-provoking, misery inducing ADA low fat diet.
In fact, as little as I like the so-called "glycemic index" which is based on non-reproducible averages of measurements of the blood sugar of normal people and has little applicability to anyone with Diabetes who has lost part of their second phase insulin release, I have to admit that even a true low glycemic diet--the so-called Mediterranean diet, which is a medium fat/slow carb diet, will do a much better job than this one does.
The fact is, this really is not a low glycemic diet, it is low glycemic only if you you compare it with a fudge sundae and soda diet which may well have been what the subjects in the study were eating before they were recruited. It is also a high fructose diet, which is bad news for anyone who believes that step one in dealing with Type 2 diabetes is to reduce insulin resistance.
Fructose was believed to be good for people with diabetes a decade ago and the ADA was slow to stop recommending fructose to people with diabetes. But now we know that eating fructose contributes to fatty liver and increases insulin resistance.
You can read a brand new discussion of new research which looks at how eating fructose changes the way that genes in the liver express in this week's edition of the Diabetes in Control newsletter.
To those who say, but what about the findings that the diet the study promoted lowered cholesterol and A1c, there is only one answer: go look at the actual data. The changes in cholesterol were "significant" only in the statistical meaning of the word. The actual change in the lipid measurements was small and triglyceride level, which are more closely linked to heart risk than LDL did not change significantly.
The changes in body weight and A1c compared to baseline are slightly better, but are probably due to the diet being used here being one that severely restricted food choices, urged people to lower calories, and told people not to eat any of the junk food that adds calories to the Standard Diet. A lower calorie very high carbohydrate diet will have less carbs than a high calorie very high carbohydrate diet and that will reduce A1c, though in this case, not enough to provide lasting health benefits.
Pit this diet against a low carb diet of any kind and you'll see how pitiful this diet really was. For that matter, pit it against a truly "low glycemic" diet--one that also has a low glycemic load and you will similarly see the limitations of this antique, failed ADA low fat diet exposed.
You don't have to take my word for it. These studies have already been done. You can find them listed here:
Studies Proving the Safety and Efficacy of the Low Carb Diet
But you don't need to read studies to find out what is a safe and effective diet for your own, unique body. Get out your blood sugar meter and test after eating. If the foods you eat keep your blood sugar under 140 mg/dl, they're good for you. If they raise your blood sugar higher than that, they aren't. And if you really want to be healthy, shoot for a lower post meal blood sugar target. Many people stay under 120 mg/dl, which appears to be the true upper end of the normal range for post meal blood sugars. Some go even lower.
And write a letter to the publishers of JAMA asking why they gave valuable page space to a study that is so obviously flawed.
It doesn't, but to see why, you have to download the entire, free, PDF, which includes the damning details that make it clear that the diet used in this study was not by any but the most twisted logic a "low glycemic diet."
To see these details and read what the participants ate in this diet study, click on the link below and then click on the PDF link to the right.
Effect of a Low–Glycemic Index or a High–Cereal Fiber Diet on Type 2 Diabetes: A Randomized Trial JAMA. 2008;300(23):2742-2753.
Despite the media spin, what this study actually did was attempt to answer a stupid question: Is a high carb diet/low fat made up predominantly of pasta, beans, carrots, pears, oranges and skim milk better for people with diabetes than a high carb/low fat diet made up of Wheetabix, potatoes, mangoes, skim milk and toast.
The answer turns out to be "yes," very slightly. This is one step away from asking if a diet made up of pasta and fruit is better than one made of hot fudge sundaes and soda. It is, but neither is a diet you would feed to someone with diabetes if you cared about their long term health.
Neither diet in the JAMA study lowered the blood sugar of the study subjects to the range that avoids complications. The average fasting glucose in the group eating the supposedly "low glycemic" diet ended up well over 130 mg/dl, and this was in a group of people taking Avandia, Actos, Metformin and sulfonylurea drugs.
With fasting blood sugars that high, the post-meal blood sugars of those eating either diet had to be spiking well over the 140 mg/dl level at which complications begin to occur and spending lots of time over the 200 mg/dl level where they become dangerous.
That the high carb/low fat diet raises blood sugars is not news. Nor is it news that it makes very little improvement in lipids compared to a lower carbohydrate diet. But what had me really scratching my head after reading this study was the definition of "low glycemic" used to craft the supposedly "low glycemic" diet used in this study. Because that diet was filled with stuff like skim milk, Carrot coins, Oranges, and tomato sauce, which even the most dedicated follower of the Glycemic Index would find baffling.
After all, doctors suggest people use orange juice to treat hypos because orange juice is one of the fastest carbs available and though oranges have fiber, any time I eat one, I see it hit my bloodstream within an hour and when it does, all 20 grams of carbohydrate make themselves known.
More "low glycemic" diet foods fed people on the low glycemic diet here were "low fat yogurt" and pears. Also jam. Also Balsamic vinaigrette salad dressing. I have eaten all these foods and tested afterwards I can tell you they will all hit my blood sugar with full force within one hour after eating.
Add to these super fast carbs the slower to digest but very high carb foods that fill out the diet, the rye pita, lentils and the full cup of spaghetti, and you have a diet that should keep blood sugars elevated for all day long without a break. No wonder that fasting blood sugars were well over 130 mg/dl despite a full load of meds. You can only imagine what blood sugars would have looked like without meds, too!
This is just plain nuts, people. This isn't a low glycemic index diet. This is the classic ADA low fat diet hiding behind a new name.
But it isn't 1998 anymore and the health claims for the low fat diet have been completely discredited. We now have a lot of high quality research showing that low carbohydrate diets with adequate protein and lots of healthy fat lower blood sugars much better than this tired old, hunger-provoking, misery inducing ADA low fat diet.
In fact, as little as I like the so-called "glycemic index" which is based on non-reproducible averages of measurements of the blood sugar of normal people and has little applicability to anyone with Diabetes who has lost part of their second phase insulin release, I have to admit that even a true low glycemic diet--the so-called Mediterranean diet, which is a medium fat/slow carb diet, will do a much better job than this one does.
The fact is, this really is not a low glycemic diet, it is low glycemic only if you you compare it with a fudge sundae and soda diet which may well have been what the subjects in the study were eating before they were recruited. It is also a high fructose diet, which is bad news for anyone who believes that step one in dealing with Type 2 diabetes is to reduce insulin resistance.
Fructose was believed to be good for people with diabetes a decade ago and the ADA was slow to stop recommending fructose to people with diabetes. But now we know that eating fructose contributes to fatty liver and increases insulin resistance.
You can read a brand new discussion of new research which looks at how eating fructose changes the way that genes in the liver express in this week's edition of the Diabetes in Control newsletter.
To those who say, but what about the findings that the diet the study promoted lowered cholesterol and A1c, there is only one answer: go look at the actual data. The changes in cholesterol were "significant" only in the statistical meaning of the word. The actual change in the lipid measurements was small and triglyceride level, which are more closely linked to heart risk than LDL did not change significantly.
The changes in body weight and A1c compared to baseline are slightly better, but are probably due to the diet being used here being one that severely restricted food choices, urged people to lower calories, and told people not to eat any of the junk food that adds calories to the Standard Diet. A lower calorie very high carbohydrate diet will have less carbs than a high calorie very high carbohydrate diet and that will reduce A1c, though in this case, not enough to provide lasting health benefits.
Pit this diet against a low carb diet of any kind and you'll see how pitiful this diet really was. For that matter, pit it against a truly "low glycemic" diet--one that also has a low glycemic load and you will similarly see the limitations of this antique, failed ADA low fat diet exposed.
You don't have to take my word for it. These studies have already been done. You can find them listed here:
Studies Proving the Safety and Efficacy of the Low Carb Diet
But you don't need to read studies to find out what is a safe and effective diet for your own, unique body. Get out your blood sugar meter and test after eating. If the foods you eat keep your blood sugar under 140 mg/dl, they're good for you. If they raise your blood sugar higher than that, they aren't. And if you really want to be healthy, shoot for a lower post meal blood sugar target. Many people stay under 120 mg/dl, which appears to be the true upper end of the normal range for post meal blood sugars. Some go even lower.
And write a letter to the publishers of JAMA asking why they gave valuable page space to a study that is so obviously flawed.
Diabetic Nerve Pain and What You Can Do About It
One of the saddest statistics about diabetes is that, at the time of their diagnosis, fully 48% of those newly diagnosed with diabetes already have signs of diabetic nerve damage.
You can see this documented in this table where "impaired foot sensitivity" is a diagnostic sign of neuropathy:
Prevalence of microvascular complications at the time of diagnosis in diabetic patients identified by screening and in general practice
which is taken from this study:
Microvascular Complications at Time of Diagnosis of Type 2 Diabetes Are Similar Among Diabetic Patients Detected by Targeted Screening and Patients Newly Diagnosed in General Practice: The Hoorn Screening Study
It is known from studies of people with Type 1 diabetes that it takes a decade of exposure to elevated blood sugars to produce neuropathy. But high blood sugars creep up on people with Type 2 diabetes, and it turns out that even blood sugars in the "prediabetic" range can cause it.
You can read more about the research that documents the relationship of high post-meal blood sugars to neuropathy HERE.
Doctors miss the early diagnosis of Type 2 diabetes in these people because they rely on the fasting glucose test, or perhaps the A1c test, to screen for diabetes.
Unfortunately, neurologists who have researched the topic have found that the incidence of neuropathy correlates entirely to rising post-meal blood sugars, not fasting glucose or A1c. As soon as post-meal blood sugars (or GTT blood sugars) go over 140 mg/dl (7.7 mmol/L) the incidence of neuropathy starts to rise. It starts with small nerve fibers and with extended exposure to high blood sugars, extends to the thicker fibers.
But even after they diagnose people with Type 2 diabetes, the treatment that doctors give their patients ensures that even those who did not have neuropathy at diagnosis will develop it over time, because most doctors who are not specialists follow the treatment guidelines provided by the American Diabetes Association (ADA). These guidelines focus entirely mainly on lowering A1c using oral drugs and when they mention post-meal blood sugars at all--which is not often, they recommend post meal blood sugar levels that are way over the blood sugar level where science has found neuropathy begins.
Symptoms of Neuropathy
Neuropathy starts out with pain and tingling in your feet. It usually is present in both feet, which can help you distinguish it from similar foot pain that can be caused by compressed nerves due to bad vertebral discs or piriformis syndrome which is likely to be present on only one side of your body.
The damage to your nerves is being caused by glucose blocking up the tiny capillaries that feed your nerves so that they do not receive the nourishment they need and start to die. Though you feel the pain in your sensory nerves, neuropathy also affects your autonomic nervous system--the nerves that control involuntary functions like heart beat and sexual response. It also turns out that the autonomic nervous system, through the vagus nerve, controls your immune system. So when your nerves are dying your immune system may not get the message that invaders have attacked your feet, which is part of what leads to the devastating infections that lead to diabetic amputations.
Treatment for Neuropathy
If you go to your doctor complaining about tingling or numbness in your feet, you are likely to be given a prescription for an expensive drug like Lyrica or Topomax. These drugs do not have any effect on the progress of your neuropathy. Instead, what they do is disrupt the pain signals being sent to your brain so that you don't feel them. They have also been linked to suicidal thinking and actions and the FDA just today published new guidelines warning of this devastating side effect in people taking these drugs.
But while you take these drugs, even though you might feel better, the nerve damage continues. Eventually your nerve pain goes away to be replaced by numbness, which is easier to live with but much worse for your health. Once your feet are numb, infection can easily take root and since your immune system is weakened, it can lead to tissue death requiring amputation.
This is very scary especially for those of you who have seen relatives lose their limbs. But the good news is that you can reverse neuropathy by lowering your post meal blood sugars.
Doctors may not tell you this because after years of urging their patients to shoot for the dangerously high ADA blood sugar targets, they have observed most of their patients develop neuropathy. This convinces them that "tight control" (as defined by the ADA) cannot prevent neuropathy. Since they assume that all people with diabetes will eventually develop it, they give you your pain pills and shoo you out of the office.
Effective Treatment for Neuropathy
Everything changes when you define "tight control" to mean "Maintaining post-meal blood sugars below the level where neuropathy begins." That level turns out to be 140 mg/dl (7.7 mmol/L). Lower your blood sugar to this level, meal after meal, and your nerves sill start to heal.
This is a good 40 mg/dl lower than the dangerously high 180 mg/dl two hours after eating which the ADA officially defines as "tight control." And when you bring your blood sugars down below 140 mg/dl and keep them there for a few months, your feet will get better.
In fact, people who have done this have reported on web discussion groups that once they get into truly good control, they can tell when their blood sugar has gone over 140 mg/dl because their feet begin to hurt. If they bring it back down, the pain stops.
If you have been living with much higher blood sugars for a while and have neuropathy that has progressed to numbness, there is one bump in the road you should be aware of. If your nerves are so damaged that they have become numb, when you start to heal them, they may hurt.
Regenerating nerves always hurt, itch or tingle. This is true whether they are regenerating from glucose poisoning or mechanical damage. If your feet start to hurt after you have lowered your blood sugar, remind yourself that this is good not bad.
It is a sign that your nerves are healing and that, even more importantly, your immune system is learning that you have feet again and will get back on the job of fighting off invaders.
If you think it is impossible to get your post-meal blood sugar down below 140 mg/dl after eating, be assured it is not. Thousands of people with diabetes--both Type 2 and Type 1--who are active on online discussion groups are doing it.
The secret is to follow a strategy like the one described here:
How to Get Your Blood Sugar Under Control
If you are taking insulin or a sulfonylurea drug like Amaryl that can cause hypos, you will have to work slowly and carefully cut back on your doses of medication as your blood sugars come down to avoid hypos. Talk to your doctor or diabetic educator about how to do this if you don't already know how.
No matter how bad your blood sugars might be now, there is some combination of dietary change, oral medication, or insulin, properly prescribed, that will bring your post-meal blood sugars down to the safe zone.
If your doctor or educator is not supportive of your desire to achieve truly safe blood sugars targets, and does not respond with enthusiasm to your desire to lower your post meal blood sugars to the safe range, find a new one who is better trained and more up-to-date, who will.
The take-away lesson here is this: It is post meal blood sugars that cause neuropathy. People can get identical A1cs with very different post meal blood sugars which is probably why the research finds there is no clear correlation between A1c and the presence of neuropathy, especially when A1c is below 8%.
Your fasting blood sugar, which is the only blood sugar many out-of-date doctors monitor, is also worthless in evaluating your neuropathy risk, because it is possible to have extremely high post meal blood sugars and completely normal fasting blood sugars. I did that myself years ago when I had fasting blood sugars of 98 mg/dl and post meal blood sugars at every meal over 250 mg/dl.
This 140 mg/dl post meal blood sugar target is very mainstream--the American Association of Clinical Endocrinologists has been recommending it for five years now and I have heard rumors that some of that organization's members would like to see it lowered even further.
I personally try to keep my blood sugar under 120 mg/dl at all times, though that is not always possible. But even with eating quite a few meals that missed that target, I have been able to maintain my A1cs in a range between 5.5% and 5.8% over the past decade, and has been enough to keep me from developing any signs of diabetic neuropathy.
I do periodically experience neuropathy caused by compressed nerves in my spine, thanks to some ruptured vertebral discs. But as long as I keep my blood sugar in the safe range, I have found that over time those nerve injuries are able to heal up, too.
Do Supplements Help?
People often write to me asking about whether there are supplements that can help with neuropathy. As is the case with any painful, chronic condition, diabetes attracts flocks of vultures eager to prey on the desperation of sufferers. These vultures will gladly sell you herbs and potions at inflated prices with the promise they will heal you.
Save your money. There are very few supplements that appear to have any affect on neuropathic pain and the evidence for them is underwhelming. You can read what researchers have found about these supplements here:
Useful Supplements for People with Diabetes
But after years of reading the discussion boards, my impression is that very few people find these supplements worth the expense, while everyone who follows the advice about modifying their diet experiences improvement. So your best bet is to put the money you would have wasted on expensive herbs and supplements into buying the foods that lower your blood sugar. It's a much better investment.
You can see this documented in this table where "impaired foot sensitivity" is a diagnostic sign of neuropathy:
Prevalence of microvascular complications at the time of diagnosis in diabetic patients identified by screening and in general practice
which is taken from this study:
Microvascular Complications at Time of Diagnosis of Type 2 Diabetes Are Similar Among Diabetic Patients Detected by Targeted Screening and Patients Newly Diagnosed in General Practice: The Hoorn Screening Study
It is known from studies of people with Type 1 diabetes that it takes a decade of exposure to elevated blood sugars to produce neuropathy. But high blood sugars creep up on people with Type 2 diabetes, and it turns out that even blood sugars in the "prediabetic" range can cause it.
You can read more about the research that documents the relationship of high post-meal blood sugars to neuropathy HERE.
Doctors miss the early diagnosis of Type 2 diabetes in these people because they rely on the fasting glucose test, or perhaps the A1c test, to screen for diabetes.
Unfortunately, neurologists who have researched the topic have found that the incidence of neuropathy correlates entirely to rising post-meal blood sugars, not fasting glucose or A1c. As soon as post-meal blood sugars (or GTT blood sugars) go over 140 mg/dl (7.7 mmol/L) the incidence of neuropathy starts to rise. It starts with small nerve fibers and with extended exposure to high blood sugars, extends to the thicker fibers.
But even after they diagnose people with Type 2 diabetes, the treatment that doctors give their patients ensures that even those who did not have neuropathy at diagnosis will develop it over time, because most doctors who are not specialists follow the treatment guidelines provided by the American Diabetes Association (ADA). These guidelines focus entirely mainly on lowering A1c using oral drugs and when they mention post-meal blood sugars at all--which is not often, they recommend post meal blood sugar levels that are way over the blood sugar level where science has found neuropathy begins.
Symptoms of Neuropathy
Neuropathy starts out with pain and tingling in your feet. It usually is present in both feet, which can help you distinguish it from similar foot pain that can be caused by compressed nerves due to bad vertebral discs or piriformis syndrome which is likely to be present on only one side of your body.
The damage to your nerves is being caused by glucose blocking up the tiny capillaries that feed your nerves so that they do not receive the nourishment they need and start to die. Though you feel the pain in your sensory nerves, neuropathy also affects your autonomic nervous system--the nerves that control involuntary functions like heart beat and sexual response. It also turns out that the autonomic nervous system, through the vagus nerve, controls your immune system. So when your nerves are dying your immune system may not get the message that invaders have attacked your feet, which is part of what leads to the devastating infections that lead to diabetic amputations.
Treatment for Neuropathy
If you go to your doctor complaining about tingling or numbness in your feet, you are likely to be given a prescription for an expensive drug like Lyrica or Topomax. These drugs do not have any effect on the progress of your neuropathy. Instead, what they do is disrupt the pain signals being sent to your brain so that you don't feel them. They have also been linked to suicidal thinking and actions and the FDA just today published new guidelines warning of this devastating side effect in people taking these drugs.
But while you take these drugs, even though you might feel better, the nerve damage continues. Eventually your nerve pain goes away to be replaced by numbness, which is easier to live with but much worse for your health. Once your feet are numb, infection can easily take root and since your immune system is weakened, it can lead to tissue death requiring amputation.
This is very scary especially for those of you who have seen relatives lose their limbs. But the good news is that you can reverse neuropathy by lowering your post meal blood sugars.
Doctors may not tell you this because after years of urging their patients to shoot for the dangerously high ADA blood sugar targets, they have observed most of their patients develop neuropathy. This convinces them that "tight control" (as defined by the ADA) cannot prevent neuropathy. Since they assume that all people with diabetes will eventually develop it, they give you your pain pills and shoo you out of the office.
Effective Treatment for Neuropathy
Everything changes when you define "tight control" to mean "Maintaining post-meal blood sugars below the level where neuropathy begins." That level turns out to be 140 mg/dl (7.7 mmol/L). Lower your blood sugar to this level, meal after meal, and your nerves sill start to heal.
This is a good 40 mg/dl lower than the dangerously high 180 mg/dl two hours after eating which the ADA officially defines as "tight control." And when you bring your blood sugars down below 140 mg/dl and keep them there for a few months, your feet will get better.
In fact, people who have done this have reported on web discussion groups that once they get into truly good control, they can tell when their blood sugar has gone over 140 mg/dl because their feet begin to hurt. If they bring it back down, the pain stops.
If you have been living with much higher blood sugars for a while and have neuropathy that has progressed to numbness, there is one bump in the road you should be aware of. If your nerves are so damaged that they have become numb, when you start to heal them, they may hurt.
Regenerating nerves always hurt, itch or tingle. This is true whether they are regenerating from glucose poisoning or mechanical damage. If your feet start to hurt after you have lowered your blood sugar, remind yourself that this is good not bad.
It is a sign that your nerves are healing and that, even more importantly, your immune system is learning that you have feet again and will get back on the job of fighting off invaders.
If you think it is impossible to get your post-meal blood sugar down below 140 mg/dl after eating, be assured it is not. Thousands of people with diabetes--both Type 2 and Type 1--who are active on online discussion groups are doing it.
The secret is to follow a strategy like the one described here:
How to Get Your Blood Sugar Under Control
If you are taking insulin or a sulfonylurea drug like Amaryl that can cause hypos, you will have to work slowly and carefully cut back on your doses of medication as your blood sugars come down to avoid hypos. Talk to your doctor or diabetic educator about how to do this if you don't already know how.
No matter how bad your blood sugars might be now, there is some combination of dietary change, oral medication, or insulin, properly prescribed, that will bring your post-meal blood sugars down to the safe zone.
If your doctor or educator is not supportive of your desire to achieve truly safe blood sugars targets, and does not respond with enthusiasm to your desire to lower your post meal blood sugars to the safe range, find a new one who is better trained and more up-to-date, who will.
The take-away lesson here is this: It is post meal blood sugars that cause neuropathy. People can get identical A1cs with very different post meal blood sugars which is probably why the research finds there is no clear correlation between A1c and the presence of neuropathy, especially when A1c is below 8%.
Your fasting blood sugar, which is the only blood sugar many out-of-date doctors monitor, is also worthless in evaluating your neuropathy risk, because it is possible to have extremely high post meal blood sugars and completely normal fasting blood sugars. I did that myself years ago when I had fasting blood sugars of 98 mg/dl and post meal blood sugars at every meal over 250 mg/dl.
This 140 mg/dl post meal blood sugar target is very mainstream--the American Association of Clinical Endocrinologists has been recommending it for five years now and I have heard rumors that some of that organization's members would like to see it lowered even further.
I personally try to keep my blood sugar under 120 mg/dl at all times, though that is not always possible. But even with eating quite a few meals that missed that target, I have been able to maintain my A1cs in a range between 5.5% and 5.8% over the past decade, and has been enough to keep me from developing any signs of diabetic neuropathy.
I do periodically experience neuropathy caused by compressed nerves in my spine, thanks to some ruptured vertebral discs. But as long as I keep my blood sugar in the safe range, I have found that over time those nerve injuries are able to heal up, too.
Do Supplements Help?
People often write to me asking about whether there are supplements that can help with neuropathy. As is the case with any painful, chronic condition, diabetes attracts flocks of vultures eager to prey on the desperation of sufferers. These vultures will gladly sell you herbs and potions at inflated prices with the promise they will heal you.
Save your money. There are very few supplements that appear to have any affect on neuropathic pain and the evidence for them is underwhelming. You can read what researchers have found about these supplements here:
Useful Supplements for People with Diabetes
But after years of reading the discussion boards, my impression is that very few people find these supplements worth the expense, while everyone who follows the advice about modifying their diet experiences improvement. So your best bet is to put the money you would have wasted on expensive herbs and supplements into buying the foods that lower your blood sugar. It's a much better investment.
December 14, 2008
Tis the Season
It's cold. It's dark. There is food everywhere, and most of it is full of flour and sugar.
If you are sticking to your diabetes diet, whatever it might be, good for you. If you aren't, well join the crowd.
I've done it both ways. I spent a couple holiday seasons keeping my carbs where they needed to be to keep my blood sugar in a reasonable range. No stuffing. No potatoes. Lots of things made with Splenda and protein powder that looked like the foods they were supposed to replace but tasted like Splenda and protein powder.
But holiday food is a big deal in our family, and invariably after passing on all the traditional foods that had been part of my holidays for the past fifty-some years, I'd end up in tears. Not a happy holiday.
I've done it the other way, too: Declared that food has no carbs on Thanksgiving and Christmas and proceeded to eat accordingly. Back in the days when my doctor wouldn't give me a prescription for insulin, eating like that was a good way to remind myself why it was that I didn't eat carbs. My blood sugars would hover near 300, I'd end up feeling like poison was flowing through my veins and awake with a massive carb hangover and rampant hunger the next day as I fought to get back on track.
At this point you might be thinking? Well, what about moderation? Why not just eat a little bit of carbs? Well, if you can do it, hurrah for you. I can't do it on the big family food holidays.
Now that I use insulin, I can eat the traditional family foods if I use my insulin pen like a pump and inject more insulin every time I eat something with carbs in it. That flattens out the blood sugars very well, so my toes, eyes and kidneys thank me, but boy does it pack on the pounds. Insulin plus carbs and fat is the recipe for weight gain, and even though the blood sugars might be under control, once you start playing "my pen is a pump" it's tough to shut off the overindulgence.
When my blood sugar log isn't full of scary numbers, it's hard to stop eating crap not only on Thanksgiving and Christmas Day but on all the days in between. Since it takes me about a week to gain a pound and a month or more of fasting and repentance (a.k.a. weight loss dieting) to lose that same pound, this is not an ideal solution, either.
So when people ask me what the best way is to handle holiday eating, my answer is, "Beats me!"
But that's largely because I know that holiday eating is one of those areas where the individual differences in our personalities really come to the fore and where there is no "one size fits all" solution, even if we share the same blood sugar issues.
The best way to decide what holiday food approach would be best for you is to take an honest look at your history with food and what you have learned in the past about what it is that you can and cannot handle.
If you have shown in the past that you can take a day or two off of your diet and get back on track, that opens up some possibilities that should not be on the table if you have a history of months-long binges that have erased other months of very hard work.
The trick here is to face facts and not to tell yourself that this year it will be different. It won't. If you binged in the past, you will binge this time too. That is why it is so important to know your own limits.
I know I can diet in January, and in April or September if I have to. Just not in November and December. I knew in the past, before I had insulin, that I could eat a high carb meal and get back on track the next day even though I also knew I would be very hungry. That gave me some options that would not be there for a person who had problems with binging.
Beyond that, I have always had one hard and fast rule: If I go off plan I measure my blood sugar one hour and two hours later.
There is nothing like seeing alarming numbers on your meter to help you get back on track. . That is the main reason that testing is so helpful to anyone who has learned that there is a connection between the amount of carbohydrate they eat and their resulting blood sugar numbers.
And if seeing high numbers for more than a meal here and there doesn't get you back on track and you are spiking over 200 mg/dl meal over meal, it is time for some tough love. If you can't stop eating the high carb stuff that you can't handle, do a Google Search on the words "Diabetic foot."
Then click on the "images" link at the top of the page. What you see there should motivate you to get back in control. Because if you eat like every day is Christmas, what you see in those harrowing pictures is what you will end up with in your stocking.
CODA: If you are seeing numbers over 200 mg/dl meal after meal and it isn't because you are eating a succession of high carb meals, it is time to insist that your doctor help you find a safe drug regimen that will get you back into control--preferably one that uses fast acting insulin--or send you to a specialist who will help you. Most people with Type 2 diabetes caused primarily by insulin resistance can recover very good control by cutting out the carbs. If you are still seeing very high blood sugars after eating lower carb meals, the chances are you are insulin deficient.
If you are sticking to your diabetes diet, whatever it might be, good for you. If you aren't, well join the crowd.
I've done it both ways. I spent a couple holiday seasons keeping my carbs where they needed to be to keep my blood sugar in a reasonable range. No stuffing. No potatoes. Lots of things made with Splenda and protein powder that looked like the foods they were supposed to replace but tasted like Splenda and protein powder.
But holiday food is a big deal in our family, and invariably after passing on all the traditional foods that had been part of my holidays for the past fifty-some years, I'd end up in tears. Not a happy holiday.
I've done it the other way, too: Declared that food has no carbs on Thanksgiving and Christmas and proceeded to eat accordingly. Back in the days when my doctor wouldn't give me a prescription for insulin, eating like that was a good way to remind myself why it was that I didn't eat carbs. My blood sugars would hover near 300, I'd end up feeling like poison was flowing through my veins and awake with a massive carb hangover and rampant hunger the next day as I fought to get back on track.
At this point you might be thinking? Well, what about moderation? Why not just eat a little bit of carbs? Well, if you can do it, hurrah for you. I can't do it on the big family food holidays.
Now that I use insulin, I can eat the traditional family foods if I use my insulin pen like a pump and inject more insulin every time I eat something with carbs in it. That flattens out the blood sugars very well, so my toes, eyes and kidneys thank me, but boy does it pack on the pounds. Insulin plus carbs and fat is the recipe for weight gain, and even though the blood sugars might be under control, once you start playing "my pen is a pump" it's tough to shut off the overindulgence.
When my blood sugar log isn't full of scary numbers, it's hard to stop eating crap not only on Thanksgiving and Christmas Day but on all the days in between. Since it takes me about a week to gain a pound and a month or more of fasting and repentance (a.k.a. weight loss dieting) to lose that same pound, this is not an ideal solution, either.
So when people ask me what the best way is to handle holiday eating, my answer is, "Beats me!"
But that's largely because I know that holiday eating is one of those areas where the individual differences in our personalities really come to the fore and where there is no "one size fits all" solution, even if we share the same blood sugar issues.
The best way to decide what holiday food approach would be best for you is to take an honest look at your history with food and what you have learned in the past about what it is that you can and cannot handle.
If you have shown in the past that you can take a day or two off of your diet and get back on track, that opens up some possibilities that should not be on the table if you have a history of months-long binges that have erased other months of very hard work.
The trick here is to face facts and not to tell yourself that this year it will be different. It won't. If you binged in the past, you will binge this time too. That is why it is so important to know your own limits.
I know I can diet in January, and in April or September if I have to. Just not in November and December. I knew in the past, before I had insulin, that I could eat a high carb meal and get back on track the next day even though I also knew I would be very hungry. That gave me some options that would not be there for a person who had problems with binging.
Beyond that, I have always had one hard and fast rule: If I go off plan I measure my blood sugar one hour and two hours later.
There is nothing like seeing alarming numbers on your meter to help you get back on track. . That is the main reason that testing is so helpful to anyone who has learned that there is a connection between the amount of carbohydrate they eat and their resulting blood sugar numbers.
And if seeing high numbers for more than a meal here and there doesn't get you back on track and you are spiking over 200 mg/dl meal over meal, it is time for some tough love. If you can't stop eating the high carb stuff that you can't handle, do a Google Search on the words "Diabetic foot."
Then click on the "images" link at the top of the page. What you see there should motivate you to get back in control. Because if you eat like every day is Christmas, what you see in those harrowing pictures is what you will end up with in your stocking.
CODA: If you are seeing numbers over 200 mg/dl meal after meal and it isn't because you are eating a succession of high carb meals, it is time to insist that your doctor help you find a safe drug regimen that will get you back into control--preferably one that uses fast acting insulin--or send you to a specialist who will help you. Most people with Type 2 diabetes caused primarily by insulin resistance can recover very good control by cutting out the carbs. If you are still seeing very high blood sugars after eating lower carb meals, the chances are you are insulin deficient.
December 9, 2008
Lots of Interesting New Studies This Week
I've just spent some time going through the medical journals, and there are quite a lot of new findings that should be of interest to people with diabetes.
I've integrated these new findings into the relevant pages on my Blood Sugar 101 web site, and also discussed them in the blog that tracks changes to the Blood Sugar 101 site. The widget below lets you easily see what's new. Just click on the entries that interest you:
I've integrated these new findings into the relevant pages on my Blood Sugar 101 web site, and also discussed them in the blog that tracks changes to the Blood Sugar 101 site. The widget below lets you easily see what's new. Just click on the entries that interest you:
December 8, 2008
More Research Shows Januvia and Glinides Inhibit Tumor Suppressor Gene DPP-4
UPDATE (April 2, 2013): Before you take Byetta, Victoza, Onglyza, or Januvia please read about the new research that shows that they, and probably all incretin drugs, cause severely abnormal cell growth in the pancreas and precancerous tumors. You'll find that information HERE.
Original post:
I spent some time this week scanning IHOP for the latest academic research about the impact of DPP-4 inhibition.
This IHOP has nothing to do with pancakes. It's a database that links to all research references related to specific genes.
Two new studies grabbed my attention and should be of great interest to anyone taking Januvia. These studies looked at the impact of inhibiting DPP-4 on the growth of two different kinds of cancers.
This is important because the way Januvia lowers blood sugar is by inhibiting DPP-4. It does this because DPP-4 is a protease (an enzyme that chops up protein chains) that, among other things, destroys a hormone, GLP-1, that helps control blood sugar levels. When you inhibit DPP-4, GLP-1 levels to rise and blood sugars drop.
But none of the drug industry-sponsored testing for the safety of Januvia looked at the other things that DPP-4 does. Fortunately, some academic researchers not-funded by drug makers are doing this and what they are finding should make any sane person stop taking Januvia.
Because it turns out that DPP-4 is also a tumor suppressor. And when you inhibit it, cells that have become cancerous get a "get out of jail free" card.
One study of prostate cancer cells studied in a culture medium concluded
Here's the abstract of that study:
CD26/dipeptidyl peptidase IV regulates prostate cancer metastasis by degrading SDF-1/CXCL12.
The other study involved melanoma cells and had this to say,
Here's the abstract of that article:
Dipeptidyl peptidase IV (DPPIV), a candidate tumor suppressor gene in melanomas is silenced by promoter methylation.
All this suggests, loud and clear, that if you want to raise GLP-1 levels it is much safer to use Byetta. Byetta is a synthetic, long-lasting form of GLP-1 which does not have any impact on your DPP-4 levels.
Another, older study points to another interesting conclusion. Metformin raises GLP-1 levels without inhibiting DPP-4.
Enhanced secretion of glucagon-like peptide 1 by biguanide compounds.
Even more interesting, another study that came up on the IHOP DPP-4 search suggests that another diabetes drug family also inhibits DPP-4. That family is the "glinide" family which includes Prandin and Starlix.
You can read the research that found this connection here:
Effects of antidiabetic drugs on dipeptidyl peptidase IV activity: nateglinide is an inhibitor of DPP IV and augments the antidiabetic activity of glucagon-like peptide-1.
Here Starlix was the drug the researchers found to have the strongest inhibitory effect on DPP-4. (Note, this statement has been corrected since this post was first made.)
But if you want to use a pill to inhibit DPP-4 there is one huge advantage to using Starlix or Prandin rather than Januvia. Is this: they have a much shorter half life in the body. The half-life of Prandin is 1 hour. The half life of Starlix is 1.5 hours. That means that if you take these drugs at meal time, they do their job and go home. So while they inhibit DPP-4, they do so for only a short period, after which the DPP-4 gene can express and produce DPP-4 again.
In contrast, the half life of Januvia is 12.5 hours and the Januvia prescribing information states, "In patients with type 2 diabetes, administration of JANUVIA led to inhibition of DPP-4 enzyme activity for a 24-hour period." Since Januvia is taken daily, this means that it inhibits DPP-4 all the time.
Ask yourself this: Do you want to permanently inhibit the activity of a tumor suppressor gene?
I don't think so. Particularly not when you realize that all the studies attesting to the safety of Januvia did not examine its impact on tumor growth. You can read more about how the safety studies avoided this issue in this old blog post:
More Evidence Connects Januvia to Cancer,
UPDATE Later the same day:
In response to an email in which I asked for more clarification about the implications of the research cited above for people taking Januvia, the researcher who authored one of these studies wrote the following:
Original post:
I spent some time this week scanning IHOP for the latest academic research about the impact of DPP-4 inhibition.
This IHOP has nothing to do with pancakes. It's a database that links to all research references related to specific genes.
Two new studies grabbed my attention and should be of great interest to anyone taking Januvia. These studies looked at the impact of inhibiting DPP-4 on the growth of two different kinds of cancers.
This is important because the way Januvia lowers blood sugar is by inhibiting DPP-4. It does this because DPP-4 is a protease (an enzyme that chops up protein chains) that, among other things, destroys a hormone, GLP-1, that helps control blood sugar levels. When you inhibit DPP-4, GLP-1 levels to rise and blood sugars drop.
But none of the drug industry-sponsored testing for the safety of Januvia looked at the other things that DPP-4 does. Fortunately, some academic researchers not-funded by drug makers are doing this and what they are finding should make any sane person stop taking Januvia.
Because it turns out that DPP-4 is also a tumor suppressor. And when you inhibit it, cells that have become cancerous get a "get out of jail free" card.
One study of prostate cancer cells studied in a culture medium concluded
By inhibiting CD26/DPPIV, invasion and metastasis of PCa cell lines [prostate cancer] were enhanced in in vitro and in vivo metastasis assays. Together, these data suggest that the degradation of CXCL12 by CD26/DPPIV may be involved in the metastatic cascades of PCa, and suggests that inhibition of CD26/DPPIV may be a trigger of PCa metastasis. [emphasis mine].This is serious stuff. What it is saying is that if you have a prostate cell that had become cancerous and then inhibit DPP-4 that will be able to invade tissue and really take off.
Here's the abstract of that study:
CD26/dipeptidyl peptidase IV regulates prostate cancer metastasis by degrading SDF-1/CXCL12.
The other study involved melanoma cells and had this to say,
Previously we have demonstrated that DPPIV abrogates growth factor independence and functions as a tumor suppressor gene in melanomas ... Further more, 5-AZA-Cdr induced increases in DPPIV levels correlated with growth inhibition and apoptosis in melanoma cells. All together these findings suggest that frequent downregulation of DPPIV expression in melanoma can be attributed, in large part, to aberrant promoter hypermethylation and this loss of DPPIV may be a critical event contributing to melanoma development. [emphasis mine]What this is saying is that if you increase DPP-4 levels, melanoma cells experience apoptosis, a fancy word for cell suicide. If you inhibit DPP-4, these cancerous cells will continue to grow.
Here's the abstract of that article:
Dipeptidyl peptidase IV (DPPIV), a candidate tumor suppressor gene in melanomas is silenced by promoter methylation.
All this suggests, loud and clear, that if you want to raise GLP-1 levels it is much safer to use Byetta. Byetta is a synthetic, long-lasting form of GLP-1 which does not have any impact on your DPP-4 levels.
Another, older study points to another interesting conclusion. Metformin raises GLP-1 levels without inhibiting DPP-4.
Enhanced secretion of glucagon-like peptide 1 by biguanide compounds.
Even more interesting, another study that came up on the IHOP DPP-4 search suggests that another diabetes drug family also inhibits DPP-4. That family is the "glinide" family which includes Prandin and Starlix.
You can read the research that found this connection here:
Effects of antidiabetic drugs on dipeptidyl peptidase IV activity: nateglinide is an inhibitor of DPP IV and augments the antidiabetic activity of glucagon-like peptide-1.
Here Starlix was the drug the researchers found to have the strongest inhibitory effect on DPP-4. (Note, this statement has been corrected since this post was first made.)
But if you want to use a pill to inhibit DPP-4 there is one huge advantage to using Starlix or Prandin rather than Januvia. Is this: they have a much shorter half life in the body. The half-life of Prandin is 1 hour. The half life of Starlix is 1.5 hours. That means that if you take these drugs at meal time, they do their job and go home. So while they inhibit DPP-4, they do so for only a short period, after which the DPP-4 gene can express and produce DPP-4 again.
In contrast, the half life of Januvia is 12.5 hours and the Januvia prescribing information states, "In patients with type 2 diabetes, administration of JANUVIA led to inhibition of DPP-4 enzyme activity for a 24-hour period." Since Januvia is taken daily, this means that it inhibits DPP-4 all the time.
Ask yourself this: Do you want to permanently inhibit the activity of a tumor suppressor gene?
I don't think so. Particularly not when you realize that all the studies attesting to the safety of Januvia did not examine its impact on tumor growth. You can read more about how the safety studies avoided this issue in this old blog post:
More Evidence Connects Januvia to Cancer,
UPDATE Later the same day:
In response to an email in which I asked for more clarification about the implications of the research cited above for people taking Januvia, the researcher who authored one of these studies wrote the following:
I agree that use of DPPIV inhibitors to treat diabetes patients needs further studies. Inhibiting DPPIV function in general(according to ours and others research) may not be a great idea. I believe that decrease or loss of DPPIV may be associated with cancer initiation or progression.Januvia is Merck's most profitable drug. You can be sure that they have not and do not plan to do any studies that could kill this particular golden goose. Even if failure to do this research might kill YOU.
We have shown that loss of DPPIV is indeed associated with melanoma, prostate and lung cancers. Importantly our work has shown that restoring DPPIV can suppress the tumor growth. I have not conducted any detailed studies with DPPIV inhibitors including Januvia, in particular. DPPIV has multiple functions. It is not known if Januvia blocks all of its functions. This warrants more studies with this drug.
December 6, 2008
New Info on How to Use Byetta for MODY!
UPDATE (April 2, 2013): Before you take Byetta, Victoza, Onglyza, or Januvia please read about the new research that shows that they, and probably all incretin drugs, cause severely abnormal cell growth in the pancreas and precancerous tumors. You'll find that information HERE.
Original Post:
Since I did so extremely well on Januvia, but had to stop taking it because of its ability to promote Melanoma by inhibiting an enzyme used to fight metatastic cells, I had hoped I could switch to Byetta. The kind of MODY I have is one that responds extremely well to beta cell stimulation by sulfs, to the point where a sulf is overwhelming even at tiny doses.
Unfortunately, when I tried Byetta two years ago, it was also overwhelming--causing me to hypo and go into a strange and unnerving mental state. The dose on the pen is set so I couldn't cut it back. I figure that since the main market for Byetta is very large, very insulin resistant Type 2s, the "small" dose was probably similar to the the Type 2 "starter dose" of insulin that is large enough to nearly kill insulin-sensitive me.
But recently I heard from a correspondent with MODY-3 who was using Byetta successfully. The starter pen dose was effective for her, but also pretty overwhelming. Her doctor (who is someone quite well known in the endocrinology community) told her how to cut the dose down on Byetta and she passed that information on to me.
It turns out, the standard 5 mc dose of Byetta is 2 units in an insulin syringe. If you draw the Byetta out with a syringe you can use partial doses. 1 unit is 1/2 a dose.
My friend was doing very well with the 1 unit dose, so I asked my doc for a prescription to try this technique. She gave me a sample, and I used 1/2 of a unit yesterday before breakfast and dinner and got very good results. Not quite normal, but competitive with what I have been seeing with insulin lately, minus the ugly peaks.
Using a syringe to remove Byetta from the vial is something the company tells you not to do. It may contaminate the Byetta. So I am putting a pen needle on the pen, shooting the Byetta into an open syringe and then carefully pushing out 1 unit before injecting it, rather than drawing the Byetta directly out of the syringe and getting all that air in it. Byetta is VERY fragile and very expensive.
The reason I wanted to try this is that for this whole past month I have been having a tough time with my insulin and seeing a lot of high numbers. I think my insulin may have been damaged by a known problem I've been having with my fridge, but whatever the problem, my insurance makes my current insulin regimen very expensive and there is no way to replace the insulin until next month. Oddly, despite its obscene cost, my insurance will only charge me $30 for Byetta. So if it works, this will be good news for me.
The other reason I wanted to try Byetta is that since switching from R to analogs, I have been battling slow but steady weight gain. Not a lot, but at my age, a pound you gain is a pound you will carry around until you get a wasting disease. So even three pounds a year--especially if it is three pounds on the tummy--is not good news. Byetta definitely took away my appetite, though at the low dose I tried I did not experience nausea.
Byetta also has the benefit of causing C-peptide secretion which may protect nerves.
I'll be reporting periodically on how this latest experiment goes.
Original Post:
Since I did so extremely well on Januvia, but had to stop taking it because of its ability to promote Melanoma by inhibiting an enzyme used to fight metatastic cells, I had hoped I could switch to Byetta. The kind of MODY I have is one that responds extremely well to beta cell stimulation by sulfs, to the point where a sulf is overwhelming even at tiny doses.
Unfortunately, when I tried Byetta two years ago, it was also overwhelming--causing me to hypo and go into a strange and unnerving mental state. The dose on the pen is set so I couldn't cut it back. I figure that since the main market for Byetta is very large, very insulin resistant Type 2s, the "small" dose was probably similar to the the Type 2 "starter dose" of insulin that is large enough to nearly kill insulin-sensitive me.
But recently I heard from a correspondent with MODY-3 who was using Byetta successfully. The starter pen dose was effective for her, but also pretty overwhelming. Her doctor (who is someone quite well known in the endocrinology community) told her how to cut the dose down on Byetta and she passed that information on to me.
It turns out, the standard 5 mc dose of Byetta is 2 units in an insulin syringe. If you draw the Byetta out with a syringe you can use partial doses. 1 unit is 1/2 a dose.
My friend was doing very well with the 1 unit dose, so I asked my doc for a prescription to try this technique. She gave me a sample, and I used 1/2 of a unit yesterday before breakfast and dinner and got very good results. Not quite normal, but competitive with what I have been seeing with insulin lately, minus the ugly peaks.
Using a syringe to remove Byetta from the vial is something the company tells you not to do. It may contaminate the Byetta. So I am putting a pen needle on the pen, shooting the Byetta into an open syringe and then carefully pushing out 1 unit before injecting it, rather than drawing the Byetta directly out of the syringe and getting all that air in it. Byetta is VERY fragile and very expensive.
The reason I wanted to try this is that for this whole past month I have been having a tough time with my insulin and seeing a lot of high numbers. I think my insulin may have been damaged by a known problem I've been having with my fridge, but whatever the problem, my insurance makes my current insulin regimen very expensive and there is no way to replace the insulin until next month. Oddly, despite its obscene cost, my insurance will only charge me $30 for Byetta. So if it works, this will be good news for me.
The other reason I wanted to try Byetta is that since switching from R to analogs, I have been battling slow but steady weight gain. Not a lot, but at my age, a pound you gain is a pound you will carry around until you get a wasting disease. So even three pounds a year--especially if it is three pounds on the tummy--is not good news. Byetta definitely took away my appetite, though at the low dose I tried I did not experience nausea.
Byetta also has the benefit of causing C-peptide secretion which may protect nerves.
I'll be reporting periodically on how this latest experiment goes.
December 1, 2008
New Study Spins Actos' Health Risk While Ignoring Its True Dangers
The bad news about Avandia's association with heart attack has been good news for Takeda, the maker of Actos. Both drugs are thiazolidinediones (TZD). They help lower blood sugar by reducing insulin resistance. Until the ACCORD study results came out last year, Avandia was prescribed far more frequently than Actos. Now, with Avandia's reputation in tatters, Takeda has been pushing doctors to switch their Type 2 patients to Actos.
The latest effort in this direction was the publication of a new study that is being spun in the media as showing the Actos is far safer than Avandia.
Here's a link to the actual study: Comparison of Cardiovascular Outcomes in Elderly Patients With Diabetes Who Initiated Rosiglitazone vs Pioglitazone Therapy. Wolfgang C. Winkelmayer, MD, ScD; Soko Setoguchi, MD, DrPH; Raisa Levin, MS; Daniel H. Solomon, MD, MPH. Arch Intern Med. 2008;168(21):2368-2375.
The study's finding was this:
1. There was no control group of people taking no TZD drug. The finding that Actos causes less heart failure than Avandia sounds like good news until you learn that other studies have found that Actos causes a lot more heart failure than taking no drug at all. In fact, heart failure appears to be a side effect of this class of drugs.
This meta-study discovered the real risks:
Thiazolidinediones and Heart Failure: A Teleo-Analysis Sonal Singh, MD, Yoon K Loke, MBBS, MD and Curt D Furberg, MD, PhD. Diabetes Care, published online ahead of print May 29, 2007
As reported by Bloomberg.com are these:
So yes, maybe Actos causes less heart failure than Avandia but it still causes unnecessary heart failure in younger people when taken even at low doses. And it causes heart failure in younger people who did not have cardiac disease before they started taking it.
2. This Study Did Not Look For The Other Well-Known Severe Side Effects of Actos. Heart failure and heart attack are severe side effects, but they are not the only serious side effects associated with Actos and Avandia.
Actos causes macular edema, which leads to blindness. Macular edema is swelling in the retina. You can read about the relationship of Actos to this side effect here:
Medscape: Glitazone Use May Be Associated With Macular Edema in Diabetics
Actos also causes osteoporosis leading to fractures, especially in older women.
This is clearly stated in the Prescribing Information published by the drug's maker:
Neither macular edema or osteoporosis were investigated in this study. Had they been, it is likely that the finding would have been that Actos caused more of these disastrous side effects.
All These Side Effects and Actos Does Little for Blood Sugar and A Lot For Weight Gain
A study that compared Actos against diet and exercise found that the drug was not as effective as diet and exercise and that, in fact, what it did was add brand new fat cells to people's upper arms and butts.
Effects of Pioglitazone Versus Diet and Exercise on Metabolic Health and Fat Distribution in Upper Body Obesity Samyah Shadid, MD and Michael D. Jensen, MD (Mayo Clinic). Diabetes Care 26:3148-3152, 2003.
This is troubling, because once you add new fat cells, they do not go away even when you diet. It is even more troubling because the Mayo Clinic study cited above also found that The group of insulin resistant volunteers in this study who took no drug but cut 500 calories a day from their diet and exercised for 45 minutes achieved far better improvements in their fasting insulin levels, their fasting triglyceride levels, and their total cholesterol than did the Actos group, while losing weight from both their waists and their "lower fat depot," which is how scientists denote the part of your body that is covered by your undies.
Finally, it is worth noting that the main reason that doctors have been recommending Avandia and Actos for the past decade is because the drugmakers convinced them that these drugs could rejuvenate failing beta cells.
This turned out to be completely false. The follow-up to the DREAM study found that as soon as people who had been taking Avandia for more than 3 years stopped taking it, they became diabetic at the same rate as those did who had not taken the drug. This makes it clear that the drug had no impact on beta cells at all.
BOTTOM LINE: There is NO reason to take either Actos or Avandia. They are both dangerous drugs that make a very small difference in blood sugars at the cost of packing extra fat on you and exposing you to the possibility of developing catastrophic side effects that may shorten your life, make you go blind, or leave you with crumbling bones.
For detailed information about the problems with Actos including links to many peer reviewed studies, including those that proved it did not regrow beta cells as claimed by the manufacturer and that it damages the bones, please read this web page:
Actos and Avandia -- Dangerous Diabetes Drugs
The latest effort in this direction was the publication of a new study that is being spun in the media as showing the Actos is far safer than Avandia.
Here's a link to the actual study: Comparison of Cardiovascular Outcomes in Elderly Patients With Diabetes Who Initiated Rosiglitazone vs Pioglitazone Therapy. Wolfgang C. Winkelmayer, MD, ScD; Soko Setoguchi, MD, DrPH; Raisa Levin, MS; Daniel H. Solomon, MD, MPH. Arch Intern Med. 2008;168(21):2368-2375.
The study's finding was this:
After adjustment for a large number of patient characteristics, Cox regression models revealed 15% greater mortality among patients who initiated therapy with rosiglitazone [Avandia]compared with pioglitazone [Actos](95% confidence interval, 5%-26%). Use of rosiglitazone was also associated with a 13% greater risk of congestive heart failure (95% confidence interval, 1%-26%). No differences between the 2 drugs were found in their rates of myocardial infarction or stroke.This makes Actos sound pretty good, doesn't it. But only if you ignore the study design. Let's look more closely at why this is a misleading study.
1. There was no control group of people taking no TZD drug. The finding that Actos causes less heart failure than Avandia sounds like good news until you learn that other studies have found that Actos causes a lot more heart failure than taking no drug at all. In fact, heart failure appears to be a side effect of this class of drugs.
This meta-study discovered the real risks:
Thiazolidinediones and Heart Failure: A Teleo-Analysis Sonal Singh, MD, Yoon K Loke, MBBS, MD and Curt D Furberg, MD, PhD. Diabetes Care, published online ahead of print May 29, 2007
As reported by Bloomberg.com are these:
The analysis in the journal Diabetes Care projected that one in every 50 patients who takes Avandia or Actos over a 26-month period would be hospitalized for heart failure. The researchers found that one-fourth of cases occur in people younger than 60. Heart failure tends to affect older people.Note this comment from the study:
Heart failure can occur even at doses below those used for therapeutic benefit, and the relatively low daily doses of pioglitazone 15-mg or rosiglitazone 2 mg are already at the top end of the dose-effect curve for triggering off episodes of heart failure.
So yes, maybe Actos causes less heart failure than Avandia but it still causes unnecessary heart failure in younger people when taken even at low doses. And it causes heart failure in younger people who did not have cardiac disease before they started taking it.
2. This Study Did Not Look For The Other Well-Known Severe Side Effects of Actos. Heart failure and heart attack are severe side effects, but they are not the only serious side effects associated with Actos and Avandia.
Actos causes macular edema, which leads to blindness. Macular edema is swelling in the retina. You can read about the relationship of Actos to this side effect here:
Medscape: Glitazone Use May Be Associated With Macular Edema in Diabetics
Actos also causes osteoporosis leading to fractures, especially in older women.
This is clearly stated in the Prescribing Information published by the drug's maker:
Fractures: In a randomized trial (PROactive) in patients with type 2 diabetes (mean duration of diabetes 9.5 years),an increased incidence of bone fracture was noted in female patients taking pioglitazone. During a mean follow-up of 34.5 months, the incidence of bone fracture in females was 5.1% (44/870) for pioglitazone versus 2.5% (23/905) for placebo. This difference was noted after the first year of treatment and remained during the course of the study. The majority of fractures observed in female patients were nonvertebral fractures including lower limb and distal upper limb. No increase in fracture rates was observed in men treated with pioglitazone 1.7% (30/1735) versus placebo 2.1% (37/1728). The risk of fracture should be considered in the care of patients, especially female patients, treated with pioglitazone and attention should be given to assessing and maintaining bone health according to current standards of care.The reason for this appears to be that the way that the TZD drugs decrease insulin resistance is by transforming bone stem cells into new fat cells into which insulin pushes glucose. Over time, the bone is weakened because the cells that should have grown into new bone have turned into fat.
Neither macular edema or osteoporosis were investigated in this study. Had they been, it is likely that the finding would have been that Actos caused more of these disastrous side effects.
All These Side Effects and Actos Does Little for Blood Sugar and A Lot For Weight Gain
A study that compared Actos against diet and exercise found that the drug was not as effective as diet and exercise and that, in fact, what it did was add brand new fat cells to people's upper arms and butts.
Effects of Pioglitazone Versus Diet and Exercise on Metabolic Health and Fat Distribution in Upper Body Obesity Samyah Shadid, MD and Michael D. Jensen, MD (Mayo Clinic). Diabetes Care 26:3148-3152, 2003.
This is troubling, because once you add new fat cells, they do not go away even when you diet. It is even more troubling because the Mayo Clinic study cited above also found that The group of insulin resistant volunteers in this study who took no drug but cut 500 calories a day from their diet and exercised for 45 minutes achieved far better improvements in their fasting insulin levels, their fasting triglyceride levels, and their total cholesterol than did the Actos group, while losing weight from both their waists and their "lower fat depot," which is how scientists denote the part of your body that is covered by your undies.
Finally, it is worth noting that the main reason that doctors have been recommending Avandia and Actos for the past decade is because the drugmakers convinced them that these drugs could rejuvenate failing beta cells.
This turned out to be completely false. The follow-up to the DREAM study found that as soon as people who had been taking Avandia for more than 3 years stopped taking it, they became diabetic at the same rate as those did who had not taken the drug. This makes it clear that the drug had no impact on beta cells at all.
BOTTOM LINE: There is NO reason to take either Actos or Avandia. They are both dangerous drugs that make a very small difference in blood sugars at the cost of packing extra fat on you and exposing you to the possibility of developing catastrophic side effects that may shorten your life, make you go blind, or leave you with crumbling bones.
For detailed information about the problems with Actos including links to many peer reviewed studies, including those that proved it did not regrow beta cells as claimed by the manufacturer and that it damages the bones, please read this web page:
Actos and Avandia -- Dangerous Diabetes Drugs
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